W2 Erectile Dysfunction (Joey) Flashcards
Slide 3
How is an erection defined?
a vascular event that is a result of increased arterial blood flow into the penis, and decreased venous blood flow out of the penis (compression of the veins)
Erections are a highly complex event, requiring:
● Intact arterial and venous system (Penile Arteries and Veins)
● Normal neurologic innervation (Dorsal Penile, Cavernosal Nerves, CNS / psych)
● Normal hormonal factors (ex. Testosterone)
● Functioning (compliant, unobstructed) erectile tissue (Corpora) Abnormalities in any or all of these can lead to Erectile Dysfunction
Slide 4
Which artery supplies the corpus cavernosum? Which is a terminal branch of?
Innervated by
Which artery supplies spongiosum
Which 2 arteries supply the glans penis
Deep penile artery supplies corpus cavernosum, it is a terminal branch of the pudendal artery
Bulbourethral artery supplies spongiosum
Dorsal penile artery and bulbourethral artery supply the glans penis
❗️[must know]
⭐️Physiology of erectile function
See my drawing
- Stimulation
- ACh released into endothelial cells
- NO synthase activation
- Increase in NO which leaves the endothelial cells
- NO travels to smooth muscle cells
- Activates guanylate cyclase
- Increase in cGMP intracellularly
- Inhibits Ca++ release from SR
- Inactivation of myosin and actin
- Smooth muscle relaxation
- Vasodilation
- Blood flows in = erection
Sexual Stim (visual, verbal/audial, tactile, thoughts, etc)
→ presynaptic neurons of neuromuscular & neuroendothelial 3Ak junction (FYI: primarily pudendal n. branches & contributions from the sympathetic trunk) release Acetylcholine into synapse of NMJ & NEJ → ACH enters endothelial cells of penile vascular tissue and activates NO Synthase → increased production of Nitric Oxide, which then easily diffuses out of endothelial cells → NO enters smooth muscle cells of penile vasculature and activates Guanylate Cyclase → Guanylate Cyclase activation increases production of intracellular cyclic Guanosine Monophosphate (cGMP) → increases in intracellular cGMP lead to prevention of intracellular calcium (Ca ++) release from the sarcoplasmic reticulum into cytoplasm → less intracellular calcium leads to decreased actin and myosin activation → smooth muscle relaxation → vasodilation of arteries → increased arterial blood flow to corpora → corporal tissue engorgement and progressive extrinsic pressure on veins reducing outflow of blood → end result: erection
https://www.youtube.com/watch?v=NAMDHH5h
Erectile dysfunction definition
What are the two types?
Slide 7 & 8
ED is defined as “the inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance (subjective)
Organic
—functional loss of a physical cause
—CV: atherosclerosis
—neurologic: diabetic neuropathy, MS, trauma below S2
—endocrine: thyroid, DM, hypogonadism
—more common in Middle Ages to elderly men >45 y/o
—gradual onset, consistent dysfunction
—no nocturnal, reflex, masturbation erection
—so many meds!
Inorganic
—psychogenic: depression, anxiety and situational stressors
—<45 y/o
—teenagers/young 20s
—rapid onset
—inconsistent
—still have nocturnal erections
slide 9
Workup, patient interview, PE
Physical Exam:
● Penile Exam
○ Visual inspection for virilization (Tanner Staging), trauma, curvature while
flaccid (may raise suspicion for Peyronie’s plaque)
○ Bilateral corpora palpation for plaques - peyronie’s
○ Tactile sensation bilaterally (ex: can pt feel tactile stimulation?)
