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Pharm 2 > Drug Box 2 > Flashcards

Drug Box 2 Flashcards

1
Q

Sufentanil Name (generic and trade)

A

Sufenta

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2
Q

Sufentanil Classification

A

Opioid Agonist

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3
Q

Sufentanil Contraindications

A

Reduce the dose/caution use in elderly, hypovolemic, patients taking sedatives or narcotics, high risk surgical patients. Sufentanil crosses the placental
barrier; Can cause respiratory depression in neonate if used during labor

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4
Q

Sufentanil Dose and Route

A

Route: IV, IM, Epidural/Spinal

Induction: intravenous: 1 to 30 mcg/kg; infusion: 0.005 to 0.015 mcg/kg/min. Epidural: bolus: 25-50 mcg; infusion: 5 to 30 mcg/hr.

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5
Q

Sufentanil MOA

A

Opioids act as agonists at specific opioid receptors at presynaptic and postsynaptic sites in the central nervous system (CNS) (mainly the brainstem and spinal cord) as well as in the periphery. These same opioid receptors normally are activated by three endogenous peptide opioid receptor ligands known as enkephalins, endorphins, and dynorphins. Opioids mimic the actions of these endogenous ligands by binding to opioid receptors, resulting in activation of pain-modulating (antinociceptive) systems

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6
Q

Sufentanil Elimination

A

Half-Life; 6 Hours Hepatic/Renal

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7
Q

Sufentanil Onset

A

1-3 mins

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8
Q

Sufentanil Peak

A

5.6 min

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9
Q

Sufentanil Duration

A

dose dependant

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10
Q

Ketamine Name (generic and trade)

A

Ketalor

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11
Q

Ketamine Classification

A

phencyclidine (PCP) derivative: Non-barbiturate dissociative anesthetic: NMDA (N-Methyl-D-Aspartate) receptor antagonist

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12
Q

Ketamine Contraindications

A

patients with CAD (inotropic effect increases cardiac myocardial O2 requirements), patients with pulmonary HTN or increased ICP

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13
Q

Ketamine Dose and Route

A

Route: primarily IV can be given PO or IM
Adult: IV: sub anesthesia analgesic dose 0.2-0.5 mg/kg, Induction of anesthesia: 1-2mg/kg IV
IM: 4-8 mg/kg; continuous infusion: 1-2 mg/kg/hr
(Flood 5th edition pages: 186-193, 259-261, 595-596)
spinal (intrathecal) 5-50 mg in 3 ml of saline (better absorption if combined with epi to slow systemic absorption)
Pediatric: same as adult: continuous infusion: 1-2 mg/kg/hr; Induction dose: 1-2 mg/kg

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14
Q

Ketamine MOA

A

exact MOA is unknown; primarily a noncompetitive antagonist for NMDA receptors, also acts on opioid, monoaminergic, muscarinic and neuronal nicotinic Ach receptors.

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15
Q

Ketamine Elimination

A

metabolized in the liver - demethylation by P450 enzymes, <5% fecal excretion, primarily excreted by the kidneys

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16
Q

Ketamine Onset

A

30-60 seconds IV, 2-4 minutes IM

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17
Q

Ketamine Peak

A

1 minute IV and 5 minutes IM

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18
Q

Ketamine Duration

A

10-20 mins

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19
Q

Ketamine Misc

A

known for emergence delirium (adjunct benzo administration may prevent delirium); causes bronchodilation and may be useful as induction drug in patients with asthma: does not produce significant respiratory depression. It commonly causes nystagmus. Does NOT trigger malignant hyperthermia. Giving a sub anesthesia dose can prevent opioid tolerance. Dont give to PTSD
Supply: 500mg/10ml

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20
Q

Flumazenil Name (generic and trade)

A

Romazicon

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21
Q

Flumazenil Classification

A

competitive benzodiazepine-receptor antagonist

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22
Q

Flumazenil Contraindications

A

Flumazenil should be avoided in patients who take oral benzodiazepines on a chronic basis and those taking antiepileptic drugs, as they are at significant risk of having a withdrawal seizure following flumazenil administration

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23
Q

Flumazenil Dose and Route

A

Route - IV
Adults- 0.2–1.0 mg IV boluses titrated to the patient’s response; up to 3 mg per hour. After an initial response, patients may become resedated once the effects of flumazenil have subsided, in which case an IV infusion of flumazenil may be administered (0.1-0.4 mg/hr) until the benzodiazepine effects have resolved. Lack of patient response after 5mg suggests that benzodiazepines are not the cause of sedation. (Flood. Pg 182, ebook).
Peds- 0.01 mg/kg up to a maximum total dose of 1 mg at a rate not exceeding 0.2mg/min. The safety and efficacy of romazicon in the reversal of conscious sedation in pediatric patients below the age of 1 year have not been established.

