Anasthetics

Question 1

what are the four different goals of anasthesia?

Answer 1

immobility
sedation
amnesia
analgesia

Question 2

to achieve immobility, what type drug do you give?

Answer 2

NMJ blockers

Question 3

to achieve sedation , what type drug do you give?

Answer 3

anesthetics

Question 4

to achieve amnesia, what type drug do you give?

Answer 4

amnestics (benzodiazapines)

Question 5

to achieve alangesia, what type drug do you give?

Answer 5

analgesics (opiods, local anesthetics)

Question 6

to achieve sedation, what target do you go after?

Answer 6

cortex, thalamus

Question 7

to achieve immobility, what target do you go after?

Answer 7

spinal cord and NMJs

Question 8

to achieve amnesia, what target do you go after?

Answer 8

hippocampus, amygdala, pre frontal cortex

Question 9

to achieve analgesia, what target do you go after?

Answer 9

spinal cord

Question 10

what are the two classes of anesthetics?

Answer 10

IV and inhaled anesthetics

Question 11

what are the two MoA of anesthetics?

Answer 11

stimulate GABA synapses to allow more Cl flow

inhibit glutamine synapses

Question 12

what is the gas anesthetic?

Answer 12

nitrous oxide

Question 13

what are the volatile liquid anasthetics?

Answer 13

fluranes

Question 14

what are the two main factors determining how quickly sedation occurs with anesthetics?

Answer 14

ventilation

drug solubility in plasma

Question 15

does faster ventilation lead to quicker or slower therapeutic concentration?

Answer 15

quicker

Question 16

does high water solubility of a drug lead to faster or slower therapeutic conc and sedation?

Answer 16

slower…because it takes longer to saturate the blood

Question 17

does high water solubility of a drug lead to faster or slower recovery from anesthetic?

Answer 17

slower

Question 18

what is the BG?

Answer 18

blood gas coefficient

Question 19

does a high or low BG coefficient mean faster sedation?

Answer 19

low BG means quicker sedation because low BG means less solubility

Question 20

what is the MAC?

Answer 20

minimum alveolar conc to achieve sedation in 50% of patients

Question 21

what is issue with MAC? what do we use instead?

Answer 21

only 50% effective…use the 1.3 MAC because it is 99% effective…multiply MAC by 1.3

Question 22

more hydrophobicity leads to higher or lower potency?

Answer 22

higher potency

Question 23

a more potent, more hydrophobic drug will have a higher or lower MAC compared to a low potent/hydrophobic drug?

Answer 23

lower MAC

Question 24

what else do fluranes induce that can be useful?

Answer 24

bronchodilation…good for obstructive lung disease patients needing anesthesia

Question 25

what is the secondary advantage of isoflurane?

Answer 25

coronary vasodilator

Question 26

name the two common toxicities of fluranes and NO

Answer 26

post operative nausea/vomit | malignant hyperthermia

Question 27

what is malignant hyperthermia?

Answer 27

opening of ryanodine channel due to anesthetic toxicity, leads to muscle rigidity, acidosis and hyperthermia

Question 28

what are the three IV anesthetics?

Answer 28

ketamine propofol thiopental

Question 29

what is MOA of ketamine?

Answer 29

glutamate inhib

Question 30

what is MOA of propofol and thiopental?

Answer 30

GABA positive modulator

Question 31

hydrophobic drugs go to these three areas...order them in sequence of time when the drug gets there after administration (lipid poor high perfusion, lipid rich, high perfusion, lipid rich poor perfusion)

Answer 31

lipid rich high perf lipid poor high perf lipid rich low perf

Question 32

propofol also has what advantage?

Answer 32

anti emetic

Question 33

what is a random toxicity of propofol? why?

Answer 33

hypersensitivity rxn to lecithin

Question 34

what is thiopental similar to in MOA?

Answer 34

benzodiazepines

Question 35

in addition to sedation, what can ketamine help with that is a goal of anesthesia?

Answer 35

amnesia and analgesia

Question 36

what is a bad tox of ketamine? who should never get it?

Answer 36

disorientation/hallucination dreams....dont give to schizos

Question 37

how does ketamine affect BP and RR and blood flow?

Answer 37

increase BP, decrease RR, increase blood flow

Question 38

how does propofol and thiopental affect BP and RR and blood flow?

Answer 38

low BP, lower RR, lower blood flow

Question 39

what is the main amnesia inducing drug?

Answer 39

midazolam

Question 40

what is the class of midazolam?

Answer 40

benzodiazepine

Question 41

what is the drug to reverse action of midazolam?

Answer 41

flumazenil

Question 42

how do opiods affect pain?

Answer 42

block ascending pain pathways and stimulate descending modulatory pain pathways

Question 43

how do opioids block the ascending pain pathway?

Answer 43

inhibit the pre synaptic glutamate release and hyper polarize post synaptic neuron

Question 44

how do opioids stimulate the descending pain modulatory pathway?

