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Pharmacology > Anesthesia > Flashcards

Anesthesia Flashcards

1
Q

The rate of onset of anesthesia from a drug like nitrous oxide or isoflurane is primarily determined by?

A

Degrees of solubility: the less soluble = the less potent (but gasses diffuse into the tissues quickly

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2
Q

Which one of the following inhalation anesthetics is most likely to produce hepatotoxicity?

a. Isoflurane
b. Enflurane
c. Halothane
d. Methoxyflurane

A

What causes hepatotoxicity:

c. Halothane (even though its no longer used)

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3
Q

What are the 4 components of the anesthetic state?

A

Amnesia - partial or complete loss of memory

Sedation - decreased level of arousal

Hypnosis - unconsiousness

Immobility - lack of respone to noxious stimuli

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4
Q

Year for Ether Anesthesia?

A

1842

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5
Q

What is an important preoperative consideration?

A

Taking a good history

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6
Q

Proposed mechanisms of action of general anesthesics:

It was hypothesized that volatile anesthetics and act nonspecifically on what component of cells?

A

Volatile anesthetics act on hydrophobic lipid components

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7
Q

Lipid solubility and relationship to potentcy?

A

More lipid soluble = more potent

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8
Q

Minimum Alveolar Concentration (MAC)

Concentration of gas in the ___ compartment that results in a ___ of response to a noxious stimulus in ___% of subjects.

Limitations: ___% of patients still respond

Absence of response to pain may ___ indicate ___ of consciousness

A

Concentration of gas in the alveolar compartment that results in a lack of response to a noxious stimulus in 50% of subjects.

Limitations:

50% of patients still respond

Absence of response to pain may NOT indicate LOSS of consciousness

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9
Q

Propsed mechanisms of action of general anesthetics:

General anesthetics increase the activity of ____ receptors and ___ channels and decrease the activity of ____ receptors and ____ receptors. Causes an increase in _____.

A

General anesthetics increase the activity of GABA receptors and potassium channels and decrease the activity of acetylcholine receptors and glutamate receptors. Causes and increase in inhibition

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10
Q

Pharmacology of general anesthetics:

What are the IV drugs?

What are the volatile drugs (inhaled)?

A

IV: thiopental, propofol, etomidate, ketamine

Volatile: halothane, isoflurane, sevoflurane, desflurane, and nitrous oxide

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11
Q

What drugs are IV?

A

Barbiturates

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12
Q

What is thiopental used for?

What drug is not around anymore?

How many methohexital drugs are used?

A

Thiopental - executions

Thiamylal - not used anymore

Methohexital - only one used

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13
Q

Barbiturates:

Terminal ___ ___ longer with continued infuction but _____ has a relatively rapid clearance.

Contraindicated in patients with?

A

Terminal half lives longer with continued infusion but methohexital has relatively rapid clearance

Contraindicated in patients with porphyria

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14
Q

Propofol:

Clearance compared to barbiturates?

What is this drug for?

A

Propofol:

Rapid clearance compared to barbiturates

Drug is good for MS

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15
Q

Etomidate:

  1. Use in patients with risk for hypotension - why?
  2. Suppression of?
A

Etomidate:

  1. CARDIOSTABLE
  2. Suppresion of adrenals!
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16
Q

Ketamine:

  1. Used in patients with risk for ___ or ___ since it increases ___ ___ and is a ____.
  2. Toxicity causes increase in ____ blood flow or emergence ____.
  3. Contraindicated in what patients?
A

Ketamine:

  1. Used in patients with risk for hypotension or bronchospasm since it increases blood pressure and is a bronchodilator.
  2. Toxicity causes increase in cerebral blood flow or emergence delirium.
  3. Contraindicated in patients with CLOSED HEAD INJURIES
17
Q

Clinical problems of IV Anesthetics:

  1. Depression of ____ and ____ drive.
  2. What does Ketamine cause?
  3. What does Etomidate cause?
A

Clinical problems of IV anesthetics:

  1. Depression of respiratory and cardiovascular drive.
  2. Ketamine - hallucinations and emergence delirium
  3. Etomidate causes adrenal suppression
18
Q

Which of the following can increase cerebral blood flow:

a. propofol
b. thiopental
c. ketamine
d. etomidate

A

Cerebral blood flow can be increased by ketamine

19
Q

Inhalation anesthetics are all part of what class?

A

Halogenated hydrocarbons

20
Q

NO: solubility? potentcy? speed of effects?

Halothane: solubility? potentcy? speed?

A

NO: very unsoluble, not very potent, but quick effects

Halothane: soluble, VERY potent, SLOW effects

21
Q

Desflurane: why is it not used for induction?

Sevoflurane: used on who? Why?

Nitrous oxide: MAC=?

A

Desflurane: strong airway irritant

Sevoflurane: used on children bc it doesnt irritate the airway

Nitrous oxide: MAC=105%

22
Q

Drugs to know?

