Drug Identification - NCLEX-PN
Card 0 of 1272
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?
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?
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.
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.
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Identify the anti-viral agent that blocks assembly of pox viruses by inhibiting viral protein synthesis.
Identify the anti-viral agent that blocks assembly of pox viruses by inhibiting viral protein synthesis.
Methisazone blocks synthesis of viral mRNA and proteins. This is especially evident in pox viruses. Methisazone has been used to treat small pox.
Methisazone blocks synthesis of viral mRNA and proteins. This is especially evident in pox viruses. Methisazone has been used to treat small pox.
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Which of the following is a common feature of the anti-viral action of AZT and acyclovir compounds?
Which of the following is a common feature of the anti-viral action of AZT and acyclovir compounds?
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.
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.
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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?
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?
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.
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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Which of the following antifungal agents interacts with cytochrome P-450 dependent sterol 14 -demethylase to inhibit ergosterol synthesis in many fungal organisms, as well as in gram-positive bacteria and protozoans?
Which of the following antifungal agents interacts with cytochrome P-450 dependent sterol 14 -demethylase to inhibit ergosterol synthesis in many fungal organisms, as well as in gram-positive bacteria and protozoans?
The mechanism of amphotericin B involves ergosterol, but the mechanism is not related to ergosterol synthesis. Amphotericin B binds to ergosterol in the cell membrane, disrupting its permeability to ions. Ketoconazole and other imidazoles interact with cytochrome P-450 to inhibit P-450 dependent synthesis of ergosterol by sterol 14-demethylase. Griseofulvin interacts with microtubular protein to inhibit fungal mitosis. Flucytosine incorporates into RNA and disrupts fungal protein synthesis. Zidovudine is used primarily as an antibiotic and not as an antifungal agent.
The mechanism of amphotericin B involves ergosterol, but the mechanism is not related to ergosterol synthesis. Amphotericin B binds to ergosterol in the cell membrane, disrupting its permeability to ions. Ketoconazole and other imidazoles interact with cytochrome P-450 to inhibit P-450 dependent synthesis of ergosterol by sterol 14-demethylase. Griseofulvin interacts with microtubular protein to inhibit fungal mitosis. Flucytosine incorporates into RNA and disrupts fungal protein synthesis. Zidovudine is used primarily as an antibiotic and not as an antifungal agent.
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Cases of invasive pulmonary aspergillosis occur in severely immunocompromised patients. The drug of choice for the treatment of these infections is
Cases of invasive pulmonary aspergillosis occur in severely immunocompromised patients. The drug of choice for the treatment of these infections is
The opportunistic mycoses are a group of fungal infections that occur almost exclusively in immunocompromised patients. A host of fungi, previously thought to be nonpathogenic, are known to be the etiologic agents of the opportunistic fungal infections. A certain few mycoses are seen with the greatest frequency and include zygomycosis, candidiasis, cryptococcosis, and aspergillosis. Aspergilli are widespread in the environment, and their conidia are easily dispersed and inhaled. These organisms are capable of causing a pulmonary infection in the immunocompromised patient, which rapidly disseminates and causes infection in virtually every organ. The drug of choice for the treatment of these infections is amphotericin B. A polyene macrolide antibiotic, amphotericin B works by forming pores in the fungal cell membrane. The other listed compounds are antifungal agents; however, their selectivity makes them unsuitable for the treatment of aspergillosis.
The opportunistic mycoses are a group of fungal infections that occur almost exclusively in immunocompromised patients. A host of fungi, previously thought to be nonpathogenic, are known to be the etiologic agents of the opportunistic fungal infections. A certain few mycoses are seen with the greatest frequency and include zygomycosis, candidiasis, cryptococcosis, and aspergillosis. Aspergilli are widespread in the environment, and their conidia are easily dispersed and inhaled. These organisms are capable of causing a pulmonary infection in the immunocompromised patient, which rapidly disseminates and causes infection in virtually every organ. The drug of choice for the treatment of these infections is amphotericin B. A polyene macrolide antibiotic, amphotericin B works by forming pores in the fungal cell membrane. The other listed compounds are antifungal agents; however, their selectivity makes them unsuitable for the treatment of aspergillosis.
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A 52-year-old man presents with a 3-day history of persistent diarrhea, having up to 7 watery bowel movements without bleeding a day. He has associated lower-abdominal cramping and notes mild nausea. He denies travel outside of the country. He does not recall eating anything unusual, and none of his family members are sick. Past medical history is significant for GERD, for which he takes protonix daily. He recently had an upper respiratory infection and completed a course of oral levofloxacin approximately 3 weeks ago. A stool sample is obtained. Stool is negative for ova and parasites, but PCR testing is positive for Clostridium difficile.
