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MOD 2 Quiz 1 > NSAIDs and DMARDs > Flashcards

NSAIDs and DMARDs Flashcards

1
Q

NSAIDs? DMARDs?

A

nonsteroidal anti inflammatory drugs

disease modifying antiherumatic drugs

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2
Q

NSAIDs use?

A

analgesic, antipyretic, anti-inflammatory
risk reduction for reinarction and stroke
closure of patent DA in neonates
treat biochemical degredation of Bartter’s syndrome
Chemoprevention of certain cancers such as colon cancer

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3
Q

NSAIDs all inhibit?

A

COX
inhibit prostaglandin synthesis largely responsible for therapeutic effect
no affect course of disease, just symptomatic relief

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4
Q

General side effect?

A

GI, Renal, CV, CNS

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5
Q

Cyclooxygenase forms?

A

COX1 COX2

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6
Q

COX-1?

A

constitutively expressed in most cells/tissues

important for normal homeostasis

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7
Q

COX-2?

A

mostly inducible
proinflammatory and mitogenic function
PGs in inflammatory sites (synociocytes, macrophages)
prevent proinflammatory cascade

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8
Q

Do you get platelet effect with COX-2?

A

no only COX-1

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9
Q

Joint inflammation from?

A

COX-2

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10
Q

Kidney damage?

A

both COX-1 and 2

inhibitors of both cause kidney damage

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11
Q

Nonselective inhibitors?

A

drugs tend to cause GI toxic, COX-1 inhibition

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12
Q

COX 2 selective?

A

better GI safety profile

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13
Q

Inhibition of PG synthesis impt in those?

A

who have stimulated PG synthesis

  • renal disease
  • Effective volume depletion
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14
Q

NSAIDs and renal function?

A 
Acute renal failure
-PGs normally oppose vasoconstriction, without goes unopposed
Hyperkalemia
Edema and Hyponatremia
Increase BP
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15
Q

Acetylsalicylic acid?

A

ASA, aspirin

nonselective, irrverisble COX inhibitor

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16
Q

Non-acetlyated salicylates?

A 
all else (but aspirin)
non selective COX inhibitors
reversible
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17
Q

Low dose aspirin?

A

cause antithromotic effects (anitplatelet)

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18
Q

High dose aspirin?

A

cause antiinflammatory effects
limited by toxicity
(interfere with uric acid elim and aggravate control of gout)

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19
Q

Salicylates Adverse effects?

A

GI toxic
increased bleeding time
renal toxic
liver toxic

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20
Q

Acute mild toxicity?

A

tinnitus (common)

headache, dizziness, drowsiness, mental confusion, sweating, nausea/vomit

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21
Q

Acid base abnormalities?

A

direct stim respiratory center
cause fall in CO2, respiratory alkalosis
componsated renal alkalosis

anion gap metabolic acidosis can follow

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22
Q

Acid/base in severe intox?

A

decrease respiration

respiratory acidosis

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23
Q

Aspirin toxicity treatment?

A 
Decontaminate (activated charcoal, gastic levage)
volume resuscitation
suplemental glucose
alkalization
hemodialysis
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24
Q

Reyes syndrome?

A

high incidence with aspirin use in children with viral illness
avoid aspirin, use acetaminophen instead

25
Q

Non-salicylate nsaids?

A

nonselective cox blockers
reversible inhibit
reversible inhibit of platelet aggegation

26
Q

Antiinflammtory effects?

A

not immediate (after steady state, 5 half lives)

decrease capillary permeable, decrease lysosomal enzyme release, decrease release of mediators from PMN

27
Q

Adverse effects Non-salicylate nsaids?

A

GI toxic- ulcers, bleeding

28
Q

Misoprostol and NSAIDs?

A

in combo for patients at high risk for GI toxicity

M- PGE analog, decrease gastric acid, stim bicarb and mucus production

29
Q

Also decrease GI toxic with NSAIDs?

A

proton pump inhibitors

need acid and pepsin to develop ulcer/lesion, decreased acid is protective

30
Q

Nephrotoxicity with Non-salicylate nsaids?

