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ABBEY MSII Unit 5 > Pharm adrenal steroids > Flashcards

Pharm adrenal steroids Flashcards

1
Q

what are the layers of the adrenal gland

A

zona glomerulosa, zona fasciculata, zona reticularis

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2
Q

what does zona glomerulosa make

A

aldosterone

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3
Q

what does zona fasciculata make

A

glucocorticoids (cortisol)

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4
Q

what does zona reticularis make

A

cortisol and androgens

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5
Q

Common enzyme for androgens and cortisol

A

17-alpha hydroxylase

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6
Q

common enzyme for aldosterone and cortisol

A

21-beta hydroxylase

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7
Q

mineralcorticoids

A

aldosterone and deoxycorticosterone (DOC)

cortisol has weak mineralcorticoid activity

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8
Q

glucocorticoids

A

cortisol

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9
Q

cortisol mechanism of action

A

works within nucleus (diffuses through membrane)

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10
Q

what controls the release of cortisol from the adrenal gland?

A

ACTH from anterior pituitary

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11
Q

what controls the release of ACTH from the anterior pituitary?

A

CRH from hypothalamus

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12
Q

glucocorticoid effects

A

stress hormone
carbohydrate metabolism
immune function

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13
Q

glucocorticoid metabolic effects

A
  • increase gluconeogenesis,
  • release amino acids through muscle catabolism,
  • inhibit peripheral glucose uptake,
  • simulate lipolysis,
  • maintain adequate glucose for brain!
  • increase blood pressure
  • decrease bone formation
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14
Q

how does glucocorticoid increase blood pressure?

A

upregulates alpha 1 receptors on arterioles and leads to increased sensitivity to norepi and epi

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15
Q

glucocorticoid anti-inflammatory effects

A

upregulation of anti-inflammatory proteins, down regulation or pro-inflammatory, decreased leukocyte presence and function at site of inflammation

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16
Q

mineralcorticoid effects

A

-active in distal convoluted and collecting tubules maintaining electrolyte balance and intravascular volume

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17
Q

what are the most significant regulators of aldosterone secretion?

A

increased potassium, angiotensin II

ACTH, sodium deficiency

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18
Q

mineralcorticoid specificity with aldosterone receptors

A

cortisol binding AR is prevented by 11 beta-hydroxysteroid dehydrogenase type 2
(cortisol –> cortisone)

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19
Q

pharmacologic uses of corticosteroids

A
  • adrenal insufficiency
  • establish diagnosis and cause of cushing’s syndrom
  • treat inflammatory, allergic, immunological disorders
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20
Q

what is the synthetic mineralcorticoid? difference from cortisol?

A

fludrocortisone

-very high mineralcorticoid effect with a longer duration of action

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21
Q

what are the disorders of adrenal function?

A

adrenocortical insufficiency
congenital adrenal hyperplasia
cushing’s syndrome
aldosteronism

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22
Q

primary vs secondary adrenocortical insufficiency

A

primary: anatomic destruction of adrenal gland (autoimmune)
secondary: decreased pituitary production of ACTH

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23
Q

causes for secondary adrenal insufficiency

A

ACTH deficiency due to iatrogenic and hypopituitarism

24
Q

primary adrenal insufficiency symptoms/signs

A

weakness, fatigue, nausea, vomiting, diarrhea, salt craving, postural dizziness, anorexia, weight loss, skin pigmentation

25
Q

primary adrenal insufficiency labs

A

hyponatremia, hyperkalemia, anemia, eosinophilia, azotemia

26
Q

secondary adrenal insufficiency symptoms/signs

A

same as primary except NO hyperpigmentation (ACTH is low not elevated) and near-normal aldosterone levels

27
Q

how to diagnose adrenal insufficiency

A

measure plasma cortisol level at baseline and 30-60 min after cosyntropin (synthetic ACTH)
if cortisol is greater than 18 = normal
if cortisol is less than 18 = abnormal

28
Q

diagnosis adrenal insufficiency: primary vs secondary

A 
primary = low cortisol and high ACTH
secondary = low cortisol and low ACTH
29
Q

causes for acute adrenal insufficiency “adrenal crisis”

A

rapid withdrawal of steroids from someone how has been on them for a long time

30
Q

signs/symptoms of adrenal crisis

A

volume depletion and hypotension, lassitude, nausea, vomiting, hyperkalemia, hyponatremia (mineralcorticoid deficiency, increased ADH)

31
Q

treatment of adrenal crisis

A
  • support with large amounts of IV fluids

- high-dose IV glucocorticoid (dexamethasone if no previous dx of adrenal insufficiency, or hydrocortisone)

32
Q

treatment of chronic adrenal insufficiency

A
  • maintenance therapy: glucocorticoid replacement (hydrocortisone 2x per day) and mineralocorticoid replacement (fludrocortison, liberal salt intake)
  • stress dosing
33
Q

congenital adrenal hyperplasia

A

inherited AR disorders caused by deficient adrenal corticosteroid synthesis d/t mutations of genes involved with adrenal steroidogenesis
-enzyme deficiency

34
Q

what is the MCC of congenital adrenal hyperplasia? what does it cause?

