Skin Quick Revision Notes PDF

SKIN QUICK REVISION NOTES DERMATOLOGY BASICS: Layers of Skin Stratum Corneum Dead layer, Flat cells, No nuclei Stratum Lucidum Palms & Soles Refractile granules of Eleidin Stratum Granulosum Keratohyalin granules – produce Fi...

SKIN QUICK REVISION NOTES DERMATOLOGY BASICS: Layers of Skin Stratum Corneum Dead layer, Flat cells, No nuclei Stratum Lucidum Palms & Soles Refractile granules of Eleidin Stratum Granulosum Keratohyalin granules – produce FilaggrinQ Lamellar granules / Odland bodies – Lipids Stratum Spinosum Desmosomes are intercellular structures which help in the attachment of keratinocytes Keratin synthesis Stratum Basale / St. Highly mitotically active (proliferating) Germinativum Epidermal Turnover Time (ETT) / Skin Doubling Time Time taken by keratinocytes to move from stratum Basale till shedding off in the environment 8 weeks (42 – 75 days)Q Epidermal turn-over is 4 days in Psoriasis.Q 2 Cerebellum Quick Revision Notes Intra Epidermal / Inter cellular K-K bridges Defect in Desmoglein (Dsg) – Pemphigus Row of tomb stone appearance seen in pemphigus as Hemidesmosomes are uninvolved.Q Cells Of Epidermis Keratinocytes Non-Keratinocytes Desmosomes Ectodermal in Langerhans cells origin Melanocytes KIF – Keratin Merkel cells intermediate filaments Characters: Langerhans cells Melanocytes Merkel cells Location Spinosum Basale Basale Origin Bone marrow (macrophages) Mesoderm Neural crest Ectoderm Components Birbeck granules tennis racquet appearance on electron Melanosomes Neurosecretory microscopy granules Function Antigen Presenting Cells Melanin Mechanoreceptors pigment (Touch): slow producing cell adapting low threshold receptors. (SALT) Example Langerhans cell histiocytosis Melanoma Merkel cell carcinoma Markers S100, CD1a, CD-207 (Langerin) Most specific markerQ S100, HMB 45 CytoKeratin - 20Q Melan- AQ  3 Skin Subcutaneous Layer Aka – PANNICULUS / HYPODERMIS / SUBCUTIS Fat lobules & their Septa form subcutaneous layer Panniculitis: Inflammation of subcutaneous layer. There are 2 types of panniculitides –– Septal Panniculitis – Erythema nodosumQ –– Lobular Panniculitis – Bazin disease Dermatopathology: Basement Membrane Junction / Stratum corneum Stratum spinosum Dermo-Epidermal Junction Hyperkeratosis: Ballooning degeneration Specialized zone connecting the epidermis & pathological thickening (intracellular edema) Dermis inside stratum spinosum Parakeratosis: Spongiosis; intercellular Layers of Dermis - retention of nucleus edema in-between cells.Q Dermis divided into 2 layers –– Superficially, Papillary dermis – Constitutes C/F Of Acantholytic Cells 1/10th portion of the dermis. 1. Oval shaped cells, –– Deep, Reticular dermis – Constitutes 2. Have large nucleus, remaining 9/10 portion of the dermis. 3. Shows perinuclear halo 4 Cerebellum Quick Revision Notes To see these cells Tzanck smear is prepared Acantholytic cells seen in (Giemsa stain) Autoimmune: pemphigus group Infection: bacterial / viral Bacterial: bullous impetigo, Staphylococcal Scalded Skin Syndrome Viral: HSV infection Genetic: Hailey hailey disease, Darier disease. Lines in Dermatology: Blaschko’s lines: Langer lines: RSTL Pathways of epidermal cell migration during Collagen fibre orientation in the dermis corresponds to embryonic development them Do not correspond to arteries/veins/nerves Applied: put incision along or parallel to these lines→ V shaped on upper spine healing better without scarringQ S shaped on abdomen Spiraled on scalp Linear on lower extremities Ex: Incontinentia pigmenti (X linked dominant inheritance)Q Diascopy: Vitro Pression Test Press the lesion with Glass slide Uses of Diascopy:  5 Skin Erythema Purpura Apple jelly nodulesQ (Extravasation of RBCs) Redness disappears: blanching RBCs degenerate along with Erythema disappears, granulomas become response staining of blood vessel wall. prominent: apple jelly nodules – Lupus vulgaris Redness persists: non blanching response Dermatological Investigations Woods lamp examination: Wavelength: 360-364nmQ Made of filter: 9% nickel oxide+ barium silicate Tzanck smear (Cyto-Diagnostic test) Microsporum Blue green Trichophyton schonleinii Dull blue Pityriasis versicolor Yellow Corynebacterium Coral red fluorescenceQ minutissimum Vitiligo Milky white Pityriasis versicolor: Yellow florescence Fluid filled lesion (Vesicle/ Bulla) →deroof the lesion → scrapping from floor & roof → Giemsa stain 6 Cerebellum Quick Revision Notes Acantholytic cells: pemphigus group & Herpes Multinucleate giant cells: HSV 1,2 & Varicella infections. infections Dermatological Therapy 1. Cryotherapy: 2. Phototherapy Agent: liquid nitrogen (-196 Celsius) UV rays Mechanism: freeze tissue → Cellular death NB-UVB (Narrow band UV B radiation) wavelength 311+-2nm Indication: Warts & keloids PUVA: Psoralen (P) (Photosensitizer) + UVA therapy wavelength 320-400nmQ Psoralen is given prior to UVA for better penetration of skin. Indications: Psoriasis, Vitiligo, Atopic dermatitis Classification Of Bullous Disorders: Intraepidermal blistering Subepidermal blistering 1. Immunobullous disorders disorders (superficial): disorders (deeper): 2. Mechanobullous disorders Pemphigus group of disorders Pemphigoid group 3. Inherited acantholytic disorders & dermatitis herpetiformis Immunobullous Disorders (Immuno=Autoimmune) Pemphigus group of disorders: Level: Intraepidermal Classification: based on the level of the split in the skin Target proteins: desmosomes (connects keratinocytes to each other)  7 Skin Acantholysis is the process by which Nikolsky Sign: desmosomes get ruptured/separated What is to be done: apply tangential pressure Desmosomes over skin What happens: upper layers of epidermis separate from lower layers Keratinocytes Pemphigus Foliaceous Pemphigus Vulgaris *First Desmoglein-1 antibody Desmoglein-3>1 antibodies Expression of Desmoglein 1 & 3 (skin / mucosa) Desmoglein-1 Desmoglein-3 Bulla Spread Sign: Skin Upper epidermis Lower epidermis What is to be done: apply lateral pressure over Oral Low concentration/ High concentration bulla mucosa absent What happens: extension of margin of bulla with P. Foliaceous P. Vulgaris irregular angulated border in case of pemphigus (Desmoglein 1 (Desmoglein 3Q vulgaris antibody) antibody) Skin split Subcorneal split Suprabasal split Desmoglein-1 Desmoglein-3>1 Mucosa No oral lesions ++ in 95% cases How to look for Acantholysis: Clinical: Lab: Asboe-Hansen sign Nikolsky sign Tzanck smear Asboe Hansen sign Histopath Bulla spread sign variation Bulla spread sign It applies to smaller, intact, tense bullae where the pressure is applied to the center of the blister. 