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Summary Table

Category	Details
Risk Factors	Age >40, diabetes mellitus, hypertension, dyslipidemia, smoking, obesity, cardiovascular disease, pelvic surgery or radiation, spinal cord injury, depression, chronic kidney disease, medications (beta-blockers, thiazides, SSRIs, spironolactone, 5-alpha reductase inhibitors)
Etiology	Vasculogenic (most common overall), neurogenic, hormonal, psychogenic, drug-induced, or mixed
Patient Presentation	Inability to achieve or maintain an erection sufficient for satisfactory sexual intercourse, often gradual onset if organic, sudden onset if psychogenic
Classic Physical Exam	May be normal; look for decreased peripheral pulses, testicular atrophy, gynecomastia, reduced secondary sexual characteristics, penile plaques (Peyronie disease), absent bulbocavernosus reflex
Key Diagnostic Results	Morning erections preserved = psychogenic; fasting glucose/HbA1c, lipid panel, serum testosterone (drawn in the morning); nocturnal penile tumescence testing distinguishes organic from psychogenic
Management	PDE-5 inhibitors (sildenafil, tadalafil) as first-line pharmacotherapy; vacuum erection devices; intracavernosal injection therapy (alprostadil); penile prosthesis for refractory cases
Keywords	"Gradual onset," "unable to maintain erection," "morning erections absent/present," "diabetes with sexual complaints," "post-prostatectomy," "bicycle injury"

1. Pathophysiology

Penile erection is fundamentally a vascular event modulated by neurologic input. Sexual stimulation triggers parasympathetic outflow via the pelvic splanchnic nerves (S2-S4), leading to release of nitric oxide (NO) from non-adrenergic, non-cholinergic nerve terminals and the endothelium of the corpus cavernosum. NO activates guanylate cyclase, which converts GTP to cyclic GMP (cGMP). Rising cGMP levels cause smooth muscle relaxation in the helicine arteries and trabecular smooth muscle of the corpora cavernosa, resulting in increased arterial inflow. As the sinusoidal spaces fill, they compress the subtunical venular plexus against the tunica albuginea, trapping blood and producing rigidity. This is the veno-occlusive mechanism.

Detumescence occurs when phosphodiesterase type 5 (PDE-5) degrades cGMP, restoring smooth muscle tone and allowing venous outflow. This is why PDE-5 inhibitors work: they block the enzyme that breaks down cGMP, thereby prolonging the erectile response. Critically, NO release must still occur for PDE-5 inhibitors to be effective, which is why sexual stimulation remains necessary even with medication.

Vasculogenic erectile dysfunction is the most common organic cause and shares the same pathophysiologic basis as atherosclerosis. Endothelial dysfunction reduces NO bioavailability, impairing smooth muscle relaxation. This is why erectile dysfunction is considered an early marker of systemic cardiovascular disease, often preceding symptomatic coronary artery disease by 3 to 5 years. Diabetes accelerates this process through both endothelial damage and peripheral neuropathy affecting the autonomic nerves to the penis.

Neurogenic causes include spinal cord injury (upper motor neuron lesions above S2-S4 may preserve reflexogenic erections but lose psychogenic erections), radical prostatectomy (damage to the cavernous nerves running along the posterolateral aspect of the prostate), and diabetic autonomic neuropathy.

Psychogenic erectile dysfunction results from excessive sympathetic tone overriding parasympathetic-mediated erection. The hallmark is preserved nocturnal and morning erections, because during REM sleep, parasympathetic activity predominates without psychologic inhibition.

2. Classification and Clinical Manifestation

Classification	Mechanism	Onset	Nocturnal Erections	Key Associations
Vasculogenic	Atherosclerosis, endothelial dysfunction, venous leak	Gradual	Absent	Diabetes, hypertension, smoking, dyslipidemia, peripheral vascular disease
Neurogenic	Damage to autonomic or somatic nerves	Variable (often sudden if post-surgical)	Absent	Spinal cord injury, radical prostatectomy, multiple sclerosis, diabetic neuropathy
Hormonal	Low testosterone, hyperprolactinemia, thyroid disorders	Gradual	Absent or diminished	Decreased libido, fatigue, gynecomastia, visual field defects (prolactinoma)
Psychogenic	Excessive sympathetic activation, performance anxiety, depression	Sudden	Preserved	Younger age, situational pattern, relationship stressors, normal libido or variable
Drug-Induced	Medication side effects altering vascular, neurologic, or hormonal pathways	Temporally related to medication initiation	Usually preserved	Beta-blockers, thiazide diuretics, SSRIs, spironolactone, ketoconazole, cimetidine, 5-alpha reductase inhibitors
Mixed	Combination of above	Variable	Variable	Most common real-world presentation, especially in older diabetic patients

A vignette featuring a young patient with sudden-onset erectile dysfunction, preserved morning erections, and no cardiovascular risk factors is pointing toward psychogenic etiology. Conversely, a middle-aged diabetic smoker with gradual onset and absent morning erections is classic vasculogenic disease.

