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  • Penis is suspended to lower ischiopubic ramii through fundiform and suspensory ligaments.
  • Ed

    1. 1. PHYSIOLOGY OF PENILE ERECTION &  PATHOPHYSIOLOGYOFERECTILE DYSFUNCTIONDr. V.Priyadarshi
    2. 2. Physiology of Penile Erection
    3. 3. An Erection Requires a CoordinatedInteraction of Multiple Organ Systems Psychological Endocrine Neurologic Vascular
    4. 4. Physiology of penile erectionSexual stimulation Nitrix oxide synthesized in nerve and vascular tissue of penis Nitrix oxide activates GTP  cGMP guanylate cyclasecGMP relaxes smooth muscles of Vasocongestion ofcorpus cavernosum/penile arterioles penile tissues 17
    5. 5. Three types of erections 1. Genital stimulated (contact or reflexogenic) - induced by tactile stimulation of the genital area. - can be preserved in upper spinal cord lesions. - usually short in duration and poorly controlled . 2.central-stimulated (noncontact or psychogenic) - more complex, - resulting from memory, fantasy, visual, or auditory stimuli. 3. central-originated (nocturnal) - can occur spontaneously without stimulation or during sleep - most sleep erections occur during REM sleep. - occurs due to differential activation of cholinergic neurons at RAS while deactivation of adrenergic and serotonergic neurons during REM sleep..
    6. 6. Internal structure of the penis: top view (internal, in (between glans and the body) pelvic cavity) Male Sexual Anatomy (cont.) (engorge with blood (head of the (expands during arousal) penis; lots of to form nerve endings) the glans)Fig 5.1a Interior structure of the penis: (a) view from above.
    7. 7. cross-section of the penis  Tube within tube pattern.  Three corpora  Thick bilayered T.albuginia with elastic fibers which can expand and strech.  Incomplete outer longitudinal layer b/w 5-7 0’clock.  Spongiosa lacking outer long. Layer of T. albuginea.  Intracavernosal pillars and incomplete incavernosal septum.  suspended to lower ischiopubic ramii through fundiform and suspensory ligaments.
    8. 8. Blood supply of penis
    9. 9. Hemodynamics of Erection In the flaccid state, the arteries, arterioles, and sinusoids are contracted. The intersinusoidal and subtunical venous plexuses are wide open, with free flow through the emissary veins. The pO2 is venous(35 mm Hg). In the erect state, the muscles of the sinusoidal wall and the arterioles relax, allowing maximal flow to the compliant sinusoidal spaces. Most of the venules are compressed b/w expanding sinusoids. Larger venules of sub tunicial plexus are sandwiched b/w the distended sinusoids and the t.albuginea that effectively reduces the venous capacity to a minimum. The pO2 here is arterial(> 90 mm Hg) and ICP >100mmHg.
    10. 10. How blood inflow helps maintainerection Inside the penis: like a tube within a tube  When the inner tube fills with blood and expands, it fills the space between the tubes and blocks the outflow of blood, helping to maintain erection.
    11. 11. Phases of the Erection Process(o) Flaccid phase Minimal arterial and venous flow; blood gas values equal those of venous blood.(1) Latent (filling) phase Increased flow in the internal pudendal artery during both systolic and diastolic phases. Decreased pressure in the internal pudendal artery; unchanged intracavernous pressure. Some elongation of the penis.(2) Tumescent phase Rising intracavernous pressure until full erection is achieved. arterial flow rate decreases as the pressure rises. When intracavernous pressure rises above diastolic pressure, flow occurs only in the systolic phases.
    12. 12. Phases of the Erection Process(3) Full erection phase Intracavernous pressure rises to as much as 80–90% of the systolic pressure. Pressure in the artery increases but remains slightly below systemic pressure. Arterial flow is much less than in the initial filling phase but is still higher than flaccid phase. The venous channels are mostly compressed. Blood gas values approach those of arterial blood.(4) Skeletal or rigid erection phase As a result of contraction of the ischiocavernous muscle, the intracavernous pressure rises well above the systolic pressure, resulting in rigid erection. almost no blood flows through the cavernous artery.(5) Initial detumescent phase After ejaculation or cessation of erotic stimuli, sympathetic discharge resumes, contraction of the smooth muscles around the sinusoids and arterioles.(5) Slow detumescent phase – slow opening of venous channels.(6) Fast detumescent phase Expelulsion of a large portion of blood from the sinusoidal and diminition of the arterial flow to flaccid leve. The penis returnsto its flaccid length and girth
    13. 13. Neurophysiology of Erection
    14. 14. Neurophysiology of ErectionPeripheral and spinal At glans penis, high density free nerve endings and receptors. Dorsal nerve of penis carries somatosensory fibers. Sympathetic innervation from T10-T12 segments. causes detumescence. Parasympathetic supply through cavernous nerve from pelvic plexus carrying S2-4segments.induces erection. Pudendal nerve from Onuf’s nucleus(S2-4) is somatomotor, supplying muscles. Contraction of the ischiocavernosus muscles produces the rigid-erection phase. Rhythmic contraction of the bulbocavernosus muscle helps in ejaculation.
