Pharm Nsaids, Acetaminophen, And Drugs Used In Rheumatoid Arthritis And Gout

Front 1

Question: These drugs are used for?

Indomethacin and celecoxib

Colchicine

Probenecid

Back 1

Nonselective COX inhibitor and COX-2 inhibitor respectfully. Both have analgesic, antipyretic, and anti-inflammatory effects.

Gout and has anti-inflammatory action

Uricosuric drug that promotes excretion of uric acid.

Front 2

Question: Among NSAIDs, aspirin is unique because it

Back 2

Irreversibly inhibits its target enzyme, cyclooxygenase.

Front 3

Question: What drug is an analgesic and antipyretic drug that lacks an anti-inflammatory action?

Back 3

Acetaminophen.

Front 4

Question: A 16 year old girl comes to the ER suffering from the effects of an aspirin overdose. What syndrome is this PT most likely to exhibit as a result of this drug overdose?

Back 4

Hyperthermia, metabolic acidosis, and coma.

Front 5

Question: What drug is most likely to increase serum concentrations of conventional doses of methotrexate, a weak acid that is primarily cleared in the urine?

Back 5

Probenecid

Front 6

Question: The main advantage of ketorolac over aspirin is that ketorolac?

Back 6

Is available in a parenteral formulation that can be injected intramuscularly or intravenously.

Note: ketorolac, with typical NSAID effects, is primary used for parenteral agent for pain management, typically for post-operative PTs.

Front 7

Question: An 18-mo-old boy dies from an accidental overdose of acetaminophen. Which of the following is the most likely cause of this PT's death?

Back 7

Liver failure.

In OD, it causes fulminant liver failure due to highly reactive metabolite after its conversion form CYP450.

Front 8

Question: In the treatment of this woman's acute attack of gout, a high dose of colchicine will reduce the pain and inflammation. However, many physicians prefer to treat acute gout with a corticosteroid or indomethacin because high doses of colchicine are likely to cause?

Back 8

Severe diarrhea.

Note: at doses needed to treat acute gout, colchicine frequently causes significant diarrhea. Such GI effects are less likely with the lower doses used in chronic gout.

Front 9

Question: Over the next 7 mo, a PT had 2 more attakcs of acute gout. her serum concentration of uric acid was elevated. The decision was made to put her on chronic drug therapy to try to prevent subsequent attacks. Which of the following drugs could be used to decrease this woman's rate of production of uric acid?

Back 9

Allopurinol.

Note:

Allopurinol, decreases uric acid production while probenecid increases uric acid excretion.

Aspirin decreases renal secretion of uric acid and raises uric acid blood level. It should not be used in gout.

Front 10

Question: A PT with early stage rheumatoid arthritis was decided to be treated with NSAID therapy.

What is the most compelling reason to avoid celecoxib in the treatment of arthritis?

Back 10

History of MI

Note: COX-2 inhibitors have a advantage over nonselective NSAIDs to reduce GI toxicity; however, they increase arterial thrombotic events.

Front 11

Question: What is the parenterally administered DMARD whose mechanism of anti-inflammatory action is antagonism of tumor necrosis factor?

Back 11

Etanercept

It binds to TNF and prevents its inflammatory effects.

Front 12

What is gout?

Back 12

Inflammatory joint disease caused by precipitation of uric acid crystals.

Treatment: focus on inflammation and elimination of uric acid.

Front 13

In terms of analgesic and anti-inflammatory effectiveness and duration of action

Ibuprofen and naproxen

Indomethacin

Ketorolac

Back 13

Has moderate effectiveness

Greater anti-inflammatory effectiveness

Greater analgesic effectiveness

Front 14

What was celecoxib design for and why was it discontinue?

Back 14

Designed as a COX-2 inhibitor so that it could lessen GI toxicity while preserving efficacy.

Unfortunately, it was shown to have a higher incidence of cardiovascular thrombotic events.

Front 15

COX-1

COX-2

Back 15

Expressed in noninflammatory cells

Activated in lymphocytes, polymorphonuclear cells, and other inflammatory cells.

Front 16

Aspirin and nonselective NSAIDs

COX-2 selective inhibitors

Back 16

Inhibit both COX-1 and COX-2, thereby, decrease prostaglandin and thromboxane.

Have less effect on the prostaglandins, particularly those in the GI tract.

Front 17

Aspirin vs. other NSAIDs

Back 17

Aspirin acetylates and thereby irreversibly inhibits COX.

NOTE: this results in a longer duration of its antiplatelet effect and its reason for its use as a antiplatelet drug.

Other NSAIDs: its inhibition on COX is reversible.

Front 18

Aspirin three therapeutic dose ranges:

Low

Intermediate

High

Back 18

Low range (<300 mg/d): effective in reducing platelet aggregation

Intermediate (300 - 2400): having antipyretic and analgesic effect

High dose (2400 - 4000): used for an anti-inflammatory effect.

Front 19

Nonselective NSAIDs can?

Back 19

Reduce polyp formation in PTs with primary familial adenomatous polyposis.

Long-term use of NSAIDs reduces the risk of colon cancer.

Front 20

What is acetylsalicylic acid MOA?

