ED can result from any single abnormality or combination of abnormalities of the four systems necessary for a normal penile erection. Vascular, neurologic, or hormonal etiologies of ED are referred to as organic ED. Patients who do not respond to psychogenic stimuli and have no organic cause for dysfunction have psychogenic ED.
The penis has two corpora cavernosa and one corpus spongiosum, which contain interconnected sinuses that fill with blood to produce an erection.
Acetylcholine works with other neurotransmitters (ie, cyclic guanylate monophosphate, cyclic adenosine monophosphate, and vasoactive intestinal polypeptide) to produce penile arterial vasodilation and ultimately an erection.
Organic ED is associated with diseases that compromise vascular flow to the corpora cavernosum (eg, peripheral vascular disease, arteriosclerosis, and essential hypertension), impair nerve conduction to the brain (eg, spinal cord injury and stroke), or impair peripheral nerve conduction (eg, diabetes mellitus). Secondary ED is associated with hypogonadism.
Psychogenic ED is associated with malaise, reactive depression or performance anxiety, sedation, Alzheimer disease, hypothyroidism, and mental disorders. Patients with psychogenic ED generally have a higher response rate to interventions than those with organic ED.
Social habits (eg, cigarette smoking and excessive ethanol intake) and medications (Table 80–1) can also cause ED.
TABLE 80–1Medication Classes That Can Cause Erectile Dysfunction |Favorite Table|Download (.pdf) TABLE 80–1 Medication Classes That Can Cause Erectile Dysfunction
|Drug Class ||Proposed Mechanism by Which Drug Causes Erectile Dysfunction ||Special Notes |
|Anticholinergic agents (antihistamines, antiparkinsonian agents, tricyclic antidepressants, phenothiazines) ||Anticholinergic activity || |
Second-generation nonsedating antihistamines (eg, loratadine, fexofenadine, or cetirizine) are associated with less erectile dysfunction (ED) than first-generation agents.
Selective serotonin reuptake inhibitor (SSRI) antidepressants cause less ED than tricyclic antidepressants. Of the SSRIs, paroxetine, sertraline, and fluoxetine cause ED more commonly than venlafaxine, nefazodone, trazodone, or mirtazapine.
Phenothiazines with less anticholinergic effect (eg, chlorpromazine) can be substituted in some patients if ED is a problem.
|Dopamine antagonists (eg, metoclopramide, phenothiazines) ||Inhibit prolactin inhibitory factor, thereby increasing prolactin levels || |
|Estrogens, antiandrogens (eg, luteinizing hormone–releasing hormone superagonists, digoxin, spironolactone, ketoconazole, cimetidine) ||Suppress testosteronemediated stimulation of libido || |
|Central nervous system depressants (eg, barbiturates, narcotics, benzodiazepines, short-term use of large doses of alcohol, anticonvulsants) ||Suppress perception of psychogenic stimuli || |
|Agents that decrease penile blood flow (eg, diuretics, peripheral β-adrenergic antagonists, or central sympatholytics [methyldopa, clonidine, guanethidine]) ||Reduce arteriolar flow to corpora || |
Any diuretic that produces a significant decrease in intravascular volume can decrease penile arteriolar flow.
Safer antihypertensives include angiotensin-converting enzyme inhibitors, postsynaptic α1-adrenergic antagonists (terazosin, doxazosin), calcium channel blockers, and angiotensin II receptor antagonists.
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