18

DERMATOLOGY1. SCABIES:a. Scabies is caused by the Acarus, Sarcoptes scabiei, with an estimated global prevalence of 300 million. The infestation causes considerable discomfort and can lead to secondary infection. Scabies spreads in households and environments where there is intimate personal contact. b. Diagnosis is made by identifying the scabietic burrow and by extracting the mite using a blunt needle. Inappropriate application of scabietic treatments can cause considerable irritation in other conditions. c. In small children the palms and soles can be involved with pustule formation Involvement of the genital area in boys is pathognomonic. The main symptom is itch. d. The clinical features include secondary eczematisation elsewhere on the body; the face and scalp are never involved, except in the case of infants. Even after successful treatment, the itch can continue and occasionally nodular lesions persist. e. Topical treatment of scabies is required for the affected individual and all asymptomatic family members/physical contacts to ensure eradication. f. Two applications 1 week apart of an aqueous solution of either permethrin or malathion to the whole body, excluding the head, are usually successful.g. If there is poor compliance, immunocompromise or heavy infestations (Norwegian scabies), systemic treatment with ivermectin (200 g/kg) as a single dose is appropriate2. MUCORMYCOSIS:a. Mucormycosis is a severe but uncommon opportunistic systemic mycosis caused by any of the Mucorales, mainly Myocladus (formerly Absidia) spp., Rhizomucor spp., Mucor spp. and Rhizopus spp. b. Disease patterns include rhinocerebral/craniofacial, pulmonary, cutaneous and systemic disease. c. All are characterised by the rapid development of severe tissue necrosis, which is almost always fatal if left untreated. d. The major predisposing factors are uncontrolled diabetes mellitus, iron chelation therapy with desferrioxamine, severe burns and, most commonly, profound immunosuppression from neutropenia or bone marrow transplant in association with the use of broad-spectrum azole prophylaxis with agents like voriconazole. e. Diagnosis is by culture, but histopathological confirmation is required as the fungi may be environmental contaminants. f. Treatment requires a combination of antifungal therapy and surgical dbridement, with correction of predisposing factor(s) if possible. g. High-dose lipid-formulated amphotericin B is used most commonly, although posaconazole is active in vitro and has been used successfully.

3. PSORIASIS.PAPER I; FEB 2013 PAPER II1. Psoriasis is a non-infectious, chronic inflammatory disease of the skin, characterised by well-defined erythematous plaques with silvery scale, with a predilection for the extensor surfaces and scalp, and a chronic fluctuating course. 2. The prevalence is approximately 2% in European populations but may be lower in African and some Asian populations, e.g. Japanese. 3. Psoriasis may start at any age but is unusual before 5 years. 4. There are two epidemiological patterns of psoriasis, sometimes referred to as type 1 and type 2. a. The first has an onset in the teenage and early adult years, often with a family history of psoriasis and an increased prevalence of the HLA group Cw6. b. The onset of the second is in the fifties or sixties, when a family history is less common and HLA Cw6 is not so prominent. 5. Aetiologya. Psoriasis is genetically complex and a large number of genes are thought to be important in its pathogenesis. b. Empirical estimates suggest that if one parent has psoriasis, then the chance of a child being affected is in the order of 1520%; if both parents have the disease, this figure rises to 50%. 6. Pathology:a. There are two key pathophysiological features in psoriatic plaques:i. The keratinocytes hyperproliferate with a grossly increased mitotic index ii. There is a large inflammatory cell infiltrate. iii. The nails of patients with psoriasis, even when clinically unaffected, grow more quickly than those of controls. b. The evidence implicating a key role for an immune pathogenesis includes the association with HLA Cw6;

