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SUM'20 Drug Boxes > Box 3 > Flashcards

Box 3 Flashcards

1
Q

Trade name for Esmolol?

A

Brevibloc

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2
Q

Esmolol classification?

A

Cardioselective Beta Blocker/B-1 adrengeric receptor antagonist

Class II anti-arrhythmic agent.

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3
Q

Esmolol MOA?

A

By blocking adrengeric activity of epi and norepi, it decreases inotropic contractility, heart rate, and conduction.

Esmolol increases atrioventricular refractory time decreases oxygen demand of the myocardium, and decreases atrioventricular conduction.

A minor Beta 2 blockade has been reported with high IV infusion doses

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4
Q

Esmolol MOA?

A

By blocking adrengeric activity of epi and norepi, it decreases inotropic contractility, heart rate, and conduction.

Esmolol increases atrioventricular refractory time decreases oxygen demand of the myocardium, and decreases atrioventricular conduction.

A minor Beta 2 blockade has been reported with high IV infusion doses

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5
Q

Indications for Esmolol use?

A

Supraventricular Tachycardia (SVT); perioperative hypertension

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6
Q

Loading dose of Esmolol (flood)

A

Loading dose: 50-300 mg/kg/min

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7
Q

Onset, peak and duration of Esmolol?

A

Rapid onset and short duration.

Onset: 1-2 minutes.
Peak effect: 5-6 minutes.
Duration: 10-20 minutes.

Do not infuse for more than 48 hours.

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8
Q

What all routes can you infuse Esmolol?

A

ONLY IV

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9
Q

Can Esmolol cause hypoglycemia? Does Esmolol cross the BBB and the placenta?

A

Yes, yes, yes

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10
Q

elimination half time of Esmolol?

A

about 9 minutes

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11
Q

How is Esmolol cleared from the plasma and tissues?

A

ester hydrolysis

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12
Q

Classification of Labetalol?

A

combined alpha and Beta- adrenergic Receptor Antagonist.

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13
Q

Contraindications of Labetalol?

A

bronchial asthma, 2nd-3rd degree heart block, hepatic failure.

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14
Q

IV dose of labetalol?

A

0.1-0.5mg/kg

start with 5-10mg

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15
Q

Labetalol MOA?

A

exhibits selective α1 and non-selective β1- and β2-adrenergic antagonist effects. Presynaptic α2 receptors are spared by labetalol such that released norepinephrine can continue to inhibit further release of catecholamines via the negative feedback mechanism resulting from stimulation of α2 receptors. α to β blocking potency ratio is 1:7 IV, 1:3 Oral

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16
Q

Labetalol IV onset, peak, duration?

A

Onset: 1-3 min.
Peak: 5-15 min.
Duration: 20 min. - 2 hours.

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17
Q

Labetalol and inhaled anesthetics?

A

anesthetic inhalants may increase hypotensive effects.

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18
Q

Labetalol typically comes in a supply of what concentration?

A

20mg/4mL

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19
Q

Classification of Metoprolol?

A

Beta blocker, Beta 1 selective

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20
Q

Contraindications to Metoprolol use?

A

COPD, CAD, Vulnerable to hypoglycemia

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21
Q

IV dose of metoprolol?

A

1mg-15mg

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22
Q

Metoprolol MOA?

A

Selective B1-Adrenergic receptor antagonist

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23
Q

Which type of metoprolol lasts longer (has a longer elimination half-time) succinate or tartrate?

A

succinate 1/2 time = 5-7 hours

tartrate 1/2 time = 2-4 hours

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24
Q

onset of metoprolol?

A

1-5 min.

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25
Q

selectivity of metoprolol based on dose?

A

Selectivity is dose related and large doses become non-selective antagonist B2 receptor as well as B1

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26
Q

Metoprolol comes in a supply concentration of what?

A

1mg/1ml (or 5mg/5ml)

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27
Q

Classification of Neostigmine?

A

Anticholinesterase agent.

increases ACH by blocking cholinesterase “what breaks it down”

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28
Q

Contraindications to Neostigmine use?

A

Use with caution in patients with bradycardia, bronchial asthma, epilepsy, cardiac arrhythmias, peptic ulcer, peritonitis, or mechanical obstruction of the intestines or urinary tract

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29
Q

Does of Neostigmine?

A

60-80 mcg/kg with a max dose of 5mg

some sources also say 40-70mcg/kg, I guess know both?

30
Q

Neostigmine MOA?

A

It inhibits AChE by forming a drug-enzyme complex that degrades in the same manner as ACh-Cholinesterase complex, thereby increasing the concentration of endogenous ACh around the cholinoreceptors

31
Q

Elimination of Neostigmine?

A

Renal excretion accounts for about 50% of the excretion of neostigmine . Renal failure decreases the plasma clearance of neostigmine as much as, if not more than, that of the long-acting neuromuscular blockers

32
Q

Neostigmine Onset with a reversal dose?

A

3-15 minutes

33
Q

What will you give with neostigmine and why?

A

To minimize the muscarinic cardiovascular side effects of acetylcholinesterase inhibitors, give with glycopyrrolate (7 to 15 µg/kg) which matches the slower acting neostigmine (40 to 70 µg/kg)

34
Q

What will an overdose of neostigmine look like and how will you treat it?

