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piggy > Micro - Antimicrobials Part 2 > Flashcards

Micro - Antimicrobials Part 2 Flashcards

1
Q

Patients with what enzyme deficiency can suffer additional toxicities of sulfonamide antibiotics?

A

People with glucose-6-phosphate dehydrogenase deficiency will get hemolytic anemia

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2
Q

Sulfonamides can cause which renal pathology?

A

Tubulointerstitial nephritis

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3
Q

What neurologic injury can sulfonamides cause in infants?

A

Kernicterus

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4
Q

How do sulfonamides affect the plasma concentration of albumin-bound drugs such as warfarin?

A

The plasma concentration of warfarin and other drugs is raised by displacement from albumin by sulfonamides

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5
Q

What skin condition can sulfonamides cause?

A

Photosensitivity

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6
Q

Which two drugs inhibit dihydrofolate reductase?

A

Trimethoprim and pyrimethamine

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7
Q

Which drugs can be dosed with sulfonamides for synergistic inhibition of bacterial DNA synthesis?

A

Trimethoprim and pyrimethamine

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8
Q

What reaction is catalyzed by dihydrofolate reductase?

A

The conversion of dihydrofolic acid to tetrahydrofolic acid

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9
Q

Why are trimethoprim and sulfamethoxazole used in combination?

A

To cause the sequential block of folate synthesis and synergistic inhibition of DNA synthesis

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10
Q

Trimethoprim-sulfamethoxazole is used to treat what pulmonary infection of HIV-positive patients?

A

Pneumocystis jirovecipneumonia

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11
Q

Trimethoprim-sulfamethoxazole is used to treat which infections?

A

Recurrent urinary tract infections, Shigella, Salmonella, and (in HIV-positive patients) Pneumocystis jiroveci pneumonia

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12
Q

What part of the body is most affected by the adverse effects of trimethoprim-sulfamethoxazole treatment?

A

The blood cell precursors in bone marrow (remember: TMP Treats Marrow Poorly)

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13
Q

What hematologic toxic effects are seen with the use of trimethoprim-sulfamethoxazole?

A

Megaloblastic anemia, leukopenia, and granulocytopenia (remember: TMP Treats Marrow Poorly)

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14
Q

The toxic bone marrow effects seen with the use of trimethoprim-sulfamethoxazole may be alleviated with the administration of what supplement?

A

Folinic acid

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15
Q

Patients who do not tolerate sulfa drugs should not be given which drugs?

A

Sulfonamide antibiotics, sulfonylureas, sulfasalazine, and most diuretics (including furosemide, thiazides, and acetazolamide)

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16
Q

Name seven examples of fluoroquinolones.

A

Ciprofloxacin, norfloxacin, ofloxacin, sparfloxacin, moxifloxacin, gatifloxacin, and enoxacin

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17
Q

Fluoroquinolones inhibit what enzyme?

A

DNA gyrase (topoisomerase II)

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18
Q

Which organisms are targeted by fluoroquinolones?

A

Gram-negative rods (in the urinary and gastrointestinal tracts) including Pseudomonas, Neisseria, and some gram-positive organisms

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19
Q

Fluoroquinolones are contraindicated in pregnant women and children because of possible damage to what structure?

A

The cartilage (remember: fluoroquinoloneshurt attachments to your Bones)

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20
Q

What musculoskeletal adverse effects are seen in adults with fluoroquinolone toxicity?

A

Tendonitis and tendon rupture

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21
Q

What musculoskeletal complaints do children with fluoroquinolone toxicity have?

A

Leg cramps and myalgias

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22
Q

What is the mechanism of action of metronidazole?

A

Toxic metabolites formed in the bacterial cell damage DNA

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23
Q

Metronidazole is used with what two agents as “triple therapy” against Helicobacter pylori?

A

Bismuth and amoxicillin; another option for triple therapy is omeprazole, amoxicillin, and clarithromycin

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24
Q

What may happen when patients taking metronidazole consume alcohol?

A

Disulfiram-like reaction

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25
Q

Name two common adverse effects of metronidazole.

A

Headache and metallic taste

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26
Q

Name six infections that are treated using metronidazole.

A

Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes, Helicobacter pylori (remember: GET GAP on the Metro)

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27
Q

What is the mechanism of action of polymyxins?

