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FHB Hormone/Repro > 75 - HPA axis and adrenal gland > Flashcards

75 - HPA axis and adrenal gland Flashcards

1
Q

In what hypothalamic nucleus is corticotrophin-releasing hormone/factor (CRH/CRF) release from?

A

PVN

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2
Q

What CRH/CRF stimulate the release of?

A

ACTH release from corticotropes in anterior pituitary

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3
Q

What is the target gland of ACTH?

What is produced?

A
  • Adrenal cortex

- Cortisol

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4
Q

What triggers CRH release?

What are some specific eg’s?

A

Stress

- Emotional, chemical (e.g. drugs of abuse), physical (e.g. temperature)

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5
Q

How many AA’s is CRH?

A

41 AAs

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6
Q

Is CRH produced by parvo or magnocellular neurons of the PVN?

A

Parvocellular (ant pit)

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7
Q

What is the pattern of CRH release from the PVN?

A

Pulsatile (results in episodic release)

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8
Q

What is the half-life of CRH?

A

~5 min

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9
Q

What type of receptor does CRH bind?

A

GPCR

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10
Q

What are the names of the 2 CRH receptors?

A

CRH R1 and CRH R2

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11
Q

Regarding CRH receptors, which binds CRH in ant pit w/higher affinity?
Which binds w/higher affinity to urocortin?

A
  • CRH R1

- CRH R2

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12
Q

What is the 2nd msger system of CRH after it binds its GPCR?

A

GPCR -> GDP -> GTP -> AC -> PKA -> L-type Ca2+ channels -> Ca2+ in -> ACTH release

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13
Q

What hormone acts synergistically w/CRH to increase amplitude of ACTH release from the ant pit?

A

AVP

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14
Q

What is the name of the receptors that cortisol binds to negatively feedback on both the hypothalamus and anterior pituitary?

A

Nuclear steroid hormone glucocorticoid receptor (GR)

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15
Q

What hormones does cortisol inhibit the synthesis and release of when it binds GRs on the PVN?

A

CRH and AVP

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16
Q

From what gene does cortisol come from?

A

POMC (pro-opiomelanocortin), along w/a number of other hormones that are important for pregnancy and fetal development

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17
Q

What are the names of the 2 receptors to which ACTH binds?

A

melanocortin 1 and 2 receptors (MC1R, MC2R)

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18
Q

Which of the 2 receptors that ACTH binds (MC1R or MC2R) have a higher affinity for ACTH?
Where is the other receptor found, which binds ACTH w/lower affinity?

A
  • MC2R: Adrenal gland

- MC1R: Skin

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19
Q

Because ACTH binds the MC1R in the skin, very high levels of ACTH can lead to ____________ of the skin.

A

Hyperpigmentation (via melanin synthesis/dispersal)

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20
Q

How is small-lung cell carcinoma related to the stress HPA axis?

A

It’s a non-pituitary tumor that autonomously makes ACTH.

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21
Q

What are the immediate, subsequent, and long-term effects of ACTH binding its high-affinity MC2R receptor in the adrenal gland?

A

IMMEDIATE:
- Increased cholesterol esterase, decreased CE synthetase, increased cholesterol xport to mito, increased cholesterol binding to P450scc, increased pregnenolone production, increased StAR (all to make steroid hormones)
SUBSEQUENT
- Increased gene TS of P450scc/c17/c11, adrenoxin, LDL and HDL receptors
LONG-TERM
- Increased size and functional complexity of organelles
- Increased size and number of cells

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22
Q

The adrenal cortex derives from the (endo/meso/ecto-derm).

A

Mesoderm

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23
Q

The adrenal medulla derives from ______________.

A

Neural crest (it’s basically modified sympathetic postganglionic neurons)

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24
Q

(adrenal cortex or medulla?)

Steroid hormones are made in the ___________, while catecholamines are processed in the ____________.

A

cortex

medulla

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25
Q

Starting from the capsule and moving in, name the 4 layers of the adrenal gland.

A

Cortex: “GFR” (80-90%)

  1. Zona glomerulosa (15%)
  2. Zona fasciculata (65-80%)
  3. Zona reticularis (
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26
Q

What hormones are found in the zona glomerulosa?

A

Mineralocorticoids (aldosterone)

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27
Q

What hormones are found in the zona fasciculata?

A

Glucocorticoids (cortisol)

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28
Q

What hormones are found in the zona reticularis?

A

Weak androgens (DHEAS)

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29
Q

What hormones are synthesized in the medulla?

A

NE/E

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30
Q

Why do you see lipid droplets on histological sections of the adrenal cortex?

