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Archive for the ‘Uncategorized’ Category

Anatomy Notes Vol.1 with Orthopaedics

Posted by Dr KAMAL DEEP on December 17, 2010

Note:-Bolded or underlined statements are previous questions.

1.Attachments on the scapula:-No attachments for Pectoralis Major.




2.SITminor(Supraspinatus,Infraspinatus,Teres Minor inserted on gretaer tubercle of humerus on posterior side of top of humerus. All have attachments on scapula.Subscapularis inserted on Lesser tubercle of humerus.Pectoralis minor is inserted on coracoid process.

3.Tip of coracoid process:- Short Head of biceps and Coracobrachialis.

4.Carpal Bones :-


Proximal row:- ScaLunaTriqPisi (Scaphoid Lunate Triquetral Pisiform):Lateral to medial

Distal Row :- Trapezium,Trapezoid,Capitate and Hamate: Lateral to medial

The pisiform is a sesamoid bone in the tendon of flexor carpi ulnaris and articulates with the anterior surface of the triquetrum.

Most common site of scaphoid fracture is :
(B)Proximal fragment
(C)Distal fragment
(D)Tilting of the lunate

Fractures of the scaphoid are the most common of carpal fractures. They usually occur in young adult men following falls on their outstretched palms. Experimental studies have shown that the force must be applied to the radial side of the palm, with the wrist extended a minimum of 95° (102). In that position, the scaphoid is the only carpal bone in contact with the radius. The proximal part of the scaphoid assumes a wedge-shaped configuration between the radius and capitate, where it is supported by the radial collateral and radiocapitate ligaments. The distal pole of the scaphoid, however, is unsupported and capsular structures in the area are lax. It is the distal pole that receives most of the applied force and the bone fractures at its most vulnerable area, its waist.

The profile of the bone is best seen on PA and posterior-oblique views with the wrist in ulnar deviation ( The posterior-oblique view visualizes the carpal bones on the radial side of the wrist, particularly the scaphoid, and the anterior-oblique view visualizes the pisiform and, to a lesser extent, the hamate)

Although radiographs taken immediately after the injury may be negative, the scaphoid should still be considered fractured until proven otherwise. Immobilize the wrist in a thumb spica splint or cast and repeat radiographs in 1 to 2 weeks. If there is a fracture, it should then be evident by the appearance of bone resorption at the fracture site. Occasionally, bone resorption does not appear until 3 weeks after the fracture, and even then radiographs may remain inconclusive. In these cases, radionuclide imaging with technetium-99m (99mTc) can be helpful (32). Although bone scans are highly sensitive and are generally positive within 24 h of a fracture, they are nonspecific. Therefore, although a fracture can be ruled out with a negative scan, a positive scan requires more specific imaging studies. Vibratory testing, using audible “intrasound” frequencies between 20 and 20,000 Hz (infrasound less than 20 Hz and ultrasound greater than 20,000 Hz are inaudible), has been shown to be effective in diagnosing occult scaphoid fractures (8). The test is considered positive when pain is sufficient to cause an immediate “positive retraction response.” The definitive test is a CT scan.

The second method of classification is based on the site of the fracture within the scaphoid, which is separated into proximal, middle, and distal thirds. Most fractures involve the middle third of the bone. They usually heal if they are not displaced, and there is no intercarpal instability.Q:- Fractures in the proximal third, sometimes referred to as the proximal pole of the scaphoid, have the highest incidence of nonunion and avascular necrosis because of the pattern of intraosseous circulation. The blood supply to the scaphoid enters dorsally and distally and traverses the bone in a proximal direction (36). Fractures in the distal third of the scaphoid are the rarest and tend to heal promptly because of the excellent blood supply in the area. Distal-third fractures include intraarticular fractures and fractures of the tubercle.

Q:-So non-union and delayed union is more common than malunion.

Avascular necrosis of the scaphoid (Priser’s disease) and of the lunate (Kienbock’s disease).

5.The anterior group of lymph nodes lie along the lateral thoracic vessels.Approximately 75% is via lymphatic vessels that drain laterally and superiorly into axillary nodes.

As indicated in Fig. 17-8, the lymph node groups are assigned levels according to their anatomic relationship to the pectoralis minor muscle(not pectoralis major). Lymph nodes located lateral to or below the lower border of the pectoralis minor muscle are referred to as level I lymph nodes, which include the axillary vein, external mammary(anterior axillary or pectoral group), and scapular groups. Lymph nodes located superficial or deep to the pectoralis minor muscle are referred to as level II lymph nodes, which include the central and interpectoral groups. Lymph nodes located medial to or above the upper border of the pectoralis minor muscle are referred to as level III lymph nodes, which consist of the subclavicular group. The plexus of lymph vessels in the breast arises in the interlobular connective tissue and in the walls of the lactiferous ducts and communicates with the subareolar plexus of lymph vessels. Efferent lymph vessels from the breast pass around the lateral edge of the pectoralis major muscle and pierce the clavipectoral fascia, ending in the external mammary (anterior, pectoral) group of lymph nodes. Some lymph vessels may travel directly to the subscapular (posterior, scapular) group of lymph nodes. From the upper part of the breast, a few lymph vessels pass directly to the subclavicular (apical) group of lymph nodes. The axillary lymph nodes usually receive >75% of the lymph drainage from the breast. The rest is derived primarily from the medial aspect of the breast, flows through the lymph vessels that accompany the perforating branches of the internal mammary artery, and enters the parasternal (internal mammary) group of lymph nodes


Axillary lymph node groups. Level I includes lymph nodes located lateral to the pectoralis minor muscle (PM); level II includes lymph nodes located deep to the PM; and level III includes lymph nodes located medial to the PM. Arrows indicate the direction of lymph flow. The axillary vein with its major tributaries and the supraclavicular lymph node group are also illustrated.

The boundaries for lymph drainage of the axilla are not well demarcated, and there is considerable variation in the position of the axillary lymph nodes. The six axillary lymph node groups recognized by surgeons (Figs. 17-7 and 17-8) are (a) the axillary vein group (lateral), which consists of four to six lymph nodes that lie medial or posterior to the vein and receive most of the lymph drainage from the upper extremity; (b) the external mammary group (anterior or pectoral group), which consists of five or six lymph nodes that lie along the lower border of the pectoralis minor muscle contiguous with the lateral thoracic vessels and receive most of the lymph drainage from the lateral aspect of the breast; (c) the scapular group (posterior or subscapular), which consists of five to seven lymph nodes that lie along the posterior wall of the axilla at the lateral border of the scapula contiguous with the subscapular vessels and receive lymph drainage principally from the lower posterior neck, the posterior trunk, and the posterior shoulder; (d) the central group, which consists of three or four sets of lymph nodes that are embedded in the fat of the axilla lying immediately posterior to the pectoralis minor muscle and receive lymph drainage both from the axillary vein, external mammary, and scapular groups of lymph nodes, and directly from the breast; (e) the subclavicular group (apical), which consists of six to twelve sets of lymph nodes that lie posterior and superior to the upper border of the pectoralis minor muscle and receive lymph drainage from all of the other groups of axillary lymph nodes; and (f) the interpectoral group (Rotter’s nodes), which consists of one to four lymph nodes that are interposed between the pectoralis major and pectoralis minor muscles and receive lymph drainage directly from the breast. The lymph fluid that passes through the interpectoral group of lymph nodes passes directly into the central and subclavicular groups.


6. Clavipectoral Fascia:-


Pierced by LTC

L-Lateral pectoral nerve

T-Thoracoacromial vessels

C—Cephalic VEIN

Clavipectoral fascia:-The clavipectoral fascia is a strong fibrous sheet behind the clavicular part of pectoralis major. It fills the gap between pectoralis minor and subclavius, and covers the axillary vessels and nerves. It splits around subclavius and is attached to the clavicle both anterior and posterior to the groove for subclavius. The posterior layer fuses with the deep cervical fascia which connects omohyoid to the clavicle and with the sheath of the axillary vessels. Medially it blends with the fascia over the first two intercostal spaces and is attached to the first rib, medial to subclavius. Laterally, it is thick and dense, and is attached to the coracoid process, blending with the coracoclavicular ligament. Between the first rib and coracoid process the fascia often thickens to form a band, the costocoracoid ligament. Below this the fascia becomes thin, splits around pectoralis minor and descends to blend with the axillary fascia and laterally with the fascia over the short head of biceps. The cephalic vein, thoraco-acromial artery and vein, and lateral pectoral nerve pass through the fascia.

7. Serratus Anterior muscle :- SERRATUS (AT = 8 Digitations from upper eight ribs)

Nerve supply:- C5,C6 and C7(long thoracic nerve)

Also called as Boxer`s muscle.-Along with the pectoralis minor the muscle pulls the scapula forwards around the chest wall to protract the upper limb(in pushing and punching movements)

Forms the Medial Wall of Axilla

Damage to the long thoracic nerve;-Because the long thoracic nerve passes down the lateral thoracic wall on the external surface of the serratus anterior muscle, just deep to skin and subcutaneous fascia, it is vulnerable to damage. Loss of function of this muscle causes the medial border, and particularly the inferior angle, of the scapula to elevate away from the thoracic wall, resulting in characteristic ‘winging’ of the scapula, on pushing forward with the arm.

True bout the Serratus anterior muscle is
A. Originates from the lower four ribs (upper 8 ribs)
B. Bipennate muscle (8 pinna)
C. Supplied by the subscapular nerve  (long thoracic nerve C5 C6 C7 roots)
D/ Helps in forced inspiration –True

Winging of scapula is due to paralysis of :
(A) Rhomboides (B) Trapezius
(C) L. dorsi (D) Serratus-anterior

8. Axilla:- The axillary inlet is oriented in the horizontal plane and is somewhat triangular in shape, with its apex directed laterally.The margins of the inlet are completely formed by bone.

  • the medial margin is the lateral border of rib I;
  • the anterior margin is the posterior surface of the clavicle;
  • the posterior margin is the superior border of the scapula The apex of the triangularly shaped axillary inlet is lateral in position and is formed by the medial aspect of the coracoid process
  • imageimage

The anterior wall is formed by pectorales major and minor, the former covering the whole wall, the latter its intermediate part. The interval between the upper border of pectoralis minor and clavicle is occupied by the clavipectoral fascia. The posterior wall is formed by subscapularis above, and teres major and latissimus dorsi below. The medial ‘wall’ is convex laterally and is composed of the first four ribs and their associated intercostal muscles, together with the upper part of serratus anterior. The anterior and posterior walls converge laterally: the ‘wall’ is narrow and consists of the humeral intertuberous sulcus. The lateral angle lodges coracobrachialis and biceps.

So lateral wall is very narrow,its actually an angle.

Contents of Axilla:-

The axilla contains the axillary vessels, the infraclavicular part of the brachial plexus and its branches, lateral branches of some intercostal nerves, many lymph nodes and vessels, loose adipose areolar tissue and, in many instances, the ‘axillary tail’ of the breast. The axillary vessels and brachial plexus run from the apex to the base along the lateral wall, nearer to the anterior wall: the axillary vein is anteromedial to the artery. The obliquity of the upper ribs means that the neurovascular bundle, after it emerges from behind the clavicle, crosses the first intercostal space: its relations are therefore different at upper and lower levels. Thoracic branches of the axillary artery are in contact with the pectoral muscles; the lateral thoracic artery reaches the thoracic wall along the lateral margin of pectoralis minor. q:-Subscapular vessels descend on the posterior wall at the lower margin of subscapularis. The subscapular and thoracodorsal nerves cross the anterior surface of latissimus dorsi at different inclinations. Circumflex scapular vessels wind round the lateral border of the scapula; posterior circumflex humeral vessels and the axillary nerve curve back and laterally around the surgical neck of the humerus.

No large vessel lies on the medial ‘wall’, which is crossed proximally only by small branches of the superior thoracic artery. The long thoracic nerve descends on serratus anterior and the intercostobrachial nerve perforates the upper anterior part of this wall, crossing the axilla to its lateral ‘wall’

9.The Brachial Plexus:-Branches of the brachial plexus may be described as supraclavicular and infraclavicular

From roots 1. Nerves to scaleni and longus colli C5, 6, 7, 8
  2. Branch to phrenic nerve C5
  3. Dorsal scapular nerve C5
  4. Long thoracic nerve C5, 6 (7)
From trunks 1. Nerve to subclavius C5, 6
  2. Suprascapular nerve C5, 6

Dorsal Scapular nerve supplies rhomboids

Long thoracic nerve supplies the serratus anterior.

Point to note nerves from roots supplies the muscles inserted into the medial margin of Scapula.

The lateral pectoral nerve is larger than the medial, and may arise from the anterior divisions of the upper and middle trunks, or by a single root from the lateral cord. Its axons are from the fifth to seventh cervical rami. It crosses anterior to the axillary artery and vein, pierces the clavipectoral fascia and supplies the deep surface of pectoralis major. It sends a branch to the medial pectoral nerve, forming a loop in front of the first part of the axillary artery  to supply some fibres to pectoralis minor.

In a postfixed plexus the contribution by T1 is large,T2 is always present,C4 is absent and C5 is reduced in size.

In a prefixed plexus the contribution by C4 is large and that from T2 is absent,

Lower subscapular nerve supplies teres major

Upper and Lower subscapular Nerve supplies Subscapular muscles.

