antiinflammatory drugs

Question 1

H1 antagonists

Answer 1

competitive inhibitors (ineffective at high histamine levels), require hepatic activation. most cross the BBB and placenta.

Question 2

use of H1 antagonist

Answer 2

type I HSR. motion sickness, vertigo. nausea, vomiting, preop sedation. OTC sleep aids, and cold remedy

Question 3

SE of the H1 antagonisrts

Answer 3

M block and sedation.

Question 4

diphenhydramine

Answer 4

strong M block. antimotion sickness. widely used OTC.

Question 5

SE of diphenhydramine

Answer 5

SEDATION

Question 6

promethazine

Answer 6

antihistamine. strong M block. some antimotion. does cause sedation. anesthetic.

Question 7

chlorpheniramine

Answer 7

some M block, some sedation, some antimotion, CNS stimulation.

Question 8

meclizine

Answer 8

some M block, some sedation, HUGE antimotion sickness. highly effective for antimotion sickness

Question 9

cetirizine/loratadine/fexofenadine

Answer 9

no CNS entry, no M block, no sedation. ONLY FOR USE ON ALLERGIES

Question 10

what inhibits phospholipase A2 and thus decreases all inflammatory mediators?

Answer 10

glucocorticoids

Question 11

what do NSAIDs do

Answer 11

nonselective inhibitors of COX1/2 decrease prostaglandins and thromboxanes. all have analgesic, antipyretic, and antiinflammatory as well as antiplatelet function by definition.

Question 12

what is the mechanism for NSAID

Answer 12

irreversible inhibition by binding covalently to serine hydroxyl

Question 13

functions of the low dose NSAID

Answer 13

antiplatelet. also decrease tubular secretion of uric acid and thus cause hyperuricemia.

Question 14

functions of moderate dose NSAID

Answer 14

analgesics and antipyresis.

Question 15

functions of high dose NSAID

Answer 15

antiinflammation. this also decreases the reabsorption of uric acid and causes uricosuria.

Question 16

what is the hallmark of reaching the antiinflammatory range of NSAID treatment

Answer 16

tinnitus.

Question 17

what is REYE syndrome

Answer 17

high dose ASA toxicity of children with viral illness. this is caused by ETC uncoupling.

Question 18

SEof ASA

Answer 18

acute gastritis, ulcers, bleeding. salicylism (tinnitus, vertigo, decrease hearing). bronchoconstriction (never use in asthmatics), HSR. increases bleeding time.

Question 19

what can we use to combat ASA gastritis

Answer 19

misoprostal.

Question 20

what is chronic ASA use associated with

Answer 20

papillary necrosis of renal tubules. this causes renal dysfunction.

Question 21

which is the worst NSAID to use for analgesia? what is the best

Answer 21

Aspirin. ketorolac

Question 22

what is the NSAID with NO renal dysfunction

Answer 22

sulindac

Question 23

what are the other SE of sulindac

Answer 23

SJS, hematoxic

Question 24

what is indomethicin

Answer 24

strong NSAID.

Question 25

what are the SE of indomethicin

Answer 25

hematoxicity thrombocytopenia, agranulocytosis.

Question 26

what is celecoxib

Answer 26

COX2 selective. there is no more efficacy than the others. but there is less GI irritation, less antiplatelet activity.

Question 27

what is the huge negative about celecoxib

Answer 27

it is associated with endothelial cell dysfunction MI and stroke.

Question 28

acetominophen

Answer 28

there is no inhibition of COX. it is completely devoid of antiinflammatory affects. it is equivalent in analgesic and antipyretic effects.

Question 29

what does acetominophen have NO functions at doing

Answer 29

no antiplatelet activity, not implicated in reye syndrome, no effects on uric acid, not bronchospasmatic, GI is low.

Question 30

what is the major SE of acetominophen

Answer 30

hepatotoxicity through depletion of glutathione

Question 31

what is the antidote to acetominophen toxicity

Answer 31

N-acetylcysteine within the first 12 hours.