Sperm Storage, Transport, and Male Sexual Dysfunction Flashcards Preview

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Flashcards in Sperm Storage, Transport, and Male Sexual Dysfunction Deck (23):

Describe the process of ejaculation based on its component parts

Sperm is produced in the testes and stored in the epipdidymis until ejaculation, where it travels via the vas deferens to the ampulla where it is combined with semen (fluid) from seminal vesicles, and together they travel through the prostate gland to the urethra


Where is sperm made?

seminiferous tubules (seperated by septa). The seminiferous tubules connect to the retes testes and then to the epididymis, consisting of a head, body and tail region


Describe seminiferous tubules

Outlining these tubules is a basement membrane lined with fibrolasts, and around/ in-between the tubules lies interstitial cells (aka Leydig cells- produce testosterone) and capillaries. Within the tubules lie nurse cells (Sertoli cells) on the periphery that help sperm production. Sperm production begins on the outer-most periphery of the tubules in sperm stem cells (spermatogonia) which develop and move inward toward a lumen of the tubule by dividing via mitosis and meiosis to produce almost-mature spermatozoa. 


What happens to spermatozoa?

It isnt properly mobile, so it goes to the epididymis to mature and for storage until ejaculation


Describe spermatogenesis

Diploid permatogonia (2N, 46) divide via mitosis to produce diploid primary spermatocytes (4N, 46) (daughter cells), which then undergo two meioses to produce haploid secondary spermatocytes (2N, 23) and finally haploid spermatids (N, 23) to complete spermatogenesis. After spermatogenesis is complete, a process called spermiogenesis begins that allows spermatids to develop into immature spermatozoa (loss of cytoplasmic contents and gain or acrosomal cap) that can travel to the epididymis

NOTE: impaired tail mobility can lead to infertility (seen in ciliary dyskinesia/Kartagener's syndrome)


Describe the other components of semen

Sperm from the vas deferens combines with seminal fluid containing fructose and prostaglandins from the seminal vesicles in the ejaculatory duct and then pass through the prostate (where prostate fluid is secreted to make up the additional 30% of the semen fluid) and then to the urethra. After passing through the prostate, the bulbo-urethral glands add a thick alkaline fluid that neutralizes an acidic fluid from the urethra

A typical ejaculation contains about 2-5 ml of semen and about 20-100 million sperm cells


How is the flaccid vs. erect state of the penis maintained

Centrally-perceived sensual stimuli are relayed to a spinal cord center involving sympathetic nerve fibers at levels T-10 to L2, and to another involving parasympathetic nerves at levels S2-S4. Tonic activity of the sympathetic neurons maintains flaccidity. Stimulation of the parasympathetic sacral segments produces erection.


Erection notes

Erection may occur in response to central stimuli (psychogenic erection) or in response to tactile stimulation of the penis via a direct sacral reflex arc (reflex erection).

In addition, nonsexual, nocturnal erections normally occur 3-4 times/night during periods of REM sleep, beginning with adolescence.

Most men are aware of an erection when they awaken in the morning. Early morning erections demonstrate physiologic ability to attain erection; asking patients about the presence or absence of erections on awakening can therefore help differentiate organic from psychogenic causes of erectile dysfunction. 


Important things to know about erection

 1) sacral parasympathetic input is responsible for tumescence (erection);

2) the thoracolumbar sympathetic pathway is responsible for detumescence (flaccid state);

and 3) emission of semen (as opposed to erection) is a sympathetic event. (mnemonic: “Point and Shoot” [parasympathetic vs. sympathetic])



What are the absolute prerequisites for erection?

 a) an adequate arterial inflow; and b) sufficient nitric oxide synthase activity to generate nitric oxide


How does erection occur?

Normally, sympathetic output maintains a flaccid state, but given an appropriate stimulus, parasympathetic putput from spinal segments S2-S4 activate NOS which promote the synthesis of NO via cGMP mechanism to produce cavernous smooth muscle relaxation and artery engorgement


What are some causes of decreased libido?

