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IV Drugs Flashcards

1
Q

Describe the metabolism of NMBs

A

Succinylcholine - plasma cholinesterase
Atracurium / Cisatracurium - Hofmann elimination
Vecuronium / Rocuronium - primarily hepatic
Pancuronium - primarily renal

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2
Q

List the cardioselective B blockers

A

Block only B1 receptors

“BEAM”

Betaxolol
Bisoprolol
Esmolol
Atenolol
Acebutolol
Metoprolol
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3
Q

Which drugs are contraindicated in Parkinson’s disease?

A

Drugs which may produce extrapyramidal effects such as dopamine antagonists droperidol, promethazine; and metoclopramide (dopamine and serotonin antagonist)

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4
Q

Describe the solubility of Midazolam

A

Water-soluble drug that is converted to a lipid-soluble drug when exposed to the blood’s pH

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5
Q

Describe the effects of anticholinergics (Atropine, Glyco, Scop)

A

Decreased gastric acid secretion

Decreased salivary secretion

Decreased LES tone

Tachycardia

Mydriasis (pupil dilation)

May cause urinary retention

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6
Q

Which anticholinesterase drug can cross the BBB?

A

Physostigmine is a tertiary amine and is able to cross the BBB (useful in treating central anticholinergic syndrome)

Neostigmine, Pyridostigmine, and Edrophonium are quarternary ammonium compounds and cannot cross the BBB

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7
Q

What makes Meperidine unique?

A

Meperidine is an opioid that is structurally similar to atropine and possess mild anticholinergic properties. Instead of the usual bradycardia seen with opioids, tachycardia can be seen with Meperidine. Meperidine can also cause decreases in contractility at large doses.

Normeperidine is a metabolite of Meperidine and can lead to delirium and seizures, especially in patients with renal or hepatic impairment

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8
Q

Does Ketamine have any active metabolites?

A

Norketamine, which is about 1/3 as potent at Ketamine

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9
Q

How does Ephedrine work to increase BP?

A

Indirectly by stimulating the release of norepinephrine from sympathetic nerve fibers and to a lesser degree, by directly binding to adrenergic receptors

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10
Q

Which induction agent is most likely to cause myocardial depression? Why?

A

Thiopental

Dose dependent negative inotropic effect results from a decrease in calcium influx in the myocardium

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11
Q

What drug should be avoided in patients taking Ecothiophate for glaucoma?

A

Succinylcholine, as it’s effects can be prolonged by Ecothiophate’s inhibition of acetylcholinesterase

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12
Q

Which muscle relaxant causes slight histamine release?

A

Atracurium

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13
Q

Termination of action of norepinephrine is achieved primarily through what mechanism?

A

80% of released norepinephrine rapidly undergoes reuptake into the sympathetic nerve terminals (uptake 1) and reenters storage vesicles for future use

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14
Q

How does Metoclopramide (Reglan) work?

A

It is a dopamine antagonist that increases lower esophageal sphincter tone and stimulates gastric and upper GI tract motility

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15
Q

How much will administration of Succinylcholine raise serum [K+]?

A

0.5 mEq/L

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16
Q

What conditions or drugs can enhance neuromuscular blockade?

A

Volatile anesthetics

Aminoglycoside antibiotics (Tobra-/Genta-/Neo-/Streptomycin)

Magnesium

Local anesthetics

Furosemide

Dantrolene

Calcium channel blockers

Lithium

Hypothermia

Hypokalemia

Acidosis

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17
Q

Laudanosine is a metabolite of which drug?

A

Atracurium

Laudanosine is a tertiary amine that can cross the BBB and cause CNS stimulation at very high levels

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18
Q

Pre-treatment with a non-depolarizing muscle relaxant will have what effect on the expected side effects of Succinylcholine?

A 
Attenuates, but does not eliminate:
Cardiac dysrhythmias
Elevations in infra gastric pressure
Elevations of ICP
Myalgias

Does not eliminate hyperkalemia

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19
Q

List the order of onset of anticholinesterase drugs

A

Edrophonium (1 to 2 minutes)
Neostigmine (7 to 11 minutes)
Pyridostigmine (16 minutes)

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20
Q

List some conditions that may lead to an increased hyperkalemic response to Succinylcholine

A 
Denervation injuries
Burns
Acute upper motor neuron injuries (stroke)
Muscle trauma
Severe abdominal infections

Risk usually peaks 10 to 50 days after injury, but should be avoided if possible anytime after 24 hours from injury

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21
Q

What is the percentage of neuromuscular receptors which may be blocked and still allow a 5 second head lift?

A

50% (considered adequate recovery)

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22
Q

What is pseudocholinesterase? Where is it produced? What is its half-life?

