Induction — Dermatology

Written by Betra Youhanna, a medical student and not a doctor — check every detail against your own teaching.

50 diseases · 13 criteria · structured C/P · Inves · Mng

C/P — Clinical Presentation

Inves — Investigations

Mng — Management

Special — Pathognomonic / disease-unique

Dermatology — Inflammatory

6 entries

Atopic Dermatitis

C/P

Chronic relapsing pruritic dermatitis; family history of atopy (asthma, allergic rhinitis)
Infants/toddlers: face, elbows, knees (crawl-rub areas)
Acute: red, dry, itchy patches; blisters → ooze → crust if scratched
Chronic: lichenification (thick skin, prominent markings) ± post-inflammatory hyperpigmentation
70% positive family history; incidence 1–20% of children

Inves

Clinical (deck defers detailed Inves/Mng to clinical sessions)
Microscopy if biopsied: spongiosis + intraepidermal vesicles (acute); marked epidermal hyperplasia + dermal fibrosis (chronic / lichen simplex chronicus)

Mng

— (deck defers to clinical sessions)

Special

Type I hypersensitivity reaction
Loss-of-function filaggrin mutation OR reduced claudin-1 expression → tight junction failure in cornified layer
Prognosis: 50% clear by 3y, 66% by 6y, 90% by 20y

Seborrhoeic Dermatitis

C/P

Greasy, white, flaky scaling over erythematous patches; usually not painful unless infected/irritated
Age peaks: babies <3 months (cradle cap), adults 30–60y
Scalp (= dandruff when mild); face (eyebrows, eyelids, forehead, nasolabial folds); chest; creases of neck/arms/legs/groin

Inves

Microscopy: subacute dermatitis with spongiosis in epidermis + hair follicle epithelium; scales in follicular ostia with neutrophils; dilated follicular ostia; epidermal hyperplasia

Mng

Special

Link to Malassezia / Pityrosporum orbiculare yeast overgrowth
Adult increase in: Parkinson's disease, facial paralysis, obesity, zinc deficiency, HIV
Infant variant = cradle cap

Allergic Contact Dermatitis (ACD)

C/P

Inflammatory eruption at site of allergen contact in pre-sensitised person
Examples: poison ivy; nickel (most common in children — snap/watch/belt/jewellery sites); periumbilical reaction from trouser belt
Acute spongiotic dermatitis pattern → subacute → chronic (resembles lichen simplex chronicus)
Other common allergens (beyond poison ivy & nickel): rubber, cosmetics, fragrances

Inves

Microscopy: marked spongiosis with vesicles; lower epidermis affected early; lymphocytes + eosinophils in infiltrate; necrotic keratinocytes absent

Mng

Special

Type IV cell-mediated delayed hypersensitivity
First exposure = sensitisation (memory T cells); second exposure = inflammatory lesion
Eosinophils on histology are the key marker vs ICD

Irritant Contact Dermatitis (ICD)

C/P

Inflammatory skin response to non-immune direct toxic effect of chemical/physical irritant
Causes: chemical burns (alkalis/acids), acute irritants (cosmetics), chronic irritants (detergents)
Diaper rash = most common infant ICD (prolonged contact with urine/stool chemicals)

Inves

Microscopy: upper-epidermis affected; marked ballooning degeneration with variable keratinocyte necrosis; neutrophils in necrotic areas; spongiosis slight/absent

Mng

Special

Direct epidermal damage: lipid barrier removal, cell membrane damage, denatured keratin
Neutrophils + upper-epidermal necrosis distinguish from ACD (which has eosinophils + lower-epidermal spongiosis)
Ulceration/erosions may be present (absent in ACD)

physiology · background · low-yield

Mechanism

Full irritant-damage mechanism set (deck gives 5): removal of surface lipids, cell-membrane damage, keratin denaturation, cytokine release and direct cytotoxic effect; barrier-penetration cascade also drives chemotaxis of PNLs within the epidermis and damage to papillary dermal blood vessels

Nummular (Discoid) Eczema

C/P

Scaly, crusted, pruritic, coin-shaped plaques

Inves

Microscopy: subacute spongiotic dermatitis

Mng

Special

Endogenous dermatitis subtype

Pemphigus Vulgaris

C/P

Skin barrier failure → fluid, protein and heat loss; portal of entry for infection (grouped with TEN + burns in this regard in the lectures)

Inves

—
Microscopy: suprabasal acantholysis (deck-flagged "V important") → early suprabasal cleft → vesicle; overlying orthokeratosis

