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61 Cards in this Set
- Front
- Back
NSAIDs are for???
A. relieve pain B. reduce inflammation C. slow disease progression, prevent bony erosions, or joint deformity D. A & B E. all of the above |
D
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Prototypical NSAID
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Ibuprofen (Motrin, Advil, Nuprin)
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MOA of NSAIDs
|
Nonselective, reversible inhibitor of Cox1
and Cox2 |
|
ADR of NSAIDs
|
– tinnitus,
– gastric ulcers, – GI bleeding, – liver and kidney damage |
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NSAIDs are superior/inferior to opiates when pain is
mediated by inflammation |
superior
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Prostacyclin (PGI2) _______
gastric acid secretion, |
inhibits
|
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PGE2 and PGF2a ________
synthesis of protective mucus in the stomach and small intestine |
stimulate
|
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NSAID Antipyretic Action
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Antipyretic effects are due to the blockade of prostaglandin synthesis at the thermoregulatory centers
|
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Thromboxane A2 ______ platelet
aggregation, |
enhances
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PGI2 __________ platelet aggregation
|
decreases
|
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prostaglandins
responsible for maintaining renal blood flow |
PGE2 and PGI2
|
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Decreased production of PGE2 and PGI2 can cause
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sodium and water retention, edema and possibly hyperkalemia
|
|
Used primarily as an anti-inflammatory agent in
the treatment of IBD as well as for rheumatoid arthritis |
Sulfasalazine
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Adverse effects of sulfasalazine include
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– GI (anorexia, nausea, vomiting, diarrhea),
• GI symptoms may be minimized by starting with low doses and taking the drug with food. – dermatologic (rash, urticaria), – hematologic (leukopenia, rare agranulocytosis), and – hepatic (elevated enzymes) effects |
|
sulfasalazine takes _______ to work
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4-8 wks
|
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mild salicylate toxicity
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– NV,
– marked hyperventilation, – headache, – mental confusion, – dizziness, and – tinnitus |
|
severe salicylate toxicity
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– restlessness,
– delirium, – hallucination, – convulsions, – coma, – respiratory acidosis,due to continued production of CO2 – metabolic acidosis, – death |
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salicylate excretion
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by urine
|
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ADR of salicylate
|
–GI
–prolonged bleeding times –Reye’s Syndrome –Hypersensitivity (asthma) –Respiratory depression (toxic doses) |
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Antacids________rate of aspirin absorption
|
reduce
|
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Probenecid/Sulfinpyrazone with aspirin result in
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decreased urate excretion
|
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Salicylates may increase plasma concentration of
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phenytoin, naproxen, sulfinpyrazone, thiopental, thyroxine, and triiodothyronine
|
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Acetaminophen is for
A. Anti-pyretic B. analgesic C. anti-inflammation D. A & B E. all of the above |
D
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MOA of acetaminophen
|
Reversible inhibition of COX in CNS better than periphery (inactivation by peroxidase
enzymes during inflammation) |
|
indication of acetaminophen
|
pt w/ liver Dz
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COX-2 selective NSAIDs
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Celecoxib (Celebrex)
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MOA of celecoxib
|
Selective reversible inhibitor of COX-2
|
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ADR of celecoxib
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Increased HTN (less renal arteriolar dilation)
Increased thrombotic events |
|
DMARDs
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hydroxychloroquine (Plaquenil),
auranofin (Ridaura), sulfasalazine (Azulfidine), minocycline (Dynacin, Minocin), methotrexate (Rheumatrex). |
|
True / False
DMARDs have immediate effect on slowing progressioin |
False
May require weeks or months for benefit |
|
MOA of
Methotrexate (Rheumatrex, Trexall) |
-- folic acid analog that inhibits