•Medications (e.g., SSRIs, anti-androgens, 5-alpha-reductase inhibitors, and opioids)
•Alcohol or other recreational drug use
•Relationship problems
•Systemic illnesses
•Testosterone deficiency


How is Erectile dysfunction (ED) defined?

Defined as the consistent or recurrent inability to acquire or sustain an erection of sufficient rigidity and duration for sexual intercourse. It is the most common sexual problem in men.


The prevalence of ED increases with age, with a range of 8% during the 3rd decade and increasing to 37% of men aged 70-75. Still, ED should not be simply be attributed to “age”.

Many of the causes of ED are more common as men age, and specific diagnoses should be identified.


In addition to age, what are the best predictors of ED?

Diabetes, hypertension, obesity, dyslipidemia, cardiovascular disease, smoking, and medication use. Of note, many of these are classic cardiovascular (CV) risk factors. It should therefore not be surprising that ED may be an early warning sign of future CV events, suggesting that CV screening of men with ED may be prudent.


How should ED be evaluated?

Evaluation of ED begins with a history (including detailed psychosexual history) and focused physical examination. The H & P has a 95% sensitivity for ED, but only a 50% specificity as to cause. Therefore, additional testing is often necessary. 

Psychogenic factors and medications are most common causes of ED that deserve special attention in the diagnostic evaluation. History should assess libido, rapidity of onset of ED, and psychosocial status and stressors. Performance anxiety is a psychogenic cause suggested by a history of no sexual problems until “one night when I could not perform” followed by persistent ED.

Complaints of ED accompanied by other times of normal erections (e.g., nocturnal or early morning erections or satisfactory erections with masturbation) is suggestive of psychogenic causes. Similarly, inability to maintain erection following vaginal penetration is most commonly due to anxiety (but may also be due to venous leak from subtunical veins). Complete loss of nocturnal erections is seen in men with neurologic or vascular causes. Men with testosterone deficiency are still capable of exhibiting some nocturnal erectile activity. 


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List the specific therapies for ED in order.

1.Oral type 5 phosphodiesterase inhibitors (e.g., sildenafil)*

2.Intraurethral alprostadil suppositories*

3.Intracavernosal vasoactive drug injection*

4.ÜVacuum erection device

5.Surgery (penile prosthesis)


How is premature ejaculation defined?

by 3 features: 1) brief ejaculatory latency; 2) lack of control of ejaculation; and 3) psychological distress in the patient and/or partner.

Approximately 30% of men describe PE, though few seek treatment. About 30% of these have concurrent ED. Couples therapy, behavioral approaches, manual techniques, topical anesthetic agents (in condoms), and SSRIs are all possible therapies.


Normally, the internal bladder neck sphincter contracts during ejaculation, ensuring the semen is propelled into the urethra. Retrograde ejaculation of semen into the bladder can instead occur if the bladder neck is damaged during prostate surgery or if there is interruption of the a-adrenergic impulses normally responsible for constriction of the bladder neck sphincter. The result may be described by patients as a “dry ejaculate”. Such men may present for evaluation of infertility.

Retrograde ejaculation is suggested by low-volume ejaculates with low sperm counts, but the presence of ample sperm in post-ejaculatory urine specimens. Not surprisingly, retrograde ejaculation may be caused by a-adrenergic blockers.


Hematospermia is the presence of blood in the semen. Although alarming to patients, it is usually benign and self-limited when seen in men under 40.


What are the main causes of hematospermia?

Infection accounts for about 40% of cases in which a cause is determined.


How should hematospermia be evaluated?

No further evaluation or treatment may be needed in younger men without risk factors for GU disease or associated symptoms.

A urinalysis, urine culture, and studies for gonorrhea and chlamydia should be obtained in patients with ongoing lower urinary tract symptoms.

Older age, suspicion of prostate cancer, or persistent or recurrent symptoms should prompt further evaluation and/or referral.