Anesthesia, Pharmacology Absite Flashcards

Front 1

What is the advantage of amide (contain "I" = lido, bupiva, mepiva) anestetics over ester (procaine, cocaine, tetracaine) anesthetics?

Back 1

PABA analog of ester anesthetics (procaine, cocaine, tetracaine) anesthetics => more likely to cause ALLERGIC RXN

Front 2

mechanism of amrinone

Back 2

Amrinone:
-Phosphodiesterase inhibitor
Inotrope, increases CO, decreases SVR

Front 3

ASA class 1 = _

Back 3

ASA class 1 =
healthy pt

Front 4

ASA class 2 = _

Back 4

ASA class 2 =
mild dz s/ limitation (HTN, DM, obesity, smokers)

Front 5

ASA class 3 = _

Back 5

ASA class 3 =
severe dz (stable angina, previous MI, moderate COPD)

Front 6

ASA class 4 = _

Back 6

ASA class 4 =
disease that is severe constant treat to life (unstable angina, renal failure, liver failure, severe COPD)

Front 7

ASA class 5 = _

Front 8

ASA class 6 = _

Back 8

ASA class 6 = organ donor

Front 9

65M on dialysis for renal failure undergoes elective AAA repair
-AAA class = _

Back 9

ASA class 3 =
severe dz (stable angina, previous MI, moderate COPD)

Front 10

50M c/ moderate COPD has ASA class _

Back 10

This patient is ASA Class III.
1. Healthy patient
2. Mild systemic disease e.g. HTN, DM
3. Severe systemic disease e.g. previous MI, stable angina, etc.
4. Severe systemic disease that is a constant threat to life e.g. renal/liver failure, unstable angina, severe COPD
5. Not expected to live 24 hours irrespective of operation
6. organ donor
An e is added to the status number to designate an emergency operation.

Front 11

mechanism of aspirin

Back 11

Aspirin:
-Irreversibly binds CYCLOOXYGENASE
-Effective for life of platelets = 7 days

Front 12

Max bupivacaine dose

Back 12

Max bupivacaine dose = 2.5 mg/Kg

Front 13

Revised Cardiac Risk Index: 6 risk factors are ……

Score _ => non-invasive stress testing
Score

Back 13

Revised Cardiac Risk Index: 6 risk factors
1. hx heart failure
2. hx CV dz
3. hx ischemic heart dz
4. IDDM
5. Pre-op Cr >2 mg/dL
6. High-risk surgery (intrathoracic, intraperitoneal, suprainguinal vascular)

Score of 2 (and definitely 3) => periop beta blockade
Score 3 or 2 + indeterminate functoinal status => non-invasive stress testing (cath if it shows severe coronary dz)

Front 14

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Back 14

Cis-atracurium is metabolized via Hoffman degradation (rxn of amide/RCONH2 -> amine/RNH2), not dependent on renal or liver fx,

Front 15

Neuromuscular blocker _ is metabolized 80% to laudanosine via Hoffman degradation

Back 15

Cisatracurium = 80% metabolized y Hoffman rearrangement/degradation
primary amide (R-C=O=NH2)-> primary amine (R-NH2)
-dependent on pH, temp of plasma
-LESS RISK FOR PT'S C/ RENAL/HEPATIC FAILURE

Front 16

Antibiotic _ can prolong neuromuscular blockade

Back 16

Clindamycin:
-Prolongs neuromuscular blockade

Front 17

patient undergoing routine lap chole develops severe hypotension, tachycardia, decreased ET CO2. (+) bilat breath sounds
-Suspect..

Back 17

CO2 embolus -> impaired gas exchange @ alveolar level -> increasing EtCO2.
-Tx: trendelenburg, L side down, 100% O2, increase minute ventilation
-Continue CPR for a long time if needed to reabsorb CO2
(if breath sounds are decreased, suspect disconnection from vent)

Front 18

Iodinated contrast => _% rate of adverse rxns
(vs. _% c/ low-osmolar non-ionic media)
_ = #1 = 4.6%
70% of rxns occur w/in _ min
_x risk c/ asthma, _x risk c/ contrast allergy or atopy

Back 18

Iodinated contrast => 13% rate of adverse rxns
(vs. 3% c/ low-osmolar non-ionic media)
Nausea = #1 = 4.6%
-Urticaria 3.2%, Itching 3%, Heat sensation 2.3%
Dyspnea 0.17%, acute hypotension 0.1%, LOX 0.02%, cardiac arrest 0.00004%
70% of rxns occur w/in 5 min
8x risk c/ asthma, 5x risk c/ contrast allergy or atopy

