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430 Cards in this Set

  • Front
  • Back
When velocity is equal to one half of its maximum (Vmax), the corresponding concentration of substrate is equal to what value?
Km
2010-228
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?
The inverse of Vmax = 1/Vmax
2010-228
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.
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
2010-228
In enzyme kinetics, competitive inhibitors _____ (resemble/do not resemble) the substrate while noncompetitive inhibitors _____ (resemble/do not resemble) the substrate.
Resemble; do not resemble
2010-228
In enzyme kinetics, the value of Km reflects the _____ of the enzyme for its substrate.
Affinity
2010-228
In enzyme kinetics, Vmax is directly proportional to the _____ _____.
Enzyme concentration
2010-228
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.
Increasing, although it will plateau when the enzyme is saturated
2010-228
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?
Km/Vmax
2010-228
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.
Do not change; decrease
2010-228
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.
Increase; do not change
2010-228
True or False? In enzyme kinetics, the lower the Km, the higher the affinity.
True
2010-228
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?
The inverse of Km = 1/Km
2010-228
After one half-life, given constant intravenous infusion of a drug, how close to steady-state is the concentration of the drug?
50% of steady-state concentration
2010-228
How many half-lives of a drug must pass before a drug infused at a constant rate reaches approximately 94% of steady-state concentration?
Four
2010-228
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).
Tissues
2010-228
After three half-lives, given constant intravenous infusion of a drug, how close to steady-state is the concentration of the drug?
87.5% of steady-state concentration
2010-228
Given the volume of distribution and clearance of a drug, how does one calculate the half-life of the drug?
Half-life = (0.7 × volume of distribution) / clearance
2010-228
What is the formula for calculating the clearance of a drug?
Clearance (L/min) = rate of elimination of drug (g/min) / plasma drug concentration (g/L)
2010-228
Drugs with a low volume of distribution, such as 4-8 L, are found in the _____ (blood/extracellular space/tissues).
Blood alone; these drugs do not distribute outside the plasma
2010-228
What is the formula for calculating the volume of distribution of a drug?
Volume of distribution = amount of drug in the body / plasma drug concentration
2010-228
What is the definition of the half-life of a drug?
The time required to reduce the amount of drug in the body by one half
2010-228
A drug with a volume of distribution of 15 L is most likely to be found in the _____ (blood/extracellular space/tissues).
Extracellular space; these drugs distribute throughout the total body water
2010-228
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
2010-229
What is the bioavailability of a drug if it is administered intravenously?
100%
2010-229
What is the formula for maintenance dose of a drug administered intravenously?
Maintenance dose = rate of elimination/bioavailability = (target plasma concentration × clearance) / bioavailability
2010-229
What is the formula for the loading dose of a drug?
Loading dose = (target plasma concentration × volume of distribution) / bioavailability
2010-229
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
2010-229
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
2010-229
In first-order elimination of drugs from the body, how does the plasma concentration of a drug change over time: linearly or exponentially?
Exponentially
2010-229
In zero-order elimination of drugs from the body, how does the plasma concentration of a drug change over time: linearly or exponentially?
Linearly
2010-229
What are three drugs that exhibit zero-order elimination?
Phenytoin and ethanol; aspirin at toxic concentrations
2010-229
Weak acids get trapped in _____ (acidic/basic) environments.
Basic
2010-229
Ionized species become trapped in urine because they are not _____ _____.
Lipid soluble; therefore, they cannot cross cell membranes
2010-229
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
2010-229
What substance is given to enhance the renal clearance of weakly acidic drugs such as phenobarbital, methotrexate, and aspirin?
Bicarbonate
2010-229
Weak bases get trapped in _____ (acidic/basic) environments.
Acidic
2010-229
What substance is given to enhance the renal clearance of weakly basic drugs such as amphetamine?
Ammonium chloride
2010-229
The products of phase II metabolism of drugs are excreted by what organ?
Kidneys
2010-229
What three types of biochemical reactions are involved in the phase II metabolism of drugs?
Acetylation, glucuronidation, and sulfation; these are conjugation reactions
2010-229
True or False? Drug products that result from phase I metabolism are water soluble.
True
2010-229
What enzyme system mediates the phase I metabolism of drugs in the body?
Cytochrome P-450
2010-229
Do geriatric patients lose the ability for phase I or phase II drug metabolism first?
Phase I
2010-229
What is the polarity of the drug products that result from phase I metabolism?
The products are slightly polar
2010-229
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
2010-229
What three types of biochemical reactions are involved in the phase I metabolism of drugs?
Reduction, oxidation, and hydrolysis
2010-229
True or False? Drug products that result from phase I metabolism are often still active.
True
2010-229
What is the definition of potency?
Amount of drug needed for a given effect
2010-229
A drug that requires a very low dose to achieve its desired effect is considered _____.
Potent
2010-229
What is the definition of efficacy?
Maximal effect a drug can produce
2010-229
In pharmacodynamics, the addition of a noncompetitive agonist _____ (increases/decreases/does not change) the efficacy of the agonist.
Decreases
2010-230
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
2010-230
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
2010-230
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
2010-230
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
2010-230
What property of a drug is determined by its therapeutic index?
Safety; drugs with higher therapeutic indices are less likely to cause toxicities
2010-230
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)
2010-230
Safer drugs have _____ (higher/lower) therapeutic index values.
Higher
2010-230
How many neurons are involved in sympathetic transmission from the spinal cord to the target organ?
Two
2010-231
What neurotransmitter mediates sympathetic tone in the cardiac muscle, smooth muscle, and glandular cells?