Mng

Special

Desmosomes between basal & overlying suprabasal cells are disrupted while hemidesmosomes remain intact → early suprabasal cleft → vesicle

Skin & Soft Tissue Infections

14 entries

Impetigo

C/P

Large epidermal blisters fill with clear fluid/neutrophils → pustule → ruptures easily → yellow crust
Scab = coagulated plasma, cell debris, extravasated blood cells

Inves

Clinical

Mng

Antistaphylococcal cover (gram-positive coverage implied by causative organism)

Special

Superficial epidermal infection; gram-positive, most commonly Staphylococcus aureus
Bullous impetigo = localised form of staphylococcal exfoliative-toxin disease (the widespread form is SSSS)

Staphylococcal Scalded Skin Syndrome (SSSS)

C/P

Widespread confluent blistering + separation of upper epidermal layers
Original infection may be occult, upper respiratory tract, or middle ear

Inves

Mng

Special

Driven by staphylococcal exfoliative toxin (cleaves desmoglein 1)
Relatively good prognosis in infants, considerable mortality in adults

Folliculitis

C/P

Pus accumulation around hair shaft
Hairy areas: buttocks, thighs, bearded face, scalp

Inves

Clinical

Mng

Special

Bacterial infection of hair follicles; most often Staphylococcus aureus

Furuncle (Boil)

C/P

Tender, indurated swelling around a hair follicle with surrounding oedema
Common on back, neck
Steps: staphylococcal pilosebaceous infection → suppuration → central necrosis → spontaneous rupture

Inves

Clinical

Mng

Removal of affected hair follicle aids drainage; incision usually not necessary
"Blind boil" (no suppuration): antistaphylococcal antibiotics

Special

Associated with debility and diabetes mellitus
Iodine application aggravates spontaneous rupture

Carbuncle

C/P

Confluent boils forming indurated masses with multiple skin openings (infective gangrene of subcutaneous tissue)
Back and nape of neck (regions with less tissue vitality)
Older diabetic patients classically

Inves

Clinical

Mng

Initial: antibiotics + local magnesium sulphate (reduces oedema, softens centre)
Non-responding: surgical — cruciate incision with corners of flaps excised for drainage

Special

Usually S. aureus (sometimes streptococci, gram-negative bacilli)
Strongly associated with poorly controlled diabetes (check BG)

Hidradenitis Suppurativa

C/P

Multiple swellings (axilla, groin, perianal) discharging pus, subsiding, recurring after months
More common in women in tropical countries (perianal form more common in men)

Inves

Clinical

Mng

Prevent: local hygiene; avoid deodorant, depilation, shaving
Antibiotics: erythromycin + metronidazole
Surgical: excision of affected skin + split thickness skin grafting if conservative fails

Special

Chronic infection of apocrine sweat glands due to duct blockage

Cellulitis (non-necrotising)

C/P

Diffusely spreading infection of dermis and soft tissues
Borders are ill-defined (unlike erysipelas)

Inves

Clinical

Mng

TOC: parenteral penicillin
Severe: protein synthesis inhibitor ± cell wall agent
Other options: antistaphylococcal penicillins, cefazolin, ceftaroline, ceftriaxone
Other causative agents to consider: Haemophilus influenzae, Pneumococcus

Special

Most frequent agent: Streptococcus pyogenes (lytic enzymes — streptokinase, DNAase, hyaluronidase — facilitate spread)
Macrolide resistance increasing

Erysipelas

C/P

Superficial cellulitis with prominent lymphatic involvement
Sharply demarcated raised border (vs ill-defined cellulitis edge)
Face, arms, legs
Local redness + swelling + regional lymphadenitis + systemic high fever, chills

Inves

Clinical

Mng

Penicillin

Special

Group A beta-haemolytic streptococci
"Cellulitis + dermal lymphatic inflammation"

Acne Vulgaris

C/P

Disorder of pilosebaceous units
More prominent in men (androgens stimulate sebum)

Inves

Clinical

Mng

Special

Multifactorial: sebum overproduction; pilosebaceous canal keratin obstruction; distension by sebum/keratin; anaerobic Propionibacterium acnes proliferation; secondary pyogenic infection

Sebaceous Cyst (Epidermal Inclusion Cyst)

C/P

Smooth, soft or firm cyst with central punctum attached to skin
Face, scalp, neck, scrotum (anywhere sebaceous glands exist)
Absent on palms and soles (no sebaceous glands)

