Pharm Final - Nsaids

Front 1

(1) what was the first antipyretic which was used for rheumatic fever (and later for gout)? (2) what drug was used primarily for its anti-inflammatory effects?

Back 1

sodium salicylate

Hint 1

acetylsalicylate (aspirin)

Front 2

(1) what is the only p-aminophenol compound still in use? (2) what were these known as?

Back 2

acetaminophen

Hint 2

coal tar analgesics

Front 3

(1) what are the 3 major properties of most NSAIDs? (2) how do they work?

Back 3

anti-inflammatory, analgesic, antipyretic

Hint 3

inhibit the enzyme cyclooxygenase > inhibit formation of prostaglandins and TxA2 > gives analgesic/antipyretic effects > contributes to anti-inflam effect

Front 4

(1) what analgesia do NSAID's provide? (2) how do they effect pain perception (nociception)?

Back 4

mild-to moderate; especially effective on integument pain (skin, teeth, muscle, joints) caused by inflam. Not effective against deep visceral pain. Cause neither tolerance nor dependence with chronic use and no effect on other senses

Hint 4

nociception is largely due to prostaglandin-mediated sensitization of nerve endings to pain-inducing effects of other mediators; NSAIDs short circuit this by blocking prostaglanding production

Front 5

(1) how do NSAID's act in antipyresis? (2) what temperature elevations are not affected by NSAID's?

Back 5

inhibits PGE2 synthesis (which causes the body temperature increase) in the hypothalamus; pyrogenic cytokines released from leudocytes (IL-1 and TNF) induce PGE2 formation.

Hint 5

exercise, increased ambient temperatures

Front 6

(1) the side effects of NSAIDs are due to what? (2) what are the most common side effects?

Back 6

inhibition of prostaglandin production

Hint 6

GI ulceration/bleeding, prolongation of bleeding time, prolongation of labor, renal problems, ischemic intestinal damamge in dogs

Front 7

(1) what is the most common problem associated with NSAID usage? (2) how do we explain this?

Back 7

GI ulceration and bleeding

Hint 7

local irritation hypothesis (local irritiation of GI mucosa > Back diffusion of acid > amplifies irritation/damage; however fails to explain parenteral administration) & prostaglandin inhibition hypothesis (inhibition of PGE2 & PGI2 by gastric mucosal cells > lose inhibition of acid secretion in stomach, lose secretion of cytoprotective mucus > increase susceptibility to damage; administering PGE1/PGE2 reduces GI damage)

Front 8

(1) what synthetic congener of PGE1 is administered with NSAIDs to minimize GI ulceration? (2) what are the side effects?

Back 8

misoprostol

Hint 8

GI discomfort, vomitting, diarrhea (may be unacceptable in large animals like horses)

Front 9

(1) how do NSAIDs affect platelet function? (2) what NSAID impacts platelets the most and why?

Back 9

block synthesis of TxA2 > increased bleeding time

Hint 9

aspirin because it irreversibly blocks inhibits platelet cyclooxygenase

Front 10

(1) why can't platelets compensate for the irreversible inactivation of cyclooxygenase through de novo synthesis? (2) how can this be taken advantage of?

Back 10

platelets cannot synthesize new proteions (lack nucleus)

Hint 10

treatment of coagulopathies including cardiac problems

Front 11

(1) what adverse effects other than GI ulceration and platelet inactivation occur with NSAIDs?

Back 11

prolong gestation and spontaneous labor, delay parturtion (inhibits prostaglandin procution), cause acute renal failure (by inhibiting PGE2 synthesis and causing ischemic renal tubular injury) , cause ischemic intestinal damage in dogs

Front 12

(1) what is the distinction between COX-1 & COX-2? (2) how was this used in pharmaceuticals?

Back 12

COX-1 is a constitutively produced enzyme present in most cells and instrucmental in protecting stomach lining and preventing ulcers while COX-2 is an inducible enzyme that is only expressed in inflamed tissues. BOTH catalyze prostaglandin and thromboxane formation

Hint 12

COX-2 inhibitors were developed with the thought that they would be ani-inflammatory but not ulcerogenic

Front 13

(1) what were the unexpected side effects for COX-2 inhibitors? (2) why did this happen?

Back 13

heart attacks, strokes, blood clots

Hint 13

COX-2 regulates PGI2 production by the vascular endothelium so inhibitors reduced it but had no effect on TxA2 production by platelets (COX-1) and COX2 derived PGI2 functions to remodel blood vessels to preserve adequate blood flow by regulating changes in smooth muscle liningins of blood vessels (due to presure related changes). = favors vasoconstriction, increased platelet aggregation/clotting, prevents necessary changes in blood vessel structure in response to pressure changes. additionally COX-2 heals GI ulcers & does intestinal repair (inducible form in gastric mucosal cells) and COX-1 w/constitutive COX-2 mechanisms in kidneys

Front 14

(1) what COX-2 inhibitors are FDA approved for treatment of osteoarthritis in dogs? (1) which one is available as a tablet and oral paste and is most COX-2 selective?

Back 14

deracoxib, fibrocoxib, meloxicam

Hint 14

Firocoxib

Front 15

(1) what drug is a COX-2 inihbitor used for post-op pain in the form of a chewable tablet (name known side effect?) (2) what COX-2 inhibitor is available as an oral suspencion and paraenteral preperation?

Back 15

Deracoxib - GI bleeding

Hint 15

Meloxicam

Front 16

(1) where is aspirin absorbed? (2) how is it processed in the body?