Answer 44

inhibit the pre synaptic GABA release

Question 45

what is the full agonist opioid?

Answer 45

fentanyl

Question 46

what is the antagonist opioid?

Answer 46

naloxone

Question 47

what is the MOA of local anesthetics?

Answer 47

block the reset of VG Na channels

Question 48

what are local anesthetics two chemical classes?

Answer 48

amide and esters

Question 49

what are the two esters that are local anesthetics?

Answer 49

procaine and cocaine

Question 50

what are the two amides that are local anesthetics?

Answer 50

lidocaine and mepivacaine

Question 51

do charged or uncharged local anesthetics cross the membrane? are local anesthetics bases or acids?

Answer 51

bases..uncharged will cross the membrane

Question 52

do charged or uncharged local anesthetics bind the VG Na channel?

Answer 52

charged

Question 53

what do you often have to add to LAs to help make them be uncharged to enter cells?

Answer 53

a bicarb solution because they are made with acidic solutions

Question 54

does LA potency increase of decrease with hydrophobicity?

Answer 54

increases with hydrophobicity

Question 55

does LA duration of action increase or decrease with hydrophobicity?

Answer 55

increases

Question 56

does time to onset of LAs increase or decrease with hydrophobicity? why?

Answer 56

increases..bc more hydrophobic offers better chance to bind with other things like proteins and make it slower to enter cells

Question 57

what are LAs often coadminstered with ? why?

Answer 57

epinephrine...bc LAs are cleared by blood flow and epinephrine leads to vasoconstriction

Question 58

does LA sensitivity increase or decrease with increased myelination and diamete?

Answer 58

sensitivity decreases as myelination and diameter increases

Question 59

what nerves are most sensitive to LAs?

Answer 59

autonomic nerves and pain nerves

Question 60

what nerves are leastsensitive to LAs?

Answer 60

motor nerve

Question 61

if a nerve depolarize faster and more often...is it more or less sensitive to LAs compared to slower ones?

Answer 61

more sensitive because VG Na channels are open and can be bound more

Question 62

peripherally acting muscle relaxants are considered what?

Answer 62

neuromusclular blockers

Question 63

name the three times neuromuscular blocking agents are used

Answer 63

endotracheal intibation mechanincal ventilation prolonged muscle relaxation during surgery

Question 64

NMBAs have what as their MOA?

Answer 64

inhibit the nAChR signaling at the motor end plate

Question 65

what are the two types of NMBAs?

Answer 65

depolarizing and non depolarizing

Question 66

what is the depolarizing NMBA?

Answer 66

succinylcholine

Question 67

what are the non depolarizing NMBAs that are steroid derivatives?

Answer 67

vecuronium pancuronium rocuronium

Question 68

how does succinylcholine work?

Answer 68

pretty much makes cell depolarize a ton and leads to one contraction then flacid paralysis

Question 69

what is a severe tox associated with succinylcholine?

Answer 69

hyperkalemia leading to cardiac arrest and malignant hyperthermia

Question 70

what are the non depolarizing NMBAs that are isoquinolones?

Answer 70

atracurium cisatracurium mivacurium tubocurarine

Question 71

how do non depolarizing NMBAs work?

Answer 71

competitive antagonist to depolarization of cells

Question 72

isoquinolone NMBAs have what two toxicities?

Answer 72

hypotension and bronchoconstriction

Question 73

steroid NMBAs have what toxicity?

Answer 73

tachycardia

Question 74

atracurium and cisatracurium have what advantage? but what disadvantage can this cause?

Answer 74

quick degradation that avoids the liver and renal clearance...breakdown product can lead to seizures

Question 75

what breaks down mivacurium?

Answer 75

pseudocholinesterase

Question 76

what can you have that leads to issue with mivacurium?

Answer 76

pseudocholinesterase deficiency AR

Question 77

aside from mivacurium what other drugs are broken down by pseudocholinesterase

Answer 77

succinylcholine and procaine/tetracaine

Question 78

what are the reversal drugs for non depol muscle relaxants?

Answer 78

neostigmine and edrophonium

Question 79

what are the two classes of spasmolytics?

Answer 79

central and peripheral acting

Question 80

name the three centrally acting spasmolytics?

Answer 80

baclofen cyclobenzaprine tizanidine

Question 81

name the peripherally acting spasmolytic?

Answer 81

dantrolene

Question 82

what is the target of tizanidine?

Answer 82

a2 receptor and decreases NT release from presynaptic neuron

Question 83

what is the target and MOA of baclofen?

Answer 83

GABAb receptor that leads to more Cl in postsynaptic neuron

Question 84

what is toxicities of cyclobenzaprine?

Answer 84

anti cholinergic like dry mouth and tachycardia

Question 85

what is dantrolenes MOA and what is it used for?

Answer 85

ryanodine receptor antagonist...used to treat malignant hyperthermia