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Endocrinology > Lecture 6: HPA Axis and Adrenal Gland - Part 2 > Flashcards

Lecture 6: HPA Axis and Adrenal Gland - Part 2 Flashcards

1
Q

What are mineralocorticoids?

A

steroid hormones that regulate sodium/water balance

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2
Q

What is the primary endogenous mineralocorticoid?

A

aldosterone

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3
Q

What is the precursor to aldosterone?

A

11-deoxycorticosterone

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4
Q

What 4 sites has high mineralocorticoid action?

A

1) distal tubule in kidney
2) colon
3) salivary ducts
4) sweat ducts

MR IS ONLY FOUND IN THESE 4 PLACES

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5
Q

What is the main target of MR action?

A

kidney (stimulates sodium and water reabsorption; also increases potassium secretion)

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6
Q

What is the main stimulator of aldosterone?

A

potassium levels

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7
Q

What stimulates renin release from the JGA of the kidney?

A

decreased blood pressure

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8
Q

What does renin do?

A

cleave angiotensinogen (from the liver) to angiotensin I

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9
Q

What converts AT1 to ATII?

A

Angtiontensin converting enzyme (ACE)

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10
Q

What does ATII do?

A

VASOCONSTRICTS and stimulates aldosterone

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11
Q

How does cortisol influence the renin-angiotensin system?

A

increases substrate of angiotensinogen

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12
Q

_________ is the primary regulator of ECV while ________ is the primary regulator of free water balance

A

aldosterone; ADH

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13
Q

What 2 things does aldosterone do?

A

1) stimulates Na+ and water reabsorption in the kidney
2) stimulates K+ excretion

NET RESULT: increases ECV and BP (sodium in extracellular space pulls water)

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14
Q

What does ADH do?

A

1) stimulates distal nephron water permeability (increases water retention)
2) decreases plasma osmolality which secondarily affects sodium conc in the blood

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15
Q

What happens when cortisol enters a mineralocorticoid cell?

A

it is deactivated to cortisone (inactive) and then flows back to the blood where it encounters another cell that converts it back to cortisol

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16
Q

What is the main hormonal actor on mineralocorticoid cells?

A

aldosterone (mineralocorticoid)

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17
Q

What form of glucocorticoid enters GC target cells?

A

cortisone (converts to cortisol by 11b-HSD1) then binds to GR

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18
Q

Which 11b-HSD is in the GC cells? Mineralocorticoid cells?

A

GC cells: 1

MC cells: 2

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19
Q

What inhibits 11B-HSD2 and what effects does that inhibition have on homeostasis?

A

carbenoxolone and licorice

block 11B-HSD2, cortisol cannot be converted to inactive cortisone so leads to increased sodium and water retention

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20
Q

What zone is right up against the medulla?

A

zona reticularis (makes weak androgens)

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21
Q

Why are androgens produced in the reticularis considered “weak?”

A

low binding affinity for androgen receptors

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22
Q

When is the adrenal gland the primary source of androgen and estrogen for women?

A

post menopausal

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23
Q

What fraction of total androgen precursors in adult male prostate come from adrenal?

A

50%

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24
Q

What is the precursor for all steroid hormones?

A

pregnenolone

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25
Q

The first step towards steroid hormone production is regulated by what?

A

ACTH

26
Q

What is CYP11A1 and what does it do?

A

converts FC to pregnenolone

it is a desmolase - cleaves cholesterol side chain

27
Q

Match aldosterone, cortisol, androstenedione with glomerulosa, fasciculata, reticulata

A

aldosterone —-> glomerulosa
cortisol —–> fasciculata
androstenedione —-> reticularis

28
Q

What is the flow from cholesterol to becoming cortisol?

A

cholesterol –> pregnenolone –> progesterone –> 17(OH) progesterone –> 11-deoxycortisol –> cortisol

29
Q

What happens in a 21a hydroxylase deficiency?

A

excess DHEA, no mineralocorticoids/GCs

most common cause of congenital adrenal hyperplasia

signs: virilization, ambiguous genitalia

30
Q

Why do androgens increase when mineralocorticoids decrease (as in a CYP21A2 deficiency?)?

