Pharm Flashcards
Tight capillary cell junctions resulting in an added barrier to the entry of drugs is most characteristic of which organ or tissue? A. Adrenal gland B. Brain C. Heart D. Liver E. Lung
B. The brain has especially tight capillary junctions as
well as glial cells that result in a blood–brain
barrier.
A prescription for which of the following drugs
requires a valid DEA number on the prescrip-
tion?
A. Amoxicillin B. Carbamazepine C. Dexamethasone D. Diphenhydramine E. Oxycodone
E. Only oxycodone is a scheduled drug, requiring
DEA registration on the part of the prescriber.
- What would be the effect of prior administra-
tion of a competitive drug antagonist on the
concentration–response profile of a drug
agonist on a graded concentration–response
curve? (Assume that both drugs act at the
same receptor.)
A. The agonist curve would shift to the left.
B. The agonist curve would shift to the right.
C. The agonist curve would not change.
D. The agonist curve would not shift but would
reach a lower maximal effect than the curve
with agonist alone.
E. The agonist curve would both shift to the left
and have a lower maximal effect.
A. The characteristic response to a competitive
antagonist is a parallel shift to the right of the
agonist curve, with the two curves reaching the
same maximal effect.
How many human drug testing phases are car-
ried out before a drug is marketed?
A. One
B. Two
C. Three
D. Four
C. The fourth phase constitutes postmarketing sur-
veillance.
In what situation is the postganglionic nerve of
the sympathetic system a cholinergic nerve?
A. The nerves to the eye
B. The nerves to the heart
C. Most nerves to blood vessels
D. Most nerves to sweat glands
E. Most nerves to salivary glands
D. This situation for sweat glands is atypical for the
sympathetic nervous system.
Which is a nicotinic receptor?
A. Receptor for the neurotransmitter at the
skeletal–neuromuscular junction
B. Receptor for the neurotransmitter at the junction
between the postganglionic sympathetic nerve
and sweat glands
C. Receptor for the neurotransmitter at the junction
between the postganglionic parasympathetic
nerve and the parotid gland
D. Receptor for the neurotransmitter at the junction
between the postganglionic sympathetic nerve
and blood vessels
E. Receptor for the neurotransmitter at the junction
between the postganglionic parasympathetic
nerve and the heart
A. Nicotinic receptors are located at the
skeletal–neuromuscular junction, ganglia, junc-
tion of the sympathetic nerve to the adrenal
gland and the adrenal chromaffin cells, as well as
in the central nervous system.
Which of the following effects is a typical effect of an antimuscarinic drug? A. Bronchoconstriction B. Lacrimation C. Miosis D. Sweating E. Urinary retention
E. All other choices are typical of muscarinic cholin-
ergic receptor agonists.
The administration of which compound will
give “epinephrine reversal” (drop in blood pres-
sure from epinephrine) if given prior to admin-
istration of epinephrine?
A. Atropine B. Guanethidine C. Propranolol D. Phenoxybenzamine E. Tyramine
D. α-Adrenoceptor blockers such as phenoxy-
benzamine will inhibit the vasoconstrictor effect of
epinephrine but not the vasodilator effect of epi-
nephrine. Therefore, the administration of
α-blockers will result in epinephrine reversal.
Atropine would have little effect since it does not
act at adrenergic receptors. Propranolol would only
block the vasodilator effect of epinephrine and the
effect of epinephrine on the heart. Guanethidine
and tyramine act largely at prejunctional sites and
don’t block adrenergic receptors.
Motor adverse effects from phenothiazine antipsychotic drugs are due to drug effects in what region of the brain? A. Chemoreceptor trigger zone B. Cerebrum C. Cerebellum D. Nigro-striatal pathway E. Mesolimbic pathway
D. The nigro-striatal pathway contains dopa-
minergic neurons—important in muscle control.
Many antipsychotic drugs block these, leading to
the motor adverse effects.
A patient is administered haloperidol. Along
with the haloperidol, the patient also receives
benztropine. What is the most likely reason for
administering the benztropine?
A. To reduce the effects of histamine release
B. To aid in the therapeutic response to
haloperidol
C. To reduce the motor adverse effects of
haloperidol
D. To overcome a decrease in salivary flow
resulting from haloperidol
E. To reduce the rate of kidney excretion of
haloperidol
C. The antimuscarinic action of benztropine tends to
reduce the Parkinsonlike symptoms and some
other motor symptoms caused by haloperidol, a
dopamine receptor blocker. It does not improve
the antipsychotic effect of haloperidol. Histamine
release appears to play little role in this interaction.
Benztropine actually reduces salivary flow and
xerostomia can easily result from its admin-
istration. Benztropine has little effect on renal
clearance of haloperidol.
The benzodiazepine receptors BZ1 and BZ2 are located on which ion channel? A. Calcium B. Chloride C. Magnesium D. Potassium E. Sodium
B. The two benzodiazepine receptor subtypes (tar-
gets for drugs such as diazepam) are located on
the same chloride channel as is the GABAA
receptor.
Methemoglobinemia is an adverse effect associ-
ated with which local anesthetic due to its
metabolism to o-toluidine? A. Lidocaine B. Mepivacaine C. Prilocaine D. Bupivacaine E. Benzocaine
C. Only prilocaine is metabolized to o-toluidine.
Which drug poses the greatest risk of a cardiac arrhythmia when administered at the same time as epinephrine? A. Desflurane B. Halothane C. Isoflurane D. Propofol E. Sevoflurane
B. Halothane sensitizes the heart to epinephrine
and other catecholamines.
Local anesthetics act on what type of receptor?
A. An ion channel receptor
B. A nuclear receptor
C. A 7-membrane domain receptor linked to Gs
D. A 7-membrane domain receptor linked to Gq
E. A membrane receptor with tyrosine kinase
activity
A. Inhibiting sodium channels leads to the inhibition
of the nerve action potential and inhibition
of nerve conduction. Sodium channels are
examples of ion channel receptors. Ion channel
receptors contain several subunits arranged in a
barrel shape. Drugs that bind to the channel can
alter conductance to the ion associated with that
channel.
Which drug lacks the amine group that other
anesthetics have and is used only topically?
A. Procaine
B. Mepivacaine
C. Lidocaine
D. Benzocaine
E. Prilocaine
D. Benzocaine lacks the amine group that procaine,
mepivacaine, prilocaine, and lidocaine have.
This amine group can become protonated, thus
making these drugs more water-soluble and
facilitating an injectible form. Benzocaine must be provided in a cream or oil-based preparation
allowing just a topical form. Procaine and
mepivacaine have poor topical anesthetic
properties.
Injecting a local anesthetic into an area of
inflammation would have which effect?
A. Increase the rate of onset of anesthesia.
B. Decrease the rate of metabolism of the
anesthetic.
C. Reduce the net anesthetic effect of the drug.
D. Reduce the vasodilator effect of the local
anesthetic.
E. Reduce the need for a vasoconstrictor with the
local anesthetic.
C. An area of inflammation is an area of low pH. The
acid environment would convert more of the
drug into the charged form, making it less able to
diffuse to the nerve cells. This would reduce the
rate of onset and the net anesthetic effect of the
drug.
Which two drugs have mechanisms of anal-
gesic action that are most similar?
A. Fentanyl, ibuprofen B. Aspirin, codeine C. Oxycodone, acetaminophen D. Ibuprofen, naproxen E. Aspirin, ibuprofen
D. All of the choices are combinations of an opioid
and an inhibitor of cyclo-oxygenase (COX), except
two: ibuprofen, naproxen and aspirin, ibuprofen.
Ibuprofen and naproxen are both reversible
inhibitors of COX, and are propionic acid deriva-
tives. Aspirin is a salicylate and is an irreversible
inhibitor.
Your patient is continually taking a small daily
dose of aspirin (82 mg) prescribed by the
patient’s physician. The object of this therapy
is most likely what mechanism?
A. To mimic the effect of endogenous endorphins
B. To inhibit the production of prostaglandin E1
C. To inhibit the production of thromboxane A2
D. To inhibit the production of arachidonic acid
E. To inhibit the production of leukotrienes
C. Thromboxane A2 increases platelet aggregation.
Its inhibition is the target of low-dose aspirin which
inhibits cyclo-oxygenase. Inhibition of this enzyme
leads to a reduction in important down stream
products, including thromboxane A2
Your patient indicates that he is taking medica-
tion for atrial fibrillation. He reports that a
blood test has indicated that he has an INR
number of 4.0. An emergency dental extraction
is now required. Which postoperative medica-
tion would pose the greatest risk for an
adverse effect in this patient? A. Acetaminophen B. Amoxicillin C. Aspirin D. Codeine E. Ibuprofen
C. The international normalized ratio (INR) value
indicates that the patient has received anticoagu-
lant therapy for his atrial fibrillation. Aspirin
increases the risk of postsurgical bleeding. The
combination of increase in prothrombin time,
surgery, and the antiplatelet effect of aspirin
make aspirin contraindicated in this situation.
Ibuprofen’s effect on the platelet is reversible,
whereas the effect of aspirin on the platelet is
irreversible. Thus, aspirin poses a greater risk
than does ibuprofen in this situation.
Which drug blocks H1 histamine receptors but is least likely to cause sedation? A. Diphenhydramine B. Hydroxyzine C. Fexofenadine D. Albuterol E. Famotidine
C. The first three choices are all H1 histamine recep-
tor blockers. Fexofenadine, however, is largely
excluded from the central nervous system, unlike
diphenhydramine and hydroxyzine. Albuterol is a
β2 adrenergic receptor agonist. Famotidine is a H2
histamine receptor antagonist.
The use of selective COX-2 inhibitors has recently been restricted or discontinued because of what type of adverse effects? A. Carcinogenesis B. Cardiovascular disorders C. Convulsive disorders D. Striated muscle disorders E. Skeletal disorders
B. The cardiovascular risks may be associated with
adverse hematologic effects, but the exact mech-
anism is not yet known.
Sodium reabsorption in the thick ascending limb
of the loop of Henle is inhibited by which drug?
A. Bumetanide
B. Chlorthalidone
C. Hydrochlorothiazide
D. Spironolactone
E. Triamterene
A. All the drugs listed are diuretics. However, only
bumetanide acts on the ascending limb of the
loop of Henle. It is called a “loop” or “high ceil-
ing” diuretic because of its site of action in the
nephron and maximal effect, respectively.
Torsades de pointes, or polymorphic ventricu-
lar tachycardia, is linked most closely to what
characteristic of the electrocardiogram? A. Inverted T wave B. Shorter P-R interval C. Shorter P-P interval D. Longer Q-T interval E. Normal electrocardiogram
D. The long Q-T interval observed as a result of cer-
tain drugs or as a hereditary condition makes the
patient more susceptible to this condition.
Which antihypertensive drug also increases bradykinin levels? A. Candesartan B. Furosemide C. Lisinopril D. Metoprolol E. Nifedipine
C. Lisinopril, by virtue of the fact that it inhibits
angiotensin-converting enzyme (ACE) (also
called peptidyl dipeptidase), inhibits the break-
down of bradykinin.
Which one of the following drugs enters the
target cell and acts on a nuclear receptor?
A. Diazepam
B. Epinephrine
C. Insulin
D. Prednisone
E. Heparin
D. Diazepam, epinephrine, and insulin act at ion
channel receptors, G-protein-linked receptors,
and tyrosine kinase-linked receptors, res-
pectively. These three receptor types are cell
surface receptors. Thyroid hormone and steroid
hormones or drugs, such as prednisone, act on
Sample Exam Answer Key ▼ 411
nuclear receptors, accounting for much of their
action. Heparin’s action is to stimulate
antithrombin III in the plasma. Its action is
extracellular.
Inhibiting a-glucosidase and reducing glucose absorption from the gastrointestinal tract is the mechanism of action of which drug? A. Acarbose B. Acetoheximide C. Glyburide D. Metformin E. Pioglitazone
A. All of the choices are oral hypoglycemic agents.
Only acarbose inhibits α-glucosidase.
Which of the following drugs blocks the aldos-
terone receptor?
A. Amiloride B. Triamterene C. Losartan D. Spironolactone E. Furosemide
D. Spironolactone, a potassium-sparing diuretic
useful in treating edema and heart failure, is
a competitive antagonist at the aldosterone
receptor.
Which drug is most selective as a glucocorticos-
teroid?
A. Aldosterone
B. Dexamethasone
C. Fludrocortisone
D. Hydrocortisone
B. Aldosterone and fludrocortisone are selective
mineralocorticosteroids. Hydrocortisone has sig-
nificant mineralocorticoid and glucocorticoid
activity. Dexamethasone has very little mineralo-
corticoid activity.
Stimulation of gluconeogenesis and lipolysis
are most characteristic of which hormone?
A. Calcitonin
B. Cortisol
C. Insulin
D. Parathyroid hormone
E. Progesterone
B. Glucocorticoids characteristically stimulate glu-
coneogenesis and lipolysis. Insulin has the oppo-
site effects. The other hormones have minor or
negligible effects.
Fanconi syndrome from outdated tetracyclines affects predominantly which organ? A. Brain B. Heart C. Kidney D. Pancreas E. Stomach
C. Renal tubular acidosis, aminoaciduria, and
hyperphosphaturia are some of the manife-
stations of proximal tubule damage in Fanconi
syndrome.
Methicillin-resistant Staphylococci are most likely to be inhibited by which drug? A. Amoxicillin B. Clarithromycin C. Clindamycin D. Vancomycin E. Penicillin V
D. Of the choices given, only vancomycin is effec-
tive against many methicillin-resistant Staphy-
lococci. Various penicillins, macrolides, and
clindamycin are ineffective.
Pick the organism that is usually clinically sen-
sitive to clarithromycin but not to penicillin V.
A. Streptococcus viridans B. Leptotrichia buccalis C. Mycoplasma pneumoniae D. Streptococcus pneumoniae E. Streptococcus pyogenes
C. Because it lacks a cell wall, Mycoplasma pneumo-
niae is not sensitive to cell wall inhibitors such as
penicillin V. The macrolides, such as clar-
ithromycin, are ribosomal protein synthesis
inhibitors that are effective against Mycoplasma
pneumoniae. Streptococcus viridans, Strep-
tococcus pneumoniae, and Streptococcus pyo-
genes are gram-positive cocci. Leptotrichia
buccalis is a gram-negative oral bacillus.
