Endocrine II Flashcards

1
Q

what is the thyroid glands secretory functional unit?

A

follicle

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2
Q

what does the thyroid follicle include?

A

cuboidal cells (follicular cells)
colloid (lumen)
c-cells (parafollicular cells)

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3
Q

cuboidal cells function

A

TG synthesis

iodine

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4
Q

colloid cell function

A

TG storage

T4/T3 storage

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5
Q

c cells function

A

calcitonin

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6
Q

what are the 8 steps to synthesis of t3/t4

A

1 TG synthesis and transport to lumen
2 Na/I cotransport into membrane
3 oxidation of I by peroxidase
4 organification of I into MIT and DIT on tyrosine on TG by peroxidase
5 coupling of MIT and DIT into t3/t4 by peroxidase
6 endocytosis of TG
7 hydrolysis and entering circ of t3/t4 by proteases
8 deiodination of MIT and DIT, recycle I and tyrosine

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7
Q

what is hashimotos thyroiditis?

levels of T4, TSH, TRH, Goiter?

A
chronic lymphocytic thyroiditis 
(primary HYPOthyroidism)
T4- decrease
TSH- increase
TRH- increase
Goiter? possible
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8
Q

what is pituitary hypothyroidism?

levels of T4, TSH, TRH, Goiter?

A
secondary hypothyroidism
T4- decrease
TSH- decrease
TRH- increase
Goiter? no
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9
Q

what is graves disease? BUG EYES

levels of T4, TSH, TRH, Goiter?

A
TSI autoimmune primary HYPERthyroidism
T4- increase
TSH- decrease
TRH- decrease
Goiter? possible
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10
Q

does the thyroid make more t4 or t3?

A

t4 90%

t3/rt3 10% (made mostly by other tissues deiodinizing)

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11
Q

if you have a t4 and you deiodinize the inner ring, is it active or inactive?

A

inactive

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12
Q

in the circulation are t3/t4 free or bound?

A

bound 70% to TBG

bound 29% to albumin

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13
Q

what are the half lives for t3/t4, why is t4 greater?

A

t4- 6 days, b/c higher affinity for TBG

t3- 1 day

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14
Q

does birth control increase or decrease TBG?

A

increase

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15
Q

does liver failure increase or decrease TBG?

A

decrease

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16
Q

to have a goiter what do you need?

A

activation of TSH receptor, by TSH or TSI

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17
Q

does t3 or t4 have greater affinity for the THR?

A

t3

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18
Q

what are the 4 B’s of normal T3 function?

A

basal metabolic rate
beta adrenergic effects
brain maturation
bone turnover– bone growth

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19
Q

when would you have an increased likelihood of fracture? hypo or hyper thyroidism?

A

BOTH

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20
Q

subclinical

A

no clinical symptoms of disease yet, but still has disease

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21
Q

what is a good starting point to test thyroid function?

A

TSH

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22
Q

Is Iodine deficiency hypo or hyper? TSH?

A

hypo, TSH increase

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23
Q

is HPA depression hypo or hyper? TSH?

A

hypo, TSH decrease

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24
Q

is pituitary adenoma hypo or hyper? TSH?

A

hyper, TSH increase

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25
Q

what are the clinical manifestations of thyroid storm?

A
fever
tachy
nausea
diarrhea
vomit
arrhythmias
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26
Q

what pts are most likely to have thyroid storm?

A

graves disease
thyroid tumor
high dose thyroid meds
subclinical hyperthyroidism

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27
Q

what are the treatments for thyroid storm? 3

A
PTU (inhibit t4/t3)
potassium iodide (wolff-chaikoff effect, too much iodine)
beta blocker (also slow t4-t3 conversion)
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28
Q

once thyroid hormones are transported to tissue cells what happens?

A

bind to hormone receptors that bind DNA and alter gene transcription

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29
Q

what are the two functional glands of the adrenal cortex?

A

cortex (3 layers that surround the medulla)

medulla (functions as modified sym. ganglion)

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30
Q

what are the 3 layers of the cortex

A

glomerulosa
fasciculata
reticularis

31
Q

which layer binds ANGII/K and what does it produce?

A
glomerulosa
aldosterone (mineralcorticoids)
32
Q

which layer binds ACTH and makes cortisol? (glucocorticoids)

A

fasciculata

33
Q

which layer binds ACTH and makes androgens?

A

reticularis

34
Q

what does the medulla bind? what does it produce?

A

Binds ACTH/cortisol/Ach

produces epo

35
Q

17alpha-OH deficient, ACTH? BP? aldosterone? androgen?

A

ACTH- increase
BP- increase
Aldosterone- increase
androgen- decrease

36
Q

21beta-OH deficient, ACTH? BP? aldosterone? androgen?

A

ACTH- increase
BP- decrease
Aldosterone- decrease
androgen- increase

37
Q

11beta-OH deficient, ACTH? BP? aldosterone? androgen?

A

ACTH- increase
BP- increase
Aldosterone- increase
androgen- increase

38
Q

what in cortisol production causes skin pigment changes?

