Pharmacology Final Practice

132 Questions

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Pharmacology Quizzes & Trivia

Questions and Answers
  • 1. 
    Characteristics of viruses:
    • A. 

      Obligate intracellular parasites that consist of double or single stranded DNA or RNA enclosed in a capsid

    • B. 

      Have lipid envelope that may contain antigenic glycoproteins

    • C. 

      Hijack host metabolic machinery

    • D. 

      Single stranded RNA only

  • 2. 
    Effective anti-viral Rx:
    • A. 

      target virus specific steps in viral replication processes

    • B. 

      Specifically inhibit virus-directed nucleic acid or protein synthesis

    • C. 

      Non-specific toxicity

    • D. 

      Selective toxicity

  • 3. 
    Anti-influenza agents:
    • A. 

      Amantadine

    • B. 

      Oseltamivir

    • C. 

      Adefovir

    • D. 

      Rimantadine

    • E. 

      Zanamivir

  • 4. 
    Anti-hepatitis Agents:
    • A. 

      Adefovir

    • B. 

      Cidofovir

    • C. 

      Entecavir

    • D. 

      Interferon

    • E. 

      Lamivudine

    • F. 

      Telbivudine

  • 5. 
    Anti-herpes virus Agents:
    • A. 

      Acyclovir

    • B. 

      Cidofovir

    • C. 

      Famciclovir

    • D. 

      Fomivirsen

    • E. 

      Zanamivir

    • F. 

      Foscarnet

  • 6. 
    Anti-herpes virus Agents:
    • A. 

      Ganciclovir

    • B. 

      Penciclovir

    • C. 

      Interferon

    • D. 

      Valacyclovir

    • E. 

      Valganciclovir

    • F. 

      Vadarabine

  • 7. 
    HSV-1:
    • A. 

      Mouth

    • B. 

      Face

    • C. 

      Skin

    • D. 

      Esophagus

    • E. 

      Hands

    • F. 

      Brain

  • 8. 
    HSV-2:
    • A. 

      Genitals

    • B. 

      Rectum

    • C. 

      Hands

    • D. 

      Menenges

    • E. 

      Brain

  • 9. 
    VZV:
    • A. 

      Cause chicken pox

    • B. 

      Cause shingles

    • C. 

      Cause retinitis

    • D. 

      Cause helminths

  • 10. 
    Rx for herpes simplex viruses act during acute phase of viral infection; with little/no efficacy during latent phase.
    • A. 

      True

    • B. 

      False

  • 11. 
    Acyclovir is the "prototype" anti-herpes Rx.
    • A. 

      True

    • B. 

      False

  • 12. 
    Acyclovir MOA:
    • A. 

      Inhibits viral RNA synthesis

    • B. 

      Guanosine analog that is converted to monophosphate form via viral thymidine kinase

    • C. 

      Acyclovir converted to the di- and tri-phosphate forms by the host cell

    • D. 

      Acyclovir tri-phosphate competes with dGTP as a substrate for viral DNA polymerase and incorporated into viral DNA --> premature DNA chain termination

    • E. 

      Acyclovir tri-phosphate irreversibly binds to the DNA polymerase, thereby inactivating the enzyme

  • 13. 
    Acyclovir Resistance:
    • A. 

      Absence or partial production of viral thymidine kinase

    • B. 

      Altered thymidine kinase substrate specificity

    • C. 

      Altered viral DNA polymerase

  • 14. 
    Acyclovir resistance in VZV due to mutations in thymidine kinase and often via mutations in DNA polymerase.
    • A. 

      True

    • B. 

      False

  • 15. 
    CMV is resistant to acyclovir since it lacks a specific viral thymidine kinase.
    • A. 

      True

    • B. 

      False

  • 16. 
    Famciclovir & Penciclovir:
    • A. 

      Acyclic guanosine nucleoside derivatives

    • B. 

      Famciclovir is orally active

    • C. 

      Penciclovir only administered topically

  • 17. 
    Famciclovir & Penciclovir MOA:
    • A. 

      Famiclovir is metabolized to penciclovir

    • B. 

      Penciclovir is monophosphorylated by viral thymidine kinase

    • C. 

      Cellular enzymes convert to triphosphate form

    • D. 

      Inhibits HSV RNA polymerase

  • 18. 
    Ganciclovir:
    • A. 

      Use against CMV

    • B. 

      Convert to triphosphate form by viral and host enzymes (uses protein kinase phosphotransferase)

    • C. 

      Inhibits viral DNA polymerase

    • D. 

