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Pharm Unit 5 > Steroids > Flashcards

Steroids Flashcards

1
Q

Cortisol

A

Class: Glucocorticoid
Mech: Binds GR, which regulates expression of genes with many effects on carbohydrate metabolism and immune function
Important SE’s: Cushing’s; glucocorticoid-induced osteoporosis; iatrogenic adrenal insufficiency
Misc: RelAnti-Inflam: 1; RelMin: 1; DoA: 8-12 hours

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2
Q

Cortisone acetate (Cortone): difference with cortisol:

A

Misc: RelAnti-Inflam: 0.8; RelMin: 0.8; DoA: 8-12 hours

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3
Q

Hydrocortisone: difference with cortisol:

A

Thera: Chronic primary adrenal insufficiency (maintenance); CAH
Misc: RelAnti-Inflam: 1; RelMin: 1; DoA: 8-12 hours

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4
Q

Prednisone (Deltasone): difference with cortisol:

A

Thera: CAH
Misc: RelAnti-Inflam: 4; RelMin: 0.8; DoA: 12-36 hours; 1/4 dose of cortisol

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5
Q

Prednisolone (Orapred): difference with cortisol:

A

Misc: RelAnti-Inflam: 4; RelMin: 0.8; DoA: 12-36 hours; 1/4 dose of cortisol

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6
Q

Methylprednisolone (Medrol): difference with cortisol:

A

Misc: RelAnti-Inflam: 5; RelMin: 0.5; DoA: 12-36 hours; 1/5 dose of cortisol

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7
Q

Triamcinolone: difference with cortisol:

A

Misc: RelAnti-Inflam: 5; RelMin: 0; DoA: 12-36 hours; 1/5 dose of cortisol

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8
Q

Dexamethasone (Decadron): difference with cortisol:

A

Thera: Emergency treatment (severe adrenal crisis, PAI); suppression test (Cushing’s); CAH
Misc: RelAnti-Inflam: 30; RelMin: 0; DoA: 8-12 hours; <1/20 dose of cortisol

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9
Q

Fludrocortisone

A

Class: Mineralocorticoid
Mech: Binds aldosterone receptor (AR) which increases Na+K+ATPase expression and increase epithelial sodium channel experession
Thera: Chronic primary adrenal insufficiency (maintenance); CAH
Important SE’s: Primary aldosteronism
Misc: RelAnti-Inflam: 10; RelMin: 125; DoA: 12-36 hours; very small dose

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10
Q

Aminoglutethide (Cytadren)

A

Mech: Blocks conversion of cholesterol to pregnenolone
Thera: Cushing’s Syndrome

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11
Q

Ketoconazole (Nizoral)

A

Class: Anti-fungal imidazole derivitive
Mech: Potent, nonselective inhibitor of adrenal and gonadal steroid synthesis
Thera: Cushing’s Syndrome

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12
Q

Mitotane (Lysodren)

A

Class: DDT insecticide relative
Mech: Nonselective cytotoxic action on adrenal cortex
Thera: Cushing’s Syndrome
Important SE’s: Bad side effect profile

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13
Q

Metyrapone (Metopirone)

A

Mech: Relatively selective inhibitor of 11-hydroxylation (interferes with cortisol and corticosterone synthesis)
Thera: Cushing’s syndrome; can use diagnostically to test anterior pituitary;
Misc: ACTH levels should rise in compensatory response to decreased cortisol and corticosterone, with precursor 11-deoxycortisol increasing also during metyrapone test

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14
Q

Mifepristone (RU-486)

A

Mech: Progesterone receptor antagonist; GR antagonist at high concentrations
Thera: Cushing’s syndrome (controls hyperglycemia secondary to hypercortisolism in those with endogenous Cushing’s syndrome who had issues with surgery); cortisol-induced psychosis
Important SE’s: Fatigue, nausea, headache, hypokalemia (moderate to severe since now crtisole can overwhelm the mineralocorticoid system), arthralgias
Other SE’s: edema and endometrial thickening in women;
Adrenal insufficiency that needs to be treated with withdrawal of mifepristone and then high-dose dexamethasone

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15
Q

Pasireotide

A

Class: somatostatin analog
Mech: Binds to somatostatin receptorand blocks release of ACTH from corticotropes
Thera: Cushing’s disease (pituitary)
Important SE’s: Hyperglycemia, GI problems

