GC065 I Have An Itchy Rash
A clinical presentation of pruritic dermatitis requiring systematic evaluation to distinguish among common causes such as eczema, contact dermatitis, urticaria, fungal infections, and scabies.
I Have an Itchy Rash — Acne, Eczema (Atopic, Irritant, Allergic Contact), and Dermatological Management
The Big Idea: This GC 065 lecture by Prof. Henry Chan covers three major dermatological domains through case-based teaching: (1) Acne vulgaris — its pathogenesis, clinical features, and treatment ladder; (2) Eczema/Dermatitis — distinguishing atopic dermatitis (AD) from seborrhoeic dermatitis (SD), and endogenous from exogenous (irritant vs. allergic contact) dermatitis; and (3) Contact dermatitis from Topical Traditional Chinese Herbal Medicine (TTCM) — a Hong Kong–relevant clinical scenario. Although the lecture title says "I have an itchy rash," the deck also covers acne (which is notably non-itchy) and laser treatment for acne scarring (fractional photothermolysis). The lecture connects to Block A dermatology PBLs, the eczema/urticaria/psoriasis sessions, and allergology fundamentals. [1]
Learning Objectives (inferred from slides + Block A notes):
- Understand the aetiology and pathogenesis of acne vulgaris
- Classify acne lesions and select appropriate topical and systemic treatments
- Differentiate atopic dermatitis from seborrhoeic dermatitis
- Classify dermatitis as endogenous vs. exogenous (irritant vs. allergic contact)
- Understand the immunology of allergic contact dermatitis (Type IV hypersensitivity)
- Know the indications for patch testing
- Recognize contact dermatitis from TTCM as a clinically relevant entity in Hong Kong
- Appreciate laser resurfacing principles for acne scarring (lower yield for written exams)
PART 1: ACNE VULGARIS
"20F, last several years noticed rash in face and trunk, non-itchy, non-tender." [1]
Key learning point: Acne is non-itchy and non-tender in most cases — this immediately separates it from eczema and other itchy rashes. 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]
Why This Matters
The massive treatment gap (91% prevalence but only 25% treated) explains why scarring is the main consequence of acne. Many patients/parents consider acne "normal for puberty" and neglect treatment. The examiner may test your understanding that early treatment prevents scarring — this is the recent clinical trend emphasized in the lecture.
The aetiology of acne involves four sequential steps: Sex hormones → Sebum production → Bacteria proliferation → Host response. [1]
| Step | Mechanism | Clinical Correlation |
|---|---|---|
| 1. Sex Hormones | Testosterone increases sebum production; definite role. Male > female. Females may flare with menses. Females with irregular periods are more resistant to treatment. | Explains why acne peaks at puberty and why hormonal therapy (anti-androgen) works in females |
| 2. Sebum Production | ↑ Sebum (hormonal, ?genetic, ?food) + dead cells → block hair follicle → comedone (blackhead/whitehead) | Comedone = the fundamental acne lesion. Blockage is the initiating event |
| 3. Bacteria Proliferation | Blocked follicle + sebum → bacteria proliferate (P. acnes, P. avidum, P. granulosum) → inflammation → red papule | Explains why antibiotics (topical and systemic) are part of the treatment ladder |
| 4. Host Response | WBC infiltration → enzyme secretion → non-specific destruction of bacteria AND dermal tissue → pustules, scarring, cyst formation | The host response, not the bacteria alone, causes tissue destruction and scarring. This is why anti-inflammatory therapy matters |
Exam High Yield
"Sebum production plays a key role in acne formation" — this is the correct answer to the lecture MCQ (Q1). Lack of cleaning is NOT the main cause. Topical steroid is NOT effective and can worsen acne (steroid acne). [1]
Clinical features of acne: Comedone → Papule → Pustule → Scarring → Cyst [1]
- Comedone: Open (blackhead) or closed (whitehead). Non-inflamed. The earliest lesion.
- Papule: Inflamed, red bump. Indicates bacterial proliferation.
- Pustule: Contains pus. Indicates host immune response.
- Cyst: Deep, painful nodule. Indicates severe inflammation extending into dermis.
- Scarring: The feared irreversible consequence. Can be atrophic (ice-pick, boxcar, rolling) or hypertrophic/keloidal.