A

some degree of
acute renal failure
analgesic nephropathy

31
Q

Indomethacin?

A

most toxic NSAIDs
not treat fever
gout, RA, other inflammation
DA in newborns

similar AE and Contra as others

32
Q

Ibuprofen (motrin)?

A

low cost, low tox
use in RA (limited, 4x day dosing)
AEs less than aspirin
may negate aspirins cardioprotective effects by antagonizing aspirins irreversible platelet inhibition

33
Q

Naproxen?

A

most frequent prescribed

half life allow 2x day dosing

34
Q

Ketorolac?

A

analgesic not antiinflam

mod to severe pain, short term (ulcers, silent bleed)

35
Q

COX 2 inhibitors?

A

induced in peripheral tissues by noxious simuli that cause inflammation and pain
have better GI safety profile
no safer to GI than nonselective

36
Q

Celecoxib?

A

celebrex
increased incidence of MIs
may be useful in treatment of certain tumors that express COX-2

37
Q

Acetaminophen?

A

not an nsaid
inhibits COX-2
no significant antiinflammatory effects
analgesic, antipyretic effects

38
Q

Use acetaminophen?

A

pain and fever relief
when aspirin cant be used
-children, patients on anticoagulants, gouty patients on uricosurics

39
Q

Adverse reactions acetaminophen?

A

dose dependent hepatic necrosis

usually in acute overdose

40
Q

Prevent severe hepatic necrosis with aceta?

A

NAC (N-acteylcystine) given within 24 hrs can protect the liver too

41
Q

Predict toxicity with acteminophen?

A

Rumack-Matthew Nomogram

42
Q

DMARDs?

A

more toxic than NSAIDs
slow progress of RA
MOA not well defined

43
Q

DMARD use for RA?

A

can slow progress if introduced early

44
Q

Methotrexate?

A

gold standard for RA treatment
initial drug for RA
anti-RA effects begin within 6 wks
lower dose than chemo treatment, still get some side effects

45
Q

Hydroxychloroquine?

A

antimalarial drug
MOA unclear
early, mild RA without poor prognostic features
can take 2-3 months to see improvement

46
Q

Hydroxychloroquine side effects?

A

GI upset
skin changes
-hyperpigmentation

47
Q

Sulfasalazine?

A

antiinflammtory agetn
MOA unclear
prefer over hydrox in pts with more symptoms and signs of actuve synovitis
clin improvement with 1-2 months

48
Q

Leflunomide?

A

option for nonresponsive or who cannot tolerate MTX
inhibit de novo synthesis pyrimidine synthesis
adverse effects-
-hypertension, hepatotoxicity

49
Q

Gold Salts?

A

MOA unclear

effective in early rapid stages of RA, short term

50
Q

Gold salts adverse?

A

toxic
less with oral but not as effective
-dermatitis, hematological abnormalities, nephrotoxicity

51
Q

Penicillamine?

A 
if gold doesnt work
chelating agent (copper poison, Wilson's disease)
MOA unclear
decrease bone destruction in RA
52
Q

Adverse Penicillamine?

A

more frequent than gold
severe side effects limit use
-GI, agranulocytosis, nephrotoxicity, allergy

53
Q

Biological DMARDs?

A

generally alter TNFalpha activity

54
Q

Etanercept?

A 
form of recombinant TNFalpha receptor
fake receptor
response may occur in a couple of wks
como with methotrexate, no increase in tox
less frequent occur SE
rash at injection site
55
Q

Infliximab?

A 
monoclonal antibody to TNFalpha
bind and neutralize free TNFalpha
adverse effects
risk of infection
hypersentivity
SLE like syndrome
56
Q

Bio modifiers adverse?

A

Heart failure and TNF inhibitors
Cancer risk-lymphoma and others
TB, invasive infection

57
Q

Anakinra?

A

IL-1 receptor antagonist
block inflammatory and immunologic rxn of IL-1 in RA
adverse effects
-pain,inflammation, erythema at injection
increased risk of infection

58
Q

Use combo of biological modifiers?

A

no increase risk of infection

MOD 2 Quiz 1 (9 decks)

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