Review of Critical Care Medicine

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Dermatology (Skin) MCQs

Posted by Dr KAMAL DEEP on December 26, 2011

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Skin is the largest organ in the body. In a 70-kg individual, the skin weighs over 5 kg and covers a surface area approaching 2 m2. Human skin consists of a stratifi ed, cellular epidermis and an underlying dermis of connective tissue.Beneath the dermis is a layer of subcutaneous fat, which is separated from the rest of the body by a vestigial layer of striated muscle. The epidermis is mainly composed of keratinocytes and is typically 0.05–0.1 mm in thickness. It is formed by division of cells in the basal layer which give rise to the spinous layer. This layer contains cells that move outwards and progressively differentiate, forming the granular layer and the stratum corneum. The cellular progression from the basal layer to the skin surface takes about 30 days but is accelerated in diseases such as psoriasis. The ‘bricklike’ shape of keratinocytes is provided by a cytoskeleton made of keratin intermediate fi laments. As the epidermis differentiates, the keratinocytes become fl attened. This process involves the fi lament aggregating protein, filaggrin, a protein component of keratohyalin granules. Indeed, keratin and fi laggrin comprise 80–90% of the mass of the epidermis. The outermost layer of the epidermis is the stratum corneum, where cells (now called corneocytes) have lost nuclei and cytoplasmic organelles. The corneocyte has a highly insoluble, cornified envelope within the plasma membrane, formed by cross-linking of soluble protein precursors, including involucrin and loricrin, the latter contributing 70–85% to the mass of the cornifi ed cell envelope; it also contains several lipids (fatty acids, sterols and ceramides) released from lamellar bodies within the upper, living epidermis. Other cells in the epidermis are the melanocytes, Langerhans’ cells and Merkel cells. Melanocytes are dendritic cells that distribute packages of melanin pigment in melanosomes to surrounding keratinocytes to give skin its colour. The number of melanocytes does not differ much between white and black skin. Rather it is the nature of the melanin and the size of the melanosomes that account for the different appearances. The Langerhans’ cells are also dendritic in nature, although these are of mesenchymal origin and originate from bone marrow. Langerhans’ cells are antigen-presenting cells and process antigens encountered by the skin to local lymph nodes and thus have a key role in adaptive immune responses in the skin. Merkel cells are probably derived from keratinocytes. They have a role as mechanosensory receptors in response to touch. Human skin contains pilosebaceous follicles and sweat glands. The hair follicles comprise pockets of epithelium that are continuous with the superficial epidermis but which also envelop a small papilla of dermis at their base. A bundle of smooth muscle, the arrector pili, extends at an angle between the surface of the dermis and a point in the follicle wall. Above the insertion, there are holocrine sebaceous glands which open into the pilary canal. In some sites, such as the axillae, the follicles may be associated with apocrine glands. Also derived from the epidermis and opening directly to the skin surface are the eccrine sweat glands. The epidermis is attached to the dermis via a complex network of proteins and glycoproteins that extend from inside basal keratinocytes into the superficial dermis. Besides adhesion, the dermal–epidermal junction components also contribute to cell migration (for example during wound healing) as well as epithelial– mesenchymal signalling events. Over 30 different macromolecules (collagens, laminins, integrins) interact within a basement membrane zone that is less than 200 μm across. The dermis is a supporting matrix or ground substance in which polysaccharides and proteins are linked to produce macromolecules that have a remarkable capacity for retaining water. The thickness of the dermis varies from less than 0.5 mm to more than 5 mm. There are two principal types of protein fibre: collagen and elastic tissue. Collagen is the major extracellular matrix protein comprising 80–85% of the dry weight of the dermis. Twenty-nine different collagens have been identified in vertebrate tissue (depicted by Roman numerals in the order of their discovery, from I to XXIX), of which at least 12 are expressed in skin. The main interstitial dermal collagens are types I and III whereas the principal basement membrane collagen (at the dermal–epidermal junction and around dermal blood vessels, nerves and appendages) is type IV collagen. Triple-helical collagen monomers polymerize into fibrils and fibres, which then become stabilized by the complex formation of both intra- and intermolecular crosslinks. Collagen fibres are extremely tough and provide skin with its tensile strength. Elastic fibres account for no more than 2–4% of the extracellular matrix in the dermis and consist of two components, elastin and elastin-associated microfibrils, which together give skin its elasticity and resilience. Elastic microfibrils are composed of several proteins, including fibrillin, which surround the elastin and which can extend throughout the dermis in a web-like configuration to the junction between the dermis and the epidermis. The dermis also contains a number of non-collagenous glycoproteins including fibronectins, fibulins and integrins. These extracellular matrix components facilitate cell adhesion and cell motility. Between the dermal collagen and elastic tissue is the ground substance made up of glycosaminoglycan/proteoglycan macromolecules. These contribute only 0.1–0.3% of the total dry weight of the dermis but provide a vital role by maintaining hydration, mostly due to the high water-binding capacity of hyaluronic acid. About 60% of the total weight of the dermis is water. The dermis has a very rich blood supply, although no vessels pass through the dermal–epidermal junction. There is a superficial and a deep vascular plexus. The motor innervation of the skin is autonomic, and includes a cholinergic component to the eccrine sweat glands and adrenergic components to both the eccrine and apocrine glands, to the smooth muscle and the arterioles and to the arrector pili muscle. The sensory nerve endings are of several kinds; some are free, some terminate in hair follicles and others have expanded tips.

Human sweat glands are generally divided into two types: apocrine and eccrine.

The eccrine gland is the primary gland responsible for thermoregulatory sweating in humans. Eccrine sweat glands are distributed over nearly the entire body surface.Acetylcholine is the primary neurotransmitter released from cholinergic sudomotor nerves and binds to muscarinic receptors on the eccrine sweat gland, although sweating can also occur via exogenous administration of α- or β-adrenergic agonists.

Mental or emotional sweating usually appears on the palms and soles.

Apart from eccrine glands, the skin also contains apocrine sweat glands. Eccrine glands do not show cytological changes during secretion whereas apocrine glands are characterized by decapitation secretion, in which part of the cell is pinched off and released into the lumen. Apocrine glands are located only in genital,axillary and mammary areas, where they are always connected to a hair follicle. Apocrine glands have a low secretory output, and hence no significant role in thermoregulation.

A flat discolouration on skin  1 cm is called
a) Macule b) Plaque c) Boil d) Papule e) Wheal

Table 51-1 Description of Primary Skin Lesions


Macule: A flat, colored lesion, <2 cm in diameter, not raised above the surface of the surrounding skin. A "freckle," or ephelid, is a prototype pigmented macule.
Patch: A large (>2 cm) flat lesion with a color different from the surrounding skin. This differs from a macule only in size.
Papule: A small, solid lesion, <0.5 cm in diameter, raised above the surface of the surrounding skin and, hence, palpable (e.g., a closed comedone, or whitehead, in acne).
Nodule: A larger (0.5–5.0 cm), firm lesion raised above the surface of the surrounding skin. This differs from a papule only in size (e.g., a dermal nevomelanocytic nevus).
Tumor: A solid, raised growth >5 cm in diameter.
Plaque: A large (>1 cm), flat-topped, raised lesion; edges may either be distinct (e.g., in psoriasis) or gradually blend with surrounding skin (e.g., in eczematous dermatitis).
Vesicle: A small, fluid-filled lesion, <0.5 cm in diameter, raised above the plane of surrounding skin. Fluid is often visible, and the lesions are translucent [e.g., vesicles in allergic contact dermatitis caused by Toxicodendron (poison ivy)].
Pustule: A vesicle filled with leukocytes. Note: The presence of pustules does not necessarily signify the existence of an infection.
Bulla: A fluid-filled, raised, often translucent lesion >0.5 cm in diameter.
Wheal: A raised, erythematous, edematous papule or plaque, usually representing short-lived vasodilatation and vasopermeability.
Telangiectasia: A dilated, superficial blood vessel.

