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*Pharmacology > Apex-IV anesthetics > Flashcards

Apex-IV anesthetics Flashcards

1
Q

2,-6 Diisopropylphenol

A

Propofol

Diso-PROPYL-phenol

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2
Q

What is the preservative in generic propofol that can precipitate bronchospasm in asthmatics?

A

Sodium metabisulfate

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3
Q

What is disodium edetate

A

The preservative found in diprivan

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4
Q

Why should generic propofol be avoided in infants?

A

Bc it’s preservative benzyl alcohol cant be given to infants

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5
Q

Induction dose of Propofol

A

1.5-2.5mg/kg IV

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6
Q

Antiemetic effects of propofol are seen at what dose?

A

10mcg/kg/min

(or 10-20mg IVP)

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7
Q

Onset of propofol

A

30-60 seconds

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8
Q

Duration of propofol

A

3-8 minutes

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9
Q

Metabolism of propofol

A

Liver (P450 enzymes)
+extrahepatic metabolism (lungs)

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10
Q

The active metabolite of propofol

A

none

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11
Q

Why is propofol likely safe to administer in those with egg allergies?

A

Bc most people with egg allergies are allergic to the albumin in the egg whites.

Egg lechin is derived from the YOLK (think yellow cap)

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12
Q

Is propofol safe to give in someone with a soy allergy? why or why not?

A

bc any soy proteins capable of producing an immune response are removed during the refining process

soy safe and peanut safe

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13
Q

3 ways to decrease burning of propofol

A
  1. Inject into a larger/more proximal vein
  2. Lidocaine prior or mixed
  3. Opioid prior
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14
Q

What is wakening from propofol due to?

A

Redistribution out of the brain

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15
Q

When must propofol in a syringe be discarded?

What about in a vial/tubing?

A

syringe- 6 hours

vial/tubing = 12 hours

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16
Q

Risk factors for Propofol infusion syndrome (6)

A

Prop > 4mg/kg/hr (67mcg/kg/min) [dose]
Inufsion > 48 hours [length]
Sepsis (inadequate o2 delivery)
continuous catecholamine infusions
High dose steroids
Significant cerebral injury

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17
Q

Explain propofol infusion syndrome

A

Prop contains long chain triglycerides (LCT)

increased LCT load impairs oxidative phosphorylation and fatty acid metabolism

  • this starves cells of o2 > esp in cardiac and skeletal muscle
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18
Q

S/S PIS

A

*Refractory bradycardia > asystole + at least one of the following:

  1. metabolic acidosis (base deficit > 10mmol/L)
  2. Rhabdo
  3. Enlarged or fatty liver
  4. Renal failure
  5. HLD
  6. Lipemia (cloudy plasma or blood) - may be an early sign
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19
Q

Tx of PIS (7)

A

D/C propofol
*Maximize gas exchange
-cardiac pacing
PDE inhibitors
Glucagon
ECMO
CRRT

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20
Q

Which drug?

A

Propofol

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21
Q

Respiratory effects of propofol

A

Decreased respiratory drive

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22
Q

CV effects of propofol (4)

A

Decreased BP, SVR, preload, contractility

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23
Q

CNS effects of propofol (5)

A

decreased CMRO2 (cerebral o2 consumption

decreased CBF, ICP, and IOP

*anticonvulsant properties (very rare reports of it inducing seizures)

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24
Q

T/F - Propofol has minor analgesic effects

A

False- none

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25
Q

PKA of propofol

A

11

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26
Q

Does propofol affect the CO2 response curve?

A

Yes, it shifts it to the right (less sensitive to CO2) > resp depression &/or apnea

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27
Q

T/F: Propofol inhibits hypoxic ventilatory drive

A

True

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28
Q

Propofol vials must be cleansed with ____% isopropyl alcohol first.

A

70%

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29
Q

What turns urine green or cloudy with propofol infusion?

*Does it indicate renal impairment or dysfunction?

A

Green = phenol exretion

Cloudy = increased uric acid secretion

*does not suggest renal impairment or dysfunction

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30
Q

Does propofol at the gaba-A receptor reduce or increase RMP?

