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Anesthesia Drugs Flashcards

0
Q

What are the effects of inhaled anesthetics?

A

Myocardial depression
Respiratory depression
Nausea/emetics
Increased cerebral flow

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1
Q

What are the inhaled anesthetics?

A 
Halothane
Enflurane
Isoflurane
Sevoflurane
Methoxyflurane
Nitrous oxide
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2
Q

What is the toxicity of halothane?

A

Hepatotoxicity

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3
Q

What is the toxicity of methoxyflurane?

A

Nephrotoxicity

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4
Q

What is the toxicity of enflurane?

A

Proconvulsant

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5
Q

What is the toxicity of inhaled anesthetics in general except for nitrous oxide?

A

Malignant hyperthermia

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6
Q

What is the danger of nitrous oxide?

A

Expansion of trapped gas in the body

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7
Q

What is seen in the liver with halothane toxicity?

A

Massive hepatic necrosis
Sx: increased LFTs, liver tenderness, hepatomegaly
Light microscopy shows widespread centrilobular hepatic necrosis

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8
Q

What are the IV anesthetics?

A 
Thiopental
BZD
Arylcyclohexylamines (ketamine)
Opioids
Propofol
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9
Q

What is the action of thiopental?

A

It is a barbiturate - so it facilitates GABA action by increasing the duration of chloride channel opening thus decreasing neuron firing

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10
Q

What is unique about thiopental?

A

It has high potency and high lipid solubility so it has rapid entry into the brain then it redistributes into the skeletal muscle and fat.

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11
Q

What is thiopental used for?

A

Induction of anesthesia

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12
Q

What is the MOA of midolazam?

A

It is a BZD so it facilitates GABA action - increases the frequency of chloride channel opening

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13
Q

What is midolazam used for?

A

Endoscopy

Adjunctively with gaseous anesthetics and narcotics

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14
Q

What are the side effects of midolozam?

A

Post op respiratory depression
Decreased BP
Amnesia

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15
Q

What is the MOA of the arylcyclohexylamines?

A

PCP analogs that act as dissociative anesthetics

They block NMDA receptors –> increase CV and cerebral blood flow

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16
Q

What are the side effects of arylcyclohexylamines?

A

Disorientation
Hallucination
Bad dreams

17
Q

What are the opioids used in anesthesia?

A

Morphine

Fentanyl

18
Q

What is propofol used for?

A

Sedation in ICU
Rapid anesthesia induction
Short procedures

19
Q

What is the MOA of propofol?

A

Potentiates GABA

20
Q

What is the advantage to propofol?

A

Less nausea than thiopental

21
Q

What are local anesthetics?

A 
Esters = -caines = procainamide, cocaine, tetracaine
Amides = 2 I's in their names = lidocaine, mepivacaine, bupivacaine
22
Q

What is the MOA of local anesthetics?

A

Block sodium channels by binding to specific receptors on inner portion of channel
They preferentially bind to inactivated sodium channels, so most effective in rapidly firing neurons.
Note: tertiary amines penetrate the bb barrier as uncharged form then bind ion channels in charged form

23
Q

Why would you give vasoconstrictors with a local anesthetic?

A

To enhance the local action and increase anesthesia of the area by decreasing the systemic concentration

24
Q

Why must more anesthetic be given when dealing with infected tissue?

A

Alkaline nature of amine anesthetics can’t penetrate because the acidic environment of the infection

25
Q

What is the order of nerve blockade?

A

Small myelinated> small unmyelinated > large myelinated > large unmyelinated

26
Q

What is the order of sensory loss?

A

Pain > temperature > touch > pressure

27
Q

What are local anesthetics used for?

A

Minor surgery

Spinal anesthesia

28
Q

What is the toxicity of local anesthetics?

A 
CNS excitation
Severe CV toxicity (bupivacaine)
HTN
Hypotension
Arrhythmias (cocaine)
29
Q

What are the drugs used for muscle paralysis during surgery.

A

NMJ blocking drugs : succinylcholine, tubocurarine, -curiums, -curoniums

30
Q

What is succinylcholine?

A

A de polarizing Ach receptor agonist

31
Q

What is the action of succinylcholine?

A

Produces sustained depolarization and prevents muscle contraction

32
Q

What are the complications of using succinylcholine?

A

Hyperkalemia, hypercalcemia, malignant hyperthermia

33
Q

What is phase I of reversal of succinylcholine blockade?

A

Prolonged depolarization

No antidote - prolonged by cholinesterase inhibitors

34
Q

What is phase II of succinylcholine reversal blockade?

A

Repolarized but blocked - Ach receptors are available but desensitized - use cholinesterase inhibitors (stigmines)

35
Q

What are the nondepolarizing NMJ blockers?

A

-curiums, tubocurarine, -curoniums

36
Q

What is the MOA of nondepolarizing NMJ blockers?

A

Compete with Ach for receptors

37
Q

How do you reverse blockade with nondepolarizing NMJ drugs?

A

Cholinesterase inhibitors

38
Q

What is the MOA of dantrolene?

A

Prevents release of calcium from sarcoplasmic reticulum in skeletal muscle

39
Q

What is dantrolene used for?

A

To tx malignant hyperthermia

Neuroleptic malignant syndrome

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