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Endo/Repro Block2 > Male Phys > Flashcards

Male Phys Flashcards

1
Q

Where does spermatogenesis occur?

A

in the seminiferous tubules of the testes

  • it is staggered thru/o the ST’s so that all developmental phases are present at 1 time
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2
Q

compare and contrast female vs male gamete prodxn

A
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3
Q

What is a spermatogenic wave?

what is the benefit behind this?

what is the daily sperm production?

How does age affect spermatogenesis?

A

spermatogenic wave time it takes for reappearance of the samee stage w/in a given segment of the seminiferous tubule

  • BENEFIT: spermatozoa are produced continually and mature sperm are always available
  • 100 million sperm produced per day!
  • spermatogenesis continues thru/o life but prodxn decreases with age
    • positively correlated with testosterone levels
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4
Q

Describe the hormonal regulation of spermatogenesis

A
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5
Q

which cell is directly related to spermatogenesis?

A

the sertoli cell!

simple linear [direct] relationship b/w sertoli cell # & daily sperm prodxn

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6
Q

which spermatogenesis cells die with age?

What consequences does this have?

A

Leydig cells!

there is a (+) linear relationship b/w leydigs and sperm prodxn:

_Consequences: _[leydig produce testosterone]

  • decreased total & free test. levels
    • leads to increased abd fat & decreased muscle mass
      • [and decreased sperm prdxn]
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7
Q

What is andropause?

What are causes it?

what are the Sx’s?

Dx?

Tx?

A

androgen deficiency with aging

  1. Cause: decrease testicular fxn
    • loss of spermatocytes, Leydigs, sertolis–>decrease test prodxn –>^^GnRH & LH/FSH
  2. Sx’s: +/- erectile dysfxn
    • weight gain [met. shifts, reduced activity & gynecomastia]
      • also due to E:test ratio changes
  3. Dx: measure morning total test [more than 1 #, follow up w/ FSH/LH levels]
  4. Tx: HRT, sleep & eat well, exercise, Viagra-like drugs for ED
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8
Q

What are testosterone target organs?

WHat organs produce 5a reductase?

A

targets: muscle, seminal vesicle, epididymis, bone

5a-reductase: prostate, external genitalia, & skin

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9
Q

What is testosterone made by?

What do some tissues convert it to?

How does it circulate through the body [form]?

What does it bind to?

A
  • test is made by leydig cells (95%) and adrenal gland (5%)
  • test –> dihydrotestosterone [DHT] in target tissues that have 5a-reductase
  • circulating testosterone is usually bound to SHBG [sex hormone binding globulin] aka androgen binding globulin ABG when made by sertolis
    • males: 0.6 mcg/dL
    • females: 0.03 mcg/dL
  • ​binds to androgen R [AR] binds all androgens–> acts a transcription factor
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10
Q

What effects do androgens have?

A
  • promote health & fxn of:
    • seminal vesicles, prostate, genital tract, external genitalia, hair growth patterns, voice change
  • Anabolic effects:
    • muscle building
        • N+ balance; increase in protein synthesis
    • bone growth & closure of epiphysis
    • Na+ & h2o retention
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11
Q

clinically when do we use androgens?

A
  • androgenic effects: hypogonadism & hypopit fxn
  • anabolic effects: trauma, debilitating dz
    • enhance athletic performance [BAD DONT DO IT]
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12
Q

wHICH HAVE ^^ 1st pass metabolism, natural vs. synthetic androgens?

A

1st pass metabolism= natural>synthetic

  • synthetics are weak or inactive metabolites?
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13
Q

What is methyl testosterone?

what is oxandrolone?

A

methyl testosterone: test. analog

  • orally active, and esterification retards absorption & metabolism
  • SE: hepatotoxic
    • acute cholestasis [1%] & ^^risk of tumor incidence
  • USE; Test. hormone replacement

oxandrolone: DHT derivitive

  • orally active, cannot be converted by aromatase
  • low risk of hepatotoxicity
  • anabolic steroid–>promotes muscle growth
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14
Q

What are advers/SE’s of androgen therapy?

A
  • Growth interruption (premature bone closure) in growing youth
    • Aromatization of androgens to estrogen occurs at bone plates
    • Estrogen is critical for epiphyseal fusion in both young men and women.
  • •Priapism
  • •Sodium & water retention
  • •Jaundice
  • •Hepatic carcinoma
  • •Hypogonadism upon cessation due to long-term reduction in HPG axis
  • •Aggressive behavior
  • •Urinary obstruction
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15
Q

What are the gender specific adverse SE’s of anabolic steroids?

A

MEN:

  • gynecomastia, testicular shrinkage, impotence, reduced sperm count
  • baldness

WOMEN:

  • menstrual irregulariteis [shorter & lighter]
  • clitorus enlargement
  • ^^facial & body hair
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16
Q

Why do androgen anabolic steroids have so many SE’s?

A
  • they can bind to AR, glucoC R, P & E R’s ==> multiple effects
  • aromatization of AAS’s can render many adverse E effects
17
Q

When would we do medical castration?

How would we do this medically?

A

Purpose:

  • interfere w/ precocious puberty
  • Tx: androgen dependent cancers
  • reduce libido

Meds:

  • AR antagonists
  • nonpulsatile GnRH agonists
  • ” “ antagoniists
18
Q

in postemenopausal women, where are nearly all estrogen/androgens made?

Would GnRH agonists/antagonists work on these pts?

A

locally in peripheral tissues from adrenal steroid precursor DHEA

  • NO, because GnRH ant-/agonists wipe out testicular prodxn of androgens but not locally
19
Q

what drug should we use if we want to shut down HPG-axis?

A

use GnRH agonist/antagonist

20
Q

if the goal is to reduce AR signaling in prostate gland what would we use?

A

AR antagonists and/or 5a reductase inhibitors and/or GnRH antagonists

21
Q

What is cyproterone acetate?

what si it used for

A

MOA: androgen antagonist

  • also has strong activity as a progestin too

USE:

  • to reduce excessive sex drive in men
  • tx hirsuitism in women [in combo with E–> shifts balance to E dominance]
22
Q

what is gonadorelin?

uses?

A

acetate salt of human recombinant GnRH–> agonist

  • bind GnRH-R’s–> stimul8 release of FSH/LH–>increase test
  • used for fxnl assessment of gonadal response
  • male infertility: 3-6 mo of pulsatile infusion improves sperm #s

**continuous delivery shuts down HPG axis, whereas pulsatile or single dose is stimulatory

23
Q

What are degarelix?

Ganirelix & Cetrorelix?

A
  • relix = GnRH antagonists
  • binds GnRH-R’s in pit–> blocks axn of GnRH–> decreases FSH/LH –> decreases test prdxn

Degarelix: for advanced prostate cancer

  • male chemical castration
  • BPH
  • assisted reprodxn under investigation

Ganirelic, CEtrorelix: assisted reprodxn 4 ovarian hyperstim=>blox premature LH surge in females

  • major diff from GnRH agonist is the antagonist DOESNT have initial LH/FSH^^ phase
24
Q

How does an erection happen?

A
25
Q
A

Endo/Repro Block2 (11 decks)

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