What is the appropriate first-line treatment in this patient?
A 52-year-old man presents with a 3-day history of persistent diarrhea, having up to 7 watery bowel movements without bleeding a day. He has associated lower-abdominal cramping and notes mild nausea. He denies travel outside of the country. He does not recall eating anything unusual, and none of his family members are sick. Past medical history is significant for GERD, for which he takes protonix daily. He recently had an upper respiratory infection and completed a course of oral levofloxacin approximately 3 weeks ago. A stool sample is obtained. Stool is negative for ova and parasites, but PCR testing is positive for Clostridium difficile.
What is the appropriate first-line treatment in this patient?
Metronidazole is correct. The patient is infected with Clostridium difficile, a Gram-positive, spore-forming bacillus. It is manifested by watery diarrhea, which left untreated can progress to fulminant colitis. Previous antibiotic use is the leading cause of Clostridium difficile, as the use of antibiotics alters the normal colonic flora, allowing Clostridium difficile to proliferate. Patients who have confirmed infection should first discontinue any offending antibiotics. The patient is then treated with either oral metronidazole or oral vancomycin. Due to its cost, oral vancomycin is typically reserved for severe or recurrent cases of Clostridium difficile.
The other choices are incorrect. Loperamide and lomotil are incorrect. These medications are both anti-motility agents. Their use is not recommended in the treatment of Clostridium difficile, as anti-motility agents have been associated with the development of toxic megacolon and systemic infection. Prednisone is incorrect. While corticosteroids have been used in severe Clostridium difficile colitis as adjunctive treatment to reduce inflammation, their use is not recommended for first-line treatment. In order to clear Clostridium difficile, the patient must undergo treatment with either metronidazole or vancomycin. Clindamycin is incorrect. Clindamycin is not active against Clostridium difficile. In fact, its use has been associated with development of Clostridium difficile.
Metronidazole is correct. The patient is infected with Clostridium difficile, a Gram-positive, spore-forming bacillus. It is manifested by watery diarrhea, which left untreated can progress to fulminant colitis. Previous antibiotic use is the leading cause of Clostridium difficile, as the use of antibiotics alters the normal colonic flora, allowing Clostridium difficile to proliferate. Patients who have confirmed infection should first discontinue any offending antibiotics. The patient is then treated with either oral metronidazole or oral vancomycin. Due to its cost, oral vancomycin is typically reserved for severe or recurrent cases of Clostridium difficile.
The other choices are incorrect. Loperamide and lomotil are incorrect. These medications are both anti-motility agents. Their use is not recommended in the treatment of Clostridium difficile, as anti-motility agents have been associated with the development of toxic megacolon and systemic infection. Prednisone is incorrect. While corticosteroids have been used in severe Clostridium difficile colitis as adjunctive treatment to reduce inflammation, their use is not recommended for first-line treatment. In order to clear Clostridium difficile, the patient must undergo treatment with either metronidazole or vancomycin. Clindamycin is incorrect. Clindamycin is not active against Clostridium difficile. In fact, its use has been associated with development of Clostridium difficile.
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Which of the following drugs is useful in treating infections from mycobacteria, which is the drug of choice in treating M. leprae?
Which of the following drugs is useful in treating infections from mycobacteria, which is the drug of choice in treating M. leprae?
Dapsone has been the world wide standard for treatment of leprosy. The other agents listed are used in treatment of tuberculosis.
Dapsone has been the world wide standard for treatment of leprosy. The other agents listed are used in treatment of tuberculosis.
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Which of the following is ototoxic and nephrotoxic?
Which of the following is ototoxic and nephrotoxic?
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.
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.
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Bacterially-acquired resistance to aminoglycoside antibiotic agents occurs by several mechanisms. From a clinical standpoint, which of these is most important?
Bacterially-acquired resistance to aminoglycoside antibiotic agents occurs by several mechanisms. From a clinical standpoint, which of these is most important?
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.
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.
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A 30-year-old man with HIV is being treated with anti-viral agents. 4 weeks after initiating therapy, he presents with weakness and fatigue. Laboratory studies reveal anemia, leukopenia and thrombocytopenia indicating bone marrow suppression. What anti-viral agent is most likely the cause of his symptoms?
