Pharmacology, Preparation for NBDE Part II

  • Category: Pharmacology, General Dentistry
  • Aim: Revising for NBDE Part II
  • Questions: 25
  • Hint: No
  • Mutiple Opportunites: No
  • Time Limit: No
  • Answer Explaining: Yes

Pharmacology

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Question 1
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
Question 1 Explanation: 
B. Nitroglycerin is a nitrovasodilator. It produces nitric oxide, which activates guanylyl cyclase which, in turn, catalyzes the production of cGMP.
Question 2

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.
Question 2 Explanation: 
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.
Question 3

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
Question 3 Explanation: 
E. Trimethoprim, by virtue of its inhibition of bacterial dihydrofolate reductase, acts synergistically with the sulfonamides.
Question 4
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
Question 4 Explanation: 
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.
Question 5
A very low blood: gas solubility coefficient (partition coefficient = OAT), analgesic effect, and a drug that inhibits methionine synthase best describes which drug?
A
Ketamine
B
Nitrous oxide
C
Halothane
D
Isoflurane
E
Propofol
Question 5 Explanation: 
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, isoflurane). Ketamine is not inhaled; rather, it is injected. It also does not inhibit methionine syn¬thase. The same is true for propofol.
Question 6
What receptor or signaling pathway is linked most directly to α2-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
Question 6 Explanation: 
A. Inhibition of adenylyl cyclase through Gi, resulting from stimulation of α2-adrenergic receptor, leads to a reduction in intracellular cAMP.
Question 7
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
Question 7 Explanation: 
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.
Question 8

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
Question 8 Explanation: 
E. Transpeptidase is the enzyme that catalyzes the peptide crosslinking of peptidoglycan. Transpeptidase, is inhibited by penicillins and cephalosporins.
Question 9
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
Question 9 Explanation: 
B. Enoxaparin is a low-molecular-weight heparin. It activates antithrombin III and inhibits factor Xa.
Question 10
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
Question 10 Explanation: 
E. Di- and trivalent cations, such as those found in oral antacids, chelate tetracyclines and prevent their absorption.
Question 11
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
Question 11 Explanation: 
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.
Question 12
A decrease in glycogenolysis in the liver would be expected from which drug?
A
Albuterol
B
Epinephrine
C
Glucagon
D
Insulin
E
Parathyroid hormone
Question 12 Explanation: 
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.

Question 13
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
Question 13 Explanation: 
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 inhalation use. Inhaled methacholine, unlike the other drugs listed, is not used therapeutically but, rather, is used to diagnose hyperactive airway.
Question 14
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
Question 14 Explanation: 
C. The use of oral ketorolac (an NSAID) is limited to continue therapy after a parenteral dose.
Question 15
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
Question 15 Explanation: 
C. Circulating muscarinic cholinergic receptor agonists stimulate these receptors on endothelial cells, leading to release of nitric oxide and vasodilation.
Question 16
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
Question 16 Explanation: 
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.
Question 17
Naloxone antagonizes the therapeutic and toxic effects of which drug?
A
Acetaminophen
B
Aspirin
C
Carbamazepine
D
Fentanyl
E
Ibuprofen
Question 17 Explanation: 
D, Naloxone is a competitive antagonist at opioid receptors.
Question 18

Dihydrofolate reductase is an enzyme inhibited by which anticancer drug?

         
A
Bleomycin
B
Cisplatin
C
Doxorubicin
D
5-fluorouracil
E
Methotrexate
Question 18 Explanation: 
E. The mammalian enzyme form of dihydrofolate reductase is the target for methotrexate. Bleomycin produces strand breaks in DNA. Cisplatin is an alkylating agent. Doxorubicin intercalates with DNA. 5-Fluorouracil, after undergoing activation, inhibits thymidylate synthase.
Question 19
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
Question 19 Explanation: 
C. Alpha adrenoceptor blockers, like phenoxybenzamine, inhibit the vasoconstrictor effect of epinephrine 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 tyramine act largely at prejunctional sites and don’t block adrenergic receptors.
Question 20

Which of the following organisms is usually sensitive to clindamycin?

A
Candida albicans
B
Klebsiella pneumoniae
C
Methicillin-resistant Staphylococcus aureus
D
Streptococcus uiridans
E
Pseudomonas aeruginosa
Question 20 Explanation: 
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 clindamycin and most traditional antistaphylococcal drugs. Candida albicans is a yeastlike fungus and is not inhibited by antibacterial drugs such as clindamycin.
Question 21
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.
Question 21 Explanation: 
E. The recently described mild analgesic effect of dextromethorphan has been linked to N-methyl- D-aspartate (NMDA) receptor antagonism in the CNS.
Question 22
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
Question 22 Explanation: 
C. Alpha adrenergic receptor stimulation accounts for the vasoconstrictor effect of levonordefrin.
Question 23
Drug agonists having the same intrinsic activity also ham the same ____.
A
Maximal effect
B
Potency
C
Receptor affinity
D
Therapeutic index
E
Aqueous solubility
Question 23 Explanation: 
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.
Question 24
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
Question 24 Explanation: 
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.
Question 25
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
Question 25 Explanation: 
C. Cyclooxygenase (COX) is a key enzyme in the synthesis of prostaglandins. Prostaglandins, including PGE2 and PGF2a, are important media­tors for such functions as pain, and are a product of COX. Aspirin inhibits both COX-1 and COX-2.
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