CFB MED08 Dermatology (i)
Dermatology is the medical specialty concerned with the diagnosis and management of diseases affecting the skin, hair, nails, and mucous membranes.
Dermatology (I): Basics of Dermatology — Comprehensive Exam-Ready Notes
The Big Idea: Before you can diagnose or treat any skin disease, you must speak the language of dermatology. This lecture is the foundational toolkit — it teaches you how to describe a skin lesion precisely, how to take a dermatological history, how to examine the skin systematically, what investigations exist, and how treatments (especially topicals) work and can harm. Everything downstream — eczema, psoriasis, bullous diseases, dermatological emergencies — depends on mastering this first lecture. [1]
Learning Objectives (from the lecture): [1]
- How to describe a lesion
- How to use descriptive terms to arrive at a correct clinical diagnosis
- How to take a dermatological history
- Common investigations in dermatology
- Treatment in dermatological conditions
"The skin is the largest organ in the body — average weight 4 kg in an adult, surface area 1.35–2 m²." [1]
Functions of the skin:
- Barrier/protection: physical barrier against microbes, chemicals, UV radiation
- Temperature regulation: via vasodilation/vasoconstriction and sweating
- Vitamin D synthesis: UVB converts 7-dehydrocholesterol in epidermis to cholecalciferol
- Sensation: touch, pain, temperature via nerve endings
- Immunological: Langerhans cells (dendritic cells in epidermis) serve as antigen-presenting cells
Why this matters for dermatology: When thinking about lesion types, think about the layer of skin involved — epidermis, dermis, or subcutis. The lecture explicitly links lesion morphology to skin structure. [1]
| Layer | Key Structures | Lesion Examples |
|---|---|---|
| Epidermis | Keratinocytes, melanocytes, stratum corneum | Macules (color change only), vesicles, scaling |
| Dermis | Collagen, blood vessels, nerves, adnexae | Papules, nodules, wheals, telangiectasia |
| Subcutis | Fat lobules, fibrous septa | Panniculitis (erythema nodosum), deep nodules |
II. Approach to Skin Disease — History & Physical Examination
A. Dermatological History
The history in dermatology is structured differently from, say, a cardiac history. The key domains, as laid out in the lecture: [1]
- Onset: When did it first appear? Sudden vs gradual onset.
- Time course: Acute vs chronic; intermittent vs persistent; seasonal variation (e.g., eczema worse in winter due to dry air).
- Site: Initial site → pattern of spread → evolution (how it changes over time).
- Aggravating factors: Scratching (Koebner phenomenon in psoriasis), cold/hot exposure, trauma, sunlight (photosensitive rashes like SLE).
- Previous treatment and response: Critical — did topical steroids help (suggests inflammatory)? Did antifungals help (suggests tinea)? [1]
- Skin symptoms: Itchiness (eczema, urticaria, scabies), pain (herpes zoster, cellulitis), paraesthesia/loss of sensation (leprosy, neuropathic conditions).
- General/constitutional symptoms:
- Acute: Fever, sweats, chills, headache, nausea/vomiting — think infection, drug reaction, or dermatological emergency.
- Chronic: Fatigue, anorexia, weight loss, malaise — think malignancy, systemic disease with skin manifestation. [1]
Why ask about prodromal symptoms?
Prodromal symptoms help differentiate diagnoses. For example, herpes zoster typically has a prodrome of burning/tingling pain in a dermatome before vesicles appear. Drug reactions (e.g., SJS/TEN) may have a prodrome of fever and malaise before the rash develops. This sequence gives you a diagnostic timeline.
- Drug allergy/food allergy: Essential because drug eruptions are extremely common and mimic many dermatoses.
- Drug history/current medications: Many drugs cause skin reactions (β-blockers, antimalarials, NSAIDs, antibiotics, lithium).
- Family/personal history: Atopy (eczema, asthma, allergic rhinitis run together), psoriasis (40% have positive family history [8]), inherited conditions (e.g., ichthyosis, epidermolysis bullosa). [1]
B. Physical Examination
"Physical examination: 4 plus cardinal features of SKIN examination: Skin + SCALP, Hair, Nail, Mucosa." [1]
This is a critical exam point — never forget to examine scalp, hair, nails, and mucosae in a dermatology station.
