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Endocrinology > Exam 3 Lesson 19 > Flashcards

Exam 3 Lesson 19 Flashcards

1
Q

Pathway from cholesterol to aldosterone/mineralocorticoids

A

Cholesterol – pregnenolone – progesterone – deoxycorticosterone – corticosterone – 18-hydroxycorticosterone – aldosterone – mineralocorticoids

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2
Q

pathway from cholesterol to cortisol/glucocorticoids

A

Cholesterol – pregnenolone – 17-hydroxypregnenolone – 17-hydroxyprogesterone – 11-deoxycortisol – cortisol/glucorticoids

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3
Q

pathway from cholesterol to androstenedione/androgens

A

Cholesterol – pregnenolone - 17-hydroxypregnenolone – Dehydroepiandrosterone – androstenedione / androgens

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4
Q

pathway from progesterone to cortisol/glucorticoids

A

Progesterone – 17-hydroxyprogesterone – 11-deoxycortisol – cortisol/glucocorticoids

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5
Q

pathway from progesterone to androstenedione/androgens

A

progesterone – 17-hydroxyprogesterone – androstenedione/androgerns

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6
Q

what does zona glomerulosa secrete? What regulates its secretion?

A

aldosterone (mineralocorticoid)/ renin-angiotensin

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7
Q

what does zona fasciculata secrete? What regulates its secretion?

A

cortisol (glucocorticoid)/ACTH

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8
Q

what does zona reticularis secrete? What regulates its secretion?

A

dehydroepiandrosterone/ACTH

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9
Q

what is congenital adrenal hyperplasia (CAH)?

A

genetic enzymatic defects in cortisol synthesis. The adrenal cortex will still respond to ACTH, so hyperplasia will develop

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10
Q

what is a cause of CAH?

A

inborn defect to 21-hydroxylase. Its precursor is converted to androgen instead. Aldosterone lacking causes hypoaldosteronism. You will see hypotension and low Na+ in plasma)

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11
Q

what are cortisol and corticosterone?

A

glucocorticoids

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12
Q

what are aldosterone and deoxycorticosterone?

A

mineralocorticoids

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13
Q

what are DHEA, DHEA-S, androstenedione?

A

androgens

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14
Q

what does cortisol regulate?

A

intermediary metabolism

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15
Q

how are cortisol effects permissive?

A

cortisol doesn’t directly initiate metabolic or circulatory processes, but it is necessary to permit their full expression

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16
Q

how does ACTH regulate cortisol?

A

ACTH has a GCPR that is coupled with Gs, which activates adenylyl cyclase, cAMP, and in turn, PKA, which turns on the cholesteryl ester hydroxylase in the lipid proteins that turn cholesteryl esters into free cholesterol. Then the free cholesterol can go on to become cortisol.

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17
Q

where does ACTH come from?

A

anterior pituitary

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18
Q

What happens to cortisol once it is secreted?

A

it can become free cortisol in the plasma. Then, it will either bind to a cotisol-binding protein or it will be absorbed by tissue.

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19
Q

which proteins bind with cortisol in the plasma?

A

Corticosteroid-binding globulin or albumin

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20
Q

how large is corticosteroid-binding globulin? Where is it synthesized and secreted?

A

50 KD, in the liver

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21
Q

11Beta-hydroxysteroid dehydrogenase

A

enzyme used to convert cortisol to cortisone and vice versa

22
Q

11beta-HSD 2

A

converts cortisol to cortisone

23
Q

11beta-HSD 1

A

converts cortisone to cortisol

24
Q

which is inactive? Cortisol or cortisone? Active?

A

cortisol is active/ cortisone is inactive.

25
Q

why can’t cortisone bind to mineralocorticoid or glucocorticoid receptors?

A

because it is inactive. Cortisol can because it is active.

26
Q

what is the half life of cortisol?

A

70-90 minutes

27
Q

how does cortisol regulate carbohydrate metabolism?

A

increases glucose supply/decreases body’s glucose utilization

28
Q

how does cortisol regulate protein metabolism?

A

decreases amino acid utilization, except in liver

29
Q

how does cortisol regulate fat metabolism?

A

increases fatty acid/glycerol mobilization; stimulates appetite and fat deposition in trunk area

30
Q

How does cortisol maintain normal vascular integrity?

A

it preserves volume of body fluids, and its absence can cause vasodilation and bp to fall

31
Q

what do glucocorticoids suppress?

A

inflammation and immune reactions

32
Q

how does cortisol affect the CNS?

A

it provides negative feedback control; modulates perceptions and emotion.

33
Q

what is cortisol important for in development?

A

development and maturation of tissues like intestinal enzymes and lung surfactants

34
Q

what happens if glucocorticoid levels are high after birth?

A

they inhibit skeletal growth

35
Q

Hypothalamic-pituitary-adrenal axis: what does hypothalamus release to pituitary?

A

CRH and vasopressin

36
Q

Hypothalamic-pituitary-adrenal axis: what does pituitary release after being stimulated?

A

ACTH

37
Q

Hypothalamic-pituitary-adrenal axis: what does adrenal gland release?

A

steroid hormones

38
Q

Hypothalamic-pituitary-adrenal axis: how does cortisol affect the axis?

A

it provides feedback inhibition

39
Q

addison disease

A

primary hypoadrenalism by adrenal cortex destruction (infection or autoimmune disease). Symptoms include low cortisol and aldosterone levels and high ACTH levels

40
Q

cushing syndrome

A

high ACTH. Stimulates glucocorticoid oversecretion

41
Q

conn syndrome

A

mineralocorticoid excess (tumor growth). Symptoms are hypertension and hypokalemia (low potassium)

42
Q

excess glucocorticoid effect: brain/CNS

A

depression/psychosis

43
Q

excess glucocorticoid effect: endocrine system

A

decrease LH, FSH, TSH release, GH secretion

44
Q

excess glucocorticoid effect: liver/ carb and lipid metabolism

A

increase in hepatic glycogen deposition; increase in peripheral insulin resistance; increase in gluconeogenesis; increase in free fatty acid production; overall diabetogenic effect

45
Q

excess glucocorticoid effect: cardiovascular/renal

A

salt and water retention; hypertension

46
Q

excess glucocorticoid effect: adipose tissue distribution

A

promotes visceral obesity

47
Q

excess glucocorticoid effect: bone and calcium metabolism

A

decrease in bone formation, decrease bone mass and osteoporosis

48
Q

excess glucocorticoid effect: growth and development

A

decrease in linear growth

49
Q

excess glucocorticoid effect: skin/muscle/connective tissue

A

protein catabolism/ collagen breakdown; skin thinning; muscular atrophy

50
Q

excess glucocorticoid effect: immune system

A

Anti-inflammatory action; immunosuppresion

Endocrinology (21 decks)

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