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Stack #197837
Erectile Dysfunction 1.10
| Question | Answer |
|---|---|
| Define erectile dysfunction. | Impotence: the total or inconsistent ability to achieve erection suitable for intercourse. |
| Describe the mechanics behind an erection. | 1.) Increases blood flow into cavernosa (dilate penile arteries, relax cavernosal smooth muscle), 2.) Decrease exit of blood from cavernosa (compress trabecular smooth muscle ag tunica albuginea) |
| What 3 things initiate an erectile state? | 1.) Genital stimuli, 2.) Sexual arousal such as thoughts, vision, 3.) Hypothalamus integrates neural input to initiate erection |
| How does genital stimuli initiate an erectile state? | Genital stimuli activate afferent fibers of pudendal nerve = S2-S4 segments of spinal cord = activates nerves that ascend to hypothalamus |
| How does sexual arousal initiate an erectile state? | Sexual arousal (thoughts, vision) stimulates the limbic system + hypothalamus |
| How does the hypothalamus help to initiate an erectile state? | The hypothalamus integrates neural input to initiate erection. DA receptors activate descending nerves that synapse with PNS + nonadrenergic noncholinergic (NANC) nerves |
| Describe how the PNS + NANC nerves are involved in initiating an erection. | ACh released fr PNS. Inhibits NE releas fr SNS. Incr NO syn w/in endo cells & release of NO in synapse of endo cells & sm muscle of penile arteries & cavernosa. Incr NO releas fr NANC in synapse. NO activ GC = Inc cGMP = Decr Ca+2 = relax sm muscle |
| Describe how ACh fr PNS + endogenous prostaglandin E1 (PGE1) lead to an erection. | It stimulates AC = cAMP = decreases intracellular Ca+2 = relaxes smooth muscle of penile arteries and cavernosa |
| How does the compression of trabecular smooth muscle contribute to an erection? | Compression of trabecular smooth muscle against tunica albuginea closes veins and accumulates blood in the sinuses of the cavernosa. |
| What does detumescence mean? | Loss of erection |
| Describe the mechanism behind a loss of erection. | Increase release of NE (during ejaculation), this stimulates A1 receptors = constricts penile arteries and contracts sinus tissue. |
| What are the 7 risk factors associated with detumescence? | Failure to fill, failure to store, psychogenic (anxiety, depression), endocrine levels, diabetes mellitus, prostatectomy, and drugs. |
| Describe how failure to fill is a risk factor for detumescence. | Failure to fill can be caused by atherosclerosis. The narrow arterial lumen lowers pressure within cavernous arteries = partial filling of sinuses = partial compression of venules. |
| Describe how failure to store is a risk factor for detumescence. | There is excessive venous outflow due to insufficient relaxation of trabecular smooth muscle. This can be a result of an hyperactive SNS or a hypoactive PNS. |
| How is diabetes mellitus a risk factor for detumescence? | Leads to neuropathy of penile nerves. There is a reduced amt of NO synthase. |
| What type of drugs are risk factors for detumescence? | Estrogens, androgens, cimetidine, spironolactone, CNS depressants, nicotine, anti-hypertensives (diuretics, B Blockers, CNS sympatholytics ie clonidine), all decrease penile blood flow, and anticholinergics. |
| What are the PDE5 inhibitor drugs? | Sildenafil (Viagra), Vardenafil (Levitra), and Tadalafil (Cialis) |
| What is the MOA for the PDE5 inhibitors? | Inhibit PDE5 = maintain cGMP levels produced during sexual stimulation. |
| What is the precaution for PDE5 inhibitors? | Priapism, which includes erections lasting over 4 hours (medical emergency) and Hypoxia, which can lead to fibrosis and scarring. |
| What are the 7 ADRs associated with PDE5 inhibitors? | Facial flushing, nasal congestion, abnormal vision, loss of blue/green color discrimination, non-arteroc ischemic optic neuropathy (NAION), sudden hearing loss, and hypotension. |
| Describe how abnormal vision is an ADR of PDE5 inhibitors. | PDE5 inhibitors can also inhibit PDE6 which has a role in phototransduction. |
