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RGU Exam 3 > Male Infertility and Erectile Dysfunction > Flashcards

Male Infertility and Erectile Dysfunction Flashcards

1
Q

Infertility Statistics

A
  • 15% of couples will be affected by infertility
  • 30% male factor alone
  • 20% male and female factors
  • 50% of all infertile couples will have an abnormal male factor
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2
Q

Male LH

A
  • Released from ant. pituitary by GnRH or LHRH
  • Pulasatile release; q60min
  • Stimulates leydig cells to produce testosterone
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3
Q

Male FSH

A
  • Released from ant. pituitary by GnRH or LHRH
  • Stimulates sertoli cells to initiate spermatogenesis
  • Inhibin- postulated as neg. feedback substance
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4
Q

Male Prolactin

A
  • Released from ant. pituitary
  • Inhibits GnRH release
  • Hyperprolactinemia produces hypogonadotropic hypogonadism
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5
Q

Male Testosterone Physiology

A
  • Circadian production; highest in am
  • Pulsatile release
  • Bound in peripheral circulation
  • Small % is unbound and bioavailable
  • Can be aromatized to estradiol and 5alpha reduced to DHT
  • Acts as neg. feedback to hypothalamus
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6
Q

Spermatogenesis

A
  • Smpermatogonia (stem cell)
  • Spermatocyte (undergo meiosis)
  • Spermatids

*develops a cap (acrosome)

*develops a tail (9 paired microtubules

*forms a blood-testes barrier

  • Process takes approx. 74 days
  • Highly sensitive to environmental factors
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7
Q

Ejacalatory Mechanism

A
  • Epididymis- maturation and storage of spermatozoa in the cauda
  • Vas deferens- transport
  • Seminal vesicles- formation of coagulum
  • Prostate- proteases for liquefaction
  • Neurologic innervation- “point and shoot”

*point = erection and is parasympathetically controlled

*shoot = ejaculation and is sympathetically controlled

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8
Q

Post-coital test

A
  • Test that looks at cervical mucus, anti-sperm antibodies
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9
Q

What disease causes congenital absence of vas deferens?

A
  • Cystic fibrosis
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10
Q

Anatomic causes of male infertility

A
  • Congenital absense of the vas
  • Cryptorchidism (absence of 1 or both testes in the scrotum
  • Ejaculatory duct obstruction
  • Varicocele
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11
Q

Behavioral and environmental causes of male infertility

A
  • Obesity
  • Environmental exposure
  • Substance abuse (opiods, exogenous T, vit. deficiencies)
  • Chemoradiation
  • Meds
  • Surgery
  • Infections/inflamation
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12
Q

Male infertility syndromes

A
  • Cystic fibrosis (autosomal recessive, congenital absence of the vas)
  • Primary ciliary dyskinesia (autosomal recessive, kartagener’s syndrome)
  • Kallmans syndrome (absence of GnRH)
  • Klinefelters syndrome (47 XXY, 48 XXXY)
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13
Q

What test is performed to examine for ejaculatory duct obstruction?

A
  • Trans rectal ultrasound (TRUS)
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14
Q

Male infertility physical exam

A
  • Signs of hypogonadism/gynecomastia
  • Testicular size

*seminiferous tubules 85% of testes volume

  • Prostate, penis, epididymis, vas (CF)
  • Spermatic cords- varicocele
  • Ejaculatory duct obstruction (TRUS)
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15
Q

Male infertility lab exam

A
  • Urinalysis
  • Semen analysis:

*2 seperate specimens, 48-72hrs of abstinence

*volume, sperm density, motility, forward progression and morphology

*leukocytes

  • Hormonal eval

*freq. of primary endocrine defects <3%

*FSH, LH, prolactin, testosterone

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16
Q

Oligospermia

A
  • Sperm density <50 million total
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17
Q

Asthenospermia

A
  • Defects in sperm motility
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18
Q

Azoospermia

A
  • Defects in sperm visualized
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19
Q

Necrospermia

A
  • Dead or immotile sperm identified
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20
Q

Tetraspermia

A
  • Defects in morphology
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21
Q

Cryptospermia

A
  • Live sperm seen in a centrifuged pellet
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22
Q

Abnormalities of seminal fluid tests

A
  • Quantitation of leukocytes in semen

*difficult to distinguish leukocytes from immature, round germ cells, use monoclonal assay

  • Antisperm antibody testing

*ASA (anti-sperm antibody) should be suspected in clumping or agglutination, diminished motility and a poor post-coital test

*blood-testis barrier is breached

*immunobead test

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23
Q

Abnormalities of sperm function tests

A
  • Sperm capacitation assays

*capacitation is the hyperactive motility w/ cellular changes before the spermatozoa can bind to the zona pellucida and undergo the acrosome reaction

