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Anesthetics - general principles
*drugs with decreased solubility in blood = rapid induction and recovery times
*drugs with increased solubility - increased potency = 1/MAC (meaning one over mac!)
Examples: N20 has low blood and lipid solubility, and thus fast induction and low potency. Halothane, in contrast, has increased lipid and blood solubility, and thus high potency and slow induction.
Inhaled anesthetics
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.
Mechanism: the lower the solubility in blood, the quicker the anesthetic induction and the quicker the recovery
Effects: Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow
Toxicity: Hepatoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), malignant hyperthermia (rare).
Intravenous anesthetics
Barbiturates: Thiopental-high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by redistribution from brain. Decreased cerebral blood flow.
Benzodiazepines: Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression and amnesia (can't you just imagine the heart walking around like the sad zoloft bubble?!)
Ketamine: a PCP analog that acts as a dissociative anesthetics. Cardiovascular stimulant. Causes disorientation, hallucination, and bad dreams (aww sad). Increased cerebral blood flow.
Opiates: Morphine, fentanyl used with other CNS depressants during general anesthesia.
Propofol: Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental.
Neuromuscular blocking drugs
Used for muscular paralysis in surgery or mechanical ventilation.
*Depolarizing: Succinylcholine
Reveral of blockade:
--Phase I (prolonged depolarization): no antidote. Block potentiated by cholinesterase inhibitors
--Phase II (repolarized but blocked): antidote consists of cholinesterase inhibitors (e.g. neostigmine)
*Nondepolarizing: Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium.
Reversal of blockade: Neostigmine, edrophonium, and other cholinesterase inhibitors
Dantrolene
Used in the treatment of malignant hyperthermia, which is caused by the concomitant use of inhation anesthetics (except N20) and succinylcholine. Also used to treat neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).
Mechanism: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
Local Anesthetics
Esters - procaine, cocaine, tetracaine
Amides - lidocaine, bupivacaine - Amides have TWO i's in name! wow thats totally unhelpful.
Mechanism: Block Na+ channels by binding to specific receptors on inner portion of channel. 3° amine local anesthetics penetrate (hee) membrane in uncharged form, then bind in charged form.
Principle: 1) In infected (acidic) tissue, anesthetics are charged and cannot penetrate membrane effectively. Therefore, more anesthetic is needed in these cases.
2) Order of nerve blockade: small diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination so small unmyelinated pain fibers > small myelinated autonomic fibers >large myelinated autonomic fibers. (duh?!) Order of loss- pain (lose first) > temperature >touch > pressure (lose last)
3) Given with vasoconstrictors (usually epinephrine) to enhance local action.
Clinical Use: Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.
Toxicity: CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, and arrhythmias (cocaine)
wow this was long...and i'm making it longer!
random fact from jessie:
whenever i type anesthetic i always think Anes The Tic...what a regal name.
Opioid analgesics
Morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan (orphan!)
Mechanism: act as agonists at opioid receptors (mu = morphine (phi morphine!) delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission.
Clinical Use: pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone).
Toxicity: Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).
NSAIDs
Ibuprofen, naproxen, indomethacin.
Mechanism: reversibly inhibit cyclooxygenase (both COX-1 and COX-2). Block prostaglandin synthesis.
Clinical use: Antipyretic, analgesis, anti-inflammatory. Indomethacin is used to close a PDA.
Toxicity: renal damage, aplastic anemia, GI distress ulcers.
COX-2 inhibitors
Celecoxib, valdecoxib
Mechanism: selectively inhibit cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and mediates inflammation and pain; spares COX-1, which helps maintain the gastric musoca. Thus, should not have the corrosive effects of the other NSAIDs on the GI lining.
Clinical use: Rheumatoid and osteoarthritis.
Toxicity: similar to other NSAIDS but maybe less GI irritation. Risk of MI and stroke with rofecoxib (now withdrawn).
Acetaminophen
Mechanism: reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.
Clinical use: Antipyretic, analgesic, but lacking anti-inflammatory properties
Toxicity: Overdose produces hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic NAPQI in liver. N-acetylcysteine is antidote - regenerates glutathione and/or binds NAPQI