ROOT VALUES :-a) Musculocutaneous nerve:-C5,C6,C7 (Branches of lateral cord)

b)Ulnar Nerve :- C7C8T1 (Medial Cord)

c) Axillary nerve :- C5C6 (POST CORD)

D) Radial nerve (c5,c6,c7,c8,t1) Post Cord

10. Erbs Paralysis:- Upper Trunk C5,C6 injury   CAUSES Policemans tip or Porters Tip hand.Arm HANGS BY SIDE,IT IS ADDUCTED AND MEDIALLY ROTATED.Supination as well as flexion is lost ,so is abduction.

11.Klumpkes Paralysis/Neurogenic Thoracic Outlet Syndrome (arterial type is also discussed in addition due to anatomic relevance) :- Lower trunk (C8T1) injury causes Claw Hand due to unapposed action of long flexors and extensors of the fingers.In a claw hand there is hyperextension at the MCP joint and flexion at the IP joints.Horners syndrome is also seen in Klumpke`s paralysis.Klumpke`s paralysis is seen in Thoracic Outlet syndrome.Thoracic outlet is an anatomic region containing First Rib,Subclavian Artery and vein Brachial Plexus,The clavicle and Lung Apex.



At the superior thoracic aperture(Thoracic Outlet) , the superior aspects of the pleural cavities, which surround the lungs, lie on either side of the entrance to the mediastinum .Structures that pass between the upper limb and thorax pass over rib I and the superior part of the pleural cavity as they enter and leave the mediastinum. Structures that pass between the neck and head and the thorax pass more vertically through the superior thoracic aperture.

True neurogenic thoracic outlet syndrome (TOS) results from compression of the lower trunk of the brachial plexus or ventral rami of the C8 or T1 nerve roots by an anomalous band of tissue connecting an elongate transverse process at C7 with the first RIB.

Patients with neurogenic thoracic outlet compression may develop shoulder and arm pain, weakness, and paresthesias. Patients with arterial compression may experience claudication, Raynaud’s phenomenon, and even ischemic tissue loss and gangrene. Venous compression may cause thrombosis of the subclavian and axillary veins; this is often associated with effort and referred to as Paget-Schroetter syndrome.(New in 17th ed Harrison Page 1571)

Adson’s test is used to assess for the presence of Thoracic Outlet Syndrome at the scalene triangle. The patient is examined standing. The examiner palpates the radial pulse while moving the upper extremity in abduction, extension, and external rotation. The patient then is asked to rotate her head toward the involved side while taking a deep breath and holding it. A positive exam will result in a diminished or absent radial pulse.

Several maneuvers that support the diagnosis of thoracic outlet compression syndrome may be used to precipitate symptoms, cause a subclavian artery bruit, and diminish arm pulses. These include the abduction and external rotation test, in which the affected arm is abducted by 90° and the shoulder is externally rotated; the scalene maneuver (extension of the neck and rotation of the head to the side of the symptoms); the costoclavicular maneuver (posterior rotation of shoulders); and the hyperabduction maneuver (raising the arm 180°).Most patients can be managed conservatively. They should be advised to avoid the positions that cause symptoms. Many patients benefit from shoulder girdle exercises. Surgical procedures such as removal of the first rib or resection of the scalenus anticus muscle are necessary occasionally for relief of symptoms or treatment of ischemia.

12.  Trapezius (Accessory Nerve,XI):- Each trapezius muscle is flat and triangularly shaped, with the base of the triangle situated along the vertebral column (the muscle’s origin) and the apex pointing toward the tip of the shoulder (the muscle’s insertion)  The muscles on both sides together form a trapezoid.

The superior fibers of trapezius, from the skull and upper portion of the vertebral column descend to attach to the lateral third of the clavicle and to the acromion of the scapula. Contraction of these fibers elevates the scapula. In addition, the superior and inferior fibers work together to rotate the lateral aspect of the scapula upward to raise the upper limbs above the head.(Overhead abduction).

Motor innervation of trapezius is by the accessory nerve (XI), which descends from the neck onto the deep surface of the muscle . Proprioceptive fibers from trapezius pass in the branches of the cervical plexus and enter the spinal cord at spinal cord levels C3 and C4.

Acting with levator scapulae, the upper fibres elevate the scapula and with it the point of the shoulder; acting with serratus anterior, trapezius rotates the scapula forward so that the arm can be raised above the head; and acting with the rhomboids, it retracts the scapula, bracing back the shoulder. With the shoulder fixed, trapezius may bend the head and neck backwards and laterally. Trapezius, levator scapulae, rhomboids and serratus anterior combine in producing a variety of scapular rotations

Clinical anatomy: testing Trapezius is palpated while the shoulder is shrugged against resistance.

13.  Rhomboideus:-Retract the scapula Supplied by dorsal Scapular nerve.

14. Clavicle:- The shaft is gently curved and in shape resembles the italic letter f, being convex forwards in its medial two-thirds and concave forwards in its lateral third.

The clavicle begins to ossify before any other bone in the body, and is ossified from three centres. The shaft of the bone is ossified in condensed mesenchyme from two primary centres, medial and lateral, which appear between the fifth and sixth weeks of intrauterine life, and fuse about the forty-fifth day. Cartilage then develops at both ends of the clavicle. The medial cartilaginous mass contributes more to growth in length than does the lateral mass: the two centres of ossification meet between the middle and lateral thirds of the clavicle. A secondary centre for the sternal end appears in late teens, or even early twenties, usually 2 years earlier in females (Fig. 49.2). Fusion is probably rapid but reliable data are lacking. An acromial secondary centre sometimes develops at c.18 to 20 years, but this epiphysis is always small and rudimentary and rapidly joins the shaft.

The clavicle is often fractured, commonly by indirect forces, as a result of a violent impact to the hand or shoulder. The break is usually at the junction of the lateral and intermediate thirds, where the curvature changes, for this is the weakest part of the bone. A fracture medial to the conoid tubercle interrupts weight transmission from the arm to the axial skeleton. The resulting deformity is caused by the weight of the arm, which acts on the lateral fragment through the coracoclavicular ligament and draws it downwards. The medial fragment, as a rule, is a little displaced.


The coracoclavicular ligament connects the clavicle and the coracoid process of the scapula. Though separate from the acromioclavicular joint, it is a most efficient accessory ligament, and maintains the apposition of the clavicle to the acromion. Its trapezoid and conoid parts, usually separated by fat or, frequently, a bursa, connect the medial horizontal part of the coracoid process and lateral end of the subclavian groove of the clavicle; these adjacent areas may even be covered by cartilage to form a coracoclavicular joint.

The coracoclavicular ligament stabilizes the acromioclavicular joint. In acromioclavicular dislocation, the ligament is torn and the scapula falls away from the clavicle. Dislocation readily recurs because of the flatness and orientation of the joint surfaces.



All of the following are branches of subclavian artery except :
(A)Vertebral artery
(B)Thyrocervical trunk
(C)Subscapular artery—-axillary artery branch
(D)Internal thoracic artery


16. Deltoid:-     ORIGIN                                                                              INSERTION                                                       NERVE                                                              ACTION

Trapezius Superior nuchal line, external occipital protuberance, medial margin of the ligamentum nuchae, spinous processes of CVII to TXII and the related supraspinous ligaments Superior edge of the crest of the spine of the scapula, acromion, posterior border of lateral one-third of clavicle Motor spinal part of accessory nerve (CN XI). Sensory (proprioception) anterior rami of C3 and C4 Powerful elevator of the scapula; rotates the scapula during abduction of humerus above horizontal; middle fibers retract scapula; lower fibers depress scapula
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 Deltoid tuberosity of humerus Axillary nerve [C5,C6] Major abductor of arm (abducts arm beyond initial 15° done by supraspinatus); clavicular fibers assist in flexing the arm; posterior fibers assist in extending the arm


The two most superficial muscles of the shoulder are the trapezius and deltoid muscles (Fig. 7.34 and Table 7.1). Together, they provide the characteristic contour of the shoulder:

  • trapezius attaches the scapula and clavicle to the trunk;
  • deltoid attaches the scapula and clavicle to the humerus

Trapezius is attached to all structures except :
(A)First rib

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Discriminatory beta-hCG level

Posted by Dr KAMAL DEEP on August 16, 2010



When the last menstrual period is unknown, serum b-hCG testing is used to define expected sonographic findings. Each institution must define a b-hCG discriminatory value, that is, the lower limit at which an examiner can reliably visualize pregnancy. At most institutions, a concentration between 1,500 and 2,000 IU/L represents this value.


Units in the above diagram is in IU/ML.So maximum levels are 120 IU/ml OR 120,000 mIU/ml OR 120,000 IU/L at 8 weeks of gestation in the above diagram.

Distinct profiles for the concentrations of human chorionic gonadotropin (hCG), human placental lactogen (hPL), and corticotropin-releasing hormone (CRH) in serum of women throughout normal pregnancy.Because hCG circulates as multiple highly related isoforms with variable cross-reactivity between commercial assays, there is considerable variation in calculated serum hCG levels among the more than 100 assays. Peak levels reach about 100,000 mIU/mL OR 100 IU/MLbetween the 60th and 80th days after the last menses (see Fig. 3–26). Beginning at about 10 to 12 weeks’ gestation, maternal plasma levels of hCG begin to decline, and a nadir is reached by about 20 weeks. Plasma levels are maintained at this lower level for the remainder of pregnancy.Current serum and urine pregnancy tests that use enzyme-linked immunosorbent assays (ELISAs) are sensitive to levels of chorionic gonadotropin of 10 to 20 mIU/mL

1. There has been much improvement in the early diagnosis of ectopic pregnancy using vaginal sonography. Its use results in earlier and more specific diagnoses of uterine pregnancy than abdominal sonography, and it has become the imaging method of choice in early pregnancy.

A.Using a vaginal transducer allows ultrasonic detection of a uterine gestation as early as 1 week after missed menses(5 WEEKS GESTATION).

B.When serum chorionic gonadotropin (B-hCG) levels exceed 1000 mIU/mL or 1 IU/ML, a gestational sac is seen half the time (De Cherney and Eichhorn, 1996). Criteria include identification of a 1- to 3-mm or larger gestational sac, eccentrically placed in the uterus, and surrounded by a decidual–chorionic reaction. A fetal pole within the sac is diagnostic, especially when accompanied by fetal heart action1.

The choice of diagnostic algorithm applies only to hemodynamically stable women; those with presumed rupture should undergo prompt surgical therapy. In a woman in whom ectopic pregnancy is suspected because of pain, bleeding, and a positive pregnancy test, performance of vaginal sonography is a logical first step. If a live uterine gestation is present, ectopic pregnancy is extremely unlikely. A heterotypic pregnancy is, of course, the rare exception (Hirsch and associates, 1992). Alternatively, if the uterus is empty, an ectopic pregnancy can be diagnosed based on visualization of an adnexal mass separate from the ovaries (Fig. 10–6).

In the event of a nondiagnostic study, subsequent management can be based on serial serum -hCG values and repeat vaginal sonography. A number of investigators have described discriminatory -hCG levels . Above these levels, failure to visualize a uterine pregnancy by transvaginal ultrasound indicates with high reliability that the pregnancy is either ectopic or nonviable. In a study by Barnhart and colleagues (1994), an empty uterus with a serum -hCG concentration of 1500 mIU/mL OR 1500 IU/L (1.5 IU/ML) or higher was 100-percent accurate in excluding a live uterine pregnancy. Thus, if the initial -hCG exceeds the discriminatory level, and no live intrauterine pregnancy is identified by vaginal sonography, the differential diagnosis is narrowed to a uterine pregnancy with a dead fetus versus an ectopic pregnancy. Early multifetal gestation, of course, remains a possibility. Uterine curettage will distinguish an ectopic from a nonliving uterine pregnancy. If an embryo, fetus, or placenta is identified, the diagnosis is apparent. When none of these is identified, tubal pregnancy is a probability.

If the initial B-hCG level is below the discriminatory value, early uterine pregnancy is a possibility, and serial assays of -hCG, in conjunction with repeat vaginal sonography, may prove useful. Kadar and Romero (1987) confirmed earlier work and demonstrated that in women with normal pregnancies, mean doubling time for -hCG in serum was approximately 48 hours(2 DAYS), and the lowest normal value for this increase was 66 percent (Table 10–2). In a series of 287 pregnant women, Barnhart and co-workers more recently (2004) reported a somewhat lower 48-hour minimum rise for a live intrauterine pregnancy of 53 percent, and a 24-hr minimum rise of 24 percent. Kadar and Romero concluded that failure to maintain this minimum rate of increased -hCG production, along with an empty uterus, was suggestive of an ectopic pregnancy. Thus, appropriately selected women in whom ectopic pregnancy is suspected, but whose initial -hCG is below the discriminatory level, may be followed expectantly. They are seen at 2- to 3-day intervals for further evaluation. If the -hCG level rises inappropriately, plateaus, or exceeds the discriminatory level without evidence of a uterine pregnancy by vaginal sonography, a live uterine pregnancy can be excluded. Then, distinction between nonliving uterine versus an ectopic pregnancy is made by uterine curettage, or in some cases, by endometrial biopsy. Barnhart and associates (2003) reported that biopsy was less sensitive than curettage.