- Appearance: Moon face/Cushingoid facies → suggests long-term steroid use (relevant if the skin disease itself was treated with steroids).
- Muscle wasting/cachexia: Think underlying malignancy (paraneoplastic dermatoses).
- Chest/abdomen: Look for surgical scars (prior operations, underlying conditions).
- Lymph node enlargement: Could indicate lymphoma (mycosis fungoides), infection, or metastatic skin cancer.
- Hepatosplenomegaly: Systemic diseases with skin manifestations (e.g., SLE, sarcoidosis, lymphoma).
- Inspection: Scan head to toes systematically.
- Palpation:
"Palpation can sometimes be more important than inspection in certain lesions (e.g., erythema nodosum — a type of panniculitis)." [1]
Why? Erythema nodosum lesions are tender, warm, subcutaneous nodules on the shins. They may look like vague areas of redness, but palpation reveals the firm, deep nodule that is pathognomonic. Similarly, morphoea (localized scleroderma) feels indurated/waxy, which you cannot appreciate by sight alone.
| Feature | What to Assess | Why It Matters |
|---|---|---|
| 1. Type of lesion | Is it flat, raised, depressed, fluid-filled? | Determines the primary morphological category → narrows DDx |
| 2. Shape, color, border | Round, annular, linear, umbilicated; red, violaceous, brown; well-demarcated vs ill-defined | Well-demarcated = psoriasis; ill-defined = eczema; violaceous = lichen planus |
| 3. Arrangement/Distribution | Grouped, scattered, dermatomal; flexural vs extensor; symmetrical vs asymmetrical | Dermatomal = herpes zoster; flexural = eczema; extensor = psoriasis |
| 4. Consistency | Firm, hard, soft, fluctuant | Hard = malignancy; fluctuant = abscess/cyst |
III. Morphology of Skin Disease — Terminology
"Accurate/precise description of the skin lesions allows good communication and achieves the accurate diagnosis." [1]
This is the core of the lecture. You must know these terms cold for exams.
Primary Lesions — Classification by Depth/Character
| Term | Definition | Key Examples |
|---|---|---|
| Macule | Flat, < 1 cm, color change only (not palpable) | Café-au-lait spots, freckles, post-inflammatory hyperpigmentation |
| Patch | Flat, > 1 cm | Vitiligo, fixed drug eruption |
| Infarct | Area of tissue necrosis from vascular occlusion | Calciphylaxis, cholesterol emboli |
| Sclerosis | Hardening/thickening of skin (can appear flat but feels indurated) | Morphoea, scleroderma |
| Telangiectasia | Visible dilated small blood vessels | Rosacea, BCC, chronic sun damage, hereditary hemorrhagic telangiectasia |
| Term | Definition | Key Examples |
|---|---|---|
| Papule | Raised, solid, < 1 cm | Molluscum contagiosum, lichen planus, scabies |
| Plaque | Raised, solid, > 1 cm, plateau-like | Psoriasis, eczema, mycosis fungoides |
| Nodule | Raised, solid, > 1 cm, round, deeper | Lipoma, erythema nodosum, BCC |
| Wheal | Transient, edematous, raised lesion (dermal edema) | Urticaria — wheals last < 24 hours |
| Vesicle | Small (< 1 cm) fluid-filled blister with clear fluid | Herpes simplex, chickenpox, eczema herpeticum |
| Bulla | Large (> 1 cm) fluid-filled blister | Bullous pemphigoid, SJS/TEN |
| Pustule | Contains purulent material | Folliculitis (infective), pustular psoriasis (non-infective) |
| Abscess | Larger collection of pus, deeper | Staphylococcal abscess |
| Cyst | Encapsulated nodule containing semisolid material | Epidermal cyst, acne cyst |
Exam Trap: Not All Pustules Are Infected
A common exam pitfall: pustular psoriasis and AGEP (Acute Generalised Exanthematous Pustulosis) produce sterile pustules. The presence of pustules does NOT automatically mean bacterial infection. Always consider non-infective causes. [2]
| Term | Definition | Key Examples |
|---|---|---|
| Petechiae | Small (< 3 mm) non-blanching macules | Thrombocytopenia, vasculitis |
| Ecchymosis | Larger (≥ 5 mm) non-blanching patches | Coagulopathy, trauma |
Why non-blanching? Purpura = extravasation of RBCs into the skin. Unlike erythema (which is vasodilation and disappears when you press — blood is pushed away), extravasated blood is outside the vessel and cannot be pushed away by pressure. This is tested with diascopy (pressing a glass slide on the lesion).