7. Factors thought to precipitate exacerbations are: a. Traumai. Lesions appear in areas of skin damage such as scratches or surgical wounds (Kbner phenomenon) when the condition is eruptingb. Infectioni. b-haemolytic streptococcal throat infections often precede guttate psoriasisc. Sunlighti. UVR rarelyd. Drugsi. Antimalarials, ii. b-adrenoceptor antagonists (b-blockers) and lithiumiii. Rebound after systemic corticosteroids or potent local corticosteroids are stoppede. Emotion: Anxiety8. Clinical featuresa. There are several different forms of psoriasis. i. Stable plaque psoriasis 1. This is the most common. Individual lesions are well demarcated and range from a few millimetres to several centimetres in diameter. They are red, with a dry silvery-white scale, which may only be obvious after scraping the surface. The elbows, knees and lower back are commonly involved. Other sites of predilection include: Scalp. Nails Flexures Palmsii. Guttate psoriasis1. This is most commonly seen in children and adolescents, and may follow a streptococcal sore throat. 2. Individual lesions are droplet shaped, seldom over 1 cm in diameter and scaly. iii. Erythrodermic psoriasis1. The skin becomes universally red or scaly, or more rarely just red with very little scale. As in other forms of erythroderma, temperature regulation becomes compromised with a danger of either hypothermia or hyperthermia.iv. Pustular psoriasis1. There are two varieties of pustular psoriasis. The generalised form is rare but serious. The onset is usually sudden, with large numbers of small sterile pustules erupting on a red base. The patient may rapidly become ill with a pyrexia coinciding with the appearance of new pustules, and will usually require urgent assessment and hospital admission. 2. A localised form, which primarily affects the palms and soles, is more common. This is chronic and comprises small sterile pustules which lie on a red base, and resolve to leave brown macules or scaling. The relationship between pustular psoriasis of the palms and the soles (palmoplantar pustulosis) and psoriasis remains disputed, although they commonly coexist. v. Arthropathy: Between 5 and 10% of individuals with psoriasis develop a chronic seronegative inflammatory arthropathy 9. Investigationsa. Biopsy is seldom necessary and contributes little. b. Throat swabbing for streptococci or other evidence of recent infection may occasionally be useful in suspected guttate psoriasis. c. Joint symptoms, unless minor, require a formal rheumatology assessment.10. General management of psoriasisa. Explanation, reassurance and instruction are vital. b. psoriasis is not lifethreatening and therefore, if the treatment is worse than the disease, it should be stopped. 11. TreatmentTreatment can be classed in four broad categories: a. Topical agents Emollients, corticosteroids, vitamin D agonists, weak tar or dithranol preparationsb. UV therapies UVB or PUVAc. Systemic agents Methotrexate, retinoids Immunosuppressives, e.g. ciclosporin, mycophenolate Newer biological agents, e.g. infliximab, etanerceptd. Intensive inpatient or day-patient care Topical agents and UVR under medical supervision12. Topical agentsa. Dithranol and tar: In Ingrams regimen, the plaques are covered with low concentrations of dithranol in a zinc oxide paste following a tar bath and UVR exposure, and then covered in talcum powder and bandages, which are left in situ for 24 hours. b. Calcipotriol is a vitamin D agonist. It seldom clears plaques of psoriasis but reduces plaque thickness and diminishes scaling. It is applied twice or once daily. It is a mainstay of primary care management of psoriasis and may be combined with corticosteroids.c. Corticosteroids ; Corticosteroids may cause local skin atrophy, and when they are stopped the psoriasis tends to return. 13. Ultraviolet and PUVA therapya. UV therapyUltraviolet radiation (UVR) is the mainstay of outpatient management of those with moderate to severe psoriasis. More recently, a particular type of UVB radiation produced by the Philips TL01 lamp (narrowband UVB), delivered 25 times a week on an outpatient basis, has become a popular treatment. b. PUVA therapyPsoralens are natural photosensitisers found in a number of plants. Psoralen molecules intercalate between the two strands of DNA and, upon excitation with UVA, photons cross-link the DNA strands. It is thus a pro-drug that is distributed throughout the body after oral administration, but only activated by UVR in skin that is exposed to UVA. The long-term hazards of PUVA therapy are the result of its mutagenicity; patients who have received a large amount of PUVA therapy, particularly maintenance therapy (continuous PUVA lasting for 6 months to a year), are at increased risk of squamous and basal cell carcinoma. 14. Systemic treatment1. Methotrexatea. Methotrexate is highly effective and is given once weekly. Its mechanism of action is primarily on the immune system rather than having a direct effect on keratinocyte or epidermal hyperproliferation. The main hazards are immunosuppression and bone marrow suppression.2. Oral retinoidsa. Oral retinoids, such as acitretin, are effective in pustular psoriasis of the palms and soles, but are potent teratogens. 3. Ciclosporina. Ciclosporin is an immunosuppressive used over a 34-month period to induce clearance or prior to treatment with other systemic agents.4. Biological therapiesa. monoclonal antibodies, fusion proteins and cytokines, have been shown to have striking activity against psoriasis and appear as effective as classical agents. Eg. i. etanercept, a human recombinant TNF receptor fusion protein, ii. infliximab is a human-murine anti-TNF- monoclonal antibody.

