Pharm: Anesthesia Flashcards Preview

Block 9 - Neuro > Pharm: Anesthesia > Flashcards

Flashcards in Pharm: Anesthesia Deck (22)
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1
Q

What factors determine the systemic distribution of a local anesthetic drug injected at one site?

A

the dosage administered
vascularity of the site of admin
strength of binding of local anesthetic to tissue
presence of vasoconstricting substances - lower systemic absorption by decreased blood flow

2
Q

How does pH affect local anesthetics?

A

cationic (charged) form of local anesthetics responsible for blocking Na channels from cytoplasmic side
pH in areas of inflammation more acidic - more anesthetic is protonated - lowers cellular concentration

3
Q

What is a separation of fxn caused by the structure of local anesthetics?

A

charged amine group provides for electrostatic block of ion conduction through voltage-gated Na channel
hydrophobic aromatic group facilitates partitioning of local anesthetic into plasma membrane of target neurons

4
Q

What is the metabolism and elimination of local anesthetics?

A

metabolic processing by plasma (for esters) or liver (for amides) enzymes to water soluble products excreted in urine
ester linked rapidly broken down in plasma by esterases
amide-linked modified and hydrolyzed in liver after traveling through circulation

5
Q

What accounts for the difference in use-dependence seen with lipophilic vs. less lipophilic drugs?

A

approach from cytoplasm - binding site only accessible in open or inactive state
approach from within membrane (lipophilic) - binding site accessible in all states, less use dependent (and less common)

6
Q

How do local anesthetics affect pain fibers without affecting others, including motor?

A

use dependence - pain fibers fire more rapidly with longer duration APs
smaller pain fibers less myelinated than motor fibers - more channels per given area

7
Q

What are the types of toxicity of local anesthetics?

A

CNS toxicity: sleepiness, light headedness, visual/auditory disturbances, restlessness, higher doses –> convulsions, CNS depression, death
neurotoxicity
CV toxicity: pacemaker malfxn, loss of contraction strength and dilation of arterioles, severe symptoms rare unless large dose
smooth muscle: inhibit contractility of bowel and intestinal, may increase tone
respiratory depression
hematologic toxicity
alleric rxns
radiculopathy
cauda equina syndrome

8
Q

What are the stages of the depth of anesthesia?

A

Stage I: decreased perception, calm
Stage II: excitement, delirium, irregular respiration, amnesia begins
Stage III: surgical anesthesia, regular or no breathing, complete absence of perception
Stage IV: medullary compression/coma

9
Q

What is the meaning of the blood:gas partition coefficient?

A

high coefficient = high solubility = low effective gas concentration = lower anesthetic effect

10
Q

What are the pharmacokinetics of anesthetic gas uptake?

A
gas inspired (Fi) --> builds in alveolus (FA) --> concentrates in arterial circulation (Fa) --> goes to brain
all values directly proportional
FA/Fi < 1 as brain concentration increases, reverse true upon emergence
Fa/FA <1 upon induction and maintenance
11
Q

What are the five major factors affecting how quickly gas builds up in the alveoli (Fi–>FA)?

A

concentration of anesthetic in inspired air
pulmonary ventilation
solubility (rate of induction inversely proportional)
pulmonary blood flow - dilution effect means high blood flow slows buildup of anesthetic
AV concentration gradient - continued gradient allows more uptake, gases distribute into various tissues according to individual partition coefficients for each tissue

12
Q

What does a V/Q mismatch cause?

A

increased A-a gradient and slows rise of Fa

13
Q

How are inhaled anesthetics eliminated?

A

once FA/Fi >1, gas will diffuse back into alveolar compartment down concentration gradient and into air
diffusion is major route
same factors that increase induction increase elimination

14
Q

What is the role of biotransformation in the pharmacokinetics of inhaled anesthetics?

A

minimal effect on elimination except halothane which has extensive metabolism

15
Q

What is the minimum alveolar concentration (MAC)?

A

measure of potency of inhalation agent
MAC of gas at which 50% of pts will not move in response to noxious stimuli
Lower MAC = more potent

16
Q

Why is respiratory depression not considered an adverse event w potent inhalation anesthetics?

A

apnea is goal because intention is to assume control of patient’s respiration w mechanical ventilation
different than IV where spontaneous respiration should be maintained

17
Q

How is malignant hyperthermia involved in inhalation anesthetics?

A

potential with any except NO
has hypercarbia, tachy, and HTN followed by hypotension
treatment = cessation of anesthetic, cooling, IV hydration, IV dantrolene (Ca channel antagonist)
risk = mutation in ryanodine receptor

18
Q

What are factors that decrease MAC?

A

elderly, opioids/benzos, acute alcohol intox, NO

19
Q

What are factors that increase MAC?

A

youth, acute cocaine use, chronic alcohol abuse, TCA’s/MAOI’s

20
Q

What is the Meyer-Overton principle of mechanism of action of inhalation anesthetics?

A

degree of lipid solubility of volatile anesthetics directly correlates with potency (MAC) - support for theory that hydrophobic gas molecules partition into cell membrane and alter permeability to alter/abate APs
= nonspecific interxn, mostly disproven

21
Q

What is the more recent theory of mechanism of action of volatile anesthetics?

A

direct interxn of gas molcules w neuronal membrane proteins to alter: ion channel activity, intracellular signaling, NT release, NT binding/reuptake
supported by steep dose-response curve

22
Q

What are the components for general anesthesia for a major surgical procedure?

A

sedative/amnestic, analgesic, induction agent, muscle relaxant, maintenance anesthetic, maybe relaxant reversal