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Erectile Dysfuntion EPIDEMIOLOGY AND PATHOPHYSIOLOGY. Dr. Anmar Nassir, FRCS(C) Canadian board in General Urology Fellowship in Andrology (U of Ottawa) Fellowship in EndoUrology and Laparoscopy (McMaster Univ ) Assisstent Prof Umm Al- Qura

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  1. Erectile DysfuntionEPIDEMIOLOGY AND PATHOPHYSIOLOGY Dr. Anmar Nassir, FRCS(C) Canadian board in General Urology Fellowship in Andrology(U of Ottawa) Fellowship in EndoUrology and Laparoscopy (McMaster Univ) Assisstent Prof Umm Al-Qura Consultant Urology King Faisal Specialist Hospital

  2. Before age 40  1- 9% • from 40 to 59  5-30% • from 60 to 69  20- 40% • men in their 70s and 80s50-75% 24 international studies between 1993 and 2003

  3. Males : 40 and 70 years • 52% reported some degree of ED. • 40  70 the probability of: • complete impotence tripled from 5.1%  15% • moderate impotence doubled from 17%  34% • minimal impotence remained constant at 17%. • By the age of 70 years 68 % have ED. 1709 noninstitutionalized men The Massachusetts Male Aging Study 1994

  4. ED in SA • 680 patients: AI El-sakka, 2004 International Journal of Impotence Research

  5. ED = consistent or recurrent inability to attain and/or maintain penile erection sufficient for sexual performance.

  6. Anatomy

  7. Physiology

  8. PENILE SMOOTH MUSCLE RELAXATION CAUSES ERECTION Sexual stimulation Sympathetic + parasymp Smooth muscle relaxation Arterial dilation + venous occlusion • Relaxation of the cavernous smooth muscle is the key to penile erection.

  9. CNS psych imagination auditory Hypothalamus tactile memory Testosterone Sexual Ctre olfactory visual Estradiol Sympathetic + parasympathetic

  10. Nitric oxide • Synthesis of NO is catalyzed by NOS, • converts l-arginine and oxygen  l-citrulline and NO. • NOS exists as three isoforms in mammals: • nNOS - in neurons cells • eNOS - in endothelial cells, • iNOS in virtually all cell types. • In the corpus cavernosum: • nNOS initiating erection • eNOS  sustaining erection. • Future: • Gene transfer of nNOS or eNOS to the penis has been shown to augment erectile responses in animal studies.

  11. Nitric oxide • Upon entering the smooth muscle cells, stimulates the production of cGMP. • Cyclic GMP • activates protein kinase G, • opens potassium channels and closes calcium channels. • Low cytosolic calcium favors smooth muscle relaxation. • The smooth muscle regains its tone when cGMP is degraded by phosphodiesterase.

  12. Phosphodiesterase • All PDEs have been identified in the corpus cavernosum • With the exception of PDE6, which is specifically expressed in photoreceptor cells. • PDE5 is the principal PDE for the termination of cavernous cGMP signaling. • Inhibition of the cGMP-catalytic activity of PDE5 by specific inhibitors has been shown to be highly effective in treating ED .

  13. Nitric Oxide-cGMP Mechanism of Corpus Cavernosal Smooth Muscle Relaxationand Penile Erection 3 1 2

  14. !!! • Other substrates relevant to vascular or cavernous smooth muscle functions are as follows: • Inositol 1,4,5-trisphosphate (IP3) receptor • IP3 receptor-associated PKG substrate (IRAG) • Phospholamban (PLB) • Heat shock-related protein (HSP20) • Myosin phosphatase (MP) • Phosphatase inhibitor-1 (PPI-1) • GTPase RhoA

  15. Etiology Etiology of Erectile Dysfunction • For simplicity, erectile dysfunction can be classified as • Organic - due to vasculogenic, neurologic, hormonal, or cavernosal abnormalities or lesions • Psychogenic - due to central inhibition of the erectile mechanism without a physical insult However, in most patients with erectile dysfunction, a combination of organic and psychogenic components is involved.