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Posted by Dr KAMAL DEEP on July 25, 2010




The CT image is a cross-sectional representation of anatomy created
by a computer-generated analysis of the attenuation of x-ray beams
passed through a section of the body. As the x-ray beam, collimated to
the desired slice width, rotates around the patient, it passes through
selected regions in the body. X-rays that are not attenuated by the
body are detected by sensitive x-ray detectors aligned 180° from the
x-ray tube. A computer calculates a “back projection” image from
the 360° x-ray attenuation profile. Greater x-ray attenuation, e.g., as
caused by bone, results in areas of high “density,” while soft tissue

[Collimation The use of lead shutters to control the effective thickness of the
X-ray beam and thus the slice thickness. Prepatient collimation is next to
the X-ray tube. Positioning of the shutters requires high precision and accuracy
as the beam will diverge, thus the shutter collimation has to be less
than the nominal slice thickness. Prepatient collimation markedly affects
patient radiation dose. Postpatient collimation is next to the detectors. This
will reduce scatter and also controls the nominal slice thickness. Thinsection
CT can be more easily acquired with postpatient collimation, but
accurate alignment between pre- and postpatient collimation is required to
optimise radiation]

structures, which have poor attenuation of x-rays, are lower in density.
The resolution of an image depends on the radiation dose, the detector
size or collimation (slice thickness), the field of view, and the matrix
size of the display. A modern CT scanner is capable of obtaining
sections as thin as 0.5–1 mm with submillimeter resolution at a speed
of 0.5–1 s per rotation; complete studies of the brain can be completed
in 2–10 s.
Helical or multidetector CT (MDCT) is now standard in most radiology
departments. Continuous CT information is obtained while the
patient moves through the x-ray beam. In the helical scan mode, the
table moves continuously through the rotating x-ray beam, generating
a “helix” of information that can be reformatted into various slice
thicknesses. Single or multiple (from 4 to 256) detectors positioned
180 degrees to the x-ray source may result in multiple slices per revolution
of the beam around the patient. Advantages of MDCT include
shorter scan times, reduced patient and organ motion, and the ability
to acquire images dynamically during the infusion of intravenous contrast
that can be used to construct CT angiograms of vascular structures
and CT perfusion images.




CT scanning produces cross-sectional images of a patient rather than the conventional shadow images of conventional radiography. Figure I-23 schematically illustrates CT scanner operation. Confusing and distracting overlying structures are eliminated. In x-ray CT scanning, a fan x-ray beam from a source rotating about the patient passes through the patient, and the exit transmission intensity is monitored by a series of detectors. Spiral CT scanners move the patient through the x-ray beam while the tube continuously rotates around the patient. The x-ray beam “cuts a slice” about 10-mm thick through the patient. The transmission at any angle can be used to calculate the average attenuation coefficient along the length of the x-ray beam. By measurement of the transmission at many angles around the patient, a complex group of mathematical equations can be solved to calculate and determine the mass attenuation coefficient of small (about 1 × 1 × 10 mm) volume elements (voxels). The final cross-sectional image is then made up of a display of the gray scale value of every voxel. For historical reasons and convenience, the attenuation coefficients are reported in terms of Hounsfield units. In Hounsfield units, bone and other dense materials are +1,000, water is equal to 0, and air is equal to –1,000. CT scanning, like digital radiography, can separate spatial and contrast resolution.

Over the last decade, computed tomography has developed rapidly,from conventional, single-slice machines through helical (spiral)
CT to the current multidetector (multislice) scanners. A number of advances in hardware and software have enabled this: in particular,
the use of slip rings to allow the scanner gantry to rotate continuously in one direction; the development of X-ray tubes with great heat capacity for long continuous X-ray exposure (up to 60 s);

Three key advances enable CT data to be acquired continuously with on-going patient movement. These are slip-ring technology, precise patient table transport, and software reconstruction algorithms.

Slip-ring technology was the fundamental step that allowed volume data acquisition and was necessary for subsequent developments described below. In older (conventional) CT systems, there was an inherent delay of 3–5 seconds between each exposure. This arose from the physical need to have cables connecting the stationary gantry and the rotating X-ray tube, detector systems, and controls (tube–detector assembly). After 1–3 exposures, depending on the cable length and other factors, the cables became wound and rotation of the tube–detector assembly had to stop, change direction, and then unwind while further exposures were taken. Not only did this result in interrupted data acquisition but occasionally led to mechanical problems. Slip-ring technology brought about a major change. It abolished the physical need for the presence of an electrical cable between the ‘on the ground’ generator and the moving tube–detector assembly. Instead, power from the generator is connected to a large stationary ring. Other large rings that house the X-ray tube, detector systems, and controls move around within the stationary ring. Power is transmitted between the stationary and moving rings by means of brushes. Hence the scene is set for continuous X-ray rotation (rather than back and forth) and continuous data acquisition.

2. Interaction of electromagnetic radiation with matter
The detection of X-rays and gamma-rays depends on the interaction of their electromagnetic fields with matter. There are three forms of photon interaction with matter that are most important in nuclear medicine: photoelectric absorption, Compton scattering, and pair production.
In a photoelectric interaction, an atom absorbs all the energy of the incident photon. The photon ceases to exist but the energy is transferred to an inner-shell electron which is ejected and is then referred to as a photoelectron. This creates a vacancy in an orbital shell which eventually leads to the emission of a characteristic X-ray ( Fig. 6.1A ).photoelectric-effect
In a Compton interaction, a photon interacts with an orbital electron and loses some of its energy which is then transferred to the electron. The photon as a result is ‘scattered’ or deflected off in a new direction with a lower energy ( Fig. 6.1B ).

In pair production, high-energy photons interact with the electric field of a nucleus ( Fig. 6.1C ); the photon transfers its energy to create a positron and an electron. Since each particle has the rest mass of an electron, 0.511 MeV, this requires a minimum photon energy of 2 × 0.511 = 1.022 MeV. Radionuclides with photons exceeding 1.02 MeV are not generally used in nuclear medicine.




2.     ULTRASONOGRAPHY:-Ultrasound is generated by piezoelectric materials which have the property of changing thickness when a voltage is applied across them. Lead zirconate titanate (PZT) is the most widely used. The crystal is mounted in a conveniently shaped holder which contains the electrodes and any associated electronics, as well as the lenses and matching layers required to improve the beam shape (see later). The whole assembly is known as the probe or transducer, although strictly the latter term should be reserved for devices that change one form of energy into another, in this case electrical to acoustic energy.

High-frequency ultrasound gives good resolution because of its short wavelength, but the rapid attenuation of high-frequency ultrasound by tissue is the limiting factor to the maximum frequency that can be used in any given clinical application. Frequencies as high as 20 MHz can be used when only a few millimetres of tissue are to be traversed, such as for imaging the eye and skin and for intravascular ultrasound (IVUS). For superficial tissues, such as the thyroid, breast and scrotum, 7–15 MHz is appropriate. For the heart, abdomen and second and third trimester obstetrics, 3–7 MHz is optimal, while for some difficult applications, such as the abdomen in obese subjects, and for transcranial studies (most of which use Doppler), one has to resort to 1.5 or 2.5 MHz transducers. This frequency limitation is being reduced by the use of coded transmit pulses, which essentially impose a signature on the pulse (for example, by making its frequency slide upwards during the pulse, so called chirp encoding) so that the receiver circuitry can detect true echoes even when they are weaker than the noise floor.

Acoustic shadowing and increased through transmission of sound (often referred to as enhancement although this term is better reserved for the signal-augmenting effects of microbubble Contrast agents) are important components of the ultrasound image. Shadowing occurs when little or no ultrasound can penetrate an interface and results in a dark band over the deeper tissues, bounded by the ultrasound beam lines, which are parallel for a linear transducer and radiating for a sector transducer ( Fig. 3A.17 ).

Acoustic Shadowing

Absorption and reflection are the two main causes of shadowing. If a portion of the tissue being imaged absorbs ultrasound faster than the background, the chosen TGC(TIME-GAIN COMPENSATION) will be insufficient to compensate properly, and therefore tissues deeper to the highly attenuating region are undercorrected and appear darker than adjacent tissue. Fibrous tissue and, to a lesser extent, fat attenuate at a higher rate than the usual 1 dB MHz-1 cm-1 and are common causes of acoustic shadowing, for example in a fatty liver, behind scars and behind scirrhous breast carcinomas. High attenuation also partly accounts for the shadows seen deep to calcific lesions such as biliary and renal stones, but here intense reflection is also a factor. Whatever proportion of the incident ultrasound is reflected is not available to continue through for imaging. For stones this amounts to about 60% of the incident energy, but for tissue–gas interfaces almost all 100% of the incident ultrasound is reflected and these produce dense shadows. In this case, the shadows are often partially filled in by reverberant echoes, which form because of the efficiency of these gas–tissue boundaries as reflectors, so that reverberation artefacts commonly occur. The noise in gas shadows has given rise to their designation as ‘dirty shadows’ in stones, as compared to the ‘clean shadows’ behind stones, and this is sometimes a useful differential diagnostic feature.
Whether a stone or gas bubble actually casts a shadow depends on its size relative to the ultrasound beam width. A significant fraction (about three quarters) of the beam must be obstructed to cause a shadow. If a stone is smaller than this, or lies away from the central axis of the beam, enough ultrasound passes beside it to insonate the deeper tissues. In practice, shadowing is usually apparent behind renal and biliary stones of 5 mm or more in diameter, and much smaller calcifications may also shadow if high-resolution transducers are used. Groups of fine calcifications can also shadow if their aggregate size and density is high enough; for example, in nephrocalcinosis.


A third important type of shadowing, ‘edge shadows’, are sometimes known as ‘refractive shadows’, a description based on one explanation of their origin. They are seen as fine, dark lines extending deep to strongly curved surfaces and do not imply attenuation or strong reflections. Cysts and the fetal skull are typical examples and fascial sheaths are often also responsible, for example the fine shadows seen beyond Cooper’s ligaments in the breast and those caused by the neck of the gallbladder. These edge shadows must be recognized as being different from attenuating and reflective shadows to avoid errors in their interpretation.

Increased through transmission is the exact opposite of attenuation shadowing: here, a region of tissue has a lower than average attenuation and so the TGC (which is adjusted to compensate for the average attenuation) is inappropriately high for that region. Thus the echoes from deeper tissues are overamplified. The phenomenon is the hallmark of cystic spaces and the ‘bright up’ is often accentuated by the darker banding lines of the edge shadows typically formed from the cyst wall ( Fig. 3A.18 )


Increased Sound Transmission

Some solid tissues also show increased sound transmission, however, usually because they have a high proportion of fluid. Many tumours fall into this category, especially fibroadenomas in the breast, and lymphomatous deposits and inflammatory masses may behave in the same way. Even those fluid cavities that contain echogenic material, such as suspended crystals in the gallbladder, pus, blood or necrotic tissue, usually still produce increased transmission, depending largely on the proportion of fluid present.


The prime determinant of the strength of ultrasonic echoes is the impedance mismatch (Z) between adjacent tissue components. At the risk of being somewhat simplistic, in practical clinical terms this may be understood as interfaces between tissues of different densities. The larger the mismatch the stronger the echo, so that interfaces between soft tissues and bone, for example, give very strong echoes and, within soft tissues, the most significant components are fibrous tissue (often in the form of the perivascular microskeleton) and fatty tissue. Thus, while uniform regions of fibre or fat are echo-poor (subcutaneous fat and retroperitoneal fibrosis are examples), admixtures between them and watery tissues give stronger echoes.
A second important factor is the concentration of the scatterers: for a given impedance mismatch, a region that contains a large number of scatterers is more echogenic than one where they are spread out. Commonly, the ‘dilution’ of scatterers is caused by an increase in water content. The low reflectivity of the congested liver in right heart failure is an example. Malignant tumours are a general case: until they grow large enough to undergo necrosis or calcification (which produce new reflectors) they tend to be echo-poor ( Fig. 3A.19 ).



Similarly, the oedematous tissues in acute inflammation give low-level echoes; examples include the echo-poor pancreas in acute pancreatitis and the segmental echo-poor regions of acute lobar nephronia in reflux nephropathy. On the other hand, the high concentration of reflectors is the cause of the echogenic kidneys in recessive (infantile) polycystic renal disease (the interfaces between the innumerable cysts cause strong echoes ( Fig. 3A.20 ));


strong echoes are also obtained from the multiple interfaces of the vessel walls of haemangiomas, and even stronger ones from angiomyolipomas, in which there is also admixed fatty tissue.

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Posted by Dr KAMAL DEEP on July 5, 2010

26. Subglottic Hemangioma:-Although rare in adults, subglottic hemangioma is the most common laryngeal and upper tracheal neoplasm in the newborn and infant. The lesion typically appears as a well-defined mass in the posterior or lateral portion of the subglottic airway ( Fig. 99–11 ). [127] [138] Although the subglottic narrowing is usually eccentric, circumferential narrowing suggestive of croup may be seen. Hemangiomas may occur on the skin or elsewhere in the body.

“Squamous papillomas, the most frequent laryngeal tumors in children, have also been reported in adults.”

Current management options that have been reported include tracheotomy, laser partial excision, open surgical resection, systemic or intralesional steroids, and systemic interferon alfa-2A

Infantile subglottic hemangiomas occur in children a few months of age and present as a lateral subglottic submucosal bluish mass, causing respiratory symptoms. These lesions, if mildly symptomatic, are managed conservatively with corticosteroids and observation. They usually involute spontaneously with time; however, a tracheotomy is occasionally needed when severe airway compromise is present. Healy and others[3] reported the use of the carbon dioxide laser for the management of this condition.[3] The carbon dioxide laser is used to vaporize the tumor until an adequate airway is achieved.
The Nd:YAG laser, although ideal for low-flow venous malformations, is not recommended for subglottic hemangiomas because these lesions are more compact capillary-type vascular lesions. The depth of penetration of the Nd:YAG laser presents a serious risk to the infant’s larynx and trachea, with potential stricture formation or tracheal perforation, and is not recommended for the management of these lesions.