A 30-year-old man with HIV is being treated with anti-viral agents. 4 weeks after initiating therapy, he presents with weakness and fatigue. Laboratory studies reveal anemia, leukopenia and thrombocytopenia indicating bone marrow suppression. What anti-viral agent is most likely the cause of his symptoms?
Zidovudine (ZDV,) formerly called azidothymidine, is active orally and is distributed to most tissues. The primary toxic side effect of ZDV is bone marrow suppression leading to anemia and neutropenia, which may require transfusions. Additional side effects include thrombocytopenia, gastrointestinal distress, headache, myalgia, acute cholestatic hepatitis, agitation, and insomnia.
The other choices are incorrect. Acyclovir is commonly used for the treatment of mucocutaneous and genital herpes lesions and for prophylaxis in AIDS. Acyclovir has no significant toxicity on the bone marrow. Nelfinavir is a protease inhibitor that is characterized by a short half-life and has a number of drug interactions but its primary adverse effect is diarrhea and it has the most favorable safety profile in pregnancy. It is not associated with bone marrow suppression. Lamivudine is a nucleoside inhibitor and is an active inhibitor of HIV reverse transcriptase. It is used in the treatment of hepatitis B virus infection. The drug is remarkably nontoxic and adverse effects are mild. Tenofovir is a nucleoside reverse transcriptase inhibitor and anti-HIV drug that competitively inhibits reverse transcriptase and causes chain termination after incorporation into DNA. Adverse side effects include gastrointestinal distress, asthenia, and headache but not anemia, leukopenia, or thrombocytopenia.
Zidovudine (ZDV,) formerly called azidothymidine, is active orally and is distributed to most tissues. The primary toxic side effect of ZDV is bone marrow suppression leading to anemia and neutropenia, which may require transfusions. Additional side effects include thrombocytopenia, gastrointestinal distress, headache, myalgia, acute cholestatic hepatitis, agitation, and insomnia.
The other choices are incorrect. Acyclovir is commonly used for the treatment of mucocutaneous and genital herpes lesions and for prophylaxis in AIDS. Acyclovir has no significant toxicity on the bone marrow. Nelfinavir is a protease inhibitor that is characterized by a short half-life and has a number of drug interactions but its primary adverse effect is diarrhea and it has the most favorable safety profile in pregnancy. It is not associated with bone marrow suppression. Lamivudine is a nucleoside inhibitor and is an active inhibitor of HIV reverse transcriptase. It is used in the treatment of hepatitis B virus infection. The drug is remarkably nontoxic and adverse effects are mild. Tenofovir is a nucleoside reverse transcriptase inhibitor and anti-HIV drug that competitively inhibits reverse transcriptase and causes chain termination after incorporation into DNA. Adverse side effects include gastrointestinal distress, asthenia, and headache but not anemia, leukopenia, or thrombocytopenia.
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Which of the following is an analog of guanine (a purine) and is transformed by viral thymidine kinase before it can inhibit viral DNA polymerase in viruses that are actively replicating?
Which of the following is an analog of guanine (a purine) and is transformed by viral thymidine kinase before it can inhibit viral DNA polymerase in viruses that are actively replicating?
The chemical type of an antiviral compound is often important in determining its potential mechanisms and, therefore, its utility against specific types of viruses. Interferon is a glycoprotein produced by many types of mammalian cells. It stimulates host mechanisms to prevent viral penetration and also inhibits viral protein synthesis. Idoxuridine, as its name implies, is a pyrimidine, which inhibits viral DNA polymerase. Zidovudine and zalcitabine are also pyrimidines, but they inhibit reverse transcriptase and act as chain terminators. Only acyclovir is a purine that requires viral thymidine kinase to be converted to an active phosphorylated form, which then inhibits viral DNA polymerase.
The chemical type of an antiviral compound is often important in determining its potential mechanisms and, therefore, its utility against specific types of viruses. Interferon is a glycoprotein produced by many types of mammalian cells. It stimulates host mechanisms to prevent viral penetration and also inhibits viral protein synthesis. Idoxuridine, as its name implies, is a pyrimidine, which inhibits viral DNA polymerase. Zidovudine and zalcitabine are also pyrimidines, but they inhibit reverse transcriptase and act as chain terminators. Only acyclovir is a purine that requires viral thymidine kinase to be converted to an active phosphorylated form, which then inhibits viral DNA polymerase.
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Which of the following anthelminthic drugs must be administered intravenously and may cause albuminuria due to accumulation in the kidney, photophobia, and papular eruption?