Back 16

stomach and upper small intestine

Hint 16

rapidly deesterfied to salicylate in plasma, liver, erythrocytes

Front 17

(1) describe the plasma half life of salicylate (2) when is aspirin used in cats?

Back 17

variable by species, can be quite long (dog = 8.6h, cat = 37.5h) and increases as dose increases

Hint 17

for its anti-platelet effects

Front 18

(1) what drug may be administered for long anti-platelet effects in cats? (2) when should it be used cautiously (in all species)?

Back 18

aspirin

Hint 18

renal/liver disease, with aminoglycoside antibiotics (nephrotoxicity), GI problems, within 2wks of a major surgical procedure

Front 19

(1) what drug irreversibly acetylate and inhibits the cyclooxygenae enzymes? (2) what might this drug be administered with?

Back 19

aspirin

Hint 19

an antaacid (Maalox) or as an enteric coated formulation (Ascriptin), but no actual evidence that it reduces GI complications

Front 20

(1) what drug is a de-esterified aspirin with a poorly understood action that includes weak cyclooxygenase inhibitor and membrane stabilization? (2) an intoxication characterized by nausea, vomiting and restlessness that may progress to a severe intoxication with alterations in acid-base balance, hyperpyrexia, CNS seizuer, and coma is called what and caused by what drug?

Back 20

salicylate

Hint 20

salicylism - aspirin overdosage (salicylate intoxication)

Front 21

(1) name the only P-aminophenol derivative currently used? (2) how is it used in vet med?

Back 21

acetaminophen (tylenol)

Hint 21

with codeine to treat pain in dogs

Front 22

(1) what drug is an analgesic and antipyretic, but has a very weak anti-inflammatory property? (2) what can occur if it is overdosed?

Back 22

acetaminophen

Hint 22

hemolysis, methemoglobinemia, hepatic and renal damage. Treat with Acetylcysteine

Front 23

(1) what drug can, if overdosed, cause hemolysis, methemoglobinemia, hepatic and renal damage and how should it be treated? In what species is it contraindicated?

Back 23

acetaminophen. Treat with acetylcystein

Hint 23

cats

Front 24

(1) what drug is an analgesic, antipyretic, and anti-inflammatory used for extended periods to treat laminitis and non articular (soft tissue) rheumatism? (2) what other species is it used in and for what?

Back 24

phenylbutazone

Hint 24

(lesser extent) in dogs to treat arthritis; only for a short period of time

Front 25

(1) what drug exhibits high plasma protein binding (drug interactions), accumulation with chronic dosing, narrow therapeutic index, high incidence of fluid retention and GI ulceration (oral and esophageal too)? (2) how is it pharmacologically active and what are the potential side effects?

Back 25

phenylbutazone

Hint 25

may be due primarily to the active metabolite oxyphenbutazone. Can cause fatal agranulocytosis and aplastic anemia (more so in humans)

Front 26

(1) name the propionic acid derivatives? (2) what are the general properties?

Back 26

naproxen, ketoprofen, flubiprofen, carproften

Hint 26

analgexic, antipyretic, anti-inflammatory

Front 27

(1) what drug is used IV in horses and to treat osteoarthritis in dogs? (2) what drug is used topically to prevent miosis during ocular surgery?

Back 27

ketoprofen

Hint 27

flurbiprofen

Front 28

(1) what drug is widely used to treat osteoarthritis and post operative pain in dugs and is under investigation in cats? (2) how does it work and what are the side effects?

Back 28

carprofen

Hint 28

controversial: somewhate COX-2 selective, stimulates glycosaminoglycans synthesis (may affect cartilage synthesis), somewhat less ulcerogenic than aspirin in dogs; hepatotoxicity may be an issue 2-3 wks post treatment

Front 29

(1) what drug is a potent, long acting agent used parenterally or orally (paste or granules) to relieve the pain of colic in horses? (2) what is the concern about this?

Back 29

flunixin

Hint 29

delay in referring for treatment = irreperable damage

Front 30

(1) what drug is used to treat endotoxic shock and reduce post surgical ocular inflammation in dogs and cats? (2) why is this controversial?

Back 30

flunixin

Hint 30

GI ulceration and renal damage with repeated dosing

Front 31

(1) what drug is a good anti-inflammatory agent in dogs for osteoarthritis that has a long duration of action, lower incidence of GI effects, and is a moderatly selective COX-2 inhibitor? (2) what drug comes as a honey-flavored oral suspension for the treatment of osteoarthritis in dogs and cats?

Back 31

etodolac

Hint 31

meloxicam

Front 32

(1) what drug comes as a paraenteral or oral form for the relief of intense, deep pain used to relieve postsurgical pain with analgesia comparable to opioids? (2) what is the concern with this drug?

Back 32

ketorolac (acular is a topical form to prevent miosis during cataract surgery)

Hint 32

ulcerogenic

Front 33

(1) what drug can be used in a topical form to prevent miosis during cataract surgery?

Back 33

ketorolac (as acular)

Front 34

(1) what NSAID is a relatively nonselective COX-1/COX-2 inhibitor that is a 5-lipoxygenase inhibitor? (2) how is it delivered?

Back 34

tepoxalin

Hint 34

rapidly disintegrating tablet

Front 35

(1) what drug can be used to treat pain and inflammation in a dog whose neck can't be fully extended (cervical pain, osteoarthritis)? (2) what is it's duration/dosing and why?

Back 35

tepoxalin

Hint 35

once a day dosing because both parent compound and major metabolite are active with >13hr half life