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Lumb and Jones Anesthesia Drugs Flashcards

1
Q

What is the mechanism of action of anticholinergics?

A

Competitively antagonize ACh at post-ganglionic muscarinic cholinergic receptors in parasympathetic NS

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2
Q

Which anticholinergic can cross the blood brain barrier?

A

Atropine

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3
Q

What is the difference in onset of action and duration between atropine and glycopyrrolate?

A

Atropine - onset fast (1 min), shorter duration (30 mins)

Glycopyrrolate - onset slower (few mins), longer duration (1h)

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4
Q

Is atropine or glycopyrrolate more potent?

A

Glycopyrrolate - 4x potency of atropine

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5
Q

Which anticholinergic causes paradoxical bradycardia?

A

Atropine - can occur initially due to AV block. Often self-limiting or can be overcome with a larger dose

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6
Q

What are the 6 types of adrenergic receptors?

A

Alpha-1

Alpha-2

Beta-1

Beta-2

Dopamine 1 (D1)

Dopamine 2 (D2)

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7
Q

Where are alpha-1 receptors located and what is their effect?

A

Smooth muscle (blood vessels, bronchi, GI, uterus, urinary) Smooth muscle contraction and vasoconstriction

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8
Q

Where are alpha-2 receptors located and what is their effect?

A

CNS, primarily cause sedation

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9
Q

Where are beta-1 receptors located and what is their effect?

A

Only in the heart. Positive inotrope and chronotrope (increases contractility)

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10
Q

Where are beta-2 receptors located and what is their effect?

A

Smooth muscle (blood vessels, bronchi, GI, uterus, urinary) and heart.

Relaxation of smooth muscle, vasodilation

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11
Q

Where are D1 receptors located and what is their effect?

A

CNS, vascular smooth muscle, kidney

Vasodilation of GI and kidney

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12
Q

Where are D2 receptors located and what is their effect?

A

CNS, vascular smooth muscle, kidney

Inhibit norepinephrine release

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13
Q

What are the 3 endogenous (naturally occurring) catecholamines?

A

Epinephrine, norepinephrine, dopamine

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14
Q

What are the different effects between low vs. high dose epinephrine?

A

Low dose - B1 and B2 effects predominate. Increased cardiac output, myocardial O2 consumption, coronary artery dilation; reduced threshold for arrhythmias

High dose - alpha 1 effects predominate. Marked rise in SVR

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15
Q

What is the predominant effect of norepinephrine?

A

Predominantly alpha-1 effects, increased SVR

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16
Q

What are the different effects of dopamine at low, mid, and high doses?

A

Low - vasodilation through activation of D1 and D2 receptors (increases renal and GI perfusion)

Intermediate - stimulates beta-1 receptors, increased contractility

High - stimulates alpha-1 receptors, vasoconstriction (increased SVR)

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17
Q

What are the effects of dobutamine?

A

Beta-1 receptor agonist - increases contractility and cardiac output. At high doses can have effects at beta-2 and alpha-1 receptors

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18
Q

What are the effects of phenylephrine?

A

Potent alpha-1 agonist, dose-dependent vasoconstriction.

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19
Q

What are the effects of ephedrine?

A

Mixed agonist - alpha 1 and 2, beta 1 and 2. Increases CO and MAP with minimal effect on SVR. Bronchodilation.

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20
Q

What are the effects of terbutaline/albuterol?

A

Beta 2 agonists - decrease bronchoconstriction. Can have B1 effects at higher doses. Can cause hypokalemia.

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21
Q

What is prazosin?

A

Alpha-1 antagonist, highly selective to bladder neck and proximal urethra to relax urethral sphincter. Can cause vasodilation of arterioles and venues and reduced SVR.

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22
Q

What is phenoxybenzamine?

A

Nonselective alpha antagonist (a1>a2). Long-acting. Used to reduce SVR (pheochromocytoma with chronic vasoconstriction)

23
Q

What are atenolol and esmolol?

A

Beta-1 antagonists - reduce HR and CO, inhibition of RAAS d/t blockade of beta-1 receptors at juxtaglomerular apparatus

24
Q

What is propranolol?

A

Non-selective beta 1 antagonist, reduces HR.

