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RRPA Pharmacology III > Adrenal Pharmacology (Exam 1) > Flashcards

Adrenal Pharmacology (Exam 1) Flashcards

1
Q

In order for corticosteroids to be released from the adrenal cortex, the hypothalamus releases _____, which stimulates the ant. pituitary to release _____, which stimulates the adrenal cortex.

A

CRF

ACTH

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2
Q

Corticosteroids refers to?

A

Steroids made by the adrenal cortex -> mineralocorticoids and glucocorticoids

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3
Q

Function of glucocorticoids?

A

metabolic, anti-inflammatory, and immunosuppressive

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4
Q

Function of mineralocorticoids?

A

Peripheral actions on salt and water metabolism

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5
Q

What are the zones of the adrenal cortex and what hormones does each produce?

A

Glomerulosa - Aldosterone
Fasiculata - Cortisol
Reticularis - DHEA

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6
Q

Where do glucocorticoids provide negative feedback?

A

At the ant pituitary on ACTH release

At the hypothalamus on CRF release

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7
Q

What hormone released by the zona fasiculata is a glucocorticoid?

A

Cortisol

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8
Q

Chronic use of GCs can cause?

A

Adrenal atrophy due to suppression of the HPA axis.

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9
Q

Insufficient adrenal response to environmental stressors known as adrenal crisis is treated with?

A

Supplemental GCs

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10
Q

Secretion or cortisol peaks when?

A

Early AM and evening

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11
Q

Cortisol in the blood is bound by _____.

A

Cortisol binding globulin (CBGs)

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12
Q

T/F? Only free cortisol is active?

A

True

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13
Q

T1/2 of cortisol?

A

60-90 minutes

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14
Q

Cortisol actions on muscle cells?

A

Decrease glucose uptake
Increase protein breakdown
Overall - Muscle wasting

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15
Q

Cortisol actions on fat cells?

A

Decrease glucose uptake
Increase fat breakdown peripherally.
Decrease fat breakdown centripetally.

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16
Q

Cortisol actions on liver cells?

A

Gluconeogenesis leading to hyperglycemia

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17
Q

Permissive effects of glucocorticoids?

A

Vasoconstrictor
Fat cell lipolytic response to epi, ACTH, GH
Normal cardiac output

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18
Q

What hormone released by the adrenal cortex is a mineralocorticoid?

A

Aldosterone

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19
Q

Effects of aldosterone?

A

Na+ reabsorption at kidney leading to increased blood volume and BP

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20
Q

Excess aldosterone would cause what symptoms?

A

Hypertension, hypokalemia, metabolic alkalosis

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21
Q

T/F? Anti-inflammatory effects of GCs can be separated from immunosuppressive effects.

A

False

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22
Q

Addison’s disease is ____ adrenal insufficiency.

A

Primary

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23
Q

Addison’s disease requires replacement of both GCs and MCs. What medications should be used to replace them?

A

Hydrocortisone or Prednisone Or Dexamethasone +/- fludrocortisone

24
Q

What medication is used for it’s anti-inflammatory/immunosuppressive properties without MC activity?

A

Dexamethasone

25
Q

Why must prednisone be given orally?

A

Gets metabolized to active form - prednisolone in the liver.

26
Q 
Rank the following drugs from most to least anti-inflammatory potency.
Dexamethasone
Cortisol
Fludrocortisone
Prednisone
Triamcinolone
Aldosterone
A 
Dexamethasone
Fludrocortisone
Triamcinolone
Prednisone
Cortisol
Aldosterone
27
Q

Rank the following drugs from most to least salt-retaining potency.

Cortisol
Fludrocortisone
Prednisone
Aldosterone

A

Aldosterone
Fludrocortisone
Cortisol
Prednisone

28
Q

What advantage do dexamethasone and prednisone have over hydrocortisone in the treatment of Addison’s disease?

A

They are longer acting than hydrocortisone

29
Q

When would you add fludrocortisone to a patients treatment for Addison’s

A

If they are hypotensive.

