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FHB Endocrinology > L72: HPA Axis and Adrenal Gland > Flashcards

L72: HPA Axis and Adrenal Gland Flashcards

1
Q

What does the HPA Axis regulate in the adrenal gland?

A

Response to stress: Catecholeamines (Epi/NE), Glucocorticoids (Cortisol)

Immune Function: Anti-inflammatory (glucocorticoids)

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2
Q

What functions of the adrenal gland are NOT regulated by the HPA Axis?

A

Maintenance of water, sodium, potassium balance and blood pressure by Mineralocorticoids (Aldosterone)

Weak Androgen production (DHEA)

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3
Q

What is the HPA Axis

A

Hypothalamic-Pituitary-Adrenal Axis

CRH made in PVN of hypothalamus -> released at median eminence-> stimulate POMC gene expression -> ACTH release from corticotropes in anterior pituitary-> ACTH stimulates Adrenal Cortex-> produce cortisol

Classic Negative Feedback Pathways: ACTH (short neg to hypothalamus CRH), Cortisol (long neg to pituitary and hypothalamus)

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4
Q

Where is CRH produced?

A

Parvocellular Neurons of the PVN

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5
Q

What does CRH do?

A

Stimulates anterior pituitary to express POMC gene -> ACTH production

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6
Q

How is CRH secreted?

A

pulsatile -> leads to episodic release of ACTH

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7
Q

What are CRH receptors? Which binds CRH with highest affinity?

A

CRH R1 and CRH R2: GPCRs

Highest affinity to CRH R1 in anterior pituitary

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8
Q

How do AVP and CRH work in conjunction?

A

Synergistic actions to increase amplitude of ACTH release from anterior pituitary

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9
Q

What does the release of cortisol lead to for AVP and CRH?

A

NEgatively inhibits the synthesis and release of CRH and AVP by binding to the nuclear steroid glucocorticoid receptor in pituitary and hypothalamus

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10
Q

How is ACTH regulated?

A

REgualted by CRH and AVP from hypothalamus

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11
Q

What is the precursor for ACTH?

A

POMC (preprohormone)

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12
Q

What does ACTH do in the adrenal gland?

A

Steroid biosynthesis: stimulate conversion of cholesterol to pregnenolone

Z.Fasciculata and Z.Reticularis: syntehsis of cortisol and DHEA

Adrenal Medulla: Convert dopamine to NE

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13
Q

Does ATCH regulate Aldosteron in the Z.Glomerulosa?

A

NO. But it does regulate the synthesis of aldosterone precursors

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14
Q

What are the receptors for ACTH?

A

MC2R(adrenal cortex):Binds with high affinity to MC2R

MC1R(skin): binds with low affinity;High levels of ACTH can lead to hyperpigmentation

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15
Q

What are hte laeyrs of the adrenal gland from inner to outer?

A

Adrenal Medulla -> ZReticularies->Z.Fasciculata->Z.Glomerulosa

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16
Q

Which artery perfuses the cortex and adrenal medulla?

A

Capsular Artery

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17
Q

How does blood flow from the capsular artery?

A

From outer cortex to adrenal core via capillary beds -> controls access of steroid hormones to general circulation

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18
Q

Where are glucocorticoids made?

A

Z.Fasciculata

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19
Q

What are the glucocorticoids?

A

Cortisol

Corticosterone

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20
Q

How are glucocorticoids transported in blood?

A

Bound to transport proteins CBG (must dissociate to be active)

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21
Q

How much of glucocorticoids are free in circulation?

A

~5%

22
Q

How are glucocorticoids released?

A

in circadian manner, peaks at around 8am

23
Q

Where are Corticosteroid binding globulins (CBG) made?

A

Liver

24
Q

How much of cortisol in circulation are bound to CBG? Albumin?

A

CBG: 90%
Albumin: 7%
Free Cortisol: 3-4%

25
Q

Which hormone does CBG bind with higher affinity with cortisol or aldosterone?

A

Cortisol (30x higher)

26
Q

How does estrogen impact CBG?

A

Decreases CBG -> increased free cortisol

27
Q

How does shock/infection affect CBG?

A

Decreases CBG levels

28
Q

What kind of receptors do glucocorticoids bind?