What is the approximate elimination half-time for penicillin V? A. 0.5 hour B. 2 hours C. 4 hours D. 8 hours E. 12 hours
A. The short elimination half-time for penicillin V is
due to rapid excretion of penicillin in the urine.
About 90% of this renal excretion is a result of
active tubular transport, a rapid and efficient
process. (Very little metabolism of penicillin
occurs.)
Which drug has an antibacterial spectrum that is limited to anaerobes? A. Amoxicillin B. Clarithromycin C. Clindamycin D. Gentamicin E. Metronidazole
E. Amoxicillin, clarithromycin, and clindamycin are
effective against some anaerobes but their spec-
trum is not limited to anaerobic bacteria.
Aminoglycosides are effective only against aer-
obes. Metronidazole’s action requires a reduced
environment. Its antibacterial spectrum is limited
to anaerobes. Metronidazole is also effective
against many parasites.
Which drugs tend to concentrate in body compartments of high pH? A. Permanently charged drugs B. Drugs that are not charged C. Weak organic acids D. Weak organic bases E. Inorganic ions
C. Only weak acids and weak bases are greatly
affected in their distribution by changes in pH.
Weak organic acids dissociate more from
protons at higher pH, making a higher percent-
age of their molecules charged. This traps them
in that compartment.
Drug agonists having the same intrinsic activity also have the same \_\_\_\_\_. A. Maximal effect B. Potency C. Receptor affinity D. Therapeutic index E. Aqueous solubility
A. Drug agonists have an intrinsic activity of greater
than 0 and less than or equal to 1. This refers to
the maximal effect attainable by the drug.
Potency and receptor affinity are not directly
related to intrinsic activity. The therapeutic index
(TI) requires a quantal dose–response curve,
unlike the other characteristics listed which
require graded concentration–response curves.
Drugs with the same intrinsic activity may vary a
great deal in their aqueous solubility.
What receptor or signaling pathway is linked
most directly to a2-adrenoceptor stimulation?
A. Gi and a reduction in cAMP
B. Gs and an increase in cAMP
C. Gq and calcium
D. Sodium ion channel
E. Membrane receptor containing tyrosine kinase
A. Inhibition of adenylyl cyclase through Gi
, result-
ing from stimulation of α2-adrenergic receptor,
leads to a reduction in intracellular cAMP.
What tissue or organ has many muscarinic receptors but lacks innervation to those receptors? A. Heart B. Parotid gland C. Blood vessels D. Sweat glands E. Urinary bladder
C. Circulating muscarinic cholinergic receptor
agonists stimulate these receptors on endothelial
cells, leading to release of nitric oxide and
vasodilation.
Which drug used in the therapy for Parkinsonism does not cross the blood–brain barrier? A. Amantadine B. Carbidopa C. L-dopa D. Selegiline E. Tolcapone
B. Carbidopa is used to inhibit dopa decarboxylase.
Its usefulness is based on reducing conversion of
L-dopa to dopamine outside the central nervous
system. Carbidopa does not penetrate the
blood–brain barrier and therefore does not inter-
fere with the beneficial effect of L-dopa in the
brain, but prevents the adverse effects of dopa-
mine in the periphery.
After an injection, which drug would be expected
to have the longest duration of action? (Assume
no vasoconstrictor was injected with the local
anesthetic.)
A. Bupivacaine
B. Lidocaine
C. Mepivacaine
D. Prilocaine
E. Procaine
A. Bupivacaine has the highest lipid solubility of the
drugs listed. This is the major chemical charac-
teristic of the local anesthetic that determines
duration of action. Procaine is the only ester
given as a choice and is rarely used.
A very low blood:gas solubility coefficient
(partition coefficient = 0.47), analgesic effect,
and a drug that inhibits methionine synthase
best describes which drug?
A. Ketamine
B. Nitrous oxide
C. Halothane
D. Isoflurane
E. Propofol
B. Nitrous oxide oxidizes the cobalt in vitamin B12,
resulting in the inhibition of methionine synthase.
Nitrous oxide has greater analgesic potency than
other inhaled anesthetics (e.g., halothane, isoflu-
rane). Ketamine is not inhaled; rather, it is
injected. It also does not inhibit methionine syn-
thase. The same is true for propofol.
Levonordefrin is added to certain cartridges
containing mepivacaine. The desired effect of
levonordefrin is due to what pharmacological
effect?
A. Inhibition of nicotinic cholinergic receptors
B. Inhibition of muscarinic cholinergic receptors
C. Stimulation of α-adrenergic receptors
D. Stimulation of β-adrenergic receptors
E. Stimulation of dopamine receptors
C. Alpha adrenergic receptor stimulation accounts
for the vasoconstrictor effect of levonordefrin.
The analgesic effects of dextromethorphan are
due to what receptor effect?
A. Gamma aminobutyric acid (GABA) receptor
antagonism.
B. Dopamine receptor antagonism.
C. Nicotinic cholinergic receptor antagonism.
D. Mu (μ) opioid receptor antagonism.
E. N-methyl-D-aspartate (NMDA) receptor
antagonism.
E. The recently described mild analgesic effect of
dextromethorphan has been linked to N-methyl-
D-aspartate (NMDA) receptor antagonism in the
CNS.
Naloxone antagonizes the therapeutic and toxic effects of which drug? A. Acetaminophen B. Aspirin C. Carbamazepine D. Fentanyl E. Ibuprofen
D. Naloxone is a competitive antagonist at opioid
receptors.
What is the mechanism of the analgesic action of aspirin? A. Stimulates μ opioid receptors B. Blocks histamine H2 receptors C. Inhibits cyclooxygenase D. Inhibits lipoxygenase E. Blocks sodium channels in nerves
C. Cyclooxygenase (COX) is a key enzyme in the
synthesis of prostaglandins. Prostaglandins,
including PGE2 and PGF2α, are important media-
tors for such functions as pain, and are a product
of COX. Aspirin inhibits both COX-1 and COX-2.
What is the clinical setting for the use of ketorolac by the oral route? A. For severe pain B. For initial treatment of pain C. To continue therapy after an IV or IM dose of ketorolac D. Only in combination with an opioid E. Only in combination with an NSAID
C. The use of oral ketorolac (an NSAID) is limited to
continue therapy after a parenteral dose.
The use of H2 histamine receptor blockers is
most clinically useful at what cell type?
A. Beta cells of the pancreas
B. Basophils
C. Mast cells
D. Juxtaglomerular cells
E. Parietal cells
E. Basophils and mast cells release histamine.
However, the cell that responds to histamine
stimulation at the H2 receptor is the parietal cell
of the stomach. Stimulation of this receptor leads
to proton release and a decrease in the pH of the
stomach lumen. H2 histamine receptor blockers
are used to reduce stomach acid.
14. Which class of antihypertensive drug most effectively reduces the release of renin from the kidney? A. β-adrenergic receptor blockers B. ACE inhibitors C. α-adrenergic receptor blockers D. Calcium channel blockers E. Angiotensin II receptor blockers
A. Renin release from the kidney is enhanced by
stimulation of the β1-adrenergic receptors in
the juxtaglomerular cells. From the above list,
only β blockers reduce renin release. Although
angiotensin converting enzyme inhibitors and
angiotensin II receptor blockers act on the
renin-angiotensin system, they do not inhibit
renin release. In fact, they tend to increase
plasma renin.
The administration of which compound will give “epinephrine reversal” (drop in blood pressure from epinephrine) if given prior to administration of epinephrine? A. Guanethidine B. Propranolol C. Phenoxybenzamine D. Tyramine
C. Alpha adrenoceptor blockers, like phenoxyben-
zamine, inhibit the vasoconstrictor effect of epi-
nephrine but not the vasodilator effect of
epinephrine. Therefore, the administration of alpha blockers results in epinephrine reversal.
Propranolol would only block the vasodilator
effect of epinephrine. Guanethidine and tyra-
mine act largely at prejunctional sites and don’t
block adrenergic receptors.
What is the mechanism of action of enoxaparin?
A. Inhibition of synthesis of clotting factors II, VII, IX,
and X
B. Activation of antithrombin III with resulting
inhibition of clotting factor Xa
C. Indirect activation of tissue plasminogen activator
D. Direct inhibition of plasminogen with resulting
degradation of fibrin
E. Dilation of coronary blood vessels
B. Enoxaparin is a low-molecular-weight heparin. It
activates antithrombin III and inhibits factor Xa.
Oropharyngeal candidiasis is an adverse effect most likely with which drug? A. Inhaled salmeterol B. Inhaled ipratropium C. Inhaled nedocromil D. Inhaled beclomethasone E. Inhaled methacholine
D. The effect of glucocorticosteroids remaining in
the mouth after inhalation is to make the oral
cavity more susceptible to fungal infection. The
mouth should be rinsed with water after inhala-
tion use. Inhaled methacholine, unlike the other
drugs listed, is not used therapeutically but,
rather, is used to diagnose hyperactive airway.
Oral antacids are most likely to reduce the absorption of which drug when it is given orally? A. Clarithromycin B. Clindamycin C. Metronidazole D. Penicillin V E. Tetracycline
E. Di- and trivalent cations, such as those found in
oral antacids, chelate tetracyclines and prevent
their absorption.
A decrease in glycogenolysis in the liver would be expected from which drug? A. Albuterol B. Epinephrine C. Glucagon D. Insulin E. Parathyroid hormone
D. A decrease in glycogen breakdown is a classic
effect of insulin. Epinephrine (by acting as an
agonist at α1- and β2-adrenergic receptors),
albuterol (by acting as an agonist at β2
-adrenergic
receptors), and glucagon (by acting at glucagon
receptors) all tend to increase glycogen.
Parathyroid hormone has little effect on
glycogenolysis.
Nitrates and nitrites have what effect on blood
vessel smooth muscle?
A. Increase in the level of intracellular calcium
B. Increase in the level of cyclic guanosine
monophosphate (cGMP)
C. Antagonism at α1-adrenergic receptors
D. Antagonism at β-adrenergic receptors
E. Inhibition of L-type calcium channels
B. Nitroglycerin is a nitrovasodilator. It produces
nitric oxide, which activates guanylyl cyclase
which, in turn, catalyzes the production of cGMP.
Clavulanic acid offers an advantage therapeutically because it has what action? A. It inhibits Streptococci at a low minimum inhibitory concentration (MIC). B. It inhibits transpeptidase. C. It inhibits penicillinase. D. It inhibits anaerobes at a low MIC. E. It inhibits DNA gyrase.
C. Clavulanic acid has very little antimicrobial activity.
Its value in combination with certain penicillins is
due to its ability to inhibit certain penicillinases.
This protects the penicillin from bacterial enzyme
attack. Transpeptidase is inhibited by β-lactams,
such as penicillin. DNA gyrase is inhibited by the
fluoroquinolones such as ciprofloxacin.
Identify the enzyme whose inhibition is most responsible for the cell wall synthesis inhibitory effect of penicillin G. A. β-lactamase B. DNA gyrase C. Nitro reductase D. Transglycosylase E. Transpeptidase
E. Transpeptidase is the enzyme that catalyzes the
peptide crosslinking of peptidoglycan. Trans-
peptidase, is inhibited by penicillins and ceph-
alosporins.
Which drug is often combined with sulfamethoxazole for the treatment of respiratory tract and urinary tract infections? A. Amoxicillin B. Ciprofloxacin C. Clindamycin D. Metronidazole E. Trimethoprim
E. Trimethoprim, by virtue of its inhibition of bacte-
rial dihydrofolate reductase, acts synergistically
with the sulfonamides.
Which of the following organisms is usually
sensitive to clindamycin?
A. Candida albicans
B. Klebsiella pneumoniae
C. Methicillin-resistant Staphylococcus aureus
D. Streptococcus viridans
E. Pseudomonas aeruginosa
D. Clindamycin is useful for some oral infections,
including those involving Streptococcus viridans.
Klebsiella pneumoniae and Pseudomonas aerug-
inosa are gram-negative rods and not subject to
clinical inhibition by clindamycin. Methicillin-
resistant Staphylococci are insensitive to clinda-
mycin and most traditional antistaphylococcal
drugs. Candida albicans is a yeastlike fungus and
is not inhibited by antibacterial drugs such as
clindamycin.
Dihydrofolate reductase is an enzyme inhibited by which anticancer drug? A. Bleomycin B. Cisplatin C. Doxorubicin D. 5-fluorouracil E. Methotrexate
E. The mammalian enzyme form of dihydrofolate
reductase is the target for methotrexate. Bleo-
mycin produces strand breaks in DNA. Cisplatin is
an alkylating agent. Doxorubicin intercalates with
DNA. 5-Fluorouracil, after undergoing activation,
inhibits thymidylate synthase.
Class of drugs most consistent in structure
local anesthetics
Ester anesthetics
procaine, tetracaine, cocaine
metabolism of esters vs amides
esters in plasma by esterases; amides (tertiary!) in liver
prilocaine side effect
methemoglobinemia
methemoglobinemia is side effect of what
prilocaine
local anesthetic overdose
myocardial depression, cardiovascular collapse, hypotensive shock
mechanism of local anesthetics
prevent generation of impulses; block Na transport
which form of anesthetic can penetrate
free base, non-ionized
absorption of local anesthetic in inflamed tissues
inflammation –> lower pH –> less non-ionized form available to penetrate
2% lidocaine - amount in one carpule?
one carpule is 1.8 mL
2% means 20 mg/mL
so 20 x 1.6 = 36 mg in one 1.8 mL carpule
Which of the following is a local anesthetic subject to inactivation by plasma esterases? a. Procaine b. Lidocaine c. Prilocaine d. Mepivacaine e. Bupivacaine
(a) Proccaine is the only ester listed – all the rest are amides
Procaine differs from lidocaine in that
a. Procaine is a p-aminobenzoic acid ester and lidocaine is not
b. Lidocaine is a meta-aminobenzoic acid ester and procaine is not
c. The duration of action of procaine is longer than that of an equal
total dose of lidocaine
d. Procaine hydrochloride is metabolized into diethylaminoethanol
and benzoic acid.