Norepinephrine
2010-231
What neurotransmitter receptor mediates parasympathetic tone in the cardiac muscle?
Muscarinic acetylcholine receptors (specifically, M2)
2010-231
At the paravertebral ganglia, the neurotransmitter _____ acts on _____ receptors to mediate sympathetic nervous system function.
Acetylcholine; nicotinic acetylcholine
2010-231
What neurotransmitter receptor mediates parasympathetic tone in the glandular cells?
Muscarinic acetylcholine receptors (specifically, M1 and M3)
2010-231
How many neurons are involved in parasympathetic transmission from the spinal cord to the target organ?
Two
2010-231
True or False? Preganglionic sympathetic axons synapse on neurons in the peripheral ganglia.
False; preganglionic sympathetic axons synapse on neurons in the paravertebral ganglia
2010-231
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
2010-231
What neurotransmitter mediates sympathetic nervous system function at the sweat glands?
Acetylcholine
2010-231
What neurotransmitter receptor mediates parasympathetic nervous system function at the peripheral ganglia?
Nicotinic acetylcholine receptors
2010-231
From which regions of the central nervous system do parasympathetic nerves originate?
Cranial and sacral regions
2010-231
How many synapses are involved in activation of the adrenal medulla?
One; the adrenal medulla releases epinephrine and norepinephrine into the blood
2010-231
What two substances are released into the blood from the adrenal medulla after the activation of the sympathetic nervous system?
Epinephrine and norepinephrine
2010-231
What neurotransmitter receptor mediates parasympathetic tone in the smooth muscle?
Muscarinic acetylcholine receptors (specifically, M3)
2010-231
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
2010-231
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
2010-231
What neurotransmitter receptor mediates sympathetic tone in the renal vascular smooth muscle?
D1 receptors
2010-231
True or False? Craniosacral parasympathetic axons synapse on neurons in the peripheral ganglia.
True
2010-231
What neurotransmitter receptor mediates sympathetic nervous system function at the sweat glands?
Muscarinic acetylcholine receptors
2010-231
What types of nerves arise from the spinal cord and innervate skeletal muscle directly?
Somatic nerves
2010-231
What neurotransmitter mediates parasympathetic nervous system function?
Acetylcholine
2010-231
From which regions of the central nervous system do sympathetic nerves originate?
Thoracic and lumbar regions
2010-231
What neurotransmitter mediates sympathetic tone in the renal vascular smooth muscle?
Dopamine
2010-231
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
2010-231
Are nicotinic acetylcholine receptors ligand-gated sodium-potassium channels or G-protein coupled receptors?
Nicotinic receptors are ligand gated sodium-potassium channels
2010-231
What enzyme is activated by diacylglycerol?
Protein kinase C
2010-232
What is the effect of increased inositol triphosphate on the intracellular concentration of calcium?
It increases the intracellular calcium concentration
2010-232
Phospholipase C catalyzes the cleavage of membrane lipids into what molecules?
Inositol trisphosphate3 and diacylglycerol
2010-232
What final effector enzyme is inhibited by receptors that are coupled with Gi proteins?
Protein kinase A
2010-232
What final effector enzyme is activated by receptors that are coupled with Gs proteins?
Protein kinase A
2010-232
Adenyl cyclase catalyzes the conversion of adenosine triphosphate into what molecule?
cAMP
2010-232
What enzyme is inhibited directly downstream of Gi-coupled receptors?
Adenyl cyclase
2010-232
What enzyme is activated directly downstream of Gs-coupled receptors?
Adenyl cyclase
2010-232
What enzyme is activated directly downstream of Gq-coupled receptors?
Phospholipase C
2010-232
What three types of receptors are coupled with Gi proteins?
a2, M2, and D2
2010-232
What five types of receptors are coupled with Gs proteins?
β1, β2, D1, H2, and V2
2010-232
What five types of receptors are coupled with Gq proteins?
α1, M1, M3, H1, and V1
2010-232
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
2010-232
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)
2010-232
What effect does V1-receptor activation have on vascular smooth muscle?
It increases vascular smooth muscle contraction
2010-232
What is the effect of H2-receptor activation?
It increases gastric acid secretion
2010-232
What are the effects of H1-receptor activation?
Pruritis, pain, nasal and bronchial mucus production, contraction of bronchioles
2010-232
What effect does D1-receptor activation have on renal vasculature?
It relaxes renal vascular smooth muscle
2010-232
What are the effects of M3-receptor activation?
Increased exocrine gland secretions, gut peristalsis, bladder contraction, bronchoconstriction, miosis, and accommodation
2010-232
What effect does M2-receptor activation have on cardiac function?
It decreases heart rate and contractility
2010-232
Where are M1-receptors located?
The central nervous system
2010-232
What effect does β2-receptor activation have on glucagon release?
It increases glucagon release
2010-232
What is the major function of β2-receptor activation on the respiratory system?
Bronchodilation
2010-232
What is the major function of β2-receptor activation on the body's vasculature?
Vasodilation
2010-232
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
2010-232
What are the major functions of α2-receptor activation?
It decreases sympathetic outflow and decreases insulin release
2010-232
What are the major effects of α1-receptor activation?