    15. 15. Neurophysiology of Erection contd .Supraspinal centers Medial Pre Optic Area (MPOA) and paraventricular nucleus (PVN) of the hypothalamus and hippocampus are important integration centers for sexual function and penile erection ( Sachs and Meisel, 1988 ; Marson et al, 1993 ) Medial preoptic area (MPOA) recognizes a sexual partner and integrate hormonal and sensory cues. Efferent pathways from the MPOA passes through the medial forebrain bundle and the midbrain tegmental region. Pathologic processes in these regions, such as PD or CVA, are often associated with ED. Paraventricular nucleus (PVN) facilitates penile erection through oxytocin neurons to spinal sympathetic efferents – Psychogenic erection that persist even in lumbar and sacral cord injuries.
    16. 16. Spinal Reflexes Involved in Stimulation of Penile Dorsal NerveStimulation Spinal Center Efferent EffectNoxious, abrupt Sacral motor Pudendal nerve Bulbocavernousstimulation neurons (motor) reflexLow-intensity Sacral 1. Pelvic nerves 1.Closure ofcontinuous (e.g., parasympathetic bladder neck andvibratory, manual) neurons and Bladder inhibition interneurons 2. Cavernous 2. Penile erection nerveHigh-intensity Sacral motor and Pudendal, pelvic, Ejaculationcontinuous parasympathetic and cavernous Thoracolumbar nerves sympathetic neurons
    17. 17. Neurotransmitters
    18. 18. NeurotransmittersPeripheral Neurotransmitters Adrenergic neurotransmission, and endothelium- derived contracting factors such as angiotensin II, PGF2α, and endothelins maintain the flaccid state. NO released from nonadrenergic, noncholinergic neurotransmission and from the endothelium is the principal neurotransmitter mediating penile erection. NO increases the production of cGMP, which in turn relaxes the cavernous smooth muscle. Detumescence after erection may be a result of cessation of NO release, the breakdown of cyclic guanosine monophosphate (cGMP) by phosphodiesterases, or sympathetic discharge during ejaculation.
    19. 19. Neurotransmitters Central Neurotransmitters Dopaminergic and adrenergic receptors promote sexual function. (Apomorphine / Yohimbine) Serotonin inhibit sexual drive. (SRI /Buspirone) Low levels of DA stimulation causes erection (D1) while higher levels or prolonged stimulation produces seminal emission ( D2 ).Act through Oxytocin release from PVA. Prolactin suppress sexual function through inhibition of dopaminergic activity in the MPOA and decreased testosterone. has a direct contractile effect on the cavernous smooth muscle. GABA, NO, Opioids and melanocortins are other modulators.
    20. 20. Physiology ofSmooth Muscle Relaxation
    21. 21. Physiology ofSmooth Muscle Relaxation▪ Relaxation of the cavernous smooth muscle is the key to penile erection.▪ Low cytosolic calcium favors smooth muscle relaxation.▪ Nitric oxide released by nNOS contained in the terminals of the cavernous nerve initiates the erection process, and nitric oxide released from eNOS in the endothelium helps maintain erection.▪ Upon entering the smooth muscle cells, NO stimulates the production of cGMP. PGE1and PGE2 activate adenyl cyclase to produce cAMP.▪ Cyclic GMP and AMP activate protein kinases A & G , which in turn opens potassium channels and closes calcium channels and sequestration of intracellular Ca by EPR. The resultant fall in intracellular calcium leads to smooth muscle relaxation.▪ The smooth muscle regains its tone when cGMP and cAMP are degraded by phosphodiesterase and it leads to detumesence. PDE5 is the principle phosphodiesterase that is inhibited by Sildenafil. Papaverine is a nonspecific phosphodiesterase inhibitor.
