"20F, last several years noticed rash in face and trunk, non-itchy, non-tender." ^[1]

Key learning point: Comedonal acne is usually not itchy. Deep inflammatory nodules can be tender, so tenderness does not exclude acne; morphology and distribution remain decisive.

Acne is often neglected because it is asymptomatic and not life-threatening, so patients and parents may dismiss it as trivial despite its psychosocial impact. Students must recognize that "I have an itchy rash" as a lecture title is somewhat misleading; acne is included because it is a major dermatological condition commonly encountered alongside eczema.

Acne is common in teenagers (~80%), male > female, with a positive family history component. ^[1]

Hong Kong data: 552 telephone interviews — 91.3% had acne, 47.6% had active acne, 48% had scars or marks, only 25% on any treatment, and only 1.8% sought medical advice. ^[1]

The slides simplify acne into four linked processes: sex-hormone signalling → increased sebum → follicular blockage/dysbiosis → host inflammation. ^[1]

Clinical features of acne: Comedone → Papule → Pustule → Scarring → Cyst ^[1]

• Comedone: Open (blackhead) or closed (whitehead). Non-inflamed. The earliest lesion.
• Papule: A small inflamed raised lesion; redness can be less conspicuous in richly pigmented skin.
• Pustule: A superficial inflammatory lesion containing visible purulent material.
• Nodule: A deep, often painful inflammatory lesion. The slides use “cyst,” but many so-called acne cysts are solid nodules rather than true epithelial-lined cysts.
• Scarring: A feared irreversible consequence. It may be atrophic (ice-pick, boxcar, rolling) or hypertrophic/keloidal.

What the Clinical Photographs Add

• The face and trunk photographs show polymorphic disease: comedones coexist with papules, pustules and deep nodules. This mixture favours acne over a monomorphic folliculitis.
• On darker skin, erythema may be subtle while post-inflammatory hyperpigmentation (PIH) is striking. PIH is not itself a scar, although both can coexist and both matter to the patient.
• The back photograph shows that truncal acne can produce both depressed scars and raised hypertrophic/keloidal scars. Examine beyond the face before grading severity.
• The severe facial case already has confluent nodules and atrophic scars: this is a visual trigger to escalate treatment early rather than waiting for symptoms, because acne can be asymptomatic while damage accumulates.

The lecture-era slides call confluent ablative resurfacing the “gold standard.” In current practice, scar treatment is individualised by scar morphology, skin type, active-acne control, downtime and risk; no single laser is best for every acne scar. ^[1]

Fractional Photothermolysis (Fraxel): Creates multiple microthermal zones (MTZs), each 50–70 microns in diameter, surrounded by viable tissue. Stratum corneum remains intact. Collagen is denatured at 400–700 microns depth. Viable cells enable rapid healing. Minimizes pain, no exudate/crusting. Treatment can be "dialed in." ^[1]

What the diagrams and serial photographs demonstrate:

• Traditional ablative destroys the entire surface → prolonged healing, high complication rate
• Fractional creates microscopic columns of thermal injury surrounded by untouched tissue → healing is driven by the surrounding viable cells → faster recovery, fewer complications
• Necrotic debris and melanin are expelled by keratinocyte migration ("unique epidermal repair")
• The deck's day-2 photograph after confluent resurfacing shows a broad oozing/crusted wound, while the week-7 image still shows marked erythema. These images explain the downtime rather than merely naming it.
• The fractional-treatment series show gradual, partial improvement after multiple sessions—not scar erasure. Before/after lighting and pose can also influence apparent response.
• Fractional procedures still cause pain, erythema, infection, scarring and dyspigmentation; PIH is especially important when counselling patients with darker skin. Treat active acne first and use an experienced procedural clinician.

For exams, understand the fractional principle rather than memorising the slide's device settings or session counts. Those parameters are not portable prescriptions.

