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🏥 DERMATOLOGY - COMPLETE EXAM NOTES

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📋 QUICK OVERVIEW TABLE

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1. ECZEMA (Atopic Dermatitis)

Definition

• Chronic, relapsing inflammatory skin disease
• Characterized by pruritus and eczematous lesions
• Word "eczema" = from Greek: "to boil forth/effervesce"

Pathophysiology (simple)

Genetic susceptibility (filaggrin mutation)
        ↓
Defective skin barrier
        ↓
Allergen penetration → IgE sensitization
        ↓
Th2 > Th1 response (IL-4, IL-13, IL-31)
        ↓
Mast cell degranulation → PRURITUS
        ↓
Scratching → Spongiosis → Lichenification (chronic)

Clinical Features by Stage

3 Age Phases:

1. Infantile (2 months - 2 years): cheeks, scalp, extensors
2. Childhood (2-10 years): flexural folds (cubital/popliteal)
3. Adolescent/Adult: hands, neck, periorbital area

Hannifin & Rajka Diagnostic Criteria

MAJOR (need 3):

1. Pruritus (itch that rashes)
2. Typical morphology + age-specific distribution
3. Chronic/relapsing course
4. Personal/family history of atopy (asthma, rhinitis)

MINOR (need 3 of 23):

• Xerosis (dry skin)
• Elevated serum IgE
• IgE skin test reactivity
• Ichthyosis / hyperlinear palms
• Keratosis pilaris
• Dennie-Morgan infraorbital fold
• Anterior subcapsular cataracts
• Orbital darkening
• White dermatographism
• Nipple eczema / Cheilitis
• Prone to S. aureus infections

Clinical Examination Findings

• Dennie-Morgan fold: extra crease below lower eyelid
• Hertoghe's sign: thinning of lateral eyebrows
• White dermatographism: white line appears after stroking skin
• Lichenification: thickened leathery skin with exaggerated markings
• Excoriations: scratch marks
• Pityriasis alba: pale hypopigmented patches (children)

Investigations

Histology Key:

SPONGIOSIS = intercellular edema in epidermis = HALLMARK of all eczemas

Treatment (Brief)

• Emollients (base of treatment)
• Topical corticosteroids (mild-moderate)
• Tacrolimus/pimecrolimus (steroid-sparing)
• Antihistamines (for pruritus)
• Dupilumab (anti-IL-4/IL-13, for severe)
• Avoid triggers

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2. URTICARIA

Definition

• Transient edematous skin lesions (wheals) from mast cell degranulation
• Can involve superficial dermis (urticaria) or deep dermis/subcutaneous tissue (angioedema)

Pathophysiology

Trigger (allergen, drug, infection, cold, pressure)
        ↓
Mast cell / Basophil degranulation
        ↓
Release of Histamine, PGs, Leukotrienes
        ↓
Vasodilation + Increased capillary permeability
        ↓
WHEAL (edema) + FLARE (erythema) + PRURITUS

Classification

URTICARIA
├── ACUTE (<6 weeks)
│    ├── Allergic (IgE-mediated): food, drugs, insect stings
│    ├── Infective: viral URI (most common in children)
│    └── Idiopathic
└── CHRONIC (>6 weeks)
     ├── Chronic Spontaneous Urticaria (CSU) - most common
     ├── Physical Urticarias
     │    ├── Dermographism (stroking)
     │    ├── Cold urticaria
     │    ├── Solar urticaria
     │    ├── Pressure urticaria
     │    └── Cholinergic urticaria (exercise/heat)
     └── Contact urticaria

Clinical Features

• Wheal: pale, raised, edematous papule or plaque, surrounded by erythematous flare
• Pruritic - intensely itchy
• Individual lesion lasts <24 hours (diagnostic criterion)
• Comes and goes at different sites
• Angioedema: involves lips, eyelids, tongue, throat (can be life-threatening)
• No surface change - skin looks normal after lesion resolves

Types - Quick Summary

Clinical Examination

• Identify wheal and flare pattern
• Look for angioedema (lips, eyes)
• Dermographism test: stroke with blunt object → wheal forms
• Ice cube test: for cold urticaria
• Check for systemic disease (thyroid, SLE, infections)

