Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

(OMS1) GIGU Exam > Lecture 23: Male Reproductive Physiology > Flashcards

Lecture 23: Male Reproductive Physiology Flashcards

1
Q

How do these contribute to male sexual differentiation?
SRY gene
AMH & testosterone

A
  • on the Y chromosome, TDF

- released by Sertoli and Leydig cells respectively > development of male tract and external genitalia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q 
Draw the trends for male gonadotropin secretion through these stages: 
Fetus 
Childhood
Puberty
Adult
Senescence
A

Ok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is puberty initiated?

A

Pulsatile GnRH > pulsatile FSH >LH > pulsatile testosterone and estradiol > puberty characteristics

Long acting GnRH does not trigger puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sertoli cells

Leydig cells

A
  • provide sperm nutrients and secrete fluid that transport sperm to epididymis
  • make and secrete testosterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Draw the synthesis of androgens in Leydig cells from cholesterol ester to DHT

A

Ok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens to testosterone after it is synthesized?

A
  • concentrated in the tubules by binding to androgen binding protein
  • bound to SHBG and albumin so it can circulate in blood (must be freed to be activated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is estrogen synthesized in males?

Why is it important?

A
  • aromatase converts testosterone to estradiol in tubules

- important in enhancing spermatogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the role of LH?

A

increase P450SCC affinity for cholesterol and synthesis of more of the enzyme > stimulate the conversion of cholesterol to pregnenolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Once in the circulation, how does Testosterone implement its effects?

A

diffuse to target cell and binds to Androgen receptors (AR) in the nucleus > direct protein synthesis in target cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the role of DHT?

A

-binds to ARs, plays role in development of fetal external genitalia, hair, sebaceous gland, prostate growth
(5a reductase deficiency causes ambiguous genitalia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are testosterone and metabolites excreted?

A

-mostly in urine (as urinary 17-ketosteroids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which androgens do these tissues produce?
Testis
Adrenal
Peripheral tissues

A
  • cholesterol to DHT/estradiol (testosterone pathway)
  • cholesterol to androstendione
  • testosterone to DHT/estradiol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the importance of testosterone during fetal development?

A

Presence of fetal testosterone during the 2nd month = development of penis and scrotum, internal male tract and testicular descent

Absence = default to female tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the importance of testosterone during puberty?

A

-responsible for muscle growth, epiphyseal plate closure, voice deepening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

BPH
cause
sx
tx

A
  • urethra constriction due to enlarged prostate, not necessarily elevated DHT, but possibly more DHT receptors
  • can’t pee like you want to pee (can be restricted or urgent)
  • 5a reductase inhibitors = inhibits DHT formation which is responsible for prostate growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Draw the pathway of testosterone action from Leydig to Sertoli cell

A

ok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the functions of Sertoli cells?

A

Supportive: blood testis barrier, phagocytosis, nutrient transfer
Exocrine (secretions) and Endocrine (intracellular mechanisms)

18
Q

Draw the male HPG axis and the main regulatory mechanisms

A

Ok

19
Q

Where does spermatogenesis happen?

A

-seminiferous tubule epithelium with spermatogenic cells and supportive Sertoli cells

20
Q

Draw the process/progression of spermatogenesis

A

Ok

21
Q

Characteristics of Division I of spermatogenesis

Characteristics of Division III of spermatogenesis

A
  • mitotic divisions, sperm proliferation (increases in puberty)
  • maturation phase/spermiogenesis (nuclear and cytoplasmic > morphologic changes on spermatids > sertoli cells release the mature spermatozoa)
22
Q

Be able to label the parts of the mature spermatozoa on the image

A

Ok

23
Q

What happens to the “leftover” residual bodies during spermiogenesis?

A

phagocytosed by Sertoli cells

24
Q 
Summary of the hormones effects on male phys: 
LH
FSH
GH
Testosterone
Estradiol
A
  • induce Leydig cells to make Testosterone
  • induces stertoli cells with primary spermatocytes to mature into spermatozoa
  • testis growth/maintenance
  • growth of germinal cells
  • enhances spermatogenesiss
25
Q

How is spermatogenesis regulated?