Fluid filled in epidermis and dermis is called
a) Wheal b) Macule c) Papule d) Vesicle

A vesicle is a circumscribed, elevated lesion that contains fluid . Often the vesicle walls are so thin that they are translucent and the serum, lymph, blood, or extracellular fluid is visible. A vesicle with a diameter greater than 0.5 cm is a bulla. Vesicles and bullae arise from cleavage at various levels of the skin; the cleavage may be within the epidermis (i.e., intraepidermal vesication), or at or below the dermal-epidermal interface (i.e., subepidermal). Cleavage just beneath the stratum corneum produces a subcorneal vesicle or bulla , as in impetigo. Intraepidermal vesication may result from intercellular edema (spongiosis), as characteristically seen in delayed hypersensitivity reactions of the epidermis (e.g., in contact eczematous dermatitis) and in pompholyx. Loss of intercellular bridges, or desmosomes, is known as acantholysis, and this type of intraepidermal vesication  is seen in pemphigus vulgaris, where the cleavage is usually just above the basal layer. In pemphigus foliaceus, the cleavage occurs just below the subcorneal layer. Viruses cause a curious “ballooning degeneration” of epidermal cells , as in herpes zoster, herpes simplex, variola, and varicella. Viral bullae often have a depressed (“umbilicated”) center. Pathologic changes at the dermal-epidermal junction may lead to subepidermal vesicles and bullae , as are seen in pemphigoid, bullous erythema multiforme, porphyria cutanea tarda, dermatitis herpetiformis, and some forms of epidermolysis bullosa. The thickness of the wall of a bulla may be estimated by its translucency and flaccidity. The amount of pressure required to collapse the lesion may help predict whether the bulla is intraepidermal or subepidermal. It has been said that a relatively large, tense bulla suggests pemphigoid, whereas a flaccid bulla suggests pemphigus. There is, however, no reliable means of distinguishing these two diseases except by histologic examination of the lesion and immunofluorescence.

A 7yr. old child presenting with recurrent dry scaly macules (white, small) on face has
a) Indeterminate Leprosy b) Post dermal leishmaniasis
c) Pitryasis alba d) Early vitiligo

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                                                                                                                        Pityriasis alba

Pityriasis alba is a common finding (5% of children) that is probably more usual in patients with the atopic diathesis .The condition appears in most instances before puberty. The face, neck, and arms are the most common sites. The lesions begin as a nonspecific erythema and gradually become scaly and hypopigmented. The hypopigmentation is transient and caused by mild dermal inflammation and the UV screening effect of the scaly skin. The condition gradually improves after puberty. Treatment consists of lubrication. Mild inflammation responds to group V topical steroids, but the degree of pigmentation is not affected by any treatment.
The condition is often confused with vitiligo and tinea versicolor. Vitiligo does not scale. The potassium hydroxide preparation is positive in tinea versicolor.
The age incidence, the fine scaling and the distribution of the lesions usually suggest the diagnosis. Conspicuous hypopigmentation may lead to a misdiagnosis of vitiligo. Naevus de pigmentosus most commonly presents at birth or before 3 years of age, and most often causes single, well-marginated lesions on the trunk .However, this condition may be difficult to distinguish from pityriasis alba when it occurs on the face and in cases of later onset. Discoid eczema in an atopic child is intensely pruritic, and the lesions are larger and more oedematous. In older children and adults, the lesions on the trunk, during their early erythematous phase, may be mistaken for psoriasis but the distribution and the relatively mild scaling should exclude this diagnosis. Mycosis fungoides, although relatively rare, may present with lesions clinically resembling pityriasis alba .This condition may also be difficult to distinguish histologically, so follow-up and repeat biopsy are sometimes required.

The test likely to help in diagnosis of a patient who presents with an itchy annular plaque on the face is:
A.Gram’s stain
B.Potassium hydroxide mount
C Tissue smear
D. Wood’s lamp examination

Woods lamp has a frequency of TN 04
a) 250 nm b) 300 nm c) 320 nm d) 360

The UV spectrum reaching the earth represents <10% of total incident solar energy and is arbitrarily divided into two major segments, UV-B and UV-A, constituting the wavelengths from 290–400 nm. UV-B consists of wavelengths between 290 and 320 nm. This portion of the photobiologic action spectrum is the most efficient in producing redness or erythema in human skin and hence sometimes is known as the "sunburn spectrum." UV-A includes wavelengths between 320 and 400 nm and is ~1000-fold less efficient in producing skin redness than is UV-B.

The wavelengths between 400 and 700 nm are visible to the human eye. The photon energy in the visible spectrum is not capable of damaging human skin in the absence of a photosensitizing chemical.

Uses of woods light includes
a) Urine examination in phorphyria b) examination of hair in T. capitis c) Sclerema d) all

A Wood’s lamp generates 360-nm ultraviolet (or "black") light that can be used to aid the evaluation of certain skin disorders. For example,

1. A Wood’s lamp will cause erythrasma (a superficial, intertriginous infection caused by Corynebacterium minutissimum) to show a characteristic coral pink color,

2. Wounds colonized by Pseudomonas to appear pale blue.

3. Tinea capitis caused by certain dermatophytes such as Microsporum canis or M. audouini exhibits a yellow fluorescence. Pigmented lesions of the epidermis such as freckles are accentuated, while dermal pigment such as postinflammatory hyperpigmentation fades under a Wood’s light.

4.Vitiligo appears totally white under a Wood’s lamp, and previously unsuspected areas of involvement often become apparent.

5.A Wood’s lamp may also aid in the demonstration of tinea versicolor and in recognition of ash leaf spots in patients with tuberous sclerosis.

A pinkish red fluorescence of urine with wood’s Lamp is seen in
a) Lead poisoning b) Porphyria cutanea tarda c) Erythromelagia d) Acrocyanosis

The wood’s lamp filter is made of AIIMS 79, PGI 80
a) Tin and chromium oxide b) Nickel oxide and silica c) Copper oxide Barium
oxide d) Zinc oxide

Coral red-fluorescence wood’s Lamp seen in

a) Porphyria cutanea tarda b) Erythrasma Livedo-reticularis
d) Hypomelanosis

Wood’s lamp (longwave ultraviolet light, “black” light) is essential for the clinical diagnosis of certain skin and hair diseases and of porphyria. Longwave ultraviolet radiation is obtained by fitting a high-pressure mercury lamp with a specially compounded filter made of nickel oxide and silica (Wood’s filter); this filter is opaque to all light except for a band between 320 and 400 nm. When using the Wood’s lamp, it is essential for the examiner to become dark-adapted in order to see the contrasts clearly. When the ultraviolet waves emitted by Wood’s lamp impinge on the skin, a visible fluorescence occurs. Wood’s lamp is particularly useful in the detection of the fluorescence of dermatophytosis ( Microsporum) in the hair shaft (green) and of erythrasma (coral red) on the skin. Wood’s lamp also helps to estimate the variation in the “whiteness” of lesions in relation to the normal skin color, in dark-skinned and especially in fair-skinned persons; for example, the lesions seen in hypomelanotic macules in tuberous sclerosis and in tinea versicolor are not as white as the macules present in vitiligo, which are typically amelanotic. Circumscribed hypermelanosis, such as ephelides and melasma, is much more evident under Wood’s lamp, and in lentigo maligna melanoma and acrolentiginous melanoma the Wood’s lamp can be used to detect the total extent of the lesion as a guide to total excision. Melanin in the dermis, as in a Mongolian sacral spot, does not become accentuated under Wood’s lamp. Therefore, it is possible to localize the site of melanin (epidermal or dermal) by use of the Wood’s lamp; this phenomenon is not evident in patients with brown or black skin. The technique is as follows: a grading (minimal, moderate, marked) of the degree of pigmentation is made with visible light and compared with a grading of the degree of color change when examined with Wood’s lamp. In epidermal melanin pigmentation the pigment grade increases from minimal to marked, but dermal melanin has the same degree of pigment in both visible light and Wood’s lamp illumination.

Patients with PCT excrete increased amounts of porphyrins in the urine, which rarely may exhibit characteristic pink-red fluorescence when examined with a Wood’s lamp.

Commonest site of Atopic dermatitis is
a) Scalp b) Elbow c) Trunk d) Ante cubital fossa

Atopic dermatitis can be best diagnosed by
a) Clinical evaluation b) Patch test c) IgE levei d)Skin Biopsy

‘Itch is the disease’ is true for

a) Atopic dermatitis b) Insect bites c) Seborrheic dermatitis d)Tinea cruris

Kaposis variceliform eruption PGI 2004
a) Atopic dermatitis b) Dermatitis herpetiformis
c) Lymphoma d) All

 

Kaposi varicelliform eruption (KVE) is the name given to a distinct cutaneous eruption caused by herpes simplex virus (HSV) type 1, HSV-2, coxsackievirus A16, or vaccinia virus that infects a preexisting dermatosis. Most commonly, it is caused by a disseminated HSV infection in patients with atopic dermatitis (AD) and, for this reason, is often referred to as eczema herpeticum (EH).