Inves

Clinical

Mng

Excision of cyst with complete cyst wall removal (retained wall = recurrence)

Special

Pathognomonic = central punctum
Complications: infection, Cock's peculiar tumour, sebaceous horn

physiology · background · low-yield

Mechanism

Retention cyst formed by obstruction of the pilosebaceous follicle → gland distends with its own secretion

Necrotising Soft Tissue Infections (NSTI / Necrotising Fasciitis)

C/P

Earliest: severe pain out of proportion to examination findings (ischaemia)
Skin often spared early (rich vascular collaterals)
Late "hard signs": blistering, crepitus, bullae, haemorrhagic blebs, obvious necrosis
Systemic: SIRS, sepsis, profound multi-organ shock

Inves

Gold standard: clinical diagnosis confirmed by operative exploration
Operative findings: pasty grey necrotic tissue; thin purulent "dishwater" fluid; lack of resistance to digital pressure along fascia; lack of bleeding; thrombosed vessels; muscles do not contract to electrocautery
"Finger test": surgeon's fingers easily dissect SC layer off deep fascia
LRINEC score (WBC, Hb, Na, glucose, creatinine, CRP); ≥6 → high suspicion (PPV 92%, NPV 96%); does not distinguish septic shock/death so don't rely solely on it
Suggestive labs: WBC ≥15,400/µL, Na <135
Imaging: plain X-ray (SC gas — specific but only 17–30% sensitivity); CT (fascial thickening/oedema, gas — high specificity, low sensitivity); MRI (T2 hyperintense signal at deep fascia/muscle — slow, don't delay surgery)
Bedside test for equivocal cases: limited 2-cm operative incision down to the superficial fascia under local anaesthesia (direct inspection when diagnosis is uncertain)
Rising WBC count + serum lactate after initial debridement → highly suggestive of ongoing NSTI progression (mandates immediate second-look operation)

Mng

Immediate aggressive surgical debridement (single most important determinant of survival; >24h delay = 9× mortality)
Excision of all necrotic skin/SC/fascia/muscle back to healthy bleeding tissue
Planned second-look operation in 12–24h after resuscitation; serial debridements until no infection
Saline-soaked gauze dressing post-debridement
Amputation (guillotine first) if limb non-viable, non-functional, or extensive proximal spread
Diverting colostomy for perineal infections (faecal contamination control)
Empiric antibiotics: gram-positive (incl MRSA) + gram-negative + anaerobic
Clindamycin attenuates exotoxins (S. aureus, hemolytic strep M proteins, clostridia)
Add doxycycline/tetracycline if Vibrio/Aeromonas suspected
Antibiotic duration: ≥48–72h after systemic signs resolve + source control complete
IVIG: theoretical benefit on streptococcal superantigens; INSTINCT study found no 6-month survival benefit
Hyperbaric O₂: theoretical benefit, failed to show mortality/LOS benefit; cost/availability limit use

Special

Hyaluronidase degrades fascial adhesions → rapid spread along fascial planes
Avascular fascia liquifies (diagnostic feature)
Anaerobic gas production (CO₂, H₂, N₂, H₂S, CH₄) → crepitus + radiographic gas
4 types:
- Type I (55–80%) — polymicrobial (Streptococcus + Bacteroides); risk factors: diabetes, obesity, immunosuppression, CKD, cirrhosis, malignancy, alcohol abuse
- Type II (10–15%) — monomicrobial (β-haemolytic Streptococcus or Staphylococcus aureus); post-trauma/surgery/IV drug use; M proteins → polyclonal T cell activation
- Type III — marine exposure (Clostridium species, Vibrio vulnificus from warm coastal seawater/raw oysters); 30–40% mortality; isolated Clostridium = up to 4× higher mortality; add tetracycline
- Type IV — Aeromonas hydrophila, Candida (immunocompromised), Zygomycetes (immunocompetent); penetrating trauma or burns; add antifungal
Obesity paradox: protective on in-hospital mortality
Paediatrics: predisposed by varicella lesions, IM injections; usually monomicrobial S. pyogenes
DKA → higher mortality, longer hospital stays
Depth spectrum: necrotising cellulitis / fasciitis / myositis — clostridial involves underlying muscle (myonecrosis), non-clostridial involves subcutaneous fascia (necrotising fasciitis); myonecrosis is a late poor-prognosis sign

physiology · background · low-yield

Mechanism

Pathophysiologic hallmarks vs uncomplicated SSTI: progressive infection, toxin production, cytokine activation, thrombosis, ischaemia, tissue destruction/death; exotoxins damage endothelium (fluid leak) and microthrombi occlude vessels reducing intravascular flow