| Term | Definition | Key Examples |
|---|---|---|
| Atrophy | Thinning of skin (loss of epidermis ± dermis) | Chronic topical steroid use |
| Erosion | Superficial loss of epidermis only (heals without scarring) | Pemphigus vulgaris |
| Ulcer | Full-thickness loss through epidermis and into dermis (heals with scarring) | Venous ulcers, arterial ulcers, pyoderma gangrenosum |
| Sinus | Tract connecting a deep abscess to the skin surface | Pilonidal sinus |
| Gangrene | Tissue necrosis | Diabetic foot, peripheral vascular disease |
Erosion vs Ulcer — A Critical Distinction
- Erosion = partial-thickness loss (epidermis only) → heals without scar
- Ulcer = full-thickness loss (into dermis) → heals with scar
- In pemphigus vulgaris, the split is intraepidermal (suprabasal) → flaccid blisters that rupture easily → erosions
- In bullous pemphigoid, the split is subepidermal → tense blisters that are harder to rupture
- This distinction directly correlates with the blister's clinical appearance and Nikolsky sign
| Term | Definition | Key Examples |
|---|---|---|
| Scale | Accumulation of dead stratum corneum | Psoriasis (silvery scale), seborrhoeic dermatitis |
| Crust | Dried serum, blood, or pus on the surface | Impetigo (honey-colored crusts), pemphigus (crusts from erosions) |
| Lichenification | Thickening of skin with accentuated skin markings from chronic rubbing | Chronic atopic dermatitis |
| Excoriation | Linear erosion from scratching | Eczema, scabies — indicates pruritus |
| Scar | Fibrous tissue replacing normal skin | Keloid, hypertrophic scar |
| Exudate | Fluid (serous, purulent, or sanguineous) oozing from lesion | Weeping eczema |
Rule of Thumb for Scarring
"Lesions don't leave scars if the injury is above the dermis." Epidermal injury alone → no scar. Dermal injury → scar. This is why pemphigus vulgaris erosions (intraepidermal) heal with post-inflammatory hyperpigmentation but generally no true scar, unless the patient scratches deeply. [3]
| Shape | Description | Classic Example |
|---|---|---|
| Round/Oval | Circular or elliptical | Nummular eczema |
| Annular | Ring-shaped (active periphery, central clearing) | Tinea corporis, granuloma annulare |
| Arciform | Arc-shaped (incomplete ring) | Erythema marginatum |
| Linear | In a line | Contact dermatitis (e.g., from plant), Koebner phenomenon |
| Umbilicated | Central depression/dimple | Molluscum contagiosum, herpes vesicle |
| Arrangement | Description | Classic Example |
|---|---|---|
| Isolated/Scattered | Random distribution | Drug eruption |
| Grouped | Clustered together | Herpes simplex |
| Herpetiform | Grouped vesicles resembling herpes | Dermatitis herpetiformis |
| Zosteriform | Following a dermatome | Herpes zoster |
| Annular | Ring arrangement | Granuloma annulare |
| Linear | In a line | Lichen striatus |
| Reticular | Net-like | Livedo reticularis |
Distribution encompasses: Extent, Pattern, and Characteristic location. [1]
| Aspect | Options | Clinical Significance |
|---|---|---|
| Extent | Generalized vs localized | Generalized = systemic cause (drug reaction, viral exanthem); localized = contact dermatitis, herpes zoster |
| Pattern | Symmetrical; exposed/photosensitive areas; pressure areas; intertriginous areas | Symmetrical = endogenous (eczema, psoriasis); photosensitive = SLE, drug photosensitivity; intertriginous = candida, inverse psoriasis |
| Characteristic location | Flexural, extensor, dermatomal, trunk, lower extremities, palms/soles, facial, genital | Flexural = eczema; extensor = psoriasis; dermatomal = zoster; palms/soles = secondary syphilis, erythema multiforme |
Color:
- Red → inflammation, infection
- Dark red → deep inflammation
- Violaceous (purple) → lichen planus, vasculitis, Kaposi sarcoma
- Brown → melanin (post-inflammatory hyperpigmentation)
- Yellow → xanthoma, jaundice
- Dark/black → melanoma, necrosis
Special color tests:
- Diascopy: Press glass slide on lesion → blanching (erythema from vasodilation) vs non-blanching (purpura from extravasated blood). This is a bedside test that differentiates vasculitis from simple inflammation.