Investigations

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3. PSORIASIS

Definition

• Chronic, recurrent, immune-mediated inflammatory skin disease
• Characterized by well-demarcated, erythematous plaques with silvery micaceous scales

Pathophysiology

Genetic (HLA-Cw6) + Triggers (stress, infection, drugs)
        ↓
APC activation → IL-23 production
        ↓
Th17 cell activation → IL-17, IL-22
        ↓
Keratinocyte hyperproliferation
        ↓
Epidermal turnover: Normal 28 days → 3-4 days in psoriasis
        ↓
Thickened, scaly plaques + Dilated capillaries

Types of Psoriasis

PSORIASIS
├── Plaque psoriasis (Psoriasis vulgaris) - 90%
├── Guttate psoriasis (drop-shaped, post strep throat)
├── Pustular psoriasis
│    ├── Generalized (von Zumbusch) - EMERGENCY
│    └── Localized (palmoplantar)
├── Erythrodermic psoriasis - EMERGENCY
├── Flexural/Inverse psoriasis
└── Nail psoriasis

Clinical Features

Classic Lesion (Plaque Psoriasis):

• Well-demarcated, salmon-pink/red plaque
• Covered with thick, silvery-white, micaceous scales
• Sites: extensor surfaces (elbows, knees), scalp, sacrum, umbilicus
• Bilateral and symmetrical

Clinical Signs:

Nail Psoriasis (seen in 50%):

• Pitting (most common) - ice pick pits
• Onycholysis - nail separation from bed
• Oil drop sign (salmon patch)
• Subungual hyperkeratosis
• Beau's lines

Psoriatic Arthritis (in ~30%):

• Asymmetric oligoarthritis (most common)
• Distal interphalangeal (DIP) joint involvement
• Sausage digits (dactylitis)
• Sacroiliitis

Clinical Examination

• Distribution: check elbows, knees, scalp, nails, flexures
• Grattage test (candle grease → membrane → Auspitz sign)
• Koebner phenomenon check
• Joint examination for psoriatic arthritis
• PASI score (Psoriasis Area and Severity Index)

Investigations

Histology Findings (KEY for exam):

• Munro microabscesses: neutrophils in stratum corneum
• Parakeratosis: nuclei retained in stratum corneum
• Acanthosis: thickening of epidermis
• Suprapapillary thinning: thinning just above dermal papillae

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4. LICHEN PLANUS

Definition

• Pruritic, inflammatory disease of skin, mucous membranes, hair follicles, and nails
• T-cell mediated (Th1 cytokines) at the dermoepidermal junction

The 6 P's of Lichen Planus (CLASSIC EXAM QUESTION)

Clinical Features

Skin Lesions:

• Small, flat-topped, polygonal, violaceous papules (0.5-1.5 cm)
• Glistening surface with fine white lines = Wickham striae
• Sites: flexor wrists (most common), forearms, ankles, trunk, glans penis
• Koebner phenomenon present

Oral Lichen Planus (very common):

• Bilateral white reticular pattern (lacy/net-like) on buccal mucosa
• Can be erosive (painful)
• Pre-malignant potential (especially erosive type)

Nail Changes (5-10%):

• Longitudinal ridging and splitting (most common)
• Pterygium formation
• Anonychia (loss of nail plate)

Variants:

Clinical Examination

• Look for 6 P's
• Oral mucosa check (reticular pattern)
• Nail examination
• Koebner phenomenon test
• Dermoscopy: Wickham striae better visualized

Investigations

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5. PEMPHIGUS

Definition

• Autoimmune bullous disease with intraepidermal blisters
• Caused by autoantibodies (IgG) against desmogleins (desmoglein 1 and 3)

Types

Pathophysiology

IgG autoantibodies against Desmoglein (3 > 1)
        ↓
Disruption of desmosome adhesion = ACANTHOLYSIS
        ↓
Keratinocytes separate from each other
        ↓
Intraepidermal blister formation
        ↓
Flaccid, easily rupturing blisters

Clinical Features (Pemphigus Vulgaris)

• Oral mucosa first (in 60% of cases) - painful erosions, months before skin
• Flaccid (easily ruptured, superficial) blisters on skin
• Blisters rupture → raw, painful erosions
• Nikolsky sign: POSITIVE (applying lateral pressure extends blister)
• Bulla spread sign (Asboe-Hansen): pressure on bulla extends it laterally
• Healing without scarring (unless secondarily infected)
• Nikolsky +ve even on normal-looking skin adjacent to lesion

