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Endo/Repro: Week 2 > Rose: Adrenal and Pancreas Physiology > Flashcards

Rose: Adrenal and Pancreas Physiology Flashcards

1
Q

What are the 3 zones of the adrenal cortex and what do they do?

A 
G= mineralcorticoids (aldosterone)
F= glucocorticoids (cortisol)
R= androgens
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2
Q

What part of the adrenal gland is a modified sympathetic ganglion that DIRECTLY releases catecholamines?

A

Medulla

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3
Q

Where is ACTH synthesized?

A

Corticotrophs

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4
Q

What is the primary ACTH receptor? Where is it expressed?

A

MC2-R (Melanocrotin receptor)

Adrenal cortex

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5
Q

Where is MC2-R also locate?

A

skin melanocytes and adipocytes (mediates stress induced lipolysis)

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6
Q

ACTH binds MC2-R then what….

A

GaPCR>
increased cAMP>
signal transduction cascade

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7
Q

How does ACTH affect CYP11A (side chain cleavage enzyme) synthesis in the adrenal cortex? Why?

A

PROMOTES synthesis

This rxn is REQUIRED for cholesterol conversion to pregnolone

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8
Q

What is the RLS in adrenal steroid syntehsis?

A

CYP11A

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9
Q

What is the primary active glucocorticoid and what does it do?

A

Cortisol>
binds glucocorticoid receptor>
increases glucose levles

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10
Q

How does cortisol promote gluconeogenesis?

A

Cortisol>
mobilizes AA from proteins>
liver>
gluconeogenesis

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11
Q

A def of cortisol may cause?

A

hypoglycemia

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12
Q

What does aldosterone do?

A

Promotes Na and H20 retention

binds mineralcorticoid receptor (MR)

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13
Q

What is the main sex steroid and what does it bind to?

A

DHEA, androstenedione and some testonsterone (minor site for estrogen synthesis)>
binds Androgen receptors

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14
Q

What percent of cortisol is bound to a carrier protein?

A

90%

60%= CBG= transcortin
30%= albumin
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15
Q

What leads to an increase in CBG?

A

estrogens

pregnancy

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16
Q

What leads to a decrease in CBG?

A

increased cortisol and liver cirrhosis

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17
Q

Where are GR located and what family do they belong to?

A

expressed in every cell in the CYTOPLASM

Nuclear receptor super family

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18
Q

What happens when hormone binds the GR?

A

Hormone binds receptor>
translocation to the nucleus>
homodimer

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19
Q

What is a homodimer?

A

TF

Binds to genes w/ GRE>
can up and down regulate trxn

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20
Q

What hormone has the highest affinity and potency for GR?

A

cortisol

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21
Q

What is an example of a MR?

A

Aldosterone REceptor

NR3C2

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22
Q

WHere are aldosterone receptors found?

A

kidney, colon, sweat glands, heart, hippocampus, brown adipose

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23
Q

Which has greater effect in mineralcorticoid responsive tissues–cortisol or aldosterone?

A

Cortisol is converted to cortisone in MCR tissues which is metabollically inactive>
cortisone has NO effect and aldosterone can act

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24
Q

What are the physiological effects of coritsol?

A
  1. carb met> increased gluconeogenesis + decreased glucose uptake by muscle and fat> increased plasma glucose
  2. fat met: increased lipolysis> increased free FA
  3. Protein met: increased proteolysis> increased N excretion
25
Q

What are the effects on the body of sustained cortisol levels?

A 
reproductive capacity
fat redistribution
muscle atrophy
collagen brkdown
bone loss
anti-inflammaotry
26
Q

What are the physiological effects of mineralcorticoids (aldosterone)?

A
  1. stimulates Kindey reabsorption of Na and water
  2. stimulates N and water reabsorption in teh colon, salivary glands, sweat glands
  3. enhances kidney K excretion
27
Q

Hypersecretion of aldosterone can lead to…

A

HTN

28
Q

What does the activity of glucocorticoid/steroid depend on?

A

tissue enzyme expression

29
Q

What does 11BHSD2 do?

A

It OXIDIZES active steroid to inactive steroid

30
Q

What tissues is 11BHSD2 active in?