Kaposi varicelliform eruption (KVE) is caused primarily by HSV-1, but can also be caused by HSV-2, coxsackievirus A16, or vaccinia virus infecting a preexisting dermatosis. Most commonly, it is caused by a disseminated HSV infection in patients with AD. For this reason, it is also referred to as EH.

KVE has also been associated with the following:

  • Pityriasis rubra pilaris

  • Neurodermatitis

  • Irritant contact dermatitis

  • Congenital ichthyosiform erythroderma

  • Ichthyosis vulgaris

  • Pemphigus foliaceus

  • Benign familial pemphigus (Hailey-Hailey disease)

  • Darier disease

  • Wiskott-Aldrich syndrome

  • Sézary syndrome

  • Seborrheic dermatitis

  • Skin grafts

  • Burns

  • Cowpox

  • Cutaneous T-cell lymphomas

  • Rosacea

    A 25 — year old presents with recurrent episodes of flexural eczema, contact urticaria, recurrent skin infections and severe abdominal cramps and diarrhea upon taking sea foods. He is suffering from All India 04
    a) Seborrheic dermatitis
    b) Atopic dermatitis
    c) Airborne contact dermatitis d) Nummular dermatitis

    Personal history of food allergy makes diagnosis of atopy more than contact dermatitis.

     

    Air-borne contact dermatitis can be diagnosed by:
    a) Skin biopsy. b) Patch test. c) Prick test. d) Estimation of serum IgE levels

    Contact dermatitis is a type of Hypersensitivity
    a) Type I b) Type II c) Type III d) Type IV

    Berloque dermatitis is due to contact with: a) Metals b) Cosmetics c) Food d) Plants

    Commonest cause of air borne contact dematitis is
    a) Crysanthemum b) Parthenium c) Calotropis d) Bourgainvilia

    Type I hypersensitivity is characterized by an allergic reaction occurring immediately following an individual’s second contact with the responsible antigen (the allergen). Upon initial exposure to a soluble allergen, B cells are stimulated to differentiate into plasma cells and produce specific IgE with the help of T cells (figure 33.2). This IgE is sometimes called a reagin, and the individual has a hereditary predisposition for its production. Once synthesized, IgE binds to the Fc receptors of mast cells (basophils and eosinophils can also be activated) and sensitizes these cells, making the individual allergic to the allergen. When a second exposure to the allergen occurs, the allergen attaches to the surfacebound IgE on the sensitized mast cells causing degranulation. Degranulation releases physiological mediators such as histamine, leukotrienes, heparin, prostaglandins, PAF (platelet-activation factor), ECF-A (eosinophil chemotactic factor of anaphylaxis), and proteolytic enzymes. These mediators trigger smooth muscle contractions, vasodilation, increased vascular permeability, and mucous secretion. The inclusive term for these responses is anaphylaxis [Greek ana, up, back, again; and phylaxis, protection]. Anaphylaxis can be divided into systemic and localized reactions. Systemic anaphylaxis is a generalized response that occurs when an individual sensitized to an allergen receives a subsequent exposure to it. The reaction is immediate due to the large amount of mast cell mediators released over a short period. Usually there is respiratory impairment caused by smooth muscle constriction in the bronchioles. The arterioles dilate, which greatly reduces arterial blood pressure and increases capillary permeability with rapid loss of fluid into the tissue spaces. Because of these reactions the individual can die within a few minutes from reduced venous return, asphyxiation, reduced blood pressure, and circulatory shock. Common examples of allergens that can produce systemic anaphylaxis include drugs (penicillin), passively administered antisera, peanuts, and insect venom from the stings or bites of wasps, hornets, or bees (figure 33.3). Localized anaphylaxis is called an atopic (“out of place”) allergy. The symptoms that develop depend primarily on the route by which the allergen enters the body. Hay fever (allergic rhinitis) is a good example of an atopic allergy involving the upper respiratory tract. Initial exposure involves airborne allergens—such as plant pollen, fungal spores, animal dander, and house dust mites—that sensitize mast cells located within the mucous membranes. Reexposure to the allergen causes the typical localized anaphylactic response.

    Once the responsible allergen has been identified, the individual should avoid contact with it. At times this is not possible, and desensitization is warranted. This procedure consists of a series of allergen doses injected beneath the skin to stimulate the production of IgG antibodies rather than IgE antibodies. The circulating IgG antibodies can then act as blocking antibodies to intercept and neutralize allergens before they have time to react with mast cell-bound IgE. Recent evidence suggests that suppressor T-cell activity also may cause a decrease in IgE synthesis. Desensitizations are about 65 to 75% effective in individuals whose allergies are caused by inhaled allergens

    Type II hypersensitivity is generally called a cytolytic or cytotoxic reaction because it results in the destruction of host cells either by lysis or toxic mediators. In type II hypersensitivity, IgG or IgM antibodies are directed against cell surface or tissue-associated antigens. They usually stimulate the complement pathway and a variety of effector cells (figure 33.5). The antibodies interact with complement (Clq) and the effector cells through their Fc regions. The damage mechanisms are a reflection of the normal physiological processes involved in interaction of the immune system with pathogens. A classic example of type II hypersensitivity is that resulting when a person receives a transfusion with blood from a donor with a different blood group.

     

    Type III hypersensitivity involves the formation of immune complexes (figure 33.6a). Normally these complexes are removed effectively by the fixed monocytes and macrophages of the monocyte-macrophage system. In the presence of excess amounts of some soluble antigens, the antigen-antibody complexes may not be efficiently removed. Their accumulation can lead to a hypersensitivity reaction from complement that triggers a variety of inflammatory processes. This inflammation causes damage, especially of blood vessels (vasculitis; figure 33.6b), kidney glomerular basement membranes (glomerulonephritis), joints (arthritis), and skin. Diseases resulting from type III reactions can be placed into three groups. First, a persistent viral, bacterial, or protozoan infection, together with a weak antibody response, leads to chronic immune complex formation and eventual deposition of the complex in host tissues. Second, the continued production of autoantibody to self-antigen during an autoimmune disease can lead to prolonged immune complex formation. This overloads the monocyte-macrophage system, and tissue deposition of the complexes occurs (e.g., in the disease systemic lupus erythematosus). Third, immune complexes can form at body surfaces (such as the lungs), following repeated inhalation of allergens from molds, plants, or animals. For example, in Farmer’s lung disease, an individual has circulating antibodies to fungi after being exposed repeatedly to moldy hay. These antibodies are primarily IgG. When the allergens (fungal spores) enter the alveoli of the lungs, local immune complexes form, leading to inflammation. Some group A streptococcal infections can produce an immunologically mediated acute glomerulonephritis. Although the mechanism is not completely understood, it is believed that complexes of antibody and streptococcal antigen are deposited within the kidney glomeruli and generate a type III hypersensitivity.