A
  1. Overdose may induce a cholinergic crisis characterized by; n&v, bradycardia/tachycardia, excessive salivation, sweating, bronchospasm, weakness and paralysis. Treated by discontinuing neostigmine and administration of atropine
35
Q

Trade name of glycopyrrolate?

A

Robinul

36
Q

Classification of glycopyrrolate?

A

Antiholinergic

37
Q

Dose of Glycopyrrolate?

A

7-15 mcg/kg per Hammon PPT

10-20 mcg/kg Nagelhout

38
Q

Glycopyrrolate MOA?

A

Synthetic quaternary ammonium compound that is an anticholinergic and blocks the effects of acetylcholines at parasympathetic sites. Reduces the rate of salivation by preventing the stimulation of acetylcholine receptors.

39
Q

Elimination of Robinul?

A

urine (85%) and feces (15%) within 48 hours

40
Q

Robinul onset, peak, duration IV?

A

Onset: 1-2 min
Peak: 30-45 min.
Duration: 2-4 hours

41
Q

Does robinul pass the placental barrier or BBB?

A

No

42
Q

Glycopyrrolate is often used with what drug to reverse NMB?

A

Neostigmine (it matches the slower time to action compared to atropine)

43
Q

glycopyrrolate comes as a supply concentration of what?

A

0.2mg/ml

44
Q

Tell me what Robinul does to smooth muscles, lower esphageal sphincter, secreations, and HR?

A

Moderate relaxation of smooth muscle. Lower esophageal sphincter relaxation. Moderate antisialagogue. Moderate increase in heart rate (Less than Atropine). Less initial tachycardia than atropine; no central nervous system effects (does not pass the blood-brain barrier). Fewer systemic side effects than atropine.

45
Q

Zofran classification?

A

serotonin receptor antagonist, anti-emetic.

46
Q

Dose of zofran IV and how/when do you give?

A

4 to 8 mg IV over 2 to 5 minutes immediately before induction. (prevention of PONV)

47
Q

MOA zofran?

A

Ondansetron is a carbazalone derivative that is structurally related to serotonin and possesses specific 5-HT3 subtype receptor antagonist properties.

48
Q

Does zofran totally eliminate the complication of PONV?

A

Although highly effective in decreasing the incidence and intensity of PONV, does not totally eliminate this complication

49
Q

How is zofran supplied?

A

4 mg/2ml

50
Q

Generic name for Decadron?

A

Dexamethasone

51
Q

classification of dexamethasone?

A

long acting corticosteroid

52
Q

Contraindications to Dexamethasone?

A

Patients with peptic ulcers, osteoporosis, psychosis, psychoneurosis, acute bacterial infections, herpes zoster, herpes simplex ulceration of the eye, and other viral infections. Use it with caution in patients with DM, chronic renal failure, or infection disease in elderly patients. May increase the risk of developing TB in patients with purified protein derivative test. They may increase the risk of development of serious or fatal infection in person exposed to viral illness such as chickenpox.

53
Q

IV or IM dose of Dexamthasone in Adults?

A

Initially 0.5-9 mg, administer over 3-5 minutes when IV.

54
Q

Dexamethasone MOA?

A

For PONV mechanism of action is unclear.

Steroids inhibit the production of prostaglandins and therefore reduce pain

55
Q

How much stronger is dexamethasone compared to endogenous cortisol?

A

25 times stronger

56
Q

What drug can prolong the analgesia from interscalene blocks using ropivacaine or bupivacaine?

A

Dexamethasone

57
Q

True or false, we know exactly how dexamethasone works?

A

False, MOA is unclear.

58
Q

Dexamethasone comes in a supply concentration of?

A

4 mg/ ml

59
Q

Sugammadex trade name?

A

Bridion

60
Q

Classification of sugammadex?

A

modified (gamma)y-cyclodextrin; selective neuromuscular blockade reversal agent.

61
Q

When is sugammadex contraindicated?

A

Renal impairment
creatinine clearance <30 ml/min
allergy
bleeding

62
Q

Dose of Sugammadex?
TOF 2/4
PTC 1-2
immediately after full induction with Roc?

A

2mg/kg TOF 2/4

4mg/kg for a deeper block at 1-2 PTC

more profound block would require range of 8-16mg/kg

63
Q

When infusing sugammadex IV over what time do you push it?

A

10 sec.

64
Q

Sugammadex MOA?

A

encapsulates/binds to steroidal neuromuscular blocking drugs (rocuronium, vecuronium, and pancuronium)

65
Q

Suggamadex elimination?

A

mainly kidneys; approx.. 70% excreted within 6 hours, >90% within 24 hours.

66
Q

Suggamadex onset of reversal?

A

within 3 minutes if dosed appropriately to level of block

67
Q

peak of sugamadex and duration?

A

works within 3 min.

Duration half life is 2 hours in an adult with normal renal function.

68
Q

Do you need to co-administer anything with Sugamadex?

A

Does not affect acetylcholinesterase, eliminating the need for the co-administration of an anticholinergic

69
Q

What do you need to make sure you tell women who you give sugamadex to?

A

If on birth control, must use non-steroidal method of contraception for at least 7 days

70
Q

Sugamadex only works on what drugs (reversal)?

A

Only works on rocuronium, vecuronium, and pancuronium

71
Q

Supply of sugamadex?

A

100mg/ml

SUM'20 Drug Boxes (6 decks)

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