(a) this is basically a true-false type question. (a) is the only
statement that is true
(a) is the only
statement that is true
Which of the following local anesthetics would be expected to produce a sensitization reaction in a patient allergic to lidocaine? a. Mepivacaine b. Tetracaine c. Procaine d. Prilocaine e. Dibucaine i. (a), (b) and (c) ii. (a), (d) and (e) iii. (b) and (c) only iv. (b), (c) and (d) v. (b), (d) and (e)
(ii) another ester vs. amide type identification question.
Lidoccaine is an amide, thus other amides will be cross-
allergenic - mepivacaine, prilocaine and dibucaine are the other
amides listed. Procaine and tetracaine are esters and will not be
cross-allergenic.
The hydrolysis of procaine occurs mainly in the
a. Liver
b. Lungs
c. Plasma
d. Muscles
e. Kidneys
(c) procaine is an ester; esters are metabolized predominately
by pseudocholinesterases in the plasma.
Which of the following is local anesthetic subject to inactivation by plasma esterases? a. Lidocaine b. Prilocaine c. Tetracaine d. Mepivacaine e. Bupivacaine
(c) esters are metabolized by plasma esterases - tetracaine is
the only ester listed, all the rest are amides
The activity of procaine is terminated by
a. Elimination by the kidney
b. Storage in adipose tissue
c. Metabolism in the liver only
d. Metabolism in the liver and by pseudocholinesterase in the
plasma
(d) remember #9 above? see the word “mainly”? same
question, but worded a little differently to throw you off. Again,
procaine is an ester; esters are metabolized predominately by
pseudocholinesterases in the plasma, but also to some extent
by esters in the liver.
All of the following factors are significant determinants of the duration
of conduction block with amide-type local anesthetics EXCEPT the
a. pH of tissues in the area of injection
b. Degree of vasodilatation caused by the local anesthetic
c. Blood plasma cholinesterase levels
d. Blood flow through the area of conduction block
e. Concentration of the injected anesthetic solution
(c) the word “EXCEPT” should alert you that this is basically a
true-false type question with 4 true statements and 1 false
statement; you just have to figure out which one! In this case,
you just have to remember that plasma cholinesterase levels
are only important for the duration of action of ester-type LAs,
not amides, which are metabolized in the liver. All the other
statements are variables which affect duration of the block, but
apply to both esters and amides.
Which of the following is contraindicated for a patient who had an
allergic reaction to procaine six months ago?
a. Nerve block with lidocaine
b. Topical application of lidocaine
c. Topical application of tetracaine
d. Infiltration with an antihistamine
(c) again, just another question that requires you to be able to
pick out an ester or an amide from a list. Since procaine is an
ester, only another ester LA would be cross-allergenic. In this
list the only ester listed is tetracaine.
Bupivacaine (Marcaine ) has all of the following properties relative to
lidocaine (Xylocaine ) EXCEPT bupivacaine
a. Is more toxic
b. Is an ester-type local anesthetic
c. Has a slower onset of action
d. Has a longer duration of action
(d) According to textbooks, local anesthetics fall into the
following classes in terms of duration of action: short: procaine;
moderate: prilocaine, mepivacaine, lidocaine; long: bupivacaine,
tetracaine, etidocaine. Statements (a), 3, and 4 would be true if
the question was comparing mepivacaine to bupivacaine, which
are structurally similar; but the comparison is to lidocaine. The
only difference that applies is duration of action ((d)),
bupivacaine is longer. (b) is wrong, both are amides.
Amide-type local anesthetics are metabolized in the
a. Serum
b. Liver
c. Spleen
d. Kidney
e. Axoplasm
(b) don’t forget: esters in plasma; amides in liver
15. The duration of action of lidocaine would be increased in the presence of which of the following medications? a. Prazosin b. Propranolol c. Hydrochlorothiazide d. Lisinopril e. Digoxin
(b) this is an interaction I tested you on several times – now you
know why! Propranolol interacts with lidocaine in two ways.
By slowing down the heart via beta receptor blockade, blood
delivery (and lidocaine) to the liver is reduced, thus lidocaine
remains in the systemic circulation longer, and can potentially
accumulate to toxic levels. Propranolol and lidocaine also
compete for the same enzyme in the liver, thus metabolism of
lidocaine can be reduced.
propranolol class
non-selective beta-blocker
slows down heart
Severe liver disease least affects the biotransformation of which of the following? a. Lidocaine b. Procaine c. Prilocaine d. Mepivacaine
(b) Answer is (b)- You should be able to recognize that all of
these drugs are local anesthetics. Local anesthetics are of one
of two types, either esters or amides. Ester types are subject to
hydrolysis in the plasma and thus have short half lives. Amides
are metabolized primarily in the liver and have longer half lives.
Thus the biotransformation (e.g., metabolism; again, the rats are
using a different word to confuse you, even though they are
asking the same basic question) of an amide type local
anesthetic would be the most altered in the presence of sever
liver disease. The key word here is “least”. Of the drugs listed,
only procaine is an ester. The rest are amides.
A patient has been given a large volume of a certain local anesthetic
solution and subsequently develops cyanosis with
methemoglobinemia. Which of the following drugs most likely was
administered?
a. Procaine
b. Prilocaine
c. Dibucaine
d. Lidocaine
e. Mepivacaine
(b)
Use of prilocaine carries the risk of which of the following adverse effects? a. Porphyria b. Renal toxicity c. Gastric bleeding d. Methemoglobinemia
(d) same as above but asked backwards. Methemoglobinemia
may result from a toluidine metabolite of prilocaine,
orthotoluidine.
which anesthetic has o-toluidine metabolite? why important?
prilocaine; metHbemia
The most probable cause for a serious toxic reaction to a local
anesthetic is
a. Psychogenic
b. Deterioration of the anesthetic agent
c. Hypersensitivity to the vasoconstrictor
d. Hypersensitivity to the local anesthetic
e. Excessive blood level of the local anesthetic
(e) Most toxic reactions of a serious nature are related to
excessive blood levels arising from inadvertent intravascular
injection. Hypersensitivity reactions (options b & c) are rare, but
excessive blood levels will induce toxic reactions like CNS
stimulation in most everyone. This is a case where option (e) is
the “best” answer, because it is more likely than the other
alternatives, which might be true, but are not as likely (e.g,
“most probable”) to happen.
- High plasma levels of local anesthetics may cause
a. Inhibition of peristalsis
b. stimulation of baroreceptors resulting in severe hypotension
c. Inhibition of the vagus nerve to the heart
d. Depression of inhibitory neurons in the CNS
(d) Initially LAs inhibit central inhibitory neurons, which results in
CNS stimulation, which can proceed to convulsions. At higher
doses, they inhibit both inhibitory and excitatory neurons,
leading to a generalized state of CNS depression which can
result in respiratory depression and death.
Unfortunately, you injected your lidocaine intra-arterially. The first
sign of lidocaine toxicity that might be seen in the patient would be
a. Elevated pulse rate
b. Sweating
c. CNS excitation
d. Cardiovascular collapse
e. CNS depression
(c) same question as above just worded differently. The intra-
arterial injection would result in the high plasma levels
mentioned in the previous question.
The first sign that your patient may be experiencing toxicity from too much epinephrine would be a. Cardiovascular collapse b. Convulsions c. Elevated pulse rate d. Slurred speech
(c) it is a sympathomimetic after all. All the other reactions are
related to elevated lidocaine levels
Which disease condition would make the patient most sensitive to the epinephrine in the local anesthetic? a. Grave’s disease b. Diabetes c. HIV d. Alcoholism e. Schizophrenia
(a) Grave’s disease is an autoimmune disease that causes
hyperthyroidism – the resulting high levels of circulating thyroid
hormone result in a hypermetabolic state with heightened
sympathetic activity, which combined with injected epinephrine
could result in a hypertensive crisis.
Cardiovascular collapse elicited by a high circulating dose of a local anesthetic may be caused by a. Syncope b. Vagal stimulation c. Histamine release d. Myocardial depression e. Medullary stimulation
(d) Cardiovascular collapse is due to a direct action of the local
anesthetic on the heart muscle itself (LA’s in toxic doses
depress membrane excitability and conduction velocity), thus
(d) is the correct answer. All of the other alternatives are indirect
ways to affect the heart.
The most serious consequence of systemic local anesthetic toxicity is
a. Vertigo
b. Hypertension
c. Hyperventilation
d. Post depressive central nervous system convulsions
e. Postconvulsive central nervous system depression
(e) Of the options listed, this is the one that will kill the patient,
which I guess makes it the most serious.
Hypotensive shock may result from excessive blood levels of each of the following local anesthetics EXCEPT a. Cocaine b. Procaine c. Lidocaine d. Tetracaine e. Mepivacaine
(a) All the listed local anesthetics except cocaine are
vasodilators, especially ester-ctype drugs such as proccaine
and the amide lidocaine. Cocaine is the only local anesthetic
that predictably produces vasoconstriction. Cocaine is also the
only local anesthetic to block the reuptake of NE into adrenergic
neurons, and thus potentiate the NE that has been released
from nerve endings
Which of the following anesthetic drugs produces powerful stimulation of the cerebral cortex? a. Cocaine b. Procaine c. Lidocaine d. Tetracaine e. Mepivacaine
(a) see explanation above *NE potentiation)
Local anesthetics block nerve conduction by
a. Depolarizing the nerve membrane to neutrality
b. Increasing membrane permeability to K+
c. Increasing membrane permeability to Na+
d. Preventing an increase in membrane permeability to K+
e. Preventing an increase in membrane permeability to Na+
(e) didn’t I make you memorize this? You should at keast
remember Na+ ions are involved, which limits your choices to
(c) and (e). (c) would increase or facilitate nervous impulse
conduction, which is the opposite of what you want the local
anesthetic to do, so pick (e).
Which of the following is true regarding the mechanism of action of
local anesthetics?
a. Usually maintain the nerve membrane in a state of
hyperpolarization
b. Prevent the generation of a nerve action potential
c. Maintain the nerve membrane in a state of depolarization
d. Prevent increased permeability of the nerve membrane to
potassium ions
e. Interfere with intracellular nerve metabolism
(b)
Local anesthetic agents prevent the generation of nerve impulses by
a. Decreasing threshold for stimulation
b. Decreasing resting membrane potential
c. Decreasing inward movement of sodium ion
d. Increasing inward movement of potassium ion
(c) Answer is (c)- straight memorization- nerve impulses are
generated by the influx of sodium resulting in depolarization.
repolarization and inactivity occurs when potassium moves out.
(sodium-potassium pump). LAs act by blocking Na+ movement.
Local anesthetics interfere with the transport of which of the following ions during drug-receptor interaction a. Sodium b. Calcium c. Chloride d. Potassium e. Magnesium
(a)
If the pH of an area is lower than normal body pH, the membrane
theory of local anesthetic action predicts that the local anesthetic
activity would be
a. Greater, owing to an increase in the free-base form of the drug
b. Greater, owing to an increase in the cationic form of the drug
c. Less, owing to an increase in the free-base form of the drug
d. Less, owing to a decrease in the free-base form of the drug
e. None of the above
(d)
A local anesthetic injected into an inflamed area will NOT give
maximum effects because
a. The pH of inflamed tissue inhibits the release of the free base
b. The drug will not be absorbed as rapidly because of the
decreased blood supply
c. The chemical mediators of inflammation will present a chemical
antagonism to the anesthetic
d. Prostaglandins stabilize the nerve membrane and diminish the
effectiveness of the local anesthetic
(a) while some of the other alternatives sound plausible, think
about the factoids you were taught about local anesthetics and
variables that affect their action. An important one was the role
of pH and ionization factors. Remember, the free base or
nonionized form is the form that passes through membranes,
yet once inside the neuron only the ionized form is effective.
Inflamed tissue has a lower pH than normal tissue and will shift
the equilibrium of the LA solution such that most of it remains
ionized and thus unavailable to penetrate
The penetration of a local anesthetic into nervous tissue is a function
of the
a. Length of the central alkyl chain
b. Lipid solubility of the ionized form
c. Lipid solubility of the unionized form
d. Ester linkage between the aromatic nucleus and the alkyl chain
e. Amide linkage between the aromatic nucleus and the alkyl chain
(c) only options (b) and (c) are relevant here - the others have
nothing to do with LA penetration into membranes. Membrane
permeability is affected by whether or not the molecule is
“charged” or ionized or not (e.g., unionized). Only the latter form
passes readily through membranes. See, they’re asking the
same thing they asked in the previous question, just coming at it
from another angle. Remember the fact and you can cover the
angles.
At a pH of 7.8, lidocaine (pKa = 7.8) will exist in
a. the ionized form
b. the nonionized form
c. an equal mixture of ionized and nonionized forms
d. a mixture 10 times more ionized than nonionized forms
(c) the ratio of ionized to unionized forms is given by the
formula log A/AH= pH-pKa. In this instance the difference
between pH and pKa is 0. Thus lidocaine will exist as an equal
mixture ( so (c) is correct). Most local anesthetics are weak
bases with pKa ranging from 7.5 to 9.5. LA’s intended for
injection are usually prepared in salt form by addition of HCl.
They penetrate as the unionized form into the neuron where
they re-equilibrate to both charged and uncharged forms inside the neuron - the positively charged ion blocks nerve conduction.
The more rapid onset of action of local anesthetics in small nerves is
due to
a. The slightly lower pH of small nerves
b. The greater surface-volume ratio of small nerves
c. The increased rate of penetration resulting from depolarization
d. Smaller nerves usually having a higher threshold
(b) - the theory
goes that there is a size dependent critical length of
anesthetic exposure necessary to block a given nerve. Small
fibers will be blocked first because the anesthetic
concentration to h critical length in a small fiber will be reached
faster than the critical length in a larger fiber. You have to
block three nodes of ranvier, and they are farther apart in
larger fibers than they are in small diameter fibers.