    Type IV hypersensitivity involves delayed T-cell-mediated immune reactions. A major factor in the type IV reaction is the time required for a special subset of TH1 cells (often called delayedtype hypersensitivity [TDTH] cells) to migrate to and accumulate near the antigens. This usually takes a day or more. Type IV reactions occur when antigens, especially those binding to tissue cells, are phagocytosed by macrophages and then presented to receptors on the TH1 cell surface in the context of class I MHC. Contact between the antigen and TH1 cell causes the cell to proliferate and release cytokines. Cytokines attract lymphocytes, macrophages, and basophils to the affected tissue. Extensive tissue damage may result. Examples of type IV hypersensitivities include tuberculin hypersensitivity (the TB skin test), allergic contact dermatitis, some autoimmune diseases, transplantation rejection, and killing of cancer cells. In tuberculin hypersensitivity a partially purified protein called tuberculin, which is obtained from the bacillus that causes tuberculosis (Mycobacterium tuberculosis; see section 39.1), is injected into the skin of the forearm (figure 33.7a). The response in a tuberculin-positive individual begins in about 8 hours, and a reddened area surrounding the injection site becomes indurated (firm and hard) within 12 to 24 hours. The TH1 cells that migrated into the injection site are responsible for the induration. The reaction reaches its peak in 48 hours and then subsides. The size of the induration is directly related to the amount of antigen that was introduced and to the degree of hypersensitivity of the tested individual. Other microbial products used in type IV skin testing are histoplasmin for histoplasmosis, coccidioidin for coccidioidomycosis, lepromin for leprosy, and brucellergen for brucellosis. Allergic contact dermatitis is caused by haptens (see figure 32.4) that combine with proteins in the skin to form the allergen that elicits the immune response. The haptens are the antigenic determinants, and the skin proteins are the carrier molecules for the haptens. Examples of these haptens include cosmetics, plant materials (catechol molecules from poison ivy and poison oak; figure 33.7b), topical chemotherapeutic agents, metals, and jewelry (especially jewelry containing nickel). Several important chronic diseases involve cell and tissue destruction by type IV hypersensitivity reactions. These diseases are caused by viruses, mycobacteria, protozoa, and fungi that produce chronic infections in which the macrophages and T cells are continually stimulated. Examples are leprosy, tuberculosis, leishmaniasis, candidiasis, and herpes simplex lesions.

  • The name sandworm eruption refers to Kerala 04
    a) Cercarial dermatitis
    b) Creeping eruption
    c) Migratory myiasis d) Guinea worm disease

  • Cutaneous larva migrans (abbreviated CLM) is a skin disease in humans, caused by the larvae of various nematode parasites of the hookworm family (Ancylostomatidae). The most common species causing this disease in the Americas is Ancylostoma braziliense.

    Colloquially called creeping eruption due to the way it looks, the disease is also somewhat ambiguously known as "ground itch" or (in some parts of the Southern USA) "sandworms", as the larvae like to live in sandy soil. Another vernacular name is plumber’s itch. The medical term CLM literally means "wandering larvae in the skin.

     

    PSORIASIS

  • Formation of spongiform microabscesses (Munro microabscesses) filled with granulocytes is a hallmark of psoriasis. The presence of these cells in psoriatic lesions is variable and becomes more pronounced with disease activity, e.g., in acute guttate or pustular psoriasis. Ultramicroscopically, degranulation is absent in these cells; instead, they appear to remain intact while migrating in response to chemotactic stimuli [CTCL:- The classic findings are characterized by finding lymphocytes with hyperchromatic and hyperconvoluted nuclei that cluster in the epidermis in microabscesses (Pautrier type)]

  • The treatment of choice for erythrodermic psoriasis is : SGPG I 04
    a) Corticosteroids b) Methotrexate c) Coaltar topically d) Topical corticosteroids

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    Koebners phenomenon is seen in a) Lichen planus b) Psoriasis c) Icthyosis d) Pitriasis rubra e) Phemphigus

    Which of the following is pruritic
    a) Lichen planus b) Psoriasis c) Icthyosis d) secondary syphilis

    Photochemotherapy is used in A189
    a) Psoriasis b) Phemphigus c) Tinea capitis d) Tinea cruris

    All are common of psoriasis except a) Nail changes b) Extensor distribution c) Arthritis d) Squamo erythematous lesions

    Psoriasis is characterised by all except a) Definite pink plaque with clear margin c) Always associated with nail infection b) In children disappears in 2 weeks to reappear again d) Involves knees and elbows

    Non-cicatrical alopecia is present in TN 90
    Scieroderma b) Lichen planus c) Psoriasis d) parvo virus

    Psoralen with UV-A is used for treating a) Porphyria b) Psoriasis c) Pemphigus d) tinea versicolor

    Psoriasis is exacerbated by
    a) Lithium b) B-Blockers c) Antimalarials d) All of the above

    The important feature of psoriasis is a) Crusting b) Scaling c) Oozing d) Erythema

    Vitamin D analogue calcitriol is useful in the treatment of
    a) Lichen planus b) Psoriasis c) Pemphigus d) Leprosy

    Kobner’s phenomenon is seen in all the following PGI -04
    a. Lichen planus b. Herpes simplex c. Human papilloma virus infection
    d. Psoriasis e. All the above

    The Koebner (isomorphic) phenomenon refers to the fact that in persons with certain skin diseases, especially psoriasis, trauma is followed by new lesions in the traumatized but otherwise normal skin, and these new lesions are identical to those in the diseased skin.The Koebner reaction occurs in traumatized normal skin in vitiligo, psoriasis, and lichen planus, among other conditions. The Koebner phenomenon may occur in recent scars or at pressure points.

    Which of the following are causes for Erythroderma? PGI-05
    a. Psoriasis b. Lichen planus c. Eczema
    d. Pityriasis rubra pilaris e. Pityriasis versicoior

    Erythroderma is the term applied to any infl ammatory skin disease that affects more than 90% of the body surface. The term exfoliative dermatitis is used synonymously, although the degree of exfoliation is sometimes quite mild.

    image

    A wide range of drugs can cause erythroderma. Among the more commonly implicated are pyrazalone derivatives such as phenylbutazone, hydantoin derivatives, carbamazepine, cimetidine, gold salts and lithium.

    Pityriasis rubra pilaris (PRP) refers to a group of chronic disorders characterized by reddish orange, scaling plaques and keratotic follicular papules

    Treatment of Pustular psoriasis is: MAHA-05
    a. Thalidomide b. Retinoids c. Hydroxyurea d. Metholtrexate

    Koebners phenomenon is seen in a) Lichen planus b) Psoriasis c) Icthyosis d) Pitriasis rubra e) Phemphigus

    Causes of Cicatricial alopecia are PGI-04
    a. Disseminated lupus erythramatosis b. Alopecia areata c. Psoriasis
    d. Lichen planus e. Androgenic alopecia

    Bulkeley membrane is seen in; DNB 89, PGI 89
    a) Psoriasis b) Pemphigus c) Tinea d) Pityriasis rubra

    IN PSORIASIS WHEN THE SCALES ARE COMPLETELY SCRAPED OFF ,THE BASEMENT MEMBRANE IS EXPOSED & SEEN AS A MOIST RED SURFACE (BULKELEY’S MEMBRANE )THROUGH WHICH DILATED CAPILLARIES CAN BE SEEN AS RED SPOTS WORONOFF’S RING – PERILESIONAL HALO IN PSORIATIC PLAQUES USUALLY AFTER TREATMENT WITH UV LIGHT.DUE TO DEFICIENCY OF PG E2. GRATTAGE TEST -POSITIVE IN PSORIASIS,ALSO CANDLE WAX SIGN PRESENT.