Treatment of Acne
Topical treatments include: Benzoyl peroxide, Antibiotics, Retinoids (Retin-A), Azelaic acid, Sulphur. [1]
| Agent | Mechanism | Key Points |
|---|---|---|
| Benzoyl Peroxide (BPO) | Reduces comedones, suppresses skin surface free fatty acids, reduces skin surface bacteria | Conc 2.5–10%. Use in combination with topical antibiotics. Irritation and dryness common. Does NOT cause antibiotic resistance — important advantage |
| Topical Retinoids (Tretinoin, Isotretinoin, Adapalene) | Reduce comedogenesis; reduce both inflamed and non-inflamed lesions | Dryness and irritation common. Avoid in pregnancy (teratogenic). Adapalene gel = new-generation retinoid, as effective as tretinoin 0.025% but fewer side effects (less scaling, irritation, erythema) |
| Topical Antibiotics (Erythromycin, Tetracycline, Clindamycin) | Anti-microbial: reduce P. acnes | Must use in combination with BPO or retinoids to reduce antibiotic resistance |
| Azelaic Acid | Keratolytic; reduces free fatty acids and bacterial load | As effective as BPO, retinoid, and tetracycline. Mild irritation common |
| Sulphur | Anti-inflammatory and mild keratolytic | Less commonly used; mentioned for completeness |
Combination is Key
Topical antibiotics should almost never be used as monotherapy — always combine with BPO or retinoids to prevent P. acnes resistance. BPO + adapalene is a commonly used fixed-dose combination.
Systemic options: Hormonal therapy, Antibiotics, Isotretinoin. [1]
Previous indications for systemic therapy: Moderate to severe acne, depression, significant post-inflammatory hyperpigmentation, acne excoriée, acne keloidalis, gram-negative folliculitis. [1]
Recent trend: Early treatment to avoid scarring. [1]
| Agent | Mechanism & Details | Side Effects |
|---|---|---|
| Hormonal Therapy (Cyproterone-containing OCP) | Anti-androgen. For females with hormonal disturbance. Takes 4–6 weeks to improve. Relapse on discontinuation. | Venous thromboembolism risk, weight gain, mood changes |
| Systemic Antibiotics (Tetracycline group, Erythromycin group) | Anti-microbial AND anti-inflammatory. | Usually GI side effects. Rarely: phototoxicity, liver damage, SLE-like syndrome (tetracyclines). Relapse on discontinuation |
| Isotretinoin (Oral) | Decreases sebaceous gland volume → ↓ sebum. Alters cutaneous immunological function. Only dermatologists can prescribe. | Teratogenicity (absolute contraindication in pregnancy — need 2 forms of contraception), cheilitis, conjunctivitis, myositis, arthralgia, hair loss, liver impairment, raised triglycerides, raised benign intracranial pressure, headache, mood changes |
Isotretinoin Side Effects — Exam Favourite
Teratogenicity is the most critical side effect of isotretinoin. Female patients of childbearing age must use two forms of contraception and have a negative pregnancy test before starting. Monitor LFTs and lipids regularly during treatment. Be aware of the association with raised intracranial pressure (pseudotumour cerebri) — presenting with headache and visual changes — and mood changes/depression (controversial but examinable). [1]
Ablative resurfacing (CO2 laser, Er:YAG laser) is the gold standard for acne scarring but has significant problems: pain, oozing, prolonged erythema, risk of infection and further scarring, downtime, pigmentary problems (especially in darker skin types). [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]
Why fractional is better than traditional ablative:
- 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")
Note: The lecture shows many before/after photos of Fraxel treatment. For the exam, understand the principle rather than memorize specific case numbers. The concept of "fractional" therapy is the key testable point.
