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68 Cards in this Set
- Front
- Back
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Anesthesia
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loss of sensation
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Analgesic
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drugs alleviates pain
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amnestic
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blunts memory
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hypnotic
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induce sleep
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induction
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onset of anesthetic
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emergence
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waking up from anesthesia
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Ideal agent:
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high anesthesia, hgh anagestion, relaxes muscle, high amnesia, rapid kinetsic, not toxicity
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Presynaptic action of volatile anesthetics
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decrease NT release in the hippocampus to produce anesthesia
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Postsynaptic actios
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inceas CL- GABA conductance for colatile agents
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Glycine receptors
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propofol and barbituates
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Nicotinic receptors
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think inhaled
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NMADA receptors
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think ketamin, NO and Xnenon
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Most IV anesthetics potentiate what
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GABA except ketamine
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Volatile Anesthetics work on what
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pre and post synaptic areas
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these three drugs work in NMDA
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ketamin NO xenon
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MAC
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Min alveolar concentration MAC-to maintain immobilithy in response to surgical incision
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MACS are what and what
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additive and effective att 1.2-1.3
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Low blood soubility
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fast gas equilibrium
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low oil solubility
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decreased potency (or higher MAC)
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inhalation gases act like what in tisseus
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equilibrize like gases
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how to measure equilibriumn
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when inhaled conc = ehaled conc
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more blood soluble
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longer equilibration
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Anesthesia does what to EEGs
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increas amp and decrease frequency
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Nitrous Oxide is...
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not soluble
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SE of NO
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supress hematopoietic system, dns syn, megaloblastic anemai
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SE of NE (air)
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replaces nitrogen in closed space can cause expansion of air probs
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Isoflurane
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less heawrt depression and more muscle relaxation
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Severflurane-type, solubility
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unhalatui, poor solubility = fast induction
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Desflurane-soluble, tyope, SE
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poor soluble, inhalation, can make tachy and irritate airways
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Benegits of inhaled anaesthetis 2
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increased muscle releaction that neuromuscl blocks to reuce iv drugs
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what SE do you need to watch for in Halothane and other voltagile agents
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heptatic dysfunction via IgG hypersensitivity with eosinopihilla
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what two drugs do you watch for flourine ion toxicity
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Enflourane and Sevoflourane
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what is malignant hyperthermia and what drugs is it associated with
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hypermetabolism of skeletal muscles associated with volatile anesthtetics and succinhyl choline
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what is malignatnt hhyperthermia genetically qassociated with
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ryanodine receptors with icreased Ca2+ releas
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what is the treatment of malignants hyperherm
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Dantrolene and treatment of metabolic acidisosi
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thiopentaol: type? kinetics?
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IV barbiturate-think rapid uptake, rapdi distribution and releases
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what does Thiopentol cause release of
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Histamine
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Methohexital: type, how to give, SE
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IV barb, can give rectal, can increase seizures
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Name 3 Benzo
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Midazlopam, Diazepam and Lorazepam
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which Benzo does not have active metabolites
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lorazepam
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what enzyme if in use by other drugs will cause increased longer sedation in Midazlopma and in Diazepam
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CYP3A$
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MOA of Ketamine
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NMDA antagonist
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How can ketamine be given
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anyway and IM whic is special
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when to use ketamine
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unstable patietns with airway probs that need spontaneous ventillation
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what is the main advantage of etomitdate
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hemodynamic and cardio stabiloty
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uses of propofol
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rapid awakening and rapid onset
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SE of propofol
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high cardiovasc depression
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what is a train of 4
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four birsts whith last amp divided by first amp contraction
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what is tetanty and what is it called over time?
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cts stim peripheral nerve amp measurement called fade of tetany over time
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Post tetany favilitation
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if second train of 4 tetany is stronger then the first = fasiculation
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depolarizing agents do they fasciualte
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yes
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depolarizing agents: what is the train of 4 ration
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1
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depolarizing agents: does it fade and is there a post tatny faciliation
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No
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how do chlinesterase inhibitors affeect depolarising drugs
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increases blockade by inhibiting metabolizinm of depolarizing agents
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what is succinhyl choline
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depolarizing agent
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succinycholine contraindication
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hyperkalemia nx can trigger malignant hypertherm
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what metabolizes succinylcholine what do you watch for
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pseudocholinesterase and prolonged paralytic response
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How do depolarizing drugs act on the nicotinic receptor
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they bind to the nicotinic receptor
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action of non-depolarizing drugs on the nicotininoc receptro
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bind but do not activate the nicotinic receptor
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NDEPO-do they cause fasiculation, how is the train ration and is tehre a fade
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no fasiculation, tain of 4 <1, positive fade of tetany
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do NONDEPO have post tetanic fasicilations?
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Non-depolarizing agents have post what ever facilations
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how do cholinesterase inhibitors affect Non-depo drugs?
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they decrease the blockage by incrasing available ach to overcome the durgs at teh junction
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Rocuronium
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short acting non-depo
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cistacurium and vercuronium
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intermediate action non-depos
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Pancuronium
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Long acting non-depo
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SE of non-depo drugs (3)
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histamin release. muscarinic and ganglion blcoks and metabolism
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how to revers non-depo blockade
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give an Achlinesterase inhibitor like Neostigme and Edrophonium
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name two drugs that are antimuscarinic agents, how to dhtey work
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atropine and glycopurrolate
-block ach at muscarinic receptors |