Which of the following statements are true regarding onset, degree
and duration of action of local anesthetics?
a. The greater the drug concentration, the faster the onset and the
greater the degree of effect
b. Local anesthetics block only myelinated nerve fibers at the nodes
of Ranvier
c. The larger the diameter of the nerve fiber, the faster the onset of
effect
d. The faster the penetrance of the drug, the faster the onset of
effect
i. (a), (b), and (c)
ii. (a), (b) and (d)
iii. (a) and (c) only
iv. (b), (c) and (d)
(ii) if you knew the fact above about small nerves, then this
question basically becomes a true false type thing, and (c) is the
false statement. (a) and (d) make logical sense so you are
stuck picking between (b) and (c). You have your pick of
memorizing the small nerve thing or the myelinated nerve nodes
of ranvier thing.
A dentist administers 1.8 ml of a 2% solution of lidocaine. How many mg of lidocaine did the patient receive? a. 3.6 b. 9 c. 18 d. 36 e. 180
(d) 2% solution = 20 mg/ml X 1.8 ml = 36 mg lidocaine.
Three ml of a local anesthetic solution consisting of 2% lidocaine with
1: 100,000 epinephrine contains how many milligrams of each?
a. 6 mg. lidocaine, 0.3 mg. epinephrine
b. 6 mg. lidocaine, 0.03 mg. epinephrine
c. 60 mg. lidocaine 0.3 mg. epinephrine
d. 60 mg. lidocaine 0.03 mg epinephrine
e. 600 mg lidocaine, 0.3 mg. epinephrine
f. 600 mg. lidocaine, 0.03 mg. epinephrine
(d) 2% lidocaine = 20 mg/ml x 3 = 60 mg lidocaine
1: 100,000 epi = 0.01 mg/ml x 3 = 0.03 mg epi
The maximum allowable adult dose of mepivacaine is 300 mg. How many milliliters of 2% mepivacaine should be injected to attain the maximal dosage in an adult patient? a. 5 b. 10 c. 15 d. 20 e. 25
(c) 2% mepivacaine = 20 mg/ml, so 300 mg / 20 mg/ml = 15 ml
A recently introduced local anesthetic agent is claimed by the
manufacturer to be several times as potent as procaine. The product
is available in 0.05% buffered aqueous solution in 1.8 ml. cartridge.
The maximum amount recommended for dental anesthesia over a 4-
hour period is 30 mg. The amount is contained in approximately how
many cartridges?
a. 1-9
b. 10-18
c. 19-27
d. 28-36
e. Greater than 36
(d) 0.05% = 0.5 mg/ml . To give 30 mg, you have to give
30mg/0.5 mg/ml or 60 ml. 1 cartridge = 1.8 ml, thus 60ml /1.8ml
= 33.3 cartridges. - first express the percentage of solution as a
fraction of 100, then add the units gm/ml. 0.05% equals 0.5 or
1/2 gms per 100 ml. The cartridge is 1.8 ml which you can
round off to almost 2 mls total. In this 2 ml you would have 1 gm
of the local anesthetic. You need to give 30 gms, which would
require 30 cartridges. The alternative that meets this answer is
(d).
According to AHA guidelines, the maximum # of carpules of
local anesthetic containing 1:200,000 epinephrine that can be used
in the patient with cardiovascular disease is
a. 1
b. 2
c. 3
d. 4
e. 11
(d) the AHA limit is 0.04 mg, compared to 0.2 mg in the healthy
patient. 1:200,000 equals 0.005 mg/ml or 0.009 per 1.8 ml
carpule. 4 carpules would thus contain 0.036 mg, which is just
below the 0.04 mg limit
Max epi that cardiovascular pts can receive (in mgs)
0.04 mg
Max epi healthy pts can receive (in mgs)
0.2 mg
how much epi in one carpule of 1:200,000
1.8 mL /200,000 = 0.9 ug of epi in one carpule - 0.009 mg
Penicillin V vs Penicillin G
G more susceptible to acid degradation, injected more often than peroral
best G- spectrum among penicillins
ampicillin
cross-allergenic with penicillin
ampicillin, cephalosporins
against penicillinase
dicloxacillin
pseudomonas-specific penicillin
carbenicllin (extended spectrum)
when prophylaxis?
NOT for joints anymore! unless complications, then refer to their surgeon
- yes for infective endocarditis; prosthetic valves, hx of infective endocarditis, cardiac transplant; congenital heart defects
1st line of abx prophylaxis
2g of amoxicillin (4 of 500mg) 1 hr before procedure
for kids: 50mg/hr before procedure
abx if penicillin allergy
clindamycin 600 mg 1 hour PO (4 x 150mg)
kids 20 mg/kg
if can’t peroral:
same dosages but 1/2 hr before procedure
procedures that don’t require prophylaxis
restorative, intracanal endo, impressions
typical penicillin VK prescription
250-500mg, q6h for 7 days
kids 20-50 mg/kg, qid
typical clinda prescription
150-300 mg, q8h for 7 days
kids 8-12 mg/kg tid or qid
typical amoxicillin prescription
500mg q8h for 7 days
kids 20-40
mechanism of penicillins
inhibit cell wall synthesis
bactericidal!
tetracycline: cidal or static?
static!
mechanism of tetracycline
inhibit protein synthesis on ribosomes; static
mechanism of antifungals
bind to ergosterol, weaken cell wall (like Nystatin)
nystatin class
antifungal
sulfonamides static or cidal?
static
sulfonamides mechanism
compete with PABA in folic acid synthesis
which drugs involved in folic acid synthesis
sulfonamides
allergy to penicillins
dermatitis, stomatitis, bronchoconstriction and cardiovascular
collapse
clindamycin side effects
GI upset and pseudomonas infection
GI upset and Pseudomonas infection whose side effects
clindamycin
most likely to give superinfection
broad spectrum, like tetracyclines
how broad in penicillin G spectrum>? superinfx likely?
narrow, unlikely
aplastic anemia whose side effects
chloramphenicol
chloramphenicol side effect
aplastic anemia
organ toxicity of tetracyclin
liver
allergic cholestatic hepatitis
erythromycin
erythromycin - cross-reactive with penicillin?
no
eryhtromycin allergy
cholestatic hepatitis
tetracyclin + penicllin interaction
cancel each other: cidal vs static
how is penicillin eliminated
renal
which drug can alter penicillin elimination
pribenecid
probenecid with penicillin elimination
can alter
what can reduce tetracylin effectiveness
antacids, dairy
antacids and dairy on tetracyclin
can reduce effectiveness
ampicillin and oral contraceptives
ampicillin decrease the effectiveness of
oral contraceptives due to suppression of normal Gl flora
involved in the recycling of active steroids from bile conjugates,
leading to more rapid excretion of the steroids from the body
erythromycin class
macrolide
macrolides can inhibit which drugs
seldane, digoxin
herpes tx
acyclovir
candidiasis tx
fluconazole, ketoconazole
fluconazole, ketoconazole class
systemic antifungals
For treating most oral infections, penicillin V is preferred to penicillin G
because penicillin V
a. Is less allergenic
b. Is less sensitive to acid degradation
c. Has a greater gram-negative spectrum
d. Has a longer duration of action
e. Is bactericidal, whereas penicillin G is not
b
The sole therapeutic advantage of penicillin V over penicillin G is
a. Greater resistance to penicillinase
b. Broader antibacterial spectrum
c. More reliable oral absorption
d. Slower renal excretion
e. None of the above
c
Which of the following penicillins is administered ONLY by deep intramuscular injection? a. Ampicillin b. Dicloxacillin sodium c. Penicillin G procaine d. Penicillin V potassium
c; Penicillin G
is destroyed by acid in the stomach resulting in variable and
irregular absorption. Penicillin V is acid stable and available for
oral use. Penicillin G procaine is typically given intramuscularly
in repository form, yielding a tissue depot from which the drug is
absorbed over hours. In this form, it cannot be given IV or
subcutaneously.
The principal difference among potassium, procaine and benzathine
salts of penicillin G is their
a. Potency
b. Toxicity
c. Duration of action
d. Antibacterial spectrum
e. Diffusion into the cerebrospinal fluid
(c) again, just asking you to know something about the various
forms of penicillin. Since in most cases you are going to use Pen
VK orally, this question is an old one showing its age and probably
not likely to appear anymore on board excams
Which of the following antibiotics is cross-allergenic with penicillin
and should NOT be administered to the penicillin-sensitive patient?
a. Ampicillin
b. Erythromycin
c. Clindamycin
d. Lincomycin
e. Tetracycline
a
Which of the following antibiotics may be cross-allergenic with penicillin? a. Neomycin b. Cephalexin c. Clindamycin d. Erythromycin e. All of the above
b
- Which of the following antibiotics shows an incidence of
approximately 8% cross-allergenicity with penicillins?
a. neomycin
b. cephalexin
c. bacitracin
d. vancomycin
e. tetracycline
b
Which of the following groups of antibiotics is related both structurally
and by mode of action to the penicillins?
a. Polymyxins
b. Cycloserines
c. Cephalosporins
d. Chloramphenicols
c
For the dentist, the most reliable method of detecting a patient’s
allergy to penicillin is by
a. Injecting penicillin intradermally
b. Taking a thorough medical history
c. Placing a drop of penicillin on the eye
d. Having the patient inhale a penicillin aerosol
e. Injecting a small amount of penicillin intravenously
(b) all of the other methods involve unacceptable risk. Once
sensitized, even a small amount can cause an allergic
response. Remember, it is not a dose-related response that
won’t be problematic if you only inject a little bit.
Which of the following antibiotics is the substitute of choice for
penicillin in the penicillin-sensitive patient?
a. Bacitracin
b. Erythromycin
c. Tetracycline
d. Chloramphenicol
CLINDAMYCIN IS BEST BUT
b
reason (b) is the right answer is that the
spectrum of activity of erthromycin is very similar to penicillin. The
others offer a much broader spectrum of coverage than we usually
require; always use the drug with the narrowest spectrum possible
that includes the microbe in question. Standards have now
changed such that clindamycin is the drug of choice in this
situation. But if they don’t include clindamycin, look for
erythromycin, or for that matter Azithromycin
Most anaphylactic reactions to penicillin occur
a. When the drug is administered orally
b. In patients who have already experienced an allergic reaction to
the drug
c. In patients with a negative skin test to penicillin allergy
d. When the drug is administered parenterally
e. Within minutes after drug administration
i. (a), (b) and (d)
ii. (b), (c) and (d)
iii. (b), (d) and (e)
iv. (b) and (e) only
v. (c), (d) and (e)
iii
Which of the following penicillins has a broader gram-negative spectrum than penicillin G? a. Nafcillin b. Ampicillin c. Cephalexin d. Methicillin e. Penicillin V
b
Which of the following penicillins has the best gram-negative spectrum? a. Nafcillin b. Ampicillin c. Methicillin d. Penicillin V e. Phenethicillin
b
Which of the following antibiotics should be considered the drug of
choice in the treatment of infection caused by a penicillinase-
producing staphylococcus?
a. Neomycin
b. Ampicillin
c. Tetracycline
d. Penicillin V
e. Dicloxacillin
e that’s really the only use for dicloxacillin
Oral infections caused by organisms that produce penicillinase should be treated with a. Ampicillin b. Dicloxacillin c. Erythromycin d. Any of the above e. Only (a) or (c) above
(b) of those listed only (b) is penicillinase resistant. Ampicillin is an
extended spectrum penicillin, and is not penicillinase resistant.
Erythromycin shouldn’t be affected by penicillinases, since it isn’t a
peniciilin, but it doesn’t work against staph for other reasons.
does erythromycin work against staph?
no
Which of the following antibiotics is LEAST effective against penicillinase-producing microorganisms? a. Ampicillin b. Cephalexin c. Methicillin d. Clindamycin e. Erythromycin
a
Which of the following is a bactericidal antibiotic used specifically in the treatment of infections caused by Pseudomonas species and indole-positive Proteus species? a. Ampicillin b. Penicillin V c. Tetracycline d. Dicloxacillin e. Carbenicillin
e
Penicillin's effectiveness against rapidly growing cells is primarily due to its effect on a. Protein synthesis b. Cell wall synthesis c. Nucleic acid synthesis d. Chelation of metal ions e. Cell membrane permeability
b
Chlortetracycline acts by interfering with
a. Cell wall synthesis
b. Nuclear acid synthesis
c. Protein synthesis on bacterial but not mammalian ribosomes
d. Protein synthesis on mammalian but not bacterial ribosomes
c
The probable mechanism of the bacteriostatic action of sulfonamides
involves
a. Disruption of the cell membrane
b. Coagulation of intracellular proteins
c. Reduction in oxygen utilization by the cells
d. Inhibition of metabolism by binding acetyl groups
e. Competition with para-aminobenzoic acid in folic acid synthesis
e
The sulfonamides act by
a. Suppressing bacterial protein synthesis
b. Inhibiting the formation of the cytoplasmic bacterial membrane
c. Inducing the formation of “lethal” bacterial proteins
d. Inducing a deficiency of folic acid by competition with para-
aminobenzoic acid
d
Which antibiotic is able to achieve a higher concentration in bone than in serum? a. penicillin b. erythromycin c. clindamycin d. metronidazole e. amoxicillin
c
drig that is able to achiebe high concentration in gingival crevicular fluid
tetracycline
Tetracycline reduces the effectiveness of concomitantly administered
penicillin by
a. Reducing absorption of penicillin
b. Increasing metabolism of penicillin
c. Increasing renal excretion of penicillin
d. Increasing binding of penicillin to serum proteins
e. None of the above
(e) tetracycline is bacteriostatic and would slow the rapid
growth of the microbial population that a bactericidal drug such
as penicillin needs to be effective, sine only when rapidly
dividing are the cells making cell walls
The action of which of the following drugs will most likely be impaired
by concurrent administration of tetracycline?
a. Clarithromycin
b. Erythromycin
c. Sulfonamide
d. Penicillin
e. Lincomycin
d
Which of the following antibiotics is most likely to cause liver damage? a. Streptomycin b. Penicillin G c. Tetracycline d. Cephalosporins e. Amphotericin B
(c) (a) streptomycin can damage the eighth nerve, affecting
both balance and hearing, but is not associated with liver
damage. (b) other than allergic reactions, penicillins are
extremely safe, with no effect on the liver. (d) the
cephalosporins are chemically related to the penicillins and
share their relatively nontoxic nature. (e) amphotericin B, is an
antifungal agent that produces such adverse side effects as
nephrotoxicity and hypokalemia, but not liver toxicity. Thus (c) is
the correct answer. Tetracyclines have been shown to be
hepatotoxic following high doses in pregnant patients with a
history of renal disease.
toxicity of streptomycin
balance and hearing
toxicity of amphetericin B
renal + hypoKemia
Which of the following erythromycins associated with an allergic cholestatic hepatitis? a. Erythromycin base b. Erythromycin stearate c. Erythromycin estolate d. Erythromycin succinate
c
Which of the following antibiotics is LEAST likely to cause superinfection? a. Gentamicin b. Tetracycline c. Penicillin G d. Streptomycin e. Chloramphenicol
c bc narrow
Gastrointestinal upset and pseudomembranous colitis has been prominently associated with a. Nystatin b. Cephalexin c. Clindamycin d. Polymyxin B e. Erythromycin
(c) The only 2 possibilities that produce GI upset are (c) and
(e). As for producing colitis, (b) and (c) are associated with this
adverse side effect. (c) is the only drug which does both,
therefore it’s the right answer.