    Antibody Brand name Approval date Type Target Indication
    (What it’s approved to treat)
    Example FDA approved therapeutic monoclonal antibodies[1]
    Abciximab ReoPro 1994 chimeric inhibition of glycoprotein IIb/IIIa Cardiovascular disease
    Adalimumab Humira 2002 human inhibition of TNF-α signaling Several auto-immune disorders
    Alemtuzumab Campath 2001 humanized CD52 Chronic lymphocytic leukemia
    Basiliximab Simulect 1998 chimeric IL-2Rα receptor (CD25) Transplant rejection
    Belimumab Benlysta 2011 human inihibition of B- cell activating factor SLE[disambiguation needed ]
    Bevacizumab Avastin 2004 humanized Vascular endothelial growth factor (VEGF) Colorectal cancer, Age related macular degeneration (off-label)
    Brentuximab vedotin Adcetris 2011 Chimeric CD30 Anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma
    Canakinumab Ilaris 2009 Human IL-1β Cryopyrin-associated periodic syndromes (CAPS)
    Cetuximab Erbitux 2004 chimeric epidermal growth factor receptor Colorectal cancer, Head and neck cancer
    Certolizumab pegol[19] Cimzia 2008 humanized inhibition of TNF-α signaling Crohn’s disease
    Daclizumab Zenapax 1997 humanized IL-2Rα receptor (CD25) Transplant rejection
    Denosumab Prolia , Xgeva 2010 Human RANK Ligand inhibitor Postmenopausal osteoporosis , Solid tumor`s bony metasteses
    Eculizumab Soliris 2007 humanized Complement system protein C5 Paroxysmal nocturnal hemoglobinuria
    Efalizumab Raptiva 2002 humanized CD11a Psoriasis
    Gemtuzumab Mylotarg 2000 humanized CD33 Acute myelogenous leukemia (with calicheamicin)
    Golimumab Simponi 2009 Human TNF-alpha inihibitor Rheumatoid arthritis, Psoriatic arthritis, and Ankylosing spondylitis
    Ibritumomab tiuxetan Zevalin 2002 murine CD20 Non-Hodgkin lymphoma (with yttrium-90 or indium-111)
    Infliximab Remicade 1998 chimeric inhibition of TNF-α signaling Several autoimmune disorders
    Ipilimumab ( MDX-101 ) Yervoy 2011 Human blocks CTLA-4 Melanoma
    Muromonab-CD3 Orthoclone OKT3 1986 murine T cell CD3 Receptor Transplant rejection
    Natalizumab Tysabri 2006 humanized alpha-4 (α4) integrin, Multiple sclerosis and Crohn’s disease
    Ofatumumab Arzerra 2009 Human CD20 Chronic lymphocytic leukemia
    Omalizumab Xolair 2004 humanized immunoglobulin E (IgE) mainly allergy-related asthma
    Palivizumab Synagis 1998 humanized an epitope of the RSV F protein Respiratory Syncytial Virus
    Panitumumab Vectibix 2006 human epidermal growth factor receptor Colorectal cancer
    Ranibizumab Lucentis 2006 humanized Vascular endothelial growth factor A (VEGF-A) Macular degeneration
    Rituximab Rituxan, Mabthera 1997 chimeric CD20 Non-Hodgkin lymphoma
    Tocilizumab ( or Atlizumab ) Actemra and RoActemra 2010 Humanised Anti- IL-6R Rheumatoid arthritis
    Tositumomab Bexxar 2003 murine CD20 Non-Hodgkin lymphoma
    Trastuzumab Herceptin 1998 humanized ErbB2 Breast cancer

     

    In addition to chimeric and humanized antibodies, there are other pharmaceutical purposes for the creation of chimeric constructs

    Etanercept:-. Etanercept, for example, is a TNFα blocker created through the combination of a tumor necrosis factor receptor (TNFR) with the immunoglobulin G1 Fc segment. TNFR provides specificity for the drug target and the antibody Fc segment is believed to add stability and deliverability of the drug.

    Alefacept:- Alefacept is a fusion protein: it combines part of an antibody with a protein that blocks the growth of some types of T cells.The exact mode of action is very complicated and involves dual mechanisms, one of which inhibits the activation of CD4+ and CD8+ T cells by interfering with CD2 on the T cell membrane thereby blocking the costimulatory molecule LFA-3/CD2 interaction. The second mechanism is inducing apoptosis of memory-effector T lymphocytes. If the T cells were to become activated they would stimulate proliferation of keratinocytes resulting in the typical psoriatic symptoms. Therefore, alefacept leads to clinical improvement of moderate to severe psoriasis by blunting these reactions.Combinations of therapeutic modalities have been utilized to meet the challenge of difficult to treat psoriasis.

    Pitting of nails is seen in PGI88
    a) Lichen planus b) Psoriasis c) Phemphigus d) Arsenic poisoning a) Leprosy

    Nail Involvement is not a feature of (UNSOLVED)?
    a) Dermatophytosis b) lichen planus c) DLE d) psoriasis

    Pterygium of nail is characteristically seen in: All India 2006
    a) Lichen planus. b) Psoriasis. c) Tinea unguium, d) Alopecia areata

    Tinea ungium effects
    A.Nail fold
    B.Nail plate
    C.Joints
    D.Inter digital space

    ONYCHOMYCOSIS
    Onychomycosis denotes any infection of the nail caused by dermatophyte fungi, nondermatophyte fungi, or yeasts. Tinea unguium, however, refers strictly to dermatophyte infection of the nail plate. The four clinical types of onychomycosis are: (1) distal subungual onychomycosis (DSO), (2) proximal subungual onychomycosis (PSO), (3) white superficial onychomycosis (WSO), and (4) candidal onychomycosis

    Least common site involvement in psoriasis is
    (A)Scalp
    (B)Nail involvement
    (C)CNS involvement
    (D)Arthritis

    Which of the following is wrong statements :
    (A)Koilonychia in Vit B12 deficiency
    (B)Oncholysis in Psoriasis
    (C)Mees lines in Arsenic poisoning
    (D)Pterygium of nails in Lichen Planus

    Griesofulvin is given for the treatment of fungal infection in finger nail dermatophytosis for :
    A.4 weeks
    B.6 weeks
    C.2 month
    D.3 month

  • Griseofulvin :-The duration of anti-fungal therapy may be 2 weeks for uncomplicated tinea corporis, 8–12 weeks for tinea capitis, or as long as 6–18 months for nail infections. Due to high relapse rates, griseofulvin is seldom used for nail infections. Common side effects of griseofulvin include gastrointestinal distress, headache, and urticaria.

  • Oral itraconazole and terbinafine are approved for onychomycosis. Itraconazole is given as either continuous daily therapy (200 mg/d) or pulses (200 mg bid for 1 week per month) administered with food. Fingernails require 2 months of continuous therapy or two pulses. Toenails require 3 months of continuous therapy or three pulses. Itraconazole has the potential for serious interactions with other drugs requiring the P450 enzyme system for metabolism. Terbinafine (250 mg/d) is also effective for onychomycosis. Therapy with terbinafine is continued for 6 weeks for fingernail infections and 12 weeks for toenail infections. Terbinafine has fewer drug-drug interactions, but caution should be used with patients who are on multiple medications.

    A middle aged man presents with paraesthesia of hands and feet. Examination reveals presence of `Mees’ lines in the nails and rain drop pigmentation in the hands. The most likely causative toxin for the above mentioned symptoms is :
    A.Lead
    B.Arsenic
    C.Thallium
    D.Mercury

  • NAIL INVOLVEMENT

    General Features of the Hair and Nails
    The distribution of the body hair, its texture, and amount should be noted as a part of the initial overall survey of the patient’s skin, as should examination of the nails. The nails (see Chap. 72) can provide evidence of latent skin disease (psoriasis, lichen planus, alopecia areata, congenital ectodermal defect), as well as suggest the presence of renal or liver disease. Beau’s lines (transverse indentations of the nails) and other variations on the theme of transverse white lines across the nails may be associated with a recent febrile or systemic illness, especially a renal or hepatic one. Telangiectasia in the periungual skin is a frequent and important diagnostic finding in systemic lupus erythematosus and dermatomyositis

    PSORIASIS:- Onychodystrophy, nail pitting, subungual keratosis, Beau’s lines (ridging), leukonychia, crumbling nail plate, and discoloration are more strongly associated with arthritis than with psoriasis alone, being found in 85 percent of those with arthritis versus 31 percent of those with the isolated cutaneous form of the disease. 47 The most prevalent findings are pitting and onycholysis. Onychodystrophy is closely related to involvement of the distal interphalangeal joint of the same digit, suggesting a broader acral dystrophic state. The appearance of onychodystrophy is closely related in time to the appearance of the arthritis.Nail pitting results from the presence of easily detachable parakeratotic cells in the superficial layers of the nail plate

    Nails in patients with alopecia areata may show fine pitting or, less commonly, mottled lunula, trachyonychia, or onychomadesis.

    Contact dermatitis of the proximal nail fold is responsible for chronic paronychia and nail plate surface abnormalities, such as irregular pitting and Beau’s lines. These are caused by mild involvement of the adjacent proximal nail matrix. Contact dermatitis of the hyponychium produces severe subungual hyperkeratosis and nail bed splinter hemorrhages. The differential diagnosis includes onychomycosis, psoriasis, parakeratosis pustulosa, pityriasis rubra pilaris, and keratoderma.

     

    Nail changes, including pitting, horizontal and longitudinal ridging, leukonychia, onycholysis, dyschromia, nail bed atrophy, and telangiectasia of the cuticle nail fold, have been observed in patients with SLE.

    DLE activity can localize to the nail unit. The nail can be impacted by other forms of cutaneous LE as well as SLE, producing nail fold erythema and telangiectasia, red lunulae, clubbing, paronychia, pitting, leukonychia striata, and onycholysis.

