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58 Cards in this Set
- Front
- Back
What is the advantage of amide (contain "I" = lido, bupiva, mepiva) anestetics over ester (procaine, cocaine, tetracaine) anesthetics?
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PABA analog of ester anesthetics (procaine, cocaine, tetracaine) anesthetics => more likely to cause ALLERGIC RXN
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mechanism of amrinone
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Amrinone:
-Phosphodiesterase inhibitor Inotrope, increases CO, decreases SVR |
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ASA class 1 = _
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ASA class 1 =
healthy pt |
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ASA class 2 = _
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ASA class 2 =
mild dz s/ limitation (HTN, DM, obesity, smokers) |
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ASA class 3 = _
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ASA class 3 =
severe dz (stable angina, previous MI, moderate COPD) |
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ASA class 4 = _
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ASA class 4 =
disease that is severe constant treat to life (unstable angina, renal failure, liver failure, severe COPD) |
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ASA class 5 = _
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ASA class 6 = _
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ASA class 6 = organ donor
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65M on dialysis for renal failure undergoes elective AAA repair
-AAA class = _ |
ASA class 3 =
severe dz (stable angina, previous MI, moderate COPD) |
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50M c/ moderate COPD has ASA class _
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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. |
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mechanism of aspirin
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Aspirin:
-Irreversibly binds CYCLOOXYGENASE -Effective for life of platelets = 7 days |
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Max bupivacaine dose
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Max bupivacaine dose = 2.5 mg/Kg
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Revised Cardiac Risk Index: 6 risk factors are ……
Score _ => non-invasive stress testing Score |
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) |
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"
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Cis-atracurium is metabolized via Hoffman degradation (rxn of amide/RCONH2 -> amine/RNH2), not dependent on renal or liver fx,
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Neuromuscular blocker _ is metabolized 80% to laudanosine via Hoffman degradation
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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 |
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Antibiotic _ can prolong neuromuscular blockade
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Clindamycin:
-Prolongs neuromuscular blockade |
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patient undergoing routine lap chole develops severe hypotension, tachycardia, decreased ET CO2. (+) bilat breath sounds
-Suspect.. |
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) |
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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 |
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 |
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Avoid pain med _ if pt is taking MAOI
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Demerol:
-Avoid for pts on MAOIs |
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mechanism of digoxin
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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 |
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Dilated/hypertrophic cardiomyopathy = contraindication for epidural b/c…
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Epidurals:
-Decrease afterload -Dilated/hypertrophic cardiomyopathy = absolute contraindication (ventricle will collapse on itself) |
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Respiratory depression with epidural is likely 2/2 drug _
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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 |
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etomidate: pros + cons
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Etomidate:
-fewer hemodyn changes and faster acting than other induction agents -long-term uses causes adrenocortical suppression |
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Halothane: toxic to the _
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Halothane:
-Hepatic toxicity |
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mechanism of indomethacin
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Indomethacin:
-Blocks PG production -Used to close PDA (effective in 70%) -Decreases renal blood flow |
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_ = pain med that increases cardiac work, O2 use, secretions
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Ketamine;
-Increases cardiac work, O2 use, secretions -No resp depression -SE: hallucinations |
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Max lidocaine dose:
-Alone -with Epi |
Max lidocaine dose:
-5 mg/Kg = 0.5 mL/Kg of 1% lidocaine -with Epi; 7 mg/Kg |
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Stages of lidocaine toxicity
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Lidocaine toxicity:
1. Perioral paresthesias 2. Visual/auditory hallucinations 3. Sedation -> unconsciousness 4. Seizures 5. Resp depression 6. Cardiac arrhythmias -> CV collapse |
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Local anesthetic mechanism
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Local anesthetics increase AP threshold in peripheral nerves =>
harder to create an AP -work poorly in acidic environments |
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Hypotension, bradycardia with epidural is 2/2 _
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LOCAL anesthetic in epidural -> hypotension, bradycardia
-Morphine is NOT the cause (CSF does not have histamine-releasing cells to produce that SE) |
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is anesthetic MAC high or low if fast onset?
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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 |
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how is anesthetic MAC defined?
