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MS 2 - Unit 5 > "Pharmacology Steroid Pharmacology Rachel L. Hopkins" > Flashcards

"Pharmacology Steroid Pharmacology Rachel L. Hopkins" Flashcards

1
Q

How do glucocorticoids increase blood pressure?

A

Glucocorticoids such as cortisol (stress hormone) upregulate alpha 1 receptors in arterioles that result in increased sensitivity to norepi and epi.

At high concentrations, they can bind to aldosterone receptors as well.

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2
Q

Do glucocorticoids increase or decrease bone formation?

A

Decrease

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3
Q

What is the result of glucocorticoids’ causing decreased leukocyte presence and leukocyte functioning at sites of inflammation?

A

Glucocorticoids are potent anti-inflammatories with immunosuppressive properties.

They upregulate anti-inflammatory proteins, and downregulate pro-inflammatory ones.

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4
Q

What are the naturally occurring mineralocorticoids in the body?

A

Aldosterone
Deoxycorticosterone
(Cortisol - weak)

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5
Q

What are the functions of mineralocorticoids in the body?

A

Active in the DCT and collecting ducts of the kidney;

Maintain electrolyte balance and intravascular volume

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6
Q

K+ and Angiotensin II have strong effects on what steroid?

A

Aldosterone

Weaker influences on aldosterone include adrenocortocitropic hormone (ACTH) and sodium deficiency

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7
Q

Cortisol and aldosterone bind to aldosterone receptors with the same affinity. Cortisol is also present in the blood about 2000x higher than aldosterone. How does the body prevent overwhelming cortisol binding?

A

11-beta-hydroxysteroid dehydrogenase type 2 converts cortisol to cortisone

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8
Q

Treatment of Adrenal insufficiency, congential adrenal insufficiency, and dianosing Cushing’s syndrome, all involve what drug class?

A

Corticosteroids

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9
Q

Class: Fludrocortisone

A

(Synthetic) Mineralcorticoid

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10
Q

MOA: Fludrocortisone

A

Binds aldosterone receptor (AR) which increases Na+K+ATPase expression and increase epithelial sodium channel experession

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11
Q

Use: Fludrocortisone

A

Chronic primary adrenal insufficiency (maintenance); CAH

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12
Q

Fludrocortisone is structurally similar to:

A

aldosterone

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13
Q

What causes primary adrenocortical insufficiency?

A

Anatomic destruction of the adrenal gland

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14
Q

What causes secondary adrenocortical insufficiency?

A

Decreased pituitary production of ACTH;

Can be iatrogenic (suppression from exogenous glucocorticoid therapy)

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15
Q

Side effects: Fludrocortisone

A

Primary aldosteronism

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16
Q

Hyponatremia, hyperkalemia, anemia, eosinophilia, azotemia, all characterize lab findings of what disorder?

A

Primary adrenal insufficiency
Signs and symptoms: weakness, fatigue, nausea, vomiting, diarrhea, salt craving, postural dizziness, anorexia, weight loss, skin pigmentation, pigmentation of mucous membranes, hypotention, vitiligo

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17
Q

How are the findings of secondary adrenal infficiency different from primary?

A 
No hyperpigmentation (ACTH is low);
Near-normal aldosterone levels
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18
Q

How is adrenal insufficiency diagnosed?

A

Test cortisol levels at baseline and 30-60 minutes after a dose of cosyntropin

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19
Q

Low cortisol, high ACTH characterizes what dx?

A

Primary adrenal insufficiency

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20
Q

Low cortisol, low ACTH characterizes what dx?

A

Secondary adrenal insufficiency

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21
Q

What is adrenal crisis?

A 
Volume depletion;
hypotension;
lassitude, nausea, vomiting;
Hyperkalemia;
Hyponatremia (mineralocorticoid deficiency, increased ADH caused by cortisol deficiency)
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22
Q

How is adrenal crisis treated?

A

High dose IV glucocorticoid (ie dexamethasone, hydrocortisone)

Do not delay treatment, as adrenal crisis is life-threatening.

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23
Q

Class: Hydrocortisone

A

Glucocorticoid

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24
Q

MOA: Hydrocortisone

A

Binds GR, which regulates expression of genes with many effects on carbohydrate metabolism and immune function

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25
Q

Uses: Hydrocortisone

A

Chronic primary adrenal insufficiency (maintenance);

CAH

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26
Q

What is the goal of treatment of chronic adrenal insufficiency?

A

To replace physiologic glucocorticoids and mineralocorticoids

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27
Q

Side effects: Hydrocortisone

A

Cushing’s;
glucocorticoid-induced osteoporosis;
iatrogenic adrenal insufficiency

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28
Q

Class: Dexamethasone

A

Glucocorticoid

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29
Q

MOA: Dexamethasone

A

Binds GR, which regulates expression of genes with many effects on carbohydrate metabolism and immune function

30
Q

Uses: Dexamethasone

A 
Emergency treatment (severe adrenal crisis, PAI); 
suppression test (Cushing's dx); 
CAH
31
Q

Side effects: Dexamethasone

A

Cushing’s;

glucocorticoid-induced osteoporosis; iatrogenic adrenal insufficiency

32
Q

What is “stress dosing?”

