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Archive for the ‘Medical’ Category

Kidney MCQs

Posted by Dr KAMAL DEEP on May 26, 2011

1.Glomerulosclerosis is a feature of –
a) Diabetes mellitus
b) Hypertension
c) Acute glomerular
d) Nephrotic syndrome
Ans is A
CAUSES OF NEPHROTIC SYNDROME in order of frequency-
Primary Glomerular Disease-Membranous glomerulonephritis,Lipoid nephrosis,Focal segmental glomerulosclerosis,Membranoproliferative glomerulonephritis,Other proliferative glomerulonephritis (focal, “pure mesangial,” IgA nephropathy)
Systemic Diseases–Diabetes mellitus,Amyloidosis,Systemic lupus erythematosus,Drugs (gold, penicillamine, “street heroin”),Infections (malaria, syphilis, hepatitis B, acquired immunodeficiency syndrome)
Malignant disease (carcinoma, melanoma),Miscellaneous (bee-sting allergy, hereditary nephritis)
*Approximate prevalence of primary disease = 95% in children, 60% in adults. Approximate prevalence of systemic disease = 5% in children, 40% in adults.
Diabetic Nephropathy
(See also Chapter 21 page 923 of robbins ) . The kidneys are prime targets of diabetes. Renal failure is second only to myocardial infarction as a cause of death from this disease. Three lesions are encountered: (1) glomerular lesions; (2) renal vascular lesions, principally arteriolosclerosis; and (3) pyelonephritis, including necrotizing papillitis.
The most important glomerular lesions are capillary basement membrane thickening, diffuse glomerulosclerosis, and nodular glomerulosclerosis. These are described in detail in Chapter 21 . The glomerular capillary basement membranes are thickened throughout their entire length. This change can be detected by electron microscopy within a few years of the onset of diabetes, sometimes without any associated change in renal function.
Diffuse glomerulosclerosis consists of a diffuse increase in mesangial matrix along with mesangial cell proliferation and is always associated with basement membrane thickening. It is found in most patients with disease of more than 10 years’ duration. When glomerulosclerosis becomes marked, patients manifest the nephrotic
Nodular glomerulosclerosis and the diffuse lesion are fundamentally similar lesions of the mesangium. The nodular lesion, however, is virtually pathognomonic of diabetes, so long as care is taken to exclude membranoproliferative (lobular) glomerulonephritis, the glomerulonephritis associated with light-chain disease, and amyloidosis. Approximately 15% to 30% of long-term patients with diabetes develop nodular glomerulosclerosis, and in most instances it is associated with renal failure
Nodular glomerulosclerosis describes a glomerular lesion made distinctive by ball-like deposits of a laminated matrix within the mesangial core of the lobule (see Fig. 21-32) . These nodules tend to develop in the periphery of the glomerulus, and since they arise within the mesangium, they push the glomerular capillary loops even more to the periphery. Often these capillary loops create halos about the nodule. This distinctive change has been called the Kimmelstiel-Wilson lesion, after the pioneers who described it. They usually contain trapped mesangial cells. Diffuse glomerulosclerosis is present in glomeruli not affected by nodular glomerulosclerosis.
Robbins 967 6th ed
Focal segmental glomerulosclerosis occurs in the following settings
in association with other known conditions, such as HIV infection and heroin addiction
Hypertension- Arteriolar nephrosclerosis (fibrnoid necrosis)


Kimmelstiel-wilson disease is diagnostic of
a)Diabetic glomerulosclerosis
b)Hypertension benign
c)Malignant hypertension
Already Described above–

Charactersitic feature of kidneys in diabetes mellitus is —(Al 89)
a)Nodular sclerosis
b)Fibrin cap
c)Papillary necrosis
d)Difuse glomendosclerosis
Ans is A…already described above

Nephrotic syndrome is caused by all except —
a) Malaria
b) Penicillamine
c) Syphilis
d) Shock
Ans is D
1.Acute nephritic syndrome—Hematuria, azotemia, variable proteinuria, oliguria, edema, and hypertension
2.Rapidly progressive glomerulonephritis–Acute nephritis, proteinuria, and acute renal failure
3.Nephrotic syndrome: >3.5 gm proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria
4.Chronic renal failure:Azotemia uremia progressing for years
5.Asymptomatic hematuria or proteinuria:Glomerular hematuria; subnephrotic proteinuria
CAUSES OF NEPHROTIC SYNDROME in order of frequency-
Primary Glomerular Disease-Membranous glomerulonephritis,Lipoid nephrosis,Focal segmental glomerulosclerosis,Membranoproliferative glomerulonephritis,Other proliferative glomerulonephritis (focal, “pure mesangial,” IgA nephropathy)
Systemic Diseases–Diabetes mellitus,Amyloidosis,Systemic lupus erythematosus,Drugs (gold, penicillamine, “street heroin”),Infections (malaria, syphilis, hepatitis B, acquired immunodeficiency syndrome)
Malignant disease (carcinoma, melanoma),Miscellaneous (bee-sting allergy, hereditary nephritis)
robbins 953 6th ed


Transitional cell carcinomas can be caused by —
a) Napthylamine
b) Smoking
c) Bilharziasis
d) Betel nut
Ans. Three options are correct i.e., ‘a, b & c’ {Ref : Robbin’s 7″/e p. 1029 & 6th/e p. 1007]
A number of factors have been implicated in the causation of transitional cell carcinoma. Some of the more important contributors include the following:
Cigarette smoking is clearly the most important influence, increasing the risk threefold to sevenfold, depending on the pack-years and smoking habits. Fifty per cent to 80% of all bladder cancers among men are associated with the use of cigarettes. Cigars, pipes, and smokeless tobacco invoke a much smaller risk.
Industrial exposure to arylamines, particularly 2-naphthylamine as well as related compounds, as pointed out in the earlier discussion of chemical carcinogenesis (Chapter 8) . The cancers appear 15 to 40 years after the first exposure.
Schistosoma haematobium infections in areas where these are endemic (Egypt, Sudan) are an established risk. The ova are deposited in the bladder wall and incite a brisk chronic inflammatory response that induces progressive mucosal squamous metaplasia and dysplasia and, in some instances, neoplasia. Seventy per cent of the cancers are squamous, the remainder being transitional cell carcinoma.
Long-term use of analgesics, implicated also in analgesic nephropathy (Chapter 21) .
Heavy long-term exposure to cyclophosphamide, an immunosuppressive agent, induces as noted hemorrhagic cystitis and increases the risk of bladder cancer.
How these influences induce cancer is unclear, but a number of genetic alterations have been observed in transitional cell carcinoma. The cytogenetic and molecular alterations are heterogeneous. Particularly common (occurring in 30% to 60% of tumors studied) are chromosome 9 monosomy or deletions of 9p and 9q as well as deletions of 17p, 13q, 11p, and 14q. [8] The chromosome 9 deletions are the only genetic changes present frequently in superficial papillary tumors and occasionally in noninvasive flat tumors.

IMPORTANT POINT IN TREATMENT OF TRANSITIONAL CELL CARCINOMA OF BLADDER:–Intravesical therapies are used in two general contexts: as an adjuvant to
a complete endoscopic resection to prevent recurrence or, less commonly,
to eliminate disease that cannot be controlled by endoscopic resection
alone. Intravesical treatments are advised for patients with recurrent disease,
>40% involvement of the bladder surface by tumor, diffuse CIS, or T1
disease. The standard intravesical therapy, based on randomized comparisons,
is bacillus Calmette-Guerin (BCG) in six weekly instillations, followed
by monthly maintenance administrations for ≥1 year

At least 95% of cancers of the oral cavity (including the tongue) are squamous cell carcinomas.A major regional predisposing influence is the chewing of betel nuts and pan in India and parts of Asia.
Though smoking is related to both types.

Commonest type of nephrotic syndrome seen in children
a) Focal
b) Diffuse
c) Minimal change
d) Proliferative
Ans. is ‘c’ i.e., Minimal change [Ref : Robbin’s rie p. 979 t (20.8) & 6THe p. 954]
Membranous glomerulonephritis is the most common cause of the nephrotic syndrome in adults. It is characterized by diffuse thickening of the glomerular capillary wall and the accumulation of electron-dense, immunoglobulin-containing deposits along the epithelial (subepithelial) side of the basement membrane.
Minimal Change Disease (Lipoid Nephrosis)This relatively benign disorder is the most frequent cause of nephrotic syndrome in children. It is characterized by diffuse loss of foot processes of epithelial cells in glomeruli that appear virtually normal by light microscopy. The peak incidence is between 2 and 6 years of age.

Basement membrane has type…. Collagen –
a) I
b) II
c) II
Ans. is ‘d’ i.e., IV [Ref : Robbin’s 7h/e p. 956 & 6e p. 931]
The glomerular capillary wall is the filtering membrane and consists of the following structures [2] (Fig. 21-2) :
A thin layer of fenestrated endothelial cells, each fenestrum being about 70 to 100 nm in diameter.
A glomerular basement membrane (GBM) with a thick electron-dense central layer, the lamina densa, and thinner electron-lucent peripheral layers, the lamina rara interna and lamina rara externa. The GBM consists of collagen (mostly type IV), laminin, polyanionic proteoglycans (mostly heparan sulfate), fibronectin, entactin, and several other glycoproteins. Type IV collagen forms a network suprastructure to which other glycoproteins attach. The building block (monomer) of this network is a triple-helical molecule made up of three alpha chains, composed of one or more of six types of alpha chains (alpha1 to alpha6 or COL4A1 to COL4A6), the most common consisting of alpha1 alpha2 alpha1 (Fig. 21-3) . [3] Each molecule consists of a 7S domain at the amino terminus, a triple-helical domain in the middle, and a globular noncollagenous domain (NC1) at the carboxyl terminus. The NC1 domain is important for helical formation and also for assembly of collagen monomers into dimers. The 7S domain, in turn, is involved in formation of tetramers, and thus a porous suprastructure evolves. Glycoproteins (laminin, entactin) and acidic proteoglycans (perlecan) attach to the collagenous suprastructure [4] (Fig. 21-4) . These biochemical determinants are critical to understanding glomerular diseases. For example, as we shall see, the NC1 domain is the antigenic site in anti-GBM nephritis; genetic defects in the alpha chains underlie some forms of hereditary nephritis; and the acidic porous nature of the GBM determines its permeability characteristics.
The visceral epithelial cells (podocytes), structurally complex cells that possess interdigitating processes embedded in and adherent to the lamina rara externa of the basement membrane. Adjacent foot processes (pedicels) are separated by 20- to 30-nm-wide filtration slits, which are bridged by a thin diaphragm.
The entire glomerular tuft is supported by mesangial cells lying between the capillaries. Basement membrane-like mesangial matrix forms a meshwork through which the mesangial cells are scattered. These cells, of mesenchymal origin, are contractile, phagocytic, and capable of proliferation, of laying down both matrix and collagen, and of secreting a number of biologically active mediators. They are, as we shall see, important players in many forms of human glomerulonephritis.

Bundles of banded fibers with high tensile strength
Skin (80%), bone (90%), tendons, most other organs
Thin fibrils; structural protein
Cartilage (50%), vitreous humor
Thin fibrils; pliable
Blood vessels, uterus, skin (10%)
All basement membranes
Amorphous/fine fibrils
2 – 5% of interstitial tissues, blood vessels
Amorphous/fine fibrils
Interstitial tissues
Anchoring filament
Dermal-epidermal junction
Probably amorphous
Endothelium-Descemet membrane
Possible role in maturation of cartilage

IMPORTANT—Three groups of macromolecules are physically associated to form the ECM: (1) fibrous structural proteins, such as the collagens and elastins; (2) a diverse group of adhesive glycoproteins, including fibronectin and laminin; and (3) a gel of proteoglycans and hyaluronan. These macromolecules assemble into two general organizations: interstitial matrix and BM (basal membrane). The interstitial matrix is present in spaces between epithelial, endothelial, and smooth muscle cells and in connective tissue. It consists of fibrillar (types I, III, V) and nonfibrillar collagen, elastin, fibronectin, proteoglycans, hyaluronate, and other components. BMs are produced by epithelial and mesenchymal cells and are closely associated with the cell surface. They consist of a network of amorphous nonfibrillar collagen (mostly type IV), laminin, heparan sulfate, proteoglycan, and other glycoproteins

Bilateral contracted kidney occurs in all except
a)Diabetes mellitus (AIIMS 90)
b)Benign nephrosclerosis
c)Chronic pyelonephritis
d)Chronic glomerular nephritis
Ans. is ‘a’ i.e., Diabetes mellitus [Ref : Chandrasoma taylor 3rd/e p. 725, table (49.2)]
Table 49–2. Differential Diagnosis of a Granular, Contracted Kidney.
ARE :-Chronic Glomerulonephritis Chronic Pyelonephritis Benign Nephrosclerosis (Hypertension)

Glomerulonephritis is due to:-
a)Type I hypersensitivity reaction
b)Type IV hypersensitivity reation
c)Immune complex deposition
d)Type V hypersensitivity reaction
Ans. is ‘c’ i.e., Immune complex deposition [Ref : Robbin’s 7/e p. 975 & 6th/e p. 943]
Immune-mediated glomerulonephritis (Chaps. 274 and275) accounts for a large fraction of acquired renal disease. The majority of cases are associated with the deposition of antibodies, often autoantibodies, within the glomerular tuft, indicating dysregulation of humoral immunity. Cellular immune mechanisms also contribute to the pathogenesis of antibody-mediated glomerulonephritis by modulating antibody production and through antibody-dependent cell cytotoxicity (see below). In addition, cellular immune mechanisms probably play a primary role in the pathophysiology of “pauci-immune” glomerulonephritides, notable for robust glomerular inflammation in the absence of immunoglobulin deposition.

Antiglomerular antibodies are present in —
a)Good pasture syndrome (Al 90)
b)Focal gloumerulonephritis
c)Membramcous glomerulonephritis
d)Membrano proliferative glomerulonephritis
RPGN may be caused by a number of different diseases, some restricted to the kidney and others systemic. [34] Although no single mechanism can explain all cases, there is little doubt that in most cases the glomerular injury is immunologically mediated. Thus, a practical classification divides RPGN into three groups on the basis of immunologic findings (Table 21-6) . In each group, the disease may be associated with a known disorder or it may be idiopathic.
Type I RPGN is best remembered as anti-GBM disease and hence is characterized by linear deposits of IgG and, in many cases, C3 in the GBM, as previously described. In some of these patients, the anti-GBM antibodies cross-react with pulmonary alveolar basement membranes to produce
Goodpasture syndrome
TYPE II RPGN (immune complex)
Systemic lupus erythematosus
Henoch-Schonlein purpura (IgA)
TYPE III RPGN (pauci-immune)
(ANCA associated)
Wegener granulomatosis
Microscopic polyarteritis nodosa
the clinical picture of pulmonary hemorrhages associated with renal failure ( Goodpasture syndrome). The Goodpasture antigen, as noted, resides in the noncollagenous portion of the alpha3 chain of collagen type IV. What triggers the formation of these antibodies is unclear in most patients. Exposure to viruses or hydrocarbon solvents (found in paints and dyes) has been implicated in some patients, as have various drugs and cancers. Cigarette smoking appears to play a permissive role, since most patients who develop pulmonary hemorrhage are smokers. There is a high prevalence of certain HLA subtypes and haplotypes (e.g., HLA-DRB1), a finding consistent with the genetic predisposition to autoimmunity. [34]
Type II RPGN is an immune complex- mediated disease. It can be a complication of any of the immune complex nephritides, including postinfectious glomerulonephritis, SLE, IgA nephropathy, and Henoch-Schonlein purpura. In some cases, immune complexes can be demonstrated, but the underlying cause is undetermined. In all of these cases, immunofluorescence studies reveal the characteristic (“lumpy bumpy”) granular pattern of staining. These patients cannot usually be helped by plasmapheresis, and they require treatment for the underlying disease.
Type III RPGN, also called pauci-immune type, is defined by the lack of anti-GBM antibodies or immune complexes by immunofluorescence and electron microscopy. Most of these patients have antineutrophil cytoplasmic antibody (ANCA) in the serum, which, as we have seen (Chapter 12) , plays a role in some vasculitides. Hence, in some cases, type III RPGN is a component of a systemic vasculitis such as Wegener granulomatosis or microscopic polyarteritis. In many cases, however, pauci-immune crescentic glomerulonephritis is isolated and hence idiopathic. More than 90% of such idiopathic cases have C-ANCA or P-ANCA in the sera.
To summarize, all three types of RPGN may be associated with a well-defined renal or extrarenal disease, but in many cases (approximately 50%) the disorder is idiopathic. Of the idiopathic cases, about one fourth have anti-GBM disease (RPGN type I) without lung involvement; another one fourth have type II RPGN; and the remainder are pauci-immune or type III RPGN. The common denominator in all types of RPGN is severe glomerular injury.


In crescentric glomerulonephritis, prognosis depends on —(AI 90)
a) Size
b) Cellularity
c) Number
d) Basement membrane break
Ans. is ‘c’ i.e., Number [Ref : Basic Robbin’s p. 453]
A crescent is a half-moon-shaped collection of cells in Bowman’s space, usually composed of proliferating parietal epithelial cells and infiltrating monocytes. Because crescentic glomerulonephritis is often associated with renal failure that progresses rapidly over week to months, the clinical term rapidly progressive glomerulonephritis and pathologic term crescentic glomerulonephritis are often used interchangeably

The epithelium in the ureter is —
a) Squamous
b) Columnar
c) Ciliated columnar
d) Transitional
Urothelium is a specialized epithelium that lines much of the urinary tract and prevents its rather toxic contents from damaging surrounding structures. It extends from the ends of the collecting ducts of the kidneys, through the ureters (p. 1277) and bladder (p. 1292), to the proximal portion of the urethra. In males it covers the urethra as far as the ejaculatory ducts, then becomes intermittent and is finally replaced by stratified columnar epithelium in the membranous urethra. In females it extends as far as the urogenital membrane. During development, part of it is derived from mesoderm and part from ectoderm and endoderm
The epithelium lining the preprostatic urethra and the proximal part of the prostatic urethra is a typical urothelium. It is continuous with that lining the bladder, and with the epithelium lining the ducts of the prostate and bulbourethral glands, the seminal vesicles, and the vasa deferentia and ejaculatory ducts. These relationships are important in the spread of urinary tract infections.
Below the openings of the ejaculatory ducts the epithelium changes to a pseudostratified or stratified columnar type, which lines the membranous urethra and the major part of the penile urethra Mucus-secreting cells are common throughout this epithelium and frequently occur in small clusters in the penile urethra. Branching tubular paraurethral glands secrete protective mucus onto the urethral epithelial lining and are especially numerous on its dorsal aspect. In older men many of the deep recesses of the urethral mucosa contain concretions similar to those found within prostatic glands (p. 1302). Towards the distal end of the penile urethra the epithelium changes once again, becoming stratified squamous in type with well-defined connective tissue papillae. This epithelium also lines the navicular fossa and becomes keratinized at the external meatus. The epithelial cells lining the navicular fossa are glycogen-rich. This may provide a substrate for commensal lactobacilli which, as in the female vagina (p. 1353), provide a defence against pathogenic organisms.
ref:-gray anatomy

Which is not a feature of benign hypertension in Kidney-

a)Hyaline arteriosclerosis
b)Interstitial lobular fibrosis
c)Medial hypertrophy of small vessels
d)Fibrinoid necrosis

Ans. is ‘d’ i.e., Fibrinoid necrosis [Ref : Robbin’s 7Th/e p. 1006, 1007 & 6e p. [snip],[snip] p. [snip]

Whether it is “essential” or of known etiology, hypertension results in
development of intrinsic lesions of the renal arterioles (hyaline arteriolosclerosis)
that eventually lead to loss of function (nephrosclerosis)…
harrison 1813 17th ed

“Essential” Hypertension (Arteriolar Nephrosclerosis)(BENIGN):-The characteristic pathology is in the afferent arterioles, which have
thickened walls due to deposition of homogeneous eosinophilic material
(hyaline arteriolosclerosis). Narrowing of vascular lumina results,
with consequent ischemic injury to glomeruli and tubules.Two processes participate in inducing the arterial lesions:
Medial and intimal thickening, as a response to hemodynamic changes, genetic defects, or both
Hyaline deposition in arterioles, caused partly by extravasation of plasma proteins through injured endothelium and partly by increased deposition of basement membrane matrix

Malignant nephrosclerosis is the form of renal disease associated with the malignant or accelerated phase of hypertension.The basis for this turn for the worse in hypertensive subjects is unclear, but the following sequence of events is suggested. The initial event appears to be some form of vascular damage to the kidneys. This most commonly results from long-standing benign hypertension, with eventual injury to the arteriolar walls, or it may spring from arteritis or a coagulopathy. In either case, the result is increased permeability of the small vessels to fibrinogen and other plasma proteins, endothelial injury, and platelet deposition. This leads to the appearance of fibrinoid necrosis


Linear deposition of lgG on glomerular basementmembrane is seen in —
b)Good pasteur’s syndrome
c)Nephrotic syndrome
d)Shunt nephritis

Ans. is ‘b’ i.e., Good pasture’s syndrome [Ref; Robbin’s 7E p. 976, 977 & 6E p. 951]

Patients who develop autoantibodies directed against glomerular
basement antigens frequently develop a glomerulonephritis termed
antiglomerular basement membrane (anti-GBM) disease. When they
present with lung hemorrhage and glomerulonephritis, they have a
pulmonary-renal syndrome called Goodpasture’s syndrome. The target epitopes for this autoimmune disease lie in the quaternary structure of α3 NC1 domain of collagen IV.

The presence of anti-GBM antibodies
and complement is recognized on biopsy by linear immunofluorescent
staining for IgG (rarely IgA).

Prognosis at presentation is worse if there are >50% crescents on renal
biopsy with advanced fibrosis, if serum creatinine is >5–6 mg/dL, if oliguria is present, or if there is a need for acute dialysis. Although frequently attempted, most of these latter patients will not respond to
plasmapheresis and steroids. Patients with advanced renal failure who
present with hemoptysis should still be treated for their lung hemorrhage,
as it responds to plasmapheresis and can be lifesaving. Treated
patients with less severe disease typically respond to 8–10 treatments
of plasmapheresis accompanied by oral prednisone and cyclophosphamide
in the first 2 weeks.

The worst prognosis for renal cell carcinoma is-

a)Vascular invasion
b)Associated with hyper calcemia
c)Presence of Hematuria
d)Size more than 5 cm.

Ans. is ‘a’ i.e., Vascular invasion [Ref : Robbin’7E. 1018 & 6E p. 993,]

Two staging systems used are the Robson classification and the American
Joint Committee on Cancer (AJCC) staging system. According to
the AJCC system, stage I tumors are <7 cm in greatest diameter and confined to the kidney, stage II tumors are ≥7 cm and confined to the
kidney, stage III tumors extend through the renal capsule but are confined to Gerota’s fascia (IIIa) or involve a single hilar lymph node
(N1), and stage IV disease includes tumors that have invaded adjacent
organs (excluding the adrenal gland) or involve multiple lymph
nodes or distant metastases
. The rate of 5-year survival varies by
stage: >90% for stage I, 85% for stage II, 60% for stage III, and 10%
for stage IV. HARRISON 593 17TH ED

Two staging systems used commonly are the Robson classification and the American Joint Committee on Cancer (AJCC) staging system. According to the former, stage I tumors are confined to the kidney; stage II tumors extend through the renal capsule but are confined to Gerota’s fascia; stage III tumors involve the renal vein or vena cava (stage III A) or the hilar lymph nodes (stage III B); and stage IV disease includes tumors that are locally invasive to adjacent organs (excluding the adrenal gland) or distant metastases. Five-year survival rate varies by stage: 66% for stage I, 64% for stage II, 42% for stage III, and 11% for stage IV. The prognosis for patients with stage IIIA lesions is similar to that of stage II disease, whereas the 5-year survival rate for patients with stage IIIB lesions is only 20%, closer to that of stage IV.
Harrison 15th ed p 607 describes Robson Classification

Minimal-change nephropathy—
a)Is the commonest cause of the nephrotic syndrome in childhood
b)Does not relapse after remission
c)Produces highly selective proteinuria
d)Does not cause depression of the serumcomplement level
e)Must always be confirmed by renal biopsy

Ans. Three options are correct i.e., a, c & d [Ref : Robbin’s 7th/e p. [snip], [snip] & 6th/e p. 954 & 956,]

MCD, sometimes known as nil lesion, causes 70–90% of nephrotic
syndrome in childhood
but only 10–15% of nephrotic syndrome in
adults.harrison 17th ed 1790

In children, the abnormal urine principally
contains albumin with minimal amounts of higher molecular weight
proteins, and is sometimes called selective proteinuria.

Relapses occur in 70–75% of children after the first remission, and
early relapse predicts multiple subsequent relapses.

Renal biopsy is a valuable tool in adults with nephrotic syndrome for establishing a definitive diagnosis, guiding therapy, and estimating prognosis. Renal biopsy is not required in the majority of children with nephrotic syndrome as most cases are due to MCD and respond to empiric treatment with glucocorticoids. harrison 15th ed 1585

Splliting of the glomerular basement membraneis seen in —
a)Acute glomerulonephritis
b)Membranous glomerulonephritis
c)Membranoproliferative glomerulonephritis
d)Good pasture’s syndrome

Ans. is ‘c’ i.e., Membranoproliferative glomerulonephritis [Ref : Robbin’s 7e p [snip] & 6e p. 959]

The glomeruli have a “lobular” appearance accentuated by the proliferating mesangial cells and increased mesangial matrix (Fig. 21-23) . The GBM is clearly thickened, often focally, most evident in the peripheral capillary loops. The glomerular capillary wall often shows a “double-contour” or “tram-track” appearance, especially evident in silver or PAS stains. This is caused by “duplication” of the basement membrane and the inclusion within the lamina rara interna of processes of cells extending into the peripheral capillary loops, so-called mesangial and monocyte interposition.

Type I MPGN, the most proliferative of the three types, shows mesangial
proliferation with lobular segmentation on renal biopsy and mesangial interposition between the capillary basement membrane
and endothelial cells, producing a double contour sometimes called
(Figs. e9-7 and e9-9). Subendothelial deposits with low
serum levels of C3 are typical, although 50% of patients have normal
levels of C3 and occasional intra-mesangial deposits.

Low serum C3 and a dense thickening of the GBM containing ribbons of dense deposits
and C3 characterize Type II MPGN, sometimes called dense deposit
disease (Fig. e9-8). Classically, the glomerular tuft has a lobular
appearance; intramesangial deposits are rarely present and subendothelial deposits are generally absent.

Proliferation in Type III MPGN is less common than the other two types and is often focal; mesangial interposition is rare, and subepithelial deposits can occur along widened segments of the GBM that appear laminated and disrupted.

The intracytoplasmic vacuoles seen in the Armmani Epstein cell are rich in –
a) Na and K’
b) Glycogen
c) Lipids
d) None of the above

ans is B

Glycogen vacuolation of the terminal part of the proxcimal convoluted tubules (loops of Henle) in diabetic patients, directly related to hyperglycemia and glycosuria..Ref INTERNET

Findings of multiple myeloma in kidney are –

a)Tubular casts
c)Wire loop lesions
d)Renal tubular necrosis

Ans. Four options are correct i.e., a, b, d & e [Ref : Robbin’s 7’/e p. 1005, 1006 & 6THe p. [snip] & [snip];Harrison 16th/e p. 1647 & 13Th/e p. 1544 for V]


Multiple Myeloma
Nonrenal malignant tumors, particularly those of hematopoietic origin, affect the kidneys in a number of ways (Table 21-11) . The most common involvements are tubulointerstitial, caused by complications of the tumor (hypercalcemia, hyperuricemia, obstruction of ureters) or therapy (irradiation, hyperuricemia, chemotherapy, infections in immunosuppressed patients). As the survival rate of patients with malignant neoplasms increases, so do these renal complications. We limit the discussion to the renal lesions in multiple myeloma that sometimes dominate the clinical picture in patients with this disease.
Renal involvement is a sometimes ominous manifestation of multiple myeloma; overt renal insufficiency occurs in half the patients with this disease. Several factors contribute to renal damage:
1.Bence Jones proteinuria and cast nephropathy. The main cause of renal dysfunction is related to Bence Jones (light-chain) proteinuria, because renal failure correlates well with the presence and amount of such proteinuria and is extremely rare in its absence. Two mechanisms appear to account for the renal toxicity of Bence Jones proteins. First, some light chains are directly toxic to epithelial cells; different light chains have different nephrotoxic potential. Second, Bence Jones proteins combine with the urinary glycoprotein (Tamm-Horsfall protein) under acidic conditions to form large, histologically distinct tubular casts that obstruct the tubular lumina and also induce a peritubular inflammatory reaction (cast nephropathy).

2.Amyloidosis, which occurs in 6% to 24% of patients with myeloma

3.Light-chain nephropathy. In some patients, light chains deposit in glomeruli in nonfibrillar forms, causing a glomerulopathy(described earlier), or around tubules, causing a tubulointerstitial nephritis.
Hypercalcemia and hyperuricemia, which are often present in these patients
4.Vascular disease in the usually elderly population affected with myeloma
5.Urinary tract obstruction with secondary pyelonephritis

Bilarerally symmmetrical contracted scarred kidney is seen in-
b)Chronic glomerulonephriris
c)End stage renal disease
d)Chronic pyelonephritis

Chronic obstructive pyelonephritis may be insidious in onset or may present the clinical manifestations of acute recurrent pyelonephritis with back pain, fever, frequent pyuria, and bacteriuria. Chronic pyelonephritis associated with reflux may have a silent onset. These patients come to medical attention relatively late in the course of their disease because of the gradual onset of renal insufficiency and hypertension or because of the discovery of pyuria or bacteriuria on routine examination. Reflux nephropathy is a common cause of hypertension in children. Loss of tubular function–in particular of concentrating ability–gives rise to polyuria and nocturia. Radiographic studies show asymmetrically contracted kidneys with characteristic coarse scars and blunting and deformity of the calyceal system.

Chronic Glomerulonephritis-The kidneys are symmetrically contracted and have diffusely granular, cortical surfaces. On section, the cortex is thinned, and there is an increase in peripelvic fat.

Cylindrical dilatation of renal tubules is seen in –
a)Polycystic disease ‘of kidney(Jipmer 95)
b)Medullary cystic disease
c)Wilms tumour
d)Lipoid nephrosis

Ans. is ‘a’ i.e., Polycystic disease of kidney [Ref : Robbin’s 7h/e p. 966 & 6ep. 940, see morphology 9th line]

This rare developmental anomaly is genetically distinct from adult polycystic kidney disease, having an autosomal recessive type of inheritance. Perinatal, neonatal, infantile, and juvenile subcategories have been defined, depending on time of presentation and presence of associated hepatic lesions. The first two are most common; serious manifestations are usually present at birth, and the young infant may succumb rapidly to renal failure.
Kidneys are enlarged and have a smooth external appearance. On cut section, numerous small cysts in the cortex and medulla give the kidney a spongelike appearance. Dilated elongated channels are present at right angles to the cortical surface, completely replacing the medulla and cortex (Fig. 21-8 C). On microscopic examination, there is saccular or, more commonly, cylindrical dilation of all collecting tubules. The cysts have a uniform lining of cuboidal cells, reflecting their origin from the collecting tubules. The disease is invariably bilateral. In almost all cases, there are multiple epithelium-lined cysts in the liver (Fig. 21-8 D) as well as proliferation of portal bile ducts.
Patients who survive infancy (infantile and juvenile form) may develop a peculiar type of hepatic fibrosis characterized by bland periportal fibrosis and proliferation of well-differentiated biliary ductules, a condition now termed congenital hepatic fibrosis. In older children, the hepatic picture in fact predominates. Such patients may develop portal hypertension with splenomegaly. Curiously, congenital hepatic fibrosis sometimes occurs in the absence of polycystic kidneys and has been reported occasionally in the presence of adult polycystic kidney disease.

FOR THE ABOVE QUESTION:-At birth the kidneys are enlarged with a smooth external surface. The distal tubules and collecting ducts are dilated into elongated cysts that are arranged in a radial fashion. As the patient ages, the cysts may become more spherical and the disease can be confused withADPKD. Interstitial fibrosis is also seen as renal function deteriorates. Liver involvement includes proliferation and dilation of small intrahepatic bile ducts as well as periportal fibrosis.


Flea bitten kidney is seen in all of following except –

a)Malignant hypertension
c)Infective endocarditis

Malignant Nephrosclerosis and Accelerated Hypertension:
On gross inspection, the kidney size is dependent on the duration and severity of the hypertensive disease. Small, pinpoint petechial hemorrhages may appear on the cortical surface from rupture of arterioles or glomerular capillaries, giving the kidney a peculiar “flea-bitten” appearance.

HUS and TTP, consumptive coagulopathies characterized by microangiopathic hemolytic anemia and thrombocytopenia, have a particular predilection for the kidney and the central nervous system, the latter especially in TTP. The kidneys of patients with HUS or TTP often exhibit a “flea-bitten” appearance, the result of multiple cortical hemorrhagic infarcts.HARRISON 15TH ED

Grossly, the kidneys in subacute bacterial endocarditis
have subcapsular hemorrhages with a “flea-bitten” appearance,
and microscopy on renal biopsy reveals a focal proliferation
around foci of necrosis associated with abundant mesangial, subendothelial,
and subepithelial immune deposits of IgG, IgM, and C3.HARR 17TH ED 1787

The pathology in the kidney in classic PAN is that of arteritis
without glomerulonephritis. In patients with significant hypertension,
typical pathologic features of glomerulosclerosis may be seen. In addition,
pathologic sequelae of hypertension may be found elsewhere in
the body.

The protein in glomerular basement membraneresponsible for charge dependent filtration is –

b)Collagen type IV

Ans. is ‘c’ i.e., Proteoglycan

Figure 21-4 ROBBINS 6TH ED P 934 :-A proposed model of the GBM molecular architecture in which type IV collagen monomers (gray) form a stable network through their NC1 domains (dimeric interactions, gray spheres) and 7S domains (tetrameric interactions) and intertwine along the triple-helical domains. Laminin monomers (red) separately form a reversible meshwork. Entactin (green) connects laminin to the collagen network and binds to perlecan (blue), an anionic heparan sulfate proteoglycan. This anionic suprastructure determines the charged porous nature of the GBM.
The major characteristics of glomerular filtration are an extraordinary high permeability to water and small solutes, accounted for by the highly fenestrated endothelium, and impermeability to proteins, such that molecules of the size of albumin (+3.6-nm radius; 70,000 MW). The latter property, called glomerular barrier function, discriminates among various protein molecules, depending on their size (the larger, the less permeable) and charge (the more cationic, the more permeable). This size- and charge-dependent barrier function is accounted for by the complex structure of the capillary wall, the collagenous porous charged suprastructure of the GBM, and the many anionic moieties present within the wall, including the acidic proteoglycans of the GBM (Fig. 21-4) and the sialoglycoproteins of epithelial and endothelial cell coats. The charge-dependent restriction is important in the virtually complete exclusion of albumin from the filtrate, because albumin is an anionic molecule of a pI 4.5. The visceral epithelial cell is important in the maintenance of glomerular barrier function: its slit diaphragm presents a distal diffusion barrier to the filtration of proteins, and it is the cell type that is largely responsible for synthesis of GBM components

Lipid cast are seen in –
a)Acute tubular necrosis
b)Nephrotic syndrome
c)Cytomegalic inclusion disease

Ans. is ‘b’ i.e., Nephrotic syndrome [Ref : Robbin’s 7e p. 979 & 6E p. 953]
Due to increased lipoproteins, lipoproteins leak across the glomerular capilary wall and the lipids appear in the urine either as free fat or as oval fat bodies representing lipoproteins absorbed by tubular epithelial cellsand then shed along with degenerated cells.

Benign hypertension is associated with –
a) Hyline arteriosclerosis
b) Fibrinoid necrosis
c) Basal ganglia
d) Periventricle

Ans. is ‘a’ i.e., Hyaline arteriosclerosis [Ref : Robbin’s 7″/e p. 1006 & 6fhle p. [snip]]

A patient presenting with haemoptysis and renal failure with anti basement membrane antibodies has –
a) Good pasture’s
b) Wegener’s
c) Churg Strauss
d) Henoch-scholein purpura

Ans. is ‘a’ i.e., Good pasture’s syndrome [Ref : Robbin’s 7/e p. 976 & 6/e p. 951]

Bilateral contracted granular kidney seen in all except-
a)Chronic Pyelonephritis
b)Chronic glomerulonephritis
c)Benign Nephrosclerosis
d)Diabetic nephropathy

Ans. is `d’ i.e., Diabetic nephropathy [Ref : Chandrasoma taylor 3”/e p. 725, table (49.2)]

already discussed

Crescents in post-streptococal glomerulonephritis are –
a)Epithelial cells
b)Mesangial cells
c)Epithelial, mesangial & macrophages
d)Macrophages only

Ans. is a and b

harrison—A crescent is a half-moon-shaped collection of cells in Bowman’s space, usually composed of proliferating parietal epithelial cells and infiltrating monocytes.The classic pathologic correlate of RPGN is crescent formation involving most glomeruli (crescentic glomerulonephritis), crescents being half-moon-shaped lesions in Bowman’s space composed of proliferating parietal epithelial cells and infiltrating monocytes (extracapillary proliferation).

robbins—Crescents are formed by proliferation of parietal cells and by migration of monocytes and macrophages into Bowman space. Neutrophils and lymphocytes may be present. The crescents eventually obliterate Bowman space and compress the glomerular tuft.

