INI CET 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. Describe the lupus band test and the characteristic cutaneous lesion of discoid lupus erythematosus.

   Lupus band test: DIF showing granular IgG/IgM and C3 deposition along the dermo-epidermal junction. Discoid LE shows well-defined erythematous plaques with adherent scale, follicular plugging, and scarring/atrophy.

2. List the characteristic cutaneous signs of dermatomyositis (including eponymous signs).

   Heliotrope rash (violaceous periorbital eyelid erythema with edema), Gottron's papules (violaceous papules over knuckles/MCP-PIP joints), shawl sign (V-neck/upper back erythema), and periungual telangiectasia with ragged cuticles. Associated with proximal muscle weakness and elevated CK; paraneoplastic in adults.

3. Which autoantibodies are associated with limited (CREST) vs. diffuse systemic sclerosis (scleroderma)?

   Limited cutaneous SSc/CREST: anti-centromere antibody. Diffuse cutaneous SSc: anti-Scl-70 (anti-topoisomerase I), associated with interstitial lung disease. Anti-RNA polymerase III is linked to renal crisis.

4. What does the CREST syndrome acronym stand for?

   Calcinosis cutis, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia.

5. What is the pathophysiology of vitiligo and the characteristic Wood's lamp finding?

   Vitiligo is autoimmune destruction of melanocytes causing well-demarcated depigmented (chalk-white) macules. Under Wood's lamp the lesions show bright/sharply accentuated blue-white fluorescence and clearer margins. Koebner phenomenon is positive.

6. Differentiate melasma from post-inflammatory hyperpigmentation in terms of cause and distribution.

   Melasma: symmetric, blotchy facial hyperpigmentation (malar, centrofacial, mandibular) triggered by UV, pregnancy/hormones, and is acquired/chronic. PIH: hyperpigmentation following inflammation/injury (e.g., acne, eczema) located at prior lesion sites; epidermal PIH improves faster than dermal.

7. What is the cornerstone topical depigmenting agent for melasma and the classic combination formulation?

   Hydroquinone (tyrosinase inhibitor) is first-line. The Kligman's formula combines hydroquinone, tretinoin, and a topical corticosteroid. Strict broad-spectrum photoprotection is essential.

8. Describe the classic clinical features and prognostic sign of alopecia areata.

   Alopecia areata: non-scarring, well-circumscribed round patches of hair loss with 'exclamation mark' hairs at the margins. It is autoimmune (T-cell mediated against the hair follicle). Ophiasis pattern and nail pitting indicate poorer prognosis; alopecia totalis/universalis are extensive variants.

9. What is the pattern and pathogenesis of androgenetic alopecia, and the two FDA-approved treatments?

   Androgenetic alopecia is patterned hair loss from dihydrotestosterone (DHT)-mediated miniaturization of follicles: bitemporal recession/vertex in men (Norwood scale), diffuse crown thinning sparing frontal line in women (Ludwig scale). FDA-approved: topical minoxidil and oral finasteride (5-alpha-reductase inhibitor).

10. Name the most common dermatophyte causing onychomycosis, the most common clinical subtype, and the gold-standard treatment.

    Trichophyton rubrum is the most common cause; distal lateral subungual onychomycosis (DLSO) is the most common subtype. Oral terbinafine is the treatment of choice (most effective for dermatophyte nail infection).

11. What is the basic defect in epidermolysis bullosa, and how are the three classic types distinguished by level of cleavage?

    EB is a group of inherited mechanobullous disorders with blistering from minor trauma. EB simplex: cleavage within the basal keratinocytes (keratin 5/14 defect, intraepidermal). Junctional EB: split within the lamina lucida (laminin-332 defect). Dystrophic EB: split below the lamina densa (type VII collagen/anchoring fibril defect, scarring/milia).

12. List the diagnostic criteria features of neurofibromatosis type 1 (NF1).

    NF1 (von Recklinghausen): >=2 of - >=6 cafe-au-lait macules (>5 mm prepubertal, >15 mm postpubertal); >=2 neurofibromas or 1 plexiform neurofibroma; axillary/inguinal freckling (Crowe's sign); optic glioma; >=2 Lisch nodules (iris hamartomas); a distinctive bony lesion; and a first-degree relative with NF1.