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24
Q

Flumazenil MOA

A

competitively inhibits the activity at the benzodiazepine recognition site on the GABA/benzodiazepine receptor complex.

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25
Q

Flumazenil Elimination

A

Flumazenil is quickly metabolized by hydroxylation through hepatic microsomal enzymes to inactive metabolites with a half-life of about 1 hour

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26
Q

Flumazenil Onset

A

1-2 minutes

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27
Q

Flumazenil Peak

A

2-10 minutes

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28
Q

Flumazenil Duration

A

30-60 minutes

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29
Q

Flumazenil Misc

A

Do not use flumazenil until the effects of neuromuscular blockade have been fully reversed. Administer it in a large vein to minimize pain at the injection site. Monitor the patient for resedation. No patient response by 5 mg total dose suggests that benzodiazepines are not the cause of sedation or cardiopulmonary depression.

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30
Q

Narcan Name (generic and trade)

A

NALOXONE

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31
Q

Narcan Classification

A

Nonselective Opioid antagonist

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32
Q

Narcan Contraindications

A

Use naloxone with caution in patients with pre-existing cardiac disease (Nagelhout Handbook, 670). After administration of naloxone, cardiovascular stimulation manifests as increased sympathetic nervous system activity, reflecting the reversal of analgesia and the sudden perception of pain. This sympathetic nervous system stimulation may manifest as; tachycardia, hypertension, pulmonary edema, cardiac dysrhythmias, and even ventricular fibrillation

33
Q

Narcan Dose and Route

A

Route: IV, IM
Dose: 1 to 4 mcg/kg IV promptly reverses opioid-induced analgesia and depression of ventilation (Flood, 245). May repeat at 2 to 3 minute intervals; response should occur with a maximum dose of 1 mg (Nagelhout Handbook, 670)
Children: 5 to 10 mcg/kg every 2 to 3 minutes as needed

34
Q

Narcan MOA

A

Naloxone is an opioid antagonist that inhibits the uptake of opioids at the opioid receptor sites (Flood, 245). The three opioid receptor sites include μ (Mμ1, Mμ2), δ (delta), and κ (kappa)

35
Q

Narcan Elimination

A

Naloxone is metabolized primarily in the liver by conjugation with glucuronic acid to form naloxone-3-glucuronide. The elimination half-time is 60-90 minutes

36
Q

Narcan Onset

A

Intravenous: 2 minutes; IM: 5 minutes

37
Q

Narcan Peak

A

5 to 15 minutes

38
Q

Narcan Duration

A

30-45 minutes. The short duration of action is presumed to be due to its rapid removal from the brain

39
Q

Narcan Misc

A

Naloxone can easily cross the placenta. For this reason, administration of naloxone to an-opioid dependent parturient (woman about to give birth) may produce acute withdrawal in the neonate

Supply: 0.4mg/ml

40
Q

Ephedrine Name (generic and trade)

A

Ephedrine

41
Q

Ephedrine Classification

A

Synthetic Noncatecholamine sympathomimetic with mixed direct and indrect actions as well as CNS effects (same class as Phynylephrine)

42
Q

Ephedrine Contraindications

A

Use cautiously in patients with hypertension and ischemic heart disease. It has unpredictable effects in patients whom endogenous catecholamines are depleted. Phenylephrine (vs Ephedrine) is preferred choice of sympathomimetic for treatment of maternal hypotension. Studies demonstrated phenylephrine is associated with lower rates of fetal acidosis vs ephedrine (Flood p.458)
Effects can be potentiated by tricyclic antidepressants and MAOI (monoamine oxidase inhibitors)

43
Q

Ephedrine Dose and Route

A

Route – IV bolus (5-10mg) for perioperative hypotension;
Oral for bronchial asthma (Beta 2 adrenergic agonist) (Flood)
IM for antiemetic effect (less sedation compared to droperidol)
Dose – 5-10mg IV bolus (p.459, Flood); 5 to 25mg (or 100-300mcg/kg) (p.635, Nagelhout)
0.5mg/kg IM for antiemetic

44
Q

Ephedrine MOA

A

indirectly stimulates alpha- and beta- adrenergic receptors; Direct stimulation of adrenergic receptors AND stimulation of release of endogenous norepinephrine (indirect acting)

45
Q

Ephedrine Elimination

A

Slower elimination compared to epinephrine; up to 40% of single dose is excreted unchanged in urine; Small quantities are metabolized by liver