Fournier's Gangrene

C/P

NSTI affecting genitourinary tract / perineum

Inves

As for NSTI

Mng

As for NSTI; orchiectomy rarely needed (testicular blood supply preserved)
Diverting colostomy often needed for soilage control

Special

Anatomical-site variant of NSTI

Ludwig Angina

C/P

NSTI involving submandibular and sublingual spaces

Inves

As for NSTI

Mng

As for NSTI

Special

Anatomical-site variant of NSTI

Diabetic Foot Infection

C/P

Diabetic patient with chronic plantar ulcer, new deep tracking, malodorous oedematous erythematous foot, extreme pain on palpation
Doppler may show biphasic pulses

Inves

Local susceptibility patterns + previous antibiotic exposure + prior pathogens guide empirical therapy

Mng

Empiric options: cefazolin, ceftriaxone, cefoxitin, ceftaroline, ampicillin-sulbactam, piperacillin-tazobactam, a carbapenem; daptomycin/linezolid with gram-negative cover
MRSA cover: vancomycin, telavancin, ceftaroline, daptomycin, tigecycline, linezolid

Special

Most common pathogen profile: gram-positive cocci
Other: gram-negative bacilli and anaerobes
Chronic wounds may have resistant pathogens
High risk for progression to NSTI of the foot (neuropathy + PVD + chronic ulcer)

Skin Malignancy & Pigment

3 entries

Malignant melanoma

Special

Failure of immune surveillance
Presents as an irregular pigmented lesion

Squamous cell carcinoma

Special

Arises from increased UV penetration & DNA damage (e.g. albino child)

Albinism

Special

Reduced melanin → increased UV penetration → predisposes to squamous cell carcinoma

Viral & Infective Skin Disease

6 entries

Eczema herpeticum

Special

Abnormal cutaneous cell-mediated immunity in an atopic patient with HSV → widespread HSV infection

Tinea corporis

Special

Annular

Herpes zoster (shingles)

Special

Dermatomal

Herpes simplex

Special

Grouped vesicles

Scabies

Special

Burrow — a tunnel dug in the skin by the scabies mite

Infective dermatitis

Special

Exogenous dermatitis (environmental factor); named at survey level only

Papulosquamous & Eczematous

9 entries

Urticaria

Special

Wheal

Psoriasis

Special

Extensor surface (outside of a joint)
May be linear in configuration
Shows Koebnerization — new lesions on previously unaffected skin secondary to trauma

Lichen planus

Special

Shows Koebnerization — new lesions on previously unaffected skin secondary to trauma

Lichen sclerosus et atrophicus (LSA)

Special

Epidermal atrophy — thin epidermis with absent rete ridges

Spongiotic dermatitis / Eczema (general concepts)

C/P

Dermatitis = inflammation of the skin
Clinically: erythema and itching

Special

Spongiotic dermatitis = spongiosis with associated inflammation; histologically spongiosis + inflammation
Accumulation of extracellular fluid (intercellular oedema) causing disruption of desmosomes
Presence of inflammatory cells within the epidermis with associated spongiosis; infiltrate both perivascular in dermis + extends into epidermis
Oedema both within and between cells → cell rupture → reticular meshwork (remnants of ruptured cell wall)
Intra-epidermal vesicle

Allergic Contact Dermatitis

Special

Pathology: inflammation initiated within the papillary dermis → exocytosis by monocytes and eosinophils

Irritant Contact Dermatitis

Special

Once irritant penetrates stratum corneum → stimulation of cytokine expression, chemotaxis of PNLs (neutrophils) within epidermis, damage of papillary dermal blood vessels + direct cytotoxic effect

Autosensitization (Id) reaction

Special

Endogenous dermatitis (constitutional + hereditary factors); named at survey level only

Asteatotic dermatitis

Special

Exogenous dermatitis (environmental factor); named at survey level only

Blistering & Severe Cutaneous Reactions

2 entries

Toxic epidermal necrolysis (TEN)

Special

Skin-barrier failure (grouped with pemphigus/burns) → fluid, protein & heat loss + portal of entry for infection

Burns

Special

Skin-barrier failure (grouped with pemphigus/TEN) → fluid, protein & heat loss + portal of entry for infection

Normal Skin Structure & Histology

10 entries

Epidermis — keratinocyte layers (normal)