      Incorporated into DNA and decrease rate of chain elongation

    • E. 

      Resistance increases with duration of Rx

  • 19. 
    CMV is deficient in thymidine kinase and uses protein kinase phosphotransferase.
    • A. 

      True

    • B. 

      False

  • 20. 
    Cidofovir:
    • A. 

      Treatment of CMV retinitis in AIDS patients

    • B. 

      Nucleotide analog of guanosine

    • C. 

      Phosphorylation not dependent upon viral enzymes

    • D. 

      IV, intravitreal and topical formulations

    • E. 

      Significant risk of liver toxicity

  • 21. 
    Fomivirsen:
    • A. 

      Antisense oligonucleotide (21 bp) directed against CMV mRNA

    • B. 

      Complementary to the mRNA sequence for major immediate-early transcriptional region of CMV → inhibits CMV replication

    • C. 

      Active against CMV strains resistant to ganciclovir, cidofovir & foscarnet

    • D. 

      2-4 week washout following cidofovir therapy is recommended to ↓ toxicity

  • 22. 
    Classes of Respiratory Virus Infections Rx based upon MOA:
    • A. 

      Inhibitors of viral un-coating

    • B. 

      Inhibitors of neuraminidase

    • C. 

      Inhibitors of RNA capping and function

  • 23. 
    Influenza A is the only form that causes pandemics.
    • A. 

      True

    • B. 

      False

  • 24. 
    Amantadine & Rimantadine:
    • A. 

      Tricyclic amines

    • B. 

      Use for Influenza A only

    • C. 

      70-90% effective in preventing infection if Rx is begun at time of, or prior to, exposure of the virus

    • D. 

      Decrease duration & severity of symptoms if started within 1st 48 hours after exposure to the virus

    • E. 

      Especially useful for high-risk patients who have not been vaccinated during epidemics

  • 25. 
    Amantadine & Rimantadine MOA:
    • A. 

      Inhibits uncoating of the viral RNA within infected host cells → prevents replication

    • B. 

      Block M2

    • C. 

      Block M1

    • D. 

      Inhibits neuraminidase

  • 26. 
    Oseltamivir & Zanamivir:
    • A. 

      Sialic acid analogs

    • B. 

      Antiviral spectrum: Influenza A and B viruses

    • C. 

      Resistance is associated with mutations in hemagglutinin and/or neuraminidase genes

    • D. 

      Most effective when administered within 24-28 hours after infection

  • 27. 
    Cleavage of sialic acid residues via neuraminidase is essential for release of virus from infected cells.
    • A. 

      True

    • B. 

      False

  • 28. 
    Oseltamivir & Zanamivir MOA:
    • A. 

      Neuraminidase inhibitors

    • B. 

      Competitively and reversibly interact with the active neuraminidase enzyme site to inhibit it’s activity

    • C. 

      Virons aggregation at the internal surface of infected cells (they cannot be released)

    • D. 

      Inhibits viral un-coating

  • 29. 
    Anti-influenza viral activities of active drug include:
    • A. 

      Inhibits guanosine triphosphate formation

    • B. 

      Prevents mRNA capping

    • C. 

      Blocks RNA-dependent RNA polymerase

    • D. 

      Inhibits cytosine triphosphate formation

  • 30. 
    Ribavirin:
    • A. 

      Synthetic guanosine analog

    • B. 

      Anti-viral spectrum: broad spectrum of DNA and RNA viruses

    • C. 

      Oral administration for hepatitis E virus

    • D. 

      Aerosolized formulation administered via nebulizer to children and infants with severe RSV bronchiolitis or pneumonia

  • 31. 
    Hepatitis B & C are most common causes of chronic hepatitis, cirrhosis and hepatocellular carcinoma.
    • A. 

      True

    • B. 

      False

  • 32. 
    Hepatitis B & C:
    • A. 

      5% of world’s population are carriers for HBV

    • B. 

      3% of world’s population is infected with HCV

    • C. 

      HBV & HCV transmssion → blood-borne

    • D. 

      Current therapies for Hepatitis B & C are suppressive rather than curative

  • 33. 
    Interferonsm (α, β, γ):
    • A. 

      Host cytokines that exert complex antiviral, immunomodulatory and antiproliferative effects

    • B. 

      Synthesized by host cells in response to various inducer stimuli

    • C. 

      Cause biochemical changes that result in reduced ability of viruses to infect cells

    • D. 

      Injectable pegylated formulations (s.c, i.m) of IFNα (IFN α-2a and α-2b) are approved for treatment of HBV and HCV infections

  • 34. 
    Interferon MOA:
    • A. 