It increases vascular smooth muscle contraction, and increases pupillary dilator muscle contraction (mydriasis)
2010-232
To what class of G-proteins are V2-receptors linked?
s
2010-232
To what class of G-proteins are V1-receptors linked?
q
2010-232
To what class of G-proteins are H2-receptors linked?
s
2010-232
To what class of G-proteins are H1-receptors linked?
q
2010-232
To what class of G-proteins are D2-receptors linked?
i
2010-232
To what class of G-proteins are D1-receptors linked?
s
2010-232
To what class of G-proteins are M3-receptors linked?
q
2010-232
To what class of G-proteins are M2-receptors linked?
i
2010-232
To what class of G-proteins are M1-receptors linked?
q
2010-232
To what class of G-proteins are β2-receptors linked?
s
2010-232
To what class of G-proteins are β1-receptors linked?
s
2010-232
To what class of G-proteins are α2-receptors linked?
i
2010-232
To what class of G-proteins are α1-receptors linked?
q
2010-232
What toxin inhibits the calcium-induced release of acetylcholine from the cholinergic nerve terminals?
Botulinum
2010-233
The entry of what ion into the nerve terminal induces the release of norepinephrine into the synaptic cleft?
Calcium
2010-233
The entry of what ion into the nerve terminal induces the release of acetylcholine into the synaptic cleft?
Calcium
2010-233
Tyrosine is converted into dopamine via what intermediate precursor?
DOPA; DOPA can be used as a pharmacologic agent to increase central nervous system dopamine
2010-233
Dopamine is converted into norepinephrine in the ______ (cytoplasm/presynaptic vesicle).
Presynaptic vesicles
2010-233
What pharmacologic agent blocks the transport of dopamine into the presynaptic vesicles in nerve terminals?
Reserpine
2010-233
What three receptor types modulate the presynaptic release of norepinephrine from the noradrenergic nerve terminals?
M2-receptors, angiotensin II receptors, and α2-receptors
2010-233
What effect does the activation of M2-receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?
It inhibits norepinephrine release
2010-233
Tyrosine is a precursor to the formation of which neurotransmitters? What is the order of their synthesis?
Tyrosine, DOPA, dopamine, norepinephrine, epinephrine
2010-233
What effect does the activation of α2-receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?
It inhibits norepinephrine release
2010-233
What pharmacologic agent stimulates the release of norepinephrine from the noradrenergic nerve terminals?
Amphetamine
2010-233
What pharmacologic agents inhibit the reuptake of norepinephrine into the nerve terminals?
Cocaine, amphetamine, and tricyclic antidepressants
2010-233
What effect does the activation of angiotensin II receptors in presynaptic sympathetic nerve terminals have on norepinephrine release?
It stimulates norepinephrine release
2010-233
What enzyme breaks down acetylcholine in the synaptic cleft? What two products result from this reaction?
Acetylcholinesterase; choline and acetate
2010-233
What pharmacologic agent blocks the uptake of choline into cholinergic nerve terminals?
Hemicholinium
2010-233
How is norepinephrine cleared form the synaptic cleft?
Diffusion, metabolism (monoamine oxidase A), and reuptake
2010-233
What pharmacologic agent blocks the conversion of tyrosine to DOPA?
Metyrosine
2010-233
What pharmacologic agent inhibits the calcium-induced release of norepinephrine from the noradrenergic nerve terminals?
Guanethidine
2010-233
Tyrosine transporters are located in the nerve terminals of what type of cells?
Noradrenergic cells; tyrosine is the precursor of norepinephrine
2010-233
What pharmacologic agent blocks the transport of acetylcholine into the presynaptic vesicles in nerve terminals?
Vesamicol
2010-233
What enzyme is responsible for the formation of acetylcholine? What are its two substrates?
Choline acetyltransferase; Acetyl-CoA and choline
2010-233
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
2010-233
Pilocarpine is effective for the treatment of narrow-angle glaucoma because it activates what muscle?
The pupillary sphincter
2010-234
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
2010-234
Indirect cholinergic agonists increase endogenous acetylcholine by inhibiting what enzyme?
Acetylcholinesterase
2010-234
Name four direct cholinergic agonists.
Bethanechol, carbachol, pilocarpine, methacholine
2010-234
Why is pyridostigmine used to treat myasthenia gravis?
It increases the amount of acetylcholine in the neuromuscular synapse, thereby increasing muscle strength
2010-234
What two direct agonist cholinomimetic drugs can be used to treat glaucoma?
Carbachol and pilocarpine
2010-234
True or False? Pilocarpine is susceptible to acetylcholinesterase.
False; pilocarpine is resistant to acetylcholinesterase
2010-234
What is a methacholine challenge test?
A test in which methacholine is inhaled to stimulate muscarinic receptors and induce bronchoconstriction to diagnose asthma
2010-234
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
2010-234
What effect does neostigmine have on the central nervous system?
None; it does not penetrate the blood-brain barrier (remember: NEO CNS = NO CNS)
2010-234
What are the clinical indications for use of neostigmine?
The treatment of postoperative and neurogenic ileus
2010-234
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

2010-234
What is the clinical indication for use of echothiophate?
The treatment of glaucoma
2010-234
Name five indirect cholinergic agonists.
Neostigmine, pyridostigmine, edrophonium, physostigmine, echothiophate
2010-234
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)
2010-234
Carbachol and pilocarpine are effective for the treatment of open-angle glaucoma because they activate what muscle?
The ciliary muscle of the eye
2010-234
True or False? The treatment of glaucoma is a clinical application of physostigmine.
True (remember: "PHYS is for the EYES")
2010-234
True or False? The treatment of myasthenia gravis is a clinical application of pyridostigmine.
True
2010-234
What mechanism underlies the symptoms of acetylcholinesterase inhibitor poisoning?
Inhibition of acetylcholinesterase leads to overactivity of the body's cholinergic systems
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
What antidote can be given to a patient who presents with diarrhea, urinary incontinence, miosis, bronchospasm, bradycardia, lacrimation, sweating, and salivation?
