442-MT1

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Author:
jgiantess
ID:
131269
Filename:
442-MT1
Updated:
2012-01-28 20:22:50
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pharmacology
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drugs
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  1. chloroform, cyclopropane, ethylene
    • inhaled anesthetics - volatile halogenated hydrocarbons
    • not used anymore.
  2. halothane:
    • inhaled anesthetics - volatile halogenated hydrocarbons
    • not used anymore.
    • highest blood/gass partition coeff (2.3) = more insoluble in gas than blood, therefore more molecules needed to dissolve in blood before increase PP significantly, and so arterial tension of gas and brain conc increases less rapidly.
    • 15-20% metabolized; mostly to trifluoracetic acid (TFA). clin sig: halothane hepatitis, nephorotox
  3. diethyl ether
    • inhaled anesthetic - volatile ether
    • not used anymore.
  4. enflurane
    • inhaled anesthetic - volatile halogenated ether
    • not really used anymore.
  5. methoxyflurane
    • inhaled anesthetic - volatile halogenated ether
    • not really used anymore.
    • 40-50% metabolized; mostly to fluoride. clinical sig: nephrotox, hepatotox
  6. isoflurane
    • inhaled anesthetic - volatile halogenated ether
    • one of 3 most commonly used ethers now (+ sevoflurane and desflurane)
    • higher Blood/Gas Partition Coeff (1.4) = more insoluble in gas than blood, therefore more molecules needed to dissolve in blood before increase PP significantly, and so arterial tension of gas and brain conc increases less rapidly.
    • 0.2% metab'd, mostly to trifluoracetic acid (TFA). low potential for tox.
  7. fluroxene
    • inhaled anesthetic - volatile halogenated ether
    • not really used anymore.
  8. sevoflurane
    • inhaled anesthetic - volatile halogenated ether
    • one of 3 most commonly used ethers now (+ isoflurane and desflurane)
    • low-med Blood/Gas Partition Coeff (0.6) = very insoluble in blood, gets to brain very fast b/c fewer molecules needed to increase partial pressure in blood.
    • 3% metabolized; mostly to fluoride (short lived). Low potential for toxicity.
    • But increased degradation by soda line (C02 absorbent in gas machine) to vinyl ether (Cpd A) --> nephrotox to rats
  9. desflurane
    • inhaled anesthetic - volatile halogenated ether
    • one of 3 most commonly used ethers now (+ sevoflurane and isoflurane)
    • low Blood/Gas Partition Coeff (0.42) = very insoluble in blood, gets to brain very fast b/c fewer molecules needed to increase partial pressure in blood.
    • very resistant to metabolism (0.02%). high molecular stability, no sig tox
  10. nitrous oxide
    • inhaled anesthetic - inorganic gas
    • incomplete: rapid onset and rapid recovery.
    • important as adjuvant to volatile agents (so that can use less of the volatile drug), but use is less because:
    • 1) green house gas
    • 2) induces post-op N&V
    • 0.0004% metabolized...to nitrogen. toxicity of free radicals?
    • low Blood/Gas Partition Coeff (0.47) = very insoluble in blood, gets to brain very fast b/c fewer molecules needed to increase partial pressure in blood.
  11. xenon
    • inhaled anesthetic - inorganic gas
    • not used much - too expensive.
  12. thiopental
    • intravenous anesthetic - barbiturate
    • rapid induction of hypnosis ("arm-brain circulation time", less than 20 seconds)
    • facilitates inhibitory neurotransmission via GABAa receptors
    • redistribution to other tissues -> pt wakes up 5mins after single IV bolus.
    • but when tissues are saturated after infusion/repeated doses, t1/2 elimination = 11 hours.
    • SE: hypotension (Pearl Harbor experience), resp depression, histamine release, arterial occlusion.
  13. propofol
    • intravenous anesthetic - most popular one now (alternative to thiopental)
    • used for sedation, induction, and maintenance of anesthesia (total IV anesthesia). smooth induction...pleasant dreams.
