Pharm Ii Rheumatoid Arthritis

Front 1

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

Back 1

D

Front 2

Prototypical NSAID

Back 2

Ibuprofen (Motrin, Advil, Nuprin)

Front 3

MOA of NSAIDs

Back 3

Nonselective, reversible inhibitor of Cox1
and Cox2

Front 4

ADR of NSAIDs

Back 4

– tinnitus,
– gastric ulcers,
– GI bleeding,
– liver and kidney damage

Front 5

NSAIDs are superior/inferior to opiates when pain is
mediated by inflammation

Back 5

superior

Front 6

Prostacyclin (PGI2) _______
gastric acid secretion,

Back 6

inhibits

Front 7

PGE2 and PGF2a ________
synthesis of protective
mucus in the stomach and
small intestine

Back 7

stimulate

Front 8

NSAID Antipyretic Action

Back 8

Antipyretic effects are due to the blockade of prostaglandin synthesis at the thermoregulatory centers

Front 9

Thromboxane A2 ______ platelet
aggregation,

Back 9

enhances

Front 10

PGI2 __________ platelet aggregation

Back 10

decreases

Front 11

prostaglandins
responsible for maintaining renal blood
flow

Back 11

PGE2 and PGI2

Front 12

Decreased production of PGE2 and PGI2 can cause

Back 12

sodium and water retention, edema and possibly hyperkalemia

Front 13

Used primarily as an anti-inflammatory agent in
the treatment of IBD as well as for rheumatoid
arthritis

Back 13

Sulfasalazine

Front 14

Adverse effects of sulfasalazine include

Back 14

– 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

Front 15

sulfasalazine takes _______ to work

Back 15

4-8 wks

Front 16

mild salicylate toxicity

Back 16

– NV,
– marked hyperventilation,
– headache,
– mental confusion,
– dizziness, and
– tinnitus

Front 17

severe salicylate toxicity

Back 17

– restlessness,
– delirium,
– hallucination,
– convulsions,
– coma,
– respiratory acidosis,due to continued production of CO2
– metabolic acidosis,
– death

Front 18

salicylate excretion

Back 18

by urine

Front 19

ADR of salicylate

Back 19

–GI
–prolonged bleeding times
–Reye’s Syndrome
–Hypersensitivity (asthma)
–Respiratory depression
(toxic doses)

Front 20

Antacids________rate of aspirin absorption

Back 20

reduce

Front 21

Probenecid/Sulfinpyrazone with aspirin result in

Back 21

decreased urate excretion

Front 22

Salicylates may increase plasma concentration of

Back 22

phenytoin, naproxen, sulfinpyrazone, thiopental, thyroxine, and triiodothyronine

Front 23

Acetaminophen is for
A. Anti-pyretic
B. analgesic
C. anti-inflammation
D. A & B
E. all of the above

Back 23

D

Front 24

MOA of acetaminophen

Back 24

Reversible inhibition of COX in CNS better than periphery (inactivation by peroxidase
enzymes during inflammation)

Front 25

indication of acetaminophen

Back 25

pt w/ liver Dz

Front 26

COX-2 selective NSAIDs

Back 26

Celecoxib (Celebrex)

Front 27

MOA of celecoxib

Back 27

Selective reversible inhibitor of COX-2

Front 28

ADR of celecoxib

Back 28

Increased HTN (less renal arteriolar dilation)
Increased thrombotic events

Front 29

DMARDs

Back 29

hydroxychloroquine (Plaquenil),
auranofin (Ridaura),
sulfasalazine (Azulfidine),
minocycline (Dynacin, Minocin),
methotrexate (Rheumatrex).

