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23 Cards in this Set

  • Front
  • Back
inflammation is characterized by:
1. heat: vasodilation
2. redness: vasodilation of capillaries to increase blood flow
3. swelling: increased vascular permeability
4. pain: hyperalgesia, sensitation of nociceptors
5. loss of function
inflammatory responses occur in 3 distinct phases
1. transient phase-local vasodilation and increased cap permeability
2. subacute phase- infiltration of leukocytes
3. chronic proliferative phase: tissue degeneration and fibrosis
mediators of inflammation
1. vasoactive amines (histamine, serotonin)
2. platelet activating factor (PAF)
3. complement system
4. kinin system
5. cytokines
6. NO
7. adhesion molecules
8. arachidonic acid metabolites (PGA and thromboxane)
Major enzymes inhibited by NSAIDs..
1. produces prostaglandins that mediate homeostatic functions
2. continuously expresssed
3. plays an important role in gastric mucosa, kidney, platelets, and vascular endothelium
1. produces prostaglandins that mediate inflammation, pain, and fever
2. induced mainly in sites of inflammation by cytokines
3. constitutive expression in brain and kidney
GI protection
GI protection, platelet function, regulation of blood flow, kidney function
platelet function, regulation of blood flow
PGE2, PGI2, TXA2, other chemical mediators
inflammation, pain, fever
adverse effects: salicylate intoxication
mild intoxication as a result of repeated high ddoses intake (headaches, dizziness, tinnitus, hearing impairment, mental confusion)

Severe effects:
-alteration of acid-base and electrolyte balance
-gastric irritation, microbleeding
-impairment of platelet function
-edema and acute renal failure (individuals with preexisting renal dysfunction or CHF)
-convulsion coma
Reye's syndrome
characterized by the acute onset of encephalopathy, liver dysfunction, and fatty infiltration of the liver adn other viscera (can be lethal)
acetominophen therapeutics
niacin tolerability
systemic mastocytosis
severe episodes of vasodilation and hypotension
different types of NSAIDs
1. salicylates
2. propionic acid derivatives
3. enolic acids (Oxicams)
4. arylacetic acid derivatives
5. selective COX-2 inhibitors
the salicylates
-has analgesic action byt lacks inflammatory action

difunisal (Dolobid)- has prolonged analagesic effect and more potent anti-inflammatory action (but GI toxicity...), used to rheumatoid and osteoarthritis

-fendosal is believed to have greater analgesic and anti-inflammatory activity than aspirin but with less GI toxicity

Salicylates are highly bound to the plasma protein albumin. Thus, it will have interactions with each other medications leading to higer free drug levels.
MOA of aspirin
covalently and irreversibly modifies both COX-1 and COX-2 by acetlyating serine-530 in the active

-acetlyation of COX-1 creates a steric block that prevents the binding of arachidonic acid at the catalytic site

-acetylation of COX-2 retains the cyclooxygenase activity although the reaction generates a different and novel product 15-R-HETE
aspirin and diabetes...
1. Aspirin should be used in any diabetic patient who has evidece of:
-a prior heart attack
-a previous bypass procedures
- a stroke, angina, claudication, or blood vessel disease

2. aspirin therapy should be considered in high-risk men and women with type 1 or type 2 diabetes. This includes diabetic patients with the following:
-a family history of heart disease
-positive protein in the urine
-high cholesterol
-over age 30
propionic acid derivatives
1. ibuprofen (Advil, Nuprin, etc...)
-prescribed for RA and osteoarthritis
-peak concentrations in plasma within 15-30 min; half life 2 h
-99% bound to plasma proteins

SE: GI effects are experienced in 5-15% of patients

Naproxen (Aleve, Naprosyn)
-peak concentrations in plasma within 2-4
-99% bound to plasma proteins
SE: GI discomfort (less than others), heartburn, N/V, and gastric bleeding
in CNS: drowsiness, headache, crosses the placenta and appears in milk of lactating women

Ketoprofen (Orudis, generic, OTC)- effected both in human and animals

-Oxaprozin (Daypro): unique in that it can be administered once daily
Arylacetic acid derivatives
1. indomethacin (Indocin)
2. Sulindac (Clinoril)
3. Ketorolac (Toradol)
4. Diclofenac (Voltaren)
5. Bromfenac (Duract)
6. Etodolac
7. Nabumetone (Relafen)
Enolic acids (Oxicams)
1. piroxican (Feldene)
long half life
additive anti-inflmmatory effects: inhibits migration of neutrophils
2. Meloxicam (Mobic)
less potent than Piroxicam
more selective COX-2 inhibitor than the other NSAIDs
Drug interactions
-most (if not all NSADs) can increase the anticoagulatnt effect of WARFARIN displacement of warfarin from plasma albumin anad the subsequent inhibition of warfarin metabolism and elimination
-potentially all NSAIDs can blunt the diuretic actions of THIAZIDES
-may enhanve the toxicity of methotrexate
-may reduce the renal elimination of Li ions
-may interfere with the anti-hypertensive actions of beta blockers, diuretics, anc ACE inhibitors
acetaminophen (APAP, paracetamol, Tylenol)
-APAP is effective as an analgesic and antipyretic
-it has little to no anti-inflammatory action
-well tolerated and lacks many of the SE of aspirin and other NSAIDs
-no gastric irritation or ulceration
-does not inhibit neutrophil activation
-no effect on CV or respiratory systems
-peak concentrations in plasma within 30-60 minutes, half life 2h
-20-50% bound to plasma proteins
-conventional oral dose 325-1000 mg, should not exceed 4000 mg
acetamenophen toxicity
-skin rash and other allergic reactions
-hepatic and renal necrosis upon OD
-due to glutathione depeletion
1)N acetyl cysteine (Mucomyst, Mucocil) is the antidote for APAP OD, replenishing of GSH