Pharm Test 2- Nsaids And Gout

Front 1

Acetylsalicylic acid (aka _____) inhibits the formation of ____ by blocking ______ enzymes.

Back 1

Aspirin; prostanoids (prostaglandins); cyclooxygenase (COX)

Front 2

Explain the three phases of inflammation. Which phase do NSAIDs work on?

Back 2

Phase 1: leukocytes bind endothelial cells, become active, and travel to the interstitium.
Phase 2: leukoctyes either phagocytise stuff or release stuff (including arachadonic acid metabolites) into the interstitium
Phase 3: endothelial injury and tissue damage result, amplifying the inflamm response;
Phase 2

Front 3

Out of the 3 COX enzymes:
1. Which is constitutively expressed?
2. Which is an inducible enzyme thought to play an important role in inflammation?

Which ones do NSAIDs block?

Back 3

1. COX1
2. COX2

COX1 and COX2

Front 4

Why are COX2 selective agents beneficial in patients with ulcers?

Back 4

because they won't block the BENEFICIAL properties COX1 enzymes exhibit in the gastric epithelial cells

Front 5

T or F: COX inhibitors can reduce renal function.

Back 5

T (in marginally functioning kidneys)

Front 6

T or F: The NSAIDs' analgesic effects are directly due to blocking PGE2 which causes hyperalgesia at sites of inflamm.

Back 6

FFF!!! (by directly inhibiting nociceptive effects at peripheral or centrl neurons)

Front 7

T or F: Aspirin is a reversible inhibitor of COX

Back 7

F...irreversible (enzyme must re-synthesize)

Front 8

Which of these drugs is devoid of antiinflammatory action and acts in the brain only as an antipyretic and analgesic.

Back 8

Acetaminophen (Tylenol)

Front 9

Chronic postoperative pain (or pain from inflamm) is well controlled except from where? What's the exception to this?

Back 9

hollow viscera; pain with menstruation

Front 10

T or F: NSAIDs arrest the progression of the underlying disease in inflammatory diseases (ex: RA)

Back 10

F!

Front 11

What two NSAIDs do NOT increase the renal clearance of urate which is beneficial for gout?

Back 11

Tolmetin and Aspirin

Front 12

T or F: COX2 selective agents and p-aminophenol derivatives are less harmful to the stomach (than the drugs blocking COX1).

Back 12

T

Front 13

COX2 selective agents have/don't have effect on TXA2 formation. They do/don't suppress PG12 activation.

What is the consequence of this?

Back 13

don't have; do suppress

PG12 NORMALLY SUPPRESSES PLATELET ACTIVATION, so if you suppress this, platelets are overactivated leading to potential thrombotic events

Front 14

NSAIDs can be used in premature babies. Why?

Back 14

premature closure of the patent ductus arteriosus

Front 15

T or F: do not use NSAIDs in acute or chronic renal failure

Back 15

T (non-selective and COX2 selective agents liked to potential renal problems)

Front 16

T or F: The metabolism of aspirin is saturable.

Back 16

T (so toxic levels can be reached rapidly)

Front 17

T or F: Aspirin irreversibly inhibits platelets.

Back 17

T

Front 18

T or F: Aspirin is more selective for COX2 than COX1.

Back 18

F!

Front 19

What's considered a high amount of aspirin which can cause death?

Back 19

10-30 grams

Front 20

What does this indicate: headache, dizziness, tinnitus, hearing loss, dimness of vision, mental confusion, lassitude, sweating, thirst, hyperventilation and nausea.

Back 20

aspirin intoxication (mild chronic symptoms)

Front 21

What is Reye's syndrome?

Back 21

linked to aspirin given to children with viral infections and fever..SO DON'T DO THIS!

Front 22

Diflusinal is a more/less potent antiinflamm agents than aspirin and has more/less side effects.

