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Spring Pharm Exam 3 > Corticosteroids > Flashcards

Corticosteroids Flashcards

1
Q

Glucocorticoid action

A

carbohydrate and protein metabolism, anti-inflammatory response (cortisol)

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2
Q

mineralocorticoid action

A

Na+ retention (Aldosterone)

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3
Q

Adrenal Androgen Increased release occurs in concert with cortisol, not aldosterone

A

:)

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4
Q

Dihydroandrostenedione (DHEA)

A

weak androgenic activity, some converted to testosterone and estradiol outside adrenal glad

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5
Q

regulates mineralocorticoid release

A

RAAS system

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6
Q

Regulation of glucocorticoid and androgen release

A

ACTH from pituitary released following CRH from hypothalamus

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7
Q

CRH is released in response to sleep-wake cycles

A

:)

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8
Q

Curculating corticosteroids (endogenous and exogenous) cause negative feedback to the release of ACTH

A

:0

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9
Q

STRESS response can override negative feedback and produce an increase release of steroids

A

:)

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10
Q

Glucocorticoid pathway is substrate limited, the rate-limiting step is…

A

Conversion of cholesterol to pregnenolone - ACTH stimulates this in zona fasiculata and reticularis

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11
Q

Mineralocorticoid Pathway is stimulated independent of ACTH, ANG II stimulates conversion of

A

cholesterol to pregnenolone and corticosterone to aldosterone

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12
Q

Glucocorticoid MOA (widely distributed receptors)

A

Steroid (S) binds intracellular receptor (R) – forms S-R complex that gets transported to nucleus – binds glucocorticoid response element on DNA – activates or inhibits gene transcription to increase or decrease protein synthesis – alters cellular function in hours or more

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13
Q

Glucocorticoid metabolic effects on carbohydrates

A 
Stimulates gluconeogenesis (in fasting state) --> increases BGL and insulin release
Stimulates gluconeogenesis and glycogen synthase --> increased liver glycogen deposition
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14
Q

Glucocorticoid metabolic effects on lipids

A

Inhibits uptake of glucose by adipocytes –> stimulates lipolysis (but NET effect is lipogenesis from increased insulin)
Greater effect on central tissues –> central obesity

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15
Q

Glucocorticoid metabolic effect on protein

A

Increased AA uptake into liver and kidney, decreased protein synthesis (except liver) –> net transfer of AA from muscle to liver
Can lead to muscle wasting and atrophy in connective tissue

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16
Q

Glucocorticoid NET physiologic results are to maintain glucose to the brain (insulin antagonism)

A

:)

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17
Q

permissive effects are…

A

responses that occur in presence of glucocorticoids but are not further stimulated with increased amount of glucocorticoids

18
Q

Permissive effects of glucocorticoids

A

vasoconstriction and bronchodilation response to catecholamines
fat cell lipolytic response to catecholamines, ACTH, GH

19
Q

Cortisol effects via mineralocorticoid receptors

A

cortisol also induces formation of mRNA to synthesize and insert membrane proteins to increase reabsorption of Na+ from renal distal tubules, loosely coupled to increased secretion of H+ and K+

20
Q

adverse effects of steroids acting on mineralocorticoid receptors

A

hypertension (fluid retention) and edema. hypokalemia, metabolic alkalosis

21
Q

for use in physiologic replacement, use an agent with both mineralocorticoid and glucocorticoid activity

A

(Cortisol aka hydrocortisone)

22
Q

For use in anti-inflammatory or immunosupressive actions, select an agent with minimal or no mineralocorticoid activity

A

(Dexamethasone)

23
Q

It is not possible to have anti-inflammatory activity without glucocorticoid activity

A

:)

24
Q

Aldosterone (longer acting: Fludrocortisone) possesses essentially all mineralocorticoid activity

A

:O

25
Q

glucocorticoid analogs: structural changes can affect receptor specificity, potency, abs, membrane permeability, elimination

A

:)

26
Q

11-hydroxy glucocorticoids are physiologically active. Examples are:

A

Cortisol, prednisolone, methylprednisolone, dexamethasone, fludrocortisone

27
Q

11-keto glucocorticoids are prodrugs that must be activated by 11-B-hydroxysteroid dehydrogenase 1 (11B-HSD1) examples are

A

Prednisone and Cortisone

28
Q

level of activity of endogenous and EXOGENOUS cortisol in various tissues can be determined by which type of 11B-HSD is expressed in the tissue

A

Helps to decipher which route to give it

29
Q

Liver has 11B-HSD1

A

Activates Prednisone and Cortisone - so can be given PO and activated via first pass. CANT activate via topical or IV

30
Q

Kidney has 11B-HSD2

A

INACTIVATES cortisol to cortisone to protect kidneys from unregulated MC activity

31
Q

Fetus/Placenta 11B-HSD2 - fetal liver (11B-HSD1) inactive

A

can treat mother without effect on baby
to treat baby: must use drug that is a poor substrate for 11B-HSD2 to it will not become inactivated (for lung development or prior to premature delivery)

32
Q

Cortisol must circulate bound to…

A

Corticosteroid binding protein and albumin. Must be bound to circulate w/o being metabolized, but must be free to diffuse into cells

33
Q

Cortisol (Hydrocortisone) Use

A

Replacement therapy and emergencies: IV and PO.

1:1 GC:MC action

34
Q

Prednisone Use

A

Most commonly used steroid burst PO agent

GC:MC 13:1. inactive until 1st pass effect in liver

35
Q

Methylprednisolone (Solu-Medrol parenteral, Medrol PO)

A

Used if parenteral desired for steroid burst. minimal MC action

36
Q

Dexamethasone (Decadron) Use

A

Most potent anti-inflammatory. Cerebral edema, chemo-induced vomiting, GREATEST suppression of ACTH secretion at pituitary. NO MC action

37
Q

Triamcinolone (Kenalog) Use

A

Excellent topical activity. POTENT systemic action. NO MC action

38
Q

Adrenal Insufficiency treatment

A

Chronic - Addison’s: Cortisol daily, increase during times of stress. Fludrocortisone (long acting) usually required for MC effect.
Acute - Life threatening. Immediate TX IV

39
Q

Adrenocortical Hyperfunction (Cushing’s Syndrome from tumor secreting ACTH or Cortisol) TX

A

Surgery is TX of choice.
Glucocorticoid synthesis inhibitors. IE: Ketoconozol
Glucocorticoid receptor antagonist: Mifepristone. NOT 1st line. Contra in pregnancy

40
Q

Adrenocortical Hyperfunction (Congenital Adrenal Hyperplasia, decreased cortisol synthesis (multiple congenital enzyme defects) –>to increased ACTH and overstimulation of adrenals) TX

A

Replace deficient steroids while minimizing adrenal sex hormone (overproduction) and glucocorticoid excess (overtreatment)
Depending on the enzyme deficiency: virulization (»androgens), hypotension (>MC)

41
Q

Adrenocortical Hyperfunction (Pheochromocytoma - excess catecholamine) TX

A

Surgery, after alpha-adrenergic receptor blockade to avoid HTN crisis in surgery
Phenoxybenzamine - irreversible A-receptor antagonist
Beta-blockers after A-adrenergic receptor block
CCB can supplement alpha and beta blockers

Spring Pharm Exam 3 (8 decks)

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