Front 19

Avoid pain med _ if pt is taking MAOI

Back 19

Demerol:
-Avoid for pts on MAOIs

Front 20

mechanism of digoxin

Back 20

Digoxin:
-Glycoside
-Inhibits Na-K ATPase -> increase Ca in heart
-Slows AV node conduction
-Inotrope, but doesn’t increase O2 consumption
-Decreases splanchnic flow -> ass'd c/ ischemic gut
-Avoid hypokalemia

Front 21

Dilated/hypertrophic cardiomyopathy = contraindication for epidural b/c…

Back 21

Epidurals:
-Decrease afterload
-Dilated/hypertrophic cardiomyopathy = absolute contraindication (ventricle will collapse on itself)

Front 22

Respiratory depression with epidural is likely 2/2 drug _

Back 22

Morphine in epidural -> respiratory depression
(less likely with Dilaudid)
-Morphine in epidural does NOT cause low BP b/c no histamine-releasing mast cells in CSF

Front 23

etomidate: pros + cons

Back 23

Etomidate:
-fewer hemodyn changes and faster acting than other induction agents
-long-term uses causes adrenocortical suppression

Front 24

Halothane: toxic to the _

Back 24

Halothane:
-Hepatic toxicity

Front 25

mechanism of indomethacin

Back 25

Indomethacin:
-Blocks PG production
-Used to close PDA (effective in 70%)
-Decreases renal blood flow

Front 26

_ = pain med that increases cardiac work, O2 use, secretions

Back 26

Ketamine;
-Increases cardiac work, O2 use, secretions
-No resp depression
-SE: hallucinations

Front 27

Max lidocaine dose:
-Alone
-with Epi

Back 27

Max lidocaine dose:
-5 mg/Kg = 0.5 mL/Kg of 1% lidocaine
-with Epi; 7 mg/Kg

Front 28

Stages of lidocaine toxicity

Back 28

Lidocaine toxicity:
1. Perioral paresthesias
2. Visual/auditory hallucinations
3. Sedation -> unconsciousness
4. Seizures
5. Resp depression
6. Cardiac arrhythmias -> CV collapse

Front 29

Local anesthetic mechanism

Back 29

Local anesthetics increase AP threshold in peripheral nerves =>
harder to create an AP
-work poorly in acidic environments

Front 30

Hypotension, bradycardia with epidural is 2/2 _

Back 30

LOCAL anesthetic in epidural -> hypotension, bradycardia
-Morphine is NOT the cause (CSF does not have histamine-releasing cells to produce that SE)

Front 31

is anesthetic MAC high or low if fast onset?

Back 31

MAC = amount of anesthetic for which 50% of patients move c/ incision
-LOW MAC: SLOW onset, more lipid soluble, more potent
-HIGH MAC (e.g. nitrous): faster onset, less lipid soluble, less potent

Front 32

how is anesthetic MAC defined?

Back 32

MAC = amount of anesthetic for which 50% of patients move c/ incision
-LOW MAC: SLOW onset, more lipid soluble, more potent
-HIGH MAC (e.g. nitrous): faster onset, less lipid soluble, less potent

Front 33

_ is related to defective ryanodine receptor on sarcoplasmic reticulum, which controls Ca release

Back 33

MALIGNANT HYPERTHERMIA: -
Defective ryanodine receptor on SR =defect in Ca metabolism ->
exposure to succinylcholine, inh anesthetic (sevo/iso/enflurane, halothane) ->
prolonged muscle excitation-contraction syndrome
1. Increase in end-tidal CO2
2. tachycardia, fever, rigidity, acidosis, hyperkalemia
-Tx: stop precipitating anesthetic/paralytic, Dantrolene (decouples excitation-contraction complez), cooking blankets, HCO3-, glucose, O2

Front 34

"medical adrenalectomy" is accomplished with 2 drugs…

Back 34

"medical adrenalectomy" is accomplished with Metyrapone, Aminoglutethimide

Front 35

Methoxyfluorane: toxic to the _

Back 35

Methoxyfluorane:
-renal toxicity

Front 36

mechanism of metoclopramide

Back 36

Metoclopramide = Reglan = DA blocker
-Increases LE sphincter tone, gastric motility

Front 37

how is misoprostil protective against peptic ulcer dz?

Back 37

Misoprostil:
-Replaces PGE2 (cytoprotective) for pt on NSAIDS, to reduce PUD

Front 38

narcotic drug _ has SE of histamine release

Back 38

Morphine:
-SE: histamine release
-active metabolites can build up in pts c/ renal failure

Front 39

Non-depolarizing paralytics are reversed by drug _

Back 39

NEOSTIGMINE
-acetylcholinesterase inhibitor
-increase acetyl choline => conteract the competitive inhibition of the non-depolarizing paralytics

Front 40

how do non-depolarizing neuromuscular blockers work?