Front 30

True / False
DMARDs have immediate effect on slowing progressioin

Back 30

False
May require weeks or months for benefit

Front 31

MOA of
Methotrexate (Rheumatrex, Trexall)

Back 31

-- folic acid analog that inhibits
dihydrofolate reductase (DHFR) and folic acid
recycling
-- inhibits purine, thymidylate, serine and
methionine synthesis--> affects dividing cells

Front 32

Methotrexate
onset

Back 32

2-3 wks

Front 33

ADR of Methotrexate

Back 33

• 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)

Front 34

Concomitant _______ may reduce some adverse effects of MTX without loss of efficacy

Back 34

folic acid

Front 35

MOA of Gold Prep

Back 35

Taken up by macrophages:
– suppresses phagocytosis and
– suppresses lysosomal enzyme activity --> (less bone and articular destruction)

Front 36

IM Gold

Back 36

– Aurothioglucose (Solganol) (suspension in oil)
– gold sodium thiomalate (Myochrysine, Aurolate) (aqueous solution)

Front 37

PO Gold

Back 37

Auranofin (Ridaura)

Front 38

ADR of Gold

Back 38

glomerulonephritis,
Nitroid rxn (flushing, edema of the tongue and lips, vomiting, profuse sweating, a fall in blood pressure, and sometimes death)

Front 39

Immunosuppressants

Back 39

• leflunomide (Arava),
• azathioprine (Imuran),
• cyclosporine (Neoral, Sandimmune) and
• cyclophosphamide (Cytoxan)

Front 40

LEFLUNOMIDE (Arava)
MOA

Back 40

inhibits pyrimidine synthesis-->
– reduces lymphocyte proliferation and
– modulation of inflammation.

Front 41

ADR of Leflunomide

Back 41

liver toxicity
alopecia
teratogenic

Front 42

AZATHIOPRINE (Imuran)
MOA

Back 42

Purine analog that is converted to 6 mercaptopurine -->
toxic to B / T cells

interferes with DNA and RNA synthesis

Front 43

AZATHIOPRINE (Imuran)
ADR

Back 43

– bone marrow suppression
• leukopenia, macrocytic anemia, thrombocytopenia,
pancytopenia,
– GI intolerance, stomatitis
– infections,
– drug fever,
– pneumonitis,
– hepatotoxicity, and
– oncogenic potential.

Front 44

CYCLOSPORINE (Sandimmune)
MOA

Back 44

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.

Front 45

CYCLOSPORINE (Sandimmune)
Indication

Back 45

Organ transplantation

Front 46

CYCLOSPORINE (Sandimmune)

Back 46

– hypertension,
– hyperglycemia,
– Nephrotoxicity,
– tremor,
– GI intolerance,
– hirsutism, and
– gingival hyperplasia.

Front 47

Compare Onsets of
1. Sulfasalazine
2. Methotrexate
3. IM gold
4. Leflunomide
5. Azathioprine
6. Cyclosporine

Back 47

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

Front 48

Anti-malarials

Back 48

Hydroxychloroquine
Chloroquine

Front 49

ADR
Hydroxychloroquine

Back 49

• 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.

Front 50

Biologics

Back 50

• Etanercept (Enbrel)
• Infliximab (Remicade)
• Anakinra (Kineret)

Front 51

Etanercept (Enbrel)

Back 51

Binds tumor necrosis factor alpha for removal by
phagocytic cells ---> decrease in tumor necrosis
factor

Front 52

Etanercept
ADR

Back 52

– discomfort at injection site,
– URI symptoms (minor),
– case reports of pancytopenia and neurological
demyelinating syndromes

Front 53

Infliximab
Combine with ?

Back 53

If not combined with methotrexate, patient
produces antibodies that inactivate infliximab

Front 54

Infliximab
ADR

Back 54

– 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)

Front 55

Anakinra (Kineret)

Back 55

interleukin-1 receptor antagonist (IL-
1RA)

Front 56

Anakinra (Kineret)
ADR

Back 56

– redness,
– swelling,
– pain

Front 57

Rituximab (Rituxan, MabThera)
ADR

Back 57

– 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

Front 58

Corticosteroids and glucose

Back 58

Regulate glucose metabolism
– decreased glucose uptake
– Increased Lipolysis
– Increased Gluconeogenesis

Front 59

Corticosteroids
ADR

Back 59

Cushing’s syndrome: hyperglycemia, fat deposition, striae, muscle wasting, osteoporosis, depression

Front 60

The newest drug that was approved by FDA

Back 60

Tocilizumab (Actemra and
RoActemra)

Front 61

Tocilizumab (Actemra and
RoActemra)
MOA

Back 61

monoclonal antibody against the interleukin-6 receptor (IL-6R)