Back 20

Irreversibly inhibits COX-1 and COX-2, which converts arachidonic acid to endoperoxides (prostaglandin precursors)

Without PGE2: decrease sensation to pain (analgesia), decrease setpoint of hypothalamic thermoregulatory center (antipyretic) and decrease protective gastric mucus (leads to gastric ulcers).

Without TXA2: decrease platelet aggregation.

Without PGI2: increase gastric acid secretion (leading to ulcers)

Front 21

SE of acetylsalicylic acid?

Back 21

GI upset (gastric ulcers), nephrotoxicity (interstitial nephritis), increase in bleeding time. Those who have hypersensitivity (esp. those with nasal polyp) can have asthma from increase in leukotrienes. Children with viral infections, can develop Reye's syndrome, resulting in rapid liver degeneration and encephalopathy. Metabolic acidosis

Front 22

What are some COX-2 selective inhibitors? And their results.

Back 22

Celecoxib, rofecoxib, and valdecoxib.

Reduce GI GI effect, including gastric ulcers and serious GI bleeding.

They carry an increased risk of MI and stroke.

It is believed that COX-2 inhibitors have a greater effect inhibitory effect on endothelial prostacyclin (PGI2) formation than on platelet TXA2 formation.

Front 23

What is the only over-the-counter NSAID available?

Back 23

Acetaminophen

Note: it lacks anti-inflammatory or anti-platelet effects.

Front 24

Acetaminophen acts via?

Back 24

Reversibly inhibits COX-1 and COX-2 in the CNS. It is largely inactivated peripherally, thus has minimal anti-inflammatory effects.

Front 25

Acetaminophen can be useful for children with?

Back 25

Viral infections instead of aspirin, to prevent Reye syndrome.

Front 26

What can prevent acetaminophen OD to prevent hepatotoxicity?

Back 26

Acetylcysteine.

It contains sulfhydryl group which binds and inactivate the toxic metabolite of acetaminophen.

Front 27

What is disease-modifying antirheumatic drugs (DMARDs)?

Back 27

Drugs that modify the inflammatory processes underlying rheumatoid arthritis; they have a slow (weeks to months) onset of clinical effects.

Anti-inflammatory actions in several connective tissue diseases.

Front 28

What is the MOA and effects of the following DMARDs?

Methotrexate

Sulfasalazine, hydroxychloroquine, cyclosporine

Rituximab

Gold compounds

Infliximab, adalimumab, and etanercept

Back 28

Reduces number of immune cells available to maintain the inflammatory response

Interferes with activity of T-cells

B-cells

Macrophages

Inhibits TNF-alpha

Front 29

What is methotrexate MOA?

Back 29

Inhibition of dihydrofolate reductase

Bone marrow suppression, hepatotoxicity, teratogenicity, pulmonary toxicity.

Used for chemotherapy, and autoimmune disorders (RA, Crohn disease, scleroderma, psoriasis).

Front 30

How do you treat gout?

Back 30

Reducing inflammation (with colchicine, NSAIDs, or glucocorticoids).

Accelerating renal excretion of uric acid (probenecid or sulfinpyrazone)

Reducing conversion of purines to uric acid by xanthine oxidase (allopurinol or febuxostat)

Front 31

What is indomethacin effect on gout?

Back 31

Reduces inflammation of acute gouty arthritis via reducing prostaglandin formation and inhibition of crystal phagocytosis by macrophages.

Note: Reversible inhibitor of COX-1 and 2; is an agent to close a patent ductus arteriosus; and labor suppressant by decreasing uterine contractions.

Front 32

What is colchicine effect on gout?

Back 32

Inhibitor of microtubule assembly, which decreases migration of leukocytes to the affected sites. Also blocks formation of leukotriene B4.

Note: Colchicine is a mitotic poison, it reacts with tubulin and interferes with microtubule assembly; therefore, cell division and motility.

Front 33

What is colchicine used for and its SE?

Back 33

Gout and familial Mediterranean fever. Also, Behcet disease and scleroderma.

Significant GI disturbances (e.g., diarrhea), liver and kidney damage in overdose.

Front 34

DOC for gout?

Back 34

NSAID or a glucocorticoid.

Colchicine causes severe diarrhea. It is used when there is a history of recurrent acute attacks.

Front 35

What are probenecid and sulfinpyrazone purpose in gout?

Back 35

They are weak acids that decreases reabsorption of uric acid in the proximal tubule by competing for reabsorption.

Front 36

What is a side effect of probenecid?

Back 36

Since they inhibit the secretion of weak acids (eg., penicillin, methotrexate), they can be used to prolong antimicrobial drug actions.

Front 37

What does xanthine oxidase perform?

Back 37

Converts hypoxanthine to xanthine to uric acid.

Front 38

What are two xanthine oxidase inhibitors?

Back 38

Allopurinol: metabolite irreversibly inhibits xanthine oxidase

Febuxostat: more selective, and reversible inhibits xanthine oxidase. Newer drug, and possibly DOC for chronic gout.

Front 39

What is the SE of Allopurinol?

Back 39

GI upset, hypersensitivity reaction AND inhibits metabolism of mercaptopurine and azathioprine, drugs that depend on xanthine oxidase for elimination.

Bone marrow suppression

Front 40

Sulfonamide drugs?

Back 40

Probenecid and sulfinpyrazone.

Also, some drugs within the diuretics, antimicrobials and hypoglycemic drugs class.