Which of the following anthelminthic drugs must be administered intravenously and may cause albuminuria due to accumulation in the kidney, photophobia, and papular eruption?
Suramin must be administered intravenously and should be used cautiously in patients with kidney disease. It inhibits protein kinases and dihydrofolate reductase and reduces ATP synthesis. It is used in the treatment of certain extra-intestinal nematodes and is probably one of the most toxic anthelminthic agents.
The other choices are incorrect. Diethylcarbamazine is rapidly absorbed following oral administration and increases the susceptibility of extra-intestinal nematodes to host antibodies. Ivermectin is used to treat _O. volvulu_s in humans and is rapidly absorbed following oral administration. The primary use of praziquantel, which is rapidly absorbed orally, is in the treatment of infection from flat worms and flukes where it reduces the resistance of the parasite to host immune mechanisms. Zidovudine is also administered orally, but is used for treatment of AIDS, where most of its toxic symptoms are hematologic.
Suramin must be administered intravenously and should be used cautiously in patients with kidney disease. It inhibits protein kinases and dihydrofolate reductase and reduces ATP synthesis. It is used in the treatment of certain extra-intestinal nematodes and is probably one of the most toxic anthelminthic agents.
The other choices are incorrect. Diethylcarbamazine is rapidly absorbed following oral administration and increases the susceptibility of extra-intestinal nematodes to host antibodies. Ivermectin is used to treat _O. volvulu_s in humans and is rapidly absorbed following oral administration. The primary use of praziquantel, which is rapidly absorbed orally, is in the treatment of infection from flat worms and flukes where it reduces the resistance of the parasite to host immune mechanisms. Zidovudine is also administered orally, but is used for treatment of AIDS, where most of its toxic symptoms are hematologic.
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A 42-year-old immigrant from Pakistan comes to your office after his wife noted hypopigmented anesthetic patches on his back. On further examination, you discover bilaterally thickened ulnar nerves. Skin biopsy reveals numerous acid-fast bacilli and a negative lepromin test. What combination of drugs would you recommend for this patient?
A 42-year-old immigrant from Pakistan comes to your office after his wife noted hypopigmented anesthetic patches on his back. On further examination, you discover bilaterally thickened ulnar nerves. Skin biopsy reveals numerous acid-fast bacilli and a negative lepromin test. What combination of drugs would you recommend for this patient?
Leprosy is of two types namely lepromatous and tuberculoid.This patient is suffering from lepromatous leprosy on account of the symmetric nerve involvement, the abundant acid fast bacilli and the negative lepromin test. The course of this subtype is progressive and malignant. In case of tuberculoid leprosy the course is more benign with cellular immunity remaining intact. The skin biopsy shows few bacilli and there is a positive skin test. Combination therapy is recommended for all types of leprosy to avoid the emergence of resistance. Cases of lepromatous leprosy are treated with a combination therapy involving the use of the following:
- Dapsone
- Rifampin
- Clofazimine
This combination is given for 2 to 3 years, ideally till the skin biopsies are negative. Cases of indeterminate (borderline) and tuberculoid leprosy are treated with a combination therapy involving the use of the following:
- Dapsone
- Rifampin
Rifampin for 6 to 12 months followed by dapsone—alone—for 2 years.
Leprosy is of two types namely lepromatous and tuberculoid.This patient is suffering from lepromatous leprosy on account of the symmetric nerve involvement, the abundant acid fast bacilli and the negative lepromin test. The course of this subtype is progressive and malignant. In case of tuberculoid leprosy the course is more benign with cellular immunity remaining intact. The skin biopsy shows few bacilli and there is a positive skin test. Combination therapy is recommended for all types of leprosy to avoid the emergence of resistance. Cases of lepromatous leprosy are treated with a combination therapy involving the use of the following:
- Dapsone
- Rifampin
- Clofazimine
This combination is given for 2 to 3 years, ideally till the skin biopsies are negative. Cases of indeterminate (borderline) and tuberculoid leprosy are treated with a combination therapy involving the use of the following:
- Dapsone
- Rifampin
Rifampin for 6 to 12 months followed by dapsone—alone—for 2 years.
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Foscarent is toxic to which of the following organs?
Foscarent is toxic to which of the following organs?
Foscarent can cause damage to the kidneys. To reduce the damaging effect, the patient may be put on intravenous fluids.
Foscarent can cause damage to the kidneys. To reduce the damaging effect, the patient may be put on intravenous fluids.
