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161-179 (all)
IV. Some diseases make inflam worse severe pain, fever, distress needs
pharmacotherapy
V. What triggers the inflammatory response?
a. Release of chemical mediators r/t pathogens, chemicals, and physical trauma
i. Histamine key mediator in inflam, released by mast cells in tsu space
under epithelial mb (skin bronchi, GIT, bv)
1. Vasodilation leaky caps affected area swell with blood
edema and pain
2. Drugs that act as antagonists at histamine receptors tx allergic
rhinitis
ii. Leukotrienes
iii. Bradykinin vasodilator cause pain; similar effects to his, (broken
down by ACE (angiotensin-converting enz)
iv. Complement cascade of 20+ protein, stim his relase
v. Prostaglandins (PG) lipid present in most tissues and stored and
released by mast cells,
1. fxn:
a. increase capillary permeability
b. Attract WBC to inflam site
c. Causes pain, induces fever
2. Drugs can target certain mediators, e.g. aspirin and ibuprofen are
PG inhibitors tx: fever, pain, inflam
b. Anaphylaxis - Rapid and large-scale of mediators SHOCK, DEATH
I. Salicylates
o Aspirin mild pain and inflammation; protect cardiovascular sys, prev DVT MI
stroke
highly used, bind to COX-1 and COX-2 prev infl PG & prolonged anti-
PLT
lg dose cause
lots adverse effect on GIT ( gastric acid secretion, irritate stomach
epigastric pain, hearburn, ulcer, bleeding.
o Buffered formulation or enteric coating to protect GIT
Salicylism syndrome tinnitus, dizziness, headache, sweating
II. Ibuprofen and Ibuprofen-like NSAIDS COX 1 and COX2 inhibition but
REVERSIBLE, treats pain, fever, inflammation
o Ibuprofen Motrin, Advil
o Ibuprofen-like NSAIDs
Low incidence of adv/e when used intermittently
s/e:
n&v (gastric ulcer, bleeding) lower incidence than aspirin
kidney toxicity (renal pt should take acetaminophen for
pain/fever)
Anti-PLT, lower risk than aspirin
can be combined with a drug that protects GIT (ibuprofen + famotidine)
o ibuprofen + other NSAIDs risk: thrombus, stroke, MI; worsen/ cause HTN