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Endocrinology > Lecture 5: HPA Axis and Adrenal Gland Part 1 > Flashcards

Lecture 5: HPA Axis and Adrenal Gland Part 1 Flashcards

1
Q

What two major functions are regulated by the HPA axis?

A

1) Adaptive response to stress

2) Immune function

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2
Q

What are the 2 legs of the adaptive response to stress?

A

1) Catecholamines (epi and NE)

2) Glucocorticoids (cortisol)

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3
Q

What is NOT regulated by the HPA axis?

A

maintenance of water, sodium, potassium balance and blood pressure

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4
Q

What is the HPA axis?

A

H - hypothalamus (CRH/CRF}
P - pituitary (ACTH)
A - adrenal

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5
Q

What promotes CRH release?

A

STRESS

hypoglycemia, emotional, physical, etc

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6
Q

What is the central regulator of the HPA axis and where is it produced?

A

CRH (made in PVN)

responsible for stimulating POMC/ACTH

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7
Q

True or false: CRH is released in a pulsatile fashion

A

TRUE (5 min half life)

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8
Q

What kind of receptor does CRH bind to?

A

GPCR

highest affinity to CRH R1

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9
Q

How does the presence of AVP affect ACTH release?

A

Amplifies it

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10
Q

What cell type in the anterior pituitary produces ACTH?

A

corticotrophs

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11
Q

What is the precursor to ACTH?

A

POMC (pre-opiomelanocortin)

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12
Q

What receptor does ACTH bind to with the highest affinity? lowest?

A

Highest: MC2R
lowest: MC1R (skin)

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13
Q

What do high levels of ACTA lead to?

A

hyperpigmentation

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14
Q

What are the immediate effects of ACTH binding to MC2R?

A

1) increased cholesterol esterase activity
2) decrease cholesterol ester synthetase
3) increase cholesterol transport into mitochondria
4) increase pregnenolone production
5) increase StAR protein (bring cholesterol from outer to inner mito)

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15
Q

What are the long term effects of ACTH action?

A

increased size and functional complexity of organelles

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16
Q

What secondary messenger does ACTH/MC2R work through?

A

cAMP

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17
Q

The adrenal cortex derives from __________ while the medulla derives from ____________

A

mesoderm; neural crest (modified sympathetic postganglionic neurons)

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18
Q

What hormones are produced in the cortex?

A

steroid hormones (aldosterone and androgens)

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19
Q

What are produced by the medulla?

A

catecholamines (epi and norepi)

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20
Q

What are the 3 parts of the adrenal cortex?

A

1) zona glomerulosa
2) zona fasciculata
3) zone reticularis

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21
Q

What is produced in the zona glomerulosa of the adrenal cortex?

A

mineralocorticoids

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22
Q

What is produced in the zona fasciculata of the adrenal cortex?

A

glucocorticoids (cortisol)

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23
Q

What is produced in the zona reticularis?

A

weak androgens (DHEAS)

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24
Q

True or false: there is a high density of lipid droplets in the adrenal cortex

A

True - site of steroid synthesis (needs cholesterol as building block)

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25
Q

Describe the blood supply to the adrenal cortex?

A

suprarenal arteries break into subcapsular plexus of capillaries (fenestrated)

second plexus forms at the zona reticularis before entering the medulla

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26
Q

Describe the blood supply to the adrenal medulla

A

DUAL BLOOD SUPPLY

bathed in blood carrying corticosteroids from cortex (which is important for conversion of NE to E)

arterioles break into fenestrated capillaries

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27
Q

Why is it important for the medulla to get the blood from the cortex?

A

it is laden with corticosteroids which are important in converting NE to E in the medulla

28
Q

When is cortisol released?

A

in response to acute or chronic stress

starvation, illness, psychological

29
Q

What receptor does cortisol bind to?

A

glucocorticoid receptor GR (high affinity) and mineralocorticoid receptor (MR) in the CYTOPLASM

30
Q

What converts cortisone to cortisol?

A

11b-HSD1

31
Q

What form of the ACTH end product is in the blood?

A

cortisone (becomes cortisol inside the cell after 11b-HSD1 acts on it)

32
Q

Is circulating cortisol bound or unbound?

A

BOUND (90% to CBG; 7% to albumin; 3% free)

33
Q

What is CBG?

A

Corticosteroid Binding Globulin (CBG) aka Transcortin

binding protein for cortisol in the blood

34
Q

Does CBG have higher affinity for cortisol or aldosterone?

A

cortisol (30x)

35
Q

What effect does estrogen have on CBG?

A

decreases it resulting in increased free cortisol

36
Q

How does shock/severe infection alter CBG?