Atropine and pralidoxime
What symptoms indicate cholinesterase inhibitor poisoning?
DUMBBELSS: Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of the skeletal muscle and the central nervous system, Lacrimation, Sweating, and Salivation
The symptoms of parathion poisoning are caused by the inhibition of what enzyme?
Acetylcholinesterase
The symptoms of organophosphate poisoning are caused by the inhibition of what enzyme?
Acetylcholinesterase
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
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
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
What is the mechanism and clinical application for benztropine?
It is a muscarinic antagonist used to reduce symptoms of Parkinson's disease
2010-235
What is the mechanism and clinical application for methscopolamine?
It is a muscarinic antagonist used to treat peptic ulcers
2010-235
What is the mechanism and clinical application for scopolamine?
It is a muscarinic antagonist used to treat motion sickness
2010-235
Which muscarinic antagonist is most commonly used to treat motion sickness?
Scopolamine
2010-235
Which muscarinic antagonist can be used to reduce urgency in patients with mild cystitis?
Oxybutynin (also glycopyrrolate)
2010-235
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
2010-235
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
2010-235
What is the mechanism and clinical application for pirenzepine?
It is a muscarinic antagonist used to treat peptic ulcers
2010-235
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
2010-235
What is the mechanism and clinical application for propantheline?
It is a muscarinic antagonist used to treat peptic ulcers
2010-235
Which muscarinic antagonist can be used to treat bladder spasms?
Oxybutynin (also glycopyrrolate)
2010-235
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
2010-235
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!)
2010-235
True or False? Atropine toxicity can cause fecal incontinence.
False; atropine toxicity causes constipation, not fecal incontinence
2010-235
True or False? Atropine toxicity can cause urinary incontinence.
False; atropine toxicity can cause urinary retention in men with prostatic hypertrophy
2010-235
True or False? Diarrhea is a sign of atropine toxicity.
False; constipation is a sign of atropine toxicity
2010-235
True or False? Increased body temperature is a sign of atropine toxicity.
True (ie, "hot as a hare")
2010-235
True or False? Dry, flushed skin is a sign of atropine toxicity.
True (ie, "dry as a bone, red as a beet")
2010-235
True or False? Disorientation is a sign of atropine toxicity.
True (ie, "mad as a hatter")
2010-235
True or False? Slower heart rate is a sign of atropine toxicity.
False; heart rate would be increased
2010-235
What is the effect of atropine on gastrointestinal motility?
It decreases motility
2010-235
According to the mnemonic DUMBBELSS, what four major physiologic processes are blocked by atropine?
Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle, Lacrimation, Sweating, and Salivation
2010-235
True or False? Cycloplegia is a sign of atropine toxicity.
True (ie, "blind as a bat")
2010-235
Atropine is used for therapeutic effect in which four organ systems?
Eyes, gastrointestinal system, respiratory system, urinary system
2010-235
What is the effect of atropine on the airway mucosa?
It decreases secretions
2010-235
Which two adverse effects of atropine are more common in elderly patients?
Urinary retention and acute angle closure glaucoma
2010-235
What is the effect of atropine on the bladder in a patient with cystitis?
It decreases urgency
2010-235
What are the two effects of atropine on the eye?
Pupil dilation, cycloplegia
2010-235
True or False? Dry mouth is a sign of atropine toxicity.
True (ie, "dry as a bone")
2010-235
What is the effect of atropine on the stomach?
It decreases acid secretion
2010-235
What type of acetylcholine receptors does hexamethonium antagonize?
Nicotinic acetylcholine receptors
2010-235
Name four toxicities of hexamethonium.
Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction
2010-235
What effect does hexamethonium have on heart rate?
can prevent bradycardia in response to increased blood pressure when pressors are given
2010-235
Isoproterenol is an agonist for which receptors?
β1- and β2-receptors equally
2010-236
Does norepinephrine have greater affinity for α-adrenergic receptors or β1-receptors?
α-Adrenergic receptors
2010-236
Which types of receptors are activated by norepinephrine?
α1- and α2-; β1-receptors (with lower affinity)
2010-236
Low doses of epinephrine are selective for _____ (α1, α2, β1, β2) adrenergic receptors.
β1
2010-236
Which types of receptors are activated by epinephrine?
α1-, α2-, β1-, and β2-receptors
2010-236
Name 11 drugs that act as direct sympathomimetics.
Isoproterenol, dobutamine, phenylephrine, epinephrine, norepinephrine, dopamine, albuterol, terbutaline, ritodrine, metaproterenol, and salmeterol
2010-236
What effect does isoproterenol have on pulse pressure and heart rate?
Increases pulse pressure and heart rate
2010-236
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
2010-236
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
2010-236
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
2010-236
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
2010-236
Is the effect of isoproterenol on β-receptors greater than, equal to, or less than its effect on α-receptors?
Greater than
2010-236
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
2010-236
What are the effects of cocaine when used topically?
Vasoconstriction and local anesthesia
2010-236
True or False? Phenylephrine can be used to treat nasal congestion.
True
2010-236
What are three clinical applications of ephedrine?
To treat nasal congestion, urinary incontinence, and hypotension
2010-236
What are the clinical indications for use of amphetamines?
Narcolepsy, obesity, attention deficit hyperactivity disorder
2010-236
By what mechanism does cocaine exert its sympathomimetic effect?
It inhibits catecholamine uptake in the nerve terminal
2010-236
By what mechanism does ephedrine exert its sympathomimetic effect?
It stimulates the release of stored catecholamines
2010-236
By what mechanism does amphetamine exert its sympathomimetic effect?