Back 40

Non-depolarizing NM blockers completitively inhibit ACh R's ->
reversed c./ Neostigmine = acetylcholinesterase inhibitor

Front 41

Vecuronium, Rocuronium, Atracurium, Mivacurium:
-mechanism
-_-acting
-#1 side effect of atracurium, mivacurium
-Advantage of vecuronium, rocuronium

Back 41

Intermediate-acting non-depolarizing inhibitors @ neuromuscular junction
-Main SE of atracurium, mivacurium -= histamine release

Front 42

mechanism of nitroglycerin = primarily acts on _

Back 42

Nitroglycerin:
-Primarily relaxes veins

Front 43

Nitrous oxide = fastest working inhlaed anesthetic
-High or low MAC?
-More or less lipid soluble?

Back 43

Nitrous oxide = fastest working inhlaed anesthetic
-Less lipid soluble => FAST onset, high MAC, less potent

Front 44

_ = long-acting somatostatin analog

Back 44

Octreotide = long-acting somatostatin analog

Front 45

mechanism of omeprazole

Back 45

Omepraszole:
-Blocks Na/H ATPase on parietal cells
-Ass'd c/ entrochromaffin hyperplasia in rats
-No e/o carcinogenesis in humans

Front 46

Pancuranium is a non-depolarising muscle relaxant (as oppose to Succinylcholine). It is also an ingredient of lethal injection e.g. capital punishment. What is the most common side effect of pancuranium?

Back 46

The most common side-effect of pancuranium is TACHYcardia, and thus increased cardiac output and hypertension.
Bradycardia is a side-effect of succinylcholine.

Front 47

Pancuronium:
-mechanism
-short or long acting?
-#1 side effect

Back 47

Pancuronium:
-Long-acting (1 hr) non-depolarizing inhbitor @ neuromuscular junction
(other 2 are doxacurium, pipecuronium)
-TACHYCARDIA = #1 side effect
Muscle weakness c/ long-term use

Front 48

Pancuronium: most common SE = _

Back 48

Pancuronium = non-depolarizing NM junction blocker
-SE: tachycardia

Front 49

1st muscles to relax after paralytics, last to recover are _

Back 49

Neck/Face muscles = 1st to relax after paralytics, last to recover

Front 50

Last muscles to relax after paralytics, 1st to recover are _

Back 50

Diaphragm muscles = last to relax after paralytics, 1st to recover

Front 51

Sodium nitroprusside: monitor for _ toxicity

Back 51

Sodium nitroprusside:
-relaxes arteries and veins
-watch for CN toxicity

Front 52

_ = non-competitive (depolarizing) inhibitor @ neuromuscular junction
Pros
Cons

Back 52

Succinyl choline = non-competitive (depolarizing) inhibitor @ neuromuscular junction
-Short duration, quickly degraded by cholinesterases
Can't be reversed

Front 53

Succinylcholine: why is it so fast on/off?

Back 53

Succinylcholine
-Non-competitive (depolarizing) inhibitor @ neuromuscular junction
-Generalized contractions
-Fast on/off, quickly degraded by cholinesterases
-Can't be reversed
-Risks of aspiration, glaucoma

Front 54

Vasopressin:
-Give with _ to avoid _

Back 54

Vasopressin:
-Reduces splanchnic blood flow, portal flow ~40%
-Useful in GI bleed
-Give with beta blocker to avoid angina

Front 55

most common organisms to grow from early post-op wound infection (i.e.PACU fever, gray watery discharge)

Back 55

Clostridium perfringens, beta hemolytic Grp A strep = pyogenes

Front 56

What drug should be used for the treatment of local anesthetic induced arrhythmias?

Back 56

Bretylium should be used for the treatment of local anesthetic induced arrhythmias

Front 57

what is the effect of halogenated anesthetics (e.g. enflurane) on ICP?

Back 57

Most halogenated anesthetics produce cerebral vasodilation leading to an increase in ICP.

Front 58

A 45 yo male with history of ESRD and on dialysis presents as a trauma activation with GCS of 6. You decide to intubate the patient and want to use a non-depolarizing muscle relaxant. Which is the best choice?

Back 58

Cis-atracurium is metabolized via Hoffman degradation (rxn of amide/RCONH2 -> amine/RNH2), not dependent on renal or liver fx