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Repro-Endo > Male Gonad Physiology > Flashcards

Male Gonad Physiology Flashcards

1
Q

Can you measure GnRH in the serum?

A

No. It’s really only present in the hypophyseal circulation from hypothal -> ant. pit.

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2
Q

What’s Kallman’s syndrome?

A

GnRH neuron precursors fail to migrate to hypothalamus (due to KAL gene mutation)

Results in congenital hypogonadism

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3
Q

In what cell type is GnRH produced?

A

Parvi-cellular hypothalmic neurons

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4
Q

What kind of receptor is the GnRH receptor?

A

GPCR using Gq (PLC, Ca2+ pathway)

Is a MEMBRANE receptor found on the Gonadatrope cell in anterior pituitary gland

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5
Q

What’s the circadian rhythm of GnRH?

A

GnRH (and thus LH and testosterone) are highest in the early morning

Levels vary throughout day
Controlled by melatonin output of pineal gland

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6
Q

What’s the pulsatile rhythm of GnRH: what rhythms favor which gonadotropins? What happens when you have excessive frequent pulses or continuous GnRH release?

A

Pulses that occur every 60-180 minutes during the day

High freq -> LH secretion
Lower freq -> FSH
Abnormal (severe stress, eg.) -> inhibition of gonadotropins

Controlled by sex steroid feedback–> Initially frequent pulses lead to increase in LH/FSH but eventually get GnRH receptor down-reg and get LOW LH and FSH

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7
Q

What’s a pharmacological GnRH receptor agonist?

A

Leuprolide

probs not important for this lecture. Used to treat hormone-dependent and for chemical castration

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8
Q

What cells does FSH stimulate in males? How about LH? What does each cell make in response to this stimulation?

A

FSH -> Sertoli -> Inhibin B

LH -> Leydig -> Testosterone

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9
Q

Are LH and FSH co-secreted?

A

No, they appear to be in different granules. (but high levels of one can have crossover effects)

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10
Q

What provides negative feedback to FSH and LH secretion?

A

FSH: inhibin B
LH: testosterone (acts on both hypothal and ant. pit.)

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11
Q

What kind of receptors are those for FSH and LH?

A

Both are GPCRs using Gs-alpha (increases cAMP)

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12
Q

Major effect of LH?

A

Increased testosterone production

Stimulates Leydig cells to produce testosterone

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13
Q

Major effect of FSH?

A

Spermatogenesis and spermiogenesis
(Acts on Sertoli Cells in the testes)
Also results in production on INHIBIN B

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14
Q

What cells in males have aromatase? What is the effect of estradiol on the HPT axis?

A

Sertoli and peripheral tissues make estradiol.

Decreases LH and FSH response to GnRH.

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15
Q

What’s the major difference in the HPT axis between pre and post-puberty?

A

Pre-puberty, GnRH secretion is very sensitive to negative feedback from steroid hormones.
Afterward, negative feedback is reset to allow larger FSH and LH pulses.

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16
Q

What induces Leydig cells to proliferate and produce T during early gestation?

A

hCG

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17
Q

Where do Leydig cells come from, embryologically?

A

Mesenchymal cells adjacent to renal system… the migrate into the intersitium around sex cords. (probably not important?)

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18
Q

6 intracellular features of Leydig cells?

A

1) Cholesterol droplets.
2) Lots of mitochondria.
3) Lots of smooth ER.
4) Lots of Golgi.
5) Lipofuscin granules.
6) Reinke’s crystals…. which are mysterious.

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19
Q

What’s the rate limiting step of steroid synthesis? What protein accomplishes this? THIS WILL BE ON EXAM***

A

Transport of cholesterol across inner mitochondrial membrane.
via Steroidogenic Acute Regulatory (StAR) protein .
(this IS probably important)

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20
Q

What does T do in the plasma?

A

It binds proteins (SHBG and albumin).
Free T has a short half-life.

Free amount is what can ACT on receptors

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21
Q

What’s more potent than T?

A

DHT

22
Q

Must the Androgen Receptor dimerize to do its work?

A

Yes, it must.

23
Q

How does proliferation of Sertoli cells change in infant vs. adults?

A

In children, Sertoli cells are very mitotic.

Sertoli proliferation stops afer the first meiotic division of germ cells (i.e. when puberty starts).

24
Q

What is the effect of Androgen Binding Protein?

A

It allows T concentration in Sertoli cells to be 100x that in the circulation.

25
Q

4 ways Sertoli cells support spermatogenesis?

A

1) Create specialize microenvironment.
2) Give lots of T to the GCs (though they don’t make it).
3) Gap junctions between Sertoli’s and GCs.
4) Transport GCs toward lumen.

26
Q

2 reasons why it’s good to have a Blood-Testis-Barrier?

A

Isolation of haploid GCs (from toxins and immune system).

