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Pharm II > local anesthetics > Flashcards

local anesthetics Flashcards

1
Q

more soluble a gas is

A

slower onset

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2
Q

less soluble

A

faster onset

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3
Q

if a drug has 1 I in the name it is an

A

Ester and is destoryed by esterase which is in every tissue in the body

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4
Q

if a drug has 2 I’s it is an

A

amide

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5
Q

esters are converted

A

in the plasma by esterase enzymes

SHORT ACTING and not widely use

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6
Q

why do amides take lober to biotransform

A

converted in the liver by amidase

compared to esters that are converted in the plamsa

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7
Q

molecules with a positive charge are what in terms of solubility

A

they are water soluble and this is a problem because you need to inject an dhope that it gets into the neuron through the neuronal sheath

if it is water soluble it will not enter

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8
Q

the target of all anesthetics is the

A

Na receptor on the axon

shut it down
keep it from firing

patient will never feel the knife

electrical conduction Na K Na K Na K

neuron goes to sleep

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9
Q

unionized is

A

not charge
which means you can go through lipid soluble layers and this is where we want the drugs at

need a buffer

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10
Q

why is a infx an issue

A

more acidic and not as infective because it is ionized right away

faovirng the charged form

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11
Q

buffering

A

makes i more basic so that you are in a state that will remain unionized and allow for a shorten onset time

charge all has to do with cell penetration

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12
Q

why would you use epinephrine w/ lidocaine

A

vasoconstriction will keep the local anesthetic at the site longer

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13
Q

DKA

A

ph at which half of the drug is ionized and half is onionized

you w

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14
Q

why doesn’t the second injc of lidocaine work as well as the first

A

because o the buffering capacity at the injection site

buffer it yourself and you won’t run into problems

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15
Q

all local anesthetics promote vasodilation except

A

cocaine

nasal surgey this is the drug of choice

this is why we use Brier’s block

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16
Q

epinephrine

A

reduces blood flow

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17
Q

co-administration with CO2 saturated solutions increases intracellular levels of local anesthetic because

A

high intracellular CO2 produces a local acidosis which causes intracellular accumulation of cationic anesthetics

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18
Q

reduced response from repeated dosing)

A

Tachyphylaxis (

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19
Q

at pH 7.5 drugs are

A

unionized and pass through lipid membranes

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20
Q

In extracellular fluids drugs are buffered from

A

6 (bottle) to 7.4

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21
Q

why can Intralipid be used to reverse bupivacaine toxicity?

A

lipid solluble and intraplipid sucks it up

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22
Q

IV anesthestics

A 
barbs (thipental methohexital)
benzo (midazolam, diazepam) GABA
propofol 
ketamine
opioid (morphine tanil)
misc sedative (etomidate)
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23
Q

inhaled anesthetics

A

make it RANE =volatile (liquid at room temp)

nitrous oxide

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24
Q

remain the primary INHIBITORY ion channels considered legitimate candidates of anesthetic action.

A

Chloride channels (γ-aminobutyric acid-A [GABAA] and glycine receptors) ETOH

and potassium channels (K2P, possibly KV, and KATP channels)

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25
Q

Excitatory ion channel targets for general anesthesia

A

Excitatory ion channel targets include those activated by acetylcholine (nicotinic and muscarinic receptors), by glutamate (amino-3-hydroxy-5-methyl-4-isoxazol-propionic acid [AMPA], kainate, and N-methyl-D-aspartate [NMDA] receptors), or by serotonin (5-HT2 and 5-HT3 receptors). Figure 25– 1 depicts the relation of these inhibitory and excitatory targets of anesthetics within the context of the nerve terminal.

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26
Q

balanced anethesia

A

inhaled anestheis
sedative hypnotic
opioid for pain mngmt
neuromuscular blocking for relaxation

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27
Q

monitored anesthesia

A

used when you need the pt conscious

local plus a sedative allowing the pt to respond

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28
Q

low vapor pressure and high boiling points are characteristics of this gas

A

volatile

and the RANEs

allows for precision

29
Q

gas works through (4)

A

CL
K channels

this means that

inside the neuron K is much higher
K flows out

brining up inhibition can be done by taking K out of the neuron

glutamate

aCH

all possible MOA

30
Q

BLUE CYLINDER

A

Nitrous Oxide

31
Q

The most important parameter that can be controlled by the anesthesiologist to change alveolar concentration quickly is

A

the inspired concentration or partial pressure.