    22. 22. Ejaculation Ejaculation: the process by which semen is expelled through the penis outside the body. Ejaculation is a separate process from orgasm, and the two may not always occur simultaneously.  It is possible for men to experience multiple orgasms w/o ejaculation. 2 phases (see next slides for details): 1) Emission phase: semen collects in the urethral bulb  This stage is usually sensed by the man as the “point of no return” 2) Expulsion phase: semen is expelled
    23. 23. Emission phase of ejaculation (phase 1) Contractions in the prostate, seminal vesicles, and vas deferens force secretions into urethral bulb. Both the internal and external urethral sphincters close, trapping semen in the urethral bulb (like a balloon)
    24. 24. Expulsion phase of ejaculation (phase 2) Collected semen is expelled out of the body by rhythmic contractions of muscles surrounding the urethral bulb and also on the urethra. External urethral sphincter relaxes to allow semen out; internal urethral sphincter stays contracted to prevent the escape of urine.
    25. 25. ErectileDysfunction
    26. 26. DefinitionsErectile dysfunction is defined as the “Inability to achieve or maintain an erectionsufficient for satisfactory sexual performance.”-The National Institutes of Health (NIH) Consensus DevelopmentConference on Impotence(December 7-9, 1992)
    27. 27. ED vs Impotence “ED is the more precise term, especially given the fact that sexual desire and the ability to have an orgasm and ejaculate may well be intact despite the inability to achieve or maintain an erection.” - American Urological Association Education and Research
    28. 28. Epidemiology
    29. 29. Incidence and prevalance Incidence of 25 to 30 per 1000 man-years -Moreira et al, 2003 ; Schouten et al, 2005 Age dependent  2%men at age <40 years  25% men age 65  75% men >75 years -Kinsey et al ,1948 Not a necessary occurrence of the aging process Rising trend of prevalance of ED -international studies reported between 1993 and 2003
    30. 30. Massachusetts Male Aging Study (MMAS) Prevalence rates of ED between the ages of 40 and 70 years, the probability of complete ED increased from 5.1% to 15%, moderate dysfunction increased from 17% to 34%, and mild dysfunction remained constant at about 17%. Crude incidence rate of impotence in white men in the United States was 25.9 cases per 1000 man- years. ED was higher for men with diabetes mellitus (50.7 cases), treated heart disease (58.3 cases), and treated hypertension (42.5 cases) per 1000 man- years.
    31. 31. Risk Factors Diabetes 27% - 59% Chronic renal failure 40% Hepatic failure 25% - 70% Multiple Sclerosis 71% Severe depression 90% Other (vascular disease, low HDL, high cholesterol) -Benet et al. Urol Clinic North Am. 1995; 151:54-61
    32. 32. Other risk factors General health status Concurrence of other genitourinary disease Psychiatric or psychologic disorders Other chronic diseases Sociodemographic conditions. Smokingng and medications Hormonal factors Endothelial dysfunction - common etiologic pathway
    33. 33. Classification
    34. 34. Classification of EDInternational society of Impotence Research Psychogenic Organic Mixed organic/psychogenic (most common type)
    35. 35. PsychogenicED
    36. 36. Psychogenic ED Sexual behavior and penile erection are controlled by the hypothalamus, the limbic system, and the cerebral cortex. Direct inhibition of the spinal erection center by the brain as an exaggeration of the normal suprasacral inhibition ( Steers, 1990 ) Excessive sympathetic outflow or elevated peripheral catecholamine levels, which may increase penile smooth muscle tone to prevent its necessary relaxation (Kim and Oh,1992)
    37. 37. Classification of EDInternational society of Impotence ResearchPsychogenic ED1. Generalized type A. Generalized unresponsiveness a. Primary lack of sexual arousability b. Aging-related decline in sexual arousability B. Generalized inhibition a. Chronic disorder of sexual intimacy2. Situational type A. Partner related a. Lack of arousability in specific relationship b. Lack of arousability due to sexual object preference c. High central inhibition due to partner conflict or threat B. Performance related a. Associated with other sexual dysfunction/s (rapid ejaculation) b. Situational performance anxiety (eg, fear of failure) C. Psychological distress or adjustment related a. Associated with negative mood state (eg, depression) b. major life stress (eg, death of partner)
    38. 38. Differentiating Psychogenicfrom Organic EDPsychogenic ED: Younger patient (<40) Preservation of morning erections and nocturnal erections Achieve erection with masturbation May be partner-specific Often sudden onset
    39. 39. Organic ED
    40. 40. Differentiating Psychogenic fromOrganic EDOrganic ED: Gradual deterioration Decrease in morning erections and nocturnal erections No erections with masturbation No loss of libido Presence of co-morbid conditions