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What is acyclovir's mechanism of action?
What is acyclovir's mechanism of action?
Acyclovir is a guanosine analog, which works by inhibiting viral DNA polymerase. This slows down the rate at which viruses can replicate. Acyclovir is used primarily in the treatment of herpes simplex viruses 1 and 2, chickenpox, and shingles.
Acyclovir is a guanosine analog, which works by inhibiting viral DNA polymerase. This slows down the rate at which viruses can replicate. Acyclovir is used primarily in the treatment of herpes simplex viruses 1 and 2, chickenpox, and shingles.
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You are a nurse in a primary care setting. One of your patients is diagnosed with hypercholesterolemia, and after failing to see cholesterol improvements with diet and exercise, is started on atorvastatin. Which of the following best describes the mechanism of action of atorvastatin?
You are a nurse in a primary care setting. One of your patients is diagnosed with hypercholesterolemia, and after failing to see cholesterol improvements with diet and exercise, is started on atorvastatin. Which of the following best describes the mechanism of action of atorvastatin?
The correct answer is "HMG-CoA reductase inhibition," as this is the accurate mechanism of action of atorvastatin, a commonly-prescribed lipid-lowering agent for patients with a number of medical conditions, including hypercholesterolemia. HMG-CoA reductase is an enzyme found within the liver that catalyzes a major reaction involved in cholesterol formation. By inhibiting this enzyme with a medication such as a statin, the new production of LDL cholesterol is decreased, and the number of LDL receptors is upregulated (which decreases circulating LDL, therefore lowering LDL cholesterol).
Atorvastatin is neither an alpha-adrenergic inhibitor, beta-adrenergic inhibitor, PPAR activator (fibrates), or Na-K-2Cl symporter inhibitor (loop diuretics).
The correct answer is "HMG-CoA reductase inhibition," as this is the accurate mechanism of action of atorvastatin, a commonly-prescribed lipid-lowering agent for patients with a number of medical conditions, including hypercholesterolemia. HMG-CoA reductase is an enzyme found within the liver that catalyzes a major reaction involved in cholesterol formation. By inhibiting this enzyme with a medication such as a statin, the new production of LDL cholesterol is decreased, and the number of LDL receptors is upregulated (which decreases circulating LDL, therefore lowering LDL cholesterol).
Atorvastatin is neither an alpha-adrenergic inhibitor, beta-adrenergic inhibitor, PPAR activator (fibrates), or Na-K-2Cl symporter inhibitor (loop diuretics).
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You are a nurse working on an inpatient medicine floor. One of your patients is advised to discuss starting gemfibrozil, a fibrate medication, after he is discharged. Which of the following best describes the mechanism of action of gemfibrozil?
You are a nurse working on an inpatient medicine floor. One of your patients is advised to discuss starting gemfibrozil, a fibrate medication, after he is discharged. Which of the following best describes the mechanism of action of gemfibrozil?
The correct answer is "Peroxisome proliferator-activated receptor (PPAR) activation," as this is the accurate mechanism of action for fibrate medications, such as gemfibrozil. Fibrates are commonly-used medications used to treat high cholesterol, as well as a number of other metabolic abnormalities in patients. Fibrates have the relatively unique property of lowering LDL (the "bad" cholesterol), increasing HDL (the "good" cholesterol), and lowering triglycerides, making them a popular choice when administered either alone, or with statin medications for patients with hypercholesterolemia.
HMG-CoA reductase inhibition is the mechanism of action of statins.
Vitamin-K-dependent clotting factor synthesis inhibition is the mechanism of action of warfarin.
Alpha-adrenergic inhibition is the mechanism of action of phenoxybenzamine, among other medications.
Beta-adrenergic inhibition is the mechanism of action of propranolol, among other medications.
The correct answer is "Peroxisome proliferator-activated receptor (PPAR) activation," as this is the accurate mechanism of action for fibrate medications, such as gemfibrozil. Fibrates are commonly-used medications used to treat high cholesterol, as well as a number of other metabolic abnormalities in patients. Fibrates have the relatively unique property of lowering LDL (the "bad" cholesterol), increasing HDL (the "good" cholesterol), and lowering triglycerides, making them a popular choice when administered either alone, or with statin medications for patients with hypercholesterolemia.
HMG-CoA reductase inhibition is the mechanism of action of statins.
Vitamin-K-dependent clotting factor synthesis inhibition is the mechanism of action of warfarin.