     

    In secondary syphilis, nail changes may result from involvement of either the nail matrix or the nail folds. In the nail plate, brittleness, splitting, onycholysis, pitting, lunular elkonyxis (pits) with fissuring, and dystrophy have been described.

    ECTRODACTYLY–ECTODERMAL DYSPLASIA–CLEFT LIP/PALATE (EEC) SYNDROME; SPLIT HAND–SPLIT FOOT–ECTODERMAL DYSPLASIA–CLEFT LIP/PALATE SYNDROME :-The nails are dystrophic in about four-fifths of individuals with transverse ridging, pitting, and slow growth

    LICHEN PLANUS OF THE NAILS Nail involvement occurs in 10 to 15 percent of patients. 23 Lichen planus limited to the nails is uncommon, and the initial involvement is followed, in many cases, by the development of typical lesions elsewhere. Lichen planus of nails is infrequent in children. Thinning, longitudinal ridging, and distal splitting of the nail plate (onychoschizia) are the most common findings. Onycholysis, longitudinal striation (onychorrhexis), subungual hyperkeratosis, or even absence (anonychia) of the nail plate can also be seen. Twenty-nail dystrophy (trachyonychia) may represent an isolated nail finding of lichen planus. Psoriasis and alopecia areata can also lead to these distinctive nail changes. Nail loss may result from ulcerative lichen planus involving the nail unit. Pterygium or forward growth of the eponychium with adherence to the proximal nail plate is a classic finding of lichen planus of the nail ( Fig. 49-12). An atrophic cicatrizing form of lichen planus with random and progressive nail loss in Asians and blacks has also been reported. The “tenting” or “pup-tent” sign is observed as a result of nail bed involvement that elevates the nail plate and may cause longitudinal splitting.

    Degeneration of basal cells occur in
    a) Lichen planus b) pemphigus c) psoriasis

    Compy’s sign (white patches due to degenerated squamous epithelium occurring on
    buccal Mucosae and gums) is seen in: JIPMER 80, AIIMS 85
    a) Moniliasis b) Pemphigus c) Lichen planus d) Measles

    30 year old male presents with pruritic flat-topped polygonal, shiny violaceous papules with flexural distribution. The most likely diagnosis is UPSC
    a) Psoriasis b) Pityriasis rosea c) lichen planus d) Lichenoid dermatitis

    Civatte bodies are found in
    a) Lichen planus b) Psoriasis c) Dermatophytosis d) Vitiligo

    Which of the following not photosensitive APPGE 04
    a) Porphyria b) DLE c) SLE d) Lichen Planus

    Causes of Cicatricial alopecia are PGI-04
    a. Disseminated lupus erythramatosis b. Alopecia areata c. Psoriasis
    d. Lichen planus e. Androgenic alopecia

    Kobner’s phenomenon is seen in all the following PGI -04
    a. Lichen planus b. Herpes simplex c. Human papilloma virus infection
    d. Psoriasis e. All the above

    Max Joseph’s space is a histopathological feature of:
    a) Psoriasis vulgaris. b) Lichen planus.
    c) Pityriasis rosea. d) Parapsoriasis.

    Wickham’s striae are seen in
    a) Lichen nitidus b)Lichen scrufosum c) Lichen planus d) DLE

    Basal cell degeneration is characteristic of
    a) Pemphigus b) Lichen planus c) Pemphigold
    d) Psoriasis

    The two major pathologic findings in lichen planus are basal epidermal keratinocyte damage and lichenoid-interface lymphocytic reaction. 1 The epidermal changes include hyperkeratosis, wedge-shaped areas of hypergranulosis, and elongation of rete ridges that resemble a sawtooth pattern .Multiple apoptotic cells or colloid-hyaline (Civatte) bodies are seen at the dermal–epidermal junction. Eosinophilic colloid bodies are present in the papillary dermis. They are PAS-positive and measure about 20 µm in diameter. A bandlike lymphocytic infiltrate is seen in the papillary dermis that abuts the epidermis. Many histiocytes and few plasma cells are seen. Plasma cells are more prominent in mucous membrane specimens. Few eosinophils are seen in drug-induced lichen planus or lichenoid drug eruptions. Melanin pigmentation is invariably present and is more pronounced in older, waning lesions and in dark-skinned individuals. Separation of the epidermis in small clefts (Max Joseph cleft formation) is occasionally seen .

    The classic cutaneous lesion of lichen planus is a faintly erythematous to violaceous, flat-topped, polygonal papule, sometimes showing a small central umbilication ( Fig. 49-1). A thin, transparent, and adherent scale may be discerned atop the lesion. Fine, whitish puncta or reticulated networks referred to as Wickham striae, named after the dermatologist who described the finding, are present over the surface of many well-developed papules. These are considered to be highly characteristic and are more easily observed after applying oil, xylene, or water and visualizing the lesions with a magnifying lens or a handheld dermatoscope. The surface alteration may result from localized thickening of the keratohyalin-containing cell layers of the stratum granulosum, although a focal increase in the activity of lichen planus may account for the morphologic alteration of Wickham striae.
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    Pterygium or forward growth of the eponychium with adherence to the proximal nail plate is a classic finding of lichen planus of the nail

    Pityriasis rosea

    Arvinder, 24 year old woman, presents with erythematous annular lesions with collarette scales predominantly arranged over trunk.
    Most likely diagnosis is
    a) Pityriasis rosea b) Pityriasis rubra pilaris c) Tenia versicolor
    d) Psoriasis

    Psoralen – A is used in the treatment of
    a) pemphigus b) Vitiligo c) pityriasis alba d) lcthyosis

    ‘Fir-tree’ type of distribution is seen in PGI 80, JIPMER 81
    a) Pityriasis Rosea b) Psoriasis c) Measles d) Secondary syhilis

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    The primary plaque (plaque primitive, herald patch, primary medallion, mother patch;)oval or round with a central, wrinkled, salmon-colored area and a darker red peripheral zone, separated by a collarette of fine scaling . The primary plaque is usually situated on the trunk in areas covered by clothes.

    Classic secondary rash small plaques resembling primary plaques in miniature, with the two red zones separated by the scaling ring,distributed with their long axes following the lines of cleavage of the skin, forming a “Christmas tree” pattern.

  • Pityriasis rubra pilaris (PRP)

  • Pityriasis rubra pilaris (PRP) refers to a group of chronic disorders characterized by reddish orange, scaling plaques and keratotic follicular papules.

    The follicular papules so characteristic of the disease soon appear as keratotic follicular plugs surrounded by erythema .The follicular papules are not always present but are very prominent in black South Africans. They are seen most commonly on the dorsal aspects of the proximal phalanges , the elbows, and the wrists. They can occur on other areas of the extremities and even the trunk but appear rarely on the face. A more widespread eruption consisting of scaling orange-red plaques is observed on the trunk and extremities and occasionally on the face. The lesions have sharp borders, and islands of normal skin within them are characteristic .The lesions may expand and coalesce  and eventually cover the entire body .The scales vary from fine to thick, the latter being particularly common on the palms and soles, which also may fissure and have an intense yellow-orange hue, and may cover the scalp in thick sheets.

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    Capture

    Tricky Question:- A forty two-year-old engineer developed redness of the glans and radial fissuring of the prepuce 2 weeks ago. A potassium hydroxide preparation of scrapings from the glans showed pseudohyphae and buds. Which one of the following systemic illness should be screened for  a) Pulmonary tuberculosis b) Diabetes mellitus AIIMS 04
    c) Systemic candidiasis d)Chronic renal failure

    Drug of choice in systemic candidiasis is
    a) Amphotericin-B b) Griseofulvin c) Nystatin d) Ketoconazole

    Griseofulvin AND Terbinafine is not effective for candidiasis,deep fungal infections or pityriasis versicolor.

    DERMATOPHYTOSIS :-This commonly involves the inguinal area, i.e., tinea cruris, but rarely causes superficial infection of the scrotum or penis. Tinea cruris is always associated with tinea pedis, the dermatophyte being transferred by the hand from the feet to the crural area. Clinically, tinea cruris presents as an erythematous to tan plaque with well-demarcated, scalloped borders advancing inferiorly down the anterior thigh. Chronic scratching may induce an eczematous dermatitis or lichen simplex chronicus on the scrotum or, less commonly, on the penis. Chronic application of topical corticosteroids can mask the clinical presentation (tinea incognito).

