GC184 Erection And Erectile Dysfunction
Erection is the neurovascular process of penile engorgement mediated by parasympathetic-induced smooth muscle relaxation and increased blood flow, while erectile dysfunction is the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance.
Erection and Erectile Dysfunction
This lecture (GC 184, Dr. Wilson Hung, Division of Urology, HKU/QMH) covers the anatomy, physiology, and biochemistry of penile erection, the definition, classification, assessment, and stepwise management of erectile dysfunction (ED) [1]. It is supplemented by the Psychiatry lecture on Sexual Function & Dysfunction (MBBS4) [2] and integrates with cardiovascular risk factor management, BPH pharmacology, endocrinology (hypogonadism/hyperprolactinaemia), and the broader context of men's health.
Why this matters for exams: ED has been directly tested in the Fourth Summative MCQ (2020 Q55, 2021 Q75) [3][4]. The lecture covers a perfect SAQ topic — a systematic walkthrough from mechanism → classification → assessment → stepwise treatment, with a clear "absolute contraindication" (nitrates + PDE5i) that examiners love.
Learning Objectives (inferred from slide scope):
- Describe penile anatomy relevant to erection.
- Explain the neurophysiology and biochemistry of erection (cGMP/cAMP pathways).
- Define ED and when it requires treatment.
- Classify ED (organic vs. psychogenic) and list risk factors.
- Outline the clinical assessment including history, examination, investigations.
- Describe the stepwise management (first → second → third line).
- Recognize absolute contraindications to PDE5 inhibitors.
- Understand ED as an early marker of cardiovascular disease.
Core Concepts and Mechanisms
The penis contains two corpora cavernosa (dorsal) and one corpus spongiosum (ventral, surrounding the urethra). The corpora cavernosa are the key erectile bodies. [1]
Key structures:
- Corpora cavernosa: Paired cylindrical bodies composed of sinusoidal spaces (lacunae) lined by endothelium and surrounded by smooth muscle. They are enclosed by the tunica albuginea — a thick, fibrous, inelastic covering.
- Corpus spongiosum: Surrounds the urethra; contributes to glans engorgement but not rigid erection.
- Tunica albuginea: Critical for the veno-occlusive mechanism — when stretched by expanded sinusoids, it compresses the subtunical venous plexus and emissary veins, trapping blood inside the cavernosa.
- Arterioles: Deep (cavernosal/helicine) arteries supply blood to sinusoids. Their smooth muscle tone determines arterial inflow.
Erection involves psychogenic stimulation (brain → spinal cord → penis) AND neurogenic activation via the cavernous nerve (S2-4). [1]
| Nerve | Origin | Function |
|---|---|---|
| Dorsal nerve of penis | From pudendal nerve | Sensory nerve — transmits pain, temperature, touch via spinothalamic tract |
| Cavernous nerves (parasympathetic) | S2-4 → pelvic plexus | Innervate corpora cavernosa → allow tumescence (erection) |
| Sympathetic nerves | T11-L2 → superior/inferior hypogastric plexus → pelvic plexus | Allow detumescence and ejaculation |
| Pudendal nerve (somatic motor) | S2-4 (Onuf's nucleus) | Innervates bulbospongiosus, ischiocavernosus, levator ani, external urethral/anal sphincter |
Why two erection centres?
- Sacral erection centre (S2-4): Mediates reflex erection from tactile/genital stimulation (parasympathetic) [5].
- Thoracolumbar erection centre (T11-L2): Mediates psychogenic erection from visual/auditory/fantasy input (sympathetic pathway that paradoxically facilitates erection through a different circuit) [5].
This is clinically important: a patient with a complete spinal cord lesion above T11 loses psychogenic erection but may retain reflex erections, and vice versa.
The key to erection is relaxation of cavernous smooth muscle. [1]
Sequence (from the lecture slides):
- Flaccid state: Arteriole wall smooth muscle and sinusoidal smooth muscle are contracted → minimal arterial inflow.
