NCLEX-RN : Drug Identification

Study concepts, example questions & explanations for NCLEX-RN

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Example Questions

Example Question #21 : Antimicrobial Pharmacology

Which of the following is ototoxic and nephrotoxic?

Possible Answers:

Erythromycin

Doxycycline

Gentamicin

Ceftriaxone

Ampicillin

Correct answer:

Gentamicin

Explanation:

Gentamicin belongs to the aminoglycoside antimicrobial agents. It is a bactericidal agent with a wide spectrum of activity against Gram-negative and Gram-positive organisms. It irreversibly inhibits protein biosynthesis by acting directly on the ribosome. Gentamicin binds receptors on the 30S subunit of the bacterial ribosome and inhibits protein synthesis through interference with the initiation complex, misreading of the code on the mRNA template, and causing polysomes to dissociate into nonfunctional monosomes.

Ototoxicity and nephrotoxicity are the most serious adverse effects of gentamicin. Ototoxicity is manifested as vestibular dysfunction, which may be due to destruction of hair cells. If renal failure is present, the probability of ototoxicity is greater.

Nephrotoxicity is more common with gentamicin than with any of the other aminoglycosides. It can produce acute renal insufficiency and tubular necrosis.

Example Question #22 : Antimicrobial Pharmacology

Bacterially-acquired resistance to aminoglycoside antibiotic agents occurs by several mechanisms. From a clinical standpoint, which of these is most important?

Possible Answers:

Retarded penetration of the drug through pores in the microbial outer membrane

Failure of the drug to penetrate the microbial cytoplasmic membrane

Alteration of microbial ribosomal structure

Inactivation by microbial enzymes

Correct answer:

Inactivation by microbial enzymes

Explanation:

The amino glycoside antibiotics include gentamicin, streptomycin, neomycin, tobramycin, kanamycin, amikacin, and netilmicin. All these drugs contain amino sugars linked to an aminocyclitol ring by glycosidic bonds. They are used primarily to treat infections caused by aerobic gram-negative bacteria, where they act to interfere with protein synthesis. The aminoglycosides diffuse through channels in the outer membrane of the bacteria and enter the periplasmic space. Subsequently, the drugs are transported across the cytoplasmic membrane by an energy-dependent transport system, which requires the bacteria to utilize oxygen. Once inside the bacterium, they bind to the 30 S ribosomal subunit and block the initiation of protein synthesis. Bacteria may acquire resistance to the action of the aminoglycosides by several different mechanisms. Penetration of the drug through the pores in the outer membrane may become retarded, but resistance of this type is unimportant clinically. Natural resistance to the aminoglycoside antibiotics can be caused by the failure of the drug to penetrate the cytoplasmic membrane. As the transport mechanism requires the utilization of oxygen, this explains the resistance of anaerobic bacteria and facultative bacteria grown under anaerobic conditions. However, the importance of this mechanism on clinically-important acquired-resistance does not appear to be significant. Resistance resulting from alterations in ribosomal structure is less clinically relevant for most infections. While an alteration in ribosomal structure can prevent binding of the drug, these alterations are not widespread. The most clinically relevant mechanism for acquired-resistance to the aminoglycoside antibiotics is the plasmid-mediated elaboration of inactivating enzymes. These enzymes may phosphorylate, adenylate, or acetylate the aminoglycoside, resulting in loss of function. This has become a source of special concern with regard to enterococcal infections, many of which are highly resistant to all aminoglycosides.

Example Question #23 : Antimicrobial Pharmacology

A 37-year-old man is admitted to the hospital after being diagnosed with tuberculosis. Before treatment is started, you inform him about the most common ways of transmitting the tubercle bacillus, as well as the medications used: isoniazid, rifampin, and pyrazinamide. What is a common side effect of rifampin therapy?

Possible Answers:

Reddish body fluids

Jaundice

Hyperuricemia

Polyneuropathy

Muscle pain

Correct answer:

Reddish body fluids

Explanation:

Initial treatment for pulmonary or extrapulmonary tuberculosis is isoniazid (INH), rifampin (RMP), and pyrazinamide (PZA) as a short-course intensive daily regimen for 2 months, followed by INH and RMP for 4 more months. The most common side effects of rifampin are reddish urine and stool, saliva, sweat, tears, diarrhea, joint pain, back pain, swelling of feet and/or legs, and blood in urine. Hyperuricemia is a major toxic effect of pyrazinamide; other toxic effects include fever, indigestion, urticaria, photosensitivity, and joint pain. Isoniazid can cause polyneuropathy, jaundice, muscle pain, confusion, and unsteady walk.

