RACE DERMATOLOGY 2024 By Dr Ashish_240520_114648.pdf

RACE: REVISION AND CHANTING EXPRESS DERMATOLOGY By Dr. Ashish Skin is the largest organ in the body: Epidermis & Dermis CoLLege Girls Study Books Layers: Stratum corneum – most superficial layer. It is underdeveloped in preterm infants for 2-3 we...

RACE: REVISION AND CHANTING EXPRESS DERMATOLOGY By Dr. Ashish Skin is the largest organ in the body: Epidermis & Dermis CoLLege Girls Study Books Layers: Stratum corneum – most superficial layer. It is underdeveloped in preterm infants for 2-3 weeks. Stratum lucidum. Stratum granulosum. Stratum spinosum (prickle cell layer) – prickle cells are keratinocytes linked by desmosomes. This layer provides mechanical strength to the skin. Stratum basalae or stratum germinatum – deepest layer, mitotic activities are more intense here. Cells Layer Derived from 1.Keratinocytes All layer's Ectoderm 2.Melanocyte St.Basale Neural crest cell 3.Merkel cells St.Basale Ectoderm 4.Langerhans cells St.Spinosum Mesoderm Cells in epidermis: 1.Keratinocyte = 90% , HALLMARK – PRESENCE OF KERATIN FILAMENT  HARD KERATIN : DISULPHIDE BONDS , STRONG , SEEN IN NAILS AND HAIR  SOFT KERATIN : DISULPHIDE BOND , WEAK , SEEN IN SKIN 2.Melanocytes – Dendritic cells in the basal layer. Synthesize – melanosome which contain – melanin   Melanocytes form melanosomes ( have melanin)  1 MELANIN UNIT CONTAINS ( 36 KERATINOCYTE )  DERIVED FROM NEURAL CREST CELLS  PRESENT IN STRATUM BASALE 3.Langerhans cells – Macrophages/antigen-presenting cells  HALLMARK = BIRBECK GRANULES ( ROD SHAPED/ RACQUET SHAPED )  PRESENT IN STRATUM SPINOSUM  MARKER = CD1a, S100  APC  PHAGOCYTOSIS Merkel’s cells –  Presents in Stratum basale  Derived from Ectoderm > Neural crest  slow adapting type 1 mechanoreceptors found in prickle cell layer. Skin Epidermal proliferation time: Or skin doubling time is 4 weeks. LAYER’S : STRATUM BASALE  Germ cell layer  Mitotically active  Single layer thickness  Degeneration of cells of Stratum Basale seen in Lichen planus STRATUM SPINOSUM : Thickest layer of epidermis STRATUM GRANULOSUM : Granules presents Are i) Keratohyalin granule : profilagrin (Deficiency leads to ICTHYOSIS VULGARIS - fishy like scale are present ) ii) Lamellar Granules ( Membrane coating granules / ODLAND BODIES ) also formed in lung ( type I Alveolar cell ) Form lipid – acts as Barrier function ( defect leads to Asteatotic Eczema ) VESICULOBULLOUS DISORDER Fluid filled lesions  Vesicles < 0.5cm size  Bulla > 0.5cm size Immunological skin diseases: Pemphigus Pemphigus Bullous Dermatitis Foliaceus vulgaris pemphigoid herpetiformis Site Subcorneal split Suprabasal split Deep Subepidermal (Stratum (stratum (subepidermal granulosum) spinosum ) spilit ) Seborrheic Flexural areas ( Areas  upper trunk) chest , neck , face , scalp Bullae Crusted erosion, Flaccid Blister Tense Papulovesicular Superficial ,Deep bullae lesion Bullae Target Antigen DSG -1 DSG -3 > DSG-1 BP180 ( BPAg2 ) , Transglutaminase BP230 (BPAg1) Sensation Painless Painful erosion Painless Extremely itchy, excoriated And itching Location Only upper layer Mucosal Lower extremities Natal cleft , Elbow , knees , of SKIN involvement – most common buttocks involvement. Buccal mucosa—most No mucosal common involvement Course Rupture Easily Erythematous Rupture is late Tendency for are seen , heals erosion , whitish And heals grouping without scarring exudate , No rapidly without tendency to heal scarring Acantholysis , Positive Positive Positive Bulla Negative Nikolsky’s Sign spread sign Association ------ ------- Lymphoma, Gluten