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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
A higher dose of ketoconazole inhibits
CYP11A1
26
inhibiting CYP11A1 results in what
inhibiting all steroidogensis
27
what is the mechanism of metyrapone
selective inhibitor of CYP11B1 reducing the biosynthesis of of cortisol
28
When do you give Metyrapone
hypercorticism resulting from either adrenal neoplasms or tumors producing ACTH ectopically
29
Name 5 side effects for Metyrapone
1. HIRSUTISM | 2. nausea, headache, sedation, rash
30
what is the Mechanism of action for mefepristone
blocks release of glucocorticoid receptors from chaperone proteins
31
What Mifepristone is an antagonist for what? side effect?
progesterone antagonist | abortion pill --> vaginal bleeding
32
when is Mifepristone perscribed
1. patients with inoperable ectopic ACTH tumor | 2. adrenal carcinomas un responsive to other treatments
33
what are the characteristics of primary adrenal insufficiency
1. high ACTH levels | 2. low glucocorticoids and mineralcorticoids
34
what is the difference between the primary and secondary insufficiency
Primary: target organ secondary: pituitary/hypothalamic
35
What is the disease seen with primary adrenal insufficiency
Addison's desase
36
What is a symptoms commonly seen in Addison's disease
hyper-pigmentation ( of hand)
37
what happens in secondary adrenal insufficiency
decreased ACTH | decreased glucocorticoid and adrenal androgens
38
what is the diagnostic test to determine difference primary and secondary insufficiency
Cosyntropin test ( synthetic ACTH)
39
How do you treat Addison's disease? what do you supplement it with and why?
1. hydrocortsone/cortisone peferred | - supplemented with fludrocortisone to giver higher mineralocorticoid effect
40
what is the treatment difference between secondary and primary
secondary: no supplement because mineralocorticoids are not needed
41
What deficiency is seen in congenital adrenal hypersplaisa
CYP21
42
what does deficiency in CYP21 cause? why?
increase 17-hydroxyprogesterone | - lack of feedback inhibition and excess ACTH
43
what are your blood levels of corticosteroids in CAH
low
44
what is the clinical presentation for congenital adrenal hyperplasia for post puberty teenagers
females: mild androgens hirsutism amenorrhea
45
What does aldosteronism cause
hypertension | hypokalemia
46
How do you treat aldosteronism
aldonsterone antagonist- Spironolactone
47
How does Spironolactone worke
it binds to the aldosterone receptor in the renal
48
when giving glucococortidoids what is the goal of the therapy
want to give minimal effective dose because of its many side effects
49
why is there still an underlying effect for therapeutic use of glucocorticoids
because you only treat the symptom
50
after failure of which less toxic substances, do you use glucocorticoids
antihistamines | Ibuprofen
51
What is the best administration of glucocorticoids that has less side effect
single large dose
52
what should you avoid when using glucocorticoid therapy?
rapid withdrawel
53
what should you be concerned with when giving glucocorticoids with the disease and testing?
suppression of signs and symptoms of disease | interfere with diagnostic tests
54
How often do you use glucocorticoid therapy for remission
use ever other day therapy
55
which part of the day should glucocorticoid administered while on remission and why
morning, to duplicate circadian rhythm
56
Why is every other day treatment given for glucocorticoid
1. reduced suppression of HPA axis 2. better compliance 3. less die effects
57
When should glucocorticoid therapy be used with cation
if viruses are contributing factor
58
what happens when you give glucocorticoid to asthma and COPD patients
low systemic side effects in inhalation: | common side effect oral candidasis
59
what happens when you give glucocorticoid to people with allergies
not used for severe allergic reaction like anaphylaxis
60
what happens when you give glucocorticoid to GI pateints
glucocorticoid may mask symptoms of intestinal perforations and peritonitis
61
what happens when you give glucocorticoid to transplant patients
ALWAYS GIVEN IN CONJUNCTION WITH OTHER AGENTS
62
what are all the corticosteroids originate from in structure
hydrocortisone
63
What is the relative anti-inflammatory potency of glucocorticoid high to low
1. Dexamethasone/betamethasone 2. Triamcinolone 3. Methylpredinosione/predinisoine/prednisone 4. cortisone 5. cortisol/hydrocortisone
64
what are the enzymes that activate/deactivate in the cortisol-cortisone shuttle
HSD1 | HSD2
65
where is HSD1 found
found in most glucocorticoid target tissues
66
where is HSD2 found
in mineralocorticoid target tissues | kidney, colon, salivary glands, placenta
67
How is cortisol transported in plasma
bound to plasma protein | CBG and albumin
68
what is the difference between giving oral and IM
IM- more prolonged effects
69
what are the adverse reactions due to long term use/dose
cushing's sydnrome
70
If a patient is on prolonged steroids, can induce osteoporosis and can occur in menopausal women, what diet will you suggest to the patient
calcium and vitamin D supplementation
71
which CYP is induced by corticosteroids and what does it metabolize
CYP3A4 | estrogen

POD exam 4 (6 decks)

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