- Sexual stimulation → parasympathetic firing (ACh):
- ACh inhibits pre-synaptic sympathetic firing (stops the "keep it flaccid" signal).
- ACh stimulates NO release from endothelium and from cavernous nerve terminals.
- Rapid increase in arterial inflow to sinusoids.
- Sinusoids fill and expand → subtunical venous plexus compressed against the tunica albuginea.
- Tunica albuginea stretched, occluding emissary veins → blood trapped inside corporeal bodies (veno-occlusive mechanism).
- Further pressure increase by contraction of the ischiocavernosus muscles (somatic, pudendal nerve) → achieves rigid erection (~200 mmHg).
Veno-Occlusive Mechanism
This is the critical concept: erection is NOT just about "more blood in." It requires trapping blood by compressing outflow veins. Failure of this mechanism → "venous leak" (cavernosal/venogenic ED). This explains why pathology of the tunica albuginea (e.g., Peyronie's disease, fibrosis) can cause ED.
4. Biochemistry of Smooth Muscle Relaxation
Two pathways mediate smooth muscle relaxation: (a) cGMP pathway activated by NO, and (b) cAMP pathway activated by PGE1. [1]
- Parasympathetic activation → ACh → stimulates NO release from endothelium and nerve terminals.
- NO diffuses into smooth muscle cells → activates soluble guanylyl cyclase → converts GTP to cGMP.
- cGMP activates protein kinase G (PKG) → opens K⁺ channels (hyperpolarization) + closes Ca²⁺ channels + sequesters Ca²⁺ into ER.
- Net effect: ↓ intracellular Ca²⁺ → smooth muscle relaxation.
- cGMP is degraded by phosphodiesterase type 5 (PDE5) → smooth muscle regains tone → detumescence.
Therefore PDE5 inhibitor has developed into drugs for treating Erectile Dysfunction. [1]
- PGE1 binds to receptor on smooth muscle cell.
- Activates adenylyl cyclase → converts ATP to cAMP.
- cAMP activates protein kinase A (PKA) → same downstream effects (K⁺ channel opening, Ca²⁺ sequestration).
- cAMP is also degraded by PDE5 (note: the slide states this, though PDE3/4 are also involved — for exam purposes, PDE5 is the key enzyme for both pathways per the lecture framing) [1].
High Yield: Why PDE5 Inhibitors Are NOT Initiators of Erection
PDE5 inhibitors do NOT initiate erection — they require sexual stimulation (which generates NO) to work. [1] This is a commonly tested discriminator. If there is no NO being produced (no sexual stimulation), there is no cGMP to protect from degradation, and the drug is useless. This also means PDE5i will NOT cause spontaneous/unwanted erections — a key counselling point.
Five phases of erection [1]:
| Phase | Term | Arterial Flow | Intracorporeal Pressure |
|---|---|---|---|
| 0 | Flaccid | Minimal | 0 |
| 1 | Latent | Increase | 0 |
| 2 | Tumescence | Decrease | Increase |
| 3 | Full erection | Minimal | ~100 mmHg |
| 4 | Rigid erection | 0 | ~200 mmHg |
| 5 | Detumescence | Minimal | Gradual decrease |
Why does arterial flow decrease in phase 2-3? Because as the sinusoids fill and pressure rises, the perfusion pressure gradient across the arterial bed decreases. In phase 4, ischiocavernosus muscle contraction actually stops all inflow and squeezes intracorporeal pressure above systolic BP.
Sympathetic firing (norepinephrine): increases intracellular calcium → activates smooth muscle contraction → responsible for detumescence. [1]
After orgasm/ejaculation, sympathetic discharge causes arteriolar and sinusoidal smooth muscle contraction → sinusoids collapse → venous drainage reopens → blood exits → flaccidity returns.