Dermatitis is classified as Endogenous (Atopic Dermatitis) or Exogenous (Primary Irritant Contact Dermatitis, Allergic Contact Dermatitis). ^[1]

Dermatitis
├── Endogenous
│   └── Atopic Dermatitis
└── Exogenous
    ├── Primary Irritant Contact Dermatitis
    │   ├── Acute Toxic
    │   └── Chronic Cumulative
    └── Allergic Contact Dermatitis (Type IV hypersensitivity)

"1-year-old Ming Ming, several months history of rash affecting face, limbs and trunk. The rash is itchy. More recently confined to flexural areas. Mother has hay fever. On aqueous cream only." ^[1]

Diagnosis: Atopic Dermatitis. Hallmark: Itch is the hallmark of atopic dermatitis. ^[1]

This comparison table is directly from the lecture slides and is extremely high yield. ^[1]

Seborrhoeic dermatitis: the deck emphasises infancy and older age, but it also commonly affects adolescents and younger adults. Malassezia and sebum-rich sites are implicated. For infantile scalp scale, use gentle washing and short-contact scale softening with an appropriate emollient/mineral oil; avoid presenting olive oil as the required treatment. A short course of low-potency topical corticosteroid for marked inflammation or an age-appropriate topical antifungal may be clinician-directed. ^[1]

Management begins with history (duration, site, exposures/occupation, atopic tendency, family history) and examination of morphology and distribution. Patch testing is reserved for suspected superimposed allergic contact dermatitis—for example persistent eyelid, facial or hand eczema—not routine AD. ^[1][11]

First-line management: Avoid irritant/allergen, Emollient, Topical steroids, Antihistamine, Potassium permanganate, Treat secondary infection. ^[1]

From Block A notes and past papers: Wet wraps may be used for severe flares, but whole-body wet wrapping with topical corticosteroid should be initiated by trained clinicians and is not first-line home therapy. Systemic corticosteroids are generally avoided for routine AD because rebound and adverse effects can outweigh short-lived benefit. ^[2][11]

Immunological basis (from Block A Allergology notes): AD combines barrier dysfunction with immune dysregulation; type 2 inflammation is especially prominent in many phenotypes. However, high IgE does not equal a causal allergy, and normal IgE does not exclude AD. ^[3]

"Ming Ming's mother is a housewife, itchy rash affecting hands, worse in winter with marked dryness." ^[1]

DDx for hand dermatitis: atopic hand eczema, primary irritant dermatitis from wet work, and allergic contact dermatitis. Patch testing is appropriate when the history/distribution suggests allergy or when dermatitis persists despite appropriate care; it is not a screening test that separates all three on its own. ^[1][13]

The three categories of dermatitis (atopic, irritant contact and allergic contact) overlap — a single patient can have more than one type simultaneously. The three-circle Venn diagram is clinically important: an atopic barrier predisposition can lower tolerance to wet work, while a specific contact allergy may be superimposed. ^[1]

The hand photograph shows palmar xerosis and superficial fissuring rather than a pathognomonic eruption. In the case context—housework, winter worsening and repeated water/detergent exposure—the image supports chronic cumulative irritant hand dermatitis, but it cannot exclude atopic or allergic components.

Delayed Type IV hypersensitivity. Host immunological response to allergen. Occurs in susceptible individuals that become sensitized. ^[1]

Two-Phase Process:

1. Sensitisation phase:

   • Hapten (small molecule allergen) penetrates skin
   • Langerhans cells (antigen-presenting cells in epidermis) pick up hapten
   • Migrate via lymphatics to regional lymph nodes
   • Present antigen to T cells → generation of allergen-specific memory T cells. The slide labels CD4+ cells, but CD8+ and other immune populations can also contribute. ^[1]

2. Elicitation phase (re-exposure):

   • On re-exposure, resident/recruited memory T cells are activated
   • Cytokine release → vascular permeability ↑ → fluid and protein leak into tissue
   • Clinical result: eczematous reaction at site of contact, typically 48–72 hours after exposure ^[1]

What the Contact-Dermatitis Photographs Add

• Face/eyelids: dramatic oedema, erythema and vesiculation can occur because eyelid skin is thin; investigate cosmetics, hair dye, airborne allergens and transferred products from the hands.
• External ear: a localised eczematous pattern should prompt exposure questions about hearing devices, earbuds, spectacles, topical medicines, hair products and metals.
• Forearm: the sharply demarcated plaque ending at an exposure boundary is a powerful clue to contact dermatitis, but geometry alone cannot distinguish allergic from irritant disease.
• Acute allergic contact dermatitis can be vesicular/weeping; chronic exposure produces scale, fissures and lichenification. Always map the rash against the suspected contact surface.