8 Cerebellum Quick Revision Notes –– Suprabasal Split - Few rounded cells in the blister cavity (Row of tombstones) : acantholytic cells Intraepidermal split Subepidermal split Thin roof Comparatively thick roof Direct immunofluorescence Flaccid bulla Tense bulla –– IgG & C3 deposited Intraepidermally & in between the keratin cells (intercellular) Wrinkling + on surface Absent –– Shows fishnet/ chicken wire patternQ Pemphigus vulgaris Primary lesions: Flaccid bullae over the normal skin →Secondary lesions: erosions (tend to extend / no tendency to heal) Site: scalp, oral mucosa (DSG-3>1), chest, trunk, flexures Buccal mucosa & Gingival mucosa can be involvedQ Treatment of Pemphigus vulgaris: Flaccid bullae with erosion which could show no tendency to heal and eventually spreading Systemic steroids (vigorous) are the main stay further on the skin treatment modality Lab: Cyclophosphamide: monitor urine routine DCP pulse: Dexamethasone Cyclophosphamide Tzanck smear (Cytodiagnostic test) Pulse –– Vesicle Deroofed - Base scraped- Giemsa 3 days admitted DCP given 27 days low dose Stain Cyclophosphamide –– Acantholytic cells/Tzanck cells- Round cell, Moderate to severe Pemphigus vulgaris prominent nucleus, perinuclear halo Rituximab (FDA approved in 2018), Anti-CD20 Histopathology of Pemphigus vulgaris (CD20 on B cells)  9 Skin Subepidermal Immuno Bullous Disorders Pemphigoid group Dermatitis herpetiformis Pemphigoid group defect lies in Basement Membrane Zone proteins KIF keratin intermediate filament Hemidesmosome complex Lamina lucida Lamina densa Sign Bullous Pemphigoid Pemphigus vulgaris Sub Lamina densa Nikolsky sign Negative Positive (acantholysis) Bulla spread Extension with Extension with Zones Components sign regular border irregular border KIF keratin intermediate Keratin 5/14, BPAG 2 & 1 Asboe Extension with Extension with filament Hansen’s sign regular border irregular border Hemidesmosome complex Investigations: Lamina lucida BPAG 2 (Transmembrane molecule), Tzanck smear: Presence of eosinophils, Absence Laminin of acantholytic cellsQ Lamina densa Laminin Histopathology Collagen 4 Subepidermal Split Sub Lamina densa Collagen 7 (anchoring fibrils) *Seven Bullous Pemphigoid Immunobullous disease with a subepidermal (deeper) split IgG is the autoantibody deposited Target protein: HemidesmosomesQ Target antigens: BPAG 2 >1 (Bullous Pemphigoid Antigen) Direct ImmunoFluorescence No acantholysis - Nikolsky sign absent –– Autoantibody: IgG, C3 - Site: Basement Membrane Zone, Linear patternQ Clinical Features 60 to 80 years of age (males=females) Primary lesions: –– Tense pruritic bullae on erythematous skin or normal skinQ 10 Cerebellum Quick Revision Notes Clinical Features Autoantibody: IgA Bullae itchy → Erosions due to scratching/ Age: children itching Morphology: Annular arrangement of vesicles Tend to heal / No tendency to extend (studded at margins) Very good prognosis Cluster of jewels / string of pearls appearance Dapsone Rx Treatment: Topical steroids Low dose oral steroids Pemphigoid Gestationis: Aka Herpes Gestationis Bullous Pemphigoid in pregnancy Target antigen BPAG2 LABD Bullous Pemphigoid Child – CBDC Adult - LAD DIF Linear Linear Autoantibody IgA IgG Dermatitis Herpetiformis aka Duhring C/F: Tense bullae & Urticarial plaques disease Periumbilical region: important site to note Chronically relapsing, itchy, subepidermal immunobullous disease Extends to the thighs & abdomen Autoantibody: IgA Treatment: systemic steroids DOC Target antigen: epidermal transglutaminase 3 1. Linear IgA Bullous Dermatosis HLA associations: HLA DQ2 DQ8Q Children: CBDC Chronic Bullous Dermatosis of childhood, Systemic important clue: gluten sensitive enteropathy (asymptomatic) Adults: LAD Linear IgA Disease Manifestations: malabsorption, diarrhea Chronic Bullous Dermatosis of abdominal pain Childhood (CBDC) Course: Chronically relapsing, itchy, subepidermal immunobullous disease 20-40 years of age M>F ratio is 2:1 C/F: Primary lesions: extremely itchy Papulo vesicles  11 Skin Treatment Gluten free diet: Avoid Barley Rye Oats, Wheat –– BROW should not be consumed DOC: DapsoneQ Mechanobullous disorders almost synonymous to Epidermolysis Bullosa Mild mechanical injury →Blisters / bullae Secondary lesions: Grouped excoriations Genetic Sites: extensor & pressure points over the trunk & extremitiesQ EB Simplex K5 / 14 Investigations: EB junctional laminin in lamina lucida Tzanck smear EB dystrophic Collagen 7Q –– Neutrophils Clues by examiner: Histopathology Consanguineous marriage→ (Genetic) –– Subepidermal split, Papillary tip microabscess: Mom → handling the baby → blisters (Mechanical neutrophils trauma induces blisters) Ix: DIF Negative Microabscess - collection of neutrophils Direct ImmunoFluorescence: –– IgA is deposited at the Basement Membrane Zone & dermal papilla granular patternQ DIF findings Dermatitis Herpetiformis LAD aka Duhring disease Autoantibody: IgA IgA Location: Basement Membrane Zone & BMZ dermal papilla