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OLD "MBS 603" > Lecture & Vodcast 3 -- Exam 5 > Flashcards

Lecture & Vodcast 3 -- Exam 5 Flashcards

1
Q

What hormone does zone 1 (Glomerulosa) in the adrenal gland secrete?

A

aldosterone

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2
Q

What hormone does zone 2 (fasciculata) in the adrenal gland secrete?

A

cortisol

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3
Q

What hormone does zone 3 (reticularis) in the adrenal gland secrete?

A

epinephrine and testosterone
** main source of epinephrine

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4
Q

What is the precursor for aldosterone, cortisol and testosterone?

A

cholesterol

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5
Q

When making aldosterone, cortisol and testosterone, cholesterol is converted into _______________ in the adrenal gland

A

pregnenolone

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6
Q

When making aldosterone, cortisol and testosterone, cholesterol is converted into pregnenolone by what enzyme in the adrenal gland?

A

P450 Scc

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7
Q

What enzyme does zone 1 (aldosterone) and zone 2 (cortisol) share when making these hormones in the adrenal gland?

A

21 hydroxylase

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8
Q

What is the enzyme zone 1 needs to make aldosterone and is the final enzyme before aldosterone is created in adrenal gland?

A

P450 aldosterone synthase

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9
Q

Does high or low Na+ passing through the glomerula (zone 1) in adrenal gland induce synthesis of aldosterone?

A

low Na+
** will stimulate reaborption

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10
Q

_____ is the actual stimulator for aldosterone secretion and not Na+ levels because its the one that binds to zone 1 cells to induce aldosterone secretion in adrenal gland

A

AT II

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11
Q

______kalemia causes opening of Ca2+ channels on zone 1 cells to start the second messenger pathway for aldosterone synthesis in adrenal gland.

A

hyperkalemia

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12
Q

What are the 4 roles of aldosterone in zone 1 of the adrenal gland?

A
  1. increase apical Na+ channels (for absorption)
  2. increase basolateral Na/K ATPase (for absorption)
  3. increase ATP (for step 2)
  4. increase apical K+ channels (K+ secretion)
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13
Q

___________ blood volume triggers zone 1 cells

A

decreased

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14
Q

What are the 3 hormones for the hypothalamic-pituitary-adrenal axis?

A

hypothalamus: CRH
pituitary: ACTH
adrenal: cortisol

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15
Q

_______glycemia induces cortisol secretion

A

hypoglycemia (cortisol raises BG)

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16
Q

What is cortisols main function?

A

raise blood glucose

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17
Q

_______ from the pituitary stimulates release of cortisol in the adrenal gland

A

ACTH

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18
Q

______ can feedback in a short loop fashion to stop CRH secretion from hypothalamus

A

ACTH

** short: pituitary –> hypothalamus

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19
Q

cortisol can feedback in a long loop fashion to stop ______ secretion from the hypothalamus

A

CRH

** long loop: periphery gland –> hypothalamus

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20
Q

What lipid binds to zone 2 cells when ACTH binds and is needed because its the precusor for the zone 2 hormone?

A

LDL (cholesterol)

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21
Q

When does cortisol peak the most?

A

right when you wake

** long fast

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22
Q

Cortisol secretion follows _______ patterns

A

feeding

  • rises between meals
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23
Q

What is cortisol’s affect on fat?

A

increases breakdown except in stomach
* to raise BG

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24
Q

What’s cortisol’s affect on protein synthesis?

A

decreases synthesis
* to raise BG

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25
Q

Why does cortisol seem to break everything down for glucose except it increases glycogen storage?

A

stores some glucose to prevent hyperglycemia

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26
Q

How does cortisol affect the immune system?

A

suppresses it

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27
Q

What is the precursor for epinephrine in zone 3 of the adrenal gland?

A

tyrosine

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28
Q

What enzyme converts tyrosine to DOPA when synthesizing epinephrine in zone 3 of the adrenal gland?

A

tyrosine hydroxylase

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29
Q

What nervous system stimulates the function of tyrosine hydroxylase in zone 3 of adrenal gland?

A

SNS
** remember we are producing epinephrine

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30
Q

What enzyme converts norepinephrine into epinephrine in the zone 3 of adrenal gland?

A

PNMT

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31
Q

Why is cortisol needed to convert norepinephrine into epinephrine even though these hormones are made in 2 different zones of the adrenal gland?

A

blood supply to the adrenal gland passes through zone 2 before it gets to zone 3 so cortisosl is carried

32
Q

Is the an aldosterone deficiency or excess?
salt craving
low sodium
acidosis
dehydration

A

deficiency

33
Q

Is the an aldosterone deficiency or excess?
Na+ retention
hypokalemia
hypertension

A

excess

34
Q

What is Addison’s disease?

A

autoimmune destruction of adrenal gland

35
Q

What is the affect of aldosterone and cortisol levels in Addison’s disease?