PART 2: ECZEMA / DERMATITIS
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]
MCQ from Lecture
"The following statement about atopic dermatitis is correct: Itch is the hallmark" — This is the correct answer (Q2). AD is NOT infective, NOT a form of allergic contact dermatitis, tends to occur in infancy (not teenagers), and dryness IS common. [1]
Atopic eczema: Associated with asthma and allergic rhinitis. Early onset (age > 2 months). Genetic predisposition. Due to immunological imbalance. Common in HK: 5–28%. [1]
HK Epidemiology: Prevalence peaks at 3–5 years, then declines through 6–7 years and 12–13 years. Asthma prevalence rises in older age groups — this illustrates the "atopic march" concept. [1]
Clinical Features
Clinical features of atopic eczema: Itchy rash; face and extensor surfaces in infants; flexural involvement in children; chronic and relapsing nature; dry skin. [1]
| Age Group | Distribution | Why |
|---|---|---|
| Infants (< 2 years) | Face, scalp, extensor surfaces | Extensor surfaces are exposed to friction (crawling); face is exposed to saliva/food |
| Children (> 2 years) | Flexural surfaces (antecubital fossae, popliteal fossae, wrists, ankles) | Flexural areas trap sweat and are subject to occlusion |
| Adults | Hands, face, flexures, may become generalized | Occupational exposure contributes |
This comparison table is directly from the lecture slides and is extremely high yield. [1]
| Feature | Atopic Dermatitis (AD) | Seborrhoeic Dermatitis (SD) |
|---|---|---|
| Onset | Starts at 3 months | Starts at 6 weeks |
| Course | Chronic | Resolves by 3 months (6–12 weeks) |
| Itch | Itchy | Non-itchy |
| Family History | Positive for atopic disease | No family history |
| Distribution | Face, flexural surfaces | Scalp, face, axilla, napkin area |
| IgE | Raised | Normal |
Seborrhoeic dermatitis: Occurs at extremes of age (infant and elderly). Aetiology thought to be associated with yeast (Malassezia). Can be difficult to differentiate from AD. Resolves within 6–12 weeks of life. Treatment: olive oil for scalp, mild potency steroid, antifungal cream, emollient. [1]
Why SD Resolves But AD Doesn't
Infantile SD is driven by transplacental maternal androgens that stimulate sebaceous glands. Once these hormones clear (~3 months), the condition resolves. AD, in contrast, is driven by an intrinsic immunological imbalance (Th2 predominance, filaggrin gene mutations, impaired skin barrier) that persists.
Management: History (duration, site, occupation, atopic tendency, FH) → Examination (distribution) → Patch test (if indicated). [1]
First-line management: Avoid irritant/allergen, Emollient, Topical steroids, Antihistamine, Potassium permanganate, Treat secondary infection. [1]
| Intervention | Rationale |
|---|---|
| Avoid irritants/allergens | Remove trigger to break the itch-scratch cycle |
| Emollients | Restore skin barrier function; reduce transepidermal water loss (TEWL). Use liberally and frequently. The cornerstone of AD management |
| Topical corticosteroids | Anti-inflammatory. Use appropriate potency for the body site (mild for face, moderate for body, potent for thick skin/lichenified areas). Step down as control is achieved |
| Antihistamines | Sedating antihistamines (e.g., chlorphenamine, hydroxyzine) help with nocturnal itch. Non-sedating (cetirizine, loratadine) for daytime. Note: antihistamines address itch but not the underlying inflammation |
| Potassium permanganate | Astringent/antiseptic soak for weeping eczema. Dries exudative lesions |
| Treat secondary infection | Impetiginized eczema (golden crusts, pustules) → topical or systemic antibiotics. Common organisms: S. aureus. Viral superinfection: eczema herpeticum (HSV) — a dermatological emergency |
From Block A notes and past papers: Wet wraps (topical steroid + wet bandaging) are used for acute severe flares. Systemic steroids are rarely used ("I hardly ever give systemic steroids to patients — only those with pemphigus/pemphigoid" — Prof. Chan). [2]
Immunological basis (from Block A Allergology notes): Atopic eczema involves a Th2-dominant immune response with elevated IgE. However, high IgE does not equal allergy — atopy is the tendency to produce more IgE, but even without identifiable triggers, patients can still have eczema (the skin barrier defect and immunological imbalance are intrinsic). [3]
PART 3: CONTACT DERMATITIS (Exogenous)
Contact Irritant Dermatitis
Non-immunological. Direct chemical or physical damage to the skin. If exposure to an irritant is sufficient, EVERYONE will develop irritant dermatitis. [1]
This is the critical distinction: irritant dermatitis is dose-dependent and universal — it does not require prior sensitization. Anyone exposed to enough detergent, water, or chemical will develop it.
| Subtype | Mechanism | Graph Pattern |
|---|---|---|
| Acute Toxic | Single high-dose exposure causes acute injury exceeding threshold for clinical disease | Sharp spike above threshold line |
| Chronic Cumulative | Repeated sub-threshold insults accumulate over time until clinical disease manifests | Stepwise rise with each insult, eventually crossing threshold |
The chronic cumulative model explains why housewives, nurses, and hairdressers develop hand dermatitis — each hand wash or chemical exposure is sub-clinical, but the cumulative damage overwhelms the skin's repair capacity.