Erectile Dysfunction: Definition, Significance, and Classification
ED: The inability to achieve and/or maintain an erection of sufficient rigidity for satisfactory sexual intercourse. [1]
However, all men, at one time or another, have had an incidence of erection failure associated with anxiety, alcohol, or fatigue — this is NOT erection dysfunction and does NOT require treatment. [1]
Treatment only required when:
- More than 3 months duration
- More than 50% of times
- Varying presentations: no erection at all; only half an erection and failure to penetrate; failure to keep the erection; varies at different times [1]
1. Common problem, especially in aging population 2. Affects physical and psychosocial health and impairs quality of life 3. Often an early (and only) manifestation of cardiovascular disease [1]
Prevalence in Hong Kong (Men's Health Survey 2002, Family Planning Association of HK) [1]:
| Age Range | Prevalence of ED |
|---|---|
| 26-30 | 18% |
| 31-40 | 29% |
| 41-50 | 38% |
| 51-60 | 47% |
| 61-70 | 61% |
ED as a cardiovascular sentinel event: The penile artery is ~1-2 mm in diameter — much smaller than coronary arteries (~3-4 mm). Atherosclerotic disease therefore manifests in penile arteries earlier than coronary arteries. ED may precede a myocardial infarction by 3-5 years. This is why "ED is often an early (and only) manifestation of cardiovascular disease" [1].
Risk Factor Increased Risk of ED (OR) Coronary Artery Disease 1.9-fold Diabetes Mellitus 2.6-fold Peripheral Vascular Disease 5.1-fold [1]
Classification
Classification of Erectile Dysfunction [1]:
Organic:
- Vasculogenic (arteriogenic, cavernosal, mixed)
- Neurogenic
- Anatomic
- Endocrinologic (e.g., hypogonadism, hyperprolactinaemia, hypothyroidism)
- Drug-induced
Psychogenic:
- Generalized
- Situational
| Category | Examples / Mechanism |
|---|---|
| Vasculogenic | Atherosclerosis (DM, HT, hyperlipidaemia, smoking) → ↓ arterial inflow; Cavernosal (venous leak) → failure of veno-occlusive mechanism |
| Neurogenic | Spinal cord injury, MS, diabetic autonomic neuropathy, pelvic surgery (radical prostatectomy damages cavernous nerves), Parkinson's |
| Anatomic | Peyronie's disease, hypospadias, micropenis |
| Endocrinologic | Hypogonadism (↓ testosterone → ↓ libido AND ↓ NO production), Hyperprolactinaemia (inhibits GnRH → secondary hypogonadism), Hypothyroidism |
| Drug-induced | Antiandrogens, antidepressants (SSRIs), antihypertensives (beta-blockers, thiazides), 5α-reductase inhibitors (finasteride/dutasteride) [1][6] |
Endothelial dysfunction is a common final pathway to ED in patients with hyperlipidaemia, diabetes mellitus, hypertension, and chronic renal failure. [1]
Why does DM cause ED? Multiple mechanisms: (1) Accelerated atherosclerosis → arterial insufficiency, (2) Autonomic neuropathy → loss of cavernous nerve function, (3) Endothelial dysfunction → ↓ NO production, (4) Advanced glycation end-products damage smooth muscle and endothelium [7].
Generalized: [1]
- Generalized unresponsiveness: Primary lack of sexual arousability; Aging-related decline
- Generalized inhibition: Chronic disorder of sexual intimacy
Situational: [1]
- Partner-related: Lack of arousability in specific relationship; sexual object preference; partner conflict
- Performance-related: Performance anxiety; associated sexual dysfunction
- Psychological distress/adjustment-related: Depression; major life stress (death of partner)
From psychiatry lecture [2]:
Psychogenic causes: Fatigue, performance anxiety/spectatoring, relationship problems, stress, lack of privacy, low self-esteem, mood disorders (anxiety, social phobia, mild depression).