A

Nuclear steroid receptor

29
Q

Where are glucocorticoid receptors found?

A

Most tissues

30
Q

What is the sequence of cortisol going to target tissue?

A

Cortisone (blood) -> Cross into target cell -> Dissociates chaperone from GR (glucocorticoid receptor) -> GR/Cortisol complex -> goes to nucleus -> act as transcription factor for gene transcription

31
Q

What converts Cortisone in the cell to Cortisol?

A

11B-HSD1

32
Q

How does cortisol affect muscle?

A

Decrease muscle mass-
Increase transcription of E3 ubiquitin ligase (MuRF-1) => Inc proteolysis

Inhibit amino acid uptake and AKT phosphorylation => decreased protein synthesis

33
Q

How does cortisol affect bone?

A

Inhibit intestinal calcium absorption
Inhibit bone formation (decrease IGF-1 receptors)
Increase bone resorption by activating osteoclasts

34
Q

How does cortisol affect immune response?

A

Inhibit inflammation and immune responses:
Binds to activated NF-kB and prevent its nuclear binding
Increases transcription of IkB (binds NF-kB in cytosol)

35
Q

How does cortisol affect the kidneys?

A

Increase GFR and increase free water clearance

36
Q

How does cortisol affect the cardiovascular system?

A

Maintain cardiac output
Increase arteriolar tone
Decrease endothelial permeability
Stimulates RBC production

37
Q

What is cortisol’s actions on metabolism?

A

Counter-regulatory to insulin: mobilize energy stores and increases plasma glucose:

Increase gluconeogenesis
Antagonize insulin action
Inhibit intestinal calcium absorption

38
Q

How does cortisol increase plasma glucose?

A

Increases tyrosine aminotransferase, PEP Carboxykinase, G6Phosphatase

Decrease GLUT4 insertion in muscle cells

39
Q

How does cortisol act on adipose tissue?

A

Increase lipolysis

Redistribute fat stores -> abdominal obesity and depletion of subcutaneous fat (thinning of limbs)

40
Q

What are the results of cortisol’s inhibition of immune function?

A

Inc anti-inflammatory cytokines
Inhibit prostaglandins
Suppress antibody formaiton
Increase neutrophils, platelets, RBCs

41
Q

What does glucocorticoid deficiency lead to in terms of cardiovascular funciton?

A

Hypotension

42
Q

What are cortisol’s actions on the CNS

A

Emotional response, perception, negative feedback on CRH and ACTH

43
Q

What is Cushing’s disease?

A

Excessive cortisol secretion due to pituitary adenoma -> get excessively high levels of ACTH

44
Q

What is cushing syndrome?

A

All others due to excess cortisol production (ex: exogenous cortisol intake) usually leads to low ACTH levels due to neg feedback.

45
Q

What happens with Cushing’s Disease?

A

Change in body fat Distribution: moon face, abdominal obesity, thin skin, bruising, buffalo hump

Osteoporosis: inhib calcium absorption in intestine

HTN: excess glucocorticoids-> activate MR(cortisol binds GR and MR equally)

Glucose intolerant: antagonzie insulin action

Purple Striae: fragile thin skin stretching over abdominal fat -> hemmorhage into striae

46
Q

What can also present similar to Cushing’s disease?

A

Long term glucocorticoid therapy treatment

47
Q

What is a consequence of prolonged glucocorticoid therapy?

A

Shutdown of HPA axis due to negative feedback on CRH and ACTH -> atrophy of Z.Fasciculata -> can’t synthesize endogenous glucocorticoids

48
Q

What is the sequence of the normal HPA Axis?

A

Hypothalamus ->CRH ->Pituitary ->ACTH -> Z.FAsciculata -> Cortisol

49
Q

What is Adrenal Insufficiency?

A

Failure of adrenal to secrete glucocorticoids, mineralocorticoids, or both

Primary: Failure at adrenal
Secondary: Failure to secrete CRH or ACTH

50
Q

What is Addison’s Disease?

A

Primary Adrenal Insufficiency due to autoimmune destruction of adrenals

51
Q

What is the most common cause of secondary Adrenal Insufficiency?

A

Sudden cessation of glucocorticoid therapy

FHB Endocrinology (10 decks)

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