A

Kidney, colon, SG, placenta, fetus

mineralcorticoid responsive tissues

31
Q

What does 11GHSD1 do?

A

Reduces inactive steroid to ACTIVE steroid

32
Q

Where is 11.BHSD1 active?

A

LIVER ADIPOSE

lung, vascular tissue, CNS

33
Q

What does most glucocorticoid metabolism ocur?

A

liver

cortisone and cortisol are rapidly conjugated>
tetrahydrocortisone and tetrahydrocortisol glucuronide/sulfate

34
Q

Are derivatives of glucocorticoid metabolism soluble in the serum?

A

YES and excreted by the kidneys

35
Q

How do you assess adrenal steroid production?

A

24 hr urine collection

36
Q

What are the main sources of cholesterol?

A

diet, liver, de novo synthesis

37
Q

What regulates side chain cleavage of cholesterol?

A

ACTH

*RATE LIMITING

38
Q

What is prenenolone?

A

common precursor to mineralcorticoids, glucocorticoids and androgens

39
Q

What step in adrenal steroidogenesis is common to all pathways?

A

cholesterol> progenolone

40
Q

What happens to pregenolone in the aldosterone pathway?

A

progesterone>
11-deoxy-corticosterone>
corticosterone>
aldosterone

41
Q

What happens to pregenolone in the cortisol pathway?

A 
→ 17α hydroxyl-pregnenolone 
→ 17α hydroxyl-progesterone 
– (*21 hydroxylase) 
→ 11-deoxycortisol 
– (*11b hydroxylase)
 → cortisol
42
Q

What happens to pregenolone in the androgen pathway?

A 
→ 17α hydroxyl-pregnenolone 
→ DHEA
 → Androestenediol 
OR  → 17α hydroxyl-pregnenolone 
→ 17α hydroxyl-progesterone 
→ androstenodione 
→ Testosterone
43
Q

What is the rate limiting enzymes involved in side chain cleavage in steroid synthesis from cholesterol?

A

CYP11A1

44
Q

What defect in steroid synthesis is responsible for 95% of genetic abnormalities and can lead to CAH?

A

CYP21A-21-hydroxylase

45
Q

What is the second MC enzymatic defect that can also cause CAH?

A

CYP11B1

46
Q

What is CYP11B2?

A

aldosterone synthase

47
Q

What are the sxs of 21 hydroxylase def?

A

decreased cortisol AND aldosterone>
virilization and HOTN (losing salt and reducing BV)

Increased: ACTH, enzymes, androgens

48
Q

What are the sxs of 11B-hydroxylase def?

A

Virilization (increased androgens)

HTN (increased deoxycorticosterone)

49
Q

What has tonic control over mineralcorticoid regulation?

A

ACTH

50
Q

What stimulates mineralcorticoid synthesis?

A

HIGH levels ACTHa nd normal level AT II» increases/maintains BP

51
Q

Does aldosterone NGB on ACTH?

A

No

52
Q

What can cause Hypercortisolism?

A
  1. Adrenal cortex: tumor/hyperplasia> excess cortisol production> cushing syndrome
  2. Pituitary adenoma (MC), hypothalamic cuase
  3. Taking steroids, morbid obesity, DM2> Cushing syndrome
53
Q

What are the effects of hypercortisolism?

A 
Moon face
bufallo hump
thin skin
high BP
red striae
pendulous abdomen
54
Q

How do you dx hypercortisolism?

A

Increased ACTH (pituitary adenoma)

Increaed cortisol (iatrogenic, adrenal gland problem)

55
Q

What causes hypocortisolism?

A
  1. immune mediated destruction of adrenal cortex> addison disease
  2. w/drawal of exog glucocorticoid> iatrogenic
56
Q

What are the effects of hypocorisolism?

A

fatigue/weakness
anorexia, wght loss
diarrhea
HYPERPIGMENTATION

57
Q

What causes hyperpigmentation observed in Addisons?

A

increased POMC>
increase in both ACTH and MSH>
hyperpigmentation via MC-R

58
Q

How do you dx Addisons?

A

decrease in cortisol and aldosterone

Endo/Repro: Week 2 (11 decks)

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