Special

Keratinizing stratified squamous epithelium; 4 keratinocyte layers, each with a specific function
Basal: site of mitosis/regeneration; single layer of elongated cells with palisaded nuclei; ~60% of basal cells proliferate (rapidly or slowly); few suprabasal cells also mitotically active
Spinous (prickle): postmitotic; develops keratin filament–desmosome complex + cornified envelope; gives the epidermis its structure
Granular: keratin formation + water barrier; cornified envelope reaches full strength
Horny: anucleated uppermost layer; basket-weave/orthokeratotic in formalin-fixed specimens (contents not fixed by formalin, washed away during processing)

Granular layer — filaggrin & Odland bodies (normal)

Special

Kerato-hyaline granules composed of profilaggrin → enzymatically converted to filaggrin (keratin-filament-aggregating matrix protein)
Filaggrin decomposes → derivatives that are sun-shielding and water-binding
Odland bodies: released from upper spinous keratinocytes, move to periphery of granular layer, discharge lipid-rich, hydrophobic (water-repelling) contents into intercellular space

Epidermal dendritic cells (normal)

Special

Melanocytes: neural-crest origin, sit in basal layer; positive for S-100, HMB-45 and Melan A; make melanosomes handed to keratinocytes, stored over the nucleus so melanin absorbs UV before it reaches DNA
Langerhans cells: bone-marrow-derived antigen-presenting cells in upper/mid epidermis; positive for CD1a; increased in contact dermatitis
Merkel cells: light-touch sensory cells at basement-membrane level, desmosomal contacts with keratinocytes; produce cytokeratin-20 (CK20) + neurosecretory granules; not detectable on routine H&E

Melanin (normal)

Special

Function = protection against solar radiation; filters light by converting radiative energy into heat
Synthesised from tyrosine: dihydroxyphenylalanine (DOPA) → dopaquinone → eumelanin

Dermis (normal)

Special

Papillary dermis: type III collagen, thin/loose bundles, less eosinophilic
Reticular dermis: type I collagen, dense/irregular bundles, eosinophilic
Elastic fibres in both layers, more numerous in the reticular dermis
Two plexi: superficial plexus (papillary dermis) and deep plexus (reticular dermis)

Skin layer thickness (normal)

Special

Epidermis: <0.1 mm on eyelids to ~1 mm on acral sites
Dermis: ~1 mm on the face to ~4 mm on the back
Subcutaneous fat: up to multiple cm — by site (thick abdominal wall, thin eyelids) and gender (females thick pubic/thigh; males thick upper arm/posterior neck)

Epidermal appendages (normal)

Special

Hair follicles: regulate body temperature, aid evaporation of sweat
Sebaceous glands: secrete sebum (fat) = lubricant for skin and hair
Eccrine sweat glands: regulation of body temperature
Apocrine glands: scent/odour glands, fully developed at puberty

Mucosa vs skin (normal)

Special

Parakeratosis is normal; no basket-weave orthokeratosis; no granular layer unless traumatised; keratinocytes appear pale from abundant glycogen; no pilosebaceous units; plasma cells are a normal part of the submucosal inflammatory infiltrate; salivary glands/ducts may be present

Desmosomes (normal)

Special

Keratinocytes adhere via desmosomes (desmoglein + desmocollin) with a keratin/tonofilament attachment-plaque complex
Basal layer anchored to the basal lamina by half-desmosomes (hemidesmosomes)
Act as intercellular cement; continuously break and reform to allow regulated upward migration of keratinocytes toward the horny layer

Skin coloration (normal)

Special

Main cause = melanin pigment; minor causes = carotenoids in epidermis, oxy-haemoglobin in dermal capillaries, deoxy-haemoglobin in dermal venules

Dermatology & Dermatopathology

13 entries

Primary lesion morphology (height x size)

Use: Core lesion-terminology decision tree by height and diameter

Raised

<0.5 cm = Papule
>0.5 cm = Nodule

Flat

<0.5 cm = Macule
>0.5 cm = Patch

Fluid-filled lesion classification

Use: Classify fluid-filled primary lesions by size and content

Fluid-filled <0.5 cm = Vesicle
Fluid-filled >0.5 cm = Bulla
Pus-filled = Pustule

Special primary lesions

Use: Disease-specific primary lesions

Burrow — tunnel dug by the scabies mite
Comedone — primary lesion of acne
Wheal — primary lesion of urticaria

Secondary lesions

Use: Lesions evolving from primary lesions

Scale — visible/palpable flake of aggregated epidermal cells
Crust — dried exudate (serum, blood or pus)
Excoriation — superficial ulceration secondary to scratching
Ulcer — loss of epidermis +/- underlying structure