A

reduces RMP (moves it further away from TP)

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31
Q

What organs are primarily responsible for propofol metabolism?

A

Liver (P450) & lungs

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32
Q

Does propofol increase or decrease the apneic threshold?

A

Increases it (more likely to become apneic)- closer to threshold = more likely to happen

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33
Q

What drug is Lusedra?

A

Fospropofol

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34
Q

Phosophono-O-methyl-2,5-Dissopropylphenol

A

Fospropofol

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35
Q

MOA of fospropofol +(onset and duration)

A

Prodrug - it’s metabolized into propofol by the enzyme Alkaline Phosphatase (in the blood)

*slower onset (5-10 mins), longer duration (15-45 mins)

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36
Q

T/F: Fospropofol is prepared as an aqueous solution

A

True - doesn’t burn or support microbial growth like propofol

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37
Q

Side effect of Fospropofol

A

Genital and anal burning

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38
Q

Initial and repeat bolus’s of fospropofol and frequency

A

initial: 6.5mg/kg

repeat bolus: 1.6mg/kg

(not more than q4min)

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39
Q

Active metabolite of fospropofol

A

Propofol

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40
Q

Fospropofol –> Propofol + _______ + ________

how is it metabolized?

A

Propofol + Formaldehyde + Phosphate

Formaldehyde is metabolized to formate and excreted in the urine

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41
Q

What drug?

A

Fospropofol

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42
Q

Primary MOA of Ketamine

A

NMDA antagonist (antagonizes glutamate, causes of dissociative state)

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43
Q

What are the secondary MOAs by which ketamine works (6)

A

Opioid (treats pain)

MAO (treats depression)

Serotonin (treats depression)

NE (SNS stimulant)

Sodium channels (SNS stimulant)

Muscarinic (increased secretions)

*think: pain, depression (2), SNS (2) & secretions

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44
Q

What happens when glutamate binds to the NMDA receptor?

Where does ketamine bind to the receptor and what happens when it does?

A

The mag core pops out and calcium and sodium enter the cell (depolarization)

Ketamine binds to the PCP receptor and when that happens, glutamate can no longer bind. Therefore, Calcium and sodium can’t enter the cell so no depolarization takes place

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45
Q

Ketamine causes dissociative anesthesia at the __________ (place in brain)

A

Thalmus

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46
Q

T/F: ketamine leaves airway reflexes intact

A

True

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47
Q

Ketamine onset:

IV:

IM:

PO:

A

IV: 30-60 seconds (same as propofol, etomidate)

IM: 3-5 minutes

PO: variable

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48
Q

Clearing organ of ketamine

A

Liver

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49
Q

Ketamine induction doses:

IV, IM, PO

A

IV: 1-2mg/kg

IM: 4-8mg/kg

PO: 10mg/kg

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50
Q

Bolus dose of ketamine

onset/duration

A
  1. 2-0.5mg/kg
    onset: 1-2 minutes

duration- 10-20 minutes

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51
Q

How long may it take after dosing ketamine to return to full orientation?

A

60-90minutes

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52
Q

T/F: Ketamine has an active metabolite

A

True : Norketamine

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53
Q

Opioid-sparing doses of ketamine

A

0.1-0.5mg/kg

1-3mcg/kg/min

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54
Q

Clearance of Ketamine

A

Liver- P450 enzymes

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55
Q

Excretion of ketamine

A

Renal *caution- active metabolite can build in renal impairment

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56
Q

T/F: Ketamine does not alter respiratory drive

A

true

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57
Q

Which IV anesthetic increases oral secretions

A

Ketamine (muscarinic effect)

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58
Q

CV effects of ketamine (4)

A

increased SNS tone, SVR, HR, CO

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59
Q

CNS effects of ketamine (4)

A

increased ICP, IOP, nystagmus, analgesia

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60
Q

Which IV anesthetic causes emergence delirium and lowers the seizure threshold

A

Ketamine

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61
Q

T/F: Ketamine should be avoided in patients with a seizure hx

A

True - lowers seizure threshold (TP drops closer to RMP)