    • also antiemetic
    • facilitates inhbitory neurotransmission via GABAa receptors
    • rapid induction of hypnosis like thiopental, even more rapid awakening after IV bolus (3mins)
    • but rapid liver metab (t1/2 = 1h), no redistb --> useful for infusion
    • SE: resp depression and apnea, hypotension (more than thiopental), injection pain, sepsis (formulation in egg lecithin and soy bean oil, supports bacterial growth)
  14. ketamine
    • intravenous anesthetic - only IV anesthetic that is anesthetic + analgesic. phencyclidine-derivative. psychomimetic drug "Angel Dust"
    • dissociative anesthesia: conscious, but cannot process/respond to sensory input (catatony, amnesia, analgesia)
    • little cardioresp depression, maintains airway reflexes, bronchodilator properties...unpleasant dreams.
    • for induction of anesthesia in trauma or shock, battlefield surgery, analgesia in burn patients, i.m induction in children.
    • MoA: antagonist at NMDA receptors (excitatory glutamate)
    • rapid induction after IV bolus (but slower than thiopental and propofol)
    • causes increased cerebral bf, oxygen consumption, ICP...dangerous when ICP high (similar to volatile anesthetics).
    • hepatic metab t1/2 3h.
    • SE: post-op disorientation, illusions, vivid dreams.
  15. pentazocine
    • opioid, agonist at K receptor, weak antagonist or partial agonist at u receptor.
    • opioid with lower abuse potential
    • high doses cause dysphoric and psychotomimetic effects (confusion, hallucinations)
    • does not block resp effects of other opioids (e.g. morphine)
    • has ceiling effect to analgesia
    • can precip withdrawal if given to a pt dependent on a u agonist
    • can be used in pts allergic to morphine
    • (K receptor agonists more effective analgesics in women than men)
  16. nalbuphine
    • opioid, agonist at K receptor, antagonist at u receptor
    • similar to pentazocine, but with less dysphoric effects
    • (K receptor agonists more effective analgesics in women than men)
  17. buprenorphine
    • opioid, partial agonist at u receptor (limited intrinsic activity), antagonist when used with a full agonist
    • analgesia similar to morphine
    • can precip mild withdrawal if given to pt receiving u agonist long-term
    • unknown whether there is a ceiling to resp depression (not major problem)
    • when d/c'd, can cause withdrawal similar to morphine but not as severe.
    • injection = analgesic; SL = tx of opioid dependence
    • metabolized by CYP3A4
  18. codeine
    • opioid, "weak"
    • converted to morphine by CYP2D6 (polymorphic gene: ultra-rapid=more SE and toxicity, slow 5-10% Caucasians=not as much analgesia as expected).
    • Drug interactions with CYP2D6 can be significant.
    • - inhibitors (amiodarone, cimetidine, SSRIs, venlafaxine, methadone)
    • - inducers rare
    • antitussive at dose >15mg q4-6h
    • chronic use in severe renal dysfunction can lead to accumulation of toxic metabolites (likely switch to hydromorphone)
    • - morphine-6-glucuronide = active metabolite: more analgesia, but more toxicity
  19. oxycodone
    • opioid, agonist at u and K receptors
    • recent high rate of abuse, but weaker than heroin in terms of high
    • CYP3A4 interactions:
    • - inhibitors: macrolides, azoles, protease inhibitors, cimetidine, grapefruit, dilt
    • - inducers: cbmzp, phenytoin, phenobarb, primidone, rifampin, St John's wort
  20. tramadol
    • opioid, centrally acting analgesic, weak u agonist
    • blocks reuptake of 5-HT and NE...not scheduled as narcotic yet
    • not studied in peds
    • reduces seizure threshold - increases risk of seizures (caution if recent head trauma, epilepsy)
    • parent compound: serotonergic effects (inhibition of CYP2D6/decrease activity INCREASES parent coompound, increase risk of serotonin syndrome esp if pt is on other serotonergic drugs SSRI, SNRI, TCA)
    • --> e.g. avoid tramadol with SSRI, but ok to give together if pt aware of sx to look for
    • active metabolite via CYP2D6: opioid actions (weak u agonism)...genetic variations and drug interactions affect analgesia
    • CI with MAOI
    • renal: decrease dose of CrCl <30ml/min
    • SE: dizziness, N/V, constipation, h/a, somnolence.