A

Methohexital

Propofol

Etomidate

Ketamine

Halothane

Isoflurane/Enflurane

Sevoflurane

Desflurane

Nitrous oxide

23
Q

Important to know about:

Methohexital?

Etomidate?

Ketamine?

Isoflurane/Enflurane?

Sevoflurane?

Desflurane?

Nitrous oxide?

A

Methohexital - ECT and Barbs

Etomidate - cardiostable and adrenosuppression

Ketamine - cardiostable and increase cerebral BF

Isoflurane/Enflurane - inhalation agents

Sevoflurane - kids (doesnt irritate airway)

Desflurane - airway irritatne

Nitrous oxide - hallmark bc not very lipid soluble

24
Q

Local anesthetics prevent/relieve pain by ___ blocking nerve ____.

Local anethetics block what channels? Can affect all ___ tissues.

Myelinated vs. Unmyelinated: A-delta and C fibers? Role of both?

A

Local anesthetics prevent/relieve pain by reversibly blocking nerve conduction

Local anesthetics block fast voltage-gated sodium channels and can affect all exciteable tissues

A-delta (small myelinated) C (unmyelinated) –> both are affected by anasthetics and transmit pain

25
Q

What specific fibers are associated with pain?

What fibers are myelinated?

Put these in order in terms of fiber suceptibility to blockade by local anesthetics: pain fibers, motor fibers, autonomic fibers, sensory fibers

A

Pain: Adelta and C

Myelinated: A and B

Autonomic fibers> pain fibers > sensory > motor

26
Q

Lidocane has an ____ link.

Procaine has an ____ link.

Where are amide type local anesthetics broken down?

What happens to ester type?

A

Lidocaine: amide link

Procaine: ester link

Amide: broken down in liver

Ester: hydrolyzed

27
Q

Drugs with short duration vs. med vs. long?

A

Pro’s are short: procaine

PriMeL is medium: PRIlocain, mepivocaine, lidocaine

BERT is long: Bupivicaine, Etidocaine, Ropivacaine, and Tetracaine

28
Q

Metabolism of amides? Problem in who?

Metabolism of esters?

Addition of a vasoconstritor to local anesthetics will ___ systemic absorption, ___ duration of anesthesia, and ___ risk of systemic toxicity.

A

Amides - degraded by CYP450 (bad for severe hepatic disease)

Esters - degraded by plasma esterases

Addition of a vasoconstrictor to local anesthetics will decrease systemic absorption, prolong duration of anesthesia, and reduce risk of systemic toxicity

29
Q

Infiltration Anesthesia has a ___ dose. To note: buvicaine has a ___ ___ dose and can cause __ ____.

Differences between epidural and spinal anesthetics?

Adverse effects when bupivacain exceeds max dose?

What can etidocain induce? what is this good for?

A

maximal; buvicaine has a small maximal dose and cause CV collapse

Epidural takes longer to work and requires more drug than spinal

Buvicaine - CARDIOTOXIC (can cause death)

Etidocaine induces motor block - good for muscle relaxation

30
Q

What is the best topical anesthetic OTC?

Toxicity of local anesthetics:

  1. What does it do to the CNS?
  2. What does it do to the CV system?

Methemoglobinemia is a potential side effect of what drugs?

A

Benzocaine

  1. CNS stimulation (restlessness, tremor, convulsions) –> depression (drowsiness, sedation, respiratory failure)
  2. Causes DECREASED conduction/force of contraction/excitability

Methemoglobinemia could be a side effect of prilocaine and benzocaine

31
Q

BE ABLE TO RECOGNIZE THE STRUCTURE OF ACETYLCHOLINE

What is the sequence of paralysis? (5 things)

What is the sequence of recovery?

What does sugammadex do?

Example of a depolarizing neuromuscular blocker?

A

Paralysis: Muscles of fine movement –> limbs –> trunk –> intercostals –> diaphragm

Recovery: Diaphragm –> intercostals… (paralysis in reverse)

Sugammadex: inactivates local anesthetics

Succinylcholine

32
Q

Succinylcholine is a depolarizing muscle _____.

With the use of succinylcholine: beware in patients with extensive ___ or ___ ___ damage and in ____.

Succinylcholine can cause?!

A

Succinylcholine is a depolarizing muscle relaxant

Bewar in patients with extensive burns or soft tissue damage and in paraplegics

Can cause malignant hyperthermia

33
Q

How do you treat malignant hyperthermia?

Succinylcholine leads to ____. Reverse how?

Non-depolarizing neuromuscular blockade: give what?

A

Treat MH with dantrolene

Succinylcholine leads to fasciculations. Reverse by just letting the drug wear off

For non-depolarizing neuromuscular blockade: give anticholinesterase (kidney, blood, liver: competitive inhibitors)

Pharmacology (24 decks)

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