Anesthetics

Question 1

What are the inhaled anesthetics?

Answer 1

Nitric oxide
Isoflurane
Sevoflurane

Question 2

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

Answer 2

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

Question 3

How is nitric oxide used as an anesthetics?

Answer 3

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

Question 4

What does blood/gas ratio means for inhaled anesthetics?

Answer 4

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

Question 5

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

Answer 5

More lipid soluble—>lower MAC—>more potent

Question 6

MAC is lower in what population?

Answer 6

Elderly/the presence of opioid or sedative

Question 7

What is midazolam used for and what is its effect?

Answer 7

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

Question 8

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

Answer 8

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

Question 9

How is etomidate compares with propofol?

Answer 9

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

Question 10

What is fentanyl?

Answer 10

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

Question 11

What is the mechanism of ketamine?

Answer 11

NMDA blocker—>IV anesthesia—>induction of anesthesia

Disassociative anesthesia—>hallucination

Question 12

What is the IV anesthesia for asthmatics?

Answer 12

Ketamine

Question 13

How do local anesthetics work?

Answer 13

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

Question 14

What toxins work similarly to local anesthetics?

Answer 14

Tetrodotoxin and saxitoxin (both from puffer fish)

Question 15

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

Answer 15

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

Question 16

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

Answer 16

They target the fiber that is firing the fastest

Question 17

What kind of fiber is most sensitive to local anesthetics?

Answer 17

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

Question 18

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

Answer 18

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

Question 19

Which class of local anesthetics cause allergy and why?

Answer 19

Esters—>they form PABA

Question 20

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

Answer 20

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

Question 21

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

Answer 21

Trick question—>NO

Question 22

What are the nondepolarizing skeletal muscle relaxants?

Answer 22

“curium” “curonium”
Atracurium
Mivacurium
Pancuronium

Question 23

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

Answer 23

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

Question 24

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

Answer 24

Succinylcholine--->noncompetitive Nm agonist 
Phase I (initial depolarization--->flaccid paralysis)---->phase II (desensitization)

Question 25

What group of drugs might increase phase I of succinylcholine?

Answer 25

AChE inhibitors

Question 26

If a pt takes a long time to recover from succinylcholine, what do you suspect?

Answer 26

Pt might have atypical pseudocholinesterase (can’t metabolize succinylcholine sufficiently)

Question 27

What are the 2 side effects of succinylcholine and how do they occur?

Answer 27

Hyperkalemia—>Na rushes into the muscles cells and K leaks out
Malignant hyperthermia—>muscle rigidity (life threatening)

Question 28

Which 3 syndromes present with malignant hyperthermia and muscle rigidity?

Answer 28

Malignant hyperthermia as a side effect of succinylcholine
Serotonin syndrome
NMS as side effect from typical antipsychotic

Question 29

What kind of pt is more susceptible for malignant hyperthermia from succinylcholine?

Answer 29

Pt with mutation in genes that code ryanodine receptors or part of L type Ca channel in skeletal muscle?

Question 30

What drug is used to treat malignant hyperthermia from succinylcholine?

Answer 30

Dantrolene—>block Ca release from SR in skeletal muscle cells

Question 31

What are the 2 centrally acting Nm blockers?

Answer 31

Benzo—>GABAa (Cl channel)
Baclofen—>GABAb (K channel)
Use for spasticity