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Flashcards in Endo Physiology Review Deck (67):
1

positive feedback

action of estrogen on LH during midcycle

2

MSH

melanocyte stimulating hormone

from anterior pituitary

3

TRH

thyrotropin releasing hormone

4

lipid soluble hormones

steroids
thyroid hormones

receptor intracellular

synthesized as needed

carried on proteins

long half life

5

water soluble hormones

peptides
proteins

receptor outer cell surface

stored in vesicles

unbound in plasma

short half life

6

plasma analysis

of hormone level

reflect time of sampling

lots of variation

7

urine analysis

catecholamines and steroid hormones

8

anterior pituitary

has portal system

hypothalamic/hypophysial portal vessels

9

posterior pituitary

supraoptic nuclei
paraventricular nuclei

10

supraoptic nuclei

produces vasopressin - ADH

posterior pituitary

11

paraventricular nuclei

produce vasopressin and oxytocin

posterior pituitary

12

actions of ADH

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

13

oxytocin actions

milk letdown

uterine contraction

14

diabetes insipidus

large volume of urine that is hypotonic

15

neurogenic DI

hypothalamic/central pathology
-unregulated ADH

low ADH

16

nephrogenic DI

unresponsive to ADH

high ADH

17

primary polyuria

increase water intake
-pathologic, habitual, psychiatric syndrome

18

diagnosis of DI

confirmed by dehydration stimulus followed by inability to concentrate urine

19

no change in urine osmolality after dehydration

think diabetes insipidus

20

urine osmolality increase after ADH administration

neurogenic diabetes insipidus

21

stimulation for GH release

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

22

inhibition of GH release

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

23

actions of GH

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

24

dopamine

inhibit prolactin release

prolactin induces dopamine synthesis

25

stimulation of prolactin release

pregnancy
breast feeding
sleep
stress
TRH
dopamine antagonists

26

inhibition of prolactin release

dopamine
bromocriptine (dopamine agonist)
somatostatin
prolactin

27

slow GnRH pulse

decreased LH
increased FSH**

28

fast GnRH pulse

decreased FSH
increased LH**

29

pulsatile GnRH release

prevents downregulation of its receptor

30

continuous infusion of GnRH

cause decrease in both LH and FSH

31

thyroglobulin

to T4 and T3

32

thyroid hormone synthesis

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

TBG

binds T3 and T4 in blood

99% bound in circulation

34

T4 vs. T3

T4 to T3 ration 10:1

however, T3 is 10x more active at receptor

tissue has deiodinase to convert T4 to T3

35

normal T4 levels

5-12 microgram/dL

36

normal T3 levels

70-190 nanogram/dL

37

euthyroid sick syndrome

hypothyroidism

pathology - increased deiodinase D3 - forms inactive rT3

38

stimulation of thyroid hormone release

TSH
thyroid stimulating Igs
increased TBG

39

inhibition of thyroid hormone release

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

40

wolf-chaikoff effect

excess iodine causes inhibition of thyroid hormone release

41

action of thyroid hormones

growth
maturation of CNS
increased metabolism
increased cardiac output

42

thyrotoxicosis

excess thyroid hormone in body

43

hot nodule

overproduction of thyroid hormone

44

granulomatous thyroiditis

painful gland

45

graves disease

autoimmune disease
-antibodies that activate TSH receptor - increased thyroid hormone release

46

hashimotos disease

alpha-TPO Abs

destruction of thyroid tissue

primary hypothyroid

47

secondary hypothyroid

pituitary insufficiency

48

zones of adrenal gland

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

medulla - catecholamines

49

excess androgens absence of glucocorticoids and mineralocorticoids

21-alpha-hydroxylase deficiency

50

increased mineralocorticoids and absence of androgens

17-alpha hydroxylase deficiency

51

stimualtion of cortisol release

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

52

inhibition of cortisol release

increased blood cortisol levels
opiods
somatostatin

53

ACTH

stimulates adrenal cortex to release aldosterone

aldosterone also stimulated by ANG II via RAAS system

54

adrenal steroid hormones

glucocorticoids
mineralocorticoids
adrenal androgens

55

glucocoticorticoids

essential for survival during fasting

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

56

metabolic response to stress

to ensure sufficient energy to meet increased demand of body

cortisol release, increased E and NE

57

chronic elevated cortisol

localized obesity
muscle wasting/weakness

elevated insulin/glucagon ratio

58

acute elevated cortisol

decreased insulin/glucagon ratio

59

primary adrenocortical insufficiency

addison disease

60

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

addison disease

increased ACTH levels
-negative feedback of decreased cortisol

61

primary adrenal hyperplasia

cushing syndrome

62

excess ACTH

cushing disease

63

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

cushing syndrome

decrased ACTH
-negative feedback of increased cortisol

64

aldosterone secreting tumor

conn syndrome

65

HTN, hypokalemia, metabolic alkalosis, decreased renin

conn syndrome

66

virilization in females

21-beta hydroxylase deficiency

67

lack of pubic hair
deficient glucocorticoids
excess mineralocorticoids

17-alpha hyedroxylase deficiency