Acne Study Guide

📖 Core Concepts Acne vulgaris: chronic blockage of hair follicles by excess sebum & dead skin cells → comedones, papules, pustules, nodules, cysts. Androgen drive: testosterone → DHT & DHEA‑S increase sebaceous gland size & sebum output. Follicular hyperkeratinization: excess keratin plugs the pilosebaceous duct → comedo formation. Cutibacterium acnes: colonizes clogged follicles, releases lipases & activates TLR‑2/4 → cytokine surge (IL‑1α, IL‑8, TNF‑α) → inflammation. Severity grading: Mild: comedones ± occasional papules/pustules (face only). Moderate: many papules/pustules on face + trunk. Severe: nodules ± extensive trunk involvement. Hormonal acne clues: onset 20‑30 y, pre‑menstrual flare, jaw‑line/chin distribution, nodular lesions. 📌 Must Remember Genetics ≈ 80 % of acne risk variation. Androgens (testosterone, DHT, DHEA‑S) = primary sebaceous stimulators. Benzoyl peroxide: kills C. acnes, no antibiotic resistance, effective 2.5‑10 % (lower = fewer side effects). Topical retinoids (adapalene, tretinoin, tazarotene) normalize keratinization; may cause initial flare. Oral isotretinoin: 4‑6 mo course, remission in majority; mandatory pregnancy prevention (iPLEDGE). Combination therapy (BPO + antibiotic or retinoid) > monotherapy; prevents resistance. COC benefit: 40‑70 % lesion reduction; third/fourth‑gen progestins preferred (anti‑androgenic). Spironolactone: 50‑200 mg/d, blocks androgen receptor; 33‑85 % lesion reduction in women. Low‑glycemic diet ↓ lesions; dairy has weak association. Scarring: occurs in 95 % of acne patients; atrophic (ice‑pick, boxcar, rolling) vs hypertrophic. 🔄 Key Processes Microcomedone formation ↑ Sebum + dead keratin → plug → follicle blockage. Superficial plug oxidizes melanin → blackhead (open comedo). Deep plug remains closed → whitehead. Bacterial‑mediated inflammation C. acnes → TLR‑2/4 activation → NF‑κB → IL‑1α, IL‑8, TNF‑α. Lipase → free fatty acids → further cytokine release. Progression to nodules/cysts Intense inflammation → follicular rupture → dermal penetration → nodule → possible cyst formation. Scar formation Inflammation → MMP activation via AP‑1 → collagen breakdown → atrophic/hypertrophic scar. Hormonal therapy action COC: ↓ ovarian androgen production & ↑ SHBG → ↓ free testosterone. Spironolactone: antagonizes androgen receptor & inhibits 5α‑reductase at higher doses. 🔍 Key Comparisons Blackhead vs Whitehead – Open comedo (oxidized melanin, visible) vs closed comedo (plug stays beneath skin). Benzoyl peroxide vs Topical antibiotics – BPO kills C. acnes without resistance; antibiotics risk resistance, need BPO adjunct. First‑gen vs Third/Fourth‑gen progestins (COC) – First‑gen: androgenic → may worsen acne; Third/Fourth‑gen: anti‑androgenic → preferred for acne. Oral isotretinoin vs Oral antibiotics – Isotretinoin: targets all pathogenic steps, used for severe/refractory disease, teratogenic; antibiotics: mainly anti‑bacterial/inflammatory, limited duration. ⚠️ Common Misunderstandings “Acne is caused by dirty skin.” – Hygiene plays little role; hormonal, inflammatory, and microbial factors are primary. “All dairy worsens acne.” – Association is modest; only certain components (whey protein, bovine IGF‑1) implicated. “Topical retinoids are unsafe in pregnancy.” – Category C; limited data but generally avoided, especially in first trimester. “Antibiotics can be used indefinitely.” – Should not exceed 3‑12 weeks without adjunct (BPO or retinoid) to prevent resistance. 🧠 Mental Models / Intuition “Four‑horse race” – Think of acne as a race among Sebum, Keratin, Bacteria, Inflammation; effective therapy tackles ≥2 horses simultaneously. “Block‑and‑burst” – Blockage → comedo → bacterial growth → inflammatory burst → possible rupture → scar. Visualizing this chain helps select where to intervene. 🚩 Exceptions & Edge Cases Pregnancy: Avoid oral isotretinoin, tetracyclines, topical retinoids; safe options = BPO, azelaic acid, certain antibiotics (azithromycin, penicillins). Women of color: PIH risk high → prioritize azelaic acid, nicotinamide, careful use of lasers to prevent hyperpigmentation. 5α‑Reductase inhibitors: Strong teratogenicity for male fetuses → limited to non‑pregnant women with strict contraception. 📍 When to Use Which Mild comedonal acne → Low‑strength BPO or topical retinoid alone. Moderate inflammatory acne → BPO + topical antibiotic or BPO + topical retinoid; add oral doxycycline if needed (≤3 mo). Severe nodulocystic acne → Oral isotretinoin ± adjunctive BPO; consider intralesional steroids for acute nodules. Hormone‑sensitive adult female acne → COC (3rd/4th‑gen progestin) ± spironolactone (if COC insufficient). Pregnant patients → BPO, azelaic acid; oral erythromycin/azithromycin for short‑term flares. 👀 Patterns to Recognize Jaw‑line/ chin distribution + pre‑menstrual flare → hormonal acne → consider COC/spironolactone. Sudden worsening after starting lithium or glucocorticoids → drug‑induced acne → review medication list. Predominance of deep, painful nodules → likely nodulocystic → need systemic therapy (isotretinoin). Persistent dark patches in darker skin → PIH → treat with azelaic acid, hydroquinone, or nicotinamide. 🗂️ Exam Traps “Benzoyl peroxide causes antibiotic resistance.” – False; it prevents resistance. “Topical retinoids are first‑line for pregnant women.” – False; they are contraindicated (Category C/X). “All oral contraceptives improve acne equally.” – False; only those with low‑androgenic or anti‑androgenic progestins are effective. “Cysts are common in acne.” – True cysts are rare; most deep lesions are nodules. “High‑glycemic diet is the main cause of acne.” – Overstated; it worsens severity but isn’t the sole cause. --- Study this guide repeatedly; focus on the “four‑horse race” model to quickly pick the right combination therapy for any severity level.