Treatment: Pattern: granular pattern Linear GENE Therapy (definitive) supportive management 12 Cerebellum Quick Revision Notes Inherited acantholytic disorders Alopecia Dariers disease or Hailey Hailey Loss of hair Keratosis disease or chronic Classification: *Cicatrix means scar follicularis benign familial pemphigus Non scarring (non-cicatricial) Inheritance AD AD Scarring (cicatricial) - Stem cells in Bulge area Defect Ca +2 ATPase Ca +2 ATPase are damaged involvement involvement Gene defect ATP 2A2 ATP 2C1 Chromosome 3 chromosome 12 Non cicatricial alopecia classification: Patchy Diffuse Patterned Systemic Alopecia areata Effluvium Androgenetic alopecia SLE Trichotillomania Anagen (chemo & Radio) Thyroid Tinea capitis (non-inflammatory) Telogen (Stress, Infections) dysfunction Secondary syphilis Alopecia Areata Exclamatory Mark Hair Sign Areata: patchy/ spotty areas of alopecia Autoimmune disease which Targets anagen hair Histopathology of Alopecia Areata bulb Peribulbar lymphocytic infiltrates Clinical Features Swarm of bees appearanceQ Circular areas of complete hair loss Nail pitting No signs of inflammation seen Regular Margin of lesions: Exclamation mark hair superficial (Geometric) Autoimmune disease Distal end broad Proximal end tapering  13 Skin Treatment Localized disease Extensive Disease Topical steroids: Clobetasol Systemic Steroids (Most potent) Q ILS (triamcinolone acetonide) Scarring Alopecia (also used for scabies) Papulosquamous disease: Lichen Plano pilaris Trichotillomania (LPP) A psychiatric condition (OCD) characterized by Granulomatous disorders: Sarcoidosis pulling out of one’s own hair (mostly in Females) Connective tissue diseases: Discoid Lupus Erythematosus, Systemic Lupus Erythematosus Infections: Tinea capitis (inflammatory): Favus, Kerion Classification Of Sweat Glands Eccrine glands Apocrine glands Site: Entire body (palms & Axilla, areola, soles) Groin Opening: Directly open onto Along Hair follicle Incomplete loss of hair in a given patch skin surface Variable lengths of hair follicles seen Nerve Cholinergic Adrenergic Perifollicular hemorrhage supply: sympathetic sympathetic Secretion Androgen Patterned Type / Non Cicatricial depends on dependent (glands Alopecia / Androgenetic AlopeciaQ present at birth→ active puberty Function Sweat production → Pheromones Thermoregulation associated with Body odour Blockage of Eccrine glands: Miliaria Male pattern AGA Female pattern AGA Hamilton Ludwig, Olsen Fronto-temporal Frontal hairline maintained recession Loss of hair over the central Balding of vertex portion of scalp 14 Cerebellum Quick Revision Notes Fox Fordyce disease: Due to obstruction of the Apocrine duct Morphology: multiple skin-colored pruritic papules Sites: Axilla, Areola of the nipple Eyelids: meibomian glands & glands of Zeis Ectopic sebaceous glands (no association with hair Prepuce: Tyson’s glands follicle) Upper lip, buccal mucosa: Fordyces spots Presents as yellow micro papules Acne Vulgaris Chronic inflammatory disease of the pilosebaceous unit Breast: Montgomery tubercles Polymorphic cutaneous lesions (Comedones = Specific lesions) Organism: Cutibacterium acnes (Propionibacterium acnes) 4 Grades Grade 1 Acne Vulgaris Open comedones Closed comedones Black because of oxidation of the sebum by the atmospheric air White  15 Skin Treatment Topical Retinoids: Vitamin A analogue (Tretinoin, Adapalene) (ISOTRETINOINis not topical) Grade 2 Acne Vulgaris Grade 3 Acne Vulgaris Grade 4 Acne Vulgaris Predominant Red Papular Lesions Prominent Pustular Lesions (Most Severe form): Nodulocystic Acne with Scars Treatment Differential Diagnosis DOC: isotretinoin = 13 Cis Retinoic acid Acne Rosacea Indication: Nodulocystic acne, resistant Morphology: Comedones Comedones absent recalcitrant acne (Usually Grade 3)Q present Papules, nodules & Most common side effect: cheilitis (dryness of Papules, pustules present lips) nodules Dose: 0.5-1 mg/kg/ body weight daily (TCD: pustules & 120-150 mg/kg body weight). scars Associations Skin greasy Erythema flushing –– Investigation when on oral retinoids for acne background: & telangiectasia Lab monitoring: Fasting lipid profile, LFT as prominentQ oral retinoids are associated with increased Distribution: Face upper Convexities of triglycerides & total cholesterolQ part of trunk face Centro facial Important Syndromes Associated with Acne chest & lesion, cheeks, nose shoulders & forehead, spares SAPHO syndrome SAHA HAIRAN periorificial area syndrome Syndrome Synovitis Hyper Acne Rosacea Acne Seborrhoea Androgenism Chronic inflammatory facial dermatoses Pustulosis Acne Insulin Sites: Centro-facial areas (convexities of the Hirsutism Resistance Hyperostosis face) Osteitis Androgenic Acanthosis Sunlight, spicy food, alcohol, stress alopecia Nigricans PAPA syndrome Abnormal vascular reactivity (flushing)Q Pyogenic Arthritis Pyoderma gangrenosum Acne 16 Cerebellum Quick Revision Notes Papulopustular stage: papules & pustules present Phymatous type: aka potato nose Lesion: skin over the nose becomes thick Otophyma - Thickening over the ear Surface of nose: prominent pores, surface Rosacea SLE nodularity Photosensitivity Present Absent Pathology: characterized by hypertrophy & fibrosis of the sebaceous gland Malar rash Triggers in Spicy food, Absent CO2 laser excision followed by resurfacing is history alcohol, TOC stress Papules & Present Absent pustules Erythema Transient / Fixed Fixed Systemic Absent Fever, arthralgia, features myalgia, oral ulcers Leukonychia / White Nails: True leukonychia Apparent leukonychia Nail matrix Nail bed Rhinophyma - Thickening over the nose Mees lines Muehrcke’s bands Half & half nails / Lindsay nails Terrys nails True Leukonychia Chronic arsenic poisoning Mees lines: horizontal, transverse white bands on the nail plate Gnathophyma - thickening over the chin  17 Skin Apparent Leukonychia Muehrcke’s bands - paired transverse white bands Half & half nails / Lindsay nails Terry’s nails Muehrcke’s bands: Conditions seen in: Hypoalbuminemia / Nephrotic syndrome/ Malnutrition Half & half nails / Lindsay nails Terry’s Nails Kidney failure Liver disease Proximal 50%: white/pale proximal (90%): white/pale Distal (50%) brown to pink distal (10%): pink to brown Pigmentary Disorders Freckles/ Lentigines ephelides Melasma Sites: Sun exposed Sun exposed & Presentation: Symmetrical hyperpigmented protected brownish macules -> Nose, malar area, and Melanocyte Normal Increased mandibular area. number Differential diagnosis: SLE Melanocyte Increased Normal Activity Seasonal Summer Constant colour variation worsening+ Associations: Xeroderma Peutz Jeghers pigmentosum syndrome Melasma SLE Malar rash Present Present Unique Brown - Black Red feature Peutz Jeghers syndrome: Autosomal Dominant Inherited Condition Characterized by mucosal lentigines and Gl polyps. Most common site for polyp is jejunum. 18 Cerebellum Quick Revision Notes Most common type of polyp is Hamartomatous Nevus of Ota: Nevus of Ito Unilateral Follows the Blue to slate grey colour posterior Follows the 1st & 2nd supraclavicular & division of Trigeminal lateral brachial nerve (ophthalmic and cutaneous nerves. Maxillary divisions). Site: upper Site: Face. shoulder and back 2/3rd of patients has Becker’s Nevus scleral involvement. Nevus of HORI = B/L CMN (Congenital BECKERS NEVUS (Puberty) Nevus of Ota Melanocytic Nevi) Acquired nevus, seen during *>20cm has higher risk puberty of malignant melanoma Black Brown Thick skin Normal Folds Normal Uni / Bilateral Unilateral Site: Chest and upper shoulder. Becker’s nevus Nevus of ITO Unilateral, brown patch Blue patch on shoulder, upper on shoulder, back back Hypertrichosis + -ve Onset: Puberty Birth Dermal Melanocytosis Proliferation of melanocytes in the dermis →Blue colour. Ceruloderma Cerulo blue, derma skin. Blue to slate grey in colour (due to Tyndall effect) Mongolian Spot: Treatment of Nevus of Ota/Ito: Q switched Nd YAG Infants laser. Common site is lumbo-sacral DISORDERS OF HYPO/ Resolves spontaneously DEPIGMENTATION Congenital Disorders Of Hypo Depigmentation. Albinism Biochemical Defect: Tyrosinase defective  19 Skin 2 types: Nevus depigmentosus / Nevus anemicus (Not 1. Ocular albinism: involvement of only the Eyes, Achromicus a Melanin disorder) (Pharmacological Defect) 2.Oculocutaneous albinism Involvement of eyes, skin Defect in the Transfer Defective Blood vessels and hair. of Melanosomes to the → Vasoconstriction Keratinocytes Congenital Onset is at birth Pale looking → Presents as Decreased Blood supply depigmented macule → Decreases colour with feathery margins. Acquired disorders of hypo/ depigmentation Vitiligo Piebaldism: Most accepted theory: Auto-antibodies destroy Major characteristic of Piebaldism is a white forelock the Melanocytes → melanocyte absent from the (a patch of white hair directly above the forehead). lesion. Autosomal dominant. Association: Thyroid dysfunction, T1DM, Defect in neural crest function. Pernicious anaemia Clinical features - Depigmented chalky white macules → Melanocytes are AbsentQ 3 varieties 1. Segmental 2. Non segmental 3. Unclassified/ undetermined Segmental Vitiligo Starts at early childhood. Unilateral, Segmental, does not cross the midline White forelock -> Characteristic lesion. Mainly over forehead Treatment - Surgical intervention melanocyte transplanting, skin grafting Islands of normal skin: Trunk, within the white patch Non-segmental Vitiligo 20 Cerebellum Quick Revision Notes Acrofacial vitiligo - Face, head, and distal extremities Mucosal vitiligo - Involves > 1 site, Vitiligo vulgaris (most common type): Symmetrically Distributed depigmented macular lesions Universal vitiligo → 80- 90% body surface area depigmented Exaggerated white fluorescence can be seen due to presence of collagen in the dermis Treatment Acrofacial Vitiligo Universal Vitiligo Based on the body surface area (BSA) involved 1. 20% BSA involved: Systemic steroids (halt the progress of disease), Azathioprine. (Chronic duration therapy) Mucosal Vitiligo Vitiligo Vulgaris NBUVB (Narrow Band UV B radiation) at 311 nm Wavelength. (Safer) Unclassified/ Undetermined Vitiligo: Focal vitiligo Small, isolated depigmented Chemical Leukoderma lesions - 1-2 over the body Melanocyte destruction due to Chemicals –– Bindi dermatitis: Para tertiary butyl phenol (PTBP) glue present destroys the melanocytes Koebner’s phenomenon Leucotrichia True Koebner’s phenomenon: Hair follicle melanocytes new lesions appear at the are involvedQ site of trauma –– Rubber footwear: Contains Mono Benzyl Ether of Hydroquinone (MBEH) causes destruction of melanocytesQ  21 Skin Alta dye has Crocein scarlet MOO & solvent –– Site: Extensors & Lumbo-sacral (Elbows, yellow 3 causes the depigmentation knees, Back)Q Psoriasis Definition: Chronic, T cell mediated inflammatory disease involving skin & multiple systems. Pustular Psoriasis Skin: Erythematous plaques with Silvery white scaling Sterile pustules (tiny pus filled lesions) with inflammatory cells (not infectious cells) Systems: Joints → Arthritis & Metabolic syndrome (Hyperlipidemia, Hyperglycemia, Trigger: sudden withdrawal of systemic hypertension, visceral obesity). steroidsQ Triggering Environmental factors Clinical features: sheets / lakes of pus 1. Seasons - Exacerbation during winters 2. Infections - HIV, Streptococcal Infection (Guttate) 3. Drugs 4. Substance abuse - Alcohol, smoking Pathogenesis Epidermis: keratinocyte hyperproliferation Dermis: inflammation Etiopathogenesis Generalized pustular psoriasis Cellular components Signaling molecules (Cytokines) Th1 IL-2, TNF alpha, IFN-gamma Acute form : Th17 