      Bind to specific IFN receptors and signal via JAK/STAT signaling pathways

    • B. 

      Nuclear translocation of cellular protein complex

    • C. 

      Bind to genes containing IFN-specific response element

    • D. 

      Synthesis > 24 proteins which contribute to viral resistance

  • 35. 
    Interferon MOA:
    • A. 

      Inhibit viral penetration

    • B. 

      Inhibit viral gene transcription

    • C. 

      Inhibit viral protein translation

    • D. 

      Inhibit viral protein processing

    • E. 

      Inhibit virus maturation

  • 36. 
    Adefovir Dipivoxil MOA:
    • A. 

      Treatment of HBV

    • B. 

      Adefovir dipivoxil enters cells and is de-esterified to adefovir

    • C. 

      Converted to tri-phosphate form which is a competitive inhibitor of viral DNA polymerase and reverse transcriptase (vs. dATP) and serves as chain terminator to viral DNA synthesis

    • D. 

      Q.d. dosing possible as di-phosphate form has long intracellular t1/2

    • E. 

      Resistance: point mutation in HBV polymerase

  • 37. 
    Lamivudine:
    • A. 

      Competitive inhibitor of HBV DNA polymerase

    • B. 

      Inhibits HIV reverse transcriptase

    • C. 

      Enhanced antiviral activity w/combo RX (adefovir or penciclovir) against hepatic adenoviruses

    • D. 

      Potently and rapidly induces viral suppression

    • E. 

      Chronic Rx associated w/lamivudine resistant strains

  • 38. 
    Although many anti-viral compounds show antiviral activity in vitro, most affect some host cell function and are associated with unacceptable toxicity in human beings.
    • A. 

      True

    • B. 

      False

  • 39. 
    Effective anti-viral agents typically have a restricted spectrum of antiviral activity and target a specific viral protein.
    • A. 

      True

    • B. 

      False

  • 40. 
    Single-nucleotide changes leading to critical amino acid substitutions in a target protein often are sufficient to cause antiviral drug resistance.
    • A. 

      True

    • B. 

      False

  • 41. 
    Current anti-viral agents inhibit active replication, so viral replication may resume following drug removal.
    • A. 

      True

    • B. 

      False

  • 42. 
    Current anti-viral agents do not eliminate non-replicating or latent virus.
    • A. 

      True

    • B. 

      False

  • 43. 
    Clinical efficacy depends on achieving inhibitory concentrations at the site of infection, usually within infected cells.
    • A. 

      True

    • B. 

      False

  • 44. 
    HIV-related disease:
    • A. 

      Human immunodeficiency viruses are lentiviruses

    • B. 

      Replication is constant following infection

    • C. 

      Current treatment strategies assume that all aspects of disease derive from direct toxic effects of HIV on host cells →CD4+ T-lymphocytes

    • D. 

      Humans are only known hosts

  • 45. 
    Most of AIDS epidemic involves HIV-1 and HIV-2.
    • A. 

      True

    • B. 

      False

  • 46. 
    Therapies for treatment of HIV infection:
    • A. 

      Goals of modern Rx: suppress replication of HIV and restore the number of CD4+ cells and immunocompentency to the patient

    • B. 

      Multi-drug regimen: “highly active antiretroviral therapy” or HAART

    • C. 

      Antiviral agents

  • 47. 
    Classes of antiretroviral Rx:
    • A. 

      Nucleoside & nucleotide reverse transcriptase inhibitors (NTRIs)

    • B. 

      Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

    • C. 

      Protease inhibitors

    • D. 

      Entry inhibitors

    • E. 

      Integrase inhibitors

  • 48. 
    Nucleoside/Nucleotie reverse transcriptase inhibitors (NRTIs):
    • A. 

      Competitive inhibition of HIV-1 reverse transcriptase

    • B. 

      NRTIs prevent infection of susceptible cells but have no effect on infected cells

    • C. 

      Require phosphorylation to triphosphate analog

    • D. 

      Block viral replication by competitively inhibiting incorporation of native nucleotides

    • E. 

      Block viral replication by terminating elongation of nascent proviral DNA as they lack a 3’-hydroxyl group

    • F. 

      Typical resistance mutations include M184V, L74V, D67N and M41L

  • 49. 
    All NRTIs may be associated with mitochondrial toxicity.
    • A. 

      True

    • B. 

      False

  • 50. 
    Nonnucleoside reverse transcriptase inhibitors (NNRTIs):
    • A. 

      Highly selective competitive inhibitors of HIV-1 and HIV-2 reverse transcriptase

    • B. 