It stimulates the release of stored catecholamines
2010-236
Amphetamine, ephedrine, and cocaine are (direct/indirect) sympathomimetics.
Indirect
2010-236
Which sympathomimetics can be used to reduce premature uterine contractions?
Terbutaline, salmeterol
2010-236
What is the clinical application for albuterol?
Acute asthma
2010-236
What are the clinical applications of phenylephrine?
Treats nasal decongestion; causes vasoconstriction; dilates pupils
2010-236
What are the clinical applications for dobutamine?
Shock, heart failure, cardiac stress testing
2010-236
True or False? Dopamine can be used to treat heart failure.
True
2010-236
What role does dopamine have in treating shock?
Increases blood pressure while maintaining renal perfusion
2010-236
What is the clinical application for isoproterenol?
Atrioventricular block
2010-236
What effect does norepinephrine have on renal perfusion?
It decreases renal perfusion
2010-236
What are the clinical applications of epinephrine?
Anaphylaxis, open-angle glaucoma, asthma, hypotension
2010-236
Ritodrine acts on _____ (α1, α2, β1, β2)-adrenergic receptors.
β2
2010-236
Metaproterenol, albuterol, salmeterol, and terbutaline are agonists for which receptors?
β2-receptors > β1-receptors
2010-236
Phenylephrine is an agonist for which receptors?
α1-receptors > α2-receptors
2010-236
Dopamine is _____ (ionotropic/not ionotropic) and _____ (chronotropic/not chronotropic), while dobutamine is _____ (ionotropic/not ionotropic) and _____ (chronotropic/not chronotropic).
Ionotropic; chronotropic; ionotropic; not chronotropic
2010-236
Dopamine is an agonist for which receptors?
β1- and β2-receptors
2010-236
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
2010-236
What are two patient populations for which α-methyldopa is indicated (as an antihypertensive)?
Renal failure patients, pregnant patients
2010-237
What is the effect of clonidine on central adrenergic outflow? Which receptor does it act on?
is an α2-agonist and decreases central adrenergic outflow; remember that the α2-receptor is responsible for negative feedback
2010-237
What are the clinical applications of α-methyldopa?
Hypertension, especially with renal disease, because it does not decrease blood flow to the kidneys
2010-237
What are the clinical applications of clonidine?
Hypertension, especially with renal disease, because it does not decrease blood flow to the kidneys
2010-237
What is the effect of α-methyldopa on central adrenergic outflow? Which receptor does it act on?
is an α2-agonist and decreases central adrenergic outflow
2010-237
What is the clinical application and mechanism of action of phentolamine?
Phentolamine is a nonselective α-blocker that is used to treat pheochromocytoma
2010-237
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 ß2, so it is completely negated by α-blockade
2010-237
What is the clinical application and mechanism of action of phenoxybenzamine?
Phenoxybenzamine is a nonselective α-blocker that is used to treat pheochromocytoma
2010-237
Why does epinephrine, a pressor, cause hypotension if a patient is pretreated with an α-blocker?
α-receptors are blocked, the β-agonist properties of epinephrine predominate and lower blood pressure
2010-237
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
2010-237
What is the clinical application and mechanism of action of mirtazapine?
Mirtazapine is an α2-selective blocker used to treat depression
2010-237
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
2010-237
What are three effects of α2-selective blocker toxicity?
Sedation, increased serum cholesterol, increased appetite
2010-237
What are two adverse effects of nonselective α-blockers?
Orthostatic hypotension and reflex tachycardia
2010-237
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
2010-237
What are three effects of α1-selective blocker toxicity?
Orthostatic hypotension (first dose only), dizziness, headache
2010-237
What are some effects of β-blocker toxicity?
Bradycardia, atrioventricular block, congestive heart failure (reduced cardiac output), sedation, sleep alteration, impotence, exacerbation of asthma
2010-238
How do β-blockers work in the setting of angina pectoris?
Decrease heart rate and contractility; decrease myocardial oxygen consumption
2010-238
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
2010-238
Which β-blocker is the shortest acting?
Esmolol
2010-238
Name five nonselective β-blockers.
Propranolol, timolol, nadolol, pindolol, and labetalol
2010-238
To which class of antiarrhythmic agents do β-blockers belong?
Class II; drugs that slow atrioventricular conduction
2010-238
What are two nonselective α- and β-antagonists?
Carvedilol, labetalol
2010-238
What is the mechanism of β-blockers in the treatment of glaucoma?
They reduce the secretion of aqueous humor, reducing intraocular pressure
2010-238
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?
ß-Blockers, such as propranolol, will reduce heart rate and consequently reduce angina
2010-238
What β-blockers have partial agonist activity?
Pindolol, Acebutolol (remember: Partial Agonist)
2010-238
Which two β-blockers are used to treat supraventricular tachycardia?
Propranolol, esmolol
2010-238
What is the mechanism of β-blockers in the treatment of supraventricular tachycardia?
They decrease atrioventricular conduction velocity
2010-238
What is the mechanism of β-blockers in treatment of hypertension?
Decreasing cardiac output and decreasing renin secretion
2010-238
What β-blocker is frequently used to treat glaucoma?
Timolol
2010-238
Name six clinical applications for β-blockers.
Hypertension, angina pectoris, myocardial infarction, supraventricular tachycardia, congestive heart failure, glaucoma
2010-238
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
2010-238
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
2010-238
Name five β1-selective antagonists.
Acebutolol, Betaxolol, Esmolol, Atenolol, Metoprolol (remember: A BEAM of β1-blockers)
2010-238
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
2010-239
What is the antidote for theophylline?