IL-17 Von Zumbusch Type Pregnancy : Th22 IL-22 Pro-inflammatory cytokines Pustular psoriasis of Pregnancy(PPP) Clinical Types of Psoriasis Or Chronic plaque psoriasis / Psoriasis Vulgaris Impetigo Herpetiformis (Misnomer) Clinical features Impetigo = Bacterial –– Lesions: Erythematous scaly papules & plaques Herpes = Viral –– Scales: micaceous silvery white scales 22 Cerebellum Quick Revision Notes Erythrodermic Psoriasis:(Red Skin) 2. Koebners phenomenon Exfoliative Dermatitis 3. Wornoff ring It is presentation (not a disease) >90% BSA Auspitz SignQ showing erythema +- Scaling Glass slide→ Scrape psoriasis lesion (Grattage There are multiple causes of erythroderma ex: test) psoriasis Accentuation of silvery white scales Burkeley membrane Pin point bleeding spots Psoriatic arthritis Koebners Phenomenon / Isomorphic Response: Clinical significance: Disease is active, so patient should be advised to avoid any unnecessary trauma Appearance of morphologically similar lesions along the lines of trauma over normal skin Types of Koebners phenomenon.Q Seronegative arthritis (RF factor negative) True Pseudo Rare causes Erosive arthritis Immunologic Autoinoculation Kaposi sarcoma, Classical joint involved: DIPQ Darier disease, Lichen nitidus Worst type: Arthritis mutilans severe destruction (shortening of digits) Psoriasis Viral infections lichen planus molluscum Dactylitis: Inflammation of digits Vitiligo contagiosum Special Signs Phenomenon features (Depigmented viral wartsQ lesions) 1. Auspitz sign  23 Skin Wornoff’s Ring Subungual hyperkeratosis: Below the nail plate material is depositedQ Hypopigmented rim around psoriasis lesions Onycholysis: separation of the nail plate from Due to abnormal prostaglandin levels in the the underlying nail bed peripheral zone of lesionsQ Oil drop sign = Salmon patch Clinical significance: Pathognomonic of nail psoriasis Description: Yellow discoloration of nail bed Nail Psoriasis Matrix Nail bed Pitting Oil drop sign (Salmon Patch) Leukonychia: white Onycholysis discoloration of nail plate Thickening of nail plate with yellow colored discoloration Subungual hyperkeratosis is also present Splinter hemorrhages Pitting of nails Lesions: Depressions in nail plate Clinical significance: MC nail change in psoriasis Types: DIC (Deep, Irregular, Coarse) (Opposite in Alopecia Areata)Q Defect: Proximal nail matrix 24 Cerebellum Quick Revision Notes Psoriasis Alopecia areata Stratum Granulosum Deep Irregular Coarse Superficial regular Absent / decreased granular Wedge shaped pits Geometric layer: psoriasis vulgaris, Hypergranulosis: lichen icthyosis vulgarisQ planusQ Regional Variation Of Psoriasis Scalp Psoriasis No alopecia present only thick micaceous scales Micro abscess Cells Disease Munroe's Neutrophils in Psoriasis microabscess stratum corneum Spongiform pustules Neutrophils in Psoriasis of KogojQ stratum spinosum Inverse Flexural psoriasis: Scaling absentQ Stratum Corneum Parakeratosis Spongiform pustules of Kogoj Hyperkeratosis: pathological thickening Parakeratosis: retention of nucleus Munros’s microabscess  25 Skin Systemic Therapy Biological agents: Targeted therapy Ustekinumab: IL-12 & 23 Guselkumab, Risankizumab, Tildrakizumab: IL- 23 GRT Infliximab, Etanercept, Adalimumab: TNF- alpha inhibitors Secukinumab, Ixekizumab: IL-17Q Brodalumab: IL-17 (R) Psoriasis important negative points: Supra Papillary Thinning Never involves CNS Histopathology of Psoriasis Never affect Mucosa (Geographic tongue) Parakeratosis: Retention of nucleus in topmost No Itching layer No Alopecia Agranulosis: Absence of stratum granulosum Auspitz’s sign is negative in Inverse and Acanthosis= Thickening of stratum Spinosum Pustular Psoriasis. Dermal papillae are enlarged resulting in Supra Lichen Planus papillary thinning Definition: chronic yet self-limiting (1-2 Dermal T-cell infiltration years) immune mediated inflammatory disease Dilated & Tortuous dermal Vessels (results in affecting the skin, mucosa & hair follicle pin point bleeding when lesion is Scraped) Provocative factors: - Most important: Dental From tip of these dermal papillae, inflammatory amalgam (Presence of mercury) Cells Come out & starts collecting in epidermis –– Infections: Hepatitis C & BQ known as spongiform pustules of kogoj generally present in stratum Spinosum + –– Drugs: AntiMalarials, ACE inhibitors, Beta Stratum Basale i e in Malpighian layer) BlockersQ Munros microabscess (Generally present in Reticulate Lacy Stratum Corneum) Pattern Treatment & Options in Psoriasis Basis: BSA 10% Dental Amalgam 1. Topicals: BSA 10% 3. Systemic agents: BSA >10% Oral involvement: 30-70% Methotrexate Psoriasis vulgaris, Pso arthritis, Reticulate lacy white pattern (net like pattern)Q (Teratogenic) Erythrodermic psoriasis Acitretin Pustular psoriasis & HIV Ulcerative / Erosive LP: premalignant lesion (chance of developing into malignancy +ve) (Teratogenic) Steroids Impetigo herpetiformis, Psoriatic Morphology erythroderma in pregnancy 6 P’s 26 Cerebellum Quick Revision Notes 1. Pruritic Nail Involvement: 2. Purple M/C finding: thinning of nail plateQ 3. Polygonal Most characteristic finding: pterygiumQ of nail 4. Plain topped wing shaped/ triangular shaped fold extend from Proximal Nail Fold→ destroys nail plate 5. Papules reaches nail bed 6. Plaques Hair Involvement: Wickham’s Striae Patient complains of Hair loss: scarring alopeciaQ Surface of LP seen with magnifying lens with (hair destroyed) oil on top of lesion: whitish linear streaks Wickham’s striaeQ Lichen Plano Pilaris Activity Perifollicular Lichenoid Papules + Scaling + Stratum Granulosum Koebners phenomenon will be positiveQ Saw-toothing rete-ridges  27 Skin Lichen Planus Psoriasis Genetic - + Itching Most Not common common++ Oral & Hair Wickhams - Striae++ Scarring Alopecia Arthropathy - + Histopathology