4. GUTATE PSORIASIS 20111. Guttate psoriasis, a variant that occurs predominantly in children, is characterized by an explosive eruption of profuse, small, oval or round lesions that morphologically are identical to the larger plaques of psoriasis. 2. Sites of predilection are the trunk, face, and proximal portions of the limbs. 3. The onset frequently follows a streptococcal infection; a culture of the throat and serologic titers should be obtained. 4. Guttate psoriasis has also been observed after perianal streptococcal infection, viral infections, sunburn, and withdrawal of systemic corticosteroid therapy. 5. Pathogenesis:a. Psoriatic skin lesions may be induced, in a genetically susceptible host, by CD4+ T cells that were initially activated by streptococcal pyrogenic exotoxins acting as superantigens. b. The source of the streptococcal antigens can be the throat or the skin. c. Some of the superantigen-activated T cells recognize streptococcal M protein in the skin and appear to have cross reactivity with an abnormal keratin that has homology with streptococcal M protein. The autoreactive T cells may be responsible for the formation and maintenance of psoriatic skin lesions. 6. D.D: The lesions may be confused with viral exanthems and pityriasis lichenoides chronica 7. Treatment: refere previos answer.a. The treatment of psoriasis should be viewed as a 3-tier process. The 1st tier is topical therapy.b. The 2nd tier of therapy is phototherapyc. Systemic therapy is the 3rd tier.

5. FOUR CAUSES OF PRURITIS WITHOUT SKIN DISEASE.Medical conditions associated with pruritusMedical condition Cause of pruritus TreatmentLiver diseaseCentral opioid effect NaltrexoneElevation in bile salts ColestyramineRifampicinSedativeantihistaminesUVB

Renal failure Unknown; unlikely to Oral activated charcoalinvolve histamineBlood diseaseAnaemia Iron deficiency Iron replacementPolycythaemia Unknownrubra veraLymphomaLeukaemia UnknownMyelomaEndocrine diseaseDiabetes mellitus May be associated Clotrimazolewith genital candidiasisThyrotoxicosis Generalised due to Emollientsdry skinHypothyroidism Localised; may be dueto CandidaCarcinoid5HT-mediatedsyndrome HIV infection Infection, infestation, Treatment ofe.g. Candidaopportunistic infectionEosinophilic folliculitis UnknownLocal corticosteroids,UVBMalignancy UnknownPsychogenic Unknown Psychotherapy,anxiolytics,antidepressants6. PEDICULOSISHead lice1. Infestation with head louse, Pediculus humanus capitis, is common; it is highly contagious, spread by direct head-to-head contact. 2. Itching of the scalp leads to scratching which causes secondary infection and cervical lymphadenopathy. 3. The diagnosis is confirmed by identifying the living louse or nymph on the scalp or on a black sheet of paper after careful fine-toothed combing of wet hair that has had conditioner applied. 4. The empty egg cases (nits) are easily seen along the hair shaft and are characteristically difficult to dislodge. 5. Treatment is recommended for the infected individual and any infected household/school contacts. Eradication in school populations has proved difficult because of poor compliance and resistance to certain treatments. 6. The standard treatments are malathion, permethrin and carbaryl in a lotion or aqueous formulation, which are applied on two separate occasions at 710 days interval. 7. Many advise rotational treatments within a community to avoid resistance. Regular wetcombing (physical removal of the live lice by regular combing of slippery, conditioned wet hair) seems less effective than pharmacological treatments. 8. Involvement of the eyebrows/eyelashes is treated by topical Vaseline 12-hourly for at least a fortnight.

Body lice1. These are similar to head lice but live on clothing, particularly in seams, and feed on the skin. They are found on individuals with poor hygiene and in overcrowded conditions. Itch is the principal symptom. The skin is excoriated and secondary infection is common. It is managed by dry cleaning and high-temperature washing or insecticide treatment of clothes.Pubic (crab) lice1. These are usually sexually acquired and cause pruritus. An aqueous-based treatment of either malathion or carbaryl is the treatment of choice, applied on two occasions to the whole body, as body hair can also be infested. 2. Contacts should also be treated.

7. STAPHYLOCOCCAL SCALDED SKIN SYNDROME. (SSSS).1. SSSS is a potentially serious exfoliating cutaneous disease that occurs predominantly in children, particularly neonates. 2. It is caused by blood-borne exfoliative toxins from a focus of infection with Staph.aureus, which specifically cleave desmoglein-1. 3. The focus of infection may be the umbilicus or urinary tract, or it may stem from colonisation of the nasopharynx. The child presents with fever, irritability, skin tenderness and, in severe cases, erythema, starting in the groin, axilla and around the mouth. Blisters and superficial erosions develop within 2428 hours, and can rapidly involve large areas of the skin with severe systemic upset. 4. Bacterial swabs should be taken from obvious primary sites of infection, the nose and throat. A skin snip should be taken for rapid histological examination. This is a sample of the superficial peeling skin removed by snipping with scissors. No local anaesthetic is required. 5. It shows a split beneath the stratum corneum, and differentiates it from toxic epidermal necrolysis in which the whole epidermis is affected. 6. Systemic antibiotics (e.g. flucloxacillin) and intensive supportive measures should be commenced at once. Bacterial swabs from nostrils, axilla and groin should be taken from the patients relatives to exclude staphylococcal carriage.