27. Management Of early Glottic Cancer:- Recent advances in microlaryngeal laser excision (laser microscopic excision, LME) of early glottic lesions and in laryngeal reconstruction after vertical partial laryngectomy (VPL) have enhanced the quality of life for patients cured of their cancer.

Curative radiotherapy is reserved for early lesions which neither impair cord mobility nor invade cartilage or cervical nodes. Cancer of the vocal cord without impairment of its mobility gives a 90% cure rate after irradiation and has the advantage of preservation of voice. Superficial exophytic lesions, especially of the rip of epiglottis, and aryepiglottic folds give 70-90% cure rate. Radiotherapy does not give good results in lesions with fixed cords, subglottic extension, cartilage invasion, and nodal metastases. These lesions require surgery.

The anterior commissure has been considered as a barrier to tumor spread or as an early pathway for cancer extension into the laryngeal framework.[29] Shvero and others[55] related that surgical treatment is preferred for cancers arising in this region because of a higher local recurrence rate and an increased risk for distant metastasis. They contend that the behavior of small cancers in this location is much different from that of other early glottic cancers.[56] Other investigators have attributed the higher rates of failure after radiotherapy for anterior commissure lesions to problems with adequate dosing.[31] [71] The distance from the anterior commissure to the skin varies greatly among patients. This variability and the thick overlying thyroid cartilage have been cited as impediments to consistent dosing of radiation to this region. Some investigators relate that modern radiotherapy techniques with improved dosimetry have adequately addressed these concerns.Radiotherapy more frequently fails to control the cancer when there is involvement of the anterior commissure, impaired vocal cord mobility, or subglottic extension.

Indications for Vertical Partial Laryngectomy and Laryngoplasty ; VPL and laryngoplasty are anterior commissure involvement, extension to the vocal process of the arytenoid, selected superficial transglottic lesions, and recurrent cancer after radiation therapy. Partial laryngectomy for recurrent cancer after radiation therapy must meet the following criteria: (a) lesion limited to one cord (may involve the anterior commissure); (b) body of arytenoid free of tumor; (c) subglottic extension no more than 5 mm; (d) mobile cord; (e) no cartilage invasion; (f) recurrence correlating with initial tumor; and (g) early complications after partial laryngectomy, including subcutaneous emphysema, bleeding, and tracheotomy tube occlusion.

Early glottic carcinoma limited to the membranous portion of the vocal fold can be cured using endoscopic surgical excision, thyrotomy with cordectomy, hemilaryngectomy, VPL with laryngoplasty, and/or radiation therapy.

About one in six patients with severe dysplasia or carcinoma in situ will develop invasive carcinoma if the only therapy used is a single vocal cord stripping or biopsy.

Microinvasive carcinoma of the true vocal fold can be managed by sequential endoscopic excisional biopsy, endoscopic laser excision, or radiation therapy

The management issues in glottic carcinoma are local control, effective management of suspected or known metastatic cervical lymph nodes, patient education concerning carcinogenic substances (usually smoking cessation therapy), and patient follow-up for the possibility of residual laryngeal cancer or second primary lesions. Tumors arising on the arytenoid, in the subglottic region, or in the supraglottic portion of the larynx do not cause hoarseness and often are diagnosed at a later stage. They have a lower cure rate because delayed diagnosis is associated with diminished therapeutic effectiveness of surgery or radiation therapy.

In general, early glottic carcinoma can be managed without total laryngectomy and without the procedures that limit vocal quality or rely on radiation therapy with its inherent problems. A broad surgical armamentarium now includes endoscopic excision, laser resection, and surgical excision, with a number of reconstructive/rehabilitative techniques to enhance postoperative function.

The relative contraindications for LME as anterior commissure involvement, subglottic extension, T3 glottic cancer, and posterior commissure involvemen

Indications for VPL and laryngoplasty are tumor involvement of the anterior commissure, extension to involve the vocal process of the arytenoid, selected superficial transglottic lesions, and carcinoma recurring after radiation therapy. The contraindications for any of these procedures include a fixed vocal cord, involvement of the posterior commissure, invasion of both arytenoid cartilages, bulky transglottic lesions, and lesions invading the thyroid cartilage

when a diagnosis of severe dysplasia or carcinoma in situ is made and when the site of the lesion involves the true vocal cord, microscopic suspension laryngoscopy with stripping of the epithelium and a closely monitored program of follow-up are indicated. The patient must be convinced of the necessity to discontinue smoking and ethanol intake and to maintain a schedule of regular visits for indirect laryngoscopy following a pattern of careful assessment every 2 or 3 months for at least 5 year

Microinvasive carcinoma can be managed by endoscopic excisional biopsy (vocal cord stripping), by laser excision endoscopically, or by radiation therapy. We prefer a protocol consisting of microscopic suspension laryngoscopy and sequential vocal cord stripping every 3 months until two consecutive epithelial stripping specimens can be confirmed to be free of malignant cells. We then monitor these patients with indirect laryngoscopy every 2 to 3 months. If any suspicious epithelial changes or significant voice changes are noted, we repeat the suspension microlaryngoscopy and biopsy.

Early invasive glottic carcinoma can be treated by endoscopic excision, laser excision, thyrotomy with cordectomy, hemilaryngectomy, VPL with laryngoplasty, or radiation therapy. Traditionally, radiation therapy has been offered as the preferred treatment for invasive epidermoid carcinoma involving the membranous portion of the mobile true vocal cord. Recently, some studies have challenged that approach, and endoscopic excision with or without the laser has been found to be equally safe and effective. Late recurrence of carcinoma and the development of second primary tumors are issues of great importance and mandate a pattern of close follow-up, regardless of the treatment chosen.
Radiation therapy is the primary treatment for glottic carcinoma in Northern Europe, with total or partial laryngectomy used for salvage of those patients who have recurrence of cancer. In other parts of the world, surgeons report wider use of VPL for early glottic carcinoma and for advanced T2 glottic lesions.

Ackerman’s Tumor
Verrucous carcinoma is known also as Ackerman’s tumor and can be distinguished histologically from other well-differentiated squamous cell carcinomas. This tumor is characterized by its rough, shaggy surface, a rounded, pushing margin, and no metastasis. Smaller lesions can be excised endoscopically; larger tumors are managed by partial laryngectomy. This tumor is less radiosensitive than ordinary squamous cell carcinoma, but radiation therapy is a reasonable alternative for treating larger tumors; total laryngectomy is reserved for large lesions that do not respond to radiation therapy.


28. Benign tumors and cysts of the esophagus are relatively rare, occurring less frequently than malignant tumors. Esophageal lesions can be classified as intraluminal, intramural, or extramural. Intramural tumors are usually asymptomatic until they become significantly enlarged. Because they are mucosally covered, it is uncommon for these tumors to be associated with ulceration and bleeding. Leiomyoma is the most common benign tumor of the esophagus, representing an intramural tumor arising from the muscularis mucosa (Fig. 56.7). In 90% of patients, it occurs in the middle or lower third of the esophagus. Patients usually present with dysphagia, although many leiomyomas are found radiographically in asymptomatic patients.

“Polyps are the most common intraluminal lesions, although papillomas, adenomas, and hemangiomas may occur. Fibrovascular polyps can grow to an enormous size and have been reported to prolapse into the hypopharynx, causing asphyxiation and death. Most polyps occur in the cervical esophagus, causing dysphagia and regurgitation. Barium swallow demonstrates an intraluminal, pedunculated mass. Most can be excised endoscopically by snaring the base of the polyp.”

29Scleroderma is a generalized collagen vascular disease in which 80% of patients eventually develop esophageal symptoms. Typically, scleroderma results in a motility disorder that causes progressive dysphagia for solids. There appears to be an increased incidence in those who also manifest the Raynaud phenomenon.
Pathologically, the smooth muscle in the gastrointestinal tract becomes atrophied. Manometric studies demonstrate diminished contractions in the LES and distal two thirds of the esophagus. Because the UES is composed of striated muscle, contraction pressures are usually normal. Although dysphagia occurs, heartburn is the more prominent symptom because LES tone is attenuated. With compromise of the LES, reflux esophagitis and its associated complications may develop.

30. The esophagus is a flexible, muscular tube that can be compressed or narrowed by surrounding structures at 3 locations (Fig. 3.90):

  • the junction of the esophagus with the pharynx in the neck;
  • in the superior mediastinum where the esophagus is crossed by the arch of aorta; in the posterior mediastinum where the esophagus is compressed by the left main bronchus;
  • in the posterior mediastinum at the esophageal hiatus in the diaphragm.

These constrictions have important clinical consequences. For example, a swallowed object is most likely to lodge at a constricted area. An ingested corrosive substance would move more slowly through a narrowed region, causing more damage at this site than elsewhere along the esophagus. Also, constrictions present problems during the passage of instruments.



Alpha-adrenergic neurotransmitters increase LES pressure and a-adrenergic blockers decrease it; b-adrenergic stimulation decreases LES pressure and b-adrenergic blockers increase it. Cholinergic mechanisms also exert control over resting LES pressure. Hormonal regulation has been studied extensively, and dozens of hormones and peptides have been found to influence LES pressure. Protein meals and antacids tend to increase LES pressure, whereas fatty meals, chocolate, ethanol, smoking, and caffeine are known to decrease LES pressure.

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Otolaryngology (ENT) MCQs & Important Points

Posted by Dr KAMAL DEEP on June 26, 2010

1.Killian Dehiscence:-

The inferior constrictor is the thickest of the three constrictor muscles, and is usually described in two parts, cricopharyngeus and thyropharyngeus. Cricopharyngeus arises from the side of the cricoid cartilage between the attachment of cricothyroid and the articular facet for the inferior thyroid cornu. Thyropharyngeus arises from the oblique line of the thyroid lamina, a strip of the lamina behind this, and by a small slip from the inferior cornu. Some additional fibres arise from a tendinous cord that loops over cricothyroid. Both cricopharyngeus and thyropharyngeus spread posteromedially to join the contralateral muscle. Thyropharyngeus is inserted into the median pharyngeal raphe and its upper fibres ascend obliquely to overlap the middle constrictor, however cricopharyngeus blends with the circular oesophageal fibres around the narrowest part of the pharynx.

Hypopharyngeal diverticula


The pharyngeal mucosa that lies between cricopharyngeus and thyropharyngeus is relatively unsupported by pharyngeal muscles and is called the dehiscence of Killian. A delay in the relaxation of cricopharyngeus, which can occur when the swallowing mechanism becomes discoordinated, generates a zone of elevated pressure adjacent to the mucosa in the dehiscence. The result is the development of a pulsion diverticulum (a pouch of prolapsing mucosa), which breaches the thin muscle wall adjacent to the sixth cervical vertebra and expands, usually a little to the left side, into the parapharyngeal potential space. This may trap portions (or all) of the passing food bolus, resulting in regurgitation of old food, aspiration pneumonia, halitosis and weight loss. Treatment may involve open excision or inversion of the pouch to prevent it filling, coupled with division of the circular fibres of cricopharyngeus, to prevent the build-up of pressure in the region and recurrence of the pouch.



2.   Killian-Jamieson diverticula (also termed “proximal lateral cervical esophageal diverticula” or “lateral diverticula from the pharyngoesophageal junction area“) have been recognized on pharyngoesophagography as variable-sized outpouchings from the lateral wall of the proximal cervical esophagus. These diverticula protrude through a muscular gap in the anterolateral wall of the cervical esophagus inferior to the cricopharyngeus and lateral to the longitudinal muscle of the esophagus just below its insertion on the posterior lamina of the cricoid cartilage. This gap (also known as the Killian-Jamieson space) should be differentiated from the muscular gap in the posterior portion of the cricopharyngeus (also known as Killian’s dehiscence), the site of development of a Zenker’s diverticulum,The recurrent laryngeal nerve enters inferiorly and laterally to the cricothyroid articulation through the Killian-Jamieson area.

3. Laimer and Hackermann:- The circular fibres of the oesophageal musculature lie below and parallel to the cricopharyngeus, but the longitudinal muscles at the upper end sweep forward to insert into the cricoid cartilage, leaving a relatively weak area, first described by Laimer and Hackermann, whose names are given to this area.Posterolateral:- Laimer-Hackermann point.


4. Reinke’s space  a potential space between the vocal ligament and the overlying mucosa.

Mucosal Cover
The mucosal cover of most of the upper airway is respiratory epithelium, with numerous mucous glands (Fig. 42.8). Over the free edge of the vocal fold, however, mucosa is adapted for periodic vibration with squamous epithelium and no mucous glands. A highly specialized lamina propria separates the epithelium from underlying muscle. The lamina propria serves as a shock absorber, so that the epithelium can vibrate freely, without restriction by the bulky underlying muscle. It contains three layers: superficial, intermediate, and deep. Each has unique mechanical properties because of varying densities of elastic and collagenous fibers. The deep layer, or vocal ligament, is the stiffest, due to a high concentration of collagen fibers. Elastic fibers are most numerous in the intermediate layer and gradually decrease toward the epithelium and muscle .The superficial layer of the lamina propria is often referred to as Reinke’s space, although it is not actually a potential space. This layer has the lowest concentration of both elastic and collagenous fibers and offers the least impedance to vibration.