    A washer man presents with thickness erosion & discoloration of web spaces of toes diagnosis is
    a) Psoriasis b) Tinea Unguum c) Both d) Candidiasis

    Tinea Capitis is caused by all except
    a) Epidermophyton b) Microsporum c) T. violaceum d) T. Schoenleinii

    Tinea capitis is caused by all except
    a) microsporum b) candida c) Epidermophyton d) Trichophyton

    Bulkeley membrane is seen in; DNB 89, PGI 89
    a) Psoriasis b) Pemphigus c) Tinea d) Pityriasis rubra

    Dhobi’s itch is:
    a) Tinea corporis b) Tinea cruris c) Tinea barbae d) Tinea capitis

    Boggy swelling on head with easily pluckable hair in a young child diagnosis a) Pyoderma capitis b) Tinea capitis c) Alopecia areata d) None

    Tinea incognito is due to inappropriate use of systemic & topical
    a) Antibiotics b) Antifungals c) Steroids d) Antiviral

    An eleven year old boy is having tinea capitis on his scalp. The most appropriate line of treatment is
    a) Oral griseofulvin therapy b) Topical griseofulvin therapy
    c) Shaving of the scalp d) Selenium sulphide shampoo

    All these fungal diseases causing tinea capitus are seen in India except PGI -04
    a. Tinea mentagrophytes b. Tinea ondoinii c. Tinea rubrum
    d. microsporum e. Epidermophyton

    Tinea versicolor is caused by PG186, AP 86, Kerala 87, AI-88, 77(90, Al 91
    a) Malaezzia furfur b) candida c) Trichophyton rubra d) Trichophyton, mentagrophyte

    Treatment of tinea versicolor
    a) Clotrimazole b) sod. sulphite c) selenium sulphide d) miconazole d) all of the above

    Girseofulvin is not useful in one of the following Karnat 89
    a) Tinea capitis b) Tinea cruris c) Tinea versicolor d) Tinea pedis

    Tinea cruris is common in a) Adult male b) Adult female c) female child d) male child

     

    While all dermatophyte species invade the stratum corneum of the skin;Epidermophyton floccosum never invades hair and only occasionally nail.T.rubrum rarely invades hair but frequently invades nail.

    Tinea Corporis:- Most commonly by T rubrum.All known dermatophytes can produce lesions of the glabrous skin.Some species have predilections for particular parts of the body; for example, M. audouinii, classically a cause of tinea capitis, and T. rubrum, which most commonly causes tinea pedis but these can, and on many occasions do, cause tinea corporis.

    Tinea capitis:-Most species of dermatophyte are capable of invading hair but some species (e.g. M. audouinii, T. schoenleinii and T. violaceum) have a distinct predilection for the hair shaft.The principal feature of tinea capitis in recent years has been the rise of M. canis as the dominant organism in infections in some parts of Europe , and the spread of T. tonsurans in urban communities in the USA . A similar rise in the prevalence of T. tonsurans has recently been recorded in urban areas of the UK and in some other European countries.T. tonsurans is now most common cause in USA.

    Imp:- Rook says M. audouinii is most common worldwide while fitzpatrick says M.canis is most common worldwide.

    Harrison says predominant organism is T. Tonsurans but it must be talking about USA though not mentioned specifically.

    E. fl occosum, T. concentricum and T. mentagrophytes var. interdigitale are exceptional in apparently never causing tinea capitis.

    image

    Tinea Barbae : The animal species T. verrucosum and T. mentagrophytes var. mentagrophytes are responsible for the great majority of cases.

    Tinea faciei:-T. mentagrophytes var. mentagrophytes and T. rubrum predominate but T. tonsurans, M. audouinii and M. canis are also common causes worldwide

    Tinea Pedis:- Three anthropophilic species, T. rubrum, T. mentagrophytes var. interdigitale and E. fl occosum, are together responsible for the vast majority of cases of foot ringworm throughout the world.

    Tinea cruris:-The causal species are those implicated in foot ringworm but in different proportions. T. rubrum is the main cause [1]; T. mentagrophytes var. interdigitale and E. fl occosum also account for some cases.

    Onychomycosis caused by dermatophytes:-The principal dermatophytes concerned are: (i) with associated foot and hand infections—T. rubrum, T. mentagrophytes var. interdigitale and E. fl occosum; (ii) with associated scalp infections—T. tonsurans, T. violaceum and T. soudanensei.

    image

    The treatment of dermatophyte infections usually involves the use of oral terbinafine, fl uconazole itraconazole, griseofulvin or one of several well-tried topical preparations .All those noted have been shown to be effective in a substantial majority of patients, provided they are used regularly.

     

    Favus. Infection with T. schoenleinii is now seen rarely and sporadically in a variety of countries, such as South Africa [32], Ethiopia, where it is still endemic, as well as the Middle East, Pakistan, USA, Canada, the UK and Australia. The classical picture of tinea capitis caused by this organism is characterized by the presence of yellowish cup-shaped crusts known as scutula.

    Tinea imbricata (Tokelau) resulting from T. concentricum, an anthropophilic dermatophyte found in southern Asia, the islands of the South Pacific and in Guatemala, southern Mexico and Brazil, causes a distinctive infection. It seems to affect mainly the native peoples of these areas, and although susceptibility may be inherited as an autosomal recessive character [13], it occurs in both sexes and at all ages. Occasional cases may be seen elsewhere in travellers from these regions [14]. The infection begins as a scaling ring; centrifugal spread follows, but within the area of central clearing a second wave of scaling soon arises. The process is repeated to give numerous concentric rings  and, as the natural history is normally extremely prolonged, the whole body may become affected. Pruritus is intense and may lead to lichenification. Hypopigmentation may accompany the lesions.

  • __________________________________________________________________________________________________________________________________________________________

     

    ALOPECIA

     

    Knowledge of the hair cycle is vital to understanding hair problems. The duration and rate of growth of the anagen (growth) phase normally vary at different body sites, in different individuals, and at various ages, and determine the ultimate length of hair in that area.

    1 Catagen is the transitional portion of the cycle between anagen and telogen and is short-lived (2 to 4 weeks) in duration. Telogen duration also varies greatly in different body sites, but interindividual variability appears more limited. In a normal scalp, telogen is assumed to last 3 to 4 months and anagen to last 3-plus years. With age, there is both a diminution in anagen duration and an increase in the time interval between two anagen cycles.

    2 At any given time, ˜90 percent of the scalp hair is in anagen and 10 percent in telogen; this is subject to some seasonal variability.

    3 At the end of anagen, each hair bulb moves from its location in the subcutaneous tissue or dermis (depth of location is determined by whether the follicle is terminal or vellus) to a more superficial location by means of shrinkage and remolding of that portion of the follicle below the “bulge” where the arrector pili muscle inserts. The concentric layers of the inner root sheath, which anchor the hair shaft in the follicle, are only present to the bottom of the isthmus of the follicle, the region to which the hair bulb ascends in telogen . Consequently, the hair shaft in telogen is no longer anchored securely in the tissue, as it was in anagen, and it may be dislodged with the gentle traction of shampooing, combing, brushing, etc. The recapitulation of the anagen follicle and initiation of growth of a new anagen hair leads to the shedding of any remaining telogen hair in the follicular canaL.

     

    image

    Non cicatrical alopecia is present in TN 90
    A) Scleroderma b) Lichen Planus c) Psoriasis d) Parvovirus

     click here. for D/D of alopecia.