      Bind directly to HIV-1 reverse transcriptase at a site adjacent to the active site

    • C. 

      Inducing a conformational change resulting in allosteric enzyme inhibition

    • D. 

      NNRTIs neither compete with nucleoside triphosphates nor require phosphorylation to be active

  • 51. 
    The major advantage of NNRTIs is its lack of effect on host blood-forming elements and lack of cross resistance with NRTIs.
    • A. 

      True

    • B. 

      False

  • 52. 
    Which of the following are NRTIs:
    • A. 

      Zidovudine/AZT

    • B. 

      Abacavir

    • C. 

      Didanosine

    • D. 

      Tenofovir

    • E. 

      Lamivudine

  • 53. 
    Which of the following are NNRTIs:
    • A. 

      Delavirdine

    • B. 

      Etravirine

    • C. 

      Efavirenz

    • D. 

      Saquinavir

  • 54. 
    Resistance of NNRTIs:
    • A. 

      K103N and Y181C mutations confer resistance across the entire class of NNRTIs except for etravirine

    • B. 

      L100I and Y188C mutations may confer cross-resistance across the entire drug class

    • C. 

      No cross-reactivity w/NRTIs

  • 55. 
    Protease Inhibitors MOA:
    • A. 

      Noncompetitively inhibit protease inhibitors

    • B. 

      Prevent the post-translational cleavage of Gag and Pol polyproteins

    • C. 

      Prevent the processing of viral proteins into functional form

    • D. 

      Production of immature, non-infectious viral particles.

    • E. 

      Active against HIV-1 & HIV-2

  • 56. 
    Protease inhibitors:
    • A. 

      A syndrome of redistribution and accumulation of body fat →central obesity, “buffalo hump”, cushings-like symptoms

    • B. 

      Most HIV protease inhibitors are substrates for the P-gp efflux pump (found in BBB) → limits brain penetration

    • C. 

      DDI are significant problem →All PI drugs are extensively metabolized by CYP3A4; some are substrates as well as inhibitors

  • 57. 
    Viral attachment to the host cell involves:
    • A. 

      Binding of the viral envelope glycoprotein complex gp160 (gp 120 + gp 41) to it’s receptor, CD4

    • B. 

      Binding induces conformational change in gp120→access to chemokine co-receptors, CCR5 or CXCR4

    • C. 

      Co-receptor binding induces further conformational changes in gp120→allows exposure of gp41 → fusion of viral envelope w/host cell membrane → entry of viral core into the cellular cytoplasm

    • D. 

      Binding of the viral envelope glycoprotein complex gp160 (gp 140 + gp 21) to it’s receptor, CD4

  • 58. 
    Which of the following are Protease inhibitors:
    • A. 

      Saquinavir

    • B. 

      Indinavir

    • C. 

      Enfuvirtide

    • D. 

      Maraviroc

  • 59. 
    Integrase inhibitors:
    • A. 

      Raltegravir specifically binds to, and inhibits integrase

    • B. 

      Resistance: Occurs with mono-Rx. Requires only single point mutation at codons 148 or 155

    • C. 

      Metabolized via UGT1A1-mediated glucuronidation; does not interact w/CYP P450 enzymes

    • D. 

      Polyvalent cations (e.g. Mg2+, Ca2+ ) may bind integrase inhibitors and alter activity

    • E. 

      DDI possible w/drugs that are strong inducers or inhibitors of UGT1A1

  • 60. 
    Chemotherapy has been the only practical way to both treat infected individuals and reduce transmission of parasitic infections.
    • A. 

      True

    • B. 

      False

  • 61. 
    Opportunistic infections with protozoa are prominent in:
    • A. 

      Infants

    • B. 

      Individuals with cancer

    • C. 

      Transplant recipients

    • D. 

      Persons with HIV infections

    • E. 

      Those receiving immunosuppressive drugs or extensive antibiotic therapy

  • 62. 
    Amebiasis:
    • A. 

      Infections caused by Entamoeba dispar (90%) and Entamoeba histolytica

    • B. 

      Humans only known hosts; fecal-oral route of infection

    • C. 

      Ingested E. histolytica cysts from contaminated food or water survive acid gastric contents

    • D. 

      Transform into trophozoites in the large intestine

  • 63. 
    Only E. histolytica infections cause human disease.
    • A. 

      True

    • B. 

      False

  • 64. 
    Classes of Amebiasis Rx:
    • A. 

      Luminal

    • B. 

      Systemic

    • C. 

      Mixed

    • D. 