A

blood flow trickles down through zones so all precursors are high (ACTH stimulates upstream pathways and enzymes that are part of pathway leading to excessive androgen production)

31
Q

What is the gene for 11 hydroxylase?

A

CYP11B1

32
Q

What happens in a 11 hydroxylase deficiency?

A

no cortisol; low aldosterone; high MR activity; increased androgens

signs: masculinzation, hypertension

33
Q

17a hydroxylase is only found where?

A

fasciculata and reticularis (NOT glomerulosa)

34
Q

What happens in a 17a hydroxylase deficiency?

A

no cortisol; high aldosterone; decreased androgens

35
Q

What is the only important enzyme found in the zona reticularis?

A

17a hydroxylase (also in fasciculata)

36
Q

Which enzyme is only found in the glomerulosa?

A

aldosterone synthase (CYP11B2)

aka 11 hydroxylase

37
Q

An 11 hydroxylase deficiency is referring to a defect where?

A

CYP11B1 in z. fasciculata

38
Q

What is the ACTH receptor?

A

MC2R

39
Q

What are the ACTH targets in the adrenal gland?

A

1) stimulates conversion of cholesterol to pregnenolone by activating StAR
2) stimulates cellular hypertrophy
3) stimulates biosynthesis of cortisol, DHEA, 11b-hydroxylase
4) stimulates conversion of dopamine to norep (medulla)

40
Q

What is the predominant catecholamine secreted from the adrenal medulla?

A

epinephrine (not norep)

41
Q

the adrenal medulla originates from ______________

A

neural crest (same type that forms sympathetic ganglia)

42
Q

Describe the morphology of the adrenal medulla cells

A

cords of polyhedral shaped epithelial cells

43
Q

What are the 3 catecholamines?

A

1) dopamine
2) norepinephrine
3) epinephrine

44
Q

What is the pathway of catecholamine synthesis?

A

tyrosine —-> XDOPA —–> Dopamine —–> Norepinephrine —–> epinephrine

45
Q

What is the rate limiting step in catecholamine synthesis?

A

tyrosine hydroxylase (converts tyrosine to XDOPA)

46
Q

Where in the body does the pathway stop at dopamine?

A

brain (dopaminergic neurons)

47
Q

Where in the body does the pathway convert dopamine to norep?

A

peripheral nerves

48
Q

What stimulates conversion of norep to ep? And where?

A

Cortisol in the adrenal medulla

49
Q

Which intermediate of the tyrsoine —> catecholamine pathway is found in greatest abundance?

A

epinephrine

50
Q

What happens to the tyrosine —-> catecholamine pathway in the absence of cortisol?

A

build up of norep

51
Q

What are the 3 main targets of epineprine?

A

1) muscle
2) liver
3) fat

52
Q

What does epinephrine do in the skeletal muscle?

A

promotes glycogenolysis (releases ATP for local energy —> cannot provide energy for the whole body because glucose 6-phosphatase is not expressed in skeletal muscle)

53
Q

What does epinephrine do on liver?

A

releases glucose into the blood

antagonize what insulin is doing

54
Q

What does epinephrine do in fat?

A

promote lipolysis

55
Q

What is the main goal of epinephrine?

A

to get energy to muscle and adequate oxygen and glucose to brain (vasoconstricts everything but coronaries)

leads to GI and bronchial muscle relaxation

increases metabolic rate

56
Q

In times of stress, cortisol increases and epinephrine __________

A

INCREASES (cortisol converts norep to ep)

57
Q

Acute stress activates the symp and stimulates the release of _____

A

NE

58
Q

What does NE do?

A

stimulates CRH to initiate HPA response to long-term stress

59
Q

What is produced when you have an excess of catecholamines produced?

A

VMA (used to clinically detect tumors producing excess EPI or NE)

60
Q

What are pheochromocytomas?

A

tumors originating from the chromaffin cells

61
Q

What are symptoms of too much catecholamine production?

A

hypertension, headaches, tachy

62
Q

Why are pheochromocytomas called the 10% tumor?

A

10% of them are malignant, bilateral, in children, familian, recur, MEN syndrome, stroke, extra-adrenal

Endocrinology (16 decks)

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