GeriQBank · Paper III · Q10
Causes of Erectile Dysfunction and Treatment Options
- Chapter
- Endocrinology, Metabolic & Reproductive Health
- Years asked
- Not recorded in the source
- Frequency
- Set 1× in Paper III (2009–2025)
As set in the university paper
What are the causes of erectile dysfunction and what treatment options are currently available?
Paper III · Continence, Bladder & Men’s Health · asked ×1 · 7-mark note · see in paper list
Detailed answer
Pro · free in betaAttempt it firstOutline your answer as a 7-mark note before revealing it — definition, causes, evaluation, management and the geriatric angle.Reveal answer
15 MARKS
High-Yield Points (Textbook Core)
A. Definition and epidemiology
Erectile dysfunction (ED) is the persistent inability to attain and maintain an erection satisfactory for sexual intercourse, present for at least 3 months.
Prevalence rises steeply with age: about 50% of non-diabetic men over 60, and 55–95% of diabetic men over 60.
Continuation of an active sex life is associated with longevity in both men and women; ED must never be dismissed as normal ageing. In women the parallel problems are vaginal atrophy, low desire, depression and SSRI effects.
Physiology: erection is parasympathetic (S2–S4) and nitric-oxide mediated → cavernosal smooth-muscle relaxation via cGMP; PDE5 degrades cGMP. Detumescence is sympathetic. This is the rationale for PDE5 inhibition.
B. Causes — organic (about 80% in the elderly)
Vasculogenic (commonest): atherosclerosis, hypertension, dyslipidaemia, smoking, diabetes, endothelial dysfunction, venous leak, pelvic irradiation, Leriche syndrome.
Neurogenic: diabetic autonomic neuropathy, stroke, Parkinson's disease, multiple sclerosis, spinal cord disease, cauda equina, and pelvic or prostate surgery (radical prostatectomy, cystectomy).
Endocrine / hormonal dysregulation: hypogonadism, hyperprolactinaemia, thyroid disease, poorly controlled diabetes.
Local and anatomical: Peyronie's disease, post-priapism fibrosis, phimosis, BPH-related lower urinary tract symptoms.
Drug-related — a particular problem in older patients: thiazide diuretics, spironolactone, beta blockers, cimetidine (all four specifically named in Pathy's), plus SSRIs, antipsychotics, antiandrogens and GnRH agonists, 5-alpha-reductase inhibitors, opioids, and older centrally acting antihypertensives. Always take an alcohol and tobacco history.
C. Causes — psychogenic
Performance anxiety, depression, bereavement and loss of a partner, relationship difficulty, and lack of privacy in institutional or multigenerational settings. Sudden onset, situational failure and preserved nocturnal or early-morning erections suggest a psychogenic component. In practice most older men have a mixed organic and psychogenic picture.
D. Evaluation
Interview the patient — and the partner where appropriate. Take a full sexual, psychosocial and drug history, and clarify whether the problem is desire, erection, ejaculation or orgasm.
Examination: secondary sexual characteristics, penis (plaques, phimosis), testicular volume and consistency, gynaecomastia, peripheral pulses, blood pressure, digital rectal examination, and a focused neurological examination including perineal sensation and bulbocavernosus reflex.
Investigations: fasting glucose/HbA1c, lipid profile, early-morning total testosterone, thyroid function; add prolactin and gonadotrophins if testosterone is low. Validated assessment: the International Index of Erectile Function (IIEF / IIEF-5).
Specialised tests — nocturnal penile tumescence, penile duplex Doppler, cavernosometry — are available through specialist ED clinics but are usually avoided in older patients, in whom extensive testing rarely changes management.
E. Treatment — a stepwise approach
Step 1 — modify reversible factors: optimise glycaemic, blood pressure and lipid control; stop smoking; reduce alcohol; weight loss and regular exercise; and substitute the offending drug (for example replace a thiazide or non-selective beta blocker — nebivolol and ARBs are more erection-friendly; use bupropion or mirtazapine rather than an SSRI for depression).
Step 2 — psychosexual counselling with the partner involved; general education about age-related sexual change; treat depression and address bereavement.
Step 3 — oral PDE5 inhibitors (first-line pharmacotherapy): Sildenafil 25–100 mg on demand, about 1 hour before intercourse; a fatty meal delays absorption. Tadalafil 10–20 mg on demand or 5 mg once daily; duration up to 36 hours, and it also improves BPH-related LUTS — often the best choice in the older man. Vardenafil and avanafil are alternatives. PDE5 inhibitors are effective in carefully selected older people with diabetes. Start at the lower dose in the elderly, in renal or hepatic impairment, and in men on alpha blockers.