Thickening of basement membrane of glomeruliis seen in –
a)IgA nephropathy
b)Membranoproliferative glomerulonephritis
c)Lipoid nephrosis
d)Post streptococcal glomerulonephrities

Ans. is ‘b’ i.e., Membranoproliferative glomerulonephritis [Ref : Robbin’s 7e p. [snip] ]

Maximum endocapillary proliferation is seen in-
a)Membranous glomerulonephritis
b)Masangioproliferative glomerulonephritis
c)Focal segmental glomerulonephritis
d)Post streptococcal glomerulonephritis

ans is D


To illustrate the importance of the speed of onset, extent, and intensity of glomerular injury, it is instructive to compare two forms of immune complex glomerulonephritis, namely, acute postinfectious glomerulonephritis and IgA nephropathy. Postinfectious glomerulonephritis is characterized by rapid and extensive formation of immune complexes throughout the glomerular capillary wall, which often provokes acute renal failure with the classic hallmarks of acute inflammation: complement activation, leukocyte recruitment, lysosomal enzyme release, free radical generation, and perturbation of vascular tone and permeability. In contrast, IgA nephropathy is characterized by slow, but sustained, formation of immune complexes, largely confined to the mesangium; less dramatic activation of complement and other secondary mediator systems; and either stability ofGFR or progressive renal insufficiency over 10 to 20 years

Interstitial nephritis is caused by –
a) Methicillin
b) Ampicillin
c) Cloxacillin
d) Pencicillin


ref. Katzung Pharmacology p. 377

SIDE EFFECTS OF PENICILLIN:-Allergy: Allergic reactions include urticaria, severe pruritus, fever, joint swelling. hemolytic anemia, nephritis, and anaphylaxis. About 5-10% of persons with a past history
of penicillin reaction have an allergic response when given a penicillin again. Methicillin causes nephritis more often than do other penicillins, and nafcillin is associated with neutropenia. Antigenic determinants include degradation products of penicillins such as penicilloic acid. Complete cross-allergenicity between different penicillins should be as-
sumed. Ampicillin frequently causes maculopapular skin rash that may not be an allergic reaction.

Interstitial nephritis
A. Allergic: antibiotics (β-lactams, sulfonamides, quinolones, rifampin),
nonsteroidal anti-inflammatory drugs, diuretics, other drugs
B. Infection: pyelonephritis (if bilateral)
C. Infiltration: lymphoma, leukemia, sarcoidosis
D. Inflammatory, nonvascular: Sjögren’s syndrome, tubulointerstitial
nephritis with uveitis

Harrison 17th ed 1753

Virtually any pharmacologic agent may
trigger allergic interstitial nephritis, which is characterized by infiltration
of the tubulointerstitium by granulocytes (typically but not invariably
eosinophils), macrophages, and/or lymphocytes and by
interstitial edema. The most common offenders are antibiotics (e.g.,
penicillins, cephalosporins, quinolones, sulfonamides, rifampin) and

Fever, arthralgias, and a pruritic erythematous
rash following exposure to a new drug suggest allergic interstitial nephritis,
although systemic features of hypersensitivity are frequently

(See also Chap. e9) Anuria suggests complete urinary tract obstruction
but may complicate severe cases of prerenal or intrinsic renal ARF.
Wide fluctuations in urine output raise the possibility of intermittent
obstruction, whereas patients with partial urinary tract obstruction
may present with polyuria due to impairment of urine concentrating
In prerenal ARF, the sediment is characteristically acellular and
contains transparent hyaline casts (“bland,” “benign,” “inactive” urine
sediment). Hyaline casts are formed in concentrated urine from normal
constituents of urine—principally Tamm-Horsfall protein, which
is secreted by epithelial cells of the loop of Henle. Postrenal ARF may
also present with an inactive sediment, although hematuria and pyuria
are common in patients with intraluminal obstruction or prostatic
disease. Pigmented “muddy brown” granular casts and casts containing
tubule epithelial cells are characteristic of ATN and suggest an ischemic
or nephrotoxic etiology. These casts are usually found in
association with mild “tubular” proteinuria (<1 g/d), reflecting impaired
reabsorption and processing of filtered proteins by injured
proximal tubules. Casts may be absent in 20–30% of patients with
ATN and are not required for diagnosis. In general, red blood cell casts
indicate glomerular injury or, less often, acute tubulointerstitial nephritis.
White cell casts and nonpigmented granular casts suggest interstitial
, whereas broad granular casts are characteristic of
chronic kidney disease and probably reflect interstitial fibrosis and
dilatation of tubules. Eosinophiluria (>5% of urine leukocytes) is a
common finding (~90%) in antibiotic-induced allergic interstitial nephritis
and can be detected with Hansel’s stain; however, lymphocytes
may predominate in allergic interstitial nephritis induced by NSAIDs
and some other drugs (i.e., ampicillin, rifampicin, and interferon α).
Occasional uric acid crystals (pleomorphic in shape) are common in
the concentrated urine of prerenal ARF but suggest acute urate nephropathy
if seen in abundance. Oxalate (envelope-shaped) and hippurate
(needle-shaped) crystals raise the possibility of ethylene glycol
ingestion and toxicity.

Acute Drug-Induced Interstitial Nephritis
This is a well-recognized adverse reaction to a constantly increasing number of drugs. First reported after the use of sulfonamides, acute tubulointerstitial nephritis most frequently occurs with synthetic penicillins (methicillin, ampicillin), other synthetic antibiotics (rifampin), diuretics (thiazides), NSAIDs (phenylbutazone), and miscellaneous drugs (phenindione, cimetidine)

Tamm-Horsefall protein is produced in-
a) Kideny
b) Liver
c) Plasma cells
d) None
Ans. is ‘a’ i.e., Kidney [Ref : Robbin’s 7h/e p. 995 & 6′”/e p. 970]

Eosinophilic hyaline casts, as well as pigmented granular casts, are common, particularly in distal tubules and collecting ducts. These casts consist principally of Tamm-Horsfall protein (a specific urinary glycoprotein normally secreted by the cells of ascending thick limb and distal tubules) in conjunction with hemoglobin, myoglobin, and other plasma proteins.

Histopathology showing large cells with plant like apperance with perinuclear halo is seen in
which type of renal cell carcinoma ?-(PGI 2K)
a) Onchocytoma
b) Granular cell carcinoma
c) Angiosarcoma
d) Chromophobic
e)Clear cell carcinoma

Ans. is ‘d’ i.e., Chromophobic [Ref : Robbin’s 7e p. 1018 & 6e p. 993]

Sub-epithelial humps are characteristic of –
a)Minimal change glomerulonephritis
b)Membranous glomerulonephritis
c)Membranoproliferative glomerulonephritis
d)Post-steptococcal glomerulonephritis

Ans. is ‘d’ i.e., Post-streptococcal glomerulonephritis [Ref : Robbin’s 7e p. 975 & 6e p. 950]

The renal biopsy in poststreptococcal glomerulonephritis demonstrates
hypercellularity of mesangial and endothelial cells, glomerular
infiltrates of polymorphonuclear leukocytes, granular subendothelial
immune deposits of IgG, IgM, C3, C4, and C5-9, and subepithelial deposits
(which appear as “humps”) (Fig. e9-4).harrison 17 e

Onion skin lesions, in the muscular layer ofarteriole, are seen in
b)Benign nephrosclerosis
c)Malignant nephrosclerosis
d). RPGN

“Malignant” Hypertension–The kidneys are characterized
by a flea-bitten appearance resulting from hemorrhages in
surface capillaries. Histologically, two distinct vascular lesions can be
seen. The first, affecting arterioles, is fibrinoid necrosis, i.e., infiltration of arteriolar walls with eosinophilic material including fibrin, thickening of vessel walls, and, occasionally, an inflammatory infiltrate (necrotizing arteriolitis). The second lesion, involving the interlobular
arteries, is a concentric hyperplastic proliferation of the cellular elements
of the vascular wall with deposition of collagen to form a hyperplastic
arteriolitis (onion-skin lesion).

Ewing sarcoma usually arises in the diaphysis of long tubular bones, especially the femur and the flat bones of the pelvis. It presents as a painful enlarging mass, and the affected site is frequently tender, warm, and swollen. Some patients have systemic findings, including fever, elevated sedimentation rate, anemia, and leukocytosis, which mimic infection. Plain x-rays show a destructive lytic tumor that has permeative margins. The characteristic periosteal reaction produces layers of reactive bone deposited in an onion-skin fashion.

In its macroscopic appearance, the renal cell carcinoma tumor is characteristic. It may arise in any portion of the kidney, but more commonly it affects the poles, particularly the upper one. Clear cell neoplasms occur as solitary unilateral lesions. They are spherical masses, 3 to 15 cm in diameter, composed of bright yellow-gray-white tissue that distorts the renal outline. There are commonly large areas of ischemic, opaque, gray-white necrosis, foci of hemorrhagic discoloration, and areas of softening. The margins are usually sharply defined and confined within the renal capsule (Fig. 21-59) . Papillary tumors can be multifocal and bilateral. They are typically hemorrhagic and cystic, especially when large. The papillae may be seen grossly as golden yellow flakes.
As tumors enlarge, they may bulge into the calyces and pelvis and eventually may fungate through the walls of the collecting system to extend even into the ureter. One of the striking characteristics of this tumor is its tendency to invade the renal vein (Fig. 21-59) and grow as a solid column of cells within this vessel. Further extension produces a continuous cord of tumor in the inferior vena cava and even in the right side of the heart.
In clear cell carcinoma, the growth pattern varies from solid to trabecular (cordlike) or tubular (resembling tubules). The tumor cells have a rounded or polygonal shape and abundant clear or granular cytoplasm; the latter on special stains contains glycogen and lipids (Fig. 21-60 A). The
tumors have delicate branching vasculature and may exhibit cystic as well as solid areas. Most tumors are well differentiated, but some show marked nuclear atypia with formation of bizarre nuclei and giant cells. Papillary carcinoma is composed of cuboidal or low columnar cells arranged in papillary formations. Interstitial foam cells are common in the papillary cores (Fig. 21-60 B). Psammoma bodies may be present. The stroma is usually scanty but highly vascularized. Chromophobe renal carcinoma is made up of pale eosinophilic cells, often with a perinuclear halo, arranged in solid sheets with a concentration of the largest cells around blood vessels (Fig. 21-60 C). Collecting duct carcinoma is a rare variant showing irregular channels lined by highly atypical epithelium with a hobnail pattern. Sarcomatoid changes arise infrequently in all types of renal cell carcinoma and are a decidedly ominous feature of these tumors.

Membranous glomerulopathy. Membranous glomerulopathy
is due to subepithelial deposits, with resulting basement membrane
reaction, resulting in the appearance of spike-like projections on
silver stain.

Poststreptococcal glomerulonephritis, lupus nephritis,
and idiopathic membranous nephritis typically are associated with immune
deposits along the GBM, while anti-GBM antibodies are produced
in anti-GBM disease. Preformed circulating immune complexes
can precipitate along the subendothelial side of the GBM, while other
immune deposits form in situ on the subepithelial side. These latter
deposits accumulate when circulating autoantibodies find their antigen
trapped along the subepithelial edge of the GBM.

Immunofluorescent and electron microscopy can detect
the presence and location of subepithelial, subendothelial, or mesangial
immune deposits, or reduplication or splitting of the basement membrane.

Membranous glomerulopathy. Membranous glomerulopathy
is due to subepithelial deposits, with resulting basement membrane
reaction, resulting in the appearance of spike-like projections on
silver stain (left). The deposits are directly visualized by fluorescent anti-
IgG, revealing diffuse granular capillary loop staining (middle). By electron microscopy, the subepithelial location of the deposits and early surrounding basement membrane reaction is evident, with overlying foot
process effacement (right). (ABF/Vanderbilt Collection.)

Postinfectious (poststreptococcal) glomerulonephritis.
The glomerular tuft shows proliferative changes with numerous
PMNs, with a crescentic reaction in severe cases (left). These
deposits localize in the mesangium and along the capillary wall in a
subepithelial pattern and stain dominantly for C3 and to a lesser extent
for IgG (middle). Subepithelial hump-shaped deposits are seen
by electron microscopy (right). (ABF/Vanderbilt Collection.)

Subendothelial deposits not seen in membranous nephritis type while spike pattern is seen there.In poststreptococcal subendothelial and subepithelial deposits are seen but there is hump of subepithelial deposits instead.
Uremia occurs when total GFR is reduced by
a) 25% b) 50%
c) 60% d) 80%

Ans. is ‘a’ i.e., 25% [Ref : Patho. Robbins 7Th/e p. 961 & 6′”/e p. 936]

It should be emphasized that the signs and symptoms of uremia
will develop at significantly different levels of serum creatinine depending
upon the patient (size, age, and sex), the underlying renal disease,
existence of concurrent diseases, and true GFR. In general, patients do not develop symptomatic uremia until renal insufficiency is usually quite severe (GFR < 15 mL/min).HARRISON 17TH ED 269

Uremia. The red cells in uremia may acquire numerous,
regularly spaced, small spiny projections. Such cells, called burr cells or echinocytes, are readily distinguishable from irregularly spiculated

Acanthocytosis. Spiculated red cells are of two types:
acanthocytes are contracted dense cells with irregular membrane projections that vary in length and width; echinocytes
have small, uniform, and evenly spaced membrane projections. Acanthocytes are present in severe liver disease, in patients with abetalipoproteinemia, and in rare patients with McLeod blood group. Echinocytes are found in patients with severe uremia, in glycolytic red cell enzyme defects, and in microangiopathic hemolytic anemia.

Clinical feature of CRF appear when renal function is reduce to
a) 70% b) 50%
c) 30% d) 20% of normal

Ans. is ‘d’ i.e., 20% of normal [Ref : Patho. Robbins 7e p. 961 & 6e p. 936]

Acute renal failure is dominated by oliguria or anuria (no urine flow), with recent onset of azotemia. It can result from glomerular (e.g., crescentic glomerulonephritis), interstitial, and vascular injury or acute tubular necrosis.

Chronic renal failure, characterized by prolonged symptoms and signs of uremia, is the end result of all chronic renal diseases.

Uremia or uraemia is a term used to loosely describe the illness accompanying kidney failure (also called renal failure), in particular the nitrogenous waste products associated with the failure of this organ.

Azotemia is another word that refers to high levels of urea, but is used primarily when the abnormality can be measured chemically but is not yet so severe as to produce symptoms. Uremia can also result in fibrinous pericarditis.

All of the following may be associated with massive proteinuria except –
b)Renal vein thrombosis
c)Polycystic kidneys
d)Polyarteritis nodosa

ans is C and D

Renal artery thrombosis may lead to mild proteinuria and hematuria, whereas renal vein thrombosis typically induces heavy proteinuria and hematuria.

Amyloidosis also ass with heavy protenuria
Polycystic Kidney ass with mild proteinuria.
PAN is also ass with mild proteinuria as it produces nephritic syndrome.
Harrison 1785 17th ed

CLINICAL SYNDROMES Various forms of glomerular injury can also be parsed into several distinct syndromes on clinical grounds (Table 277-2). These syndromes, however, are not always mutually exclusive.There is an acute nephritic syndrome producing 1–2 g/24 h ofproteinuria,hematuria
with red blood cell casts, pyuria,
hypertension, fluid retention, and a rise in serum creatinine associated with a reduction
in glomerular filtration. If glomerular inflammation develops slowly, the serum creatinine will rise gradually over many weeks, but if the serum creatinine rises quickly, particularly over a few days, acute
nephritis is sometimes called rapidly progressive glomerulonephritis (RPGN); the histopathologic term crescentic glomerulonephritis
refers to the clinical occurrence of RPGN in a patient with this characteristic glomerular lesion. When patients with RPGN present with lung hemorrhage from Goodpasture’s syndrome, antineutrophil cytoplasmic antibodies (ANCA) small-vessel vasculitis, lupus erythematosus, or cryoglobulinemia, they are often diagnosed as
having a pulmonary-renal syndrome. Nephrotic syndrome describes the onset of heavy proteinuria (>3.0 g/24 h), hypertension,hypercholesterolemia, hypoalbuminemia, edema/anasarca, and microscopic hematuria;if only large amounts of proteinuria
are present without clinical manifestations, the condition is sometimes called nephrotic-range proteinuria. The glomerular filtration
rate (GFR) in these patients may initially be normal or, rarely, higher than
normal, but with persistent hyperfiltration and continued nephron loss, it typically declines over months to years. Patients
with a basement membrane syndrome either have genetically abnormal basement membranes or an autoimmune response to
basement membrane collagen IV associated with microscopic hematuria, mild to heavy proteinuria, and hypertension with variable elevations in serum creatinine. Glomerular-vascular syndrome describes patients
with vascular injury producing hematuria and moderate proteinuria. Affected individuals can have vasculitis, thrombotic microangiopathy, antiphospholipid syndrome, or, more commonly, a systemic disease
such as atherosclerosis, cholesterol emboli, hypertension, sickle cell anemia, and autoimmunity. Infectious diseases-asso-ciated syndrome is most important if one has an international perspective.Save for subacute bacterial endocarditis in the Western Hemisphere, malaria and schistosomiasis may be the most commoncauses of glomerulonephritis throughout the world, closelyfollowed by HIV and chronic hepatitis B and C. These infectiousdiseases produce a variety of inflammatory reactions in glomerular capillaries, ranging from nephrotic syndrome to acute nephritic injury,and yield urinalyses that demonstrate a combination of hematuria and proteinuria.

Wilm’s tumour may be associated with all except –
a)Genitourinary anomalies
b)Beckwith’s syndrome

Ans. is ‘d’ i.e., Glaucoma [Ref Patho Robins 7e p. 504, 505 & 6e p. 488 ]

Wilms’ tumor is the most common primary renal tumor of childhood, usually diagnosed between the ages of 2 and 5 years.

Neuroblastoma is one of the most common childhood solid tumors and is the most common tumor diagnosed in infants less than 1 year of age

Neoplasms that exhibit sharp peaks in incidence in children younger than 10 years of age include (1) leukemia (principally acute lymphoblastic leukemia); (2) neuroblastoma; (3) Wilms’ tumor; (4) hepatoblastoma; (5) retinoblastoma; (6) rhabdomyosarcoma; (7) teratoma; (8) Ewing sarcoma; and, finally, posterior fossa neoplasms–principally (9) juvenile astrocytoma, (10) medulloblastoma, and (11) ependymoma

Hemangiomas: (benign) are the most common tumors of infancy.

The risk of Wilms’ tumor is increased in association with at least three recognizable groups of congenital malformations exhibiting aberrations in at least two distinct chromosomal loci.
1.The first group of patients have the WAGR syndrome characterized by aniridia, genital anomalies, and mental retardation and have a 33% chance of developing Wilms’ tumor.
2.A second group of patients at risk for Wilms’ tumor have the Denys-Drash syndrome, which is characterized by gonadal dysgenesis (male pseudohermaphroditism) and nephropathy leading to renal failure. The majority of these patients develop Wilms’ tumors.
3.Clinically distinct from these previous two groups of patients but also having an increased risk of developing Wilms’ tumor are those children with Beckwith-Wiedemann syndrome, characterized by enlargement of body organs, hemihypertrophy, renal medullary cysts, and abnormal large cells in adrenal cortex (adrenal cytomegaly).

Which one the following variants of renal cell carcinoma has the worst prognosis –
)a) Papillary b) Tubuloalveolar
c) Chromophobe d) Sacromatoid

no idea

Renal cell neoplasia represents a heterogeneous group of tumors with
distinct histopathologic, genetic, and clinical features ranging from
benign to high-grade malignant (Table 90-3). They are classified on
the basis of morphology and histology. Categories include clear cell
carcinoma (60% of cases), papillary tumors (5–15%), chromophobic
tumors (5–10%), oncocytomas (5–10%), and collecting or Bellini
duct tumors (<1%). Papillary tumors tend to be bilateral and multifocal.
Chromophobic tumors have a more indolent clinical course, and
oncocytomas are considered benign neoplasms. In contrast, Bellini
duct carcinomas, which are thought to arise from the collecting ducts
within the renal medulla, are very rare but very aggressive. They tend
to affect younger patients.

The renal tumour which has multicentric origin –a)Wilm’s tumour(TN [snip])
b)Transitional cell carcinoma
c)Squamous cell carcinoma
d)Renal cell carcinoma


Related to the molecular genetic and corresponding heterogeneity of Wilms’ tumor is the recognition of a premalignant or precursor lesion in many of these cases– nephroblastomatosis. This term refers to multicentric or diffuse foci of immature nephrogenic elements within areas of otherwise non-neoplastic kidney parenchyma. [86] Recognition of this lesion is important because its presence implies a substantially increased risk of developing a Wilms’ tumor.
MORPHOLOGY.–Grossly, Wilms’ tumor tends to present as a large, solitary, well-circumscribed mass, although 10% are either bilateral or multicentric at the time of diagnosis. On cut section, the tumor is soft, homogeneous, and tan to gray with occasional foci of hemorrhage, cyst formation, and necrosis

In an adult Unilateral smooth contracted kidney with hypertension is seen in.-
a) Stenosis of renal artery
b) Chr. GN
c) Renal cell CA
d) Pyelonephritis

Ans. is ‘a’ i.e., Stenosis of renal artery [ Ref : Robbin’s Illustrated r/e p. 1009 & 63/4 p. [snip], 976]

The ischemic kidney is usually reduced in size and shows signs of diffuse ischemic atrophy, with crowded glomeruli, atrophic tubules, interstitial fibrosis, and focal inflammatory infiltrate. The arterioles in the ischemic kidney are usually protected from the effects of high pressure, thus showing only mild arteriolosclerosis, in contrast to the contralateral nonischemic kidney, which may exhibit hyaline arteriolosclerosis, depending on the severity of the preceding hypertension.

Crescents are derived from –
a)Epithelial cells + fibrin + macrophage
b)Mesangium + fibrin + macrophage
c)Tubule + mesangiaum + fibrin
d)Mesangiaum + fibrin

Ans. is ‘a’ i.e., Epithelium cells + fibrin + macrophage [Ref : Robbin’s Illustrated 7h/e p. 977 & 6e p.951]


Disease that recurs after transplantation of kidney is –
a) DM b) MPGN
c) SLE d) Mesangial

Ans. Two options are correct i.e., ‘a & b’ [Ref :Robbin’s Illustrated 7e p. 985, 984 & 6th/e p. 958, 959]”Diabetic lesions may recur in the renal allografts (r/e p. 992, 6e p. 968)”
“There is high incidence of recurrence in transplant patients in membranoproliferative glomerulonephritis,particularly in dense deposit disease”. —> (7″/e p. [snip], 6th/e p. 959)
“In focal segmental glomerulosderosis recurrences are seen in 25% to 50% of the patients receivingallograpts” r/e p. [snip], 6th/e p. 958

Disease that recurs after transplantation of kidney is –
a) DM b) MPGN
c) SLE d) Mesangial



While 1-year transplant survival is excellent, most recipients experience
progressive decline in kidney function over time thereafter. Chronic renal
transplant dysfunction can be caused by recurrent disease, hypertension,
cyclosporine or tacrolimus nephrotoxicity, chronic immunologic
rejection, secondary focal glomerulosclerosis, or a combination of these
. Chronic vascular changes with intimal proliferation
and medial hypertrophy are commonly found. Control of systemic and
intrarenal hypertension with ACE inhibitors is thought to have a beneficial
influence on the rate of progression of chronic renal transplant dysfunction.
Renal biopsy can distinguish subacute cellular rejection from
recurrent disease or secondary focal sclerosis.

All are true about minimal change GN except-

a)Selective proteinuria
b)IgG deposition in mesangium
c)Common in age group 2-9 years .
d)Responds to steroids

Ans. is ‘b’ i.e., IgG deposition in mesangium [ Ref : Robbin’s Illustrated 7h/e p. [snip]-[snip] & 6e p. 955]

In children, the abnormal urine principally contains albumin with minimal amounts of higher molecular weight proteins, and is sometimes called selective proteinuria.

Prednisone is first-line therapy, and other immunosuppressive
drugs, such as cyclophosphamide, chlorambucil, and mycophenolate
mofetil, are saved for frequent relapsers, steroid-dependent, or steroid resistant patients.

MCD, sometimes known as nil lesion, causes 70–90% of nephrotic
syndrome in childhood
but only 10–15% of nephrotic syndrome in
In reflux nephropathy, glomerular lesion is-
a) Focal G.N.
b) Membranous G.N.
c) Membrano proliferative G.N.
d) Minimal change disease

1014.Ans. is ‘a’ i.e., Focal G.N. [ Ref : Robbin’s Illustrated 7e p. 1000, 1001 & &6e p. 977]

1810 HARRISON 17TH ED…..Vesicoureteral Reflux (See also Chap. 283) When the function of the ureterovesical junction is impaired, urine may reflux into the ureters due to the high intravesical pressure that develops during voiding. Clinically, reflux is often detected on the voiding and postvoiding films obtained during intravenous pyelography, although voiding cystourethrography may be required for definitive diagnosis. Bladder infection may ascend the urinary tract to the kidneys through incompetent ureterovesical sphincters. Not surprisingly, therefore, reflux is often discovered in patients with acute and/or chronic urinary tract infections. With more severe degrees of reflux, characterized by dilatation of ureters and renal pelves, progressive renal damage often appears. Uncertainty exists as to the necessity of infection in producing the scarred kidney of reflux nephropathy.
Substantial proteinuria is often present, and glomerular lesions
similar to those of idiopathic focal glomerulosclerosis (Chap. 277)
are often found in addition to the changes of chronic tubulointerstitial
Surgical correction of reflux is usually necessary only with the
more severe degrees of reflux since renal damage correlates with the extent of reflux. Obviously, if extensive glomerulosclerosis already exists,
urologic repair may no longer be warranted
True about membranous GN are following except-
a)Thickening of B.M
b)Deposition between endothelium and B.M.
c)Most common cause of nephrotic syndrome in adults
d)Seen in SLE, tumors, drugs

Ans. is “b’ i.e., Deposition between endothelium and B.M. f Ref :Robbin’s illustrated 7Th/e p.[snip], [snip] & 6th/e p. 954]

Already discussed
In membranous glomerulopathy only subepithelial deposits seen.Not subendothelial.

Glomerulonephritis associated with AIDS is-

a) Focal segmental GN
d) Membranous GN

Ans. is ‘a’ i.e., Focal segmental GN [ Ref : Robbin’s Illustrated 7h/e p. [snip], [snip] & 6th/e p. 958,”Now collapsing glomerulopathy is the hall mark of AIDS”Harrison 15thle p. 1887]

Subepithelial deposits in kidney are seen in ALL EXCEPT-a)MPGN-1
b)GPS (good-pasture synd)
d)Membranous GN


There are no subepithelial deposits.

Crescents formed in bowmans space

Kidney disease with autosomal dominant inheritance
a) Juvenile nephrolithiasis
c) Medullary sponge kidney
d) Nephronopthisis

Ans. Two options are correct i.e., ‘b & c’ [ Ref : Robbin’s Illustrated 7h/e p. 962 & 6th/e p. 941]

Nephronophthisis (NPHP) is the most common genetic cause of ESRD in childhood and adolescence.Five distinct genetic mutations with autosomal recessive inheritance have been identified (Table 278-1 harrison 17th ed p.1799). Although their precise functions are unclear,
the defective protein products, named nephrocystins and inversin,
localize to the primary cilium and associated basal body of renal
epithelial cells, similar to the polycystins and fibrocystin.

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Surgery MCQs

Posted by Dr KAMAL DEEP on May 23, 2011


HTSs rise above the skin level but stay within the confines of the original wound and often regress over time. Keloids rise above the skin level as well, but extend beyond the border of the original wound and rarely regress spontaneously .Both HTSs and keloids occur after trauma to the skin, and may be tender, pruritic, and cause a burning sensation. Keloids are 15 times more common in darker-pigmented ethnicities, with individuals of African, Spanish, and Asian ethnicities being especially susceptible. Men and women are equally affected. Genetically, the predilection to keloid formation appears to be autosomal dominant, with incomplete penetration and variable expression

Keloids tend to occur 3 months to years after the initial insult, and even minor injuries can result in large lesions

HTSs usually develop within 4 weeks after trauma. The risk of HTSs increases if epithelialization takes longer than 21 days.

Keloids can result from surgery, burns, skin inflammation, acne, chickenpox, zoster, folliculitis, lacerations, abrasions, tattoos, vaccinations, injections, insect bites, ear piercing, or may arise spontaneously.even minor injuries can result in large lesions.Certain body sites have a higher incidence of keloid formation, including the skin of the earlobe as well as the deltoid, presternal, and upper back regions. They rarely occur on eyelids, genitalia, palms, soles, or across joints. Keloids rarely involute spontaneously, whereas surgical intervention can lead to recurrence, often with a worse result.Keloid scars tend to occur above the clavicles, on the trunk, on the upper extremities, and on the face

HTSs They usually occur across areas of tension and flexor surfaces, which tend to be at right angles to joints or skin creases.. A hypertrophic scar can occur anywhere on the body.



Opposite Views?

Sabiston :-Histologically, both HTSs and keloids demonstrate increased thickness of the epidermis with an absence of rete ridges. There is an abundance of collagen and glycoprotein deposition. Normal skin has distinct collagen bundles, mostly parallel to the epithelial surface, with random connections between bundles by fine fibrillar strands of collagen. In HTSs, the collagen bundles are flatter, more random, and the fibers are in a wavy pattern. In keloids, the collagen bundles are virtually nonexistent, and the fibers are connected haphazardly in loose sheets with a random orientation to the epithelium. The collagen fibers are larger and thicker and myofibroblasts are generally absent.

After secretion into the ECM, specific proteases cleave the propeptides of the procollagen molecules to form collagen monomers. These monomers assemble to form collagen fibrils in the ECM, driven by collagen’s tendency to self-assemble. Covalent cross-linking of the lysine residues provides tensile strength. The extent and type of cross-linking vary from tissue to tissue. In tissues such as tendons, where tensile strength is crucial, collagen cross-linking is extremely high. In mammalian skin, the fibrils are organized in a basket-weave pattern to resist multidirectional tensile stress. In tendons, on the other hand, fibrils are in parallel bundles aligned along the major axis of tension

Schwartz :-Keloids and hypertrophic scars have stretched collagen bundles aligned in the same plane as the epidermis, as opposed to normal scar tissue, where the collagen bundles are randomly arrayed and relaxed. In addition, keloid scars have thicker, more abundant collagen bundles that form acellular nodelike structures in the deep dermal portion of the keloid lesion. The center of keloid lesions also contains a paucity of cells in comparison to hypertrophic scars, which have islands composed of aggregates of fibroblasts, small vessels, and collagen fibers throughout the dermis.



Keloid scars is made up of –
a) Dense collagen b) Loose fibrous tissue
c Granulamatous tissue d) Loose areolar tissue

What is true about keloids – (JIPMER 95)
a)It appears immediately after surgery
b)It appears a few days after surgery
c)It is limited in its distribution (grows beyond the limits of the original wound)
d) it is common in old people

Keloid is best treated by – (UPSC 95)
a)Intrakeloidal injection of triamcinolone
b)Wide excision and grafting
c)Wide excision and suturing
d)Deep X-ray therapy

The following statement about keloid is true- A) They do not extend in normal skin   (extreme overgrowth of scar tissue that grows beyond the limits of the original wound)

b)Local recurrence is common after excision

c) They often undergo malignant change

d) They are more common in whites than in blacks


The best cure rate in keloids is achieved by –
a)Superficial X – ray therapy (UPSC 2001)
b)Intralesional injection of triamcinolone
d)Excision and radiotherapy

Combination is always better.

Surgery:-Excision alone of keloids is subject to a high recurrence rate, ranging from 45 to 100%. There are fewer recurrences when surgical excision is combined with other modalities such as intralesional corticosteroid injection, topical application of silicone sheets, or the use of radiation or pressure

Radiation:-Poor results with 10 to 100% recurrence when used alone. It is more effective when combined with surgical excision. Given the risks of hyperpigmentation, pruritus, erythema, paresthesias, pain, and possible secondary malignancies, radiation should be reserved for adults with scars resistant to other modalities.

Combination therapies:- Intralesional corticosteroid injections decrease fibroblast proliferation, collagen and glycosaminoglycan synthesis, the inflammatory process, and TGF levels. When used alone, however, there is a variable rate of response and recurrence, therefore steroids are recommended as first-line treatment for keloids and second-line treatment for HTSs if topical therapies have failed. Intralesional injections are more effective on younger scars. They may soften, flatten, and give symptomatic relief to keloids, but they cannot make the lesions disappear nor can they narrow wide HTSs. Success is enhanced when used in combination with surgical excision. Serial injections every 2 to 3 weeks are required.

Sabiston:- Intralesional injection of steroids into a keloid scar can inactivate and shrink the scar; such therapy is not indicated for hypertrophic scars.

Scars that are perpendicular to the underlying muscle fibers tend to be flatter and narrower, with less collagen formation than when they are parallel to the underlying muscle fibers. The position of an elective scar can be chosen in such a way to make a narrower and less obvious scar in the distant future. As muscle fibers contract, the wound edges become reapproximated if they are perpendicular to the underlying muscle. If, however, the scar is parallel to the underlying muscle, contraction of that muscle tends to cause gaping of the wound edges and leads to more tension and scar formation.



Primary closure of incised wounds must be done in –
a) 2 hrs b) 4 hrs
c) 6 hrs d) 12 hrs
e) 16 hrs

(Because of the fear of bacterial invasion, primary wound closure beyond 6 to 8 hours after injury was historically proscribed. However, several scientific studies have since shown that when blood supply to a wound is adequate and bacterial invasion is absent, wounds can be safely closed at any time after proper débridement and irrigation)

The tensile strength of wound reaches that of normal tissue by – (PGI 88)
) 6 weeks
c) 4 months
b) 2 months
d) 6 months


In the healing of a clean wound the maximum immediate strength of the wound is reached by –
a) 2 – 3 days b) 4 – 7 days
10 – 12 days d) 13 – 18 days

21 days is ans

The tensile strength of the wound starts and increases after – (MAHE 05)
a)Immediate suture of the wound
b)3 to 4 days
c)7-10 days
d 6 months

see figure

When is the maximum collagen content of wound
tissue – (PGI 81, ROHTAK 87)
a)Between 3rd to 5th day
b)Between 6th to 17th day
C) Between 17th to 21st day d) None of the above

In a sutured surgical wound, the process of epithelialization is completed within – (UPSC 07)
a) 24 hours b) 48 hours
c) 72 hours d) 96 hours

Ref schwartz Epithelialization:- While tissue integrity and strength are being re-established, the external barrier must also be restored. This process is characterized primarily by proliferation and migration of epithelial cells adjacent to the wound The process begins within 1 day of injury and is seen as thickening of the epidermis at the wound edge.Re-epithelialization is complete in less than 48 hours in the case of approximated incised wounds, but may take substantially longer in the case of larger wounds, in which there is a significant epidermal/dermal defect.

Sabiston : – Finally, adequate dressing of the closed wound isolates it from the outside environment. Providing an appropriate dressing for 48 to 72 hours can decrease wound contamination. However, dressings after this period increase the subsequent bacterial count on adjacent skin by altering the microenvironment underneath the dressing.

Following are required for wound healing except – a) Zinc
b) Copper c) Vitamin C d) Calcium

Copper is also a component of ferroprotein, a transport protein involved in the basolateral transfer of iron during absorption from the enterocyte. As such, copper plays a role in iron metabolism, melanin synthesis, energy production, neurotransmitter synthesis, and CNS function; the synthesis and cross-linking of elastin and collagen :- Harrison

Copper Deficiency:- Anemia, growth retardation, defective keratinization and pigmentation of hair, hypothermia, degenerative changes in aortic elastin, osteopenia, mental deterioration.

Patient has lacerated untidy wound of the leg and attended the casualty after 2 ‘hours. His wound (AIIMS 84)should be –
a) Sutured immediately  b) Debrided and sutured immediately  c) debrided and sutured secondarily d) Cleaned and dressed

Wound healing is worst at –
(ALL INDIA 93) a) Sternum b) Anterior neck
c) Eyelid d) Lips

After closing deep tissues and replacing significant tissue deficits, skin edges should be reapproximated for cosmesis and to aid in rapid wound healing. Skin edges may be quickly reapproximated with stainless steel staples or nonabsorbable monofilament sutures. Care must be taken to remove these from the wound before epithelialization of the skin tracts where sutures or staples penetrate the dermal layer. Failure to remove the sutures or staples by 7 to 10 days after repair will result in a cosmetically inferior wound

(Anatomic areas where tension is excessive are avoided if possible. The shoulders, back, and anterior chest are high tension and mobile areas where wide scarring is difficult to avoid. Patients are also questioned as to propensity for development of hypertrophic scars or keloid formation. Ears, anterior chest, and shoulders are areas prone to these problematic scars)

Sabiston :-Wound strength increases rapidly within 1 to 6 weeks and then appears to plateau up to 1 year after the injury .When compared with unwounded skin, tensile strength is only 30% in the scar. An increase in breaking strength occurs after approximately 21 days, mostly as a result of cross-linking.The rate of collagen synthesis declines after 4 weeks and eventually balances the rate of collagen destruction by collagenase (MMP-1). At this point the wound enters a phase of collagen maturation.

Taylor:-The tensile strength of the young scar is only about 10% that of normal skin. Scar strength increases to about 30–50% of normal skin by 4 weeks and to 80% after several months.

Robbins:-We now turn to the questions of how long it takes for a skin wound to achieve its maximal strength, and which substances contribute to this strength. When sutures are removed, usually at the end of the first week, wound strength is approximately 10% of the strength of unwounded skin, but it increases rapidly over the next 4 weeks. This rate of increase then slows at approximately the third month after the original incision and then reaches a plateau at about 70 to 80% of the tensile strength of unwounded skin, which may persist for life.

Schwartz:-Wound strength and mechanical integrity in the fresh wound are determined by both the quantity and quality of the newly deposited collagen. The deposition of matrix at the wound site follows a characteristic pattern: Fibronectin and collagen type III constitute the early matrix scaffolding, glycosaminoglycans and proteoglycans represent the next significant matrix components, and collagen type I is the final matrix. By several weeks postinjury the amount of collagen in the wound reaches a plateau, but the tensile strength continues to increase for several more months.20 Fibril formation and fibril cross-linking result in decreased collagen solubility, increased strength, and increased resistance to enzymatic degradation of the collagen matrix. Scar remodeling continues for many (6 to 12) months postinjury, gradually resulting in a mature, avascular, and acellular scar. The mechanical strength of the scar never achieves that of the uninjured tissue.