  21. morphine
    • opioid, strong u agonist
    • morphine-6-glucuronide: active, toxic metabolite
    • renal dysfxn: accumulation of toxic metabolite --> SE
  22. hydromorphone
    • opioid, strong u agonist
    • safe for renal dysfxn (palliative, end-of-life)
    • less SE than morphine in some pts (sedation, N, constip)
    • given po, sc, im iv, pr
  23. meperidine
    • opioid, u agonist and NMDA antagonist, 5-HT reuptake blocker
    • rapid onset, short duration, not for chronic pain, but for acute pain/alternative in cases of morphine allergy
    • NOT to use in renal dysfxn: toxpic metabolite normeperidine accumulates.
    • serotonin syndrome can occur if also taking antidepressants (TCA, SSRI, SNRI)
    • CI with MAOI
    • safe in morphine allergy
    • cardiovascular SE: antimuscarinic (tachycardia), negative inotropic effects.
  24. fentanyl
    • opioid, strong u agonist
    • transdermal: onset is delayed initially...wait for 6 days before adjust dose.
    • not for opioid naive pts or acute pain
    • not studied in peds
    • heat increases absorption from patch
    • if pain irritates skin: use steroid spray or wait 1min for alcohol in patch to evaporate.
  25. methadone
    • opioid, agonist at u and delta receptors, NMDA antagonist
    • blocks reuptake of 5-HT and NE
    • used tor treatment of opioid dependence, good for both pain and addiction, or pts in pain with hx of addition
    • works better for difficult-to-treat pain e.g. cancer/neuropathic (b/c of activity at other receptors)
    • long t1/2 - wait 4 days before changing dose
    • resp depression possible
    • SE: usual opioid SE as well as QT prolongation, swearing, antichol effects, arrhythmias, MI, seizures
    • interactions: CI with amiodarone (b/c methadone QT prolong + amio pro-arrhythmic = increase risk of sig vent arrhythmias that cause death)
    • other interactions: cleared through CYP3A4, CYP2D6 inhibitor, serotonin syndrome
  26. COX non-selective
    • inhibit both COX-1 and COX-2
    • risk of GI ulceration
    • inhibit platelet aggregation
  27. COX-2 selective
    • limit GI ulceration because homeostatic GI protection is mediated by COX-1.
    • older COX-2 NSAIDs showed increased CVD rates...COX-2 inhibitors do not inhibit platelet aggreg.
    • newer evidence: Swedish cohort - COX-2 inhibs no increased risk of MI, stroke, or heart failure without prior CVD dx.
    • Increased risk of afib, but also seen in traditional NSAIDs too.
  28. ASA
    • NSAID
    • irreversibly blocks COX enzymes by acetylation
    • low doses (<325mg) preferntially blocks COX-1 on platelets...blocks TXA2 production, and decrease platelet aggregation and vasodilation. Duration of effect is related to platelet lifetime = 7 days.
    • Therefore, stop ASA 7-14 days before major surgery.
  29. acetaminophen
    • analgesic and antipyretic activity, but no anti-inflamm
    • raises threshold to painful stimuli
    • MoA
    • 1) weakly inhibits COX-1 and COX-2 by reducing cyclooxygenase to inactive form and block prostaglandin synth.
    • 2) inhibit COX-3, found in high concs in brain and heart...but unlikely to be main mechanism because only a weak producer of PGE2.
    • 3) activate descending endogeous opioid pathways + synergistic action at level of spinal cord.
    • 4) endogenous serotonergic descending pain inhibitory pathway originating from periaqueductal gray in midbrain.
    • 5) inhibition of NO pathway...which facilitates transmission of nociception.
    • 6) metabolite of acetam blocks reuptake of endocannabinoid...indirectly activating cannabinoid CB1 receptors and --> analgesic, antipyretic
    • 7) metabolite activates transient receptor potential vanilloid 1 in vitro...antinociceptive.
    • SE rare at therapeutic doses: rash, neutropenia, thrombocytopenia.

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