8. SKIN CHANGES IN ENDOCRINE DISEASES. PAPER II AUG 20101. Thyrotoxicosis may lead to multiple cutaneous manifestations, including hair loss, pretibial myxedema, onycholysis and acropachy.2. In patients with hypothyroidism, there is hair loss, the skin is cold and pale, with myxedematous changes, mainly in the hands and in the periorbital region. 3. The striking features of Cushing syndrome are centripetal obesity, moon facies, buffalo hump, supraclavicular fat pads, and abdominal striae. 4. In Addison disease, the skin is hyperpigmented, mostly on the face, neck and back of the hands. 5. Virtually all patients with acromegaly have acral and soft tissue overgrowth, with characteristic findings, like macrognathia and enlarged hands and feet. The skin is thickened, and facial features are coarser. 6. Conditions leading to hyperandrogenism in females present as acne, hirsutism and signs of virilization (temporal balding, clitoromegaly).7. A prominent feature of hypopituitarism is a pallor of the skin with a yellowish tinge. The skin is also thinner, resulting in fine wrinkling around the eyes and mouth, making the patient look older. 8. Primary hyperparathyroidism is rarely associated with pruritus and chronic urticaria. In hypoparathyroidism, the skin is dry, scaly and puffy. Nails become brittle and hair is coarse and sparse. 9. Pseudohypoparathyroidism may have a special somatic phenotype known as Albright osteodystrophy. This consists of short stature, short neck, brachydactyly and subcutaneous calcifications. 10. Some of the cutaneous manifestations of diabetes mellitus include necrobiosis lipoidica diabeticorum, diabetic dermopathy, scleredema adultorum and acanthosis nigricans.

9. PEMPHIGUS VULGARIS. FEB 20101. Pemphigus is an uncommon autoimmune disorder that can present with mucosal symptoms only, usually in the mouth. 2. It is due to:a. IgG1 and IgG4 autoantibodies, directed against desmogleins-1 and 3 and causing intra-epidermal blistering b. it can also be drug-induced (e.g. by penicillamine or captopril) c. It is rarely associated with an underlying malignancy (paraneoplastic pemphigus). 3. In pemphigus foliaceus, a very superficial form, the autoantibodies are directed solely against desmoglein-1, therefore affecting only the most superficial epidermis.Clinical features and diagnosis1. Flaccid blisters occur on the skin, usually on the upper trunk and back. As the blisters are superficial, they are fragile and may look like erosions. 2. The Nikolsky sign is positive. 3. Mucosal involvement can be severe, increasing the morbidity and risk of mortality. Pemphigus can be associated with other autoimmune disorders and full assessment for these is mandatory. Investigations1. In the acute situation, histology from a Tzank smear (taken from the base of the blister with a scalpel) reveals acantholysis, i.e. separation of the epidermal cells. 2. Disease activity can be monitored by measuring the level of circulating autoantibody in serum by indirect immunofluorescence. 3. Investigations should also include full blood count, ESR, urea and electrolytes, liver function tests, chest X-ray and other imaging, particularly if paraneoplastic pemphigus is suspected.Management1. Systemic treatment with high-dose oral steroids is required, but the disease is more difficult to control than BP and life-long treatment is generally required. 2. Azathioprine and cyclophosphamide are alternatives. Intravenous IgG may be used to gain rapid control in severe cases.