Factors That Inhibit Wound Healing





Local tension

Diabetes mellitus

Ionizing radiation

Advanced age


Vitamin deficiencies:- Vitamin C Vitamin A

Mineral deficiencies:-Zinc Iron

Exogenous drugs:-Doxorubicin (Adriamycin) Glucocorticosteroids

suture marks are to be avoided, skin sutures should be removed by -  a) hours b) 1 week
2 weeks d) 3 weeks

Epidermal skin sutures function for fine alignment of skin edges. Interrupted sutures are less constrictive than running sutures. The needle enters and exits the skin at 90 degrees in order to evert the skin edges. These skin sutures are removed as soon as adequate intrinsic bonding strength is sufficient. Skin sutures left in place too long result in an unsightly track pattern. On the other hand, sutures removed prematurely risk wound dehiscence. Nonabsorbable sutures on the face are typically removed after 5 days. Sutures in the hand, foot, or across areas that are acted on by motion are left for 14 days or longer .Alternatively, by employing the running intradermal suturing technique, the time constraints of suture removal may be disregarded, and these sutures may be left in place for a longer time without risking a track pattern scar. Finally, epidermal approximation can be achieved without suture using a medical-grade cyanoacrylate adhesive such as Dermabond. Such adhesives are applied across the coapted skin edges only and contribute no tensile strength. Tape closure strips such as Steri-Strips can be applied at the completion of wound closure to help splint the coapted skin edges.

 Guidelines for Day of Suture Removal by Area
Scalp 6-8
Ear 10-14
Eyelid 3-4
Eyebrow 3-5
Nose 3-5
Lip 3-4
Face (other) 3-4
Chest, abdomen 8-10
Back 12-14
Extremities 12-14
Hand 10-14
Foot, sole 12-14

A patient with grossly contaminated wound presents 12 hours after an accident. His wound should be managed by – (UPSC 96)
a)Thorough cleaning and primary repair
b)Thorough cleaning with debridement of all dead and devitalised tissue without primary closure
c)Primary closure over a drain
d)Covering the defect with split skin graft after cleaning

Management of an open wound seen 12 hrs. after
the injury – (AIIMS 87)
b)Debridement and suture
c)Secondary suturing
d)Heal by granulation

Delayed wound healing is seen in all except-(AP 96)
a) Malignancy b) Hypertension
c) Diabetes d) Infection

All of the following favour postoperative wound dehiscence except – (Karnat 05)
b)Vitamin B complex deficiency

Fibroblast in healing wound derived from –
a) Local mesenchyme b) Epithelium (PGI 98)
c) Endothelial d) Vascular fibrosis

(Sabiston) Fibroplasia:- Fibroblasts are specialized cells that differentiate from resting mesenchymal cells in connective tissue; they do not arrive in the wound cleft by diapedesis from circulating cells. After injury, the normally quiescent and sparse fibroblasts are chemoattracted to the inflammatory site, where they divide and produce the components of the ECM.The primary function of fibroblasts is to synthesize collagen, which they begin to produce during the cellular phase of inflammation. The time required for undifferentiated mesenchymal cells to differentiate into highly specialized fibroblasts accounts for the delay between injury and the appearance of collagen in a healing wound. This period, generally 3 to 5 days, depending on the type of tissue injured, is called the lag phase of wound healing.The rate of collagen synthesis declines after 4 weeks and eventually balances the rate of collagen destruction by collagenase (MMP-1). At this point the wound enters a phase of collagen maturation. The maturation phase continues for months or even years. Glycoprotein and mucopolysaccharide levels decrease during the maturation phase, and new capillaries regress and disappear. These changes alter the appearance of the wound and increase its strength.

Degloving injury is – (KERALA 2K)
a) Surgeon made wound b) Lacerated wound
c) Blunt injury d) Avulsion injury
e)Abrasive wound

Avulsion injuries are open injuries where there has been a severe degree of tissue damage. Such injuries occur when hands or limbs are trapped in moving machinery, such as in rollers, producing a degloving injury. Degloving is caused by shearing forces that separate tissue planes, rupturing their vascular interconnections and causing tissue ischaemia. This most frequently occurs between the subcutaneous fat and deep fascia. Degloving injuries can be open or closed. Degloving can be localised or circumferential. It can occur only in the single, subcutaneous plane, but where present in multiple planes, such as between muscles and fascia and between muscles and bone, is an indication of a severe high-energy injury with a limited potential for primary healing. Similar injuries occur as a result of runover road traffic accident injuries where friction from rubber tyres will avulse skin and subcutaneous tissue from the underlying deep fascia (Fig. 3.11). The history should raise the examiner’s suspicion and it is often possible to pinch the skin and lift it upwards revealing its detachment from the normal anchorage. The danger of degloving or avulsion injuries is that there is devascularisation of tissue and skin necrosis may become slowly apparent in the following few days. Even tissue that initially demonstrates venous bleeding may subsequently undergo necrosis if the circulation is insufficient. Treatment of such injuries is to identify the area of devitalised skin and to remove the skin, defat it and reapply it as a full-thickness skin graft. Avulsion injuries of hands or feet may require immediate flap cover using a one-stage microvascular tissue transfer of skin and/or muscle.

In treatment of hand injuries, the greatest priority is – (A1 96)
a)Repair of tendons
b)Restoration of skin cover
c)Repair of nerves
d) Repair of blood vessels

During the surgical procedure – (AIIMS 83)
a)Tendons should be repaired before nerves
b)Nerves should be repaired before tendons
c)Tendons should not be repaired at the same time
d)None is true

In hand injuries first to be repaired is – (A195)
a) Bone b) Tendon
c) Muscle d) Nerve

In the case of injuries, treatment is directed at the specific structures damaged: skeletal, tendon, nerve, vessel, and integument. In emergency situations, the goals of treatment are to maintain or restore distal circulation, obtain a healed wound, preserve motion, and retain distal sensation. Stable skeletal architecture is established in the primary phase of care because skeletal stability is essential for effective motion and function of the extremity. This also results in reestablishing skeletal length, straightening deformities, and correction of compression or kinking of nerves and vessels. Arteries are also repaired in the acute phase of treatment to maintain distal tissue viability. Additionally, extrinsic compression on arteries must be released emergently such as in compartment pressure problems. In clean-cut injuries, tendons can be repaired primarily. In situations in which there is a chance that tendon adhesions may form, such as when there are associated fractures, it is nonetheless better to repair tendons primarily with preservation of their length and if necessary at a later date to perform tenolysis. However, when there are open and contaminated wounds or a severe crushing injury, it is best to delay repair of both tendon and nerve injuries

Prevention of wound infection done by –
a)Pre-op shaving (PGI  05)
b)Pre-op antibiotic therapy
c)Monofilament sutures
d)Wound apposition

SSIs are the most common nosocomial infection in our population and constitute 38% of all infections in surgical patients. By definition, they can occur anytime from 0 to 30 days after the operation or up to 1 year after a procedure that has involved the implantation of a foreign material (mesh, vascular graft, prosthetic joint, and so on). Incisional infections are the most common; they account for 60% to 80% of all SSIs and have a better prognosis than organ/space-related SSIs do, with the latter accounting for 93% of SSI-related mortalities.

Preoperative shaving has been shown to increase the incidence of SSI after clean procedures as well. This practice increases the infection rate about 100% as compared with removing the hair by clippers at the time of the procedure or not removing it at all, probably secondary to bacterial growth in microscopic cuts. Therefore, the patient is not shaved before an operation. Extensive removal of hair is not needed, and any hair removal that is done is performed by electric clippers with disposable heads at the time of the procedure and in a manner that does not traumatize the skin

1.Basic principles include size of the OR, air management (filtered flow, positive pressure toward the outside, and air cycles per hour), equipment handling (disinfection and cleansing), and traffic rules. All OR personnel wear clean scrubs, caps, and masks, and traffic in and out of the OR is minimized.

2.The CDC recommends the use of chlorhexidine showers, and it is reasonable to implement such a policy, particularly in patients who have been in the hospital for a few days and in those in whom an SSI will cause significant morbidity (cardiac, vascular, and prosthetic procedures). Skin preparation of the surgical site is done with a germicidal antiseptic such as tincture of iodine, povidone-iodine, or chlorhexidine. An alternative preparation is the use of antimicrobial incise drapes applied to the entire operative area. Traditionally, the surgical team has scrubbed their hands and forearms for at least 5 minutes the first time in the day and for 3 minutes every consecutive time.

3.As many as 90% of an operative team puncture their gloves during a prolonged operation. The risk increases with time, as does the risk for contamination of the surgical site if the glove is not changed at the moment of puncture. The use of double gloving is becoming a popular practice to avoid contamination of the wound, as well as exposure to blood by the surgical team. Double gloving is recommended for all surgical procedures.Instruments that will be in contact with the surgical site are sterilized in standard fashion, and protocols for flash sterilization or emergency sterilization, or both, must be well established to ensure the sterility of instruments and implants.

Local Wound Related:-Intraoperative measures include appropriate handling of tissue and assurance of satisfactory final vascular supply, but with adequate control of bleeding to prevent hematomas/seromas. Complete débridement of necrotic tissue plus removal of unnecessary foreign bodies is recommended, as well as avoiding the placement of foreign bodies in clean-contaminated, contaminated, or dirty cases. Monofilament sutures have proved in experimental studies to be associated with a lower rate of SSI. Sutures are foreign bodies that are used only when required. Suture closure of dead space has not been shown to prevent SSI. Large potential dead spaces can be treated with the use of closed-suction systems for short periods, but these systems provide a route for bacteria to reach the wounds and may cause SSI. Open drainage systems (e.g., Penrose) increase rather than decrease infections in surgical wounds and are avoided unless used to drain wounds that are already infected.

In heavily contaminated wounds or wounds in which all the foreign bodies or devitalized tissue cannot be satisfactorily removed, delayed primary closure minimizes the development of serious infection in most instances. With this technique, the subcutaneous tissue and skin are left open and dressed loosely with gauze after fascial closure. The number of phagocytic cells at the wound edges progressively increases to a peak about 5 days after the injury. Capillary budding is intense at this time, and closure can usually be accomplished successfully even with heavy bacterial contamination because phagocytic cells can be delivered to the site in large numbers. Experiments have shown that the number of organisms required to initiate an infection in a surgical incision progressively increases as the interval of healing increases, up to the fifth postoperative day.

Finally, adequate dressing of the closed wound isolates it from the outside environment. Providing an appropriate dressing for 48 to 72 hours can decrease wound contamination. However, dressings after this period increase the subsequent bacterial count on adjacent skin by altering the microenvironment underneath the dressing.

Elective cholecystectomy is – (APPG 06)
a) Clean contaminated b) Clean
Dirty d) Contaminated

Which one of the following surgical procedures is considered to have a clean-contaminated wound ?

a),Elective open cholecystectomy for cholelithiasis
b)Hemiorrhaphy with mesh repair
c)Lumpectomy with axillary node dissection
d)Appendectomy with walled off abscess

The accepted range of infection rates has been 1% to 5% for clean, 3% to 11% for clean-contaminated, 10% to 17% for contaminated, and greater than 27% for dirty wounds.

Table 14-2 Surgical Wound Classification According to Degree of Contamination
Clean An uninfected operative wound in which no inflammation is encountered and the respiratory, alimentary, genital, or infected urinary tract is not entered. Wounds are closed primarily and, if necessary, drained with closed drainage. Surgical wounds after blunt trauma should be included in this category if they meet the criteria
Clean-contaminated An operative wound in which the respiratory, alimentary, genital, or urinary tract is entered under controlled conditions and without unusual contamination
Contaminated Open, fresh, accidental wounds. In addition, operations with major breaks in sterile technique or gross spillage from the gastrointestinal tract and incisions in which acute, nonpurulent inflammation is encountered are included in this category
Dirty Old traumatic wounds with retained devitalized tissue and those that involve existing clinical infection or perforated viscera. This definition suggests that the organisms causing postoperative infection were present in the operative field before the operation

Staphylococcus aureus remains the most common pathogen in SSIs, followed by coagulase-negative staphylococci, enterococci, and Escherichia coli. However, for clean-contaminated and contaminated procedures, E. coli and other Enterobacteriaceae are the most common cause of SSI.


The Vitamin which has inhibitory effect on wound healing is – (MAHE 05)
a) Vitamin-A b) Vitamin-E
c) Vitamin-C d) Vitamin B-complex

Golden period for treatment of open wounds is
….hours – (AIIMS 86, 88)
a) 4 b) 6
c) 12 d) 24

In the first 4 hours after a breach in an epithelial surface and underlying connective tissues made during surgery or trauma, there is a delay before host defences can become mobilised through acute inflammatory, humoral and cellular processes. This period is called the ‘decisive period’ and it is during these first 4 hours after incision that bacterial colonisation and established infection can begin. It is logical that prophylactic antibiotics will be most effective during this time.

Abbey-Estlander flap is used in the reconstruction
of- (AI 05)
a) Buccal mucosa b) Lip
c) Tongue d) Palate

In defects of less than one third the horizontal length, enough redundancy is present to allow primary closure. More complex decisions must be made for defects that are between one third and two thirds of the total lip length. The two categories of lip flap technique are transoral cross-lip flaps and circumoral advancements flaps. Cross-lip flaps include the Abbé flap and the Estlander flap. The Abbé flap was originally designed to reconstruct central upper lip (tubercle) defects with lower lip full-thickness tissue vascularized by one of the labial arteries.The technique requires a second-stage procedure for division of the pedicle. The Estlander flap is similar in principle but is based laterally at the oral commissure and is used to reconstruct lateral upper or lower lip lesions. Both the Estlander and Abbé flaps are denervated, but sensation and perhaps even motor function return over months.The Karapandzic technique is an advancement-rotation flap technique designed for central lower lip defects. Although good function, sensation, and mobility are preserved, a side effect is reduction in the size of the oral aperture. The Webster-Bernard technique uses cheek tissue advancement flaps to replace defects with full-thickness or partial-thickness cheek incisions extended laterally from the commissure (Fig. 45-34). When performed bilaterally, both the Karapandzic and the Webster-Bernard methods can be used to reconstruct a complete upper or lower lip.



Abbé flap upper lip reconstruction. A. Defect and flap design.                     B. Rotation of the flap and primary closure of the donor site.                                     C. Division of the pedicle (after 2 to 3 weeks) and final insetting.

Cock’s peculiar tumour is-(UPSC 86,NIMHANS 87,
a)Papilloma Kerala 87, TN 90 )
b)Infected sebaceous cyst
d)Sqaumous cell carcinoma (RESEMBLES SCC but it’s not SCC)


Epidermoid cyst(syn. sebaceous cyst, wen)
These cysts contain keratin and its breakdown products, surrounded by a wall of stratified squamous keratinising epithelium (the commonly used term sebaceous cyst is incorrect — these cysts only rarely have associated sebaceous glands and do not contain sebum). Epidermoid cysts often have a punctum. They are inherited in an autosomal dominant fashion. The common sites are the face, neck, shoulders and chest, areas favoured by acne vulgaris. Lesions may be solitary but are commonly multiple. They enlarge slowly and may become inflamed and tender from time to time. Suppuration may occur. The contents of an infected cyst become semiliquid and usually very foetid. Recurrent infective episodes cause the cyst wall to become adherent to surrounding subcutaneous tissue, and consequently more difficult to remove. If ulceration occurs it can resemble squamous cell carcinoma to which the term ‘Cock’s peculiar tumour’ may be applied .The contents of a cyst sometimes escape slowly from the duct orifice and dry in successive layers on the skin, forming a ‘sebaceous horn’.Treatment is by surgical excision (except if inflamed, when it is better incised and drained). This can be performed under local anaesthesia; an ellipse of skin including the punctum is removed with the cyst. Unless the wall is completely removed, recurrence is likely.

Cause of persistance of a sinus or fistulae includes-
a)Foreign body (JIPMER 86)
b)Non dependentt drainage
c)Unrelieved Obstruction
d)Presence of malignancy
e)All of the above


Sinuses and fistulas
A sinus is a blind track (usually lined with granulation tissue) leading from an epithelial surface into the surrounding tissues. Pathological sinuses must be distinguished from normal anatomical sinuses (e.g. the frontal and nasal sinuses). A fistula  is an abnormal communication between the lumen or surface of one organ and the lumen or surface of another, or between vessels. Most fistulas connect epithelial­lined surfaces .Sinuses and fistulas may be congenital or acquired. Forms which have a congenital origin include preauricular sinuses, branchial fistulas , tracheo-oesophageal fistulas  and arteriovenous fistulas.The acquired forms often follow inadequate drainage of an abscess. Thus, a perianal abscess may burst on the surface and lead to a sinus (erroneously termed a blind external ‘fistula’). In other cases, the abscess opens both into the anal canal and on to the surface of the perineal stem resulting in a true fistula-in-ano .Acquired arteriovenous fistulas are caused by trauma or operation (for renal dialysis).
  Persistence of a sinus or fistula
  The reason for this will be found among the following:
•  a foreign body or necrotic tissue is present, e.g. a suture, hairs, a sequestrum, a faecolith or even a worm (see below);
•  inefficient or nondependent drainage: long, narrow, tortuous track predisposes to inefficient drainage;
•  unrelieved obstruction of the lumen of a viscus or tube distal to the fistula;
•  high pressure, such as occurs in fistula-in-ano due to the normal contractions of the sphincter which force faecal material through the fistula;
•  the walls have become lined with epithelium or endothelium (arteriovenous fistula);
•  dense fibrosis prevents contraction and healing;
•  type of infection, e.g. tuberculosis or actinomycosis;
•  the presence of malignant disease
•  ischaemia;
•  drugs, e.g. steroids, cytotoxics;
•  malnutrition;
•  interference, e.g. artefacta;
•  irradiation, e.g. rectovaginal fistula after treatment for a carcinoma of the cervix;
•  Crohn’s disease;
• high-output fistula, e.g. duodenocutaneous fistula.

Premalignant conditions of the skin include –
a)Bowen disease (JIPMER 86)
b)Pagel’s disease of nipple
d)Solar keratosis
e)All of the above

Premalignant lesions :-Actinic keratoses
Bowen’s disease
Erythroplasia of Querat
Chronic scars(A carcinoma which develops in a scar (Marjolin’s ulcer) )
Sebaceous epidermal naevus


Melanoma should be excised with a margin of –
a) 2 cm b) 5 cm (UPSC 88)
c) 7 cm d) 10 cm



Harrison also recommends same treatment for Melanoma as described in above figure.

Hidradenitis suppurativa. is found to occur in – (JIPMER 86, AIMS 87)
a) Axilla b) Circumanal
c) Scalp d) Groin

Hidradenitis suppurativa. :- This is a chronic infection of apocrine glands around the anal margin giving rise to numerous sinuses. The mons pubis and groin can also be affected. After excision of the area, granulation and healing ate accelerated by using Silastic foam dressing (Hughes).

The term universal tumour refers to – (PGI 88)
a) Adenoma b) Papilloma
c) Fibroma d) Lipoma

A lipoma is a slowly growing tumour composed of fat cells adult type. Lipomas may be encapsulated or diffuse. It occur anywhere in the body where fat is found and earn tl titles of the ‘universal tumour’ or the ‘ubiquitous tumour The head and neck area, abdominal wall and thighs are particularly favoured sites.

Hydrocele is a type of ….cyst – (PGI 88)
a) Retention b) Distension
c) Exudation d) Traumatic

Acquired cysts
Retention cysts are due to the accumulated secretion of a gland behind an obstruction of a duct. Examples are seen in the pancreas, the parotid, the breast, the epididymis and Bartholin’s gland. A sebaceous cyst starts with the obstruction of a sebaceous gland, but this is followed by the down-growth and the accumulation of desquamated epidermal cells, thus turning it into an epidermoid cyst. In the epididymis, if the retention cyst contains sperms, it is known as a ‘spermatocele’.

Distension cysts occur in the thyroid from dilatation of the acini, or in the ovary from a follicle. Lymphatic cysts and cystic hygromas are distension cysts.

Exudation cysts occur when fluid exudes into an anatomical space already lined by endothelium, e.g. hydrocele, a bursa, or when a collection of exudate becomes encrusted.

Cystic tumours. Examples are cystic teratomas (dermoid cyst of the ovary) and cystadenomas (pseudomucinous and serous cystadenoma of the ovary).
Ganglia. Implantation dermoids arise from squamous epithelium which has been driven beneath the skin by a penetrating wound. They are classically found in the fingers of women who sew assiduously and metal workers.


Sebaceous cyst does not occur in the …. – (PGI 88)
a) Scalp b) Scrotum
c) Back d) Sole

Sebaceous cysts are common in the scrotal skin. They are usually small and multiple.

Fordyce spots are – (All India 95)
a)Ectopic sebaceous glands
b)Ectopic eccrine
c)Ectopic apocrine
d)Ectopic mucossal glands

Broke’s tumor is a tumor of–
a)Superficial dermal vesels
b)Sweat glands
c)Hair follicles
d)Sebaceous glands


Commonest site for rodent ulcer is – (PGI 88)
a) Inner canthus b) Outer canthus
c) Angle of mouth d) Cheek

Squamous cell carcinoma can arise from-(PGi88)
a)Long standing venous ulcers
b)chronic lupus vulgaris
c)Rodent ulcer
d)All of the above

There is a strong correlation with damage to the skin by the sun , and can be experimentally produced by ultraviolet light. Occa­sionally it arises as a complication of long-standing chronic granulomas, such as syphilis, lupus vulgaris and leprosy, chronic ulcers, osteomyelitis, Hydradenitis suppurativa, long-standing venous ulcers or old burn scars

The best results in treatment of capillary nevus have been achieved by – (AIIMS 84)
a)Full thickness skin graft
d)Argon laser treatment

Capillary malformation, usually referred to as a port-wine stain or nevus flammeus, is the most common type of vascular malformation

Vascular malformations:-These are structural and morphological anomalies due to faulty embryological morphogenesis. The lesions are present at birth, grow commensurate with the child and do nor regress. They can lead to underlying soft tissue or bony hypertrophy, nodular development and discoloration as a consequence of blood vessel ectasia with age. The natural history of these lesions is determined by their haemodynamic and Iymphodynamic characteristics.
• High-flow lesions include arterial malformations and arteriovenous malformations (arterial plexiform angiomas, cirsoid aneurysm).
• Low-flow lesions include lymphatic (LM) venous (VM) and capillary (CM — port-wine stain). Frequently these lesions combine arterial, venous and lymphatic elements.
Port-wine stains:-Port-wine stains are intradermal capillary mal­formations that change very little throughout life, although the colour may alter a little and they may become nodular in some areas. Treatment is for reason of appearance. Treatment of choice for these lesions is the use of the pulsed tunable dye laser.

Eleven month old child presents with erythematous lesion with central clearing which has been decreasing in size – (Al 97)
a)Strawberry angioma
c)Portwine stain
d)Cavernous haemangioma

Malignant melanoma most often develops from –
a)Hairy naevus (SGPGI 05)
b)Junctional naevus
c)Intradermal naevus
d)Blue naevus


The aim of differential diagnosis is to distinguish benign pigmented lesions from melanoma and its precursor. If melanoma is a consideration, then biopsy is appropriate. Some benign look-alikes may be removed in the process of trying to detect authentic melanoma. Table 83-5 summarizes the distinguishing features of benign lesions that may be confused with melanoma.


Full thickness skin graft can be taken from the following sites except – (AIIMS 87)
a) Elbow b) Back to neck
c) Supraclavicular area d) Upper eyelids

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Anatomy Thorax

Posted by Dr KAMAL DEEP on May 17, 2011


The horizontal plane passing through the disc that separates thoracic vertebrae TIV and TV is one of the most significant planes in the body (Fig. 3.10) because it:

  • passes through the sternal angle anteriorly, marking the position of the anterior articulation of the costal cartilage of rib II with the sternum. The sternal angle is used to find the position of rib II as a reference for counting ribs (because of the overlying clavicle, rib I is not palpable);
  • separates the superior mediastinum from the inferior mediastinum and marks the position of the superior limit of the pericardium;
  • marks where the arch of the aorta begins and ends;
  • passes through the site where the superior vena cava penetrates the pericardium to enter the heart;
  • is the level at which the trachea bifurcates into right and left main bronchi;
  • marks the superior limit of the pulmonary trunk.


The major structures found in the superior mediastinum include:

  • thymus,
  • right and left brachiocephalic veins,
  • left superior intercostal vein,
  • superior vena cava,
  • arch of the aorta with its three large branches,
  • trachea,
  • esophagus,
  • phrenic nerves,
  • vagus nerves,
  • left recurrent laryngeal branch of the left vagus nerve, (not right one as left vagus goes very low down to present in sup aperture giving rec branch there)
  • thoracic duct, and
  • other small nerves, blood vessels, and lymphatics





The commonest variation in the arteries arising from the arch of aorta is:
A.Absence of brachiocephalic trunk
B.Left vertebral artery arising from the arch
C.Left common carotid artery arising from brachio cephalic trunk
D.Presence of retroesophageal subclavian artery

Branches Three branches arise from the convex aspect of the arch: the brachiocephalic trunk, left common carotid and left subclavian arteries (Figs 31.15, 60.6). They may branch from the beginning of the arch or the upper part of the ascending aorta. The distance between these origins varies, the most frequent being approximation of the left common carotid artery to the brachiocephalic trunk.

Primary branches from the aortic arch may be reduced to one, but more commonly two. The left common carotid may arise from the brachiocephalic trunk (7%). More rarely, the left common carotid and subclavian arteries may arise from a left brachiocephalic trunk, or the right common carotid and right subclavian may arise separately, in which case the latter more often branches from the left end of the arch and passes behind the oesophagus. The left vertebral artery may arise between the left common carotid and the subclavian arteries. Very rarely, external and internal carotid arteries arise separately, the common carotid being absent on one or both sides, or both carotids and one or both vertebral arteries may be separate branches. When a ‘right aorta’ occurs, the arrangement of its three branches is reversed. The common carotids may have a single trunk. Other arteries may branch from it, most commonly one or both bronchial arteries and the thyroid ima artery.

An analysis of variation in branches from 1000 aortic arches showed the usual pattern in 65%; a left common carotid shared the brachiocephalic trunk in 27% (contrast percentage quoted above) and the four large arteries branched separately in 2.5%. The remaining 5% showed a great variety of patterns, the most common (1.2%) being symmetric right and left brachiocephalic trunks




Figure 59.5 Transverse section of thorax through the middle of the fourth thoracic vertebra and aortic arch; obtained by computed tomography.


Transverse section of thorax at the level of the lower border of the fourth thoracic vertebra, just at the level of the tracheal bifurcation; obtained by computed tomography.


Transverse section of thorax at the upper border of the sixth thoracic vertebra, below the carina at the level of the pulmonary trunk and the right main pulmonary artery; obtained by computed tomography


Transverse section of thorax through the lower portion of the seventh thoracic vertebra, passing through the aortic root; obtained by computed tomography

The structure found in a cross-section of the thorax at
T4 vertebra is :
A.Azygos vein
B.Brachiocephalic artery
C.Arch of the aorta
D.Left Subclavian artery

Azygous vein also present at T4 level but more accurate answer is arch of aorta. As azygous is at lower level of T4.

The hilum of the right lung is arched by
A.Recurrent laryngeal nerve
B.Azygos vein
C.Thoracic duct
D.Vagus nerve

Bochdalek hernia occurs in
A.Anterolateral part of diaphragm
B.Posterolateral part of diaphragm
C.Retrosternal area
D.Posterior to diaphragm


A diaphragmatic hernia is defined as a communication between the abdominal and thoracic cavities with or without abdominal contents in the thorax  The etiology may be congenital or traumatic. The symptoms and prognosis depend on the location of the defect and associated anomalies. The defect may be at the esophageal hiatus (hiatal), paraesophageal (adjacent to the hiatus), retrosternal (Morgagni), or at the posterolateral (Bochdalek) portion of the diaphragm. The term congenital diaphragmatic hernia (CDH) typically refers to the Bochdalek form. These lesions may cause significant respiratory distress at birth, can be associated with other congenital anomalies, and have a significant mortality and long-term morbidity. The overall survival from the CDH Study Group is 67%. The Bochdalek hernia accounts for up to 90% of the hernias seen in the newborn period, with 80–90% occurring on the left side


The separation of the pleural and peritoneal cavities is effected by development of the diaphragm (Fig. 65.1). This forms from a portion of the septum transversum mesenchyme above the developing liver. The septum transversum is a population of mesenchymal cells that arises from the coelomic wall of the caudal part of the pericardial cavity. As the population proliferates, it forms a condensation of mesenchyme, caudal to the pericardial cavity and extending from the ventral and lateral regions of the body wall to the foregut. Dorsal to it on each side is the relatively narrow pleuroperitoneal canal. The endodermal hepatic bud grows into the caudal part of the septum transversum, whereas the cranial portion will form the diaphragm.

Medial to the pleuroperitoneal canals are the oesophagus and stomach with their dorsal mesentery and, at the root of the latter, the dorsal aorta. Dorsolateral to the canals are the pleuroperitoneal membranes, which remain small. Dorsally are the mesonephric ridges, suprarenal (adrenal) glands and gonads. Just as the enlargement of the pleural cavity cranially and ventrally is effected by a process of burrowing into the body wall, so its caudodorsal enlargement is effected in the same way. The expanding pleural cavities extend into the mesenchyme dorsal to the suprarenal glands, the gonads and (degenerating) mesonephric ridges. Thus somatopleuric mesenchyme is peeled off the dorsal body wall to form a substantial portion of the dorsolumbar part of the diaphragm. The pleuroperitoneal canal is closed by the fusion of its edges, which are carried together from posterolaterally to anteromedially by growth of the organs surrounding it and in particular that of the suprarenal gland. The right pleuroperitoneal canal closes earlier than the left, which presumably explains why an abnormal communication persisting between the pleural and peritoneal cavities is more frequently encountered on the left.

The diaphragm is a dome-shaped musculotendinous structure that is derived from four distinct fused structures. The septum transversum gives rise to the central tendon and separates the pericardial and peritoneal cavities. The central tendon constitutes 30% of the diaphragm and is the largest portion. The pleuroperitoneal membranes give rise to the dorsal lateral portions of the diaphragm; this separates the paired pleural cavities and the “fetal diaphragm” at approximately 8 wk gestation. The esophageal mesentery forms the dorsal crura and the intercostal muscle groups give rise to the muscular portion of the diaphragm. CDH may be due to defective formation of the pleuroperitoneal membrane. When the abdominal contents return to the abdomen from the umbilical sac at 10 wk gestation, herniation of the abdominal contents may occur.


Anteriorly, the costal cartilages of ribs I to VII articulate with the sternum.


The costal cartilages of ribs VIII to X articulate with the inferior margins of the costal cartilages above them.

Ribs XI and XII are called floating ribs because they do not articulate with other ribs, costal cartilages, or with sternum. Their costal cartilages are small, only covering their tips.

There are twelve pairs of ribs, each terminating anteriorly in a costal cartilage

Although all ribs articulate with the vertebral column, only the costal cartilages of the upper seven ribs, known as true ribs, articulate directly with the sternum. The remaining five pairs of ribs are false ribs:

  • the costal cartilages of ribs VIII to X articulate anteriorly with the costal cartilages of the ribs above;
  • ribs XI and XII have no anterior connection with other ribs or with the sternum and are often called floating ribs.



A, Superior and B, inferior aspects of the first rib. (Photographs by Sarah-Jane Smith.)

The superior surface of the rib is characterized by a distinct tubercle, the scalene tubercle, which separates two smooth grooves that cross the rib approximately midway along the shaft. The anterior groove is caused by the subclavian vein, and the posterior groove is caused by the subclavian artery. Anterior and posterior to these grooves, the shaft is roughened by muscle and ligament attachments.

The insertion of scalenus medius on the elongated rough area behind the groove for subclavian artery.

The external border is convex, thick posteriorly and thin anteriorly. It is covered behind by scalenus posterior descending to the second rib. The first digitation of serratus anterior is, in part, attached to it, behind the subclavian (arterial) groove. The internal border is concave and thin, and the scalene tubercle is near its midpoint. The suprapleural membrane, which covers the cervical dome of the pleura, is attached to the internal border.

The superior surface of the flattened shaft is crossed obliquely by two shallow grooves, separated by a slight ridge, which usually ends at the internal border as a small pointed projection, the scalene tubercle, to which scalenus anterior is attached. The groove anterior to the scalene tubercle forms a bed for the subclavian vein, and the rough area between this and the first costal cartilage gives attachment to the costoclavicular ligament and, more anteriorly, to subclavius. The subclavian artery and (usually) the lower trunk of the brachial plexus pass in the groove behind the tubercle. Behind this, scalenus medius is attached as far as the costal tubercle.

  • the superior costal facets on the body of vertebra TI are complete and articulate with a single facet on the head of its own rib-in other words, the head of rib I does not articulate with vertebra CVII;
  • similarly, vertebra TX (and often TIX) articulates only with its own ribs and therefore lacks inferior demifacets on the body;
  • vertebrae TXI and TXII articulate only with the heads of their own ribs-they lack transverse costal facets and have only a single complete facet on each side of their bodies.

Costal cartilages articulate with small concavities on the lateral sternal borders (chondrosternal articulations, Fig. 57.16). Perichondrium and periosteum are continuous. The first sternocostal joint is an unusual variety of synarthrosis, often inaccurately called a synchondrosis. The second to seventh costal cartilages articulate by synovial joints

The manubriosternal joint lies between the manubrium and sternal body, and is usually a symphysis. The bony surfaces are covered by hyaline cartilage and connected by a fibrocartilage

COSTOCHONDRAL JUNCTIONS :- Artificially separated from its rib, a costal cartilage has a rounded end that fits a reciprocal depression in the rib. Periosteum and perichondrium are continuous across the costochondral junctions, and the collagen of the osseous and cartilaginous matrices blend. No movement occurs at costochondral junctions.

Intercostal muscles

The intercostal muscles are three flat muscles found in each intercostal space that pass between adjacent ribs (Fig. 3.27). Individual muscles in this group are named according to their positions:

  • the external intercostal muscles are the most superficial;
  • the internal intercostal muscles are sandwiched between the external and innermost muscles

External intercostal muscles :-The eleven pairs of external intercostal muscles extend from the inferior edges of the ribs above to the superior surfaces of the ribs below. When the thoracic wall is viewed from a lateral position, the muscle fibers pass obliquely anteroinferiorly (Fig. 3.27). The muscles extend around the thoracic wall from the regions of the tubercles of the ribs to the costal cartilages, where each layer continues as a thin connective tissue aponeurosis termed the external intercostal membrane. The external intercostal muscles are most active in inspiration.

Internal intercostal muscles :-The eleven pairs of internal intercostal muscles pass between the most inferior lateral edge of the costal grooves of the ribs above, to the superior surface of the ribs below. They extend from parasternal regions, where the muscles course between adjacent costal cartilages, to the angle of the ribs posteriorly (Fig. 3.27). This layer continues medially toward the vertebral column, in each intercostal space, as the internal intercostal membrane. The muscle fibers pass in the opposite direction to those of the external intercostal muscles. When the thoracic wall is viewed from a lateral position, the muscle fibers pass obliquely posteroinferiorly. The internal intercostal muscles are most active during expiration.



Intercostal nerves and associated major arteries and veins lie in the costal groove along the inferior margin of the superior rib and pass in the plane between the inner two layers of muscles.

In each space, the vein is the most superior structure and is therefore highest in the costal groove. The artery is inferior to the vein, and the nerve is inferior to the artery and often not protected by the groove. Small collateral branches of the major intercostal nerves and vessels are often present superior to the inferior rib below.

Innervation of the thoracic wall is mainly by the intercostal nerves, which are the anterior rami of spinal nerves T1 to T11 and lie in the intercostal spaces between adjacent ribs. The anterior ramus of spinal nerve T12 (the subcostal nerve) is inferior to rib XII

A typical intercostal nerve passes laterally around the thoracic wall in an intercostal space. The largest of the branches is the lateral cutaneous branch, which pierces the lateral thoracic wall and divides into an anterior branch and a posterior branch that innervate the overlying skin

In addition to innervating the thoracic wall, intercostal nerves innervate other regions:

  • the anterior ramus of T1 contributes to the brachial plexus;
  • the lateral cutaneous branch of the second intercostal nerve (the intercostobrachial nerve) contributes to cutaneous innervation of the medial surface of the upper arm;
  • the lower intercostal nerves supply muscles, skin, and peritoneum of the abdominal wall

Vessels that supply the thoracic wall consist mainly of posterior and anterior intercostal arteries, which pass around the wall between adjacent ribs in intercostal spaces (Fig. 3.29). These arteries originate from the aorta and internal thoracic arteries, which in turn arise from the subclavian arteries in the root of the neck. Together, the intercostal arteries form a basket-like pattern of vascular supply around the thoracic wall.

Posterior intercostal arteries originate from vessels associated with the posterior thoracic wall. The upper two posterior intercostal arteries on each side are derived from the supreme intercostal artery, which descends into the thorax as a branch of the costocervical trunk in the neck. The costocervical trunk is a posterior branch of the subclavian artery (Fig. 3.29).

The remaining nine pairs of posterior intercostal arteries arise from the posterior surface of the thoracic aorta. Because the aorta is on the left side of the vertebral column, those posterior intercostal vessels passing to the right side of the thoracic wall cross the midline anterior to the bodies of the vertebrae and therefore are longer than the corresponding vessels on the left.

In addition to having numerous branches that supply various components of the wall, the posterior intercostal arteries have branches that accompany lateral cutaneous branches of the intercostal nerves to superficial regions.

Venous drainage :-

Venous drainage from the thoracic wall generally parallels the pattern of arterial supply 

Centrally, the intercostal veins ultimately drain into the azygos system of veins or into internal thoracic veins, which connect with the brachiocephalic veins in the neck.

Often the upper posterior intercostal veins on the left side come together and form the left superior intercostal vein, which empties into the left brachiocephalic vein.

Similarly, the upper posterior intercostal veins on the right side may come together and form the right superior intercostal vein, which empties into the azygos vein.