Configuration / pattern of skin lesions

Use: Describe the arrangement/pattern of lesions

Symmetrical vs asymmetrical
Flexural (atopic dermatitis) vs Extensor (psoriasis)
Grouped — herpes simplex
Linear — psoriasis
Dermatomal — herpes zoster
Serpiginous
Arcuate
Annular — tinea corporis
Koebnerization — new lesions on previously unaffected skin secondary to trauma (lichen planus, psoriasis)

Distribution descriptors

Use: Describe where and how varied lesions are

Localized (e.g. tumours) vs Generalized (e.g. rash)
Photosensitive
Monomorphic vs Pleomorphic

Lesion description checklist

Use: Further points to describe every lesion

Site
Colour
Shape
Surface — rough/smooth/verrucous
Texture
Temperature
Consistency — soft/firm/hard

Functions of the skin & consequences of impaired function

Use: 7 skin functions each mapped to a disease of malfunction

7 functions

Physical barrier — keeps microorganisms/chemicals out, body fluids/protein in
Thermoregulation
Reduces UV penetration & DNA damage
Vitamin D production
Sensory organ
Surface for grip
Immune surveillance

Disease of malfunction

Barrier loss — pemphigus vulgaris / TEN / burns (fluid, protein & heat loss + portal of entry for infection)
Barrier loss in atopic patient → 2ry Staph infection
Abnormal cutaneous cell-mediated immunity — eczema herpeticum (atopic + HSV)
Increased UV penetration — albino child with SCC
Failure of immune surveillance — malignant melanoma

Common microscopic (dermatopathology) terminology

Use: Glossary of terms used to microscopically describe skin lesions

Acanthosis: increased thickness of the spinous layer
Epidermal atrophy: thin epidermis with absent rete ridges
Orthokeratosis: normal basket-weave appearance of the horny layer
Hyperkeratosis: thickening of the horny layer
Parakeratosis: retention of nuclei within the horny layer
Hypergranulosis: thickened granular layer
Acantholysis: separation of keratinocytes from desmosome disruption → intra-epidermal blisters
Spongiosis: intercellular oedema; excessive → intraepidermal vesicles
Exocytosis: inflammatory cells within a spongiotic epidermis
Reticular degeneration: inter- and intracellular oedema with keratinocyte rupture, leaving a reticulum of remaining cell membranes
Ballooning degeneration: accumulation of intracellular fluid in response to cell injury

Five mechanisms of blister formation

Use: Framework for the pathogenesis of blisters

1. Spongiosis (intercellular oedema) with associated exocytosis (e.g. eosinophils)
2. Reticular degeneration: inter + intracellular oedema → cell rupture → intraepidermal vesicle
3. Acantholysis: loss of cell cohesion → clefts/suprabasal vesicles
4. Cytolysis: disruption of keratinocytes by friction or heat (e.g. irritant contact dermatitis, upper-epidermal necrosis + spongiosis)
5. Basement-membrane-zone disruption (e.g. ballooning degeneration of the basal layer)

Blister size definitions

Use: Size cut-offs for blistering lesions

Blister = fluid-filled cavity, intra- or sub-epidermal
Vesicle: <0.5 cm
Bulla: >0.5 cm

Histological staging of spongiotic dermatitis (Acute / Subacute / Chronic)

Use: Stage spongiotic dermatitis by its histological features

Acute

Normal stratum corneum
Normal epidermal thickness
Inter- & intra-cellular oedema
Reticular degeneration
Intraepidermal vesicles
Perivascular infiltrate of lymphocytes + histiocytes
Dermal oedema

Subacute

Start of regeneration = epidermal hyperplasia
Smaller-sized vesicles
Areas of spongiosis & exocytosis

Chronic

Increased stratum corneum thickness
Marked epidermal hyperplasia
NO spongiosis or vesicles
Dermal fibroblastic reaction (result of itching)

Aetiological classification: Endogenous vs Exogenous dermatitis

Use: Classify dermatitis by cause/aetiology

Dermatitis classified by 3 bases

(1) Stage
(2) Cause / aetiology
(3) Morphology

Endogenous (constitutional + hereditary)

Atopic
Seborrheic
Discoid (nummular)
Dyshidrotic (pompholyx / palmoplantar eczema)
Autosensitization (Id) reaction

Exogenous (environmental)

Contact (allergic + irritant)
Infective
Asteatotic