endocrine lecture3 Flashcards

1
Q

what kind of hormone is glucagon?

A

peptide

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2
Q

what cells release glucagon?

A

alpha cells of the islets of langerhans

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3
Q

main stimulus for glucagon release?

A

drop in blood glucose

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4
Q

what is the GLUT found on pancreatic alpha cells?

A

GLUT4 (insulin dependent)

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5
Q

how does diabetes get exacerbated by glucagon?

A

low insulin –> no block on glucagon –> more and more glucagon –> higher blood glucose

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6
Q

what is the main glucagon receptor?

A

G protein receptor (Gs) (stimulates adenlyl cyclase)

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7
Q

glucagon’s main role occurs where in the body?

A

the liver, it has very few effects in the periphery and is not in appreciable concentrations there either

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8
Q

what does glucagon do in the liver?

A

activates the enzymes responsible for the reversal of insulin’s actions

  • glycogen breakdown
  • gluconeogenesis
  • beta oxidation of fatty acids –> acetyl CoA –> ketones
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9
Q

what GLUT occurs on liver cells?

A

GLUT2 (insulin independent)

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10
Q

structure of thyroid hormone?

A

2 tyrosine residues linked together by an ether, and iodonated

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11
Q

Is thyroid hormone water soluble?

A

no, but its not super hydrophobic either.

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12
Q

what cell type produces thyroid hormones?

A

follicular cell

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13
Q

iodo residue are generally in the ___ and ___ position on thyroid hormone?

A

3 and 5

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14
Q

which is the active thyroid hormone? T3 or T4?

A

T3 (3,5,3-triiodothyronine)

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15
Q

How does iodide get into the cell?

A

an Na+/iodide symporter, then Na+ is pumped out (REQUIRES ATP)

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16
Q

what is thyroperoxidase?

A

enzyme that converts iodide to active iodide, and attaches it to thyroid hormone. Also catalyzes the ether link between tyrosine residues

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17
Q

what is thyroglobulin?

A

protein made by follicular cell, which has tyrosine residues. Secreted INTO THE LUMEN of the follicle

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18
Q

what is “luminal colloid” made of?

A

thyroglobulin

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19
Q

does the lumen of the follicle have any free thyroid hormone?

A

NO, they are all bound up in thyroglobulin molecules. Must be endocytosed and processed in lysosomes to become free hormone

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20
Q

what does thyroid hormone do once its in the blood?

A

99% is bound up 1% is free

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21
Q

what does thyroid hormone do at its target cells?

A
  • binds to intracellular receptors in the nucleus
  • change gene expression
  • primary controller of basal metabolic rate
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22
Q

does T4 have any function?

A

yes, it is de-iodonaated in the target cells into the active form T3

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23
Q

will increased thyroid hormone cause higher or lower metabolic rate?

A

higher

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24
Q

what are the “permissive effects” of T3?

A

basically it means that Thyroid hormone is essential for the proper function of many other hormones (GH, epi, catecholamines)

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25
Q

how is thyroid hormone regulated?

A

hypothalamus (TRH–>thyrotropes–>TSH)

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26
Q

what kind of molecule is TSH?

A

peptide

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27
Q

what receptors does TSH use?

A

G protein receptors

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28
Q

how does TSH affect the thyroid gland?

A

regulates the number of follicle cells, levels of enzymes, levels of thyroglobulin, and iodide transport

29
Q

what is “organification of iodide”?

A

taking inorganic iodide and putting it into the organic molecule

30
Q

What causes HYPO-thyroidism?

A
  • endemic (water doesnt have enough iodide)
  • pituitary dysfunction
  • autoimmune (Hashimotos thyroiditis)
31
Q

what is the result of HYPO-thyroidism?

A
  • Cretinism (mental retardation)
  • enlarged thyroid gland
  • goiter
32
Q

levels of T3/T4, and TSH in case of endemic HYPO-thyroidism (low iodide)?

A
  • low T3/T4

- high TSH (disinhibited)

33
Q

levels of T3/T4, and TSH in case of panhypopituitarism HYPO-thyroidism

A
  • low T3/T4

- low TSH (since the problem is at the pituitary

34
Q

levels of T3/T4, and TSH in case of autoimmune HYPO-thyroidism?

A
  • low T3/T4

- high TSH

35
Q

What can cause HYPER-thyroidism?