A

decreased

36
Q

Does Addison’s disease cause increasing weight or decreasing weight?

A

decreasing

  • cannot regulate hunger due to low cortisol levels
37
Q

Does Addison’s disease cause high or low blood glucose?

A

low (no cortisol to increase it)

38
Q

What is affect of ACTH levels in Addison’s Disease?

A

high because the adrenal gland is what is messed up so no cortisol is being produced causing excessive secretion of ACTH by pituitary

39
Q

What is Cushing’s syndrome?

A

excess cortisol

40
Q

In Cushing’s syndrome, what are the levels of ACTH, cortisol, and adrogens?

A

increased

41
Q

What would happen to ATII and ACTH and testosterone levels if there is a 21-hydroylase deficiency?

A

ATII and ACTH would be high (they are upstream of issue) which drives production of pregnenolone (precursor for adrenal cortisol and adlosterone) which will make a TON of testosterone

42
Q

What do alpha cells produce in the pancreas?

A

glucagon

43
Q

What do beta cells produce in the islet of the pancreas?

A

insulin

44
Q

What do delta cells produce in the islet of the pancreas?

A

somatostatin

45
Q

The islets of the pancreas receive stimulation for para sympathetic and sympatheic NS because cells there produce ________ and _________

A

insulin
glucagon

46
Q

What is the role of glucagon?
What about insulin?

A

glucagon: raise BG
insulin: lower BG

47
Q

What are the 2 ways glucagon can raise BG?

A

glycogenolysis
gluconeogenesis

48
Q

Where are most of glucagon’s effects felt?

A

liver

49
Q

Why does glucagon function the most in the liver?

A

first location glucagon goes when its released

50
Q

Is hexokinase inhibited or activated in glucagon conditions?

A

inhibited (dont want to uptake glucose)

51
Q

Does glycogen levels increase or decrease in glucagon conditions?

A

decrease (breaks it down for glucose)

52
Q

Is acetyl coA carboxylase inhibited or activated in glucagon conditions?

A

inhibited to prevent malonyl coA from storing glucose as triglycerides

53
Q

What happens to malonyl coA if glucagon has inhibited cetyl coA carboxylase?

A

it goes through beta oxidation to generate ketone bodies

54
Q

Rising ketone levels turn off _______ to prevent ketoacidosis

A

glucagon

55
Q

What glucose transporter is insulin-independent?

A

GLUT2

56
Q

What is the role of the ATP-sensitive K+ channels in insulin secretion?

A

formation of ATP (from glycolysis products) closes K+ channel which allows for an influx of Ca2+ = depolarization = release of insulin

57
Q

When glucagon is high it can stimulate ________ to prevent hyperglycemia

A

insulin

58
Q

__________ ________ can activate insulin and glucagon

A

amino acids

59
Q

When insulin binds to its receptor it phosphorylates IRS which induces transcription of ….

A

GLUT 4

60
Q

What glucose transporter is insulin-dependent?

A

GLUT4

61
Q

What tissue type has GLUT 4?

A

muscle tissue (prevents excessive glucose uptake)
adipose tissue

62
Q

Why can glucose never leave muscle cells?

A

it doesn’t have a G6Pase

63
Q

What is insulin’s affect on lipids in muscle tissue?

A

increases lipogenesis

64
Q

What is insulin’s affect on protein synthesis in muscle tissue?

A

increases

65
Q

What tissue contains GLUT2?

A

liver

66
Q

What is insulins affect on glycogen in the liver?

A

increases storage

67
Q

What is insulin’s affect on acetyl coA carboxylase?

A

increases it = increased triglyceride

68
Q

Somatostatin is not a primary regulator of insulin and glucagon because it’s meant for _______ __________

A

fine tuning

69
Q

Glucagon __can/can’t__ directly stimulate insulin but insulin ___can/can’t___ stimulate glucagon

A

can
can’t

70
Q

Do type I diabetics have high or low insulin levels?

A

low
* destruction of beta cells

71
Q

Do type I diabetics have high or low ketone bodies?

A

high
* no insulin to turn it off

72
Q

Do type I diabetics have insulin resistance?

A

no

73
Q

How does metformin function as a diabetic drug?

A

reduces liver gluconeogenesis

74
Q

How does Sulfonylureas function as a diabetic drug?

A

blocks ATP-sensitive K+ channel to induce insulin secretion
* increases intracellular ca2+ to induce insulin secretion

75
Q

How does DPP-4 inhibitors function as a diabetic drug?

A

reduces gluconeogensis in liver
blocks DPP-4 = more insulin

76
Q

How does SGLT2 inhibitors function as a diabetic drug?

A

increases glucose excretion

77
Q

How does GLP-1 agonist function as a diabetic drug?

A

synthetic GLP-1 increases insulin secretion
reduces gastric emptying

OLD "MBS 603" (22 decks)

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