Allows separate microenvironment (so SC can nurse germ cells to maturity)

27
Q

Which germ cells replicate to maintain a supply of stem cells?

A

Type Ad (dark)

28
Q

Which germ cells replicate to produce a clonal population that goes on to meiosis / differentiation?

A 
Type Ap (pale)
...once they differentiate, they're called Type B.
29
Q

Review: What does spermiogenesis refer to?

A

Morphological changes of spermatid into actual spermatozoan.

30
Q

4 stages of spermiogenesis?

A

Golgi phase - polarity established.
Cap phase - nucleus condensation, acrosomal cap.
Acrosome - tail develops, acrosome matures
Maturation - extrusion of excess cytoplasm (residual bodies)

31
Q

Can exogenous testosterone induce spermatogenesis in pre-pubertal males?

A

No, but T-producing Leydig tumors can. The T has to be local due to the whole Testosterone Binding Protein thing…

32
Q

What is primary hypogonadism? Signs?

A

Testicular defect causing infertility.

Signs: Infertility precedes low T, FSH is often elevated (due to decreased Inhibin being made by SC’s)

33
Q

What is secondary hypogonadism? Signs?

A

Not enough gonadotropins or GnRH. T often low.
Infertility and T occur simultaneously.
FSH and LH are low or inappropriately normal.

34
Q

How do you diagnose hypogonadism?

A

Multiple morning measurements of T, “consistent signs and symptoms,” infertility…

  • Oligo or azoospermia may also suggest infertility
35
Q

Sequelae of hypogonadism?

A

It varies with time of onset… but predicable defects in internal and external sexual development.

1) 1st Trimester: Ambiguous genitalia, hypospadias
2) 2/3rd Trimester: Micropenis, undescended testes
3) Childhood: Delayed/abesent puberty, small penis, eunuchoid body proportions
4) Adult: Gynecomastia, infertility, low libido, loss of body hair, ED, hot flashes

36
Q

What are FSH, LH, and T levels in isolated spermatogenic failure?

A

Only FSH is elvated. Others normal

37
Q

What are FSH, LH, and T levels in isolated obstructive infertility?

A

All normal

38
Q

What are FSH, LH, and T levels in testicular failure (primary hypogonadism)?

A

FSH and LH high, but T remains low.

39
Q

What are FSH, LH, and T levels in secondary hypogonadism?

A

FSH and LH are low or normal, T is low.

40
Q

What are 2 common causes of congenital primary hypogonadism?

A 
Klinefelter syndrome (47 XXY)
Cryptorchidism
41
Q

3+ causes of acquired primary hypogonadism?

A

Torsion
Chemotherapy/medications/toxins
Mumps orchitis
Other: (trauma, radiation, cancer, etc. etc.)

42
Q

Causes of secondary hypogonadism?

A

There are lots:
Kallman’s syndrome (no GnRH producing neurons)
Anything that damages pituitary/hypothalmus (masses, infection, metabolic)
Medications (esp. opiates)

43
Q

What was mentioned as a genetic cause of infertility?

A

Y chromosome microdeletions

these mutations a probably hard to pass on…

44
Q

3 treatments for hypogonadism?

A

1) T replacement (may help symptoms but worsen infertility).
2) Gonadotropin replacement (if secondary) for fertility.
3) Testicular sperm extraction (TESE).

45
Q

What is a hormone?

A

Chemical messenger with specific action (i.e. causes conformational change in a receptor)

46
Q

What 2 types of receptors do hormones act on (i.e. what 2 did he mention in lecture)?

A

1) Act on MEMBRANE receptors that go via 2nd messenger signaling (GPCR)
2) Nuclear receptors (such as steroids)

47
Q

What is co-secreted with GnRH?

A

56AA GAP (GnRH Associated Protein)

48
Q

WHERE is GnRH secreted into?

A

Hypothalamo- Hypophyseal Portal System

Is the connection between brain and pituitary gland (capillary systems that are connected at both ends but don’t go through heart)

49
Q

What is the structure of LH and FSH? What are they structurally similar to? What is different?

A
  • Glycoproteins made of Alpha and Beta subunits
  • Common Alpha unit with hCG and TSH
  • Beta unit is unique and confers activity (what is measured for hCG in pregnancy test)
50
Q

4 Big Features of Sertoli Cells?

A

1) They are POLARIZED–> helps coordinate timeline of sperm maturation, can adapt shape
2) Secrete substances that support/nourish sperm (cytokine, prostaglandins)
3) Make Inhibin B, AMH, and contain aromatase so they make Estradiol (may have role in sperm maturation)
4) Determine Testes volume (dependent on # of Sertoli and germ cells )- make up 1/3rd of germinal epithelium

51
Q

Causes of congenital primary hypogonadism?

A
  • Klinefelter (XXY)- incomplete puberty, infertility, eunuchoid body, cyrptorchidism (at risk for testicular cancer)

Repro-Endo (60 decks)

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