    41. 41. Classification of EDInternational society of Impotence ResearchOrganic ED 1. Neurogenic 2. Hormonal 3. Arterial 4. Cavernosal (venogenic) 5. Drug induced
    42. 42. Neurogenic 10% to 19% of ED is neurogenic ( Abicht 1991 ; Aboseif et al, 1997 ). Pathologic processes in the region of higher center, such as Parkinsons disease, stroke, encephalitis, or temporal lobe epilepsy ,tumors, dementias, Alzheimers disease, and trauma . Spinal cord injuries: 5% - 80% Reflexogenic erection is preserved in 95% of patients with complete upper cord lesions but in only about 25% of those with complete lower cord lesions. ( Eardley and Kirby, 1991 ). disorders at the spinal level e.g., spina bifida, disk herniation, syringomyelia, tumor, transverse myelitis, and multiple sclerosis Injury to cavernosal nerve and pelvic plexus in pelvic surgery ( Iatrogenic ED)
    43. 43. Iatrogenic impotence resulting fromvarious pelvic surgical procedures radical prostatectomy - 43% to 100% Nerve sparing radical prostatectomy -30% to 50% perineal prostatectomy for benign disease - 29% abdominal perineal resection -15% to 100% external sphincterotomy at the 3 and 9 oclock positions -2% to 49%
    44. 44. Hormonal Hypogonadism is a not-infrequent finding in the impotent population. Testosterone enhances sexual interest, increases the frequency of sexual acts, and increases the frequency of nocturnal erections but has little or no effect on fantasy- induced or visually stimulated erections. However, exogenous testosterone therapy in impotent men with borderline-low testosterone levels reportedly has little effect ( Graham and Regan, 1992 ). Hyperprolactinemia,results in both reproductive and sexual dysfunction and is associated with low circulating levels of testosterone, which appear to be secondary to inhibition of gonadotropin-releasing hormone secretion by the elevated prolactin levels. In hypothyroidism, low testosterone secretion,increased circulating estrogen and elevated prolactin levels contribute to ED.
    45. 45. Arteriogenic Atherosclerotic or traumatic arterial occlusive disease of the hypogastric-cavernous-helicine arterial tree can decrease the perfusion pressure and arterial flow to the sinusoidal spaces, This increases the time to maximal erection and decreases the rigidity of the erect penis. An atherosclerotic process may decrease expansibility of cavernous smooth muscles by decreasing NOS activity. Common risk factors associated with arterial insufficiency include hypertension, hyperlipidemia, cigarette smoking, diabetes mellitus, blunt perineal or pelvic trauma, and pelvic irradiation. As, ED and cardiovascular disease share the same risk factors, ED may present as a manifestation of generalized or focal arterial disease (Sullivan et al,1999).
    46. 46. Cavernous (Venogenic) Failure of adequate venous occlusion is one of the most common causes of vasculogenic impotence ( Rajfer et al, 1988 ). Veno-occlusive dysfunction : degenerative tunical changes, fibroelastic structural alterations (increased deposition of collagen and decreased elastic fiber) , insufficient trabecular smooth muscle relaxation, and venous shunts. Degenerative changes as old age, and diabetes or traumatic injury to the tunica albuginea (penile fracture) can impair the compression of the subtunical and emissary veins. In Peyronies disease, the inelastic tunica albuginea may prevent the emissary veins from closing. ( Metz et al, 1983 ).
    47. 47. Diabetes and ED The prevalence of ED is three times higher in diabetic men (28% versus 9.6%) ( Feldman et al, 1994 ), occurs at an earlier age, and increases with disease duration. Associated with a decreased desire and orgasmic dysfunction as well . ED occurs due to dysfunction of one or a combination of : psychologic function, CNS function, androgen secretion, peripheral nerve activity, endothelial cell function, and smooth muscle contractility ( Dunsmuir and Holmes, 1996 ). A higher odds ratio is seen with insulin-dependent diabetes mellitus; diabetes present for over 10 years; fair or poor control based on glycosylated hemoglobin; management by means other than diet; a history of diabetes-related arterial, renal, or retinal disease and neuropathy; and concurrent cigarette smoking.
    48. 48. Drug induced ED Most common cause of ED in men >50 years. Antihypertensives - thiazides - β- Blockers - α1 blockers - α2 agonist - ACE inhibitor and AT II antagonists Antipsychotics Antidepressants. -Tricyclics - Monoamine oxidase inhibitors - Selective serotonin reuptake inhibitors (SSRIs) Anxiolytics Antiandrogens Digitalis Opioids Protase inhibitors Tobbaco and alcohol H2 receptor antagonist
    49. 49. THANK YOU!

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