sensitive Eosinophils enteropathy, ( high ) + HLA DQ2 B8 neutrophils Immunofluorescene IgG Deposits in IgG Deposits in IgG against IgA Deposits in dermo study epidermis epidermis BPAg-2 Gene epidermal junction Basement At papillary tip membrane Treatment Systemic steroid Systemic steroid Topical steroid Dapsone. Avoid Gluten Sign Elicited  NIKOLSKY SIGN: Tangential pressure on normal skin - peeling of skin / bulla formation   Bulla spread sign : putting lateral pressure on the bulla , angulated spread seen  Asboe Hansen Sign : i) done in small lesion , Vertical pressure is applied. Fishnet appearance on immunofluorescence Linear IgA Diseases  Antigen : LAD -1  IgA Against BPAg2  String of pearl or beads appearance --- Age group – “ Bimodal “ – children  chronic bullous diseases of childhood Adult - LAD  Site : In children  STARTS IN PERIORAL AREA  On histopathology : Subepidermal Spilt  On DIF : Linear deposit of IgA TREATMENT : DAPSONE PAPULOSQUAMOUS DISORDERS Psoriasis Characterized by erythematous, sharply demarcated papules and rounded plaques, covered by silvery scales. The lesions are pruritic. Pathology: There is increase in epidermal proliferation rate (skin doubling time reduced to 4 days). Thickness is increased from normal 3-4 cells to 12- 15 cells. Stratum corneum is parakeratotic and contains microabscesses of neutrophils (Munro microabscess). Types: 1. Stable plaque – most common type. Sites – extensor aspects of elbows, knees, gluteal cleft and the scalp. 2. Eruptive or guttate psoriasis – most common in children and young adults. Involves the trunk, may follow a streptococcal URTI. 3. Erythrodermic psoriasis. 4. Pustular psoriasis –This follows an exacerbating episodes, e.g. infection, withdrawal of steroids, etc. Most commonly occurs on palms and soles. May be generalized. 5. Inverse psoriasis – Non-scaly, red lesions in flexural areas, e.g. inframammary region Etiology: 1. Idiopathic – may have positive family history. 2. External factors – infection, stress. 3. Drugs – antimalarials, beta blockers, lithium. Clinical feature: Pruritus. Auspitz sign – removal of scales causes pinpoint bleeding. Koebner or isomorphic phenomenon – development of lesions in traumatic skin. Nail involvement – punctuate pitting (thimble pitting), onycholysis, subungual hyperkeratosis, ‘oil drop’ sign (yellow discoloration). Psoriatic arthropathy – seen in 5-10 percent cases, most commonly involves the small bones in hands; sacroilitis.  X-ray bone: shows ‘opera glass’ hand, ‘pencil in cup’ appearance of hands. Treatment: Topical therapy – glucocorticoids, vitamin D analogue (calcipitriol). Phototherapy – UVB radiation. Combination of UVA radiation and oral/topical psoralen (PUVA) is known as photochemotherapy. Methotrexate is used in – erythrodermic psoriasis, pustular psoriasis and psoriatic arthritis. Retinoids are used in – pustular psoriasis (drug of choice in this condition). Lichen Planus This is characterized by pruritic, polygonal, flat-topped, violaceous papules. Sites: Wrists, shins, lower back and genitalia. Etiology: Drugs, chronic graft-versus-host disease, chronic viral hepatitis (hepatitis C). Pathology: Subepidermal lymphocyte infiltration. Degeneration of the basal cell layer. Increased thickness of the stratum granulosum. Civatte bodies are seen. There is hyperpigmentation of the residual skin. Clinical feature: Intense itching. Wickham’s striae – gray lines on lesions. Oral mucosa – white net-like eruption. Scalp – scarring alopecia. Nail – subungual hyperkeratosis, dystrophy of nail, pterygeum, onychorrhexis, anychia. Koebner’s