Figure 3.30 Veins of the thoracic wall.                                                                                                                                                             Recess

The largest and clinically most important recesses are the costodiaphragmatic recesses, which occur in each pleural cavity between the costal pleura and diaphragmatic pleura . The costodiaphragmatic recesses are the regions between the inferior margin of the lungs and inferior margin of the pleural cavities. They are deepest after forced expiration and shallowest after forced inspiration.

During quiet respiration, the inferior margin of the lung crosses rib VI in the midclavicular line, rib VIII in the midaxillary line, and then courses somewhat horizontally to reach the vertebral column at vertebral level TX. From the midclavicular line and around the thoracic wall to the vertebral column, the inferior margin of the lung can be approximated by a line running between rib VI, rib VIII, and vertebra TX. The inferior margin of the pleural cavity at the same points is rib VIII, rib X, and vertebra TXII. The costodiaphragmatic recess is the region between the two margins.

The right costo-phrenic recess extends up to the level of which rib in the mid-axillary line



imageFigure 60.12 Principal elements of the fibrous skeleton of the heart. For clarity, the view is from the right posterosuperior aspect. Perspective causes the pulmonary anulus to appear smaller than the aortic anulus, whereas in fact the reverse is the case. Consult text for an extended discussion. Key: red, mitral and aortic ‘anuli’; blue, tricuspid and pulmonary ‘anuli’; green, tendon of the infundibulum. (Copyright from The Royal College of Surgeons of England. .)image




                                          Left Dominance

Variations in the distribution patterns of coronary arteries

Several major variations in the basic distribution patterns of the coronary arteries occur:

  • The distribution pattern described above for both right and left coronary arteries is the most common and consists of a right dominant coronary artery. This means that the posterior interventricular branch arises from the right coronary artery. The right coronary artery therefore supplies a large portion of the posterior wall of the left ventricle and the circumflex branch of the left coronary artery is relatively small.
  • In contrast, in hearts with a left dominant coronary artery, the posterior interventricular branch arises from an enlarged circumflex branch and supplies most of the posterior wall of the left ventricle (Fig. 3.73).
  • Another point of variation relates to the arterial supply to the sinu-atrial and atrioventricular nodes. In most cases, these two structures are supplied by the right coronary artery. However, vessels from the circumflex branch of the left coronary artery occasionally supply these structures


Anterior views of the coronary arterial system, with the principal variations. The right coronary arterial tree is shown in magenta, the left in full red. In both cases posterior distribution is shown in a paler shade. A, The most common arrangement. B, A common variation in the origin of the sinuatrial nodal artery. C, An example of left ‘dominance’ by the left coronary artery, showing also an uncommon origin of the sinu-atrial artery.



 B. Left anterior oblique view of right coronary artery. C. Right anterior oblique view of left coronary artery


From two to nine large left anterior ventricular arteries branch at acute angles from the anterior interventricular (descending) artery and cross the anterior aspect of the left ventricle diagonally; larger terminals reach the rounded (obtuse) left border. One is often large and may arise separately from the left coronary trunk (which then ends by trifurcation). This left diagonal artery, reported in 33-50% or more individuals, is sometimes duplicated (20%). A small left conus artery frequently leaves the anterior interventricular (descending) artery near its start, and anastomoses on the conus with its counterpart from the right coronary artery and with the vasa vasorum of the pulmonary artery and aorta. The anterior septal branches leave the anterior interventricular (descending) artery almost perpendicularly, and pass back and down in the septum, usually supplying its ventral two-thirds. Small posterior septal branches from the same source supply the posterior one-third of the septum for a variable distance from the cardiac apex.

The circumflex artery, comparable to the anterior interventricular (descending) in calibre, curves left in the atrioventricular groove, continuing round the left cardiac border into the posterior part of the groove and ending left of the crux in most hearts, but sometimes continuing as a posterior interventricular (descending) artery. Proximally, the left atrial auricle usually overlaps it. In c.90%, a large ventricular branch, the left marginal artery, arises perpendicularly from the circumflex artery and ramifies over the rounded ‘obtuse’ margin, supplying much of the adjacent left ventricle, usually to the apex. Smaller anterior and posterior branches of the circumflex artery also supply the left ventricle. Anterior ventricular branches (from one to five, commonly two or three) course parallel to the diagonal artery, when it is present, and replace it when it is absent. Posterior ventricular branches are smaller and fewer; the left ventricle is partly supplied by the posterior interventricular (descending) artery. When this is small or absent, it is accompanied or replaced by an interventricular continuation of the circumflex artery, which is frequently double or triple. The circumflex artery may supply the left atrium via anterior, lateral and posterior atrial branches.

The right coronary artery supplies the right atrium and right ventricle, the sinu-atrial and atrioventricular nodes, the interatrial septum, a portion of the left atrium, the posteroinferior one-third of the interventricular septum, and a portion of the posterior part of the left ventricle

The distribution pattern of the left coronary artery enables it to supply most of the left atrium and left ventricle, and most of the interventricular septum, including the atrioventricular bundle and its branches.

Occlusion of the ant descending branch of LAD will
lead to infarction of which area?
A.Posterior part of the interventricular septum
Anterior wall of the left ventricle
C.Lateral part of the heart
D.Inferior surface of right ventricle

All of the following are true about coronary artery except :
A.Right coronary artery lies in right anterior coronary salcus
B.Left anterior descending artey is a branch of left coronary artery
C.Usually 3 obtuse marginal arteries arise from left coronary artery   It is single.Diagonal branches are 2-3 sometimes.
D.In 85% cases posterior descending
interventricular artery arises from right co. art.

The right coronary artery supplies all of the following parts of the conducting system in the heart except:
A.SA Node
B.AV Node
C.AV Bundle
D.Right Bundle branch

Most commonly, the right coronary artery supplies all the right ventricle (except a small region right of the anterior interventricular groove), a variable part of the left ventricular diaphragmatic aspect, the posteroinferior one-third of the intraventricular septum, the right atrium and part of the left, and the conducting system as far as the proximal parts of the right and left crura. Left coronary distribution is reciprocal, and includes most of the left ventricle, a narrow strip of right ventricle, the anterior two-thirds of the interventricular septum and most of the left atrium

As the right and left bundle branches runs in Interventricular septum so it must be supplied by Left coronary artery

The middle cardiac vein is located at the:
A.Anterior interventricular sulcus
B.Posterior interventricular sulcus
C.Posterior AV groove
D.Anterior AV groove

Right coronary artery

The right coronary artery originates from the right aortic sinus of the ascending aorta. It passes anteriorly and to the right between the right auricle and the pulmonary trunk and then descends vertically in the coronary sulcus, between the right atrium and right ventricle .On reaching the inferior margin of the heart, it turns posteriorly and continues in the sulcus onto the diaphragmatic surface and base of the heart. During this course, several branches arise from the main stem of the vessel:

  • an early atrial branch passes in the groove between the right auricle and ascending aorta, and gives off the sinu-atrial nodal branch, which passes posteriorly around the superior vena cava to supply the sinu-atrial node;
  • a right marginal branch is given off as the right coronary artery approaches the inferior (acute) margin of the heart and continues along this border toward the apex of the heart;
  • as the right coronary artery continues on the base/diaphragmatic surface of the heart, it supplies a small branch to the atrioventricular node before giving off its final major branch, the posterior interventricular branch, which lies in the posterior interventricular sulcus.

The left coronary artery originates from the left aortic sinus of the ascending aorta. It passes between the pulmonary trunk and the left auricle before entering the coronary sulcus. While still posterior to the pulmonary trunk, the artery divides into its two terminal branches, the anterior interventricular and the circumflex

  • the anterior interventricular branch (left anterior descending artery-LAD), which continues
  • around the left side of the pulmonary trunk and descends obliquely toward the apex of the heart in the anterior interventricular sulcus during its course, one or two large diagonal branches may arise and descend diagonally across the anterior surface of the left ventricle;
  • the circumflex branch, which courses toward the left, in the coronary sulcus and onto the base/diaphragmatic surface of the heart and usually ends before reaching the posterior interventricular sulcus-a large branch, the left marginal artery, usually arises from it and continues across the rounded obtuse margin of the heart

The coronary sulcus circles the heart, separating the atria from the ventricles. As it circles the heart, it contains the right coronary artery, the small cardiac vein, the coronary sinus, and the circumflex branch of the left coronary artery.

The anterior and posterior interventricular sulci separate the two ventricles-the anterior interventricular sulcus is on the anterior surface of the heart and contains the anterior interventricular artery and the great cardiac vein, and the posterior interventricular sulcus is on the diaphragmatic surface of the heart and contains the posterior interventricular artery and the middle cardiac vein

  • the right and left margins are the same as the right and left pulmonary surfaces of the heart;
  • the inferior margin is defined as the sharp edge between the anterior and diaphragmatic surfaces of the heart (Figs 3.56 and 3.58)-it is formed mostly by the right ventricle and a small portion of the left ventricle near the apex;
  • the obtuse margin separates the anterior and left pulmonary surfaces (Fig. 3.56)-it is round and extends from the left auricle to the cardiac apex (Fig. 3.58), and is formed mostly by the left ventricle and superiorly by a small portion of the left auricle




Details of coronary distribution require integration into a concept of total cardiac supply. Most commonly, the right coronary artery supplies all the right ventricle (except a small region right of the anterior interventricular groove), a variable part of the left ventricular diaphragmatic aspect, the posteroinferior one-third of the intraventricular septum, the right atrium and part of the left, and the conducting system as far as the proximal parts of the right and left crura.

Left coronary distribution is reciprocal, and includes most of the left ventricle, a narrow strip of right ventricle, the anterior two-thirds of the interventricular septum and most of the left atrium. As noted (Figs 60.23, 60.24), variations in the coronary arterial system mainly affect the diaphragmatic aspect of the ventricles; they consist of the relative ‘dominance’ of supply by the left or the right coronary artery. The term is misleading, as the left artery almost always supplies a greater volume of tissue.

.In ‘right dominance’, the posterior interventricular (descending) artery is derived from the right coronary; in ‘left dominance’ it derives from the left. In the so-called ‘balanced’ pattern, branches of both arteries run in or near the groove. Less is known of variation in atrial supply because the small vessels involved are not easily preserved in the corrosion casts that are used for analysis. In more than 50% of individuals, the right atrium is supplied only by the right coronary; in the remainder the supply is dual. More than 62% of left atria are largely supplied by the left and c.27% by the right coronary; in each group a small accessory supply from the other coronary artery exists, and 11% are supplied almost equally by both arteries. Sinu-atrial and atrioventricular supplies also vary. Various studies have reported that the right and left coronary arteries supply the sinu-atrial node in 51-65% and 35-45% respectively (fewer than 10% of nodes receive a bilateral supply). The atrioventricular node is supplied by the right coronary (80-90%) and left coronary arteries (10-20%).




The large majority of cardiac veins drain into the wide coronary sinus, c.2 or 3 cm long, lying in the posterior atrioventricular groove between the left atrium and ventricle (Figs 60.2, 60.25). The sinus opens into the right atrium between the opening of the inferior vena cava and the right atrioventricular orifice; the opening is guarded by an endocardial fold (semilunar valve of the coronary sinus; Fig. 60.7). Its tributaries are the great, small and middle cardiac veins, the posterior vein of the left ventricle and the oblique vein of the left atrium; all except the last have valves at their orifices.

The great cardiac vein begins at the cardiac apex, ascends in the anterior interventricular groove to the atrioventricular groove and follows this, passing to the left and posteriorly to enter the coronary sinus at its origin .It receives tributaries from the left atrium and both ventricles, including the large left marginal vein that ascends the left aspect (‘obtuse border’) of the heart

The small cardiac vein lies in the posterior atrioventricular groove between the right atrium and ventricle and opens into the coronary sinus near its atrial end (Fig. 60.25). It receives blood from the posterior part of the right atrium and ventricle. The right marginal vein passes right, along the inferior cardiac margin (‘acute border’). It may join the small cardiac vein in the atrioventricular groove, but more often opens directly into the right atrium

The middle cardiac vein (Fig. 60.25) begins at the cardiac apex, and runs back in the posterior interventricular groove to end in the coronary sinus near its atrial end.

Posterior vein of the left ventricle  The posterior vein of the left ventricle (Fig. 60.25) is found on the diaphragmatic surface of the left ventricle a little to the left of the middle cardiac vein. It usually opens into the centre of the coronary sinus, but sometimes opens into the great cardiac vein.

Oblique vein of the left atrium  The small vessel that is the oblique vein of the left atrium (Fig. 60.25) descends obliquely on the back of the left atrium to join the coronary sinus near its end. It is continuous above with the ligament of the left vena cava. The two structures are remnants of the left common cardinal vein.


The anterior cardiac veins drain the anterior part of the right ventricle. Usually two or three, sometimes even five, they ascend in subepicardial tissue to cross the right part of the atrioventricular groove, passing deep or superficial to the right coronary artery. They end in the right atrium, near the groove, separately or in variable combinations. A subendocardial collecting channel, into which all may open, has been described. The right marginal vein courses along the inferior (‘acute’) cardiac margin, draining adjacent parts of the right ventricle, and usually opens separately into the right atrium. It may join the anterior cardiac veins or, less often, the coronary sinus. Because it is commonly independent, it is often grouped with the small cardiac veins, but it is larger in calibre, being comparable to the anterior cardiac veins or even wider.


The existence of small cardiac veins, opening into all cardiac cavities, has been confirmed, but they are more difficult to demonstrate than larger cardiac vessels. Their numbers and size are highly variable: up to 2 mm in diameter opening into the right atrium and c.0.5 mm into the right ventricle. Numerous small cardiac veins have been identified in the right atrium and ventricle, but they are rare in the left atrium and left ventricle

The toughest layer of the esophagus is the

IInd constriction in oesophagus is seen at the following site :
(A)Where it crosses left main bronchus
(B)Crossing of aorta
(C)At pharyngoesophageal junction
(D)Where it pierces the diaphragm

Oesophagus is constricted at the beginning (15 cm (6 in) from the incisor teeth), where it is crossed by the aortic arch (22.5 cm (9 in) from the incisor teeth), where it is crossed by the left principal bronchus (27.5 cm (11 in) from the incisors) and as it passes through the diaphragm (40 cm (16 in) from the incisors). …ref gray

there are 3 constrictions ;second one by aortic arch and bronchus…..ref schwartz and sabiston…


                                           Schwartz                                                                                                                                                                                                   Gray



Oesophagus receives supply from all of the following except :
(A)Bronchial artery
(B)Internal mammary artery
(C)Inferior phrenic artery
(D)Inferior thyroid artery

The cervical oesophagus is supplied by the inferior thyroid artery. The thoracic oesophagus is supplied by bronchial arteries and oesophageal arteries. There are four or five oesophageal arteries, which arise anteriorly from the aorta and descend obliquely to the oesophagus. They form a vascular chain on the oesophagus that anastomoses above with the oesophageal branches of the inferior thyroid arteries and below with ascending branches from the left phrenic and left gastric arteries.(The arterial supply and venous drainage of the esophagus in the posterior mediastinum involves many vessels. Esophageal arteries arise from the thoracic aorta, bronchial arteries, and ascending branches of the left gastric artery in the abdomen)

In a patient with a tumor in superior mediatinurn compressing the superior vena cava, all of the following veins would serve as alternate pathways for the blood to return to the right atrium, except:         AI 2003

A.Lateral thoracic vein
B.Internal thoracic vein
C.Hemiazygos vein
D.Vertebral venous plexus


All of the above can provide alternate pathways.

Im not able to find the answer to this Question

EXPLAINATION GIVEN BELOW:- Reference Snell Anatomy



The possible collateral circulations of the superior and interior venae cavae. Note the alternative pathways that exist for blood to return to the right atrium of the heart if the superior vena cava becomes blocked below the entrance of the azygos vein (upper black bar). Similar pathways exist if the inferior vena cava becomes blocked below the renal veins (lower black bar). Note also the connections that exist between the portal circulation and the systemic veins in the anal canal.

The inferior vena cava is commonly compressed by the enlarged uterus during the later stages of pregnancy. This produces edema of the ankles and feet and temporary varicose veins. Malignant retroperitoneal tumors can cause severe compression and eventual blockage of the inferior vena cava. This results in the dilatation of the extensive anastomoses of the tributaries (see CD Fig. 8-3). This alternative pathway for the blood to return to the right atrium of the heart is commonly referred to as the caval–caval shunt. The “same pathway” comes into effect in patients with a superior mediastinal tumor compressing the superior vena cava. “Clinically”, the enlarged subcutaneous anastomosis between the lateral thoracic vein, a tributary of the axillary vein, and the superficial epigastric vein, a tributary of the femoral vein, may be seen on the thoracoabdominal wall (see CD Fig. 8-3). “Anatomically” many are present.

Reference Snell

Chronic thrombosis of the inferior vena cava

A medical student was asked to inspect the abdomen of two patients. On the first patient he noted irregular veins radiating from the umbilicus. On the second patient he noted irregular veins, coursing in a caudal to cranial direction, over the anterior abdominal wall from the groin to the chest. He was asked to explain his findings and determine the significance of these features.

In the first patient the veins were draining radially away from the periumbilical region. In normal individuals, enlarged veins do not radiate from the umbilicus. In patients with portal hypertension the portal venous pressure is increased as a result of hepatic disease. Small collateral veins develop at, and around, the obliterated umbilical vein. These veins pass through the umbilicus and drain onto the anterior abdominal wall, forming a portosystemic anastomosis. The eventual diagnosis for this patient was cirrhosis of the liver.

The veins draining in a caudocranial direction on the anterior abdominal wall in the second patient is not a typical appearance of veins on the anterior abdominal wall. When veins are so prominent it usually implies that there is an obstruction to the normal route of venous drainage and an alternative route has been taken. Typically, blood from the lower limbs and the retroperitoneal organs drains into the inferior cava and from here to the right atrium of the heart. This patient had a chronic thrombosis of the inferior vena cava preventing blood returning to the heart by the ‘usual’ route.

Blood from the lower limbs and the pelvis may drain via a series of collateral vessels, some of which include the superficial inferior epigastric veins, which run in the superficial fascia. These anastomose with the superior, superficial, and deep epigastric venous systems to drain into the internal thoracic veins, which in turn drain into the brachiocephalic veins and the superior vena cava.

After the initial inferior vena cava thrombosis, the veins of the anterior abdominal wall and other collateral pathways hypertrophy to accommodate the increase in blood flow.

52-year-old man presented with headaches and shortness of breath. He also complained of coughing up small volumes of blood. Clinical examination revealed multiple dilated veins around the neck. A chest radiograph demonstrated an elevated diaphragm on the right and a tumor mass, which was believed to be a primary bronchogenic carcinoma.


By observing the clinical findings and applying anatomical knowledge, the site of the tumor can be inferred.

The multiple dilated veins around the neck are indicative of venous obstruction. The veins are dilated on both sides of the neck, implying that the obstruction must be within a common vessel, the superior vena cava. Anterior to the superior vena cava in the right side of the chest is the phrenic nerve, which supplies the diaphragm. Because the diaphragm is elevated, suggesting paralysis, it is clear that the phrenic nerve has been involved with the tumor.


Four pairs of lumbar veins collect blood by dorsal tributaries from the lumbar muscles and skin. These branches anastomose with tributaries of the lumbar origin of the azygos and hemiazygos veins .The abdominal tributaries to the lumbar veins drain blood from the posterior, lateral and anterior abdominal walls, including the parietal peritoneum. Anteriorly, the abdominal tributaries anastomose with branches of the inferior and superior epigastric veins. These anastomoses provide routes of continued venous drainage from the pelvis and lower limb to the heart in the event of inferior vena caval obstruction. The abdominal tributaries drain into the superior epigastric veins and hence via the internal thoracic veins to the superior vena cava, whereas the dorsal tributaries carry blood into the azygos and hemiazygos system and hence into the superior vena cava. Near the vertebral column, the lumbar veins drain the vertebral plexuses and are connected by the ascending lumbar vein, which is a vessel running longitudinally anterior to the roots of the transverse processes of the lumbar vertebrae

Collaterals in inferior vena caval occlusion

Occlusion of the inferior vena cava may follow thrombosis resulting from hypercoagulable conditions, or embolism from lower limb or pelvic thromboses. The increased pressure within the lower body circulation leads to oedema of the legs and back, without ascites. Collateral venous circulation is established through a wide range of anastomoses between branches that drain ultimately to the superior vena cava. The lumbar veins connect to branches of the superior epigastric, circumflex iliac, lateral thoracic and posterior intercostal veins. They also anastomose with tributaries of the azygos, hemiazygos and lumbar azygos veins. The interconnecting vertebral venous plexuses provide an additional route of collateral circulation between the vena cavae



Superior vena caval obstruction is characterized by headaches, facial congestion and facial oedema. It is often caused by bronchial carcinoma involving the right upper lobe of the lung or metastatic involvement of the right paratracheal lymph nodes causing circumferential narrowing or complete obstruction of the superior vena cava. This impairs venous drainage of the head, neck and upper arms. This is usually considered to be an oncological emergency and symptoms may be relieved by insertion of a vascular stent or by radiotherapy to the affected region after a tissue diagnosis is established.

The level of SVC obstruction relative to the insertion of the azygous vein is predictive of the patient’s degree of symptoms. Obstruction of the SVC above the insertion of the azygous vein may cause fewer symptoms, because the azygous vein provides venous drainage for the head and upper extremities. If the level of obstruction is below the azygous vein, then venous drainage occurs via collaterals to the inferior vena cava.

.An obstructed superior vena cava (SVC) initiates collateral venous return to the heart from the upper half of the body through 4 principal pathways. The first and most important pathway is the azygous venous system, which includes the azygous vein, the hemiazygous vein, and the connecting intercostal veins. The second pathway is the internal mammary venous system plus tributaries and secondary communications to the superior and inferior epigastric veins. The long thoracic venous system, with its connections to the femoral veins and vertebral veins, provides the third and fourth collateral routes, respectively


The thoracic part is very short, partly inside and partly outside the pericardial sac. The extrapericardial part is separated from the right pleura and lung by the right phrenic nerve. The intrapericardial part is covered, except posteriorly, by inflected serous pericardium. The venous drainage from the tissues below the diaphragm finally ends in the inferior vena cava. The inferior vena cava traverses the diaphragm at the level of the eight and ninth thoracic vertebrae between the right and central tendon of the diaphragm (p. 1081). It then passes through the pericardium and drains into the inferoposterior part of the right atrium.


In obstruction of the upper inferior vena cava, the azygos and hemiazygos veins and vertebral venous plexuses are the main collateral channels maintaining venous circulation. They connect the superior and inferior venae cavae and communicate with the common iliac vein by the ascending lumbar veins and with many tributaries of the inferior vena cava.

Veins of the vertebral column form intricate plexuses along the entire column, external and internal to the vertebral canal. Both groups are devoid of valves, anastomose freely with each other, and join the intervertebral veins. Interconnections are widely established between these plexuses and longitudinal veins early in fetal life. When development is complete, the plexuses drain into the caval and azygos/ascending lumbar systems via named veins which accompany the arteries described above. The veins also communicate with cranial dural venous sinuses and with the deep veins of the neck and pelvis. The venous complexes associated with the vertebral column can dilate considerably, and can form alternative routes of venous return in patients with major venous obstruction in the neck, chest or abdomen. The absence of valves allows pathways for the wide and sometimes paradoxical spread of malignant disease and sepsis. Pressure changes in the body cavities are transmitted to these venous plexuses and thus to the CSF, though the cord itself may be protected from such congestion by valves in the small veins which drain from the cord into the internal vertebral plexus.

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Posted by Dr KAMAL DEEP on March 25, 2011

1. How strenuous is the physical activity required
to elicit symptoms? The classification provided by the New
York Heart Association has been found to be useful in describing
functional disability

New York Heart Association Functional Classification

Class I

  No limitation of physical activity

  No symptoms with ordinary exertion

Class II

  Slight limitation of physical activity

  Ordinary activity causes symptoms

Class III

  Marked limitation of physical activity

  Less than ordinary activity causes symptoms

  Asymptomatic at rest

Class IV

  Inability to carry out any physical activity without discomfort

  Symptoms at rest

Modified from The Criteria Committee of the New York Heart Association

Limitation of physical activity & symptom association alongwith is basis of NYHA classification.

Important point for MCQ:- if symptoms occurs on More than ordinary activity or on heavy exertion ,they are not part of NYHA.

2. Loud first heart sound is heard in – a)Mitral stenosis b)M.R.
d)Calcified mitral leaflet

ANS IS A i.e mitral stenosis

The intensity of the first heart sound (S1) is influenced by (1) the position of the mitral leaflets at the onset of ventricular systole:- [The loud S1 in mitral stenosis usually signifies that the valve is pliable and that it remains open at the onset of isovolumetric contraction because of the elevated left atrial pressure.]; if AV flow is increased because of high cardiac output or prolonged because of mitral stenosis.;S1 is louder if diastole is shortened because of tachycardia ,or if atrial contraction precedes ventricular contraction by an unusually short interval, reflected in a short PR interval

(2) the rate of rise of the left ventricular pressure pulse;A soft S1may be due to slow rise of the left ventricular pressure pulse AND a long PR interval,

In short PR interval and Tachycardia both position and rate of rise of left ventricular pressure pulse increases the First heard sound loudness

(3) the presence or absence of structural disease of the mitral valve; a Soft S1 may be due to imperfect closure due to reduced valve substance, as in mitral regurgitation.S1 is also soft when the anterior mitral leaflet is immobile because of rigidity and calcification, even in the presence of predominant mitral stenosis.

(4) the amount of tissue, air, or fluid between the heart and the stethoscope.:-A soft S1may be due to poor conduction of sound through the chest wall.


Schematic diagrams of the configurational changes in carotid pulse and their differential diagnoses. Heart sounds are also illustrated. . S4, fourth heart sound; S1, first heart sound; A2 aortic component of second heart sound; P2 pulmonic component of second heart sound.


A. Normal


B. Aortic stenosis. Anacrotic pulse with slow upstroke to a reduced peak.


C. Bisferiens pulse with two peaks in systole. This pulse is rarely appreciated in patients with severe aortic regurgitation



D. Bisferiens pulse in hypertrophic obstructive cardiomyopathy. There is a rapid upstroke to the first peak (percussion wave) and a slower rise to the second peak (tidal wave).



E. Dicrotic pulse with peaks in systole and diastole. This waveform may be seen in patients with sepsis or during intra-aortic balloon counterpulsation with inflation just after the dicrotic notch


Commonest cause of pulsus paradoxus is – (A192)
a) Pericardial effusion
b) Adhesive pericarditis
c) Constrictive peircarditis
d) Chylopericardium

Pulsus paradoxus refers to a fall in systolic pressure >10 mmHg with inspiration that is seen in patients with pericardial tamponade but also is described in those with massive pulmonary embolism, hemorrhagic shock, severe obstructive lung disease, and tension pneumothorax. Pulsus paradoxus is measured by noting the difference between the systolic pressure at which the Korotkoff sounds are first heard (during expiration) and the systolic pressure at which the Korotkoff sounds are heard with each heartbeat, independent of the respiratory phase. Between these two pressures, the Korotkoff sounds are heard only intermittently and during expiration. The cuff pressure must be decreased slowly to appreciate the finding. It can be difficult to measure pulsus paradoxus in patients with tachycardia, atrial fibrillation, or tachypnea. A pulsus paradoxus may be palpable at the brachial artery or femoral artery level when the pressure difference exceeds 15 mmHg. This inspiratory fall in systolic pressure is an exaggerated consequence of interventricular dependence.

Pulsus bisferiens may be seen in all except

a)Combined AS+AR (PGI 80, UPSC 83)
b) Hypertrophic subaortic stenosis
c) Normal individuals
d) None of the above

Pulsus paradoxius is associated witha)
Cardiac tamponade (JIPMER 81, AMU 89)
b) Patent ductus arteriosus
c) Hypertension
d) ASD
e) VSD

Opening snap in mitral area corresponds toa)
‘X’ descent in JVP (JIPMER 93)
b) ‘A’ wave in JVP
c) Dicrotic notch of carotid pulse
d) ‘C’ point of apex cardiogram

Pulses bisferiens is seen in – (PGI 89)
a) AS b) MR
c) AR d) Hypertrophic cardiomyopathy

A palpable double systolic arterial pulse, the so-called bisferiens pulse, excludes pure or predominant AS and signifies dominantAR.

Anacrotic pulse in felt in- (NIMHANS 88)
a) AR b) MR
c) MS d) AS

This wave form is characterised by a slow upstroke. It is particularly prominent in the brachial and carotid pulses. The time taken to reach the peak is prolonged and the entire wave is flattened and of small amplitude. Slow rising pulses are less obvious in the peripheral pulses.

Possible causes include :-

  • Aortic valve stenosis – in this condition the rate of ejection of blood into the aorta is decreased so that the duration of the ejection is prolonged. The amplitude of the pulse is diminished as a consequence
  • poorly functioning left ventricle may give rise to a slow rising wave form due to slow ejection from the poorly functioning ventricle

Pulses alternans is seen in – (NIMHANS 88)
a) Left ventricular failure b) Digitalis poisoning
c) AS with AR d) MS with MR

Pulses paradoxus is seen in – (NIMHANS 88)
a) Mitral stenosis b) Artrial fibrillation
c) Aortic stenosis d) Asthma

Varying pulse pressure with normal rhythum is
seen in – (JIPMER 78, PGI 87, 93)
a) Left ventricular failure b) Asthma
c) Respiratory failure d) Cardiac tamponade

Water hammer pulse is seen in all except –
a) AR b) Anaemia (CMC 98)
c) Pregnancy d) MR
e) MS

Pulsus bisiferians is best felt at – (AIIMS 98)
a) Carotids b) Radial
c) Brochial d) Femoral

Dicrotic pulse is seen in – (Jipmer 2K)
a) Cardiac tamponade
b) Aortic regurgitation
c) Dilated cardiomyopathy
d) Retrictive cardiomyopathy

A bifid pulse is easily appreciated in patients on intra-aortic balloon counterpulsation (IABP), in whom the second pulse is diastolic in timing.

The dicrotic pulse has two palpable waves, one in systole and one in diastole. It usually denotes a very low stroke volume, particularly in patients with dilated cardiomyopathy.

True about pulsus paradoxus is – (PGI 98)
a) Arm-tongue circulation time is increased
b)inc. Stroke volume
c) Seen in constrictive pericarditis
d)inc. HR

Pulsus alternans occurs in – (PGI 98)
a) Constrictive pericarditis b) Viral myocarditis
c) Hypokalemia d) MI

Water hammer pulse seen in – (Aiims May 07)
a) Aortic stenosis
b) Aortic regurgitation
c) Aortic stenosis and Aortic regurgitation
d) Mitral regurgitation

Which one of the following does not cause pulsus
paradoxus ? (UPSC 07)
a) Severe aortic regurgitation
b) Cardiac tamponade
c) Constrictive pericardities
d) Acute severe bronchial asthma

Pulsus paradoxus seen in – • (PGI June 06)
a) Cardiac tamponade
b) Constrictive pericarditis
d) AR
e) Severe asthma

One of the following is not an indicator of the severity
of asthma – (AIIMS 78, PGI 81)
a) Use of accessory muscles
b) Pulsus paradoxus
c) Cyanosis
d) Systolic hypertension

A post-operative cardiac surgical patient developed
sudden hypotension, raised central venous pressure,
pulsus paradoxus at the 4 post operative hour. The
most probable diagnosis is:
A. Excessive mediastinal bleeding
B. Ventricular dysfunction
C. Congestive cardiac failure
D. Cardiac tamponade

Pulse pressure in a particular vessel is determined
chiefly by – (Bihar 91)
a) Distance from heart
b) Frictional characteristics lumen
c) Distensibility
d) Cross sectional area

The arterial pulse pressure in the femoral artery
is normally – (PGI 91)
a) Less than the pulse pressure in the upper aorta
b) Less than 20 mm Hg
c) Greater than the pulse pressure in the upper aorta
d) Equal to the pressure in the upper aorta
e) None of the above

Blood pressure is defined as the product of –
a) Systolic pressure x pulse (PGI 98)
b) Diastolic pressure x pulse rate
c) Pulse pressure x pulse rate
d) Cardiac output x peripheral resistance

Best artery to palpate for pulse in infants is –
a) Femoral a b) Radial a (PGI 2000)
c) Carotid a d) Brachial a

All of following tend to increase in old age
except – (Delhi 96)
a) Residual volume b) Systolic BP
c) Pulse pressure d) Vital capacity

Which tends to decrease with increasing
age – (AIIMS 85)
a) Vital capacity b) Systolic B.P.
c) Pulse pressure d) Residiial volume


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Posted by Dr KAMAL DEEP on February 14, 2011

1.Body Composition


Note :- Proteins are not in interstitial fluid (because there are more proteins in plasma than in interstitial fluid, there is a Donnan effect on ion movement across the capillary wall also.)

60% Water (40%ICF;20%ECF(15%Interstitial plus 5% Plasma Volume) 18% Protein Fat 15% Minerals 7%

TBW 60%—measured by D20,HEAVY WATER.It is ECF PLUS ICF.

ICF (40%)—Measured by TBW minus ECF.It cannot be measured directly just like interstitial fluid.

ECF (20%) –Measured by Inulin (Mannitol and sucrose have also been used to measure this space though not as much accurate as inulin)

ECF=Interstitial Fluid(15%) Plus Plasma Volume(5%).

Interstitial Fluid is measured by ECF minus Plasma Volume.It cannot be measured directly just like intracellular fluid.

Plasma Volume(3.5 liters ;5% of body weight) can be measured using dyes Evans Blue(T-1824).It can also be measured by serum albumin labeled with radioactive iodine.

In short TBW(D20,Titanium oxide and aminopyrine),ECF(INULIN,MANNITOL,SUCROSE),PLASMA(T-1824,ALBUMIN) can be measured directly by bracketed methods while Intracellular fluid(TBW-ECF)and interstitial fluid(ECF –PLASMA) can be derived from them indirectly by subtraction methods.

TBW= 40-45 LITRES;60% of body weight; (Intracellular Fluid=28.8Litres Plus Interstitial Fluid =10.5 Liters Plus Blood plasma=3.5 Liters) where ECF(interstitial plus blood plasma) is 14 L or another name is sucrose space in a 70 KG MAN.

Total Blood volume = 3500 Multiply 100/100-38 where 38 is hematocrit.Hematocrit is percentage of blood volume that is made up of red blood cells..So Total blood volume equals 5645 ml.In other words TTAL  is about 8% of body weight in which 5% part is plasma volume and 3 % is red cell volume.

The water content of lean body tissue is constant at 71-72 ml/100g of tissue.

Q:-Most accurate measurement of extracellular fluid
volume (ECF) can be done by using – (AIIMS 03)
a) Sucrose b) Mannitol
c) Inulin d) Aminopyrine

Ans is C i.e. INULIN

Q:- In an adult man 70kgs, the extracellular
fluid volume will be about – (Karn PG MEE 2006)
a) 42L b) 25L
c) 15L d) 121L  Ans is not A as given in guides…Thanks to

Q:-Which of the following methods is not used for measurement of body fluid volumes –
a) Aminopyrine for total body water-true (AIIMS May 05)
b)Inulin for extracellular fluid-true
c)Evans blue for plasma volume-true
d)albumin for blood volume-false it is used for plasma volume   Ans is D

Note:- Red cell volume can be determined by subtracting the plasma volume from the total blood volume..Total blood volume was determined by plasma volume and hematocrit.A commonly used tag is 15Cr,a radioactive isotope of chromium that is attached to the cells by incubating them in a suitable chromium solutions.Isotopes of iron and phosphorus and antigenic tagging have also been employed.

Heavy water (D20) or Deuterium Oxide is most frequently used for measuring the TBW.Titanium oxide and aminopyrine have also been used for this purpose.

Solvent Drag:- When solvent is moving along one direction,it tends to drag along some molecules of solute.

Q:- The percentage of the circulating blood volume in the venous system and splanchnic vessels is
normally between – (JIPMER 70, AMU 88)
a) 20-30% b) 40-50%
c) 60-70% d) None of these

Ans is c

Q:-Splanchnic vessels and venules contain what percentage of blood volume – (AMC 86,87)
a) 10-20 %
b) 20-30 %
c) 40-50 % d) 60-70 %

Ans is b given…..

Two different answers

Because different questions.

Veins are also called “capacitance vessels” because most of the blood volume (60%) is contained within veins.the splanchnic circulation contains about 25—30% of the total blood volume.

Q:-Osmolarity is – (JIPMER 98)
a)Osmolarity per kg of solvent
b)Osmolarity per litre of solvent
c)Moles per kg of solvent
d)Moles per litre of solvent

The osmolal concentration of a substance in a fluid is measured by the degree to which it depresses the freezing point, with 1 mol of an ideal solution depressing the freezing point 1.86 °C. The number of milliosmoles per liter in a solution equals the freezing point depression divided by 0.00186

Osmolarity is the number of osmoles per litre of the solution.

Osmolality is the number of osmoles per kg of the solvent.

Therefore, osmolarity is affected by the volume of the various solutes in the solution and the temperature, while the osmolality is not.

Osmotically active substances in the body are dissolved in water, and the density of water is 1, so osmolal concentrations can be expressed as osmoles per liter (Osm/L) of water. In this book, osmolal (rather than osmolar) concentrations are considered, and osmolality is expressed in milliosmoles per liter (of water).

Note that although a homogeneous solution contains osmotically active particles and can be said to have an osmotic pressure, it can exert an osmotic pressure only when it is in contact with another solution across a membrane permeable to the solvent but not to the solute.

Q:-A solution contains 1 gram-mole of magnesium sulfate per liter. Assuming full ionization of this compound , calculate the osmotic pressure of the solution (1 mosmole/liter concentration is equivalent to 19.3 mm.IIg osmotic pressure) – (AI 86)
a) 19.3 mm Hg b) 3.86 mm Hg
c) 19.300 mm Hg d) 38.600 mm Hg
e) 57.900 mm Hg

Ans is D  19.3 MULTIPLY BY 2

Magnesium sulfate (or magnesium sulphate) is a chemical compound containing magnesium, sulfur and oxygen, with the formula MgSO4 SUPPLYING 2 Osm

If a solute is a nonionizing compound such as glucose, the osmotic pressure is a function of the number of glucose molecules present. If the solute ionizes and forms an ideal solution, each ion is an osmotically active particle. For example, NaCl would dissociate into Na+ and Cl ions, so that each mole in solution would supply 2 Osm. One mole of Na2SO4 would dissociate into Na+, Na+, and SO42– supplying 3 Osm..

