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POD exam 4 > Corticosteroids 2 > Flashcards

Corticosteroids 2 Flashcards

1
Q

What are glucocorticoid levels in the body through out the day

A

morning - high

evening - low

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2
Q

How does glucocorticoid act on the target cell

A
  • bind to cytoplasmic receptor ( glucorticoid receptor)

- complex to nucleus

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3
Q

What are 2 main non-endocrine use for glucocorticoid drug

A
  1. increases lipocortin levels

2. reduces NF-Kappa B levels

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4
Q

what is the effect of increased levels of lipocortin

A

inhibits phospholipase A2 activity

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5
Q

What is the effect of decreased phospholipase A2

A
  1. decreased arachindonic acid

2. decreases production of ecosanoids

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6
Q

Decreased levels of NF-Kappa B levels leads to decreases in what?

A
  1. proteolytic enzyme
  2. vasoactive cytokines
  3. chemoatractict cytokines
  4. COX-2
  5. NOS
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7
Q

What modulates the mineralocorticoid system

A

renin-angiotensin system

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8
Q

Aldosterone is found where in the nephron

A

distal tubules and collecting ducts

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9
Q

Aldosterone promotes the excretion of what ion

A

potassium

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10
Q

What stimulates the secretion of aldosterone

A
  1. hyperkalemia
  2. decrease plasma volume indirectly
  3. hyponatremia
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11
Q

What are levels of mineralocorticoids throughout the day

A

constant

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12
Q

name a disease with excess glucocorticoids

A

Cushing’s syndrome

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13
Q

name 2 diseases with insufficient glucocorticoids

A
  1. Addison’s

2. Congenital Adrenal Hyperplasia (CAH)

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14
Q

clinical manifestations for Cushing syndrome

A
  1. fat re disposition
  2. moon face
  3. hyperglycemia
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15
Q

What are the major causes of Cushing disease

A
  1. corticosteroid therapy - most common
  2. adrenocorticoal adenoma/carcinoma
  3. pituatary hypersecretion ACTH
  4. hypothalamic hyper secretion CRH
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16
Q

how do you treat Cushing? side effects

A

cortisol synthesis inhibitors

-can precipitate adrenal insufficiency

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17
Q

what are the two diagnostic tests

A
  1. Dexamethasone test

2. Metyrapone test (diagnostic)

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18
Q

Explain the Dexamethasone test

A
  1. inject high potency glucocorticoid
  2. inhibit ACTH (negative feedback inhibition)
  3. then determine cortisol levels
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19
Q

Does Dexamathasone interfere with lab tests for cortisol

A

no

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20
Q

Which test determines if you have cushing’s and which test differentiates the type of cushing’s

A
  1. low dose test and overnight test

2. high dose test

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21
Q

What are the inhibitors of cortisol production

A

Aminoglutethimide
keotconazole
metyrapone

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22
Q

what are the inhibitors of cortisol action

A

Mifepristone

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23
Q

mechanisms of action for aminoglutethimide

A

inhibits CYP11A1

CYP11B1 - lesser degree

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24
Q

mechanism of action for ketoconazole

A
  1. inhibit anti-fungal CYP17

2. inhibit corticotroph adenylate cyclase activation

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25
Q

A higher dose of ketoconazole inhibits

A

CYP11A1

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26
Q

inhibiting CYP11A1 results in what

A

inhibiting all steroidogensis

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27
Q

what is the mechanism of metyrapone

A

selective inhibitor of CYP11B1 reducing the biosynthesis of of cortisol

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28
Q

When do you give Metyrapone

A

hypercorticism resulting from either adrenal neoplasms or tumors producing ACTH ectopically

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29
Q

Name 5 side effects for Metyrapone

A
  1. HIRSUTISM

2. nausea, headache, sedation, rash

30
Q

what is the Mechanism of action for mefepristone

A

blocks release of glucocorticoid receptors from chaperone proteins

31
Q

What Mifepristone is an antagonist for what? side effect?