phenomenon / isomorphic phenomenon  present in vitiligo , psoriasis , lichen planus. treatment – phototherapy Course: Spontaneous remission occurs in most cases. Treatment: Topical glucocorticoids. For systemic disease – systemic steroids Pityriasis Rosea Etiology – unknown. This is characterized by annular lesions of 2-6 cm diameter (the herald patch) followed by smaller annular or popular lesions, predominantly on the trunk along the cleavage lines. Lesions are erythematous with fine branny scales. Rarely involves the palms and soles (c.f. secondary syphilis). Common in young adults and in women. Course – usually self-limiting. Lesions on the back are parallel to the ribs giving a ‘Christmas tree’ appearance. Treatment : self limiting Pityriasis Rubra Pilaris Clinical feature: Orange-red perifollicular papules. Site: Generalized, first involves the face and scalp. Characteristically, islands of normal skin are spared – ‘skip lesions’. Others – wax like keratoderma. Seen in: middle aged and elderly. Diagnosis: Skin biopsy. Treatment: Isotretinoin, methotrexate. INFECTIONS Bacterial infections A. Erythrasma  Causative organism: Corynebacterium minutissinum  SITES : Axilla , groins , inflammatory Areas , toe cleft FEATURES : i) Well demarcated erythema to brown itchy ii) On wood lamp : coral red fluorescence due to Coproporphyrin III  TREATMENT : Topical azole , Clindamycin , oral erythromycin.  B. IMPETIGO Bullous Impetigo Non – Bullous impetigo Seen in Newborn , children Pre -schooler Caused by Staph aureus Strep. pyrogens > Staph Site Bulla ( superficial rupture ) Small vesicles  rupture the skin lesions are the site Raw erosion with honey of infection, more localized, coloured / golden yellow presents with honey-colored crusts crusts. No lymphadenopathy Lymphadenopathy Complication : PSGN Polycyclic erosion present. Impetigo Most common skin infection in children. a. Non-bullous impetigo: Causative organism – Streptococcus pyogenes, Staphylococcus aureus. Features – superficial skin infection with honey coloured crusted papules. Complication – acute glomerulonephritis. b. Bullous impetigo: Causative organism – coagulase positive group II Staphylococcus aureus. Clinical feature – tense, clear bullae. Management : 1. Topical  Fusidin , Mupirocin , bacitracin 2. Systemic  cloxacillin , cephalexin , erythromycin. Erysipelas / Cellulitis  Causative organism – Streptococcus pyogenes (most common), Staphylococcus aureus (very rare).  Soft tissues infection  Warm , tender plaques + fever and constitutional symptoms  Site : LL > UL > FACE  Predisposing lesions – chronic lymphedema. ERYSIPELAS CELLULITIS  Group B Hemolytic strep  Staph / strep  Involves Superficial dermis +  Involves Deep +dermis + lymphatics subcutaneous tissues  Well demarcated  Not well demarcated  Superficial vesiculations  Crusting +pustules Treatment  Systemic antibodies  Nsaids. Fungal infection Limited to outermost layer of skin , hair , nail and mucosa membrane i) SUPERFICIAL : stratum corneum Inflammation minimal Eg:- pityriasis versicolor , Tinea nigra ,Piedra ii) CUTANEOUS : Inflammation Eg: dermatophyte Candida A. Pityriasis Versicolor : (Scaling colours)  Etiology : Malassezia globosa > M. furfur  Scales : Fine branny scales.  Lesions : Hypo + Hyper pigmented macules.  M/c site : Trunk.  Ix : 10% KOH mount : Short hyphae + Round spores.  Spaghetti meat ball appearance.  Wood’s lamp : Yellow fluorescence.  Rx : Topical (1st line) : Azoles + Selenium sulphide.  