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MQW U5 > Pharm - Steroids > Flashcards

Pharm - Steroids Flashcards

1
Q

3 Zona of Adrenal Cortex from Outside In:

A

Glomerulosa — Fasciculata — Reticularis

15% — 75% — 10%

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2
Q

Main hormone(s) of each adrenal cortex

A 
Glomerulosa = aldosterone (mineralcorticoid)
Fasciculata = cortisol (glucocorticoid)
Reticularis = cortisol and Androgens

remember: salty dinner, sweet desert, sex

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3
Q

Where and on what hormones does cortisol have negative feedback effects?

A

Hypothalamus – CRH (corticotropin releasing hormone)

Anterior Pituitary – ACTH

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4
Q

How and through what receptor do glucocorticoids affect BP?

A

Increases BP – a1 adrenergic receptors on arterioles –> increased sensitivity to NE and Epi

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5
Q

Glucocorticoids (increase/decrease) gluconeogenesis

A

Increase gluconeogensis – MORE GLUCOSE FOR BRAIN

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6
Q

Glucocorticoids (increase/decrease) amino acid release through muscle catabolism

A

Increase

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7
Q

Glucocorticoids (increase/decrease) peripheral glucose uptake

A

Decrease – MORE FOR BRAIN

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8
Q

Glucocorticoids (increase/decrease) lipolysis

A

Increase – less fat, more SUGAR for brain

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9
Q

Glucocorticoids (increase/decrease) bone Formation

A

Decrease

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10
Q

Glucocorticoids (increase/decrease) anti-inflammatory proteins

A

Increase – up-regulation

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11
Q

Glucocorticoids (increase/decrease) pro-inflammatory proteins

A

Decrease – downregulation

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12
Q

2 Naturally occurring mineralcorticoids:

A
  • -Aldosterone

- -Deoxycorticosterone

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13
Q

(High/Low) potassium upregulates aldosterone

A

High

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14
Q

Blood concentration of [cortisol/aldosterone] is higher

A

Cortisol – 2000fold higher than Aldosterone

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15
Q

What prevents cortisol from binding to aldosterone receptors?

A

11B-hydroxysteroid dehydrogenase TYPE 2 – converts intracellular cortisol to cortisone

–Type 1 reverses

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16
Q

What commonly used corticosteroid has 0 mineralcorticoid activity (relative to cortisol)?

A

Dexamethasone – 30 anti-inflammatory, 0 mineralcorticoid, 36-72hr

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17
Q

What commonly used corticosteroid has the highest mineralcorticoid activity (relative to cortisol)

A

Fludrocortisone – 10 anti-inflammatory, 125 mineralcorticoid

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18
Q

Cause of primary vs. secondary adrenocortical insufficiency:

A

Primary – anatomic destruction of adrenal gland

Secondary – decreased pituitary production of ACTH

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19
Q

[Primary/Secondary] Adrenal insufficiency causes hyperpigmentation

A

Primary – hyperpigmented skin, hand creases, and nails

20
Q

Cortisol and ACTH levels in Primary adrenal insufficiency

A
  • -Low cortisol – can’t make

- -High ACTH – can’t use

21
Q

Cortisol and ACTH levels in Secondary adrenal insufficiency

A
  • -Low cortisol – doesn’t make

- -low ACTH – doesn’t make

22
Q

What is Cosyntrpin test and how does it work?

A

ACTH stimulation test to determine primary vs 2ndary adrenal insufficiency

  • -Primary = No increase in Cortisol
  • -2ndary = Increase in Cortisol
23
Q

Na and K changes in acute Adrenal Insufficiency “Adrenal Crisis”

A
  • -Hyperkalemia

- -Hyponatremia – b/c high ADH from cortisol deficiency, low mineralcorticoid

24
Q

CAH inheritence is [autosomal/x-linked] [dominant/recessive]

A

Autosomal recessive

25
Q

Most common form of CAH involves what enzyme?

A

21-hydroxylase deficiency

26
Q

What is increased in most common form of CAH?