A

progesterone antagonist

abortion pill –> vaginal bleeding

32
Q

when is Mifepristone perscribed

A
  1. patients with inoperable ectopic ACTH tumor

2. adrenal carcinomas un responsive to other treatments

33
Q

what are the characteristics of primary adrenal insufficiency

A
  1. high ACTH levels

2. low glucocorticoids and mineralcorticoids

34
Q

what is the difference between the primary and secondary insufficiency

A

Primary: target organ
secondary: pituitary/hypothalamic

35
Q

What is the disease seen with primary adrenal insufficiency

A

Addison’s desase

36
Q

What is a symptoms commonly seen in Addison’s disease

A

hyper-pigmentation ( of hand)

37
Q

what happens in secondary adrenal insufficiency

A

decreased ACTH

decreased glucocorticoid and adrenal androgens

38
Q

what is the diagnostic test to determine difference primary and secondary insufficiency

A

Cosyntropin test ( synthetic ACTH)

39
Q

How do you treat Addison’s disease? what do you supplement it with and why?

A
  1. hydrocortsone/cortisone peferred

- supplemented with fludrocortisone to giver higher mineralocorticoid effect

40
Q

what is the treatment difference between secondary and primary

A

secondary: no supplement because mineralocorticoids are not needed

41
Q

What deficiency is seen in congenital adrenal hypersplaisa

A

CYP21

42
Q

what does deficiency in CYP21 cause? why?

A

increase 17-hydroxyprogesterone

- lack of feedback inhibition and excess ACTH

43
Q

what are your blood levels of corticosteroids in CAH

A

low

44
Q

what is the clinical presentation for congenital adrenal hyperplasia for post puberty teenagers

A

females: mild androgens
hirsutism
amenorrhea

45
Q

What does aldosteronism cause

A

hypertension

hypokalemia

46
Q

How do you treat aldosteronism

A

aldonsterone antagonist- Spironolactone

47
Q

How does Spironolactone worke

A

it binds to the aldosterone receptor in the renal

48
Q

when giving glucococortidoids what is the goal of the therapy

A

want to give minimal effective dose because of its many side effects

49
Q

why is there still an underlying effect for therapeutic use of glucocorticoids

A

because you only treat the symptom

50
Q

after failure of which less toxic substances, do you use glucocorticoids

A

antihistamines

Ibuprofen

51
Q

What is the best administration of glucocorticoids that has less side effect

A

single large dose

52
Q

what should you avoid when using glucocorticoid therapy?

A

rapid withdrawel

53
Q

what should you be concerned with when giving glucocorticoids with the disease and testing?

A

suppression of signs and symptoms of disease

interfere with diagnostic tests

54
Q

How often do you use glucocorticoid therapy for remission

A

use ever other day therapy

55
Q

which part of the day should glucocorticoid administered while on remission and why

A

morning, to duplicate circadian rhythm

56
Q

Why is every other day treatment given for glucocorticoid

A
  1. reduced suppression of HPA axis
  2. better compliance
  3. less die effects
57
Q

When should glucocorticoid therapy be used with cation

A

if viruses are contributing factor

58
Q

what happens when you give glucocorticoid to asthma and COPD patients

A

low systemic side effects in inhalation:

common side effect oral candidasis

59
Q

what happens when you give glucocorticoid to people with allergies

A

not used for severe allergic reaction like anaphylaxis

60
Q

what happens when you give glucocorticoid to GI pateints

A

glucocorticoid may mask symptoms of intestinal perforations and peritonitis

61
Q

what happens when you give glucocorticoid to transplant patients

A

ALWAYS GIVEN IN CONJUNCTION WITH OTHER AGENTS

62
Q

what are all the corticosteroids originate from in structure

A

hydrocortisone

63
Q

What is the relative anti-inflammatory potency of glucocorticoid high to low

A
  1. Dexamethasone/betamethasone
  2. Triamcinolone
  3. Methylpredinosione/predinisoine/prednisone
  4. cortisone
  5. cortisol/hydrocortisone
64
Q

what are the enzymes that activate/deactivate in the cortisol-cortisone shuttle

A

HSD1

HSD2

65
Q

where is HSD1 found

A

found in most glucocorticoid target tissues

66
Q

where is HSD2 found

A

in mineralocorticoid target tissues

kidney, colon, salivary glands, placenta

67
Q

How is cortisol transported in plasma

A

bound to plasma protein

CBG and albumin

68
Q

what is the difference between giving oral and IM

A

IM- more prolonged effects

69
Q

what are the adverse reactions due to long term use/dose

A

cushing’s sydnrome

70
Q

If a patient is on prolonged steroids, can induce osteoporosis and can occur in menopausal women, what diet will you suggest to the patient

A

calcium and vitamin D supplementation

71
Q

which CYP is induced by corticosteroids and what does it metabolize

A

CYP3A4

estrogen

POD exam 4 (6 decks)

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