PDE5 inhibitor contraindications and cautions: absolute — any nitrate or nicorandil (risk of profound hypotension), and riociguat. Caution with alpha blockers (separate dosing), recent myocardial infarction or stroke, unstable angina, severe aortic stenosis, hypotension, and retinitis pigmentosa. Side effects: headache, flushing, dyspepsia, nasal congestion, blue-tinged vision (sildenafil), back and muscle ache (tadalafil), and rarely non-arteritic anterior ischaemic optic neuropathy and sudden sensorineural hearing loss.
Step 4 — testosterone replacement where the man is genuinely hypogonadal: it improves libido and may restore responsiveness to a previously failed PDE5 inhibitor. It is not a treatment for ED with normal testosterone.
Step 5 — second-line therapies: intracavernosal alprostadil injection (most effective non-surgical option; warn about priapism), intraurethral alprostadil (MUSE), and the vacuum erection device — particularly valuable in older men on nitrates or anticoagulants and after radical prostatectomy.
Step 6 — penile prosthesis (inflatable or malleable) for refractory ED, with high satisfaction rates. Penile revascularisation is reserved for younger men with isolated post-traumatic arterial insufficiency. Low-intensity shockwave therapy, platelet-rich plasma and stem-cell “restorative” therapies remain investigational and should not be offered as established treatment.
Latest Updates (2023–Present)
Princeton IV Consensus (Kloner et al., J Sex Med 2024; Mayo Clin Proc 2024) — ED is formally recognised as an ASCVD risk-enhancing factor. Men aged 40–79 with ED and no overt cardiac disease should undergo formal 10-year ASCVD risk estimation, with coronary artery calcium scoring as a risk modifier in those calculated to be low risk. Sexual intercourse represents only 2–3 METs, comparable to climbing two flights of stairs or walking 1.6 km in 20 minutes, and is safe in stable cardiovascular disease.
PDE5 inhibitors appear cardioprotective. A 2023 meta-analysis of 16 cohort studies (1,257,759 subjects, median follow-up 4.3 years) found PDE5 inhibitor use associated with reduced MACE (RR 0.78) and reduced all-cause mortality (RR 0.70). This reframes them as more than a symptomatic drug — though randomised confirmation is still awaited, and signals are neutral or unfavourable in HFpEF and after stroke. EAU 2025 Sexual and Reproductive Health guideline — many apparent “non-responders” are simply inadequately treated: verify dosing, timing and at least 4–6 adequate attempts, and try more than one molecule or schedule before declaring failure. Efficacy is lower where diabetes, obesity and cardiovascular disease are poorly controlled, so comorbidities must be optimised concurrently. Testosterone therapy may be used as an initial treatment where ED coexists with biochemical hypogonadism.
ICSM 2024 (Fifth International Consultation on Sexual Medicine) — choice among PDE5 inhibitors should be driven by patient preference, anticipated frequency of activity, desired duration of action, response to a therapeutic trial, partner factors and cost; testosterone monotherapy has only a limited role in isolated ED. A dedicated 2025/2026 ICSM statement addresses sexuality and sexual health specifically in older adults. Combination or dual PDE5 inhibitor regimens (daily low-dose tadalafil plus on-demand sildenafil) are being studied for on-demand non-responders, particularly in diabetes — including Indian cohort data (Lucknow, 2025).
Current Practice Update
Issue Textbook position Current practice (2023–present)
Meaning of ED A complex multifactorial A sentinel marker of endothelial dysfunction and an ASCVD sexual problem risk-enhancing factor — triggers formal cardiovascular risk assessment PDE5 inhibitors Effective symptomatic Same, plus observational evidence of reduced MACE and all-therapy in selected older cause mortality diabetic men Defining failure Move to second-line if oral Must first confirm correct dose, timing and ≥4–6 attempts, and therapy fails trial a second molecule Testosterone Adjunct in the hypogonadal May be an initial treatment when ED coexists with proven man hypogonadism; not for isolated ED Restorative therapies Not discussed Shockwave, PRP and stem-cell therapy formally reviewed and classed as investigational Exam One-Liners Erection = parasympathetic, nitric oxide, cGMP; PDE5 breaks cGMP down.
Commonest organic cause in the elderly is vasculogenic; commonest reversible cause is drugs. Preserved morning erections point to a psychogenic component.
Nitrates + PDE5 inhibitor = absolutely contraindicated.
Tadalafil 5 mg daily treats ED and LUTS together — ideal in the older man with BPH. Vacuum device is the safe option in men on nitrates or anticoagulants.
ED precedes coronary events by about 3–5 years — assess cardiovascular risk in every man who presents with it.
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References
- PAPERS-2-3-4_COMBINED.pdf — page 804
- GeriQBank source PDF — p. 804
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