3. Diagnostic Workup

Test	Purpose	When to Order
Fasting glucose / HbA1c	Screen for diabetes	All patients
Lipid panel	Assess cardiovascular risk	All patients
Morning serum total testosterone	Screen for hypogonadism	All patients; must be drawn before 10 AM due to diurnal variation
Free testosterone, LH, FSH, prolactin	Distinguish primary vs. secondary hypogonadism, screen for prolactinoma	When total testosterone is low
Thyroid function tests	Rule out thyroid dysfunction	When clinically suspected
Nocturnal penile tumescence (NPT) testing	Distinguish organic from psychogenic	When diagnosis is uncertain
Duplex Doppler ultrasonography of penile arteries	Evaluate arterial inflow and veno-occlusive function	When vascular etiology needs confirmation before intervention
Penile angiography	Gold standard for vascular anatomy	Rarely used; reserved for young patients being considered for vascular reconstructive surgery

The workup begins with a thorough history and physical examination, which alone can often distinguish organic from psychogenic causes. The single most important question on the exam is whether the patient has preserved morning or nocturnal erections. If yes, the neurologic and vascular apparatus is intact, and the cause is likely psychogenic.

Laboratory evaluation is the best initial step in all patients. The baseline panel includes fasting glucose or HbA1c, a lipid panel, and a morning serum total testosterone. Testosterone must be drawn in the morning (before 10 AM) because levels peak in the early morning and decline throughout the day. A low total testosterone should be confirmed with a repeat measurement, followed by free testosterone, LH, FSH, and prolactin to differentiate primary hypogonadism (high LH/FSH, low testosterone) from secondary hypogonadism (low or inappropriately normal LH/FSH, low testosterone). An elevated prolactin level raises concern for a prolactinoma and warrants MRI of the pituitary.

Nocturnal penile tumescence (NPT) testing is the most accurate test to distinguish organic from psychogenic erectile dysfunction. A normal man has 3 to 5 erections per night during REM sleep. Absence of these erections confirms organic pathology. This test is rarely needed clinically but is high-yield for examination purposes.

Duplex Doppler ultrasonography with intracavernosal injection of a vasoactive agent (prostaglandin E1) is the best initial vascular study. It measures peak systolic velocity (PSV) in the cavernosal arteries. A PSV below 25 cm/s suggests arteriogenic insufficiency, while failure of the veins to compress (persistent diastolic flow) suggests venous leak.

4. Management and Treatment

Line of Therapy	Intervention	Details
Lifestyle modification	Weight loss, exercise, smoking cessation, alcohol reduction	First step for all patients; can improve erectile function independently
Medication adjustment	Discontinue or substitute offending drugs	Switch beta-blockers, thiazides, SSRIs if temporally related
First-line pharmacotherapy	PDE-5 inhibitors	Sildenafil 50 mg (range 25-100 mg) taken 1 hour before intercourse; tadalafil 10-20 mg (or 5 mg daily for continuous use)
Second-line	Intracavernosal injection (alprostadil/prostaglandin E1), intraurethral suppository (MUSE), vacuum erection device	Alprostadil 10-20 mcg injected into the corpus cavernosum; maximum 3 times per week
Third-line	Penile prosthesis (inflatable or semi-rigid)	Definitive surgical option for refractory cases
Hormonal	Testosterone replacement therapy	Only for documented hypogonadism; does not replace PDE-5 inhibitors if vascular cause coexists
Psychogenic	Cognitive behavioral therapy, sex therapy, couples counseling	First-line for psychogenic erectile dysfunction; may combine with PDE-5 inhibitors

Lifestyle modification is the foundational intervention. Weight loss alone in obese men has been shown to improve erectile function. Exercise improves endothelial function and NO bioavailability. All modifiable cardiovascular risk factors should be addressed.

PDE-5 inhibitors are first-line pharmacotherapy. Sildenafil, vardenafil, and avardenafil require on-demand dosing (taken 30-60 minutes before sexual activity), while tadalafil has a long half-life (17.5 hours) allowing both on-demand use and daily low-dose (5 mg) administration. These drugs work by inhibiting the degradation of cGMP, but they require baseline NO release from sexual stimulation to be effective.