A

They bind to the cell membrane, disrupting the osmotic properties of the bacterial cell (remember: PolyMYXins MIXup membranes)

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28
Q

Polymyxins are _____ (anionic/cationic) basic proteins that act like _____ (detergents/enzymes).

A

Cationic; detergents

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29
Q

What kind of infection are polymyxins used to treat?

A

Resistant gram-negative infections

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30
Q

What are the two major toxicities of polymyxins?

A

Neurotoxicity and acute renal tubular necrosis

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31
Q

What antimicrobial is used as prophylaxis against Mycobacterium tuberculosis infection?

A

Isoniazid

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32
Q

What antimicrobial is used as prophylaxis against Mycobacterium avium-intracelulare infection?

A

Azithromycin

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33
Q

Which drugs can be used to treat Mycobacterium leprae infection?

A

Dapsone, rifampin, and clofazimine

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34
Q

What are the four medications commonly used to treat Mycobacterium avium-intracellulare infection?

A

Azithromycin, rifampin, ethambutol, and streptomycin

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35
Q

Name five drugs that are commonly used as first-line antituberculosis treatment.

A

Isoniazid (INH), Streptomycin, Pyrazinamide, Rifampin, Ethambutol (remember: INH-SPiRE)

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36
Q

All antituberculosis drugs have what potential toxicity?

A

Hepatotoxicity

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37
Q

Name an important adverse effect of ethambutol.

A

Optic neuritis causing red-green color blindness

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38
Q

Ketoconazole can be used to treat which four systemic fungal infections?

A

Blastomycosis, coccidioidomycosis, histoplasmosis, and candidal infection

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39
Q

Aside from treating fungal infection, what else can ketoconazole be used to treat?

A

Hypercortisolism, due to its inhibition of hormone synthesis

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40
Q

What three toxicities are associated with the use of azole drugs?

A

The inhibition of hormone synthesis (gynecomastia), liver dysfunction (the inhibition of cytochrome P450), and fevers/chills

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41
Q

What two azoles are commonly used to treat topical fungal infections?

A

Clotrimazole and miconazole

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42
Q

Name six azole antifungal drugs.

A

Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole and voriconazole

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43
Q

Flucytosine works by inhibiting _____ synthesis by conversion to 5-fluorouracil, which competes with _____.

A

DNA; uracil

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44
Q

Clinically, flucytosine is used to treat what broad category of infections?

A

Systemic fungal infections such as Candida and Cryptococcus

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45
Q

What toxicities are associated with flucytosine treatment?

A

Nausea, vomiting, diarrhea, and bone marrow suppression; flucytosine is an antimetabolite and has many of the same toxicities as chemotherapy

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46
Q

Which drug is flucytosine frequently paired with to treat systemic fungal infections?

A

Amphotericin B

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47
Q

How does caspofungin work?

A

Inhibits the synthesis of -glucan, which inhibits synthesis of the fungal cell wall

48
Q

Clinically, caspofungin is used when a patient in infected with what organism?

A

Invasive aspergillus infections

49
Q

Terbinafine inhibits which enzyme?

A

Squalene epoxidase

50
Q

Terbinafine is used as treatment for infection with what organisms?

A

Terbinafine is used as treatment for infection with what organisms?
Dermatophytoses (onychomycosis)

51
Q

By interfering with microtubule function, griseofulvin disrupts which biologic process in fungi?

A

Mitosis

52
Q

Griseofulvin deposits in which tissues?

A

Keratin (nails); therefore, it is helpful in treatment of onychomycosis

53
Q

Griseofulvin is used to treat which infections?

A

Superficial dermatophyte infection (ringworm, tinea)

54
Q

Griseofulvin _____ (increases/decreases) warfarin metabolism because it _____ (increases/decreases) the activity of cytochrome P450.

A

Increases; increases

55
Q

Name three toxicities associated with griseofulvin.

A

Headaches, confusion, and carcinogenicity

56
Q

What patient population should griseofulvin not be given to?

A

Pregnant mothers (it is teratogenic)

57
Q

Uncoating of a virus is blocked by which antiviral agent?

A

Amantadine

58
Q

Amantadine specifically treats which infection by blocking viral uncoating?

A

Influenza A

59
Q

Nucleic acid synthesis is blocked by which two antiviral classes?