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62
Q

True/Fale: Ketamine is a safe drug to give in someone with acute intermittent porphyria

A

False

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63
Q

2-(o-cholophenyl)- 2 (methylamino) cyclohexanone hydrochloride

A

Ketamine

*It’s called ketamine because it has a ketone group and an amine group

2-(o-cholophenyl)- 2 (methylamino) cyclohexanone hydrochloride

(you can also maybe use cyclohexanone thinking your brain feels like a cyclone on ketamine)

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64
Q

Which Iv induction agent is a Arylcyclohexylamine

(amine group + cyclone)

A

Ketamine

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65
Q

Which drug is a phencyclidine derivative?

A

Ketamine (PCP derivitive)

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66
Q

PKA of ketamine

A

7.5 (basic bitches love ketamine)

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67
Q

T/F: ketamine is a racemic mixture

A

True

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68
Q

Which drug

A

Ketamine

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69
Q

5 patient populations to avoid ketamine in

A
  1. CAD (indirect sympathomimetic - increases cardiac workload and O2 consumption)
  2. Pt’s with hx seizures (lowers threshold for seizures)
  3. Increased ICP
  4. Hypertensive patients
  5. Pt’s with RV failure (increases pulm vas resistance)

(sub hypnotic doses <0.5mg/kg usually don’t activate the SNS)

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70
Q

2 ways ketamine effects the lungs

A
  1. bronchodilation (good for asthma/COPD)
  2. increased pulm. vasc resistance (caution in severe RV failure/pulm HTN)
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71
Q

T/F: ketamine is direct myocardial depressent

A

True! It will be seen in patients with depleted catecholamine stores (sepsis, hf, sympathectomy) - need an intact SNS to have the sympathomimetic effects

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72
Q

How does ketamine affect the CO2 response curve

A

It doesn’t

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73
Q

T/F ketamine is a good choice for ocular surgery

A

False- causes nystagmus

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74
Q

Best way to prevent emergence delirium and hallucinations associated with ketamine

A

Benzos (midaz > diaz)

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75
Q

Risk factors for emergence delirium from ketamine (4)

A

age > 15

female

ketamine dose > 2mg/kg

hx personality disorder

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76
Q

Does ketamine relieve somatic or visceral pain more?

A

Somatic

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77
Q

What agent prevents opioid-induced hyperalgesia as seen after remi infusions?

A

Ketamine

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78
Q

Which induction agent blocks central sensitization and wind-up in the dorsal horn of the spinal cord?

A

Ketamine

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79
Q

Plasma protein binding of:

Dexmedetomidine, Midazolam, Diazepam, Lorazepam, Propofol, Etomidate, Ketamine

A

Propofol & Diazepam = 98%

Midazolam & Dexmedetomidine = 94%

Lorazepam = 90%

Etomidate = 75%

*Ketamine = 12%

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80
Q

MOA of etomidate

A

GABA-A agonist

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81
Q

Onset of Etomidate

A

30-60 seconds (same as propofol and ketamine)

82
Q

Duration of Etomidate

A

3-8 mins (slightly shorter than prop due to metablism by liver + esterases)

83
Q

Clearance/Metabolism of Etomidate

A

Liver AND plasma Esterases

84
Q

3 E’s of Etomidate

A

Etomidate

Emetic

Esterases

85
Q

Induction dose of Etomidate

A

0.2-0.4mg/kg

86
Q

Respiratory effects of etomidate

A

mild respiratory depression

87
Q

CV effects of etomidate

A

minimal

88
Q

CNS effects of Etomidate (4)

A

decreased CMRO2

decreased CBF (cerebral vasoconstriction)

decreased ICP

may activate seizure foci

89
Q

Which drug

A

Etomidate

90
Q

Active metabolite of etomidate

A

None

91
Q

T/F - rapid awakening following etomidate is due to metabolism, not redistribution

A

False - it’s due to redistribution

92
Q

R-1-Methyl-1 (a-methylbenzyl) imidazole-5-carboxylate

A

Etomidate

R-1-Methyl-1 (a-methylbenzyl) imidazole-5-carboxylate

93
Q

Class of etomidate

A

Imidazole

Aciditic pH > ring opens > increased water solubility

physiologic pH > ring closes> increased lipid solubility

(open and water goes in, closes and can cross lipid membranes)

94
Q

Mechanism by which etomidate causes adrenocortical supression

A

Inhibits 11-beta hydroxylase

(no cortisol or aldosterone synthesis)

95
Q

Which anesthetic agent increases mortality in patients with Addisonian crisis?