30
Q

T/F? DHEA can help with mood and well being in all patients with Addison’s.

A

False - only in some women

31
Q

Treatment for adrenal crisis?

A

Volume replenishment
Large amounts of IV hydrocortisone if pervious diagnosis
Dexamethasone if no previous diagnosis

32
Q

Why does the treatment differ for patients with a previous diagnosis of Addison’s?

A

Dexamethasone does not interfere with cortisol labs

33
Q

Cushing’s disease is _____ hypercortisolism

A

Secondary

34
Q

Treatment of choice for Cushing’s?

A

Surgery

35
Q

What types of medications can be used for adjunctive therapy or pharmacotherapy in inoperable cases of Cushing’s?

A

Cortisol synthesis inhibitors
GC receptor antagonists
Somatostatin analogs

36
Q

What cortisol synthesis inhibitors are used early? late?

A

Early - ketoconazole

late - Metyrapone, etomidate

37
Q

What medication is a GC receptor antagonist?

A

Mifepristone (RU-486)

38
Q

What medication is a somatostatin analog that is used in Cushing’s?

A

Pasireotide

39
Q

Is the dose of ketoconazole higher or lower in Cushing’s when comparted to the antifungal dose?

A

Higher

40
Q

Adverse reactions to ketaconazole?

A

headache, n/v, gynecomastia, impotence, reversible hepatotoxicity.

41
Q

Adverse reactions to metyrapome?

A

Hirsutism in women, Na+ retention and HTN

42
Q

Congenital adrenal hyperplasia is treated with?

A

Cortisol +/- fludrocortisone

43
Q

Before surgery for a pheochromocytoma, what medications need to be given?

A

An alpha blocker - phenoxybenzamine (or terazosin/doxazosin)
A beta blocker - Metoprolol (or labetalol)
+/- nicardipine depending on BP

44
Q

If a pheochromocytoma is inoperable, what medication would be added?

A

Metyrosine (catecholamine synthesis inhibitor

45
Q

Treatment of choice for adrenomedullary hyperfunction?

A

Surgery

46
Q

In Congenital adrenal hyperplasia is cortisol synthesis and secretion increased or decreased

A

It is decreased, which results in INCREASED ACTH and then ADRENAL HYPERPLASIA

47
Q

What would you see with a 21-hydroxylase deficiency?

A
  1. No cortisol synthesis —– > increased ACTH—-> allowing excess androgen——> VIRILIZING
  2. No desoxycorticosterone OR aldosterone synthesis ——-> DECREASED MC activity ——-> Hypotension
48
Q

What would you see with 17a-hydroxylase deficency?

A
  1. No cortisol synthesis —– > increased ACTH—–> INCREASED desoxycorticosterone——> INCREASED MC ACTIVITY———> Hypertension
  2. No adrenal androgen synthesis—-> NON-VIRILIZING
49
Q

what would you see with 11-hydroxylase deficency?

A
  1. No cortisol synthesis —– > increased ACTH—-> allowing excess androgen——> VIRILIZING
  2. No cortisol synthesis —– > increased ACTH—–> INCREASED desoxycorticosterone——> INCREASED MC ACTIVITY———> Hypertension
50
Q

is Phenoxybenzamine a reversible or irreversible α1-α2 receptor antagonist?

A

irreversible

51
Q

________ is a competitive inhibitor of catecholamine synthesis

A

Metyrosine

52
Q

What effect does physiologic levels of cortisol have on Carbohydrate?

A

increased gluconeogenesis—-> increased blood glucose (increased insulin)

53
Q

What effect does physiologic levels of cortisol have on protein?

A

increased AA uptake into liver and kidney

DECREASED protein synthesis (except liver)

54
Q

What effect does physiologic levels of cortisol have on lipids?

A
  1. increase lipolysis (peripherally)—-> increased fatty acids
55
Q

What is the Net Physiologic Result of physiologic levels of glucocorticoids?

A

Maintenance of glucose supply to brain

RRPA Pharmacology III (9 decks)

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