A

17-hydroxy-progesterone and androgens (DHEA, androstenedione, testosterone, estradiol)

27
Q

In Cushing’s Syndrome, glucocorticoids are [increased/decreased]

A

Increased – too much adrenal cortex activity

28
Q

ACTH dependent Cushing’s Syndrome causes:

A
  • -Pituitary adenoma (Cushing’s Disease)

- -Ectopic ACTH production (small cell lung Cx, bronchial carcinoid)

29
Q

ACTH independeing Chushing’s Syndrome causes:

A
  • -Adrenal adenoma

- -Adrenal carcinoma

30
Q

Characteristics of abdominal striae in Cushing’s Syndrome

A
  • -Greater than 1cm in width

- -Violaceous color

31
Q

4 Diagnostic tests for Cushing’s Syndrome

A

1–ACTH
2–24hr urine free cortisol excretion
3–Low dose overnight dexamethasone suppression test
4–Midnight salivary cortisol level test

**Need 2+ tests for diagnosis

32
Q

ACTH dependent Cushing’s Syndrome has what ACTH and Cortisol levels?

A
  • -High ACTH

- -High Cortisol

33
Q

ACTH independent Cushing’s Syndrome has what ACTH and Cortisol levels?

A
  • -Low ACTH

- -High Cortisol

34
Q

What is the mechanism of Metyrapone?

A
  • -Selective inhibitor of 11-hydroxylase
  • -Results in increased 11-deoxycortisol
  • -Increased ACTH due to lower feedback inhibition
35
Q

This drug for Cushing’s Syndrome was developed as a progesterone receptor antagonist, but has glucocorticoid receptor antagonist activity at higher concentrations

A

Mifepristone (RU-486)

36
Q

This drug for Cushing’s Syndrome blocks conversion of cholesterol to pregnenolone

A

Aminoglutethimide

37
Q

This drug for Cushing’s Syndrome is a potent, nonselective inhibitor of adrenal and gonadal steroid synthesis; imidazole derivative

A

Ketoconazole – antifungal

38
Q

This drug for Cushing’s Syndrome is a DDT insecticide relative w/ bad side effect profile

A

Mitotane – nonselective cytotoxic action on adrenal cortex

39
Q

This drug for Cushing’s Syndrome binds to somatostatin receptors to block release of ACTH

A

Pasireotide – high affinity for somatostatin receptor subtype 5

40
Q

Classic presentation of Primary aldosteronism:

A

Hypertension w/ hypokalemia

41
Q

2 Drugs used for medical management of Primary Aldosteronism:

A
  • -Spirinolactone – aldosterone receptor blocker

- -Eplerenone – less anti-androgen effect

42
Q

What Cushing Syndrome cause leads to bilateral adrenal atrophy?

A

Exogenous corticosteroids ( low ACTH)

No atrophy causes:

  • -Primary adrenal adenoma/hyperplasia/carcinoma
  • -Cushing Disease (ACTH secreting pituitary adenoma)
  • -Paraneoplastic ACTH secretion
43
Q

[FA]

Cortisol mnemnoic: BIG FIB

A

Blood pressure = increased
Insulin resistance
Gluconeogenesis + lipolysis, proteolysis –> hyperglycemia
Fibroblast activity –> striae
Inflammatory and Immune =
—inhibit leukotriene, prostaglandin synthesis
—inhibit WBC adhesion –> neutrophilia
—block histamine release from mast cells
—reduce eosinophils
—block IL-2 producction
Bone formation = decreased ( low osteoblast activity)

44
Q

Scenario: Already know high 24hr urine cortisol, high midnight salivary cortisol and no suppression w/ overnight low-dose dexamethasone test.

  • -What if ACTH is low?
  • -What if ACTH is high?
A

Low ACTH = think adrenal tumor or exogenous glucoccorticoid cause

High ACTH = high dose dexamethasone suppression to differentiate Cushing disease (suppressed) vs. ectopic secretion (no suppression)

45
Q

How is metyrapone stimulation test used?

A

Metyrapone given to block 11-hydroxylase (11-deoxycortisol–>cortisol)

Normal: low cortisol, compensatory high ACTH, 11-deoxycortisol

Primary adrenal insufficiency: high ACTH, low 11-deoxycortisol

2ndary adrenal insufficiency: low ACTH, low 11-deoxycortisol

MQW U5 (8 decks)

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