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Kaplan Section 4 Chapter 1 CNS Pharm - Anesthetics

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Answer
What is the MAC value?   Minimal alveolar anesthetic concentration (% of inspired air) at which 50% of pts do not respond to a surgical stimulus. Measures potency of an anesthetic. The lower the MAC value, the stronger the anesthetic.  
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Name 6 inhaled anesthetics in MAC order   In order of decreasing MAC value (increasing potency): NO, Des Sevo, En, Iso, Halo. Nitrous oxide, desflurane, Sevoflurane, Enflurane, Isoflurane, Haloflurane. ISOdora has SEVeral HALOs, so has NO DESire to ENhale that cigarette.  
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Name 6 inhaled anesthetics in blood-gas solubility order   In order of decreasing rate of onset/recovery: Des, NO, Sevo, Iso, En, Halo. Desire NOthing and SEVer all ties with IsoEnHalo.  
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What does the blood-gas ratio tell you about the anesthetic?   Rate of onset and recovery of inhaled anesthetics. The more soluble a gasin the blood, the longer that drug takes to exert its effects on the CNS or other body tissues (it wants to stay in ght  
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Which inhaled anesthetic has the lowest potency?   NO - but relatively fast, so often used in combo with other anesthetics  
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What are the cardiovascular effects of NO?   Minimal  
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Which inhaled anesthetic has the most rapid onset and recovery? Adverse effects?   Desflurane, but causes airway irritation and coughing  
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What are the cardiovascular effects of Desflurane?   Vasodilation and increased HR (reflex?)  
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Which inhaled anesthetics cause vasodilation and increased heart rate?   Desflurane and Haloflurane  
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Which inhaled anesthetics cause decreased heart rate?   Sevoflurane, Enflurane, Haloflurane  
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Which inhaled anesthetic sensitizes the heart to catecholamines?   Haloflurane  
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Which inhaled anesthetic causes tonic/clonic muscle spasms?   Enflurane  
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Which inhaled anesthetic causes bronchiolar secretions and spasms?   Isoflurane  
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Which inhaled anesthetic causes hepatitis?   Haloflurane  
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Which inhaled anesthetic causes malignant hyperthermia?   Haloflurane  
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Which inhaled anesthetic causes cardiac arrhythmias?   Haloflurane  
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What are the three actions of inhaled anesthetics?   1. lowers response to increased PCO2, 2. increase cerebral blood flow, 3. relax uterine smooth muscle  
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Name the 5 IV anesthetics   Thiopental, Midazolam, Propofol, Fentanyl, Ketamine. Rich-as-MIDAs THIO PROPOsed to FEN-yen while on IV special K (ketamine).  
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Which IV anesthetic should be used for induction? Why?   Thiopental (barbiturate). Highly lipid soluble, but RAPID onset and SHORT-acting. RAPID recovery (redistribution from CNS to peripheral tissues).  
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Which IV anesthetic should be used for preoperative sedation? Why?   Midazolam (BZ). Allows conscious sedation and anterograde amnesia.  
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Which IV anesthetic should be used for outpatient surgery? Why?   Propofol. Very rapid onset and recovery. Can be used both for induction and maintenance. Has antiemetic effects.  
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Which IV anesthetic is a potent analgesic?   Fentanyl. An opioid analgesic, but shorter duration of action than most opioids.  
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Which is the only anesthetic to cause CV stimulation?   Ketamine (NMDS receptor antagonist)  
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How is thiopental eliminated from the body?   Liver metabolism  
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What is the effect of thiopental?   Depresses respiratory and cardiac function, but does not increase cerebral blood flow.  
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What is the effect of midazolam?   Depresses respiratory function.  
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How do you reverse the effects of midazolam?   Flumazenil. (BZ receptor antagonist)  
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Which anesthetic causes dissociative amnesia?   Ketamine (NMDA receptor antagonist). Dissociative: drug which reduces (or blocks) signals to the conscious mind from other parts of the brain. State of sensory deprivation and dissociation can facilitate hallucinations & dreamlike states.  
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Adverse effects of fentanyl   Can cause chest wall rigidity with IV use (can also be used orally or delivered through a patch)  
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What is neurolept anesthesia?   Intravenous sedation - partially conscious. Uses combination of fentanyl, droperidol, and NO.  
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What are the properties of ketamine?   rapid onset and short-duration, causes amensia, catatonia, and analgesia.  
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What are emergence reactions?   Occurs with ketmine use - vivid dreams and hallucinations. Can be offset by BZ's.  
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Esters and amides are what kind of anesthetic? How can you tell the difference?   Local anesthetics. Esters have one i (procaine, cocaine, benzocaine), amides have >1 i's (lidocaine, bupivacaine, mepivacaine).  
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How are esters metabolized?   by plasma and tissue esterases  
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How are amides metabolized?   liver amidases  
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What is the mechanism of local anesthetics (LA)?   LA must first be in nonionized form to cross lipid bilayer of axon --> gets into cell --> becomes ionized --> binds to component of Na channel on inner side of membrane --> binds in INACTIVATED state (M open h closed) --> block reactivation  
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Increases in extracellular acidity does what to the effectiveness of local anesthetics?   Increased acidity would protonate the LA's (which are usually weak bases), so they can't cross the lipid bilayer to bind to the inactivated Na channel --> decrease LA activity  
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Which nerve fibers are most sensitive to the actions of local anesthetics? List in order of sensitivity.   Nerve fibers of smaller diameter and higher firing rates are the most sensitive to blockade. Order of sensitivity: type B and C > A delta > A beta and gamma > A alpha  
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What happens when local anesthetics are coadministered with a adrenoceptor agonists (such as epinephrine)?   LA absorption into systemic circulation decreases --> prolong LA effects, decreases toxicity.  
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Adverse effects of local anesthetics   Neuro: dizzines, nystagmus, sensory impairment, seizures. CV: CV depression, except for cocaine, which increases HR and BP. Allergies: esters --> PABA --> people are allergic to PABA  
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What is tetrodotoxin?   toxin from puffer fish. Binds externally to READY state (M closed, h open) of Na channels in both cardiac and nerve cell membranes --> block Na influx --> no depolarization --> no conduction  
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What is saxitoxin?   toxin from dinoflagellates in "red tide". Binds externally to READY state (M closed, h open) of Na channels in both cardiac and nerve cell membranes --> block Na influx --> no depolarization --> no conduction  
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What is ciguatoxin?   toxin from exotic fish and Moray eels. Binds in the Na channel in the OPEN state (both M and h are open) --> persistent depolarization --> channel inactivation  
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What is batrachotoxin?   toxin from south American frogs. Binds in the Na channel in the OPEN state (both M and h are open) --> persistent depolarization --> channel inactivation  
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