Systemic : Fluconazole, itraconazole for recurrence. B. Candidiasis :  ORAL CANDIDIASIS Intertrigo/ Vulvovaginal Candidal flexural candidiasis balanoposthitis candidiasis  AFFECTS THE In female  Radial fissuring ORAL MUCOSA  macerated premenstrual around prepuce. plaques + discharge A/s with DM. Satellite pustules  WHITISH Curdy  CONCAVE Thicky curdy whitish There are small crumbly Patch borders on discharge superficial vesicals /  On removal of opposing papules / pustules patch surface  on rupture - erythematous  Peeling frayed peeling edges base. edges  are seen. Subcorneal  Associated itching and Soreness On investigation: - KOH mount : Budding yeast cells & Pseudohyphae On culture  Creamy white colonies Rx : Fluconazole/Clotrimazole C. Dermatophytosis SKIN HAIR NAIL TRICHOPHYTON + + + MICROSPORON + + - EPIDERMOPHYTON + - + D. TINEA INFECTION  Tinea Capitis =Head is involved DOC – GRISEOFLUVIN  Tinea mannum = Hands  Tinea Pedis = Feet  Tinea unguium = Nail  Tinea Cruris = Inguinal Area DOC = TERBINAFINE > ITRACONAZOLE SUBCUTANEOUS MYCOSES : 1.Sporotrichosis/ Rose Gardener’s disease  Etiology : Sporothrix schenckii  Lesions : Nodulo-ulcerative (Along lymphatics of extremities).  HPE : Asteroid body.  Rx : Itraconazole. 2.CHROMOBLASTOMYCOSIS  Etiology : Dermataceous fungi in Vegetative trauma  Lesions : Verrucous plaques + Black dots on surface.  Ix : KOH mount → Medlar/Sclerotic, Copper penny bodies  Rx : Itraconazole. Mycobacterial Skin Infection 3. Lupus Vulgaris (M/c in adults).  Lupus vulgaris: most common form of cutaneous TB  Lesion : Annular infiltrated plaques with peripheral extension.  M/c sites : Face, buttocks & Extremities  Diascopy : Apple jelly nodules. 4. Scrofuloderma (M/c in child).  Commonly present with sinus M/c site : Cervical LN Scrub Typhus :  Cause : Orientia tstsugamushi  Vector : Trombiculid mite  Skin lesion : Eschar + erythema  Rx : Doxycycline (DOC)  Pregnancy : Azithromycin  Note : Central scarring → Lupus Vulgaris  Central clearing → Tinea  Central crusting → Leishmaniasis PARASITIC SKIN INFECTIONS Scabies Causative organism: Itch mite – Sarcoptes scabiei. Incubation period: 2-3 weeks. Pathology: The fertilized female makes the characteristic skin burrow in stratum corneum. Clinical feature: Intense pruritus, worse at night and after a hot shower. Burrows – seen most commonly on interdigital webs, flexor aspects of wrists. Site: the face, scalp, neck, palms and soles are spared except in children. Nodular scabies – affects the scrotum. Norwegian scabies – hyperinfestation with thousands of mites, seen in steroid therapy, immunodeficiency or AIDS Treatment: Gamma-Benzene hemachloride (lindane) 1% solution (side effects – seizures and aplastic anemia). 5% permethrin cream – drug of choice. Benzyl benzoate. Ivermectin. SEXUALLY TRANSMITTED DISEASES SYPHILIS:  Caused by TREPONEMA PALLIDUM  C/F: PAINLESS CHANCRE +PRESENT Primary syphilis  IP : 9-90 days  C/F : Hard chancre (single, clean based,  indurated, non-tender, not bleed on touch)  Inguinal LN : B/L, enlarged, non-tender  rubbery LN.  IOC : Dark ground microscopy.  Slender organisms  (corkscrew motility). Secondary syphilis  Hematogenous spread. Constitutional symptoms.  Rash : Symmetric, non pruritic, polymorphic  (except vesicles & bulla). Palms & soles involved.  Generalised LNpathy (epitrochlear LN ++)  IOC : VDRL/ Rapid plasma reagin test (RPR).  Note : IOC for neurosyphilis : CSF-VDRL.  Rx= For early latent syphilis Inj.Benzathine penicillin single dose  Late syphilis 3 dose of Inj benzathine penicillin weekly once  Except neurosyphilis - Aqueous crystalline penicillin. Dark field microscopy : Corkscrew motility Chancroid  Etiology : Hemophilus ducreyi.  