A

tumor of thyroid
tumor if pituitary
graves disease (antibodies mimic TSH)

36
Q

what is the mechanism of graves disease?

A

antibodies simulate TSH. these are called TSI’s (thyroid stimulating immunoglobulins)

37
Q

levels of T3/T4, and TSH in case of thyroid tumor?

A
T3/T4 = high
TSH = low
38
Q

levels of T3/T4, and TSH in case of in case of pituitary tumor?

A
T3/T4 = high
TSH = high
39
Q

levels of T3/T4, and TSH in case of graves disease?

A
T3/T4 = high
TSH = low
40
Q

overall symptoms of HYPO-thyroidism?

A

low BMR, lethargy

41
Q

overall symptoms of HYPER-thyroidism?

A

high BMR, agitated

42
Q

adrenal gland is located where?

A

on top of kidney

43
Q

what are the 2 parts of the adrenal?

A

Cortex (steroids)

medulla (epinephrine)

44
Q

what are the 3 parts of the adrenal cortex?

A
zona glomerulosa (mineralocortocoids)
zona fasciculata (gluccocortocoids)
zona reticularis (sex steroids)
45
Q

what is the main mineralocortocoid?

A

aldosterone

46
Q

what is the main gluccocortocoid?

A

cortisol

47
Q

what are the main sex steroids?

A

androgens

48
Q

what controls the level of aldosterone?

A

renin angiotensin system

49
Q

why is cortisol important?

A

it regulates the stress response

50
Q

how is cortisol carried in the serum?

A

cortisol binding globulin (90% bound)

51
Q

what does cortisol do when it reaches its target?

A

enters cell, binds to receptor, goes to nucleus

  • counters the action of insulin
  • potentiates effects of epinephrine
  • increases gluconeogenesis
  • stimulates glycogen breakdown
  • protein breakdown in skeletal muscle
  • stimulates FFA breakdown
  • antiinflammatory effect
52
Q

what happens in HYPER-cortisol?

A
  • redistribute fat (buffalo hump, moon face, centripetal redistrubutions of fat)
  • inhibits fibroblasts in the skin (thin skin, easy bruising)
  • increases heart rate/contractility (upregulates B adrenergic receptors thereby potentiating epinephrine
  • controls RBC production (polycythemia / anemia)
  • antagonizes Vit D
53
Q

how does cortisol have an antiinflammatory effect?

A

-inhibits prostaglandin synthesis, therby preventing vascular permeablity increaes

54
Q

how does cortisol have immunosupressive effects?

A

inhibits T-cells

55
Q

what is the cortisol synthesis pathway?

A

hypothalamus –> CRH–> ant. pituitary (POMC) –> ACTH –> zona fasciculata–> cortisol –>negative feedback

56
Q

what does ACTH do to the adrenal cortex?

A
  • regulates number of cells

- regulates enzyme activity

57
Q

what regualtes ACTH production?

A

only cortisol levels

58
Q

what can cause HYPO-cortisol?

A

-Addison’s disease (autoimmune destroction of cortex)

59
Q

levels of cortisol, ACTH, and aldosterone in addisons disease?

A

cortisol down
ACTH up
aldosterone down

60
Q

levels of cortisol, ACTH, and aldosterone in hypo-pituitarism?

A

low cortisol
ACTH down
aldosterone normal

61
Q

what can cause HYPER-cortisol?

A

adrenal tumor
pituitary problem (cushings disease)
exogenous cushings

62
Q

what is addisons?

A

HYPO-cortisol

63
Q

what is cushings DISEASE

A

HYPER-cortisol cause by pituitary dysfunction

64
Q

levels of cortisol, ACTH, and aldosterone in adrenal tumor HYPER-cortisol

A

high cortisol
low ACTH
high aldosterone

65
Q

levels of cortisol, ACTH, and aldosterone in pituitary dysfunction HYPER-cortisol?

A

high cortisol
high ACTH
normal aldosterone

66
Q

levels of cortisol, ACTH, and aldosterone in exogenous cushings HYPER-cortisol?

A

high cortisol
low ACTH
normal aldosterone

67
Q

general symtoms of HYPER-cortisol?

A

immune supression

hyperglycemia

68
Q

what is cushings SYNDROME?

A

the constellation of problems caused by HYPER-cortisol in general