Indications for patch test: Dermatitis of hands, feet, face, and legs that persists; chronic medicament usage; atypical or persistent discoid eczema. ^[1]

Patch-test methodology and interpretation:

• A baseline series plus exposure-, occupation- and region-specific allergens is applied under occlusion, usually to unaffected upper-back skin.
• Current ESCD best practice uses 2 days of occlusion and at least two readings: typically D2, D3/D4 and ideally around D7 because some allergens react late. ^[13]
• The photograph of chambers on the back shows why careful site mapping is essential. After removal, each square is graded morphologically; pressure erythema or an irritant reaction can mimic positivity.
• A positive test means sensitisation. Label it current, past or unknown relevance by linking it to the patient's products and distribution before recommending avoidance.
• Patch testing reproduces a delayed type IV reaction; skin-prick testing addresses immediate IgE-mediated allergy and is a different test.

Screening Series Allergens (lecture list): ^[1]

The screening list printed in this 2023 deck contains older names and preservatives. Contemporary baseline series are revised over time and should be supplemented for local exposures rather than memorised as a fixed universal panel.

2019 Fourth Summative Mini Case — Case Three (3-year-old Michael): ^[4]

• Itchy rash for 6 months, flexural distribution, dry skin, excoriation, pustules (secondary infection)
• Temperature 39.5°C, WBC 19.2 (neutrophilia + eosinophilia)
• Diagnosis: Atopic dermatitis with secondary bacterial infection (impetiginized eczema)
• Physical signs to look for: Erythema, excoriation, lichenification, xerosis (dryness), flexural distribution, vesicles/pustules (secondary infection), weeping/crusting
• Lecture-era exam investigations: the past-paper answer may mention CBC, swab and total IgE. In current care, neither eosinophilia nor total IgE confirms AD; do not routinely swab an initial suspected bacterial flare, and do not prescribe antibiotics for colonisation alone. Culture is more useful for recurrent, severe, atypical or treatment-unresponsive infection. ^[12]

2021 Fourth Summative MCQ — Dermatology EMQ: ^[5]

• Perilesional skin biopsy from atopic dermatitis → Spongiosis within the epidermis (answer H)
• This tests histopathology knowledge: spongiosis = intercellular oedema in the epidermis = hallmark of eczema/dermatitis

2025 Fourth Summative SAQ — Q8: ^[6]

• 6-year-old with cough, runny nose, difficulty breathing, and intermittent rash over antecubital fossae → atopic march (eczema → allergic rhinitis → asthma)

Approach to any skin problem: ^[7]

1. Identify the primary lesion (macule, papule, patch, plaque, vesicle, bulla, pustule, nodule)
2. Identify secondary changes (scaling, crusting, excoriation, lichenification, erosion, ulceration)
3. Note the distribution (flexural vs. extensor, truncal, acral, dermatomal, photodistributed)
4. Consider the morphological pattern (annular, linear, grouped, disseminated)

Biopsy of eczema shows spongiosis — intercellular oedema between keratinocytes in the epidermis. This is the histological hallmark.

• Topical steroids: finger-tip unit (FTU) for dosing guidance
• Steroid potency ladder: mild (hydrocortisone 1%) → moderate → potent → superpotent
• Topical calcineurin inhibitors (tacrolimus, pimecrolimus) — steroid-sparing agents, particularly useful for face and intertriginous areas where steroid atrophy is a concern
• For chronic urticaria: 2nd-generation antihistamines, up to 4× standard dose ^[8]

• Atopy ≠ Allergy: Atopy is the genetic tendency to mount IgE responses. High IgE does not automatically mean clinical allergy. Eczema can persist even without identifiable allergens. ^[3]
• Clinical differentiation of Type I vs. Type IV reactions is the most important takeaway from the allergology lecture.