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USMLE Step 1 -- OLD TEST > Pharmacology > Flashcards

Pharmacology Flashcards

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USMLE® Step 1 flashcards
1
Q

In enzyme kinetics, competitive inhibitors _____ (resemble/do not resemble) the substrate while noncompetitive inhibitors _____ (resemble/do not resemble) the substrate.

A

Resemble; do not resemble

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2
Q

In enzyme kinetics, the value of Km reflects the _____ of the enzyme for its substrate.

A

Affinity

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3
Q

True or False? In enzyme kinetics, the lower the Km, the higher the affinity.

A

True

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4
Q

In enzyme kinetics, Vmax is directly proportional to the _____ _____.

A

Enzyme concentration

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5
Q

In enzyme kinetics, a graph of substrate concentration on the x-axis and velocity of the reaction on the y-axis has _____ (increasing/decreasing) velocity as substrate is increased.

A

Increasing, although it will plateau when the enzyme is saturated

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6
Q

When velocity is equal to one half of its maximum (Vmax), the corresponding concentration of substrate is equal to what value?

A

Km

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7
Q

In enzyme kinetics, the y-intercept of a graph that plots the inverse of velocity on the y-axis and the inverse of substrate concentration on the x-axis is equal to what value?

A

The inverse of Vmax = 1/Vmax

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8
Q

In enzyme kinetics, the x-intercept of a graph that plots the inverse of velocity on the y-axis and the inverse of substrate concentration on the x-axis is equal to what value?

A

The inverse of Km = 1/Km

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9
Q

In enzyme kinetics, the slope of a graph that plots the inverse of velocity on the y-axis and the inverse of substrate concentration on the x-axis is equal to what value?

A

Km/Vmax

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10
Q

In enzyme kinetics, a competitive inhibitor _____ (cannot/can) be overcome by increasing the concentration of substrate; a noncompetitive inhibitor _____ (cannot/can) be overcome by increasing the concentration of substrate.

A

Can; cannot. This is because competitive inhibitors bind the active site of the enzyme, competing with the substrate, whereas noncompetitive inhibitors bind elsewhere on the enzyme and so are not affected by substrate concentration

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11
Q

In enzyme kinetics, competitive inhibitors _____ (increase/decrease/do not change) the Vmax of the reaction, while noncompetitive inhibitors _____ (increase/decrease/do not change the Vmax of the reaction.

A

Do not change; decrease

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12
Q

In enzyme kinetics, competitive inhibitors _____ (increase/decrease/do not change) the Km of the reaction, while noncompetitive inhibitors _____ (increase/decrease/do not change the Km of the reaction.

A

Increase; do not change

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13
Q

What is the formula for calculating the volume of distribution of a drug?

A

Volume of distribution = amount of drug in the body / plasma drug concentration

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14
Q

Drugs with a low volume of distribution, such as 4-8 L, are found in the _____ (blood/extracellular space/tissues).

A

Blood alone; these drugs do not distribute outside the plasma

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15
Q

A drug with a volume of distribution of 15 L is most likely to be found in the _____ (blood/extracellular space/tissues).

A

Extracellular space; these drugs distribute throughout the total body water

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16
Q

In a 75 kg man, a drug has a volume of distribution of 40 L. It can be expected to be found in _____ (blood/extracellular space/tissues).

A

Tissues

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17
Q

What is the formula for calculating the clearance of a drug?

A

Clearance (L/min) = rate of elimination of drug (g/min) / plasma drug concentration (g/L)

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18
Q

What is the definition of the half-life of a drug?

A

The time required to reduce the amount of drug in the body by one half

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19
Q

How many half-lives of a drug must pass before a drug infused at a constant rate reaches approximately 94% of steady-state concentration?

A

Four

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20
Q

Given the volume of distribution and clearance of a drug, how does one calculate the half-life of the drug?

A

Half-life = (0.7 × volume of distribution) / clearance

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21
Q

After one half-life, given constant intravenous infusion of a drug, how close to steady-state is the concentration of the drug?

A

50% of steady-state concentration

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22
Q

After three half-lives, given constant intravenous infusion of a drug, how close to steady-state is the concentration of the drug?

A

87.5% of steady-state concentration

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23
Q

What is the formula for the loading dose of a drug?

A

Loading dose = (target plasma concentration × volume of distribution) / bioavailability

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24
Q

What is the formula for maintenance dose of a drug administered intravenously?

A

Maintenance dose = rate of elimination/bioavailability = (target plasma concentration × clearance) / bioavailability

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25
Q

How do loading and maintenance doses of drugs differ for patients with hepatic and renal disease?

A

For both hepatic and renal disease, loading dose does not change, but maintenance dose decreases

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26
Q

What is the bioavailability of a drug if it is administered intravenously?

A

100%

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27
Q

In zero-order elimination of drugs from the body, what is the relationship between the rate of elimination and the drug concentration?

A

The rate of elimination is constant regardless of drug concentration

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28
Q

What are three drugs that exhibit zero-order elimination?

A

Phenytoin and ethanol; aspirin at toxic concentrations

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29
Q

In first-order elimination of drugs from the body, what is the relationship between the rate of elimination and the drug concentration?

A

The rate of elimination is directly proportional to the drug concentration; a constant fraction (rather than a constant amount) is eliminated

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30
Q

In zero-order elimination of drugs from the body, how does the plasma concentration of a drug change over time: linearly or exponentially?

A

Linearly

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31
Q

In first-order elimination of drugs from the body, how does the plasma concentration of a drug change over time: linearly or exponentially?

A

Exponentially

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32
Q

Weak acids get trapped in _____ (acidic/basic) environments.

A

Basic

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33
Q

Weak bases get trapped in _____ (acidic/basic) environments.

A

Acidic

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34
Q

What substance is given to enhance the renal clearance of weakly acidic drugs such as phenobarbital, methotrexate, and aspirin?

A

Bicarbonate

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35
Q

What substance is given to enhance the renal clearance of weakly basic drugs such as amphetamine?

A

Ammonium chloride

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36
Q

Ionized species become trapped in urine because they are not _____ _____.

A

Lipid soluble; therefore, they cannot cross cell membranes

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37
Q

A 24-year-old man attempts suicide by consuming a small bottle of aspirin. After three hours he thinks better of it, and comes to the emergency room. He is put in your care, and you start him on intravenous saline with bicarbonate. By what mechanism does this help him?

A

Bicarbonate alkalinizes the lumen of his nephrons, which traps acetylsalicylic acid within the lumen because it is a weak acid and is ionized in a basic environment

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38
Q

What three types of biochemical reactions are involved in the phase I metabolism of drugs?

A

Reduction, oxidation, and hydrolysis

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39
Q

What is the polarity of the drug products that result from phase I metabolism?

A

The products are slightly polar

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40
Q

True or False? Drug products that result from phase I metabolism are water soluble.

A

True

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41
Q

True or False? Drug products that result from phase I metabolism are often still active.

A

True

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42
Q

What enzyme system mediates the phase I metabolism of drugs in the body?

A

Cytochrome P-450

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43
Q

What three types of biochemical reactions are involved in the phase II metabolism of drugs?

A

Acetylation, glucuronidation, and sulfation; these are conjugation reactions

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44
Q

Do geriatric patients lose the ability for phase I or phase II drug metabolism first?

A

Phase I

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45
Q

Phase I metabolism of drugs yields _____ (nonpolar/slightly polar/very polar) molecules that are _____ (inactive/often still active), whereas phase II metabolism of drugs yields _____ (nonpolar/slightly polar/very polar) molecules that are _____ (inactive/often still active).

A

Slightly polar; often still active; very polar; inactive

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46
Q

The products of phase II metabolism of drugs are excreted by what organ?

A

Kidneys

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47
Q

What is the definition of efficacy?

A

Maximal effect a drug can produce

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48
Q

What is the definition of potency?

A

Amount of drug needed for a given effect

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49
Q

A drug that requires a very low dose to achieve its desired effect is considered _____.

A

Potent

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50
Q

True or False? In pharmacodynamics, when a competitive antagonist is given, the maximal effect of an agonist is decreased regardless of how much additional agonist is given.

A

False; the maximal effect of an agonist is still achievable in the presence of a competitive antagonist if increased amounts of the agonist are given

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51
Q

What is the effect of a noncompetitive antagonist on the position of an agonist’s dose-response curve?

A

It vertically shrinks; the agonist’s efficacy is decreased

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52
Q

In pharmacodynamics, the addition of a noncompetitive agonist _____ (increases/decreases/does not change) the efficacy of the agonist.

A

Decreases

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53
Q

How does the efficacy of a partial agonist relate to the efficacy of a full agonist of the same receptor?

A

A partial agonist has a lower maximal efficacy than a full agonist

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54
Q

How does the potency of a partial agonist relate to the potency of a full agonist of the same receptor?

A

A partial agonist may be more potent than, less potent than, or equally as potent as a full agonist

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55
Q

What property of a drug is determined by its therapeutic index?

A

Safety; drugs with higher therapeutic indices are less likely to cause toxicities

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56
Q

What is the formula that describes the therapeutic index of a drug?

A

TI (therapeutic index) = LD50 (median toxic dose) / ED50 (median effective dose) (remember: TILE)

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57
Q

Safer drugs have _____ (higher/lower) therapeutic index values.

A

Higher

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58
Q

From which regions of the central nervous system do parasympathetic nerves originate?

A

Cranial and sacral regions

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59
Q

From which regions of the central nervous system do sympathetic nerves originate?

A

Thoracic and lumbar regions

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60
Q

What types of nerves arise from the spinal cord and innervate skeletal muscle directly?

A

Somatic nerves

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61
Q

How many neurons are involved in parasympathetic transmission from the spinal cord to the target organ?

A

Two

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62
Q

True or False? Craniosacral parasympathetic axons synapse on neurons in the peripheral ganglia.

A

True

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63
Q

What neurotransmitter mediates parasympathetic nervous system function?

A

Acetylcholine

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64
Q

What neurotransmitter receptor mediates parasympathetic nervous system function at the peripheral ganglia?

A

Nicotinic acetylcholine receptors

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65
Q

What neurotransmitter receptor mediates parasympathetic tone in the cardiac muscle?

A

Muscarinic acetylcholine receptors (specifically, M2)

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66
Q

What neurotransmitter receptor mediates parasympathetic tone in the smooth muscle?

A

Muscarinic acetylcholine receptors (specifically, M3)

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67
Q

What neurotransmitter receptor mediates parasympathetic tone in the glandular cells?

A

Muscarinic acetylcholine receptors (specifically, M1 and M3)

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68
Q

Somatic nerves that arise from the spine innervate skeletal muscle. What neurotransmitter receptor, which is located on skeletal muscle, receives this input?

A

Nicotinic acetylcholine receptors

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69
Q

How many neurons are involved in sympathetic transmission from the spinal cord to the target organ?

A

Two

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70
Q

Where is the first synapse after the spinal cord in sympathetic innervation of an organ?

A

Preganglionic sympathetic axons synapse on neurons in the paravertebral ganglia

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71
Q

True or False? Preganglionic sympathetic axons synapse on neurons in the peripheral ganglia.

A

False; preganglionic sympathetic axons synapse on neurons in the paravertebral ganglia

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72
Q

At the paravertebral ganglia, the neurotransmitter _____ acts on _____ receptors to mediate sympathetic nervous system function.

A

Acetylcholine; nicotinic acetylcholine

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73
Q

What neurotransmitter mediates sympathetic nervous system function at the sweat glands?

A

Acetylcholine

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74
Q

What neurotransmitter receptor mediates sympathetic nervous system function at the sweat glands?

A

Muscarinic acetylcholine receptors

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75
Q

What neurotransmitter mediates sympathetic tone in the cardiac muscle, smooth muscle, and glandular cells?

A

Norepinephrine

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76
Q

What are four cell types in which α- and β-adrenergic receptors mediate sympathetic tone?

A

Cardiac muscle, smooth muscle, glandular cells, and terminal ends of neurons

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77
Q

What neurotransmitter mediates sympathetic tone in the renal vascular smooth muscle?

A

Dopamine

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78
Q

What neurotransmitter receptor mediates sympathetic tone in the renal vascular smooth muscle?

A

D1 receptors

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79
Q

What two substances are released into the blood from the adrenal medulla after the activation of the sympathetic nervous system?

A

Epinephrine and norepinephrine

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80
Q

How many synapses are involved in activation of the adrenal medulla?

A

One; the adrenal medulla releases epinephrine and norepinephrine into the blood

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81
Q

Are nicotinic acetylcholine receptors ligand-gated sodium-potassium channels or G-protein coupled receptors?

A

Nicotinic receptors are ligand gated sodium-potassium channels

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82
Q

Are muscarinic acetylcholine receptors ligand-gated sodium-potassium channels or G-protein-coupled receptors?

A

Muscarinic acetylcholine receptors are G-protein-coupled receptors that act through second messengers

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83
Q

To what class of G-proteins are α1-receptors linked?

A

q

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84
Q

To what class of G-proteins are α2-receptors linked?

A

i

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85
Q

To what class of G-proteins are β1-receptors linked?

A

s

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86
Q

To what class of G-proteins are β2-receptors linked?

A

s

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87
Q

To what class of G-proteins are M1-receptors linked?

A

q

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88
Q

To what class of G-proteins are M2-receptors linked?

A

i

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89
Q

To what class of G-proteins are M3-receptors linked?

A

q

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90
Q

To what class of G-proteins are D1-receptors linked?

A

s

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91
Q

To what class of G-proteins are D2-receptors linked?

A

i

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92
Q

To what class of G-proteins are H1-receptors linked?

A

q

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93
Q

To what class of G-proteins are H2-receptors linked?

A

s

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94
Q

To what class of G-proteins are V1-receptors linked?

A

q

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95
Q

To what class of G-proteins are V2-receptors linked?

A

s

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96
Q

What are the major effects of α1-receptor activation?

A

It increases vascular smooth muscle contraction, and increases pupillary dilator muscle contraction (mydriasis)

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97
Q

What are the major functions of α2-receptor activation?

A

It decreases sympathetic outflow and decreases insulin release

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98
Q

What are the major functions of β1-receptor activation?

A

It increases heart rate and contractility, increases renin release from the kidneys, and increases lipolysis of adipose tissue

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99
Q

What is the major function of β2-receptor activation on the body’s vasculature?

A

Vasodilation

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100
Q

What is the major function of β2-receptor activation on the respiratory system?

A

Bronchodilation

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101
Q

What effect does β2-receptor activation have on glucagon release?

A

It increases glucagon release

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102
Q

Where are M1-receptors located?

A

The central nervous system

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103
Q

What effect does M2-receptor activation have on cardiac function?

A

It decreases heart rate and contractility

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104
Q

What are the effects of M3-receptor activation?

A

Increased exocrine gland secretions, gut peristalsis, bladder contraction, bronchoconstriction, miosis, and accommodation

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105
Q

What effect does D1-receptor activation have on renal vasculature?

A

It relaxes renal vascular smooth muscle

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106
Q

What are the effects of H1-receptor activation?

A

Pruritis, pain, nasal and bronchial mucus production, contraction of bronchioles

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107
Q

What is the effect of H2-receptor activation?

A

It increases gastric acid secretion

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108
Q

What effect does V1-receptor activation have on vascular smooth muscle?

A

It increases vascular smooth muscle contraction

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109
Q

The activation of what two types of G-protein-coupled receptors can increase vascular smooth muscle contraction? Which receptors mediate vascular relaxation?

A

α1- and V1-receptors increase contraction; relaxation is mediated by β2, and D1 (renal only)

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110
Q

What is the effect of V2-receptor activation? Where are they located?

A

It increases water permeability and reabsorption in the collecting tubules of the kidney

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111
Q

What five types of receptors are coupled with Gq proteins?

A

α1, M1, M3, H1, and V1

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112
Q

What five types of receptors are coupled with Gs proteins?

A

β1, β2, D1, H2, and V2

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113
Q

What three types of receptors are coupled with Gi proteins?

A

a2, M2, and D2

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114
Q

What enzyme is activated directly downstream of Gq-coupled receptors?

A

Phospholipase C

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115
Q

What enzyme is activated directly downstream of Gs-coupled receptors?

A

Adenyl cyclase

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116
Q

What enzyme is inhibited directly downstream of Gi-coupled receptors?

A

Adenyl cyclase

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117
Q

Adenyl cyclase catalyzes the conversion of adenosine triphosphate into what molecule?

A

cAMP

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118
Q

What final effector enzyme is activated by receptors that are coupled with Gs proteins?

A

Protein kinase A

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119
Q

What final effector enzyme is inhibited by receptors that are coupled with Gi proteins?

A

Protein kinase A

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120
Q

Phospholipase C catalyzes the cleavage of membrane lipids into what molecules?

A

Inositol trisphosphate3 and diacylglycerol

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121
Q

What is the effect of increased inositol triphosphate on the intracellular concentration of calcium?

A

It increases the intracellular calcium concentration

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122
Q

What enzyme is activated by diacylglycerol?

A

Protein kinase C

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123
Q

What pharmacologic agent blocks the uptake of choline into cholinergic nerve terminals?

A

Hemicholinium

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124
Q

What enzyme is responsible for the formation of acetylcholine? What are its two substrates?

A

Choline acetyltransferase; Acetyl-CoA and choline

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125
Q

What pharmacologic agent blocks the transport of acetylcholine into the presynaptic vesicles in nerve terminals?

A

Vesamicol

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126
Q

The entry of what ion into the nerve terminal induces the release of acetylcholine into the synaptic cleft?

A

Calcium

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127
Q

What toxin inhibits the calcium-induced release of acetylcholine from the cholinergic nerve terminals?

A

Botulinum

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128
Q

What enzyme breaks down acetylcholine in the synaptic cleft? What two products result from this reaction?

A

Acetylcholinesterase; choline and acetate

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129
Q

Tyrosine transporters are located in the nerve terminals of what type of cells?

A

Noradrenergic cells; tyrosine is the precursor of norepinephrine

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130
Q

Tyrosine is a precursor to the formation of which neurotransmitters? What is the order of their synthesis?

A

Tyrosine, DOPA, dopamine, norepinephrine, epinephrine

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131
Q

What pharmacologic agent blocks the conversion of tyrosine to DOPA?

A

Metyrosine

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132
Q

Tyrosine is converted into dopamine via what intermediate precursor?

A

DOPA; DOPA can be used as a pharmacologic agent to increase central nervous system dopamine

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133
Q

What pharmacologic agent blocks the transport of dopamine into the presynaptic vesicles in nerve terminals?

A

Reserpine

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134
Q

Dopamine is converted into norepinephrine in the ______ (cytoplasm/presynaptic vesicle).

A

Presynaptic vesicles

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135
Q

The entry of what ion into the nerve terminal induces the release of norepinephrine into the synaptic cleft?

A

Calcium

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136
Q

What pharmacologic agent inhibits the calcium-induced release of norepinephrine from the noradrenergic nerve terminals?

A

Guanethidine

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137
Q

What pharmacologic agent stimulates the release of norepinephrine from the noradrenergic nerve terminals?

A

Amphetamine

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138
Q

How is norepinephrine cleared form the synaptic cleft?

A

Diffusion, metabolism (monoamine oxidase A), and reuptake

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139
Q

What pharmacologic agents inhibit the reuptake of norepinephrine into the nerve terminals?

A

Cocaine, amphetamine, and tricyclic antidepressants

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140
Q

What three receptor types modulate the presynaptic release of norepinephrine from the noradrenergic nerve terminals?

A

M2-receptors, angiotensin II receptors, and α2-receptors

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141
Q

What effect does the activation of α2-receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?

A

It inhibits norepinephrine release

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142
Q

What effect does the activation of angiotensin II receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?

A

It stimulates norepinephrine release

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143
Q

What effect does the activation of M2-receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?

A

It inhibits norepinephrine release

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144
Q

The norepinephrine-mediated activation of α2-receptors on presynaptic sympathetic nerve terminals is an example of a mechanism of what type of feedback?

A

Negative feedback

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145
Q

Name four direct cholinergic agonists.

A

Bethanechol, carbachol, pilocarpine, methacholine

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146
Q

What is the clinical application of bethanechol?

A

Treatment of postoperative and neurogenic ileus and urinary retention (remember: Beth Anne, call (bethanechol) me if you want to activate your Bowels and Bladder)

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147
Q

What is the mechanism of action of bethanechol?

A

Bethanechol is a direct cholinergic agonist resistant to acetylcholinesterase that works on receptors in the bowel and bladder

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148
Q

What two direct agonist cholinomimetic drugs can be used to treat glaucoma?

A

Carbachol and pilocarpine

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149
Q

Carbachol and pilocarpine are effective for the treatment of open-angle glaucoma because they activate what muscle?

A

The ciliary muscle of the eye

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150
Q

What is a methacholine challenge test?

A

A test in which methacholine is inhaled to stimulate muscarinic receptors and induce bronchoconstriction to diagnose asthma

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151
Q

Pilocarpine is effective for the treatment of narrow-angle glaucoma because it activates what muscle?

A

The pupillary sphincter

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152
Q

True or False? Pilocarpine is susceptible to acetylcholinesterase.

A

False; pilocarpine is resistant to acetylcholinesterase

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153
Q

Name five indirect cholinergic agonists.

A

Neostigmine, pyridostigmine, edrophonium, physostigmine, echothiophate

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154
Q

What are the clinical indications for use of neostigmine?

A

The treatment of postoperative and neurogenic ileus

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155
Q

True or False? The treatment of myasthenia gravis is a clinical application of pyridostigmine.

A

True

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156
Q

Which anticholinesterase is used to diagnose myasthenia gravis? Why?

A

Edrophonium; the effects last for minutes and if weakness is transiently reversed it is diagnostic of myasthenia gravis

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157
Q

True or False? The treatment of glaucoma is a clinical application of physostigmine.

A

True (remember: “PHYS is for the EYES”)

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158
Q

Which pharmacologic agent is used to treat atropine overdose?

A

Physostigmine, because it crosses the blood-brain barrier and is able to reverse central nervous system as well as peripheral nervous system effects

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159
Q

What is the clinical indication for use of echothiophate?

A

The treatment of glaucoma

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160
Q

Indirect cholinergic agonists increase endogenous acetylcholine by inhibiting what enzyme?

A

Acetylcholinesterase

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161
Q

Why is pyridostigmine used to treat myasthenia gravis?

A

It increases the amount of acetylcholine in the neuromuscular synapse, thereby increasing muscle strength

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162
Q

What effect does neostigmine have on the central nervous system?

A

None; it does not penetrate the blood-brain barrier (remember: NEO CNS = NO CNS)

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163
Q

What is the clinical application and mechanism of action of topical atropine, homatropine, and tropicamide?

A

These drugs antagonize muscarinic receptors in the eye to produce mydriasis and cycloplegia

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164
Q

What is the mechanism and clinical application for benztropine?

A

It is a muscarinic antagonist used to reduce symptoms of Parkinson’s disease

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165
Q

What is the mechanism and clinical application for scopolamine?

A

It is a muscarinic antagonist used to treat motion sickness

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166
Q

What is the mechanism and clinical application for ipratropium?

A

It is a muscarinic antagonist used to treat asthma and chronic obstructive pulmonary disease (remember: I PRAY I can breathe soon!)

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167
Q

What is the mechanism and clinical application for methscopolamine?

A

It is a muscarinic antagonist used to treat peptic ulcers

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168
Q

What is the mechanism and clinical application for oxybutynin?

A

It is a muscarinic antagonist used to reduce urgency in mild cystitis and reduce bladder spasms

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169
Q

What is the mechanism and clinical application for glycopyrrolate?

A

It is a muscarinic antagonist used to reduce urgency in mild cystitis and reduce bladder spasms

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170
Q

What is the mechanism and clinical application for pirenzepine?

A

It is a muscarinic antagonist used to treat peptic ulcers

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171
Q

What is the mechanism and clinical application for propantheline?

A

It is a muscarinic antagonist used to treat peptic ulcers

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172
Q

Which muscarinic antagonist can be used to reduce urgency in patients with mild cystitis?

A

Oxybutynin (also glycopyrrolate)

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173
Q

Which muscarinic antagonist is most commonly used to treat motion sickness?

A

Scopolamine

174
Q

Which muscarinic antagonist can be used to treat bladder spasms?

A

Oxybutynin (also glycopyrrolate)

175
Q

You recently prescribed haloperidol to your patient to treat his schizophrenia, but he has since developed Parkinson’s-like motor adverse effects. What drug could you add to his regimen to treat this?

A

Benztropine

176
Q

Atropine is used for therapeutic effect in which four organ systems?

A

Eyes, gastrointestinal system, respiratory system, urinary system

177
Q

What are the two effects of atropine on the eye?

A

Pupil dilation, cycloplegia

178
Q

What is the effect of atropine on the airway mucosa?

A

It decreases secretions

179
Q

What is the effect of atropine on the stomach?

A

It decreases acid secretion

180
Q

What is the effect of atropine on gastrointestinal motility?

A

It decreases motility

181
Q

What is the effect of atropine on the bladder in a patient with cystitis?

A

It decreases urgency

182
Q

According to the mnemonic DUMBBELSS, what four major physiologic processes are blocked by atropine?

A

Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle, Lacrimation, Sweating, and Salivation

183
Q

True or False? Increased body temperature is a sign of atropine toxicity.

A

True (ie, “hot as a hare”)

184
Q

True or False? Slower heart rate is a sign of atropine toxicity.

A

False; heart rate would be increased

185
Q

True or False? Dry mouth is a sign of atropine toxicity.

A

True (ie, “dry as a bone”)

186
Q

True or False? Dry, flushed skin is a sign of atropine toxicity.

A

True (ie, “dry as a bone, red as a beet”)

187
Q

True or False? Cycloplegia is a sign of atropine toxicity.

A

True (ie, “blind as a bat”)

188
Q

True or False? Diarrhea is a sign of atropine toxicity.

A

False; constipation is a sign of atropine toxicity

189
Q

True or False? Disorientation is a sign of atropine toxicity.

A

True (ie, “mad as a hatter”)

190
Q

Which two adverse effects of atropine are more common in elderly patients?

A

Urinary retention and acute angle closure glaucoma

191
Q

True or False? Atropine toxicity can cause urinary incontinence.

A

False; atropine toxicity can cause urinary retention in men with prostatic hypertrophy

192
Q

True or False? Atropine toxicity can cause fecal incontinence.

A

False; atropine toxicity causes constipation, not fecal incontinence

193
Q

What type of acetylcholine receptors does hexamethonium antagonize?

A

Nicotinic acetylcholine receptors

194
Q

What effect does hexamethonium have on heart rate?

A

It can prevent bradycardia in response to increased blood pressure when pressors are given

195
Q

Name four toxicities of hexamethonium.

A

Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction

196
Q

Name 11 drugs that act as direct sympathomimetics.

A

Isoproterenol, dobutamine, phenylephrine, epinephrine, norepinephrine, dopamine, albuterol, terbutaline, ritodrine, metaproterenol, and salmeterol

197
Q

Which types of receptors are activated by epinephrine?

A

α1-, α2-, β1-, and β2-receptors

198
Q

Low doses of epinephrine are selective for _____ (α1, α2, β1, β2) adrenergic receptors.

A

β1

199
Q

Which types of receptors are activated by norepinephrine?

A

α1- and α2-; β1-receptors (with lower affinity)

200
Q

Does norepinephrine have greater affinity for α-adrenergic receptors or β1-receptors?

A

α-Adrenergic receptors

201
Q

Isoproterenol is an agonist for which receptors?

A

β1- and β2-receptors equally

202
Q

Which types of receptors does dopamine activate, and how strongly does it activate them relative to one another?

A

D1 = D2 receptors > β-receptors > α-receptors

203
Q

Dopamine is an agonist for which receptors?

A

β1- and β2-receptors

204
Q

Dopamine is _____ (ionotropic/not ionotropic) and _____ (chronotropic/not chronotropic), while dobutamine is _____ (ionotropic/not ionotropic) and _____ (chronotropic/not chronotropic).

A

Ionotropic; chronotropic; ionotropic; not chronotropic

205
Q

Phenylephrine is an agonist for which receptors?

A

α1-receptors > α2-receptors

206
Q

Metaproterenol, albuterol, salmeterol, and terbutaline are agonists for which receptors?

A

β2-receptors > β1-receptors

207
Q

Ritodrine acts on _____ (α1, α2, β1, β2)-adrenergic receptors.

A

β2

208
Q

What are the clinical applications of epinephrine?

A

Anaphylaxis, open-angle glaucoma, asthma, hypotension

209
Q

What effect does norepinephrine have on renal perfusion?

A

It decreases renal perfusion

210
Q

What is the clinical application for isoproterenol?

A

Atrioventricular block

211
Q

What role does dopamine have in treating shock?

A

Increases blood pressure while maintaining renal perfusion

212
Q

True or False? Dopamine can be used to treat heart failure.

A

True

213
Q

What are the clinical applications for dobutamine?

A

Shock, heart failure, cardiac stress testing

214
Q

What are the clinical applications of phenylephrine?

A

Treats nasal decongestion; causes vasoconstriction; dilates pupils

215
Q

What is the clinical application for albuterol?

A

Acute asthma

216
Q

Which sympathomimetics can be used to reduce premature uterine contractions?

A

Terbutaline, salmeterol

217
Q

Amphetamine, ephedrine, and cocaine are (direct/indirect) sympathomimetics.

A

Indirect

218
Q

By what mechanism does amphetamine exert its sympathomimetic effect?

A

It stimulates the release of stored catecholamines

219
Q

By what mechanism does ephedrine exert its sympathomimetic effect?

A

It stimulates the release of stored catecholamines

220
Q

By what mechanism does cocaine exert its sympathomimetic effect?

A

It inhibits catecholamine uptake in the nerve terminal

221
Q

What are the clinical indications for use of amphetamines?

A

Narcolepsy, obesity, attention deficit hyperactivity disorder

222
Q

What are three clinical applications of ephedrine?

A

To treat nasal congestion, urinary incontinence, and hypotension

223
Q

True or False? Phenylephrine can be used to treat nasal congestion.

A

True

224
Q

What are the effects of cocaine when used topically?

A

Vasoconstriction and local anesthesia

225
Q

Is the effect of epinephrine on β-receptors greater than, equal to, or less than its effect on α-receptors?

A

Equal to, except at low doses, at which epinephrine is selective for β1

226
Q

Is the effect of isoproterenol on β-receptors greater than, equal to, or less than its effect on α-receptors?

A

Greater than

227
Q

What are the effects of norepinephrine on heart rate, systolic and diastolic blood pressure, and pulse pressure?

A

It increases systolic and diastolic blood pressure, slightly increases pulse pressure (systolic increases more than diastolic), and reduces heart rate by causing reflex bradycardia

228
Q

What are the effects of epinephrine on heart rate, systolic and diastolic blood pressure, and pulse pressure?

A

It increases systolic blood pressure, decreases diastolic blood pressure, greatly increases pulse pressure, and increases heart rate

229
Q

Why does norepinephrine administration result in reflex bradycardia?

A

Norepinephrine raises blood pressure, causing a vagal response that leads to reflex bradycardia via increased parasympathetic input to the heart

230
Q

Epinephrine causes an increase in heart rate via which receptor subtype?

A

β1 receptors; although epinephrine exhibits affinity for both β subtypes, it is selective for β1 at low doses, leading to tachycardia

231
Q

What effect does isoproterenol have on pulse pressure and heart rate?

A

Increases pulse pressure and heart rate

232
Q

What is the effect of clonidine on central adrenergic outflow? Which receptor does it act on?

A

It is an α2-agonist and decreases central adrenergic outflow; remember that the α2-receptor is responsible for negative feedback

233
Q

What are the clinical applications of clonidine?

A

Hypertension, especially with renal disease, because it does not decrease blood flow to the kidneys

234
Q

What is the effect of α-methyldopa on central adrenergic outflow? Which receptor does it act on?

A

It is an α2-agonist and decreases central adrenergic outflow

235
Q

What are the clinical applications of α-methyldopa?

A

Hypertension, especially with renal disease, because it does not decrease blood flow to the kidneys

236
Q

What are two patient populations for which α-methyldopa is indicated (as an antihypertensive)?

A

Renal failure patients, pregnant patients

237
Q

What is the clinical application and mechanism of action of phenoxybenzamine?

A

Phenoxybenzamine is a nonselective α-blocker that is used to treat pheochromocytoma

238
Q

Would you use phenoxybenzamine or phentolamine before removal of a pheochromocytoma? Why?

A

Phenoxybenzamine, because it is irreversible. Phentolamine is reversible, so the high levels of catecholamines released during surgery would overcome the α-block

239
Q

What is the clinical application and mechanism of action of phentolamine?

A

Phentolamine is a nonselective α-blocker that is used to treat pheochromocytoma

240
Q

What are two adverse effects of nonselective α-blockers?

A

Orthostatic hypotension and reflex tachycardia

241
Q

What are the clinical applications and mechanisms of action of prazosin, doxazosin, and terazosin?

A

They are each an α1-selective blocker used to treat hypertension and urinary retention in benign prostatic hyperplasia

242
Q

What are three effects of α1-selective blocker toxicity?

A

Orthostatic hypotension (first dose only), dizziness, headache

243
Q

What is the clinical application and mechanism of action of mirtazapine?

A

Mirtazapine is an α2-selective blocker used to treat depression

244
Q

What are three effects of α2-selective blocker toxicity?

A

Sedation, increased serum cholesterol, increased appetite

245
Q

What is the net effect of epinephrine on blood pressure before and after nonselective α-blockade? Why?

A

Before α-blockade, epinephrine increases blood pressure; after α-blockade, it decreases blood pressure. This is because epinephrine also activates β2, which lowers blood pressure and is not blocked

246
Q

What is the net effect of phenylephrine on blood pressure before and after nonselective α-blockade? Why?

A

Before a-blockade, phenylephrine increases blood pressure; after a-blockade, it has little effect on blood pressure. This is because phenylephrine is specific for a and does not activate ﾧ2, so it is completely negated by α-blockade

247
Q

Why does epinephrine, a pressor, cause hypotension if a patient is pretreated with an α-blocker?

A

If α-receptors are blocked, the β-agonist properties of epinephrine predominate and lower blood pressure

248
Q

Name six clinical applications for β-blockers.

A

Hypertension, angina pectoris, myocardial infarction, supraventricular tachycardia, congestive heart failure, glaucoma

249
Q

Which two β-blockers are used to treat supraventricular tachycardia?

A

Propranolol, esmolol

250
Q

What β-blocker is frequently used to treat glaucoma?

A

Timolol

251
Q

How do β-blockers work in the setting of angina pectoris?

A

Decrease heart rate and contractility; decrease myocardial oxygen consumption

252
Q

A 63-year-old patient is referred to you from the emergency room for long-term care after his first myocardial infarction. Is a β-blocker suggested or contraindicated for this patient?

A

Suggested; after myocardial infarction, patients should receive β-blockers to decrease risk of mortality

253
Q

What is the mechanism of β-blockers in the treatment of supraventricular tachycardia?

A

They decrease atrioventricular conduction velocity

254
Q

To which class of antiarrhythmic agents do β-blockers belong?

A

Class II; drugs that slow atrioventricular conduction

255
Q

How does the use of β-blockers affect the progression of congestive heart failure?

A

Slows progression of heart failure; β-blockers reduce cardiac output but have proven benefit in congestive heart failure

256
Q

What is the mechanism of β-blockers in the treatment of glaucoma?

A

They reduce the secretion of aqueous humor, reducing intraocular pressure

257
Q

Why should β-blockers be used with caution in diabetic patients?

A

β-Blockers should be used with caution in diabetic patients because they can block initial warning signs of hypoglycemia such as increased heart rate and diaphoresis

258
Q

Name five nonselective β-blockers.

A

Propranolol, timolol, nadolol, pindolol, and labetalol

259
Q

Name five β1-selective antagonists.

A

Acebutolol, Betaxolol, Esmolol, Atenolol, Metoprolol (remember: A BEAM of β1-blockers)

260
Q

Which β-blocker is the shortest acting?

A

Esmolol

261
Q

What β-blockers have partial agonist activity?

A

Pindolol, Acebutolol (remember: Partial Agonist)

262
Q

What are two nonselective α- and β-antagonists?

A

Carvedilol, labetalol

263
Q

A patient with a history of Graves’ disease (hyperthyroidism) presents with chest pain. Her resting heart rate is 128 beats per minute, her blood pressure is 120/80 mmHg, and her respiratory rate is 18 breaths per minute. You order thyroid-stimulating hormone and thyroxine tests. What class of drugs would address her cardiac problems while you await the lab results?

A

ﾧ-Blockers, such as propranolol, will reduce heart rate and consequently reduce angina

264
Q

What is the mechanism of β-blockers in treatment of hypertension?

A

Decreasing cardiac output and decreasing renin secretion

265
Q

What are some effects of β-blocker toxicity?

A

Bradycardia, atrioventricular block, congestive heart failure (reduced cardiac output), sedation, sleep alteration, impotence, exacerbation of asthma

266
Q

What symptoms indicate cholinesterase inhibitor poisoning?

A

DUMBBELSS: Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of the skeletal muscle and the central nervous system, Lacrimation, Sweating, and Salivation

267
Q

What mechanism underlies the symptoms of acetylcholinesterase inhibitor poisoning?

A

Inhibition of acetylcholinesterase leads to overactivity of the body’s cholinergic systems

268
Q

The symptoms of parathion poisoning are caused by the inhibition of what enzyme?

A

Acetylcholinesterase

269
Q

The symptoms of organophosphate poisoning are caused by the inhibition of what enzyme?

A

Acetylcholinesterase

270
Q

A child ingests insecticide and presents with diarrhea, abdominal pain, wheezing, pinpoint pupils, and copious tears and salivation. What medication should he be given?

A

Atropine and pralidoxime

271
Q

What antidote can be given to a patient who presents with diarrhea, urinary incontinence, miosis, bronchospasm, bradycardia, lacrimation, sweating, and salivation?

A

Atropine and pralidoxime

272
Q

Why is it important to give pralidoxime as well as atropine in organophosphate poisoning?

A

Because organophosphates are irreversible inhibitors of acetylcholinesterase and pralidoxime helps to regenerate functional acetylcholinesterase

273
Q

Atropine is used as an antidote for what kind of poisoning? By what mechanism does it accomplish this?

A

Organophosphate/anticholinesterase inhibitor poisoning; it inhibits muscarinic acetylcholine receptors

274
Q

Pralidoxime is used as an antidote for what kind of poisoning? By what mechanism does it accomplish this?

A

Organophosphate/cholinesterase inhibitor poisoning; it regenerates active acetylcholinesterase

275
Q

What is the antidote for acetaminophen overdose?

A

N-acetylcysteine

276
Q

What are the two treatments for salicylate overdose?

A

Alkalinization of urine and dialysis if necessary

277
Q

What compound is used to alkalinize urine?

A

NaHCO3; weak acids are better excreted when the urine is alkaline

278
Q

What is the treatment for amphetamine overdose?

A

NH4Cl

279
Q

Amphetamines are _____ (acidic/basic); therefore, overdose is treated with _____ (NH4Cl/NaHCO3) to _____ (acidify/alkalinize) the urine.

A

Basic; NH4Cl; acidify

280
Q

What are the two antidotes for anticholinesterase toxicity?

A

Atropine to block cholinergic receptors and pralidoxime to regenerate acetylcholinesterase

281
Q

What are the antidotes for organophosphate poisoning?

A

Atropine and pralidoxime; organophosphates inhibit acetylcholinesterase

282
Q

What is the antidote for toxicity caused by anticholinergic agents?

A

Physostigmine; it inhibits acetylcholinesterase, increasing the available acetylcholine to overcome anticholinergic toxicity

283
Q

Physostigmine is the antidote for toxicity caused by what two types of agents?

A

Antimuscarinic agents and anticholinergic agents

284
Q

What is the antidote for β-blocker toxicity?

A

Glucagon

285
Q

What are five treatments for digitalis toxicity?

A

Stop the medication; normalize the potassium level; give the patient lidocaine; give the patient anti-digoxigenin Fab fragments; give the patient magnesium

286
Q

What is the antidote for iron toxicity?

A

Deferoxamine, a chelating agent

287
Q

What are four treatments for lead poisoning?

A

Edetate calcium disodium, dimercaprol, succimer, and penicillamine

288
Q

Penicillamine is the antidote for toxicity caused by what substances?

A

Copper, arsenic, gold

289
Q

What are three treatments for arsenic poisoning?

A

Dimercaprol, succimer, penicillamine

290
Q

What are two treatments for mercury poisoning?

A

Dimercaprol and succimer

291
Q

What are three treatments for gold poisoning?

A

Dimercaprol, succimer, penicillamine

292
Q

Dimercaprol and succimer are the antidotes for toxicity caused by what substances?

A

Mercury, arsenic, gold

293
Q

The combination of thiosulfate and nitrite is the antidote for toxicity caused by what substance?

A

Cyanide

294
Q

Hydroxocobalamin is the antidote for toxicity caused by what substance?

A

Cyanide

295
Q

What are the treatments for cyanide poisoning?

A

Hydroxocobalamin, or a combination of nitrite and thiosulfate

296
Q

What is the treatment for methemoglobinemia?

A

Methylene blue, vitamin C

297
Q

Methylene blue is used to treat elevated serum levels of what substance?

A

Methemoglobin

298
Q

What are the treatments for carbon monoxide poisoning?

A

100% oxygen and hyperbaric oxygen

299
Q

What are the treatments for methanol and ethylene glycol (antifreeze) poisoning?

A

Ethanol, dialysis, and fomepizole

300
Q

Fomepizole is an antidote for toxicity caused by what substances?

A

Methanol, ethylene glycol

301
Q

What are the antidotes for opioid overdose?

A

Naloxone or naltrexone

302
Q

Naloxone is the antidote for overdose of what substance?

A

Opioids

303
Q

What is the antidote for benzodiazepine overdose?

A

Flumazenil; it reduces the action of benzodiazepines at γ-aminobutyric acid receptors

304
Q

Flumazenil is the antidote for overdose of what substance?

A

Benzodiazepines

305
Q

What is the treatment for tricyclic antidepressant overdose?

A

Sodium bicarbonate; it can prevent cardiac arrhythmias

306
Q

Alkalinization of the serum with sodium bicarbonate is a treatment for overdose with what class of antidepressant medications?

A

Tricyclic antidepressants; the alkalinization can prevent cardiac arrhythmias

307
Q

What is the reversal agent for heparin?

A

Protamine

308
Q

Protamine is used to reverse the effects of what pharmacologic agent?

A

Heparin; however, it does not reverse low-molecular-weight heparin

309
Q

What agents are used to reverse the effects of warfarin?

A

Vitamin K and fresh frozen plasma

310
Q

Vitamin K is used to reverse the effects of what pharmacologic agent?

A

Warfarin

311
Q

What agent is used to reverse the effects of both tissue plasminogen activator and streptokinase?

A

Aminocaproic acid

312
Q

Aminocaproic acid is used to reverse the effects of what two pharmacologic enzymes?

A

Tissue plasminogen activator and streptokinase

313
Q

What is the antidote for theophylline?

A

β-Blockers

314
Q

A woman brings her 3-year-old son to the emergency room because she found him eating pills out of the acetaminophen bottle. She is not sure how many he ate, but says that the bottle was almost empty by the time she got to him, and that he was eating them one hour ago. Which drug should be administered to minimize further liver toxicity?

A

N-acetylcysteine

315
Q

Which component of multivitamins is the most likely to cause fatal overdose in children?

A

Iron

316
Q

What is the mechanism of cell death in iron poisoning?

A

Peroxidation of membrane lipids

317
Q

What will a patient with acute iron poisoning present with?

A

Gastric bleeding

318
Q

After gastrointestinal bleeding in the acute phase of iron poisoning, what is the progression of the clinical presentation?

A

Metabolic acidosis followed by gastrointestinal strictures and obstruction

319
Q

Which antidepressants can cause tachycardia due to anticholinergic action?

A

Tricyclic antidepressants

320
Q

Which drugs can cause coronary vasospasm?

A

Cocaine and sumatriptan

321
Q

Which drugs can cause cutaneous flushing as an adverse effect?

A

Vancomycin, adenosine, niacin, calcium channel blockers (remember: VANC)

322
Q

Which drugs cause dilated cardiomyopathy?

A

Doxorubicin (Adriamycin), daunorubicin

323
Q

Which drugs can cause torsades de pointes?

A

Class III (sotalol) and class IA (quinidine) antiarrhythmic agents, cisapride

324
Q

What cardiac adverse effect can result from either cocaine or sumatriptan use?

A

Coronary vasospasm

325
Q

What is the major adverse effect of niacin use?

A

Flushing

326
Q

Which drugs can cause agranulocytosis as an adverse effect?

A

Clozapine, carbamazepine, colchicine, propylthiouracil, methimazole

327
Q

Which drugs (or exposures) can cause aplastic anemia as an adverse effect?

A

Chloramphenicol, benzene, nonsteroidal antiinflammatory drugs, propylthiouracil, methimazole

328
Q

Which antihypertensive drug can cause hemolytic anemia?

A

α-Methyldopa

329
Q

Which antibiotic can cause “grey baby syndrome”?

A

Chloramphenicol

330
Q

Which drugs can cause hemolytic anemia in G6PD-deficient patients?

A

Isoniazid, Sulfonamides, Primaquine, Aspirin, Ibuprofen, Nitrofurantoin (remember: hemolysis IS PAIN)

331
Q

Which drugs can cause megaloblastic anemia?

A

Phenytoin, Methotrexate, Sulfa drugs (remember: Having a blast with PMS)

332
Q

What is a major adverse effect of oral contraceptives?

A

Thrombotic events such as deep vein thrombosis and pulmonary embolus

333
Q

Which antihypertensive drug can cause chronic cough?

A

Angiotensin-converting enzyme inhibitors

334
Q

What is the advantage of angiotensin II receptor blockers (like losartan) over angiotensin-converting enzyme inhibitors?

A

Angiotensin II receptor blockers are often prescribed as an alternative renoprotective antihypertensive medication in patients with angiotensin-converting enzyme inhibitor-induced cough

335
Q

Which drugs can cause pulmonary fibrosis?

A

Bleomycin, busulfan, amiodarone

336
Q

What adverse effect would you suspect in a newly jaundiced patient recently started on azithromycin?

A

Acute cholestatic hepatitis

337
Q

Which drugs (or exposures) can cause hepatic necrosis?

A

Halothane, valproic acid, acetaminophen, Amanita phalloides

338
Q

What effect can isoniazid have on the liver?

A

Hepatitis

339
Q

Which drugs can cause pseudomembranous colitis?

A

Clindamycin and ampicillin are commonly implicated, but many antibiotics can be responsible

340
Q

Administration of clindamycin or ampicillin can cause overgrowth of which bacteria in the colon?

A

Clostridium difficile, which leads to pseudomembranous colitis

341
Q

What adverse effect occurs when exogenous glucocorticoids are rapidly withdrawn?

A

Adrenocortical insufficiency due to long-term hypothalamic-pituitary-adrenal axis suppression; this is why steroids are usually tapered as opposed to abruptly discontinued

342
Q

Which drugs are known to cause gynecomastia?

A

Spironolactone, Digitalis, Cimetidine, Alcohol (chonic use), estrogens, Ketoconazole (remember: Some Drugs Create Awesome Knockers)

343
Q

Which drugs can cause hot flashes?

A

Tamoxifen, clomiphene

344
Q

Which drug can cause gingival hyperplasia?

A

Phenytoin

345
Q

Which drugs can cause gout?

A

Furosemide and thiazide diuretics

346
Q

Osteoporosis can be caused by long-term use of which drugs?

A

Steroids, heparin

347
Q

Which drugs induce photosensitivity?

A

Sulfonamides, Amiodarone, Tetracyclines (remember: SAT for a photo)

348
Q

Which drugs can cause Stevens-Johnson syndrome?

A

Ethosuximide, lamotrigine, carbamazepine, phenobarbital, phenytoin, sulfa drugs, penicillin, allopurinol; think anticonvulsants and antibiotics

349
Q

Which drugs can cause a lupus-like syndrome?

A

Hydralazine, Isoniazid, Procainamide, Phenytoin (remember: it’s not HIPP to have lupus)

350
Q

Which adverse effects of fluoroquinolones are specific to children?

A

Tendonitis, tendon rupture, and cartilage damage

351
Q

Which drug can cause Fanconi’s syndrome if taken after its expiration date?

A

Tetracycline

352
Q

Which drugs can cause interstitial nephritis?

A

Methicillin, nonsteroidal antiinflammatory drugs, and furosemide

353
Q

Which two drugs can cause hemorrhagic cystitis?

A

Cyclophosphamide and ifosfamide

354
Q

Which drug is administered to prevent hemorrhagic cystitis from the use of ifosfamide or cyclophosphamide?

A

Mesna

355
Q

Name two drugs that can cause cinchonism.

A

Quinidine and quinine; cinchonism describes headache and tinnitus

356
Q

Which adverse effect of lithium can cause hypernatremia?

A

Diabetes insipidus

357
Q

Name two drugs that can cause diabetes insipidus.

A

Lithium and demeclocycline

358
Q

Name three drugs that can cause seizures.

A

Bupropion, imipenem/cilastatin, isoniazid

359
Q

Which class of drugs can result in tardive dyskinesia?

A

Antipsychotics

360
Q

What drugs can cause a disulfiram-like reaction?

A

Metronidazole, certain cephalosporins, procarbazine, first-generation sulfonylureas

361
Q

Polymyxins are toxic to which organ systems?

A

Neural and renal; as a result it is usually only used topically

362
Q

Which drugs can cause both ototoxicity and nephrotoxicity?

A

Aminoglycosides, vancomycin, loop diuretics, cisplatin

363
Q

A 60-year-old man presents with sudden severe great toe pain. On microscopy, an aspirate of the joint shows crystals. His medications include daily baby aspirin, a thiazide diuretic to control hypertension, a ﾧ-blocker to control a cardiac arrhythmia, and a nonsteroidal antiinflammatory drug for joint pain. Which of these medications likely contributed to his presentation?

A

Thiazide diuretics

364
Q

What are the seven most common drugs that induce cytochrome P450 enzyme activity?

A

Quinidine, Barbituates, St. John’s Wort, Phenytoin, Rifampin, Griseofulvin, Carbamazepine (remember: Queen Barb Steals Phen-phen and Refuses Greasy Carbs)

365
Q

What are the six most common substances that inhibit cytochrome P450 enzyme activity?

A

Sulfonamides, Isoniazid, Cimetidine, Ketoconazole, Erythromycin, Grapefruit juice, Acute alcohol use (remember: Inhibit yourself from drinking beer from a KEG because it makes you Acutely SICk)

366
Q

Which drug can both induce and inhibit different forms of cytochrome P450 enzymes? Is induction or inhibition its more significant effect?

A

Quinidine; induction is more significant

367
Q

Ethylene glycol is converted to oxalic acid by which enzyme?

A

Alcohol dehydrogenase

368
Q

Alcohol dehydrogenase converts ethylene glycol into what?

A

Oxalic acid

369
Q

What substance is converted to oxalic acid by alcohol dehydrogenase?

A

Ethylene glycol; it is usually found in antifreeze

370
Q

What are two adverse effects of oxalic acid?

A

Acidosis and nephrotoxicity; oxalic acid crystalizes in the kidney to cause damage

371
Q

What enzyme converts methanol to formaldehyde and formic acid?

A

Alcohol dehydrogenase

372
Q

What does alcohol dehydrogenase convert methanol into?

A

Formaldehyde and formic acid

373
Q

What are two adverse effects of formaldehyde and formic acid?

A

Severe acidosis, retinal damage

374
Q

Alcohol dehydrogenase converts what alcohol into formaldehyde and formic acid?

A

Methanol

375
Q

What enzyme converts ethanol to acetaldehyde?

A

Alcohol dehydrogenase

376
Q

Acetaldehyde dehydrogenase converts what substrate into acetic acid?

A

Acetaldehyde

377
Q

What does alcohol dehydrogenase convert ethanol into?

A

Acetaldehyde

378
Q

What enzyme that is involved in ethanol metabolism is inhibited by disulfiram?

A

Acetaldehyde dehydrogenase

379
Q

Ethanol competes with what endogenous hormone substrate for binding in renal tubules?

A

Antidiuretic hormone; the result is a diuretic effect

380
Q

Alcohol dehydrogenase converts what alcohol into acetaldehyde?

A

Ethanol

381
Q

What are four adverse effects of acetaldehyde?

A

Nausea, headache, vomiting, hypotension

382
Q

Alcohol dehydrogenase is involved in the metabolism of what three alcohols?

A

Ethylene glycol, methanol, and ethanol

383
Q

Alcohol dehydrogenase is inhibited by what drug?

A

Fomepizole; the drug can be used to prevent toxicities of methanol and ethylene glycol ingestions

384
Q

Acetaldehyde dehydrogenase is inhibited by what drug?

A

Disulfiram; the drug worsens the adverse effects of alcohol use and is also called Antabuse

385
Q

What enzyme converts acetaldehyde to acetic acid?

A

Acetaldehyde dehydrogenase

386
Q

What does acetaldehyde dehydrogenase convert acetaldehyde into?

A

Acetic acid

387
Q

Name the eight drugs that can cause allergic reactions in patients with known sulfa allergies.

A

Celecoxib, probenicid, furosemide, thiazides, trimethoprim/sulfamethoxazole, sulfonylureas, sulfasalazine, and sumitriptan

388
Q

What are some clinical manifestations of sulfa allergic reactions?

A

Fever, pruritic rash, Stevens-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, uriticaria (hives)

389
Q

A patient presents to the emergency room with a fever, intensely pruritic rash, and urticaria. You ask her what medications she is taking, and she replies, “I can’t remember the names, but I just switched to a different type of diuretic.” What is a possible drug-related cause of her symptoms?

A

She is allergic to sulfa drugs and was just switched to furosemide or a thiazide

390
Q

Penicillins are typically named with what suffix?

A

The suffix -cillin; such as methicillin

391
Q

Drugs used for the treatment of erectile dysfunction are typically named with what suffix?

A

The suffix -afil; such as sildenafil

392
Q

Drugs used for inhalational general anesthesia are typically named with what suffix?

A

The suffix -ane; such as halothane

393
Q

Phenothiazines are typically named with what suffix?

A

The suffix -azine; phenothiazines are neuroleptics such as chlorpromazine

394
Q

Benzodiazepines are typically named with what suffix?

A

The suffix -azepam; such as diazepam

395
Q

Antifungals are typically named with what suffix?

A

The suffix -azole; such as ketoconazole

396
Q

Some antibiotics that inhibit protein synthesis are named with what suffix?

A

The suffix -cycline; such as tetracycline

397
Q

Barbiturates are typically named with what suffix?

A

The suffix -barbital; such as phenobarbital

398
Q

Drugs used for local anesthesia are typically named with what suffix?

A

The suffix -caine; such as lidocaine

399
Q

Butyrophenones are typically named with what suffix?

A

The suffix -operidol; neuroleptics such as haloperidol

400
Q

Trichloroacetic acids are typically named with what suffix?

A

The suffix -ipramine; such as Imipramine

401
Q

Protease inhibitors are typically named with what suffix?

A

The suffix -navir; such as saquinavir

402
Q

β-Antagonists are typically named with what suffix?

A

The suffix -olol; such as propranolol

403
Q

Drugs that end in -azine are generally what class of drug?

A

Phenothiazines (neuroleptics, antiemetics)

404
Q

Cardiac glycosides are typically named with what suffix?

A

The suffix -oxin; such as digoxin

405
Q

Drugs that end in -azole are generally what class of drug?

A

Antifungals

406
Q

Drugs that end in -barbital are generally what class of drug?

A

Barbiturates

407
Q

Drugs that end in -caine are generally what class of drug?

A

Local anesthetic

408
Q

Drugs that end in -cillin are generally what class of drug?

A

Penicillins

409
Q

Methylxanthines are typically named with what suffix?

A

The suffix -phylline; such as theophylline

410
Q

Drugs that end in -cycline are generally what class of drug?

A

Antibiotic or protein synthesis inhibitors at the 30s subunit of the ribosome

411
Q

Drugs that end in -ipramine are generally what class of drug?

A

Tricyclic antidepressants

412
Q

Angiotensin-converting enzyme inhibitors are typically named with what suffix?

A

The suffix -pril; such as captopril

413
Q

ﾧ2-Agonists are typically named with what suffix?

A

The suffix -terol; such as albuterol

414
Q

Drugs that end in -navir are generally what class of drug?

A

Protease inhibitors

415
Q

Drugs that end in -olol are generally what class of drug?

A

β-Antagonists

416
Q

Drugs that end in -operidol are generally what class of drug?

A

Butyrophenones (neuroleptics)

417
Q

Drugs that end in -oxin are generally what class of drug?

A

Cardiac glycosides (inotropic agents)

418
Q

H2-antagonists are typically named with what suffix?

A

The suffix -tidine; such as cimetidine

419
Q

Drugs that end in -phylline are generally what class of drug?

A

Methylxanthines

420
Q

Drugs that end in -pril are generally what class of drug?

A

Angiotensin-converting enzyme inhibitors

421
Q

Pituitary hormones are typically named with what suffix?

A

The suffix -tropin; such as somatotropin

422
Q

Drugs that end in -terol are generally what class of drug?

A

β2-Agonists

423
Q

Drugs that end in -tidine are generally what class of drug?

A

Histamine2 antagonists

424
Q

α1-Antagonists are typically named with what suffix?

A

The suffix -zosin; such as prazosin

425
Q

Drugs that end in -triptyline are generally what class of drug?

A

Tricyclic antidepressants

426
Q

Drugs that end in -tropin are generally what class of drug?

A

Pituitary hormones

427
Q

Drugs that end in -zosin are generally what class of drug?

A

α1-Antagonists

428
Q

Drugs that end in -afil are generally used for what purpose?

A

Erectile dysfunction

429
Q

Drugs that end in -ane are generally used for what purpose?

A

Inhalational general anesthesia

430
Q

Drugs that end in -azepam are generally what class of drug?

A

Benzodiazepines

USMLE Step 1 -- OLD TEST (17 decks)

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