DR1.1-2 | Acne — Practice Quiz

Correct. Non-inflammatory lesions only (open + closed comedones), no papules/pustules = IGA Grade 2 (mild). The step-therapy ladder places this patient on topical monotherapy.

IGA grade 2 (mild) is characterised by non-inflammatory lesions only (open/closed comedones) with no papules or pustules. Grade 1 permits only very rare comedones.

Re-read the IGA grading criteria. The key discriminator between grades 1 and 2 is lesion number; between grade 2 and 3 is the presence of any inflammatory lesions (papules/pustules).

Correct. Follicular hyperkeratinisation forms the microcomedone, the precursor lesion from which all acne lesions evolve. Sebum excess and C. acnes colonisation amplify the process but are not the primary trigger.

The initiating event in acne pathogenesis is abnormal follicular keratinocyte differentiation causing hyperkeratinisation — the microcomedone — not sebum excess or bacterial colonisation, which are downstream.

While C. acnes, sebum, and inflammation are all involved, the very first structural event in the pilosebaceous unit is abnormal shedding of follicular keratinocytes causing the microcomedone.

Correct. For moderate inflammatory acne unresponsive to topical therapy, the step-therapy ladder calls for oral antibiotics (doxycycline or minocycline) combined with a topical retinoid and/or BPO. This covers the bacterial and keratolytic pillars simultaneously.

Moderate inflammatory acne (IGA 3) that has failed an adequate topical trial steps up to a systemic oral antibiotic combined with a topical retinoid. Isotretinoin is reserved for severe/recalcitrant disease.

Isotretinoin is for severe or recalcitrant acne. Topical antibiotic + BPO is the next step for mild-moderate unresponsive disease, but this patient's bilateral inflammatory acne calls for systemic therapy.

Correct. 'Sandwich' application (cleanser → dry skin → retinoid at night) minimises retinoid dermatitis. Sunscreen is mandatory. The most common early adverse effect is irritant retinoid dermatitis, not photosensitisation per se, but UV exposure worsens dryness and erythema.

Topical retinoids cause retinoid dermatitis (dryness, peeling, erythema) especially on moist skin. Correct application is pea-sized amount on DRY skin at night; daytime sunscreen is mandatory due to photosensitivity.

Applying tretinoin to moist skin dramatically increases irritation. Avoiding it entirely in summer is not the recommendation; daily SPF 30+ sunscreen while using any retinoid is.

Correct. The black colour of an open comedone results from melanin within the plug and oxidation of sebaceous lipids, not dirt — an important patient education point.

An open comedone (blackhead) is a widened follicular ostium plugged with keratin and oxidised lipid; the black colour is due to melanin and oxidation of lipids, NOT dirt. A closed comedone (whitehead) is covered by intact epidermis.

Distinguish carefully: open comedone = blackhead (oxidised plug, no infection); closed comedone = whitehead (intact epidermis over the plug). Papules and pustules are inflammatory lesions, not comedones.

Correct. This patient has three red flags for hyperandrogenism (perimenstrual flare, hirsutism, irregular cycles). Serum androgens (free/total testosterone, DHEAS) are the first-line screen; PCOS workup may follow.

Acne is usually a clinical diagnosis requiring no investigation. However, hormonal screen (androgens) is indicated when there are features suggesting hyperandrogenism: irregular periods, hirsutism, acne resistant to treatment, or adult-onset acne in females.

In uncomplicated acne, no investigation is needed. But signs of hyperandrogenism mandate a hormonal screen — not a skin biopsy (which is never routine) and not a swab (bacterial cultures are for acne fulminans or suspected gram-negative folliculitis).

Correct. BPO is an oxidising agent; the free radicals it releases are bactericidal against the anaerobic C. acnes. Crucially, bacteria cannot develop resistance to oxidative killing — unlike antibiotic-based agents.

BPO kills C. acnes through oxidative burst (free radical release) — a non-antibiotic mechanism that does NOT induce resistance. This is why BPO is combined with topical antibiotics to prevent resistance emergence.

5-alpha reductase inhibition describes the mechanism of flutamide/finasteride (hormonal agents). Normalising keratinocyte differentiation is the retinoid mechanism. Ribosomal 30S binding describes tetracyclines/macrolides.

Correct. Pregnancy is the absolute contraindication to isotretinoin (teratogenicity: craniofacial and cardiac defects, microtia, CNS malformations). Elevated triglycerides and depression are relative contraindications requiring monitoring and counselling, not absolute exclusions. Concurrent tetracyclines are contraindicated due to pseudotumour cerebri risk, not isotretinoin itself.

Isotretinoin is a known teratogen (category X). Pregnancy is the ONE absolute contraindication — two forms of contraception + monthly pregnancy tests are mandated for all women of childbearing potential (iPLEDGE or equivalent programme).

While elevated triglycerides and depression require careful monitoring during isotretinoin therapy, they are not absolute contraindications. Pregnancy, however, is absolute.

Correct. Comedones are the hallmark of acne vulgaris. Rosacea has papules, pustules, flushing, and telangiectasia — but NO comedones. If you cannot find a comedone, reconsider the diagnosis.

Comedones are the pathognomonic lesion of acne vulgaris. Their absence should prompt consideration of mimics: rosacea (papulopustular, no comedones), perioral dermatitis, gram-negative folliculitis, or steroid acne.

Papules/pustules and facial distribution are shared by multiple conditions. The single most useful discriminator is the comedone — present in acne vulgaris, absent in rosacea and perioral dermatitis.