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Physio Review > Endo/Repro > Flashcards

Endo/Repro Flashcards

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1
Q

5 cell types of the anterior pituitary

A

acidophils
somatotrope- GH
lactotrope- prolactin

basophils
gonadotrope- LH/FSH
corticotrope- ACTH
thyrotrope- TSH

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2
Q

list 4 steroid hormones, where they act

A

GCs, androgens, estrogens, vit D

nuclear receptors, slow effects

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3
Q

what does cortisol stimulate

A
  • gluconeogenesis, lipolysis, proteolysis

- inhibits NFkappaB by binding to Ikappab promoter, forming complexes with it outside cell

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4
Q

4 layers of the adrenal gland and what it produces

A

glomerulosa- aldosterone, MRs
fasiculata- GRs
reticulata- weak androgens

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5
Q

common effects of adrenal cortex enzyme deficiencies

A
  • no CORT

- adrenal hyperplasia due to excess ACTH

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6
Q

ACTH receptor

A

MC2R

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7
Q

21 hydroxylase deficiency

A
  • no cortisol or aldosterone, increased androgens
  • hypotension, hyperkalemia
  • high renin
  • masculinization
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8
Q

11-hydroxylase deficiency

A
  • no cortisol, low aldosterone, high MR activity (11-DOC), increased androgens
  • hypertension, hypokalemia
  • masculinization
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9
Q

17 hydroxylase deficiency

A
  • no cortisol , low aldosterone, high 11-DOC
  • hypertension, hypokalemia
  • feminization
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10
Q

cushing’s syndrome vs cushing’s disease; symptoms

A
  • when ACTH comes from the pituitary, it’s cushing’s disease
  • hypertension (cort stimulating alpha adrenergics) , central obesity, thinning of skin, hyperglycemia, insulin resistance
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11
Q

what is required for the NE to E conversion in the adrenal medulla?

A

cortisol

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12
Q

excess VMA in the urine, what do you suspect

A

pheochromocytoma, excess degradation of NE/E

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13
Q

thyroid hormone synthesis; what all steps are dependent upon

A

trap, transport, (oxidize iodide- TPO) iodinate (organification-TPO), conjugate (TPO), endocytose, proteolysis, secrete; everything dependent on TSH

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14
Q

T3 vs T4

A

T3- MIT-DIT

T4- DIT-DIT

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15
Q

type 1, 2, 3 deiodinase

A

1) outer and inner rings, makes T3/RT3, liver, kidney, thyroid, skeletal muscle
2) outer- pituitary, brain, heart, placenta
3) inner- brain, skin, placenta

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16
Q

actions of T3

A

increases BMR, increases brain maturation, increase beta adrenergic receptors

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17
Q

what stimulates prolactin; what inhibits it

A

stimulates- TRH, GH
inhibits- dopamine

lactation inhibited by estrogen and progesterone

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18
Q

where do the incretins come from?

A

glucagon gene, GLP1 & GLP2 activated in the intestines in response to low glucose

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19
Q

transcription factor which increase glucokinase?

A

SREPB1 in WAT

PPAR gamma increases adipocytes

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20
Q

targets of PTH

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A

kidney- increases Ca reabsorption, Pi excretion

bone- releases Ca

21
Q

targets of vitamin d

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A

chief cells- inhibits PTH
bone- mobilizes Ca
gut- increases Ca and Pi absorption

22
Q

estrogens effects of Ca2+ regulation

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A

increases 1alphahydroxylase activity, stimulates OPG, decreases bone loss

23
Q

endocrine disrupters

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A

PCBs compete with TBG

DES synthetic estrogen

24
Q

what does the product of epsilon cells in the stomach do?

