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Medical Physiology > Exam #4: Male Reproductive Physiology > Flashcards

Exam #4: Male Reproductive Physiology Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the function of the epididymis?

A

Remember that the epididymis connects the rete testis to the vas deferens. The functions of the epididymis include:

  • Storage, maturation and transporation of sperm
  • Development of sperm motility
  • Reabsorption of aging sperm

*Note that H+ ions are secreted to maintain the sperm in an inactive state

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2
Q

What is the function of the vas deferes?

A

Remember that the Vas deferens connects the epididymis to the seminal vesicles. The functions of the Vas Deferens include:

  • Storage of sperm in the ampulla
  • Transportation of sperm

*Note that the ampulla contracts during ejaculation to propel sperm into the proximal urethra/ allows sperm to mix with prostatic and seminal vesicle fluids

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3
Q

What is the function of the seminal vesicle?

A
  • The seminal vesicle produces roughly 60% of the fluid portion of the ejaculate i.e. semen
  • Seminal fluid or semen consists of:
    1) Fructose= energy for sperm
    2) Prostaglandin= make the cervical environment more favorable for sperm survival & promote peristalsis of the uterus/ fallopian tubes
    3) Fibrinogen= coagulation of semen that holds semen in deeper regions of the vagina and cervix
    4) Seminogelin= suppresses motility of sperm in the coagulated semen
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4
Q

What is the function of the prostate gland?

A

The prostate gland secretes a milky fluid that constitutes roughly 39% of the fluid of semen and contains:

1) Ca++
2) Citrate
3) Prostatic acid phosphatase
4) Profibrinolysin= activated to plasmin that dissolves coagulated semen & frees sperm
5) HCO3 (bicarbonate)= neutralizes the acidic environment of the cervix, allowing sperm to become more motile
6) Prostate Specific Antigen (PSA)= hydrolyzes seminogelin, which causes sperm to become more motile

*****Note that PSA is a biomarker for prostate cancer

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5
Q

What is the function of the bulbouretheral gland?

A

Secretion of mucous into the urethra upon arousal

  • Functions as a lubricant in the urethra
  • Cleans the lumen of the urethra

*Note that the bulbouretheral gland is also known as “Cowper’s Gland”

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6
Q

What are Leydig cells? What is the function of the Leydig cells?

A
  • Endocrine cells that secrete testosterone
  • These cells are contained within the “peritubular compartment” of the testes, or the spaces between the tubules of the testes
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7
Q

What are Sertoli cells? What is the function of the Sertoli cells?

A
  • Sertoli cells are cells contained with in the seminiferous tubules, or in the “intratubular space”
  • Functions
    1) This is where spermatogenesis occurs
    2) Production and secretion of Androgen Binding Protein (ABP), which binds and concentrates testosterone in the area of spermatogenesis
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8
Q

Where is GnRH synthesized and released?

A

Hypothalamus

*Note that it is released in a pulsatile fashion that is controlled by the pulse generator in the hypothalamus

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9
Q

What is the function of GnRH?

A

Influences the release of the pituitary gonadotropes

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10
Q

Where is LH produced?

A

Anterior pituitary

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11
Q

What is the function of LH?

A
  • Binds receptors on Leydig cells and stimulates testosterone production/ secretion
  • Testosterone then diffuses to Sertoli cells to facilitate spermatogenesis
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12
Q

Where is FSH produced?

A

Anterior Pituitary

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13
Q

What is the function of FSH?

A

Stimulation of Sertoli cells to produce ABP

- ABP concentrates testosterone at the site of spermatogenesis

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14
Q

Why is it important to pulsatile secretion of GnRH?

A
  • Constant high levels of GnRH causes a desensitization of GnRH receptors
  • This can lead to a reduction in LH and FSH release
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15
Q

Outline the specific mechanism of action of LH on Leydig cells.

A

LH induces cholesterol to be converted into Testosterone

  • LH binds to a GPCR on the Leydig cell
  • cAMP increases (Gas)
  • PKA increases
  • Increased synthesis of steroidogenic enzymes that control testosterone synthesis

*Note that the testosterone produced by the Leydig cells with diffuse into the Stertoli cells and stimulate spermatogenesis

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16
Q

What is Estradiol? Where is Estradiol produced and what is its function?

A

Estradiol is a product of testosterone

  • Estradiol is produced in the Sertoli cells
  • Sertoli cells contain the enzyme Aromatase
  • Aromatase converts Testosterone into Estradiol
  • Estradiol diffuses back into the Leydig cells
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17
Q

Outline the specific mechanism of action of FSH on Sertoli cells.

A

Like LH, FSH binds to a GPRC on the Steroli cells

  • Gas subunit activation increases cAMP
  • PKA is increased
  • Aromatase, ABP, and Inhibin are all produced in response to FSH binding to the Steroli cell
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18
Q

How is Testosterone synthesized? Draw & label the synthesis pathway of Testosterone & DHT synthesis. What is the rate-limiting enzyme?

A
  • The rate limiting step of the production of Testosterone is the conversion of cholesterol to pregnolone via Cholesterol desmolase
  • Pregnolone is converted by 17alpha-hydroxylase into intermediate products
  • 3B-hydroxysteroid dehydrogenase (3B-HSD) makes Androstenedione
  • 17B-Hydroxysteroid dehydrogenase cleaves Androstenedione into Testosterone

*****Note that Testosterone is converted into the DHT by 5a-reductase

19
Q

How does testosterone production change throughout life?

A
  • Spike in the fetal development to form male genitalia
  • Spike in the neonate
  • Spike in puberty and reaches a peak in adulthood

*Note that Testosterone production is not constant throughout the day either

20
Q

How is testosterone transported in the blood?