      Cilliary

  • 65. 
    Luminal is effective against amebas in liver and intestinal wall.
    • A. 

      True

    • B. 

      False

  • 66. 
    Metronidazole:
    • A. 

      Nitroimidizone compound that is mixed amebicide of choice for treating amebic infections as it kills E. histolytica trophozoites

    • B. 

      Taken up by the parasite and is non-enzymatically reduced by reacting with reduced ferredoxin

    • C. 

      Reduction causes the production of reduced cytotoxic compounds that bind to protein and DNA→ cell death

  • 67. 
    Which of the following are mixed amebicides:
    • A. 

      Metronidazole

    • B. 

      Tinidazole

    • C. 

      Iodoquinol

  • 68. 
    Which of the following are Luminal Amebicides:
    • A. 

      Iodoquinol

    • B. 

      Chloroquine

    • C. 

      Paromomycin sulfate

  • 69. 
    A luminal amebicides should be administered for asymptomatic colonization state following the treatment of invasive intestinal or extra-intestinal amebic disease is complete.
    • A. 

      True

    • B. 

      False

  • 70. 
    Iodoquinol:
    • A. 

      Halongenated 8-hydroxy quinolone

    • B. 

      Amebicidal against E. histolytica (luminal trophozoites and cyst forms)

    • C. 

      Chelate ferrous ions required for metabolism

  • 71. 
    Paromomycin sulfate:
    • A. 

      Aminoglycoside antibiotic effective only against luminal forms of E. histolytica (and tapeworm)

    • B. 

      Not significantly absorbed from the GI tract

    • C. 

      Blocks protein synthesis

  • 72. 
    Systemic Amebicides:
    • A. 

      Chloroquine + metronidazole + diloxanide furoate cocktail

    • B. 

      Emetine and dehydroemetine

    • C. 

      Metronidazole + Tinidazole

  • 73. 
    Chloroquine + metronidazole + diloxanide furoate cocktail:
    • A. 

      Treat and prevent amebic liver abscesses

    • B. 

      Eliminates trophozoites in liver abscesse

    • C. 

      Not useful in treating luminal amebiasis

  • 74. 
    Emetine and dehydroemetine:
    • A. 

      Protein synthesis inhibitors that block chain elongation

    • B. 

      Due to major toxicity, used only under unusual circumstances where severe amebiasis requires effective therapy and metronidazole cannot be use

    • C. 

      Should be used for minimal treatment period (3-5 d) under supervision

  • 75. 
    Trypanosomiasis:
    • A. 

      Trypanosomiasis (African sleeping sickness)

    • B. 

      Chagas’ disease (Central & South American)

    • C. 

      Available therapies for are seriously deficient in efficacy, safety, or both

  • 76. 
    Trypanosomiasis (African Sleeping Sickness):
    • A. 

      Caused by Trypanosoma brucei gambiense and Trypanosoma brucei rhodiense

    • B. 

      Transmitted via bite of the tsetse fly

    • C. 

      Live and grow in blood → CNS → inflammation of brain and spinal cord →lethargy → continuous sleep

    • D. 

      Stage 1: fever, enlarged lymph nodes & spleen, myocarditis

  • 77. 
    Pentamidine isethionate:
    • A. 

      Drug of choice to treat early hemolymphatic stage of West African sleeping sickness (T. brucei gambiense)

    • B. 

      Inferior to suramin for treatment of early East African sleeping sickness (T. brucei rhodiense)

    • C. 

      Should be used for Stage 2 disease w/CNS involvement

  • 78. 
    Pentamidine isethionate MOA:
    • A. 

      T. brucei concentrate pentamidine via energy-dependent, high affinity uptake system

    • B. 

      MOA not well defined, but drug appears to bind to parasite DNA

    • C. 

      Interferes w/DNA, RNA and protein synthesis

  • 79. 
    Suramin:
    • A. 

      Used in the prophylaxis and early treatment of African sleeping sickness

    • B. 

      Highly reactive; inhibits many enzymes involved in energy metabolism e.g. glycerol phosphate dehydrogenase

    • C. 

      Requires close patient monitoring

  • 80. 
    Melarsoprol:
    • A. 

      Derivative of mersalyl oxide, a trivalent arsenical

    • B. 

      Use limited to treatment of late Stage 1 sleeping sickness

    • C. 

      MOA: reacts with sulfhydryl groups of enzymes (parasite and host)

    • D. 

      Resistance due to ↓ permeability

    • E. 

      Mammalian cells may be less permeable to drug vs. parasite

    • F. 