10. URTICARIA Feb 2009 pII1. Urticaria refers to an area of focal dermal oedema secondary to a transient increase in capillary permeability. 2. On certain body sites such as the lips or hands, the oedema spreads deeper and is referred to as angioedema. 3. By definition, the swelling lasts less than 24 hours. 4. Acute urticaria may be associated with angioedema of the lips, face, throat and rarely wheezing, abdominal pain, headaches and even anaphylaxis. 5. Whilst severe angioedema can be life-threatening due to respiratory obstruction, this is extremely rare in a dermatological context Causes: Acute and chronic urticaria1. Autoimmune due to production of antibodies that cross-link the IgE receptor on mast cells2. Allergens (in foods, inhalants and injections)3. Drugs: aspirin; NSAID 4. Contact, e.g. animal saliva, latex5. Physical, e.g. heat, cold, pressure, sun, water6. Infection, e.g. viral hepatitis, infectious mononucleosis, HIV seroconversion7. Other conditions, e.g. systemic lupus erythematosus (SLE), pregnancy, intestinal parasites8. Idiopathic9. Urticarial vasculitisa. Hepatitis Bb. SLEc. IdiopathicPathogenesis of urticaria. 1. Type I hypersensitivity causing massive degranulation and sometimes anaphylaxis. 2. Basic pathology is mast cell degranulation and release of histamine and other mediators like a. prostaglandinsb. leukotrienesc. chemotactic cytokinesd. Heparine. 5-hydroxytryptaminef. Proteases3. Spontaneous mast cell degranulation occurs in chronic urticaria. 4. Chemical mast cell degranulation due to drugs5. Autoimmunity accounts for 30% of chronic urticaria.Clinical features:1. Clinical types:1. < 24 hours (urticaria)2. 24 hours (urticarial vasculitis)3. < 6 weeks (acute urticaria)4. 6 weeks (chronic urticaria)2. Knowing the length of time that an individual weal lasts may be of some use in distinguishing urticaria from urticarial vasculitis. Urticarial vasculitis is much less common than urticaria, and many patients are unable to distinguish the development of new weals and disappearance of old ones, from individual weals which persist for more than 1 day. 3. The physical urticarias can be identified by asking appropriate questions and subsequent challenge testing. 4. A family history must be sought in cases of angioedema. 5. There is an autoimmune pathogenesis for the most common form of disease, chronic idiopathic urticaria, which is defined by the presence of urticarial episodes for more than 6 weeks; self-reacting antibodies appear to cause cross-linking of the surface IgE receptor on mast cells with subsequent cellular degranulation.Investigations1. Full blood count, including eosinophil count in case of underlying parasites 2. Erythrocyte sedimentation rate (esr): may be elevated in cases of vasculitis 3. Urea and electrolytes, thyroid and liver function tests:may reveal an underlying systemic disorder 4. Total IgE and specific IgE to possible allergens, e.g shellfish or peanuts5. Antinuclear factor: may be positive in chronic urticaria or urticarial vasculitis6. CH50: indicates the level of complement activation; C3 and C4 levels may reveal complement consumption 7. C1 esterase inhibitor: may be quantitatively reduced or more rarely functionally deficient, as in hereditary angioedema8. Skin biopsy: helpful if urticarial vasculitis is suspected9. Appropriate challenge test: to confirm physical urticarias.10. Frequently no cause can be found for acute episodes, whereas in chronic urticaria an autoimmune pathogenesis will account for the majority of cases.Management1. Non-sedative antihistamines, such as loratadine, fexofenadine or cetirizine, are effective for one-third of patients with chronic urticaria; 2. H2 -blocker such as cimetidine or ranitidine may be added to antihistamines3. Mast cell stabilisers or protease and leukotriene inhibitors are used but efficacy is not clear. 4. Systemic corticosteroids are widely prescribed for urticaria, although there is little evidence of benefit. 5. Patients with a history of life-threatening angioedema or anaphylaxis, as is seen in allergy to peanuts and wasp stings, should carry a self-administered injection kit of adrenaline (epinephrine). 6. Urticaria may be precipitated by aspirin or NSAIDs. If there is a clear history of these agents precipitating attacks, they should be avoided, and even in the absence of a clear history it may be advisable to suggest alternatives such as paracetamol. Codeine and opioids can also induce urticaria.

11. TENIA CAPITIS APRIL 92

1. Dermatophytes are fungi capable of causing superficial skin infections known as ringworm or dermatophytosis. 2. The causative fungi belong to three genera a. Microsporum b. Trichophyton c. Epidermophyton 3. Clinical forms of cutaneous infection include tinea corporis (involvement of the body), tinea capitis (scalp involvement), tinea cruris (groin involvement), tinea pedis (involvement of the feet) and onychomycosis (nail involvement)4. Pathogenesisa. Caused by dermatophytic fungi; common etiologic agents are T. tonsurans (anthropophilic) and Microsporum canis (zoophilic)b. Transmission is person-to-person or fomites such as combs, clothing, bedding, toys and furniture Asymptomatic individuals, especially family members, act as reservoirs for infection (~25% of family members affected)5. Clinical features:a. They are variable due to associated inflammation, with patchy hair loss and some scaling. Affected individuals should have the area scraped and affected hairs plucked for mycological microscopy and culture. b. Endothrix (within the hair shaft) infections, e.g. Trichophyton tonsurans, cause relatively uninflamed patchy baldness with breakage of the hairs at the skin surface (black dot). c. There is no fluorescence under Woods light. d. Ectothrix (outside the hair shaft) species of fungi, such as Microsporum audouinii (anthropophilic), show minimal inflammation; Microsporum canis (from dogs and cats) infections are more inflamed and can be identified by green fluorescence with Woods light. e. Kerions are boggy, highly inflamed areas of tinea capitis and are usually caused by zoophilic (from animals, e.g. cattle ringworm) species of fungi (e.g. Trichophyton verrucosum) painful, inflamed, crusted mass with purulent discharge; often with associated fever and regional lymphadenopathy f. Favus is inflammation and scarring characterized by yellow cup-shaped crusts (scutula), around a hair; . 6. Diagnosisa. Clinical examinationb. KOH preparation: observe spores within brokenoff hairs, rarely hyphaec. Culture collect specimen by rubbing a sterile cotton swab over the scalp and inoculating in fungal media or DTMd. Skin biopsy may be necessary to confirm diagnosis in unusual cases, especially Majocchi granuloma7. Treatmenta. It is systemic with oral terbinafine, griseofulvin or itraconazole. b. Topical therapy, such as an antifungal shampoo, is recommended as an adjunct and arachis oil is used to remove crusting. c. Kerions sometimes require short courses of oral corticosteroids in addition to systemic antifungal therapy to reduce the inflammation.8. Prognosisa. Usually resolves without permanent alopecia b. With severe inflammatory disease, scarring and permanent hair loss may occur, but tends to be rare and spotty

