General Anesthetics I & II Flashcards Preview

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Flashcards in General Anesthetics I & II Deck (30):
1

Nitrous oxide has what chemical structure?

It is cyclic!

2

More potent anesthetics are __________ soluble in oil.

more

3

Which general anesthetics are more potent, nitrous oxide or halogenated compounds?

Halogenated compounds; in fact, nitrous oxide is only used in combination with other compounds

4

It used to be thought that general anesthetics interacted with the lipid layer, but research on luciferase contradicted this. Describe!

General anesthetics inhibit luciferase, which is intracellular. This indicates that general anesthetic must pass into cells.

5

What evidence suggests that general anesthetics must fit into a receptor pocket?

- Some compounds that are bigger but differ only in size (that is, they have similar chemical composition and properties) will not induce the anesthetic properties of smaller counterparts.

- Some anesthetics are fixed in membranes, whereas they would be freely diffusible if they just interacted with lipid membranes.

- General anesthetics are saturable, whereas they would not be if they were merely interacting with the lipid membrane.

- Only one enantiomer works, which would not be the case if volatile anesthetics only disrupted lipid membranes.

6

Halothane does what to GABA?

It prolongs GABA current.

7

At clinically relevant levels, what do general anesthetics do?

- Potentiate glycine channels
- Inhibition of acetylcholine receptors
- Potentiation of TASK-1 potassium channels

8

What concentration is needed to achieve anesthesia?

~ 100 mM

9

What are the stages of anesthesia?

I: analgesia
II: excitement, delirium
III: surgical anesthesia
IV: medullary paralysis and death

10

Describe the usefulness of knowing the oil:gas coefficient and blood:gas coefficient.

The oil:gas coefficient tells you potency, while the blood:gas coefficient tells you speed of onset and offset.

11

There are four phases of anesthesia uptake. List them and explain the properties that affect each.

- Phase I: inhalation (lung factors / ventilation rate)
- Phase II: uptake of blood from alveoli
- Phase III: uptake from blood to tissues
- Phase IV: distribution to tissues

12

Nitrous oxide has a _____________ blood:gas coefficient than the halogenated general anesthetics.

lower

13

The initial rise in arterial concentration of anesthetic _____________ with increase in pulmonary blood flow.

decreases

14

True or false: the primary route of elimination for volatile anesthetics is hepatic.

False – you breathe it out

15

The only gaseous anesthetic is ______.

nitrous oxide

16

What is the concentration effect of N2O?

N2O gets taken up faster than expected.

17

Describe diffusion hypoxia.

When anesthetic is terminated, the leaving N2O pushes oxygen out of the alveoli.

18

Which of the halogenated compounds has the lowest risk of hepatotoxic and nephrotoxic effects?

Isoflurane

19

The therapeutic indices of general anesthetics are __________.

extremely narrow – typically 2-4, meaning only twice the effective dose can kill someone

20

How is it possible to use general anesthetics with such a narrow therapeutic index?

There is a very steep dose-response curve, such that 99% of patients are anesthetized at 1.3 MAC.

21

What advantage did halothane have over the previous surgical anesthetic in use?

It is not flammable, and the previous anesthetic in common use – cyclopropane – was, occasionally resulting in operating room explosions.

22

Summarize the evidence that suggests that there is no receptor for volatile anesthetics.

- Drugs with specific receptor targets are effective at around 0.1 mM, while general anesthetics need to be at roughly 100 mM to work.

- There is no antidote/antagonist for volatile anesthetics.

23

The MAC is ___________ to the oil:gas coefficient.

inversely proportional

24

It is thought that volatile anesthetics interact with the _______________ of proteins.

lipophilic parts – both in transmembrane and intracellular proteins

25

True or false: general anesthetics lead to conduction block.

False. Anesthetized patients have normal action potential conduction.

26

Why is anesthetic uptake by fatty tissues slow?

Because the solubility of anesthetics in fat is high, and they can thus take in much anesthetic; also, fatty tissues are less well perfused than fat.

27

Describe the second-gas effect.

N2O gets pulled in faster than expected, and it can pull in another gas if co-administered (such as isoflurane).

28

For what side effects was chloroform discontinued?

Hepatotoxicity and cardiac arrhythmias

29

Desflurane has the benefit of _______________ but the drawback of _______________.

no liver toxicity; pungent odor which causes throat irritation

30

What is pharmacodynamically important about the acetylcholine-blocking drugs?

They don't cross the BBB! (Otherwise they would have terrible cortical effects.)

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