of L.P S.C -- ++ Hyperkeratosis in SC Parakeratosis Wedge shaped Hypergranulosis in SG S.C Munroe’s -- ++ Thickening of SS: Acanthosis Microabscess Saw toothing rete ridges Stratum Hyper.G Hypo.G Granulosum Band like lymphocytic infiltrate at Dermo Epidermal JunctionQ Stratum Irregular Regular Spinosum Acanthosis Acanthosis Basal cell degenerationQ Rete Saw tooth++ Elongation Necrotic keratinocytes / colloid bodies / +(Camel foot) Civatte bodiesQ S. Basale Interface Artefactual cleft at Dermo Epidermal Junction: dermatitis++ Max joseph spaceQ Melanin P’s in Lichen Planus incontinence++ P/Flexors, Purple, Pruritic, Plane topped, Polygonal, Papules, Plaques, Pterygium, Pup tent Pityriasis Rosea sign, Acute self-limiting (6-12 weeks) disease, Pigmentation (lesions heal with Etiology: M/C viral trigger: HHV 7,Q hyperpigmentation). Morphology / course: P’s in Lichen Planus NOT POLYHEDRAL  Treatment Limited: topical steroids & ILS for Hypertrophic LPQ Widespread disease: systemic steroids Phototherapy & Steroid sparing agents like Mtx & Dapsone. 1st lesion: Annular Herald patch/ mother patch *Chronic Inflammatory Disease, Papulo-squamous 1-2 weeks laterQ Disorders are common for psoriasis & lichen planus Secondary lesion: scaly papules →oval annular plaques→ mild pigmentary changes → fades slowly in 6-12weeks. 28 Cerebellum Quick Revision Notes Scales: collarette (collar like) → outer edge: within the active margin of lesion (attached)Q Inner edge: Free Distribution of lesions Christmas tree pattern Downwards & outwards from the spine--> along the lines of Langer (lines of skin tension) >90% of body surface area gets involved (parallel to the ribs) (erythroderma) Islands of sparing (some patches of the body are spared) Palms & soles - thick skin Palmoplantar keratoderma PRP sandal Pityriasis Rubra Pilaris: Clinical features: hyperkeratotic perifollicular papules (Nutmeg Grater appearance) Eczema Response of skin to Endogenous (internal) or exogenous (external) Stimuli. All eczema is dermatitis, but NOT ALL dermatitis is eczema Initially discrete → Progress to form confluent orange red erythema in cephalo-caudal direction Etiologic Classification Exogenous Endogenous Contact Dermatitis Seborrheic dermatitis/dandruff Photodermatitis Stasis eczema Phytodermatitis Asteatotic eczema Pityriasis alba Nummular eczema Pompholyx  29 Skin Morphological classification of eczema: Acute Eczema SubAcute Eczema Chronic Eczema Erythema. Erythema LichenificationQ Edema. Scaling Chronic Itching → Skin → Safety Vesicles. measure Oozing 1. Thick skin 2. Hyperpigmentation 3. Exaggerated skin markings Crusting HPE: Spongiosis intercellular edema between cellsQ Contact Dermatitis: 2 types ICD (Irritant contact dermatitis) ACD (Allergic contact dermatitis) Affects All who are exposed Affects genetically predisposed (Atopy +ve) Reason Non-immunologic (direct tissue Immunologic (Type IV hypersensitivity reaction damage) Sensitization needed Lesions Restricted to site of contact Tends to disseminate beyond the site of contact Complaints More burning More itching Examples Diaper dermatitis: Involves convex Hair dye: PPD (para phenylene diamine) areas Sparing the folds Diagnosis Patch Test 30 Cerebellum Quick Revision Notes Important Examples of Allergens causing ACD Substance in the air→ settles on the exposed parts of the skin→ ABCD Hair dye: PPD (para phenylene diamine)Q Plant: Parthenium hysterophorus (congress Metal: Nickel (most common) grass / communist plant)Q Topical antibiotic: Neomycin. Cement: Potassium dichromate. Bindi: PTBP (para tertiary butyl Phenol)Q. Seborrheic Dermatitis/Dandruff Feature: Inflammatory response of seborrheic areas to Malassezia. Yeast Sites: Scalp, face, nasolabial folds, Retro- auricular region. Scales Greasy yellow Severe disease: Seen in Parkinson’s disease, HIV infection Patch test: Principle → Type 4 Hypersensitivity Reaction. Method: Allergens are applied over the patient’s back & wait for type 4 / Delayed hypersensitivity Infantile Seborrheic Dermatitis: Cradle Cap Stasis Eczema Synonym: Gravitational/ varicose eczema. Association: chronic venous insufficiency Patch test reading –– Read at: 48 hours/ 2 days –– Best read at: 96 hours/ 4 days. Lipodermatosclerosis or inverted champagne bottle Airborne Contact Dermatitis Sesquiterpene lactone appearance SQL  31 Skin Atopic Dermatitis Pityriasis (Scaling) Alba (White) Chronic, relapsing, inflammatory skin disease Child, with facial Pityriasis alba Indeterminate It is classified as an endogenous eczema Hypopigmented leprosy triggered by Exogenous factors. patches Lesions Multiple Single Atopy: Localized form of type 1 hypersensitivity reaction. Scaling + - Atopic triad Atopy + - Recurrent allergic rhinitis (upper respiratory tract). Sensation Intact Normal / Atopic asthma/ bronchial asthma (lower Impaired respiratory tract) Skin Atrophy Absent Present Skin allergies Phases Clinical features Characteristic features Nummular Eczema Aka Discoid Eczema Infantile (3 Extremely itchy Clears in 40% by Lesions: Coin shaped lesions with Well months) exudative lesions age of 18 months demarcated edges.Q ,60% changes to Birth - 2 years bilaterally Differential diagnosis: Tinea. symmetrical on childhood pattern face cheeks & Pompholyx aka dyshidrotic eczema extensors sparing Lesions: Intensely pruritic & also painful deep- diaper area. Seated vesicles at Sides of digits having sago Childhood Red oozy papules May start denovo grain like Appearance 2yrs- puberty plaques in cubital M/C in people with history of atopy & popliteal fossa (Flexures) Adult Lichenified Less common > puberty flexural lesions 32 Cerebellum Quick Revision Notes Infantile Phase: white line Appears due to vasoconstriction. Normal skin: On stroking, Wheal flare response. Headlight Sign shows sparing of