12. DRUG ERUPTIONS APR 2000

Cutaneous drug reactions are common and almost any drug can cause them. They should be included in the differential diagnosis of most skin diseases. Although the mechanisms are poorly understood, drug eruptions may be classified as shown in Box 27.40.Clinical features and investigationsMechanism of drug eruptions: 1. Non-immunological (non-allergic)a. Pharmacological effect: Striae due to corticosteroids; mouth ulcers due to methotrexateb. Drug overdose or failure to eliminate: Morphine rashes with liver disease/failurec. Drug interaction: Bruising with warfarin and aspirin d. Idiosyncratic reaction: Drug-induced variegate porphyriae. Phototoxic reaction: Chlorpromazine-induced light reactionsf. Altered skin mycology: Tetracyclines and vaginal candidiasisg. Exacerbation of pre-existing skin condition: Lithium and -blocker worsen psoriasis2. Immunological (allergic)a. Immediate hypersensitivity: Penicillin-induced urticariab. Immune complex reaction: Drug-induced vasculitis or erythema multiformec. Delayed hypersensitivity: Drug-induced exfoliative dermatitis or photoallergic reactionsClinical patterns of drug eruptions1. Toxic erythemaa. Erythematous plaques: Antibiotics (especially ampicillin)b. Morbilliform, sometimes with urticarial or erythema multiforme-like elements: Sulphonamides, thiazide diuretics, para-aminosalicylic acid (PAS)2. Urticariaa. Itchy weals, sometimes accompanied by angioedema: i. Salicylates, codeine and NSAIDs ; ii. Antibiotics, dextran and ACE inhibitors3. Erythema and scalinga. Small, scaly, pink papules to large, scaly,red papules: i. Antibiotics (e.g. penicillins, sulphonamides including co-trimoxazole)ii. Gold, penicillamine and NSAIDs, particularly ibuprofeniii. Anticonvulsants, ACE inhibitors, barbiturates, anti-thyroid drugs and cytokine modulators, e.g. adalimumab4. Allergic vasculitisa. Painful, palpable purpura developing into necrotic ulcers: Sulphonamides, indometacin, phenytoin and oral contraceptives5. Erythema multiforme: a. Target-like lesions and bullae on the extensor aspects of the limbs: Sulphonamides and barbiturates6. Purpura:a. Widespread purpura in the absence of thrombocytopenia or a coagulation defect: Thiazides, sulphonamides, sulphonylureas, adalimumab, infliximab, barbiturates and quinine7. Bullous eruptionsa. May be associated with erythema and Purpura: Barbiturates; Penicillamine8. Exfoliative dermatitisa. Universal redness and scaling, shivering PAS, isoniazid and gold9. Acute generalised exanthematous pustulosis/toxic pustulodermaa. Rapid onset of sterile, non-follicular pustules on an erythematous base: Ampicillin/amoxicillin, quinolones, sulphonamides, pristinamycin, terbinafine Diltiazem and hydroxychloroquine10. Fixed drug eruptionsa. Round, erythematous, sometimes bullous plaques developing at same site every time drug is given; Pigmentation on resolution: Tetracyclines, sulphonamides Quinine and barbiturates 11. Acneiform eruptionsa. Rash resembles acneb. Lithium and anticonvulsantsc. Oral contraceptive, androgenic or glucocorticoid steroidsd. Antituberculosis drugs, biological therapy (cetuximab)12. Toxic epidermal necrolysisa. Rash resembles scalded skin: Barbiturates, phenytoin, lamotrigine, fluoxetine Penicillin, co-trimoxazole, nevirapine and allopurinol13. Hair lossa. Diffuse: Cytotoxic agents, infliximab and acitretin Anticoagulants, antithyroid drugs and oral contraceptives14. Hypertrichosis: a. Excessive hair growth in non-androgenic distribution: Diazoxide, minoxidil and ciclosporin15. Photosensitivity: a. Rash limited to exposed skin: Thiazide diuretics and phenothiazines Tetracyclines, sulphonamides and nalidixic acid NSAIDs, retinoids and psoralens16. Pigmentation a. Amiodarone Slate-grey; exposed sitesb. Arsenic Diffuse bronze pigmentation with superimposedc. raindrop depigmentationd. Bleomycin Often flexural; browne. Busulfan Diffuse brownf. Chloroquine Blue-grey; exposed sites17. Psoriasiform rash a. Rash like psoriasis: Lithium, -blockers and anti-TNF- therapy (infliximab)Diagnostic clues to drug eruptions a. Past history of reaction to suspected drugb. Introduction of suspected drug a few days before onset of rashc. Recent prescription of a drug commonly associated with rashes (e.g. penicillin, sulphonamide, thiazide, allopurinol)d. Symmetrical eruption which fits with a well-recognised pattern caused by a current drugManagementa. The first step is to withdraw the suspected drugb. In the case of suspected drug-induced photodermatoses, phototesting should be carried out when the patient is on the drug, and then again at a later date when the drug has been withdrawn. c. Drug withdrawal may not be easy, or even possible if there is no alternative available. The decision will depend on many factors, including the severity and nature of the drug reaction, its potential reversibility and the probability that the drug caused the reaction. d. Supportive treatment with antihistamines or a course of systemic corticosteroids may be indicated, depending on the type of skin reaction.

