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15 Cards in this Set

  • Front
  • Back
Three major components of acute responses
1) Change in vascular caliber
2) Change in microvasculature (gaps allow plasma proteins/leukocytes to leave circulation)
3) Emigration of leukocytes out of microcirculation and accumulation at focus of injury
Inflammatory Mediators
1) Arachidonic acid metabolites (COX products, lipoxygenase products)
2) Cytokines
3) Vasoactive amines
4) Others (bradykinin, plasma proteases, clotting factors, PAF, nitric oxide)
Points of Intervention
1) Production of mediators
2) Action of mediators
3) Adhesion molecules
Arachadonic acid metabolism
1) Leukotrienes
2) Prostaglandins and thromboxane
3) These lipid mediators are:
a) synthesized de novo
b) released rapidly
c) labile
PGH synthase
An enzyme comprising both COX and peroxidase activity
Compare and contrast COX-1 and COX-2
1) COX-1 is constitutively expressed
2) COX-2 is inducible and is considered to be more important than COX-1 in inflam responses and assoc fever and pain.
3) Both convert AA to PGG2
4) Different aa sequence, products of different genes
5) Different functions
NSAID: Mechanism of Action
1) Inhibition of COX w/ consequent reduction in synthesis of PGs
2) direct effects on inflam cells
3) changes in gene expression (inhibition of transcription factor, NF-kappa B)
Therapeutic uses: Fever
1) Affect body temp incr due to inflam, tissue damage or dz
2) Mech of antipyresis
fever results from resetting the temp reg. center in the hypothalamic region of the brain
Therapeutic uses: Pain
1) mild to moderate pain
2) Mech of analgesia
a) physiological concentrations of PGs do not produce pain
b) PGs at site of inflam increase sensitivity of peripheral sensory nerve endings to algesic stimuli
c) Inhibition of PG synthesis returns nociceptors to normal sensitivity
NSAIDS vs. opioids
NSAIDS do not cause respiratory depression or tolerance or physical dependence, no sedation.
Therapeutic uses: Inflammation
1) Arthritis
2) Pain from inflammation
1) Absorption, distribution
a) well absorbed in GI
b) highly bound to plasma protein
2) Metabolism, Excretion
a) species differences in clearance rates
b) largely cleared via hepatic metabolism and urinary excretion of conjugates
c) some undergo enterohepatic circulation
Potential adverse side effects
1) Gastric or intestinal irritation
2) Increased bleeding time
3) Prolonged gestation
4) Renal injury/failure
Mechanism of Gastric/Intestinal Irritation
a) Decreased synthesis of cytoprotective PGs

Prevent by:
1) coadministration of a PGE analog (misoprostol)
2) selective blockade of COX-2
Treatment of NSAID poisoning
1) removal of drug from stomach w/ emetic or gastric lavage
2) correction of dehydration
3) correction of acid-base balance
4) forced diuresis