Alpha-adrenergic inhibition is the mechanism of action of phenoxybenzamine, among other medications.
Beta-adrenergic inhibition is the mechanism of action of propranolol, among other medications.
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You are the nurse taking care of a patient hospitalized for a deep vein thrombosis. You are reviewing his discharge medications, and counsel him about the benefits and risks associated with apixaban. Which of the following is a major possible adverse effect associated with apixaban?
You are the nurse taking care of a patient hospitalized for a deep vein thrombosis. You are reviewing his discharge medications, and counsel him about the benefits and risks associated with apixaban. Which of the following is a major possible adverse effect associated with apixaban?
The correct answer is "bleeding."
Apixaban is a novel anti-coagulant medication that functions by directly inhibiting factor Xa in the clotting cascade. You can remember this mechanism of action by noting the letters "Xa" in apiXaban. Apixaban is used with increasing frequency now in the treatment of deep vein thrombosis, pulmonary embolism, and atrial fibrillation. A very serious potential adverse effect of apixaban though is that since it is an anticoagulant agent, it can predispose to serious bleeding events. Furthermore, one of the biggest dangers of apixaban is that there is no readily available antidote for it yet, and as such if a bleeding event occurs, there is no simple way to reverse it, as there is with other anti-coagulants like warfarin or heparin.
Thrombosis, myocardial infarction, and ischemic stroke are all typically thrombotic (e.g. clot-related) issues. Apixaban may be used in the treatment of conditions associated with clotting, but is not known to cause clots, as it is an anti-coagulant.
Apixaban has no known association with bowel movement frequency.
The correct answer is "bleeding."
Apixaban is a novel anti-coagulant medication that functions by directly inhibiting factor Xa in the clotting cascade. You can remember this mechanism of action by noting the letters "Xa" in apiXaban. Apixaban is used with increasing frequency now in the treatment of deep vein thrombosis, pulmonary embolism, and atrial fibrillation. A very serious potential adverse effect of apixaban though is that since it is an anticoagulant agent, it can predispose to serious bleeding events. Furthermore, one of the biggest dangers of apixaban is that there is no readily available antidote for it yet, and as such if a bleeding event occurs, there is no simple way to reverse it, as there is with other anti-coagulants like warfarin or heparin.
Thrombosis, myocardial infarction, and ischemic stroke are all typically thrombotic (e.g. clot-related) issues. Apixaban may be used in the treatment of conditions associated with clotting, but is not known to cause clots, as it is an anti-coagulant.
Apixaban has no known association with bowel movement frequency.
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You are a nurse taking care of a patient during a rapid response call. The patient is bradycardic and you are asked to administer atropine. Which of the following best describes the mechanism of action of atropine?
You are a nurse taking care of a patient during a rapid response call. The patient is bradycardic and you are asked to administer atropine. Which of the following best describes the mechanism of action of atropine?
The correct answer is "Muscarinic acetylcholine receptor antagonist," as this accurately describes the mechanism of action of atropine.
Atropine is an anticholinergic medication used for a number of reasons, including to treat bradycardia, various nerve agent poisonings, and intraoperatively at times to diminish the amount of saliva generated. Typical anticholinergic medication side effects can be associated with atropine including pupil dilation, urine retention, dry mouth, constipation, and tachycardia.
Muscarinic acetylcholine receptor agonist is incorrect as this is the opposite of how atropine works.
Beta-adrenergic blocker is incorrect. This class of medications would actually serve to decrease heart rate, which would be highly dangerous in a patient whose reason for intervention is bradycardia.
Neither alpha-adrenergic blockade nor monoamine oxidase inhibition describes the mechanism of action of atropine.
The correct answer is "Muscarinic acetylcholine receptor antagonist," as this accurately describes the mechanism of action of atropine.
Atropine is an anticholinergic medication used for a number of reasons, including to treat bradycardia, various nerve agent poisonings, and intraoperatively at times to diminish the amount of saliva generated. Typical anticholinergic medication side effects can be associated with atropine including pupil dilation, urine retention, dry mouth, constipation, and tachycardia.
Muscarinic acetylcholine receptor agonist is incorrect as this is the opposite of how atropine works.
Beta-adrenergic blocker is incorrect. This class of medications would actually serve to decrease heart rate, which would be highly dangerous in a patient whose reason for intervention is bradycardia.
Neither alpha-adrenergic blockade nor monoamine oxidase inhibition describes the mechanism of action of atropine.
Compare your answer with the correct one above