Male Physiology Flashcards

1
Q

Male reproductive hormones and where they come from

A

hypothalamus: GnRH
ant pituitary: FSH and LH
testes: inhibin b and testosterone

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2
Q

FSH function

A

acts on Sertoli cells
promotes Sertoli function (spermatogenesis)
Sertoli secrete inhibin b
inhibin b is negative feedback to prevent further FSH secretion from pituitary (but no feedback to GnRH)

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3
Q

LH function

A

acts on Leydig cells
promotes Leydig function (testosterone release)
testosterone acts on many body tissues
testosterone feeds back onto BOTH hypothalamic GnRH and pituitary LH

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4
Q

How does an increase in testosterone above normal levels possibly cause infertility?

A

testosterone feeds back onto hypothalamic GnRH
prevents downstream release of FSH
less stimulation of Sertoli cells

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5
Q

Which loop FSH/LH has long feedback loop onto hypothalamus

A

testosterone feeds back all the way to hypothalamus (and ant pituitary ie LH release)
inhibin b from Sertoli cells only feeds back onto FSH release from ant hypothalamus

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6
Q

How long does it take for sperm to get from little baby sperm all the way to mature sperm?

A

2 months

this is important because toxic exposure can decrease sperm production for up to 2 months until new sperm are produced

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7
Q

Why are sperm not destroyed by the man’s immune system?

A

Sertoli cells create a blood-testes barrier

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8
Q

Sertoli cells make men men embryologically

how

A

Sertoli cells secrete Müllerian inhibiting substance

prevents from embryo remaining female

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9
Q

Spermatogenesis is sensitive to what hormone level

A

testosterone

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10
Q

Why does taking exogenous testosterone cause testicular atrophy

A

decreases GnRH and LH levels
testicles not stimulated to produce testosterone
tissue isn’t needed to it atrophies

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11
Q

Inhibin b is produced by

A

Sertoli cells

in response to FSH

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12
Q

Testosterone is produced by

A

Leydig cells

in response to LH

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13
Q

Testosterone is anabolic/catabolic

A

anabolic

promotes protein synthesis and muscle growth

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14
Q

How does testosterone affect bones

A

testosterone promotes closure of epiphyseal plates

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15
Q

How to test for hypotestosteronemia

A

> 1 low testosterone value
==> follow up with FSH/LH levels
*really LH is the one that matters

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16
Q

How is testosterone transported in the blood

A

on SHBG (sex hormone binding globulin)

17
Q

The testosterone receptor is what type of receptor

A

nuclear receptor

creates homodimer

18
Q

GnRH receptor

A
Gq receptor (queer)
activates PKC
19
Q

Why are oral androgens hard to do?

A

first pass metabolism

20
Q

Methyl-testosterone
MOA
Tox

A

MOA: testosterone replacement
Tox: hepatotoxic

21
Q

Oxandrolone
MOA
TU
Tox

A

MOA: DHT derivative, cannot be converted w/ aromatase
TU: muscle growth
Tox: decreased risk of hepatotox compared to methyltestosterone

22
Q

Flutamide
MOA
TU
Tox

A

MOA: antagonist at androgen receptor
TU: prostate ca
Tox: gynecomastia, hepatotox

23
Q

Bicalcutamide
MOA
TU
Tox

A

MOA: antagonist at androgen receptor
TU: prostate ca
Tox: gynecomastia, hepatotox

24
Q

Nilutamide
MOA
TU
Tox

A

MOA: antagonist at androgen receptor
TU: prostate ca
Tox: gynecomastia, hepatotox

25
Q

Spironolactone and androgens

Tox

A

androgen antagonist, 17α reductase inhibitor, and 17,20-desmolase inhibitor
Tox: gynecomastia

26
Q

Gonadorelin
MOA
TU

A

MOA: GnRH agonist
TU: functional assessment of gonadal response, male infertility (when given in pulsitile nature)

27
Q

Which drug can be given to help with male infertility

A

gonadorelin

GnRH agonist

28
Q

Leuprolide
MOA
TU

A

MOA: GnRH synthetic agonist
TU: castration for cancer, initial surge in FSH and LH followed by desensitization for androgens

29
Q

-relix (degarelix, ginirelix, cetrorelis)
MOA
TU

A

MOA: GnRH antagonists
TU: advanced prostate cancer (degarelix)

30
Q

Finasteride
MOA
TU
Tox

A

MOA: 5α-reductase inhibitor (prevents testosterone -> DHT conversion)
TU: BPH, male pattern baldness

31
Q

Ketoconazole and adrogens

A

prevents androgen synthesis via 17,20-desmolase inhibition

32
Q

Tamsulosin
MOA
TU

A

MOA: α1a,d antagonist on prostate, vs α1b on vascular receptors
TU: BPH

33
Q

-fils (sildenafil, vardenafil, tadalafil)
MOA
TU
Tox

A

MOA: phosphodiesterease 5 inhibitors
TU: erectile dysfunction
Tox: headache, flushing, dyspepsia, cyanopia (blue-tinted vision), LIFE THREATENING HYPOTENSION in patients taking nitrates