Symptoms that may be characterized as allergic manifestations
during penicillin therapy are
a. Deafness, dizziness and acute anemia
b. Crystalluria, nausea, vomiting and anaphylactic shock
c. Oliguria, hematuria, bronchoconstriction and cardiovascular
collapse
d. Dermatitis, stomatitis, bronchoconstriction and cardiovascular
collapse
d
Aplastic anemia is a serious toxic effect that occurs particularly after
a course of treatment with which of the following antibiotics?
a. Penicillin
b. Lincomycin
c. Tetracycline
d. Streptomycin
e. Chloramphenicol
e
Each of the following is a side effect of prolonged tetracycline
hydrochloride therapy EXCEPT:
a. Suprainfection
b. Photosensitivity
c. Vestibular disturbances
d. Discoloration of newly forming teeth
e. Gastrointestinal symptoms (when administered orally)
c
tetracycline side effects
Suprainfection
b. Photosensitivity
d. Discoloration of newly forming teeth
e. Gastrointestinal symptoms (when administered orally)
Colitis that results following clindamycin therapy is caused by an overgrowth of a. C. dificile b. Staph aureus c. Pseudomonas d. Candida albicans
a
Which antibiotic is appropriate for premedication in the penicillin allergic patient? a. Cephalexin b. Clindamycin c. Erythromycin d. Amoxicillin e. Ampiciilin
b
- Acyclovir is useful for treating
a. Candidiasis
b. Colitis
c. Herpes simplex
d. HIV
e. ANUG
c
A distinct advantage that tetracyclines have over penicillins is that
tetracyclines
a. Have no side effects
b. Do not cause superinfections
c. Are safer to use during pregnancy
d. Have a wider range of antibacterial activity
e. Produce higher blood levels faster after oral administration
(d) broad spectrum vs. narrow spectrum. Tetracyclines certainly
have more side effects than penicillin, and are certainly one of the antibiotics to avoid during pregnancy.
Which of the following has the broadest antimicrobial spectrum?
a. Vancomycin (Vancocin )
b. Clindamycin (Cleocin )
c. Erythromycin (Erythrocin )
d. Chlortetracycline (Aureomycin )
e. A third generation cephalosporin
(d) Answer is (d)- remember, tetracyclines are broad spectrum
antibiotics effective against both gram-negative and gram-
positive cocci and bacilli. Clindamycin has a spectrum of activity
similar to erthyromycin and vancomycin, which is less than that
of the tetracylines, mainly affecting gram-positive
microorganisms. Ist generation cephalosporins are effective
against both gram-negative and gram-positive organisms, but
the third generation ones have increased activity against gram-
negative but greatly decreased activity against gram-positive
microorganisms.
Sulfonamides and trimethoprim are synergistic bacteriostatic agents
because in bacteria they
a. Both inhibit folic acid synthesis
b. Interfere sequentially with folinic acid production
c. Are both antimetabolites of para-aminobenzoic
d. Are both inhibitors of dihydrofolic acid reductase
e. Are both transformed in vivo into a single active compound
b
Which of the following substances is the most effective agent against
fungus infections of the mucous membrane?
a. Nystatin ointment
b. Undecylenic acid
c. Polymyxin ointment
d. Saturated magnesium sulfate
e. 10 per cent aluminum chloride solution
a
The most desirable property of an antibiotic when used to treat an
odontogenic infection is
a. Rapid absorption
b. Little allergenicity
c. Ability to achieve and maintain adequate concentrations at the
site of infection
d. Lack of significant binding to plasma proteins
e. No effects on drug metabolism
c
- Nystatin is of greatest clinical usefulness in treating
a. viral infections
b. fungal infections
c. spirochetal infections
d. Bacterroides infections
e. penicillin resistant gram positive infections
b
Which of the following drugs chelates with calcium?
a. Erythromycin
b. Polymyxin B
c. Tetracycline
d. Penicillin G
e. Chloramphenicol
c
Which of the following is NOT characteristic of tetracycline antibiotics?
a. Absorption is impaired when taken with antacids
b. Theypredisposetomonilialsuperinfection
c. They form a stable complex with the developing tooth matrix
d. They have a low tendency for sensitization, but a high
therapeutic index
e. They are effective substitutes for penicillin prophylaxis against
infective endocarditis
Answer is (e)- Again, the important phrase in the question is not (Hey, just Wayne and Garth). Obviously the fact that you will remember about tetracylines is that they can discolor teeth in the fetus when taken by the mother during pregnancy. But don’t circle that answer because (a) is also characteristic of tetracyclines (they are the most likely of all the antibiotics to cause superinfection), and is an annoying side effect in adults resulting from alteration of the oral, gastric and intestinal flora. The real answer is (e). Tetracyclines are not the drug of choice for prophylaxis against infective endocarditis. This is due to streptococcal infection. 15-20% of group A streptococci are resistant to tetracyclines, but none are resistant to penicillin or erythromycin. Recently a non-streptococcal induced subacute bacterial endocarditis has been identified, especially in juvenile periodontitis patients. The causative bacterium is not susceptible to penicillin or erythromycin. It may be necessary to treat predisposed patients with tetracycline for a few weeks, and then follow this with a course of penicillin or erythromycin. Remember that these drugs are antagonistic to each other and thus can’t be used concurrently. Penicillin is a bactericidal drug which kills or destroys microorganisms by interfering with the synthesis or function of the cell wall, cell membrane or both. Thus it is most effective against bacteria that are multiplying. Tetracycline is a bacteriostatic antibiotic that acts by inhibiting the growth and multiplication of organisms by inhibiting protein synthesis by binding reversibly to the 30 S subunit of the bacterial ribosome. When the two types are given together, their effectiveness is negated or reduced.
The concurrent administration of penicillin G and probenecid results in
a. Increased metabolism of penicillin G.
b. Increased renal excretion of probenecid
c. Decreased renal excretion of penicillin G
d. Decreased bactericidal effect of penicillin G
e. Increased excretion of probenecid in the feces
C
Interaction between penicillin and probenicid is best described by which of the following mechanisms?
a. competition at the receptor site
b. acceleration of drug biotransformation c. alteration in the acid-base balance
d. alteration in the rate of renal clearance
Answer is (d)- penicillin is metabolized in the liver, but it rapidly disappears from the blood due to rapid clearance by the kidneys. 90% is excreted by tubular secretion. Thus patients with renal disease will show high blood levels of penicillin. Similarly, probenicid, a uricosuric agent (a drug which tends to enhance the excretion of uric acid by reducing renal tubular transport mechanisms), reduces the renal clearance of penicillins. And you wondered why we had those lectures on pharmacokinetics!
- When broad-spectrum antibiotics are administered with coumarin anticoagulants, the anticoagulant action may be
a. b. c. d.
Reduced because of enhanced hepatic drug metabolism
Reduced because of increased protein-binding Increased because of reduction of vitamin K sources Increasedbecauseofdecreasedrenalexcretionofthe anticoagulant
C
therapeutic effectiveness of which of the following drugs will be
most affected by concomitant ingestion of antacids?
a. Cephalexin b. Erythromycin c. Tetracycline d. Sulfisoxazole e. Penicillin V
C
Erythromycin should be avoided in the patient taking
a. Aspirin
b. Seldane
c. Benadryl
d. Ibuprofen
e. Propranolol
(b) remember the famous erythromycin –Seldane potentially lethal interaction, whereby erythromycin blocks the metabolism of Seldane to its antihistamine metabolite – it stays unmetabolized and causes cardiac arrthymias. Of course this question could have many other options listed, since erythromycin decreases the metabolism of so many other useful drugs, such as digoxin.
Atenolol class and use
Cardioselective beta-blocker, HTN
metoprolol too
reduces cardiac output
Propranolol class use
non-selective beta-blocker, htn, angina, also paroxysmal tachy
reduces cardiac output and renin release
Lisinopril class use
Ace inhibitor, HTN
also congestive heart failure
Furosemide class use
Loop diuretic, HTN
Prazosine class use
selective Alpha-1 - blocker, HTN
inhibits NE release
Guanethidine class use
Neuro inhibitor, severe HTN
Cardioselective beta-blockers
Metaprolol, atenolol
Angina meds
Nitroglycerin, propranolol, Ca-channel blockers (verapamil)
Verapamil class use
Ca-channel blocker, angina
also supraventricular tachyarrhythmia, paroxysmal tachycardia, afib
lidocaine use
ventricular arrhythmias
phenytoin use
reverse digitalis induced arrhythmias
quinidine use
supraventricular tachyarrhythm, afib
digitalis (=digoxin) use
afib, paroxysmal tachy
it’s a glycoside
tx for ventircular arrhythmias
lidocaine
tx to reverse digitalis induced arrhythmia
phenytoin
tx for supraventricular tachyarrhythmias
quinidine, verapamil
tx for afib
quinidine, verapamil, digoxin
tx for paroxysmal tachycardia
verapamil, digoxin, propranolol
tx for congestive heart failure
glycosides (digoxin, digitalis) and ACE inhibitors (captopril)
glycosides use
digitalis, digoxin – congestive heart failure;
afib, paroxysmal tachy
type 1a antiarrhythmics - example, mechanism
quinidine: prolongs refractory period
type 2a antiarrhytmics - example, mechanism
lidocaine: decreases excitability
digitalis mechanism
for afib: decreses rate of AV conduction
for congestive heart failure: increase force of contraction (+ inotropic) –> inhibit Na/K ATPase –> increased Ca influx. reduce compensatory changes in CHF (heart size, rate, edema)
what is angina:
insufficient oxygen for myocardium
nitroglycerin mechanism
direct vasodilatory action on smooth muscla in coronary arteries –> increases oxygen supply
propranolol mechanism
reduces oxygen demand – reduces chronotropic response to epi and stress
Ca channel blockers mechanism
decrease oxygen demand –> reduce afterload –> reduce peripheral resistance via vasodilation
ACE inhibitors mechanism
blocks conversion of angiotensin 1 to 2 (latter is potent constrictor)
methyldopa class mechanism
alpha 2 agonist, centrally reduces sympathetic outflow
cloidine class mechanism
alpha 2 agonist, centrally reduces sympathetic outflow
diuretics mechanism
decrease the renal absorption of sodium, thus resulting
in fluid loss and a reduction in blood volume. This decreases
the work the heart has to pump. Also have weak dilatory
action.
types of diuretics and examples
thiazides - chlorothiazide
loop - furosemide
K sparing - spironolactone
spironolactone class
K sparing diuretic
Quinidine is principally used to treat
a. Hypertension
b. Angina pectoris
c. Congestive hear failure
d. Supraventricular tachyarrhythmias
(d) by elimination. Hypertension ((a)) is treated primarily with
beta blockers such as propranolol. Angina is primarily treated
with nitroglycerin, while digoxin (digitalis) is the drug of choice for
congestive heart failure. Quinidine is classed as an antiarrthymic
drug (Type I-blocks sodium channels). It reduces automaticity
and responsiveness and increases refractoriness. It also has an
antimuscarinic action preventing the bradycardia that follows
vagal stimulation.
Quinidine is used to treat
a. Hypertension
b. Angina pectoris
c. Atrial fibrillation
d. Ventricular fibrillation
e. Congestive hear failure
c
tx for ventricular arrhythmias
lidocaine
Verapamil is most efficacious in the treatment of
a. Atrial fibrillation
b. Atrial tachycardia
c. Ventricular tachycardia
d. Catecholamine-induced arrhythmias
a
Which of the following drugs is most useful in treating or preventing angina pectoris? a. Digitalis b. Quinidine c. Propranolol d. Procainamide e. Pentobarbital
c
Each of the following drugs can be used in the prevention and treatment of angina pectoris EXCEPT a. Digitalis b. Propranolol c. Nitroglycerin d. Isosorbide dinitrate e. Pentaerythritol tetranitrate
a
All of the following drugs are useful in the treatment of hypertension EXCEPT a. Ephedrine b. Reserpine c. Methyldopa d. Thiazide diuretics
a
Digitalis is useful in the treatment of which of the following conditions?
a. Atrial fibrillation
b. Congestive heart failure
c. Paroxysmal atrial tachycardia
d. All of the above
d
All of the following drugs are useful in the treatment of cardiac arrhythmias EXCEPT
a. Digitalis
b. Lidocaine
c. Phenytoin
d. Procainamide
e. Aminophylline
e
The drug of choice for initial therapy for mild hypertension is
a. Reserpine
b. Guanethidine
c. Phenobarbital
d. Chlorothiazide
e. lpha-methyldopa
d
Which of the following antihypertensives are usually reserved for
treatment of severe hypertension?
a. Sedatives and reserpine
b. Thiazide diuretics and reserpine
c. Sedatives and thiazide diuretics
d. Guanethidine and ganglionic blocking agents
d
Which of the following beta-adrenergic receptor blocking agents is thought to be cardioselective? a. Nadolol b. Timolol c. Metoprolol d. Propranolol
c
Antiarrhythmic drugs, such as quinidine, suppress certain cardiac
arrhythmias by
a. Stimulating the beta-adrenergic receptor
b. Suppressing cardiac ATP-ase activity
c. Increasing ectopic pacemaker activity
d. Increasing the refractory period of cardiac muscle
d
Most drugs useful in the treatment of cardiac arrhythmias act
primarily by
a. Blocking Purkinje fibers
b. Blocking the alpha-adrenergic receptor
c. Suppressing SA node impulse formation
d. Causing a positive inotropic effect
e. Increasing the refractory period of cardiac muscle
e
The most important pharmacologic action of drugs that suppress
cardiac arrhythmias is
a. Blockade of the vagus nerve
b. Stimulation of cardiac ATP-ase activity
c. Blockade of the Beta-adrenergic receptor
d. Stimulation of the beta-adrenergic receptor
e. Increased refractory period of cardiac muscle
e
Lidocaine produces its antiarrhythmic effects by
a. Increasing AV conduction
b. Decreasing cardiac excitability
c. Increasing cardiac conduction velocity
d. Increasing spontaneous pacemaker activity
(b) arrhythmias are defined as any abnormality of the normal sinus rhythm of the heart due to disease or injury induced
damage to the impulse conducting systems. They also result
from the development of ectopic pacemakers or abnormal
pacemaker rhythms. Drugs such as lidocaine are used to
normalize these rhythms. Lidocaine, a local anesthetic,
depresses cardiac excitability, answer (b). The refractory period
of cardiac muscle is increased, thus slowing the heart down. All
of the other alternatives given would exacerbate the arrhythmia.