Q:-When solvent is moving in one direction, the
solvent tends to drag along some molecules of solute. This is called – (PGI 81„AMU 86)
a) Filtration b) Osmosis
c) Dorman effect d) Solvent drag

D is ans

Q:-Osmolality of plasma in a normal adult (in m
Osm/L) is – (Delhi 87)
a) 250 -270
b) 270 – 290
c) 300 -310 d)310-330

The freezing point of normal human plasma averages –0.54 °C, which corresponds to an osmolal concentration in plasma of 290 mOsm/L

It is important to note the relative contributions of the various plasma components to the total osmolal concentration of plasma. All but about 20 of the 290 mOsm in each liter of normal plasma are contributed by Na+ and its accompanying anions, principally Cl and HCO3. Other cations and anions make a relatively small contribution. Although the concentration of the plasma proteins is large when expressed in grams per liter, they normally contribute less than 2 mOsm/L because of their very high molecular weights. The major nonelectrolytes of plasma are glucose and urea, which in the steady state are in equilibrium with cells. Their contributions to osmolality are normally about 5 mOsm/L each but can become quite large in hyperglycemia or uremia.

Gibbs-donnan Equation

Donnan Effect

When an ion on one side of a membrane cannot diffuse through the membrane, the distribution of other ions to which the membrane is permeable is affected in a predictable way. For example, the negative charge of a nondiffusible anion hinders diffusion of the diffusible cations and favors diffusion of the diffusible anions. Consider the following situation,


in which the membrane (m) between compartments X and Y is impermeable to charged proteins (Prot–) but freely permeable to K+ and Cl–. Assume that the concentrations of the anions and of the cations on the two sides are initially equal. Cl– diffuses down its concentration gradient from Y to X, and some K+ moves with the negatively charged Cl– because of its opposite charge. Therefore




that is, more osmotically active particles are on side X than on side Y.

Donnan and Gibbs showed that in the presence of a nondiffusible ion, the diffusible ions distribute themselves so that at equilibrium their concentration ratios are equal:




This is the Gibbs–Donnan equation. It holds for any pair of cations and anions of the same valence.

The Donnan effect on the distribution of ions has three effects in the body introduced here and discussed below. First, because of charged proteins (Prot–) in cells, there are more osmotically active particles in cells than in interstitial fluid, and because animal cells have flexible walls, osmosis would make them swell and eventually rupture if it were not for Na, K ATPase pumping ions back out of cells. Thus, normal cell volume and pressure depend on Na, K ATPase. Second, because at equilibrium the distribution of permeant ions across the membrane (m in the example used here) is asymmetric, an electrical difference exists across the membrane whose magnitude can be determined by the Nernst equation. In the example used here, side X will be negative relative to side Y. The charges line up along the membrane, with the concentration gradient for Cl– exactly balanced by the oppositely directed electrical gradient, and the same holds true for K+. Third, because there are more proteins in plasma than in interstitial fluid, there is a Donnan effect on ion movement across the capillary wall.

Nernst equation deals with – (JIPMER 92)
a)Oxygen uptake
b)Chloride shift
c)Cellular ATP levels
d)Plasma bicarbonate level

The forces acting across the cell membrane on each ion can be analyzed mathematically. Chloride ions (Cl) are present in higher concentration in the ECF than in the cell interior, and they tend to diffuse along this concentration gradient into the cell. The interior of the cell is negative relative to the exterior, and chloride ions are pushed out of the cell along this electrical gradient. An equilibrium is reached between Cl influx and Cl efflux. The membrane potential at which this equilibrium exists is the equilibrium potential. Its magnitude can be calculated from the Nernst equation, as follows:



ECl = equilibrium potential for Cl
R = gas constant
T = absolute temperature
F = the faraday (number of coulombs per mole of charge)
ZCl = valence of Cl (–1)
[Clo] = Cl concentration outside the cell
[Cli] = Cl concentration inside the cell

The equilibrium potential for Cl (ECl), calculated from the standard values listed in Table 1–1, is –70 mV, a value identical to the measured resting membrane potential of –70 mV. Therefore, no forces other than those represented by the chemical and electrical gradients need be invoked to explain the distribution of Cl across the membrane

Table 1–1 Concentration of Some Ions Inside and Outside Mammalian Spinal Motor Neurons.


Ion Concentration (mmol/L of H2O) Equilibrium Potential (mV)
Inside Cell Outside Cell
Na+ 15.0 150.0 +60
K+ 150.0 5.5 –90
Cl 9.0 125.0 –70

The magnitude of membrane potential at any given time depends,of course,upon the distribution of Na+,K+ and CL-

Table 4–1 Nerve Fiber Types in Mammalian Nerve.a


Fiber Type Function Fiber Diameter (micronm) Conduction Velocity (m/s) Spike Duration (ms) Absolute Refractory Period (ms)
Alpha Proprioception; somatic motor 12–20 70–120
Beta Touch, pressure 5–12 30–70 0.4–0.5 0.4–1
Gamma Motor to muscle spindles 3–6 15–30
Delta Pain, cold, touch 2–5 12–30
B Preganglionic autonomic 3–15 1.2 1.2
Dorsal root Pain, temperature, some mechano-reception 0.4–1.2 0.5–2 2 2
Sympathetic Postganglionic sympathetic 0.3–1.3 0.7–2.3 2 2

aA and B fibers are myelinated; C fibers are unmyelinated.

Table 4–3 Relative Susceptibility of Mammalian A, B, and C Nerve Fibers to Conduction Block Produced by Various Agents.


Susceptibility to: Most Susceptible Intermediate Least Susceptible
Hypoxia B A C
Pressure A B C
Local anesthetics C B A


A) Arrangement of thin (actin) and thick (myosin) filaments in skeletal muscle (compare to Figure 5–2). B) Sliding of actin on myosin during contraction so that Z lines move closer together. C) Detail of relation of myosin to actin in an individual sarcomere, the functional unit of the muscle. D) Diagrammatic representation of the arrangement of actin, tropomyosin, and troponin of the thin filaments in relation to a myosin thick filament. The globular heads of myosin interact with the thin filaments to create the contraction. Note that myosin thick filaments reverse polarity at the M line in the middle of the sarcomere, allowing for contraction.

The width of the A bands is constant




During phases 0 to 2 and about half of phase 3 (until the membrane potential reaches approximately –50 mV during repolarization), cardiac muscle cannot be excited again; that is, it is in its absolute refractory period. It remains relatively refractory until phase 4. Therefore, tetanus of the type seen in skeletal muscle cannot occur. Of course, tetanization of cardiac muscle for any length of time would have lethal consequences, and in this sense, the fact that cardiac muscle cannot be tetanized is a safety feature.

Cardiac muscle is a collection of individual cells (cardiomyocytes) that are linked as a syncytium by gap junctional communication.

  • Smooth muscle cells are largely under control of the autonomic nervous system.
  • There are two broad categories of smooth muscle cells: unitary and multiunit. Unitary smooth muscle contraction is synchronized by gap junctional communication to coordinate contraction among many cells. Multiunit smooth muscle contraction is coordinated by motor units, functionally similar to skeletal muscle.
  • Smooth muscle cells contract through an actomyosin system, but do not have well-organized striations. Unlike skeletal and cardiac muscle, Ca2+ regulation of contraction is primarily through phosphorylation–dephosphorylation reactions
  • the excitation–contraction coupling in unitary smooth muscle can occur with as much as a 500-ms delay. Thus, it is a very slow process compared with that in skeletal and cardiac muscle, in which the time from initial depolarization to initiation of contraction is less than 10 ms
  • Unitary smooth muscle is characterized by the instability of its membrane potential and by the fact that it shows continuous, irregular contractions that are independent of its nerve supply. This maintained state of partial contraction is called tonus, or tone. The membrane potential has no true “resting” value, being relatively low when the tissue is active and higher when it is inhibited, but in periods of relative quiescence values for resting potential are on the order of –20 to –65 mV. Smooth muscle cells can display divergent electrical activity



EEG records showing the alpha and beta rhythms. When attention is focused on something, the 8–13 Hz alpha rhythm is replaced by an irregular 13–30 Hz low-voltage activity, the beta rhythm.EEG records showing the alpha and beta rhythms. When attention is focused on something, the 8–13 Hz alpha rhythm is replaced by an irregular 13–30 Hz low-voltage activity, the beta rhythm.

1.A person falling asleep first enters stage 1, the EEG begins to show a low-voltage, mixed frequency pattern. A theta rhythm (4–7 Hz) can be seen at this early stage of slow-wave sleep. Throughout NREM sleep, there is some activity of skeletal muscle but no eye movements occur.

2.Stage 2 is marked by the appearance of sinusoidal waves called sleep spindles (12–14 Hz) and occasional high voltage biphasic waves called K complexes.

3.In stage 3, a high-amplitude delta rhythm (0.5–4 Hz) dominates the EEG waves.

4.Maximum slowing with large waves is seen in stage 4. Thus, the characteristic of deep sleep is a pattern of rhythmic slow waves, indicating marked synchronization; it is sometimes referred to as slow-wave sleep. Whereas theta and delta rhythms are normal during sleep, their appearance during wakefulness is a sign of brain dysfunction

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Forensic Medicine Notes & MCQs Part 1 (IPCs and Courts)

Posted by Dr KAMAL DEEP on February 1, 2011

1.In case of death in lock up, the inquest is held by –
a) A Police officer b) Magistrate (PGI 86)
c) Panchayat officer d) District Attorney

2.In India, inquest is carried out by all except –
a) Police b) Coroner (AIIMS 91)
c) Doctor d) Magistrate

3.The enquiry into the circumstances of death is
called – (TN 91)
a) Homicide enquiry b) Inquest report
c) Open verdict d) Adjounred verdict

4.The common type of inquest in India is –
a) Coroner’s inquest – (Karn 94)
b) Police inquest
c) Judicial magistrate inquest
d) Medical examiner’s inquest

5.In India, magrstrate inquest is done in the following
cases except – (A1 05)
a) Exhumation cases
b) Dowry deaths within 5 years of marriage
c) Murder cases
d) Death of a person in police custody

U/S 174 Cr.P.C-Police to enquire -Under section 174(subsection 3) Cr.P.C, it’s mandatory provision which requires that the body of a woman, who has committed suicide within seven years of her marriage, has to be subjected to postmortem examination and the inquest also has to be held.

U/S 176 Cr.P.C.-Inquiry by Magistrate into cause of death:-[When any person dies while in the custody of the police or when the case is of the nature referred to in clause (i) o or clause (ii) of sub-section (3) of section 174] the nearest Magistrate empowered to hold inquests shall, and in any other case mentioned in sub-section (1) of section 174, any Magistrate so empowered may hold an inquiry into the cause of death either instead of, or in additional to, the investigation held by the police officer; and if he does so, he shall have all the powers in conducting it which he would have in holding an inquiry into an offence.

Magistrate’s inquest means an inquiry conducted by a magistrate to ascertain matters of fact. It is commonly held in the following cases: Admission of a mentally ill person in a psychiatric hospital or a psychiatric nursing home under certain provisions of the Mental Health Act, 1987; Death of a convict in jail; Death of a person in police custody or during police interrogation; Death as a result of police shooting killing; Exhumation cases and Dowry deaths under section Sec 176 Criminal Procedure Code, 1973.


Important Crpc Sections:-

193 crpc–Perjury means giving willful false evidence by a witness while under oath, the witness is liable to be prosecuted for perjury and the imprisonment may extend to seven years. This falls under 193 of Penal Code

Section 53:- Examination at the request of police

Section 54:- Examination at the request of accused (imp:-NOT victim)


44-Injury Body Mind Reputation Property
84-Criminal responsibility of insane

85-Involuntary Drunkeness

86-Voluntary Drunkensess

312-316 Deals with criminal abortion

317- Abandoning of child by parents

318- Concealment of death of infant

definition of rape is sec 375
punishment for rape is sec 376
sec 377
is about unnatural sexual offences
Sections 354 (molestation),Section 354 of the IPC considers the assault or criminal force to woman with the intention to outrage her modesty. This offense is considered less serious than Rape.

Section 509. Word, gesture or act intended to insult the modesty of a woman.– Whoever, intending to insult the modesty of any woman, utters any word, makes any sound or gesture, or exhibits any object, intending that such word or sound shall be heard, or that such gesture or object shall be seen, by such woman, or intrudes upon the privacy of such woman, shall be punished with simple imprisonment for a term which may extend to one year, or with fine, or with both.

506 (2) (criminal intimidation)
The India Penal Code 1860 does not recognise child abuse. Only rape and sodomy can lead to criminal conviction
Section 5 of the Immoral Traffic Prevention Act 1956 prescribes punishment of not less than 7 years for inducing a child into prostitution, but does not directly address child abuse.
Most of these forms of child abuse are sought to be covered under sec. 354 of the Indian Penal Code as a violation of a woman’s modesty. Though offences under Sec. 354 of the IPC are cognizable, they are also bailable, allowing the perpetrator to abscond before the case comes up in court.

300-Defines MURDER
Section 302. Punishment for murder

Section 304:- Punishment for 299

Section 304. Punishment for culpable homicide not amounting to murder

Whoever commits culpable homicide not amounting to murder shall be punished with 1 [imprisonment for life ],or imprisonment of either description for a term which may extend to ten years, and shall also be liable to fine, if the act by which the death is caused is done with the intention of causing death, or of causing such bodily injury as is likely to cause death,Or with imprisonment of either description for a term which may extend to ten years, or with fine, or with both, if the act is done with the knowledge that it is likely to cause death ,but without any intention to cause death, or to cause such bodily injury as is likely to cause death

Sec 304 A Death due to negligent act (Medical or any)-2yrs punishment:-

Section 304A. Causing death by negligence
1[304A. Causing death by negligence.

Whoever causes the death of any person by doing any rash or negligent act not amounting to culpable homicide, shall be punished with imprisonment of either description for a term which may extend to two years, or with fine, or with both.]

Medical negligence falls under section 304A

Sec 304 b is dowry death- 7 yrs to Life  imprisonment

Section 320. Grievous hurt.

Section 312. Causing miscarriage
Section 37. Co-operation by doing one of several acts constituting an offence–A and B agree to murder Z by severally and at different times giving him small doses of poison. A and B administer the poison according to the agreement with intent to murder Z. Z dies from the effects of the several doses of poison so administered to him. Here A and B intentionally co-operates in the commission of murder and as each of them does an act by which the death is caused, they are both guilty of the offence though their acts are separate.

IPC Crimes
(i) Procuration of minor girls (section 366-A IPC)
(ii) Importation of girls ((Sec. 366-B IPC) 

SLL Crimes
(i) Immoral Trafficking (Prevention) Act 1956
(ii) Child Marriage Restraint Act, 1929.
Section 366B. Importation of girl from foreign country
1[366B. Importation of girl from foreign country. Whoever imports into 2[India] from any country outside India 3[or from the State of Jammu and Kashmir] any girl under the age of twenty-one years with intent that she may be, or knowing it to be likely that she will be, forced or seduced to illicit intercourse with another person, 4[***] shall be punishable with imprisonment which may extend to ten years and shall also be liable to fine.]
Section 366A. Procreation of minor girl
1[366A. procreation of minor girl.:–Whoever, by any means whatsoever, induces any minor girl under the age of eighteen years to go from any place or to do any act with intent that such girl may be, or knowing that it is likely that she will be, forced or seduced to illicit intercourse with another person shall be punishable with imprisonment which may extend to ten years, and shall also be liable to fine.]

Section 372. Selling minor for purposes of prostitution, etc
Section 373. Buying minor for purposes of prostitution, etc.

Section 299. Culpable homicide

Who ever causes death by doing an act with the intention of causing death, or with the intention of causing such bodily injury as is likely to cause death, or with the knowledge that he is likely by such act to cause death, commits the offence of culpable homicide.

Section 300. Murder

Except in the cases hereinafter excepted, culpable homicide is murder, if the act by which the death is caused is done with the intention of causing death, or-2ndly If it is done with the intention of causing such bodily injury as the offender knows to be likely to cause the death of the person to whom the harm is caused, or-3rdly If it is done with the intention of causing bodily injury to any person and the bodily injury intended to be inflicted is sufficient in the ordinary course of nature to cause death, or-4thly If the person committing the act knows that it is so imminently dangerous that it must, in all probability, cause death or such bodily injury as is likely to cause death, and commits such act without any excuse for incurring the risk of causing death or such injury as aforesaid.


(a) A shoots Z with the intention of killing him. Z dies in consequence. A commits murder.
(b) A, knowing that Z is labouring under such a disease that a blow is likely to cause his death, strikes him with the intention of causing bodily injury. Z dies in consequence of the blow. A is guilty of murder, although the blow might not have been sufficient in the ordinary course of nature to cause the death of a person in a sound state of health. But if A, not knowing that Z is labouring under any disease, gives him such a blow as would not in the ordinary course of nature kill a person in a sound state of heath, here A, although he may intend to cause bodily injury, is not guilty of murder, if he d8id not intend to cause death, or such bodily injury as in the ordinary course of nature would cause death.
(c) A intentionally gives Z a sword-cut or club-wound sufficient to cause the death of a man in the ordinary course of nature. Z dies in consequence. Here, A is guilty of murder, although he may not have intended to cause Z’s death.
(d) A without any excuse fires a loaded connon into a crowd of persons and kills one of them. A is guilty of murder, although he may not have had a premeditated design to kill any particular individual.

Exception I-When culpable homicide is not murder-Culpable homicide is not murder if the offender, whilst deprived of the power of self-control by grave and sudden provocation, causes the death of the person who gave the provocation or causes the death of any other person by mistake or accident.
The above exception is subject to the following provisos :–
First-That the provocations not sought or voluntarily provoked by the offender as an excuse for killing or doing harm to any person.
Secondly-That the provocation is not given by anything done in obedience to the law, or by a public servant in the lawful exercise of the powers of such public servant.
Thirdly-That the provocations not given by anything done in the lawful exercise of the right of private defence.
Explanation-Whether the provocation was grave and sudden enough to prevent the offence from amounting to murder is a question of fact.

Culpable Homicide not Amounting to Murder is an offence under s.304 of the Indian Penal Code. It applies to an event where the death is intentional but does not come within the IPC definition of Murder.

Murder versus Culpable Homicide:

Murder (defined under Section 300) and culpable homicide (defined under Section 299) are two offences under the Indian Penal Code the distinction between which has always been perplexing to the law students.

Section 299 and Section 300 IPC deals with the definition of culpable homicide and murder respectively. Section 299 defines culpable homicide as the act of causing death; (i) with the intention of causing death or (ii) with the intention of causing such bodily injury as is likely to cause death or (iii) with the knowledge that such act is likely to cause death. The bare reading of the section makes it crystal clear that the first and the second clause of the section refer to intention apart from the knowledge and the third clause refers to knowledge alone and not intention. Both the expression “intent” and “knowledge” postulate the existence of a positive mental attitude which is of different degrees. The mental element in culpable homicide i.e. mental attitude towards the consequences of conduct is one of intention and knowledge. If that is caused in any of the aforesaid three circumstances, the offence of culpable homicide is said to have been committed. Section 300 IPC, however, deals with murder although there is no clear definition of murder provided in Section 300 IPC. It has been repeatedly held by this Court that culpable homicide is the genus and murder is species and that all murders are culpable homicide but not vice versa. Section 300 IPC further provides for the exceptions which will constitute culpable homicide not amounting to murder and punishable under Section 304. When and if there is intent and knowledge then the same would be a case of Section 304 Part I and if it is only a case of knowledge and not the intention to cause murder and bodily injury, then the same would be a case of Section 304 Part II. The aforesaid distinction between an act amounting to murder and an act not amounting to murder has been brought out in the numerous decisions.

————(a) 300 (amounting to murder).Definition

Section 299(culpable homicide)

————b) 304  (not amounting to murder).Punishment for 299 if not (a)

_______c) 302 Punishment if (a)

Which carries more weight in a court of law –
a) Dying declaration (PGI 87)
b) Dying deposition
c) Both carry the-same weight
d) Both are not significant

Dying declaration is very important documentary evidence. It is hearsay evidence but even then it is given a lot of weightage in the court proceedings. Recording of dying declaration is very important. If it is recorded properly by the proper person keeping in mind the essential ingredients of the dying declaration it retains its full value. Missing any single ingredients of dying declaration makes it suspicious and offenders are likely to get the benefits of its shortcomings.

Its admissibility is explained in the section 32 (1) of Indian Evidence Act. According to this section when the statement is made by a person as to the cause of his death, or any of the circumstances of the transaction which resulted in his death, in cases in which the cause of that person’s death comes into question. Such statements are relevant whether the person who made this was expecting death or not [1]. In English law he must be under expectation of death only then this declaration is valid.

This can be best certified by the doctor who knows best about the condition of the patient. But even in conditions where it was not possible to take fitness from the doctor, dying declarations have retained their full sanctity if there are other witnesses to testify that victim was in such a condition of the mind which did not prevent him from making statement. Medical opinion cannot wipe out the direct testimony of the eyewitness stating that the deceased was in fit and conscious state to make the dying declaration.

It is best that it is recorded by the magistrate but if there is no time to call the magistrate due to the deteriorating condition of the victim it can be recorded by anybody e.g. public servant like doctor or any other person. Courts discourage the recording of dying declaration by the police officers but if there is no body else to record it dying declarations written by the police officers are also considered by the courts. If these are not recorded by the magistrate it is better that signatures of the witnesses are taken who are present at the time of recording it.

Ideally it should be recorded by executive magistrate. [But if magistrate is not available, it can be recorded by doctor himself or if the patient is not in the hospital it can also be recorded by any person present near the patient.] Doctor has to certify be ‘compos mentis’ .During recording police, relatives should not be present there. .It should be recorded in the presence of magistrate, doctor & 2 disinterested witness. .No oath is administered & leading questions are not permitted. .It is recorded in Question & answer form in the vernacular of patient.

At the end it is read over to the patient & is signed by the magistrate, doctor & 2 disinterested witness. If the patient dies during recording Dr. should certify that pt. is dead & incomplete declaration is signed by all the concerned. The date, time & place of recording is noted & report is sent to magistrate (if not present) in a sealed cover. If the pt. survives after recording, the declaration looses its value, because now he can be called to the court for evidence where cross examination will be possible.However under section 157 IEA,the declaration may still be relied upon to corroborate the statement of the complainant at the time of oral examination.

Ref:-JIAFM, 2004; 26(1). ISSN 0971-0973
Dr. R.K.Gorea, Professor and Head, Forensic Medicine, GMC, Patiala
Dr. O.P.Aggarwal, Professor, Forensic Medicine, M.M. Medical College, Mullana, Ambala

DYING DEPOSITION It is defined as the deposition (statement on oath) made by a person likely to die bcoz of some unnatural act done on his body,narrating the cause of his likely unnatural death to the magistrate, in the +nse of accused & lawyers of both parties who can cross examine the pt. Precautions- It should by magistrate, in the +nse of accused & lawyers of both parties. Dr. has to be +ntthrough out the procedure & has to certify the pt. in compos mentis. Oath is administered to the pt. Cross examination includes leading questions.Any person may be present during recording .No witness required. Recording is done as per the procedure of court & hence almost it seems that a court is +nt at bedside of pt.

Importance-Dying deposition is having more value than that of dying declaration bcoz, It is recorded by magistrate. In the +nseof accused & lawyers of both parties. It is recorded after cross examination. It retains its value even if pt. survives bcozcross examination has already been done.

The power of Amnesty for capital punishment
is vested with – . (AMU 88)
a) The president b) Supreme court
c) High court d) The governer

Amnesty is a legislative or executive act by which a state restores those who may have been guilty of an offense against it to the positions of innocent people. It includes more than pardon, in as much as it obliterates all legal remembrance of the offense.

Courts can only give stay order pending hearing for a lower court order.

Conduct money is paid to expert witness with
summons from – (AI 90)
a) Civil court b) Criminal court
c) High court d) Sub magistrate

Conduct money is the money paid by the court of law to the witness who is under summon or subpoena to meet his travelling expenses from his place of residence to the court, and back . In CIVIL cases , this is paid to witness at the time the summon is served on him . If this amount is not paid to him/her, he/she may ignore the summons, if he/she so desire. If he/she feels the sum is inadequate can inform the court accordingly & get it enhanced . In CRIMINAL cases however, no such fee is given usually, & it is bounden duty of every citizen to attend the court whenever summoned.(It may however be noted that provision is made by government under section 312 of Crpc for payment of reasonable expenses of an expert witness attending before any criminal court.Payment of reasonable expenses of an expert witness in magistrate courts in summons cases is provided for under section 254(3) and in warrant cases under section 243 (3) CrPC.)


Death sentence can be awarded by – (Kerala 91)
a) First class magistrate
b) Second class magistrate
c) Session court
d) Chief judicial magistrate

Important POINTS:-

1.A session court cannot commute death sentence.How can it commute a death sentence when it is the lowest court to announce the death sentence.

2.President cant Give death sentence It can give amnesty/mercy plea.

3.Additional session court have same power as session court

4.Assistant session court has lower power.

5.None of the magistrate can give death sentence or Life imprisonment

6.CJM power:- 7 years,fine without limit

1st class Judicial magistrate power:- 3 years,upto Rs 5000

2nd class Jud Mag:- 1 Year Max, upto 1000

  1. According to Indian Majority Act 1875, a person attains majority when he/she attains the age of 18 years.
  2. According to Section 4(a) of the TheHindu Minority and Guardianship Act 1956, a person who is below 18 years of age is a minor.


According to Section 363-A of I.P.C, kidnapping or maiming of a minor for the purpose of begging is an offence. If the person merely kidnaps, the sentence is 10 years and fine. If he maims, the sentence is life imprisonment and fine. For the purposes of this section a minor is a female below 18 years (or a male below the age of 16 years). This is an interesting section, as the ages for minors are different for males and females.

However Sections 87 IPC mentions eighteen years as the age for giving consent for acts not intended and not known to be likely to cause death or grievous hurt. These acts are not necessarily for the benefit of the person . Hence Section 87 IPC is not applicable to the medical profession as here (in Section 87 IPC), the acts are NOT done for the person’s benefit. .

According to Section 87 of I.P.C, a person under the age of 18 years can not give valid consent whether express or implied to suffer any harm which may result from an act not intended or not known to cause death or grievous hurt (example: fencing)’

According to Section 89 of I.P.C, a child below 12 years can not give valid consent to suffer any harm which may occur from an act done in good faith and for its benefit(as a general physical examination by a doctor,surgical operations).


The age of a 16 years old female is best determined
by the radiograph of – (PGI 87)
a) Lower end of radius and Ulna
b) Upper end of humerus
c) Upper end of radius and Ulna
d) Xiphisternum

Female                       Male

Elbow     13-14 yrs                   15-17 yrs

Wrist:-    16-17 years                18-19 yrs

Shoulder      17-18                   19-20 yrs

Crest of Ilium 18-19                  20-21yrs

Ref Parikh

Elbow(13-14)—Wrist(16-17)—Shoulder(17-18)—Crest of ilium(18-19) Add plus 2 for Males

By 13-14 years the epiphysis at the elbow join their respective shafts in Females. In males by 16-18 yrs.,all the epiphysis at the elbow (except the medial epicondyle),head of the femur,and lower end of tibia join the respective shafts.

The age of a 15 year old female is best determined
by the radiograph of –

a) Lower end of Radius and Ulna
b) Upper end of humerus
c) Upper end of Radius and Ulna??? NOT SURE
d) Xiphisternum

Ossification centre appearing just before birth is—LOWER END OF FEMUR

Capitate and hamate ossify at the age of 4 months,so before 4 months of age,no bone is seen on radiography

Pre-auricular sulcus is used for – (AMJ 88)
a) Determination of Race
b) Determination of age
c) Determination of sex
d) None of the above

The narrow part of the pelvic surface, between the auricular surface and the upper rim of the greater sciatic notch, often shows a rough preauricular sulcus for the lower fibers of the anterior sacroiliac ligament, more apparent in females.

In forensic practice, identification of human skeletal remains (which are sometimes fragmentary) usually involves diagnosis of sex, and this is most certainly established from the pelvis. Even parts of the pelvis may be useful. Several studies of metrical characteristics in various pelvic regions have been made, leading to the production of various indices. The ilium has received particular attention, e.g. one index compares the pelvic and sacroiliac parts of the bone. A line is extended back from the iliopectineal eminence to the nearest point on the anterior auricular margin and thence to the iliac crest. The auricular point divides this chilotic line into anterior (pelvic) and posterior (sacral) segments, each expressed as a percentage of the other. Chilotic indices display reciprocal values in the sexes: the pelvic part of the chilotic line is predominant in females, and the sacral part in males. Detailed metrical studies of the ilium have indicated its limited reliability in ‘sexing’ pelvis. However, the higher incidence and definition of the female preauricular sulcus is recognized.The desirability of correlating all available metrical data is to be emphasized; when a range of pelvic data can be combined, especially if they are metrical, 95% accuracy should be achieved. Complete accuracy has been claimed when the rest of the skeleton is available. Assessment of sex from isolated and often incomplete human remains is less reliable.




Males:-Suprapubic arch narrow,V shaped,angle not more than about 70 degrees and hence less Distance between ischia,Greater sciatic notch is narrow,deep,and less than right angle.Obturator foramina ovoid.Ischial Tuberosities inverted

Females:- Suprapubic arch wide,U shaped,angle more than a right angle and hence more distance between ischia.Greater sciatic notch is wide shallow and almost a right angle or more.Obturator foramina triangular.Ischial Tuberosity everted.


Structure of the bony pelvis. A. In women. B. In men. The angle formed by the pubic arch can be approximated by the angle between the thumb and index finger for women and the angle between the index finger and middle finger for men as shown in the insets.

Skull:- Orbital opening big and rectangular in males while it is rounded and small in females.Muscle attachments are more pronounced in males.

Cephalic index(for the determination of race) is obtained by multiplying the maximum transverse breadth by 100 and dividing it by maximum AP Length. A skull is dolichocephalic(long headed)—70-74.9 seen in Aryans,aborigines,and blacks.

Mesaticephalic is medium long headed—75—79.9—seen in European,, Indians and Chinese.

Mongolian- is Brachycephalic——index is more than 80or above..(transverse diameter approaches 80 per of AP length).

100 % sex differentiation is not possible by pelvis alone.Entire skeleton is needed.

According to Krogman:- Pelvis alone—95%

                                   Skull alone—90%

                                   Long bones alone—80%

                                   Pelvis and Skull—98%, Entire skeleton—100%

A method of sexing of bones by the use of medullary index has also been described.The humerus,radius,ulna,and tibia are the most reliable bones for this purpose.

Medullary index:- Diameter of medulla/diameter of whole bone multiply by 100

There is thinning of cortex in old age so it may also give some idea about age.

Medullary index of Hair is used to distinguish between animal or human hair.In animals it is more than 0.5 while in humans it is less than 0.3.

In human hair,only the cortex is pigmented;the medulla is narrow ,absent or pigmented.In Negros’s fragmentation of medulla of scalp hair is seen.


Temporary—Lower central incisors,2(6-8 months)—-Upper central incisors,2(7-9 months)———Upper Lateral incisors,2(7-9 months)———Lower lateral incisors,2(10-12 months)——-First molars,4(12-14 months)———Canines,4(17-18 months)——-Second Molars,4(20-30 months)

Permanent—-First Molars,4(6-7 years)—At new place

                   Central incisors,4(6-8 years)—Replacement

                   Lateral incisors,4(8-9 years)—Replacement

                  First bicuspids/premolars,4(9-11 years)—-Replaces 1st temp molar

                  Second bicuspids/premolars,4(10-12 years)-Replaces second temp molars

                  Canines,4(11-12 years)—-Replaces temp canines

                   Second molars,4(12-14 years)—-At new place

                  Third Molars,4(17-21 years)—— At new place

All permanent molars are additions at new place not replacements behind the second temporary molars.

There is no temporary premolars or bicuspids.Only permanent.

Premolars replaces first and second temporary molars.

The best method to determine age up to 14 years is DENTITION.


The temporary teeth begin to shed from the 6th to 7th years after the eruption of first molar behind the second “temporary” molar teeth and all temporary teeths have shed when permanent canines appears.Period of mixed dentition is from 6-11 years.

MOST IMPORTANT POINT:-From the age of 6 years till the age of 12 years-The total number of teeth remains 24 in number as 4 permanent molars in 6 years are added at new place other permanent teeth’s replaces temporary teeths; so total number doesn’t changes after addition of first permanent molars till the appearance of second molars at the age of 12-14 years.

A girl of 10 years will have 24 teeth—16 permanent and 8 temporary teeths


M      -7 yrs—-NEW PLACE







Q:-Second molar erupts at – (A1 91)
a) 6 years b) 12 years
c) 18 to 22 years d) 25 to 28 years

20 permanent teeth and 8 temporary teeth are
seen at the age of – (Kerala 2001)
a)10yrs  b) 11 yrs
c) 9 v s dl 12 yrs

First permanent tooth to arise- (JIPMER 02)
a) Incisor b) Canine
c) Premolar d) Molar

Among the secondary changes in tooth the most
useful one for age determination is – (Corned 08)
a) Attrition
b) Secondary dentine deposition
c) Root resorption
d) Root transparency

On tenth day of a tooth being knocked out, the local
clinical finding will be – (AIIMS 81, Kerala 89)
a) Tooth socket being filled up by tissue
b) Blood clots in the socket
c) Alvoelar process smooth
d) Fluid blood in the socket

In antemortem tooth loss or extraction of the
alveolus is – (Karnataka 02)
a) Smooth
b) Sharp and feathered
c) Does not show any injury
d) sMay have a regular or an irregular appearance

When a tooth has been knocked out,bleeding from its socket stops in about one to two days and a clot is formed.The clot is obliterated by fibrous tissue in about 14 days.The socket is completely filled with gradual new bone in about a  year,as seen on X-RAY examination.

Eruption of temporary teeth will be completed by

a)One to one and half year (JIPMER 81,
b) Two to two and half years Kerala 90)
c) Three to four years
d) Four to five years

A girl of 10 years wilt have —- permanent and
–temporary teeth – (PGI 79, DNB 90)
a) 8,12 b)8,16
c) 12,12 d) 16,8

A child at the age of 7 years has how many teetha)
16 b) 20 (PGI 83, UPSC 81)
C) 24 d) 28

IMPORTANT:- A boy has 20 permanent and 8 temporary teeth
his age would be –
‘ (APPPGE 04)
a) 9 years b) 10 years
c) 11 years d) 12 years

Answer in guides is 10 years.But answer is d i.e.12 years.

The total number of teeths is 28 in this Q

“In question there should have been 16 permanent and 8 temp teeth.If there are 20 permanent teeth there should be 4 temp teeth. But since there is total number of 28 teeth,A second molars must have got erupted also so age must be 12 years.8 temporary teeth i.e canines and second temp molars also get replaced as late as 12 years.So period of mixed dentition persists till about 12 to 13 years.The bicuspids are most irregular and are of little value in fixing age.”

8 TEMP TEETH are still here so 4 temporary canines and 4  temporary second molars are not replaced by 4 permanent canines and  4 permanent second premolars respectively but 4 second permanent molars have got erupted at new place making total number to 28 .since 24 teeth are till 12 years of age only. so age is 12 years.



Number of deciduous teeth is – (JIPMER 95)
a) 20 b) 24
C) 28 d) 32

Tattoo is useful in identifying body – (A1 91)
a) Living b) Dead
c) Decomposed d) Burnt

Tattoo marks on unidentified putrefied bodies may be photographed with a sharp definition if the loose epidermis is first removed and the design on the dermis recorded.

Blackening and tattooing of skin and clothing can
be best demonstrated by –  (A1 03)
a) LuminoI spray
b) Infra red photography
c) Ultra violet light
d) Magnifying lens

To reveal latent tattoo marks,the use of high-contrast photography,computer image enhancement,ultraviolet lamp or infra-red photography is helpful.

Tattooing is seen surrounding the wound of
entrance from a revolver or pistol, if the weapon
is discharged up to distance of – (COMEDK 05)
a) 10 cm b) 30 cm
c) 50 cm d) 90 cm

Rigor mortis

Rigor mortis is simulated by – (AIIMS 92)
a) Mummification b) Algor mortis
c) Cadaveric spasm d) All of the above

Stiffening and shortening of muscles.

After death ATP is resynthesized for a short period of time depending upon the glycogen available locally,but after this glycogen is used up,ATP cannot be resynthesized.This leads to fusion of myosin and actin filaments into a dehydrated stiff gel resulting in condition known as RIGOR MORTIS.

imp-it is due to decreased ATP not due to increase.

It can be broken down by mechanical force.

In the involuntary muscles,rigor mortis appear in the heart within an hour after death.

In the voluntary muscles sequence is as follows:-

EYELIDS(3-4 HRS)—->FACE(4-5 HRS)—->NECK AND TRUNK—->(5-7 HRS)——>MUSCLES OF UPPER EXTREMITIES—->(7-9 HRS),—-> of the legs(9-11hrs)—–>FINGERS AND TOES(11-12 HRS)

In india rigor mortis commences within 2-3 hrs,takes about 12 hrs to develop from head to toes,persist for another 12 hrs and takes about 12 hrs to pass off.

So if rigor mortis has not set in,the time since death would be within 2 hours and if it has affected the whole body,the time since death would be within about 12- 24 hrs.

Rigor mortis in fetus develops after attaining 7 months of age.

As a general rule,the longer it takes to appear for rigor,the longer it lasts and vive  versa.

In chronic diseases and convulsive disorders,rigor appears early and passes off quickly due to depletion of  glycogen stores.In strychnine poisoning,rigor sets in almost immediately and passes off early.

In cases of sudden death,in healthy adults,a late onset and long duration is usual.

In death from drowning,rigor appears early due to muscular exhaustion but lasts longer due to coldness of water.

Rigor is frequently absent in septicemic conditions.