A

Testosterone binds albumin in the blood & SHBG (sex-hormone-binding globulin)
- Note that the MAJORITY of testosterone is BOUND to albumin or SHBG, only a small amount is actually available

21
Q

Why is there a decrease in testosterone production with age?

A
  • Synthesis of Testosterone decreases with age
  • Increased SHBG with age leads to a decrease in the bioavaliablity of Testosterone

Thus, there is a combinatorial effect of these two mechansisms

22
Q

What is the risk of testosterone replacement therapy?

A

Increased risk of prostate cancer

23
Q

What is the mechanism of Testosterone when it reaches a target cells?

A

1) Diffuses across membrane of target cell (lipophilic)
2) Binds to the androgen receptor in the nucleus
3) Altered gene transcription

24
Q

How does the affinity of DHT for the androgen binding receptor compare to Testosterone?

A

The affinity of DHT is far greater than that of Testosterone

25
Q

What receptor does estradiol bind to?

A

Estrogen receptor

26
Q

What are the effects of Testosterone?

A
  • Internal Genitalia
  • Skeletal muscle= increased mass and strength during puberty
  • Erythropoiesis= increased production of RBCs, which is why males have a higher hematocrit than females
  • Bone= strengthens bone
27
Q

What are the effects of DHT?

A

External Genitalia

Hair= increased male hair growth during puberty

28
Q

What are the effects of Estradiol?

A
  • Bone= main regulator of bone i.e. increased bone density and epiphyseal closure
  • Libido
29
Q

What are the metabolic effects of testosterone?

A
  • Stimulates resting metabolic rate

- Inhibits lipid accumulation in adipocytes, stimulates lipolysis, and inhibits differentiation of adipocyte precursors

30
Q

Describe the hormonal control of spermatogenesis.

A

Testosterone & FSH act on the Sertoli cells to induce spermatogenesis
Testosterone
- Stimulates transcription of genes in Sertoli cells that mediate spermatogenesis
- Gets converted to estradiol via Aromatase, which is thought to facilitate spermatogenesis

FSH

  • Increases synthesis of ABP–>concentration of Testosterone
  • Aromatase= Testosterone–>Estradiol
31
Q

Why can anabolic steroid administration reduce spermatogenesis?

A

Anabolic steroids are a derivative of Testosterone that inhibits LH & FSH production via a negative feedback mechanism

  • Decrease in testosterone
  • Decreased FSH –> significant decrease in ABP

**Unable to concentrate Testosterone at the site of spermatogenesis without ABP

32
Q

Describe the process of spermatogenesis.

A

1) Spermatogonia= primordial germ cells that have migrated to the basal compartment of the seminiferous tubules
2) Primary spermatocyte= passes through tight junctions into the adluminal compartment
3) Secondary spermatocyte= 1st round of meiosis
4) Spermatid= 2nd round of meiosis

Maturation of spermatids via spermiogenesis= differentiated mature sperm that are released into the lumen of the seminiferous tubules

33
Q

What is spermiation?

A

Release of mature sperm (spermatozoa) into the lumen of the seminifierous tubules

34
Q

What is spermiogenesis? What are the steps of spermiogenesis?

A

Spermiogenesis is the process by which spermatids differentiate into spermatozoa or mature sperm
- Under the control of FSH

1) Acrosomal vesicle buds off the golgi apparatus to form the acrosomal cap
2) Centrioles bud to form the flagellum

35
Q

Why are tight junctions between Sertoli cells important?

A

Tight junctions provide the blood-testis barrier; after genetic recombination the sperm cells are different enough from self that the body would mount an immune response against them if these tight junctions did not exist

36
Q

What is the spermatogenic wave?

A
  • Spermatogenesis occurs along the length of the tubules in successive cycles
  • New cycles are initiated every 2-3 weeks

This ensures that males are always fertile

37
Q

What is hypergonadism?

A

Excess androgen activity that can lead to precocious puberty

Causes include:

  • Hypothalamic tumor treated with long term agonist that desensitizes receptors
  • Mutations of LH receptor
  • Congenital adrenal hyperplasia
  • Androgen-producing tumors
38
Q

What is primary hypogonadism?

A

Testicular dysfunction leads to a decrease in testosterone production caused by Cryptorchidism or Kleinfelter’s (males with an additional X chromosome)

  • Decreased Testosterone leads to lack of negative feedback thus:
  • Increased GnRH
  • Increased LH & FSH

*Also called hypergonadotropic hypogonadism

39
Q

What is secondary hypogonadism?

A

Decrease in circulating gonoadotropins due to a lesion in then hypothalamus or the pituitary gland

  • Decrease in circulating gonadotropes
  • Decreased testosterone in the setting of low LH & FSH

*Also called hypogonadotropic hypogonadism

40
Q

What are the stages of the male sexual act? Note whether the stage is PNS, SNS, or spinal reflex induced.

A
  • Erection- PNS
  • Lubrication- PNS
  • Emission- SNS
  • Ejaculation- Spinal reflex
41
Q

Describe the anatomy of an erection.

A

1) During arousal there is a PNS induced dilation of the penile arteries or the corpus cavernosum and corpus spongiosum
2) Veins are compressed, maintaining erection

42
Q

What terminates an erection?

A

Vasoconstriction mediated by the SNS

43
Q

What is the molecular mechanism of an erection?

A
  • PNS releases: ACh, NO, and VIP that cause dilation in the cavernous smooth muscle
  • NO activates guanylyl cyclase, causing an increase in cGMP
  • cGMP decreases Ca++
  • Decreased Ca++ leads to smooth muscle relaxation

*Note that cGMP is broken down by a phosphodiesterase

44
Q

What is the mechanism of viagra?

A

Antagonism of the phosphdiesterase the breaksdown cGMP

Medical Physiology (74 decks)

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