When digitalis is used in atrial fibrillation, the therapeutic objective is
to
a. Abolish cardiac decompensation
b. Inhibit vagal impulses to the heart
c. Decrease the rate of A-V conduction
d. Increase the rate of cardiac repolarization
e. Produce a decrease in the rate of atrial contraction
c
Nitroglycerin dilates the coronary arteries in angina pectoris by
a. Decreasing the heart rate reflexly
b. Increasing the metabolic work of the myocardium
c. Direct action on smooth muscle in the vessel walls
d. Increasing the effective refractory period in the atrium
e. Blocking beta-adrenergic receptors
c
Propranolol is of value in treating angina pectoris because it
a. Has a direct action on vascular smooth muscle
b. Blocks autoregulatory mechanisms in the heart
c. Inhibits oxygen metabolism in cardiac cells
d. Provides relief within seconds of an acute anginal attack
e. Prevents chronotropic responses to endogenous epinephrine
emotions and exercise
e
Administration of angiotensin results in
a. Anti-inflammatory effects
b. Antihistaminic effects
c. Increased blood pressure
d. Increased heart rate
e. A sedative effect
c
The primary antihypertensive effect of captopril (Capoten) is due to accumulation of a. Serotonin b. Angiotensin I c. Angiotensin III d. Bradykinin metabolites
b
Administration of angiotensin results in
a. A sedative effect
b. Increased heart rate
c. Increased blood pressure
d. Antihistaminic effects
e. Anti-inflammatory effects
c
Which of the following is NOT characteristic of the thiazide diuretics?
a. Increase renal excretion of sodium and chloride
b. Increase renal excretion of potassium
c. Increase the toxicity of digitalis
d. Exacerbate existing diabetes
e. Cause hypokalemia
f. Cause hypoglycemia
(f) first off, how can you have an option (f)?! (a) is how diuretics
lower BP, (b) is why they can cause hypokalemia, which is
conveniently option (e), and hypokalemia can potentiate digitalis
induced arrythmias option(c). Theyy apparently can also cause
hyperglycemia, which would relate to option (d). How the heck
are you supposed to remember all of this?
thiazide on blood sugar
hyperglycemia
thiazide and digitalis
thiazide increases K excretio –> can exacerbte digitalis toxicity
The most useful diuretic drugs act by
a. Increasing the glomerular filtration rate
b. Decreasing the renal reabsorption of sodium
c. Decreasing the renal excretion of chloride
d. Increasing the renal reabsorption of potassium
e. Increasing the secretion of antidiuretic hormone
(b) people with high BP are always told to reduce salt intake,
since high sodium levels cause fluid retention which can
increase BP, so ipso facto, reducing renal reabsorption of
sodium makes BP go down
Which of the following drugs act by inhibiting renal reabsorption of sodium? a. Urea b. Chlorothiazide c. Theophylline d. digitalis glycosides e. Procainamide
b
Digoxin exerts its positive inotropic effect by
a. Activation of adenylcyclase
b. Inhibition of phosphodiesterase
c. An agonist effect of beta-receptors
d. Inhibition of Na+, K+ ATPASE leading to increased calcium
influx
e. Decreasing the amount of calcium available for excitation-
contraction coupling
Answer is (d)- Remember, cardiac glycosides such as digoxin
are used in the treatment of congestive heart failure, which is
the failure of the heart to function adequately as a pump and
thus maintain an adequate circulation. Cardiac glycosides are
thought to act by altering calcium ion movement, with a desired
effect of increasing the force of contraction of the myocardium
(e.g. the inotropic effect). While several of the alternatives
involve calcium, the way digoxin does it is via (d), inhibition of
Na+, K+ ATPase, resulting in an increase of calcium ion influx
into the cardiac cells, and a subsequent enhancement of the
contractile mechanism. (a) is the way epinephrine works.
Digitoxin is effective in the treatment of cardiac failure because it
a. Is primarily a diuretic
b. Reduces the ventricular rate
c. Decreases abnormal cardiac rhythms
d. Produces peripheral vasoconstriction
e. Has a positive cardiac inotropic action
e
The primary action of therapeutic doses of digitalis on cardiac muscle
is an increase in
a. Force of contraction
b. Ventricular excitability
c. Refractory period of the atrial muscle
d. Refractory period of the ventricular muscle
e. Rate of conduction of impulse to the muscle
a
The beneficial effects of digitalis in congestive heart failure result in
part from the fact that digitalis causes
a. A decrease in end-diastolic volume
b. A decrease in end-diastolic pressure
c. An increase in stroke volume and cardiac output
d. A decrease in central venous pressure
e. A decrease in rate of the hear where tachycardia exists
i. (a), (b) and (c)
ii. (a) and (c) only
iii. (c) and (d)
iv. (e) only
v. All of the above
v
The cardiac glycosides will increase the concentration of which ion in an active heart muscle? a. Sodium b. Bromide c. Calcium d. Chloride e. Potassium
c
Which of the following ions augments the inotropic effect of digitalis?
a. Sodium
b. Lithium
c. Calcium
d. Chloride
e. Magnesium
c
In the treatment of congestive heart failure, digitalis glycosides
generally decrease all of the following EXCEPT
a. Edema
b. Urine flow
c. Heart size
d. Heart rate
e. Residual diastolic volume
b
The mechanism of action of prazosin, an antihypertensive agent is to
a. Block beta-adrenergic receptors
b. Inhibit formation of angiotensin II
c. Inhibit nerve-induced release of norepinephrine
d. Stimulate central inhibitory alpha-adrenergic receptors
e. Inhibit the postsynaptic action of norepinephrine on vascular
smooth muscle
e
Which of the following owes a significant amount of its
antihypertensive effect to a central action?
a. Methyldopa
b. Metoprolol
c. Hydralazine
d. Propranolol
e. Guanethidine
(a) All of these drugs are used to treat hypertension, but act by
different mechanisms. (a), methyldopa, is the drug with central
action- it alters CNS control of blood pressure by acting on
cardioregulatory and vasomotor systems of the brain by
stimulating alpha2 receptors in the brain stem. Clonidine is the
usual drug that is involved in this particular question. (b)
metropolol is a selectively blocks beta-1 receptors in the heart to
reduce cardiac output. (c) hydralazine has a direct action on
vascular smooth muscle to reduce hypertension via
vasodilation. (d) propranolol blocks beta receptors in the heart,
while (e) guanethidine prevents the release and causes
depletion of catecholamines taken up into storage vesicles and
is released like a false transmitter. It does not cross the blood-
brain barrier.
Which of the following drugs is thought to reduce arterial blood pressure by activating alpha receptors in the vasomotor center of the medulla? a. Prazosin b. Clonidine c. Propranolol d. Guanethidine e. Chlorothiazide
b
Propranolol (Inderal) can be useful in the treatment of hypertension
because it blocks
a. Alpha-1 adrenergic receptors
b. Sodium reabsorption in the kidney
c. The release of renin from juxtaglomerular cells
d. The release of norepinephrine from nerve terminals
e. The reflex tachycardia seen with the use of other
antihypertensives
i. (a) and (b)
ii. (a) and (d)
iii. (b), (c) and (d)
iv. (c), (d) and (e)
v. (c) and (e) only
(v) Answer is (v)- You should immediately recognize that
propranolol is the prototypic beta-adrenergic receptor blocker,
thus any answer with alternative a (i and ii) is wrong. Similarly, d
is wrong as well-propranolol is a competitive beta- receptor
blocker- it has no effect on NE release. Another drug used for
hypertension, Clonidine, acts via this mechanism by stimulating
alpha-2 autoreceptors. Thus ii, iii, and iv are wrong. This leaves
(v) as the only possible right answer. Indeed, aside from
blocking beta-1 receptors, blocking of renin release is thought to
be the other mechanism whereby beta-blockers alter
hypertension.
One of the proposed mechanisms of the antihypertensive effect of
beta-adrenergic receptor blocking agents is
a. Sedation
b. A diuretic effect
c. An antirenin effect
d. A vagal blocking effect
e. An increase in cardiac output
c
Selective beta-1 adrenergic agonists will produce which of the following effects? a. Glycogenolysis b. Increased cardiac output c. Decreased diastolic pressure d. Decreased peripheral resistance e. Relaxation of bronchial smooth muscle
b
Ototoxicity with deafness may encountered occasionally in patients
taking which of the following diuretic agents?
a. Osmotic
b. Thiazide
c. Mercurial
d. High-ceiling
d
Symptoms of digitalis toxicity include all of the following EXCEPT
a. Extrasystoles
b. Nausea and vomiting
c. Yellow-green vision
d. A-V conduction block
e. Decreased P-R interval
e
Administration of which of the following drugs increases the likelihood of a toxic response to digitalis? a. Diazepam b. Lidocaine c. Spironolactone d. Chlorothiazide e. Acetylsalicylic acid
(d) Chlorthiazide is a diuretic which causes potassium loss or
hypokalemia. This results in greater penetration of digitalis into
the myocardium, and thus potential toxicity.
aspirin vs acetaminophen
acetaminphen - no anti-inflammatory activity
no GI upset
is hepatotoxic
The therapeutic effect of the salicylates is explained on the basis of the
ability of the drug to
a. Activate autonomic reflexes
b. Uncouple oxidative phosphorylation
c. Inhibit the synthesis of prostaglandins
d. Competitively antagonize prostaglandins at the receptor site
c
The mechanism of the antipyretic action of salicylates probably results
from
a. Inhibition of prostaglandin synthesis in the CNS affecting
hypothalamic temperature regulation
b. Inhibition of bradykinin in the periphery leading to sweating
c. Depression of oxidative enzymes leading to decreased heat
production
d. Suppression of cholinergic mediators in the hypothalamus
e. Stimulation of norepinephrine in the hypothalamus
a
The antipyretic action of salicylates is explained in part by
a. Analgesia leading to sedation
b. Increased blood flow through the hypothalamus
c. Cutaneous vasodilation leading to increased heat loss
d. Depression of oxidative processes leading to decreased heat
production
c
The locus of action of aspirin’s central antipyretic effect is the
a. Brain stem
b. Hypothalamus
c. Basal ganglia
d. Limbic system
e. Cerebral cortex
b
t regulation center in CNS
hypothalamus
A patient who has been taking large quantities of aspirin might show
increased postoperative bleeding because aspirin inhibits
a. Synthesis of thromboxane A2 and prevents platelet
aggregation
b. Synthesis of prostacyclin and prevents platelet aggregation
c. Synthesis of prostaglandin and prevents production of blood
platelets
d. Thrombin and prevents formation of the fibrin network
e. G.I. absorption of vitamin K and prevents synthesis of blood
clotting factors
(a) The first fact you must remember is that aspirin prevents
platelet aggregation- this limits your choices to (a) and (b). They
hope to confuse you by using prostacylin, but of course you
know that this is wrong immediately, the right word is
prostaglandin, as in (c), but you have already eliminated that
choice because it doesn’t mention prevention of platelet
aggregation. Thus, even if you didn’t remember that
thromboxane A2 induces platelet aggregation, and aspirin
blocks this action, you could get the answer by elimination. (d) is
how heparin works, while (e) is how coumarin works.
Anti-inflammatory agents, such as aspirin, interfere with hemostasis by
a. Activating antithrombin
b. Preventing vasoconstriction
c. Inhibiting thrombin generation
d. Inhibiting platelet aggregation
e. Inhibiting polymerization of fibrin
d
Which of the following anti-inflammatory agents does NOT act
primarily by inhibiting activity of prostaglandin synthetase?
a. Diflunisal
b. Ibuprofen
c. Triamcinolone
d. Oxyphenbutazone
e. Acetylsalicylic acid
(c) triamcinolone is a corticosteroid. Corticosteroids inhibit
phospholipase A2, the enzymatic step that precedes
prostaglandin synthetase. Diflunisal is a salicylate analgesic, like
aspirin.
A nonsteroidal, anti-inflammatory agent that appears to produce fewer
gastrointestinal disturbances than high does of aspirin is
a. Ibuprofen
b. Probenecid
c. Pentazocine
d. Acetaminophen
e. Phenylbutazone
(a) you might be tempted to answer acetaminophen, because it
doesn’t cause GI upset, but remember it is also not anti-
inflammatory. The answer is ibuprofen.
Prolonged use of which of the following drugs does NOT cause a
predisposition to gastric irritation and bleeding?
a. Phenytoin
b. Ibuprofen
c. Indomethacin
d. Phenylbutazone
e. Acetylsalicylic acid
(a) This is a straight drug identification question. Answers 2-5
are all non-steroidal antiinflammatory drugs which cause gastric
irritation and bleeding due to their effects on prostaglandin
synthesis in the mucosal wall of the gut. # , phenytoin, is an
anti-convulsant-its major side effect that often appears as a
question on boards is the production of gingival hyperplasia.
