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P1: Endo > Steroids of Adrenal Cortex > Flashcards

Steroids of Adrenal Cortex Flashcards

1
Q

What are the steroids of the adrenal cortex

A

→ Glucocorticoids - cortisol
→ Mineralocorticoids - aldosterone
→ androgens

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2
Q

What does aldosterone do?

A

→ Maintains blood volume by regulating Na+

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3
Q

Where does the blood flow in the adrenal medulla?

A

→ Outer cortex to inner medulla

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4
Q

What does steroid hormone synthesis always start with?

A

→ Cholesterol

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5
Q

What does the cortex secrete?

A

→ Steroid hormones

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6
Q

What does the medulla secrete?

A

→ Adrenaline

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7
Q

What is the pathway in the zona glomerulosa?

A 
Cholesterol
↓
Pregnenolone
↓
Progesterone
↓
Deoxycorticosterone
↓
Corticosterone
↓
Aldosterone
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8
Q

What is the zona fasciculata pathway?

A 
Progesterone
↓
17 OH progesterone
↓
Deoxycortisol
↓
Cortisol
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9
Q

What is the zona reticularis pathway?

A 
Pregnenolone
↓
17 OH pregnenolone
↓
DHEA
↓
Androstenedione
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10
Q

What is the function of mineralocorticoid?

A

→ Na+ retention
→ Active Na+ reabsorption
→ Active secretion of K+

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11
Q

What is the juxtaglomerular apparatus stimulated by?

A

→ Increased sympathetic activity
→ Decreased perfusion pressure
→ Decreased Na+ and Cl-

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12
Q

What stimulates aldosterone secretion?

A

→ K+

aldosterone secretion is NOT significantly affected by changes in plasma Na concentration

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13
Q

How does aldosterone work to retain Na+?

A

→ Increases Na+/K+/ATPase activity on the apical side

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14
Q

Why does cortisol not work in the kidney?

A

→ Cortisol levels are higher
→ Cortisol can stimulate the mineralocorticoid receptor
→ cortisol in the kidney gets converted to inactive cortisone
→ by 11 beta HSD 2

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15
Q

What is the syndrome of apparent mineralocorticoid excess?

A

→ Too much cortisol in the kidney

→ High BP

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16
Q

What family is the glucocorticoid receptor a part of?

A

→ Nuclear receptor super family

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17
Q

What are the 3 structural elements of the glucocorticoid receptor?

A

→ Ligand binding
→ DNA binding
→ N- terminal transcription co-factor binding

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18
Q

What do the glucocorticoid receptors do when the ligand binds?

A

→ Receptors dimerize

→ Translocate to nucleus

19
Q

What is transactivation?

A

→ Glucocorticoid enhances transcription of the target gene

20
Q

What is transrepression?

A

→ Glucocorticoid represses the transcription of the target gene

21
Q

What are the functions of glucocorticoids?

A 
→ Decreased glucose uptake
→ Increased proteolysis
→ Stimulates lipolysis
→ Gluconeogenesis
→ Maintaining glucose
22
Q

What does hypocortisolism lead to?

A

→ hypotension

→ Inappropriate vasodilation

23
Q

What are prostaglandins and leukotrienes derived from?

A

→ Lipid derived compounds

24
Q

What is the first molecule to be synthesized in the inflammation pathway?

A

→ Arachidonic acid

25
Q

What effect does cortisol have on the inflammation pathway?

A

→ Cortisol increases the expression of ANNEXIN - 1

→ Annexin 1 downregulates arachidonic acid

26
Q

What is the pathway for the production of cortisol?

A 
→ Hypothalamus makes CRH
→ CRH stimulates anterior pituitary
→ Anterior pituitary makes ACTH
→ ACTH stimulates the adrenal cortex
→ Adrenal cortex makes cortisol
27
Q

What is primary adrenal insufficiency?

A

→ Addisons disease

28
Q

What is secondary adrenal insufficiency?

A

→ Hypopituitarism
→ RAAS defect
→ Enzyme defect in steroid synthesis

29
Q

What are the clinical features of Addisons?

A 
→ Low adrenal steroids
→ high ACTH
→ Plasma Na+ - low
→ Plasma K+ - normal - high
→ high renin
30
Q

When there is very low cortisol what two hormones are high?

A

→ ADH - plasma dilution so low Na+
cortisol inhibits ADH
→ ACTH

31
Q

What is the ACTH receptor a part of?

A

→ Melanocortin group of receptors

32
Q

Why does Addisons cause hyperpigmentation?

A

→ Excess circulating ACTH
→ Binds to melanocortin receptors
→ Pigmentation

33
Q

What is Cushings disease due to?

A

→ Secondary

→ Increased ACTH due to pituitary adenoma

34
Q

What is ACTH independent hypercortisolism?

A

→ Adrenal adenoma

→ Iatrogenic

35
Q

What are clinical features of hypercortisolism?

A 
→ Hypertension
→ Hyperglycaemia
→ truncal obesity
→ Fatigue, Muscle weakness
→ Virilization
→ Depression
36
Q

What do low doses of dexamethasone usually do?

A

→ Suppress ACTH secretion via negative feedback

37
Q

What suppresses ACTH secretion in Cushings and why?

A

→ a higher dose of dexamethesone
→ Pituitary cells have increased
→ more cortisol/dexamethesone is needed for a negative feedback

38
Q

What happens if a high dose of dexamethesone does not suppress ACTH?

A

→ Ectopic source of ACTH

39
Q

What effect does cortisol have on NO synthesis in the CVS?

A

have effect on NO synthesis so too much NO and inappropriate vasodilation.

40
Q

What is the effect of glucocorticoids inhibit?

A

→inhibit the inflammatory response by inducing annexin-1 which inhibits phospholipase A2

→inhibits induction of COX

41
Q

What happens when cortisol is very low?

A

CRH is high, and ADH rises and hyponatremia

42
Q

Explain the rationale behind the low dose dexamethasone suppression test work

A

Dexamethasone: exogenous steroid. Act like cortisol

Low doses will normally supress ACTH secretion via negative feedback

43
Q

How is ectopic ACTH linked with Cushing’s syndrome?

A

pituitary adenoma results in increased ACTH secretion, which drives excess cortisol production from adrenal cortex

Negative feedback loop is still intact, but greater mass of ACTH-secreting pituitary cells means set point is higher.

P1: Endo (12 decks)

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