Example Question #24 : Antimicrobial Pharmacology

A nurse in your office may have been exposed to blood from a patient with AIDS. She was administering an antibiotic injection intramuscularly to a HIV-positive patient and accidentally sustained a needle prick injury. As part of her post-exposure prophylaxis therapy, you instruct her to begin daily tenofovir. What is the mode of action of this medication?

Possible Answers:

Prevents the virus from entering the cells

Is incorporated into viral DNA as a purine analog causing chain termination

Blocks the viral enzyme in reverse transcriptase

Cannot be phosphorylated by host cell enzymes

Is an extremely effective inhibitor of the host cell RNA polymerase

Correct answer:

Blocks the viral enzyme in reverse transcriptase

Explanation:

Tenofovir is categorized as a nucleoside analogue reverse transcriptase inhibitor (NRTIs). An NRTI’s mechanism of action is to block reverse transcriptase, an enzyme that enables the human immunodeficiency virus 1 (HIV-1) to flourish. This enzyme aids the HIV virus in making a copy of DNA from the viral RNA, and this DNA is incorporated into the host genome. The effectiveness has been found in a review conducted by the Centers for Disease Control and Prevention to be so effective that “pre-exposure prophylaxis can potentially be a vital option for HIV prevention in pearly at very high risk for infection, whether through sexual transmission or injecting drug use.”

In regards to Post-Exposure Prophylaxis (PEP), The United States Public Health Service recommend the use of tenofovir, emtricitabine, or a combination drug of these two medications—plus raltegravir for PEP in occupational exposure scenarios.

Example Question #21 : Antimicrobial Pharmacology

Which of the following antifungal agents is associated with bone marrow suppression and renal failure?

Possible Answers:

Flucytosine

Amphotericin B

Miconazole

Itraconazole

Ketoconazole

Correct answer:

Flucytosine

Explanation:

All of the drugs are antifungal agents but only flucytosine has been associated with bone marrow suppression and synergizes with other drugs which suppress bone marrow functions. Miconazole and ketoconazole may produce hepatotoxicity, gastro-intestinal upset and headaches. Amphotericin B may produce nephrotoxicity while itraconazole is associated with gastro-intestinal upset and rare liver dysfunction.

Example Question #26 : Antimicrobial Pharmacology

The tetracyclines are a group of widely used broad spectrum antibiotics. Antimicrobial activity of tetracyclines involves which of the following mechanisms?

Possible Answers:

Inhibition of microbial protein synthesis

Inhibition of microbial DNA gyrase

Inhibition of microbial cell wall synthesis

Inhibition of microbial folic acid synthesis

Inhibition of cell membrane function

Correct answer:

Inhibition of microbial protein synthesis

Explanation:

The tetracycline antibiotics possess a wide range of antimicrobial activity against gram-positive and gram-negative bacteria, as well as Rickettsia, Mycoplasma, Chlamydia, Ureaplasma, some atypical mycobacteria, and amoebae. These drugs are primarily bacteriostatic and act by inhibiting microbial protein synthesis. The tetracyclines, after active transport into the cell, bind to the 30 S ribosomal subunit. This prevents the access of aminoacyl tRNA to the acceptor site on the mRNA-ribosome complex, inhibiting the addition of amino acids to the growing peptide chain. This effect is, for the most part, reversible and removal of the drug results in loss of action.

The other mechanisms listed are utilized by other antimicrobial agents. For example, all beta-lactam drugs are selective inhibitors of cell wall synthesis, and therefore active against growing bacteria. Sulfonamides are structural analogs of PABA that is necessary for folic acid synthesis. By competitive inhibition, the drug interferes with folic acid synthesis. Folic acid is an important precursor to the synthesis of nucleic acids. Quinolones are examples of antibiotics which inhibit bacterial DNA synthesis by blocking of the DNA gyrase. Antibiotics—polymyxin and colistin—and the antifungal agent amphotericin B act by inhibiting cell membrane function.

Example Question #27 : Antimicrobial Pharmacology

You are prophylactically treating an 84-year-old man with amantadine and vaccination for avoidance of an upcoming influenza outbreak. The patient is to receive 100 mg b.i.d. for 8 days. What is the antiviral effect of amantadine?

Possible Answers:

Amantadine prevents viral uncoating and inhibits production of viral mRNA

Amantadine binds to ICAM-1, preventing viral attachment

Amantadine is phosphorylated by viral thymidine kinase and used as a defective guanosine analog in viral DNA synthesis

Amantadine binds to the hydrophobic sites on the influenza virus capsule. This destabilizes the virus, not allowing it to attach to the cell

Amantadine serves as a "cap" to viral mRNA and prevents binding of reverse transcriptase

Correct answer:

Amantadine prevents viral uncoating and inhibits production of viral mRNA

Explanation:

Amantadine only works after viral attachment to the cell, preventing viral uncoating. It is also believed to interfere with viral mRNA production. Amantadine is effective against influenza virus A.