13. What is the most common skin cancer overall, its typical clinical appearance, and its metastatic potential?

    Basal cell carcinoma is the most common. Classic nodular BCC: a pearly/translucent papule with rolled borders, telangiectasia, and central ulceration ('rodent ulcer'). It is locally invasive but rarely metastasizes.

14. What are the key risk factors and precursor lesion for cutaneous squamous cell carcinoma?

    Risk factors: chronic UV exposure, immunosuppression (transplant patients), HPV, chronic wounds/scars (Marjolin's ulcer), and arsenic. The precursor is actinic keratosis; SCC in situ is Bowen's disease. SCC has higher metastatic potential than BCC, especially on lip/ear.

15. What are the ABCDE criteria for melanoma and the single most important histologic prognostic factor?

    ABCDE: Asymmetry, Border irregularity, Color variegation, Diameter >6 mm, Evolution/change. The most important prognostic factor is Breslow thickness (tumor depth in mm); ulceration and mitotic rate also matter.

16. Name the four major clinicopathologic subtypes of melanoma and which is most common vs. most aggressive.

    Superficial spreading (most common, ~70%), nodular (most aggressive, vertical growth from onset), lentigo maligna (sun-damaged skin of elderly, best prognosis), and acral lentiginous (palms/soles/nails; most common type in dark-skinned and Indian patients).

17. What is the mechanism of action of botulinum toxin type A in cosmetic use?

    Botulinum toxin A cleaves SNAP-25, a SNARE protein, blocking presynaptic release of acetylcholine at the neuromuscular junction, causing temporary chemodenervation/muscle relaxation. Effect onset is ~3-7 days and lasts ~3-4 months.

18. For cosmetic botulinum toxin, name the most common treated areas and a serious complication to avoid in the upper face.

    Common areas: glabellar frown lines, forehead horizontal lines, and lateral canthal lines (crow's feet). A key complication is eyelid/brow ptosis from diffusion to the levator palpebrae superioris or frontalis muscle; injections must respect safe distances from the orbital rim.

19. What is the most commonly used dermal filler material, what enzyme reverses it, and a feared vascular complication?

    Hyaluronic acid (HA) is the most common dermal filler; it is reversible with hyaluronidase. The most feared complication is intravascular injection causing vascular occlusion, leading to skin necrosis or blindness (retinal artery occlusion), most dangerous in the glabella and nose.

20. Classify chemical peels by depth and give a representative agent for each.

    Superficial (epidermis): glycolic acid, salicylic acid, Jessner's solution, 10-30% TCA. Medium (papillary to upper reticular dermis): 35-50% TCA, often combined with Jessner's. Deep (mid-reticular dermis): phenol (Baker-Gordon). Deeper peels give better results for scarring/wrinkles but higher complication (scarring, dyspigmentation) risk.

21. What is the frosting endpoint in TCA chemical peeling and what does it indicate?

    Frosting is whitening of the skin from protein coagulation/keratin denaturation by trichloroacetic acid. The degree of frosting (Level I = erythema with streaky frost; II = white frost with erythema; III = solid white frost) correlates with peel depth.

22. What Wood's lamp color is characteristic of erythrasma, and what organism causes it?

    Erythrasma fluoresces coral-red/pink under Wood's lamp due to coproporphyrin III produced by Corynebacterium minutissimum. It presents as well-demarcated reddish-brown patches in intertriginous areas.

23. What is the Nikolsky sign and in which conditions is it positive?

    Nikolsky sign is dislodgement/sliding of the superficial epidermis with lateral shearing pressure on perilesional skin, indicating epidermal fragility/acantholysis. Positive in pemphigus vulgaris, staphylococcal scalded skin syndrome, and toxic epidermal necrolysis.

24. Compare the targeted molecular cytokines in biologic therapy for psoriasis (TNF, IL-17, IL-23, IL-12/23).

    TNF-alpha inhibitors: adalimumab, etanercept, infliximab. IL-12/23 (p40): ustekinumab. IL-17 inhibitors: secukinumab, ixekizumab. IL-23 (p19): guselkumab, risankizumab. The IL-23/Th17/IL-17 axis is central to psoriasis pathogenesis.

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