- Wood's lamp: UV light (365 nm) → certain organisms fluoresce (e.g., coral-red for erythrasma caused by Corynebacterium minutissimum; bright green for Microsporum species in tinea capitis); also enhances contrast in pigmentary disorders (vitiligo appears bright white). [1]
Border:
- Well-demarcated: Psoriasis, tinea, fixed drug eruption
- Ill-defined: Eczema, cellulitis
Consistency:
- Firm → dermatofibroma
- Hard → malignancy (BCC, SCC)
- Soft/fluctuant → lipoma, cyst
IV. Investigations in Dermatology
"Ix: usually limited and not routine → clinical data of paramount importance." [7]
Most dermatological diagnoses are clinical. Investigations serve to confirm the diagnosis, identify the causative organism, or assess systemic involvement.
- CBC: Eosinophilia (drug reaction, atopic dermatitis, parasites); leukocytosis (infection); thrombocytopenia (purpura)
- LRFT (Liver and Renal Function Tests): Baseline before starting systemic therapy (methotrexate → hepatotoxic; cyclosporine → nephrotoxic)
- Serology: Autoantibodies (ANA for SLE, anti-skin antibodies for pemphigus/pemphigoid); syphilis serology; HIV
- Urinalysis, stool: Systemic involvement assessment
| Investigation | What It Detects | Clinical Use |
|---|---|---|
| Skin biopsy | Histopathology — the gold standard for many dermatoses | Differentiates psoriasis from eczema; diagnoses bullous diseases, vasculitis, malignancy |
| Gram stain of crust | Bacterial morphology | Impetigo, infected wounds |
| KOH preparation | Fungal hyphae/yeast forms | Tinea (dermatophyte infection), candidiasis |
| Tzanck smear | Multinucleated giant cells | HSV, VZV (but cannot distinguish between them — PCR is more specific) |
| Culture (wound swab/tissue) | Bacterial, mycobacterial, fungal organisms | Identifies specific pathogen and antibiotic sensitivities |
| Wood's lamp | Fluorescence pattern | Erythrasma (coral-red), tinea capitis (Microsporum = green), vitiligo (enhanced depigmentation) |
| Scraping for scabies/mites | Identifies Sarcoptes scabiei mite, eggs, or fecal pellets | Scabies diagnosis |
| Patch test | Identifies Type IV (delayed) hypersensitivity allergens | Allergic contact dermatitis — applied for 48 hours, read at 48 and 96 hours |
| Acetone whitening | Test for nickel sensitivity | Dimethylglyoxime test — rub acetone-moistened swab on metal object |
High Yield: Patch Test vs Prick Test vs RAST
- Patch test = Type IV delayed hypersensitivity (allergic contact dermatitis) — allergen applied to skin for 48h [1]
- Skin prick test = Type I immediate hypersensitivity (IgE-mediated, e.g., food allergy, drug allergy) — read at 15-20 min
- RAST (Radioallergosorbent test) = measures serum-specific IgE — unreliable as noted by senior notes [7]
- The key differentiator tested in exams: timing — Type I occurs within minutes to 1 hour; Type IV occurs after 48-72 hours [9]
| Condition | Histopathological Finding |
|---|---|
| Bullous pemphigoid | IgG deposition along basement membrane zone; subepidermal blister with eosinophils |
| Pemphigus vulgaris | IgG deposition at intercellular layer of epidermis; suprabasal acantholysis |
| Atopic dermatitis (eczema) | Spongiosis within the epidermis |
| Psoriasis | Psoriasiform hyperplasia with absent granular layer |
| Erythema nodosum | Septal panniculitis without vasculitis |
| Erythema induratum | Lobular panniculitis with vasculitis |
| Lupus panniculitis | Lobular panniculitis without vasculitis |
V. Treatment in Dermatology
| Category | Options |
|---|---|
| No treatment | Observation (some benign lesions, e.g., seborrhoeic keratosis) |
| Topical medication | Emollients, steroids, antifungals, antibiotics, retinoids, calcineurin inhibitors |
| Systemic medication | Oral steroids, immunosuppressants (methotrexate, cyclosporine, azathioprine), biologics |
