Acne vulgaris shows up everywhere on the wards and on Step—because it’s the classic example of a follicular disorder driven by hormones, keratin plugging, bacteria, and inflammation. If you can explain why comedones form and how that changes treatment, you’ll pick up easy points and avoid common traps (like using topical antibiotics alone).
Quick Definition (Step-friendly)
Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit characterized by:
- Comedones (open/closed) ±
- Inflammatory papules/pustules
- Nodules/cysts (severe) → scarring
High-yield locations: face, chest, upper back (high density of sebaceous glands).
Pathophysiology: The 4 Core Mechanisms (memorize these)
Acne is driven by four interacting processes:
- Follicular hyperkeratinization → clogged pore (microcomedone)
- Increased sebum production (androgen-mediated)
- Cutibacterium acnes (formerly Propionibacterium acnes) proliferation
- Inflammation (innate immune activation, rupture of follicle)
How lesions form (connect to what you see)
- Closed comedone (whitehead): keratin/sebum plug under the skin surface
- Open comedone (blackhead): plug exposed to air → oxidized melanin/lipids (not dirt)
- Papules/pustules: inflammation around plugged follicle
- Nodules/cysts: deeper inflammation/rupture → higher scarring risk
Epidemiology & Triggers (what Step likes)
Who gets it?
- Most common in adolescents (androgen surge), but can persist into adulthood.
- Female adult acne is common (consider hormonal patterns).
Common exacerbating factors
- Androgens (puberty, PCOS, exogenous anabolic steroids)
- Occlusion/friction (helmets, masks) → acne mechanica
- Comedogenic cosmetics
- Medications (very testable):
- Glucocorticoids → “steroid acne” (often monomorphic papules)
- Lithium
- Phenytoin
- Isoniazid
- Androgens/testosterone
- (Also seen clinically: EGFR inhibitors → acneiform eruption)
Clinical Presentation (pattern recognition)
Lesions
- Noninflammatory: open/closed comedones
- Inflammatory: erythematous papules, pustules
- Severe: nodules/cysts, sinus tracts, scarring
Distribution
- Face (T-zone), chest, upper back, shoulders
Red flags to prompt extra workup (Step-style)
Consider hyperandrogenism if acne is:
- Sudden onset, severe, or refractory
- Associated with hirsutism, irregular menses, androgenic alopecia
Possible causes: PCOS, congenital adrenal hyperplasia, androgen-secreting tumor.
Diagnosis (usually clinical)
Diagnosis is clinical—you don’t need cultures for routine acne.
When to consider labs/imaging
If signs of androgen excess:
- Total/free testosterone, DHEA-S, ± 17-hydroxyprogesterone (depending on vignette)
- Evaluate for PCOS if oligo/anovulation + hyperandrogenism
Differential Diagnosis (common Step confusions)
| Condition | Key Clue | Comedones? | Typical Trigger/Setting |
|---|---|---|---|
| Acne vulgaris | Mixed lesions: comedones + papules/pustules | Yes | Adolescence; androgen influence |
| Rosacea | Facial flushing + telangiectasias; papules/pustules | No | Hot drinks, alcohol, heat; adults |
| Folliculitis | Pustules centered on hair follicles | No | Shaving, hot tubs (Pseudomonas) |
| Perioral dermatitis | Papules around mouth; spares vermilion border | No | Topical steroids, cosmetics |
| Hidradenitis suppurativa | Painful nodules, sinus tracts in axilla/groin | No | Smoking, obesity; apocrine areas |
High-yield discriminator: comedones = acne vulgaris (not rosacea).
Treatment: Step 1/2 Algorithm You Can Apply in Vignettes
General principles
- Treat the microcomedone foundation: topical retinoids
- Don’t use topical antibiotics alone → resistance
- Escalate based on severity and scarring risk
First-line Topicals (mild acne)
Topical retinoids (adapalene, tretinoin, tazarotene)
- Mechanism: normalize follicular keratinization, prevent comedones
- AEs: irritation, dryness, photosensitivity
- Pregnancy: avoid (especially tazarotene)
Benzoyl peroxide
- Mechanism: bactericidal (free radicals), comedolytic; reduces resistance risk
- AEs: dryness, bleaching fabrics
Topical antibiotics (clindamycin, erythromycin)
- Use only in combination with benzoyl peroxide ± retinoid
High-yield combo: retinoid at night + benzoyl peroxide in morning.