Surroundings effect:-Rigor is delayed by cold and accelerated by heat.

It should be differentiated from other causes of postmortem muscular stiffening or condition simulating rigor mortis such as:
a)Cadaveric spasm.

Cadaveric spasm OR Instantaneous rigor
It is the muscular stiffening in special muscles and special type of death.
* It occurs in voluntary muscles and in cases of deaths accompanied with violence (violent death).
*Accompanied by severe mental and nervous excitation.

-It occurs as a continuation of the antemortem contraction of muscles Justbefore death without passing the stage of primary flaccidity.
-Cadaveric spasm records the last act of life Justbefore death.

Cadaveric spasm cannot be fabricated.
-Cadaveric spasm occurs in injuries of the CNS, drowning, suicide, struggling homicide and such cases of death with nervous over stimulation.

Medicolegal importance
cadaveric spasm
1-In cases of drowning, the dead animal keeps the mouth grasping some aquatic plants, weeds, and mud which is a sure sign of drowning.
2-In human forensic medicine, the hand of the victim is seen firmly grasping the weapon in suicide or the cloths or hairs of the assailant in homicide.

When a group of muscles of a dead body were in
state of strong contraction immediately prior to
death and remain so even after death, the condition
is termed as – (AIIMS May 05)
a) Gas stiffening b) Rigor mortis
c) Cadaveric spasm d) Cold stiffening

b)Cold stiffening.

Cold stiffening of muscles is due to the effect of very low temperature or freezing. It is reversible if the dead body warmed, the dead body then passes the primary flaccidity and rigor mortis as soon as thawing takes place.

c)Heat stiffening.Exposure of a body to intense heat results in heat stiffening due to coagulation of the muscle protein. Shortening of the muscles due to the effect of heat or fire of hot liquids. Heat coagulation or stiffening persists till the beginning of secondary flaccidity.

Cold stiffening may be associated with –
a) Trench foot (AIIMS 80, AMC 85)
b) Immersion foot
c) Body rigid, heavy and stiff
d) .Any of the above

It’s a POST-MORTEM finding

Rigor mortis is simulated by – (AIIMS 92)
a) Mummification b) Algor mortis
c) Cadaveric spasm d) All of the above

Rigor moreis in a foetus develops after
attaining – (TN 02)
a) 3 months of age b) 4 months of age
c) 7 months of age d) 10 months of age

Rigor mortis develops …. after death-(PGI 86,87)
a) 1/2- 1 hr. b) 1 to 2 hrs
c) 3 to 6 hrs. d) 12 hrs.

Rigor mortis first starts in – (PGI 81, AIIMS82)
a) Upper eyelids b) Lower eyelids
c) Lower limbs d) Fingers

Prolongation of Rigor mortis is seen in – (PGI 03)
a) Lead b) Arsenic
c) Mercury d) Copper

Delayed rigor mortis occurs with – (UP 07)
a) Vegetables poisons b) Strychnine
c) Opium d) Septicemia

Pugilistic attitude is due to – (PGI 99)
a) Coagulation of proteins b) Cadaveric spasm
c) Rigor mortis d) Coagulation of fats

Seen in heat stiffening

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Gynaecology & Obstetrics Notes

Posted by Dr KAMAL DEEP on January 21, 2011

1. Feto maternal transfusion is demonstrated in the mother by: a) Coombs test b) Kleihauer count c) Electrophoretic methods, d) reticulocyte count

Fetal red cells in the maternal circulation can be identified by use of the acid elution principle first described by Kleihauer, Brown, and Betke, or any of several modifications. Fetal erythrocytes contain hemoglobin F, which is more resistant to acid elution than hemoglobin A. After exposure to acid, only fetal hemoglobin remains. Fetal red cells can then be identified by uptake of a special stain and quantified on a peripheral smear (Fig. 29–7). This test is very accurate unless the maternal red cells carry excess fetal hemoglobin as the result of a hemoglobinopathy.

During all pregnancies, very small volumes of blood cells escape from the fetal intravascular compartment across the placental barrier into the maternal intervillous space. This observation is important for several reasons. It is the cause of maternal red cell isoimmunization, as discussed in Isoimmunization.Choavaratana and colleagues (1997) performed serial Kleihauer–Betke tests in 2000 pregnant women and found that, although the incidence of fetal–maternal hemorrhage in each trimester was high, the volume transfused from fetus to mother was very small .

D-positive fetal red blood cells in D-negative maternal blood can be detected by the rosette test. Maternal red cells are mixed with anti-D antibodies, which coat any fetal (D-positive) cells present in the sample. Indicator red cells bearing the D-antigen are then added, and rosettes form around the fetal cells as the indicator cells attach to them by the antibodies. Rosettes indicate that fetal D-positive cells are present.



Broad ligament
The broad ligament is a sheet-like fold of peritoneum, oriented in the coronal plane that runs from the lateral pelvic wall to the uterus, and encloses the uterine tube in its superior margin (Fig. 5.50). The part of the broad ligament between the origin of the mesovarium and the uterine tube is the mesosalpinx.
The peritoneum of the mesovarium becomes firmly attached to the ovary as the surface epithelium of the ovary. The ovaries are positioned with their long axis in the vertical plane. The ovarian vessels, nerves, and lymphatics enter the superior pole of the ovary from a lateral position and are covered by another raised fold of peritoneum, which with the structures it contains forms the suspensory ligament of ovary (infundibulopelvic ligament).
The inferior pole of the ovary is attached to a fibromuscular band of tissue (the ligament of ovary), which courses medially in the margin of the mesovarium to the uterus and then continues anterolaterally as the round ligament of uterus (Fig. 5.50). The round ligament of uterus passes over the pelvic inlet to reach the deep inguinal ring and then courses through the inguinal canal to end in connective tissue related to the labium majus in the perineum. Both the ligament of ovary and the round ligament of uterus are remnants of the gubernaculum, which attached the gonad to the labioscrotal swellings in the embryo.




Between the perineal membrane and the membranous layer of superficial fascia is the superficial perineal pouch, and the principal structures in this pouch are the erectile tissues of the penis and clitoris and associated skeletal muscles

Structures in the superficial perineal pouch

The superficial perineal pouch contains:

  • erectile structures that join together to form the penis in men and the clitoris in women; and
  • skeletal muscles that are associated mainly with parts of the erectile structures attached to the the perineal membrane and adjacent bone

The superficial perineal pouch contains three pairs of muscles: the ischiocavernosus, bulbospongiosus, and superficial transverse perineal muscles

3.Lymph Nodes:-Lymphatic channels from superficial tissues of the penis  drain mainly into superficial inguinal nodes, as do lymphatic channels from the scrotum or labia majora.

The glans penis,clitoris, labia minora, and the terminal inferior end of the vagina drain into deep inguinal nodes

Lymphatics from the testes drain via channels that ascend in the spermatic cord, pass through the inguinal canal, and course up the posterior abdominal wall to connect directly with lateral aortic and preaortic nodesaround the aorta, at approximately vertebral levels L1 and L2.

Lymphatics from most pelvic viscera drain mainly into lymph nodes distributed along the internal iliac and external iliac arteries and their associated branches (Fig. 5.67), which drain into nodes associated with the common iliac arteries and then into nodes associated with the lateral surfaces of the abdominal aorta. In turn, these lateral aortic nodes drain into the lumbar trunks, which continue to the origin of the thoracic duct at approximately vertebral level T12.

Lymphatics of vulva transverse the labia from medial to lateral side. The lymphatic drainage of the labia proceeds to the upper vulva and mons, then to the inguinal and femoral nodes with both superficial and deep lymph nodes.

The last deep femoral node is called the Cloquet’s node; spread beyond this node affects the lymph nodes of the pelvis. The tumor may also invade adjacent organs such as the vagina, urethra, and rectumand spread via their lymphatic.

Vessels from the lower part of the uterine body pass mostly to the external iliac nodes, with those from the cervix. From the upper part of the body, the fundus and the uterine tubes, vessels accompany those of the ovaries to the lateral aortic and pre-aortic nodes. A few pass to the external iliac nodes. The region surrounding the isthmic part of the uterine tube is drained along the round ligament to the superficial inguinal nodes.





4.Pelvic Floor

The muscles that span the pelvic floor are collectively known as the pelvic diaphragm(Fig. 38-8). This diaphragm consists of the levator ani and coccygeus muscles along with their superior and inferior investing layers of fasciae. Inferior to the pelvic diaphragm, the perineal membrane and perineal body also contribute to the pelvic floor.

Perineal body —The perineal body is an ill-defined but important connective tissue structure into which muscles of the pelvic floor and the perineum attach. It is positioned in the midline along the posterior border of the perineal membrane, to which it attaches. The posterior end of the urogenital hiatus in the levator ani muscles is also connected to it.

The deep transverse perineal muscles intersect at the perineal body; in women, the sphincter urethrovaginalis also attaches to the perineal body. Other muscles that connect to the perineal body include the external anal sphincter, the superficial transverse perineal muscles and the bulbospongiosus muscles of the perineum.

Urogenital Diaphragm/Triangular Ligament:-The perineal membrane is related above to a thin space called the deep perineal pouch (deep perineal space) which contains a layer of skeletal muscle and various neurovascular elements. The deep perineal pouch is open above and is not separated from more superior structures by a distinct layer of fascia. The parts of perineal membrane and structures in the deep perineal pouch, enclosed by the urogenital hiatus above, therefore contribute to the pelvic floor and support elements of the urogenital system in the pelvic cavity, even though the perineal membrane and deep perineal pouch are usually considered parts of the perineum.

5.Benign ovarian teratomas are usually cystic structures that on histologic examination contain elements from all three germ cell layers. The word teratoma was first advanced by Virchow and translated literally means “monstrous growth.” Teratomas of the ovary may be benign or malignant. Although dermoid is a misnomer, it is the most common term used to describe the benign cystic tumor, composed of mature cells, whereas the malignant variety is composed of immature cells (immature teratoma). Dermoid is a descriptive term in that it emphasizes the preponderance of ectodermal tissue with some mesodermal and rare endodermal derivatives. Malignant teratomas that are immature are usually solid with some cystic areas and histologically contain immature or embryonic-appearing tissueBenign teratomas may undergo malignant transformation. This occurs in approximately 1% to 2% of dermoids, usually in women over age 40.

6.because of their relative prevalence, dermoids are the tumor most frequently reported in a series of women with adnexal torsion. However, the relative risk of adnexal torsion is higher with parovarian cysts, solid benign tumors, and serous cysts of the ovary. The right ovary has a greater tendency to twist (3 to 2) than does the left ovary. Torsion of a malignant ovarian tumor is comparatively rare.Adnexal torsion occurs most commonly during the reproductive years, with the average patient being in her mid-20s.Pregnancy appears to predispose women to adnexal torsion, with approximately one in five women being pregnant when the condition is diagnosed. Most susceptible are ovaries that are enlarged secondary to ovulation induction during early pregnancy.

7.Ovarian Abnormalities in pregnancy

The best treatment of an asymptomatic ovarian cyst in the first trimester
a) Immediate laparotomy b) Laporatomy in second trimester…ANS
c) Laparotomy after delivery d) Leave it alone till it becomes symptomatic

D-nothing should be left alone.They should be observed serially with imaging techniques, and resection is performed if they grow, begin to look suspicious, or become symptomatic

Any type of ovarian mass may complicate pregnancy


Early in pregnancy, ovarian enlargement less than 6 cm in diameter usually is the consequence of corpus luteum formation. With the advent of high-resolution sonography, Thornton and Wells (1987) proposed a conservative approach to management based on ultrasonic characteristics. They recommend resection of all cysts suspected of rupture or torsion, those capable of obstructing labor, and measuring more than 10 cm in diameter because of the increased risk of cancer in large cysts. Cysts 5 cm or less could be left alone, and indeed, most undergo spontaneous resolution


It seems reasonable to remove all ovarian masses over 10 cm because of the substantive risk of malignancy. Tumors from 6 to 10 cm should be carefully evaluated for the possibility of neoplastic disease by ultrasound, MRI, or both. If evaluation suggests a neoplasm, then resection is indicated. If the corpus luteum is removed before 10 weeks, then 17-OH-progesterone, 250 mg intramuscularly, is given weekly until 10 weeks. Cystic masses that are thought to be benign or are less than 6 cm are observed serially with imaging techniques, and resection is performed if they grow, begin to look suspicious, or become symptomatic. In general, we have performed elective surgery at 16 to 20 weeks. Most masses that will regress will have done so by that time.

8.OCP—-Decreased risk of endometrial and ovarian cancer

INCREASES—liver, cervix, and breast cancer

Tamoxifen is an antagonist of the estrogen receptor in breast tissue via its active metabolite, hydroxytamoxifen. In other tissues such as the endometrium, it behaves as an agonist(increases endometrial ca risk but decreases breast cancer risk), hence tamoxifen may be characterized as a mixed agonist/antagonist.

OESTROGEN UNOPPOSED INCREASES RISK OF breast and endometrial cancer

9.Women with TOA most commonly present with lower abdominal pain and with unilateral or bilateral adnexal masses. Fever and leukocytosis may be absent. Abscess rupture causes severe pain with chills, fever, and progressive peritonitis. If large volumes of pus are released into the peritoneal cavity, infection may spread upward along the colonic gutters to form subphrenic abscesses that cause shoulder pain. Sonography is typically diagnostic.

25-year old married infertile woman having regular menstruation, fever. lower abdominal pain and dysmenorrhoea presents herself at the OPD. On examination, there are bilateral soft tender masses of 3″ diameter in both fornices and uterus is of normal size. The most likely diagnosis is,
a) Cystic ovaries b) Tubo-ovarian masses
c) Ectopic pregnancy d) Tuberculous salpingitis

10.The size of ovum is : a) 0.133 mm, b) 0.144 mm, c) 0.2 mm, d) None of the above

The mature ovum  measures 120-130 u/0.133 mm

11.The second maturation division of the human ovum occurs at the time of: a) fertilisation b) implantation c) ovulation d) puberty.


This protein hormone has structural features that are similar to insulin and insulin-like growth factors I and II. Its major biological action is remodeling of the connective tissue of the reproductive tract, thus allowing accommodation of pregnancy and successful parturition (Weiss and colleagues, 1993). Relaxin is secreted by the corpus luteum, decidua, and placenta in a pattern similar to that of chorionic gonadotropin (hCG). It is also secreted by the heart, and increased levels have been found in association with heart failure (Fisher and co-workers, 2002).

The role of relaxin during human pregnancy is not completely defined, however, it is known to have effects on the biochemical structure of the cervix (Bell and colleagues, 1993). The hormone also affects myometrial contractility, which may be implicated in preterm birth. Increases in peripheral joint laxity during human pregnancy do not correlate with serum relaxin levels (Marnach and co-workers, 2003; Schauberger and colleagues, 1996

13.Females with diabetes, hypertension or taking diet rich in fat are at higher risk. This is called Corpus cancer syndrome which consist of obesity, hypertension and diabetes.

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Posted by Dr KAMAL DEEP on January 20, 2011

1. Actions of CRH on the Fetal Adrenal Gland

As discussed in Chapter 3 (see Fetal Adrenal Glands), the human fetal adrenal glands are morphologically, functionally, and physiologically remarkable organs. At term, the fetal adrenal glands weigh the same as those in the adult and are similar in size to the adjacent fetal kidney. The daily production of steroids by the fetal adrenal glands near term is estimated to be 100 to 200 mg/day, which is higher than the 30 to 40 mg/day seen in adult adrenals at rest. Within the fetal adrenal gland, steroidogenic function and zonation are different from the adult. For example, significant amounts of cortisol are not produced in the fetal adrenal gland until the last trimester. As a result, fetal cortisol levels increase during the last weeks of gestation (Murphy, 1982). During this same period, levels of dehydroepiandrosterone sulfate (DHEA-S) production also are increasing significantly, leading to increases in maternal estrogens, particularly estriol. The increase in adrenal activity occurs in contrast to fetal adrenocorticotropic hormone (ACTH) levels which do not increase until the stress of actual labor.

This substantial growth and increased steroid synthesis during latter gestation is at a time when fetal plasma ACTH levels appear to decline (Winters and co-workers, 1974). Thus, many investigators have surmised that there must be growth and steroidogenesis stimuli for these glands in addition to ACTH. Two observations have made it extremely likely that factors secreted by the placenta play a key role in the regulation of steroidogenesis during late gestation. First, the fact that ACTH levels do not increase significantly during the last part of gestation makes it likely that growth and differentiation of the fetal adrenal glands are influenced by factors secreted by the placenta. Second, the fetal zone of the adrenal gland undergoes rapid involution immediately after birth when placenta-derived factors are no longer available. Many believe that CRH of placental origin is one of the critical components that facilitates fetal adrenal hypertrophy and increased steroidogenesis late in gestation. Indeed, in vitro studies have shown that CRH is able to stimulate fetal adrenal DHEA-S and cortisol biosynthesis (Parker and associates, 1999; Smith and co-workers, 1998). The ability of CRH to regulate the adrenal glands and of the adrenals to regulate placental production of CRH has led to the idea of a feed-forward endocrine cascade that occurs late in gestation (Fig. 6–19).

Placental CRH has been proposed to play several roles in the regulation of parturition. First, placental CRH may enhance fetal cortisol production, which would provide positive feedback on the placenta to produce more CRH. The resulting high level of CRH may modulate myometrial contractility. Second, cortisol has been proposed to affect the myometrium indirectly by stimulating the membranes to increase prostaglandin synthesis. Third, CRH has been shown to stimulate fetal adrenal C19-steroid synthesis, leading to increased substrate for placental aromatization. The resulting elevation in estrogens would shift the estrogen-to-progesterone ratio and promote the expression of a series of contractile proteins in the myometrium, leading to a loss of myometrial quiescence.

Ref:- Williams


Maternal plasma levels of prolactin increase markedly during the course of normal pregnancy. Serum concentration levels are usually 10-fold greater at term—about 150 ng/mL—compared with normal nonpregnant women. Paradoxically, after delivery, the plasma prolactin concentration decreases even in women who are breast feeding. During early lactation, pulsatile bursts of prolactin secretion occur apparently in response to suckling. The physiological cause of the marked increase in prolactin prior to parturition is not entirely certain. It is known, however, that estrogen stimulation increases the number of anterior pituitary lactotrophs and may stimulate the release of prolactin from these cells (Andersen, 1982). Thyroid-releasing hormone also acts to cause an increased prolactin level in pregnant compared with nonpregnant women, but the response decreases as pregnancy advances (Andersen, 1982; Miyamoto, 1984). Serotonin also is believed to increase prolactin, and prolactin-inhibiting factor (dopamine) inhibits its secretion.

The principal function of maternal serum prolactin is to ensure lactation. Early in pregnancy, prolactin acts to initiate DNA synthesis and mitosis of glandular epithelial cells and the presecretory alveolar cells of the breast. Prolactin also increases the number of estrogen and prolactin receptors in these same cells. Finally, prolactin promotes mammary alveolar cell RNA synthesis, galactopoiesis, and production of casein and lactalbumin, lactose, and lipids (Andersen, 1982). Kauppila and co-workers (1987) found that a woman with an isolated prolactin deficiency failed to lactate after two pregnancies, establishing the absolute necessity of prolactin for lactation but not for successful pregnancy outcome.

Prolactin is present in amnionic fluid in high concentrations. Levels of up to 10,000 ng/mL are found at 20 to 26 weeks, thereafter, levels decrease and reach a nadir after 34 weeks. Several investigators have presented convincing evidence that the uterine decidua is the site of prolactin synthesis in amnionic fluid (see Chap. 3, Decidual Prolactin Production). Although the exact function of amnionic fluid prolactin is not known, it has been suggested that amnionic fluid prolactin impairs the transfer of water from the fetus into the maternal compartment, thus preventing fetal dehydration during late pregnancy when amnionic fluid is normally hypotonic.


3.Fetal Heart Rate Patterns   ;-It is now generally accepted that interpretation of fetal heart rate patterns can be problematic because of the lack of agreement on definitions and nomenclature (Freeman, 2002). The National Institute of Child Health and Human Development Research Planning Workshop (1997) brought together investigators with expertise in the field to propose standardized, unambiguous definitions for interpretation of fetal heart rate patterns during labor. The definitions proposed as a result of this workshop will be used in this chapter. It is important to recognize that interpretation of electronic fetal heart rate data is based on the visual pattern of the heart rate as portrayed on chart recorder graph paper. Thus, the choice of vertical and horizontal scaling greatly affects the appearance of the fetal heart rate. Scaling factors recommended by the workshop are 30 beats per minute (beats/min or bpm) per vertical cm (range, 30 to 240 beats/min) and 3 cm/min chart recorder paper speed. Fetal heart rate variation is falsely displayed at the slower 1 cm/min paper speed when compared with that of the smoother baseline recorded at 3 cm/min (Fig. 18–6). Thus, pattern recognition can be considerably distorted depending on the scaling factors used.


Fetal heart rate obtained by scalp electrode and recorded at 1 cm/min compared with that of 3 cm/min chart recorder paper speed.

Baseline Fetal Heart Activity

Baseline fetal heart activity refers to the modal characteristics that prevail apart from periodic accelerations or decelerations associated with uterine contractions. Descriptive characteristics of baseline fetal heart activity include rate, beat-to-beat variability, fetal arrhythmia, and distinct patterns such as sinusoidal or saltatory fetal heart rates.


With increasing fetal maturation, the heart rate decreases. This continues postnatally such that the average rate is 90 beats/min by age 8 (Behrman, 1992). Pillai and James (1990) longitudinally studied fetal heart rate characteristics in 43 normal pregnancies. The baseline fetal heart rate decreased an average of 24 beats/min between 16 weeks and term, or approximately 1 beat/min per week. It is postulated that this normal gradual slowing of the fetal heart rate corresponds to maturation of parasympathetic (vagal) heart control (Renou and co-workers, 1969).

The baseline fetal heart rate is the approximate mean rate rounded to increments of 5 beats/min during a 10-minute tracing segment. In any 10-minute window, the minimum interpretable baseline duration must be at least 2 minutes. If the baseline fetal heart rate is less than 110 beats/min, it is termed bradycardia; if the baseline rate is greater than 160 beats/min, it is termed tachycardia. The average fetal heart rate is considered to be the result of tonic balance between accelerator and decelerator influences on pacemaker cells. In this concept, the sympathetic system is the accelerator influence, and the parasympathetic system is the decelerator factor mediated via vagal slowing of heart rate (Dawes, 1985). Heart rate also is under the control of arterial chemoreceptors such that both hypoxia and hypercapnia can modulate rate. More severe and prolonged hypoxia, with a rising blood lactate level and severe metabolic acidemia, induces a prolonged fall of heart rate due to direct effects on the myocardium.


During the third trimester, the normal mean baseline fetal heart rate has generally been accepted to be between 120 and 160 beats/min. The lower normal limit is disputed internationally with some investigators recommending 110 beats/min (Manassiev, 1996). Pragmatically, a rate between 100 and 119 beats/min, in the absence of other changes, usually is not considered to represent fetal compromise. Such low but potentially normal baseline heart rates also have been attributed to head compression from occiput posterior or transverse positions, particularly during second-stage labor (Young and Weinstein, 1976). Such mild bradycardias were observed in 2 percent of monitored pregnancies and averaged about 50 minutes in duration. Freeman and colleagues (2003) have concluded that bradycardia within the range of 80 to 120 beats/min with good variability is reassuring. Interpretation of rates less than 80 beats/min is problematic, and such rates generally are considered nonreassuring.

Some causes of fetal bradycardia include congenital heart block and serious fetal compromise. Figure 18–7 shows bradycardia in a fetus dying from placental abruption. Maternal hypothermia under general anesthesia for repair of a cerebral aneurysm or during maternal cardiopulmonary bypass for open-heart surgery also can cause fetal bradycardia (see Chap. 44, Valve Replacement During Pregnancy). Sustained fetal bradycardia in the setting of severe pyelonephritis and maternal hypothermia also has been reported (Hankins and co-workers, 1997). These infants apparently are not harmed by several hours of such bradycardia.

Fetal bradycardia measured with a scalp electrode in a pregnancy complicated by placental abruption and subsequent fetal death.


Fetal tachycardia is defined as a baseline heart rate in excess of 160 beats/min. The most common explanation for fetal tachycardia is maternal fever from amnionitis, although fever from any source can increase baseline fetal heart rate. Such infections also have been observed to induce fetal tachycardia before overt maternal fever is diagnosed (Gilstrap and associates, 1987). Fetal tachycardia caused by maternal infection typically is not associated with fetal compromise unless there are associated periodic heart rate changes or fetal sepsis.

Other causes of fetal tachycardia include fetal compromise, cardiac arrhythmias, and maternal administration of parasympathetic (atropine) or sympathomimetic (terbutaline) drugs. The key feature to distinguish fetal compromise in association with tachycardia seems to be concomitant heart rate decelerations. Prompt relief of the compromising event, such as correction of maternal hypotension caused by epidural analgesia, can result in fetal recovery.

Wandering Baseline

This baseline rate is unsteady and “wanders” between 120 and 160 beats/min (Freeman and colleagues, 2003). This rare finding is suggestive of a neurologically abnormal fetus and may occur as a preterminal event.

Beat-to-Beat Variability

Baseline variability is an important index of cardiovascular function and appears to be regulated largely by the autonomic nervous system (Kozuma and colleagues, 1997). That is, sympathetic and parasympathetic “push-pull,” mediated via the sinoatrial node, produces moment-to-moment or beat-to-beat oscillation of the baseline heart rate. Such irregularity of the heart rate is defined as baseline variability. Variability is further divided into short term and long term.

Short-term variability reflects the instantaneous change in fetal heart rate from one beat—or R wave—to the next. This variability is a measure of the time interval between cardiac systoles (Fig. 18–8). Short-term variability can most reliably be determined to be normally present only when electrocardiac cycles are measured directly with a scalp electrode. Long-term variability is used to describe the oscillatory changes that occur during the course of 1 minute and result in the waviness of the baseline (Fig. 18–9). The normal frequency of such waves is three to five cycles per minute (Freeman and co-authors, 2003).

It should be recognized that precise quantitative analysis of both short- and long-term variability presents a number of frustrating problems due to technical and scaling factors. For example, Parer and co-workers (1985) evaluated 22 mathematical formulas designed to quantify heart rate variability and most were unsatisfactory. Consequently, most clinical interpretation is based on visual analysis with subjective judgment of the smoothness or flatness of the baseline. According to Freeman and colleagues (2003), there is no current evidence that the distinction between short- and long-term variability has any clinical relevance. Similarly, the NICHD Workshop (1997) did not recommend differentiating short- and long-term variability because in actual practice they are visually determined as a unit. The workshop panel defined baseline variability as those baseline fluctuations of two cycles per minute or greater. They recommended the criteria shown in Figure 18–10 for quantification of variability. Normal beat-to-beat variability was accepted to be 6 to 25 beats/min.



Grades of baseline fetal heart rate variability (irregular fluctuations in the baseline of 2 cycles per minute or greater) together with a sinusoidal pattern. The sinusoidal pattern differs from variability in that it has a smooth, sinelike pattern of regular fluctuation and is excluded in the definition of fetal heart rate variability. (1) Undetectable, absent variability; (2) minimal  5 beats/min variability; (3) moderate (normal), 6 to 25 beats/min variability; (4) marked, > 25 beats/min variability; (5) sinusoidal pattern. (From National Institute of Child Health and Human Development Research Planning Workshop, 1997.)

Several physiological and pathological processes can affect or interfere with beat-to-beat variability. Dawes and co-workers (1981) described increased variability during fetal breathing. In healthy infants, short-term variability is attributable to respiratory sinus arrhythmia (Divon and co-workers, 1986). Fetal body movements also affect variability (Van Geijn and co-workers, 1980). Pillai and James (1990) reported increased baseline variability with advancing gestation. Up to 30 weeks, baseline characteristics were similar during both fetal rest and activity. After 30 weeks, fetal inactivity was associated with diminished baseline variability and conversely, variability was increased during fetal activity. Fetal gender does not affect heart rate variability (Ogueh and Steer, 1998).

It is important to recognize that the baseline fetal heart rate becomes more physiologically fixed (less variable) as the rate increases. Conversely, there is more instability or variability of the baseline at lower heart rates. This phenomenon presumably reflects less cardiovascular physiological wandering as beat-to-beat intervals shorten due to increasing heart rate.

Diminished beat-to-beat variability can be an ominous sign indicating a seriously compromised fetus. Paul and co-workers (1975) reported that loss of variability in combination with decelerations was associated with fetal acidemia. They analyzed variability in the 20 minutes preceding delivery in 194 pregnancies. Decreased variability was defined as 5 or fewer beats/min excursion of the baseline (see Fig. 18–10), whereas acceptable variability exceeded this range. Fetal scalp pH was measured 1119 times in these pregnancies, and mean values were found to be increasingly more acidemic when decreased variability was added to progressively intense heart rate decelerations. For example, mean fetal scalp pH of about 7.10 was found when severe decelerations were combined with 5 beats/min or less variability compared with a pH about 7.20 when greater variability was associated with similarly severe decelerations.

Severe maternal acidemia also can cause decreased fetal beat-to-beat variability, as shown in Figure 18–11 in a mother with diabetic ketoacidosis. The precise pathological mechanisms by which fetal hypoxemia results in diminished beat-to-beat variability are not totally understood.

Interestingly, mild degrees of fetal hypoxemia have been reported actually to increase variability, at least at the outset of the hypoxic episode (Murotsuki and co-authors, 1997). According to Dawes (1985), it seems probable that the loss of variability is a result of metabolic acidemia that causes depression of the fetal brainstem or the heart itself. Thus, diminished beat-to-beat variability, when a reflection of compromised fetal condition, likely reflects acidemia rather than hypoxia.

A common cause of diminished beat-to-beat variability is analgesic drugs given during labor (see Chap. 19, Parenteral Agents). A large variety of central nervous system depressant drugs can cause transient diminished beat-to-beat variability. Included are narcotics, barbiturates, phenothiazines, tranquilizers, and general anesthetics. Diminished variability occurs regularly within 5 to 10 minutes following intravenous meperidine administration, and the effects may last up to 60 minutes or longer depending on the dosage given (Petrie, 1993). Butorphanol given intravenously diminishes fetal heart rate reactivity (Schucker and colleagues, 1996). Hill and colleagues (2003), in a study performed at Parkland Hospital, found that 5 beats/min or less variability occurred in 30 percent of women given continuous intravenous meperidine compared with 7 percent in those given continuous labor epidural analgesia using 0.0625-percent bupivacaine and 2 g/mL of fentanyl.

Magnesium sulfate, widely used in the United States for tocolysis as well as management of hypertensive women, has been arguably associated with diminished beat-to-beat variability. Hallak and colleagues (1999) randomly assigned 34 normal, nonlaboring women to standard magnesium sulfate infusion versus isotonic saline. Magnesium sulfate was associated with statistically decreased variability only in the third hour of the infusion. However, the average decrease in variability was deemed clinically insignificant because the mean variability was 2.7 beats/min in the third hour of magnesium infusion compared with 2.8 beats/min at baseline. Magnesium sulfate also blunted the frequency of accelerations.

It is generally believed that reduced baseline heart rate variability is the single most reliable sign of fetal compromise. For example, Smith and co-workers (1988) performed a computerized analysis of beat-to-beat variability in growth-restricted fetuses before labor. They observed that diminished variability (4.2 beats/min or less) that was maintained for 1 hour was diagnostic of developing acidemia and imminent fetal death. By contrast, Samueloff and associates (1994) evaluated variability as a predictor of fetal outcome during labor in 2200 consecutive deliveries. They concluded that variability by itself cannot be used as the only indicator of fetal well-being. Conversely, they also concluded that good variability should not be interpreted as necessarily reassuring.

In summary, beat-to-beat variability is affected by a variety of pathological and physiological mechanisms. Variability has considerably different meaning depending on the clinical setting. The development of decreased variability in the absence of decelerations is unlikely to be due to fetal hypoxia (Davidson and co-workers, 1992). A persistently flat fetal heart rate baseline—absent variability—within the normal baseline rate range and without decelerations may reflect a previous insult to the fetus that has resulted in neurological damage (Freeman and colleagues, 2003).

Periodic Fetal Heart Rate Changes

The periodic fetal heart rate refers to deviations from baseline that are related to uterine contractions. Acceleration refers to an increase in fetal heart rate above baseline and deceleration to a decrease below baseline rate. The nomenclature most commonly used in the United States is based upon the timing of the deceleration in relation to contractions—thus, early, late, or variable in onset related to the corresponding uterine contraction. The waveform of these decelerations is also significant for pattern recognition. In early and late decelerations, the slope of fetal heart rate change is gradual, resulting in a curvilinear and uniform or symmetrical waveform. With variable decelerations, the slope of fetal heart rate change is abrupt and erratic, giving the waveform a jagged appearance. It has been proposed that decelerations be defined as recurrent if they occur with 50 percent or more of contractions in any 20-minute period (NICHD Research Planning Workshop, 1997).

Another system now used less often for description of decelerations is based on the pathophysiological events considered most likely to cause the pattern. In this system, early decelerations are termed head compression, late decelerations are termed uteroplacental insufficiency, and variable decelerations become cord compression patterns. The nomenclature of type I (early), type II (late), and type III (variable) “dips” proposed by Caldeyro-Barcia and co-workers (1973) is not used in the United States.


An acceleration is a visually apparent abrupt increase—defined as onset of acceleration to a peak in less than 30 seconds—in the fetal heart rate baseline (NICHD Research Planning Workshop, 1997). According to Freeman and co-authors (2003), accelerations most often occur antepartum, in early labor, and in association with variable decelerations. Proposed mechanisms for intrapartum accelerations include fetal movement, stimulation by uterine contractions, umbilical cord occlusion, and fetal stimulation during pelvic examination. Fetal scalp blood sampling and acoustic stimulation also incite fetal heart rate acceleration (Clark and co-workers, 1982). Finally, acceleration can occur during labor without any apparent stimulus. Indeed, accelerations are common in labor and nearly always associated with fetal movement. These accelerations are virtually always reassuring and almost always confirm that the fetus is not acidemic at that time.

Accelerations seem to have the same physiological explanations as beat-to-beat variability in that they represent intact neurohormonal cardiovascular control mechanisms linked to fetal behavioral states. Krebs and co-workers (1982) analyzed electronic heart rate tracings in nearly 2000 fetuses and found sporadic accelerations during labor in 99.8 percent. The presence of fetal heart accelerations during the first or last 30 minutes, or both, was a favorable sign for fetal well-being. The absence of such accelerations during labor, however, is not necessarily an unfavorable sign unless coincidental with other nonreassuring changes. There is about a 50-percent chance of acidemia in the fetus who fails to respond to stimulation in the presence of an otherwise nonreassuring pattern (Clark and colleagues, 1984; Smith and colleagues, 1986).

Early Deceleration

Early deceleration of the fetal heart rate consists of a gradual decrease and return to baseline associated with a contraction (Fig. 18–14). Such early deceleration was first described by Hon (1958). He observed that there was a drop in heart rate with uterine contractions and that this was related to cervical dilatation. He considered these findings to be physiological.

Figure 18–14.image


Feature s of early fetal heart rate deceleration. Characteristics include gradual decrease in the heart rate with both onset and recovery coincident with the onset and recovery of the contraction. The nadir of the deceleration is 30 seconds or more after the onset of the deceleration.

Freeman and co-authors (2003) defined early decelerations as those generally seen in active labor between 4 and 7 cm dilatation. In their definition, the degree of deceleration is generally proportional to the contraction strength and rarely falls below 100 to 110 beats/min or 20 to 30 beats/min below baseline. Such decelerations are uncommon during active labor and are not associated with tachycardia, loss of variability, or other fetal heart rate changes. Importantly, early decelerations are not associated with fetal hypoxia, acidemia, or low Apgar scores.

Head compression probably causes vagal nerve activation as a result of dural stimulation and that mediates the heart rate deceleration (Paul and co-workers, 1964). Ball and Parer (1992) concluded that fetal head compression is a likely cause not only of the deceleration shown in Figure 18–14 but also of those shown in Figure 18–15, which typically occur during second-stage labor. Indeed, they observed that head compression is the likely cause of many variable decelerations classically attributed to cord compression.

Figure 18–15.


Two different fetal heart rate patterns during second-stage labor that are likely both due to head compression. Maternal bearing-down efforts correspond to the spikes with uterine contractions. Fetal heart rate deceleration C is consistent with the pattern of head compression shown in Figure 18–12. Deceleration B, however, is “variable” in appearance because of its jagged configuration and may also represent cord occlusion.

Late Deceleration

The fetal heart rate response to uterine contractions can be an index of either uterine perfusion or placental function. A late deceleration is a smooth, gradual, symmetrical decrease in fetal heart rate beginning at or after the peak of the contraction and returning to baseline only after the contraction has ended (American College of Obstetricians and Gynecologists, 1995b). In most cases, the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively (Fig. 18–16). The magnitude of late decelerations is rarely more than 30 to 40 beats/min below baseline and typically not more than 10 to 20 beats/min. Late decelerations usually are not accompanied by accelerations.

Figure 18–16.


Features of late feta l heart rate deceleration. Characteristics include gradual decrease in the heart rate with the nadir and recovery occurring after the end of the contraction. The nadir of the deceleration occurs 30 seconds or more after the onset of the deceleration.

Myers and associates (1973) studied monkeys in which they compromised uteroplacental perfusion by lowering maternal aortic blood pressure. The time interval, or lag period, from the onset of a contraction to the onset of a late deceleration was directly related to basal fetal oxygenation. They demonstrated that the length of the lag phase was predictive of the fetal PO2 but not fetal pH. The lower the fetal PO2 prior to contractions, the shorter the lag phase to onset of late decelerations. This lag period reflected the time necessary for the fetal PO2 to fall below a critical level necessary to stimulate arterial chemoreceptors, which mediated decelerations.

Murata and co-workers (1982) also showed that a late deceleration was the first fetal heart rate consequence of uteroplacental-induced hypoxia. During the course of progressive hypoxia that led to death over 2 to 13 days, the monkey fetuses invariably exhibited late decelerations before the development of acidemia. Variability of the baseline heart rate disappeared as acidemia developed.