Each of the following agents has been associated with gastric irritation EXCEPT a. Aspirin b. Alcohol c. Ibuprofen d. Indomethacin e. Acetaminophen
(e) note the difference in this question and #11 and 12.
Ibuprofen was previously the answer to “shows reduced GI
irritation”, but it does cause some, which you have to remember
to answer #12 and this question. So aspirin and ibuprofen are
out. Indomethacin is a very strong NSAID that causes lots of GI
irritation, so much that use is limited in humans, so it is out.
What about alocohol vs. acetaminophen. Well, you should really
know that acetaminophen is usually the answer to these types
of analgesics questions, but if you didn’t know that, perhaps may know that alcohol also causes GI irritation, so it is out.
Which of the following is NOT produced by excessive doses of acetylsalicylic acid?
a. Delirium
b. Tinnitus
c. Hypothermia
d. Hyperventilation
e. Metabolic acidosis
(c) it only lowers your temperature if you have a fever,, taking
aspirin does not have any effect on body temperature in the
non-feverish patient, but high doses can cause all the other
effects listed.
All of the following are pharmacologic and toxicologic properties of aspirin EXCEPT a. Tinnitus b. Analgesia c. Salicylism d. Antipyresis e. Suppression of the immune response
e
Therapeutic effects of aspirin include
a. Analgesia
b. Tranquilization
c. Pyretic action
d. Anti-inflammatory action
e. Antirheumatic action
i. (a), (b) and (c)
ii. (a), (c) and (d)
iii. (a), (d) and (e)
iv. (b), (c) and (d)
v. (b), (d) and (e)
iii
All of the following are pharmacologic or toxicologic properties of acetylsalicylic acid EXCEPT a. Tinnitus b. Analgesia c. Antipyresis d. Methemoglobinemia e. Inhibition of prostaglandin synthesis
d
All of the following are possible effects of aspirin EXCEPT
a. Reduction of fever
b. Shortening of bleeding time
c. Suppression of inflammatory response
d. Bleeding from the gastronintestinal tract
e. Increase in the renal excretion of uric acid at high doses
b
Of the following, aspirin does NOT cause
a. Occult bleeding
b. Nausea and vomiting
c. Acid-base disturbance
d. Suppression of the cough reflex
e. Decreased tubular reabsorption of uric acid
d
Answer is (d)- (a) & (b) are the major side effects of aspirin (resulting from the inhibition of prostaglandin synthesis) for the
majority of people, and one reason for the popularity of aspirin
alternatives such as acetaminophen and ibuprofen, which
produce these effects to a lesser extent. # 3 & 5 may also be
seen following larger doses of aspirin. (d) is not seen with
aspirin, but is a major therapeutic use of narcotic opiates such
as codeine. I guess they are hoping that you will get the effects
of codeine and aspirin mixed up, since the two are often
compared and contrasted as moderate pain relievers.
Which of the following is NOT true about acetaminophen?
a. Is a non-prescription drug
b. Is cross-allergenic with aspirin
c. Possesses both analgesic and antipyretic effects
d. May induce methemoglobinemia at high doses
e. May be the pharmacologically active form of acetophenetidin
(phenacetin)
(b) because it ain’t a salicylate, but the other statements are true
Which of the following is NOT true regarding acetaminophen?
a. It has antipyretic properties
b. It may induce methemoglobinemia
c. It can be combined with codeine
d. It has anti-inflammatory properties
e. It is not cross-allergenic with aspirin
d
The most prominent acute toxic effect associated with acetaminophen use is a. Hemorrhage b. Renal necrosis c. Hepatic necrosis d. Gastric ulceration e. Respiratory alkalosis
(c) Remember, acetaminophen (tylenol) is an aspirin
alternative. Alternatives 1, 4, 5 are side effects of aspirin-type
drugs. The popularity of acetaminophen as an aspirin alternative
is because the incident of such effects with this drug is very low.
However, because acetaminophen can undergo
biotransformation to a toxic intermediate, hepatic and renal
necrosis have been reported, especially after very high doses.
(c), hepatic necrosis is the most prominent, especially when
combined with alcohol consumption, since the alcohol induces
the liver enzymes which make the hepatotoxic metabolites of
acetaminophen
Which of the following anti-inflammatory agents does NOT act
primarily by inhibiting the activity of cyclooxygenase?
a. Ibuprofen
b. Diflunisal
c. Prednisone
d. Indomethacin
e. Phenylbutazone
Answer is (c)- (a), 2, 4, and 5 are NSAIDS that reduce
inflammation by reducing prostaglandin synthesis by blocking
the activity of cyclooxygenase. Prednisone is a corticosteroid. Corticosteroids are potent nonspecific inhibitors of the
inflammatory process, acting at a variety of point throughout the
inflammatory process. Although they do reduce prostaglandin
production as well, they do this by a mechanism other then
blocking cyclooxygenase, probably by inhibiting the release of
the fatty acid substrate for prostaglandin synthesis.
24. Which of the following is the most appropriate drug to use to lower fever in a child under 12? a. Aspirin b. Ibuprofen c. Acetaminophen d. Salicylate e. Diflunisal
(c) acetaminophen is the best choice. Aspirin is contraindicated due to
the potential for causing Reye’s syndrome. Ibuprofen is approved,
but usually not the #1 choice. The others would be inappropriate as
well.
- Which analgesic from the following list has the longest half-life?
a. Acetaminophen
b. Aspirin
c. Diflunisal (Dolobid)
d. Ibuprofen
(c) Diflunisal can be taken twice a day, the others three-four times a
day is required.
Occurrence of which of the following is LEAST characteristic of narcotic ingestion? a. Vomiting b. Diarrhea c. Urinary retention d. Bronchiolar constriction e. Increase in intracranial pressure
(b) Again, the key word is least. Narcotics, in the form of
paregoric (tincture of opium), and Lomotil (loperamide) are over
the counter oral preparations for the treatment of diarrhea.
Opiates act on receptors in the gut to produce constipation.
Thus (b) is obviously wrong. All of the other answers are side
effects of opiate administration.
Therapeutic doses of morphine administered intramuscularly may produce a. Constipation b. Euphoria c. Dysphoria d. Mental clouding e. Decreased response to pain i. (a) and (b) only ii. (a), (b) and (d) iii. (a), (d) and (e) iv. (c), (d) and (e) v. All of the above
v
Which of the following are pharmacologic effects of morphine?
a. Respiratory depression
b. Euphoria
c. Sedation
d. Constipation
e. Dysphoria
i. (a), (b) and (c)
ii. (a), (b) and (d)
iii. (a) and (e)
iv. (c), (d) and (e)
v. All of the above
v
Which of the following drugs acts to suppress the cough reflex?
a. ASA
b. Codeine
c. Meperidine
d. Acetaminophen
e. Phenyibutazone
(b) the only drugs that do this are opioids, and codeine and
merperidine are the two opioids on the list. Of the two, codeine
is much better at this than meperidine.
Morphine binds to which site to produce analgesia?
a. By binding to specific receptors in the CNS
b. By decreasing the influx of sodium
c. By decreasing the synthesis of prostaglandins
d. By decreasing nerve activatin at the site of injury
(a) They might reword the question in a way that asks you to
remember that the specific receptors are the mu receptors.
Morphine causes vomiting by
a. A direct irritant action on the gastric mucosa
b. Stimulation of the nodose ganglion of the vagus nerve
c. Stimulation of the medullary chemoreceptor trigger zone
d. Direct stimulation of the gastrointestinal musculature
c
The decrease in ventilation caused by morphine, meperidine and
some of the related opioids depends chiefly upon
a. Depression of cortical activity
b. Peripheral blockade of chemoreceptor impulses
c. An increase in carbon dioxide concentration in the blood
d. Blockade of afferent autonomic impulses from the lungs
e. Loss of sensitivity of the medullary respiratory center to carbon
dioxide
e
Small doses of barbiturates and morphine depress respiration
primarily by
a. A parasympathominetic action
b. Inhibiting the Herine-Bueuer reflex
c. Rendering the aortic chemoreceptor system insensitive to O2
d. Rendering the respiratory centerin the brain stem less sensitive
to changes in CO2
e. A specific effect at myoneural junctions of phrenic and
intercostal nerves
d
Which of the following are pathognomonic symptoms of narcotic
overdose?
a. Miosis, coma and depressed respiration
b. Mydriasis, coma and smooth muscle spasms
c. Mydriasis, coma and depressed respiration
d. Miosis, convulsions and depressed respiration
e. Mydriasis, convulsions and depressed respiration
a
The cause of death with opioid intoxication is
a. Oxygen apnea
b. Cardiac arrest
c. Terminal convulsions
d. Circulatory collapse
e. Respiratory depression
e
opioids decrease the response of respiratory centers in the
brainstem to the carbon dioxide tension of the blood, and also
depresses pontine and medullary centers regulating respiratory
frequency. Opioids do not cause oxygen apnea, ((a)), they can
be convulsive, but not terminally so ((c)), they are stabilizing on
the heart and some are actually used in open-heart surgery
((b)), and they do not cause circulatory collapse ((d)).
Which of the following is an opioid that has both agonistic and antagonistic activities? a. Codeine b. Methadone c. Naloxone d. Meperidine e. Pentazocine
(e) This is an example of the type of question where the drug
class is given. You are asked to not only identify a drug from the
list as being from this class, but additionally that it has the
properties that are given in the question that distinguish it from
the other drugs of the class that are listed as alternatives. In this
example, there is only one drug which meets this criterion. All
are drugs which act via opiate receptors, but 3 are agonists ((a),
(b), (d)), 1 is an antagonist only ((c)). (e) pentazocine is the only
drug which has both types of action, and is the one drug left by
the process of elimination.
A heroin-dependent patient should NOT be given nalbuphine (Nubain
) for pain because
a. It has no analgesic properties
b. It may produce respiratory depression
c. As a mixed agonist-antagonist, it can elicit withdrawal
symptoms
d. The high abuse potential of nalbuphine may add to the patient’s
problems
c
A patient while not currently taking drugs has a history (6 months ago) of narcotic dependency. Which of the following analgesics should be avoided in this patient? a. Aspirin b. Pentazcine c. propoxyphene d. Indomethacin e. Acetaminophen f. None of the above
b
Which of the following statements does NOT characterize
pentazocine?
a. It is equianalgesic with codeine
b. It is a partial opioid antagonist
c. Its abuse potential is less than that of heroin
d. It may induce dysphoria and mental aberrations
e. It is effective only on parenteral administration
(e) lot of memorization required here for a drug that isn’t
used that much. I guess it was big news when these
questions were written many years ago and they seemed
hopeful, since statement (c) was true and was
therapeutically an advantage, but it soon became apparent
that (d) was also true
The antagonist of choice in the treatment of opioid overdosage is
a. Naloxone
b. Nalorphine
c. Pentazocine
d. Levallorphan
e. Propoxyphene
(a) nalorphine and pentazocine are mixed agonist-antagonists,
levallorphan is an opioid agonist, as is propoxyphene
Which of the following is a complete antagonist of the opioid receptor
and the agent of choice in the treatment of narcotic overdose?
a. Naloxone
b. Nalorphine
c. Cyclazocine
d. Levallorphan
e. None of the above
a
Methadone is used in detoxification (drug withdrawal) of patients
physically dependent on morphine because methadone
a. Precipitates withdrawal reactions
b. Antagonizes the depressant actions of morphine
c. Will not in itself produce physical dependence
d. Withdrawal reactions are less intense and stressful than those of
morphine
(d) This is an example of the kind of question that requires that
you have memorized a fact about a particular drug, in this case
the fact is (d). Methadone you will remember is not an
antagonist like naloxone- it is a full agonist with analgesic
properties, just like morphine. When taken orally it is not
euphoric in addicts, but acts just like morphine to produce
tolerance and physical dependence. Withdrawal is less severe
than with morphine because methadone has a much longer half
life. Facts 1, 2, and 3 would be met by an antagonist such as
naloxone, or perhaps even a mixed agonist-antagonist such as
pentazocine.
Which of the following drugs is currently widely used in treating opioid-dependent individuals? a. Codeine b. Methadone c. Alphaprodine d. Pentazocine e. Meperidine
b
- Meperidine (Demerol) is
a. An antidepressant
b. An opioid analgesic
c. A sedative
d. A long-acting local anesthetic
e. An antipsychotic
b
sympathetic receptors
ganglionic ACh nicotine
end-organ ACh muscarinic
parasympathetic receptors
ganglionic ACh nicotine
end-organ usually adrenergic: except sweat glands ACh muscarinic
motor neuron receptors
muscular ACh nicotine
Atropine and propantheline exert their effects on peripheral structures
by
a. preventing release of acetylcholine
b. preventing synthesis of acetylcholine
c. enhancing destruction of acetylcholine
d. competeing with acetylcholine for receptor sites
e. producing physiologic effects opposite to those of acetylcholine
(d) - (a) is wrong- botulinum toxin does this. (b) is wrong-
hemicholinium works this way. (c) is wrong- ACh is broken
down almost instantaneously, so it is almost impossible to
enhance its destruction. (e) is wrong-these drugs don’t have
any actions of their own, they just prevent ACh effects by
blocking receptors: atropine and propantheline are
postganglionic muscarinic receptor blockers-thus the answer is
(d).
Neostigmine produces its effect by
a. depressing acetylcholinesterase release
b. inhibiting acetylcholinesterase activity
c. increasing the rate of acetylcholine synthesis
d. acting like acetylcholine at ganglionic sites
e. increasing the amount of acetylcholine released from nerve
terminals
(b) – neostigmine is a cholinesterase inhibitor like physostigmine. These differ from the insecticides and nerve
gases listed below in that they are reversible and can be used
clinically; the latter are irreversible.