Delayed Type IV hypersensitivity. Host immunological response to allergen. Occurs in susceptible individuals that become sensitized. [1]
Two-Phase Process:
-
Sensitization 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 specific memory CD4+ T cells [1]
-
Elicitation Phase (Re-exposure):
- On re-exposure, memory CD4+ 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]
Type I vs. Type IV — Exam Discriminator
Type I (Immediate/IgE-mediated): Onset within minutes to 1 hour. Urticaria, angioedema, anaphylaxis. Mast cell/histamine-mediated.
Type IV (Delayed/T-cell-mediated): Onset 48–72 hours. Eczematous reaction. T-cell and cytokine-mediated.
The history (timing of onset after exposure) is the key clinical differentiator. This is the most important part of the allergology lecture per the Block A notes. [3]
Indications for patch test: Dermatitis of hands, feet, face, and legs that persists; chronic medicament usage; atypical or persistent discoid eczema. [1]
Exam MCQ from Lecture
"Patch test should be considered for patients with discoid eczema" — Correct answer (Q3). Patch test is NOT useful for acne, NOT applied for only 1 hour (it is applied for 48 hours, read at 48h and 96h), NOT for all children with AD, and NOT for detecting food allergy (food allergy is Type I — use skin prick test or specific IgE). [1]
Patch Test Methodology:
- Allergens from a standardized screening series are applied to the back under occlusion
- Removed at 48 hours, read at 48h and 96h (delayed type reaction needs time)
- Positive result: eczematous reaction at test site
Screening Series Allergens (lecture list): [1]
| Category | Examples |
|---|---|
| Metals | Potassium dichromate, Cobalt, Nickel |
| Rubber chemicals | Mercapto mix, Thiuram mix, Mercaptobenzothiazole |
| Medicaments | Neomycin, Benzocaine |
| Cosmetics | Parabens mix, Quaternium 15 |
| Balsams | Balsam of Peru |
| Others | Colophony, Fragrance mix, Formaldehyde, PPD (paraphenylenediamine), Epoxy resin, Primin |
Nickel is the most common contact allergen worldwide — found in jewelry, belt buckles, jean buttons.
Case 4
"Ming Ming's father injured his knee, seen by Chinese Herbalist. At the site where he applied TTCM, he developed itchy rash." [1]
Contact dermatitis from TTCM: Popular in Asian countries (HK, Singapore, Malaysia). Easily obtained OTC. Contact dermatitis not uncommon. [1]
| Use of TTCM | Common Allergens/Issues |
|---|---|
| For aches and pain | Contains camphor, menthol, essential oil. Cross-reactivity with fragrances or Balsam of Peru can occur |
| For orthopedic injury | Contains > 10 herbs. Allergic contact dermatitis to mastic and myrrh reported |
| For skin disease (eczema, psoriasis, tinea) | May contain contaminants: steroids, NSAIDs, keratolytic agents. Both irritant and allergic contact dermatitis reported |
Hong Kong Context
TTCM causing contact dermatitis is a distinctly HK-relevant clinical scenario. The examiner loves this because: (1) it tests your awareness of alternative medicine use in the local population; (2) it tests cross-reactivity concepts (Balsam of Peru); and (3) the contamination issue (steroids in herbal remedies) is a public health concern. On patch testing, you might find positivity to fragrance mix or Balsam of Peru as the causative allergen.
Integration with Related Material
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
- Investigations: CBC (eosinophilia), skin swab for C/S (to guide antibiotic therapy), total IgE (supporting evidence for atopy)
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]
- Identify the primary lesion (macule, papule, patch, plaque, vesicle, bulla, pustule, nodule)
- Identify secondary changes (scaling, crusting, excoriation, lichenification, erosion, ulceration)
- Note the distribution (flexural vs. extensor, truncal, acral, dermatomal, photodistributed)
- 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.
