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RDS Test 1 > B8.006 Male Reproductive Endocrinology > Flashcards

B8.006 Male Reproductive Endocrinology Flashcards

1
Q

THE KEY RELATIONSHIP SLIDE

A

LH stimulates leydig cells
FSH stimulates sertoli cells
inhibin B from sertoli cells inhibits FSH release
T from Leydig cells inhibits GnRH and LH release

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2
Q

what do sertoli cells produce

A

AMH (in fetal development)
androgen binding protein (ABP)
inhibin B

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3
Q

receptors on sertoli cells

A

FSH

androgen receptors

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4
Q

receptors on leydig cells

A

LH receptors

-LH and hCG both bind this receptor

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5
Q

normal range of total T

A

160-950 ng/dl

3 fold range

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6
Q

normal range of free T

A

50-210 ng/dl

about 1/10 of total

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7
Q

factors that stimulate GnRH release in men

A

NE
neuropeptide Y
leptin (from adipocytes)

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8
Q

factors that inhibit GnRH release in men

A 
B-endorphin
prolactin
IL-1
GABA
dopamine
nicotine
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9
Q

LH circulation

A

unbound in plasma
20-30 min half life
higher amplitude fluctuations in levels than FSH

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10
Q

FSH circulation

A

unbound in plasma
3-4 hour half life
levels more stable and show less variability than LH

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11
Q

how gonadotropins act

A
  1. bind to cell membrane G-protein coupled receptors
  2. activates adenylate cyclase and leads to an increase in the formation of cAMP
  3. rise in cAMP activated protein kinase A and subsequent kinase-mediated protein phosphorylation
  4. transcription factor phosphorylation leads to gene transcription
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12
Q

high levels of LH

A

precocious puberty
primary testicular failure
castration

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13
Q

low levels of LH

A

kallmann syndrome
hyperprolactinemia
primary pituitary failure

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14
Q

3 principal hormones produced by adult testis

A
  1. T
  2. estradiol (minor)
  3. inhibin B
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15
Q

how does LH stimulate T biosynthesis

A

increases mobilization and transport of cholesterol into the steroidogenic pathway
stimulates gene expression and activity of steroidogenic enzymes

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16
Q

steroidogenic acute regulatory protein (StAR)

A

key role in transfer of cholesterol from the outer to the inner mitochondrial membrane

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17
Q

what enzyme makes T from androstenedione

A

17 b hydroxysteroid dehydrogenase

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18
Q

how T acts

A
  1. enters cell by passive diffusion (lipid soluble)
  2. dissociates heat shock protein complex from cytosolic androgen receptor
  3. receptor dimerizes, translocates to the nucleus, and binds to DNA regulatory elements
  4. activation of gene transcription
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19
Q

symptoms of low T

A

decreased morning erections
ED
decreased frequency of sexual thoughts

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20
Q

importance of inhibin B

A

main function: suppress the secretion of FSH from the pituitary
levels correlate with total sperm count and testicular volume, can be used as an index of spermatogenesis

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21
Q

activin

A

locally (pituitary) produced peptide that antagonizes inhibin B action, resulting in stimulation of FSH release

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22
Q

result of taking anabolic steroids on fertility

A

T levels in the blood are artificially raised
pituitary reduces pulsatile LH secretions
testicular leydig cells reduce testosterone secretion
local testicular concentration of androgens drop below the levels needed to support spermatogenesis
sperm quality and quantity drop
testicles may shrink over time

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23
Q

circulation of T

A

most is bound to plasma proteins
1. sex hormone binding globulin (SHBG) (60%)
2. albumin (38%)
3. free (2%)
albumin and free are considered bioavailable

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24
Q

SHBG levels during maturation

A

fetal SHBG is low
levels rise after birth and remain high through childhood
at puberty, SHBG levels halves in girls and goes down to a quarter in boys
rises again with age, so older men have less bioavailable T

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25
Q

key steps of T metbaolism

A

in target cells:
-can have direct androgen receptor mediated effect
-can be converted to DHT by 5ar
-can be converted to estradiol by aromatase
in liver:
-degraded to ketosteroids or polar metabolites that are excreted in urine

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26
Q

estradiol in males

A

majority produced in adipose tissue through aromatization of T

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27
Q

type II 5ar

A

generates 3x more DHT than type I and is critical for sexual differentiation of male external genitalia

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28
Q

functions of T in males

A

controls sexual differentiation, libido, pubertal growth of the larynx, anabolic effects in muscle and erythropoiesis, stimulation of spermatogenesis

29
Q

effects of T on bones

A

increases osteoblast lifespan and proliferation

enhances bone formation

30
Q

effects of estrogen in males

A

critical sex hormone in the pubertal growth spurt, skeletal maturation, accrual of peak bone mass, and maintenance of bone mass in the adult
stimulates chondrogenesis in the epiphysial growth plate, increasing pubertal linear growth

31
Q

effects of DHT

A

external genitalia and prostate development, descent of the testes, phallic growth, male pattern balding, development of facial, pubic, and underarm hair, activity of sebaceous glands

32
Q

what type of virus is mumps

A

enveloped
negative sense
RNA
infects cells via sialic acid receptor, which is present on most animal cells

33
Q

mumps orchitis

A

most common extra salivary gland inflammation caused by mumps infection
occurs 1-2 weeks after parotitis

34
Q

effect of mumps on testicles

A

well known for testicular tropism
induces inflammation, decreases androgen production, and degenerates seminiferous epithelium, which can lead to sterility
can replicate within leydig cells and be associated with a decrease in T production
of those affected, 30-50% show a degree of testicular atrophy

