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Today we are going to talk about the main medicines that can cause, erectile dysfunction. There are really key things you should know. the key with erectile dysfunction is drugs that affect the nervous system, and some that lower testosterone levels, or inhibit testosterone action can cause ED. It is estimated that 25 percent of cases of erectile dysfunction are because of medications and may be reversible by decreasing dose or changing the medicine. Medication induced erectile dysfunction is widely prevalent and is caused by medications from a variety of medical fields. Finasteride and dutasteride had the highest reported causes of erectile dysfunction. Finasteride and dutasteride work by irreversibly binding to an enzyme 5-α reductase, thereby preventing the conversion of testosterone to dihydrotestosterone which the more potent form of testosterone. Finasteride binds to type II 5 α reductase which is found mostly in the prostate and genital tract. Dutasteride binds to both type 1 (found mostly in extraprostatic tissues) and type II 5 α reductase. dihydrotestosterone is vital for physiologic erections as it activates nitric oxide synthase and increases blood flow in cavernosal tissue. patients on finasteride are more likely to have a loss of libido, ejaculatory disorder, and erectile dysfunction. Neuropsychiatric medications accounted for the second common cause of erectile dysfunction. The antipsychotic paliperidone and the selective serotonin reuptake inhibitors citalopram and sertraline were found to have elevated high rate of erectile dysfunction. In addition, there are many neuropsychiatric medications with high frequencies of erectile dysfunction including escitalopram, quetiapine, olanzapine, fluoxetine, venlafaxine, risperidone, aripiprazole, gabapentin, pregabalin, and oxycodone. Neuropsychiatric medication induced erectile dysfunction is a well described phenomenon. Neuropsychiatric medications have a variety of adverse effects due to the multiple receptors targeted throughout the body. These receptors include central and peripheral serotonergic, adrenergic, dopaminergic, cholinergic, histaminergic, and melanocortin receptors. Antipsychotics inhibit dopamine receptors with varying potency, which results in both direct and indirect inhibition of erections. Dopamine is known to play an important role in emotional sexual behavior and may also directly facilitate erections. Antipsychotics can cause hyperprolactinemia by inhibiting D2 receptors in the tuberoinfundibular system. This leads to decreased gonadotropin production and secondary hypogonadism. The different antipsychotics affect various receptors and this may have varying side effects. For example, the antipsychotics that block α1 adrenergic receptors may cause retrograde ejaculation but not erectile dysfunction. Benzodiazepines may cause sexual dysfunction from potentiation of GABA in the reticular and limbic system and by affecting the serotonin and dopaminergic pathways. Cardiological medications accounted some of rug induced erectile dysfunction. Beta blockers have been shown to be associated with ED, likely secondary to suppression of central nervous system sympathetic outflow. Non–cardioselective beta antagonists like propranolol have a higher incidence of erectile dysfunction than cardioselective beta antagonists which avoid beta 2 inhibition resulting in vasoconstriction of the corpora cavernosa. Nebivolol has the greatest selectivity for beta 1 receptors as well as endothelial nitric oxide vasodilatory effects, and has been shown to have a positive effect on erections. thiazide diuretics can also induce erectile dysfunction. In contrast, there is less evidence that loop diuretics such as furosemide cause ED, which should be considered by physicians treating hypertensive men. Some data suggests that ejaculatory dysfunction with calcium channel blockers (from decreased bulbocavernosus muscle force). Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are common antihypertensives that may actually improve erectile function. Angiotensin converting enzyme inhibitors prevent the formation of angiotensin II while angiotensin receptor blockers block the peripheral vasoconstriction caused by angiotensin II. Without angiotensin IIs effects, there is less penile vasoconstriction and collagen remodeling of the corpora cavernosa. In most studies, ACE inhibitors and ARBs have not been associated with ED and some studies even showed a beneficial effect. Medicines used for Dermatology and Immunology can also cause erectile dysfunction. Isotretinoin is a sebum suppressive medication used for acne which can also lead to erectile tretinoin. It is possible that acne is related to depression, which is a known risk factor for ED. Adalimumab can also cause ED. Adalimumab is a tumor necrosis factor (TNF) α blocker.