Likely Exam Questions
-
Which of the following plays the key role in acne formation?
- A. Poor hygiene → Wrong (common misconception)
- B. Fungal infection → Wrong
- C. Sebum production → CORRECT [1]
- D. Viral infection → Wrong
- E. Topical steroid use → Wrong
-
A 3-year-old with itchy flexural rash, dry skin, and a mother with hay fever. Most likely diagnosis? → Atopic dermatitis
-
Patch test is indicated for which of the following? → Persistent discoid eczema / persistent hand dermatitis [1]
-
Histological hallmark of eczema/dermatitis? → Spongiosis (intercellular oedema in epidermis) [5]
-
Describe the 4-step pathogenesis of acne vulgaris. (4 marks) → Sex hormones → ↑ sebum production → bacterial proliferation (P. acnes) → host immune response (WBC infiltration, enzyme release, tissue destruction)
-
List 5 side effects of oral isotretinoin. (5 marks) → Teratogenicity, cheilitis, raised triglycerides, liver impairment, mood changes, raised intracranial pressure, conjunctivitis, arthralgia
-
Compare atopic dermatitis and seborrhoeic dermatitis in infants. (Table format, 5 features) → Use the AD vs SD table from lecture
-
A housewife presents with chronic hand dermatitis. What investigations would you perform and why? → Patch test to exclude allergic contact dermatitis. Skin scraping/KOH if tinea suspected. Consider skin swab if secondary infection.
-
3-year-old with itchy flexural rash, fever 39.5°C, pustules. Diagnosis? Investigations? Management? → Atopic dermatitis with secondary bacterial infection. CBC (expect eosinophilia, neutrophilia), skin swab C/S. Treat infection (oral flucloxacillin/co-amoxiclav), continue emollients, topical steroids once infection controlled.
-
A man develops itchy rash at site of TTCM application on knee. What is the mechanism? How do you investigate? → Allergic contact dermatitis (Type IV hypersensitivity). Patch test with standard series + TTCM components. Cross-reactivity with Balsam of Peru or fragrances possible.
High Yield Summary
Acne: 4-step pathogenesis (hormones → sebum → bacteria → host response). Topical first-line: BPO + retinoid ± antibiotic. Systemic for moderate-severe: antibiotics, hormonal therapy, isotretinoin (dermatologist only; teratogenic). Early treatment prevents scarring.
Atopic Dermatitis: Itchy (hallmark), chronic/relapsing, flexural in children, associated with atopic triad (eczema/asthma/allergic rhinitis), raised IgE, FH positive. Management: emollients + topical steroids + antihistamines + avoid triggers + treat secondary infection.
AD vs SD: AD starts 3m, chronic, itchy, ↑IgE, flexural, FH+. SD starts 6 weeks, resolves by 3m, non-itchy, normal IgE, scalp/axilla/napkin, yeast-associated.
Contact Dermatitis: Irritant = non-immunological, dose-dependent, everyone susceptible. Allergic = Type IV delayed hypersensitivity, sensitization then elicitation, 48–72h onset. Investigate with patch test.
TTCM Contact Dermatitis: HK-relevant. Cross-reactivity with Balsam of Peru. TTCM for skin disease may contain steroid contaminants.
Patch Test: Indicated for persistent hand/foot/face dermatitis, chronic medicament use, atypical discoid eczema. NOT for food allergy, NOT for acne. Applied 48h, read 48h and 96h.
Active Recall - I Have an Itchy Rash
[1] Lecture slides: GC 065. I have an itchy rash.pdf (all pages) [2] Senior notes: Block A - I have an itchy rash (eczema, urticaria, tinea infection and psoriasis).pdf (p1) [3] Senior notes: Block A - Fundamentals of Allergology.pdf (p3) [4] Past papers: 2019 Fourth Summative Mini Case.pdf (p15–19) [5] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (p37) [6] Past papers: 2025 Fourth Summative SAQ.pdf (p10) [7] Senior notes: Block A - Dermatology PBL 1.pdf (p4) [8] Senior notes: Block A - Treatments for skin diseases (eczema, psoriasis and urticaria).pdf (p46)
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