A

Steroidogenic cells need cholesterol to make steroids

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31
Q

What is the name of the type of cell in the medulla that makes NE/E?

A

Chromaffin cells

32
Q

Explain the adrenal cortex and medulla blood supply. (2 things)

A

Dual blood supply

  • There are 2 plexi that come into the cortex; this will come down and bath the medulla in corticosteroids (important for NE -> E conversion)
  • There is also a separate artery that goes straight to medulla
33
Q

What are glucocorticoids bound to in blood? (2 names + generic)

A

CBG/transcortin (90%)

- Also 7% to albumin

34
Q

In what manner/pattern are glucocorticoids released?

A

Circadian manner, peaking around 8AM

35
Q

Cortisol binds w/high affinity to what 2 receptors in the cytoplasm?

A
  • Glucocorticoid receptor (GR)

- Mineralocorticoid receptor (MR)

36
Q

Where are MRs found? Where are GRs found?

A

GR are everywhere, MR are restricted to where aldosterone acts. (recall, CRH and AVP closely related)

37
Q

To which “family” does CBP/transcortin belong?

A

Serpin family: serine protease inhibitor, NOT a protease inhibitor

38
Q

How does estrogen affect CBP during pregnancy, and how does this affect cortisol?

A

Decreases it, increasing serum cortisol

39
Q

Besides estrogen, what medical conditions can decrease CBP?

A
  • Shock
  • Severe infection
  • Hepatitis
40
Q

If cortisol is mostly bound by CBP, how could this alter the effects of another major hormone?

A

Since cortisol binds MRs and GRs, there will be less cortisol in the blood to compete w/aldosterone for binding to the MRs

41
Q

What type of receptor of GR?

A

Nuclear steroid receptor

- Ubiquitously expressed in most tissues

42
Q

What occurs when cortisol binds GR, mechanistically?

A

Cortisol binding dissociates GR from chaperone proteins (ie HSPs) in cytoplasm
- Cortisol:GR complex translocates to nucleus and acts as TS factor on gene promoters

43
Q

Cortisol is a pleiotropic hormone. What are some of its affects on muscle?

A

Maintain m. fcn/decrease m. mass

44
Q

Cortisol is a pleiotropic hormone. What are some of its affects on bone?

A
  • Decrease bone formation

- Increase bone resorption

45
Q

Cortisol is a pleiotropic hormone. What are some of its affects on CT?

A

Decrease CT

46
Q

Cortisol is a pleiotropic hormone. What are some of its affects on inflammation/immune system?

A

*Inhibit inflammatory/immune responses

47
Q

Cortisol is a pleiotropic hormone. What are some of its affects on the CV system?

A
  • Maintain CO
  • Increase arteriole tone
  • Decrease endothelial permeability
48
Q

Cortisol is a pleiotropic hormone. What are some of its affects on pregnancy?

A

Facilitate maturation of the fetus

49
Q

Cortisol is a pleiotropic hormone. What are some of its affects on the kidney?

A
  • Increase GFR

- Increase free water clearance

50
Q

Cortisol is a pleiotropic hormone. What are some of its affects on brain/mood?

A

Modulate emotional tone, wakefulness

51
Q

What are cortisol’s effects on metabolism?
(How is it closely related to another important metabolic hormone?)
- state how it affects sugar, lipids, protein, Ca2+

A

Metabolic Actions – potent counter-regulatory hormone to insulin. (antagonizes insulin action)

  • Mobilizes energy stores: increase plasma glucose = “glucocorticoid” (cortex of adrenal)
  • Increase GNG and plasma glucose levels
  • Increase lipolysis
  • Breaks down muscle protein - proteolysis
  • *Redistributes fat – abdominal obesity, depletion of subcutaneous fat
  • Inhibits intestinal calcium absorption
52
Q

What are the 3 enzymes gluconeogenic enzymes that cortisol stimulates the production of?

A
  • Glucose-6-phosphatase
  • PEP carboxykinase
  • Tyrosine aminotransferase (malate shuttle)
53
Q

What is the molecular mechanism that regulate insulin antagonism by cortisol in myocytes?