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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 |
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_ is related to defective ryanodine receptor on sarcoplasmic reticulum, which controls Ca release
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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 |
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"medical adrenalectomy" is accomplished with 2 drugs…
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"medical adrenalectomy" is accomplished with Metyrapone, Aminoglutethimide
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Methoxyfluorane: toxic to the _
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Methoxyfluorane:
-renal toxicity |
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mechanism of metoclopramide
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Metoclopramide = Reglan = DA blocker
-Increases LE sphincter tone, gastric motility |
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how is misoprostil protective against peptic ulcer dz?
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Misoprostil:
-Replaces PGE2 (cytoprotective) for pt on NSAIDS, to reduce PUD |
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narcotic drug _ has SE of histamine release
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Morphine:
-SE: histamine release -active metabolites can build up in pts c/ renal failure |
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Non-depolarizing paralytics are reversed by drug _
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NEOSTIGMINE
-acetylcholinesterase inhibitor -increase acetyl choline => conteract the competitive inhibition of the non-depolarizing paralytics |
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how do non-depolarizing neuromuscular blockers work?
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Non-depolarizing NM blockers completitively inhibit ACh R's ->
reversed c./ Neostigmine = acetylcholinesterase inhibitor |
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Vecuronium, Rocuronium, Atracurium, Mivacurium:
-mechanism -_-acting -#1 side effect of atracurium, mivacurium -Advantage of vecuronium, rocuronium |
Intermediate-acting non-depolarizing inhibitors @ neuromuscular junction
-Main SE of atracurium, mivacurium -= histamine release |
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mechanism of nitroglycerin = primarily acts on _
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Nitroglycerin:
-Primarily relaxes veins |
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Nitrous oxide = fastest working inhlaed anesthetic
-High or low MAC? -More or less lipid soluble? |
Nitrous oxide = fastest working inhlaed anesthetic
-Less lipid soluble => FAST onset, high MAC, less potent |
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_ = long-acting somatostatin analog
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Octreotide = long-acting somatostatin analog
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mechanism of omeprazole
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Omepraszole:
-Blocks Na/H ATPase on parietal cells -Ass'd c/ entrochromaffin hyperplasia in rats -No e/o carcinogenesis in humans |
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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?
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The most common side-effect of pancuranium is TACHYcardia, and thus increased cardiac output and hypertension.
Bradycardia is a side-effect of succinylcholine. |
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Pancuronium:
-mechanism -short or long acting? -#1 side effect |
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 |
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Pancuronium: most common SE = _
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Pancuronium = non-depolarizing NM junction blocker
-SE: tachycardia |
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1st muscles to relax after paralytics, last to recover are _
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Neck/Face muscles = 1st to relax after paralytics, last to recover
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Last muscles to relax after paralytics, 1st to recover are _
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Diaphragm muscles = last to relax after paralytics, 1st to recover
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Sodium nitroprusside: monitor for _ toxicity
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Sodium nitroprusside:
-relaxes arteries and veins -watch for CN toxicity |
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_ = non-competitive (depolarizing) inhibitor @ neuromuscular junction
Pros Cons |
Succinyl choline = non-competitive (depolarizing) inhibitor @ neuromuscular junction
-Short duration, quickly degraded by cholinesterases Can't be reversed |
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Succinylcholine: why is it so fast on/off?
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Succinylcholine
-Non-competitive (depolarizing) inhibitor @ neuromuscular junction -Generalized contractions -Fast on/off, quickly degraded by cholinesterases -Can't be reversed -Risks of aspiration, glaucoma |
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Vasopressin:
-Give with _ to avoid _ |
Vasopressin:
-Reduces splanchnic blood flow, portal flow ~40% -Useful in GI bleed -Give with beta blocker to avoid angina |
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most common organisms to grow from early post-op wound infection (i.e.PACU fever, gray watery discharge)
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Clostridium perfringens, beta hemolytic Grp A strep = pyogenes
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What drug should be used for the treatment of local anesthetic induced arrhythmias?
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Bretylium should be used for the treatment of local anesthetic induced arrhythmias
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what is the effect of halogenated anesthetics (e.g. enflurane) on ICP?
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Most halogenated anesthetics produce cerebral vasodilation leading to an increase in ICP.
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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?
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Cis-atracurium is metabolized via Hoffman degradation (rxn of amide/RCONH2 -> amine/RNH2), not dependent on renal or liver fx
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