Clinical Signs - KEY FOR EXAM

Investigations

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6. BULLOUS PEMPHIGOID

Definition

• Autoimmune bullous disease with subepidermal blisters
• Autoantibodies (IgG) against BP180 (BPAG2/type XVII collagen) and BP230 (BPAG1)

Differences: Pemphigus vs Pemphigoid

Clinical Features (Pemphigoid)

• Prodrome: pruritic urticarial plaques (weeks before blisters)
• Then: tense large blisters on erythematous or normal-appearing skin
• Sites: inner thighs, flexures, axillae, abdomen, forearms
• Oral involvement: in ~20-40% (milder)
• Lesions heal without scarring
• Nikolsky sign: NEGATIVE
• Significant peripheral blood eosinophilia

Investigations

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7. MYCOTIC SKIN DISEASES (Fungal Infections)

Classification

FUNGAL SKIN DISEASES
│
├── DERMATOPHYTOSES (Tinea)
│    ├── Tinea capitis (scalp)
│    ├── Tinea corporis (body/trunk)
│    ├── Tinea cruris (groin - "jock itch")
│    ├── Tinea pedis (feet - "athlete's foot")
│    ├── Tinea unguium/Onychomycosis (nails)
│    └── Tinea manuum (hands)
│
├── CANDIDIASIS
│    ├── Oral thrush
│    ├── Vulvovaginitis
│    ├── Diaper rash (infants)
│    └── Intertrigo
│
└── TINEA VERSICOLOR (Malassezia furfur)
     - NOT a true dermatophyte

Causative Organisms

Clinical Features

Tinea Corporis:

• Annular lesion with central clearing and scaling border (ringworm appearance)
• Pruritic, spreading outward
• Transmitted person-to-person, from animals, fomites

Tinea Capitis:

• Scaly patches of alopecia in children
• May have kerion (inflammatory, pustular boggy mass)
• Wood's lamp: Microsporum fluoresces green

Tinea Cruris:

• Sharply marginated, erythematous, scaly plaques in inguinal region
• Central clearing possible
• Does NOT involve scrotum (unlike candidiasis)

Tinea Pedis:

• Interdigital maceration and scaling (between 4th-5th toes most common)
• Moccasin type: diffuse scaling of sole
• Vesicular type: vesicles on instep

Tinea Versicolor:

• Multiple, slightly scaly macules - hypopigmented (on dark skin) OR hyperpigmented (on fair skin)
• Trunk predominantly
• KOH: "spaghetti and meatballs" appearance (short hyphae + yeast cells)

Onychomycosis:

• Distal lateral subungual (most common)
• Yellow-brown discoloration, subungual hyperkeratosis, onycholysis

Clinical Examination

• Pattern and distribution of lesions
• Take scrapings from active border/leading edge
• Wood's lamp examination (Microsporum: green fluorescence; tinea versicolor: yellow-green)

Investigations

KOH Prep Key Points:

• Scrape leading edge of lesion
• Tinea versicolor = "spaghetti and meatballs" (hyphae + yeast cells)
• Dermatophytes = branching septate hyphae

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8. LEPROSY (Hansen's Disease)

Causative Agent

• Mycobacterium leprae (acid-fast bacillus)
• Obligate intracellular organism
• Cannot be cultured in vitro
• Incubation period: 2-7 years (longest of all bacterial diseases)

Classification

WHO Classification (Practical - used in field):

Ridley-Jopling Classification (5 types):

TUBERCULOID (TT)            BORDERLINE           LEPROMATOUS (LL)
High immunity                                      Low immunity
Few, well-defined lesions ←→ BT → BB → BL → LL → Many, poorly-defined
Loss of sensation                                  No loss of sensation initially
AFB negative               Mixed                  AFB strongly positive
Lepromin +ve                                      Lepromin negative

Clinical Features

Skin Lesions:

• TT: Single or few, well-defined, hypopigmented/erythematous patch, completely anaesthetic (no sensation), no hairs/sweat
• LL: Numerous, small, shiny, symmetrical nodules/plaques, skin infiltration
  • Leonine facies: thickened corrugated facial skin
  • Saddle nose deformity: nasal cartilage destruction
  • Loss of eyebrows (madarosis)
  • Ear lobe thickening

