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REM II > hormones > Flashcards

hormones Flashcards

1
Q

What does oxytocin do?

A

Works on the breast to eject milk

positive feedback with contraction strength

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2
Q

what cell in the breast tissue does oxytocin act on?

A

myoepithelial cells

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3
Q

What area in the breast tissue does PRL work on?

A

alveolar

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4
Q

What area is MSH produced in AP?

A

Pars Nervosa

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5
Q

What nucleus releases ADH?

A

Supraoptic

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6
Q

What nucleus releases oxytocin?

A

paraventricular

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7
Q

What antibody do you test for with graves dz

A

TSI

TSHR

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8
Q

What antibody test do you run for hashimotos?

A

Anti TPO

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9
Q

What is the release pattern of GH?

A

pulsatile; peaks during sleep

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10
Q

What are release triggers for GH?

A 
stress
exercise
DEC glucose/FA
high protein meal
fasting 
ghrelin 
levodopa
apomorphine
bromocriptine
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11
Q

What pathway does GH work through when it binds to its receptor?

A

JAK/STAT (nontyrosine kinase)

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12
Q

What are the actions of GH?

A

decreases adiposity

decreases glucose use (inc BG)

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13
Q

What are the actions of IGF1?

A

inc lean muscle mass
inc linear growth
inc organ growth

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14
Q

What can inc GH cause?

A

children: gigantism
adults: acromegaly

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15
Q

What are the characteristics of congenital short stature?

A

normal GH

lack of IGF1 during puberty

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16
Q

What pathway/receptor does GHRH work through?

A

G protein

cAMP and inc Ca

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17
Q

Is there anything that inhibits GH release?

A

YES! somatostatin

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18
Q

What is the release pattern for PRL

A

pulsatile

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19
Q

What pathway does PRL work through?

A

JAK/STAT (non tyrosine kinase receptor)

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20
Q

What does PRL do?

A

breast development
milk production
inhibition of gonadotropins

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21
Q

What stimulates PRL release?

A

suckling, stimulation, stress, sleep, neurogenic reflex, phenothiazines, INC estrogen, pregnancy

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22
Q

what inhibits PRL? non hormonal inhibition?

A

dopamine, bromocriptine, apomorphine

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23
Q

What can excess PRL cause?

A

galactorrhea, infertility, amenorrhea, decreased libido, dec spermatogenesis

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24
Q

What two things are associated with inc PRL?

A

prolactinomas, empty sella syndrome

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25
Q

What receptor does TRH work through?

A

g prot to IP3 to inc Ca

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26
Q

What receptor does TSH work through?

A

g prot to cAMP

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27
Q

What are the actions of thyroid hormones?

A

bone and CNS maturation
inc BMR ( inc heat production)
Inc CO
inc metabolism

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28
Q

What are the symptoms of hyperthyroidism?

A 
wt loss
sweating
inc CO
tremor/muscle weakness
exopthalmos
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29
Q

What are the symptoms of hypothyroidism

A 
wt gain
cold sensitivity
lethargy, mental slowness
drooping eyelids
myxedema
growth retardation
mental retardation
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30
Q

What is the treatment for graves?

A

PTU

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31
Q

What is the effect of hyperthyroidism on T4, TSH, and binding proteins?

A

T4-high
TSH-low
proteins- normal

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32
Q

What is the effect of hypothyroidism on T4, TSH, and binding proteins?

A

T4-low
TSH-high
proteins-normal

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33
Q

What will happen with a cholesterol desmolase deficiency?

A

rate limiting step from cholesterol to pregnenolone

fatal

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34
Q

What will happen with a 3 beta hydroxy steroid dehydrogenase deficiency?

A 
no cortisol
no aldo
no androgens
DHEA build up
fatal
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35
Q

what will happen with a 17 alpha hydroxylase deficiency?

A

very low cortisol and androgens
inc aldo
both sexes have female phenotype
hypokalemia

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36
Q

What will happen with a 21 beta hydroxylase deficiency?

A

very low cortisol and aldo (na loss and hypotension)
DHEA and androgen build up (virilization, hirsutism, amenorrhea)
females born with ambiguous genitalia and raised as male
associated with congenital adrenal hyperplasia

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37
Q

What will happen with a 11 beta hydroxylase deficiency?

A 
inc deoxycorticosterone (na ret and htn)
inc DHEA and androgens (virilization)
very low aldo and cortisol (as its the final enzyme needed to create them)
38
Q

What enzyme deficiency is most common?

A

21 beta hydroxylase

39
Q

What stim aldo?

A

ang II

40
Q

what downregulates aldo?

A

ANP

41
Q

what are the effects of cortisol?

A 
inhibits protein synth
promotes FA use
dec glucose use
stim gluconeogenesis
antiinflammatory
42
Q

What receptor does CRH work through?

A

g prot to cAMP to ca

43
Q

what receptor does ACTH work through

A

g prot to cAMP

44
Q

what is the release pattern of cortisol?

A

circadian rhythm

45
Q

what are stimulators of cortisol?

A

stress, DEC glucose

46
Q

what happens when you lose cortisol?

A

circulatory failure
inability to readily mobilize energy sources
inhibits t cell production

47
Q

what is the most common cause of congenital adrenal hyperplasia

A

21 beta hydroxylase

48
Q

what is released from the adrenal medulla?