25
What is sotalol?
Class III anti-arrhythmic (K channel blocker), non-selective beta 1 antagonist. Used to treat ventricular arrhythmias
26
What is the MoA of phenothiazines?
Block dopamine (D2) receptors. Blockade of alpha-1, muscarinic, and H1 receptors may also contribute to sedation
27
How does acepromazine cause decreased blood pressure?
Alpha-1 antagonism. Also causes splenic engorgement which can reduce PCV 20-30%
28
What is the MoA of benzodiazepines?
Enhance GABA(A) receptor affinity for GABA (inhibitory neurotransmitter, prevents propagation of action potentials)
29
Which benzodiazepine should be used for patients with liver dysfunction?
Midazolam
30
What is the MoA of alpha-2 agonists?
Decrease norepinephrine release in the CNS - causes sedation, muscle relaxation, analgesia, decreased HR and after load. Can also have effects on alpha 1 receptors - causes vasoconstriction, hypertension, arrhythmias
31
Why do alpha-2 agonists cause bradycardia?
Hypertension from alpha-1 agonism in periphery causes reflex bradycardia
32
T/F: Opioids cross the blood-placental barrier
TRUE. Can cause respiratory depression in neonates
33
How do opioids cause ileus and vomiting?
Inhibit release of motility modifying neurotransmitters causing increased segmental contractions and decreased propulsive contractions
34
Which opioids are considered full mu agonists?
Morphine, oxymorphone, hydromorphone, fentanyl, methadone, meperidine, hydrocodone, codeine, oxycodone, remifentanil
35
Why is morphine the preferred opioid for epidurals?
Highly hydrophilic - slower onset of analgesia and longer duration of action (compared to lipophilic opioids). Analgesia for 12-24 hours.
36
What is the difference between remifentanil and fentanyl?
Remifentanil metabolized primarily by extrahepatic metabolism by plasma esterases
37
What is the MoA of tramadol?
In humans - metabolized to M1 (pure mu agonist). Dogs do not produce enough M1 metabolite to be effective analgesic, cats do. Also acts as serotonin and norepinephrine reuptake inhibitors
38
What is dantrolene?
Peripherally acting skeletal muscle relaxation, ryanodine receptor antagonist. Used for treatment of malignant hyperthermia
39
What is doxapram?
CNS stimulant (analeptic). Increases minute ventilation by increasing tidal volume and respiratory rate. Used for neonatal resuscitation and laryngeal paralysis airway exam.
40
What is the MoA of vasopressin?
Acts on V1a receptors (vascular smooth muscle), V1b receptors (anterior pituitary), and V2 receptors (renal collecting ducts). Causes potent vasoconstriction.
41
What is the MoA of gabapentin?
Structural analogue of GABA, inhibition of N-type voltage dependent neuronal calcium channels. Causes reduced release of excitatory and inhibitory neurotransmitters.
42
What is the MoA of amantadine?
Dopamine agonist, NMDA receptor antagonism.
43
What are depolarizing neuromuscular blockers?
Depolarizing drugs bind to receptor and cause activation. Not susceptible to breakdown by acetylcholinesterase so repolarization of the muscle membrane cannot occur (succinylcholine). Generalized fasciculations --> flaccid paralysis. Trigger for malignant hyperthermia.
44
What are neuromuscular blockers?
Bind to ACh receptors at the neuromuscular junction and antagonize the action of ACh --> prevents muscle contraction
45
What are nondepolarizing neuromuscular blockers?
Bind to the receptor but do not activate it (atracurium, vecuronium). Causes progressive muscle weakness --> flaccid paralysis. Smoother onset of neuromuscular blockade
46
What is Hoffman elimination of atricurium?
Elimination of atricurium independent of hepatic or renal biotransformation
47
What is the MoA of barbiturates?
Activate GABA(A) receptors causing CNS depression (propofol).
48
How is propofol metabolized?
Rapid distribution to CNS, then redistributed from brain to other tissues in the body. Undergoes hepatic metabolism and renal excretion (except cats: metabolism in lungs)
49
What is the MoA of dissociative anesthetics?
NMDA antagonists - prevents glutamate (excitatory neurotransmitter) from binding (ketamine, tiletamine). Good for decreasing hyperalgesia and allodynia, do not provide good primary somatic analgesia.
50
What is the MoA of etomidate? What is the effect of etomidate on the adrenal glands?
GABA(A) agonist. Can cause adrenal suppression for up to 6 hours.
51
What is the MoA of alfaxalone?
Steroid anesthetic - enhances GABA and glycine-mediated CNS depression. Rapidly metabolized
52
What is the MoA of local anesthetics?
Ion channel blockers - primarily block Na channels to impede membrane depolarization and creation of action potentials
53
T/F: C fibers are more susceptible to blockade by local anesthetics than A fibers
FALSE. A fibers more susceptible to blockade
54
What is the difference between lidocaine and bupivicaine?
Lidocaine - fast onset, duration ~ 1hr Bupivicaine - highly lipophilic, 4x as potent as lidocaine, slower onset of action (20-30 mins), longer duration (3-10 hours)

Phase 1 Drugs (4 decks)

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