A

Etomidate

96
Q

A single dose of etomidate suppresses adrenocortical function for how long?

A

5-8 hours (some texts say up to 24 hours)

97
Q

T/F- etomidate does not cause seizures if the patient does not have a history of seizures

A

True

-but can be useful for mapping seizure foci

98
Q

T/F: etomidate can cause acute intermittent porphyria

A

True

99
Q

T/F- etomidate can cause myoclonus

A

True

100
Q

T/F- etomidate is a good agent for septic patients

A

False- septic patients rely on the intrinsic stress response to keep them alive, don’t want to knock it out

101
Q

Which induction agents have a sulfur molecule in the second position? (2)

What does that do?

A

Thiopental, Thiamylal

-increases lipid solubility and potency

102
Q

Anesthetic management of acute intermittent porphyria

A
  1. Liberal hydration
  2. Glucose (reduces alasynthase activity)
  3. Heme Arginate
  4. Prevent hypothermia
103
Q

which agents are unsafe to give in patients with a history of acute intermittent porphyria (7)

A

BBEACKK

Barbituates, Birth control pills, Etomidate, Amiodarone, CCBs, Ketamine, Ketorolac

(everything else is safe- volatiles, nitrous, NMB, reversals, narcotics, midaz, ondansetron, vasopressors, betablockers)

104
Q

What is a key enzyme in porphyrin metabolism

(what condition)

A

Alasynthase

(acute intermittent porphyria)

105
Q

MOA of thiopental and where specifically

A

GABA-A agonist

106
Q

Onset of thipental

A

30-60 seconds (same as prop, etomidate, ketamine)

107
Q

duration of thiopental

A

5-10 minutes

108
Q

Clearance/metabolism of thiopental

A

Liver

109
Q

Induction dose of thiopental

A

2.5-5mg/kg IV

110
Q

Respiratory effects of thiopental (2)

A

Decreased resp drive & HISTAMINE RELEASE > bronchoconstriction

111
Q

CV effects of thiopental

A

Hypotension and myocardial depression

112
Q

T/F - thiopental preserves the baroreceptor reflex

A

True (unlike propofol, so lesser degree of hypotension bc HR will increase)

113
Q

CNS effects of thiopental (2)

A

Decreased ICP

hyperalgesia

114
Q

Active metabolite of thiopental

A

none- except in really high does > pentobarb i think

115
Q

What can intra-arterial injection of thiopental cause?

A

Intense vasoconstriction and crystal formation leading to tissue necrosis

(tx of vasodilator - phentolamine or stellate ganglion block)

116
Q

What is the gold-standard for ECT and why?

A

Methohexital- it decreases seizure threshold and produces a better quality seizure

117
Q

What does adding a methyl group on the nitrogen do to barbituates? Example?

A

Decreases seizure threshold, increase potency

Methohexital

118
Q

2 Oxybarbituates and their chemical composition

A

Methohixital and PENTObarbital

*there is an oxygen molecule in the 2nd position

119
Q

Best way to determine which position is what (barbiuate structure)

A

5 = R>R; then cockwise to 6, 1 , 2, 3, 4

120
Q

What does hypotension of thiopental mainly a result from

A

Venodilation (decreased preload)

(myocardial depression is a secondary cause)

121
Q

How does thiopental affect the CO2 response curve?

A

Shifts it to the right

122
Q

5-ethyl-S-(1-methybutyl)- 2- thiobarbituric acid

A

Thiopental

5-ethyl-S-(1-methybutyl)- 2- thiobarbituric acid

123
Q

What drug?