32
Q

stages of anesthesia

A

stage I analgesia without amnesia
stage II excitement delirious and vocalizing but amnesic
stage III surgical
stage IV medullary depression CNS depression and death

33
Q

what can be used to determine whether a pt is in surgical anesthesia

A

pupil size

most reliable is loss of response to noxious stimuli (trapezius muscle squees) and restablishment of regular respiratory pattern

34
Q

which stage of amnesthia do you want to skip

A

2!

most dangerous

35
Q

MAC

A

minimum alveolar concentration
the alveolar concentration at one atmosphere that produced immobility in 50% of pts expose

this is how they measure potency

36
Q

pharmakodynamis

A

drug does to the body

37
Q

kinetics

A

body does to the drug

38
Q

concentration for gas

A

partial pressure

concentration at sea level

39
Q

factors that effect movement of the gas into the CNS

A

solubility- based on blood solubility
concentration in inspired air
pulmonary ventilation
arteriovenous concentration gradient

40
Q

if gas is highly soluble

A

slow induction

halothane

41
Q

if gas is poorly solluble

A

rapid induction

42
Q

nitrous oxide induction is

A

rapid because it does not like the blood

43
Q

why would you use nitrous oxide first and halothane second

A

balanced anesthesia

44
Q

primary target of gasses

A

Cl

negative

45
Q

FLUR toxicity of gas anasthetic

A

worry about the kidney

46
Q

liver toxicity with this gas

A

halothane

may induce immune mediated cause of hepatitis

nurses that administer this start to make antibodies against it

47
Q

malignant hypothermia toxicity is caused by

A

genetic disorder of skeletal muscle and can be induced by general anesthetics and succinylcholine

48
Q

how to we tx malignant hypothermia caused by anesthetics

A

dantrolene

49
Q

what are the sxs of malingnant hyperthermia

A 
tachy
HTN
muscl rigidity
hyperthermia
hyperkalemia
acidosis
50
Q

chronic toxicity of general anesthetics

A

mutagenisity
carcinogenesity
reproductive organs

51
Q

two most widly used barbiturates iv anesthetic

A

thiopental and methohexital

52
Q

thiopental is used

A

for the induction of anesthesia

acts through GABA
blocks sodium gated ion channels

53
Q

this benzo is most widly used benzo anesth

A

medazolam

54
Q

drug blocks excitatory NT glutamic acid at NMDA receptors

A

Ketamine

dissociative anesthesia
vivd dreasm

55
Q

5 desired effects of anesthesia

A 
unconsciousness,
amnesia, 
analgesia, 
inhibition of autonomic reflexes
 and skeletal muscle relaxation).
56
Q

fosproprofol

A

prodrug that reduces incidence of injection site pain

removal of phosphate

57
Q

what MUST be used with etomidate

A

opioid
no analgesic effect

but used

58
Q

pre synaptic homeostatic biofeedback mechanism is utilized in this alpha 2 targeting drg

A

dexmedetomidine–> ALPHA 2

receptro on the nueron that is releasing the neurotransmitter
doubles back and bins to itself

raises blood pressure

alpha

59
Q

succinylcholine is the DOC

A

for intubation in the ER

60
Q

tubocurarine moa

A

neuromuscular blocking

antagonist and nondepolorizing

all that end in curarine

61
Q

suzzinylcholine moa

A

excess depolarization leading to muscle paralysis
depolarizing

ONLY ONE THAT WORKS LIKE THIS

TOO MUCH KEEPS BINDING
Keeps the channel open

62
Q

ADRs succinylchlinr

A

HYPERKALEMIA

63
Q

muscle relaxant that can lead to what in hemiparaiasis pts

A

and neuronal injuries cause increase expression of NT receptors

and can lead to lifethreatenting hyperkalemia in pts with succinylcholine

64
Q

spasmolytic for chronic use

A

diazepam

65
Q

spasmolytic that acts on GABAb

A

baclofen

66
Q

GABAa receptor agonist

A

diazepam
valieum

can be used for anxiety at low levels (less than 5)

and at 60 it’s a sedative

67
Q

phase I blocking is

A

depolarizing

68
Q

Phase II is

A

desnesitizing

69
Q

what drugs enhance neuromuscular blockade

A

AG

Pharm II (16 decks)

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