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Summer Pharm - Exam 2 > Glucocorticoids/Anti-Inflammatory Agents > Flashcards

Glucocorticoids/Anti-Inflammatory Agents Flashcards

1
Q

glucocorticoid drugs target the same receptor as endogenous cortisol, which is

A

GC-R

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2
Q

activation of GC-R receptor

is necessary for __

A

anti-inflammatory actions

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3
Q

what receptor is responsible for ADRs of glucocorticoids

A

GC-R

same as anti inflammatory

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4
Q

short to med acting glucocorticoids

A

hydrocortisone (cortisol)

prednisone

methylprednisone

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5
Q

intermediate-acting glucocorticoid to know

A

triamcinolone

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6
Q

long-acting glucocorticoid to know

A

dexamethasone

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7
Q

which 2 glucocorticoids have no topical use

A

cortisone

prednisone

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8
Q

major regulator of aldosterone synthesis

A

angiotensin II

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9
Q

effect of GC on the adrenal gland

A

suppression

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10
Q

t/f: endogenous AND exogenous GC also suppress ACTH release

A

T!

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11
Q

chronic use of pharmacologic doses of GCs can suppress __,

which leads to no ACTH and __

A

HPA axis

adrenal hypertrophy

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12
Q

if the adrenal gland is suppressed, the patient is reliant on

A

exogenous GCs

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13
Q

insufficient adrenal response to environmental stressors is called

A

adrenal crisis

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14
Q

tx for adrenal crisis

A

exogenous GCs

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15
Q

t/f: pharmacologic doses of GCs can cause iatrogenic Cushing’s

A

T!

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16
Q

excess GC use causes (7)

A

hyperglycemia

muscle wasting

central obesity

insomnia/dpn/euphoria

OP

ulcers

iatrogenic hyperaldosteronism → fluid retention, hypokalemia, metabolic alkalosis

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17
Q

bad AI/IS effects of GCs (3)

A

decrease healing

diminish immunoprotection

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18
Q

clinical value of GCs

A

suppress chronic inflammation

suppress AI rxns

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19
Q

GCs inhibit synthesis of both

A

PGs (prostaglandins)

LTs (leukotrienes)

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20
Q

which to GCs require activation in the liver

A

prednisone → prednisolone

cortisone → hydrocortisone

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21
Q

which form of GCs are inactive

A

11-keto

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22
Q

which functional group is required for activation of GCs

A

OH → hydroxyl

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23
Q

mc used oral GC used for steroid burst therapy

A

prednisone

24
Q

which steroid has minimal MC action

A

methylprednisone

dexamethasone

25
Q

IV form of methylprednisolone

A

solu-medrol

26
Q

oral form of methylprednisolone

A

medrol

27
Q

clinical use of cortisol (hydrocortisone)

A

replacement therapy → emergencies

28
Q

how is cortisol administered (2)

A

oral

parenteral

29
Q

which GC has no topical activity

A

prednisone

needs to be converted in the liver

30
Q

most potent GC

A

dexamethasone (Decadron)

31
Q

uses of dexamethasome

A

cerebral edema

chemo-induced vomiting

32
Q

which GC has greatest suppression of ACTH secretion at pituitary

A

dexamethasone (decadron)

33
Q

which GC has excellent systemic AND topical activity, but no MC action

A

triamcinolone

34
Q

non-adrenal collagen-vascular disorder to know

A

RA

35
Q

order of tx for RA (4)

A
  1. NSAIDs
  2. GCs as bridge
  3. MTX (DMARD)
  4. Etanercept and Infliximab
36
Q

when are DMARDs added to RA tx

A

when dx is certain → suppress dz progression

37
Q

how are GCs used for RA (2)

A

as a bridge until DMARDs take effect

adjunctive when dz persists

38
Q

__ side effects vary w. agent

but __ side effects are unavoidable

A

MC

GC

39
Q

list GC agents in order of least to most MC effect

A

cortisol

prednisone

methylprednisone/dexamethasone

40
Q

how is dosage figured out w. GC

A

trial and error → re-evaluation

41
Q

when should you reduce dose of GC

A

as soon as therapeutic dosages are obtained

42
Q

if a larger initial dose is needed, what GC should you choose

A

one w. little MC action

43
Q

how do you minimize adrenal suppression of GC

A

alternate day schedule

44
Q

how do you minimize dz rebound and adrenal crisis (insufficiency)

A

terminate gradually

45
Q

major consideration in deciding route of GC administration

A

minimize systemic actions

46
Q

routes of administration for GC (7)

A

oral

topical

ophthalmic

intra-articular

enemas

inhalants

nasal sprays

47
Q

mc rout of administration when systemic actions are desired

A

oral

also IV/IM

48
Q

what 4 things can cause systemic effects of topical GCs

A

potent agent

long term use

occlusive dressings

large area of application

49
Q

route of GC administration for OA/RA

A

intra-articular

50
Q

why would you use a GC enema

A

UC

51
Q

what determines adverse effects of GCs (2)

A

dose

duration

52
Q

what s.e can you expect w. GC use >2-4 weeks

A

iatrogenic Cushing’s → DM like state

HPA axis suppression

mood disturbance

increased infxn risk

impaired wound healing/increased bruising

OP

cataracts

skin atrophy/collagen loss

growth retardation

peptic ulcers

moon facies

53
Q

which 2 GC cause the most HPA suppression

A

dexamethasone

betamethasone

may also cause decrease in GH

54
Q

what reduces peptic ulcer risk w. long term GC use

A

antacids

55
Q

what decreases risk of OP w. long term GC use

A

bisposphanates

56
Q

what s.e of GC are seen w. burst therapy

A

GI upset

insomnia

DPN

HTN

hyperglycemia

Summer Pharm - Exam 2 (12 decks)

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