The most critical contraindication to PDE-5 inhibitors is concurrent use of nitrates (nitroglycerin, isosorbide mononitrate/dinitrate). Both PDE-5 inhibitors and nitrates cause vasodilation through the NO-cGMP pathway. Combined use produces severe, potentially fatal hypotension. Patients must not take nitrates within 24 hours of sildenafil or vardenafil, or within 48 hours of tadalafil. Alpha-blockers are a relative contraindication and require dose titration and interval separation to avoid orthostatic hypotension.

Intracavernosal injection of alprostadil (prostaglandin E1) is the most effective non-surgical treatment. Alprostadil directly stimulates adenylate cyclase, increasing cAMP independently of the NO pathway, which is why it works even when PDE-5 inhibitors fail. The primary risk is priapism (erection lasting more than 4 hours), which is a urologic emergency treated with corporal aspiration and injection of a sympathomimetic agent (phenylephrine, an alpha-1 agonist).

Testosterone replacement is indicated only when erectile dysfunction occurs in the setting of documented hypogonadism (two morning testosterone levels below the lower limit of normal, typically below 300 ng/dL). Contraindications to testosterone replacement include prostate cancer, breast cancer, polycythemia (hematocrit above 50%), untreated obstructive sleep apnea, and men actively trying to conceive (exogenous testosterone suppresses spermatogenesis via negative feedback on LH/FSH).

Penile prosthesis is reserved for patients who fail all conservative and pharmacologic therapies. The inflatable three-piece prosthesis provides the most natural cosmetic and functional result.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Hypogonadism (isolated)	Low testosterone causes decreased libido, which can be confused with erectile dysfunction	Primary complaint is decreased libido and fatigue, not difficulty with erection mechanics; morning testosterone will be low; erections may still be achievable with adequate stimulation
Peyronie Disease	Patients report difficulty with intercourse	Complaint is penile curvature or pain during erection, not inability to achieve erection; palpable fibrous plaque along the tunica albuginea
Depression	Decreased libido and sexual dysfunction overlap	Presence of anhedonia, sleep disturbance, appetite changes, psychomotor retardation; SSRI treatment itself may worsen erectile dysfunction
Premature Ejaculation	Both are "sexual dysfunction"	The erection is normal; the issue is ejaculation occurring before desired, not inability to maintain erection
Peripheral Vascular Disease	Shares risk factors (diabetes, smoking, atherosclerosis)	Presents with claudication, diminished distal pulses, ABI below 0.9; may coexist with vasculogenic erectile dysfunction but is a separate diagnosis
Prolactinoma	Causes erectile dysfunction through hyperprolactinemia	Look for galactorrhea, visual field defects (bitemporal hemianopia), and very high prolactin levels; MRI shows pituitary mass
Neurogenic Bladder	Overlaps with diabetic autonomic neuropathy	Presents with urinary retention, overflow incontinence, post-void residual volume elevated; may coexist

6. Traps and High-Yield Pearls

The most common way students lose points on this topic is by failing to identify the absolute contraindication of concurrent nitrate use with PDE-5 inhibitors. A vignette will describe a patient with known coronary artery disease on isosorbide mononitrate who presents with erectile dysfunction. The question asks for the next best step: the answer is not sildenafil. Instead, consider intracavernosal alprostadil, a vacuum device, or referral for medication adjustment by cardiology.

A second frequent trap is the patient with erectile dysfunction and low testosterone. Students jump to testosterone replacement, but the question may embed a contraindication such as a history of prostate cancer, elevated hematocrit, or desire for fertility. In the fertility scenario, exogenous testosterone suppresses the HPG axis and worsens azoospermia. The correct answer is clomiphene citrate (a selective estrogen receptor modulator that stimulates endogenous LH/FSH secretion) or referral to a reproductive endocrinologist.

Another tested concept is recognizing erectile dysfunction as an independent predictor of future cardiovascular events. A vignette may describe a relatively young, otherwise healthy man with new erectile dysfunction and no other symptoms. The next best step is cardiovascular risk assessment, including fasting glucose, lipid panel, and blood pressure screening. Do not treat the erectile dysfunction in isolation without addressing the underlying vascular risk.

Finally, know the distinction between psychogenic and organic causes. Preserved nocturnal or morning erections in a young patient with sudden onset and situational pattern equals psychogenic. Gradual onset, absent nocturnal erections, and cardiovascular risk factors equals organic. NPT testing is the most accurate test to confirm this distinction, though it is rarely needed when the history is clear.

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