● Testicular exam
○ Size (testicular volume, if low vol think about T production)
● Cardiovascular exam (general)
○ Palpating peripheral pulses (ex: pedal pulses, if diminished, think PAD)
Do you have nocturnal erections?
helps to determine which type
Standard work up for ED
“Standard” Metabolic Workup for ED:
Hemoglobin A1c, Lipid Panel, Fasting AM T level (before 10 am)
—If low T found, confirm finding with second AM T level at least 1 wk later,CBC, LFTs, fasting AM prolactin x2, gonadotropins (more detail in next lecture), +/- PSA if rapid onset ED and pt at risk for PCa
May consider PSA regardless in M 50-69 yo who is at high risk for PCa
Rapid onset ED you’d want to get a PSA
First line treatment for ED
[slide 11]
always lifestyle modification
Remove offending medications
Make sure you know the physiology of erection
Know the negative feedback loop as well (detumescence)
Slide 12
Detumescence
—decreased ACh release
—decreased cGMP formation
—increased degradation of cGMP by phosphodiesterase
—return of normal SR calcium release intracellularly
—return to baseline actin and my son activation
—contraction of arteries
—boner goes away
❗️[must know]
Erectile dysfunction
What is the treatment?
What are 2 side effects?
What is the biggest DDI that you MUST know about!!
[slide 14]
Phosphodiesterase Inhibitors
● Inhibit the enzyme phosphodiesterase in the physiologic erectile function pathway
○ Phosphodiesterase-5 is normally involved in degradation of cGMP in the vascular smooth muscle of
the penis
○ Inhibition of PDE-5 leads to increased cGMP —> decreased SR Ca++ dump —> decreased actin and myosin activation —> relaxation of vascular smooth muscle —> promote and prolong erection
Examples:
○ Sildenafil (Viagra) - 20 mg - 100 mg PO PRN 1-2 hours prior to sexual activity
○ Tadalafil (Cialis) - 5 mg - 20 mg PO PRN 1-2 hours prior to sexual activity, > half life than sildenafil
○ Others: Avanafil (Stendra - works fast, but expensive), Vardenafil (Levitra - similar to cialis)
Side effects/risks
Severe: Hypotension, Priapism (erection lasting >4 hours)
⚠️HIGH RISK DDI: ⚠️
Nitrates - concomitant use should be avoided (>24 hrs)
If a patient comes into the ED w/ suspicion of MI, must ask if they’ve taken a PDE-5 inhibitor. If you administer nitric oxide, you could cause profound hypotension and kill them!!!
Non-PDE5 inhibitor pharm therapies for ED
Which one can lead to priapism and necrosis?
—Intraurethral prostaglandin / alprostadil injection
—Intracavernosal Injections (aka ICI). They work too well, can lead to priapism and cause tissue necrosis.
—Vacuum Erectile Device (VED)
Less invasive, Rx free, but “unnatural” erection from venous blood - corporal fibrosis possible long term, possibly making efficacy of Rx options in the future less viable
Surgical Options: LAST LINE
—Implantable penile prosthesis (IPP) - rigid vs inflatable, VERY PAINFUL post-op course, high risk of infxn
—Vascular surgery - rare but may have greater role in future
Peyronie’s disease: what is it?
2/2 ?
What do you find on PE?
Tx? 3
priapism: duration?
A/w which ED treatment?
How is this treated?
penile fracture : what is disrupted in the anatomy?
[slide 16, know this]
Peyronie’s Disease:
An acquired curvature of the penis (not present at birth), often 2/2 recurrent microtraumas to penile corpora during sexual activity, w/ subsequent deposition of focal areas of scar tissue, once it starts it is often progressive
Hallmark is distinguishable palpable penile plaque on PE (corpora) — ED distal to the plaque
TX: NSAID, vitamin E and collagenase injections to breakdown the plaque
Priapism
—erection that lasts > 4 hours.
—prolonged untreated priapism may lead to profound corporal ischemia → necrosis → death of penile tissue
—Commonly associated with ICI use - must warn all patients using ED meds however as possible with any of them
● MEDICAL EMERGENCY warrants immediate ER visit and Urology Consult - may need alpha agonist injection (phenylephrine), corporal irrigation, surgical treatment
Penile Fracture
Penile fracture is a LARGE physical disruption of the penile tunica albuginea 2/2 direct blunt force trauma to an erect penis (often during sexual activity, falls), this is a surg emergency, often leads to a peyronie’s-like dz state (ED, pain w/ erection, etc)