The physical properties of the vocal fold are crucial in determining vocal function. During normal modal phonation, the mucosa undulates freely over the underlying vocal ligament and vocalis muscle. Hirano’s[16] important histologic studies showed that this is possible because mucosa and muscle are separated by a specialized layer of connective tissue that serves as a shock absorber. This highly specialized tissue is characterized by stratified concentrations of elastin and collagen. The most superficial layer is made up of loosely connected fibers of collagen and elastin. This layer also is known as Reinke’s space. The intermediate layer is predominantly composed of elastic fibers, and the deep layer is constructed of densely arranged collagen fibers. Together, the intermediate and deep layers form the vocal ligament.

5. Androphonia can be corrected by:- TYPE 4 THYROPLASTY

Lengthening the vocal folds and elevating vocal pitch may be achieved by advancing the anterior commissure or by cricothyroid approximation. Lengthening procedures have been advocated for vocal fold bowing resulting from aging or trauma, postsurgical defects, androphonia, and gender transformation

In most cases of unilateral vocal fold paralysis, no therapy is needed. When indicated, medialization of the cord is the goal. Thyroplasty type I or arytenoid adduction are the procedures of choice

Isshiki and colleagues categorized four types of thyroplastic surgeries. Type 1 provides lateral compression to the paralyzed cord, narrowing the glottic chink; type 2 creates a lateral expansion of the glottis; type 3 shortens and relaxes the cords bilaterally; and type 4 lengthens and stretches the cords. Based on a comparison of these surgeries in treating unilateral vocal fold paralysis in canines, Isshiki recommends using type 1 thyroplasty for unilateral recurrent paralysis, and type 1 and type 4 together for combined unilateral superior and recurrent laryngeal nerve paralysis. In this study, the degree of voice improvement was evaluated subjectively as improved or rough, and the mechanical effect of the larynx was studied only with laryngoscopy.

Surgical procedures that enhance glottic closure are important in the management of aspiration. The procedures most commonly used are vocal cord augmentation with gelatin foam sponge, polytetrafluoroethylene (PTFE), fat, or other substances and vocal cord medialization by means of laryngeal framework surgery. Injection of gelatin foam into the true vocal fold provides bulk for approximately 6 weeks; therefore it is best used in the management of aspiration due to what is believed to be temporary vocal cord paralysis (19). Permanent medialization can be performed by means of injection of PTFE; however, vocal cord medialization with thyroplasty is the standard technique in most medical centers. Medialization can be performed by means of vocal cord medialization with a prosthesis placed within the laryngeal framework (thyroplasty), rotation of the arytenoid cartilage (arytenoid adduction), or a combination of the two procedures.

Isshiki type III thyroplasty is a laryngeal framework surgical procedure that lowers a patient’s pitch.Issiki type III thyroplasty on a patient with mutational voice disorder and  The results :fundamental frequency (Fo), shimmer parameter(SP), and normalized noise energy b(NNEb) decreased after the operation. Since this procedure was effective not only for lowering vocal pitch, but also for improving hoarseness, it might be a good choice for treatment of patients with mutational voice disorders, especially those with laryngeal noise.

So type 3 thyroplasty can be used in gender transformation,mutational falsetto and spasmodic dysphonia.

6. Adenoid Cystic Carcinoma:-Adenoid cystic carcinoma accounts for 30% of minor salivary gland tumors, approximately 15% of submandibular gland tumors, and 2% to 6% of parotid gland neoplasms. Adenoid cystic carcinoma has a slow but prolonged course with frequent recurrences. Perineural extension, although seen in squamous cell carcinoma and other malignancies, is most common in adenoid cystic carcinoma, allowing tumors to spread through the parapharyngeal space or intracranially. CT signs of perineural extension include obliteration of the normal fat plane beneath the stylomastoid foramen and tumor enhancement along the course of the facial nerve, with resultant facial paralysis.Adenoid cystic carcinomas of the sinonasal tract comprise 20% of all adenoid cystic carcinomas arising in the head and neck. They are characterized by early spread to neurovascular structures, submucosal spread, and advanced stage at the time of diagnosis.Adenoid cystic carcinoma is the most common malignant epithelial neoplasm of the lacrimal gland, representing about 25% of all epithelial neoplasms. Malignant mixed cell carcinomas, adenocarcinomas, and mucoepidermoid carcinomas are also found. Patients with malignant epithelial tumors of the lacrimal gland typically present with progressive proptosis of less than 12 months’ duration.

Mucoepidermoid carcinoma is the most common malignant tumor involving the parotid gland and the second most common malignant tumor of the submandibular gland, after adenoid cystic carcinoma. Between 6% and 9% of all major salivary gland neoplasms are mucoepidermoid carcinomas (1). Sixty percent to 70% are located in the parotid gland. The palate is the next most frequent site.

Adenoid cystic carcinoma (cylindroma) accounts for about 6% of all salivary gland neoplasms. Adenoid cystic carcinoma occurs less commonly than mucoepidermoid carcinoma in the parotid gland, but it represents the most common malignancy of the submandibular gland and the minor salivary glands

Acinic cell carcinoma represents 1% of all salivary gland neoplasms and 2% to 4% of parotid gland neoplasms (1). Ninety percent to 95% of these tumors arise in the parotid gland, with the remainder found in the submandibular gland. Acinic cell carcinoma of the minor salivary glands is rare.

Most salivary gland tumors develop in the parotid gland.

Most salivary gland neoplasms are benign.

7. Otoacoustic emissions testing also is used for infant screening. Its popularity for screening is based on the fact that it is a noninvasive measure of cochlear (outer hair cell) function and thus is representative of peripheral hearing. Otoacoustic emissions tests are independent of neural and central auditory system effects, can be relatively low cost to administer, and can be performed over a relatively broad, frequency-specific range (1,000 to 6,000 Hz). Unlike the ABR, OAE amplitudes are more robust at birth than in adulthood.
Transient evoked otoacoustic emissions (TEOAEs) are used in the most common OAE screening test of infants (15), although distortion product otoacoustic emissions (DPOAEs) tests continue to increase in popularity. Transient evoked oto-acoustic emissions are reported to have excellent sensitivity (90% to 100%), with specificity in the range of 82% to 84% (16). Initial failure rates for OAE screening vary considerably; reports range from 10% to 40% (17). Factors that influence the success of OAE testing include the noise level in the test environment, vernix in the external auditory meatus, middle-ear dysfunction, and reduced responses for very low-birth-weight or premature infants.

Otoacoustic emissions are low-intensity sounds produced by the cochlea in response to an acoustic stimulus. A moderate-intensity click or an appropriate combination of two tones can evoke outer hair cell movement, or motility (2,10). Outer hair cell motility affects basilar membrane biomechanics; the result is a form of intracochlear energy amplification and cochlear tuning for precise frequency resolution. Outer hair cell motility generates mechanical energy within the cochlea that is propagated outward through the middle ear system and the tympanic membrane to the ear canal. Vibration of the tympanic membrane produces an acoustic signal (the OAE), which can be measured with a sensitive microphone.

8.Antrum of highmore= Maxillary Sinus

9.Vidian NERVE:- Nerve of pterygoid canal;

Pterygopalatine ganglion

The pterygopalatine ganglion is the largest of the peripheral parasympathetic ganglia. It is placed deeply in the pterygopalatine fossa, near the sphenopalatine foramen, and anterior to the pterygoid canal and foramen rotundum. It is flattened, reddish-grey in colour, and lies just below the maxillary nerve as it crosses the pterygopalatine fossa. The majority of the ‘branches’ of the ganglion are connected with it morphologically, but not functionally, because they are primarily sensory branches of the maxillary nerve. Thus they pass through the ganglion without synapsing, and enter the maxillary nerve through its ganglionic branches, but they convey some parasympathetic fibres to the palatine, pharyngeal and nasal mucous glands.

Preganglionic parasympathetic fibres destined for the pterygopalatine ganglion run initially in the greater petrosal branch of the facial nerve, and then in the nerve of the pterygoid canal (Vidian nerve), after the greater petrosal unites with the deep petrosal nerve. The nerve of the pterygoid canal enters the ganglion posteriorly. Postganglionic parasympathetic fibres leave the ganglion and join the maxillary nerve via a ganglionic branch, then travel via the zygomatic and zygomaticotemporal branches of the maxillary nerve to the lacrimal gland (see Fig. 30.6A). Preganglionic secretomotor fibres of uncertain origin also travel in the nerve of the pterygoid canal. They synapse in the pterygopalatine ganglion, and postganglionic fibres are distributed to palatine, pharyngeal and nasal mucous glands via palatine and nasal branches of the maxillary nerve

10. Most common site of osteoma is frontal sinus.

Benign bone tumors of the paranasal sinuses are of fibroosseous or of giant cell origin. Fibroosseous lesions include osteoma, osteochondroma, ossifying fibroma, and fibrous dysplasia. Giant cell lesions include giant cell granuloma and brown tumor. Osteoma, a common lesion, is benign proliferation of mature bone. It occurs almost exclusively in the head and neck, particularly in the frontal and ethmoidal sinuses. Compact osteoma and ivory osteoma are seen as extremely dense, well-defined masses within the paranasal sinuses (Fig. 29.18). Cancellous osteoma is variable in density on plain radiographs and CT because of the presence of a fibrous component. They can even appear as a soft-tissue density on plain radiographs, but CT shows the ossific character. Multiple osteomas of the face and skull are one of the many manifestations of Gardner syndrome. Osteochondroma can occur in the nose and paranasal sinuses. As in other locations, it is heterogeneously calcified and is pedunculated.

Most (90%) patients with fibrous dysplasia are asymptomatic. When symptomatic, patients may have local swelling, pain, displaced teeth, or nerve-compression symptoms. The most commonly affected bones are the ribs and femur for monostotic fibrous dysplasia and the femur and tibia for polyostotic fibrous dysplasia.
About 25% of patients with fibrous dysplasia have head and neck involvement. The maxilla is the bone most often affected, followed by the mandible. Painless asymmetric swelling is common.
The typical radiographic finding is an expanded osseous lesion with a poorly defined margin covered by an eggshell-thin cortex. Fibrous dysplasia also may present radiographically as a pagetoid lesion or as a sclerotic lesion. It should be considered when the paranasal sinuses are involved if radiographic studies show a calcified, thick, enlarged sinus margin and a ground-glass appearance of the mass inside the sinus.

11. Prolonged use of vasoconstrictor nose drops leads to rebound phenomenon :-

Of the topical drugs, cocaine and over-the-counter nasal decongestants commonly cause drug-induced rhinitis. Rhinitis medicamentosa is caused by prolonged use of topical vasoconstricting agents such as cocaine, oxymetazoline hydrochloride, and phenylephrine hydrochloride, as well as others derived from sympathomimetic amines and imidazoles. Patients with chronic nasal obstruction due to anatomic abnormalities such as deviated septum or due to use of medications may be tempted to use these fast-acting topical sprays or drops for longer than is recommended by the manufacturer, usually 3 days. Tachyphylaxis—the rapid reduction in drug effect after administration of several doses—may prompt the patient to use vasoconstricting agents for extended periods. This causes further rebound effects due to down-regulation of nasal mucosal a-adrenergic receptors. Rhinitis medicamentosa is caused by refractory vasodilatation of mucosal blood vessels or excessive mucosal edema. With prolonged vasoconstriction, mucosal arterioles and vessels become fatigued and hypoxic, subsequently vasodilating to resupply nutrients to the highly vascular mucosa. However, as vascular cells vasodilate, they become increasingly permeable and allow an excessive amount of water to off-load into the hypertonic nasal mucosa. Mucosal injury, such as loss of cilia, metaplasia, or fibrosis, can occur as a more serious consequence of prolonged hypoxia owing to the use of vasoconstrictors. Abuse of cocaine also irritates and inflames the mucosa and can lead to septal perforation.

12.Choanal Atresia:-Choanal atresia, first reported in 1830, occurs in 1 in 5000 to 8000 live births.

CHARGE association (coloboma [of eyes], hearing deficit, choanal atresia, retardation of growth, genital defects [males only], endocardial cushion defect)

Other anomalies associated with choanal atresia include polydactyly, nasal-auricular and palatal deformities, Crouzon’s syndrome, craniosynostosis, microencephaly, meningocele, meningoencephalocele, facial asymmetry, hypoplasia of the orbit and midface, cleft palate, and hypertelorism.

The four parts of the anatomic deformity include a narrow nasal cavity, lateral bony obstruction by the lateral pterygoid plate, medial obstruction caused by thickening of the vomer, and membranous obstruction. Histopathologic studies reveal the lateral pterygoid plate and posterior vomer are expanded by endochondral bone formation and are invested by a delicate fibroepithelial membrane that obstructs the choanae.No cartilage or bony islands are identified in the membrane.Although several theories concern the embryogenesis of choanal atresia, it is generally thought to be secondary to persistence of the nasobuccal membrane. Between the third and fourth weeks of gestation, the nasal placodes, which are ectodermal thickenings on either side of the midline, invaginate
to form nasal pits. These enlarge and burrow into the mesoderm of the developing face, and primitive nasal pouches are formed. These pouches lie immediately above the buccal cavity, and the floor thins to form a nasal and oral cavity separated only by the thin nasobuccal membrane. This membrane normally ruptures between the fifth and sixth weeks of gestation to produce choanae. Failure of this membrane to rupture causes atresia.