      Parasite enzymes appear more sensitive to the drug

  • 81. 
    Which of the following are treatment of African sleeping sickness:
    • A. 

      Suramin

    • B. 

      Melarsoprol

    • C. 

      Pentamidine isethionate

  • 82. 
    Chaga's disease:
    • A. 

      Caused by Trypanosoma cruzi (flagellate protozoan)

    • B. 

      Primarily transmitted by feces of bugs e.g. “kissing bug”

    • C. 

      No vaccine available; management via insecticides

    • D. 

      Acute may be asymptomatic and is largely undiagnosed

    • E. 

      Chronic disease (may take many years to develop)

  • 83. 
    Nifurtimox:
    • A. 

      Least commonly prescribed drug to treat Chagas’ (acute stage disease)

    • B. 

      Efficacy for treatment of chronic stage is poor

    • C. 

      MOA: oxidative stress → futile redox cycling

    • D. 

      Suppressive, not curative, therapy

  • 84. 
    Benznidazole:
    • A. 

      Recommended for prophylaxis in hematopoietic stem cell transplant recipients (donors may not be treated/cured)

    • B. 

      MOA: may involve oxidative stress (inhibit specific reductase enzymes)

    • C. 

      Nitroimidizone derivative that is alternative choice for treatment of acute and indeterminate phases of Chagas’ disease

  • 85. 
    Leishmaniasis:
    • A. 

      Major syndromes : cutaneous, mucocutaneous, diffuse cutaneous, and visceral (kala azar) forms

    • B. 

      The mucocutaneous, diffuse cutaneous, and visceral forms of the disease do not resolve without therapy

    • C. 

      Cutaneous forms of leishmaniasis generally are self-limiting, with cures occurring 3-18 mo. post- infection

    • D. 

      Visceral leishmaniasis caused by L. donovani is fatal unless treated

  • 86. 
    Which of the following are used for Chaga's infection:
    • A. 

      Nifurtimox

    • B. 

      Benznidazole

    • C. 

      Miltefosine

  • 87. 
    Sodium stibogluconate:
    • A. 

      First line therapy for cutaneous and visceral leishmaniasis

    • B. 

      MOA: not well established. Some evidence for inhibition of glycolysis via phosphofructokinase inhibition.

    • C. 

      Requires parenteral administration

  • 88. 
    Miltefosine:
    • A. 

      Potential targets include protein kinase C and lipid and phosphatidylcholine biosynthesis pathways

    • B. 

      Resistance associated with a point mutation in the expression of a miltefosine transporter, specifically a P-type ATPase, leading to ↓ uptake of miltefosine

    • C. 

      Used to treat Chaga's infections

  • 89. 
    Amphotericin B is the antifungal agent that is second line Rx for visceral and mucotaneous forms of leishmaniasis.
    • A. 

      True

    • B. 

      False

  • 90. 
    Trichomoniasis:
    • A. 

      Caused by the flagellated protozoan Trichomonas vaginalis

    • B. 

      Trichomoniasis is a sexually transmitted disease

    • C. 

      Only trophozoite forms of T. vaginalis have been identified in infected secretions

    • D. 

      Metronidazole remains the drug of choice for the treatment of trichomoniasis

  • 91. 
    Giardiasis:
    • A. 

      Caused by flagellated protozoan Giardia intestinalis

    • B. 

      Most commonly reported intestinal protozoal infection in the US

    • C. 

      Infection from ingestion of the cyst form of the parasite found in fecally contaminated water or food

    • D. 

      Least commonly reported intestinal protozoal infection in the US

  • 92. 
    Giardiasis Rx:
    • A. 

      Metronidazole is the treatment of choice for giardiasis

    • B. 

      A single dose of tinidazole probably is superior to metronidazole for the treatment of giardiasis due to single dose efficacy and better toleration

    • C. 

      Tinidazole is not approved for children under 12 years of age

  • 93. 
    Severe cardiomyopathy is a symptom of Chaga's disease.
    • A. 

      True

    • B. 

      False

  • 94. 
    Melarsoprol is a trivalent sodium drug used to treat late Stage 2 African Sleeping Sickness and reacts with the sulfhydral groups of enzymes in both the parasite and host.
    • A. 

      True

    • B. 

      False

  • 95. 
    Suramin is for the treatment of early East African sleeping sickness and should not be used for Stage 2 of Trypanosomiasis (CNS involvement). The MOA involves the inhibition of enzymes such as glycerol phosphate dehydrogenase leading to the inhibition of energy metabolism.
    • A. 

      True

    • B. 

