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Physiology 606 > Male Repro Disorders > Flashcards

Male Repro Disorders Flashcards

1
Q

Sertoli cell functions:

  • Forms _____
  • Nourishes _____
  • ____ function (defective cells, cytoplasm)
  • Produces _____ _____ fluid (unique)
  • Produces _____ _____ protein - brings androgens into semiferousl tubules
  • Site of hormonal action on spermatogenesis
  • Secretes ____ ____ factor in fetus
A
  • Blood testis barrier
  • developing sperm cells (lactate)
  • phagocytic
  • seminiferous tubule
  • androgen binding protein
  • mullerian-inhibiting factor
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2
Q

explain the biosynthesis of androgens (testosterone)

A

CHL –> PREG –> 17-hydroxypreg –> DHEA –> androstenedione –> testosterone

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3
Q

testosterone effects vs DHT effects?

A

testosterone: gonadotropin regulation, spermatogenesis, sexual differentiation (wolffian stimulation)
DHT: external virilization, sexual maturation at puberty

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4
Q

testosterone receptors (androgen receptors) have higher affinity for ______, but _____ is low in blood concentration

A

DHT, DHT

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5
Q

adipose tissue is high in _____ activity

A

aromatase, leads to higher E2 levels

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6
Q

regulation of testicular function:

  • _____ and ____
  • Pulsatile secretion of _____ —–> ______, _____
  • feedback control of testicular function via _____ and _____
A
  • FSH, LH
  • GnRH—> LH, FSH
  • testosterone (leydig cells) and inhibin (Sertoli cells)
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7
Q

_____ selectively inhibits LH secretion

______ selectively inhibits FSH secretion

A

testosterone

inhibin

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8
Q

____ acts on leydig cells leading to testosterone production

____ acts on Sertoli cells leading to production of inhibin

A

LH

FSH

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9
Q

_______ maintains high [testosterone] in seminiferous tubule

A

androgen binding protein

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10
Q

____ and ____ initiate puberty

A

FSH and testosterone

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11
Q

______ important for mitosis/meiosis

______ involved in spermatid remodeling/maturation

A

testosterone

FSH

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12
Q

pathological changes in male reproductive system

  • Fetal stage: _____ and _____
  • pubertal stage: ____ and _____
A
  • sexual differentiation and cryptochordism

- absence or precocity of puberty (disfunction of gonadostat) and/or feminizing or masculinizing possible

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13
Q

Hypogonadism - infertility:

  • Much more common than hypergonadism
  • Non-endocrine usually arise in _____ (endocrine occur ____)
  • commonly reduced _____ or _____ sperm
  • causes: _____ or _____ defects (trauma, viral orchitis, radiation, chemotherapy, autoimmune, environment toxins, systemic diseases)
A

-adults (endocrine causes occur earlier)

  • quantity/motility of sperm
  • structural or acquired defects
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14
Q

Endocrine Hypogonadism:

  • prepubertal –> ________
  • adult –> _______
  • Primary hypogonadism: (________hypogonadism) = ______ (e.g Klinefelter’s syndrome), ____ levels of LH and FSH
  • Secondary hypogonadism (_________ hypogonadism) = loss of _______ (e.g., Kallman’s syndrome)
A
  • failure of sexual maturation = eunuchoidism
  • infertility
  • hypergonadotrophic hypogonadism: testicular failure, HIGH levels of FSH/LH
  • hypogonadotrophic hypogonadism: loss of FSH/LH
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15
Q

clinical features of eunuchoidism:

  • eunuchoidal skeleton = ______, _________
  • lack of ______
  • ____ voice
  • ____ genitalia
  • poor ______ development
  • increased _____
A
  • elongation, failure of epiphyseal plate to close due to lack of androgens
  • lack of adult body hair distribution
  • high-pitched voice
  • infantile genitalia
  • poor muscle development/strength
  • baby fat: androgens are lipolytic, when absent leads to persistent baby fat
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16
Q

endocrine hypergonadism:

  • hypersecretion rare in adults
  • more common, dramatic in youth (_____/____)
  • _______ (neurogenic (tumor in pit or hypothalamus) or idiopathic (gonadostat reset too early) = excessive pituitary LH/FSH)
  • _______(LH tumors or adrenal androgens - congenital adrenal hyperplasia)
A
  • sexual development/cessation of growth
  • precocious puberty
  • pseudo-precocious puberty
17
Q

defects in androgen target tissues:

  • leads to partial or total loss of _____
  • causes male ____________
  • Major causes –> ________ or ________
A
  • androgen action
  • Pseudohermaphroditism (male appears to have both male and female sex characteristics)
  • 5 alpha-reductase deficiency or target resistance to androgens
18
Q

5alpha-reductase deficiency:

  • loss of _______
  • 46, XY Male with ________
  • Normally differentiated ____,____
  • ambiguous _____
  • Puberty - striking but selective signs of ______ (deep voice, muscle mass, penis enlarges, libido increases) why?
A
  • testosterone conversion to DHT
  • Pseudohermaphroditism (autosomal recessive)
  • testes, male ducts
  • external genitalia
  • masculinization, bc they are testosterone driven, not DHT driven
19
Q

Target organ resistance to androgens:

  • 46, XY male with ______
  • elevated _____ + ____ levels
  • Produces “____ ____ ____”
  • abdominal ____, vestigial ____
  • unambiguous ______, blind _____
A
  • X-Linked recessive disorder (androgen receptor on X-chromosome from mother)
  • androgen and LH levels (and estrogen) - (because no androgen receptor in brain to cause negative feedback)
  • “testicular feminization syndrome”
  • abdominal testes, vestigial Wolffian Ducts
  • unambiguous female genitalia, blind vagina
  • Mullerian ducts don’t develop bc MIF is still present
20
Q

differentiate between a 5alpha-reductase deficiency and a target resistance to androgens.

A
  • with a 5alpha-reductase deficiency testosterone is present and producing effects, but not DHT. Thus, you have initial (pre-birth) testosterone effects which masculines repro tract, ext. genitalia, and decent of testes (normal differentiated testes and male ducts). Once puberty starts the patient will develop deep voice, muscle mass, penis enlarges and libido increases.
  • with target resistance to androgens (basically no effects of testosterone): elevated androgen levels and LH, but absence of virilization, abdominal testes, vestigial wolffian ducts, and FEMALE GENITALIA, BLIND VAGINA.
21
Q

what are the two causes of endocrine hypergonadism?

A
  • precocious puberty: results from a neurogenic cause (tumor on pit or hypo) OR idiopathic origin.
  • Pseudoprecocious puberty: LH tumors or adrenal androgens (CAH)
22
Q

non-reproductive effects of androgens in male

A
  • protein anabolic effect
  • bone growth at puberty
  • closes epiphyseal plates after being converted to estrogen by aromatase
  • may induce aggressive behavior

Physiology 606 (12 decks)

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