| Surgical | Excision, incision & drainage, curettage, electrocauterization, cryotherapy |
| Phototherapy | UVB, PUVA, Re-PUVA, methotrexate-phototherapy |
| Laser therapy | Pigment laser, vascular laser, fractional ablative laser |
| Other | Chemical peeling, liposuction, autologous hair transplant, epidermal graft (vitiligo), iontophoresis, vaccines, Botox, fillers |
"Rule of thumb: wet lesions (e.g., weeping/burn) — use high-water content applications; dry lesions — use ointment base." [1]
Oil content spectrum (decreasing oil, increasing water): Oil > Ointment > Paste > Cream > Lotion > Collodion > Gel
| Base | Water Content | Oil Content | Best For |
|---|---|---|---|
| Ointment | Low | High | Dry, chronic, lichenified skin (e.g., chronic eczema); provides occlusion → enhances drug absorption |
| Cream | Moderate | Moderate | General use; most cosmetically acceptable |
| Lotion/Gel | High | Low | Wet/weeping lesions, hairy areas, burns |
Why does this matter? Occluding a wet/weeping lesion with ointment traps moisture → maceration → worsens infection. Conversely, applying lotion to dry, cracked skin provides insufficient moisturization.
Components of topical preparations: [1]
- Active ingredients: Corticosteroid, dithranol/tar, antiseptics, antibiotics, antifungals, antivirals, retinoid acid, benzoyl peroxide
- Other components: Preservatives (can cause allergic contact dermatitis), vehicles, fragrances (another common allergen)
This is extremely high yield for exams. The HK steroid ladder is commonly tested.
| Class | Potency | Steroid Example | Trade Name |
|---|---|---|---|
| Class IV | Mild (mildest) | 1% hydrocortisone acetate | — |
| Class III | Moderate | 0.05% clobetasone butyrate | Eumovate |
| Class II | Potent | 0.25% fluocinolone acetonide | Synalar |
| Class I | Very potent | 0.05% clobetasol propionate | Dermovate |
High Yield: Steroid Potency Selection Principles
- Face, genitalia, flexures: Use mild (Class IV: hydrocortisone) — thin skin absorbs more → higher risk of atrophy and striae
- Body/trunk: Use moderate (Class III: Eumovate)
- Palms, soles (thick skin): May need potent (Class II) or very potent (Class I) because thick stratum corneum limits absorption
- Absorption by body site (from Ryan Ho): sole of foot 0.14%, palm 0.83%, forearm 1%, scalp 3.5%, forehead 6%, mandible 13%, genitalia 42% [7]
- Duration: Intermittent with tapering — avoid continuous use (→ tolerance + rebound)
Adverse Effects of Topical Steroids [1]
"LOCAL: Aggravation of infection (cellulitis, impetiginised eczema, eczema herpeticum), skin atrophy, striae, telangiectasia, tachyphylaxis, rebound phenomenon on withdrawal." [1]
| Local Effect | Mechanism |
|---|---|
| Infection aggravation | Steroids suppress local immune response → allows bacteria (impetiginised eczema), viruses (eczema herpeticum), fungi (tinea incognito) to flourish |
| Skin atrophy | Steroids inhibit collagen synthesis by fibroblasts → thinning of dermis |
| Striae | Dermal collagen breakdown → permanent stretch marks (irreversible!) |
| Telangiectasia | Loss of dermal support → superficial vessels become visible |
| Tachyphylaxis | Reduced response with chronic continuous use → need to take "steroid holidays" |
| Rebound phenomenon | Sudden withdrawal → flare of disease worse than original (especially dangerous in psoriasis → can trigger erythroderma or pustular psoriasis) |
Tinea Incognito
Applying topical steroids to a fungal infection (misdiagnosed as eczema) partially suppresses inflammation → the rash looks atypical and is harder to diagnose → this is called "tinea incognito." Always do KOH preparation before starting steroids on an annular, well-demarcated, scaly lesion to exclude tinea. [1]
These apply to both oral/systemic AND excessive topical steroid use (especially potent steroids over large areas, under occlusion, or on thin skin).