Choanal atresia can be diagnosed in several ways. The most simple method is to attempt to pass a small catheter through the nose into the nasopharynx. The patient may also be examined with a rigid or flexible endoscope, operating microscope, mirror examinations or digital examination. An outmoded method of diagnosis is radiography using radiopaque contrast material instilled into the nasal cavity with the patient in a supine position. Computed tomography (CT) is the radiographic procedure of choice. It is superior in that it can show the nature and thickness of the obstructing segment.[4] [12] CT also has been shown to correlate anatomically with histologic sections ( Fig. 7–3 ).
Management of these patients can be immediate and definitive. Unilateral atresia is rarely emergent. The repair is generally delayed for at least 1 year, which allows the operative site to enlarge to approximately twice the size of that of a newborn and reduces the risk of postoperative stenosis. Immediate management of bilateral atresia involves training the infant to breathe through the mouth with the aid of an indwelling oral appliance such as a McGovern nipple.In an emergency, the infant can be stimulated to cry; if this is unsuccessful, a finger can be inserted into the mouth until an airway is established.

Surgical repair of choanal atresia includes transnasal, transpalatal, transantral, and transseptal approaches. Transpalatal approaches are traditionally reserved for older patients because of orthodontic growth and development may be interrupted.Compared with the transpalatal approach, transnasal repair has been associated with a higher rate of restenosis and a need for serial dilations.However, with the use of endoscopes, the operating microscope, and otologic instruments and drills via the transnasal approach, comparable results are achievable.Although many methods are described, the key points are removal and shortening of the posterior bony septum and removal of the superior-lateral nasal wall and lateral pterygoid plate.

Roederer First Described Choanal atresia.

Computed tomographic scan shows bilateral choanal atresia and medial displacement of the lateral walls of the nasopharynx

choanal atresia

The site of choanal atresia is just in front of the posterior end of nasal septum.

13. The velopharyngeal mechanism is a muscular valve that expands from the hard palate to the pharynx back wall and is located in the portion of the vocal tract called velopharynx. The patient with labiopalatine cleft may have changes of the velopharyngeal mechanism damaging the speech intelligibility, that is, when there is not the suitable closing of the velopharyngeal sphincter the air flow gets around by the nasal cavities. The term velopharyngeal dysfunction is used to express its inadequacies resulting from the lack of the soft palate tissue to complete the correct velopharyngeal closing (velopharyngeal insufficiency) or the neuromuscular incompetence with the velopharyngeal structures motion (velopharyngeal incompetence).The structural abnormalities resulting from the cleft palate reflect some changes in the speech and the most common ones are associated to the velopharyngeal dysfunction, such as hypernasality, the emission of audible air and the articulatory and compensatory disturbances. The occlusal and dental deformities may also damage the phonemes articulation and because of this reduce the speech understanding.

The hypernasality is one of the speech symptoms resulting from the velopharyngeal dysfunction, where the oral phonemes nasal resonance occurs for the lack of sealing between the oral and nasal cavity.

Palatal clefting and velopharyngeal insufficiency are relative contraindications to adenoidectomy.Also acute infection(acute sinusitis),BIFID UVULA an significant H/O nasal regurgitation in an infant.

14.   ELECTROCOCHLEOGRAPHY:-For more than 30 years, ECochG has been used to assess peripheral auditory function. The examination is performed most often for intraoperative monitoring of cochlear and eighth-nerve status and in the diagnosis of Ménière disease .The three major components of the ECochG are the cochlear microphonic, summating potential, and action potential. The cochlear microphonic and summating potential reflect cochlear bioelectric activity. The action potential is generated by synchronous firing of distal afferent eighth-nerve fibers and is equivalent to ABR wave I (Fig. 132.5). The typical ECochG analysis technique in neurotology requires determination of the amplitude of the summating potential and the action potential from a common baseline. The ratio of the summating potential to the action potential (SP/AP) is calculated and reported as a percentage. Normal ranges and cutoffs for SP/AP ratio have been reported for each electrode type. Abnormal SP/AP ratio values are defined as more than 50% for the ear canal electrode type, more than 40% for a tympanic membrane electrode, and more than 30% for a transtympanic needle electrode.The authors also determined normative ranges for absolute SP amplitude from responses to tone bursts. Using a criterion of 0.35 or less for a normal SP:AP ratio and 0.5 or larger for a definitely abnormal test.One of the main clinical applications of electrocochleography is in the differential diagnosis of hydropic conditions of the cochlea that may be associated with Ménière’s disease or other pathologies. It is believed that the presence of hydrops affects the elasticity of the basilar membrane and contributes to the increased amplitude of the SP relative to that of the AP. A relatively large SP:AP ratio is considered diagnostic of endolymphatic hydrops.[7A] The SP:AP amplitude ratio is used instead of the absolute amplitude of the SP in order to avoid contamination of this measurement by interpatient variability. Thus patients with endolymphatic hydrops are thought to exhibit relatively larger SP:AP ratios.

15.AUDITORY BRAINSTEM RESPONSE:-The ABR is a surface-recorded averaged response representing the activity of the distal portion of the auditory pathway. As a rule, five to seven peaks occurring within a time frame of less than 10 ms make up the ABR. For neurodiagnostic purposes, the first five positive polarity peaks (waves I through V) are typically considered.

The ABR may be recorded with standard or disposable surface electrodes placed high on the forehead below the hairline or at the vertex (noninverting electrode); on the medial surface of the ipsilateral earlobe; or on the medial surface of the contralateral earlobe (ipsilateral and contralateral inverting electrodes) and on the center of the forehead (ground electrode). These electrodes may be used for a typical two-channel montage with the ipsilaterally referenced channel emphasizing wave I (synonymous to the N1 of the electrocochleogram) and the contralaterally referenced channel emphasizing the separation between waves IV and V.

Investigations by Moller and Jannetta[36] suggest that the neural generators of peaks I through V originate from the cochlear nerve through the nucleus of the lateral lemniscus in the midbrain. Waves I and II of the ABR reflect the activation of the distal and proximal segments of the cochlear nerve, respectively. The two action potentials generated by the cochlear nerve may be attributed to the change from Schwann’s cell endoneurium peripherally to the neuroglial cover of the proximal segment of the nerve. This shift occurs near the porus acusticus and contributes to a change in neural conduction properties. Waves III and IV reflect the activation of the cochlear nucleus complex and the superior olivary complex.

Moller and Jannetta’s study also indicates that wave V is associated primarily with the activation of the lateral lemniscus and not the inferior colliculus as was previously considered.

A well-formed and clear wave I at a delayed latency value for the maximum stimulus intensity level is characteristic of conductive or mixed hearing loss. When wave I is small and poorly formed but interwave latency values are within normal limits (the wave I through V latency value less than 4.60 ms), high-frequency sensory (cochlear) hearing loss is suspected. Delayed interwave latency values are the signature of retrocochlear auditory dysfunction. Abnormal delays between the early wave components (I through III) are consistent with posterior fossa lesions that involve the eighth cranial nerve or lower brainstem, whereas prolonged latency of waves III through V suggests intraaxial auditory brainstem dysfunction.

A primary goal in any neurodiagnostic evaluation of ABR is to record a clear and reliable wave I component. Wave I is the benchmark for peripheral auditory function. Subsequent interwave latencies offer indices of retrocochlear (eighth cranial nerve and brainstem) function that are relatively unaffected by conductive or sensory hearing loss. The likelihood that wave I is recorded is enhanced through use of ear canal or tympanic membrane electrode designs and through alterations in the test protocol, such as a slower stimulus rate, rarefaction stimulus polarity, and maximum stimulus intensity level.

Assessment of ABR continues to be a readily available, relatively inexpensive, and reasonably sensitive procedure for initial diagnostic evaluation of eighth-nerve and auditory brainstem status in the care of patients with retrocochlear signs and symptoms.  Assessment of ABR is also valuable in electrophysiologic monitoring of the eighth cranial nerve and auditory brainstem function during neurotologic operations such as vestibular nerve section and posterior tumor removal.

16. CSF Rhinorrhoea:-

Traumatic cerebrospinal fluid rhinorrhea:-The roof of the ethmoid and the cribriform plate are the most frequent sites of CSF rhinorrhea.

Nontraumatic cerebrospinal fluid rhinorrhea:-Rhinorrhea from tumors or hydrocephalus occurs as a result of increased intracranial pressure, leading to continued erosion and weakening of bone with the eventual development of a fracture and a CSF fistula. The cribriform plate and roof of the ethmoid, which are the thinnest areas of bone at the base of the skull, are the most frequent sites of nontraumatic CSF rhinorrhea

Benign tumors of the nose are rare in comparison with malignant growths. The most common benign tumors (in decreasing order of frequency) are osteoma, hemangioma, papilloma, and angiofibroma. The two tumors of greatest interest are the inverted papilloma and the juvenile nasopharyngeal angiofibroma.

Inverted papilloma-Most authorities consider the inverted papilloma a true neoplasm. Other names used for this growth are schneiderian papilloma, papillary sinusitis, polyp with inverting metaplasia, benign transitional cell growth, epithelial papilloma, inverted schneiderian papilloma, soft papilloma, transitional cell papilloma, squamous papillary epithelioma, papillary fibroma, papillomatosis, and cylindrical cell carcinoma

18.Trotter syndrome (sinus of Morgagni syndrome) May be seen with tumors of the nasopharynx that block the eustachian tube and produce a conductive hearing loss secondary to middle-ear fluid. Other symptoms may be pain in the distribution of the ophthalmic branch of the trigeminal nerve, decreased mobility of the soft palate(X NERVE), and possibly trismus.

19.Nonsurgical treatment includes nasal CPAP therapy (Fig. 50.4) and various appliances. Nasal CPAP therapy is almost never used for nonapneic snoring, but it may be a more cost-effective alternative than separate bedrooms or divorce in patients who have failed all other types of treatment. Alternatively, numerous oral appliances, nasal splints, and positioning devices have been demonstrated to be effective in the treatment of snoring and OSAS.

.Nasal CPAP is still considered the first-line therapy in OSAS. Nasal CPAP corrects obstructive respiratory events and improves morbidity associated with OSAS. Compliance with treatment remains a serious problem in patients using nasal CPAP.

20.When great force is directed from the inferior aspect to the external nose, the nasal bones can be driven into the frontal and ethmoidal skeleton at the anterior base of the skull. This type of injury produces comminution and displacement of the nasal, frontal, and ethmoid bones with telescoping and splaying of these structures. Injury to the nasofrontal duct or cribriform plate can be associated with these complex fractures. One or both medial canthal ligaments can attach to fragments that become loosened, causing pseudohypertelorism. The Horner muscle inserts on the medial ligament and is partially responsible for this deformity. The medial canthus comprises the medial canthal tendon and the nasolacrimal sac and canaliculi. The intercanthal distance usually is equivalent to the interpalpebral distance or half of the interpupillary distance. Associated injuries include CSF rhinorrhea, anosmia, ocular injury, interruption of the lacrimal system, and cerebral contusion.

The most commonly performed surgical procedure for OSAS is the UPPP. Laser-assisted uvulopalatoplasty and other outpatient palatal procedures are effective in the treatment of snoring and in the treatment of OSAS in well-selected patients.

21.Fry using cadaveric cartilage, and retrospective clinical data suggested that injury to the septal surface can activate interlocked stresses that will cause the cartilage to twist.Classic work by Fry emphasizes the importance of scoring the concave or compressed side.

Fry`s principle

Fry suggested that septal cartilage has an intrinsic tension, the result of a built-in system of interlocking stresses that contribute to cartilage “memory.” Mostly, septal cartilage lies straight, the effect of balanced tension created by the even distribution of internal stresses. If one side of cartilage is interrupted by partial-thickness injury or incisions, an imbalance occurs, and the opposite side assumes dominance. Microfractures sustained early in life simulate partial-thickness cuts. These often result in unfurling of septal cartilage on the side of injury and may lead to substantial deviation of the septum as growth accentuates the deformity . The origin of intrinsic cartilage stress, although not fully understood, has been attributed to the histologic lamination of chondrocytes at the periphery of the septal cartilage. More recent evidence, however, suggests that cartilage tension is the product of cellular and molecular events that govern the composition and arrangement of the extracellular matrix.

Although valuable, intrinsic tension cannot be used as the sole basis for the correction of a septal deformity. The straightening effect of partial-thickness incisions on the concave side of deviated cartilage is unpredictable and influenced by confounding factors. The magnitude, arrangement, and distribution of intrinsic cartilage stresses vary among different areas of the septum and among septa in different patients. Furthermore, the effect of fibrous ingrowth into fracture lines, contracture of the investing perichondrium, and the calcification or thickening of injured cartilage should be factored into the surgical equation for straightening septal cartilage. Generally, full-thickness incisions created on the concave side, carried to but not through the opposite mucoperichondrium, are most effective in dispelling cartilage tension and are more reliable than partial-thickness cuts for straightening bent cartilage.