C/F : Soft chancre (mutiple, necrotic, non-indurated, tender, bleed on touch).  Inguinal LN : U/L Bubo + concommitant genital ulcer.  Gram stain : Gram -ve coccobacilli (pool of fish/ railroad track app).  Rx : T. Azithromycin 1g stat. Lymphogranuloma venerum  Chlamydia trachomatis L1, L2, L3  C/F : 1° stage : Single painless transient ulcer.  2°/ inguinal stage : Bubo (2/3rd U/L > 1/3rd B/L).  No concomitant genital ulcer.  Groove sign be seen.  3° stage : Genital elephantiasis.  Males : Saxophone penis  Females : Esthiomene  IOC : NAAT.  Rx : Doxycycline 100mg BD x 3 weeks Donovanosis/ Granuloma inguinale  Klebsiella granulomatis. IP : 8 - 80 days.  Ulcer : Single painless, beefy red, exuberrant granulation tissue. Bleeds on touch.  Inguinal LN : Normal. Pseudo bubo +nt (s/c nodule on groin).  Crushed tissue smear (Giemsa) : Pund cells with intra-cellular donovan bodies (closed safety pin app.)   Rx : Azithromycin till the ulcer heals. 1 g/wk x 3 wks (OR) 500 mg/day x 3 wks. Gonococcal urethritis  Neisseria gonorrhoeae  Gram negative intracellular diplococci  Inj. Ceftriaxone 500mg IM + Doxy 100 mg BD x one week (If Chlamydia is not excluded) Non-gonococcal urethritis  Chlamydia trachomatis D-K (M/c), Ureaplasma urealyticum, Mycoplasma genitalium, Trichomonas vaginalis  Scanty mucoid discharge  Numerous PMNs. Absence of GNICDC  Azithromycin 1g stat (or) Doxy 100 mg BD x 1 wk Herpes genitalis : Etiology : HSV-2 (90%), HSV-1 (10%). Vesicles → Rupture → Multiple, grouped, tender ulcers (polycyclic margins). Inguinal LN : B/L enlarged, tender. Diagnosis : Tzank smear - Multinucleated giant cells (MNG). Rx : T. Acyclovir 400 mg TDS x 7 days. PIGMENTARY DISORDERS Disorder of hyperpigmentation : MELASMA Lesion : Symmetrical Hyperpigmented macules. Site : Malar, Nose, Mandibular area In Pregnancy : Chloasma In Chikungunya : Chick sign (On nose) FRECKLES  Melanocyte number Normal  Melanocyte activity increase  Associated with Xeroderma Pigmentosa LENTIGENS  Melanocyte Activity : Normal  Peutz jegher syndrome (AD + Mucosal lentigenes +  Hamartomatous GI polyps) MONGOLION Dermal Melanocytosis : (Aka Ceruloderma) Blue SPOT slate grey coloured lesions. i. Mongolian spot : Age : Infants. Site : Lower back Fate : Spontaneous resolution BECKER’S Genetics : Acquired NEVUS Surface : Unilateral Hypertrichosis Site : Chest & Upper shoulder. Congenital Genetics : Congenital Melanocytic Surface : Hypertrichosis with Well Nevus demarcated borders (CMN) : Giant CMN : Size > 20 cm → 2.5% risk of melanoma. Disorders of Hypo/Depigmentation : a.Albinism Defect in : Tyrosinase. Types : Occular → Only eyes Occulo-cutaneous → Eyes, skin & hair. b.Piebaldism Inheritance : AD Defect : Neural crest Lesion : White Forelock c. Nevus Defective transfer of melanosomes to Keratinocytes. pigmentosus d.. Nevus Congenital white patch d/t vasoconstriction. Anemicus e. Vitiligo Acquired autoimmune destruction of melanocytes. f. Nevus of Symmetry : Unilateral, Nerve V1, V2 of trigeminal N ota Site Face & (sclera in 2/3rds) g. Nevus of Symmetry: Unilateral, Post. Supra clavicular N, Lat. Brachial ito cutaneous N , Shoulder, Scapular region SKIN APPENDAGES  HAIR  NAIL  GLAND HAIR CYCLE I ) ANAGEN :GROWTH 3YEARS II) CATAGEN : -INVOLUTION -3WEEKS III) TELOGEN  RESTING = 3MONTHS ALOPECIA Normal hair growth: Phases – Anagen = growing phase. Telogen = resting phase. Catagen = involution phase. Etiology: a. Non-scarring alopecia – Alopecia areata – autoimmune disease, ‘exclamation mark’ hair. a. Non-cicatricial alopecia (Non