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Musculoskeletal > Pharm: DMARDS and NSAIDS > Flashcards

Pharm: DMARDS and NSAIDS Flashcards

1
Q

NSAIDs

A

non-steroidal anti-inflammatory drugs: anti-inflammatory, analgesic, antipyretic
COX inhibitors
hepatic metabolism
effects: reduce urinary metabolites of PGI2 and TXA2, inhibit platelets
AE: GI, RENAL, increase bleeding time, increase BP, increase CV risk in those on aspirin regimen, liver (low risk in most)
CI: decrease clearance of lithium and methotrexate
monitor: LFTs, serum creatinine/BUN, stool guaiac
*does not slow progression of RA

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2
Q

DMARDs (non-biological)

A

disease modifying anti rheumatic drugs
AE: BLOOD DYSCRASIA
monitor: CBC

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3
Q

biological DMARDs

A

DMARDs with specific epitopes
AE: immunosuppression, infection
other: blood dyscrasia and malignancy
CI: vaccine

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4
Q

acetaminophen

A

NSAID
NO anti-inflammatory effect
NOT used for arthritis
AE: GI in IV use, renal rarely, HEPATIC

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5
Q

aspirin

A

NSAID
irreversibly acetylates COX
platelet does not have a nucleus and cannot regenerate COX-1
MI prophylaxis
AE: hepatic (Reye’s: flu), salicylate poisoning
monitor: serum salicylate

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6
Q

diclofenac

A

NSAID
short acting
low GI risk
AE: high dose: vascular event

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7
Q

ibuprofen

A

NSAID
COX inhibitor
AE: high risk GI, high dose: vascular event

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8
Q

indomethacin

A

NSAID

AE: most adverse effects of all NSAIDs

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9
Q

ketoprofen

A

NSAID

short acting

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10
Q

ketorolac

A

NSAID

COX-1 inhibitor

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11
Q

naproxen

A

NSAID
AE: high risk GI
*NO CV risk increase even with high dose

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12
Q

piroxicam

A

NSAID

LONG ACTING

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13
Q

sulindac

A

NSAID

AE: HEPATIC (hypersensitive)

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14
Q

celecoxib

A

NSAID
selective COX-2 inhibitor
low GI risk
AE: vascular event

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15
Q

methotrexate

A

DMARD (non-biological)
DHFR inhibitor, adenosine inhibition
polyglutamation to remain intracellular
AE: bleeding, opportunistic infections, malignant lymphoma, GI, fatal dermatologic rxns, PULMONARY, TERATOGEN
CI: liver problems, alcoholic, renal failure, vaccinations (suboptimal), pregnancy, breast feeding
monitor: LFT, serum uric acid, serum creatinine/BUN

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16
Q

hydroxychloroquine

A 
DMARD (non-biological)
intracellular vacuole alkalization (need acidic for assembly of MHC)
AE: blood dycrasias, CNS, EYE
CI: liver, alcoholism, EYE 
Tx: malaria, RA, SLE
monitor: OPHTHALMOLOGIC exam
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17
Q

leflunomide

A

DMARD (non-biological)
inhibits dihydroorotate dehydrogenase: inhibits pyrimidine synthesis
urocosic effect
AE: LFT, TERATOGEN
CI: immune suppression, infection
monitor: LFT, pregnancy test, electrolytes

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18
Q

sulfasalazine

A

DMARD (non-biological)
metabolized by colon bacteria to mesalamine that inhibits PG and LT produciton
acetylated
CI: renal, hypersensitivity to salicylate or sulfonamide
monitor: LFT, serum creatinine/BUN, urinalysis

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19
Q

betamethasone

A

DMARD
POTENT
long T1/2: poor solubility
corticosteroid

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20
Q

cortisone

A

DMARD

corticosteroid

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21
Q

dexamethasone

A

DMARD
POTENT
long t1/2: poor solubility
corticosteroid

22
Q

hydrocortisone

A

DMARD
low potency
SHORT t1/2
corticosteroid

23
Q

methylprednisolone

A

DMARD

corticosteroid

24
Q

prednisolone

A

DMARD

corticosteroid

25
Q

prednisone

A

DMARD

corticosteroid

26
Q

triamcinolone

A

DMARD

corticosteroid

27
Q

abatacept

A

CTLA4
binds CD80/86 to prevent T-cell co-stimulatory signal engaging with CD28
AE: maltose complicates blood glucose test