| Describe how non-arteroc ischemic optic neuropathy (NAION) is an ADR of PDE5 inhibitors. What is NAION? | NAION is permanent blurred vision with or without loss of vision. The onset is w/in 2 hrs to 7 days after dose (initial or even after several years of Rx). The MOA is that NO-induced vasodilation may disrupt autoregulation of eye microvasculature. |
| What are the drug interactions with PDE5 inhibitors? | Do not take w/ A-blockers. A1B blocker = vasodilation = hypotension. A1A blocker = less vasodilation. Tamsulosin (Flomax): A1A>A1B. Do not take Viagra w/in 4 hrs of a blocker. Little evidence of enhanced hypotensive effect w/B blockers or ACE inhibitors. |
| What are the 4 warnings associated with the PDE5 inhibitors? | MI, ventricular arrhythmia, sudden cardiac death, and nitrates (nitroglycerin, isosorbide). |
| Why is it unsafe to take nitrates with a PDE5 inhibitor? | Organic nitrates supply extra NO to stimulate GC = increase cGMP = low BP. Nitrates increase NO synthesis and PDE5 inhibitors decrease metabolism of cGMP |
| When might a doctor consider initiating a nitrate Rx with a pt on PDE5 inhibitor? | A doctor may consider initiation after more than 24 hrs after cessation of sildenafil..maybe longer is pt has an extended half life |
| What are the alprostadil drugs? | The alprostadil (prostaglandin E1, PGE1) drugs include: MUSE (Medicated Urethral System for Erection), Caverject Injection (intracavernosal), Edex Injection (intracavernosal), and Alprox TD cream. |
| What is the MOA for the MUSE pellet? | It stimulates smooth muscle AC = increases cAMP = decreases intracellular Ca+2 = dilates penile arteries |
| Which drug is considered the "last resort" for ED? Why? | Caverject is considered the last resort. Over 50% drop out in 6 months. It is a maintenance Rx: nmt 3x/week and 24 hrs between doses. |
| What is the contraindication for caverject? | Pregnancy because it stimulates the uterus |
| What is the Yohimbine drug for ED? | Yohimbine (Yocon, Aphrodyne) |
| What's the MOA for Yohimbine? | It is an A2 blocker: hypothalamus + other nuclei associated with libido/erection block CNS presynaptic A2 receptors = decrease discharge of peripheral SNS |
| What is the trade name for Papaverine? | Papaverine (Pavabid Injection) |
| What's the MOA for Pavabid injection (cavernosal)? | Inhibits cavernosal PDE5 |
| Is Papaverine ever used as monotherapy? | Infrequently used as a monotherapy due to ADRs. Combine with PGE1 and you can reduce the dose of papaverine by 66%. |
| What is the trade name for phentolamine? | Phentolamine (Spontane, Vasomax) |
| What's the MOA for phentolamine? | It's a non-selective A-blocker; It reduces peripheral SNS-induced vasoconstriction of penile arteries. |
| Is phentolamine used as a mono-therapy for ED? | No. It's combined with Rx vasodilators or smooth muscle relaxants. |
| What are the ADRs associated with Phentolamine? | nasal congestion and facial flushing |
| What combination product is out there for ED? What is the ratio of the combined drugs? | There is a Papaverine-Phentolamine mixture that has an efficacy greater than the mono-therapy of either drug. In terms of pharmacy compounding, there is a 30:1 papaverine-phentolamine ratio |
| What is Testoderm-TTS (transdermal testosterone system) indicated for? | Pts with hypogonadism with low serum levels of testosterone. |
| What are the contraindications for Testoderm-TTS? | BPH, due to stimulation of prostate growth |
| What is the trade name for Apomorphine? | Uprima |
| What is the MOA for Uprima? | D1/D2 agonist in the hypothalamus; It activates nuclei of the hypothalamus that are responsible for erection |
| Is apomorphine ever used as an alternative to PDE5 inhibitors? | Seldomly |
| What is Sildenafil (Revatio) indicated for? | Pts with pulmonary arterial hypertension |
| What's the MOA for Revatio? | It inhibits PDE5 / increases cGMP within pulmonary vascular smooth muscle = vasodilation |
Created by:
hcp1227
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