scarring) : 1. Patchy : Alopecia areata, Trichotillomania, 2° syphillis, Non inflammatory type of Tinea capitis (Black dot & Grey patch) 2. Diffuse : Secondary to stressor events. Anagen effluvium (2°to chemo/radiotherapy; occurs after 3-4 weeks) Telogen effluvium (2° to systemic stress- COVID 19, pregnancy; 3-4 months). Alopecia areata : Autoimmune disorder that targets the anagen hair bulb. Circular patch of complete hair loss. Exclamation mark hair with broad distal & tapering proximal end. Nail findings : Fine, regular superficial pits. Rx : For localised : Intralesional steroids like Triamcinolone. For extensive disease : Systemic steroids Male androgenetic alopecia (Hamilton classification) ----> Fronto temporal recession Balding of vertex. Female androgenetic alopecia (Ludwig classification) ----> Frontal hairline maintained. Diffuse thinning along central scalp Telogen effuvium: Diffuse hair loss occuring 2-3 months after a precipitating stimulus like infections, childbirth, surgery, hemorrage or emotional stress. Treatment: Alopecia areata – minoxidil. Androgenetic alopecia – topical minoxidil ± isotretinoin, finasteride, cyproterone acetate. Nail disorders : 1. Leukonychia : White nails. 2. Mees lines : Transverse white bands a/w Chronic arsenic poisoning. 3. Muehrcke’s Bands : Transverse paired white bands in Hypoalbuminemia. 4. Lindsay’s nails : Proximal half white, distal half brown ; in chronic renal failure. 5. Terry’s nails : Proximal 90% white, distal brown band ; in chronic liver failure. 6. Half & half nails - chronic renal failure 7. Paronchyia- Infection of Nail bed 8. Subungal hyperkeratosis- thickening of nails 9. Nail psoriasis- oildrop / salmon patch Cutaneous drug reactions Fixed drug eruption : Type IV Hypersensitivity reaction. Drugs : NSAIDs, Cotrimoxazole, Tetracyclines. Morphology : Circular dusky plaque. Recurs at the same site (FIXED). Heals with a very characteristic hyperpigmentation Erythema nodosum : Red tender nodules (anterior aspect of leg). MC cause : Idiopathic. MC infection trigger : Streptococci. Lofgren’s syndrome : Fever+ B/L Hilar LN + Arthritis + Erythema nodosum. Necrobiosis lipoidica diabeticorum : Waxy yellow plaque + surface telangiectasia over anterior aspect of leg. A/W diabetes mellitus. Pretibial myxoedema/ Thyroid dermopathy : Diffuse, non pitting edema. A/W Graves disease. Phrynoderma : Hyperkeratotic follicular papules. A/W essential fatty acid/ Vit A deficiency. Site: Elbows and Knees. Atopic Dermatitis Positive family history. Infantile pattern: involves face, neck, extensor surfaces and groin. Childhood pattern: involves flexural skin, particularly in the antecubital fossa and popliteal fossa. Type 1 Hypersensitivity Contact Dermatitis Delayed type of hypersensitivity mediated by memory T cells. Most common metal causing contact dermatitis in nickel. Most common site affected is hand. Most common cause of air-borne contact dermatitis– perthenium. Most common cause of contact dermatitis in Indian women – detergent. Barloque dermatitis due to cosmetics. Diagnosis: Patch test. HISTAMINE RELATED DISORDER 1. Urticaria : (Dermal edema)  Type I hypersensitivity mediated by histamine.  