22.Nasofrontal-Ethmoidal Fractures:-When great force is directed from the inferior aspect to the external nose, the nasal bones can be driven into the frontal and ethmoidal skeleton at the anterior base of the skull. This type of injury produces comminution and displacement of the nasal, frontal, and ethmoid bones with telescoping and splaying of these structures. Injury to the nasofrontal duct or cribriform plate can be associated with these complex fractures. One or both medial canthal ligaments can attach to fragments that become loosened, causing pseudohypertelorism. The Horner muscle inserts on the medial ligament and is partially responsible for this deformity. The medial canthus comprises the medial canthal tendon and the nasolacrimal sac and canaliculi. The intercanthal distance usually is equivalent to the interpalpebral distance or half of the interpupillary distance. Associated injuries include CSF rhinorrhea, anosmia, ocular injury, interruption of the lacrimal system, and cerebral contusion.



24.The narrow lumen of a child’s trachea and other obvious anatomic differences prompted the development of plastic tracheostomy tubes for pediatric use rather than a small adult metal tracheostomy tube. A soft pliable tube more easily conforms to the shape of the infant’s or child’s trachea. Multiple lengths with various inner and outer diameters are important for the age range and the developing child. A pediatric polyvinyl chloride tracheostomy tube was introduced in 1965 by Aberdeen and was the beginning of the development of more modern pediatric tracheostomy tubes. Polyvinyl chloride (Shiley and Portex) and silastic tubes (Argyle and Bivona) are more pliable and tend to collect less secretions. They do not have an inner cannula and, because of their increased malleability, may allow easier accidental decannulation. The smaller tracheostomy tubes generally have no cuff. Both the Shiley and Bivona tubes are available in pediatric standard sizes and neonatal assorted sizes. The softer silicone tube may be especially important in a child with spinal abnormalities with an abnormally shaped or deviated trachea. Holinger and Jackson metal tracheostomy tubes have inner cannulas and may be important in reconstructive procedures when a stent may be wired to the tracheostomy tube. The inner cannula provides a method of cleaning the tube lumen with the tracheostomy that is left in place for long periods of stenting. More conformity and standardization to standard endotracheal tube size and numbering system have developed, but further progress is needed.

25. Esophageal Atresia and Tracheoesophageal TES:- The most commonly seen variety is EA with distal TEF (type C), which occurs in approximately 85% of the cases in most series. The next most frequent is pure EA (type A), occurring in 8 to 10% of patients, followed by TEF without EA (type E). The latter occurs in 8% of cases and is also referred to as an H-type fistula, based on the anatomic similarity to that letter (Fig. 39-9). EA with fistula between both the proximal and distal ends of the esophagus and trachea (type D) is seen in approximately 2% of cases, and type B, EA with TEF between the proximal esophagus and trachea, is seen in approximately 1% of cases.

image image image image image

The five varieties of esophageal atresia (EA) and tracheoesophageal fistula (TEF). A. Isolated EA.(SECOND MOST COMMON) B. EA with TEF between the proximal segment of the esophagus and the trachea. C. EA with TEF between the distal esophagus and the trachea(MOST COMMMON) D. EA with fistula between both the proximal and distal ends of the esophagus and the trachea. E. TEF without EA (H-type fistula).(THIRD MOST COMMON)

The anatomic variant of EA-TEF in the infant predicts the clinical presentation. When the esophagus ends either as a blind pouch or as a fistula into the trachea (as in types A, B, C, and D), infants present with excessive drooling, followed by choking or coughing immediately after feeding is initiated as a result of aspiration through the fistula tract.

Air in the distal intestine indicates either a patent esophagus or a fistula to the respiratory tract. In type C TEF, as the neonate coughs and cries, air is transmitted through the fistula into the stomach, which results in abdominal distention. As the abdomen distends, it becomes increasingly more difficult for the infant to breathe. This leads to further atelectasis, which compounds the pulmonary dysfunction. In patients with the C and D varieties, the regurgitated gastric juice passes through the fistula, collecting in the trachea and lungs and leading to a chemical pneumonitis, which further exacerbates the pulmonary status


Type C esophageal atresia with tracheoesophageal fistula. Note the catheter coiled in the upper pouch and the presence of gas below the diaphragm, which confirms the presence of the tracheoesophageal fistula.

The diagnosis of EA is confirmed by the inability to pass an orogastric tube into the stomach (Fig. 39-10). The dilated upper pouch occasionally may be seen on a plain chest radiograph. If a soft feeding tube is used, the tube will coil in the upper pouch, which provides further diagnostic certainty. An important alternative diagnosis that must be considered when an orogastric tube does not enter the stomach is that of an esophageal perforation. This problem can occur in infants after traumatic insertion of a nasogastric or orogastric tube. In this instance, the perforation classically occurs at the level of the piriform sinus, and a false passage is created that prevents the tube from entering the stomach. Whenever there is any diagnostic uncertainty, a contrast study can confirm the diagnosis of EA and occasionally document the TEF; however, the obvious risks of aspiration associated with an undrained blind pouch cannot be overstated. The presence of a TEF can be demonstrated clinically by the finding of air in the GI tract. This can be proven at the bedside by percussion of the abdomen and confirmed by plain abdominal radiograph. Occasionally, a diagnosis of EA-TEF can be suspected prenatally on ultrasonographic evaluation. Typical features include failure to visualize the stomach and the presence of polyhydramnios. These findings reflect the absence of efficient swallowing by the fetus.

In a child with EA, it is important to identify whether coexisting anomalies are present. These include cardiac defects in 38%, skeletal defects in 19%, neurologic defects in 15%, renal defects in 15%, anorectal defects in 8%, and other abnormalities in 13%

The timing of repair is influenced by the stability of the patient’s condition. Definitive repair of the EA-TEF is rarely a surgical emergency. If the child is hemodynamically stable and is oxygenating well, definitive repair may be performed within 1 to 2 days after birth.

Management in the Preterm Infant:-

The ventilated premature neonate with EA-TEF and associated hyaline membrane disease is a patient who may develop severe, progressive cardiopulmonary dysfunctionThe tracheoesophageal fistula can worsen the fragile pulmonary status as a result of recurrent aspiration through the fistula and increased abdominal distention, which impairs lung expansion. Moreover, the elevated airway pressure that is required to ventilate these patients can worsen the clinical course by forcing air through the fistula into the stomach, which exacerbates the degree of abdominal distention and compromises lung expansion. In this situation, the first priority is to minimize the degree of positive pressure needed to adequately ventilate the child. This can be accomplished using high-frequency oscillatory ventilation.

The wall of the oesophagus consists of four coats. The inner mucosal layer, lined by stratified squamous epithelium, is demarcated by a well-developed muscularis mucosae from the submucous coat which is the toughest layer of the wall and contains the larger blood vessels and a plexus of nerves corresponding to Meissner’s plexus in the intestine. Throughout the oesophagus small mucous glands lie in the submucous layer, their ducts passing through the muscularis mucosae to open on the surface. Commonly each duct passes through a small nodule of lymphoid tissue. At the upper and lower ends of the oesophagus there are also present small tubulo-racemose glands which lie entirely within the mucosa, not penetrating the muscularis mucosae, and are similar in character to the cardiac glands of the stomach. Round the mouths of these glands the lining of the oesophagus often consists of columnar epithelium, closely resembling that of the stomach. Its presence may explain the occurrence of adenocarcinomata in the oesophagus (I9 of 267 carcinomata, or 7 per cent, reported by Watson, I933).

The toughest layer of the esophagus is the

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Orthopaedics MCQs

Posted by Dr KAMAL DEEP on May 21, 2010


1. In transverse fracture of the patella the treatment is

a)Excision of a small fragment
b)Wire fixation
c)Plaster cylinder


Transverse Patellar Fracture


Transverse fractures of the patella  are the result of an indirect force, usually with the knee in flexion. Fracture may be caused by sudden voluntary contraction of the quadriceps muscle or sudden forced flexion of the leg with the quadriceps contracted. The level of fracture is commonly in the middle. Associated tearing of the patellar retinacula depends upon the force of the initiating injury. The activity of the quadriceps muscle causes upward displacement of the proximal fragment, the magnitude of which depends on the extent of the retinacular tear.


Clinical Findings 

Swelling of the anterior knee region is caused by hemarthrosis and hemorrhage into the soft tissues overlying the joint. If displacement is present, the defect in the patella can be palpated, and active extension of the knee is lost. A straight leg raise may be preserved if the retinacula is intact.


Nondisplaced fractures can be treated with a walking cylinder cast or brace for 6-8 weeks followed by knee rehabilitation. Open reduction is indicated if the fragments are displaced > 3 mm or if articular step-off is > 2 mm. The fragments must be accurately repositioned to prevent early posttraumatic arthritis of the patellofemoral joint. If the minor fragment is small (no more than 1 cm in length) or severely comminuted, it may be excised and the quadriceps or patellar tendon (depending upon which pole of the patella is involved) sutured directly to the major fragment. Whenever possible, internal fixation of anatomically reduced fragments should be done, allowing early motion of the knee joint. This is best achieved by figure-of-eight tension banding over two longitudinal parallel K-wires.

Accurate reduction of the articular surface must be confirmed by lateral radiographs taken intraoperatively.

2. Comminuted Patellar Fracture

Comminuted fractures of the patella are usually caused by a direct force. Most often, little or no separation of the fragments occurs because the quadriceps retinaculum is not extensively torn. Severe injury may cause extensive destruction of the articular surface of both the patella and the opposing femur.

If comminution is not severe and displacement is insignificant, immobilization for 8 weeks in a cylinder extending from the groin to the supramalleolar region is sufficient.

Severe comminution can often be treated with ORIF with addition of a cerclage wire, but on rare occasions excision of the patella and repair of the defect by imbrication of the quadriceps expansion is the only viable alternative. Excision of the patella can result in decreased strength, pain in the knee, and general restriction of activity. No matter what the treatment, high-energy injuries are frequently complicated by chondromalacia patella and patellofemoral arthritis. Note:-Satisfactory results have been reported with use of the tension band wire and its modification in treating comminuted and displaced patellar fractures although most authors recommend patellectomy when less than half of the articular surface of the patella remains intact


2. Communited fracture of patella is treated by-

A)Tension wire bandage
b)Surgery and immobilisation


3. Recurrent dislocation of patella is most often associated with-
a)Abnormally high patella
b)Abnormally low patella
c)Bow leg
d)Quadriceps contracture


The majority of patients with complaints of patellar pain and instability will have objective abnormalities of the extensor mechanism and patellofemoral joint. These abnormalities are preexisting and developmental. Major examples include a shallow trochlea, an increased quadriceps angle (Q-angle), a vastus medialis obliquus (VMO) deficiency, and a patella alta(high)


PATELLA ALTA:- The Patella is high-lying in the shallower part of intercondylar groove.


The indication for arthroscopic lateral release (Fig. 87.10) is a tight lateral retinaculum that is producing the patient’s symptoms, which have not responded to appropriate nonoperative treatment. If it is not tight, don’t release it. If the patient has a large Q angle as well, an isolated lateral release will not be sufficient; the tibial tubercle will usually have to be moved also.


4.Clergymen’s knee is due to involvement of-

a)Prepatellar Bursa c)Suprapatellar
b) Intrapatellar bursa d) Infrapatellar bursa



5.Treatment of displaced transverse fracture of patella –
a) POP b) Tension band wiring
c) Screw d) Patellectomy

Ans given in guides is a b and d but its wrong as  # is displaced

Nondisplaced fractures can be treated with a walking cylinder cast or brace for 6-8 weeks followed by knee rehabilitation. Open reduction is indicated if the fragments are displaced > 3 mm or if articular step-off is > 2 mm. The fragments must be accurately repositioned to prevent early posttraumatic arthritis of the patellofemoral joint. If the minor fragment is small (no more than 1 cm in length) or severely comminuted, it may be excised and the quadriceps or patellar tendon (depending upon which pole of the patella is involved) sutured directly to the major fragment. Whenever possible, internal fixation of anatomically reduced fragments should be done, allowing early motion of the knee joint. This is best achieved by figure-of-eight tension banding over two longitudinal parallel K-wires



6 Which one of the following structures is at least risk of damage in knee dislocation? (UPSC 02)
a)Cruciate ligaments
b)Common peroneal nerve
d)Popliteal artery

Ans. is ‘c’ i.e., Patella [Ref : Apley’s 8e p. 713, Adam’s outline of fracture p. 237]

Normally the knee is held stable by –
I) Its strong ligaments (the two cruciate ligaments, the medial and lateral ligaments and the joint capsule) and
ii) Protective control of powerful Quadriceps muscle.
Dislocation is possible only if some or all of the ligaments are ruptured.
Dislocation usually occurs in the posterolateral or anteromedical direction
Complications of knee dislocation
Most feared complication of knee dislocation are – .
.Injury to the popliteal artery
.Injury to the major nerve trunks behind the knee (all of these are especially vulnerable when the tibia is displaced backwards)
Also know
Nerve trunks in posterior relation to the knee joint
.Tibial nerve (at the middle)
.Common peroneal nerve (posterolaterally)



TABLE :- Anatomic classification of knee dislocations
Type Injury Intact Structures
I Single cruciate and collateral Single cruciate and collateral
II ACL and PCL Collaterals
V Fracture dislocation Variable
C Arterial injury Variable
N Nerve injury Variable

The anatomic system takes into account the soft tissue and is seen in Table . Type III injuries are most common, with type IIIL having a poor outcome when compared to type IIIM. There is a high incidence of arterial injury (on average, 33%) including intimal tears rather than complete disruptions.