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16
Q

Spironolactone (Aldactone)

A

Mech: Aldosterone receptor antagonist
Thera: Primary aldosteronism
Important SE’s; Anti-androgenic

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17
Q

Eplerenone (Inspra)

A

Mech: Aldosterone receptor antagonist
Thera: Primary aldosteronism
Misc: More specific; less anti-androgenic effect than spironolactone

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18
Q

Glucocorticoids bind to _____, which proceeds to _____ and head into the ____ to activate _____

A

glucocorticoid receptor; dimerize; nucleus; GRE (glucocorticoid response element)

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19
Q

Glucocorticoid effects:

A
  1. Carb metabolism: increase gluconeogenesis, release aa’s through muscle catabolism, inhibits peripheral glucose uptake, stimulate lipolysis (FOR THE BRAIN)
  2. Immune function
  3. Anti-inflamm effects (upreg anti-inflamm proteins, downreg pro-inflamm proteins, decrease leukocyte presence and function at inflamm sites)
  4. Fetal development (LUNGS especially)
  5. Cognitive function/CNS effects
20
Q

Mineralocorticoids:

A

Aldo and deoxycorticosterone (DOC) naturally occur; cortisol has WEAK mineralocorticoid activity

21
Q

Mineralocoid mech of action and effects:

A
  1. Binds to AR particularly in principle cells of distal convoluted and collecting tubules in the kidney
  2. AR activated means more Na/K ATPase expression and more epi Na channel expression;
    You maintain electrolytes and intravascular volume (increased Na resorption, with water following to increase ECV and increase renal excretion of K)
22
Q

Although cortisol at higher levels than aldo, what allows for aldosterone to bind to AR knowing they have similar affinities for the receptor?

A

Use 11beta-hydroxysteroid DH type 2 to convert cortisol to cortisone

23
Q

Most significant regulators of aldosterone secretion:

A
  1. Concentration of K ions in EC fluid (small increase leads to aldo secretion strongly stimulated
  2. AII;
    other factors are ACTH and Na deficiency
24
Q

In general, what do glucocorticoids do?

A
  1. Establish diagnosis and cause of Cushing’s
  2. Treat adrenal insufficiency and CAH;
  3. in general, can treat inflamm, allergic, immunological disorders at supraphysiologic doses
25
Q

Disorders of adrenal function often

A

treated and/or diagnosed using corticosteroids

26
Q

ACTH dependent vs. ACTH independent causes of Cushing’s syndrome; what are the ACTH and cortisol levels in either:

A
  1. Pituitary adenoma (Cushing’s DISEASE)
  2. Ectopic ACTH production;
  3. adrenal adenoma
  4. adrenal carcinoma;
    IATROGENIC Cushing’s syndrome;

high ACTH and cortisol in dependent; low ACTH and high cortisol in independent

27
Q

Diagnosis of Cushing’s syndrome:

A
  1. 24-hr urine free cortisol excretion
  2. low-dose overnight dexamethasone suppression teset
  3. midnight salivary cortisol level;
    diagnosis requires AT LEAST TWO positive tests
28
Q

Difference b/w primary and secondary adrenocortical insufficiency causes; consequence of either:

A
  1. Primary will have decreased cortisol and aldo production with HIGH ACTH levels
  2. Secondary with decreased pituitary production of ACTH and decreased production primarily of cortisol (not as much aldo);
    can’t handle physiologic stress like trauma or infection, and leads to life-threatening shock
29
Q

Causes of secondary adrenal insufficiency:

A
  1. suppression from exogenous glucocorticoid therapy
  2. Hypopituitarism: removal of pituitary adenoma, pituitary tumors or surgery (craniopharyngiomas), pituitary apoplexy among others
30
Q

Difference in symptoms with secondary adrenal and primary adrenal insufficiency:

A
  1. No hyperpigmentation (ACTH not elevated)

2. Near-normal aldo levels

31
Q

Adrenal crisis and the signs/symptoms:

A
  1. Lack of cortisol: most common if primary adrenal insufficiency;
  2. LIFE-THREATENING emergency, and needs immediate treatment;
    volume depletion and hypotension, N/V, hyperkalemia, hyponatremia (mineralocorticoid deficiency and increased ADH b/c of cortisol deficiency)
32
Q

Causes of adrenal crisis (acute adrenal insufficiency) and how can we diagnose it:

A
  1. Think sepsis, surgical stress, trauma
  2. hemorrhagic destructino of gland like WF syndrome or anticoag therapy or caog disorder
  3. Rapid withdrawal of steroids;
    give synthetic ACTH to see if cortisol levels get spiked (normal) or not
33
Q

Adrenal insufficiency differences in primary and secondary:

A
  1. Primary with decreased cortisol, HIGH ACTH

2. secondary with decreased cortisol, ACTH

34
Q

Treatment of chronic primary adrenal insufficiency:

A
  1. Glucocorticoid replacement (physiologic); monitor clinical symptoms and morning ACTH
  2. Mineralocorticoid replacement: liberal salt intake; fludrocortisone; keep an eye on supine/standing BP and serum K and plasma renin;
    if a minor febrile illness, increase glucocorticoid dose for the few days of illness, but NOT mineralocorticoid;

educate pt about the disease and also use medical alert bracelet/necklace

35
Q

Adrenal crisis treatment:

A

DO NOT DELAY treatment while waiting for definitive proof of diagnosis;
Need support with large amounts of IV fluids, and hypotonic saline will worsen hyponatremia;
also need high-dose IV glucocorticoid and gradual tapering to maintenance dose

36
Q

When to screen for primary aldosteronism:

A
  1. HTN with hypokalemia
  2. Treatment with resistant HTN
  3. Adrenal incidentaloma
  4. HTN of early onset (160 systolic, >100 diastolic)
  5. Also considering secondary HTN
37
Q

Screening tests for primary aldosteronism:

A
  1. Plasma aldo concentration
  2. Plasma renin activity
  3. 24-hr urine collection for aldo and Na
38
Q

Treatment of primary aldo:

A
  1. Surgery (unilateral adenoma)

2. Med (bilateral adrenal hyperplasia): spironolactone and eplerenone (latter less antiandrogenic)

39
Q

21-hydroxylase deficiency: mech and symptoms:

A
  1. defective conversion of 17-hydroxyprogesterone to 11-deoxycortisol (and progesterone to DOC)
  2. Increased adrenal androgens produce hirsutism and/or other forms of virilization
40
Q

CAH with 21-hydroxylase deficiency early and late onset, and diagnosis:

A

Early: virilizing with clitoral enlargement, labial fusion, urogenital sinus, sexual ambiguity; salt wasting crisis and hypotension
Late: think high DHEAS, androstenedione leading to sexual precocity or hirsutism or irregular menstruation; hyponatremia, hyperkalemia, increased renin in salt wasters;
Diag: increased response of plasma 17-hydroxyprogesterone to ACTH (cosyntropin stimulation test)

41
Q

Treat 21-hydroxylase deficiency:

A
  1. Steroids (dexamethasone, prednisone, hydrocortisone)
  2. In salt-wasting, need fludrocortisone
  3. Treat gluco and mineralo deficiency if there
  4. Give steroids to suppress ACTH production and reduce androgen overproduction
42
Q

Toxicity of corticosteroids; acute SE’s:

A
  1. Can get iatrogenic Cushing’s syndrome (osteoporosis, diabetes, infections) with supraphysiological steroid doses
  2. Withdrawal of steroid therapy resulting in adrenal insufficiency;
    insomnia, behavior changes (hypomania, acute psychosis), acute peptic ulcers, acute pancreatitis (rare at high dose)
43
Q

Prolonged CS use complications:

A
  1. peptic ulcer
  2. masking symptoms of infection
  3. severe myopathy
  4. nausea
  5. depression
44
Q

Alternate day therapy indicated for

A

minimizing SE’s of HPA suppression and iatrogenic Cushings syndrome, NOT for adrenal insufficiency; we use prednisone, prednisolone, methylprednisolone

We need a Head Coach, not an Assistant

45
Q

Withdrawal from steroid therapy; how to avoid:

A

Anorexia, NV, weight loss, lethargy, headache, fever, joint or muscle pain, postural hypotension;
suggests glucocorticoid dependence even with normal or high plasma cortisol levels;
could be during withdrawal or treatment of Cushing’s syndrome;
TAPER THERAPY very slowly, and during recovery you’ll have hypothalamic pituitary function coming back before adrenocortical function, and pts at risk of ADRENAL crisis

Pharm Unit 5 (9 decks)

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