A

Pseudocholinesterase (also known as plasma cholinesterase or butyrylcholinesterase) is an enzyme found in plasma that metabolizes acetylcholine, succinylcholine, ester-type local anesthetics, heroin, and cocaine
- Does NOT metabolize Remifentanil or Esmolol (red cell esterase for both)

It is produced by the liver

Its half-life is approximately 8 to 16 hours

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23
Q

How do NSAIDs work?

A

NSAIDs inhibit cyclooxygenase, which is necessary for prostaglandin synthesis

Prostaglandins are mediators of pain and inflammation and act at the site of injury (peripherally)

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24
Q

Why is Succinylcholine avoided in children?

A

Fear of un-diagnosed muscular dystrophy that could lead to sever hyperkalemia and cardiovascular collapse
- hyperkalemia is 2/2 rhabdomyolysis

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25
Describe the onset of paralysis in central vs peripheral muscles
Neuromuscular blockade develops faster, lasts a shorter time, and recovers more quickly in the central muscles of the airway than in more peripheral muscle groups Observation of the pattern of blockade of the orbicularis oculi is similar to that of the laryngeal muscles and diaphragm
26
How does Pancuronium effect the cardiovascular system?
Pancuronium may cause increased heart rate, MAP, and CO Several mechanisms for this, including a vagolytic effect, norepinephrine release, and decrease reuptake of norepinephrine
27
Which opioid is resistant to reversal with naloxone?
Buprenorphine
28
What is Fospropofol an what are it's advantages?
Fospropofol is a prodrug of Propofol Because it is water soluble, it causes no pain on injection and carries no risk of hypertriglyceridemia, PE, or sepsis
29
Describe Clonidine
a2 agonist Primarily stimulates central adrenergic receptors and decreases sympathetic response Decreases MAC requirements Decreases extremes in blood pressure Has analgesic properties and decreases opioid requirements Can decrease post-anesthetic shivering Can be given orally, IV, epidurally, intrathecally, and in peripheral nerve blocks When given intrathecally, has been shown to decrease persistent postsurgical pain
30
What is the dibucaine number?
A test to evaluate function of pseudocholinesterase 80 - normal function (up to 10 minutes of paralysis) 50 to 60 - heterozygous (up to 30 minutes of paralysis) 20 - atypical pseudocholinesterase (over 3 hours of paralysis)
31
List the a blockers
Phentolamine - short-acting non-selective antagonist used primarily in hypertensive emergencies from pheochromocytoma Phenoxybenzamine - long-acting non-selective antagonist (irreversible) that is commonly used for pre-operative treatment of pheochromocytoma Prazosin/Terazosin/Doxazosin - selective a1 antagonists used most commonly for BPH Mirtazapine - selective a2 antagonist used in the treatment of depression
32
How does Norepinephrine work?
Mostly alpha stimulation Results in increased SVR
33
How does Epinephrine work?
Mostly beta-1 stimulation - increased cardiac output At high doses, alpha effects increase - increased SVR
34
How does Isoproterenol work?
Non-selective B-agonist Results in increased cardiac output and decreased SVR
35
How does Dobutamine work?
B1-receptor agonist Increases CO with little change in SVR
36
How does Dopamine work?
``` Low doses (up to 5 nanos) stimulate DA receptors - vasodilation ``` ``` Middle doses (5-10) stimulate beta-1 receptors - increases CO ``` ``` High doses (>10) stimulate alpha receptors - increased SVR ```
37
Which opioid receptor responsible for increase in prolactin?
u1-receptor
38
Which opioid receptor responsible for respiratory depression, muscle rigidity, constipation, and biliary spasm?
u2-receptor
39
Which opioid receptor responsible for dysphoria and sedation?
k-receptors
40
Describe the phases of depolarizing blockade
Phase I - occurs with depolarization of the postjunctional membrane Phase II - occurs when the postjunctional membranes have become repolarized but do not respond normally to acetylcholine Phase II blockade responds similarly to non-depolarizing blockade
41
List the induction doses of common agents
Propofol: 1.5 - 2.5 mg/kg Thiopental: 3 - 6 mg/kg Etomidate: 0.2 - 0.5 mg/kg Ketamine: 1 -2 mg/kg
42
What is Thiopental? How does it work? What is unique about it?
A barbiturate Binds to GABAa receptor, increasing duration of opening of a chloride-specific ion channel Causes hypotension via vasodilation, with profound reflex tachycardia Decreases ICP more than BP, thus maintaining CPP Contraindicated in porphyria and sulfa allergy
43
What is Midazolam? How does it work? What is unique about it?