A large number of clinical circumstances can result in late decelerations. Generally, any process that causes maternal hypotension, excessive uterine activity, or placental dysfunction can induce late decelerations. The two most common causes are hypotension from epidural analgesia and uterine hyperactivity caused by oxytocin stimulation. Maternal diseases such as hypertension, diabetes, and collagen-vascular disorders can cause chronic placental dysfunction. A rare cause is severe chronic maternal anemia without hypovolemia. Placental abruption can cause acute late decelerations (Fig. 18–17).

Figure 18–17.


Late decelerations due to uteroplacental insufficiency resulting from placental abruption. Immediate cesarean delivery was performed. Umbilical artery pH was 7.05 and the PO2 was 11 mm Hg.

Variable Decelerations

The most common deceleration patterns encountered during labor are variable decelerations attributed to umbilical cord occlusion. Melchior and Bernard (1985) identified variable decelerations in 40 percent of over 7000 monitor tracings when labor had progressed to 5 cm dilatation and in 83 percent by the end of the first stage. Variable deceleration of the fetal heart rate is defined as a visually apparent abrupt decrease in rate. The onset of deceleration commonly varies with successive contractions (Fig. 18–18). The duration is less than 2 minutes.

Figure 18–18.


Features of variable fetal heart rate decelerations. Characteristics include abrupt decrease in the heart rate with onset commonly varying with successive contractions. The decelerations measure  15 beats/min for 15 seconds or longer with an onset to nadir phase of less than 30 seconds. Total duration is less than 2 minutes.

Very early in the development of electronic monitoring, Hon (1959) tested the effects of umbilical cord compression on fetal heart rate (Fig. 18–19). Similar complete occlusion of the umbilical cord in experimental animals produces abrupt, jagged-appearing deceleration of the fetal heart rate (Fig. 18–20). Concomitantly, fetal aortic pressure increases. Itskovitz and co-workers (1983) observed that variable decelerations in fetal lambs occurred only after umbilical blood flow was reduced by at least 50 percent.

Figure 18–19.


Fetal heart rate effects of compression of a prolapsed umbilical cord in a 25-week footling breech. Panel A shows the effects of 25-second compression compared with those of 40 seconds in panel B. (Redrawn from Hon, 1959, with permission.)

Figure 18–20.


Total umbilical cord occlusion (arrow) in the sheep fetus is accompanied by increase in fetal aortic blood pressure. Blood pressure changes in the umbilical vessels are also shown. (From Kunzel, 1985, with permission.)

Two types of variable decelerations are shown in Figure 18–21. The deceleration denoted by A is very much like that seen with complete umbilical cord occlusion in experimental animals (see Fig. 18–20). Deceleration B, however, has a different configuration because of the “shoulders” of acceleration before and after the deceleration component. Lee and co-workers (1975) proposed that this variation of variable decelerations was caused by differing degrees of partial cord occlusion. In this physiological scheme, occlusion of only the vein reduces fetal blood return, thereby triggering a baroreceptor-mediated acceleration. Subsequent complete occlusion results in fetal systemic hypertension due to obstruction of umbilical artery flow. This stimulates a baroreceptor-mediated deceleration. Presumably, the aftercoming shoulder of acceleration represents the same events occurring in reverse (Fig. 18–22).

Figure 18–21



Varying (variable) fetal heart rate decelerations. Deceleration B exhibits “shoulders” of acceleration compared with deceleration A.

Figure 18–22.


Schematic representation of the fetal heart rate (FHR) effects of partial occlusion (PO) and complete occlusion (CO) of the umbilical cord. (FSBP = fetal systemic blood pressure; UA = umbilical artery; UC = uterine contraction; UV = umbilical vein.) (From Lee and co-authors, 1975, with permission.)

Ball and Parer (1992) concluded that variable decelerations are mediated vagally and that the vagal response may be due to chemoreceptor or baroreceptor activity, or both. Partial or complete cord occlusion produces an increase in afterload (baroreceptor) and a decrease in fetal arterial oxygen content (chemoreceptor). These both result in vagal activity leading to deceleration. In fetal monkeys the baroreceptor reflexes appear to be operative during the first 15 to 20 seconds of umbilical cord occlusion followed by decline in PO2 at approximately 30 seconds, which then serves as a chemoreceptor stimulus (Mueller-Heubach and Battelli, 1982).

Thus, variable decelerations represent fetal heart rate reflexes that reflect either blood pressure changes due to interruption of umbilical flow or changes in oxygenation. It is likely that most fetuses have experienced brief but recurrent periods of hypoxia due to umbilical cord compression during gestation. The frequency and inevitability of cord occlusion undoubtedly has provided the fetus with these physiological mechanisms as a means of coping. The great dilemma for the obstetrician in managing variable fetal heart rate decelerations is determining when variable decelerations are pathological. The American College of Obstetricians and Gynecologists (1995b) has defined significant variable decelerations as those decreasing to less than 70 beats/min and lasting more than 60 seconds.

Other fetal heart rate patterns have been associated with umbilical cord compression. Saltatory baseline heart rate (Fig. 18–23) was first described by Hammacher and co-workers (1968) and linked to umbilical cord complications during labor. Saltatory derives from the Latin and French words meaning “to leap.” The pattern consists of rapidly recurring couplets of acceleration and deceleration causing relatively large oscillations of the baseline fetal heart rate. We also observed a relationship between cord occlusion and the saltatory pattern (Leveno and associates, 1984). In the absence of other fetal heart rate findings, these do not signal fetal compromise. Lambda is a pattern involving an acceleration followed by a variable deceleration with no acceleration at the end of the deceleration. This pattern typically is seen in early labor and is not ominous (Freeman and colleagues, 2003). This lambda pattern may result from mild cord compression or stretch. Overshoot is a variable deceleration followed by acceleration. The clinical significance of this pattern is controversial (Westgate and colleagues, 2001).

Figure 18–23.


Saltatory baseline fetal heart rate showing rapidly recurring couplets of acceleration combined with deceleration.

Prolonged Deceleration

Shown in Figure 18–24, this pattern is defined as an isolated deceleration lasting 2 minutes or longer but less than 10 minutes from onset to return to baseline (NICHD Research Planning Workshop, 1997). Prolonged decelerations are difficult to interpret because they are seen in many different clinical situations. Some of the more common causes include cervical examination, uterine hyperactivity, cord entanglement, and maternal supine hypotension.

Figure 18–24.


Prolonged fetal heart rate deceleration due to uterine hyperactivity. Approximately 3 minutes of the tracing are shown, but the fetal heart rate returned to normal after uterine hypertonus resolved. Vaginal delivery later ensued.

Epidural, spinal, or paracervical analgesia may induce prolonged deceleration of the fetal heart rate. For example, Eberle and colleagues (1998) reported that prolonged decelerations occurred in 4 percent of normal parturients given either epidural or intrathecal labor analgesia. Hill and colleagues (2003) observed prolonged deceleration in 1 percent of women given epidural analgesia during labor at Parkland Hospital. Other causes of prolonged deceleration include maternal hypoperfusion or hypoxia from any cause, placental abruption, umbilical cord knots or prolapse, maternal seizures including eclampsia and epilepsy, application of a fetal scalp electrode, impending birth, or even maternal Valsalva maneuver.

The placenta is very effective in resuscitating the fetus if the original insult does not recur immediately. Occasionally, such self-limited prolonged decelerations are followed by loss of beat-to-beat variability, baseline tachycardia, and even a period of late decelerations, all of which resolve as the fetus recovers. Freeman and co-authors (2003) emphasize rightfully that the fetus may die during prolonged decelerations. Thus, management of prolonged decelerations can be extremely tenuous. Management of isolated prolonged decelerations is based upon bedside clinical judgment, which inevitably will sometimes be imperfect given the unpredictability of these decelerations.



Table 18–5. Guidelines for Intrapartum Fetal Heart Rate Surveillance


Surveillance Low-Risk Pregnancies High-Risk Pregnancies
Acceptable methods
  Intermittent auscultation Yes Yes
  Continuous electronic monitoring (internal or external) Yes Yes
Evaluation intervalsa
  First-stage labor (active) 30 min 15 minb
  Second-stage labor 15 min 5 minb

aFollowing a uterine contraction.

bIncludes tracing evaluation and charting when continuous electronic monitoring is used.

Adapted from the American College of Obstetricians and Gynecologists (1995b).


Table 18–1. NICHD Research Planning Workshop (1997) Fetal Heart Rate Patterns


Pattern Workshop Interpretations
Normal Baseline 110–160 beats/min
Variability 6–25 beats/min
Accelerations present
No decelerations
Intermediate No consensus
Severely abnormal Recurrent late or variable decelerations with zero variability
Substantial bradycardia with zero variability

4. Doppler Velocimetry

The Doppler shift is a phenomenon that occurs when a source of light or sound waves is moving relative to an observer; the observer detects a shift in the wave frequency. Similarly, when sound waves strike a moving target, the frequency of the sound waves reflected back is shifted proportionate to the velocity and direction of the moving target. Because the magnitude and direction of the frequency shift depend on the relative motion of the moving target, the velocity and direction of the target can be determined.

Important to obstetrics, Doppler may be used to determine the volume and rate of blood flow through maternal and fetal vessels. In this situation, the sound source is the ultrasound transducer, the moving target is the column of red blood cells flowing through the circulation, and the reflected sound waves are observed by the ultrasound transducer. Two types—continuous and pulse wave Doppler—are used in medicine.

Continuous wave Doppler equipment has separate crystals: one that transmits a high-frequency sound wave, and another that continuously receives signals. It can record high frequencies using low power output and is easy to use. Unfortunately, it is nonselective, recognizing all signals along its path, and does not allow visualization of the blood vessel(s). In m-mode echocardiography, continuous wave Doppler is used to evaluate motion through time. It defines blood flow through the heart, but because the cardiac structures are not visualized, it requires the correlation of the sequence of waveforms produced with the sequence of structures interrogated by the sound wave.

Pulse wave Doppler has equipment that uses only one crystal, which transmits the signal and then waits until the returning signal is received before transmitting another one. It is more expensive and requires higher power, but allows precise targeting and visualization of the vessel of interest. Pulse wave Doppler also can be configured to allow color-flow mapping, in which computer software displays blood flowing away from the transducer as blue and blood flowing toward the transducer as red.

Various combinations of continuous wave Doppler, pulse wave Doppler, color-flow Doppler, and real-time ultrasound are commercially available and are loosely referred to as duplex Doppler.

Clinical Applications

The Doppler equation shown in Figure 16–17 contains the variables that affect the Doppler shift. An important source of error when calculating flow or velocity is the angle between sound waves from the transducer and flow within the vessel—termed the angle of insonation and abbreviated as theta (). Because cosine  is a component of the equation, measurement error becomes large when the angle of insonation is not close to zero. The practical solution to this problem has been the use of ratios to compare different waveform components—allowing cosine  to cancel out of the equation. Figure 16–18 is a schematic of the Doppler waveform and describes the three ratios commonly used. The simplest is the systolic–diastolic ratio (S/D ratio), which compares maximum (peak) systolic flow with end-diastolic flow, thereby evaluating downstream impedance to flow.




Doppler waveforms from normal pregnancy. Shown clockwise are normal waveforms from the maternal arcuate, uterine, and external iliac arteries, and from the fetal umbilical artery and descending aorta. Reversed end-diastolic flow velocity is apparent in the external iliac artery, whereas continuous diastolic flow characterizes the uterine and arcuate vessels. Finally, note the greatly diminished end-diastolic flow in the fetal descending aorta. (From Copel and colleagues, 1988.)

Umbilical Artery

This vessel normally has forward flow throughout the cardiac cycle, and the amount of flow during diastole increases as gestation advances. Thus the S/D ratio decreases, from about 4.0 at 20 weeks to 2.0 at term. The S/D ratio is generally less than 3.0 after 30 weeks (Fleischer and associates, 1986). Umbilical artery Doppler may be a useful adjunct in the management of pregnancies complicated by fetal growth restriction. As presented in Chapter 15 (see Umbilical Artery Doppler Velocimetry), umbilical artery velocimetry has been subjected to more rigorous assessment than has any previous test of fetal health (Alfirevic and Neilson, 1995). It is, however, not recommended for screening of low-risk pregnancies or for complications other than growth restriction.

Umbilical artery Doppler is considered abnormal if the S/D ratio is above the 95th percentile for gestational age. In extreme cases of growth restriction, end-diastolic flow may become absent or even reversed (Fig. 16–20). These are ominous findings and should prompt a complete fetal evaluation—almost half of cases are due to fetal aneuploidy or a major anomaly (Wenstrom and associates, 1991). In the absence of a reversible maternal complication or a fetal anomaly, reversed end-diastolic flow suggests severe fetal circulatory compromise and usually prompts immediate delivery. Sezik and colleagues (2004) recently reported that fetuses of preeclamptic women who had absent or reversed end-diastolic flow were more likely to have hypoglycemia and polycythemia.


Umbilical artery Doppler waveforms. A. Normal diastolic flow. B. Absence of end-diastolic flow. C. Reversed end-diastolic flow. (Courtesy of Dr. Diane Twickler.)

Ductus Arteriosus

Doppler evaluation of the ductus arteriosus has been used primarily to monitor fetuses exposed to indomethacin and other nonsteroidal anti-inflammatory agents. Indomethacin, which is used for tocolysis, causes constriction of the ductus in sheep and human fetuses (Huhta and colleagues (1987). The resulting increased pulmonary flow may cause reactive hypertrophy of the pulmonary arterioles, and eventually pulmonary hypertension develops (see Chap. 36, Prostaglandin Inhibitors). In a study of 61 indomethacin-treated pregnant women, Vermillion and colleagues (1997) reported that half of exposed fetuses developed ductal constriction. Fortunately, this complication is largely reversible if medication is discontinued before 32 weeks (Moise, 1993).

Middle Cerebral Artery

Peak systolic velocity in the middle cerebral artery is increased with fetal anemia because of increased cardiac output and decreased blood viscosity (Segata and Mari, 2004). Velocity measurements are generally problematic because a high insonating angle introduces considerable error. Middle cerebral artery measurements are an exception, however, because the path of the artery often presents a very low angle of insonation.

Mari and colleagues (1995) performed velocity studies in 135 normal fetuses and 39 with alloimmunization. They reported that all anemic fetuses had peak systolic velocity above the normal mean. This prompted a collaborative study of 376 pregnancies by Mari and colleagues (2000). Using a threshold of 1.50 multiples of the median (MoM), they correctly identified all fetuses with moderate or severe anemia with a false-positive rate of 12 percent. Other investigators have since reported similar results (Abdel-Fattah, 2002; Bahado-Singh, 2000; Cosmi, 2002; Deren and Onderoglu, 2002, and all their associates).

It also has been hypothesized that Doppler evaluation of blood flow through cerebral vessels might be used to detect altered cerebral circulation before there is hypoxemia significant enough to alter the fetal heart rate pattern. The cerebroplacental ratio has been introduced as an indicator of brain sparing in fetuses with growth restriction and as a predictor of adverse perinatal outcome (Bahado-Singh and colleagues, 1999; Gramellini and associates, 1992). Currently, the American College of Obstetricians and Gynecologists (1999) considers antepartum surveillance with cerebral artery Doppler velocimetry to be investigational.

Uterine Artery

Uterine blood flow increases from 50 mL/min early in gestation to 500 to 750 mL/min by term. The uterine artery Doppler waveform is unique and characterized by high diastolic flow velocities similar to those in systole, and by highly turbulent flow, which displays a spectrum of many different velocities (Fig. 16–21). Increased resistance to flow and development of a diastolic notch have been associated with pregnancy-induced hypertension (Arduini, 1987; Fleischer, 1986; Harrington, 1996; North, 1994, and all their colleagues). In a recent study, Zeeman and co-authors (2003) confirmed that increased impedance of uterine artery velocimetry at 16 to 20 weeks was predictive of superimposed preeclampsia developing in women with chronic hypertension. Whether it will be clinically helpful to predict preeclampsia in this manner is yet unclear.

5. Screening for Common Congenital Abnormalities

The vast majority of cases of NTDs, Down syndrome, and many other fetal abnormalities are found in families with no prior history of birth defects. Prenatal evaluation of only women at high risk for these complications would thus fail to identify most affected pregnancies. Couples with no family history of genetic abnormalities can now be offered prenatal screening tests for certain fetal disorders. Screening tests by design do not provide a diagnosis, but rather identify individuals with risk high enough to benefit from a definitive diagnostic test. According to Wald and associates (1997), genetic screening tests should meet criteria generally accepted for other types of screening tests:

  1. The disorder is well defined and serious.
  2. Treatment or prevention is available but not possible without the screening test.
  3. The screening test is cost effective and reliable.
  4. The subsequent diagnostic test is reliable.

That said, Caughey and collaborators (2004) interviewed 447 women of all ages with undetermined genetic risk. They reported that half were willing to undergo invasive prenatal diagnostic testing. One third of women aged 35 years or older expressed a willingness to pay partially or completely for such testing. Such requests present a conundrum for prenatal diagnostic centers and each should have a protocol to cover these exigencies.

Neural-Tube Defects (NTDs)

At least 95 percent of children with NTDs are born into families with no prior history. Prior to the late 1970s, identification of affected pregnancies was not possible. At that time, Brock and associates (1972, 1973) reported that both amnionic fluid and maternal serum alpha-fetoprotein (AFP) levels were much higher in pregnancies complicated by fetal anencephaly and other NTDs. The first large prospective trial of maternal serum screening was the UK Collaborative Study on Alpha-fetoprotein in Relation to Neural-tube Defects (1977). The utility of maternal serum AFP screening for NTDs was subsequently confirmed by others and adopted in the United States and Europe (Burton and associates, 1983; Haddow and colleagues, 1983; Milunsky and co-workers, 1980).

Alpha-Fetoprotein (AFP)

This glycoprotein is synthesized early in gestation by the fetal yolk sac and later by the fetal gastrointestinal tract and liver (see Chap. 4). It normally circulates in fetal serum and passes into fetal urine and thus into amnionic fluid. Although its function is unknown, AFP is the major serum protein in the embryo-fetus, analogous to albumin. Its concentration increases steadily in both fetal serum and amnionic fluid until 13 weeks, after which these levels rapidly decrease (Burton, 1988). AFP passes into the maternal circulation by diffusion across the placental membranes and also may be transported via the placental circulation (Brumfield and colleagues, 1990). AFP is found in steadily increasing quantities in maternal serum after 12 weeks (Fig. 13–2). Open fetal body wall defects uncovered by integument permit additional AFP to leak into the amnionic fluid, and maternal serum AFP levels are increased.

Maternal Serum AFP Screening

Maternal screening is offered between 14 and 22 weeks. Maternal serum AFP is measured in nanograms per milliliter and reported as a multiple of the median (MoM) of the unaffected population. Converting the results to MoM normalizes the distribution of AFP levels and permits comparison of results from different laboratories and populations. Factors that influence the maternal serum AFP level include weight, race, and diabetic status, as well as the gestational age and number of fetuses. Using a maternal serum AFP level of 2.0 or 2.5 MoM as the upper limit of normal, most laboratories report a screen-positive rate of 3 to 5 percent, a sensitivity of at least 90 percent, and a positive-predictive value of 2 to 6 percent (Milunsky and associates, 1989).

Evaluation of an elevated maternal serum AFP begins with a basic ultrasonographic examination to determine fetal age and viability and the number of fetuses (Fig. 13–3). Underestimating gestational age accounts for a large proportion of abnormal test results. In such cases, the laboratory can usually generate a corrected report when given accurate pregnancy dating criteria. If the initial specimen was obtained prior to 14 weeks, a repeated specimen is necessary. The distributions of maternal serum AFP levels in affected and unaffected pregnancies overlap considerably (Fig. 13–4). If the level falls within the range of the overlap—the indiscriminate zone of 2.5 to 3.5 MoM—then repeating the measurement may determine whether the pregnancy is really at risk. Because repeated measurements tend to regress toward the mean of the population to which they belong, a truly elevated maternal serum AFP level will remain so in the repeated sample, whereas levels from an unaffected pregnancy have a tendency to normalize .

Maternal serum AFP levels greater than 3.5 MoM need not be repeated, because levels this high are outside the AFP distribution of unaffected pregnancies and clearly indicate increased fetal risk. In general, the likelihood that the fetus is affected increases in proportion to the AFP level. In a study of 773 women with elevated serum AFP levels, Reichler and colleagues (1994) reported that there was a progressive increase in the frequency of NTDs, ventral wall defects, and other anomalies as maternal serum AFP levels rose (Fig. 13–5). About 40 percent of pregnancies were abnormal when the AFP level was greater than 7 MoM.

Other causes of elevated levels that can be determined by ultrasonography include fetal death, multiple gestations, structural defects, and placental abnormalities

Table 13–7. Conditions Associated with Abnormal Maternal Serum Alpha-Fetoprotein Concentrations

Elevated Levels

Neural-tube defects

Pilonidal cysts

Esophageal or intestinal obstruction

Liver necrosis

Cystic hygroma

Sacrococcygeal teratoma

Abdominal wall defects—omphalocele, gastroschisis

Urinary obstruction

Renal anomalies—polycystic or absent kidneys

Congenital nephrosis

Osteogenesis imperfecta

Congenital skin defects

Cloacal exstrophy

Chorioangioma of placenta

Placental abruption

Placenta accreta



  Multifetal gestation

Low birthweight

  Fetal death

Improper adjustment for low maternal weight

Underestimated gestational age

Maternal hepatoma or teratoma

Low Levels

Chromosomal trisomies

Gestational trophoblastic disease

Fetal death

Improper adjustment for high maternal weight

Overestimated gestational age

Recommendations for Screening

The American College of Obstetricians and Gynecologists (2003) recommends that all pregnant women be offered second-trimester maternal serum AFP screening. It should be performed within a protocol that includes quality control, counseling, follow-up, and high-resolution ultrasonography. Because only 1 in 16 to 1 in 33 women with an elevated serum AFP level actually has an affected fetus, women should be counseled regarding the high false-positive rates, the risks of amniocentesis, and the rationale for the screening program.

Ultrasonographic Examination

After confirming the gestational age and establishing fetal number and viability, the fetus is evaluated by targeted ultrasonography. Anencephaly, other major cranial defects, and most spine defects can be readily identified (Figs. 13–6 and 13–7). In 99 percent of cases, open spine lesions are associated with one or more of five specific cranial anomalies detected by ultrasonography (Watson and associates, 1991). As detailed in Chapter 16 (see Neural-Tube Defects), these include frontal notching, also called the lemon sign; small biparietal diameter; ventriculomegaly; obliteration of the cisterna magna; and elongated cerebellum, the banana sign (Fig. 13–8). These cranial anomalies are most clearly visible in the second trimester, and some, such as the lemon sign, may resolve later in pregnancy.


Cranial ultrasound in a fetus with Arnold–Chiari malformation showing frontal scalloping (lemon sign) on the left and effacement of the cisterna magna (banana sign) on the right. (Courtesy of Dr. Jodi Dashe.)

In the early days of AFP screening, an elevated maternal serum AFP level prompted amniocentesis to determine the amnionic fluid AFP level. If the AFP level was elevated, then an assay for acetylcholinesterase was done. These tests were considered diagnostic for fetal NTD. Today, however, nearly 100 percent of NTDs are identified by ultrasonography used alone (Nadel and colleagues, 1990; Sepulveda and associates, 1995). Citing this high detection rate, several authorities conclude that a woman with an elevated maternal serum AFP level and a normal ultrasonographic examination need not undergo amniocentesis for amnionic fluid AFP measurement. Instead, she could be counseled that the risk of an NTD is reduced by 95 percent when no spine defects or cranial findings are seen ultrasonographically (Hogge, 1989; Morrow, 1991; Van den Hof, 1990, and their colleagues).

By contrast, a number of other studies report considerably less than a 100-percent ultrasonographic detection rate for structural fetal anomalies, especially before 22 weeks. For example, only 17 percent of all fetal anomalies were identified in the Routine Antenatal Diagnostic Imaging with Ultrasound (RADIUS) trial (Chap. 16, Clinical Applications). VanDorsten and colleagues (1998) reported only a 48-percent ultrasonographic detection rate for all fetal anomalies diagnosed. Platt and co-workers (1992) reported that 6 of 161 cases of open spina bifida were not recognized in a screening program. Accordingly, many recommend that an amniocentesis for amnionic fluid AFP be offered to all women with elevated maternal serum AFP levels. Women considering amniocentesis should be informed that amnionic fluid AFP measurement will detect only open spine defects, and not the 3 to 5 percent of defects that are covered by skin (Crandall and Matsumoto, 1984).


Amnionic fluid AFP levels are measured if an NTD is suspected, if the maternal serum AFP is elevated and the ultrasonographic examination is nondiagnostic, or simply because the maternal serum AFP is elevated, as discussed previously. An elevated amnionic fluid AFP level prompts assay of the same sample for acetylcholinesterase. After ruling out blood contamination, the presence of this enzyme verifies that exposed neural tissue or another open fetal defect is present.

Because NTDs carry a small associated risk of aneuploidy, and aneuploidy would change the prognosis and likely pregnancy management, ultrasonographic identification of a fetal NTD should prompt fetal karyotyping. In a review of more than 17,000 prenatal diagnosis cases, Hume and associates (1996) observed a 2-percent rate of aneuploidy in the 106 fetuses with an isolated NTD. Harmon and colleagues (1995) found that 7 of 43 fetuses with isolated NTDs were aneuploid.

Some clinicians determine the fetal karyotype whenever both maternal serum and amnionic fluid AFP levels are elevated, even if the amnionic fluid acetylcholinesterase assay is negative and an open NTD has thus been ruled out. Gonzalez and associates (1996) reported that in women with elevated serum and amnionic fluid AFP levels and normal ultrasonographic examinations, the incidence of chromosomal abnormalities was elevated fivefold above background risk.

Incidental Fetal Karyotype

If a woman with a normal targeted ultrasonographic examination has undergone amniocentesis for amnionic fluid AFP just because her maternal serum AFP level was elevated, and the amnionic fluid AFP level is normal, fetal karyotyping is controversial. Thiagarajah and colleagues (1995) studied 658 such women and concluded that there was no justification for routine fetal karyotyping. In contrast, Feuchtbaum and associates (1995) reviewed 8097 pregnancies complicated by elevated maternal serum AFP levels. In the pregnancies in which the elevated maternal serum AFP level was “unexplained” because there was no fetal NTD or ventral wall defect and the amnionic fluid AFP level was normal, the rate of chromosomal anomalies was 1.1 percent, or twice as high as that of the general population.

Incidental Amnionic Fluid AFP Measurement

When amniocentesis is performed primarily for genetic analysis, amnionic fluid AFP is often routinely measured. This practice may not be cost-effective. Shields and colleagues (1996) reviewed almost 7000 women who underwent second-trimester amniocentesis for fetal karyotyping. They reported that measurement of amnionic fluid AFP did not increase the detection of anomalies. Similarly, Silver and associates (2001) performed a retrospective analysis of 2769 amnionic fluid specimens and reported that incidental amnionic fluid AFP measurement identified only one NTD not detected by ultrasonography. They estimated that routine amnionic fluid AFP measurement cost $219,000 per informative case.

Unexplained Elevated Abnormal Maternal Serum AFP Levels

Even if there are no obvious fetal abnormalities, several large studies have shown that unexplained high maternal serum AFP levels often forecast a poor pregnancy outcome. These outcomes include low birthweight, oligohydramnios, placental abruption, and fetal death (Katz, 1990; Simpson, 1991; Waller, 1991, each with their associates). According to Wenstrom and co-workers (1992), the first maternal serum AFP level is the most predictive, and serial measurements are not helpful. Simpson and colleagues (1991) reported that second-trimester, but not third-trimester, maternal serum AFP elevation levels were associated with preterm ruptured membranes, preterm birth, and low-birthweight infants. Ramus and associates (1996) studied 241 women with unexplained serum AFP elevations and reported that they had a higher incidence of preterm delivery than women who had normal levels—22 versus 11 percent. The incidence of preterm delivery was highest (47 percent) in the 38 women who had both unexplained elevated serum levels and placental sonolucencies on ultrasonographic examination.

Although elevated maternal serum AFP levels in these cases are assumed to result from placental damage or dysfunction, neither the etiology of the elevated maternal serum values nor the most appropriate management for these women is clear. In these cases, no specific program of maternal or fetal surveillance favorably affects pregnancy outcomes (American College of Obstetricians and Gynecologists, 1996; Cunningham and Gilstrap, 1991).

Management of the Fetus with an NTD

Other than termination of pregnancy, options for pregnancies complicated by an NTD have traditionally been limited. Anencephaly, exencephaly, and iniencephaly are lethal, but some women elect to continue these pregnancies. Routine prenatal care is given, but interventions for fetal indications are not recommended as they will not change fetal outcome.

Counseling and decision making in the case of an isolated fetal spine defect are more difficult. Such women may benefit from counseling by a pediatric neurosurgeon, neurologist, or other specialists in pediatric development. The fully informed couple is more likely to make their best decision and to be prepared for the range of possible pregnancy outcomes. With continued pregnancy, antenatal care is designed to detect changes in fetal status that might alter the timing or route of delivery. Generally, the goal is delivery at term, but rapidly increasing ventriculomegaly may prompt delivery before term so that a shunt can be placed. Fetal heart rate testing is problematic because heart rate patterns in anomalous fetuses can be difficult to interpret (Vindla and associates, 1997).

The optimal timing and method of delivery remain controversial. All studies of delivery methods for fetuses with NTDs are retrospective and suffer from various biases. That said, an equal number of reports support cesarean versus vaginal delivery (Bensen and co-workers, 1988; Luthy and colleagues, 1991; Sakala and Andree, 1990). Theoretically, cesarean delivery might reduce the risk of mechanical trauma and infection of the fetal spine and also allow precise timing of delivery so that appropriate consultants can be available. Optimally, the delivery time and method should be determined on a case-by-case basis by the team that ultimately will care for the woman and her neonate. Team members should include maternal–fetal medicine specialists, neonatologists, neurosurgeons, and others. Fetal surgical repair of meningomyelocele is discussed later (see Neural-Tube Defects).

Down Syndrome

Before the mid-1980s, amniocentesis for fetal karyotyping was generally offered only to women aged 35 years and older. After Merkatz and colleagues (1984) reported that pregnancies with fetal Down syndrome were characterized by low maternal serum AFP levels, prenatal NTD screening was expanded to include Down syndrome screening in women aged younger than 35 years. Cuckle (1984) and Haddow (1983) and their associates confirmed this finding, and most NTD screening programs now include Down syndrome screening.

Screening program results show that detection rates are highest when maternal age-related risk is incorporated because it is the most powerful predictor of aneuploidy. Ultimately, the Down syndrome risk for each woman is estimated by multiplying her maternal age-related risk by a likelihood ratio determined by her serum AFP level (New England Regional Genetics Group, 1989). Women with a calculated Down syndrome risk greater than a predetermined threshold are offered amniocentesis for fetal karyotyping. This screening threshold is typically equal to the midtrimester or term Down syndrome risk of a 35-year-old woman.

Multiple-Marker Screening

Fetal aneuploidy alters serum analytes other than AFP. If a fetus has Down syndrome, second-trimester serum levels of chorionic gonadotropin (hCG) are usually higher and those of unconjugated estriol are lower than expected (Bogart and colleagues, 1987; Wald and associates, 1988a, 1988b). The individual predictive values of hCG, estriol, and AFP for detecting Down syndrome are low, but when combined they can frequently distinguish euploid fetuses from those with Down syndrome.

The most common second-trimester screening protocol in current use, variously called the expanded AFP test, AFP plus, triple screen, or multiple-marker screening test, is based on a composite likelihood ratio determined by levels of all three analytes. The maternal age-related risk is then multiplied by this ratio. The screening threshold chosen may be the midtrimester risk of a 35-year-old woman. More frequently, a threshold is chosen because it results in the optimal combination of a high detection rate with a low screen-positive rate. The risk threshold of about 1:200 is selected most often because, at a 5-percent screen-positive rate, the Down syndrome detection rate is 60 percent in women younger than 35 years. In women older than 35 years, the multiple-marker test detects more than 75 percent of fetuses with Down syndrome and a portion of other aneuploidies as well, although at a detection rate close to 25 percent (Haddow and co-workers, 1994). The multiple-marker test has been validated and has become the preferred second-trimester Down syndrome screening test in most centers (Burton, 1993; Cheng, 1993; Wenstrom, 1993, and their colleagues).

There are several permutations of the multiple-marker test in current use. Some centers offer AFP and hCG testing alone, and others use estriol measurement as a third marker. Some prefer to measure the free -subunit of hCG (-hCG) instead of the intact hCG molecule, and others add inhibin as a fourth analyte (Wald and colleagues, 1996; Wenstrom and associates, 1999b). Other multiple-marker screening tests have been used that combine maternal serum analytes, ultrasonographic measurement of the nuchal fold, long bone measurements, and other parameters (Bahado-Singh and colleagues, 2001; Morris and co-workers, 2001). Several investigative protocols are subsequently discussed.

In most series, only 6 percent of all screen-positive samples are associated with an affected fetus. Thus, a positive screening test indicates increased risk but not necessarily fetal Down syndrome. Conversely, a negative screening test indicates no increased risk, but does not mean that the fetus is normal. Once gestational age is confirmed by ultrasonography, women with a positive screening test should be offered amniocentesis for karyotyping (American College of Obstetricians and Gynecologists, 1996).

Serum Screening in Women Older Than 35 Years

The basis of any multiple-marker algorithm is the maternal age-related risk. Thus, the multiple-marker screening test identifies a higher proportion of fetal Down syndrome cases—at least 80 percent—in women aged 35 years and older than in younger women (Haddow and co-workers, 1994). Although the detection rate increases along with maternal age, so does the screen-positive rate. For example, about 25 percent of women aged 35 years and older will have a test result indicating increased risk. Although some older women will opt for empirical amniocentesis regardless of screening results, others find that serum screening facilitates the decision to undergo invasive testing.

First-Trimester Down Syndrome Screening

Early identification of fetal aneuploidy is desirable for many reasons, including the availability of more options for pregnancy termination. First-trimester screening protocols in current use include maternal serum analyte screening, ultrasonographic evaluation, or a combination of both. Urinary screening has been studied, but the results were disappointing. The most discriminatory first-trimester maternal serum analytes appear to be free -hCG and pregnancy-associated plasma protein A (PAPP-A) (Haddow and associates, 1998; Wald and colleagues, 1998). Measurement of the nuchal translucency (NT), an echolucent area seen in longitudinal views of the back of the neck, is also highly discriminatory (Snijders and colleagues, 1998). If the NT measurement is expressed as an MoM, it can be combined with serum analytes to calculate a composite risk.

Two large trials of combined first-trimester ultrasonographic and serum screening have documented its efficacy. First Trimester Maternal Serum Biochemistry and Fetal Nuchal Translucency Screening Study, referred to as the “BUN study,” reported by Wapner and co-workers (2003) was a multicenter trial that enrolled 8514 women who underwent screening between 74 and 97 days of gestation. Individual risks of fetal Down syndrome and trisomy 18 were calculated based on age, first-trimester levels of free -hCG and PAPP-A, and NT measurement. Women determined to be screen positive were offered fetal karyotyping. Using a Down syndrome risk cutoff of 1:270, 85 percent of Down syndrome cases were identified at a false-positive rate of 9.4 percent. When the false-positive rate was held at 5 percent, the detection rate was 79 percent. Importantly, 91 percent of trisomy 18 cases were identified at a false-positive rate of 2 percent. Because of the high incidence of spontaneous pregnancy loss in aneuploid pregnancies, performing fetal karyotyping after first-trimester screening likely resulted in the identification of some aneuploid pregnancies that would otherwise have been lost spontaneously. This outcome can be viewed either positively or negatively.

The FASTER (First- and Second-Trimester Evaluation of Risk) trial was reported by Malone and colleagues (2003a, 2003b). This multicenter trial included 33,557 women, and it took a slightly different approach. All women participating in the trial underwent both first-trimester screening—which included free -hCG, PAPP-A, NT measurement, and maternal age—and second-trimester screening with hCG, AFP, estriol, and inhibin, along with maternal age. If either test was positive, fetal karyotyping was offered. The investigators then evaluated the screen-positive and detection rates for first-, second-, and combined first- and second-trimester screening. They found that the best results were obtained when women had combined both first- and second-trimester screening—the Fully Integrated Test—and then underwent definitive testing if its result was positive. The integrated test yielded a Down syndrome detection rate of 90 percent at a screen-positive rate of 5.4 percent. Importantly, the investigators determined that NT measurement was difficult to do accurately and reproducibly (D’Alton and associates, 2003). Further, not only did NT measurement medians vary from center to center and operator to operator, but NT medians obtained by a single operator varied over time. The authors therefore concluded that NT measurement should be performed only by operators with specific training and that measurement medians for individual operators should be monitored carefully and adjusted as necessary.

In addition to drifting NT medians, problems with first-trimester screening include a relatively narrow gestational age window for screening—approximately 10 to 13 weeks—and variability in NT measurement resulting from poor visibility, suboptimal fetal position, or inconsistent measurement technique. Accurate assessment of gestational age is essential. The American College Obstetricians (2004) emphasizes that appropriate training, monitoring systems, and counseling must be provided.

Elective Genetic Amniocentesis in Women Younger Than 35 Years

Some women younger than 35 years may request amniocentesis for fetal karyotyping despite reassuring maternal serum screening and ultrasonographic findings. Caughey and colleagues (2004) interviewed 447 women of all ages with undetermined genetic risk and reported that half were willing to undergo invasive prenatal diagnostic testing. One third of women aged 35 years or older expressed a willingness to pay partially or completely for such testing. These investigators concluded that guidelines should be expanded to offer testing for a genetic diagnosis, not only for screening. Others believe that each case must be evaluated individually, and each center must develop its own protocol to handle such requests (Pauker and Pauker, 1994).