A

MSH

39
Q

how much of cortisol is protein bound?

A

CBG 92% (less available)

albumin 8%(bioavailable)

40
Q

when is cortisol highest in the day

A

morning

41
Q

what are the critical effects of cortisol? BIG FIB

A
BIG
increase in BP
increase in Insulin resistance
increase in Glucose
FIB
decrease in Fibroblasts (stretch marks)
decrease in Inflammation and immunity
decrease in Bone formation
BONUS:
impaired learning/mem
42
Q

what things make cortisol anti inflammitory

A
stabilizes lysosomal membranes
decrease capillary permi
decrease WBC migration
decrease lymphocyte prolif
decrease in interleukin, histamine, prostaglandin
43
Q

if you are fasting and have acute stress what are the results?

A

liberation of all forms of energy: increase EPI/NE
liver- glycogen to glucose
sm- protein breakdown, glycogen to glucose
adipose- fat breakdown

44
Q

if you are overfed and chronically stressed

A

muscle wasting/ IR/ weight gain: decrease EPI/NE
CNS- increase appetite
liver- increase glycogen synthesis
sm- protein breakdown, decrease glucose uptake
adipose- decrease fat breakdown, TG synthesis, decrease glucose uptake

45
Q

what is cushings syndrome usually caused by

A

ACTH secreting tumor
adrenocortical hyperplasia
excess cortisol

46
Q

what does cushings disease look like?

A
unusual obesity
striae 
bone loss
muscle wasting
buffalo hump
diabetes
47
Q

what can increase aldosterone?

A

**mostly RAAS ANGII
increases serum K
increases ACTH

48
Q

what does aldosterone do to Na and K?

A

increases Na reabsorption

increases K secretion

49
Q

what is the half life of aldosterone?

A

20min

50
Q

how do corticoid receptors fx?

A

hormone binds to receptor in cytosol and sends regulatory proteins that allow the hormone-receptor complex to bind to DNA and alter transcription

51
Q

does aldosterone bind MR or GR?

A

MR

52
Q

does cortisol bind MR or GR?

A

MR and GR

53
Q

what is addisons disease caused by?

A

autoimmune attack on adrenal cortex

decreased cortisol and aldosterone

54
Q

what are the symptoms of addisons disease?

A

hypoglycemia
increased lymphocytes
hyperK
hypoNa
increase ACTH (increase MSH, why JFK had tan)
decrease vascular response to adrenergics

55
Q

short term stress response

A

adrenal medulla releases EPI
increase BP, HR, breakdown of glucose, metabolic rate
changes in blood flow to vital organs
dilate bronichioles

56
Q

long term stress response

A
retention of Na and water
increase in BP
protein and fat into glucose 
increase blood sugar
decreased immune system
57
Q

what is the major storage site for calcium and phosphate?

A

bone as hydroxyapatite (HA)

58
Q

free calcium vs protein bound calcium vs complexed calcium

A

free 50%
PB 40%
complex 10%

59
Q

free phosphate vs protein bound phosphate vs complexed phosphate

A

free 80%
PB 10%
complex 10%

60
Q

how does thyroid regulate Calcium?

A

c cells release calcitonin and lowers calcium

61
Q

how does parathyroid regulate phosphate and calcium?

A

chief cells release parathyroid hormone and increase phosphate and calcium

62
Q

how do the skin, liver and kidney regulate phosphate and calcium?

A

skin intakes Vit D
liver converts to 25OHVitD3
kidney converts to active VitD3

63
Q

how does the bone regulate phosphate?

A

osteocytes secrete FGF23 that regulate phosphate

64
Q

what is the normal blood calcium level?

A

10mg/100mL

65
Q

what is used theraputically to prevent bone loss? shows no clinical symptoms when deficient..

A

calcitonin

66
Q

what increased PTH?

A

hypocalcemia

hyperphosptemia

67
Q

what decreases PTH?

A

hypercalcemia

increases in Vit D and FGF23

68
Q

mechanism of action for release of PTH

A
Calcium binds to receptor on chief cell
second messanger IP3 releases intracell calcium
this inhibits production of PTH
DAG stimulates PKC to inhibit exocytosis
this inhibits release of PTH
69
Q

what stimulates the kidney to produce calcitriol?

A

PTH

70
Q

what inhibits the kidney to produce calcitriol?

A

increased Calcium
increased calcitriol
increased FGF23

71
Q

if you have negative Calcium balance what happens?

A

increase in PTH, increase in calcitriol

increase in bone breakdown, renal reabsorbtion

72
Q

if you have positive calcium balance what happens?

A

increase calcitonin, increase in calcitriol

inhibit osteoclasts and bone breakdown, promotes intestinal and renal reabsorbtion

73
Q

what does FGF23 do?

A

when PTH,Pi, and Vit D are elevated it lowers phosphate levels,
inhibiting renal reabsorbtion, PTH and Vit D

74
Q

what if you have uncontrolled hyperphosphatemia?

A

typical in CKD

increase PTH, bone loss, vascular calcification, death