      False

  • 96. 
    The MOA of Iodoquniol appears to chelate ferrous ions required for metabolism.
    • A. 

      True

    • B. 

      False

  • 97. 
    Paramomycin is a(n) aminoglycoside antibiotic that block protein synthesis.
    • A. 

      True

    • B. 

      False

  • 98. 
    Metronidazole is a luminal amebicide that is non-enzamatically reduced by reacting with reduced ferredoxin generated by pyruvate oxido-reductase. This reduction produces reduced cytotoxic compounds that bind to protein and DNA, inducing cell death. 
    • A. 

      True

    • B. 

      False

  • 99. 
    Miltefosine is a treatment of Leishmaniasis which targets Protein Kinase C, Lipid and Phosphotidylcholine biosynthesis pathways
    • A. 

      True

    • B. 

      False

  • 100. 
    Trichomoniasis is a(n) sexually transmitted disease. 
    • A. 

      True

    • B. 

      False

  • 101. 
    The most commonly reported intestinal protozoal infection in the US is Giardiasis. 
    • A. 

      True

    • B. 

      False

  • 102. 
    Either a 5-day course of Tinidazole or a single dose of Metronidazole will treat Giardiasis. 
    • A. 

      True

    • B. 

      False

  • 103. 
    Which of the following are Plasmodium parasites involved in Malarial infections:
    • A. 

      Falciparum

    • B. 

      Vivax

    • C. 

      Malariae

    • D. 

      Knowlesi

  • 104. 
    In P. falciparum and P. malariae infections, only 1 cycle of liver cell invasion and multiplication occurs, and liver infection ceases spontaneously in < 4 weeks.
    • A. 

      True

    • B. 

      False

  • 105. 
    Which 2 plasmodial parasites are notably dormant and is not eradicated by most drugs? 
    • A. 

      Falciparum

    • B. 

      Malariae

    • C. 

      Vivax

    • D. 

      Ovale

  • 106. 
    Malarial infected mosquitos inject merozoites which then invade the liver and produce sporozoites. 
    • A. 

      True

    • B. 

      False

  • 107. 
    Only erythrocytic parasites cause clinical illness.
    • A. 

      True

    • B. 

      False

  • 108. 
    Merozoites become trophozoites (actively feeding and growing) in RBC, and when the RBC ruptures, other RBC’s become infected.
    • A. 

      True

    • B. 

      False

  • 109. 
    Anti-malarial agents:
    • A. 

      Method of treatment (prophylaxis or treatment) and general mechanism (stage of life cycle of parasite they affect)

    • B. 

      Eliminate both hepatic and erythrocytic stages

    • C. 

      Few available agents are causal prophylactic drugs → capable of preventing erythrocytic infection

  • 110. 
    Which of the following are anti-malarial drugs:
    • A. 

      Tissue schizonticides

    • B. 

      Blood schizonticides

    • C. 

      Gametocides

  • 111. 
    _______________ are drugs that eliminate developing or dormant liver forms of malaria
    • A. 

      Tissue schizonticides

    • B. 

      Blood schizonticides

    • C. 

      Gametocides

  • 112. 
                                         are drugs that act on erythrocytic parasites.
    • A. 

      Tissue schizonticides

    • B. 

      Blood schizonticides

    • C. 

      Gametocides

  • 113. 
                                         are drugs that kill sexual stages and prevent transmission to mosquitoes.
    • A. 

      Tissue schizonticides

    • B. 

      Blood schizonticides

    • C. 

      Gametocides

  • 114. 
    Quinolines have been the mainstay of anti-malarial chemotherapy for nearly 400 years.
    • A. 

      True

    • B. 

      False

  • 115. 
    The “treatment of choice” (both treatment and prophylaxis) for active gametocytes involved in malaria is                                     .
    • A. 

      Quinine

    • B. 

      Quinidine

    • C. 

      Chloriquine

  • 116. 
    The MOA of Chloroqiune is to bind to heme and prevent its bio-crystalization into                         . The accumulation of free heme leads to the lysis of RBCs and the parasite.
    • A. 

      Hemoglobin

    • B. 

      Heme

    • C. 

      Amino Acids

    • D. 

      Hemozoin

  • 117. 
    Chloroquine PK:
    • A. 

      Rapidly and completely absorbed

    • B. 

      Crosses BBB and placenta

    • C. 

      Accumulates in tissues (large VD) including erythrocytes, liver, spleen, kidney, lung, melanocytes and leukocytes

    • D. 

