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Phase 1 Drugs > Lumb and Jones Anesthesia Drugs > Flashcards

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
Q

What is sotalol?

A

Class III anti-arrhythmic (K channel blocker), non-selective beta 1 antagonist. Used to treat ventricular arrhythmias

26
Q

What is the MoA of phenothiazines?

A

Block dopamine (D2) receptors. Blockade of alpha-1, muscarinic, and H1 receptors may also contribute to sedation

27
Q

How does acepromazine cause decreased blood pressure?

A

Alpha-1 antagonism. Also causes splenic engorgement which can reduce PCV 20-30%

28
Q

What is the MoA of benzodiazepines?

A

Enhance GABA(A) receptor affinity for GABA (inhibitory neurotransmitter, prevents propagation of action potentials)

29
Q

Which benzodiazepine should be used for patients with liver dysfunction?

A

Midazolam

30
Q

What is the MoA of alpha-2 agonists?

A

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
Q

Why do alpha-2 agonists cause bradycardia?

A

Hypertension from alpha-1 agonism in periphery causes reflex bradycardia

32
Q

T/F: Opioids cross the blood-placental barrier

A

TRUE. Can cause respiratory depression in neonates

33
Q

How do opioids cause ileus and vomiting?

A

Inhibit release of motility modifying neurotransmitters causing increased segmental contractions and decreased propulsive contractions

34
Q

Which opioids are considered full mu agonists?

A

Morphine, oxymorphone, hydromorphone, fentanyl, methadone, meperidine, hydrocodone, codeine, oxycodone, remifentanil

35
Q

Why is morphine the preferred opioid for epidurals?

A

Highly hydrophilic - slower onset of analgesia and longer duration of action (compared to lipophilic opioids). Analgesia for 12-24 hours.

36
Q

What is the difference between remifentanil and fentanyl?

A

Remifentanil metabolized primarily by extrahepatic metabolism by plasma esterases

37
Q

What is the MoA of tramadol?

A

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
Q

What is dantrolene?

A

Peripherally acting skeletal muscle relaxation, ryanodine receptor antagonist. Used for treatment of malignant hyperthermia

39
Q

What is doxapram?

A

CNS stimulant (analeptic). Increases minute ventilation by increasing tidal volume and respiratory rate. Used for neonatal resuscitation and laryngeal paralysis airway exam.

40
Q

What is the MoA of vasopressin?

A

Acts on V1a receptors (vascular smooth muscle), V1b receptors (anterior pituitary), and V2 receptors (renal collecting ducts). Causes potent vasoconstriction.

41
Q

What is the MoA of gabapentin?

A

Structural analogue of GABA, inhibition of N-type voltage dependent neuronal calcium channels. Causes reduced release of excitatory and inhibitory neurotransmitters.

42
Q

What is the MoA of amantadine?

A

Dopamine agonist, NMDA receptor antagonism.

43
Q

What are depolarizing neuromuscular blockers?

A

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
Q

What are neuromuscular blockers?

A

Bind to ACh receptors at the neuromuscular junction and antagonize the action of ACh –> prevents muscle contraction

45
Q

What are nondepolarizing neuromuscular blockers?

A

Bind to the receptor but do not activate it (atracurium, vecuronium). Causes progressive muscle weakness –> flaccid paralysis. Smoother onset of neuromuscular blockade

46
Q

What is Hoffman elimination of atricurium?

A

Elimination of atricurium independent of hepatic or renal biotransformation

47
Q

What is the MoA of barbiturates?

A

Activate GABA(A) receptors causing CNS depression (propofol).

48
Q

How is propofol metabolized?

A

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
Q

What is the MoA of dissociative anesthetics?

A

NMDA antagonists - prevents glutamate (excitatory neurotransmitter) from binding (ketamine, tiletamine). Good for decreasing hyperalgesia and allodynia, do not provide good primary somatic analgesia.

50
Q

What is the MoA of etomidate? What is the effect of etomidate on the adrenal glands?

A

GABA(A) agonist. Can cause adrenal suppression for up to 6 hours.

51
Q

What is the MoA of alfaxalone?

A

Steroid anesthetic - enhances GABA and glycine-mediated CNS depression. Rapidly metabolized

52
Q

What is the MoA of local anesthetics?

A

Ion channel blockers - primarily block Na channels to impede membrane depolarization and creation of action potentials

53
Q

T/F: C fibers are more susceptible to blockade by local anesthetics than A fibers

A

FALSE. A fibers more susceptible to blockade

54
Q

What is the difference between lidocaine and bupivicaine?

A

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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