13. HYPOPIGMENTED SKIN LESIONS AUG 20041. The main disorders to consider are albinism and vitiligo. However, a number of others may produce secondary hypopigmentation:2. Pityriasis alba, a type of eczema presenting as depigmented areas on the face, particularly in children, with or without scale3. Pityriasis versicolor, a yeast infection characterised by hyperpigmentation early in its pathogenesis but leading to multiple areas of hypopigmentation on the trunk, particularly the back4. Idiopathic guttate hypomelanosis, characterised by numerous small areas of depigmentation in areas of skin that have been exposed to the sun5. Very rarely, phenylketonuria and hypopituitarism.Oculocutaneous albinism1. Albinism results from a range of genetic abnormalities leading to reduced melanin biosynthesis in the skin and eyes; the number of melanocytes is normal (in contrast to vitiligo). 2. There are a number of different forms of albinism, and considerable variation even within one genetic type. 3. Albinism is usually inherited as an autosomal recessive trait. a. Type 1 albinism is due to a defect in the tyrosinase gene, whose product is rate-limiting in the production of melanin. Affected individuals have an almost complete absence of pigment in the skin and hair at birth, with resulting pale skin and white hair, and failure of melanin production in the iris and retina. Patients have photophobia, poor vision not correctable with refraction, rotatory nystagmus, and an alternating strabismus associated with abnormalities in the decussation of nerve fibres in the optic tract. b. A second form of albinism is due to a defect in the P gene, which encodes an ion channel protein in the melanosome. Patients may have gross reduction of melanin in the skin and in the eyes, but may be more mildly affected than type 1 albinos. 4. Establishing the subtype of albinism requires genetic analysis, as there is considerable heterogeneity in the phenotype of the various subtypes. 5. Oculocutaneous albinos are at grossly increased risk of sunburn and skin cancer. In equatorial regions, many die from squamous cell carcinoma or, more rarely, melanoma in early adult life. They may, however, show pigmented melanocytic naevi and may freckle in response to sun damage.Management1. Avoidance of sun exposure with protective clothing and hats is important, as is a lifestyle that avoids the midday sun in particular, with indoor rather than outdoor occupations. Sunblocks may be useful but can be expensive. 2. Early diagnosis and treatment of skin tumours is essential.Vitiligo1. Vitiligo is an acquired condition in which circumscribed depigmented patches develop; it affects 1% of the population world-wide. 2. Unlike albinism, vitiligo involves focal areas of melanocyte loss. 3. There may be a positive family history of the disorder in those with generalised vitiligo, and this type is associated with autoimmune diseases such as diabetes, thyroid and adrenal disorders, and pernicious anaemia. 4. Trauma and sunburn may precipitate the appearance of vitiligo. 5. A number of hypotheses have been advanced to explain the pathogenesis, including that the melanocytes are the target of a cellmediated autoimmune attack, but why only focal areas are affected remains unexplained.Clinical assessment1. Segmental vitiligo is restricted to one part of the body but not necessarily a dermatome. Generalised vitiligo is often symmetrical and frequently involves the hands, wrists, knees and neck, as well as the area around the body orifices. The hair of the scalp and beard may also depigment. 2. The patches of depigmentation are sharply defined, and in Caucasians may be surrounded by light brown caf au lait hyperpigmentation. 3. Some spotty perifollicular pigment may be seen within the depigmented patches and is sometimes the first sign of repigmentation. 4. Sensation in the depigmented patches is normal (unlike in tuberculoid leprosy). Examination with a Woods light enhances the contrast between the pigmented and non-pigmented skin. 5. The course of vitiligo is unpredictable but most patches remain static or enlarge; a few repigment spontaneously.Management1. This is unsatisfactory. Protecting the patches from excessive sun exposure with clothing or sunscreen may be helpful in reducing episodes of burning and potential skin cancer. 2. Camouflage cosmetics may also be helpful, particularly in those with dark skin, as can potent topical corticosteroids. 3. Phototherapy with PUVA (psoralen + UVA) or more recently narrow band UVB has been used but evidence is limited. PUVA therapy increases pigmentation in normal skin, so the cosmetic effect (an increase in contrast) may actually be worse than no treatment, except in very dark-skinned individuals. When repigmentation occurs, it is frequently seen as small foci of dark areas of skin surrounding hair follicles within the vitiliginous area. 4. The absence of whiteness of the hairs in the area of vitiligo is a good prognostic feature. Transplantation, using a range of techniques including split-skin grafts and blister roof grafts, is occasionally used on to dermabraded recipient skin. 5. The impact of vitiligo differs markedly between populations. In the Indian subcontinent, the effects of vitiligo are more readily discernible than in pale-skinned individuals in northern Europe. 6. Depigmentation is also seen in leprosy, which means that individuals with vitiligo are often stigmatised. The use of more novel treatments, such as grafting, is often pursued more extensively in such populations.Other hypopigmented conditions:1. Tinea versicolor: Infection of the skin by Trichophyton Manifests as patchy hypopigmentation and sometimes hyperpigmentation Commonly found on the trunk 2. Pityriasis alba Related to eczema Hypopigmented patches on the face 3. Postinflammatory hypopigmentation May occur after any type of cutaneous inflammation More obvious in dark-skinned individuals Duration is weeks to months 4. Post-topical steroid hypopigmentation Topical steroids, particularly fluorinated, may cause thinning, atrophy, and hypopigmentation with prolonged use More common on the face and perineum 5. Tuberous sclerosis (TS) A neurocutaneous disorder affecting the brain, eyes, kidney, skin, and heart Systemic symptoms are preceded by ash-leaf macules, which are usually present in affected infants Other skin findings are shagreen patches, adenoma sebaceum, periungual fibromas Mental retardation, seizures are common 6. P artial albinism (piebaldism) Eg> Waardenburg syndromeWhite forelock, nonpigmentad patches on the face, trunk, elbows, and knees Facial dysmorphism, a white forelock, and hypopigmentation May be accompanied by hearing deficit

