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59 Cards in this Set

  • Front
  • Back
common precursor for prostaglandin and leukotriene synthesis
phospholipid membrane FA cleaved by PLA2 to form AA
Where does the PG/LT pathway diverge
catabolism of arachidonic acid by either PGH Synthase or lipooxegenase
What steps of the PG/LGT are most sensitive to drug intervention?
COX1 and COX2
cell that does not synthesize eicosanoid
erythrocytes
properties of eicosanoids
locally-acting, G-protein mediated, degraded quickly
Action of PGI2
1) vasodilation (BF maintainance)
2) reversal of platelet aggregation
PGI2 agonists
Epoprostenol
Action of PGE1
1) vasodilation
2) GI protectant
3) bronchodilation
4) blocks platelet aggregation
PGE1 agonists
Misoprostol, Alprostadil, also PGE1 directly used for platelet harvesting and aggregation (MAP)
Action of PGE2
1) vasodilation
2) bronchodilation
3) GI protectant
Epoprostenol
PGI2
rapid reversal of pulmonary hypertenstion (vasodilation)
PGE2 agonists
dinoprostone
Dinoprostone
induce labor, 2nd trimester abortion
Misoprostol
used to decrease gastric ulceration
Alprostadil
inproves BF, platelet anti-aggregant, can maintain patent ductus arteriosus, used for mel impotence but pain directly at site of injection
Drug that can maintain a patent ductus arteriosus
Alprostadil
Action of PGF2
1) vasoconstrictor
2) bronchoconstrictor
PGF2 agonists
Latanoprost
Latanoprost
used to treat glaucoma but only used topically because it will cause bronchoconstriction
Action of TXA2
1) platelet aggregant
2) vasoconstriction
3) bronchoconstrictor
action of COX
converstion of AA to PGG2
action of peroxidase
conversion of PGG2 to PGH2
COX blockers (general categories)
NSAIDS or COX-2 selective blockers
Effects of COX blockers
1) analgesic (inhibition of PG)
2) antipyretic (reset set point of PGE2)
3) Anti-inflammatory by reducing leukocyte activation/interaction with endothelial cells
Respiratory effects of Aspirin
increased respiration which causes respiratory alkalosis
GI effects of Aspirin
cramping, nausea, vomiting, gastric ulceration
How does Aspirin cause increased respiration and how does this affect the kidneys?
it uncouples oxidative phosphorylation and causes increased CO2 which sitmulates the respiratory center; kidneys excrete bicarb to compensate for respiratory alkalosis
used to close a patent ductus arteriosus
indomethacin
Mechanisms of aspirin on COX
1) irreversible acetylation
2) metabolism in to salicylic acid which reversibly inhibits COX
Ulceration of what can occur with aspirin?
Gastric but not duodenal
Effects of aspirin in pegnancy?
When used in the last trimester, aspirin cuases prolonged gesation, labor, and increased maternal blood loss.
effects of Salicylism toxicity?
tinnitus, hearing loss, vertigo
effects of salicylate poisoning?
inhibition of respiratory center due to uncompensated respiratory acidosis and DEATH
How is metabolic acidosis caused in salicylate poisoning?
Krebs cycle inhibition which causes acidic byproduct buildup
Patients with this triad have a higher incidence of hypersensitivity of aspirin
Chronic rhinitis
Asthma
Polyp
Absorption and metabolizm of aspirin.
Upper SI, metabolized in liver.
Drugs enhanced by aspirin
anticoagulants and oral hypoglycemics
Drugs inhibited by aspirin
probenecid and sulfinpyrazone
Treatment of acetominaphen toxicity
N-acetylcysteine
Amount of acetaminophen considered toxic to liver
<10g or >10g with alohol
What are DMARDS?
disease modifying anti rheumatic drugs
What are the anti TNFs?
infliximab, adalimumab, and etanercept
How are COX2 selective blockers cardiotoxic?
they block COX2 production of PGI2 which is antithrombotic without blocking COX1 production of thromboxane
Why are non-aspirin nsaids not cardioprotective?
their effects are reversible
How does aspirin enhance resolution phase mediation?
blockage of PG synthesis allows AA to be used for lipoxin and resolvin synthesis instead.
What enzyme is responsible for making resolution phase mediators?
COX-2, therefore selective inhibition of this may be :(
NSAID associated with acute renal failure
indomethacin
What drugs can be used to minimize NSAID GI ulceration?
misoprostol or omeprazole
arthrotec
combo drug with diclofenac and mistoprostol
What are the side effects of aspirin?
inhibition of platelets, inhibition of uterine motility,
hypersensitivity reaction
What renal problems may NSAIDS cause?
in norm ppl, nothing. In those with CHF, liver cirrhosis, and renal disease, the vasoconstriction caused by PGE1/2 inhibition will cause decreased RPF and precipitate acute renal failure
Indomethacin
acetic acid NSAID associated with acute renal failure
Classifications of NSAIDS:
Carboxylic acid
Propionic Acid
Acetic Acid
What are the 4 criteria that need to be met for classification of rhematoid arthritis?
-Rheumatic Factor > 95th percentile
-Stiffness in morning > 1 hr for at least 6 weeks
- Hand arthritis
- Joint erosion
- Symmetrical arthritis
- Subcutaneous nodules
- Swelling of >14 joints
What is OA and its most common treatment?
sequence of disorters that affect weight bearing joints treated with acetaminophen
Ultrasonography is used to:
detect erosions in early rheumatoid arthritis and is 6x more sensitive than conventional readiographs
What is the step down combination therapy for RA?
" Slowly Make Progress "

Sulfasalazine (2g/day)
Methotrexate (7.5 mg/ week for 40 weeks)
Prednisone (60 mg/day for 28 weeks)
Two treatments that ensure long term prognosis for RA?
1) step down combo therapy
2) biological agents
What biological agents are used for RA?
Anti-TNF drugs, Anti IL-1 drugs