β-Blockers
2010-239
Aminocaproic acid is used to reverse the effects of what two pharmacologic enzymes?
Tissue plasminogen activator and streptokinase
2010-239
What agent is used to reverse the effects of both tissue plasminogen activator and streptokinase?
Aminocaproic acid
2010-239
Vitamin K is used to reverse the effects of what pharmacologic agent?
Warfarin
2010-239
What agents are used to reverse the effects of warfarin?
Vitamin K and fresh frozen plasma
2010-239
Protamine is used to reverse the effects of what pharmacologic agent?
Heparin; however, it does not reverse low-molecular-weight heparin
2010-239
What is the reversal agent for heparin?
Protamine
2010-239
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
2010-239
What is the treatment for tricyclic antidepressant overdose?
Sodium bicarbonate; it can prevent cardiac arrhythmias
2010-239
Flumazenil is the antidote for overdose of what substance?
Benzodiazepines
2010-239
What is the antidote for benzodiazepine overdose?
Flumazenil; it reduces the action of benzodiazepines at γ-aminobutyric acid receptors
2010-239
Naloxone is the antidote for overdose of what substance?
Opioids
2010-239
What are the antidotes for opioid overdose?
Naloxone or naltrexone
2010-239
Fomepizole is an antidote for toxicity caused by what substances?
Methanol, ethylene glycol
2010-239
What are the treatments for methanol and ethylene glycol (antifreeze) poisoning?
Ethanol, dialysis, and fomepizole
2010-239
What are the treatments for carbon monoxide poisoning?
100% oxygen and hyperbaric oxygen
2010-239
Methylene blue is used to treat elevated serum levels of what substance?
Methemoglobin
2010-239
What is the treatment for methemoglobinemia?
Methylene blue, vitamin C
2010-239
What are the treatments for cyanide poisoning?
Hydroxocobalamin, or a combination of nitrite and thiosulfate
2010-239
Hydroxocobalamin is the antidote for toxicity caused by what substance?
Cyanide
2010-239
The combination of thiosulfate and nitrite is the antidote for toxicity caused by what substance?
Cyanide
2010-239
Dimercaprol and succimer are the antidotes for toxicity caused by what substances?
Mercury, arsenic, gold
2010-239
What are three treatments for gold poisoning?
Dimercaprol, succimer, penicillamine
2010-239
What are two treatments for mercury poisoning?
Dimercaprol and succimer
2010-239
What are three treatments for arsenic poisoning?
Dimercaprol, succimer, penicillamine
2010-239
Penicillamine is the antidote for toxicity caused by what substances?
Copper, arsenic, gold
2010-239
What are four treatments for lead poisoning?
Edetate calcium disodium, dimercaprol, succimer, and penicillamine
2010-239
What is the antidote for iron toxicity?
Deferoxamine, a chelating agent
2010-239
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
2010-239
What is the antidote for β-blocker toxicity?
Glucagon
2010-239
Physostigmine is the antidote for toxicity caused by what two types of agents?
Antimuscarinic agents and anticholinergic agents
2010-239
What is the antidote for toxicity caused by anticholinergic agents?
Physostigmine; it inhibits acetylcholinesterase, increasing the available acetylcholine to overcome anticholinergic toxicity
2010-239
What are the antidotes for organophosphate poisoning?
Atropine and pralidoxime; organophosphates inhibit acetylcholinesterase
2010-239
What are the two antidotes for anticholinesterase toxicity?
Atropine to block cholinergic receptors and pralidoxime to regenerate acetylcholinesterase
2010-239
Amphetamines are _____ (acidic/basic); therefore, overdose is treated with _____ (NH4Cl/NaHCO3) to _____ (acidify/alkalinize) the urine.
Basic; NH4Cl; acidify
2010-239
What is the treatment for amphetamine overdose?
NH4Cl
2010-239
What compound is used to alkalinize urine?
NaHCO3; weak acids are better excreted when the urine is alkaline
2010-239
What are the two treatments for salicylate overdose?
Alkalinization of urine and dialysis if necessary
2010-239
What is the antidote for acetaminophen overdose?
N-acetylcysteine
2010-239
What will a patient with acute iron poisoning present with?
Gastric bleeding
2010-239
What is the mechanism of cell death in iron poisoning?
Peroxidation of membrane lipids
2010-239
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
2010-239
Which component of multivitamins is the most likely to cause fatal overdose in children?
Iron
2010-239
Which drugs can cause Stevens-Johnson syndrome?
Ethosuximide, lamotrigine, carbamazepine, phenobarbital, phenytoin, sulfa drugs, penicillin, allopurinol; think anticonvulsants and antibiotics
2010-240
Which drugs induce photosensitivity?
Sulfonamides, Amiodarone, Tetracyclines (remember: SAT for a photo)
2010-240
Osteoporosis can be caused by long-term use of which drugs?
Steroids, heparin
2010-240
Which drugs can cause gout?
Furosemide and thiazide diuretics
2010-240
Which drug can cause gingival hyperplasia?
Phenytoin
2010-240
Which drugs can cause hot flashes?
Tamoxifen, clomiphene
2010-240
Which drugs are known to cause gynecomastia?
Spironolactone, Digitalis, Cimetidine, Alcohol (chonic use), estrogens, Ketoconazole (remember: Some Drugs Create Awesome Knockers)
2010-240
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
2010-240
Administration of clindamycin or ampicillin can cause overgrowth of which bacteria in the colon?
Clostridium difficile, which leads to pseudomembranous colitis
2010-240
Which drugs can cause pseudomembranous colitis?
Clindamycin and ampicillin are commonly implicated, but many antibiotics can be responsible
2010-240
What effect can isoniazid have on the liver?
