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
IV form of methylprednisolone
solu-medrol
26
oral form of methylprednisolone
medrol
27
clinical use of cortisol (hydrocortisone)
replacement therapy → emergencies
28
how is cortisol administered (2)
oral parenteral
29
which GC has no topical activity
prednisone *needs to be converted in the liver*
30
most potent GC
dexamethasone (Decadron)
31
uses of dexamethasome
cerebral edema chemo-induced vomiting
32
which GC has greatest suppression of ACTH secretion at pituitary
dexamethasone (decadron)
33
which GC has excellent systemic AND topical activity, but no MC action
triamcinolone
34
non-adrenal collagen-vascular disorder to know
RA
35
order of tx for RA (4)
1. NSAIDs 2. GCs as bridge 3. MTX (DMARD) 4. Etanercept and Infliximab
36
when are DMARDs added to RA tx
when dx is certain → suppress dz progression
37
how are GCs used for RA (2)
as a bridge until DMARDs take effect adjunctive when dz persists
38
\_\_ side effects vary w. agent but __ side effects are unavoidable
MC GC
39
list GC agents in order of least to most MC effect
cortisol prednisone methylprednisone/dexamethasone
40
how is dosage figured out w. GC
trial and error → re-evaluation
41
when should you reduce dose of GC
as soon as therapeutic dosages are obtained
42
if a larger initial dose is needed, what GC should you choose
one w. little MC action
43
how do you minimize adrenal suppression of GC
alternate day schedule
44
how do you minimize dz rebound and adrenal crisis (insufficiency)
terminate gradually
45
major consideration in deciding route of GC administration
minimize systemic actions
46
routes of administration for GC (7)
oral topical ophthalmic intra-articular enemas inhalants nasal sprays
47
mc rout of administration when systemic actions are desired
**oral** also IV/IM
48
what 4 things can cause systemic effects of topical GCs
potent agent long term use occlusive dressings large area of application
49
route of GC administration for OA/RA
intra-articular
50
why would you use a GC enema
UC
51
what determines adverse effects of GCs (2)
dose duration
52
what s.e can you expect w. GC use \>2-4 weeks
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
which 2 GC cause the most HPA suppression
dexamethasone betamethasone *may also cause decrease in GH*
54
what reduces peptic ulcer risk w. long term GC use
antacids
55
what decreases risk of OP w. long term GC use
bisposphanates
56
what s.e of GC are seen w. burst therapy
GI upset insomnia DPN HTN hyperglycemia