A

*Decrease GLUT-4 receptors on their membrane (decreases glucose uptake in muscle cells to maintain plasma glucose)

54
Q

In terms of gene TS, how does cortisol affect muscle cells? (should prob memorize)

A
  • Cortisol increases TS of MuRF-1 (an E3 ubiquitin ligase), stimulating proteolysis
  • Cortisol simultaneously inhibits AA uptake and AKT-P’lation, resulting in decreased protein synthesis
55
Q

How does cortisol stimulate lipolysis in adipose tissue? (3 genes + 1 other function that affect appearance)

A
  1. Increases TS of Mg11 gene- MAG lipase
  2. Increases TS of Lipe gene- HSTL
  3. Increases TS of Angpt14 gene- increases cAMP and activates HSLT
  4. Redistributes fat stores (abdominal obesity, thinning of limbs due to loss of sub-Q fat)
56
Q

By what cellular mechanism to glucocorticoids inhibit inflammation?

(anti-inflammatory effects are the primary reason glucocorticoids are given)

A

GR increases IκB transcription, preventing NF-κB nuclear translocation and thus blocking TS of inflammatory cytokines

57
Q

Besides blocking the synthesis of pro-inflammatory cytokines such as prostaglandins, how else do glucocorticoids affect the immune system and the blood?

A
  • Stimulates anti-inflammatory cytokines
  • Suppresses AB production
  • Increases neutrophils, platelets, and RBCs.
58
Q

By what process does cortisol affect intestinal Ca?

A

Inhibits intestinal Ca2+ absorption thru transcellular transport

59
Q

By what process does cortisol affect bone Ca? (2 ways)

A
  • Inhibits bone formation by decreasing IGF-I receptors

- Increases bone resorption by activating osteoclasts

60
Q

What is the general reasoning behind cortisol’s effects on blood flow to the brain/heart?

A

During physical stress, want blood to flow to brain/heart, away from periphery.

61
Q

Besides shunting blood to the brain/heart, what (3) effects does cortisol have on the vasculature?

A
  • Stimulates red blood cell production
  • Maintains responsiveness to catecholamine pressor effects (constrict peripheral vessels via alpha-adrenergic receptors; dilate coronary arteries in heart via beta-adrenergic receptors; Glucocorticoid excess = increased blood pressure/HTN)
  • Maintains vascular integrity and reactivity
62
Q

What psychiatric conditions could stimulate cortisol release?

A

Depression, anxiety, nervousness, panic, rage/aggression

63
Q

What defines Cushing disease vs Cushing syndrome?

A
  • “Cushing disease” – excessive cortisol secretion due to pituitary adenoma
  • “Cushing syndrome” – all other excess glucocorticoid etiologies
64
Q

What are the major sx of Cushing dz/syndrome?

A
  • Change in body fat distribution: moon face, buffalo hump, abdominal obesity, thin skin, bruising
  • Inhibition of intestinal Ca2+ absorption: osteoporosis
  • Hypertension: excess glucocorticoids activate MR
  • Glucose intolerant: antagonism of insulin action
  • Purple Striae – Fragile thin skin stretches over increased abdominal fat, vessels hemorrhage into striae
65
Q

What is the most common cause of Cushing syndrome?

A

Long-term glucocorticoid therapy

66
Q

What are some eg’s where you would use glucocorticoid therapy?

A

Medical Emergencies:

High acute dose to treat septic shock, severe asthma, severe autoimmune disease flare

67
Q

What are the long-term side effects of glucocorticoids?

68
Q

What is the danger of giving too much exogenous cortisol?

A

Lots of negative feedback…cells die and atrophy, pts no longer make their own glucocorticoids (Therefore pts must be weaned off slowly)

69
Q

What are some effects of chronic glucocorticoid administration, in terms of inflammation?
The immune system?
The adrenal gland?
Pre-term infants?

A
  • Anti-inflammatory
  • Immunosuppressive
  • Adrenal insufficiency
  • Pre-term infants – improved lung function
70
Q

Which of the following glucocorticoids has the strongest potency and is therefore mainly used for diagnositcs?
Cortisol, prednisone, dexamethasone, methylprednisone, fludrocortisone

A

Dexamethasone

71
Q

Which of the following glucocorticoids has the weakest potency?
Cortisol, prednisone, dexamethasone, methylprednisone, fludrocortisone

72
Q

What is adrenal insufficiency (AI)?

What are the names of the 2 types?

A

Failure of adrenal to secrete glucocorticoids, mineralocorticoids, or both
- Primary and secondary

73
Q

What is the difference b/w primary and secondary adrenal insufficiency?

A
  • Primary: failure at the adrenal gland

- Secondary: failure to secrete ACTH or CRH

74
Q

Is Addison’s dz a primary or secondary adrenal insufficiency?

A

Primary: autoimmune destruction of adrenals

70% of primary AI cases

75
Q

What’s the most common cause of secondary adrenal insufficiency?

A

*Sudden cessation of glucocorticoid therapy

FHB Hormone/Repro (16 decks)

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