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

B8.006 Male Reproductive Endocrinology Flashcards

(68 cards)

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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
key steps of T metbaolism
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
26
estradiol in males
majority produced in adipose tissue through aromatization of T
27
type II 5ar
generates 3x more DHT than type I and is critical for sexual differentiation of male external genitalia
28
functions of T in males
controls sexual differentiation, libido, pubertal growth of the larynx, anabolic effects in muscle and erythropoiesis, stimulation of spermatogenesis
29
effects of T on bones
increases osteoblast lifespan and proliferation | enhances bone formation
30
effects of estrogen in males
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
effects of DHT
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
what type of virus is mumps
enveloped negative sense RNA infects cells via sialic acid receptor, which is present on most animal cells
33
mumps orchitis
most common extra salivary gland inflammation caused by mumps infection occurs 1-2 weeks after parotitis
34
effect of mumps on testicles
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
effects of mumps orchitis on HP axis
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
testosterone peaks throughout the male lifetime
12-18 weeks of gestation 1st postnatal month 30 years old
37
fetal testosterone peak
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
primary sexual differentiation
differentiation of sex organs in utero
39
secondary sexual differentiation
differentiation of body parts, other than sex organs, that occurs at puberty
40
LH stimulation in newborn males
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
activation of HPG axis at puberty in males
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
initial phase of puberty
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
pubertal growth
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
sexual maturity
``` 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
nocturnal penile erections test
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
males aged 30
T stars decreasing around age 30 100 ng/dl per decade decreased T and increased SHBG, so less bioavailable T
47
population level changes in T over time
decreasing | maybe due to obesity
48
sexual senescence
``` 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
symptoms of andropaus
``` 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
precocious puberty
rare in males consequence of T excess appearance of male secondary sex characteristics before age 9
51
2 types of precocious puberty
``` gonadotropin dependent (most common) gonadotropin independent ```
52
known causes of precocious puberty
hypothalamic tumors LH receptor activating mutations congenital adrenal hyperplasia androgen producing tumors
53
hypogonadotropic hyogonadism
results from dysfunction at the level of the hypothalamus or pituitary
54
hypergonadotropic hyogonadism
dysfunction at the level of the testis
55
kallmann syndrom
delayed or absent puberty imapaired sense of smell hypogonadotropic hyogonadism: lack of production of hypothalmic hormones that direct sexual development
56
puberty in kallmann syndrome
do not develop secondary sex characteristics
57
genetics of kallmann syndrome
x linked recessive | males more commonly affected
58
hyperprolactinemia
in both sexes results in both reproductive and sexual dysfunction because high levels of prolactin inhibit GnRH release
59
klinefelters
46 XXY frequently diagnosed at puberty low T, elevated LH, FSH, and E2
60
characteristics of people with klinefelters
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
androgen insensitivity syndrome
x linked due to androgen receptor mutations considerable heterogeneity in presentation, phenotypes reflect varying severity of AR mutations
62
complete AIS
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
47, XYY syndrome
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
clinical presentation of low T in early childhood
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
androgen deficiency in the adult after normal virilization
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
definition of hypogonadism
T < 265 ng/dl | should receive replacement therapy
67
risks of T replacement therapy
``` prostate diseases: BPH and prostate cancer polycythemia sleep apnea gynecomastia acne liver diseases ```
68
essential testis derived hormones that regulate male sexual development
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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