Systemic adverse effects include: Adrenal suppression, Cushing's syndrome, growth retardation, hypertension, DM/glucose intolerance, acneiform eruption, hirsutism, skin atrophy, striae, muscle wasting, scalp hair loss/thinning, poor wound healing, osteoporosis, AVN of hip, infection, GI complications (gastritis, GI bleeding), cataracts, glaucoma, CNS effects (agitation, insomnia). [1]
"Esterified steroids (new formula): quickly metabolized by skin cells, thus not systemically absorbed/distributed." [1]
This is an important concept — newer esterified steroids (e.g., methylprednisolone aceponate) are designed to be potent locally but are rapidly deactivated when they enter the bloodstream, reducing systemic side effects. This is particularly useful for children and for sensitive areas.
| Agent | Use | Notes |
|---|---|---|
| Tar, salicylic acid | Psoriasis (keratolytic) | Salicylic acid dissolves keratin → removes scale |
| Calcipotriol | Psoriasis (vitamin D analogue) | Reduces keratinocyte proliferation |
| Benzyl benzoate | Scabies treatment | Applied whole body below neck |
| Antiseptics | Iruxol, silver nitrate | Wound care |
| Antifungals | Imidazoles (clotrimazole), miconazole | Tinea, candida |
| Antibiotics | Neomycin, gentamicin, fusidic acid (Fucidin), mupirocin (Bactroban) | Impetigo, infected eczema |
| Antiviral | Acyclovir cream | HSV — limited efficacy topically; systemic acyclovir is preferred for significant infections |
| Retinoid derivative | Adapalene (Differin) | Acne — avoid pregnancy, advise contraception, potential teratogenicity |
| Benzoyl peroxide | Acne | Bactericidal against P. acnes; can bleach clothing |
| Sulphur | Various (scabies, acne) | Traditional agent |
Retinoid Teratogenicity
All retinoids (topical or systemic) are teratogenic. Women of childbearing age must use reliable contraception. Isotretinoin (systemic) requires a pregnancy test before starting, monthly during treatment, and contraception for 1 month after stopping. Acitretin (used in psoriasis) requires contraception for 3 years after stopping because it is stored in fat. [1]
| Type | Mechanism | Indications |
|---|---|---|
| Narrowband UVB (NB-UVB) | UV light induces immunosuppression in the skin; inhibits T cell proliferation | Psoriasis, eczema, vitiligo, cutaneous T-cell lymphoma |
| PUVA | Psoralen (photosensitizer) + UVA → cross-links DNA in proliferating cells | Psoriasis, vitiligo, mycosis fungoides |
| Re-PUVA | Retinoid + PUVA → combination allows lower UV doses | Severe psoriasis |
| MTX + phototherapy | Methotrexate + phototherapy | Recalcitrant psoriasis |
Risks of phototherapy: Skin aging, increased skin cancer risk with cumulative doses (especially PUVA), phototoxic burns.
