pharm - anesthesia

8 terms by rmathew1 

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NO vs Halothane

NO

MAC - 104% (weakest); blood gas ratio 0.5 (faster) Specific characteristics - rapid onset and recovery (inducer), may cause diffusional hypoxia so increase fiO2 with administration, spontaneous abortion

Halothane

MAC - 0.8%, blood gas ratio 2.3, CV effects - sensitizes heart to catecholamines; specific characteristics - may cause malignant hyperthermia and arrythmias

IV anesthetics

thiopental - barbiturate used for induction, rapid onset so don't have to worry about P450

midazolam - benzo used for preop sedation, antergrade amnesia, induction, and outpatient surgery (give too much, flumazenil is antitode)

propofol - "looks like milk", anesthesia, antiemetic, CNS and cardiac depressant

fentanyl(s) - opiate for anesthesia and analgesia, depresses resp function

ketamine (special k) - dissociative anesthetic, NMDA receptor blocker, cause emergent delirium and hallucinations, cause cardiovascular stimulation (can maintain CV while doing surg), increase intracranial pressure

sodium channel toxins

tetrodotoxin (and saxitoxin) - block activated Na channels (Ia) and decrease sodium influx

ciguatoxin (and batrachotoxin) - bind to activated Na channels and prolong sodium influx

esters vs amides

esters metabolized by plasma and tissue esterases (Cocaine)

amides metabolized by liver amidases (i before caine is and amide) (lidocaine)

mechanism - non ionized form crosses axonal membrane and inside ionized form blocks the inactivated Na channel

nerve fiber sensitivity - smaller diameter (builds up faster) and higher firing rates more sensitive

type B and C > type Ad> type Aa (recovery in reverse order)

absorption - coadministration of alpha1 agonist (like epi) decreases the absorption into systemic circulation, prolongs effect and decreases toxicity (cocaine doesn't need an a1 agonist)

side effects - neurotoxicity, CV toxicity, allergies via esters via PABA/paraaminobenzoic acid formation

sulfonamides are PABA analogs

skeletal muscle relaxants - non depolarizing

work like myasthenia gravis, nicotinic blockers, d-tubocurarine is the prototype, reversible with AChE inhibitors, progressive paralysis (with tropism for face, limbs and resp muscle), no effects on cardiac and smooth muscle, no CNS effects

atracurium - safe in hepatic or renal impairment, spontaneous inactivation to laudanosine, (laudanosine can cause seizures)

mivacurium - shortest duration and metabolized by cholinESTERASES; can reverse block

skeletal muscle relaxants - depolarizing (non competitive)

nicotinic agonists, only way to stop block is for drug to go away

succinylcholine (may cause cholinergic crisis/flaccid paralysis)

phase I - depolarization, phase 2 - desensitization

AChE inhibitors increase phase I; have no effect on phase II

hydrolyzed by pseudocholinESTERASE

caution atypical cholinesterase aka slow therefore may need to by intubated, hyperkalemia augments depolarization, and malignant hyperthermia

centrally acting skeletal muscle relaxant

baclofen - works on GABAb and causes spasticity

malignant hyperthermia

a life threatening syndrome with muscle rigidity, hyperthermia, HTN, acidosis, and hyperkalemia

genotypic susceptibility may be related to mutations in the genes encoding ryanodine receptors

tx: dantrolene blocks Ca release from the SR, also used in neuroleptic malignant syndrome

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