Moderate Acne (inflammatory): Add Oral Therapy
Oral tetracyclines (doxycycline, minocycline)
- Mechanism: inhibit bacterial protein synthesis + anti-inflammatory
- AEs (Step classics):
- Photosensitivity (doxycycline)
- GI upset, esophagitis (take with water, stay upright)
- Teeth discoloration, inhibited bone growth
- Contraindications: pregnancy, children <8
- Pair with topical retinoid + benzoyl peroxide
Hormonal Therapy (especially in females)
Combined oral contraceptives (COCs)
- ↓ ovarian androgen production; ↑ SHBG → ↓ free testosterone
- Great for patients with acne + menstrual-related flares.
Spironolactone
- Mechanism: androgen receptor blocker; inhibits 5α-reductase activity clinically
- AEs: hyperkalemia, menstrual irregularities, breast tenderness
- Contraindication: pregnancy (risk of feminization of male fetus)
Step tie-in: Acne + hirsutism + irregular menses → think PCOS → COCs ± spironolactone.
Severe Acne / Nodulocystic Acne: Isotretinoin (the board favorite)
Isotretinoin is for:
- Severe nodulocystic acne
- Acne with scarring
- Refractory acne
Mechanism (high-yield)
- Decreases sebum production (shrinks sebaceous glands)
- Normalizes keratinization
- Decreases C. acnes
- Anti-inflammatory
Adverse effects (memorize)
- Teratogenicity (major)—requires strict pregnancy prevention (iPLEDGE)
- Dry skin, cheilitis
- Hypertriglyceridemia
- Hepatotoxicity (↑ LFTs)
- Arthralgias/myalgias
- Mood changes (association noted; test stems sometimes include depression)
Monitoring (Step-relevant)
- Pregnancy tests (before + during)
- LFTs and lipid panel (triglycerides)
Special Scenarios & Pearls
“Steroid acne”
- Often monomorphic inflammatory papules on chest/back after systemic steroids
- Treat by addressing trigger + standard acne therapies
Scarring prevention is treatment urgency
- Nodules/cysts → early isotretinoin consideration to prevent permanent scarring
Post-inflammatory hyperpigmentation
- Common in darker skin tones; treat inflammation early
- Retinoids + sun protection help over time
High-Yield Associations (rapid review list)
- Comedones are the key lesion that separates acne from rosacea.
- Androgens increase sebum → puberty, PCOS, anabolic steroids.
- C. acnes contributes, but acne is not “just infection” → retinoids are foundational.
- Tetracyclines: photosensitivity + teeth/bone effects; avoid pregnancy/kids.
- Isotretinoin: teratogen + hyperTG + hepatotoxicity → iPLEDGE, lipids/LFTs.
- Topical antibiotics must be paired with benzoyl peroxide to reduce resistance.
First Aid Cross-References (where this lives conceptually)
While page numbers vary by edition, acne content is typically integrated across:
- Dermatology—Acne/Rosacea: comedones vs rosacea (no comedones)
- Pharmacology—Retinoids: isotretinoin AEs (teratogenicity, hyperTG, hepatotoxicity)
- Antibiotics—Tetracyclines: photosensitivity, teeth discoloration, contraindications
- Endocrine—PCOS/Hyperandrogenism: acne + hirsutism + irregular menses
Use this as your mental map: lesion type → severity → therapy ladder → classic adverse effects.
Mini Self-Check (Step-style)
- Teen with open/closed comedones and inflammatory papules: best initial long-term controller?
- Topical retinoid
- Adult with facial flushing, telangiectasias, papules/pustules but no comedones: diagnosis?
- Rosacea
- Severe nodulocystic acne with scarring + elevated triglycerides during treatment: culprit med?
- Isotretinoin