Neurologic Examination. Neurologic examination includes a thorough evaluation of the peroneal nerve, including EHL and tibial anterior strength and sensation to the EHL and tibialis anterior strength. There is a 14% to 35% incidence of injury; the most common occurrence is type III L (varus) as a result of traction. The tibial nerve may be involved and can be assessed with FHL and gastrocnemius/soleus strength along with sensation over the lateral border and planter surface of the foot.


7.Transverse fracture of patella in a young adult. What is the treatment of choice?
a) Tension band wiring b) Cylinder cast
c) Patellectomy d) Conservative


8.Treatment of fracture patella in.24 year old young male is –

a)Patellectomy if undisplaced
b)No treatment required
c)Internal fixation if communited fracture
d)POP in full extension


9.In a young patient, transverse fracture of patella is best treated by –
b)Application of cylindrical POP cast
c)Strict bed rest with quandriceps exercises
d)Tension band wiring following by POP cast

ans given is C in guides but i think its wrong.

Whenever possible, internal fixation of anatomically reduced fragments should be done, allowing early motion of the knee joint.


10.The most common cause for anterior knee pain is –
a)Prepatellar bursitis
b)Congenital discoid meniscus
c)Plica syndrome
d)Chondromalacia patellae

Ref Apley p. 469-470]


The plica syndrome
.The plica is remnant of an embryonis synovial partition which persists into adult life.
.During development of embryos the knee is divided into three cavities
.a large Suprapatellar pouch and beneath this
.Medial and lateral comparments.
.These three cavities are separated from each other by membranous septa. Later these partitions disappear leaving a single cavity. But sometimes part of septum may persist as a synovial pleat or plica.
.This is seen in over 20% people.The plica in itself is not pathological. But if acute trauma, repetitive strain or some underlying disorder causes inflammation the plica may become oedematous, thickened and eventually fibrosed. It then acts as a light bowstring impinging on other structures in the joint and causing further synovial irritation.
Clinical feature
.An adolescent or young adult complains of an ache in the front of the knee with intermittent episodes of clicking or `giving way’ there may be history of trauma or markedly increased activity
.Symptoms are aggravated on exercise or climbing stairs
.The most characteristic feature is tenderness near upper pole of the patella.



11.Usual site of Tubercular bursitis –
a) Prepatelar b) Subdeltoid
c) Subpatellar d) Trochanteric
e) None


12.Usual site of TB bursitis –
a) Prepatellar b) Subacromial
c) Subdeltoid d) Subpatellar
e) Trochanteric


13.Housemaids knee is inflammation of bursa –
a) Subpatellar b) Suprapatellar
c) Infrapatellar d) Pre patellar


14.Patella is at a higher level in –
a)Recurrent dislocation
b)Nail-patella syndrome
c)Rheumatoid arthritis
d)Plica syndrome



15.Nail patella syndrome is characterised by –
a) Iliac horn b) Sacral horn
c) Absent patella d) Knee deformity
e) Dislocation of patella


The hallmark features of this syndrome are poorly developed fingernails, toenails, and patellae (kneecaps).

Bones and joints
Patellar involvement is present in approximately 90% of patients; however, patellar aplasia occurs in only 20%.
In instances in which the patellae are smaller or luxated, the knees may be unstable.
The elbows may have limited motion (eg, limited pronation, supination, extension).
Subluxation of the radial head may occur.
Arthrodysplasia of the elbows is reported in approximately 90% of patients.
General hyperextension of the joints can be present.
Exostoses arising from the posterior aspect of the iliac bones are present in as many as 80% of patients; this finding is considered pathognomonic for the syndrome.


16. Patellar tendon bearing P.O.P. cast is indicated in the following fracture :
C.Medial malleolus

Ans is B



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Pathology MCQs

Posted by Dr KAMAL DEEP on March 16, 2010

1. The following are example of apoptosis except-
a)Graft versus host disease(JIPMER 2002)
b)Menstrual cycle
c)Pathological atrophy following duct obstruction
d)Tumour necrosis

Type :- Controversial Question

Ans is None


There are two principal patterns of cell death, necrosis and apoptosis.

 Necrosis or coagulation necrosis is the more common type of cell death after exogenous stimuli, occurring after such stresses as ischemia and chemical injury. It is manifested by severe cell swelling or cell rupture, denaturation and coagulation of cytoplasmic proteins, and breakdown of cell organelles.

 Apoptosis occurs when a cell dies through activation of an internally controlled suicide program. It is a subtly orchestrated disassembly of cellular components designed to eliminate unwanted cells during embryogenesis and in various physiologic processes. Doomed cells are removed with minimum disruption to the surrounding tissue. It also occurs, however, under pathologic conditions, in which it is sometimes accompanied by necrosis. Its chief morphologic features are chromatin condensation and fragmentation. Although the mechanisms of necrosis and apoptosis differ, as we shall see, there is
considerable overlap between these two processes. Recently, a new term has been introduced– oncosis–to define the prelethal changes preceding necrotic cell death. [2] These are characterized by cell swelling ( oncos, Greek for swelling) and can be distinguished from the prelethal changes in apoptosis, associated largely with cell shrinkage. Whether the term will achieve the status sought by its creators is still unclear.

Apoptosis was initially recognized in 1972 by its distinctive morphology and named after the Greek designation for "falling off." [33] [33A] It is a form of cell death designed to eliminate unwanted host cells through activation of a coordinated, internally programmed series of events effected by a dedicated set of gene products. It occurs in the following general settings: (1) during development; (2) as a homeostatic mechanism to maintain cell populations in tissues; (3) as a defense mechanism such as in immune reactions;  when cells are damaged by disease or noxious agents; and (5) in aging. [34] [35] It is responsible for numerous physiologic, adaptive, and pathologic events, including the following:

The programmed destruction of cells during embryogenesis, including implantation, organogenesis, developmental involution, and metamorphosis. Although apoptosis is a morphologic event, which may not always underlie the functionally defined "programmed cell death" of embryologists, the terms are currently used synonymously by most workers.

1.Cell deletion in proliferating cell populations, such as intestinal crypt epithelia.

2.Cell death in tumors, most frequently during regression but also in tumors with active cell growth.

3.Death of neutrophils during an acute inflammatory response.

4.Death of immune cells, both B and T lymphocytes after cytokine depletion, as well as deletion of autoreactive T cells in the developing thymus.

5.Cell death induced by cytotoxic T cells, such as in cellular immune rejection and graft-versus-host disease.

6.Pathologic atrophy in parenchymal organs after duct obstruction, such as occurs in the pancreas, parotid gland, and kidney.

7.Cell injury in certain viral diseases, as for example in viral hepatitis, in which apoptotic cells in the liver are known as Councilman bodies.

8.Cell death produced by a variety of injurious stimuli that are capable of producing necrosis, but when given in low doses. For example, heat, radiation, cytotoxic anticancer drugs, and hypoxia can induce apoptosis if the insult is mild, but large doses of the same stimuli result in necrotic cell death.

9. Hormone-dependent involution in the adult, such as endometrial cell breakdown during the menstrual cycle, ovarian follicular atresia in the menopause, the regression of the lactating breast after weaning, and prostatic atrophy after castration.


2. True about apoptosis-(PGI 03)
a)Migration of Leukocytes
b)End products are phagocytosed by macrophage
c)Intranuclear fragmentation of DNA
d)Activation of caspases
e)Annexin V is marker of apoptopic cell

Ans is B , C D and E


The following morphologic features, some best seen with the electron microscope, characterize cells undergoing apoptosis .

Cell shrinkage. The cell is smaller in size; the cytoplasm is dense; and the organelles, although relatively normal, are more tightly packed.

Chromatin condensation. This is the most characteristic feature of apoptosis. The chromatin aggregates peripherally, under the nuclear membrane, into well-delimited dense masses of various shapes and sizes (Fig. 1-17) . The nucleus itself may break up, producing two or more fragments.

Formation of cytoplasmic blebs and apoptotic bodies. The apoptotic cell first shows extensive surface blebbing, then undergoes fragmentation into a number of membrane-bound apoptotic bodies composed of cytoplasm and tightly packed organelles, with or without a nuclear fragment.

Phagocytosis of apoptotic cells or bodies by adjacent healthy cells, either parenchymal cells or macrophages. The apoptotic bodies are rapidly degraded within lysosomes, and the adjacent cells migrate or proliferate to replace the space occupied by the now deleted apoptotic cell.
Plasma membranes are thought to remain intact

Apoptosis is the endpoint of an energy-dependent cascade of molecular events, initiated by certain stimuli, and consisting of four separable but overlapping components

Signaling pathways that initiate apoptosis (TNF,FAS,INJURY,WITHDRAWAL OF GROWTH FACTORS)

Control and integration, in which intracellular positive and negative regulatory molecules inhibit, stimulate, or forestall apoptosis and thus determine the outcome (bcl PROTEINS ETC)

A common-execution phase consisting of the actual death program and accomplished largely by the caspase family of proteases

Removal of dead cells by phagocytosis


3. Morphological changes of apoptosis include –
a)Membrane blebs(PGI 02)
c)Nuclear fragmentation
d)Spindle formation
e)Cell swelling

Ans is A and C


4. Starting point of apoptosis for programme cell death is -(PGI 97)
a)Activation of endonuclease
b)Release of enzyme
c)Accumulation of calcium
d)Destruction by macrophages

Ans is A


5. One of the following is an apoptosis inhibitor gene

a) p53′      b) BcL-2          (SGPGI 04)
c) Rb        d) c-Myc


Ans is B

Control and Integration Stage of APOPTOSIS STAGE 2.
This is performed by specific proteins that connect death signals to the execution program. These proteins are important because their actions may result in either "commitment" (i.e., determination of the inevitability of cell death) or abortion of potentially lethal signals. The proteins involved in this regulation have clinical significance: by determining the life or death of cell communities involved in important biologic processes (such as the immune response or cancer), they can affect the outcomes of disease.
There are commonly two broad schemes for this stage, which are not mutually exclusive. One involves the direct transmission of signals by specific adapter proteins to the execution mechanism, as described for the Fas-Fas ligand model and target cell killing by cytotoxic T lymphocytes (see later). [46] [47] [48] The second involves members of the Bcl-2 family of proteins [49] which play major and ubiquitous roles in apoptotic regulation largely by regulating mitochondrial function. [50] As previously described (see Fig. 1-4 ), death agonists can generate signals that affect mitochondria in two ways (Fig. 1-21) :

Apoptotic signals result in mitochondrial permeability transitions. [50A] Formation of pores within the inner mitochondrial membrane results in reduction of membrane potential and mitochondrial swelling.

The signals also cause increased permeability of outer mitochondrial membranes, releasing an apoptotic trigger, cytochrome c, from mitochondria into the cytosol.  Cytochrome c is located between the inner and outer mitochondrial membranes and is an integral but soluble component of the respiratory pathway. Cytochrome c release precedes the morphologic changes of apoptosis, showing that it occurs early, consistent with a regulatory function


Several proteins regulate such mitochondrial permeability events, but the most important are members of the Bcl-2 family, detailed in Chapter 8 and involved in an important way in cancer formation. Bcl-2, the mammalian homolog of the anti-apoptotic ced-9 gene in C. elegans, is situated in the outer mitochondrial membrane, endoplasmic reticulum, and nuclear envelope. Its function is regulated by other family members. By selectively binding to Bcl-2, these related proteins can alter Bcl-2’s activities and either promote apoptosis (e.g., Bax, Bad) or inhibit the process (e.g., Bcl-XL). Bcl-2 suppresses apoptosis in two ways: by direct action on mitochondria to prevent increased permeability, and by effects mediated by interactions with other proteins. Indeed, it is thought that mitochondrial permeability is determined by the ratio of pro-apoptotic and anti-apoptotic members of the Bcl-2 family in the membrane. [49] [50]
In certain cells Bcl-2 can also suppress apoptosis by serving as a docking protein, binding proteins from the cytosol and sequestering them on the mitochondrial membrane (Fig. 1-21) . Protein binding may modulate the function of Bcl-2 itself or target the docked protein for interaction with other proteins. Notable among these Bcl-2-binding proteins is the pro-apoptotic protease activating factor (Apaf-1), the mammalian homolog of the nematode gene ced-4. [53] [54] This protein also associates with inactive zymogen forms of certain initiator caspases (e.g., caspase 9), so called to distinguish them from the execution caspases described later. It is speculated that when cytochrome c is released from mitochondria by death signals, it binds Apaf-1 and activates it, triggering an initiator caspase and setting in motion the proteolytic events that kill the cell (Fig. 1-21) . In this scenario, Bcl-2 binding protects because it sequesters Apaf-1 and inhibits its catalytic caspase-triggering function, even if cytochrome c has leaked out of mitochondria.

The two scenarios for the anti-apoptotic actions of Bcl-2, that is, to directly prevent cytochrome c release and to inhibit Apaf-1-induced caspase activation despite cytochrome c release, are not mutually exclusive. [52] Other important proteins are also involved in apoptotic regulation. These include the p53 protein and certain mammalian homolog of viral protease inhibitor proteins.



6.The process of programmed gene directed celldeath characterized by cell-shrinkage, nuclearcondensation and fragmentation is known as –

a) Necrosis b) Chromatolysis
c) Pyknosis d) Apoptosis

Ans is D


7. Internucleosomal Cleavage of DNA is characteristicof-(AIIMS NOV 05)
a)Reversible cell injury
b)Irreversible cell injury

Ans is D

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