Periorbital, Extensor is involved due to crawling perioral & perinasal areaQ Childhood & Adult phase Investigations: Investigation of Choice: Clinical examination Diagnostic criteria of atopic dermatitis, proposed Ophthalmic manifestations: By Hanifin and Rajka.Q Conical cornea/keratoconus Pruritus: Hallmark (intermittent & intense, Termed as itch that rashes) Typical morphology & distribution with 3 Phases. Chronic or chronically relapsing Dermatitis Personal/family history of atopy Minor Diagnostic criteria: Xerosis: Dry skin. Allergic shiners & salute - over the nose Ichthyosis: Fish like scales. Allergic Shiner Allergic Salute White dermographism: On stroking the skin,  33 Skin Shield cataract/ anterior subcapsular cataract Dermographism: writing on skin possible Angioedema: Quincke edema: C1 esterase deficiency is seenQ Infraorbital fold of skin: Dennie-Morgan’s fold Swelling ++, Symptoms: non itchy, but painful, Edema: Deeper location (subcutaneous) Hereditary Angioedema: No urticaria or itching Lateral madarosis: Hertoghe’s sign due to continuous Familial & sudden rubbing Subglottic area involvement possible → airway blockage → life threatening (Immediate Rx) Cutaneous Mastocytosis: Urticaria Pigmentosa Mast cell proliferationQ Children Summary Of Ophthalmic Manifestations C-Kit gene mutations seen Conical cornea/keratoconus. Multiple hyperpigmented macules + over trunk Shield cataract/ anterior subcapsular cataract Darier sign: rubbing dark lesions->histamine release- >erythema with urticarial haloQ Infraorbital fold of skin: Dennie-Morgan’s foldQ Lateral madarosis: Hertoghe’s sign due to continuous rubbing Treatment Topical - Emollients (decreases dry skin), Topical steroids (anti-inflammatory) Urticaria IgE-mediated Type 1 hypersensitivity reaction -->degranulation of mast cells--> histamine Triple response--> Erythema -->Flare -->WhealQ Transient wheals ( 5mm, Post pubertal > 15 mm Lesions: Soft, skin coloured, non-tender, papules or nodules which are Benign tumours of connective tissue of Peripheral nerve sheath. Ocular Manifestation In Nf-I: Lisch iris nodules: Pigmented iris hamartomas Optic pathway glioma. Ophthalmology ref: slit lamp Examination. Proptosis seen Visual acuity Normal Diagnosis: 2 or more of 7 of following: 6 or more café au lait macules → 5 mm (prepubertal age) → 15 mm (post pubertal age)  35 Skin 2 or more neurofibromas of any type OR 1 A first-degree relative (parent, sibling, plexiform neurofibroma offspring) with NF1 by the above criteria. 2 or more Lisch nodules Tuberous Sclerosis Complex Aka Bourneville’s/ Freckling in the axillary or inguinal regions Epiloia / Vogt’s Triad Optic glioma Autosomal Dominant Disease. A distinctive osseous lesion such as sphenoid TSC Chromosome dysplasia or thinning of the long bone cortex with or without pseudoarthrosis 1 9 2 16 Ash leaf macules Adenoma sebaceum Shagreen patch Koenen’s tumours (KT) Earliest skin lesion Facial angiofibroma Collagenoma Periungual fibroma Lance ovate shape: Oval On Characteristic Lesions Leathery one side, Pointed on another –– Proliferation of blood plaque, side. vessels and fibrous tissue Located in lumbosacral –– Lesions are symmetrical region. –– Reddish-brown papules. Ash leaf macules Mental retardation “AASK ME SEGAR” Adenoma sebaceum Epilepsy Shagreen patch SEGA Koenen’s tumours (KT) Rhabdomyoma Sturge weber /Encephalo Trigeminal angiomatosisQ Sporadic since Birth Low flow capillary Vascular malformation 1 CNS: Epilepsy 2 Eyes: Glaucoma 3 Cutaneous: Facial PWS (U/L) pink-red overtime turning to purplish. Ichthyosis classification Prognosis: Permanent skin disease Congenital: Discussed in table. Management: PDL Acquired: Hypo thyroidism, Leprosy, (autonomic dysfunction), Hodgkin’s lymphoma, HIV, Drugs 36 Cerebellum Quick Revision Notes Icthyosis Vulgaris X linked Icthyosis Lamellar Icthyosis (Most common) (I nigra) Inheritance AD XLR AR Onset 3-12 months age Staphylococcus aureus Etiology: Always staphylococcus aureus (70,71) Toxin: exfoliative Toxin A ( DSG-1) Seen in children Seen in children Site: Face Site: Face Trunk Lesion: golden brown or honey coloured crust Q Lesion: Superficial flaccid bullae ruptures to give varnish coloured thin crust Bullous Impetigo Hypopyon sign: pus settles in the lower half of the bulla due to gravityQ. Topical Antibacterials: Fucidic acid Mupirocin: Retapamulin Ozenoxacin: quinolone drug, Currently available in India 38 Cerebellum Quick Revision Notes Erysipelas: St Anthony’s fire Cellulitis Level: upper half of the dermis + lymphatics (superficial) Level: lower half of the dermis + subcutaneous tissue Etiology: GABHS Etiology: GABHS Staphylococcus aureus (rare) (Hyaluronidase) Spreading infections Margin: ill defined, diffuse Margin: well defined, raised margin with clear demarcation between involved & normal skin MILIAN EAR SIGN;Q Staphylococcal Scalded Skin Syndrome Staph aureus → Epidermolytic toxin / Exotoxin → (SSSS) Blood →Targets skin → Target protein desmosomes → Target antigen: DESMOGLEIN-1 upper RITTERS DISEASE / Pemphigus neonatorumQ epidermis→ Subcorneal split Definition: Acute skin exfoliation secondary Lesions: initially, periorificial erythema, skin to toxin producing strains of staphylococcus tenderness (due to acantholysis) aureus (scald=burn) If untreated, progresses to epidermolysis Etiology: Staphylococcus aureus Gram +ve (sheet like epidermal peeling) organism Exotoxins True Nikolsky sign Pathogenesis: –– Focus / Source of infection: Distant staphylococcal infection in ear or conjunctiva –– Epidermolytic toxin (exotoxin) produced from the foci spreads through blood & targets the skin Target protein: Desmosomes in the epidermis Target antigen: Desmoglein -1 in upper epidermis Disease process: Acantholysis (subcorneal Mucosa: normal (periorificial crusting+) (because