Endo Physiology Review Flashcards

1
Q

positive feedback

A

action of estrogen on LH during midcycle

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2
Q

MSH

A

melanocyte stimulating hormone

from anterior pituitary

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3
Q

TRH

A

thyrotropin releasing hormone

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4
Q

lipid soluble hormones

A

steroids
thyroid hormones

receptor intracellular

synthesized as needed

carried on proteins

long half life

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5
Q

water soluble hormones

A

peptides
proteins

receptor outer cell surface

stored in vesicles

unbound in plasma

short half life

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6
Q

plasma analysis

A

of hormone level

reflect time of sampling

lots of variation

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7
Q

urine analysis

A

catecholamines and steroid hormones

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8
Q

anterior pituitary

A

has portal system

hypothalamic/hypophysial portal vessels

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9
Q

posterior pituitary

A

supraoptic nuclei

paraventricular nuclei

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10
Q

supraoptic nuclei

A

produces vasopressin - ADH

posterior pituitary

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11
Q

paraventricular nuclei

A

produce vasopressin and oxytocin

posterior pituitary

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12
Q

actions of ADH

A

released with increased serum osmolality

acts on principal cells - distal tubule kidney - V2 receptors
-increased expression of aquaporin 2 channels

increase water resorption**

also contraction of vascular smooth m to protect against volume depletion

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13
Q

oxytocin actions

A

milk letdown

uterine contraction

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14
Q

diabetes insipidus

A

large volume of urine that is hypotonic

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15
Q

neurogenic DI

A

hypothalamic/central pathology
-unregulated ADH

low ADH

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16
Q

nephrogenic DI

A

unresponsive to ADH

high ADH

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17
Q

primary polyuria

A

increase water intake

-pathologic, habitual, psychiatric syndrome

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18
Q

diagnosis of DI

A

confirmed by dehydration stimulus followed by inability to concentrate urine

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19
Q

no change in urine osmolality after dehydration

A

think diabetes insipidus

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20
Q

urine osmolality increase after ADH administration

A

neurogenic diabetes insipidus

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21
Q

stimulation for GH release

A
decreased glucose concentration
decreased fatty acid concentration
arginine
fasting/starvation
puberty hormones
exercise
stress
sleep
alpha-adrenergic agonists
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22
Q

inhibition of GH release

A
increased glucose concentration
increased fatty acid concentration
obesity
senescence
somatostatin
somatomedins
GH
beta-adrenergic agonists
pregnancy
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23
Q

actions of GH

A

diabetogenic effect - insulin resistance

decreased glucose uptake - more in blood
increased lipolysis
increased blood insulin

increased protein synthesis and organ growth - through IGF-1

  • increased AA uptake
  • increased DNA, RNA, protein synthesis
  • increased lean body mass and organ size

increased linear growth - action of IGF-1

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24
Q

dopamine

A

inhibit prolactin release

prolactin induces dopamine synthesis

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25
Q

stimulation of prolactin release

A
pregnancy
breast feeding
sleep
stress
TRH
dopamine antagonists
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26
Q

inhibition of prolactin release

A

dopamine
bromocriptine (dopamine agonist)
somatostatin
prolactin

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27
Q

slow GnRH pulse

A

decreased LH

increased FSH**

28
Q

fast GnRH pulse

A

decreased FSH

increased LH**

29
Q

pulsatile GnRH release

A

prevents downregulation of its receptor

30
Q

continuous infusion of GnRH

A

cause decrease in both LH and FSH

31
Q

thyroglobulin

A

to T4 and T3

32
Q

thyroid hormone synthesis

A

thyroglobulin exocytosis to lumen
iodine into cell and oxidized (- by PTU)
iodine into MIT and DIT (- by PTU)