Back 22

more; less

Front 23

Acetaminophen does not inhibit peripheral COX enxymes. What two things, then, does it not do compared to other NSAIDs?

Back 23

doesn't inhibit platelet aggregation and doesn't cause severe GI symptoms like other NSAIDs. (all the others can cause GI problems except this one)

Front 24

What should you give children with viral infections who need analgesic and antipyretic drugs?

Back 24

Acetaminophen (also, adjunct in gout and good for salicylate toxicities...also for those who have ulcers/bleeding problems)

Front 25

Acetaminophen: during hepatic metabolism, N-acetyl-benzoquinoneimine builds up and can cause ___ ___ ___ and possibly ___ ___ ___. What must you give the pt to avoid more damage?

Back 25

Fatal hepatic necrosis and possibly Acute renal failure; N-acetylcysteine (Mucosil) (as well as gastric lavage)

Front 26

Propionic acid derivatives are primarily represented by ____ and are better/not better tolerated than aspirin and indomethacin

Back 26

ibuprofen; better

Front 27

What is the dose range of Ibuprofen (Motrin, Advil)?

Back 27

1200-3200mg/day

Front 28

What NSAID may be associated with increased cardiovascular risk compared to palcebo?

Back 28

Naproxene (Aleve, Naprosyn) (although later he says all NSAIDs that inhibit COX2 with exception of aspirin need a black box label for this...)

Front 29

What's a HIGH POTENCY propionic acid derivative?

Back 29

Ketoprofen (Orudis)

Front 30

Tolmetin: what are the indications? adverse effects in the CNS?

Back 30

rheumatic disease + juvenile form; nervousness and anxiety

Front 31

What propionic acid derivative that is a potent analgesic used short term for moderately severe acute pain?

Back 31

Ketorolac (Toradol)

Front 32

What is the adverse effect of taking Diclofenac (Cataflam, Voltarin)?

Back 32

severe hepatic reactions

Front 33

What is gout caused by?

Back 33

uric acid crystals in joints and cartilage(-->inflamm response)...this is due to hyperuricemia caused either by increased production of uric acid or decreased excretion.

Front 34

Therapeutic approch to tx gout:
1. Reduce inflamm (what 3 agents?)
2. Increase the elimination of uric acid (what 2 agents?)
3. Decrease the production of uric acid (what agent?)

Back 34

1. NSAIDs, glucocorticoids, colchicine
2. probenecid, sulfinpyrazone
2. allopurinol

Front 35

How does Colchicine (Colbenemid) relieve the pain and inflamm assoc with acute gouty arthritis?

Back 35

It bind to and blocks tubulin (preventing leukocyte migration)

Front 36

T or F: Colchicine alleviates pain in all forms of arthritis.

Back 36

F! only gouty

Front 37

The acute intoxication of ____ include burning throat pain, bloody diarrhea, shock and fatal ascending CNS depression.

Back 37

Colchicine

Front 38

What NSAID inhibits the phagocytosis of urate crystals as well as inhibit prostaglandins (having an advantage)?

Back 38

Indomethacin

Front 39

T or F: Aspirin should NOT be used in gout

Back 39

T (retention of uric acid in the kidney)

Front 40

Probenecid and Sulfinpyrazone can cause ______, so you need to keep urine volume up.

Back 40

kidney stones

Front 41

Allopurinol inhibits ____ ____ which prevents __________________.

Back 41

xanthine oxidase; uric acid biosynthesis

Front 42

What drug has the same mechanism of action as Allopurinol but is a more potent and selectiv inhibitor? Do you need to adjust the dose in renal impairment?

Back 42

Febuxostat (uloric); NO

Front 43

________ is only used in chronic gout in patients refractive to more traditional therapy. What does it do? What's the adverse effect?

Back 43

Pegloticase (Krystexxa); recomdinant urate oxidase taking urate-->allantoin which is eliminated; since it's a recombinant drug, hypersensitivity and infusion rxns