A

Purine/pyrimidine analogs and reverse transcriptase inhibitors; usually antiretroviral drugs

60
Q

Viral release from cells is blocked by which group of antiviral inhibitors?

A

Neuraminidase inhibitors (influenza)

61
Q

What is the mechanism of action of amantadine when used as an antiviral agent?

A

Blocking viral penetration/uncoating (remember: “a man to dine” takes off his coat)

62
Q

Amantadine is used to treat which two diseases?

A

Influenza A and Parkinsons disease

63
Q

What three toxicities are associated with amantadine?

A

Ataxia, dizziness, and slurred speech; (remember: Amantadine blocks influenza A, and rubellA and causes problems with the cerebellA)

64
Q

Which has fewer central nervous system adverse effects, amantadine or rimantidine?

A

Rimantidine, because it does not cross the blood-brain barrier

65
Q

What is the mechanism of viral resistance to amantadine?

A

Mutated M2 protein has made 90% of all influenza A strains resistant to amantadine

66
Q

In addition to use as an antiviral agent, why is amantadine useful in Parkinsons disease?

A

It causes release of dopamine from nerve terminals

67
Q

Which enzymes do zanamivir and oseltamivir (Tamiflu) inhibit?

A

Influenza neuraminidase, decreasing release of progeny virus

68
Q

Which strains of influenza do zanamivir and oseltamivir (Tamiflu) inhibit?

A

Both influenza A and B

69
Q

The mechanism of action of ribavirin is through inhibiting the synthesis of _____ nucleotides by competitively inhibiting the enzyme _____ _____ _____.

A

Guanine; inosine monophosphate dehydrogenase

70
Q

Which two infections is ribavirin used to treat?

A

Chronic hepatitis C virus and respiratory syncytial virus

71
Q

What is a potential toxicity of ribavirin use?

A

Hemolytic anemia

72
Q

What patient population should ribavirin not be given to?

A

Pregnant mothers (it is teratogenic)

73
Q

What is the mechanism of action of acyclovir?

A

Acyclovir is a guanosine analog that terminates chains of viral DNA into which it is incorporated

74
Q

Name three viruses for which acyclovir is used.

A

Herpes simplex virus, varicella zoster virus, and Epstein-Barr virus

75
Q

Should acyclovir be used to treat herpes zoster?

A

No; famciclovir is more effective

76
Q

What is the mechanism of resistance developed by viruses to counteract acyclovir?

A

Loss of viral thymidine kinase

77
Q

True or False? Acyclovir is effective against latent herpes simplex virus and varicella-zoster virus infections.

A

False; it has no effect on latent forms of these infections

78
Q

Acyclovir is used to treat herpes infections in what areas/organs?

A

Mucocutaneous (cold sores), genital, herpes simplex virus encephalitis

79
Q

Why does acyclovir interfere with viral DNA synthesis and not human DNA synthesis?

A

Acyclovir requires monophosphorylation by herpes simplex virus/varicella zoster virus thymidine kinase and formation of a triphosphate form by cellular enzymes

80
Q

How do viruses develop resistance to acyclovir?

A

Lack of thymidine kinase

81
Q

How does ganciclovir work?

A

Ganciclovir is a guanosine analog that inhibits viral DNA polymerase

82
Q

Which viral infection is ganciclovir used to treat?

A

Cytomegalovirus (in immunocompromised patients)

83
Q

What four toxicities are associated with ganciclovir use?

A

Leukopenia, neutropenia, thrombocytopenia, and renal toxicity

84
Q

Leukopenia, neutropenia, thrombocytopenia, and renal toxicity

A

Mutated viral DNA polymerase, lack of viral kinase

85
Q

Which drug is more toxic, acyclovir or ganciclovir?

A

Ganciclovir

86
Q

What modifications must ganciclovir undergo before becoming active?

A

Formation of a 5’ -monophosphate by either herpes simplex virus/varicella zoster virus thymidine kinase or cytomegalovirus viral kinase and a triphosphate by cellular kinases; this process ensures that it targets viral replication and spares human cells.

87
Q

Foscarnet ____ (does/does not) require activation via phosphorylation by viral kinase.

A

Does not

88
Q

Foscarnet inhibits viral _____ (DNA/RNA) polymerase by binding to the _____ binding site of viral kinase.