Types: i. Dermographism – triple response to minor strokes on the skin. ii. Solar urticaria. iii. Cold urticaria. iv. Cholinergic urticaria. Lesion : Wheal → Itchy transient plaque with central pallor & peripheral erythema. Dermographism : Stroking the skin with a blunt object → exaggerated wheal flare. Wood’s Lamp Generates 360 nm UV rays (black). Use: i. Coral red color – erythrasma. ii. Pale blue – pseudomonas wounds. iii. Yellow color – tinea capitis. iv. Pinkish red – porphyria cutanea tarda (urine). v. Others – tinea versicolor – pale yellow. vi. Ash leaf spots. Patch Test Skin hypersensitivity test (delayed type). Readings are made after 48 hours. Use: In the diagnosis of contact dermatitis. Staphylococcal Scalded Skin Syndrome (SSSS) Also termed as Ritter’s disease in neonates and toxic epidermal necrolysis in adults. Causative organism: Staphylococcus aureus phage group. II. Pathology: Infection is extracutaneous (conjunctivitis, otitis media, pharyngitis, etc.) and the cutaneous lesions are sterile. i) Target Dsg1 ii) Sepration of keratinocyte( intraepidermal just beneath granular layer) iii) Peeling of skin ( Nikolsky sign +) Clinical feature: Flaccid bullae and exfoliation of superficial epidermis. There is no mucosal involvement or systemic features (c.f. TEN). Mediator: Staphylococcal exfoliative toxin. III. TZANCK SMEAR – Acantholytic cells + but no inflammatory cells. Toxic Epidermal Necrolysis (TEN) Cause:  Drugs (most common) – phenytoin. Infections. Clinical feature: Widespread bullae with erythema and sloughing. Oral mucosa frequently involved. Systemic features are frequent and associated with high mortality. Diagnosis: SSSS and TEN are differentiated by punch biopsy with frozen section. SSSS involves – stratum corneum. TEN involves – stratum basale/germinatum. Erythema Multiforme Cause: 1. Herpes simplex virus – most common cause. 2. Drugs – sulfonamides. 3. Internal malignancy 4. Inflammatory bowel disease. 5. UV light. Clinical feature: Target or iris lesions. Vesicles and bullae.  Most commonly seen on palms, hands, soles, extensor forearms (most commonly the face and upper limbs). Hemorrhagic crust on the lips. Examples: Steven-Johnson syndrome. Toxic epidermal necrolysis. Toxic Shock Syndrome Cause: i. Staphylococcus producing TSS toxin1 or enterotoxin B or C. Most common clinical setting is menstruation. ii. Streptococcus pyogenes – producing pyrogenic exotoxin A. Clinical feature: Fever, macular red rash, hypotension, multiorgan failure. Hansens disease ( LEPROSY)  Chronic, inflammatory granulomatous disease.  Organism : o Mycobacterium leprae o M. lepramatosis  Ridley Jopling classification (Based on CMI) : TT, BT, BB, BL, LL TYPES OF LEPROSY FEATURES Tuberculoid (TT) 1-3 skin lesions. Annular plaque with central clearing & well-defined margin. A/w : Granuloma, anesthesia, alopecia, anhydrosis. Side profile : Saucer right way up appearance. Borderline tuberculoid (BT) 3-10 lesions. Well/ not so well-defined margins. Satellite lesions present. AKA Dimorphous leprosy. Mid-borderline (BB) : 10-30 lesions. (Polymorphic). Geographic map like appearance. Inner punched out margin (swiss cheese appearance).  Borderline lepromatous (BL) Skin lesions & Nerve thickening almost symmetrical. Inverted saucer appearance. Lepromatous (LL) : Systemic disease. Symmetrical. Early features : Epistaxis, pedal edema. Late features : Leonine facies, glove & stocking neuropathy  Nerve Bx → Radial cutaneous nerve or Sural nerve  Deformities :. Saddle nose , Madarosis Trophic ulcer. Foot drop (common peroneal nerve. PAUCIBACILLARY MULTIBACILLARY SKIN LESIONS 1-5 >6 NERVES NO NERVES / 1 NERVE >1 NERVE SSS Of AFB -VE +VE Duration of treatment 6 MONTH 12 MONTH No. of drugs given 3 3 TREATMENT :  Rifampicin (D1 : 600 mg/month),  Dapsone (D1-D28 : 100 mg/day)  Clofazamine (D1 : 300 mg/month; D2-D28 : 50 mg/day)  Chemoprophylaxis (for contact ≥2 yrs) : Single dose Rifampicin (except in TB, leprosy pts). Thanking you …..