50% due to organic causes, 50% psychogenic; organic causes often give rise to psychogenic causes as well. [2]
Organic: more gradual onset — affects non-coital erection [1] Psychogenic: often sudden onset — ask for any nocturnal or early morning erection [1]
| Feature | Organic | Psychogenic |
|---|---|---|
| Onset | Gradual | Sudden |
| Nocturnal/morning erections | Absent | Present (key discriminator) |
| Erection with masturbation | Poor | Normal |
| Situation-dependent | All situations | Specific situations |
| Libido | May be normal (unless endocrine) | Usually normal |
| Risk factors | DM, HT, smoking, etc. | Anxiety, depression, relationship issues |
High Yield Discriminator
Presence of morning erection suggests PSYCHOGENIC cause — because nocturnal erections (REM-associated) rely on intact vascular/neural pathways. If these pathways work during sleep, the organic apparatus is intact, and the problem is likely psychological. The 2020 MCQ Q55 option D tests exactly this: "Presence of morning erection suggest organic cause for ED" — this is FALSE (it suggests psychogenic) [3].
Clinical Approach
Assessment of ED: what is necessary [1]:
- Confirm the diagnosis — sexual history
- Ascertain the severity — IIEF score
- Identify treatable conditions leading to ED — DM, HT, hyperlipidaemia, hypogonadism, depression etc.
- Identify causes which may be amenable to specific treatment — vascular anomalies needing reconstructive surgery, endocrine problems, psychogenic causes
Sexual history: [1]
- Clarify symptoms: erectile / ejaculation / orgasm or desire problem?
- Psychosocial context of the problem
- Chronology (gradual vs. sudden)
- Severity
- Define patient's needs and expectations
Medical history: [1]
- Aging
- HT, DM
- Arteriosclerosis — hyperlipidaemia
- Smoking
- Depression
- Pelvic injury
- Neurologic/endocrine diseases
- Recreational drugs, other drug history
Typical patient (from the lecture) [1]:
55 years old, DM, HT, gradual deterioration of erectile function for 1 year, now unable to maintain erection for satisfactory intercourse.
The International Index of Erectile Function (IIEF-5) is a 5-question validated self-report questionnaire [1]. Scores range from 5-25:
| IIEF-5 Score | Severity |
|---|---|
| 22-25 | No ED |
| 17-21 | Mild ED |
| 12-16 | Mild-moderate ED |
| 8-11 | Moderate ED |
| 5-7 | Severe ED |
Examination: [1]
- Usually not need to be complete
- Genital exam (look for Peyronie's plaques, testicular size, hypospadias)
- Blood pressure
- Secondary sexual characteristics — gynecomastia, body hair distribution, fat distribution (signs of hypogonadism/hyperprolactinaemia)
Investigations
Blood tests: FBS, lipid profile [1] +/- Testosterone — if ↓ libido, small testes [1]
Since 50% organic, most clients need to check for blood glucose, lipid profile, hormones, ECG [2]
Rare — referred if failed oral therapy, may need endocrine workup [1]
- If testosterone normal → full endocrine evaluation usually unnecessary
- Prolactin assessment (hyperprolactinaemia → secondary hypogonadism)
- Thyroid disease
- Pituitary and hypothalamic disease
Unnecessary in most cases [1]
- Indications: select patients requiring penile vascular surgery, medicolegal reasons, patient request
- Doppler USG scan — assesses penile arterial sufficiency and veno-occlusive dysfunction
- DICC (Dynamic Infusion Pharmacocavernosometry and Cavernosography) — gold standard for diagnosing venous leak
- Penile arteriography
Man achieves rigid erection 4-5 times during night [1]
- Rigiscan — electronic device that records episodes of nocturnal erection
- Now usually reserved for medicolegal cases (e.g., rape cases, industrial accident compensation)
2021 MCQ Q75: What Investigations Before Treatment?
For a 50-year-old man with 6-month insidious-onset ED, no morning erection, preserved libido/ejaculation/orgasm, unremarkable exam — the answer is A: Baseline blood tests including fasting blood glucose, lipid profiles ONLY [4]. You do NOT need DICC, NPT, or penile duplex before starting first-line treatment. Those are reserved for specific indications (surgical candidates, medicolegal).