A

Thiopental (Sulfur molecule in second position)

(increased lipid solubility and potency)

124
Q

Active metabolite of thiopental

A

after normal dose - none

after high dose - pentobarbital

125
Q

PKA of thiopental

water soluble or lipid soluble

A

9 (highly alkaline)

water soluble

126
Q

5 CNS effects of thiopental

A

Decreased CMRO2

decreased CBF (cerebral vasoconstriction)

decreased ICP (used to treat increased ICP)

decreased EEG activity (can cause burst suppression or isoelectric EEG)

no analgesia (may increase pain perception)

127
Q

Does thiopental provide neuroprotection?

A

For focal ischemia - yes (CEA, temporary occlusion of cerebral arteries)

Global ischemia- no (cardiac arrest)

128
Q

Acute interittent porphyria is made worse by what 4 things

A
  1. ALA synthase stimulation
  2. Emotional stress
  3. Prolonged NPO status
  4. CYP450 induction
129
Q

What is caused by a defect in heme synthesis that promises accumulation of heme precursors?

A

Acute Intermittent porphyria

130
Q

S/S of acute intermittent porphyria (3 body systems)

A
  1. GI: Severe abdominal pain (most common and usually first), N/B
  2. CNS: anxiety, confusion, seizures, psychosis, coma
  3. PNS: skeletal muscle weakness (risk of resp failure), bulbar weakness (risk of aspiration)
131
Q

Barbituates: What does adding a phenyl group at the carbon in the 5 position do? Example?

A
132
Q

T/F regional anesthesia is contraindicated in those with a history of acute intermittent poryphria

A

False- but many clinicians avoid it bc it may be difficult to distinguish block-related complications from an acute porphyria attack

133
Q

Induction dose of methohexital

A

1-1.5mg/kg

134
Q

Which barbituate is excreted unchanged in the urine?

A

Phenobarbital (P450 enzymes metabolize all the others- this one is an outlier)

135
Q

T/F: Precedex produces reliable amnesia

A

False

136
Q

MOA of precedex and where

A

Alpha-2 agonist

>decreases cAMP

>inhibits the locus coeruleus in the PONS (sedation)

>agonizes alpha 2 in the dorsal horn of the spinal cord (analgesia)

137
Q

Onset and duration of precedex

A

onset 3-5 mins
Peak 5-10 mins
duration 10-20 minutes

138
Q

Clearence/metabolism of Precedex

A

Liver

139
Q

Active metabolite of precedex

A

None

140
Q

Loading and maintenance dose of precedex

A

Loading: 1mcg/kg over 10 minutes

Maintenance: 0.4-0.7mcg/kg/hr

141
Q

T/F - precedex preserves respiratory drive

A

True

142
Q

CV effects of precedex

A

Bradycardia and hypotension

(transient HTN can occur with rapid administration due to peripheral alpha 2 receptors and increase calcium response)

143
Q

T/F: precedex decreases ICP

A

False- no effect on ICP

144
Q

Which induction agent has antishivering properties?

A

Precedex

145
Q

T/F: precedex has limited effects on evoked potentials

A

True

146
Q

(s)-4-1 [1-(2,3- Dimethylphenylethyl)- 1H- imizole - monohydrochloride

A

(s)-4-1 [1-(2,3- Dimethylphenylethyl)- 1H- imidazole - monohydrochloride

D+ imidazole = Dexmedetomidine

147
Q

Precedex PKA

acid or base

A

7.1 - acid

water soluble

148
Q

What drug

A

Precedex

149
Q

How does precedex produce analgesia?

A

By alpha-2 stimulation in the dorsal horn of the spinal cord

>reduces substance P and glutamate release

150
Q

What IV anesthetic is useful for a “wake-up” test (ie scoliosis surgery)

A

Precedex

151
Q

How can you give dexmedetomidine to a child without an IV?

A

Via nasal or buccal route

1-2mcg/kg 1 hour before surgery

152
Q

Rank the half life of each (longest to shortest):

Lorazepam, diazepam, midazolam

A

Diazepam, Lorazepam, Midazolam

(think we use midaz for this reason and diaz is a disaster bc of its long elimination half life )

153
Q

What explains the long half life of diazepam and what is it?