coupling rxns (- by PTU)
DIT and DIT - T4
MIT and DIT - T3

endocytosis of thyroglobulin
proteolysis of thyroglobulin - release T3 and T4

33
Q

TBG

A

binds T3 and T4 in blood

99% bound in circulation

34
Q

T4 vs. T3

A

T4 to T3 ration 10:1

however, T3 is 10x more active at receptor

tissue has deiodinase to convert T4 to T3

35
Q

normal T4 levels

A

5-12 microgram/dL

36
Q

normal T3 levels

A

70-190 nanogram/dL

37
Q

euthyroid sick syndrome

A

hypothyroidism

pathology - increased deiodinase D3 - forms inactive rT3

38
Q

stimulation of thyroid hormone release

A

TSH
thyroid stimulating Igs
increased TBG

39
Q

inhibition of thyroid hormone release

A
iodine deficiency
deiodinase deficiency
excess iodine intake (wolf-chaikoff effect)
perchlorate
thiocyanate
PTU
decreased TBG
T3
40
Q

wolf-chaikoff effect

A

excess iodine causes inhibition of thyroid hormone release

41
Q

action of thyroid hormones

A

growth
maturation of CNS
increased metabolism
increased cardiac output

42
Q

thyrotoxicosis

A

excess thyroid hormone in body

43
Q

hot nodule

A

overproduction of thyroid hormone

44
Q

granulomatous thyroiditis

A

painful gland

45
Q

graves disease

A

autoimmune disease

-antibodies that activate TSH receptor - increased thyroid hormone release

46
Q

hashimotos disease

A

alpha-TPO Abs

destruction of thyroid tissue

primary hypothyroid

47
Q

secondary hypothyroid

A

pituitary insufficiency

48
Q

zones of adrenal gland

A

cortex - GFR
zona glomerulosa - aldosterone
zona reticulata - cortisol
zona reticularis - androgens

medulla - catecholamines

49
Q

excess androgens absence of glucocorticoids and mineralocorticoids

A

21-alpha-hydroxylase deficiency

50
Q

increased mineralocorticoids and absence of androgens

A

17-alpha hydroxylase deficiency

51
Q

stimualtion of cortisol release

A
decreased blood cortisol
sleep-wake transition
stress - hypoglycemia, surgery, trauma
psychiatric disturbance
ADH
alpha-adrenergic agonist
beta-adrenergic antagonist
serotonin
52
Q

inhibition of cortisol release

A

increased blood cortisol levels
opiods
somatostatin

53
Q

ACTH

A

stimulates adrenal cortex to release aldosterone

aldosterone also stimulated by ANG II via RAAS system

54
Q

adrenal steroid hormones

A

glucocorticoids
mineralocorticoids
adrenal androgens

55
Q

glucocoticorticoids

A

essential for survival during fasting

increase protein catabolism
decrease protein synthesis
increase lipolysis
decrease glucose utilization by tissues

56
Q

metabolic response to stress

A

to ensure sufficient energy to meet increased demand of body

cortisol release, increased E and NE

57
Q

chronic elevated cortisol

A

localized obesity
muscle wasting/weakness

elevated insulin/glucagon ratio

58
Q

acute elevated cortisol

A

decreased insulin/glucagon ratio

59
Q

primary adrenocortical insufficiency

A

addison disease

60
Q
hypoglycemia
anorexia, weight loss, N/V
weakness
hypotension
hyperkalemia
metabolic acidosis
decreased pubic hair
hyperpigmentation
A

addison disease

increased ACTH levels
-negative feedback of decreased cortisol

61
Q

primary adrenal hyperplasia

A

cushing syndrome

62
Q

excess ACTH

A

cushing disease

63
Q
hyperglycemia
muscle wasting
central obesity
moon facies
buffalo hump
osteoporosis
striae
virilization
HTN
A

cushing syndrome

decrased ACTH
-negative feedback of increased cortisol

64
Q

aldosterone secreting tumor

A

conn syndrome

65
Q

HTN, hypokalemia, metabolic alkalosis, decreased renin

A

conn syndrome

66
Q

virilization in females

A

21-beta hydroxylase deficiency

67
Q

lack of pubic hair
deficient glucocorticoids
excess mineralocorticoids

A

17-alpha hyedroxylase deficiency