Management of Erectile Dysfunction
General advice and measures for ED: [1]
- Smoking and alcohol cessation
- Increase exercise
- Identify treatable causes and manage (IHD, PVD, DM etc.)
- Manage the psychological aspect of ED, be it a cause or its effect
Mainstay treatment for couple with psychosexual, relationship, and performance problems [1]
- Often restores sexual function
- Additional physical measures may be needed
- Drug may help some men overcome psychological problems by demonstrating erection is possible
First Line: PDE5 Inhibitors
Results in smooth muscle relaxation from inhibiting the degradation of cGMP [1] NOT initiators of erection — requires sexual stimulation (NO) [1]
| Feature | Sildenafil (Viagra) | Vardenafil (Levitra) | Tadalafil (Cialis) | Avanafil (Spedra) |
|---|---|---|---|---|
| Onset of action | 25 min | 25 min | 30 min | ~15 min |
| Duration of effectiveness | 5 hours | 5 hours | 36 hours | ~6 hours |
| Starting dose | 50 mg | 10 mg | 20 mg | 100 mg |
| Titration | Up/down to 100/25 mg | Up/down to 20/5 mg | Down to 10 mg | Up to 200 mg |
| Take before sex | 1 hour | 25-60 min | 30 min - 36 hours | 15-30 min |
| Max dosing frequency | Once per day | Once per day | Once per day | Once per day |
Achieves successful intercourse ~70% [1] 50% in DM, post-radical prostatectomy patients [1]
Why tadalafil is unique: Its 36-hour duration allows more spontaneous sexual activity — nicknamed "the weekend pill." It is also licensed for daily use at low dose (5 mg) for BPH with LUTS [6].
Side Effect Prevalence Mechanism Headache 9-15% PDE5 in cerebral vessels Flushing 4-12% Vasodilation Nasal congestion 1-10% Vasodilation Abnormal vision ~2% (sildenafil, vardenafil ONLY) Cross-reactivity with PDE6 in retina Back pain/myalgia 6% (tadalafil ONLY) Cross-reactivity with PDE11 in skeletal muscle [1]
Side Effect Discriminators for Exams
Visual disturbance (blue-tinged vision, "blue haze") → PDE6 cross-reactivity → sildenafil and vardenafil only. Back pain/myalgia → PDE11 → tadalafil only. These are classic MCQ discriminators.
Method of administration: [1]
- Check for absolute contraindications
- "One hour" before sexual intercourse
- Sexual stimulation is necessary
- Must not take more than one dose in every 24 hours
- Warn about possible side effects — avoid driving/operating machinery after administration
ABSOLUTE: Concomitant intake of ANY form of nitrates [1] Will lead to cGMP accumulation, profound hypotension and possible death [1]
Why? Nitrates generate NO → ↑ cGMP production. PDE5i blocks cGMP breakdown. Together, you get massively excessive cGMP → catastrophic smooth muscle relaxation in systemic vasculature → severe hypotension → cardiovascular collapse. This applies to GTN spray, ISDN, ISMN, and even amyl nitrite ("poppers").
Absolute Contraindication — Most Tested Point
This is the single most important clinical safety point of the entire lecture and has been directly tested. A patient on ANY form of nitrate therapy (including GTN spray for angina) CANNOT take PDE5 inhibitors. If a patient on sildenafil develops chest pain, you MUST NOT give GTN — manage with other anti-anginals. Separate PDE5i from nitrates by at least 24 hours (48 hours for tadalafil due to long half-life).
Relative contraindications/cautions (from BPH slide and clinical practice) [6]:
- Alpha-blockers for BPH/HT → additive hypotension; separate dosing by ≥ 6 hours (or use uroselective alpha-blockers like tamsulosin which have less interaction)
- Severe cardiovascular disease / recent MI / unstable angina
- Severe hepatic impairment
- Retinitis pigmentosa (PDE6 is crucial in photoreceptors)
- Concurrent use of potent CYP3A4 inhibitors (ketoconazole, ritonavir) → ↑ PDE5i levels
A vacuum device creates negative pressure around the penis → draws blood into corpora cavernosa → a constriction band is placed at the base to maintain the erection [1].
- Non-invasive, no systemic side effects
- Erection may feel "cold" at tip (trapped venous blood)
- Constriction band should not be left on > 30 minutes (risk of ischaemia)
- Good option for men who cannot take medications
Use LI-SWT with/without PDE5Is in patients with mild vasculogenic ED or as an alternative first-line therapy in well-informed patients who do not wish or are not suitable for oral vasoactive therapy or desire a curable option. (Weak recommendation) [1]
Use LI-SWT with/without PDE5Is in vasculogenic ED patients who are poor responders to PDE5Is. (Weak recommendation) [1]
Mechanism: Acoustic waves promote neovascularisation and improve endothelial function in penile tissue. Evidence is emerging but still has weak recommendation strength.
Alprostadil (Prostaglandin E1):
- Elicits smooth muscle relaxation using the cAMP pathway, independent of NO [1]
- Caverject (alprostadil injection) — only approved form of injectable for ED
- Produces erections in 70-80% of patients, even in DM and post-RP patients
- Need titration of dosage (5-20 μg)
Side effects: [1]
- Painful erection
- Prolonged erections (5%)
- Priapism (1%)
- Penile fibrosis (2%)
Why is ICI second-line? Because it requires self-injection into the penis (patient acceptance is lower), and it carries risk of priapism (a urological emergency). However, it works independently of the NO pathway, making it useful when PDE5i fails (e.g., severe neurogenic ED post-radical prostatectomy where NO generation is eliminated).
Priapism from ICI
Priapism = prolonged erection > 4 hours. This is ischaemic (low-flow) priapism — blood is trapped, becomes deoxygenated, and if not treated promptly → corporal fibrosis → permanent ED. Treatment: aspiration of blood from corpora cavernosa ± intracavernosal phenylephrine (alpha-agonist → causes smooth muscle contraction → detumescence).
Note: Topical/intraurethral alprostadil is no longer available in HK [1].
90-95% of inflatable prosthesis implants produce erections suitable for intercourse [1] Satisfaction rates 80-90% [1]
Complications: [1]
- Bleeding, infection, erosion of the prosthesis requiring removal
- Rarely mechanical failure leading to re-operation
Types:
- Malleable (semi-rigid): Simple rods that are bent up or down. Simpler but always semi-rigid.
- Inflatable (3-piece): Fluid reservoir in abdomen, pump in scrotum, cylinders in corpora. Most natural-feeling erection.
This is truly last-resort — it destroys the natural erectile tissue, making it irreversible.
Vascular reconstruction surgery [1] — reserved for very select young patients (e.g., post-traumatic arterial injury causing ED in a young man). NOT performed for age-related atherosclerotic ED.
Summary of Pathophysiology of ED: [1]
- Prevalence increases with aging
- Symptom of many underlying important diseases (DM, IHD)
- Condition affects penile nerve, artery, endothelium, smooth muscle, or tunica albuginea can cause ED
- Endothelial dysfunction is a common final pathway to ED in patients with hyperlipidaemia, DM, HT, and chronic renal failure
- Drugs most commonly associated with ED include antiandrogens, antidepressants, and antihypertensives
Integration with Related Material
- Tadalafil (PDE5i) is dual-indicated for ED + BPH/LUTS — it improves both conditions via smooth muscle relaxation in prostate and bladder [6].
