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Pharmacology > Pharm A Test 1 > Flashcards

Pharm A Test 1 Flashcards

1
Q

Which subset of pharmacology deals with absorption, distribution, metabolism, and excretion

A

Pharmacokinetics

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2
Q

What subset of pharmacology deals with intrinsic sensitive/responsiveness of the body’s receptors to a drug

A

Pharmacodynamics

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3
Q

What type of receptor is a Beta adrenergic receptor

A

Membrane receptor

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4
Q

What type of receptor is a GABA receptor

A

Ligand-gated ion channel

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5
Q

What type of receptor regulates Na+ channels

A

Voltage-gated ion channels

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6
Q

What is an example of a drug that blocks voltage-gated ion channels

A

Local anesthetics (Lidocaine)

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7
Q

What is the definition of enantiomers

A

2 molecules with the same chemical composition but different orientations - mirror images

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8
Q

What is a racemic mixture

A

When 2 enantiomers are present in equal proportion

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9
Q

A drug that combines directly with its receptor to trigger a response is what type of agonist

A

Directly acting receptor agonist

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10
Q

A drug that produces its physiologic response by increasing the concentration of endogenous substrate (NT or hormone) at receptor site is what type of agonist

A

Indirectly acting receptor agonist

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11
Q

What type of agonist is phenylephrine

A

Direct - binds to alpha receptors and directly activates them

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12
Q

What type of agonist is ephedrine

A

Indirect - evokes the release of norepinephrine from post synaptic nerve endings

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13
Q

What type of antagonism can be overcome by increasing the agonist concentration at the receptor site

A

Competitive

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14
Q

What type of antagonism cannot be overcome by agonists

A

Noncompetitive

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15
Q

Is neostigmine a competitive or noncompetitive antagonist

A

Competitive

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16
Q

What is a hyperactive response

A

An unusually low dose of drug triggers a pharmacological effect. Occurs in very sensitive patients

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17
Q

What is a hypersensitive response

A

An allergic response to a drug

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18
Q

What is a hyporeactive response

A

The patient requires larger doses for desired effect, often due to tolerance

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19
Q

What is a tachyphylactic response

A

Decrease effectiveness of a drug with multiple doses

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20
Q

What is an example of a drug with a tachyphylactic effect

A

Ephedrine

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21
Q

What is an additive effect of drugs

A

A second drug administered with an initial drug with produce an effect equal to the sum of the 2 doses if administered independently

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22
Q

What is a synergistic effect of drugs

A

2 drugs administered together may produce a greater effect than if they were given alone

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23
Q

What is an example of 2 drugs, when given together, that will produce a synergistic effect on respiratory rate

A

Versed and fentanyl

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24
Q

What is an antagonist effect of drugs

A

2 drugs administered together will have a lesser effect than either given alone

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25
Q

What is a prodrug

A

Pharmacologically inactive compounds designed to maximize the amount of active species that reaches its site of action. The metabolite has the clinical effect

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26
Q

How are drugs administered enterally

A

Via the alimentary tract

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27
Q

What are 3 examples of enteral routes of administration

A

Oral, rectal, sublingual

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28
Q

Which enteral route of administration is subject to first pass hepatic metabolism?

A

Oral, because drugs from GI enter the portal vein

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29
Q

What is an advantage of sublingual administration of drugs

A

Rapid absorption through buccal mucosa and bypasses the liver, dumps directly into SVC

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30
Q

What types of patients might require a drug to be administered rectally

A

Pediatric/uncooperative patients, patients who are vomiting

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31
Q

What are some examples of parenteral routes of administration

A

IV, IM, SC, pulmonary, intra-arterial, intrathecal, nasal, topical, transdermal

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32
Q

What is the difference between topical and transdermal routes of administration

A

Topical administration is for a local effect at the application site. Transdermal administration is for a systemic effect

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33
Q

What are 3 site-specific factors that affect absorption

A

1) Blood flow from the site
2) Surface area for absorption
3) Solubility of the drug at the site