A

~ 48 hours

and because it undergoes enterohepatic recirculation

154
Q

8-chloro-6-2(2-flurophenyl)-1-methyl-4-H-imidazol [1,5-a][1,4] benzodiazepine

A

8-chloro-6-2(2-flurophenyl)-1-methyl-4-H-imidazol [1,5-a][1,4] benzodiazepine

Midazolam

155
Q

MOA of midazolam

how does it differ from other IV anesthetics

A

GABA-A agonist

*increases FREQUENCY of channel opening > neuronal hyperpolarization

(other agents usually increase the amount of time the channel is open)

156
Q

Midazolam IV sedation vs IV induction doses

A

Sedation : 0.01- 0.1mg/kg

Induction: 0.1-0.4mg/kg

157
Q

Dose of PO sedation of midaz in kids

A

0.5-1mg/kg

158
Q

PO bioavialability of Midazolam

A

50% due to significant first past metabolism

159
Q

Onset and duration of Midazolam

A

Onset: 30-60 seconds (same as most others)

Duration: 30-60 minutes

160
Q

Clearence/Metabolism of Midazolam

A

Liver (P450 enzymes) and Intestines (P450 enzymes)

161
Q

Active metabolite of Midazolam

A

1- hydroxymidazolam

(1/2 potency of midaz, rapid conjugated itno inactive compound, renal failure prolonged the effect)

162
Q

T/F- sedation doses of midazolam bare little effect on CNS, Resp , and CV systems

A

True

163
Q

T/F - benzos cause retrograde amnesia

A

False- anterograde

164
Q

Can midaz produce isoelectric EEG?

A

No- prop and barbituates can

165
Q

T/F- midazolam provides minimal analgesia

A

False

166
Q

Which IV anesthetic provides spinally mediated skeletal muscle relaxation that can be useful in CP patients

A

Benzos/Midaz

167
Q

Why is propylene glycol added to diazepam and lorazepam but not midazolam?

A

To increase water solublity

but midaz contains an imidazole ring which makes it water soluble inside the vial and lipid soluble inside the bloodstream

168
Q

What limits the usefulness of lorazepam as an anticonvulsant?

A

It’s slow onset

169
Q

What is an ultra-short acting benzo with high affinity for the GABA-A receptor and is indicated for induction and maintenance for adults undergoing procedural sedation lasting less than 30 minutes (endoscopy, bronchoscopy)

A

Remimazaolam

170
Q

T/F benzodiazepems can cause a syngergystic respiratory depression when combined with other sedatives/opioids

A

True * pts with COPD are more sensitive to this

171
Q

Which Drug?

A

Midazolam

172
Q

Order of potency from greatest to least: Midazolam, Diazepam, Lorazepam

A

Lorazepam > Midazolam > Diazepam

173
Q

Which benzo must be protected from light after being removed from its packaging?

A

Remimazolam

174
Q

What is similar to remifentanyl but provides no analgesia and is used for sedation but is metabolized by the non-specific plasma esterases?

A

Remimazolam

175
Q

Remimazolam is contraindicated in patients with a history of severe hypersensitivity to what?

A

Dextran 40

176
Q

T/F: Remimazolam can be reversed with flumazenil

A

True

177
Q

Primary metabolite of Remimazolam and how is it excreted?

A

CNS 7056 - excreted in urine

178
Q

After reconsitution, the single-use vial must be discarded if not used within how many hours for remimazolam?

A

8 hours

179
Q

t 1/2life of remimazolam

A

0.5-2 minutes

180
Q

Peak sedation occurs in how many minutes after administration of Remimazolam?

A

3-3.5 minutes

181
Q

Induction of procedural sedation for Remimazolam

Maintenance infusion rate

A

5mg Iv over 1 minute

(can reduce to 2.5-5mg in sicker patients)

Maintenance- 2.5mg IV over 15 seconds with time lapse of 2 minutes between doses

182
Q

A patient is experiencing a prolonged recovery from midazolam sedation. What is the initial dose of flumazenil (mg)?