A

The adjustment of dosing of glucocorticoids when a person with chronic adrenal insuffiency is ill.

33
Q

What is the most common congenital adrenal hyperplasia?

A

21-hydroxylase deficiency, which results in the overproduction of androgens

(converts progesterone to DOC…–> aldosterone AND converts 17-OH-progesterone to 11-deoxycortisol…–> cortisol)

34
Q

How is 21-hydroxylase defiency treated?

A

Dexamethasone, prednisone or hydrocortisone.

Sometimes fludrocortisone is used if salt-wasting is occurring

Giving steroids suppresses ACTH and reduces overproduction of androgens

35
Q

Cushing’s disease is caused by:

A

pituitary adenoma

ACTH-dependent glucocorticoid excess

36
Q

Cushing’s syndrome, when paraneoplastic, is caused by:

A

Small cell lung carcinoma, bronchial carcinoid

These involve ectopic ACTH production

37
Q

Adrenal adenoma and adrenal carcinoma both product what kind of Cushing’s syndrome?

A

ACTH-independent

38
Q

Weight gain, menstrual irregularity, hirsutism, psychiatric dysfunction, backache, muscle weakness, fractures and loss of scalp hair all charactterize what diagnosis?

A

Cushing’s syndrome

Also…
truncal obesity, plethora, moon face, HTN, bruising, thinning sking, red-purple striae (like stretch marks), proximal myopathy, ankle edema, hump on back, impaired glucose tolerance, diabetes, infections, osteoporisis, renal calculi, cataracts and glaucoma

39
Q

How is Cushing’s syndrome diagnosed?

A

Administer ACTH and monitor 24-hour cortisol excretion in urine; or
overnight dexamethasone test; or
midnight salivary cortisol test
2 of these tests must be +

40
Q

Uses: Aminoglutethimide

A

Cushing’s syndrome

41
Q

MOA: Aminoglutethimide

A

Blocks conversion of cholesterol to pregnenolone

42
Q

Uses: Ketoconazole

A

Cushing’s syndrome

43
Q

MOA: Ketoconazole

A

Potent, nonselective inhibitor of adrenal and gonadal steroid synthesis

44
Q

Class: Ketoconazole

A

Anti-fungal imidazole derivitive

45
Q

Class: Mitotane

A

DDT insecticide relative

46
Q

MOA: Mitotane

A

Nonselective cytotoxic action on adrenal cortex

47
Q

Uses: Mitotane

A

Cushing’s syndrome

48
Q

Which treatment for Cushing’s syndrome is known to have a bad side effect profile?

A

Mitotane

49
Q

MOA: Metyrapone

A

Relatively selective inhibitor of 11-hydroxylation (interferes with cortisol and corticosterone synthesis)

50
Q

Uses: Metyrapone

A

Cushing’s syndrome

51
Q

T/F: Metyrapone can be used diagnostically to test anterior pituitary function.

A

True

52
Q

MOA: Mifepristone

A

Progesterone receptor antagonist; GR antagonist at high concentrations
–created generalized glucocorticoid resistance

53
Q

Uses: Mifepristone

A

Cushing’s (controls hyperglycemia secondary to hypercortisolism)

54
Q

When is Mifepristone indicated?

A

To control hyperglycemia secondary to hypercortisolism in adults with endogenous Cushing’s syndrome who have failed or are not candidates for surgery;
Cortisol-induced psychosis

55
Q

Side effects: Mifepristone

A

Fatigue, nausea, headache, hypokalemia (moderate to severe), arthralgias, edema, endometrial thickening in women;
adrenal insufficiency

56
Q

Class: Pasireotide

A

Somatostatin analog

57
Q

MOA: Pasireotide

A

Binds to somatostatin receptor (subtype 5) and blocks release of ACTH from corticotropes

58
Q

Uses: Pasireotide

A

Cushing’s syndrome

59
Q

Side effects: Pasireotide

A

hyperglycemia;

GI symptoms

60
Q

Primary aldosteronism is characterized by:

A

High aldosterone and low renin;
HTN;
hypokalemia

61
Q

When should primary aldosteronism be in the differential?

A

HTN with hypokalemia
Tx resistant HTN
HTN

62
Q

Surgery may be indicated in the treatment of primary aldosteronism if:

A

the source is a unilateral adenoma

63
Q

Medical treatment is indicated for primary aldosteronism if:

A

the source is bilateral adrenal hyperplasia

64
Q

MOA: Spironolactone

A

Aldosterone receptor antagonist

65
Q

Use: Spironolactone

A

Primary aldosteronism

66
Q

Side effects: Spironolactone

A

Anti-androgenic

67
Q

MOA: Eplerenone

A

Aldosterone receptor antagonist

68
Q

Uses: Eplerenone

A

Primary aldosteronism

Less anti-androgen effects

69
Q

Toxicity from glucocorticoids can result in:

A

Insomnia;
Behavior changes (is hypomania, psychosis);
Peptic ulcers;
Pancreatitis

70
Q

Patients who are withdrawn from long-term and/or high steroid therapy are at risk for:

A

Adrenal crisis

MS 2 - Unit 5 (21 decks)

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