local anesthetics Flashcards by Lux Smith

more soluble a gas is

slower onset

How well did you know this?

Not at all

Perfectly

less soluble

faster onset

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

if a drug has 2 I’s it is an

amide

How well did you know this?

Not at all

Perfectly

esters are converted

in the plasma by esterase enzymes

SHORT ACTING and not widely use

How well did you know this?

Not at all

Perfectly

why do amides take lober to biotransform

converted in the liver by amidase

compared to esters that are converted in the plamsa

How well did you know this?

Not at all

Perfectly

molecules with a positive charge are what in terms of solubility

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

How well did you know this?

Not at all

Perfectly

the target of all anesthetics is the

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

How well did you know this?

Not at all

Perfectly

unionized is

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

need a buffer

How well did you know this?

Not at all

Perfectly

why is a infx an issue

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

faovirng the charged form

How well did you know this?

Not at all

Perfectly

buffering

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

How well did you know this?

Not at all

Perfectly

why would you use epinephrine w/ lidocaine

vasoconstriction will keep the local anesthetic at the site longer

How well did you know this?

Not at all

Perfectly

DKA

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

you w

How well did you know this?

Not at all

Perfectly

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

because o the buffering capacity at the injection site

buffer it yourself and you won’t run into problems

How well did you know this?

Not at all

Perfectly

all local anesthetics promote vasodilation except

cocaine

nasal surgey this is the drug of choice

this is why we use Brier’s block

How well did you know this?

Not at all

Perfectly

epinephrine

reduces blood flow

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

reduced response from repeated dosing)

Tachyphylaxis (

How well did you know this?

Not at all

Perfectly

at pH 7.5 drugs are

unionized and pass through lipid membranes

How well did you know this?

Not at all

Perfectly

In extracellular fluids drugs are buffered from

6 (bottle) to 7.4

How well did you know this?

Not at all

Perfectly

why can Intralipid be used to reverse bupivacaine toxicity?

lipid solluble and intraplipid sucks it up

How well did you know this?

Not at all

Perfectly

IV anesthestics

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

How well did you know this?

Not at all

Perfectly

inhaled anesthetics

make it RANE =volatile (liquid at room temp)

nitrous oxide

How well did you know this?

Not at all

Perfectly

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

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

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

How well did you know this?

Not at all

Perfectly

Excitatory ion channel targets for general anesthesia

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.

balanced anethesia

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

monitored anesthesia

used when you need the pt conscious local plus a sedative allowing the pt to respond

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

volatile and the RANEs allows for precision

gas works through (4)

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

BLUE CYLINDER

Nitrous Oxide

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

the inspired concentration or partial pressure.

stages of anesthesia

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

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

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

which stage of amnesthia do you want to skip

2! | most dangerous

MAC

minimum alveolar concentration the alveolar concentration at one atmosphere that produced immobility in 50% of pts expose this is how they measure potency

pharmakodynamis

drug does to the body

kinetics

body does to the drug

concentration for gas

partial pressure concentration at sea level

factors that effect movement of the gas into the CNS

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

if gas is highly soluble

slow induction | halothane

if gas is poorly solluble

rapid induction

nitrous oxide induction is

rapid because it does not like the blood

why would you use nitrous oxide first and halothane second

balanced anesthesia

primary target of gasses

Cl | negative

FLUR toxicity of gas anasthetic

worry about the kidney

liver toxicity with this gas

halothane may induce immune mediated cause of hepatitis nurses that administer this start to make antibodies against it

malignant hypothermia toxicity is caused by

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

how to we tx malignant hypothermia caused by anesthetics

dantrolene

what are the sxs of malingnant hyperthermia

``` tachy HTN muscl rigidity hyperthermia hyperkalemia acidosis ```

chronic toxicity of general anesthetics

mutagenisity carcinogenesity reproductive organs

two most widly used barbiturates iv anesthetic

thiopental and methohexital

thiopental is used

for the induction of anesthesia acts through GABA blocks sodium gated ion channels

this benzo is most widly used benzo anesth

medazolam

drug blocks excitatory NT glutamic acid at NMDA receptors

Ketamine dissociative anesthesia vivd dreasm

5 desired effects of anesthesia

``` unconsciousness, amnesia, analgesia, inhibition of autonomic reflexes and skeletal muscle relaxation). ```

fosproprofol

prodrug that reduces incidence of injection site pain removal of phosphate

what MUST be used with etomidate

opioid no analgesic effect but used

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

dexmedetomidine--> ALPHA 2 receptro on the nueron that is releasing the neurotransmitter doubles back and bins to itself raises blood pressure alpha

succinylcholine is the DOC

for intubation in the ER

tubocurarine moa

neuromuscular blocking antagonist and nondepolorizing all that end in curarine

suzzinylcholine moa

excess depolarization leading to muscle paralysis depolarizing ONLY ONE THAT WORKS LIKE THIS TOO MUCH KEEPS BINDING Keeps the channel open

ADRs succinylchlinr

HYPERKALEMIA

muscle relaxant that can lead to what in hemiparaiasis pts

and neuronal injuries cause increase expression of NT receptors and can lead to lifethreatenting hyperkalemia in pts with succinylcholine

spasmolytic for chronic use

diazepam

spasmolytic that acts on GABAb

baclofen

GABAa receptor agonist

diazepam valieum can be used for anxiety at low levels (less than 5) and at 60 it's a sedative

phase I blocking is

depolarizing

Phase II is

desnesitizing

what drugs enhance neuromuscular blockade