DES- split) MOGLEIN-1 is expressed in low concentration in the History of distant infection like conjunctivitis/ Mucosa) otitis media Constitutional symptoms like fever  39 Skin Differential Diagnosis: Staphylococcal Scalded Toxic Epidermal Skin Syndrome Necrolysis Sheet like epidermal Sheet like epidermal peeling & Constitutional peeling & Constitutional symptoms symptoms CHILD ADULTS with Drug Normal mucosa History Rx → Parenteral Mucosal involvement Acute Paronychia Antibiotics is prominent with It is an acute infection of the nail folds hemorrhagic crusts Etiology: staphylococcus aureus Reiter’s Syndrome Predisposing factors: Thumb sucking/ Nail It is a reactive arthritis; - biting. C/F –– Erythema around nail folds → pus collection/ purulent discharge at nail folds Arthritis Complications may include: osteitis, lymphangitis. Conjunctivitis Rx → Without abscess: Topical antibacterials Urethritis –– Abscess formation: Surgical incision & Balanitis drainage Infections Keratoderma Cutaneous Corynebacterial Infections ErythrasmaQ Trichomycosis axillaris/ Pitted keratolysis Trichobacteriosis axillaris Etiology: Corynebacterium Not a fungal infection Etiology: Micrococcus/Kytococcus minutissimum Etiology: Corynebacterium tenuis sedentarius Lesion: asymptomatic C/F: yellow concretions/deposits C/F: pits or depressions in Hyperpigmented or over hair shafts stratum corneum (due to Erythematous macules with site axilla keratolysis due to serine Creasing / wrinkling on surface Sweat may be yellow, Black or red proteases)Q Sites: axilla, inguinal region, toe → stain clothes Also complain of malodour & web spaces maceration (Predilection to folds) Sites: soles & palms (associated Woods lamp: coral red with hyperhidrosis) fluorescence (due to coproporphyrin-III) 40 Cerebellum Quick Revision Notes ErythrasmaQ Trichomycosis axillaris/ Pitted keratolysis Trichobacteriosis axillaris Scrub Typhus Infectious disease presenting clinically with Fever Etiology: Orientia tsutsugamushi Vector: trombiculid miteQ Infective form of mite: chiggers (larval form) Clinical presentation: Causality with fever, CNS symptoms Lesion: Eschar (erythema surrounding black Cutaneous anthrax scab)Q Etiology: Bacillus anthracis Lesion: malignant pustule (misnomer) 3 types: Cutaneous, Inhalational, GI Anthrax Painless papule→ eschar → rim of vesicles DOC: Doxycycline Differential diagnosis for eschar: Cutaneous anthrax Brown recluse spider bite (poisonous spider) Scrub typhus  41 Skin Pseudomonas infections Ecthyma gangrenosum Hot tub folliculitis Green nail syndrome Pseudomonas septicaemia: Bathing/shower in an ill Pyocyanin pigment produced by Immunocompromised pts → maintained spa pseudomonasQ haemorrhagic necrosis of the skin Sites: bathing area / trunk Necrotic crusted ulcers are seen. 1. Ecthyma gangrenosum Tuberculosis Verrucosa Cutis: Post Ecthyma gangrenosum: Pseudomonas primary form Ecthyma pyogenicum: Staphylococcus Anatomists’ / Pathologists wart: verrucous means rough or uneven surface. Ecthyma contagiosum: Parapox virus (Orf virus goat sheep handling+)Q Seen in anatomists due to handling of dead bodies as M. Tuberculosis gets inoculated on skin, Meningococcemia Lesion: indurated verrucous plaque Etiology: Neisseria meningitidis Site: on distal or acral extremities Fever + signs of meningitis like neck rigidity Diascopy: petechial / purpuric lesion Angular cutaneous infarctsQ Features Tuberculosis Common warts Verrucosa Cutis Discharge + - Cutaneous TB Classification: Based on Induration + - mode of acquisition Scarring + - Exogenous (TB Chancre, TuBerculosis Verrucosa Number Single Multiple Cutis, Lupus Vulgaris) Endogenous (Scrofuloderma, Orificial TB, Lupus Vulgaris) Tuberculids (Lichen scrofulosorum, Papulonecrotic Tuberculid, Bazin disease) 42 Cerebellum Quick Revision Notes Lupus Vulgaris One margins EXTENDS, other margin SCARS, Asymmetrical lesion. Most common form of cutaneous Tuberculosis in adultsQ Route of spread: Endogenous (Blood spread) > exogenous Patients CMI (cell mediated immunity) is high, so, this is paucibacillary (less bacilli) form of cutaneous TB Scrofuloderma: AKA (Tubercular lymphadenitis) MC form of cutaneous Tuberculosis in children CMI is LOW, so Multibacillary status Lesion: red/ violaceous annular infiltrated plaque Mode of spread: Direct extension of infection to the skin from an underlying Tuberculosis (Active margins), One margins EXTENDS, other focus (lymph node, bone, joint) margin SCARS MC focus of infection: Cervical lymph nodes Centre: atrophy & scarring with Peripheral extension MC site: Neck & axilla Sites: face buttocks, & extremities C//F: Painless subcutaneous swellings → rupture into overlying skin → discharging sinuses / Diascopy: test where a glass slide is pressed ulcers / fibrotic scars. over the lesion Lesion colour changes to Golden brown colour which are called as apple jelly nodules. Erythema induratum of Bazin Erythema nodosum Red & Tender nodules Lobular panniculitis Septal panniculitis Posterior aspect of leg Anterior aspect of legQ Ulcers heal with Scarring No ulcers, Nodules heal without scarring  43 Skin Exogenous Hematogenous spread Tuberculosis MB Lupus Vulgaris PB Chancre TuBerculosis PB Miliary MB Verrucosa Cutis Tuberculosis & Gumma Endogenous Tuberculids –– KOH mount in Pityriasis Versicolor: Short hyphae + round spores, Giving a Spaghetti & Scrofuloderma MB Lichen Rarely Meatball appearanceQ scrofulosorum seen Periorificial MB Papulonecrotic Tuberculosis Bazin disease Pityriasis versicolor Etiology –– Malassezia globosa > furfur. Asymptomatic Perifollicular scaly macules seen. Fine/ Branny / Furfuraceous scales Hypopigmented > Hyperpigmented maculesQ Treatment of pityriasis versicolor Pityriasis versicolor –– 1st line: Colour of lesions –– Azoles like Ketoconazole, Clotrimazole are the mainstay.Q