Erectile dysfunction: the key points

Definition: ED is the inability to achieve or maintain an erection rigid enough for satisfactory intercourse. The Goldman-Cecil definition is "inability to obtain rigidity sufficient to permit coitus of adequate duration to satisfy himself and his partner."

1. ED is a vascular problem until proven otherwise.

An erection needs four systems working: vascular, neurologic, endocrine, and usually psychological. The vascular system is the one that most often fails.
Risk factors are diabetes, smoking, obesity, a sedentary lifestyle, hypertension, CAD and stroke. Prevalence rises with age: 2% at 40-49, 6% at 50-59, 17% at 60-69 and 39% at 70 or older (Textbook of Family Medicine 9e, p. 1260).
The textbook's phrase is "What is bad for the heart is bad for the penis." ED can be an early warning of cardiovascular disease, so assess cardiovascular risk in every patient.

2. Physiology (the mechanism behind treatment).

Parasympathetic stimulation releases nitric oxide (NO) from nerves and endothelium. NO raises cGMP in cavernosal smooth muscle, which relaxes it.
Blood flows into the corpora, compresses the emissary veins against the tunica albuginea, and traps blood. This produces the erection.
PDE-5 breaks down cGMP. PDE-5 inhibitors block that breakdown, so erection is easier to achieve and maintain.

3. First-line treatment is a PDE-5 inhibitor.

The drugs are sildenafil, tadalafil, vardenafil and avanafil.
They need sexual stimulation to work. They do not cause erections by themselves.
Contraindication: nitrates (any form). The combination can cause life-threatening hypotension, as Tintinalli's emphasizes. Use caution with alpha-blockers and in unstable cardiac disease.
Fix reversible factors too: stop smoking, lose weight, exercise, and control diabetes and blood pressure.

4. Check for drug causes (Textbook of Family Medicine 9e, Table 42-4). Common culprits:

Antihypertensives (beta-blockers, thiazides, clonidine, methyldopa)
SSRIs and TCAs
Antipsychotics
Spironolactone
5-alpha-reductase inhibitors
GnRH agonists
Opioids
Fibrates

5. Evaluation.

Take a history covering onset (sudden suggests psychogenic, gradual suggests organic), nocturnal or morning erections, libido, and smoking, alcohol and drugs.
Screen for depression and anxiety.
Make sure the complaint is really ED and not premature ejaculation. Patients often confuse the two.
Examine the genitalia, pulses and neurologic status.
Check glucose or HbA1c, lipids and morning testosterone.

6. If PDE-5 inhibitors fail or are contraindicated. I am adding this from general knowledge, not from the textbook passages I read:

Vacuum devices
Intracavernosal alprostadil
Intraurethral alprostadil
Penile prosthesis
Testosterone replacement if hypogonadism is confirmed
Psychosexual therapy

Recent evidence: A 2026 umbrella review of ED treatments (PMID 41792626) covers current treatment options. I only saw its title and metadata, not its content, so I can't say whether it changes anything above. I found nothing else recent that contradicts the textbook content.

If you are studying for an exam or want a clinical algorithm, tell me which and I can go deeper on workup or second-line therapy.

In need to go deep and how I differentiate between the couse like into organic or psychological in history or PE or investigation

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AUA EAU erectile dysfunction guideline diagnosis organic vs psychogenic history physical examination testosterone penile duplex

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Organic vs psychogenic ED: history, examination and investigations

The caveat first: these features point you in a direction. They do not give a diagnosis. Campbell-Walsh states that "often ED cannot be fully dichotomized into psychogenic and organic categories" (Campbell-Walsh Urology, Ch. 69, p. 2015). Most patients are mixed. A man with a vascular cause develops performance anxiety, and that makes the problem look psychogenic.

1. History (the most useful step)

Classic discriminators (Campbell-Walsh Urology, Table 69.4, p. 2015):

Feature	Psychogenic	Organic
Onset	Sudden	Gradual
Course	Complete, immediate loss	Incremental progression
Pattern	Situational (partner- or context-specific)	Global (every situation)
Waking erections	Present	Poor or absent

Questions that sort the cause:

Morning and nocturnal erections. These occur in REM sleep and need an intact neurovascular axis. Present and normal points to psychogenic. Absent or weak points to organic (Harrison's 22E, p. 3201).
Erections with masturbation, fantasy or visual stimulation. Good erections here but failure with a partner suggest psychogenic (Smith and Tanagho's General Urology 19e).
Situational vs consistent. Failure with one partner but not another, or with a new partner, suggests psychogenic. Consistent failure suggests organic (Harrison's).
Onset linked to a trigger.
- Psychogenic triggers: bereavement, divorce, job or money stress, a relationship conflict, a single bad episode.
- Organic triggers: pelvic or spinal trauma, prostate or bowel surgery, pelvic radiation, or starting a new drug.
Partial erections and progression. A gradual loss of rigidity, or inability to sustain nocturnal, coital or self-stimulated erections, suggests organic (Harrison's).
Libido. Low libido with ED suggests hypogonadism. It is often the earliest sign of low testosterone (Harrison's).
Ejaculation and orgasm. These are usually preserved in vascular ED. Absent or abnormal ejaculation raises the possibility of a neurogenic, drug or surgical cause.
Psychological state. Ask about depression, anxiety, performance anxiety, guilt, fear, and religious or parental inhibition (Smith and Tanagho's). Also ask about the relationship and the partner's health.
Risk factors for organic disease.
- Diabetes, hypertension, dyslipidaemia, CAD and peripheral vascular disease
- Smoking, obesity, alcohol and drugs
- Neurologic disease and prior pelvic, bladder, bowel or vascular surgery
- LUTS/BPH, which is strongly associated with ED
Medications (Textbook of Family Medicine 9e, Table 42-4): beta-blockers, thiazides, SSRIs, antipsychotics, spironolactone, 5-alpha-reductase inhibitors, GnRH agonists and others.

Lifelong vs acquired: Lifelong (primary) ED from the first attempt suggests a psychological cause or a congenital or anatomic problem. Acquired ED needs a search for what changed.

Use a questionnaire. The IIEF-5 (SHIM) grades severity: 5 to 7 severe, 8 to 11 moderate, 12 to 16 mild to moderate, 17 to 21 mild, 22 to 25 no ED. It measures severity and treatment response. It does not separate organic from psychogenic.

2. Physical examination

A normal examination does not exclude organic ED, and an abnormal one does not exclude a psychological contribution. Look for the following.

System	What to check	What it points to
Vascular	Blood pressure, BMI and waist, femoral and pedal pulses, carotid bruits	Vasculogenic ED
Endocrine	Small or soft testes, gynecomastia, reduced body hair, poor virilization, eunuchoid habitus (Klinefelter, Kallmann), thyroid enlargement	Hypogonadism
Neurologic	Perineal and genital sensation, anal sphincter tone, bulbocavernosus reflex (squeeze the glans and feel the anal sphincter contract), peripheral neuropathy	Neurogenic ED, including diabetic neuropathy
Penis	Palpate along the corpora for plaques; look for chordee, curvature or micropenis	Peyronie disease or an anatomic problem
Prostate	Digital rectal examination	BPH or prostate disease

Sources: Campbell-Walsh Urology p. 2015-2016; Textbook of Family Medicine 9e, p. 1261; Harrison's 22E, p. 3201.

A completely normal examination in a young man with sudden onset, situational ED and normal morning erections makes psychogenic ED more likely.

3. Investigations

Baseline labs. Order these for everyone. They look for organic causes and do not separate organic from psychogenic.

Fasting glucose or HbA1c, and a lipid profile
Renal function, liver enzymes and a full blood count
Morning total testosterone. If it is low, measure free or bioavailable testosterone, LH and FSH, and prolactin (Campbell-Walsh p. 2016; Harrison's p. 3201).
TSH if there is clinical suspicion
PSA when prostate disease is suspected or testosterone therapy is planned
Urine dipstick for glucosuria

Testosterone pitfalls (Textbook of Family Medicine 9e):

Only about 7% of men with ED have low testosterone.
Total testosterone can mislead because it is highly bound to SHBG.
Replacement is considered when the level is below 300 ng/dL and ED is present.

Specialized tests. Most men do not need these. The treatment plan can usually be made without them (Campbell-Walsh p. 2017). Reserve them for young men, trauma or surgical cases, medicolegal cases, PDE-5 inhibitor failures, and before surgery such as a penile prosthesis or revascularization.

Test	What it tells you
Nocturnal penile tumescence and rigidity (NPTR, RigiScan)	Measures the number, duration, rigidity and circumference of nocturnal erections. About 80% occur in REM sleep, and the average man has 3 to 5 episodes a night lasting 30 to 60 minutes. A full erection means the neurovascular axis is intact, so a normal result points to psychogenic ED. It was designed to separate the two. It is now used mostly in medicolegal and complicated cases (Smith and Tanagho's).
Intracavernosal injection with penile duplex ultrasound	Assesses arterial inflow and venous leak after a vasoactive injection. A good rigid erection with normal flow argues against a vascular cause.
Dynamic infusion cavernosometry and cavernosography (DICC)	Used for venous leak, mainly before vascular surgery.
Biothesiometry, bulbocavernosus reflex latency, dorsal nerve conduction	Assess penile sensation and nerve function in suspected neurogenic ED. They rarely change management (Smith and Tanagho's).
Audiovisual sexual stimulation (AVSS) testing	Assesses erectile response under controlled stimulation.
Psychological or psychosexual assessment	A skilled interview is the mainstay. Subtypes are generalized vs situational and lifelong vs acquired.

Campbell-Walsh Table 69.5 grades NPTR, ICI with duplex, DICC and bulbocavernosus reflex latency as B. It grades biothesiometry, dorsal nerve conduction and CC-EMG as C. Arteriography and AVSS are C, and CT/MR angiography is D.

From general knowledge, not the passages I read. Check these against your own source:

On penile Doppler after injection, a peak systolic velocity above about 30 cm/s suggests adequate arterial inflow. An end-diastolic velocity above about 5 cm/s suggests venous leak.
On NPTR, a normal result is generally taken as at least 60% tip rigidity lasting at least 10 minutes.

4. Putting it together

Picture	Likely cause
Sudden onset, situational, good morning erections, young, stressor present, normal examination	Psychogenic
Gradual, global, poor or absent morning erections, risk factors (DM, smoking, HTN, CAD), older	Organic, usually vasculogenic
Low libido, small testes, gynecomastia	Hypogonadism (check testosterone, LH, prolactin)
ED with pelvic surgery or radiation, spinal injury, diabetic neuropathy, absent bulbocavernosus reflex	Neurogenic
Curvature, painful erection, plaque	Peyronie disease
Organic risk factors plus performance anxiety	Mixed (the commonest picture)

For mixed ED, treat both components. Psychosexual therapy added to a PDE-5 inhibitor improves adherence and reduces performance anxiety.

I didn't re-run the recent-evidence check this time. The PubMed search in my first answer found no recent evidence that contradicts these classical textbook criteria. I can go deeper on penile Doppler interpretation or on work-up of the young man with ED if you want.

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