46
Q

Ephedrine Onset

A

IV: Immediate;
IM: Few minutes

47
Q

Ephedrine Peak

A

Immediate IM: 10-20 minutes

48
Q

Ephedrine Duration

A

Duration of ephedrine is 10 to 60 min after intravenous administration

49
Q

Ephedrine Misc

A

Ephedrine doesn’t cause hyperglycemia (unlike epinephrine); Pupillary dilation occurs, and CNS stimulation does occur occasionally. (Flood p.459)
Second dose produces a less intense CV response (tachyphylaxis)
Supply: 50mg/ml

50
Q

Epinephrine Name (generic and trade)

A

Epinephrine Hydrochloride (Adrenaline Chloride)

51
Q

Epinephrine Classification

A

Endogenous Catecholamine

52
Q

Epinephrine Dose and Route

A

Concentration: 1:1000 (1 mg/ml) 20 kg = 0.2 ml and 1:10,000 (0.1mg/ml) 20 kg = 2 ml
Dose: Inotropic support: 2-20mcg/min or 0.1-1mcg/kg/min.
Anaphylaxis: 100-300 mcg IV push. >10mcg/min- major α effects=vasoconstriction.
Dose limit for exogenous Epinephrine: 6 mcg/kg for Iso, Des, Sevo. ( Nagelhout ,554)
Route: IV, SuQ, IM. *Et-Tube (Flood, 449 and Nagelhout 557)

53
Q

Epinephrine MOA

A

MOA: α1, α2, ß1, ß2 and ß3 adrenergic; However more direct β than α stimulation resulting in: ↑ CO/HR/contractility (Flood, 454)

54
Q

Epinephrine Elimination

A

Renal

55
Q

Epinephrine Onset

A

immediate

56
Q

Epinephrine Peak

A

3 mins

57
Q

Epinephrine Duration

A

5-10 mins

58
Q

Epinephrine Misc

A

Use in cardiac arrest, anaphylaxis, Inotropic support, to increase duration of local anesthetics and for bronchodilation. Carefully administer in patients with MI/angina (worsens), Hyperthyroidism and Diabetes. Watch for arrhythmias and Hypertension. Hypokalemia due to the activation of the Na+/K+ ATPase.

59
Q

Neo-Synephrine Name (generic and trade)

A

Phenylephrine

60
Q

Neo-Synephrine Classification

A

Synthetic noncatecholamines, Alpha1 adrenergic agonist

61
Q

Neo-Synephrine Contraindications

A

Use phenylephrine with extreme caution in elderly patients and patients with hyperthyroidism, bradycardia, partial heart block, or severe arteriosclerosis.

62
Q

Neo-Synephrine Dose and Route

A

Dose: Intravenous bolus 10-200mcg IV bolus (Range between all text books) 50-100mcg “majority of the time,” per Dr. Hammon, IV infusion 20-100mcg/min (Flood), do not exceed 0.5mg initial dose or repeat sooner than 15 minutes (Nagelhout handbook).

Route:
Intravenous.
topical (nose spray/eye drops)

63
Q

Neo-Synephrine MOA

A

Stimulates alpha1 adrenergic receptors by a direct effect

64
Q

Neo-Synephrine Elimination

A

Renal

65
Q

Neo-Synephrine Onset

A

Immediate

66
Q

Neo-Synephrine Peak

A

1 min

67
Q

Neo-Synephrine Duration

A

15-20 mins

68
Q

Neo-Synephrine Misc

A

Supply: 10mg/ml

Phenylepherine stimulates alpha 1 receptors by direct effect, MINIMAL effects on beta receptors.

69
Q

Atropine Name (generic and trade)

A

Atropine Sulfate

Atro-Pen

70
Q

Atropine Classification

A

Anticholinergic - competitive acetylcholine antagonist at muscarinic receptors

71
Q

Atropine Contraindications

A

angle closure glaucoma
acute hemorrhage
tachycardia
obstructive disease in the GI tract

72
Q

Atropine Dose and Route

A

Adult: 0.4 - 0.6 mg IV (Nurse Anesthesia pg. 162)
Pedi: 0.02 mg/kg PO, IV, IM (Nurse Anesthesia pg. 1124)
Route
IV method preferred; it can be given PO, IM, or endotracheal (from all resources)

73
Q

Atropine MOA

A

Antagonists of acetylcholine at muscarinic receptors by inhibiting the action of acetylcholine at postganglionic sites and inhibition of action of neurotransmitter on postsynaptic receptor M1, M2

74
Q

Atropine Elimination

A

Mostly metabolized by the liver, the remaining 30 - 50% is excreted unchanged by the kidneys

75
Q

Atropine Onset

A

1-2 mins

76
Q

Atropine Peak

A

2-4 mins

77
Q

Atropine Duration

A

1-2 hours

78
Q

Atropine Misc

A

May cause transient bradycardia with low doses

79
Q

Atropine Misc

A

May cause transient bradycardia with low doses

Supply: 0.4mg/ml

Pharm 2 (13 decks)

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