Nerve Involvement (KEY):

• Great auricular nerve (most commonly enlarged)
• Ulnar nerve: clawing of ring + little fingers
• Radial nerve: wrist drop
• Common peroneal nerve: foot drop
• Facial nerve: lagophthalmos (inability to close eye)

Lepra Reactions:

TYPE 1 (Reversal reaction)         TYPE 2 (Erythema Nodosum Leprosum - ENL)
- Cell-mediated                    - Immune complex-mediated
- BT, BB, BL types                 - LL, BL types
- Pre-existing lesions get         - Tender, erythematous nodules
  red, swollen, painful             on extensor surfaces
- Nerve function worsens           - Fever, malaise
- TX: Prednisolone                 - TX: Thalidomide / Prednisolone

Clinical Examination - Leprosy

1. Inspect all skin (look for hypopigmented patches)
2. Sensation testing: touch/pin prick/temperature
3. Palpate peripheral nerves (thickening)
4. Motor function: grip strength, foot movements
5. Eyes: check for lagophthalmos
6. Nose: saddle nose, nasal discharge
7. Ear lobes: thickening in lepromatous

Investigations

MDT (Multi-Drug Therapy) WHO Regimen:

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9. VITILIGO

Definition

• Acquired pigmentary disorder
• Depigmented white patches due to destruction of melanocytes
• Autoimmune in nature

Pathophysiology

Genetic predisposition + Environmental trigger
        ↓
Autoimmune T-cell attack on melanocytes
        ↓
Melanocyte destruction
        ↓
Melanin absent in patches
        ↓
White, chalk-like depigmented patches

Epidemiology

• Onset: childhood or young adulthood (peak 10-30 years)
• Prevalence: 0.5-1% worldwide; >8% in some parts of India
• Equal in males and females

Types of Vitiligo

Clinical Features

• Chalk-white depigmented patches with normal/hyperpigmented border
• Smooth convex margins
• Hairs in affected area also turn white (leukotrichia)
• Rarely: red inflammatory border
• Trichrome vitiligo: tan zone between normal and depigmented skin (early)
• Koebner phenomenon: new lesions at sites of trauma
• Associated with: thyroid disease (Hashimoto's, Graves'), diabetes T1, Addison's, pernicious anemia, alopecia areata

Clinical Examination

• Distribution pattern (symmetric vs segmental)
• Check for leukotrichia
• Wood's lamp: enhances depigmentation (chalk-white fluorescence) - most useful in fair-skinned individuals
• Check thyroid (goiter), look for associated autoimmune diseases
• Ophthalmology exam (uveitis association)

Investigations

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10. CELLULITIS

Definition

• Acute bacterial infection of dermis and subcutaneous tissue
• Non-necrotizing (unlike necrotizing fasciitis)
• Most common organisms: Streptococcus pyogenes (~75%), S. aureus (MRSA in at-risk)

Pathophysiology

Breach in skin (wound, tinea pedis, ulcer, insect bite)
        ↓
Bacterial entry (Strep, Staph)
        ↓
Spread through tissue planes (dermis, subcutaneous)
        ↓
Inflammatory response → Erythema, Warmth, Edema, Pain
        ↓
± Lymphangitis → Regional lymphadenopathy
        ↓
± Bacteremia → Sepsis (immunocompromised)

Clinical Features

Classic Features (SWELLING + WARMTH):

• Spreading erythema - poorly demarcated (unlike erysipelas)
• Edema - pits on pressure
• Warmth and tenderness
• Induration (infiltrated area)
• Systemic: fever, chills, malaise
• Portal of entry (tinea pedis, wound, ulcer) often visible

Progression:

Mild erythema + tenderness
        ↓
Intense erythema, spreads rapidly
        ↓
Edema, vesicle formation, rupture
        ↓
Possible lymphangitis (red streaks toward lymph nodes)
        ↓
± Abscess formation (central fluctuance)

Sites:

• Lower leg (most common) - often from tinea pedis
• Orbit (orbital cellulitis - emergency)
• Face
• Post-traumatic site