 

Example Question #21 : Antimicrobial Pharmacology

A patient comes to your office with a severe eye infection. You prescribe eyedrops containing a mixture of the antibiotics gramicidin, neomycin, and polymyxin B. What does the mechanism by which neomycin acts as an anti-bacterial agent involve?

Possible Answers:

Inhibiting protein synthesis

Stimulating translation

Forming a channel in the membrane

Preventing cell wall synthesis

Inhibiting DNA replication

Correct answer:

Inhibiting protein synthesis

Explanation:

Transport antibiotics act as carriers of ions across membranes (e.g. valinomycin) or by forming channels in the membrane that allow ions to cross the membrane (example-gramicidin A). Gramicidin affects cell membrane permeability while polymyxin B interferes with bacterial cell wall production. These transport antibiotics, also called ionophores, are secreted by many microorganisms and disable other species by making their membranes permeable to ions. These antibiotics show high specificity for specific ions. Carriers bind ions on one side of the membrane and shuttle the ion across the membrane. The carrier antibiotics are donut shaped with a hydrophilic center where the ion binds and a hydrophobic periphery that allows the antibiotic to traverse the membrane.

The channel forming antibiotics form a β-helix that forms a "hole" in the membrane through which ions can move. These channels open and close and the accompanying ion movements can be detected by measuring the conductance across the membrane. The transport antibiotics have been a very useful tool for cell biologists and physiologists studying the movement of ions across biological membranes under a variety of conditions. Both types of antibiotics insert into the lipid bilayer but do not alter the composition of the membrane lipids. Penicillin is an antibiotic that acts by inhibiting cell wall synthesis by inhibiting the enzyme glycopeptide transpeptidase. Neomycin is an aminoglycoside antibiotic that binds to the 30S subunit of the ribosome inhibiting protein synthesis.

Example Question #161 : Pharmacology

Which of the following is a common feature of the anti-viral action of AZT and acyclovir compounds?

Possible Answers:

Are active in the unphosphorylated form

Act by alkylating viral DNA

Are analogues of purine nucleotides

Block virus from entering cells

Must be activated by host cell enzymes to be effective

Correct answer:

Must be activated by host cell enzymes to be effective

Explanation:

3'-azido-3'-deoxythymidine (AZT) is a nucleoside analog that blocks HIV replication by inhibiting the RNA-dependent polymerase, HIV-DNA polymerase. The DNA polymerase from HIV is 100-fold more sensitive to AZT than the host polymerase. AZT is a pyrimidine analog that is phosphorylated to AZT-triphosphate by cellular enzymes and acts as a competitive inhibitor of the reverse transcriptase. AZT can be incorporated into viral DNA and cause chain termination because its structure lacks the 2' hydroxyl needed for addition of the next nucleotide by the polymerase.

In addition to nucleoside analogues, HAART also contains non-nucleoside reverse transcriptase inhibitors and protease inhibitors that block cleavage of the precursors of the viral coat proteins, preventing proper viral assembly. Maraviroc blocks a specific cell receptor needed by HIV to enter the host cell.

Example Question #31 : Antimicrobial Pharmacology

A 32-year-old female presents to your clinic with recurrent bacterial cystitis. You culture Proteus sp. from the bladder and start her on amikacin. She presents 1 week later, with no improvement. Resistance to amikacin can occur by several methods. Which one of the following methods best describes a mechanism in which an organism can become resistant to amikacin?

Possible Answers:

Loss of the receptor on the 50S ribosomal sub-unit

Enzymatic hydrolysis by % lactamase-producing bacteria

Decrease in solubility in the bacterial cell membrane

Degradation of amikacin by bacterial peroxidase

Inactivation of amikacin by bacterial acetylation

Correct answer:

Inactivation of amikacin by bacterial acetylation

Explanation:

Amikacin binds to the 30S ribosomal sub-unit, not the 50S.

Enzymatic hydrolysis by % lactamase-producing bacteria targets penicillins.

Bacterial resistance to amikacin can be mediated through loss of a receptor by which amikacin binds the 30S ribosomal subunit, interference with membrane transport, and bacterial acetylation, adenylation, or phosphorylation.

Amikacin is resistant to peroxidase.

Amikacin is only marginally soluble in the bacterial cell membrane to begin with.

 

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