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88 CASE 88


A 60-year-old man visits his primary care physician complaining of an inability to have sex with his wife.


The patient reports an inability to achieve erections in at least 75% of intercourse attempts over the past 6 months and a complete absence of nocturnal erections.


He has a 3-year history of hypertension, which has been controlled by a calcium channel blocker. In addition, the patient has mild hyperlipidemia, which is controlled with dietary modification. He has a 1-year history of chest pain with moderate physical exertion and is being treated with aspirin and nitroglycerin. He is a social drinker and smokes one pack of cigarettes per day.






PATHOPHYSIOLOGY OF KEY SYMPTOMS


The male erection response is due to the engorgement of blood vessels in the corpus cavernosa (see Fig. 87-1). These vascular changes require the interplay of the vascular endothelial cells, sympathetic and parasympathetic nervous system, the central nervous system, and a permissive role played by the endocrine system. Disorders in any of these systems can result in erectile dysfunction, defined as “an inability to achieve and maintain an erection sufficient for satisfactory sexual performance.”


The penis is normally in a flaccid state, in which sympathetic nervous system tone constricts the smooth muscle of the penile erectile tissue, limiting blood flow into the corpus cavernosa. Endothelin and prostaglandins produced in the vascular wall augment the arteriolar vasoconstriction.


Appropriate psychologic or tactile stimulation causes an increase in parasympathetic activity and a withdrawal of sympathetic tone. The neurally mediated vasodilation causes blood to become trapped in the corpus cavernosa, leading to an erection.


The erectile response is initiated by an increase in parasympathetic nerve activity working through the NANC (nonadrenergic, noncholinergic) neurotransmitters, predominantly nitric oxide (NO) and vasoactive intestinal peptide (VIP). An increase in the activity of the NANC nerves dilates the vascular smooth muscle and causes an increase in blood flow. The increase in blood flow creates a shear stress on the vascular endothelium, stimulating NO production by the endothelial cells. It is the endothelial NO that mediates the maintenance of an erection (Fig. 88-1).


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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 88

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