A

0.2mg IV

then titrated in 0.1mg increments until desired response is achieved

183
Q

How does flumazenil work?

A

It is a competitive antagonist of the GABA-A receptor and used to reverse sedative effects of benzos

184
Q

What’s the caution with flumazinil?

A

It can cause seizures in benzo dependent patients

185
Q

Duration of action of flumazinil

A

30-60 minutes (which is why repeat dosing may be necessary)

186
Q

T/F: flumazinil does NOT increase the SNS tone, anxiety or neuroendocrine evidence of stress

A

True (unlike narcan)

187
Q

Administering an induction dose of which agent is LEASt likely to produce a rise in PaCO2?

Midaz, ketamine, prop, etomidate

A

Ketamine

188
Q

Which anesthetic agent changes from a water-soluble drug to a lipid-soluble drug after IV injection?

A

Midazolam

-has an imidazole ring, which gives it it’s hydrophilic and lipophilic properties

189
Q

What is the primary pathway of etomidate metabolism?

A

Hydrolysis

Biotransformation is the result of ester hydrolysis at the ethyl-ester side chain.

Plasma esterases and hepatic microsomal enzymes drive the reaction

*Remember - Etomidate = esterases; esterases = hydrolysis !

190
Q

How long will an oral dose of lorazepam maintain a therapeutic plasma concentration?

A. 2-4 hours

B. 6-12 hours

C. 12-24 hours

D. 24-48 hours

A

D. 24-48 hours

PO lorazepam:

Dose = 50mcg/kg 0.05mg/kg

Cp Peak = 2-4 hours

Cp Therapeutic = 24- 48 hours

IV Lorazepam

Dose = 1-4mg

Cp peak = 20-40 minutes (hours vs minutes)

Cp Theraputic = 6-10 horus

191
Q

The excretion of an acidic drug will be faster if
A. the urine output is decreased
B. the urine is alkaline
C. the urine is acidic
D. the liver blood flow is decreased

A

B. the urine is alkaline

192
Q

The absorption and distribution of a drug would fall under the study of
A. pharmacokinetics
B. distributive science
C. pharmacogenomics
D. pharmacodynamics

A

A. pharmacokinetics

193
Q

If you divide the LD50 (lethal dose for 50% of the population) by the ED50 (effective dose for 50% of the population), you are calculating the
A. plasma concentration
B. therapeutic index
C. efficacy index
D. safety margin

A

B. therapeutic index

194
Q

Which body fluid normally has a higher concentration of protein?
A. intracellular fluid
B. interstitial fluid
C. urine
D. plasma

A

A. intracellular fluid

195
Q

The plasma half-life of a drug is directly proportional to its
A. molecular weight
B. rate of metabolism
C. volume of distribution
D. rate of clearance

A

C. volume of distribution

(and decreased clearance (inversely related)

196
Q

Presystemic elimination would be most likely to occur in a drug administered
A. orally
B. intramuscularly
C. subcutaneously
D. intravenously

A

A. orally

197
Q

The termination of action of thiopental is due to
A. metabolism
B. renal excretion
C. biliary excretion
D. redistribution

A

D. redistribution

198
Q

Which of the following plasma proteins binds preferably to acidic drugs?
A. Albumin
B. Transcortin
C. Beta-globulin
D. Alpha-1 acid glycoprotein

A

A. Albumin

199
Q

Which one of the following is a Phase II reaction?

A. Oxidation
B. Hydrolysis
C. Reduction
D. Conjugation

A

D. conjugation

(Phase 1 HORs)

200
Q

What is the major intracellular anion?
A. chloride
B. phosphate
C. sodium
D. potassium

A

Phosphate

*don’t get tripped up; Anion = a negatively charged ion

201
Q

Ideally, a medication used for a transdermal application has
A. a pH between 10 and 12
B. a daily dose requirement between 15 and 20 mg
C. absolutely no water-solubility characteristics
D. a molecular weight less than 1000 daltons

A

D

Daily dose <10mg

*Pharmacology (25 decks)

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