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Orthopaedics MCQs

Posted by Dr KAMAL DEEP on January 17, 2011

Q1.Non dynamic splint is – a) Banjo b) Opponons c) Cock-up d) Brand



Principles of treatment Ref:- Chapman Ortho

Radial Nerve Palsy:-

The importance of maintaining supple joints free of deformity cannot be overemphasized. Use splints and physical therapy while awaiting nerve recovery and before considering tendon transfers. Splinting must be individualized. A simple palmar cock-up splint may increase the grip strength 3 to 5 times . Most patients are well served by such a splint. A patient requiring greater excursion of the fingers may prefer a dynamic splint with extension assists for the wrist and metacarpophalangeal joints.

dynamic splint

2.Commonest fractures in childhood is – a) Femur b) Distal humerus
c) Clavicle d) Radius

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Anatomy Notes Vol.2

Posted by Dr KAMAL DEEP on December 19, 2010

1.  Nerves of Upper Limbs



2. Musculocutaneous Nerve Supplies Lateral Side of Forearm Also.



Important See the Diagram:- All muscles of thumb are supplied (pollicis) are supplied by Median Nerve except which causes adduction(Ulnar Nerve)..Obviously Ulnar nerve is a medial nerve it supplies the Adductor Pollicis as adduction is towards medial.

Q:-Median nerve supplies all muscles of the thumb except :
(B)Flexor-pollicis brevis
(C)Opponens pollicis
(D)Adductor pollicis…….ans

Median nerve injury at “wrist”, is commonly tested by :-
Contraction of abductor pollicis brevis…….ans
(B)Contraction of flexor pollicis brevis
(C)Loss of sensation on palm
(D)Loss of sensation on ring finger

The median nerve is vulnerable to division from lacerations at the wrist. Division leads to paralysis of the lumbricals to the index and middle fingers and the thenar muscles (apart from adductor pollicis), as well as loss of sensation to the thumb, index, middle and radial half of the ring fingers. The radial half of the hand becomes flattened as a result of wasting of the thenar muscles and the adducted posture of the thumb.

Pen Test :- Detects the median Nerve injury.It tests the integrity of abductor pollicis brevis


First and Second Lumbricals are Also supplied by Median Nerve

Rest all intrinsic muscles including all interossie are supplied by ULNAR NERVE.

Flexor Pollicis Brevis Superficial head supplied by Median Nerve while deep head by Ulnar Nerve.

Flexor Pollicis “Longus” supplied by Median Nerve.


Radial Nerve supplies all the extensors and also the ABDUCTOR POLLICIS “LONGUS.”

Pollicis “Longus” muscles are supplied by respective chief muscles of forearm like abductor pollicis longus by radial nerve and flexor pollicis longus by median nerve.




3. Ring Finger tip supplied by Median nerve and Ulnar Nerve

4.Dorsum of middle finger is supplied by radial nerve and ulnar nerve and median nerve.

5.Deltoid Muscle Origin is Just outer to the Insertion of Trapezius muscle:-

Origin of Deltoid:-Inferior edge of the crest of the spine of the scapula, lateral margin of the acromion, anterior border of lateral one-third of clavicle

Insertion of Trapezius:-Superior edge of the crest of the spine of the scapula, acromion, posterior border of lateral one-third of clavicle

Function of Deltoid:-Major abductor of arm (abducts arm beyond initial 15° done by supraspinatus); clavicular fibers (Anterior Fibers) assist in flexing the arm; posterior fibers assist in extending the arm.

All of the following features can be observed after the injury to axillary nerve, except:
A.Loss of rounded contour of shoulder
B.Loss of sensation along lateral side of upper arm
C.Loss of overhead abduction
D.Atrophy of deltoid muscle

6. Sub acromial bursa:-

All of the following structures may be compressed during flexion and abduction of shoulder joint except :
(A)Suprascapular nerve
(B)Long head of biceps tendon
(C)Supraspinatus tendon


Coronal section through the left shoulder joint

Rotator cuff impingement syndrome

The Subacromial space is defined by the humeral head inferiorly, and the anterior edge and inferior surface of the anterior third of the acromion, coracoacromial ligament and acromioclavicular joint superiorly. It is occupied by the supraspinatus tendon, subacromial bursa, tendon of the long head of biceps brachii, and the capsule of the shoulder joint. Rotator cuff impingement syndrome is a painful disorder caused by severe or chronic impingement of the rotator cuff tendons under the coracoacromial arch (Michiner et al 2003). The cuff normally impinges against the coracoacromial arch when the humerus is abducted, flexed and internally rotated. This is known as the impingement position. The supraspinatus tendon is anatomically affected most by the impingement, which interestingly also coincides with an area of reduced vascularity in this tendon. Severe impingement can be caused by osteoarthritic thickening of the coracoacromial arch; inflammation of the cuff from disorders such as rheumatoid arthritis; and prolonged overuse in the impingement position, e.g. in cleaning windows, which, when associated with a tendinopathy from age-related degenerative changes within the tendon, can lead to subsequent partial or complete tears of the cuff. Clinically, this condition causes tenderness over the anterior portion of the acromion, and pain which typically occurs on abducting the shoulder between 60° and 120° (the painful arc).




The fibrous membrane of the joint capsule is thickened:

  • anterosuperiorly in three locations to form superior, middle, and inferior glenohumeral ligaments, which pass between the superomedial margin of the glenoid cavity to the lesser tubercle and inferiorly related anatomical neck of the humerus
  • superiorly between the base of the coracoid process and the greater tubercle of the humerus (the coracohumeral ligament);
  • between the greater and lesser tubercles of the humerus (transverse humeral ligament)-this holds the tendon of the long head of the biceps brachii muscle in the intertubercular sulcus

Rotator Interval (In Detail)

7. Rotator Interval  in detail :-The rotator cuff interval is a triangular space between the subscapularis and supraspinatus tendons and the base of the coracoid process, covered by the rotator interval capsule, whose main component is the coracohumeral ligament (CHL). The rotator cuff interval is a triangular space created by the intervention of the coracoid process between the subscapularis and supraspinatus muscles and tendons. The floor of the rotator cuff interval is the cartilage of the humeral head, and the roof of the rotator cuff interval is the rotator interval capsule, which links the subscapularis and supraspinatus tendons and is composed of two layers: the CHL on the bursal side and the fasciculus obliquus on the articular side.The rotator interval is an anatomic region in the anterosuperior aspect of the glenohumeral joint that represents a complex interaction of the fibers of the coracohumeral ligament, the superior glenohumeral ligament, the glenohumeral joint capsule, and the supraspinatus and subscapularis tendons. As basic science and clinical studies continue to elucidate the precise role of the rotator interval, understanding of and therapeutic interventions for rotator interval pathology also continue to evolve. Lesions of the rotator interval may result in glenohumeral joint contractures, shoulder instability, or in lesions to the long head of the biceps tendon. Long-term clinical trials may clarify the results of current surgical interventions and further enhance understanding of the rotator interval.

Rotator interval contents
• Coracohumeral ligament
• Superior glenohumeral ligament
• Long head biceps tendon



The rotator cuff interval is a triangular space between the subscapularis and supraspinatus tendons and the base of the coracoid process, covered by the rotator interval capsule, whose main component is the coracohumeral ligament (CHL). The rotator cuff interval contains the long head of the biceps tendon (LBT) and the superior glenohumeral ligament (SGHL) [16]. The relationships between the CHL, the SGHL, and the LBT are complex and may be difficult to analyze on MRI because of the variable appearance of the CHL.







8. Intermuscular Spaces:- Quadrangular space (from posterior) :-




Quadrangular space (from anterior):-


When viewed from anteriorly, its boundaries are formed by:

  • the inferior margin of the subscapularis muscle;
  • the surgical neck of the humerus;
  • the superior margin of the teres major muscle;
  • the lateral margin of the long head of the triceps brachii muscle

In the posterior scapular region, its boundaries are formed by:

  • the inferior margin of teres minor;
  • the surgical neck of the humerus;
  • the superior margin of teres major;
  • the lateral margin of the long head of triceps brachii.

9. Axillary nerve may be damaged by dislocation of shoulder or by the fracture neck of the humerus.Deltoid is paralyzed with loss of abduction at the shoulder.The rounded contour is lost leading to FLAT SHOULDER.There is sensory loss over lower half of the deltoid.

10.Anastomosis around the scapula:-




Deep branch of Transverse cervical artery makes anastomosis with suprascapular artery and circumflex scapular artery.This is an anastomosis between first part of subclavian artery and third part of axillary artery.

Q:- Subscapular artery is a branch of third part of axillary artery not sublclavian artery.Important Point

The thoraco-acromial artery is a short branch which arises from the second part of the axillary artery.

The suprascapular artery usually arises from the thyrocervical trunk of the subclavian artery, although it may arise from the third part of the subclavian artery

The lateral thoracic artery arises from the second part of the axillary artery

The superior thoracic artery is a small vessel which arises from the first part of the axillary artery near the lower border of subclavius.



The subscapular artery is the largest branch of the axillary artery. It usually arises from the third part of the axillary artery at the distal (inferior) border of subscapularis, which it follows to the inferior scapular angle, where it anastomoses with the lateral thoracic and intercostal arteries and the deep branch of the transverse cervical artery.

The other terminal branch of the subscapular artery, the thoracodorsal artery(DNB2010), follows the lateral margin of the scapula, posterior to the lateral thoracic artery, between latissimus dorsi and serratus anterior. Before entering the deep surface of latissimus dorsi, it supplies teres major and the intercostals and sends one or two branches to serratus anterior. It enters latissimus dorsi muscle with the thoracodorsal nerve: this constitutes the principle neurovascular pedicle to the muscle. It provides numerous musculocutaneous perforators which supply the skin over the superior part of latissimus dorsi. The intramuscular portion of the artery anastomoses with intercostal arteries and lumbar perforating arteries.

11. All the following are true about musculocutaneous nerve injury at shoulder except:  IMPORTANT Q
A.Loss of flexion at shoulder………ANS
B.Loss of flexion of forearm
C.Loss of supination of forearm
D.Loss of sensation on radial side of forearm

The main muscles producing flexion at shoulder are :- Pectoralis major clavicular head and Clavicular or anterior fibers of deltoid….IMP…Accesory muscle producing flexion at shoulder is Coracobrachialis supplied by Musculocutaneous nerve.

Flexion at forearm is lost as it supplies brachialis as well as Biceps brachii.

Supination is lost as Biceps brachii main action is supination when the forearm is flexed.(Supination is brought about by supinator and biceps brachii.Slow supination with elbow extended is done by supinator while rapid supination is done by biceps when arm is flexed against resistance.

Musculocutaneous nerve is injured at the lateral cord of brachial plexus, positive clinical findings would be
(A)Loss of flexion at shoulder
(B)Sensory loss on the radial side of the forearm….ANS
(C)Loss of extension of forearm
(D)Loss of extension of the wrist

The nerve involved in anterior dislocation of the shoulder is
A.Radial nerve
B.Axillary nerve
C.Ulnar nerve
D.Musculocutaneous nerve………ANS

Following anterior dislocation of the shoulder,a pt develops weakness of flexion at elbow and lack of sensation over the lateral aspect forearm; nerve injured is:
A.Radial nerve
B.Musculocutaneous nerve….ANS
C.Axillary nerve
D.Ulnar nerve

Interscalene approach to brachial plexus block does not provide optimal surgical anaesthesia in the area of distribution of which of the following nerve

Injury to radial nerve in lower part of spiral groove:
A.Spares nerve supply to extensor carpi radialis longus
B.Results in paralysis of anconeus muscle
C.Leaves extensions at elbow joint intact
D.Weakens pronation movement

An interscalene brachial plexus block relies on dispersion of the larger volume of local anesthetic within the interscalene groove to accomplish blockade of the brachial plexus.Each trunk divides onto an anterior and a posterior division behind the clavicle, at the apex of the axilla. Within the axilla, the divisions combine to produce the three cords, which are named lateral, medial, and posterior, according to their relationships to the axillary artery. From there on, individual nerves are formed as these neuronal elements descend distally.The interscalene approach to brachial plexus blockade results in consistent anesthesia of the shoulder, arm, and elbow. The interscalene block is not recommended for hand surgery; more distal approaches to the brachial plexus should be used instead (e.g., infraclavicular, axillary). T2 area is not anesthetized.(intercostobrachial nerve area is proper answer.In the above choices Ulnar nerve is the closest to the root values.


Miller says “Although this approach can be used for forearm and hand surgery, blockade of the inferior trunk (C8 through T1) is often incomplete and requires supplementation at the ulnar nerve for adequate surgical anesthesia in that distribution.”

Anatomy:-Between the scalene muscles, these nerve roots unite to form three trunks, which emerge from the interscalene space to lie cephaloposterior to the subclavian artery as it courses along the upper surface of the first rib. Therefore, the “superior” (C5 and C6), “middle” (C7), and “inferior” (C8 and T1) trunks are arranged accordingly and are not in a strict horizontal formation, as often depicted. At the lateral edge of the first rib, each trunk forms anterior and posterior divisions that pass posterior to the midportion of the clavicle to enter the axilla. Within the axilla, these divisions form the lateral, posterior, and medial cords, named for their relationship with the second part of the axillary artery.

12. Ligament of Struther`s:-Struther, ligament of: fibrous band (occasionally ossified) running between medial epicondyle and shaft of the humerus.

Struthers’ ligament is a ligament that extends between the shaft of the humerus and the medial epicondyle of the humerus.It is not a constant ligament and can be acquired or congenital. Its clinical significance arises form the fact that the median nerve, passes in the space between the ligament and the humerus, and in this space the nerve may be compressed leading to supracondylar process syndrome.The ligament is usually ignored and not mentioned due to the fact that its not always found.

Coracobrachialis is more important morphologically than functionally.It represent the medial compartment of the arm.In some animals the muscle is tricipital.In man the upper two heads have fused,but the musculocutaneous nerve passes between the remnants of these two heads.The third head (and the lowest) head of the muscle has  disappeared in man.Occasional persistence of the lower head is associated with the presence of the so called “ligament of struthers” which is a fibrous band extending from the suprocondylar process to the medial epicondyle of the humerus.Supracondylar process seen in 1%.The third head of the coracobrachialis is inserted into this ligament.The lower part of the pronator teres muscle takes origin from the same ligament.The median nerve,or the brachial artery,or both pass subjacent to the ligament.The ligament of struther is in fact a part of the tendon of the dorso-epitrochlearis which is related to the latissimus dorsi


13.Musculocutaneous Nerve lies laterally to the Axillary Artery….IMPORTANT POINT.





Musculocutaneous, median, and ulnar nerves in the arm.

The ulnar nerve enters the arm with the median nerve and axillary artery (Fig. 7.67). It passes through proximal regions medial to the axillary artery. In the middle of the arm, the ulnar nerve penetrates the medial intermuscular septum and enters the posterior compartment where it lies anterior to the medial head of the triceps brachii muscle. It passes posterior to the medial epicondyle of the humerus and then into the anterior compartment of the forearm.

The radial nerve originates from the posterior cord of the brachial plexus and enters the arm by crossing the inferior margin of the teres major muscle alongwith profunda brachii vessels in the lower triangular space ,the medial border of the space formed by the triceps and lateral border by humerus with apex down and base formed by the Teres Major above.  . As it enters the arm, it lies posterior to the brachial artery. Accompanied by the profunda brachii artery, the radial nerve enters the posterior compartment of the arm by passing through the triangular interval.As the radial nerve passes diagonally, from medial to lateral, through the posterior compartment, it lies in the radial groove directly on bone. On the lateral side of the arm, it passes anteriorly through the lateral intermuscular septum and enters the anterior compartment where it lies between the brachialis muscle and a muscle of the posterior compartment of the forearm-the brachioradialis muscle, which attaches to the lateral supraepicondylar ridge of the humerus. The radial nerve enters the forearm anterior to the lateral epicondyle of the humerus, just deep to the brachioradialis.The radial nerve at the elbow lies deep in a groove between brachialis and brachioradialis proximally and extensor carpi radialis distally. It divides into the superficial terminal branch and the posterior interosseous nerve just anterior to the lateral epicondyle

Radial nerve injury in the arm:-The radial nerve is tightly bound with the profunda brachii artery between the medial and lateral heads of the triceps brachii muscle in the radial groove. If the humerus is fractured the radial nerve may become stretched or transected in this region leading to permanent damage and loss of function. This injury is typical (Fig. 7.69) and the nerve should always be tested when a fracture of the midshaft of the humerus is suspected. The patient typically presents with wrist drop (due to denervation of the extensor muscles) and sensory changes over the dorsum of the hand.

In the arm and forearm the median nerve is usually not injured by trauma because of its relatively deep position. The commonest neurologic problem associated with the median nerve is compression beneath the flexor retinaculum at the wrist (carpal tunnel syndrome).


Muscle Origin Insertion Innervation Function
Brachioradialis Proximal part of lateral supraepicondylar ridge of humerus and adjacent inter-muscular septum Lateral surface of distal end of radius Radial nerve [C5,C6] before division into superficial and deep branches Accessory flexor of elbow joint when forearm is mid-pronated
Extensor carpi radialis longus Distal part of lateral supraepicondylar ridge of humerus and adjacent intermuscular septum Dorsal surface of base of metacarpal II Radial nerve [C6,C7] before division into superficial and deep branches Extends and abducts the wrist
Extensor carpi radialis brevis Lateral epicondyle of humerus and adjacent intermuscular septum Dorsal surface of base of metacarpals II and III Deep branch of radial nerve [C7,C8] before penetrating supinator muscle Extends and abducts the wrist
Extensor digitorum Lateral epicondyle of humerus and adjacent intermuscular septum and deep fascia Four tendons, which insert via ‘extensor hoods’ into the dorsal aspects of the bases of the middle and distal phalanges of the index, middle, ring, and little fingers Posterior interosseous nerve [C7,C8] Extends the index, middle, ring, and little fingers; can also extend the wrist
Extensor digiti minimi Lateral epicondyle of humerus and adjacent intermuscular septum together with extensor digitorum Dorsal hood of the little finger Posterior interosseous nerve [C7,C8] Extends the little finger
Extensor carpi ulnaris Lateral epicondyle of humerus and posterior border of ulna Tubercle on the base of the medial side of metacarpal V Posterior interosseous nerve [C7,C8] Extends and adducts the wrist
Anconeus Lateral epicondyle of humerus Olecranon and proximal posterior surface of ulna Radial nerve [C6 to C8] (via branch to medial head of triceps brachii) Abduction of the ulna in pronation; accessory extensor of the elbow joint

There is some variation in the level at which branches of the radial nerve arise from the main trunk in different subjects. Branches to extensor carpi radialis brevis and supinator may arise from the main trunk of the

radial nerve or from the proximal part of the posterior interosseous nerve, but almost invariably above the arcade of Frohse.

Arcade of Frohse, sometimes called the supinator arch is the most superior part of the superficial layer of the supinator muscle, and is a fibrous arch over the posterior interosseous nerve. The arcade of Frohse is the most frequent site of posterior interosseous nerve entrapment, and is believed to play a role in causing progressive paralysis of the posterior interosseous nerve, both with and without injury.


The deep branch of radial nerve may be damaged during an operation for exposure of the head of the radius.Since the extensor carpi radialis longus and brevis are spared wrist drop does not occur.

 A patient is brought to the emergency with history of trauma to his right upper limb. Extension of metacarpophalangeal is lost. There is no wrist drop and extension of IP joint is normal. The most likely nerve involved is :
(A)Ulnar nerve
(B)Median nerve
Radial nerve
(D)Posterior-interosseous nerve

Injury to radial nerve in lower part of spiral groove:
A.Spares nerve supply to extensor carpi radialis longus
B.Results in paralysis of anconeus muscle
C.Leaves extensions at elbow joint intact
D.Weakens pronation movement

One of the branches to the medial head of the triceps brachii muscle arises before the radial nerve’s entrance into the posterior compartment and passes vertically down the arm in association with the ulnar nerve

Damage to the radial nerve in the spinal groove spares which muscle
A.Lateral head of triceps
B.Long head of triceps
C.Medial head of triceps

Controversial Question

Injury to radial nerve in lower part of spiral groove:
A.Spares nerve supply to extensor carpi radialis longus— True
B.Results in paralysis of anconeus muscle—false Upper part of groove branch is given
C.Leaves extensions at elbow joint intact—-False  Weakens
D.Weakens pronation movement—-false Median nerve supplies pronators


RADIAL NERVE (see above diagram) :-The radial nerve descends behind the third part of the axillary artery and the upper part of the brachial artery, anterior to subscapularis and the tendons of latissimus dorsi and teres major. With the profunda brachii artery it inclines dorsally, passing through the triangular space below the lower border of teres major, between the long head of triceps and the humerus. Here it supplies the long head of triceps, and gives rise to the posterior cutaneous nerve of the arm (not forearm)which supplies the skin along the posterior surface of the upper arm. It then spirals obliquely across the back of the humerus, lying posterior to the uppermost fibres of the medial head of triceps which separate the nerve from the bone in the first part of the spiral groove. Here it gives off a muscular branch to the lateral head of triceps and a branch which passes through the medial head of triceps to anconeus. On reaching the lateral side of the humerus it pierces the lateral intermuscular septum to enter the anterior compartment; it then descends deep in a furrow between brachialis and proximally brachioradialis, then more distally extensor carpi radialis longus. Anterior to the lateral epicondyle it divides into superficial and deep terminal rami.

The branches of the radial nerve in the upper arm are: muscular, cutaneous, articular and superficial terminal and posterior interosseous.

Muscular branches :-Muscular branches supply triceps, anconeus, brachioradialis, extensor carpi radialis longus and brachialis in medial, posterior and lateral groups. Medial muscular branches arise from the radial nerve on the medial side of the arm. They supply the medial and long heads of triceps; the branch to the medial head is a long, slender filament which, lying close to the ulnar nerve as far as the distal third of the arm, is often termed the ulnar collateral nerve. A large posterior muscular branch arises from the nerve as it lies in the humeral groove. It divides to supply the medial and lateral heads of triceps and anconeus, that for the latter being a long nerve which descends in the medial head of triceps and partially supplies it; it is accompanied by the middle collateral branch of the profunda brachii artery and passes behind the elbow joint to end in anconeus. Lateral muscular branches arise in front of the lateral intermuscular septum; they supply the lateral part of brachialis, brachioradialis and extensor carpi radialis longus.



15. Pronator teres in addition to the main pronator of forearm also causes flexion at elbow joint.

16.”D”eep muscles of the front of forearm (Flexor digitorum  Profundus & Flexor pollicis longus)  acts on the “D”istal IP joint.

17. Flexor digitorum superficialis acts on the Proximal IP joint.

18.Flexor “carpi” radialis:- Flexes the wrist and abductor of the wrist.RADIALIS(RADIUS) acts laterally.Carpi—so acts on wrist.

Palmaris Longus:- Absent in 10% of subjects.

Flexor carpi ulnaris:-Flexes and adduct the wrist.Ulnaris—so adduct.Carpi –so flexes the wrist.

All muscles except the flexor carpi ulnaris in the forearm are supplied by the median nerve.

The pisiform bone is a seasmoid bone in the tendon of Flexor carpi ulnaris.

19.The Cubital Fossa:-The cubital fossa is an important area of transition between the arm and the forearm. It is located anterior to the elbow joint and is a triangular depression formed between two forearm muscles:

  • the brachioradialis muscle originating from the lateral supraepicondylar ridge of the humerus;
  • the pronator teres muscle originating from the medial epicondyle of the humerus image


20. Ape thumb Deformity:-   Injury of median nerve at wrist leads to wasting of thenar muscles and the thumb is adducted and laterally rotated.:- ABDUCTION IS LOST,OPPOSITION IS LOST,FLEXION IS LOST.Ape hand deformity is a deformity in humans who cannot move the thumb outside of the plane of the palm. It is caused by inability to oppose the thumb and the limited abduction of the thumb.


              Ape Hand Deformity



Flexion and extension should be confined to motion at the interphalangeal or metacarpophalangeal joints (Fig. 53.49A-C). Palmar abduction (Fig. 53.49D, E), in which the first metacarpal moves away from the second at right angles to the plane of the palm, and radial abduction (Fig. 53.49D, F), in which the first metacarpal moves away from the second with the thumb in the plane of the palm, occur at the carpometacarpal joint. The opposite of radial abduction is ulnar adduction, or transpalmar adduction, in which the thumb crosses the palm towards its ulnar border. In clinical practice the term adduction is generally used without qualification. Circumduction describes the angular motion of the first metacarpal, solely at the carpometacarpal joint, from a position of maximal radial abduction in the plane of the palm towards the ulnar border of the hand, maintaining the widest possible angle between the first and second metacarpals (Fig. 53.49G). Lateral inclinations of the first phalanx maximize the extent of excursion of the circumduction arc. Opposition is a composite position of the thumb achieved by circumduction of the first metacarpal, internal rotation of the thumb ray and maximal extension of the metacarpophalangeal and interphalangeal joints (Fig. 53.49H). Retroposition is the opposite to opposition (Fig. 53.49I). Flexion adduction is the position of maximal transpalmar adduction of the first metacarpal: the metacarpophalangeal and interphalangeal joints are flexed and the thumb is in contact with the palm (Fig. 53.49J).



Most branches to the muscles in the superficial and intermediate layers of the forearm originate medially from the nerve just distal to the elbow joint:

  • The largest branch of the median nerve in the forearm is the anterior interosseous nerve, which originates between the two heads of pronator teres, passes distally down the forearm with the anterior interosseous artery, innervates the muscles in the deep layer (flexor pollicis longus, the lateral half of flexor digitorum profundus, and pronator quadratus) and terminates as articular branches to joints of the distal forearm and wrist.
  • A small palmar branch originates from the median nerve in the distal forearm immediately proximal to the flexor retinaculum , passes superficially into the hand and innervates the skin over the base and central palm. This palmar branch is spared in carpal tunnel syndrome because it passes into the hand superficial to the flexor retinaculum of the wrist.
    Since the terminal phalanges of little and ring fingers are supplied by ulnar nerve(Ulnar nerve supplies the medial half of digital profundus muscle) These Fingers DIP are spared in Median nerve injury.

Also the PIP joint of thumb is spared as flexor pollicis brevis deep supplied by ulnar nerve.

There is one IP joint  in the thumb and MCP joint.Flexor pollicis brevis causes flexion at MCP jt. and Flexor pollicis longus causes flexion at IP joint of thumb.Both supplied by Median nerve.

So thumb is adducted(abduction is lost due to abductor pollicis brevis paralysisi) and laterally rotated 9as medial rotation by the opponens pollicis is lost.)

Flexor pollicis brevis :The flexor pollicis brevis muscle is distal to abductor pollicis brevis.It originates mainly from the tubercle of the trapezium and adjacent flexor retinaculum, but it may also have deeper attachments to other carpal bones and associated ligaments. It inserts into the lateral side of the base of the proximal phalanx of the thumb. The tendon often contains a sesamoid bone(DNB 2010).Flexor pollicis brevis flexes the metacarpophalangeal joint of the thumb.


22. Extensor Hoods:-


The tendons of the extensor digitorum and extensor pollicis longus muscles pass onto the dorsal aspect of the digits and expand over the proximal phalanges to form complex ‘extensor hoods‘ or ‘dorsal digital expansions‘ .

Because force from the small intrinsic muscles of the hand is applied to the extensor hood distal to the fulcrum of the metacarpophalangeal joints, the muscles flex these joints .Simultaneously, the force is transferred dorsally through the hood to extend the interphalangeal joints. This ability to flex the metacarpophalangeal joints, while at the same time extending the interphalangeal joints, is entirely due to the intrinsic muscles of the hand working through the extensor hoods. This type of precision movement is used in the ‘upstroke’ when writing a ‘t’.

In the index, middle, ring, and little fingers, the lumbrical, interossei, and abductor digiti minimi muscles attach to the extensor hoods. In the thumb, the adductor pollicis and abductor pollicis brevis muscles insert into and anchor the extensor hood.

Q:-The lumbricals muscles extend the MCP joints and extend the IP joints of the digit in which they insert.

23. Anatomical Snuff Box:-

Regarding the anatomical snuff box which of the following is true:
(A)Abductor Pollicis longus forms the posterior wall. (it forms the anterior wall)
(B)Abductor pollicis longus and Extensor pollicis brevis form the anterior wall. ….ans
(C)Basilus vein forms the roof.            (its cephalic not basilic)
(D)Floor is formed by Extensor carpi radialis longus and brevis.??

Basilic vein is on the ulnar side not on the radial side-Remember


The ‘anatomical snuffbox’ is a term given to the triangular depression formed on the posterolateral side of the wrist and metacarpal I by the extensor tendons passing into the thumb . Historically, ground tobacco (snuff) was placed in this depression before being inhaled into the nose. The base of the triangle is at the wrist and the apex is directed into the thumb. The impression is most apparent when the thumb is extended:

  • the lateral border is formed by the tendons of the abductor pollicis longus and extensor pollicis brevis;
  • the medial border is formed by the tendon of the extensor pollicis longus;
  • the floor of the impression is formed by the scaphoid and trapezium, and distal ends of the tendons of the extensor carpi radialis longus and extensor carpi radialis brevis.

The radial artery passes obliquely through the anatomical snuffbox, deep to the extensor tendons of the thumb and lies adjacent to the scaphoid and trapezium.

Terminal parts of the superficial branch of the radial nerve pass subcutaneously over the snuffbox as does the origin of the cephalic vein from the dorsal venous arch of the hand.


After passing around Lister’s tubercle, the tendon of extensor pollicis longus crosses the tendons of extensor carpi radialis brevis and longus obliquely .When the thumb is fully extended the tendon is separated from extensor pollicis brevis by a triangular depression or fossa, the so-called ‘anatomical snuff-box’. Bony structures can be felt in the floor of this fossa by deep palpation. In proximal to distal order they are the radial styloid, the smooth convex articular surface of the scaphoid, the trapezium, and the base of the first metacarpal. The latter are more easily felt during metacarpal movement, while the scaphoid is more easily felt during adduction and abduction of the hand

The tendon of extensor pollicis brevis can be felt at the radial border of the anatomical snuff-box, lying medial to the tendon of abductor pollicis longus, when the metacarpophalangeal joint of the thumb is extended against resistance

The tendon of extensor pollicis longus can be palpated at the ulnar border of the anatomical snuff-box when the thumb is extended at the interphalangeal joint against resistance.




24.The carpal tunnel contains all of the following important structures except:
A.Median Nerve.
B.Flexor pollicis longus.
Flexor carpi radialis.
D.Flexor digitorum superficialis.



The structures passing superficial to the flexor retinaculum are:- a)the tendon of the palmaris longus b)the palmar cutaneous branch of the median nerve c)the palmar cutaneous branch of the ulnar nerve d)the ulnar vessels e) the ulnar nerve.

The ulnar artery, ulnar nerve, and tendon of palmaris longus pass into the hand anterior to the flexor retinaculum and therefore do not pass through the carpal tunnel .

The four tendons of the flexor digitorum profundus, the four tendons of the flexor digitorum superficialis, and the tendon of the flexor pollicis longus pass through the carpal tunnel, as does the median nerve,Others are radial bursa and ulnar bursa

All the tendons of the flexor digitorum profundus and flexor digitorum superficialis are surrounded by a single synovial sheath; a separate sheath surrounds the tendon of the flexor pollicis longus. The median nerve is anterior to the tendons in the carpal tunnel.

The tendon of flexor carpi radialis is surrounded by a synovial sheath and passes through a tubular compartment formed by the attachment of the lateral aspect of the flexor retinaculum to the margins of a groove on the medial side of the tubercle of trapezium.It lies between the retinaculum and its deep slip,in the grrove on the trapezium.

25. Ofcourse the lumbricals do not insert into the thumb as polllicis has its own separate  thenar muscles.

So 1st lumbricals insert into 2nd MCP joint and so-on so that the 4th lumbrical inserted into the 5th MCP joint..

So 1st lumbicals acts on the index finger but not the thumb or 1st MCP joint,,,imp.They arise from the tendon of the Flexor digitorum profundus (as FLEX DIGITORUM PROFUNDUS is obviously inserted into the 2nd to 5th digits)and inserted into the DDE(dorsal digital expansion of Extensor digitorum.

26.Palmar interossei are abductors while Dorsal interossei are adductors of the fingers

27. All Interossei and lumbricals Flex the MCP and Extend the IP joint.

28.Midpalmar Space:-Laterally by the intermediate palmar septum attaching the palmar aponeurosis to the third metacarpal bone.

Medially by the the medial palmar septum.



The radial artery curves around the lateral side of the wrist, passes over the floor of the anatomical snuffbox and into the deep plane of the palm by penetrating anteriorly through the back of the hand . It passes between the two heads of the first dorsal interosseous muscle and then between the two heads of the adductor pollicis to access the deep plane of the palm and form the deep palmar arch.

Allen’s test:-To test for adequate anastomoses between the radial and ulnar arteries, compress both the radial and ulnar arteries at the wrist, then release pressure from one or the other, and determine the filling pattern of the hand. If there is little connection between the deep and superficial palmar arteries only the thumb and lateral side of the index finger will fill with blood (become red) when pressure on the radial artery alone is released

The deep palmar arch passes medially through the palm between the metacarpal bones and the long flexor tendons of the digits. On the medial side of the palm, it communicates with the deep palmar branch of the ulnar artery .


Anconeus is a small, triangular muscle posterior to the elbow joint and is partially blended with triceps (Figs 52.15, 52.17). Anconeus arises by a separate tendon from the posterior surface of the lateral epicondyle of the humerus. Its fibres diverge medially towards the ulna, covering the posterior aspect of the annular ligament, and are attached to the lateral aspect of the olecranon and proximal quarter of the posterior surface of the shaft of the ulna.


The extent to which anconeus fuses with triceps or extensor carpi ulnaris is variable


Anconeus assists triceps in extending the elbow joint. Its major function is not clear, but it may be the control of ulnar abduction in pronation, which is necessary if the forearm is to turn over the hand without translating it medially. In this way a tool can be revolved ‘on the spot’ or it can be swept through an arc.Anconeus abducts the ulna during pronation to maintain the center of the palm over the same point when the hand is flipped.


Which is true about synovial joint ? :
(A)Stability is inversely proportional to mobility.FALSE*(The mechanical function of the synovial joints is to permit motion whilst carrying functional loads and remaining stable)
(B)Hyaline cartilage covers articular surface of all synovial joints.TRUE—MOSTLY
(C) Metacarpo-phalangeal joint is a hinge joint. FALSE IT IS CONDYLOID
(D)”Cartilage usually divides the joint into two cavities”FALSE-ARTICULAR DISC DIVIDES.


A and B are purely diagrammatic and not related to particular joints. C, however, is a simplified representation of some features of an elbow joint but the complicated contours due to the olecranon, coronoid and radial fossae and profiles of articular fat pads present in a true section have been omitted.

Articular surfaces are mostly formed by a special variety of hyaline cartilage, reflecting their preformation as parts of cartilaginous models in embryonic life. Exceptionally, surfaces of the sternoclavicular and acromioclavicular joints and both temporomandibular surfaces are covered by dense fibrous tissue which contains isolated groups of chondrocytes and little surrounding matrix – a legacy of their formation by intramembranous ossification. Articular cartilage has a wear-resistant, low-frictional, lubricated surface, which is slightly compressible and elastic and is thus ideally constructed for easy movement over a similar surface. It is also able to absorb large forces of compression and shear generated by gravity and muscular power.

A fibrous capsule completely encloses a joint except where it is interrupted by synovial protrusions; the exceptions are described with the individual joints. The capsule is composed of parallel but interlacing bundles of white collagen fibres which form a cuff whose ends are attached continuously round the articular ends of the bones concerned.

An articular disc or meniscus occurs between articular surfaces where congruity is low. It consists of fibrocartilage, where the fibrous element is usually predominant, and is not covered by synovial membrane. A disc may extend across a synovial joint, dividing it structurally and functionally into two synovial cavities. Discs are connected at their periphery to fibrous capsules, usually by vascularized connective tissue, so that they become invaded by vessels and afferent and motor (sympathetic) nerves; sometimes the union is closer and stronger, as in the knee and temporomandibular joints. Their main part contains few cells, but their surfaces may be covered by an incomplete stratum of flat cells, continuous at the periphery with adjacent synovial membrane

Synovial Joints Joint capsule containing synovial membrane and
synovial fluid
1. Gliding Flattened or slightly curved articulating surfaces Sliding Intercarpal and intertarsal joints
2. Hinge Concave surface of one bone articulates with Bending motion in one plane Knee; elbow; joints of phalanges
convex surface of another
3. Pivot Conical surface of one bone articulates with Rotation about a central axis Atlantoaxial joint; proximal
depression of another radioulnar joint
4. Condyloid Oval condyle of one bone articulates with Movement in two planes Radiocarpal joint;
elliptical cavity of another metacarpophalangeal joint
5. Saddle Concave and convex surface on each Wide range of movements Carpometacarpal joint of thumb
articulating bone
6. Ball-and-socket Rounded convex surface of one bone articulates Movement in all planes and Shoulder and hip joints
with cuplike socket of another rotation


           Saddle joint-CARPOMETACARPAL                                                   BALL & SOCKET                                                                    HINGE                                                  CONDYLOID(ELLIPSOID)-MCP


                            PIVOT  atlas with the axis                                                                        GLIDING-intercarpal

Ellipsoid joints:- Ellipsoid joints are biaxial, and consist of an oval, convex surface apposed to an elliptical concavity, e.g. radiocarpal and metacarpophalangeal joints. Primary movements are about two orthogonal axes, e.g. flexion-extension, abduction-adduction, which may be combined as circumduction; rotation around the third axis is largely prevented by general articular shape.

Plane joints(GLIDING) :- Plane joints are appositions of almost flat surfaces (e.g. intermetatarsal and some intercarpal joints). Slight curvature is usual, although often disregarded, and movements are considered to be pure translations or sliding between bones. However, in precise dynamics even slight curvatures cannot be ignored

Ginglymi (hinge) joints:- Ginglymi resemble hinges and restrict movement to one plane, i.e. they are uniaxial. They have strong collateral ligaments to aid this, e.g. interphalangeal and humero-ulnar joints. The surfaces of such biological hinges differ from regular mechanical cylinders in that their profiles are not arcs but varyingly spiral, and therefore motion is not truly about a single axis.

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