A benzodiazepine Binds to GABAa receptor, increasing the frequency of opening of a chloride-specific ion channel Water-soluble, but converts to lipid-soluble drug at physiologic pH Produces anterograde amnesia Pts with kidney failure may accumulate high levels of metabolite a-hydroxymidazolam
44
What is Ketamine? How does it work? What is unique about it?
Analog of phencyclidine (PCP) Acts as an NMDA receptor antagonist, giving it some additional analgesic properties Dissociates thalamus from limbic cortex, creating a state of dissociative anesthesia Has an active metabolite, norketamine Increases BP, HR, CO, PA pressures, and myocardial work - Indirectly via stimulation of sympathetic nerves and inhibition of norepinephrine reuptake - Direct myocardial depressant effects only apparent during catecholamine depletion Bronchodilator, but also increases secretions Increases cerebral O2 consumption, CBF, and ICP Tolerance may develop after multiple exposures within a short period of time Intra-operative infusions at sub-anesthetic doses have been shown to have opioid sparing effects
45
What is Etomidate? How does it work? What is unique about it?
A carboxylated imidazole ring Binds to subunit of GABAa receptor, increasing the receptor's affinity for GABA Minimal effects on the CV system compared to other induction agents Can cause pain on injection, myoclonus, and adrenal suppression of cortisol and aldosterone synthesis via inhibition of 11-B-hydroxylase
46
What is Propofol? How does it work? What is unique about it?
An alkylphenol Allosterically increases the binding affinity of the GABAa receptor for GABA Long-term infusion has been associated with Propofol Infusion Syndrome - lactic acidosis, hyperkalemia, rhabdomyolisis, lipemia, and death Causes decreased BP via decreased SVR, decreased preload, and decreased contractility Has antipruritic and antiemetic properties
47
Describe the mechanism of depolarizing vs non-depolarizing muscle relaxants
Depolarizing relaxants (Succinylcholine) resemble ACh and act as receptor agonists - Cause continuous end-plate depolarization via the opening of peri-junctional Na+ channels - After initial opening and excitation, Na+ channels inactivate and cannot re-open until end-plate repolarizes Non-depolarizing relaxants bind ACh receptors,but do not cause the necessary conformational change - Act as competitive antagonists
48
List the intubating doses of NMBs
``` Succinylcholine: 1 - 2 mg/kg Atracurium: 0.4 - 0.5 mg/kg Cisatracurium: 0.1 - 0.15 mg/kg Pancuronium: 0.1 mg/kg Vecuronium: 0.1 mg/kg Rocouronium: 0.6 mg/kg ```
49
What type of drug is Succinylcholine? What is unique about it?
The only depolarizing NMB currently in use Consists of 2 joined ACh molecules Is rapidly metabolized by plasma pseudocholinesterase Many side effects - Cardiac arrhythmias, especially bradycardia - Fasciculations and subsequent myalgias - Increased intra-gastric, intra-ocular, and intra-cerebral pressures - Hyperkalemia - Possible trigger of MH
50
Describe the types of non-depolarizing NMBs
Benzylisoquinolones - Atracurium - Cisatracurium Aminosteroids - Pancuronium - Vecuronium - Rocuronium
51
What type of drug is Atracurium? What is unique about it?
An intermediate-acting benzylisoquinolone Metabolized by both nonspecific ester hydrolysis and by Hofmann elimination - Unaffected by renal or hepatic function Triggers dose-dependent histamine release, resulting in hypotension and tachycardia (bronchospasm in asthmatics) Toxic metabolite called laudanosine that can accumulate in individuals with renal failure
52
What type of drug is Cisatracurium? What is unique about it?
An intermediate-acting benzylisoquinolone Metabolized by Hofmann elimination Does not cause histamine release
53
What type of drug is Pancuronium? What is unique about it?
A long-acting aminosteroid Mostly renal metabolism Causes vagal blockade and sympathetic stimulation, leading to hypertension and tachycardia
54
What type of drug is Vecuronium? What is unique about it?
An intermediate-acting aminosteroid Mostly hepatic metabolism Has an active metabolite
55
What type of drug is Rocuronium? What is unique about it?
An intermediate-acting aminosteroid Mostly hepatic metabolism Can be given "double-dose" with onset of action that almost approaches that of Succinylcholine
56
What are the side effects of cholinesterase inhibitors (ie. Neostigmine, Edrophonium, Pyridostigmine)?
Bradycardia Bronchospasm and increased respiratory secretions Increased GI activity (nausea/vomiting/incontinence)
57
Define half-life. What are the 2 types?
Half-life (t1/2) is the time it takes for blood levels of drug to decrease to half of what it was at equilibrium Alpha (distribution) half-life is due to distribution to tissue reservoirs Beta (elimination) half-life is due to the drug being metabolized and excreted