"Laser therapy depends on the chromophore: melanin, hemoglobin, water." [1]
| Laser Type | Target Chromophore | Wavelength | Indications |
|---|---|---|---|
| Pigment laser | Melanin | 1064 nm, 755 nm | Freckles, lentigines, solar lentigo |
| Vascular laser (PDL) | Hemoglobin | 595 nm | Port-wine stain, hemangioma, keloid scar, rosacea |
| Fractional ablative laser | Water | CO₂ or Erbium | Acne scars, skin resurfacing — minimizes downtime |
| Treatment | Indication |
|---|---|
| Iontophoresis | Hyperhidrosis (excess sweating of palms/soles) — uses electrical current to deliver ions through skin |
| Vaccines | VZV (chickenpox prevention, shingles prevention); melanoma vaccine (immunotherapy) |
| Botox injection | Hyperhidrosis (blocks acetylcholine release at neuromuscular junction of eccrine sweat glands); cosmetic wrinkle reduction |
| Fillers | Cosmetic volume restoration |
| Chemical peeling | Skin rejuvenation |
| Epidermal graft | Vitiligo (transplant melanocytes from normal skin to depigmented areas) |
Anti-pruritic effect — important in eczema, urticaria, drug eruptions.
| Generation | Sedation | Examples | Key Points |
|---|---|---|---|
| 1st generation | Sedating | Chlorpheniramine (Piriton), polaramine, hydroxyzine (Atarax), promethazine (Phenergan), doxepin (anxiolytic effect) | Must warn patient not to drive if taking sedating antihistamines [1] |
| 2nd generation | Low-sedating/non-sedating | Cetirizine (Zyrtec), loratadine (Clarityne), fexofenadine (Telfast) | For patients who need to be alert, drive, or operate machinery [1] |
Antihistamine in Eczema
In atopic dermatitis, the itch is mainly mediated by cytokines (IL-31, TSLP) rather than histamine. Antihistamines in eczema work primarily through their sedative effect (1st gen), helping patients sleep rather than directly blocking the itch pathway. This is why senior dermatologists say antihistamines for eczema are "mainly as sedative." [2]
For chronic urticaria: 2nd generation antihistamines are first-line, can be uptitrated to up to 4 times the standard dose before adding other agents. [10]
VII. Integration with Related Material
The GC lecture on skin rash covers:
- Skin basics (overlaps with this lecture)
- Cutaneous manifestation of systemic disease
- Life-threatening dermatoses (blistering diseases, erythroderma)
- Common dermatoses
- Treatment in dermatology
This Derm I lecture provides the foundational vocabulary needed for GC 085 and GC 065 (itchy rash).
Derm II focuses on dermatological emergencies — SJS/TEN, erythroderma, pemphigus/pemphigoid, eczema herpeticum. Understanding the basics from Derm I is prerequisite.
Expands on management of eczema, psoriasis, and urticaria. Key addition: biologics (dupilumab for eczema, anti-IL-17/23 for psoriasis, omalizumab for chronic urticaria).
EMQ themes commonly tested:
- Match description → diagnosis (2019 MCQ Q1-2: neurofibromatosis, spider naevi) [4]
- Match histopathology → diagnosis (2021 MCQ: bullous pemphigoid, erythema nodosum, psoriasis) [5]
- Identify skin lesion type from clinical photo or description
- Topical steroid potency and adverse effects
- Drug allergy workup (2025 MCQ Q82: LTT for delayed drug hypersensitivity) [14]
- Skin cancer identification (2023 Q61: BCC vs SCC vs melanoma) [6]
| Trap | Correct Understanding |
|---|---|
| Confusing macule and patch | Macule < 1 cm; Patch > 1 cm — same thing, just size difference |
| Confusing vesicle and bulla | Vesicle < 1 cm; Bulla > 1 cm — both contain clear fluid |
| All pustules = infection | NO — pustular psoriasis and AGEP have sterile pustules |
| Blanching vs non-blanching | Erythema = blanching (vasodilation); Purpura = non-blanching (extravasated blood) |
| Erosion vs ulcer | Erosion = epidermis only → no scar; Ulcer = into dermis → scars |
| Well-demarcated vs ill-defined | Well-demarcated = psoriasis, tinea; Ill-defined = eczema |
| Flexural vs extensor | Flexural = eczema; Extensor = psoriasis |
| Dermovate is "mild" | NO — Dermovate (clobetasol propionate) is the MOST potent (Class I) |
| Hydrocortisone is "potent" | NO — 1% hydrocortisone is the MILDEST (Class IV) |
| Antihistamines "treat" eczema itch | They mainly provide sedation; eczema itch is cytokine-mediated, not purely histamine-mediated |
High Yield Summary
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Key takeaways from Dermatology I
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Summary
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- History: Onset, time course, site, spread, aggravating factors, prior treatment, drug/allergy/family history, symptoms (itch, pain, constitutional).