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A

ghrelin- inhibits insulin release by reducing the amount of intracellular Ca2+

25
which gene in linked with type 2 diabetes?
TCF72
26
what happens if, while genital ducts are maturing they encounter testosterone? antimullerian hormone? what produces each?
w/ testosterone from leydig cells (normally from testes), keep wolffian ducts w/ antimullerian hormone from sertoli cells- degrade mullarian ducts
27
what does 5 alpha reductase do?
converts testosterone to more potent DHT, which is important for male genitalia development via androgen receptors
28
where does spermatogenesis occur?
seminiferous tubules
29
what do coelomic epithelium cells become?
sertoli cells in male, granulosa cells in female (nurse cells)
30
what do mesenchymal cells become?
leydig cells in males, theca cells in females (hormone cells)
31
what converts testosterone to estadiol?
aromatase
32
what does testosterone do during fetal development?
epididymis vas deferens seminal vesicles
33
what does DHT do during fetal development?
penis/urethera scrotum prostate
34
what does testosterone do during puberty?
``` penis seminal vesicles musculature voice skeleton spermatogenesis ```
35
what does DHT do during puberty?
``` scrotum prostate male pattern baldness happy trail beards sebaceous glands ```
36
where does GnRH come from? what is it inhibited/stimulated by?
- arcuate nucleus and preoptic area of hypothalamus; - inhibitors: dopamine, endorphins, CRH stimulator: NE
37
hormone actions during follicular phase
1) GnRH causing FSH/LH release (pulsatile) 2) increasing FSH/LH stimulate ovary to develop follicle 3) follicle secretes E2 (estradiole) 4) E2 has positive feedback on follicle BUT 5) E2 has negative feedback (with inhibin) on pituitary/hypothalamus on FSH cells - keeps volume down as capacity builds (LH rising)
38
hormone actions during ovulatory phase
1) E2 gets past a certain threshold for a sustained period of time, switches to positive feedback (timing determined by ovary) 1b) increase GnRH receptors on gonadotrophs 2) get LH surge - reinforcing self and E2 3) causes rupture of follicle 4) everything dips because it's all disorganized
39
hormone actions during luteal phase
1) corpus luteum becomes dominant- makes E2 (not as high as surge) and progesterone (off the charts) 2) switch back to inhibition, get little LH/FSH/GnRH 3) no LH causes corpus luteum to degrade 4) once CL degrades, lose E2 and progesterone, FSH levels recover 5) lose functional endometrial layer
40
what are the actions of estradiol secreted by the dominant follicle?
- inhibits growth of other follicles - makes mucus thin - prepares fallopian tubes - potentiates action of progesterone so uterus goes into secretory mode - primes GnRH action on LH surge to get more LH
41
how does high insulin impact ovaries? what do you treat with?
stimulates androgen production, causing impaired follicle development and no ovulation; follicles degrade into cysts and ovaries double in size - treat with metformin
42
two exocytotic events during the fertilization process
1) Exocytosis of spermatozoan internal membrane contents- allows sperm to attach to zona pellucida 2) Exocytosis of oocyte’s internal vesicles- harden the rest of the zona pellucida (Ca2+ mediated- also triggers second meiotic division after metaphase II)
43
what happens during adhesion?
- zona pellucida dissolves - Il-1 increases integrins in endometrial cells - osteopontin (bridging molecules) binds integrins together - trophopblasts develop
44
what happens during penetration?
- stromal cells of endometrium enlarge to form the decidua (progesterone-promoted) and secrete nutrients (source until placenta) - cells preform some endocrine functions (e.g. prolactin)
45
what happens during invasion?
- find balance between decidual cells and trophoblast migration - trophoblasts differentiate into syncytiotrophoblasts (like pituitary- most endocrine functions, makes hCG/hCL) and cytotrophoblasts (like hypothalamus- CRH, TRH, somatostatins)
46
what is hPL?
HCS aka human placental lactogen (HPL) - similar to growth hormone - stimulates lipolysis and has anti-insulin effects on maternal metabolism - leads to increase in plasma glucose and FFA for fetus - cause of gestational diabetes
47
how is estriol produced?
mom's cholesterol (LDL)- pregnenolone in placenta- converted by fetal adrenal to DHEA-S- converted by fetal liver to oh-DHEA-S- sulfer removed by placenta- placenta makes estriol
48
T/F Maternal oxytocin initiates labor
FALSE- released in bursts once labor beings, has positive feedback loop, stimulating prostaglandin release - stimulus is distention of the cervix: Ferguson reflex

Physio Review (6 decks)

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