MBBS Dermatology Flashcards

24 sample cards from the Dermatology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Differentiate erysipelas from cellulitis.

   Erysipelas involves the upper dermis and superficial lymphatics with a sharply demarcated, raised border (usually Strep pyogenes); cellulitis involves the deeper dermis and subcutis with poorly defined borders.

2. What organism causes staphylococcal scalded skin syndrome (SSSS) and what mediates the skin separation?

   Staphylococcus aureus producing exfoliative (epidermolytic) toxins that cleave desmoglein-1, causing superficial intraepidermal separation.

3. What virus causes molluscum contagiosum and what is the characteristic lesion?

   A poxvirus (Molluscum contagiosum virus); lesions are dome-shaped, pearly papules with central umbilication.

4. Differentiate herpes simplex (HSV) primary infection from herpes zoster.

   HSV causes grouped vesicles on an erythematous base (orolabial/genital), reactivating from sensory ganglia; herpes zoster (shingles) is VZV reactivation causing a painful dermatomal vesicular eruption.

5. What virus causes warts (verrucae) and what histologic feature is characteristic?

   Human papillomavirus (HPV); koilocytes (vacuolated keratinocytes) are characteristic.

6. Name the common dermatophytes causing tinea infections and the diagnostic test.

   Trichophyton, Microsporum, and Epidermophyton; diagnosed by KOH (potassium hydroxide) preparation showing septate hyphae.

7. What organism causes pityriasis (tinea) versicolor and what is its KOH appearance?

   Malassezia furfur (yeast); KOH shows a 'spaghetti and meatballs' pattern of short hyphae and round spores.

8. What is the causative organism of cutaneous candidiasis and a typical clinical feature?

   Candida albicans; intertriginous erythema with satellite pustules/papules in skin folds.

9. What autoantibodies are most specific/sensitive for systemic lupus erythematosus (SLE)?

   Anti-dsDNA and anti-Smith (anti-Sm) are most specific; ANA is most sensitive (screening).

10. Describe the classic cutaneous feature of acute cutaneous lupus and the lesion of discoid lupus.

    Acute: malar (butterfly) rash sparing the nasolabial folds. Discoid lupus: well-defined erythematous plaques with adherent scale, follicular plugging, and scarring/atrophy.

11. What histopathologic/immunofluorescence finding supports lupus skin involvement?

    Interface (vacuolar) dermatitis with a positive lupus band test (granular IgG/IgM and C3 deposition at the dermoepidermal junction).

12. List the hallmark cutaneous signs of dermatomyositis.

    Heliotrope rash (violaceous periorbital edema), Gottron papules (over MCP/IP joints), shawl sign, V-sign, and periungual telangiectasia.

13. What muscle enzyme elevations and antibodies are associated with dermatomyositis?

    Elevated creatine kinase (CK) and aldolase; anti-Jo-1 (associated with interstitial lung disease) and anti-Mi-2 antibodies.

14. Why is dermatomyositis clinically important to investigate beyond the skin and muscle?

    It is associated with an increased risk of underlying internal malignancy, warranting age-appropriate cancer screening.

15. Differentiate limited from diffuse systemic sclerosis (scleroderma).

    Limited (CREST) has skin involvement distal to elbows/knees and face with anti-centromere antibodies; diffuse has widespread proximal skin involvement with anti-Scl-70 (anti-topoisomerase I) and higher risk of early internal organ disease.

16. What does the CREST acronym in limited scleroderma stand for?

    Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia.

17. What is the pathophysiology of vitiligo?

    Autoimmune destruction of melanocytes, producing well-demarcated depigmented (chalk-white) macules and patches.

18. What examination tool accentuates vitiligo lesions and how do they appear?

    Wood's lamp (UVA light); depigmented patches show bright blue-white fluorescence with sharp accentuation, especially in fair skin.

19. What is melasma and what factors commonly trigger or worsen it?

    Acquired symmetrical hyperpigmentation, typically facial; triggered/worsened by UV exposure, pregnancy ('chloasma'), and hormones (OCPs/estrogen).

20. What is the first-line topical depigmenting agent for melasma and a common triple-combination?

    Hydroquinone; the classic triple combination is hydroquinone + tretinoin + a topical corticosteroid (Kligman's formula), plus strict photoprotection.

21. What is post-inflammatory hyperpigmentation (PIH) and the mechanism?

    Acquired excess melanin (or dermal melanin deposition) following cutaneous inflammation or injury (e.g., acne, eczema), due to stimulated melanocyte activity and pigment incontinence into the dermis.

22. What is the characteristic clinical presentation of alopecia areata?

    Sudden, well-circumscribed patches of non-scarring hair loss, often with 'exclamation mark' hairs at the margins.

23. What is the underlying mechanism of alopecia areata and a common nail finding?

    T-cell mediated autoimmune attack on hair follicles (loss of immune privilege); nail pitting is a common associated finding.

24. Define alopecia totalis and alopecia universalis.

    Alopecia totalis = complete loss of all scalp hair; alopecia universalis = loss of all body and scalp hair.

What this deck covers

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