Anesthetics Flashcards

1
Q

What are the inhaled anesthetics?

A

Nitric oxide
Isoflurane
Sevoflurane

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2
Q

What is MAC (minimal alveolar concentration) in terms of inhaled anesthetics? and how is it related to potency?

A

Minimal alveolar con. when 50% of pt do not response surgical stimulus
High MAC—>lower potency

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3
Q

How is nitric oxide used as an anesthetics?

A

Use with other inhaled anesthetics since it has a really high MAC

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4
Q

What does blood/gas ratio means for inhaled anesthetics?

A

The lower the ratio—>the faster the onset/recovery

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5
Q

The more lipid or water soluble the anesthetics, the lower the MAC?

A

More lipid soluble—>lower MAC—>more potent

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6
Q

MAC is lower in what population?

A

Elderly/the presence of opioid or sedative

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7
Q

What is midazolam used for and what is its effect?

A
IV anesthetics (short acting benzo)--->preoperative sedation
Anterograde amnesia (don't remember anything after taking the drug)--->date rape drug or use it before colonoscopy
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8
Q

What is propofol and its mechanism? can you use it for pt with pre existing cardiac disease?

A

IV anesthetics for induction and maintenance of anesthesia
GABAa agonist
Antiemetic
No—>it is a cardiac depressant

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9
Q

How is etomidate compares with propofol?

A

All GABAa agonist but etomidate is not a cardiac depressant—>use for pt with pre existing cardiac disease

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10
Q

What is fentanyl?

A

IV anesthesia (opiate) use for induction and maintenance of anesthesia

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11
Q

What is the mechanism of ketamine?

A

NMDA blocker—>IV anesthesia—>induction of anesthesia

Disassociative anesthesia—>hallucination

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12
Q

What is the IV anesthesia for asthmatics?

A

Ketamine

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13
Q

How do local anesthetics work?

A

Weak bases—>basic environment (nonionized form) to cross axonal membrane—>then ionized form to be active—>prolong inactivated state of the Na channel—>prevent them from returning to rest

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14
Q

What toxins work similarly to local anesthetics?

A

Tetrodotoxin and saxitoxin (both from puffer fish)

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15
Q

What are the 2 classes of local anesthetics and how to distinguish them? and how are they metabolized?

A

Esters—>have one “i” in their names—>metabolized by plasma and tissue esterases
Amide—>have more than one “i” in their names—>metabolized by liver amidases

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16
Q

What are the similarity between antiarrhythmia/antiepileptic/local anesthesia in terms of nerve fiber sensitivity?

A

They target the fiber that is firing the fastest

17
Q

What kind of fiber is most sensitive to local anesthetics?

A

The smaller/faster the more sensitive
Type B/C (pain)—>type A delta—>type A beta and gamma—>type A alpha (motor)
Recovery is the reverse

18
Q

Local anesthetics should be taken with __ to prevent it from entering the systemic circulation? and which local anesthetics do not need to do that?

A

Alpha 1 agonist (vasoconstrict)
Cocaine does not need to be taken with alpha 1 agonist—>it blocks Na channel and also prevent uptake of NE (vasoconstrict)—>nasal ischemia

19
Q

Which class of local anesthetics cause allergy and why?

A

Esters—>they form PABA

20
Q

How do nondepolarizing skeletal muscle relaxants work? how do you reverse the affects? what muscles do they work on?

A

Block the 2 alpha subunits of Nm receptor—>competitive antagonist
Reverse the affect with AChE inhibitors
Only skeletal muscles—>no cardiac and smooth muscle

21
Q

Do nondepolarizing skeletal muscle relaxants have any CNS effects? if yes what are they?

A

Trick question—>NO

22
Q

What are the nondepolarizing skeletal muscle relaxants?

A

“curium” “curonium”
Atracurium
Mivacurium
Pancuronium

23
Q

Which nondepolarizing Nm blockers can be used with pt with liver/renal disease? and why?

A

Atracurium—>spontaneous metabolize to laudanosine—>may cause seizure

24
Q

What is the depolarizing Nm blocker? how does it work?

A
Succinylcholine--->noncompetitive Nm agonist 
Phase I (initial depolarization--->flaccid paralysis)---->phase II (desensitization)
25
What group of drugs might increase phase I of succinylcholine?
AChE inhibitors
26
If a pt takes a long time to recover from succinylcholine, what do you suspect?
Pt might have atypical pseudocholinesterase (can't metabolize succinylcholine sufficiently)
27
What are the 2 side effects of succinylcholine and how do they occur?
Hyperkalemia--->Na rushes into the muscles cells and K leaks out Malignant hyperthermia--->muscle rigidity (life threatening)
28
Which 3 syndromes present with malignant hyperthermia and muscle rigidity?
Malignant hyperthermia as a side effect of succinylcholine Serotonin syndrome NMS as side effect from typical antipsychotic
29
What kind of pt is more susceptible for malignant hyperthermia from succinylcholine?
Pt with mutation in genes that code ryanodine receptors or part of L type Ca channel in skeletal muscle?
30
What drug is used to treat malignant hyperthermia from succinylcholine?
Dantrolene--->block Ca release from SR in skeletal muscle cells
31
What are the 2 centrally acting Nm blockers?
Benzo--->GABAa (Cl channel) Baclofen--->GABAb (K channel) Use for spasticity