    Scarring hair loss
    Primary
    Lymphocyte associated
    • Lichen planus
    • Lupus erythematosus
    • Pseudopelade of Brocq
    • Follicular mucinosis
    Neutrophil associated
    • Folliculitis decalvans
    • Diffecting folliculitis
    • Folliculitis keloidalis nuchae
    Secondary
    • Trauma
    • Radiotherapy
    • Some dermatophyte infections
    • Primary neoplasia
    • Secondary neoplasia (metastasis)

     

    Non-scarring hair loss
    On an abnormal scalp
    Psoriasis
    • Seborrhoeic dermatitis
    • Some dermatophyte infections
    • Traction alopecia
    On a normal scalp
    Diffuse
    • Telogen hair loss
    • Anagen hair loss
    Patchy
    Alopecia areata
    • Triangular alopecia
    • Trichotillomania
    Secondary syphilis
    With a distinct pattern
    • Male pattern baldness
    • Female pattern baldness
    Other causes of hair loss
    • Hair shaft abnormalities
    • Congenital hypotrichosis
    • Loose anagen syndrome
    Table

    Causes of Alopecia


    I. Nonscarring alopecia
    A. Primary cutaneous disorders
    1. Telogen effluvium
    2. Androgenetic alopecia
    3. Alopecia areata
    4. Tinea capitis
    5. Traumatic alopeciaa
    B. Drugs
    C. Systemic diseases
    1. Systemic lupus erythematosus
    2. Secondary syphilis
    3. Hypothyroidism
    4. Hyperthyroidism
    5. Hypopituitarism
    6. Deficiencies of protein, iron, biotin, and zinc
    II. Scarring alopecia
    A. Primary cutaneous disorders
    1. Cutaneous lupus (chronic discoid lesions)b
    2. Lichen planus
    3. Central centrifugal cicatricial alopecia
    4. Folliculitis decalvans
    5. Linear scleroderma (morphea)
    B. Systemic diseases
    1. Discoid lesions in the setting of systemic lupus erythematosusb
    2. Sarcoidosis
    3. Cutaneous metastases

    a Most patients with trichotillomania, pressure-induced alopecia, early stages of traction alopecia.

    b While the majority of patients with discoid lesions have only cutaneous disease, these lesions do represent one of the 11 American College of Rheumatology criteria (1982) for systemic lupus erythematosus.

    Alopecia areata is treated by
    a) minoxidil b) Tranquilizers
    c) whitfields oinment d) parenternal penicillin

    Treatment of alopecia areata is with either immunosuppressives (local or systemic) or with irritants/immunogens, and is generally tailored to the severity of the disease. For localized patchy alopecia areata, intralesional steroids given at 4- to 6-week intervals are usually effective, with the main side effect being local dermal/subcutaneous atrophy related to the depth and concentration of injected steroid. Topical glucocorticoids classes I to V are also effective but take several months for initiation of hair growth, rather than the weeks for intralesional steroids. Side effects of topical steroids are generally limited to acne/hypertrichosis on the face from inadvertent transfer from the scalp and local epidermal atrophy with the more potent steroids. Systemic steroids, particularly short courses (less than 8 weeks) of tapering doses, are often used either alone or in conjunction with topical agents. In this setting, acne and weight gain are commonly seen side effects. PUVA is another immunosuppressant treatment that may be effective in alopecia areata, particularly in patients with extensive scalp and body hair loss. Between 30 and 80 treatments may be necessary before hair induction occurs, and there is an increased risk of photodamage/photoaging and skin cancer with PUVA use. The immunostimulation of topical irritants, especially anthralin, or topical immunogens (diphencyprone, squaric acid dibutylester) can be very effective in alopecia areata, but their use runs the risk of intolerable irritation if the dose titration is inappropriate. The particular mechanism of action of contact dermatitis that makes it a treatment for alopecia areata is purely speculative at this time, but it may include enhanced clearance of the putative follicular antigens through recruitment of new T cells and antigenic competition and interference with the initial or continued production of proinflammatory cytokines by the follicular keratinocytes. Five percent topical minoxidil, as a nonspecific hair growth promoter, may be a useful drug as a single agent or as an adjuvant with topical anthralin. There is a low incidence of local dryness/irritation and facial hypertrichosis with topical minoxidil. Although rare, the potential for systemic effects of topical minoxidil, particularly in young children, must be considered and the total amount applied kept to the recommended = 2 mL/day. Patients with alopecia areata need psychological support and physical means of camouflaging their hair loss. The latter often requires the use of a wig, which should be considered an integral part of treatment in patients with extensive scalp hair loss.

    Alopecia areata is due to a) Estrogen Stimulation c) Lichenoid reaction D) Androgen stimulation
    d)auto immune

    The pathogenesis of alopecia areata is still obscure, although most authors tend to classify alopecia areata as an autoimmune disease. As opposed to normal hairs, strong major histocompatibility complex (MHC) class I and class II immunoreactivity are found in lesional alopecia areata follicles, which also display aberrant expression of adhesion molecules known to direct hematopoietic cell migration.

    Pseudo pelade is synonym of: AIIMS 81, PGI 84
    a) Alopecia steatoides b) Premature alopecia c) Traction d) Cicatricial

    image

    Pseudopelade of Brocq is a rare clinical syndrome of scarring alopecia and fibrosis, in which distinct pathologic features are absent. It is generally accepted that pseudopelade of Brocq is the end stage of follicular fibrosis caused by a primary inflammatory dermatosis such as lichen planus, lupus erythematosus, pustular-scarring forms of folliculitis, or fungal infections, including favus, scleroderma, and sarcoidosis.

    PSEUDOPELADE OF BROCQ In clinical terms, pseudopelade of Brocq implies flesh- to pink-colored, irregularly shaped alopecia that may begin in a moth-eaten pattern with eventual coalescence into larger patches of alopecia . There has been considerable debate as to the specificity of this diagnosis versus an assignation of the term to describe all noninflammatory scarring alopecias, including the end-stage of a variety of initially inflammatory conditions. Histologically, the lesions are characterized by a perifollicular and perivascular lymphocytic infiltrate primarily at the level of the follicular infundibulum, loss of sebaceous epithelium, and fibrotic streams into the subcutis without interface or follicular plugging changes. 103 Elastin stains may distinguish pseudopelade (persistent elastic fibers around the midshaft of the follicle) from lichen planopilaris and lupus erythematosus (loss of elastic fibers in this location). 104 Direct immunofluorescence is negative in the majority of cases. It is unclear what treatment specifically helps.

     

    Cradle cap is a special form of:
    a) Pityriasos capitis b) Cephalohematoma
    d) Down’s syndrome c) Alopecia steatoides

    Boggy swelling on head with easily pluckable hair in a young child diagnosis a) Pyoderma capitis b) Tinea capitis c) Alopecia areata d) None

    Exclamation mark hairs are seen in
    a) Syphilis b) Alopecia areata c) Psoriasis d) Dermatophytosis

    image

    These short broken hairs, whose distal ends are broader than the proximal ends, illustrate their inherent sequence of events: follicular damage in anagen and then a rapid transformation to telogen. White or graying hairs are frequently spared and probably account, in cases of fulminant alopecia areata, for the mysterious phenomenon of “going gray overnight.” There is an increased incidence of autoimmune diseases in patients with alopecia areata, particularly thyroid-related disease, and there is a higher prevalence of pigmentary defects in patients with alopecia areata. 53 Nails in patients with alopecia areata may show fine pitting or, less commonly, mottled lunula, trachyonychia, or onychomadesis.

     

    Exclamatory Point hairs are seen in TN 2003
    a) Alopecia areata b) lcthyosis Vulgaris c) Tinea capitis
    d) Dermatomyositis

    Alopecia aerata is SGPGI 04
    a) Cicatrical scar b) Non cicatrical c) Fungal infection d) None

    Causes of Cicatricial alopecia are PGI-04
    a. Disseminated lupus erythramatosis b. Alopecia areata c. Psoriasis
    d. Lichen planus e. Androgenic alopecia
    Ref: Harrison 15th edn. page 316

    Exclamation mark" hairs are seen in? Karnat-05
    a. Tinea capitis b. Alopecia areata c. Lichen planus pilaris d. Trichotillomania

    Which of the following conditions causes alopecia without scarring? J&K-05
    a. DLE b. Herpes Zoster c. Alopecia areata d. Lichen planus pilaris

    Piebaldism refers to KARNATAKA – PGMEE – 2006.
    a. Androgenetic alopecia b. Erythema nodosum leprosum
    c. Association of vitiligo with white forelock d. None of the above
    (Ref. Harrison’s 16th edition page 968, 971)

    Which of the following is contraindicated in Androgenic Alopecia :
    (A)Testosterone
    (B)Cyproterone
    (C)Acetate Finasteride
    (D)Minoxidil

    A man aged 30years presents with, alopecia, boggy scalp swelling and easily pluckable hair. Next step in establishing Diagnosis would be
    A.KOH smear
    B.Culture sensitivity
    C.Biopsy
    D.None of the above

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