- 5α-reductase inhibitors (finasteride, dutasteride) for BPH can cause ED (side effect) — important to counsel patients [6].
- Alpha-blockers for BPH can cause ejaculatory dysfunction (retrograde ejaculation) — not the same as ED but patients may confuse them [6].
- TURP complications include ED and retrograde ejaculation [6].
- Hyperprolactinaemia → inhibits GnRH → ↓ LH/FSH → secondary hypogonadism → ↓ libido + ED. Treatment: dopamine agonist (cabergoline/bromocriptine) [8].
- Hypogonadism → testosterone replacement therapy (if confirmed low T with symptoms). Monitor PSA (risk of prostate cancer/BPH) and DEXA (osteoporosis if untreated) [9].
- Klinefelter syndrome (47,XXY) → small firm testes, hypergonadotrophic hypogonadism → ED [10].
- Leriche syndrome: Aorto-iliac occlusion → triad of bilateral buttock claudication, absent femoral pulses, and ED [11].
- ED shares risk factors with CAD and should prompt cardiovascular risk assessment.
- Lesion above T11: Loss of psychogenic erection, may retain reflex erection (S2-4 intact).
- Lesion at S2-4: Loss of reflex erection, may retain psychogenic erection (T11-L2 intact).
- Complete lower motor neuron lesion: Loss of both → ICI or prosthesis needed [5].
- 4-phase sexual response cycle: Desire → Excitement → Orgasm → Resolution [12].
- ED occurs in the excitement phase. Distinguish from disorders of desire (low libido), orgasm, or ejaculation.
- SSRIs cause ED + delayed ejaculation + anorgasmia — very common exam point.
Exam Intelligence
| Trap | Why Students Fall For It | Correct Answer |
|---|---|---|
| "Morning erection = organic ED" | Seems logical that if you can get an erection, everything is fine organically | WRONG — morning erection means organic apparatus is INTACT → suggests PSYCHOGENIC cause |
| "PDE5i causes erection without stimulation" | Students forget the mechanism | PDE5i only works when NO is being produced (requires sexual stimulation) |
| "Penile prosthesis before ICI" | Students mix up the stepwise order | ICI (2nd line) must be tried before prosthesis (3rd line) |
| "Vascular tests are routine for ED" | Over-investigating | Most patients need only FBS + lipid profile ± testosterone; vascular tests reserved for surgical candidates/medicolegal |
| "Alpha-blockers cause ED" | Confused with ejaculatory dysfunction | Alpha-blockers mainly cause retrograde ejaculation; ED is "controversial" per BPH lecture |
| "All PDE5i cause visual disturbance" | Generalizing side effects | Only sildenafil and vardenafil (PDE6 cross-reactivity) |
| "Tadalafil has 5-hour duration" | Not reading the table carefully | Tadalafil = 36 hours; sildenafil and vardenafil = 5 hours |
- PDE5i + nitrates → absolute contraindication (not just relative)
- NPT/Rigiscan → medicolegal use, not routine clinical practice
- ICI works independently of NO (cAMP pathway) — use when PDE5i fails
- Penile prosthesis: 90-95% functional, 80-90% satisfaction but irreversible
Past Paper Questions
"Which of the following statements regarding erectile dysfunction (ED) is correct?" [3]
A. Ischaemic heart disease is not an associated disease. B. Phosphodiesterase-5 inhibitors drug treatment is the usual first line treatment for most patients with ED. C. Penile prosthesis could be performed before trial for intracavernosal injection of prostaglandin E1. D. Presence of morning erection suggest organic cause for ED.