Hepatitis
2010-240
Which drugs (or exposures) can cause hepatic necrosis?
Halothane, valproic acid, acetaminophen, Amanita phalloides
2010-240
What adverse effect would you suspect in a newly jaundiced patient recently started on azithromycin?
Acute cholestatic hepatitis
2010-240
Which drugs can cause pulmonary fibrosis?
Bleomycin, busulfan, amiodarone
2010-240
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
2010-240
Which antihypertensive drug can cause chronic cough?
Angiotensin-converting enzyme inhibitors
2010-240
What is a major adverse effect of oral contraceptives?
Thrombotic events such as deep vein thrombosis and pulmonary embolus
2010-240
Which drugs can cause megaloblastic anemia?
Phenytoin, Methotrexate, Sulfa drugs (remember: Having a blast with PMS)
2010-240
Which drugs can cause hemolytic anemia in G6PD-deficient patients?
Isoniazid, Sulfonamides, Primaquine, Aspirin, Ibuprofen, Nitrofurantoin (remember: hemolysis IS PAIN)
2010-240
Which antibiotic can cause "grey baby syndrome"?
Chloramphenicol
2010-240
Which antihypertensive drug can cause hemolytic anemia?
α-Methyldopa
2010-240
Which drugs (or exposures) can cause aplastic anemia as an adverse effect?
Chloramphenicol, benzene, nonsteroidal antiinflammatory drugs, propylthiouracil, methimazole
2010-240
Which drugs can cause agranulocytosis as an adverse effect?
Clozapine, carbamazepine, colchicine, propylthiouracil, methimazole
2010-240
What is the major adverse effect of niacin use?
Flushing
2010-240
What cardiac adverse effect can result from either cocaine or sumatriptan use?
Coronary vasospasm
2010-240
Which drugs can cause torsades de pointes?
Class III (sotalol) and class IA (quinidine) antiarrhythmic agents, cisapride
2010-240
Which drugs cause dilated cardiomyopathy?
Doxorubicin (Adriamycin), daunorubicin
2010-240
Which drugs can cause cutaneous flushing as an adverse effect?
Vancomycin, adenosine, niacin, calcium channel blockers (remember: VANC)
2010-240
Which drugs can cause coronary vasospasm?
Cocaine and sumatriptan
2010-240
Which antidepressants can cause tachycardia due to anticholinergic action?
Tricyclic antidepressants
2010-240
Name three drugs that can cause seizures.
Bupropion, imipenem/cilastatin, isoniazid
2010-241
Which adverse effects of fluoroquinolones are specific to children?
Tendonitis, tendon rupture, and cartilage damage
2010-241
Name two drugs that can cause diabetes insipidus.
Lithium and demeclocycline
2010-241
Which adverse effect of lithium can cause hypernatremia?
Diabetes insipidus
2010-241
Which drug can cause Fanconi's syndrome if taken after its expiration date?
Tetracycline
2010-241
Which class of drugs can result in tardive dyskinesia?
Antipsychotics
2010-241
What drugs can cause a disulfiram-like reaction?
Metronidazole, certain cephalosporins, procarbazine, first-generation sulfonylureas
2010-241
Which drugs can cause interstitial nephritis?
Methicillin, nonsteroidal antiinflammatory drugs, and furosemide
2010-241
Name two drugs that can cause cinchonism.
Quinidine and quinine; cinchonism describes headache and tinnitus
2010-241
Which drugs can cause both ototoxicity and nephrotoxicity?
Aminoglycosides, vancomycin, loop diuretics, cisplatin
2010-241
Which two drugs can cause hemorrhagic cystitis?
Cyclophosphamide and ifosfamide
2010-241
Polymyxins are toxic to which organ systems?
Neural and renal; as a result it is usually only used topically
2010-241
Which drugs can cause a lupus-like syndrome?
Hydralazine, Isoniazid, Procainamide, Phenytoin (remember: it's not HIPP to have lupus)
2010-241
Which drug is administered to prevent hemorrhagic cystitis from the use of ifosfamide or cyclophosphamide?
Mesna
2010-241
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 ß-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
2010-241
What are the seven most common drugs that induce cytochrome P450 enzyme activity?
Quinidine, Barbituates, St. John's Wort, Phenytoin, Rifampin, Griseofulvin, Carbamazepine (remember: Queen Barb Steals Phen-phen and Refuses Greasy Carbs)
2010-241
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
2010-241
What are the six most common substances that inhibit cytochrome P450 enzyme activity?
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)
2010-241
What are two adverse effects of formaldehyde and formic acid?
Severe acidosis, retinal damage
2010-242
What substance is converted to oxalic acid by alcohol dehydrogenase?
Ethylene glycol; it is usually found in antifreeze
2010-242
What does alcohol dehydrogenase convert ethanol into?
Acetaldehyde
2010-242
Alcohol dehydrogenase is involved in the metabolism of what three alcohols?
Ethylene glycol, methanol, and ethanol
2010-242
Alcohol dehydrogenase converts ethylene glycol into what?
Oxalic acid
2010-242
Alcohol dehydrogenase is inhibited by what drug?
Fomepizole; the drug can be used to prevent toxicities of methanol and ethylene glycol ingestions
2010-242
What does alcohol dehydrogenase convert methanol into?
Formaldehyde and formic acid
2010-242
Acetaldehyde dehydrogenase is inhibited by what drug?
Disulfiram; the drug worsens the adverse effects of alcohol use and is also called Antabuse
2010-242
What are four adverse effects of acetaldehyde?
