Human Sexuality
A board-focused tour of human sexuality: the Masters & Johnson response cycle, parasympathetic-vs-sympathetic control (\"point and shoot,\" with somatic pudendal expulsion), psychogenic vs organic erectile dysfunction, drug-induced dysfunction, and the sildenafil–nitrate rule.
Why this matters on Step 1
On Step 1, human sexuality is tested through the Masters & Johnson response cycle, the autonomic control of erection and ejaculation, the split between psychogenic and organic sexual dysfunction, drug-induced effects, and normal changes with aging. The reliable exam hooks: parasympathetic erection / sympathetic emission ("point and shoot"), preserved nocturnal/morning erections pointing to a psychogenic cause, SSRIs, antipsychotics, and antihypertensives as classic culprits, and the potentially fatal sildenafil–nitrate interaction. Master these decision points and the vignettes become pattern recognition.
Masters & Johnson sexual response cycle:
- Excitement — arousal; penile erection, clitoral engorgement, vaginal lubrication, nipple erection, ↑ HR/BP
- Plateau — sustained peak arousal; testes elevate; "sex flush"; ↑ muscle tension
- Orgasm — rhythmic pelvic/genital contractions; emission + expulsion in men
- Resolution — return to baseline; men enter a refractory period (lengthens with age); women lack one → may be multiorgasmic
Autonomic/somatic control (male):
- Erection = parasympathetic (pelvic splanchnics, S2–S4; NO → ↑cGMP → cavernosal smooth-muscle relaxation → arterial inflow)
- Emission = sympathetic (hypogastric nerve, L1–L2; also closes the bladder neck to prevent retrograde flow)
- Expulsion (ejaculation) = somatic (pudendal nerve → rhythmic bulbospongiosus contraction)
- PDE5 inhibitors (sildenafil) block cGMP breakdown → sustained erection
"Point and Shoot" — autonomic control of the male sexual response:
- Point = Parasympathetic → erection (S2–S4, pelvic nerve)
- Shoot = Sympathetic → emission (L1–L2, hypogastric nerve; closes bladder neck)
- Somatic pudendal nerve → rhythmic bulbospongiosus contraction (expulsion) + genital sensation
Clinical tie-in: parasympathetic damage or anticholinergic drugs → erectile dysfunction; sympathetic injury (retroperitoneal lymph-node dissection) or α-blockers (bladder-neck relaxation) → retrograde or failed ejaculation.
Psychogenic vs organic ED
| Feature | Psychogenic ED | Organic ED |
|---|---|---|
| Onset | Sudden | Gradual |
| Situational | Yes (partner-specific) | No — all settings |
| Nocturnal/morning erections | Preserved | Reduced/absent |
| Erection with masturbation | Normal | Impaired |
| Typical causes | Anxiety, depression, relationship stress | Diabetes/vascular, neurologic, meds, low testosterone |
| Next step | Reassurance, sex therapy, treat mood | Vascular/endocrine workup; PDE5 inhibitor |
Vignette: A 44-year-old man reports 3 months of inability to maintain an erection with his partner, beginning after he lost his job. He has firm morning erections and normal erections during masturbation. Exam, fasting glucose, and testosterone are normal.
Dx: Psychogenic erectile dysfunction. Preserved nocturnal/morning erections confirm intact vascular, neurologic, and hormonal pathways — the deficit is situational and anxiety-driven.
Next step: Address psychosocial stressors and performance anxiety (sex therapy, treat depression) — not a vascular or endocrine workup. A PDE5 inhibitor may serve as an adjunct, not the primary fix.
Vignette: A 63-year-old man with stable angina on isosorbide dinitrate requests sildenafil for erectile dysfunction.
Decision: PDE5 inhibitors are contraindicated with nitrates — nitrates raise cGMP (NO donor) while PDE5 inhibitors block its breakdown → additive cGMP-mediated vasodilation → life-threatening hypotension.
Next step: Do not co-prescribe. Conversely, if a man who recently took sildenafil or vardenafil (within 24 h; 48 h for the longer-acting tadalafil) presents with chest pain, withhold nitrates and manage ischemia by other means. Optimize modifiable ED risk factors and consider non-nitrate anti-anginal therapy.
Classic culprits:
- SSRIs — ↓ libido, delayed orgasm/anorgasmia (exploited to treat premature ejaculation); switch to or augment with bupropion (or mirtazapine) — least sexual dysfunction
- Antipsychotics — D2 blockade of tuberoinfundibular dopamine → hyperprolactinemia → ↓ libido, ED, galactorrhea, gynecomastia (esp. risperidone)
- Antihypertensives — β-blockers, thiazides, clonidine, spironolactone → ED; ACEi/ARB and CCB relatively spare
- Antiandrogens — finasteride, spironolactone, ketoconazole → ↓ libido/ED
- Trazodone — priapism (also intracavernosal alprostadil, sickle cell, PDE5 inhibitors)
- Alcohol — "provokes the desire, but takes away the performance": ↑ desire, ↓ performance
Normal aging (sexual activity persists):
- Men: slower/less firm erection, need more direct stimulation, longer refractory period, less forceful ejaculation
- Women: ↓ estrogen → vaginal dryness and mucosal thinning/atrophy → dyspareunia (lubricant/topical estrogen helps)
Paraphilic disorders (≥6 mo of intense atypical arousal) — diagnosed only if causing distress/impairment or acting on nonconsenting persons: exhibitionistic, voyeuristic, frotteuristic, pedophilic, sexual sadism/masochism, fetishistic, transvestic. An atypical interest alone is not a disorder.
Gender dysphoria — marked, distressing incongruence between experienced and assigned gender ≥6 mo; being transgender without distress/impairment is not, by itself, a disorder.
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