Drugs Used in Anesthesia Flashcards
What does MAC stand for?
minimal alveolar anesthetic concentration
What does the MAC value mean when assessing inhaled anesthetics mean?
in essence the ED50 amount of drug effective in 50% population; therefore it is a measure of potency.
the lower the MAC the more potent the drug is
What does the blood-gas ratio indicate?
rate of onset and recovery
the lower the blood gas ratio the faster the onset and recovery of the drug
What is midazolam used for in regards to IV anesthesia?
- preoperative sedation
- anterograde amnesia
Uses of propofol?
- induction and maintenance of anesthesia
- antiemetic
- CNS and cardiac depressant
What class of drugs would fentanyl fall under?
opiate
Use for Fentanyl?
induction and maintenance of anesthesea
MOA ketamine?
NMDA receptor antagonist
S/E ketamine?
cardiovascular stimulation
inc. intracranial pressure
hallucination
Name some IV anesthetics?
midazolams (and other BZs)
Propofol
Fentanyl
ketamine
What are the 2 types of local anesthetics?
esters and amides
How do you remember drugs that are esters from amides?
Amides has I in name. They are local anesthetics with 2 I’s in them
Esters has no I; they are local anesthetics with 1 I in their name
TTD is found where and MOA?
tetrodotoxin (from puffer fish)
blocks activated Na+ channels
Saxitoxin is found where and what is the MOA?
- algae toxin, “red tide”
- block activated Na+ channels
How do local anesthetics use MOA and ionization to effect change on sodium channels?
the nonionized form of the drug crosses the axonal membrane; then once inside the nerve the ionized for blocks inactivated Na+ channels
Which nerve fibers are most sensivitive to blockade by local anesthetics?
smaller diameter
What is the order of sensitivity to nerve fibers blockade by local anesthetics? What is the order at which they recover?
type B and C > type Ad > type Ab and Ag > type Aa
recovery is in reverse
B& C pain fibers
Ad = pain and T
Ab and Ag = touch and pressure
Aa=motor neurons
S/E of local anesthetics.
neurotoxicity
cardiovascular toxicity (bradycardia)
Allergies (esters via PABA formation)
What is the prototype non depolarizing competitive antangoist NM relaxant drug?
rocuronium
Train of four effect with non depolarizing nicotinic antagonists?
shows fade; progressive paralysis (face, limbs, respiratory muscle)
Describe metabolism of atracurium. How may its metabolism benefit a patient? Drawbacks?
Hoffman reaction.
spontaneous inactivation to laudanosine so safe in hepatic or renal impairment
Laudanosine may cause seizures
Cisatracurium benefit over atracurium?
forms less laudanosine
Describe phase one of depolarizing (non competitive) nicotinic agonists (succinylcholine)?
depolarization, fasciculation, prolong depolarization, flaccid paralysis
Describe phase II of succinylcholine use?
desensitization
Name some centrally acting sk. muscle relaxants and MOA
BZs through GABA - A receptors
Baclofen through GABA-B receptors
Uses for centrally acting sk muscle relaxants?
spasticity
Malignant hyperthermia symptoms?
muscle rigidity, hyperthermia, hypertension, acidosis, and hyperkalemia
Genotypic susceptibility to malignant hyperthermia may be because of what?
encoding ryanodine receptors and/or a protein component of L-type calcium channel in sk muscle
Dantrolene MOA?
decreases sk. muscle contractility by blocking Ca2+ release from SR