35
Q

effects of mumps orchitis on HP axis

A

low T levels
elevated LH levels
exaggerated pituitary response to LHRH stimulation in the acute phase
T concentrations return to normal after several months, but mean FSH and LH remain increased 10-12 months after acute phase

36
Q

testosterone peaks throughout the male lifetime

A

12-18 weeks of gestation
1st postnatal month
30 years old

37
Q

fetal testosterone peak

A

needed for mesonephric (wolffian) duct development
-complete rescue of mesonephric duct, form epididymis, vas deferens, seminal vesicles and prostate
DHT required for development of external genitalia

38
Q

primary sexual differentiation

A

differentiation of sex organs in utero

39
Q

secondary sexual differentiation

A

differentiation of body parts, other than sex organs, that occurs at puberty

40
Q

LH stimulation in newborn males

A

days after birth, newborn baby boys have high LH levels that stimulate Leydig cells to release high levels of testosterone
maybe to “masculinize” the CNS

41
Q

activation of HPG axis at puberty in males

A

puberty is triggered by increased pulsatile GnRH secretion from the hypothalamus
leptin, an adipose hormone, may be a permissive factor in timing the activation for the GnRH pulse generator

42
Q

initial phase of puberty

A

plasma LH levels increase primarily during sleep
nocturnal penile erections increase in frequency
LH surges occur throughout the day and result in increased circulating T

43
Q

pubertal growth

A

increased gonadal steroids at puberty is accompanied by an increase in growth hormone secretion from somatotropes within the anterior pituitary
together, GH and gonadal steroids induce normal pubertal growth

44
Q

sexual maturity

A 
achieved at approximately 18 years
plasma levels of T from 300-1200
sperm production is optimal
plasma gonadotropins are normal
most sexual anatomic changes are complete
45
Q

nocturnal penile erections test

A

literally there has to be a better way to test this than by putting STAMPS AROUND A FUCKING PENIS but i guess thats where we’re at in modern medicine
do it for 3 nights

46
Q

males aged 30

A

T stars decreasing around age 30
100 ng/dl per decade
decreased T and increased SHBG, so less bioavailable T

47
Q

population level changes in T over time

A

decreasing

maybe due to obesity

48
Q

sexual senescence

A 
changes established by age 50
decreased T:E2 ratio
decreased LH pulse frequency
loss of diurnal rhythm of T secretion
diminished accumulation of 5ar steroids in repro tissues
49
Q

symptoms of andropaus

A 
diminished sexual desire
decreased intellectual activity
fatigue
depression
decreased lean body mass
skin alterations
decreased body hair
decreased bone mineral density and osteoporosis
increased visceral fat and obesity
50
Q

precocious puberty

A

rare in males
consequence of T excess
appearance of male secondary sex characteristics before age 9

51
Q

2 types of precocious puberty

A 
gonadotropin dependent (most common)
gonadotropin independent
52
Q

known causes of precocious puberty

A

hypothalamic tumors
LH receptor activating mutations
congenital adrenal hyperplasia
androgen producing tumors

53
Q

hypogonadotropic hyogonadism

A

results from dysfunction at the level of the hypothalamus or pituitary

54
Q

hypergonadotropic hyogonadism

A

dysfunction at the level of the testis

55
Q

kallmann syndrom

A

delayed or absent puberty
imapaired sense of smell
hypogonadotropic hyogonadism: lack of production of hypothalmic hormones that direct sexual development

56
Q

puberty in kallmann syndrome

A

do not develop secondary sex characteristics

57
Q

genetics of kallmann syndrome

A

x linked recessive

males more commonly affected

58
Q

hyperprolactinemia

A

in both sexes results in both reproductive and sexual dysfunction because high levels of prolactin inhibit GnRH release

59
Q

klinefelters

A

46 XXY
frequently diagnosed at puberty
low T, elevated LH, FSH, and E2

60
Q

characteristics of people with klinefelters

A

tall
less muscle mass and facial and body hair
broader hips than other males
small testicles
breast development
children may have weak muscle tone and delated development of motor skills such as sitting, standing, and walking

61
Q

androgen insensitivity syndrome

A

x linked
due to androgen receptor mutations
considerable heterogeneity in presentation, phenotypes reflect varying severity of AR mutations

62
Q

complete AIS

A

testes present and functional
no uterus, fallopian tubes, or upper vagina (mullerian development blocked by MIS)
inactive AR = inactive T
external genitalia is female, no epididymis, vas deferens, or seminal vesicles (mesonephric duct does not develop)

63
Q

47, XYY syndrome

A

symptoms are usually few and odten not diagnosed
taller than average, acne, increased risk of learning problems (IQ slightly lower than siblings)
average height = 6’3”

64
Q

clinical presentation of low T in early childhood

A

early childhood: short, lack of deepening of voice, female distribution of hair, anemia, underdeveloped muscles, and genitalia with delayed or absent onset of spermatogenesis and sexual function

65
Q

androgen deficiency in the adult after normal virilization

A

decrease in bone mass, decreased bone marrow activity (anemia), alterations in body composition associated with muscle weakness and atrophy, changes in mood and cognitive function, and regression of sexual function and spermatogenesis

66
Q

definition of hypogonadism

A

T < 265 ng/dl

should receive replacement therapy

67
Q

risks of T replacement therapy

A 
prostate diseases: BPH and prostate cancer
polycythemia
sleep apnea
gynecomastia
acne
liver diseases
68
Q

essential testis derived hormones that regulate male sexual development

A
  1. androgens: differentiation of epididymis, vas deferens, prostate and seminal vesicles
  2. MIS: embryonic development
  3. IGF3: aids descent of testicles into the scrotum

RDS Test 1 (22 decks)

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