dihydrofolate reductase (DHFR) and folic acid recycling -- inhibits purine, thymidylate, serine and methionine synthesis--> affects dividing cells |
|
Methotrexate
onset |
2-3 wks
|
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ADR of Methotrexate
|
• Toxicities are GI
– stomatitis, diarrhea, nausea, vomiting • hematologic – thrombocytopenia, leukopenia, • pulmonary – fibrosis, pneumonitis, and • hepatic – elevated enzymes, rare cirrhosis. – Liver injury tests (AST or ALT) |
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Concomitant _______ may reduce some adverse effects of MTX without loss of efficacy
|
folic acid
|
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MOA of Gold Prep
|
Taken up by macrophages:
– suppresses phagocytosis and – suppresses lysosomal enzyme activity --> (less bone and articular destruction) |
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IM Gold
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– Aurothioglucose (Solganol) (suspension in oil)
– gold sodium thiomalate (Myochrysine, Aurolate) (aqueous solution) |
|
PO Gold
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Auranofin (Ridaura)
|
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ADR of Gold
|
glomerulonephritis,
Nitroid rxn (flushing, edema of the tongue and lips, vomiting, profuse sweating, a fall in blood pressure, and sometimes death) |
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Immunosuppressants
|
• leflunomide (Arava),
• azathioprine (Imuran), • cyclosporine (Neoral, Sandimmune) and • cyclophosphamide (Cytoxan) |
|
LEFLUNOMIDE (Arava)
MOA |
inhibits pyrimidine synthesis-->
– reduces lymphocyte proliferation and – modulation of inflammation. |
|
ADR of Leflunomide
|
liver toxicity
alopecia teratogenic |
|
AZATHIOPRINE (Imuran)
MOA |
Purine analog that is converted to 6 mercaptopurine -->
toxic to B / T cells interferes with DNA and RNA synthesis |
|
AZATHIOPRINE (Imuran)
ADR |
– bone marrow suppression
• leukopenia, macrocytic anemia, thrombocytopenia, pancytopenia, – GI intolerance, stomatitis – infections, – drug fever, – pneumonitis, – hepatotoxicity, and – oncogenic potential. |
|
CYCLOSPORINE (Sandimmune)
MOA |
Reduces production of IL-2 which is required for
T-cell activation and cellular immunity Direct effects on B cells, macrophages, bone, and cartilage cells. |
|
CYCLOSPORINE (Sandimmune)
Indication |
Organ transplantation
|
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CYCLOSPORINE (Sandimmune)
|
– hypertension,
– hyperglycemia, – Nephrotoxicity, – tremor, – GI intolerance, – hirsutism, and – gingival hyperplasia. |
|
Compare Onsets of
1. Sulfasalazine 2. Methotrexate 3. IM gold 4. Leflunomide 5. Azathioprine 6. Cyclosporine |
1. Sulfasalazine: 4-8 wks
2. Methotrexate: 2-3 wks 3. IM gold: 12-24 wks 4. Leflunomide: <4 wks 5. Azathioprine: 3-4 wks 6. Cyclosporine: 4-12 wks |
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Anti-malarials
|
Hydroxychloroquine
Chloroquine |
|
ADR
Hydroxychloroquine |
• GI
– nausea, vomiting, diarrhea, • Ocular – accommodation defects, benign corneal deposits, blurred vision, scotomas, night blindness, rare retinopathy, – Periodic ophthalmologic examinations are necessary for early detection of reversible retinal toxicity. • Dermatologic – rash, alopecia, skin pigmentation, and • Neurologic – headache, vertigo, insomnia effects. |
|
Biologics
|
• Etanercept (Enbrel)
• Infliximab (Remicade) • Anakinra (Kineret) |
|
Etanercept (Enbrel)
|
Binds tumor necrosis factor alpha for removal by
phagocytic cells ---> decrease in tumor necrosis factor |
|
Etanercept
ADR |
– discomfort at injection site,
– URI symptoms (minor), – case reports of pancytopenia and neurological demyelinating syndromes |
|
Infliximab
Combine with ? |
If not combined with methotrexate, patient
produces antibodies that inactivate infliximab |
|
Infliximab
ADR |
– injection site irritation (adalimumab and etanercept),
– worsening congestive heart failure (infliximab), – blood disorders, lymphoma, – demyelinating diseases, and – increased risk of infection / serious infection (potentially fatal) |
|
Anakinra (Kineret)
|
interleukin-1 receptor antagonist (IL-
1RA) |
|
Anakinra (Kineret)
ADR |
– redness,
– swelling, – pain |
|
Rituximab (Rituxan, MabThera)
ADR |
– Severe infusion reactions
– Cardiac arrest – Tumor lysis syndrome, causing acute renal failure – Infections • Hepatitis B reactivation • Other viral infections • Progressive multifocal leukoencephalopathy (PML – pulmonary toxicity |
|
Corticosteroids and glucose
|
Regulate glucose metabolism
– decreased glucose uptake – Increased Lipolysis – Increased Gluconeogenesis |
|
Corticosteroids
ADR |
Cushing’s syndrome: hyperglycemia, fat deposition, striae, muscle wasting, osteoporosis, depression
|
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The newest drug that was approved by FDA
|
Tocilizumab (Actemra and
RoActemra) |
|
Tocilizumab (Actemra and
RoActemra) MOA |
monoclonal antibody against the interleukin-6 receptor (IL-6R)
|