Anesthetics Concepts – Flashcards
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What is the mechanism of action of general anesthetics?
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Thought to increase activity of GABA receptors and potassium channels and decrease the activity of acetylcholine and glutamate receptors
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What general areas are responsible for the actions of anesthetics?
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Amnesia and unconsciousness: brain Immobilization and analgesia: spinal cord
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What is balanced anesthesia?
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Using multiple drugs/methods of anesthesia to maximize desired actions and minimize undesired actions
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What are the general anesthetics that are administered intravenously?
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Thiopental, propofol, etomidate, ketamine, (methohexital)
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What are the general anesthetics that are inhaled ("volatile anesthetics")?
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Isoflurane, sevoflurane, desflurane, nitrous oxide, (halothane, methoxyflurane, enflurane)
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How is the half-life of thiopental influenced by infusion duration?
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The longer the infusion, the longer the half-life due to the redistribution of thiopental
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Describe the therapeutic window for inhalation anesthetics.
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Generally fairly narrow
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What form of an inhaled anesthetic distributes out of the lungs and into the blood and brain?
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The insoluble gas contributes to the partial pressure and is distributed
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What effect does solubility of an inhaled anesthetic have on recovery time?
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The lower the blood solubility, the shorter the recovery time When a gas is more soluble, it will fall out of the delivery stream
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What effect will a high blood/gas partition coefficient have on the action of an inhaled anesthetic?
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The higher the blood/gas partition coefficient, the longer to reach equilibrium, the longer to induce anesthesia, and the longer the duration of action
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What effect does ventilation have on time to reach anesthetic equilibrium?
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An increased ventilator rate will decrease the time to reach anesthetic equilibrium -with each breath there is a new bolus of drug
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What effect will increased cardiac output have on the time to reach anesthetic equilibrium?
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An increased cardiac output can delay the time to reach anesthetic equilibrium
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How is potency of inhaled anesthetics compared?
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Using MACs
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What is a MAC?
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The minimum alveolar concentration resulting in a lack of response to a noxious stimulus in 50% of subjects. (This can be used to compare potencies or to combine anesthetics: MACs can be added).
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What drugs are associated with malignant hyperthermia?
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Halogenated inhalation anesthetics and succinylcholine
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What is the treatment for malignant hyperthermia?
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Dantrolene
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How is local anesthesia defined?
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The loss of sensation in a body part without the loss of consciousness or the impairment of central control of vital functions
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By what mechanism do local anesthetics prevent (or relieve pain)?
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Reversibly block nerve conduction via inhibition of voltage-gated sodium channel activity
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What effect do local anesthetics have on the sodium channel?
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Stabilize the inactive state of the channel
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Where on the sodium channel do local anesthetics bind?
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Within the channel - the local anesthetic must gain access through the open channel
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What is meant by "use-dependence" of local anesthetics?
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Local anesthetics are more effective when nerves are firing more frequently due to the necessity of an open channel in order to gain access to the local anesthetic binding site
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What tissues can be blocked by local anesthetics?
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Sensory nerves, motor nerves, central nervous system, cardiovascular system, other smooth muscle, skeletal muscle
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What is the order of functional block by local anesthetics?
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Pain, autonomic C fibers -> cold -> warmth -> touch -> deep pressure -> motor In general, small fibers are more susceptible to blockade by local anesthetics than large fibers
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What is the order of recovery from local anesthetic block?
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Motor -> deep pressure -> touch -> warmth -> cold -> pain, autonomic C fibers
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Which local anesthetics are amides?
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Lidocaine, bupivacaine, ropivacaine, prilocaine (note the extra "i")
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Which local anesthetics are esters?
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Procaine, cocaine, benzocaine, tetracaine
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The pKa of a local anesthetic influences what parameter?
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Time of onset
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What effect would a decrease in pH have on a local anesthetic?
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Local anesthetics are weak bases so would be protonated and charged Charged form crosses membranes poorly Charged form binds sodium channel
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The lipid solubility of a local anesthetic influences what parameter?