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34
Q

Where does the majority of a drug stay if it has a small volume of distribution

A

In the plasma

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35
Q

How does a high volume of distribution affect the elimination half-life

A

The greater the Vd, the longer the half-life

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36
Q

What does it mean if a drug has a high volume of distribution

A

It indicates that the drug is extensively taken up by tissues

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37
Q

What is the Compartment Models Theory

A

The body is composed of multiple compartments having calculated volumes and we can examine the pharmacokinetics of drugs in terms of what compartments they travel to

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38
Q

Which compartment, central or peripheral, has a rapid uptake of drug

A

Central

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39
Q

What fluids and tissues are included in the central compartment

A

Intravascular fluids and highly perfused tissues like lungs, heart, brain, liver

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40
Q

What percentage of total cardiac output goes to the central compartment

A

75%

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41
Q

The central compartment makes up what percentage of body mass

A

10%

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42
Q

What tissues are included in the peripheral compartment

A

Less vascular tissues like fat bone, and inactive skeletal muscle

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43
Q

From which compartment are drugs eliminated

A

Central compartment

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44
Q

What is the basic concept of volume of distribution

A

The total approximation of all the compartments to which a drug goes. Relates the amount of drug in the body to the concentration in the blood

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45
Q

What is the “distribution phase” of drug metabolism

A

Immediately after administration, movement from central to peripheral compartments

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46
Q

What is the “elimination phase” of drug metabolism

A

More gradual, as drug is removed from circulation

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47
Q

What type of drugs does albumin carry

A

Acidic

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48
Q

Which protein carries basic drugs

A

Alpha-1-acid glycoproteins

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49
Q

How is degree of protein binding and volume of distribution related

A

They are inversely proportional

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50
Q

Do drugs cross membranes when they are bound or unbound

A

Unbound

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51
Q

How does ionization affect drug action?

A

Whether or not it exists predominately in an ionized vs nonionized state affects how well it permeates membranes

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52
Q

What 2 things determine the degree of ionization of a drug?

A

pKa of substrate, pH of surrounding fluid

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53
Q

Which form of drug, ionized or nonionized, is more lipid soluble

A

Nonionized form

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54
Q

When pKa and pH are identical, which form (ionized or nonionized) is the drug in?

A

It exists in both forms

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55
Q

Acidic drugs are highly ionized at ______ pH, while basic drugs are ionized at ____ pH

A

alkaline (high) pH, acidic (low) pH

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56
Q

What is ion trapping

A

If a membrane separates areas of 2 differing pHs, the nonionized portion of a drug diffuses and equilibrates but the ionized form doesn’t

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57
Q

What occurs in Phase I of metabolic biotransformation

A

The drug is converted to a polar metabolite

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58
Q

What occurs in phase II of metabolic biotransformation

A

Conjugate with endogenous substrate to water soluble

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59
Q

What are the 4 major types of drug metabolism

A

Oxidation, reduction, conjugation, hydrolysis

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60
Q

What are 2 reactions that aid in the clearance of drugs from plasma

A

Ester hydrolysis, Hofmann elimination of cisatricurium

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61
Q

What are some signs of anxiety

A

Diaphoresis (sweating), hyperventilation, tachycardia

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62
Q

What is the onset time of IV midazolam

A

30-60 seconds

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63
Q

What is the peak time of IV midazolam

A

3-5minutes

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64
Q

What is the duration of IV midazolam

A

15-80 minutes

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65
Q

What is the trade name of Lorazepam

A

Ativan

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66
Q

What is the onset time of IV Lorazepam

A

1-2 minutes

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67
Q

What is the peak time of IV Lorazepam

A

20-30 minutes

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68
Q

What is the duration of IV Lorazepam

A

6-10 hours

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69
Q

What is the trade name of Diazepam

A

Valium

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70
Q

How is diazepam usually administered

A

Preop po

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71
Q

What is the half life of midazolam

A

1.9 hours

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72
Q

What is the half life of diazepam

A

43 hours

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73
Q

What is the half life of lorazepam

A

14 hours

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74
Q

Benzodiazepines are _____ soluble at a pH over 6

A

Lipid soluble

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75
Q

Benzodiazepines are ____ soluble at a pH below 6

A

Water soluble

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76
Q

What receptors are affected by benzodiazepines

A

GABAa

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77
Q

Where are most GABAa receptors located

A

Cerebral cortex

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78
Q

Binding of benzodiazepines to GABAa receptors cause what?

A

Hyper polarization of cell

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79
Q

What percentage of receptors are occupied by benzos to treat anxiolysis

A

20%

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80
Q

What percentage of receptors are occupied by benzos to cause sedation

A

30-50%

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81
Q

What percentage of receptors are occupied by benzos to cause unconsciousness

A

60%

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82
Q

What do benzodiazepines cause?

A

Sedation, hypnosis, anxiolysis, anticonvulsant, anterograde amnesia

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83
Q

What are the main clinical uses of benzos

A

Relief of anxiety, sedation and amnesia before procedures

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84
Q

What is the per kilo dose for preop midazolam in kids

A

0.5mg/kg

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85
Q

What is the max dose of midazolam in kids

A

15mg

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86
Q

Which route of administration causes 50% of the drug to be cleared by first pass metabolism?

A

PO (orally)

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87
Q

What 3 things determine the distribution of benzos

A

Lipid solubility, rapid redistribution from brain, volume of distribution

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88
Q

How does the volume of distribution in elderly and obese patients affect the pharmacokinetics of benzos

A

They have a larger volume of distribution so there may be a longer duration of action

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89
Q

What is the percentage of protein binding in benzo metabolism

A

90-98%

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90
Q

What molecule is a main player in the metabolism of benzos in the liver?

A

Cyt P450

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91
Q

How does alcohol affect the clearance of benzos

A

It increases clearance

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92
Q

How are benzo metabolites excreted

A

In the urine

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93
Q

How do benzos affect cerebral blood flow, cmro2, and MAC requirements

A

Decrease cmro2 and cbf, decrease MAC by 30%

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94
Q

How do benzos affect ventilation

A

Can have a dose dependent decrease

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95
Q

How do benzos affect BP and HR

A

Minor decrease in BP and increase in HR

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96
Q

How do benzos work as anti-convulsants?

A

Facilitate the actions of inhibitory GABA

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97
Q

What is the drug and dose that is effective to treat lidocaine toxicity, DTs, and status epilepticus

A

Diazepam 0.1mg/kg IV

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98
Q

Midazolam is __ times more potent than Valium (diazepam)

A

2-3x

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99
Q

What benzos can be used to treat insomnia

A

Oxazepam, flurazepam

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100
Q

What unwanted side effects can be caused by diazepam (valium) and lorazepam (ativan)

A

Thrombophlebitis and venous irritation

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101
Q

What drug is used as a reversal of benzos and what is the dose/max dose?

A

Flumazenil, 0.1-0.2 mg IV - up to 3mg

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102
Q

What types of patients should you try to avoid or limit giving benzos?

A

Elderly, obese, liver failure, acutely intoxicated or recovering alcoholics

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103
Q

What patients might require more benzos?

A

Chronic alcoholic

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104
Q

What barbiturate induction drug is used in electric convulsive therapy?

A

Methohexital

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105
Q

What is the trade name of methohexital

A

Brevital

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106
Q

What is the pH of thiopental?

A

10.5

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107
Q

Why does thiopental burn so bad upon injection?

A

Its pH is so much higher than blood

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108
Q

What would happen if you put thiopental in the same IV line with another drug such as fentanyl?

A

They would crystallize

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109
Q

How long will thiopental last at room temperature?

A

~24 hours

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110
Q

How does thiopental affect GABA receptors?

A

It binds to GABAa and enhances the inhibitory action of GABA in the CNS, which decreases neuronal activity

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111
Q

How does thiopental affect chloride channels?

A

Opens chloride channels and increases the time that they are open, prolonging the inhibitory effect of the GABA channel

112
Q

How does thiopental affect the sympathetic nervous system?

A

Decreases sympathetic nerve signal transmission.

113
Q

How does thiopental’s lipid solubility affect the onset time?

A

It is very lipid soluble so it has a very quick onset

114
Q

What percentage of thiopental is protein bound?

A

80%

115
Q

How does thiopental’s lipid solubility affect its uptake into the brain?

A

There is very quick uptake into the brain due to the high lipid solubility

116
Q

How do people “wake up” from thiopental?

A

It is redistributed from the CNS into other tissues such as fat

117
Q

What is the IV induction dose of thiopental?

A

3-5mg/kg

118
Q

What is the onset time of thiopental?

A

30-40 seconds

119
Q

What is the peak time of thiopental?

A

1 minute

120
Q

What is the duration of thiopental?

A

5-8 minutes

121
Q

How is thiopental metabolized?

A

Slowly by the liver

122
Q

Does thiopental produce active metabolites?

A

No

123
Q

How does thiopental affect elderly and patients with liver dysfunction?

A

It hangs around longer due to decreased blood flow to the liver

124
Q

How is thiopental eliminated?

A

By the kidneys

125
Q

Besides induction of anesthesia, what is another use for thiopental?

A

Treatment of increased intracranial pressure

126
Q

What is focal ischemia?

A

When a blood clot or clamp has reduced flow to a certain area of the brain

127
Q

What is global ischemia?

A

When blood flow to the entire brain is stopped, commonly caused by cardiac arrest

128
Q

What is a normal cerebral perfusion pressure?

A

80-100mmHg

129
Q

What is a normal intracranial pressure for a supine patient?

A

8-12mmHg

130
Q

Approximately what percentage of cardiac output does the brain receive?

A

15%

131
Q

What is the cerebral blood flow rate under normal circumstances?

A

50mL/100g/min

132
Q

What percentage of cerebral blood flow goes to the gray matter of the brain?

A

80%

133
Q

What percentage of cerebral blood flow goes to the white matter of the brain?

A

20%

134
Q

What percentage of the brain’s energy consumption is used to support electrophysiologic function?

A

60%

135
Q

Suppression of cerebral metabolism causes what effect on cerebral blood flow?

A

A reduction in cerebral blood flow

136
Q

What is the mean arterial range of cerebral blood flow?

A

65-150mmHg

137
Q

What is the PaCO2 range of cerebral blood flow?

A

25-70mmHg

138
Q

When PaO2 reduces to below __mmHg, CBF increases dramatically

A

60mmHg

139
Q

How does temperature change affect cerebral blood flow?

A

Primarily by suppressing cerebral metabolism

140
Q

What is one of the best things you can do to the brain if it is going to be ischemic during surgery?

A

Cool it down to reduce its metabolism and blood flow

141
Q

What percentage of oxygen goes to maintaining neuronal electrical activity?

A

60%

142
Q

What percentage of oxygen goes to maintaining cellular integrity of brain cells?

A

40%

143
Q

How does PaCO2 affect cerebral blood flow?

A

PaCO2 varies DIRECTLY with arterial CO2 tension. High PaCO2 levels (hypercapnia) increases blood flow to the brain, low PaCO2 decreases blood flow to the brain

144
Q

How do you calculate cerebral perfusion pressure (CPP)?

A

CPP=MAP-ICP (if no ICP, CVP can be used as substitute)

145
Q

How does ICP therapy with thiopental affect the brain?

A

Decreases metabolic O2 requirements, decreases cerebral blood flow

146
Q

What is the only induction drug that increases cerebral blood flow?

A

Ketamine

147
Q

What type of ischemia is cerebral protection via thiopental useful for?

A

Focal ischemia

148
Q

What surgeries benefit from cerebral protection from focal ischemia via thiopental?

A

Carotid endarterectomy, thoracic aneurysm resection, cerebral aneurysm clipping

149
Q

What are the cardiovascular side effects of thiopental?

A

Decreased blood pressure, increased heart rate

150
Q

What chemical does thiopental cause a release of?

A

Histamine

151
Q

How does thiopental affect body temperature?

A

Decreases body temperature due to vasodilation

152
Q

How does thiopental affect CMRO2?

A

Decreases CMRO2 (cerebral metabolic rate) by up to 55%

153
Q

What are the 2 reasons not to use thiopental?

A

1) Causes hangover

2) Acute intermittent porphyria

154
Q

What causes Acute Intermittent Porphyria?

A

A deficiency in the enzyme porphobilogen deaminase

155
Q

What are the symptoms of Acute Intermittent Porphryia?

A

Chronic diffuse pain

156
Q

Is methohexital more or less lipid soluble than thiopental? How does this affect its distribution?

A

More lipid soluble so it hangs around in the CNS longer than thiopental before it gets redistributed to peripheral compartments

157
Q

What is the IV induction dose of methohexital?

A

1-1.5mg/kg

158
Q

What is a common side effect of methohexital?

A

Hiccups

159
Q

What component of propofol makes it burn upon injection?

A

Glycerol

160
Q

What component of propofol supports bacterial growth?

A

Egg phosphatide

161
Q

The shelf life of propofol depends on what component?

A

The amount/type of bacterial retardant

162
Q

How does propofol work in the CNS?

A

Decreases the rate of dissociation of GABA from the receptor, thereby increasing the duration of the GABA-activated opening of the Cl- channel with resulting hyperpolarization of cell membranes

163
Q

What is the onset time of propofol?

A

30 seconds

164
Q

When is the peak effect of propofol?

A

90-100 seconds

165
Q

What is the duration of propofol?

A

5-10 minutes

166
Q

What is the distribution half life of propofol?

A

2-8 minutes

167
Q

What is the half life of prolonged infusions of propofol?

A

40 minutes

168
Q

How is propofol metabolized?

A

By the liver and some by the lungs

169
Q

Does propofol cross the placenta?

A

Yes, but there are no deleterious side effects to the baby because they can distribute propofol as well

170
Q

What percent decrease in propofol dosing should you consider for elderly patients?

A

25-50%

171
Q

Why do elderly patients require a decrease in propofol dosing?

A

They have a smaller central distribution volume and decreased clearance

172
Q

How does propofol affect memory?

A

Causes anterograde amnesia (forget everything from that point forward)

173
Q

How does propofol affect the cardiovascular system?

A

Decreases blood pressure, increases heart rate

174
Q

How does propofol affect the pulmonary system?

A

Big increase in propofol can cause a big drop in respiratory rate and tidal volume

175
Q

How does propofol affect the hepatic/renal system?

A

Decreases blood flow to these systems

176
Q

How does propofol affect hypoxic pulmonary vasoconstriction?

A

It remains in tact

177
Q

What is a major side effect of propofol injection?

A

Pain on injection

178
Q

What is the induction dose of propofol?

A

1-2.5mg/kg

179
Q

What is the dosing rate of propofol for IV sedation?

A

25-100mcg/kg/min

180
Q

What is the dosing rate of propofol for a general anesthetic TIVA?

A

100-200mcg/kg/min

181
Q

What is the normal limit on how long you should run someone on a propofol infusion?

A

72 hrs, after that you worry about hyperlipidemia

182
Q

How much propofol would be useful to treat PONV?

A

10-15mg

183
Q

What is the dose of propofol for antipruritic (anti-itching) effects?

A

10mg

184
Q

Other than induction, anti-itching and anti-emetic, what are other uses of propofol?

A

Anticonvulsant and treatment of bronchoconstriction

185
Q

What is the solubility of etomidate in solution? In plasma?

A

Water soluble in solution, lipid soluble in plasma

186
Q

What makes etomidate burn so badly?

A

It is made up of 35% glycerol

187
Q

How does etomidate work in the CNS to induce anesthesia?

A

Depresses reticular activating systems and mimics the CNS inhibitory effects of GABA

188
Q

What is the onset of etomidate?

A

30 seconds

189
Q

When is the peak effect of etomidate?

A

1 minute

190
Q

What is the duration of etomidate?

A

3-5 minutes

191
Q

How protein bound is etomidate?

A

76-77%

192
Q

What is the elimination half life of etomidate?

A

2.6 hours

193
Q

In patients with what comorbidity would you want to decrease the dose of etomidate?

A

End stage liver failure b/c etomidate could have an exaggerated effect

194
Q

How is etomidate metabolized?

A

Hydrolysis, hepatic enzymes

195
Q

How is etomidate eliminated?

A

Water soluble metabolites are eliminated by the kidneys

196
Q

How does etomidate affect cerebral blood flow and metabolism?

A

Decreases by 35-45%

197
Q

How does etomidate affect an EEG? What patients should you be cautious with using it?

A

Increases excitatory spikes in an EEG, caution in seizure patients

198
Q

What system of the body is etomidate known for keeping stable?

A

Cardiovascular

199
Q

How does etomidate affect ventilation?

A

Patients maintain respiratory rate

200
Q

What muscular side effect is caused by etomidate?

A

Myoclonus

201
Q

What induction drug causes adrenocortical suppression?

A

Etomidate

202
Q

Why does etomidate cause adrenocortical suppression?

A

It inhibits 11-beta hydroxylase enzyme

203
Q

Besides myoclonus, burning, and cortisol depression - what are some other side effects of etomidate?

A

Nausea and hiccups

204
Q

In what clinical situations would it be beneficial to use etomidate?

A

Challenging cardiac cases. hypovolemic trauma patients, and burn patients during mask ventilation

205
Q

What is the non-barbiturate induction agent with analgesic effects?

A

Ketamine

206
Q

What is the main neurologic effect of ketamine?

A

Emergence delerium

207
Q

How does ketamine affect MAO?

A

Inhibits norepi uptake which is why blood pressure doesn’t decrease

208
Q

How does ketamine affect muscarinic receptors?

A

Slightly antagonizes

209
Q

How does ketamine affect NMDA receptors?

A

Non-competitive antagonist to NMDA receptors

210
Q

How does ketamine affect opioid receptors?

A

Slightly agonizes

211
Q

What is the onset time of IV ketamine?

A

30 seconds

212
Q

What is the onset time of IM ketamine?

A

3-4 minutes

213
Q

What is the duration of IV ketamine?

A

5-10 minutes

214
Q

What is the duration of IM ketamine?

A

12-25 minutes

215
Q

What is the solubility of ketamine?

A

Lipid soluble

216
Q

Is ketamine highly protein bound?

A

No, only 27%. there is a lot of free drug to bind to different receptors

217
Q

What is the elimination time of ketamine?

A

2.5 hrs

218
Q

How is ketamine metabolized?

A

By hepatic C450 enzymes

219
Q

What is the active metabolite produced by ketamine metabolism?

A

Norketamine - builds up if you run an infusion of ketamine

220
Q

How is ketamine eliminated?

A

Kidneys

221
Q

What is the analgesic infusion dose of ketamine?

A

0.1-0.5mg/kg/hr

222
Q

Is ketamine better for somatic or visceral pain?

A

Somatic

223
Q

What receptors does ketamine bind to if used in an epidural/spinal?

A

Mu receptors

224
Q

What is the IV induction dose of ketamine?

A

1-2mg/kg

225
Q

What is the IM induction dose of ketamine?

A

4-8mg/kg

226
Q

How does ketamine affect intracranial pressure?

A

Increases it by increasing cerebral blood flow and cerebral metabolism

227
Q

How does ketamine affect EEG?

A

Has an excitatory effect on EEG

228
Q

Should ketamine be used for burst suppression?

A

No b/c of the excitatory effects on the EEG

229
Q

Should ketamine be used for SSEP?

A

Yes b/c it helps with the strength of the signal

230
Q

How does ketamine affect ventilation?

A

No depression, until you get to very high end of IV doses

231
Q

How does ketamine affect the airway?

A

Increased secretions, bronchodilation

232
Q

How does ketamine affect the cardiovascular system?

A

Increases BP (mainly systolic), HR, CO

233
Q

What are risk factors of emergence delirium with ketamine?

A

Patients over 15, females, high doses of ketamine, underlying personality disorder

234
Q

What can prevent emergence delirium caused by ketamine?

A

Versed

235
Q

What are some patients who would benefit from induction with ketamine?

A

Burn patients, children, asthmatics

236
Q

What patients/surgeries should you NOT induce with ketamine?

A

1) Elevated ICP/cranial mass
2) Open eye injury
3) Heart disease
4) Vascular aneurysms
5) Psychotic disease

237
Q

What is the IV induction dose of etomidate?

A

0.2-0.6mg/kg

238
Q

What class of drug is dexmedetomidine?

A

Alpha 2 agonist

239
Q

What properties does dexmedetomidine possess?

A

Anxiolytic, anesthetic, hypnotic, analgesic

240
Q

What is the dosing of dexmedetomidine?

A

1mcg/kg over 10 minutes

241
Q

What is the dosing of a dexmedetomidine infusion?

A

0.2-0.7mcg/kg/hr

242
Q

What are the cardiovascular effects of dexmedetomidine?

A

Bradycardia and hypotension

243
Q

Why should you not use ketamine on patients with a bad heart?

A

It is a myocardial depressant

244
Q

How is flumazenil metabolized?

A

By hepatic enzymes. It is metabolized faster than benzos

245
Q

What happens on the monitors after there has been a maximum reduction in cerebral blood flow and metabolism?

A

The EEG flatlines

246
Q

What are the target channels of local anesthetics?

A

Voltage gated Na+ ion channels

247
Q

What is the bacterial retardant in propofol?

A

Disodium edetate

248
Q

What non-barbiturate induction drug causes hiccups?

A

Etomidate

249
Q

What can you not mix midazolam with to make an oral preparation?

A

Grape fruit juice

250
Q

What barbiturate induction drug could you use for burst suppression?

A

Thiopental

251
Q

Which induction drug is metabolized by hydrolysis and hepatic enzymes?

A

Etomidate

252
Q

What are 2 examples of a prodrug?

A

ACE inhibitors, insulin

253
Q

What causes the difference in effect of the same drug administered PO vs. IV?

A

First pass metabolism

254
Q

What does the absorption rate of drugs administered IM and SUBQ depend on?

A

Blood flow rate

255
Q

What are examples of drugs given transdermally?

A

Nicotine and fentanyl patches

256
Q

Which benzo is used for seizure suppression?

A

Diazepam

257
Q

What is the dose of diazepam for seizure suppression?

A

0.1mg/kg

258
Q

What is an example of a drug that requires an enzyme for drug/receptor interaction

A

Phosphodiesterase inhibitor - Milrinone

259
Q

What barbiturate induction drug is supplied as an anhydrous powder and must be refrigerated before use?

A

Thiopental

260
Q

What are normal CMRO2 (cerebral metabolic rate of oxygen) values?

A

3-3.5mL/100g/min

261
Q

What is normal cerebral venous PO2?

A

32-44mmHg

262
Q

What is normal cerebral venous SO2?

A

55-70%

263
Q

Cerebral blood flow is tightly coupled to what?

A

Cerebral metabolism

264
Q

What patients would you want to use propofol carefully with?

A

Patients with cardiovascular disease, sepsis, respiratory disease, increased ICP, hypovolemia, hyperlipidemia

265
Q

What neuro surgery would you want to use propofol carefully in?

A

If they are seizure mapping in a patient with seizure disorder. The propofol’s anticonvulsant properties could hinder the procedure

266
Q

What induction drug should you NOT use if your patient is steroid depleted, on chronic steroids, or immunosuppressed?

A

Etomidate because it decreases circulating levels of cortisol

267
Q

What monitor would become inactive if you tried to use it after administering ketamine?

A

BIS

268
Q

What induction drug would be useful for patients who are on chronic opioids for pain?

A

Ketamine

269
Q

Which induction drug does not have GABA effects?

A

Ketamine

270
Q

What induction drug would you avoid in a patient with schitzophrenia?

A

Ketamine

271
Q

What induction drug would you avoid in a patient with Addison’s Disease?

A

Etomidate b/c they are immunosuppresed

272
Q

What induction drug would be good for a patient with critical aortic stenosis?

A

Etomidate

273
Q

What induction drug would be good for a patient with Down’s syndrome?

A

Ketamine IM

274
Q

What induction drug would be useful in a patient having a spinal fusion with MEP monitoring?

A

Ketamine

275
Q

What induction drug would you avoid in an emergent cerebral aneurysm clipping with burst suppression needed?

A

Ketamine

Pharmacology (6 decks)

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