A

epi and norepi

49
Q

what is released from the zona glomerulosa

A

aldo

50
Q

what is released from the zona fasciculata

A

cortisol

51
Q

what is released from the zona reticulata

A

androgens

52
Q

what are the signs of cushings?

A

moon face, striae, truncal obesity, HTN, osteoporosis, protein depletion, mental abnormalities, DM hirsutism
hypokalemia and alkalosis

53
Q

what is the most common cause of cushings?

A

prednisone use

54
Q

what is the best way to test for cushings?

A

24 hr cortisol

55
Q

What are the steps for suspected hyperadrenalism?

A

1- low dose dexamethasone suppression test (if normal, not cushings)
2- 24 hr urine cortisol (if normal, not cushings)
3- high dose of dexamethasone suppression test

56
Q

What do the results of the high dose dexamethasone test signify:

1) >50% decrease in cortisol
2) no response
3) ACTH level high
4) ACTH level reduced

A

1) cushings due to pituitary adenoma
2) ACTH secreting tumor
3) ACTH secreting tumor from another source ie lung
4) adrenal tumor

57
Q

What is conn’s syndrome? how is it diagnosed

A

inc levels of aldo
primary hyperaldosteronism
inc ratio PAC/PRA = 25-50

58
Q

how do you test for primary aldosteronism?

A

saline suppression test
measure PAC
if falls below 5- normal
if remains above 10- primary

59
Q

How do you test for pheochromocytoma?

A

24 metanephrine and catecholamine urine collection

60
Q

how do you confirm pheo presence?

A

give clonidine to suppress

MRI or CT

61
Q

What test should you always run with a suspected pheo?

A

MIBG to see if theres any extra adrenal tumors

62
Q

What are the actions of PTH in the kidney?

A

inc Ca reabsorption
inc PO4 excretion
inc act of vit D

63
Q

What are the actions of PTH in the GI tract?

A

inc vit D -> inc Ca absorption

64
Q

what are the action of PTH on the bone?

A

inc bone resorption
through osteoblast cytokines to osteoclasts
RANKL binding RANK

65
Q

What is measured to see if bone is being broken down?

A

alkaline phosphatase

66
Q

what is the job of calcitonin?

A

antagonizes PTH
dec bone resorption
dec kidney reabsorption of Ca

67
Q

how does PTH respond in acidosis?

A

inc ionized Ca

so no PTH release

68
Q

how does PTH respond in alkalosis?

A

dec ionized Ca

inc PTH release

69
Q

what cells secrete PTH?

A

chief cells

70
Q

Other than calcium, what stimulates PTH?

A

dec Mg

inc PO4

71
Q

what does dec PO4 do?

A

inc vit d activation

72
Q

what does inc PTHrP signify?

A

malignancy

73
Q

What pathway does Ca inhibition of PTH work through?

A

G prot with IP3 releases Ca and inhibits PTH release

stim by Ca

74
Q

what pathway does PTH work through on the kidney?

A

g prot to camp to protein kinase to phos of phosphate/Na symporter dec the phos reabsorption

75
Q

what is the treatment for hypoparathyroidism

A

Vit D

Ca supplement

76
Q

what do the labs look like for primary hyperparathyroidism (PTH, Ca, P, Vit D)

A

inc PTH
inc Ca
dec P
inc Vit D

77
Q

what do the labs look like for secondary hyperparathyroidism (PTH, Ca, P, Vit D)

A

inc PTH
dec Ca
dec P
dec Vit D

78
Q

what do the labs look like for primary hypoparathyroidism (PTH, Ca, P, Vit D)

A

dec PTH
dec Ca
inc P

79
Q

what do the labs look like for secondary hypoparathyroidism (PTH, Ca, PO4, Vit D)

A

dec PTH
inc Ca
inc P
Inc Vit D possibly

80
Q

what do the labs look like for pseudo hypoparathyroidism (PTH, Ca, P, Vit D)

A

*resistance to PTH
inc PTH
dec Ca
inc P

81
Q

what do the labs look like for postmeno/immobilization hypoparathyroidism (PTH, Ca, P, Vit D)

A

dec PTH
inc Ca
inc P
*bone being broken down

82
Q

what do the labs look like for inc PTHrP hypoparathyroidism (PTH, Ca, P, Vit D)

A 
dec PTH
inc Vit D
inc Ca
inc urine phosphate
dec P
*acts like PTH
83
Q

what do the labs look like for renal failure (PTH, Ca, P, Vit D)

A

inc PTH
dec Vit D
dec Ca, due to dec in Vit D
dec P

84
Q

What is familial hypocalciuria hypercalcemia?

A

mutated Ca receptor -> inc Ca levels

takes mores Ca to turn off PTH than normal

85
Q

what stim act of Vit D

A

inc PTH
dec Ca
dec P

86
Q

what 3 things stimulate insulin secretion?

A

inc blood glucose
inc CCK, GIP
inc parasympathetic activity

87
Q

what is insulins action on hepatocytes/

A

inc hexokinase which leads to inc glycogen

88
Q

how does dec insulin lead to polyphagia?

A

insulin usually feeds back to the hypothalamus to tell you that you are full
when there is none, the body thinks theres low glucose and tells you to eat

89
Q

how does dec insulin lead to polyuria and polydipsia

A

inc blood glucose leads to diuresis and inc plasma osmolarity both lead to thirst center activation

90
Q

how does dec insulin lead to kussmaul breathing

A

leads to inc ketones -> metabolic acidosis -> inc RR

REM II (11 decks)

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