  • Sperm penetration assay (Humster test)

*sperm are mixed w/ zona free hamster ovum

*timed penetration of the ovum

*SPA has a high predictive value for IVF outcome

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24
Q

Male infertility genetic factors

A
  • 13% of men w/ obstructed azoospermia and 6% of men w/ severe oligospermia have microdeletions of the “Y” chromosomes
  • Klinefelter’s syndrome (XXY) can be found in 4-10% of men w/ non-obstructive azoospermia
  • Congenital b/l absence of the vas deferens is caused by a mutation of the gene for cystic fibrosis transmembrane conductance regulator (CFTR)
  • Careful consideration must be given to the potential for transmission of undesirable genes
25
Q

Germinal Aplasia FSH, LH and Testosterone Levels compared to normal

A
  • FSH = Elevated
  • LH = Normal
  • Testosterone = Normal or decreased
26
Q

Testicular Failure FSH, LH and Testosterone Levels compared to normal

A
  • FSH = Elevated
  • LH = Normal or elevated
  • Testosterone = Normal or decreased
27
Q

Hypogonadotropic Hypogonadism FSH, LH and Testosterone Levels compared to normal

A
  • FSH = Decreased
  • LH = Decreased
  • Testosterone = Decreased
28
Q

Hypergonadotropic Hypogonadism FSH, LH and Testosterone Levels compared to normal

A
  • FSH = elevated
  • LH = Elevated
  • Testosterone = Low-normal or decreased
29
Q

Varicocele

A
  • Most common surgically correctable cause of male infertility
  • 33% of infertile males
  • 15% in general pop.
  • 90% left sided
  • 50-90% show improved semen analysis
  • 30-50% pregnancy rates
30
Q

Hyperprolactinemia treatment

A
  • Disease which can contribute to male infertility
  • Bromocriptine
31
Q

Kallmann’s syndrome treatment

A
  • Disease which can contribute to male infertility
  • Gonadotropin (hCG) followed by hMG (pergonal)
32
Q

Antisperm antibodies treatment

A
  • Disease state which can contribute to male infertility
  • Steroids
33
Q

Retrograde ejaculation treatment

A
  • Can be caused by damage to the bladder neck
  • Antihistamine and alpha stimulation

*used to attempt to tighten the bladder neck

34
Q

Congenital adrenal hyperplasia treatment

A
  • Glucocorticoids
35
Q

Male Infertility Emperic Therapy

A

30-40% of infertile couples have no discernable etiology

  • Anti-estrogens- clompiphene, tamoxifen
  • hCG, hMG
  • GnRH, LHRH
  • Kallikrein
  • Testosterone rebound
36
Q

Intracytoplasmic Sperm Injection

A
  • Partial zona dissection, subzonal insertion
  • Significant improvement in IVF results w/ severe male factor
  • 1 sperm is injected into the cytoplasm of 1 egg
  • Sperm may be obtained directly from epididymis
  • 66-70% fertilization rate
  • “There no longer seems to be any category of male factor infertility that cannot be treated w/ ICSI”
  • Extremely expensive
37
Q

Erectile Dysfunction Diagnosis Statistics

A
  • In the US, 83% of ED is not diagnosed
  • Only 10-11% of total ED pop. is treated
38
Q

Erectile Dysfunction Definition

A
  • The inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance
39
Q

Erectile Dysfunction Prevalence

A
  • Occurs in ~5% of men at age 40, w/ prevalence increasing to b/w 15-25% by age 65
  • Community samples indicate a prevalence of 4-10%
  • Prevalence of ED increases w/ age, but ED is not an invevitable and untreatable consequence of aging
40
Q

3 Neuroeffector systems control smooth muscle relaxation and penile blood flow

A
  • Adrenergic fibers
  • Cholinergic fibers
  • Nonadrenergic-noncholinergic (NANC) fibers
  • Vasodilation mediated by nitric oxide and cGMP following activation of cholinergic and NANC fibers
  • Prostaglandin E1: relaxes corpus cavernosum
  • Flaccid state: penis under venous O2 tension and pressure
41
Q

Causes of ED

A
  • Vascular disease
  • Neuropathy
  • Iatrogenic factors
  • Congenital abnormalities
  • Peyronie’s disease
  • Psychological processes
  • Drugsd
42
Q

Treatment for ED

A

First-line therapeutic options

  • Oral therapy: PDE5 inhibitors
  • Psychosexual therapy
  • Vacuum constriction devices