Nausea, headache, vomiting, hypotension
2010-242
What does acetaldehyde dehydrogenase convert acetaldehyde into?
Acetic acid
2010-242
Acetaldehyde dehydrogenase converts what substrate into acetic acid?
Acetaldehyde
2010-242
Alcohol dehydrogenase converts what alcohol into acetaldehyde?
Ethanol
2010-242
Alcohol dehydrogenase converts what alcohol into formaldehyde and formic acid?
Methanol
2010-242
Ethylene glycol is converted to oxalic acid by which enzyme?
Alcohol dehydrogenase
2010-242
Ethanol competes with what endogenous hormone substrate for binding in renal tubules?
Antidiuretic hormone; the result is a diuretic effect
2010-242
What enzyme that is involved in ethanol metabolism is inhibited by disulfiram?
Acetaldehyde dehydrogenase
2010-242
What enzyme converts ethanol to acetaldehyde?
Alcohol dehydrogenase
2010-242
What are two adverse effects of oxalic acid?
Acidosis and nephrotoxicity; oxalic acid crystalizes in the kidney to cause damage
2010-242
What enzyme converts acetaldehyde to acetic acid?
Acetaldehyde dehydrogenase
2010-242
What enzyme converts methanol to formaldehyde and formic acid?
Alcohol dehydrogenase
2010-242
What are some clinical manifestations of sulfa allergic reactions?
Fever, pruritic rash, Stevens-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, uriticaria (hives)
2010-242
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
2010-242
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
2010-242
Drugs that end in -azepam are generally what class of drug?
Benzodiazepines
2010-243
Drugs that end in -ane are generally used for what purpose?
Inhalational general anesthesia
2010-243
Drugs that end in -afil are generally used for what purpose?
Erectile dysfunction
2010-243
Drugs that end in -zosin are generally what class of drug?
α1-Antagonists
2010-243
Drugs that end in -tropin are generally what class of drug?
Pituitary hormones
2010-243
Drugs that end in -triptyline are generally what class of drug?
Tricyclic antidepressants
2010-243
α1-Antagonists are typically named with what suffix?
The suffix -zosin; such as prazosin
2010-243
Drugs that end in -tidine are generally what class of drug?
Histamine2 antagonists
2010-243
Drugs that end in -terol are generally what class of drug?
β2-Agonists
2010-243
Pituitary hormones are typically named with what suffix?
The suffix -tropin; such as somatotropin
2010-243
Drugs that end in -pril are generally what class of drug?
Angiotensin-converting enzyme inhibitors
2010-243
Drugs that end in -phylline are generally what class of drug?
Methylxanthines
2010-243
H2-antagonists are typically named with what suffix?
The suffix -tidine; such as cimetidine
2010-243
Drugs that end in -oxin are generally what class of drug?
Cardiac glycosides (inotropic agents)
2010-243
Drugs that end in -operidol are generally what class of drug?
Butyrophenones (neuroleptics)
2010-243
Drugs that end in -olol are generally what class of drug?
β-Antagonists
2010-243
Drugs that end in -navir are generally what class of drug?
Protease inhibitors
2010-243
ß2-Agonists are typically named with what suffix?
The suffix -terol; such as albuterol
2010-243
Angiotensin-converting enzyme inhibitors are typically named with what suffix?
The suffix -pril; such as captopril
2010-243
Drugs that end in -ipramine are generally what class of drug?
Tricyclic antidepressants
2010-243
Drugs that end in -cycline are generally what class of drug?
Antibiotic or protein synthesis inhibitors at the 30s subunit of the ribosome
2010-243
Methylxanthines are typically named with what suffix?
The suffix -phylline; such as theophylline
2010-243
Drugs that end in -cillin are generally what class of drug?
Penicillins
2010-243
Drugs that end in -caine are generally what class of drug?
Local anesthetic
2010-243
Drugs that end in -barbital are generally what class of drug?
Barbiturates
2010-243
Drugs that end in -azole are generally what class of drug?
Antifungals
2010-243
Cardiac glycosides are typically named with what suffix?
The suffix -oxin; such as digoxin
2010-243
Drugs that end in -azine are generally what class of drug?
Phenothiazines (neuroleptics, antiemetics)
2010-243
β-Antagonists are typically named with what suffix?
The suffix -olol; such as propranolol
2010-243
Protease inhibitors are typically named with what suffix?
The suffix -navir; such as saquinavir
2010-243
Trichloroacetic acids are typically named with what suffix?
The suffix -ipramine; such as Imipramine
2010-243
Butyrophenones are typically named with what suffix?
The suffix -operidol; neuroleptics such as haloperidol
2010-243
Drugs used for local anesthesia are typically named with what suffix?
The suffix -caine; such as lidocaine
2010-243
Barbiturates are typically named with what suffix?
The suffix -barbital; such as phenobarbital
2010-243
Some antibiotics that inhibit protein synthesis are named with what suffix?
The suffix -cycline; such as tetracycline
2010-243
Antifungals are typically named with what suffix?
The suffix -azole; such as ketoconazole
2010-243
Benzodiazepines are typically named with what suffix?
The suffix -azepam; such as diazepam
2010-243
Phenothiazines are typically named with what suffix?
The suffix -azine; phenothiazines are neuroleptics such as chlorpromazine
2010-243
Drugs used for inhalational general anesthesia are typically named with what suffix?
The suffix -ane; such as halothane
2010-243
Drugs used for the treatment of erectile dysfunction are typically named with what suffix?
The suffix -afil; such as sildenafil
2010-243
Penicillins are typically named with what suffix?
The suffix -cillin; such as methicillin
2010-243