14. HIRSUTISM OCT 2003 Major points1. Hirsutism is a condition of unwanted, male-pattern hair growth in women. Hirsutism results in excessive amounts of coarse and pigmented hair on body areas where men typically grow hair face, chest and back2. Hair in masculine pattern in females on face,chest, upper back, abdomenSigns of virilization may also include: 3. Deepening voice4. Balding5. Acne6. Decreased breast size7. Enlargement of the clitorisPathogenesis: 1. Abnormality of pituitary, adrenal glands or ovary with increase in male hormonesDiagnosis1. History2. Physical examination3. Women approaching menopause or in the early years of menopause may develop coarse chin or other unwanted facial hair, but this isn't considered hirsutism4. Laboratory tests: serum testosterone and free testosterone, dehydroepiandrosterone sulfate, cortisol levels, urinary 17-ketosteroids, luteinizing hormone, follicle stimulating hormone, prolactin levels and pelvic ultrasound examinationDifferential diagnosis1. polycystic ovary syndrome in teens 2. Genetic predisposition in some ethnic groups3. Congenital adrenal hyperplasia4. Cushing syndrome5. Hyperprolactinemia6. Ovarian and adrenal tumors7. Medications. Some medications can cause hirsutism. One such drug is danazol, which is used to treat women with endometriosis.Treatment1. Removal of excess hair: shaving, epilation, chemical depilatories, threading, waxing, electrolysis, laser hair removal2. Oral contraceptives and weight reduction in PCODPrognosis1. Depends upon etiology of hirsutism, usually permanent2. Hirsutism can sometimes be emotionally distressing. Some women feel self-conscious about having unwanted body hair. Also, although hirsutism doesn't cause physical complications, the underlying cause of a hormonal imbalance can.

15. CLUBBING - OCT 03

1. Hippocrates described the phenomenon in a patient with empyema 2. Digital clubbing, alternatively called Hippocratic fingers, watch-glass nails, or drumstick fingers,2 can be an isolated finding or may occur as part of the syndrome of hypertrophic osteoarthropathy (HOA). 3. HOA is characterized by periostosis of long bones,joint pain, and clubbing; it may be primary, also known as pachydermoperiostosis, or secondary to a variety of disease processes. Primary HOA is an autosomal dominant disorder that presents in otherwise healthy children as clubbing, periostosis4. Clubbing develops in five steps: 1. Fluctuation and softening of the nail bed (increased ballotability)2. Loss of the normal