A
  • Spermatogenesis maintained by high conc. of T diffusing into Sertoli to drive maturation of sperm
  • Circulating and exogenous testosterone inhibits the activity of Hyp and AP > decrease T diffusing to Sertoli > decrease conecntration of T > decrease spermatogenesis
26
Q

What happens in the epidydymis?

A

sperm released from testis mature for a month here via increasing their motility and decapacitation (strengthening the sperm acrosome)

27
Q

Draw the trend of testosterone and sperm production throughout life

A

Ok

28
Q

What is the role of the seminal vesicles?

A

-prostaglandins from seminal vesicles reacts with cervical mucus to increase receptiveness to sperm penetration (thin the mucus out) > results in peristalsi in the uterus and tubes to propel sperm to ovary to meet egg

29
Q

What is the role of the prostate gland?

A
  • releases alkaline fluids to neutralize acidity of the seminal fluid which helps sperm motility
  • semen is a mixture of fluids from vas deferens, seminal vesicles and prostate + millions of sperm
30
Q

How is the male tract different from the female tract?

A

lumen is continuous through entire pathway and connects to the urinary tract (urine and semen both exit at urethra)

31
Q

Pathway of sperm out of the body:

A

tubules > epididymis > vas deferens > ejaculatory duct > 3 regions of male urethra

32
Q

What structures are responsible for mediating an erection?

A

2 corpora cavernosas + 1 corpus spongiosum - made up of potential cavernous spaces that can accommodate blood

33
Q

Physiology of erection:

A

PNS > NO to arteries supplying the cavernous spaces > Gc > cGMP > decrease Ca2+ in cell

effects: SM relaxation/vasodilation > increased vascular perm. > blood leaks to cavernous spaces > compresses veins > stimulates penile muscle contraction at base = erection

34
Q

Physiology of emission (semen motility before and during ejaculation)

A

SNS > SM peristaltic contraction @ vas deferens and entire tract to propel the semen out

*internal sphincter of bladder closes to prevent release of semen in bladder

35
Q

Physiology of ejaculation:

A

somatic motor neurons > rhythymic contraction of bulbospongiosus and ischiocavernosus muscles > propel semen out

36
Q

What does capacitation mean?

How is this achieved?

A
  • mature sperm activates repressed capabilities that are by contact with female fluids
  • wash inhibitory factors away, weaken acrosome by losing cholesterol, increase membrane permeability to Ca2+ to increase sperm motility
37
Q

Describe the sperm acrosome reaction

A

-Acrosomal head of sperm releases hyaluronidase (destroys the hyaluronic acid polymers around egg) and proteolytic enzymes (digest proteins that adhere the ovum) to penetrate the egg

38
Q

What happens if testosterone deficiency happens at …

2-3 months gestation
3rd trimester
puberty
post-puberty

A
  • male genitalia ambiguity
  • testicular descent problems (cryptochordism) and micropenis
  • poor secondary characteristics, eunuchoid features - looking prepubescent with features of opposite sex
  • decreased libido, erectile dysfunction, infertility
39
Q

Kallman’s syndrome:

A
  • hypogonadotropic hypothalamic dysfunction/secondary hypogonadism
  • GnRH neurons fail to migrate to hypothalamus during development. low GnRH > delayed/absent puberty, impaired smell
40
Q

Kleinfelter syndrome/seminiferous tubular dysgenesis

A

-primary hypogonadism.testicular dysfunction

  • XXY, phenotypically male, but low T due to destruction of tubules > reduced testes development and spermatogenesis
  • FSH, LH usually high trying to stimulate T release
41
Q

Male pattern baldness

Testicular tumor:

Germinal epithelial tumor

A
  • caused by increased DHT, treated with 5a reductase inhibitor
  • tumor produces more T than normal
  • no hormones produced
42
Q

What is andropause?

A

decreased LH sensitivity as men age

(OMS1) GIGU Exam (40 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions