Pharmacology 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
2
Q
In enzyme kinetics, the value of Km reflects the _____ of the enzyme for its substrate.
A
Affinity
3
Q
True or False? In enzyme kinetics, the lower the Km, the higher the affinity.
A
True
4
Q
In enzyme kinetics, Vmax is directly proportional to the _____ _____.
A
Enzyme concentration
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
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
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
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
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
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
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
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
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
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
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
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
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)
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
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
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
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
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
23
Q
What is the formula for the loading dose of a drug?
A
Loading dose = (target plasma concentration × volume of distribution) / bioavailability
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
25
How do loading and maintenance doses of drugs differ for patients with hepatic and renal disease?
For both hepatic and renal disease, loading dose does not change, but maintenance dose decreases
26
What is the bioavailability of a drug if it is administered intravenously?
100%
27
In zero-order elimination of drugs from the body, what is the relationship between the rate of elimination and the drug concentration?
The rate of elimination is constant regardless of drug concentration
28
What are three drugs that exhibit zero-order elimination?
Phenytoin and ethanol; aspirin at toxic concentrations
29
In first-order elimination of drugs from the body, what is the relationship between the rate of elimination and the drug concentration?
The rate of elimination is directly proportional to the drug concentration; a constant fraction (rather than a constant amount) is eliminated
30
In zero-order elimination of drugs from the body, how does the plasma concentration of a drug change over time: linearly or exponentially?
Linearly
31
In first-order elimination of drugs from the body, how does the plasma concentration of a drug change over time: linearly or exponentially?
Exponentially
32
Weak acids get trapped in _____ (acidic/basic) environments.
Basic
33
Weak bases get trapped in _____ (acidic/basic) environments.
Acidic
34
What substance is given to enhance the renal clearance of weakly acidic drugs such as phenobarbital, methotrexate, and aspirin?
Bicarbonate
35
What substance is given to enhance the renal clearance of weakly basic drugs such as amphetamine?
Ammonium chloride
36
Ionized species become trapped in urine because they are not _____ \_\_\_\_\_.
Lipid soluble; therefore, they cannot cross cell membranes
37
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?
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
38
What three types of biochemical reactions are involved in the phase I metabolism of drugs?
Reduction, oxidation, and hydrolysis
39
What is the polarity of the drug products that result from phase I metabolism?
The products are slightly polar
40
True or False? Drug products that result from phase I metabolism are water soluble.
True
41
True or False? Drug products that result from phase I metabolism are often still active.
True
42
What enzyme system mediates the phase I metabolism of drugs in the body?
Cytochrome P-450
43
What three types of biochemical reactions are involved in the phase II metabolism of drugs?
Acetylation, glucuronidation, and sulfation; these are conjugation reactions
44
Do geriatric patients lose the ability for phase I or phase II drug metabolism first?
Phase I
45
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).
Slightly polar; often still active; very polar; inactive
46
The products of phase II metabolism of drugs are excreted by what organ?
Kidneys
47
What is the definition of efficacy?
Maximal effect a drug can produce
48
What is the definition of potency?
Amount of drug needed for a given effect
49
A drug that requires a very low dose to achieve its desired effect is considered \_\_\_\_\_.
Potent
50
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.
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
51
What is the effect of a noncompetitive antagonist on the position of an agonist's dose-response curve?
It vertically shrinks; the agonist's efficacy is decreased
52
In pharmacodynamics, the addition of a noncompetitive agonist _____ (increases/decreases/does not change) the efficacy of the agonist.
Decreases
53
How does the efficacy of a partial agonist relate to the efficacy of a full agonist of the same receptor?
A partial agonist has a lower maximal efficacy than a full agonist
54
How does the potency of a partial agonist relate to the potency of a full agonist of the same receptor?
A partial agonist may be more potent than, less potent than, or equally as potent as a full agonist
55
What property of a drug is determined by its therapeutic index?
Safety; drugs with higher therapeutic indices are less likely to cause toxicities
56
What is the formula that describes the therapeutic index of a drug?
TI (therapeutic index) = LD50 (median toxic dose) / ED50 (median effective dose) (remember: **TILE**)
57
Safer drugs have _____ (higher/lower) therapeutic index values.
Higher
58
From which regions of the central nervous system do parasympathetic nerves originate?
Cranial and sacral regions
59
From which regions of the central nervous system do sympathetic nerves originate?
Thoracic and lumbar regions
60
What types of nerves arise from the spinal cord and innervate skeletal muscle directly?
Somatic nerves
61
How many neurons are involved in parasympathetic transmission from the spinal cord to the target organ?
Two
62
True or False? Craniosacral parasympathetic axons synapse on neurons in the peripheral ganglia.
True
63
What neurotransmitter mediates parasympathetic nervous system function?
Acetylcholine
64
What neurotransmitter receptor mediates parasympathetic nervous system function at the peripheral ganglia?
Nicotinic acetylcholine receptors
65
What neurotransmitter receptor mediates parasympathetic tone in the cardiac muscle?
Muscarinic acetylcholine receptors (specifically, M2)
66
What neurotransmitter receptor mediates parasympathetic tone in the smooth muscle?
Muscarinic acetylcholine receptors (specifically, M3)
67
What neurotransmitter receptor mediates parasympathetic tone in the glandular cells?
Muscarinic acetylcholine receptors (specifically, M1 and M3)
68
Somatic nerves that arise from the spine innervate skeletal muscle. What neurotransmitter receptor, which is located on skeletal muscle, receives this input?
Nicotinic acetylcholine receptors
69
How many neurons are involved in sympathetic transmission from the spinal cord to the target organ?
Two
70
Where is the first synapse after the spinal cord in sympathetic innervation of an organ?
Preganglionic sympathetic axons synapse on neurons in the paravertebral ganglia
71
True or False? Preganglionic sympathetic axons synapse on neurons in the peripheral ganglia.
False; preganglionic sympathetic axons synapse on neurons in the paravertebral ganglia
72
At the paravertebral ganglia, the neurotransmitter _____ acts on _____ receptors to mediate sympathetic nervous system function.
Acetylcholine; nicotinic acetylcholine
73
What neurotransmitter mediates sympathetic nervous system function at the sweat glands?
Acetylcholine
74
What neurotransmitter receptor mediates sympathetic nervous system function at the sweat glands?
Muscarinic acetylcholine receptors
75
What neurotransmitter mediates sympathetic tone in the cardiac muscle, smooth muscle, and glandular cells?
Norepinephrine
76
What are four cell types in which α- and β-adrenergic receptors mediate sympathetic tone?
Cardiac muscle, smooth muscle, glandular cells, and terminal ends of neurons
77
What neurotransmitter mediates sympathetic tone in the renal vascular smooth muscle?
Dopamine
78
What neurotransmitter receptor mediates sympathetic tone in the renal vascular smooth muscle?
D1 receptors
79
What two substances are released into the blood from the adrenal medulla after the activation of the sympathetic nervous system?
Epinephrine and norepinephrine
80
How many synapses are involved in activation of the adrenal medulla?
One; the adrenal medulla releases epinephrine and norepinephrine into the blood
81
Are nicotinic acetylcholine receptors ligand-gated sodium-potassium channels or G-protein coupled receptors?
Nicotinic receptors are ligand gated sodium-potassium channels
82
Are muscarinic acetylcholine receptors ligand-gated sodium-potassium channels or G-protein-coupled receptors?
Muscarinic acetylcholine receptors are G-protein-coupled receptors that act through second messengers
83
To what class of G-proteins are α1-receptors linked?
q
84
To what class of G-proteins are α2-receptors linked?
i
85
To what class of G-proteins are β1-receptors linked?
s
86
To what class of G-proteins are β2-receptors linked?
s
87
To what class of G-proteins are M1-receptors linked?
q
88
To what class of G-proteins are M2-receptors linked?
i
89
To what class of G-proteins are M3-receptors linked?
q
90
To what class of G-proteins are D1-receptors linked?
s
91
To what class of G-proteins are D2-receptors linked?
i
92
To what class of G-proteins are H1-receptors linked?
q
93
To what class of G-proteins are H2-receptors linked?
s
94
To what class of G-proteins are V1-receptors linked?
q
95
To what class of G-proteins are V2-receptors linked?
s
96
What are the major effects of α1-receptor activation?
It increases vascular smooth muscle contraction, and increases pupillary dilator muscle contraction (mydriasis)
97
What are the major functions of α2-receptor activation?
It decreases sympathetic outflow and decreases insulin release
98
What are the major functions of β1-receptor activation?
It increases heart rate and contractility, increases renin release from the kidneys, and increases lipolysis of adipose tissue
99
What is the major function of β2-receptor activation on the body's vasculature?
Vasodilation
100
What is the major function of β2-receptor activation on the respiratory system?
Bronchodilation
101
What effect does β2-receptor activation have on glucagon release?
It increases glucagon release
102
Where are M1-receptors located?
The central nervous system
103
What effect does M2-receptor activation have on cardiac function?
It decreases heart rate and contractility
104
What are the effects of M3-receptor activation?
Increased exocrine gland secretions, gut peristalsis, bladder contraction, bronchoconstriction, miosis, and accommodation
105
What effect does D1-receptor activation have on renal vasculature?
It relaxes renal vascular smooth muscle
106
What are the effects of H1-receptor activation?
Pruritis, pain, nasal and bronchial mucus production, contraction of bronchioles
107
What is the effect of H2-receptor activation?
It increases gastric acid secretion
108
What effect does V1-receptor activation have on vascular smooth muscle?
It increases vascular smooth muscle contraction
109
The activation of what two types of G-protein-coupled receptors can increase vascular smooth muscle contraction? Which receptors mediate vascular relaxation?
α1- and V1-receptors increase contraction; relaxation is mediated by β2, and D1 (renal only)
110
What is the effect of V2-receptor activation? Where are they located?
It increases water permeability and reabsorption in the collecting tubules of the kidney
111
What five types of receptors are coupled with Gq proteins?
α1, M1, M3, H1, and V1
112
What five types of receptors are coupled with Gs proteins?
β1, β2, D1, H2, and V2
113
What three types of receptors are coupled with Gi proteins?
a2, M2, and D2
114
What enzyme is activated directly downstream of Gq-coupled receptors?
Phospholipase C
115
What enzyme is activated directly downstream of Gs-coupled receptors?
Adenyl cyclase
116
What enzyme is inhibited directly downstream of Gi-coupled receptors?
Adenyl cyclase
117
Adenyl cyclase catalyzes the conversion of adenosine triphosphate into what molecule?
cAMP
118
What final effector enzyme is activated by receptors that are coupled with Gs proteins?
Protein kinase A
119
What final effector enzyme is inhibited by receptors that are coupled with Gi proteins?
Protein kinase A
120
Phospholipase C catalyzes the cleavage of membrane lipids into what molecules?
Inositol trisphosphate3 and diacylglycerol
121
What is the effect of increased inositol triphosphate on the intracellular concentration of calcium?
It increases the intracellular calcium concentration
122
What enzyme is activated by diacylglycerol?
Protein kinase C
123
What pharmacologic agent blocks the uptake of choline into cholinergic nerve terminals?
Hemicholinium
124
What enzyme is responsible for the formation of acetylcholine? What are its two substrates?
Choline acetyltransferase; Acetyl-CoA and choline
125
What pharmacologic agent blocks the transport of acetylcholine into the presynaptic vesicles in nerve terminals?
Vesamicol
126
The entry of what ion into the nerve terminal induces the release of acetylcholine into the synaptic cleft?
Calcium
127
What toxin inhibits the calcium-induced release of acetylcholine from the cholinergic nerve terminals?
Botulinum
128
What enzyme breaks down acetylcholine in the synaptic cleft? What two products result from this reaction?
Acetylcholinesterase; choline and acetate
129
Tyrosine transporters are located in the nerve terminals of what type of cells?
Noradrenergic cells; tyrosine is the precursor of norepinephrine
130
Tyrosine is a precursor to the formation of which neurotransmitters? What is the order of their synthesis?
Tyrosine, DOPA, dopamine, norepinephrine, epinephrine
131
What pharmacologic agent blocks the conversion of tyrosine to DOPA?
Metyrosine
132
Tyrosine is converted into dopamine via what intermediate precursor?
DOPA; DOPA can be used as a pharmacologic agent to increase central nervous system dopamine
133
What pharmacologic agent blocks the transport of dopamine into the presynaptic vesicles in nerve terminals?
Reserpine
134
Dopamine is converted into norepinephrine in the ______ (cytoplasm/presynaptic vesicle).
Presynaptic vesicles
135
The entry of what ion into the nerve terminal induces the release of norepinephrine into the synaptic cleft?
Calcium
136
What pharmacologic agent inhibits the calcium-induced release of norepinephrine from the noradrenergic nerve terminals?
Guanethidine
137
What pharmacologic agent stimulates the release of norepinephrine from the noradrenergic nerve terminals?
Amphetamine
138
How is norepinephrine cleared form the synaptic cleft?
Diffusion, metabolism (monoamine oxidase A), and reuptake
139
What pharmacologic agents inhibit the reuptake of norepinephrine into the nerve terminals?
Cocaine, amphetamine, and tricyclic antidepressants
140
What three receptor types modulate the presynaptic release of norepinephrine from the noradrenergic nerve terminals?
M2-receptors, angiotensin II receptors, and α2-receptors
141
What effect does the activation of α2-receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?
It inhibits norepinephrine release
142
What effect does the activation of angiotensin II receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?
It stimulates norepinephrine release
143
What effect does the activation of M2-receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?
It inhibits norepinephrine release
144
The norepinephrine-mediated activation of α2-receptors on presynaptic sympathetic nerve terminals is an example of a mechanism of what type of feedback?
Negative feedback
145
Name four direct cholinergic agonists.
Bethanechol, carbachol, pilocarpine, methacholine
146
What is the clinical application of bethanechol?
Treatment of postoperative and neurogenic ileus and urinary retention (remember: **Beth Anne, call (bethanechol)** me if you want to activate your **Bowels** and **Bladder**)
147
What is the mechanism of action of bethanechol?
Bethanechol is a direct cholinergic agonist resistant to acetylcholinesterase that works on receptors in the bowel and bladder
148
What two direct agonist cholinomimetic drugs can be used to treat glaucoma?
Carbachol and pilocarpine
149
Carbachol and pilocarpine are effective for the treatment of open-angle glaucoma because they activate what muscle?
The ciliary muscle of the eye
150
What is a methacholine challenge test?
A test in which methacholine is inhaled to stimulate muscarinic receptors and induce bronchoconstriction to diagnose asthma
151
Pilocarpine is effective for the treatment of narrow-angle glaucoma because it activates what muscle?
The pupillary sphincter
152
True or False? Pilocarpine is susceptible to acetylcholinesterase.
False; pilocarpine is resistant to acetylcholinesterase
153
Name five indirect cholinergic agonists.
Neostigmine, pyridostigmine, edrophonium, physostigmine, echothiophate
154
What are the clinical indications for use of neostigmine?
The treatment of postoperative and neurogenic ileus
155
True or False? The treatment of myasthenia gravis is a clinical application of pyridostigmine.
True
156
Which anticholinesterase is used to diagnose myasthenia gravis? Why?
Edrophonium; the effects last for minutes and if weakness is transiently reversed it is diagnostic of myasthenia gravis
157
True or False? The treatment of glaucoma is a clinical application of physostigmine.
True (remember: "PHYS is for the EYES")
158
Which pharmacologic agent is used to treat atropine overdose?
Physostigmine, because it crosses the blood-brain barrier and is able to reverse central nervous system as well as peripheral nervous system effects
159
What is the clinical indication for use of echothiophate?
The treatment of glaucoma
160
Indirect cholinergic agonists increase endogenous acetylcholine by inhibiting what enzyme?
Acetylcholinesterase
161
Why is pyridostigmine used to treat myasthenia gravis?
It increases the amount of acetylcholine in the neuromuscular synapse, thereby increasing muscle strength
162
What effect does neostigmine have on the central nervous system?
None; it does not penetrate the blood-brain barrier (remember: NEO CNS = NO CNS)
163
What is the clinical application and mechanism of action of topical atropine, homatropine, and tropicamide?
These drugs antagonize muscarinic receptors in the eye to produce mydriasis and cycloplegia
164
What is the mechanism and clinical application for benztropine?
It is a muscarinic antagonist used to reduce symptoms of Parkinson's disease
165
What is the mechanism and clinical application for scopolamine?
It is a muscarinic antagonist used to treat motion sickness
166
What is the mechanism and clinical application for ipratropium?
It is a muscarinic antagonist used to treat asthma and chronic obstructive pulmonary disease (remember: **I PRAY** I can breathe soon!)
167
What is the mechanism and clinical application for methscopolamine?
It is a muscarinic antagonist used to treat peptic ulcers
168
What is the mechanism and clinical application for oxybutynin?
It is a muscarinic antagonist used to reduce urgency in mild cystitis and reduce bladder spasms
169
What is the mechanism and clinical application for glycopyrrolate?
It is a muscarinic antagonist used to reduce urgency in mild cystitis and reduce bladder spasms
170
What is the mechanism and clinical application for pirenzepine?
It is a muscarinic antagonist used to treat peptic ulcers
171
What is the mechanism and clinical application for propantheline?
It is a muscarinic antagonist used to treat peptic ulcers
172
Which muscarinic antagonist can be used to reduce urgency in patients with mild cystitis?
Oxybutynin (also glycopyrrolate)
173
Which muscarinic antagonist is most commonly used to treat motion sickness?
Scopolamine
174
Which muscarinic antagonist can be used to treat bladder spasms?
Oxybutynin (also glycopyrrolate)
175
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?
Benztropine
176
Atropine is used for therapeutic effect in which four organ systems?
Eyes, gastrointestinal system, respiratory system, urinary system
177
What are the two effects of atropine on the eye?
Pupil dilation, cycloplegia
178
What is the effect of atropine on the airway mucosa?
It decreases secretions
179
What is the effect of atropine on the stomach?
It decreases acid secretion
180
What is the effect of atropine on gastrointestinal motility?
It decreases motility
181
What is the effect of atropine on the bladder in a patient with cystitis?
It decreases urgency
182
According to the mnemonic **DUMBBELSS**, what four major physiologic processes are blocked by atropine?
**D**iarrhea, **U**rination, **M**iosis, **B**ronchospasm, **B**radycardia, **E**xcitation of skeletal muscle, **L**acrimation, **S**weating, and **S**alivation
183
True or False? Increased body temperature is a sign of atropine toxicity.
True (ie, "hot as a hare")
184
True or False? Slower heart rate is a sign of atropine toxicity.
False; heart rate would be increased
185
True or False? Dry mouth is a sign of atropine toxicity.
True (ie, "dry as a bone")
186
True or False? Dry, flushed skin is a sign of atropine toxicity.
True (ie, "dry as a bone, red as a beet")
187
True or False? Cycloplegia is a sign of atropine toxicity.
True (ie, "blind as a bat")
188
True or False? Diarrhea is a sign of atropine toxicity.
False; constipation is a sign of atropine toxicity
189
True or False? Disorientation is a sign of atropine toxicity.
True (ie, "mad as a hatter")
190
Which two adverse effects of atropine are more common in elderly patients?
Urinary retention and acute angle closure glaucoma
191
True or False? Atropine toxicity can cause urinary incontinence.
False; atropine toxicity can cause urinary retention in men with prostatic hypertrophy
192
True or False? Atropine toxicity can cause fecal incontinence.
False; atropine toxicity causes constipation, not fecal incontinence
193
What type of acetylcholine receptors does hexamethonium antagonize?
Nicotinic acetylcholine receptors
194
What effect does hexamethonium have on heart rate?
It can prevent bradycardia in response to increased blood pressure when pressors are given
195
Name four toxicities of hexamethonium.
Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction
196
Name 11 drugs that act as direct sympathomimetics.
Isoproterenol, dobutamine, phenylephrine, epinephrine, norepinephrine, dopamine, albuterol, terbutaline, ritodrine, metaproterenol, and salmeterol
197
Which types of receptors are activated by epinephrine?
α1-, α2-, β1-, and β2-receptors
198
Low doses of epinephrine are selective for _____ (α1, α2, β1, β2) adrenergic receptors.
β1
199
Which types of receptors are activated by norepinephrine?
α1- and α2-; β1-receptors (with lower affinity)
200
Does norepinephrine have greater affinity for α-adrenergic receptors or β1-receptors?
α-Adrenergic receptors
201
Isoproterenol is an agonist for which receptors?
β1- and β2-receptors equally
202
Which types of receptors does dopamine activate, and how strongly does it activate them relative to one another?
D1 = D2 receptors \> β-receptors \> α-receptors
203
Dopamine is an agonist for which receptors?
β1- and β2-receptors
204
Dopamine is _____ (ionotropic/not ionotropic) and _____ (chronotropic/not chronotropic), while dobutamine is _____ (ionotropic/not ionotropic) and _____ (chronotropic/not chronotropic).
Ionotropic; chronotropic; ionotropic; not chronotropic
205
Phenylephrine is an agonist for which receptors?
α1-receptors \> α2-receptors
206
Metaproterenol, albuterol, salmeterol, and terbutaline are agonists for which receptors?
β2-receptors \> β1-receptors
207
Ritodrine acts on _____ (α1, α2, β1, β2)-adrenergic receptors.
β2
208
What are the clinical applications of epinephrine?
Anaphylaxis, open-angle glaucoma, asthma, hypotension
209
What effect does norepinephrine have on renal perfusion?
It decreases renal perfusion
210
What is the clinical application for isoproterenol?
Atrioventricular block
211
What role does dopamine have in treating shock?
Increases blood pressure while maintaining renal perfusion
212
True or False? Dopamine can be used to treat heart failure.
True
213
What are the clinical applications for dobutamine?
Shock, heart failure, cardiac stress testing
214
What are the clinical applications of phenylephrine?
Treats nasal decongestion; causes vasoconstriction; dilates pupils
215
What is the clinical application for albuterol?
Acute asthma
216
Which sympathomimetics can be used to reduce premature uterine contractions?
Terbutaline, salmeterol
217
Amphetamine, ephedrine, and cocaine are (direct/indirect) sympathomimetics.
Indirect
218
By what mechanism does amphetamine exert its sympathomimetic effect?
It stimulates the release of stored catecholamines
219
By what mechanism does ephedrine exert its sympathomimetic effect?
It stimulates the release of stored catecholamines
220
By what mechanism does cocaine exert its sympathomimetic effect?
It inhibits catecholamine uptake in the nerve terminal
221
What are the clinical indications for use of amphetamines?
Narcolepsy, obesity, attention deficit hyperactivity disorder
222
What are three clinical applications of ephedrine?
To treat nasal congestion, urinary incontinence, and hypotension
223
True or False? Phenylephrine can be used to treat nasal congestion.
True
224
What are the effects of cocaine when used topically?
Vasoconstriction and local anesthesia
225
Is the effect of epinephrine on β-receptors greater than, equal to, or less than its effect on α-receptors?
Equal to, except at low doses, at which epinephrine is selective for β1
226
Is the effect of isoproterenol on β-receptors greater than, equal to, or less than its effect on α-receptors?
Greater than
227
What are the effects of norepinephrine on heart rate, systolic and diastolic blood pressure, and pulse pressure?
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
What are the effects of epinephrine on heart rate, systolic and diastolic blood pressure, and pulse pressure?
It increases systolic blood pressure, decreases diastolic blood pressure, greatly increases pulse pressure, and increases heart rate
229
Why does norepinephrine administration result in reflex bradycardia?
Norepinephrine raises blood pressure, causing a vagal response that leads to reflex bradycardia via increased parasympathetic input to the heart
230
Epinephrine causes an increase in heart rate via which receptor subtype?
β1 receptors; although epinephrine exhibits affinity for both β subtypes, it is selective for β1 at low doses, leading to tachycardia
231
What effect does isoproterenol have on pulse pressure and heart rate?
Increases pulse pressure and heart rate
232
What is the effect of clonidine on central adrenergic outflow? Which receptor does it act on?
It is an α2-agonist and decreases central adrenergic outflow; remember that the α2-receptor is responsible for negative feedback
233
What are the clinical applications of clonidine?
Hypertension, especially with renal disease, because it does not decrease blood flow to the kidneys
234
What is the effect of α-methyldopa on central adrenergic outflow? Which receptor does it act on?
It is an α2-agonist and decreases central adrenergic outflow
235
What are the clinical applications of α-methyldopa?
Hypertension, especially with renal disease, because it does not decrease blood flow to the kidneys
236
What are two patient populations for which α-methyldopa is indicated (as an antihypertensive)?
Renal failure patients, pregnant patients
237
What is the clinical application and mechanism of action of phenoxybenzamine?
Phenoxybenzamine is a nonselective α-blocker that is used to treat pheochromocytoma
238
Would you use phenoxybenzamine or phentolamine before removal of a pheochromocytoma? Why?
Phenoxybenzamine, because it is irreversible. Phentolamine is reversible, so the high levels of catecholamines released during surgery would overcome the α-block
239
What is the clinical application and mechanism of action of phentolamine?
Phentolamine is a nonselective α-blocker that is used to treat pheochromocytoma
240
What are two adverse effects of nonselective α-blockers?
Orthostatic hypotension and reflex tachycardia
241
What are the clinical applications and mechanisms of action of prazosin, doxazosin, and terazosin?
They are each an α1-selective blocker used to treat hypertension and urinary retention in benign prostatic hyperplasia
242
What are three effects of α1-selective blocker toxicity?
Orthostatic hypotension (first dose only), dizziness, headache
243
What is the clinical application and mechanism of action of mirtazapine?
Mirtazapine is an α2-selective blocker used to treat depression
244
What are three effects of α2-selective blocker toxicity?
Sedation, increased serum cholesterol, increased appetite
245
What is the net effect of epinephrine on blood pressure before and after nonselective α-blockade? Why?
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
What is the net effect of phenylephrine on blood pressure before and after nonselective α-blockade? Why?
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
Why does epinephrine, a pressor, cause hypotension if a patient is pretreated with an α-blocker?
If α-receptors are blocked, the β-agonist properties of epinephrine predominate and lower blood pressure
248
Name six clinical applications for β-blockers.
Hypertension, angina pectoris, myocardial infarction, supraventricular tachycardia, congestive heart failure, glaucoma
249
Which two β-blockers are used to treat supraventricular tachycardia?
Propranolol, esmolol
250
What β-blocker is frequently used to treat glaucoma?
Timolol
251
How do β-blockers work in the setting of angina pectoris?
Decrease heart rate and contractility; decrease myocardial oxygen consumption
252
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?
Suggested; after myocardial infarction, patients should receive β-blockers to decrease risk of mortality
253
What is the mechanism of β-blockers in the treatment of supraventricular tachycardia?
They decrease atrioventricular conduction velocity
254
To which class of antiarrhythmic agents do β-blockers belong?
Class II; drugs that slow atrioventricular conduction
255
How does the use of β-blockers affect the progression of congestive heart failure?
Slows progression of heart failure; β-blockers reduce cardiac output but have proven benefit in congestive heart failure
256
What is the mechanism of β-blockers in the treatment of glaucoma?
They reduce the secretion of aqueous humor, reducing intraocular pressure
257
Why should β-blockers be used with caution in diabetic patients?
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
Name five nonselective β-blockers.
Propranolol, timolol, nadolol, pindolol, and labetalol
259
Name five β1-selective antagonists.
**A**cebutolol, **B**etaxolol, **E**smolol, **A**tenolol, **M**etoprolol (remember: **A BEAM** of β1-blockers)
260
Which β-blocker is the shortest acting?
Esmolol
261
What β-blockers have partial agonist activity?
**P**indolol, **A**cebutolol (remember: **P**artial **A**gonist)
262
What are two nonselective α- and β-antagonists?
Carvedilol, labetalol
263
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?
ﾧ-Blockers, such as propranolol, will reduce heart rate and consequently reduce angina
264
What is the mechanism of β-blockers in treatment of hypertension?
Decreasing cardiac output and decreasing renin secretion
265
What are some effects of β-blocker toxicity?
Bradycardia, atrioventricular block, congestive heart failure (reduced cardiac output), sedation, sleep alteration, impotence, exacerbation of asthma
266
What symptoms indicate cholinesterase inhibitor poisoning?
**DUMBBELSS**: **D**iarrhea, **U**rination, **M**iosis, **B**ronchospasm, **B**radycardia, **E**xcitation of the skeletal muscle and the central nervous system, **L**acrimation, **S**weating, and **S**alivation
267
What mechanism underlies the symptoms of acetylcholinesterase inhibitor poisoning?
Inhibition of acetylcholinesterase leads to overactivity of the body's cholinergic systems
268
The symptoms of parathion poisoning are caused by the inhibition of what enzyme?
Acetylcholinesterase
269
The symptoms of organophosphate poisoning are caused by the inhibition of what enzyme?
Acetylcholinesterase
270
A child ingests insecticide and presents with diarrhea, abdominal pain, wheezing, pinpoint pupils, and copious tears and salivation. What medication should he be given?
Atropine and pralidoxime
271
What antidote can be given to a patient who presents with diarrhea, urinary incontinence, miosis, bronchospasm, bradycardia, lacrimation, sweating, and salivation?
Atropine and pralidoxime
272
Why is it important to give pralidoxime as well as atropine in organophosphate poisoning?
Because organophosphates are irreversible inhibitors of acetylcholinesterase and pralidoxime helps to regenerate functional acetylcholinesterase
273
Atropine is used as an antidote for what kind of poisoning? By what mechanism does it accomplish this?
Organophosphate/anticholinesterase inhibitor poisoning; it inhibits muscarinic acetylcholine receptors
274
Pralidoxime is used as an antidote for what kind of poisoning? By what mechanism does it accomplish this?
Organophosphate/cholinesterase inhibitor poisoning; it regenerates active acetylcholinesterase
275
What is the antidote for acetaminophen overdose?
*N*-acetylcysteine
276
What are the two treatments for salicylate overdose?
Alkalinization of urine and dialysis if necessary
277
What compound is used to alkalinize urine?
NaHCO3; weak acids are better excreted when the urine is alkaline
278
What is the treatment for amphetamine overdose?
NH4Cl
279
Amphetamines are _____ (acidic/basic); therefore, overdose is treated with _____ (NH4Cl/NaHCO3) to _____ (acidify/alkalinize) the urine.
Basic; NH4Cl; acidify
280
What are the two antidotes for anticholinesterase toxicity?
Atropine to block cholinergic receptors and pralidoxime to regenerate acetylcholinesterase
281
What are the antidotes for organophosphate poisoning?
Atropine and pralidoxime; organophosphates inhibit acetylcholinesterase
282
What is the antidote for toxicity caused by anticholinergic agents?
Physostigmine; it inhibits acetylcholinesterase, increasing the available acetylcholine to overcome anticholinergic toxicity
283
Physostigmine is the antidote for toxicity caused by what two types of agents?
Antimuscarinic agents and anticholinergic agents
284
What is the antidote for β-blocker toxicity?
Glucagon
285
What are five treatments for digitalis toxicity?
Stop the medication; normalize the potassium level; give the patient lidocaine; give the patient anti-digoxigenin Fab fragments; give the patient magnesium
286
What is the antidote for iron toxicity?
Deferoxamine, a chelating agent
287
What are four treatments for lead poisoning?
Edetate calcium disodium, dimercaprol, succimer, and penicillamine
288
Penicillamine is the antidote for toxicity caused by what substances?
Copper, arsenic, gold
289
What are three treatments for arsenic poisoning?
Dimercaprol, succimer, penicillamine
290
What are two treatments for mercury poisoning?
Dimercaprol and succimer
291
What are three treatments for gold poisoning?
Dimercaprol, succimer, penicillamine
292
Dimercaprol and succimer are the antidotes for toxicity caused by what substances?
Mercury, arsenic, gold
293
The combination of thiosulfate and nitrite is the antidote for toxicity caused by what substance?
Cyanide
294
Hydroxocobalamin is the antidote for toxicity caused by what substance?
Cyanide
295
What are the treatments for cyanide poisoning?
Hydroxocobalamin, or a combination of nitrite and thiosulfate
296
What is the treatment for methemoglobinemia?
Methylene blue, vitamin C
297
Methylene blue is used to treat elevated serum levels of what substance?
Methemoglobin
298
What are the treatments for carbon monoxide poisoning?
100% oxygen and hyperbaric oxygen
299
What are the treatments for methanol and ethylene glycol (antifreeze) poisoning?
Ethanol, dialysis, and fomepizole
300
Fomepizole is an antidote for toxicity caused by what substances?
Methanol, ethylene glycol
301
What are the antidotes for opioid overdose?
Naloxone or naltrexone
302
Naloxone is the antidote for overdose of what substance?
Opioids
303
What is the antidote for benzodiazepine overdose?
Flumazenil; it reduces the action of benzodiazepines at γ-aminobutyric acid receptors
304
Flumazenil is the antidote for overdose of what substance?
Benzodiazepines
305
What is the treatment for tricyclic antidepressant overdose?
Sodium bicarbonate; it can prevent cardiac arrhythmias
306
Alkalinization of the serum with sodium bicarbonate is a treatment for overdose with what class of antidepressant medications?
Tricyclic antidepressants; the alkalinization can prevent cardiac arrhythmias
307
What is the reversal agent for heparin?
Protamine
308
Protamine is used to reverse the effects of what pharmacologic agent?
Heparin; however, it does not reverse low-molecular-weight heparin
309
What agents are used to reverse the effects of warfarin?
Vitamin K and fresh frozen plasma
310
Vitamin K is used to reverse the effects of what pharmacologic agent?
Warfarin
311
What agent is used to reverse the effects of both tissue plasminogen activator and streptokinase?
Aminocaproic acid
312
Aminocaproic acid is used to reverse the effects of what two pharmacologic enzymes?
Tissue plasminogen activator and streptokinase
313
What is the antidote for theophylline?
β-Blockers
314
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?
N-acetylcysteine
315
Which component of multivitamins is the most likely to cause fatal overdose in children?
Iron
316
What is the mechanism of cell death in iron poisoning?
Peroxidation of membrane lipids
317
What will a patient with acute iron poisoning present with?
Gastric bleeding
318
After gastrointestinal bleeding in the acute phase of iron poisoning, what is the progression of the clinical presentation?
Metabolic acidosis followed by gastrointestinal strictures and obstruction
319
Which antidepressants can cause tachycardia due to anticholinergic action?
Tricyclic antidepressants
320
Which drugs can cause coronary vasospasm?
Cocaine and sumatriptan
321
Which drugs can cause cutaneous flushing as an adverse effect?
Vancomycin, adenosine, niacin, calcium channel blockers (remember: **VANC**)
322
Which drugs cause dilated cardiomyopathy?
Doxorubicin (Adriamycin), daunorubicin
323
Which drugs can cause torsades de pointes?
Class III (sotalol) and class IA (quinidine) antiarrhythmic agents, cisapride
324
What cardiac adverse effect can result from either cocaine or sumatriptan use?
Coronary vasospasm
325
What is the major adverse effect of niacin use?
Flushing
326
Which drugs can cause agranulocytosis as an adverse effect?
Clozapine, carbamazepine, colchicine, propylthiouracil, methimazole
327
Which drugs (or exposures) can cause aplastic anemia as an adverse effect?
Chloramphenicol, benzene, nonsteroidal antiinflammatory drugs, propylthiouracil, methimazole
328
Which antihypertensive drug can cause hemolytic anemia?
α-Methyldopa
329
Which antibiotic can cause "grey baby syndrome"?
Chloramphenicol
330
Which drugs can cause hemolytic anemia in G6PD-deficient patients?
**I**soniazid, **S**ulfonamides, **P**rimaquine, **A**spirin, **I**buprofen, **N**itrofurantoin (remember: hemolysis **IS PAIN**)
331
Which drugs can cause megaloblastic anemia?
**P**henytoin, **M**ethotrexate, **S**ulfa drugs (remember: Having a **blast** with **PMS**)
332
What is a major adverse effect of oral contraceptives?
Thrombotic events such as deep vein thrombosis and pulmonary embolus
333
Which antihypertensive drug can cause chronic cough?
Angiotensin-converting enzyme inhibitors
334
What is the advantage of angiotensin II receptor blockers (like losartan) over angiotensin-converting enzyme inhibitors?
Angiotensin II receptor blockers are often prescribed as an alternative renoprotective antihypertensive medication in patients with angiotensin-converting enzyme inhibitor-induced cough
335
Which drugs can cause pulmonary fibrosis?
Bleomycin, busulfan, amiodarone
336
What adverse effect would you suspect in a newly jaundiced patient recently started on azithromycin?
Acute cholestatic hepatitis
337
Which drugs (or exposures) can cause hepatic necrosis?
Halothane, valproic acid, acetaminophen, *Amanita phalloides*
338
What effect can isoniazid have on the liver?
Hepatitis
339
Which drugs can cause pseudomembranous colitis?
Clindamycin and ampicillin are commonly implicated, but many antibiotics can be responsible
340
Administration of clindamycin or ampicillin can cause overgrowth of which bacteria in the colon?
*Clostridium difficile*, which leads to pseudomembranous colitis
341
What adverse effect occurs when exogenous glucocorticoids are rapidly withdrawn?
Adrenocortical insufficiency due to long-term hypothalamic-pituitary-adrenal axis suppression; this is why steroids are usually tapered as opposed to abruptly discontinued
342
Which drugs are known to cause gynecomastia?
**S**pironolactone, **D**igitalis, **C**imetidine, **A**lcohol (chonic use), estrogens, **K**etoconazole (remember: **S**ome **D**rugs **C**reate **A**wesome **K**nockers)
343
Which drugs can cause hot flashes?
Tamoxifen, clomiphene
344
Which drug can cause gingival hyperplasia?
Phenytoin
345
Which drugs can cause gout?
Furosemide and thiazide diuretics
346
Osteoporosis can be caused by long-term use of which drugs?
Steroids, heparin
347
Which drugs induce photosensitivity?
**S**ulfonamides, **A**miodarone, **T**etracyclines (remember: **SAT** for a photo)
348
Which drugs can cause Stevens-Johnson syndrome?
Ethosuximide, lamotrigine, carbamazepine, phenobarbital, phenytoin, sulfa drugs, penicillin, allopurinol; think anticonvulsants and antibiotics
349
Which drugs can cause a lupus-like syndrome?
**H**ydralazine, **I**soniazid, **P**rocainamide, **P**henytoin (remember: it's not **HIPP** to have lupus)
350
Which adverse effects of fluoroquinolones are specific to children?
Tendonitis, tendon rupture, and cartilage damage
351
Which drug can cause Fanconi's syndrome if taken after its expiration date?
Tetracycline
352
Which drugs can cause interstitial nephritis?
Methicillin, nonsteroidal antiinflammatory drugs, and furosemide
353
Which two drugs can cause hemorrhagic cystitis?
Cyclophosphamide and ifosfamide
354
Which drug is administered to prevent hemorrhagic cystitis from the use of ifosfamide or cyclophosphamide?
Mesna
355
Name two drugs that can cause cinchonism.
Quinidine and quinine; cinchonism describes headache and tinnitus
356
Which adverse effect of lithium can cause hypernatremia?
Diabetes insipidus
357
Name two drugs that can cause diabetes insipidus.
Lithium and demeclocycline
358
Name three drugs that can cause seizures.
Bupropion, imipenem/cilastatin, isoniazid
359
Which class of drugs can result in tardive dyskinesia?
Antipsychotics
360
What drugs can cause a disulfiram-like reaction?
Metronidazole, certain cephalosporins, procarbazine, first-generation sulfonylureas
361
Polymyxins are toxic to which organ systems?
Neural and renal; as a result it is usually only used topically
362
Which drugs can cause both ototoxicity and nephrotoxicity?
Aminoglycosides, vancomycin, loop diuretics, cisplatin
363
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?
Thiazide diuretics
364
What are the seven most common drugs that induce cytochrome P450 enzyme activity?
**Q**uinidine, **B**arbituates, **S**t. John's Wort, **P**henytoin, **R**ifampin, **G**riseofulvin, **C**arbamazepine (remember: **Q**ueen **B**arb **S**teals **P**hen-phen and **R**efuses **G**reasy **C**arbs)
365
What are the six most common substances that inhibit cytochrome P450 enzyme activity?
**S**ulfonamides, **I**soniazid, **C**imetidine, **K**etoconazole, **E**rythromycin, **G**rapefruit juice, **Acute** alcohol use (remember: **Inhibit** yourself from drinking beer from a **KEG** because it makes you **Acute**ly **SIC**k)
366
Which drug can both induce and inhibit different forms of cytochrome P450 enzymes? Is induction or inhibition its more significant effect?
Quinidine; induction is more significant
367
Ethylene glycol is converted to oxalic acid by which enzyme?
Alcohol dehydrogenase
368
Alcohol dehydrogenase converts ethylene glycol into what?
Oxalic acid
369
What substance is converted to oxalic acid by alcohol dehydrogenase?
Ethylene glycol; it is usually found in antifreeze
370
What are two adverse effects of oxalic acid?
Acidosis and nephrotoxicity; oxalic acid crystalizes in the kidney to cause damage
371
What enzyme converts methanol to formaldehyde and formic acid?
Alcohol dehydrogenase
372
What does alcohol dehydrogenase convert methanol into?