A

decreases it

37
Q

Where are glucocorticoids made?

A

zona fasciculata (F makes G)

38
Q

When does cortisol peak in humans?

A

8am

39
Q

When is cortisol active?

A

when it dissociates from CBG and is free cortisol

40
Q

What effect does cortisol have on bone?

A

decrease bone formation and increase bone resorption

41
Q

What effect does cortisol have on connective tissue?

A

decreases it

42
Q

What effect does cortisol have on the brain?

A

modulates emotional tone, wakefulness

43
Q

What effect does cortisol have on the kidney?

A

increases glomerular filtration and free water clearance

44
Q

What effect does cortisol have on the fetus?

A

facilitates maturation

45
Q

What effect does cortisol have on the heart?

A

maintains cardiac output, increases arteriolar tone, decreases entothelial permeability

46
Q

What effect does cortisol have on inflammatory and immune response?

A

INHIBITS it

immunosuppressive drug

47
Q

How do glucocorticoids influence plasma glucose levels?

A

counter regulates insulin - mobilizes glucose to the plasma (why it is called glucocorticoid)

  • increases gluconeogenesis and plasma glucose levels
  • increases lipolysis
  • increases proteolysis
  • redistributes fat (abdominal obesity)
  • antagonizes insulin
  • inhibits intestinal calcium absorption
48
Q

How does cortisol increase gluconeogenesis?

A

stimulates these enzymes:

1) glucose 6-phosphatase
2) phosphoenolpyruvate carboxykinase
3) tyrosine aminotransferase

49
Q

How does cortisol decrease glucose uptake in muscle cells?

A

inhibits GLUT4 insertion in membrane

does this to maintain plasma glucose

50
Q

How does cortisol contribute to proteolysis?

A

increases MuRF1 (E3 ubiquitin ligase) to promote protein degradation

51
Q

How do glucocorticoids promote lipolysis in adipocytes?

A

activates the transcription of Lipe, MgII, and Angptl4.

Lipe and MgII are enzymes in the lipolytic pathway

Angptl4 is a secreted protein that binds to a receptor to increase cAMP levels in adipocytes which phosphorylates Lipe via PKA

52
Q

Cortisol binds to the GR inside the cell, kicking HSP off and moving the coritosl-GR complex into the nucleus. How does this complex act as a transcription factor?

A

decreases transcription of IL1B and TNF genes

increases IKB gene expression (which sequesters NFKB, preventing it from having its inflammatory response)

53
Q

How does cortisol have an anti-inflammatory response?

A

sops up NFkB by increasing expression of IKB

54
Q

What are the 5 mechanisms for cortisol action on the immune system?

A

1) decrease inflammation
2) stimulates anti-inflammatory cytokines
3) inhibits prostaglandins
4) suppresses antibody production
5) increases neutrophils, platelets, RBCs

55
Q

How does cortisol inhibit bone formation? increase bone resorption?

A
  • decreases IGF-1 receptors

- activates osteoclasts

56
Q

What effects does cortisol have on cardiovascular health?

A

stimulates RBC production
maintains responsiveness to catecholamine pressor effects (constricts peripheral vessels via alpha adrenergic receptors; dilates coronaries via beta adrenergic)

57
Q

Glucocorticoid excess leads to hypo or hypertension?

A

HYPER (increased bp)

58
Q

What is Cushing Disease? How does it differ from Cushing syndrome?

A

excessive cortisol secretion due to pituitary adenoma

syndrome = all other reasons for excess cortisol

59
Q

What are some of the symptoms of Cushing Disease?

A
  • change in body fat distribution
  • hypertension
  • glucose intolerant
  • purple striae
60
Q

When are glucocorticoids needed?

A
  • septic shock, severe asthma, severe autoimmune disease

- anti-inflammatory, immunosuppressive, adrenal insufficiency, pre-term infants

61
Q

Why is it so important for patients to be weaned from glucocorticoid therapy?

A

glucocorticoids inhibit CRH which inhibits ACTH which feeds zona fasciculata so that zone starts to atrophy

62
Q

Describe primary adrenal insufficiency

A

failure at adrenal end (cannot secrete glucocorticoids, mineralocorticoids, or both)

63
Q

What is an example of primary adrenal insufficiency?

A

Addison’s Disease (autoimmune destruction of adrenals)

64
Q

Describe secondary adrenal insufficiency

A

failure to secrete CRH or ACTH

most common cause = sudden cessation of glucocorticoid therapy

65
Q

When is too long to be on glucocorticoids?

A 
3 weeks
(zona fasciculata starts to atrophy at 3 weeks and stops making endogenous cortisol)

Endocrinology (16 decks)

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