58
What is the equation for volume of distribution (Vd)?
(amount of drug in the body) / (concentration of drug in plasma)
59
What does the volume of distribution (Vd) tell us about the amount of drug in plasma vs tissue?
Small Vd - drug stays mainly in plasma, with little in tissues Medium Vd - similar concentration of drug in plasma and tissue Large Vd - drug mostly in tissues, with little staying in the plasma
60
What is the equation for half-life?
t1/2 = 0.69 x (volume of distribution/clearance)
61
What is the mechanism of Acetazolamide?
Inhibits carbonic anhydrase Results in decreases H+ secretion and increased loss of Na, HCO3-, and water
62
What is Amiloride? Any side effects?
A K+ sparing diuretic that inhibits the epithelial Na channel (ENaC), reducing Na reabsorption Can result in hyperkalemia
63
What is Amiodarone? How does it work? Any side effects?
An anti-arrhythmic that blocks myocardial K and Ca channels, slowing conduction speed in SA node causing prolongation of the refractory period Can cause hypotension and bradycardia Associated with abnormal TFTs, PFTs, and LFTs
64
Describe anti-platelet drug mechanisms
ASA/NSAIDs: Inhibit COX, decreasing TXA2 Clopidogrel/Prasugrel/Ticlopidine: Block ADP receptor, decreasing activation of platelets Abciximab/Eptifibatide/Tirofiban: Inhibit glycoprotein IIb/IIIa, decreasing platelet aggregation
65
What type if drugs are Hydrochlorthiazide and Metolazone? Any side effects?
Thiazides diuretics that inhibit the Na-Cl cotransporters of the renal tubules Results in decreases reabsorption of Na and Cl Can cause hypercalcemia and hyperglycemia
66
What type of drug is Furosemide? Any side effects?
A loop diuretic that inhibits the Na-K-2Cl cotransporter Results in decreased Na and H2O reabsorption Can cause metabolic alkalosis due to increased Cl excretion
67
How do burns effect NMB?
More sensitive to succinylcholine More resistant to non-depolarizing NMBs
68
How does Phenytoin effect NMB?
Acute administration potentiates the effects of NMBs Chronic administration results in decreased effect of NMBs
69
What is unique about Alfentanil?
Rapid onset due to very low pKa Very short duration of action due to very low volume of distribution
70
How does renal failure effect Neostigmine
Neostigmine is almost completely eliminated by the kidneys Renal failure prolongs the duration of action of Neostigmine - dosage must be reduced around 50 to 75%
71
Why is fentanyl a "short-acting" opioid when it has the same elimination half-life of Morphine and Dilaudid?
Fentanyl is much more lipophilic so it has a much shorter alpha-half-life (distribution)
72
Why is it okay to use Succinylcholine in pregnant women?
An insignificant amount of Succinylcholine crosses the placenta due to its high ionization and low lips solubility
73
List the drugs that should be dosed based on ideal body weight (IBW)
Propofol (infusion) Vecuronium Rocuronium Remifentanil
74
If you use succinylcholine to re-intubate a patient after reversal with neostigmine, how is the duration of action of succinylcholine affected and why?
Prolonged duration of action due to Phase 1 Block augmentation
75
Which pressor increases cerebral oxygenation in addition to increasing CPP?
Vasopressin
76
Why is sodium bicarbonate given? What are its effects?
Sodium bicarbonate is often given peri-operatively to correct an acidosis Associated with a transient increase in paCO2, EtCO2, and intracranial pressure Can cause hypotension due to hypocalcemia, ventricular depressant effects, and redistribution of blood volume from pulmonary vasculature
77
Describe sodium nitroprusside toxicity
Sodium nitroprusside administration has potential for causing toxicity due to accumulation of its metabolic byproducts: cyanide and thiocyanate Cyanide toxicity: - elevated mixed venous oxygen - tachyphylaxis to SNP - metabolic acidosis - flushing Thyiocyanate toxicity: - hypoxia - nausea - tinnitus - muscle spasm
78
What are the pharmacologic implications of major burns?
Severe burns lead to hypoalbuminemia, which can increase the free fraction of anesthetic drugs - lower doses of benzos required - higher doses of opioid required due to tolerance, despite higher free fraction Increased catecholamine and corticosteroid levels - insulin resistance, usually requiring larger doses Proliferation of extrajunctional Ach receptors - exagerated response to succinylcholine - resistance to non-depolarizing NMBs
79
What is the correct de-fasciculating dose for non-depolarizing NMBs prior to giving succinylcholine?
10% of ED95 dose | - NOT 10% of intubating dose

Anesthesiology (12 decks)

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