28
Q

adalimumab

A

TNFa mAb

29
Q

anakinra

A

IL-1 antagonist

AE: blood dycrasias

30
Q

certolizumab

A

TNFa mAb
AE lacking?: CV
AE: blood dycrasias

31
Q

etanercept

A

TNFa inhibitor: false TNF receptor
AE lacking?: CV
Postlewaite uses this TNFa inhibitor before others: variable suppression so less infection

32
Q

golimumab

A

TNFa mAb
AE lacking?: lupus like syndrome
AE: LFT

33
Q

infliximab

A

TNFa mAb
CI: HEART FAILURE
AE: LFT

34
Q

apremilast

A

oral
PDE4 inhibitor
CYP substrate
Pgp
Tx: psoriatic arthritis and plaque psoriasis
AE: WEIGHT LOSS, depression, suicide ideation

35
Q

rituximab

A

CD20 mAb (B cell)
need CONTRACEPTION (up to 4-6 mo. after ending)
AE: Steven-Johnson syndrome, epidermal necrolysis, CV, blood dycrasias
CI: PREGNANCY

36
Q

tocilizumab

A

IL-6 mAb
AE: blood dycrasias
monitor: LFT, serum lipids

37
Q

PGE2

A

activation of inflammatory cells
cytoprotective
mucus secretion, bicarb release, initiation of repair

38
Q

How do COX-2 selective inhibitors differ from traditional NSAIDs?

A

inhibit prostacyclin without thromboxane inhibition: pro-thrombotic state
NO: GI toxicity, platelet inhibition, increase bleeding time, normal urinary TXA2 metabolites

39
Q

How do NSAIDs damage the gastric mucosa?

A

direct chemical irritation and inhibition of PGE2

causes: ulceration and gastric bleeds

40
Q

risk factors for adverse GI events with NSAIDs

A
  1. prolonged use, max dose
  2. age, male
  3. GI Hx
  4. comorbidity: CV, HTN, diabetes, hepatic, renal
  5. alcohol, smoking
  6. use of aspirin, warfarin, oral corticosteroids, SSRIs, venlafaxine, duloxetine
41
Q

ways to reduce GI toxicity of NSAIDs

A
  1. enteric coating
  2. FDA says: milk/ food
    Sweatman says: empty stomach to reduce doses
  3. PG analog (misoprostol)
  4. H2 antagonist
  5. PPI (BEST)
42
Q

COX-1

A

platelet
TXA2 production
prothrombotic

43
Q

COX-2

A

endothelial
PGI2 (prostacyclin) production
antithrombotic

44
Q

How can NSAIDs cause RENAL toxicity?

A

PGI2 and E2 are released in abnormal conditions and maintain renal blood flow and GFR
inhibition of PGs can damage kidney
Sx: hematuria, pyuria, white cell casts, proteinuria, etc.

45
Q

salicylate poisoning

A

ASPIRIN overdose
stimulate medullary respiratory system: hyperventilation
RESPIRATORY ALKALOSIS
uncoupling of oxidative phosphorylation: METABOLIC ACIDOSIS
cerebral and pulmonary edema, CV collapse
sign: RINGING of EARS
prolonged prothrombin time

46
Q

Tx for RA

What if this Tx fails?

A

early aggressive therapy

  1. DMARD: methotrexate (or hydroxychoroquine: less AE)
  2. addition: NSAID and corticosteroid
  3. failure with traditional approach: biological as mono therapy or with methotrexate
47
Q

How does adenosine inhibition help in RA?

A

METHOTREXATE
inhibits lymphocyte proliferation and suppresses IL-1, IFN-y and TNF
increase IL-4

48
Q

corticosteroids

A

inhibit: Nf-kb, AP-1, NF-AT: reduced TNFa, IL-1, IL-6
upregulate: RANKL, M-CSF
Src inhibition; intercalate plasma and mitochondrial membrane
Tx: RA
AE: osteoporosis, cushingoid, diabetes, obesity, lipid profile
(reduce with localized injection depot), hyperglycemia, weight gain
monitor: osteoporosis, fasting blood sugar levels, glaucoma risk, ankle edema

49
Q

TNFa inhibitors AE

A

malignancy
lupus-like syndrome
CV: CHF, hypotension, angina, dysrhythmia

50
Q

Drugs with AE of blood dyscrasias

A 
anakinra
certolizumab
rituximab
tocilimumab
non-biologic DMARDs
51
Q

Drugs need to monitor LFT

A

golimumab
infliximab
tocilimumab

52
Q

Drugs self-administered SC

A 
injection site rotation
abatacept
adalimumab
anakinra
certolizumab
etanercept
golimumab

Musculoskeletal (13 decks)

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