Second-line therapeutic options

  • Intraurethral therapy
  • Injection therapy
  • Combination therapy

Third-line therapeutic options

  • Surgery
43
Q

Vascular Surgery for ED

A
  • Generally considerd low success
  • May be used to correct demonstrated venous leakage
  • May have a limited role in correcting congenital vascular abnormalities or traumatic injury
  • Long-term outcome may be poor
44
Q

ED Hormonal Therapy

A
  • Androgenic steroids
  • May be effective in a small fraction of ED pts. w/ documented hypogonadism
  • Oral, parenteral, transdermal preparations available
45
Q

ED Hormonal Therapy ADRs

A
  • Androgenic steroids can suppress remaining endogenous androgen production
  • May be metabolized to estradiol w/ potentially detrimental effects on sexual function
  • May increase risk of prostate hypertrophy
  • Oral therapy may lead to liver dysfunction
46
Q

Vacuum Constriction Devices for ED

A
  • Most common device used for ED
  • No tests required beyond initial evaluation
  • High success rate, pt. satisfaction

*90% achieve erections sufficient for intercourse

*>80% of pts. cont. use

47
Q

Vacuum Constriction Devices for ED Adverse Effects

A
  • Hematoma, ecchymosis, and petechiae
  • Pain, numbness of penis; blocked and/or painful ejaculation; pulling of scrotal tissue into the vacuum cylinder
48
Q

Penile Implants for ED

A
  • 2 types: semirigid and multicomponent inflatable
  • Pt. satisfaction rates range from 81-97%
  • Avg. functional life of prostheses is 7-10yrs
  • Useful in pts who fail or refuse other treatments
  • Requires pt./partner screening and education
49
Q

Penile Implant Complications

A
  • Perioperative infection (~2%)
  • Device malfunction (~4%)
  • Repeat surgery (~9%)
50
Q

Vasoactive Intracavernosal Pharmacotherapy for ED

A
  • Intracavernosal injection of vasoactive agent (eg, alprostadil, phentolamine, papavarine)
  • Relaxes cavernous and arterial smooth muscle
  • Allows filling of the penile sinusoids w/ blood and restriction of venous outflow
  • Agents may be used alone or in combination to increase efficacy and reduce adverse events
  • Alprostadil most common; up to 94% efficacy
  • Effective in pts. w/ neurogenic, vascular, hormonal and psychogenic dysfunction
51
Q

Vasoactive Intracavernosal Pharmacotherapy Disadvantages

A
  • Poor long-term tolerability: many pts. stop therapy during the 1st yr
  • Bruising
  • Prolonged erection
  • Pain
  • Induration, plaque or nodule
  • Curvature of the penis
  • Superfical infection
  • Dizziness
52
Q

Oral Pharmacologic Treatments for ED

A
  • Yohimbine
  • Trazodone
  • L-arginine
  • FDA-approved agents; PDE-5

*sildenafil (viagra)

*vardenafil (levitra)

*tadalifil (cialis)

*avanafil (stendra)

53
Q

First-Line Treatment for ED

A
  • PDE5 inhibitors
54
Q

PDE5 Inhibitors MOA Graph

A
  • PDE 5 inhibition causes cGMP accumulation ⇒ Increased cGMP accumulation relaxes the smooth muscle in the corpus cavernosum ⇒ Blood flow and erection are facilitated
55
Q

Adverse Events with PDE5 Inhibitors

A
  • Headache
  • Facial flushing
  • Dyspepsia
  • Rhinitis/congestion
  • Back pain
  • Myalgia
  • Vision disturbance
56
Q

PDE5 Inhibitors Pharmacodynamic Interactions

A
  • PDE5 inhibitors, nitrates and alpha-blockers all can cause vasodilation and decrease BP
  • Nitrates stimulate cGMP production by delivering nitric oxide
  • PDE5 inhibitors reduce breakdown of cGMP

*systemic vasodilatory properties may result in transient decreases in BP in healthy

  • Alpha-blockers inhibit pressor effects of epinephrine, leading to a fall in peripheral vascular resistance and venous return

*assoc. w/ first-dose postural hypotension and syncope

  • Additive effects of combining these classes of agents may cause increased risk for postural hypotension and syncope
57
Q

PDE5 Inhibitors Metabolism

A
  • PDE5 inhibitors are metabolized by cytochrome P450 enzymes in the liver, primarily CYP3A4
  • Drugs that inhibit CYP3A4 will cuase decrease clearance of PDE5 inhibitors

*erythromycin

*ketoconazole

*itraconazole

*ritonavir

*indinavir

58
Q

Stepa after a patient failes PDE-5 inhibitor therapy

A
  • Reeducate and re-challenge w/ same agent
  • Switch to another PDE-5 inhibitor
  • Try diff. therapeutic approach

*vacuum constriction devices

*PGE1 injections

*implants

RGU Exam 3 (19 decks)

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