A

21-hydroxylase deficiency

cuases inability to make aldosterone and cortisol which causes increased androgens

35
Q

what is measured for diagnosis of 21-hydroxylase deficiency?

A

17-OH-progesterone (if it is raised means there is 21-hydroxylase deficiency)

36
Q

21-hydroxylase deficiency treatment

A

steroids (dexmethasone, prednisone, hydrocortisone)

if salt-wasting, also add fludrocortisone

37
Q

glucocorticoid excess

A

Cushing’s syndrome
caused by 1. ACTH dependent (pituitary adenoma or ectopic ACTH production)
2. ACTH independent (adrenal adenoma and adrenal carcinoma)
3. iatrogenic

38
Q

signs and symptoms of Cushing’s syndrome

A

weight gain (truncal), moon face, HTN, bruising, thin skin, striae, ankle edema, proximal myopathy, hirsutism, psychiatric dysfxn, backache, muscle weakness, loss of scalp hair, fractures

39
Q

cushing disease

A

pituitary ademona causing the glucocorticoid excess

40
Q

diagnosis of cushing’s syndrome

A

-ACTH (high = dependent, low = independent)
-24-hr urine free cortisol excretion
-low-dose overnight dexamethasone suppression test (less than 1.8 is normal)
-midnight salivary cortisol level
need at least TWO of these tests positive

41
Q

medical treatment of cushing’s syndrome

A 
aminoglutethimide
ketoconazole
mitotane
metyrapone
mifepristone
42
Q

aminoglutethimide mechanism and use

A

blocks conversion of cholesterol to pregnenolone (treats cushing’s)

43
Q

ketoconazole mechanism and use

A

antifungal imidazole derivative. potent, nonselective inhibitor of adrenal and gonadal steroid synthesis (treats cushing’s)

44
Q

mitotane mechanism and use

A

related to DDT insecticides. nonselective cytotoxic action on adrenal cortex - bad SE (treats cushing’s)

45
Q

metyrapone mechanism and use

A

relatively selective inhibitor of 11-hydroxylation. interferes with cortisol and corticosterone synthesis
-can be used diagnostically to test anterior pituitary (ACTH levels should rise in compensatory response to decreased cortisol and corticosterone as should precursor 11-deoxycortisol)
(treats cushing’s)

46
Q

mifepristone mechanism

A

initally developed as progesterone receptor antagnoist

-has glucocorticoid receptor antagonist activity at higher concentrations (only binds glucocorticoid receptor)

47
Q

mifepristone use

A

cushing’s syndrome - controls hyperglycemia secondary to hypercortisolism in adults with endogenous cushing’s syndrome who have failed or are not candidates for surgery
-also used for rapid treatment of cortisol-induced psychosis

48
Q

mifepristone side effects

A

fatigue, nausea, headache, hypokalemia, arthralgias, edema and endometrial thickening
also: adrenal insufficiency

49
Q

pasireotide mechanism and uses

A

somatostatin analog binds to somatostatin receptors and blocks release of ACTH from the corticotropes via high affinity for somatostatin receptor subtype 5
use: cushing’s disease pituitary

50
Q

pasireotide side effects

A

hyperglycemia and gastrointestinal symptoms

51
Q

aldosteronism

A

increased aldosterone, decreased renin d/t HTN and hypokalemia

52
Q

when to screen for primary aldosteronism

A
  • HTN with hypokalemia
  • resistant HTN
  • adrenal incidentaloma
  • HTN early onselt
  • severe HTN
53
Q

treatment for priamry aldosteronism

A

surgery for unilateral adenoma and medical for bilateral adrenal hyperplasia (spironolactone and eplerenone - aldosterone receptor blocking agents)

54
Q

difference between spironolactone and eplerenone

A

eplerenone is newer with less antiandrogen effects

55
Q

nonendocrinologic use of corticosteroids

A

for suppressing inflammatory and immune response

56
Q

acute side effects of corticosteroids

A

insomnia, behaviour changes (hypomania, acute psychosis), acute peptic ulcers, acute pancreatitis (rare)

57
Q

withdrawal from steroid therapy

A
  • adrenal suppression can occur after 2 weeks
  • withdrawal syndrome of anorexia, nausea, vomiting, weight loss, lethargy, headache, fever, joint or muscle pain, postural hypotension d/t dependence
  • need to taper off steroid therapy (2-12 months)

ABBEY MSII Unit 5 (8 decks)

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