Formaldehyde and formic acid
373
What are two adverse effects of formaldehyde and formic acid?
Severe acidosis, retinal damage
374
Alcohol dehydrogenase converts what alcohol into formaldehyde and formic acid?
Methanol
375
What enzyme converts ethanol to acetaldehyde?
Alcohol dehydrogenase
376
Acetaldehyde dehydrogenase converts what substrate into acetic acid?
Acetaldehyde
377
What does alcohol dehydrogenase convert ethanol into?
Acetaldehyde
378
What enzyme that is involved in ethanol metabolism is inhibited by disulfiram?
Acetaldehyde dehydrogenase
379
Ethanol competes with what endogenous hormone substrate for binding in renal tubules?
Antidiuretic hormone; the result is a diuretic effect
380
Alcohol dehydrogenase converts what alcohol into acetaldehyde?
Ethanol
381
What are four adverse effects of acetaldehyde?
Nausea, headache, vomiting, hypotension
382
Alcohol dehydrogenase is involved in the metabolism of what three alcohols?
Ethylene glycol, methanol, and ethanol
383
Alcohol dehydrogenase is inhibited by what drug?
Fomepizole; the drug can be used to prevent toxicities of methanol and ethylene glycol ingestions
384
Acetaldehyde dehydrogenase is inhibited by what drug?
Disulfiram; the drug worsens the adverse effects of alcohol use and is also called Antabuse
385
What enzyme converts acetaldehyde to acetic acid?
Acetaldehyde dehydrogenase
386
What does acetaldehyde dehydrogenase convert acetaldehyde into?
Acetic acid
387
Name the eight drugs that can cause allergic reactions in patients with known sulfa allergies.
Celecoxib, probenicid, furosemide, thiazides, trimethoprim/sulfamethoxazole, sulfonylureas, sulfasalazine, and sumitriptan
388
What are some clinical manifestations of sulfa allergic reactions?
Fever, pruritic rash, Stevens-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, uriticaria (hives)
389
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?
She is allergic to sulfa drugs and was just switched to furosemide or a thiazide
390
Penicillins are typically named with what suffix?
The suffix *-cillin*; such as methicillin
391
Drugs used for the treatment of erectile dysfunction are typically named with what suffix?
The suffix *-afil*; such as sildenafil
392
Drugs used for inhalational general anesthesia are typically named with what suffix?
The suffix *-ane*; such as halothane
393
Phenothiazines are typically named with what suffix?
The suffix *-azine*; phenothiazines are neuroleptics such as chlorpromazine
394
Benzodiazepines are typically named with what suffix?
The suffix *-azepam*; such as diazepam
395
Antifungals are typically named with what suffix?
The suffix *-azole*; such as ketoconazole
396
Some antibiotics that inhibit protein synthesis are named with what suffix?
The suffix *-cycline*; such as tetracycline
397
Barbiturates are typically named with what suffix?
The suffix *-barbital*; such as phenobarbital
398
Drugs used for local anesthesia are typically named with what suffix?
The suffix *-caine*; such as lidocaine
399
Butyrophenones are typically named with what suffix?
The suffix *-operidol*; neuroleptics such as haloperidol
400
Trichloroacetic acids are typically named with what suffix?
The suffix *-ipramine*; such as Imipramine
401
Protease inhibitors are typically named with what suffix?
The suffix *-navir*; such as saquinavir
402
β-Antagonists are typically named with what suffix?
The suffix *-olol*; such as propranolol
403
Drugs that end in *-azine* are generally what class of drug?
Phenothiazines (neuroleptics, antiemetics)
404
Cardiac glycosides are typically named with what suffix?
The suffix *-oxin*; such as digoxin
405
Drugs that end in *-azole* are generally what class of drug?
Antifungals
406
Drugs that end in *-barbital* are generally what class of drug?
Barbiturates
407
Drugs that end in *-caine* are generally what class of drug?
Local anesthetic
408
Drugs that end in *-cillin* are generally what class of drug?
Penicillins
409
Methylxanthines are typically named with what suffix?
The suffix *-phylline*; such as theophylline
410
Drugs that end in *-cycline* are generally what class of drug?
Antibiotic or protein synthesis inhibitors at the 30s subunit of the ribosome
411
Drugs that end in *-ipramine* are generally what class of drug?
Tricyclic antidepressants
412
Angiotensin-converting enzyme inhibitors are typically named with what suffix?
The suffix *-pril*; such as captopril
413
ﾧ2-Agonists are typically named with what suffix?
The suffix *-terol*; such as albuterol
414
Drugs that end in *-navir* are generally what class of drug?
Protease inhibitors
415
Drugs that end in *-olol* are generally what class of drug?
β-Antagonists
416
Drugs that end in *-operidol* are generally what class of drug?
Butyrophenones (neuroleptics)
417
Drugs that end in *-oxin* are generally what class of drug?
Cardiac glycosides (inotropic agents)
418
H2-antagonists are typically named with what suffix?
The suffix *-tidine*; such as cimetidine
419
Drugs that end in *-phylline* are generally what class of drug?
Methylxanthines
420
Drugs that end in *-pril* are generally what class of drug?
Angiotensin-converting enzyme inhibitors
421
Pituitary hormones are typically named with what suffix?
The suffix *-tropin*; such as somatotropin
422
Drugs that end in *-terol* are generally what class of drug?
β2-Agonists
423
Drugs that end in *-tidine* are generally what class of drug?
Histamine2 antagonists
424
α1-Antagonists are typically named with what suffix?
The suffix *-zosin*; such as prazosin
425
Drugs that end in *-triptyline* are generally what class of drug?
Tricyclic antidepressants
426
Drugs that end in *-tropin* are generally what class of drug?
Pituitary hormones
427
Drugs that end in *-zosin* are generally what class of drug?
α1-Antagonists
428
Drugs that end in *-afil* are generally used for what purpose?
Erectile dysfunction
429
Drugs that end in *-ane* are generally used for what purpose?
Inhalational general anesthesia
430
Drugs that end in *-azepam* are generally what class of drug?
Benzodiazepines
