NSAIDs and DMARDs Flashcards

(58 cards)

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
Non-salicylate nsaids?
nonselective cox blockers reversible inhibit reversible inhibit of platelet aggegation
26
Antiinflammtory effects?
not immediate (after steady state, 5 half lives) decrease capillary permeable, decrease lysosomal enzyme release, decrease release of mediators from PMN
27
Adverse effects Non-salicylate nsaids?
GI toxic- ulcers, bleeding
28
Misoprostol and NSAIDs?
in combo for patients at high risk for GI toxicity | M- PGE analog, decrease gastric acid, stim bicarb and mucus production
29
Also decrease GI toxic with NSAIDs?
proton pump inhibitors | need acid and pepsin to develop ulcer/lesion, decreased acid is protective
30
Nephrotoxicity with Non-salicylate nsaids?
some degree of acute renal failure analgesic nephropathy
31
Indomethacin?
most toxic NSAIDs not treat fever gout, RA, other inflammation DA in newborns similar AE and Contra as others
32
Ibuprofen (motrin)?
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
Naproxen?
most frequent prescribed | half life allow 2x day dosing
34
Ketorolac?
analgesic not antiinflam | mod to severe pain, short term (ulcers, silent bleed)
35
COX 2 inhibitors?
induced in peripheral tissues by noxious simuli that cause inflammation and pain have better GI safety profile no safer to GI than nonselective
36
Celecoxib?
celebrex increased incidence of MIs may be useful in treatment of certain tumors that express COX-2
37
Acetaminophen?
not an nsaid inhibits COX-2 no significant antiinflammatory effects analgesic, antipyretic effects
38
Use acetaminophen?
pain and fever relief when aspirin cant be used -children, patients on anticoagulants, gouty patients on uricosurics
39
Adverse reactions acetaminophen?
dose dependent hepatic necrosis | usually in acute overdose
40
Prevent severe hepatic necrosis with aceta?
NAC (N-acteylcystine) given within 24 hrs can protect the liver too
41
Predict toxicity with acteminophen?
Rumack-Matthew Nomogram
42
DMARDs?
more toxic than NSAIDs slow progress of RA MOA not well defined
43
DMARD use for RA?
can slow progress if introduced early
44
Methotrexate?
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
Hydroxychloroquine?
antimalarial drug MOA unclear early, mild RA without poor prognostic features can take 2-3 months to see improvement
46
Hydroxychloroquine side effects?
GI upset skin changes -hyperpigmentation
47
Sulfasalazine?
antiinflammtory agetn MOA unclear prefer over hydrox in pts with more symptoms and signs of actuve synovitis clin improvement with 1-2 months
48
Leflunomide?
option for nonresponsive or who cannot tolerate MTX inhibit de novo synthesis pyrimidine synthesis adverse effects- -hypertension, hepatotoxicity
49
Gold Salts?
MOA unclear | effective in early rapid stages of RA, short term
50
Gold salts adverse?
toxic less with oral but not as effective -dermatitis, hematological abnormalities, nephrotoxicity
51
Penicillamine?
``` if gold doesnt work chelating agent (copper poison, Wilson's disease) MOA unclear decrease bone destruction in RA ```
52
Adverse Penicillamine?
more frequent than gold severe side effects limit use -GI, agranulocytosis, nephrotoxicity, allergy
53
Biological DMARDs?
generally alter TNFalpha activity
54
Etanercept?
``` 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
Infliximab?
``` monoclonal antibody to TNFalpha bind and neutralize free TNFalpha adverse effects risk of infection hypersentivity SLE like syndrome ```
56
Bio modifiers adverse?
Heart failure and TNF inhibitors Cancer risk-lymphoma and others TB, invasive infection
57
Anakinra?
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
Use combo of biological modifiers?
no increase risk of infection