A

DNA; pyrophosphate (remember: FOScarnet is a pyroFOSphate analog)

89
Q

For which two infections is foscarnet used?

A

Cytomegalovirus retinitis in the immunocompromised and acyclovir-resistant herpes simplex virus

90
Q

What is the major toxicity of foscarnet?

A

Nephrotoxicity

91
Q

Mutation in which enzyme allows cytomegalovirus or herpes simplex virus to be resistant to foscarnet treatment?

A

DNA polymerase

92
Q

Protease inhibitors end in which suffix?

A

-navir (remember: NAVIR [never] Tease a ProTEASEinhibitor)

93
Q

Name five protease inhibitors.

A

Saquinavir, ritonavir, indinavir, nelfinavir, and amprenavir

94
Q

What are the major toxicities of most protease inhibitors?

A

Gastrointestinal intolerance (nausea, diarrhea), hyperglycemia, and lipid abnormalities

95
Q

What adverse effect is specific to indinavir?

A

Thrombocytopenia

96
Q

Name six nucleoside reverse transcriptase inhibitors.

A

Zidovudine, didanosine, zalcitabine, stavudine, lamivudine, and abacavir (remember: Have YOU DINED[vudine] with my NUCLEAR family?)

97
Q

Name three nonnucleoside reverse transcriptase inhibitors.

A

Nevirapine, Efavirenz, Delavirdine (remember: Never Ever Deliver nucleosides)

98
Q

Reverse transcriptase inhibitors prevent which viral process from occurring?

A

Incorporation of viral DNA into the host genome

99
Q

What toxicities are associated with both nucleoside and nonnucleoside reverse transcriptase inhibitors?

A

Neutropenia, anemia, and peripheral neuropathy

100
Q

Which cause lactic acidosis: nucleoside reverse transcriptase inhibitors or nonnucleoside reverse transcriptase inhibitors?

A

Nucleoside reverse transcriptase inhibitors

101
Q

Which cause rash: nucleoside reverse transcription inhibitors or nonnucleoside reverse transcriptase inhibitors?

A

Nonnucleoside reverse transcriptase inhibitors

102
Q

What nucleoside reverse transcriptase inhibitor used to treat HIV can cause a megaloblastic anemia?

A

Zidovudine

103
Q

What is the name of the combination therapy that is used to treat HIV and that includes a cocktail of protease inhibitors and reverse transcriptase inhibitors?

A

Highly active antiretroviral therapy

104
Q

Which nucleoside reverse transcriptase inhibitor is used for general prophylaxis and during pregnancy to reduce fetal transmission risk?

A

Zidovudine

105
Q

At what point should highly active antiretroviral therapy be initiated in an HIV-positive individual?

A

When the viral load is high or when CD4+ cell count is < 500 cells/mm³

106
Q

In the treatment of HIV infection, what viral process does enfuvirtide inhibit?

A

Fusion

107
Q

What toxicities are associated with enfuvirtide?

A

Hypersensitivity reactions, subcutaneous injection site reaction, increased risk of bacterial pneumonia

108
Q

How does enfuvirtide block entry and replication of viruses?

A

Binding the gp41 subunit, inhibiting the conformational shift required for CD4 cell fusion

109
Q

When is enfuvirtide used clinically?

A

It is added to other antiretroviral drugs when standard regimens have failed

110
Q

How can the bone marrow suppression associated with reverse transcriptase inhibitors be reduced?

A

By treatment with granulocyte-macrophage colony-stimulating factor and erythropoietin

111
Q

What viral process is blocked by enzyme inhibition with protease inhibitors?

A

Maturation of new viruses

112
Q

What are interferons?

A

Endogenous human glycoproteins that induce an anti-viral state in cells

113
Q

What two clinical conditions are treated by interferon therapy?

A

Chronic hepatitis B and C virus infections and Kaposi sarcoma

114
Q

What clinical condition is treated by interferon beta-1a therapy?

A

Multiple sclerosis

115
Q

What clinical condition is treated by interferon γ therapy?

A

Nicotinamide adenine dinucleotide phosphate oxidase deficiency

116
Q

What is the major toxicity of the interferons?

A

Neutropenia

117
Q

In addition to blocking viral DNA and RNA synthesis, interferons also induce what enzyme to encourage viral mRNA degradation?

A

Ribonuclease

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