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Potency (more hydrophobic = more potent but also more adverse)
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Protein binding and hydrophobicity of a local anesthetic influence what parameter?
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Duration of action
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What is the difference in metabolism of local anesthetics that are amides versus those that are esters?
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Amides undergo hepatic metabolism Esters are hydrolyzed by cholinesterases in plasma (and lesser in CNS)
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What effect would the addition of a vasoconstrictor have on the action of a local anesthetic?
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Decrease systemic absorption/redistribution Prolong duration of the anesthesia Reduce risk of systemic toxicity
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How do local anesthetics produce toxicity?
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Generally systemic: may be CNS stimulation -> depression, CV depression (decreased inotropy, chronotropy, BP), decreased contraction of smooth muscle (e.g. bowel and uterus), hypersensitivity (dermatitis, asthma)
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What drugs are associated with methemoglobinemia?
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Prilocaine and benzocaine
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What is an EMLA?
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"Eutectic mixture (low melting point) of local anesthetics" containing lidocaine and prilocaine which allows anesthetic action to 5 mm depth after topical administration which bridges the gap between topical and infiltration anesthesia
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What is the major indication of neuromuscular blockers?
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To paralyze/relax skeletal muscle and prevent movement in patients under general anesthesia for surgical procedures
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How does the use of a neuromuscular blocker affect the use of other anesthetics?
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Allows for the use of less general anesthetic - "lighter" anesthesia
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Do neuromuscular blockers have analgesic properties?
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No
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Do neuromuscular blockers produce sedation?
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No
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What is the sequence of paralysis when using neuromuscular blockers?
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Muscles of fine movement (eyes, jaw, larynx, fingers) -> limbs -> trunk -> intercostals -> diaphragm
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What is the sequence of recovery when using neuromuscular blockers?
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Diaphragm -> intercostals -> trunk -> limbs -> muscles of fine movement (eyes, jaw, larynx, fingers) Breathing recovers first
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What is the difference between a non-depolarizing neuromuscular blocker and a depolarizing one?
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Non-depolarizing neuromuscular blocker acts as a classical antagonist and just blocks access to the receptor Depolarizing neuromuscular blocker first activates the receptor but because of continued activation (due to slow hydrolysis relative to ACh) the end-plate doesn't "reset" and further activation is prohibited
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How are the non-depolarizing neuromuscular blockers eliminated?
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Most are eliminated renal EXCEPT: Rocuronium and vecuronium: hepatic metabolism Atracurium: spontaneous breakdown (hofmann elimination) and plasma esterases
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What drugs can be used to reverse the effects of non-depolarizing neuromuscular blockers?
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Cholinesterase inhibitors such as neostigmine acting by increasing ACh in the synaptic cleft which can then out-compete the non-depolarizing neuromuscular blocker for binding to the nicotinic receptor.
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What concerns are there regarding the administration of a cholinesterase inhibitor to hasten recovery from non-depolarizing neuromuscular blocker?
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Muscarinic effects: bradycardia, bronchoconstriction, salivation, nausea, diarrhea, etc. so administer with muscarinic antagonist
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Which neuromuscular blocker has the shortest time to onset?
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Succinylcholine
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Which neuromuscular blocker has the shortest duration of action?
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Succinylcholine
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What is the initial response with administration of succinylcholine?
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Wave of fasciculation due to *initial activation* of the nicotinic receptor and subsequent depolarization of the membrane
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What is the effect of cholinesterase inhibitors on succinylcholine effects?
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During Phase 1 block (depolarization block) cholinesterase inhibitors can intensify the block During Phase 2 block (receptor desensitization) cholinesterase inhibitors can reverse the block
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What are examples of skeletal muscle relaxants?
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Baclofen and dantrolene
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What are the major determinants of inhalation anesthetic concentration?
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Inspired anesthetic concentration Alveolar ventilation Blood/gas solubility Pulmonary perfusion (cardiac output) - (maybe b/c there is faster redistribution so drug gets to tissues faster where it is soluble)
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