EXAM #2: ADRENAL PHYSIOLOGY Flashcards

1
Q

Identify the main steroid hormones produced and secreted by each of the zones of adrenal cortex.

A
Glomerulosa= Aldosterone 
Fasiculata= Cortisol 
Reticularis= Androgens
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2
Q

Recognize and describe the control mechanisms of the hypothalamus-pituitary-adrenal (HPA) axis.

A

Hypothalamus= CRH
Anterior Pituitary= ACTH
Adrenal Cortex= Cortisol and Androgen production

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3
Q

What increases CRH secretion?

A

1) Stress

2) Circadian rhythms

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4
Q

When is CRH synthesis the highest?

A

AM

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5
Q

What is the mechanism by which ACTH increases adrenal steroid synthesis.

A
  • ACTH activates receptors on cortical cells, specifically Melanocortin-2 receptor
  • Steroidogenic enzyme expression is INCREASED
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6
Q

What cleaves cholesterol in the synthesis of the cortical steroids? What is the product?

A

Cholesterol Desmolase– Pregnenolone

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7
Q

Pregnenolone is shunted down the Glucocorticoid and Androgen synthetic pathways by what enzyme i.e. what shunts this pathway to the left?

A

17 a-hydoxylase

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8
Q

After 3B hydroxysteroid dehydrogenase, what are the next two enzymes that continue the production of the Corticosteroids down their biosynthetic pathway?

A

21 hydroxylase and 11 B-hydroxylase

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9
Q

What converts adrostiendione to Testosterone?

A

17B-hydroxysteroid dehydrogenase

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10
Q

What enzymes are unique to producing Aldosterone?

A

Aldosterone synthase i.e. 18 hydroxylase and 18B-hydrox dehydrogenase

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11
Q

What is the major Glucocorticoid?

A

Cortisol

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12
Q

What is the rate limiting step of Cortisol/Glucocorticoid synthesis?

A

Cholesterol desmolase i.e. cholesterol to pregnenolone

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13
Q

What is the difference between the outcome of chronically low ACTH and elevated ACTH on the morphology of the adrenal gland?

A
Low= atrophy
High= hyperplasia
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14
Q

What are the major effects of increased cortisol? What is the mnemonic to remember these effects?

A

Cortisol is a BIG FIB

1) Blood pressure increased
2) Insulin resistance
3) Gluconeogenesis, lipolysis, proteolysis
4) Fibroblast activity increased
5) Immune system decreased
6) Bone resorption

*Cortisol increases beta-adrenergic receptors

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15
Q

How does cortisol increase blood glucose?

A

1) Increases enzymes and substrates (amino acids and adipose) that drive gluconeogenesis
2) Decreased glucose utilization by most cells

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16
Q

What is the main mineralcorticoid?

A

Aldosterone

*Note that some of the intermediates in the mineralcorticoid pathway have activity e.g. DOC

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17
Q

What is the name of synthetic aldosterone?

A

Fludrocortisone

18
Q

What are the two major regulators that increase Aldosterone?

A

1) Angiostenin II

2) Elevated K+

19
Q

What sets off the RAAS to ultimately increase ANGII?

A

Decreased renal perfusion pressure

20
Q

What are the major effects of Aldosterone?

A

1) Increase Na+ and water reabsorption

2) Excretion of K+

21
Q

In an enzymatic deficiency of Aldosterone, what is the expected response of Renin?

A

Increased Renin production

22
Q

What are the two major actions of Aldosterone outside fo the kidney?

A

1) Conserve Na+ in sweating

2) Conserve/prevent loss of Na+ in stool

23
Q

Describe the functions and physiological significance of both 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD type I) and 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD type II).

A
  • Cortisol can bind mineralcorticoid receptor
  • 11β-HSD type II inactivates cortisol to cortisone in mineralcorticoid rich tissues
  • 11β-HSD type I activates cortisone to cortisol in glucocorticoid rich tissues
24
Q

What are the physiologic effects of 17α-hydroxylase deficiency?

A

1) Increased mineralcorticoids
2) Hypokalemia
3) Increased blood pressure
4) Decreased cortisol
5) Decreased androgens

25
Q

What is the clinical presentation of 17α-hydroxylase deficiency in males?

A
  • Ambiguious genitalia

- Undescended testes

26
Q

What is the clinical presentation of 17α-hydroxylase deficiency in females?

A

Lack of secondary sexual characteristics

27
Q

What are the physiologic effects of 21-hydroxylase deficiency in males?

A

1) Decreased mineralcorticoids
- Increased K+
- Decreased BP
2) Decreased cortisol
3) Increased androgens

28
Q

What is the clinical presentation of 21-hydroxylase deficiency in females?

A
  • Salt wasting

- Females have male genitalia (virilization)

29
Q

What lab is diagnostic for 21-hydroxylase deficiency?

A

17-OH progesterone

30
Q

What are the physiologic effects of 11β-hydroxylase deficiency?

A

1) Decreased aldosterone but increased DOC (precursor mineralcorticoid)
- Increased K+
- BUT INCREASED BP
2) Decreased cortisol
3) Increased androgens

31
Q

What is the clinical presentation of 11β-hydroxylase deficiency?

A

Virilization

32
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease?

A
Disease= increased cortisol due to pituitary tumor
Syndrome= excessive endogenous or exogenous cortisol not from the pituitary
33
Q

In Cushing’s Disease, what is the expected result of a high dose dexamethasone suppression test?

A

50% reduction in ACTH and cortisol

34
Q

In an adrenal adenoma, what is the expected result of a high dose dexamethasone suppression test?

A

No reduction in cortisol or ACTH

*ACTH will be low

35
Q

In ectopic ACTH production, what is the expected result of a high dose dexamethasone suppression test?

A

No reduction in cortisol or ACTH

*ACTH will be high

36
Q

In iatrogenic cushing’s syndrome, what is the expected result of a high dose dexamethasone suppression test?

A

No reduction in ATCH or cortisol

*ACTH will be low

37
Q

What catecholamine is predominantly produced by the chromaffin cells of the adrenal medulla?

A

Epinephrine

38
Q

What enzyme catalyzes the rate-limiting step of catcholamine synthesis?

A

Tyrosine hydroxylase

39
Q

How does NE get converted to Epi?

A

PNMT

40
Q

What is required for the activation of PNMT?

A

Cortisol

41
Q

Draw the major catabolic pathways of the catecholamines.

A

N/A

42
Q

Which catecholamines have a greater effect at alpha and beta receptors?

A
Alpha= NE 
Beta= Epi