  16. A functional classification of impotence. • Note that it is unlikely for an individual patient’s impotence to derive solely from one source

  17. Causes of ED

  18. Major organic causes of ED

  19. ED in SA • 680 patients: • Significant association to severity of ED: • diabetes, • hypertension, • dyslipidemia, • smoking, • increased BMI, AI El-sakka, 2004 International Journal of Impotence Research

  20. Organic vs. psychogenic causes for ED

  21. Psychogenic dysfunction • Two possible mechanisms to explain the inhibition of erection: • Direct inhibition of the spinal erection center by the brain • exaggeration of the normal suprasacral inhibition • Excessive sympathetic outflow or elevated peripheral catecholamine levels, • increase penile smooth muscle tone to prevent its necessary relaxation.

  22. Organic dysfunction Diabetes Mellitus • Diabetes mellitus is a common chronic disease • Affecting 0.5% to 2% worldwide. • The overall prevalence of DM in KSA is 23.7%. • males  26.2% • females  21.5%. Saudi Med J. 2004 Al-Nozha et al

  23. Organic dysfunction Diabetes Mellitus • The prevalence of ED is three times higher in diabetic men (28% versus 9.6%) • occurs at an earlier age, • increases with disease duration, being approximately 15% at age 30 and rising to 55% at 60 years

  24. Chronic Renal Failure • Sexual dysfunction has been reported in 20% to 50% of men with chronic renal failure

  25. Cavernous (Venogenic) • Failure of adequate venous occlusion is the most common causes of vasculogenic impotence. • It may result from: • degenerative tunical changes: Peyronie's disease, old age, and diabetes • fibroelastic structural alterations, • traumatic injury to the tunica albuginea: penile fracture • insufficient trabecular smooth muscle relaxation: anxious individuals with excessive adrenergic tone patients with inadequate neurotransmitter release • venous shunts

  26. Anti HTN and ED • The underlying disorder may be more relevant for ED than the medication. • Thiazide diuretic • Associated with higher rates of ED, • This may be reduced by combination therapy and weight loss. • The α1 blockers and Angiotensin II receptor blocker • Tend to improve sexual functioning • Calcium Channel Blockers • No adverse effect on erection

  27. Effect of Antihypertensive

  28. Antipsychotics • The prevalence of sexual dysfunction ranged from 40% to 70%. • Newer agents such as clozapine showed a lower reduction in sexual desire. • The group taking risperidone had the greatest decrease in erectile frequency.

  29. Antidepressants • Tricyclics • Antagonize 5-HT receptors. • Controlled clinical studies suggest that orgasmic disorders in both sexes are frequent, explaining the use of these drugs as inhibitors of ejaculation

  30. Antidepressants • Monoamine oxidase inhibitors • associated with higher rates of orgasmic dysfunction in controlled trials

  31. Antidepressants • Selective serotonin reuptake inhibitors(SSRIs) • Commonly used to treat depression. • They inhibit the reuptake of 5-HT into CNS neurons produce stimulatory effects on 5-HT receptors. • 50% of patients experience a change in sexual function • mainly anorgasmia, • adverse effects can be modified by co-treatment with sildenafil

  32. Antidepressants • SSRIs differ in their ability to cause ED. • A high incidence has been observed in patients treated with paroxetine • A lesser impact has been reported with citalopram. • Thus, the ability to produce ED and the mechanism by which SSRIs cause ED may differ with the specific SSRI compound.

  33. Antidepressants • Recently developed antidepressants such as mirtazapine and nefazodone tend to have beneficial effects on sexual function, • Possibly by activating the 5-HT1 C receptor, • augments sexual response, • But still antagonize the 5-HT2 C receptor.

  34. Tobacco • Tobacco induce vasoconstriction and penile venous leakage. • Smokers reported an inverse correlation between nocturnal erection (both rigidity and duration) and the number of cigarettes smoked per day: • men who smoked more than 40 had the weakest and shortest nocturnal erections.

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