Answer: B
Rationale:
- A is FALSE — IHD is strongly associated (OR 1.9)
- B is CORRECT — PDE5i is the standard first-line pharmacological treatment
- C is FALSE — penile prosthesis is 3rd line; ICI is 2nd line and must be tried first
- D is FALSE — morning erection suggests the organic mechanism is intact → points to PSYCHOGENIC cause
"A 50-year-old married gentleman with good past health complains of a 6-month history of erectile dysfunction with an insidious onset and progressive severity. There is no morning erection but libido, ejaculation and orgasmic response are preserved. Physical examination is unremarkable. He is keen to have treatment for his erectile dysfunction. Which should be the investigation(s) before embarking on treatment?" [4]
A. Baseline blood tests including fasting blood glucose, lipid profiles only B. Baseline blood tests including fasting blood glucose, lipid profiles and then dynamic infusion cavernosometry C. Baseline blood tests including fasting blood glucose, lipid profiles and then nocturnal penile tumescence testing D. Baseline blood tests including fasting blood glucose, lipid profiles and then penile duplex ultrasonography
Answer: A
Rationale:
- The lecture explicitly states that vascular tests (DICC, penile duplex) are "unnecessary in most cases" and reserved for surgical candidates/medicolegal reasons.
- NPT is reserved for medicolegal cases.
- For a straightforward presentation, only baseline bloods (FBS, lipid profile) are needed before starting first-line treatment (PDE5i).
- The absence of morning erection in this case suggests an organic cause (likely vascular given age and insidious onset), but this does not change the investigation approach — you still just need basic bloods.
High Yield Summary
- Erection = smooth muscle relaxation of corpora cavernosa via cGMP (NO-mediated) and cAMP (PGE1-mediated) pathways.
- PDE5 degrades cGMP → PDE5 inhibitors block this → sustain erection. They are NOT initiators — need sexual stimulation.
- ED definition: Inability to achieve/maintain erection for satisfactory intercourse, > 3 months, > 50% of attempts.
- ED is a cardiovascular sentinel: Often the earliest sign of systemic atherosclerosis. Always check FBS, lipids.
- Organic vs. Psychogenic: Morning erections present → psychogenic. Gradual onset → organic. Sudden onset → psychogenic.
- Classification: Vasculogenic (commonest organic), neurogenic, endocrinologic, drug-induced, anatomic, psychogenic.
- Assessment: Sexual history, IIEF-5, medical history (DM/HT/smoking/drugs), genital exam, BP, FBS, lipids, ± testosterone.
- Treatment ladder: 1st line = PDE5i / VCD / LI-SWT → 2nd line = ICI (alprostadil) → 3rd line = penile prosthesis.
- ABSOLUTE contraindication to PDE5i: Concurrent nitrate use → fatal hypotension.
- Side effects: Headache, flushing, nasal congestion (all PDE5i); visual changes (sildenafil/vardenafil = PDE6); back pain (tadalafil = PDE11).
- Tadalafil: 36-hour duration (vs. 5 hours for sildenafil/vardenafil). Also used for BPH/LUTS.
- ICI (alprostadil): Works via cAMP, independent of NO → useful when PDE5i fails. Risk of priapism (1%).
Active Recall - Lecture Notes
[1] Lecture slides: GC 184. Erection and erectile dysfunction.pdf [2] Lecture slides: MBBS4 Sexual function t Dysf140824.pdf [3] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q55) [4] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Q75) [5] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Localization of lesion, p1100) [6] Lecture slides: Benign Prostatic Hyperplasia.pdf; MBBS Final MB (Surgery) (Felix PY Lai).pdf (p834) [7] Senior notes: Maksim Medicine Notes.pdf (Diabetic complications, p89); Ryan Ho Endocrine.pdf (p98) [8] Senior notes: Maksim Medicine Notes.pdf (Hyperprolactinaemia, p105-107); Ryan Ho Endocrine.pdf (p110) [9] Senior notes: Maksim Medicine Notes.pdf (Hypogonadism, p103) [10] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Klinefelter, p843) [11] Senior notes: Ryan Ho Cardiology.pdf (PAD/Leriche syndrome, p206) [12] Senior notes: Ryan Ho Psychiatry.pdf (Sexual dysfunction, p232)
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