      Parent drug and active metabolites primarily excreted in urine

  • 118. 
    Chloroquine resistance in P. Falciparum is associated with an alteration of the chloroquine transporter protein                          , thus decreasing the ability of the parasite to accumulate the drug. 
    • A. 

      CG1

    • B. 

      CG2

    • C. 

      CG3

  • 119. 
    Nearly all human deaths due to malaria caused by P. falciparum, a strain which is becoming increasingly resistant to current malarial chemotherapy.
    • A. 

      True

    • B. 

      False

  • 120. 
    Quinine is derived from the powdered bark of the South American                          tree.
    • A. 

      Woodworm

    • B. 

      Cocoa

    • C. 

      Cinchona

    • D. 

      Guava

  • 121. 
    Quinidine is a stereoisomer of quinine and is more potent and more toxic.
    • A. 

      True

    • B. 

      False

  • 122. 
    Quinine and quinidine:
    • A. 

      Act primarily against asexual erythrocytic forms with little efficacy on hepatic forms of malarial parasites

    • B. 

      Especially valuable for parenteral treatment of severe disease due to drug-resistant P. faliciparum

    • C. 

      Not suitable for prophylaxis due to toxicity and short t1/2

    • D. 

      MOA similar to Chloroquine

  • 123. 
    Mefloquine:
    • A. 

      Used for prophylaxis and treatment of drug-resistant P. falciparum and P. vivax malaria

    • B. 

      Racemic mixture of 4 optical isomers with similar anti-malarial potency

    • C. 

      Potent blood schizonticide, no efficacy against early hepatic stages and mature gametocytes

    • D. 

      MOA similar to chloroquine

  • 124. 
                             is a blood schizonticide with no resistance historically that is used in combo therapy for drug–resistant malarial infections.
    • A. 

      Artemisinin

    • B. 

      Mefloquine

    • C. 

      Quinine

  • 125. 
    Artemisinin:
    • A. 

      Potency in vivo is 10X-100X greater than other anti-malarials

    • B. 

      Act against the asexual erythrocytic stage of P. vivax and P. falciparum

    • C. 

      Gametocidal activity but do not affect either primary or latent liver stages

    • D. 

      Cleavage of the compound’s endoperoxide bridge by heme iron from parasitized erythrocytes, resulting in free radical production

    • E. 

      The free radicals (and direct binding of the drug itself) cause damage to proteins in the parasite

  • 126. 
    Pyrimethamine is a(n)                                      that acts as a blood schizonticide and works by potently, yet selectively, inhibiting plasmodial dihydrofolate reductase.
    • A. 

      Anti-folate agent

    • B. 

      Anti-chelating agent

    • C. 

      Anti-inflammatory

  • 127. 
    Pyrimethamine:
    • A. 

      Acts as a strong sporonticide in the mosquito’s gut when the mosquito ingests it from the human host

    • B. 

      Effective solo Rx for P. falciparum and in combo with a sulfonamide for P. malariae

    • C. 

      Potently inhibits plasmodial dihydrofolate reductase at much lower concentrations than needed to inhibit the mammalian enzyme

    • D. 

      Resistance due primarily to mutations in dihydrofolate reductase and dihydropteroate synthase

  • 128. 
    Tetracyclines are particularly useful for the treatment of the acute malarial attack caused by multi-drug resistant strains of P. falciparum that also show partial resistance to quinine.
    • A. 

      True

    • B. 

      False

  • 129. 
    Tetracycline is a(n)                                      that inhibits protein synthesis in a plasmodial prokaryotic-like organelle (apicoplast) and should be used in combo therapy for the treatment of malaria. It can be used solo for prophylaxis in chloroquine and mefloquine resistant strains.
    • A. 

      Antibiotic

    • B. 

      Antimalaria

    • C. 

      Antiviral

  • 130. 
    Class                          anti-malarials are useful for asexual, erythrocytic forms causing the clinical manifestation, but are not reliable against latent liver stages or P. falciparum gametocytes.
    • A. 

      1

    • B. 

      2

    • C. 

      3

    • D. 

      4

  • 131. 
    This class of anti-malarials targets both asexual erythrocytic forms and primary liver stages for P. falciparum. Treatment is reduced to several days (vs. weeks.)
    • A. 

      Class 1

    • B. 

      Class 2

    • C. 

      Class 3

  • 132. 
    1.     Primaquine is an example of a class              anti-malarial therapy with efficacy for primary and latent liver stages and gametocytes. It is most commonly used for P. Vivax and P. Ovale to eradicate the hynozoites responsible for relapsing infection.
    • A. 

      1

    • B. 

      2

    • C. 

      3