Organophosphate insecticides and nerve gases inhibit the action of which of the following enzymes? a. adenylate cyclase b. monoamine oxidase c. phosphodiesterase d. acetylcholinesterase e. carbonic anhydrase
d
Drugs which are additive with or potentiate the effects of acetylcholine include (a) methacholine (b) scopolamine (c) pralidoxime (d) neostigmine (e) pilocarpine 1. (a), (b), and (c) 2. (a), (c), and (d) 3. (a), (d) and (e) 4. (b), (d), and (e) 5. (c), (d) and (e)
(3) drugs which potentiate cholinergic stimulation can do so by
being either direct acting cholinergic agonists, acting on the
cholinergic receptor, or by indirectly increasing the duration of
action Ach by preventing its enzymatic degradation.
Methacholine and pilocarpine are direct-acting cholinergic
agonists, whereas neostigmine acts indirectly. Scopolamine is a
muscarinic antagonist like atropine, and will reduce or block
cholinergic action via direct receptor antagonism. Pralidoxime is
a chemical antidote used to regenerate AchE after nerve gas or
insecticide exposure.
Which of the following drugs is best to administer after poisoning by an
organophosphate cholinesterase inhibitor?
a. atropine
b. phenytoin
c. pralidoxime
d. propantheline
e. phenobarbital
c
Which of the following acts by antagonizing cholinesterase?
a. atropine
b. muscarine
c. neostigmine
d. pilocarpine
e. acetylcholine
c
When neostigmine is administered before acetylcholine, the action of
acetylcholine will be
a. blocked
b. enhanced and prolonged
c. less intense and of shorter duration
d. none of the above. The action of acetylcholine is not affected by
neostigmine
(b) the action will be prolonged because neostigmine prevents
its breakdown by AchE! Its action would be blocked by atropine
or scopolamine
Neostigmine can stimulate denervated skeletal muscle because it
a. is a congener of acetylcholine
b. is a competitive blocking agent
c. has no effect on acetylcholinesterase
d. is more potent than diisopropylfluorophosphate
e. is capable of acting directly on the end-plate
(e)a strange and amazing truth! Denerevated means the
skeletal muscle is not receiving neural input, and thus
stimulating a cholinergic neuron to release Ach which would
then stimulate the NMJ can’t happen. But if you inject a drug
which can stimulate the nicotinic receptors directly then you can
see an effect on the muscle. Neostigmine is one of those
anticholinesterases that can act like Ach at nicotinic receptors,
in addition to prolonging the action of Ach itself by blocking the
acetylcholinesterase that is trying to break the Ach down.
Which of the following is used to prevent laryngospasm?
a. atropine
b. epinephrine
c. diazepam (Valium)
d. neostigmine (Prostigmine)
e. succinylcholine (Anectine)
(e) What is needed is a skeletal muscle relaxant. This requires a
drug that acts at the neuromuscular junction. Of those listed,
only succinylcholine (e) is in this category. (a) atropine is a
cholinergic (Muscarinic) receptor blocker, (b) epinephrine is an
adrenergic agonist, and (c) diazepam is a benzodiazepine, and
(d) is an anticholinesterase.
In treating xerostomia, which of the following might be prescribed?
a. atropine
b. ephedrine
c. neostigmine
d. scopolamine
e. mecamylamine
(c) salivation is typically considered to be a cholinergic
response. Xerostomia is too little saliva and thus one could use
a cholinergic agonist to stimulate more saliva secretion
(assuming there is functional salivary gland tissue, which may
not be the case in patients that have been subject to radiation
therapy!) From the list, only neostigmine would produce a
cholinergic effect, since it is an indirect acting cholinergic
agonist. Of the others, atropine and scopolamine are cholinergic
antagonists, and are actually used to reduce salivation,
mecamylamine is a ganglionic blocker (not the action we desire,
too non-specific, and a blocker at that!). Ephedrine is a mixed
acting adrenergic agonist.
Which of the following drugs is most likely to dry secretions in the oral cavity? a. diazepam b. promethazine c. physostigmine d. propantheline e. diphenhydramine
d
The most useful drug to induce salivation is one which has properties that are a. adrenergic b. cholinergic c. ganglionic blocking d. adrenergic blocking e. cholinergic blocking
b
Drugs that are commonly used in the control of excessive salivation include (a) meprobamate (b) atropine (c) methantheline (d) codeine (e) chlorpromazine 1. (a) and (b) only 2. (a), (b), and (c) 3. (b) and (c) only 4. (b), (c), and (d) 5. (d) and (e)
(3) you are probably thinking, who the hell ever heard of
meprobamate and methantheline, or for that matter,
chlorpromazine! Well, these are drugs that may have been
useful in the olden days, but would be probably replace in this
type of questions by more modern equivalents. But of course
you should figure out that atropine (b), being the prototype
anticholinergic drug has to be one of the answers. So option 5
has to bee incorrect, since it does not include atropine. Now
only the most corrupt dentist would prescribe codeine to reduce
salivation, so #4 should also be incorrect – that leaves 1, 2, or 3.
So see, you didn’t even have to recognize that chlorpromazine
is an antipsychotic drug. So what is meprobamate – if we can
eliminate that one then we are down to only option 3 as a
possible answer. Meprobamate happens to be an antianxiety,
skeletal muscle relaxant drug sometimes used by dentists to
treat muscle spasms associated with TMD – also has use for
external sphincter spasticity – imagine! But it doesn’t seem to
have anticholinergic activity that is significant enough to cause
significant reduction of saliva. Methantheline, in contrast, is
Banthine, a synthetic version of atropine! So option 3, atropine
and methantheline are the drugs for this purpose.
Administration of ganglionic blocking agents will result in
a. miosis
b. diarrhea
c. copious salivation
d. orthostatic hypotension
e. enhanced activity of the parasympathetic nervous system
(d) a ganglionic blocker, since it acts by preventing cACh from
stimulating nicotinic receptors at the ganglia level will have both
anticholinergic and antiadrenergic effects. Options a, b, c, and e
are symptoms of cholinergic stimulation, and thus can’t be right.
Option (d), the remaining answer, is an antiadrenergic effect,
arising from decreases in sympathetic tone to the vasculature
Tachycardia in a patient administered with atropine or scopolamine
results from
a. release of adrenal catecholamines
b. blockade of vagus nerve activity
c. blockade of the nicotinic cholinergic receptor
d. stimulation of the alpha adrenergic receptor
e. stimulation of the beta adrenergic receptor
(b) - Atropine and scopolamine are muscarinic cholinergic
receptor blockers. Just knowing that eliminates all the
alternatives except (b). But you should also remember that
heart rate is kept under tight reflexive control: any sudden
increase in HR usually stimulates baroreceptors to send a
signal to the vagus nerve to stimulate the heart to slow it back
down. This reflex is cholinergically mediated, and will be blocked
by cholinergic blockers such as atropine. Even when given in
the absence of higher than normal heart rate, atropine will block
the normal cholinergic control over the heart, leaving the
sympathetic system in charge with a resulting tachycardia.
All of the following are possible effects of cholinomimetic drugs
except
a. mydriasis
b. bradycardia
c. increased peristalsis
d. stimulation of sweat glands
e. increased secretion by bronchial glands
(a) - The first thing you have to know is that a cholinomimetic drug is one that mimics the action of acetylcholine, the
endogenous neurotransmitter in the parasympathetic or
cholinergic nervous system. The acronym for remembering the
effects of cholinergic stimulation is SLUD, or increased
salivation, lacrimation, defecation, and urination. The heart is the
exception in that activity or heart rate is decreased
(bradycardia)- thus since the question asks for an effect which
does not occur with cholinergic stimulation, that leaves (a) as
the only possibility. Miosis, not mydriasis, occurs with
cholinergic stimulation.
A paralyzing dose of succinylcholine initially elicits
a. CNS stimulation
b. CNS depression
c. decreased salivation
d. muscle fasiculation
e. extrapyramidal reactions
(d) because succinylcholine (SUX) is an agonist at nicotinic
receptors, so the initial response is muscle stimulation. But the
NMJ rapidly depolarizes due to the inability of the plasma
cholinesterase to break down the SUX, which isjust two
molecules of acetylcholine fused together – the other
information has no relevance unless you’re just stuck thinking
“gee, I know that SUX has something to do with autonomics but
not sure exactly what!”
Based on its known mechanism and sites of action, scopolamine should theoretically be useful in (a) treatment of peptic ulcer (b) providing euphoria and amnesia prior to surgery (c.) relieving bronchoconstriction (d) relieving some of the symptoms of Parkinson disease (e) visualization of the retina 1.. (a), (b), (d) and (e) 2.. (a), (b), and (e) only 3. (a),and (c) 4. (b) and (e) only 5. All of the above
5
Symptoms of poisoning by an organophosphate insecticide include all of the following except: a. skeletal muscle fasiculation b. excessive salivation c. bronchoconstriction d. hot, dry skin e. diarrhea
(d) organophosphates kill you from too much cholinergic
stimulation (SLUD). Option (a) is from nicotinic receptor
stimulation, (b) and (c) and (e) are also cholinergic stimulation.
Option (d) is an atropine, anticholinergic type reaction and thus
doesn’t fit the pattern of responses given.
All of the following symptoms are associated with neostigmine poisoning except a. diarrhea b. salivation c. convulsions d. bonchiolar constriction e. skeletal muscle paralysis
(e) basically the same question as the preceding question, they
just changed organophosphate insecticides to neostigmine. The
difference is that neostigmine is a reversible anticholinesterase,
whereas insecticides are irreversible. But again, the question
just basically wants you to recognize two things – that
neostigmine is an indirect acting cholinergic drug and then know
what the symptoms of cholinergic stimulation are. But even if
you didn’t know those facts you might be able to get if you
remember that neostigmine is a drug that is used to reverse the
skeletal muscle paralysis produced by drugs of the curare class
– the non-depolarizing neuromuscular junction blockers
Symptoms of atropine poisoning in man include
(a) decreased intraocular pressure
(b) burning dry mouth
(c) nausea, vomiting and diarrhea
(d) hyperthermia
(e) orthostatic hypotension
1. (a) and (c)
2. (b) and (d)
3. (b), (d), and (e)
4. (d) and (e)
5. All of the above
(2) glandular secretions are generally under cholinergic control,
so sweating and salivation are greatly reduced by the
anticholinergic drug atropine. So if you can’t salivate or sweat,
you very possible will show what kind of symptoms? How about
a burning dry mouth and hyperthemia? Nausea and vomiting
are cholinergic overdose, as is orthostatic hypotension.
The most likely signs or symptoms of overdosage with atropine are
a. CNS excitation and tachycardia
b. intestinal cramps and diarrhea
c. skin rash and cutaneous itching
d. ptyalism and increased sweating
e. constriction of the pupils and blurring of vision
(a) just when you thought you could get by with the anti-SLUD
strategy, they then expect you to remember that atropine
overdose causes CNS excitation and tachycardia? Actually,
that is one of the interesting diffs between atropine and
scopolamine, and the reason that scopolamine is used for
sedation, while atropine isn’t (b) and (e) are cholinergic
stimulation I think, (c) is histamine produced, while I haven’t got
a clue what “ptyalism” is – do you? But I do know that if atropine
causes dry hot skin because it prevents sweating then (d) can’t
be right!
Disorientation, confusion and hallucinations resulting from an
overdose of scopolamine are most efficaciuosly treated by
administering
a. atropine
b. levodopa
c. acetylcholine
d. physostigmine
(d) so ya gotta know scopolamine is anticholinergic, so ya need
a cholinergic agonist, either direct or indirect to overcome its
effects. The options in the list are c and (d). Acetylcholine won’t
work because it gets broken down way to rapidly by
acetylcholinesterase, and thus is useless to inject.
Physostigmine will work since it is an indirect
acetylcholinesterase.
The immediate cause of death from irreversible cholinesterase
inhibitors is
a. shock
b. convulsion
c. cardiac arrhythmia
d. respiratory paralysis
e. dehydration from vomiting and diarrhea
(d) - while some of these are indeed associated with
organophosphate toxicity, the immediate cause of death is due
to (d), which results from the stimulation of nicotinic receptors at
the neuromuscular junction resulting in paralysis of skeletal
muscles.
Each of the following is a symptom of cholinergic crisis except
a. bradycardia
b. lacrimation
c. vasoconstriction
d. extreme salivation
e. weakness of voluntary muscles
(c) this is an except question, don’t miss that word! So looking
at the list, we got the S (option d) and the L (option b) from
SLUD, so we are left with (a), c, and (e) as possibles. (e) results
from cholinergic stimulation of the NMJ, so that can’t be it. (a) or
bradycardia, can occur from too much cholinergic stimulation of
the heart (that’s why atropine is useful in surgery, to reverse the
bradycardia that sometimes arises. So, by default,
vasoconstriction is the exception we are looking for.
Succinylcholine is a short-acting neuromuscular junction blocking
agent useful for providing a brief paralysis to aid in intubating
patients. It is short-acting because
a. it is subject to rapid metabolism in the liver
b. it rapidly redistributes away from the NMJ
c. it is subject to inactivation by plasma esterases
d. it undergoes rapid inactivation in the GI tract
(c) that’s why it is long-acting in patient’s that have a deficiency in
this enzyme
Atropine-like drugs are classed as
a. anti-adrenergic
b. cholinomimetic
c. sympatholytic
d. anti-cholinergic
e. sympathomimetic
d
reserpine class action
adrenergic blocker
inhibits NE reuptake, depletes NE
guanethidine clss action
adrenoblocker, inhibits catecholamine release
alpha methyldopa effect
adrenoblocker
which adrenomimetics block NE reuptake
cocaine, TCAs
which adrenomimetics stimulate release of stored NE
amphetamine, ephedrine, tyramine
which adrenomimetics block destruction of NE
MAOIs
in presence of alpha blocker, what happens to epi
decrease in blood pressure bc beta-dilatio predominates
a1 stimulation
vasoconstriction, urinary retention, mydriasis
b1 stimulation
increased heart rat
b2 stimulation
broncho and vasodilation
a1 block
vasodilation
b1 block
decreased heart rate
b2 block
bronchoconstriction
levodopa
Parkinson’s tx
can enter brain
carbidopa given to divert peripheral decarboxylase activity
sympathomimetic
toxicity: face twitches, mental disturbances, nausea vomiting, cardiac arrhythmias