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Summary
- 2. Examination: Always check Skin + Scalp + Hair + Nails + Mucosa. Use inspection AND palpation.
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Summary
- 3. 4 Cardinal Features: Type of lesion, Shape/Color/Border, Arrangement/Distribution, Consistency.
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Summary
- 4. Lesion terminology: Know flat (macule/patch), raised (papule/plaque/nodule/wheal/vesicle/bulla/pustule/cyst), depressed (erosion/ulcer/atrophy), secondary (scale/crust/lichenification/excoriation).
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Summary
- 5. Distribution clues: Flexural = eczema; Extensor = psoriasis; Dermatomal = zoster; Photosensitive = SLE; Symmetrical = endogenous.
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Summary
- 6. Investigations: Clinical diagnosis is paramount. Biopsy, KOH, Tzanck smear, Wood's lamp, patch test for specific indications.
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Summary
- 7.
- Topical treatment: Match base to lesion (wet → wet, dry → ointment).
- Know steroid potency ladder (Class IV = mildest hydrocortisone → Class I = most potent Dermovate).
- Know local and systemic side effects of steroids.
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Summary
- 8. Antihistamines: 1st gen = sedating (warn about driving); 2nd gen = non-sedating (safe for daytime use).
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Summary
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- Phototherapy: UVB, PUVA, Re-PUVA for psoriasis, eczema, vitiligo.
- Summary
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- Retinoids are teratogenic — contraception mandatory.
Active Recall - Dermatology I: Basics of Dermatology
[1] Lecture slides: CFB (MED08) Dermatology (I).pdf (all pages) [2] Senior notes: Maksim Medicine Notes.pdf (Dermatology section, pp. 66-68) [3] Senior notes: Block A - Dermatology PBL 2.pdf (p. 1, erosion/crust/scarring discussion) [4] Past papers: 2019 Fourth Summative MCQ.pdf (Section B, Q1-2) [5] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Section B, Q1-5) [6] Past papers: 2023 Fourth Summative MCQ.pdf (Q61) [7] Senior notes: Ryan Ho Fundamentals.pdf (pp. 412, 419) [8] Senior notes: Ryan Ho Rheumatology.pdf (p. 120, psoriasis genetics) [9] Senior notes: Block A - Fundamentals of Allergology.pdf (p. 3, Type I vs Type IV timing) [10] Senior notes: Block A - Treatments for skin diseases (eczema, psoriasis and urticaria).pdf (p. 46) [11] Lecture slides: GC 085. Skin rash_Doctor I have a rash.pdf (p. 5) [12] Lecture slides: CFB (MED09) Dermatology (II).pdf (p. 2) [13] Past papers: 2025 Fourth Summative MCQ.pdf (Q82, Q21-25) [14] Past papers: 2025 Fourth Summative MCQ.pdf (Q82)
CFB OPHTH01 Common Eye Diseases
Common eye diseases encompass frequently encountered ophthalmic conditions—such as cataracts, glaucoma, conjunctivitis, diabetic retinopathy, and age-related macular degeneration—that affect vision and ocular health across the general population.
CFB MED09 Dermatology (II)
This is a medical education module covering advanced dermatology topics, including inflammatory skin disorders, autoimmune skin diseases, skin infections, and dermatologic manifestations of systemic conditions.