Erysipelas vs Cellulitis

Clinical Examination

• Measure and mark the erythema border (monitor spread)
• Temperature, HR, BP (systemic involvement)
• Assess for fluctuance (abscess)
• Look for portal of entry
• Lymph node examination
• Look for lymphangitis (red streaks)

Investigations

Treatment (Brief):

• Mild, outpatient: Dicloxacillin or Cephalexin 5 days
• Severe, inpatient: IV penicillin / clindamycin
• MRSA suspected: Trimethoprim-sulfamethoxazole, doxycycline, or vancomycin
• Mark borders, elevate limb

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COMPARISON TABLES FOR EXAM

Bullous Diseases Quick Comparison

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Psoriasis vs Lichen Planus Quick Comparison

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Investigation Summary

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Skin Signs - Must Know Table

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Direct Immunofluorescence Patterns

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FLOW DIAGRAMS - APPROACH TO DIAGNOSIS

Approach to Blistering Disorder:

BLISTER
    ↓
Is Nikolsky sign POSITIVE?
    ↓                    ↓
   YES                   NO
    ↓                    ↓
INTRAEPIDERMAL       SUBEPIDERMAL
(Pemphigus)          (Pemphigoid)
    ↓                    ↓
DIF: IgG            DIF: Linear IgG
intercellular        at BMZ
(fishnet)
    ↓                    ↓
ELISA: Dsg3/Dsg1    ELISA: BP180/BP230

Approach to Hypopigmented Patch:

HYPOPIGMENTED PATCH
         ↓
Sensation intact or lost?
    ↓              ↓
  INTACT          LOST
    ↓               ↓
Wood's lamp?    Leprosy
    ↓
Chalk white (depigmented)?
    ↓                ↓
  YES               NO
    ↓               ↓
VITILIGO        Pityriasis alba /
                Tinea versicolor

Approach to Scaly Skin Lesion:

SCALY LESION
      ↓
Annular with central clearing?
    ↓              ↓
   YES              NO
    ↓               ↓
KOH prep       Silvery scales on
positive?      extensor surface?
    ↓                ↓
TINEA            PSORIASIS
(fungal)      (check Auspitz sign)
                   ↓
           Flat-topped violaceous
           papules on flexors?
                   ↓
            LICHEN PLANUS
           (check Wickham striae)

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QUICK REVISION POINTS (EXAM READY)

• Hallmark histology = SPONGIOSIS
• Hannifin-Rajka: 3 major + 3 minor
• "Itch that rashes"
• Dennie-Morgan fold = double fold under eyelid

• Lesion lasts <24 hours
• Wheal + Flare = histamine
• HAE = C1 esterase inhibitor deficiency
• Autoimmune CSU: anti-FcεRI or anti-IgE antibodies

• HLA-Cw6
• Auspitz sign (pinpoint bleeding)
• Munro microabscesses (histology)
• Psoriatic arthritis: DIP joints, sausage digits

• 6 P's: Pruritic, Purple, Planar, Polygonal, Papules, (+Wickham striae)
• Oral: white reticular lace pattern (pre-malignant if erosive)
• Associated with Hepatitis C

• Nikolsky sign POSITIVE
• DIF: fishnet/chicken wire pattern (intercellular IgG)
• Mouth first in PV
• Acantholysis = key pathology

• Elderly patients
• Tense blisters, Nikolsky NEGATIVE
• DIF: linear IgG at BMZ
• Eosinophilia common
• BP180 and BP230 antigens

• KOH prep = most important investigation
• Tinea versicolor = spaghetti and meatballs on KOH
• Microsporum = green fluorescence on Wood's lamp
• Onychomycosis = Trichophyton rubrum (most common)

• M. leprae, cannot be cultured in vitro
• Loss of sensation = key clinical feature
• Ridley-Jopling: TT, BT, BB, BL, LL
• Lepromin test = CMI assessment, NOT diagnosis
• MDT: PB (6 months), MB (12 months)
• Type 1 reaction = reversal; Type 2 = ENL

• Autoimmune melanocyte destruction
• Wood's lamp enhances white patches
• Associated with thyroid disease, T1DM, Addison's
• Segmental type = does NOT respond to treatment as well

• Poorly defined margins (vs. erysipelas = well-defined)
• Most common: lower leg, from tinea pedis portal
• Streptococcus = 75% of cases
• Mark borders to monitor progression

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