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42 Cards in this Set

  • Front
  • Back
Prototypical opioid?
Uses other than analgesia for opioids?
1) Cough suppressant
2) Component of anesthesia
3) Decreases GI motility
4) Adjunct to pulmonary edema
5) Drug abuse
3 Major type of opiod receptors?
1) Mu
2) Kappa
3) Delta
Mu opioid
1) Strongest analgesic
2) Most and most severe sideE
3) Resp. depression, constipation, increased risk
Side effects of Mu opioids
Resp. depression, Constipation, Highest risk of dependence
Kappa opiod
Analgesia, sedation, psychotropic
Less likely to have as severe SE as Mu
Delta opiod
Analgesic, SideE are least severe.
No risk for resp. depression, no psychotropic effects
Describe a Mixed opioid
Opioid is agonist to 1 or more receptor and antagonist to others.

i.e, Agonist = kappa; antagonist = Mu
Opiod mechanism?
Binds to opioid G-coupled protein receptor
Opioids affect on presynpatic transmission of pain?
G-proteins inhibit the release of Ca++ and cAMP release this causes less neurotransmitter release
Opioid's effect on postsynaptic neuron?
The G-proteins create an outflux of K+ which causes hyperpolarization making it more difficult of a synapse to occur.
A way that opiods can alter descending pathways?
Via disinhibition. The G-protein coupled receptors disinhibit descending pain control pathways.
Mild-to-moderate agonist (i.e. codeine)
Works for all receptors but has a lower affinity -> lower efficacy
Which opioid receptors lead to possible CV problems?
Define tolerance
Requires a greater dose for the same functional effect
Opioid withdrawal symptoms?
Flu-like symptoms, irritability, insomnia, tachycardia, uncontrollable yawning, muscle aches
Strong opioid agonist used to taper for addicts
Buprenophine. A mixed agonist-antagonist - partial Mu agonist and Kappa antagonist.
Prototypical NSAID?
Uses/Effects of NSAIDS?
1) Decreased inflammation
2) Analgesic
3) Decreased fever (antipyretic)
4) Anticoagulant
Mechanism of NSAIDS?
Anti-inflammatory/analgesic d/t inhibition of eicosanoid synthesis
3 Eicosanoids?
Porstaglandins, Thrombaxanes, Leuokotrienes
Endogenous lipidlike compound that is pro-inflammatory
Vasoconstriction & Platelet aggregation
Pro-inflammatory (esp. in air way)
Function (PGs &TXs)
Cause inflammation, pain, fever, menstral problems, clots.
Brief description of how PGs and TXs are formed?
Arachadonic acids (phospholipase) -> COX (cycloxagenase) -> Variety of PGs and TXs
Which pathway formed from arachadonic acid creates leukotrienes?
The LOX pathway (lipoxygenase)
Which two eicosanoids are inhibited with NSAIDS?
PGs and TXs
Which COX is normally produced in our bodies?
Why do NSAIDS cause GI disturbances?
b/c NSAIDS often inhibit COX-1s and COX-1s help supply the protective lining to our GI tract
Two conditions that ASA may cause Renal and/or liver problems?
1) Pre-existing disease
2) decreased body water
signs/symptoms of ASA OD?
HAs, decreased hearing, confusion, GI distress, possible metabolic acidosis & dehydration
What can induce Reye syndrome?
Adversion to ASA in children. The children can be intolerant (supersensitive) to the drug. Usually onsets after flu or chicken pox.
Adverse effects of celebrex?
1) MI
2) Stroke
Why are COX-2 inhibitors potentially very harmful?
Because the cause a shift that favors increased platelet aggregation which increases the pt's risk of clotting.
Popular analgesic OTC that is not an NSAIDS?
Acetaminophen (Tylenol/Excedrin)
Anti-inflammatory effects of acetaminophen?
There are none
Risk of high doses of acetaminophen?
Liver toxicity
Mechanism of acetaminophen?
Inhibits COX, probably inhibits PGs may preferentially inhibit CNS PGs (COX-3?)
What is odd about the pharmacokinetics of ASA?
1) Most is bound to plasma proteins
2) Unbound drug is hydrolyzed in the blood and not the liver
Which chemical in the breakdown of acetaminophen is responsible for liver toxicity?
NAPQI (must be conjugated for detoxification and excretion).