DA Exam II Anti-malarial Agents Part 2

Card Set Information

Author:
Anonymous
ID:
134608
Filename:
DA Exam II Anti-malarial Agents Part 2
Updated:
2012-02-12 08:48:38
Tags:
HUSOP
Folders:

Description:
DA Exam II Anti-malarial Agents Part 2
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user Anonymous on FreezingBlue Flashcards. What would you like to do?


  1. Name the two species variations of Plasmodium that, once the tissue schizonts leave the liver, that
    organ is devoid of parasites and there are no relapses of malaria.
    P. falciparum and P. malariae
  2. _______ and ______ are two species variations of Plasmodium where parasites persist in
    the liver and relapses of malaria can occur years later.
    P. vivax and P. ovale
  3. For species P. falciparum, P. vivax, and P. ovale it takes about _____ hours to generate new schizonts to ruptures while for __________ it takes about 72 hours.
    48; P. malariae
  4. Name the two ways anti-malaria drugs are classified.
    1) State of the parasite targeted 2) Use (prophylaxis or treatment)
  5. How many agents kill sporozoites?
    None
  6. Prophylaxis is to prevent the _____________ stage of the disease.
    Erythrocytic
  7. __________ can kill both liver and erythrocyte forms of the organism.
    • No one drug (so at least two drugs are required for
    • treatment)
  8. Class I anti-malarial drugs are effective against which form of the organism and what are they used for?
  9. Asexual erythrocytic; Can treat or prevent symptomatic malaria
  10. Why are class I drugs given prophylatically for several weeks after potential exposure?
    To ensure asymptomatic phase is complete before stopping.
  11. Class II and III anti-malarial drugs are effective against the ___________ form of the organism plus the liver phase of ______________ which allows for a shorter post-exposure dosing schedule.
    Asexual erythrocytic; P. falciparum
  12. Name the only class III anti-malarial drug, what it is
    effective for and what it is used for.
    • Primaquine; primary liver infections and the latent
    • hypnozoites & erythrocytic gametocytes; Clear the liver to prevent relapses
  13. List examples of class I drugs.
    Artemisinin, Pyrimethamine, Chloroquine, Quinine, Tetracycline
  14. Artemisinin has a potency of _______ fold greater than other traditional class I agents and acts rapidly against which phase of the organism?
    10-100; Asexual erythrocytic (no effect on liver stage organism)
  15. _________ within the parasite catalyzes cleavage of an ________ bridge in the artemisinin molecule.
    Heme iron; endoperoxide
  16. Once the endoperoxide bridge is cleaved in the artemisinin molecule, the rearrangement produces a ___________ radical that ________ parasitic macromolecules. Name one target of this.
    Carbon-centered; alkylates; ortholog of sarco/endoplasmic reticulum Ca++-ATPase
  17. In the body, artemisinin is converted to ________ which has anti-malarial activity.
    Dihydroartemisinin
  18. Aretmisinin is indicated for the initial treatment of what type of infections?
    P. falciparum
  19. What is ACT? Why is it used?
    Artemisinin combination therapy; artemisinin is used to rapidly reduce (incompletely) the level of parasite burden while another agent is used to eliminate organisms at other phases. It will also help prevent resistance.
  20. List examples of class II drugs.
    Atovaquone and Proguanil
  21. __________ is a highly lipophilic analog of ubiquinone.
    Atovaquone
  22. Atovaquone is active against liver stage of P. falciparum, but not ___________ hypnozoites.
    P. vivax
  23. Atovaquone acts at the _____________________ of the malaria mitochondria to inhibit ____________ which collapses the mitochondrial membrane potential and stop _____ production.
    Cytochrome bc1; electron transport; ATP
  24. Atovaquone can be administered with a ________ to get a more complete collapse of membrane potential.
    Biguanide (such as proguanil)
  25. Resistance to Atovaquone can occur rapidly due to _________ in the _____________ gene.
    Mutations; cytochrome b
  26. Pyrimethamine is a class ___ drug based on its
    _______________ structure.
    I; Diaminopyrimidine ring
  27. Although resistance is fairly widespread, pyrimethamine is used in combination with _______ helps to synergize its action.
    Sulfadoxine
  28. Pyrimethamine works by inhibiting what type of activity? This activity takes place in humans, so why can it still be used?
    • Dihydrofolate reductase; It inhibits the dihydrofolate
    • reductase activity of plasmodia at concentrations far less than human enzymes.
  29. Dihydrofolate reductase activity is present in the same
    protein as _________ which will be suppressed as well.
    Thymidylate synthase
  30. What is the effect of adding a sulfonamide to pyrimethamine?
    It blocks two steps in nucleotide biosynthesis
  31. Describe the two steps in nucleotide biosynthesis blocked by giving a combination of pyrimethamine and sulfonamide.
    Step one: sulfonamides inhibit dihydropteroic acid formation from p-aminobenzoate by dihydropteroate synthase. Step two: pyrimethamine inhibits dihydrofolate reductase reducing tetrahydrofolate formation. (Results in a late effect on plasmodial development to schizonts in the liver and erythrocytes)
  32. Combination therapy of pyrimethamine and sulfonamide or sulfone is restricted to treatment of _________-resistant P. falciparum.
    Chloroquine
  33. Proguanil is use for P. falciparum infections and controls which two stages?
    Primary liver and asexual erythrocyte
  34. What is the active metabolite of proguanil?
    Cycloguanil
  35. For proguanil, _________ selectively inhibits plasmoidial dihydrofolate reductase-thymidylate shynthetase causing ______ synthesis to be inhibited.
    Triazine metabolite; DNA (along with folate cofactors)
  36. Proguanil is metabolized by ______ to cycloguanil. About 20% of which two ethnicities are deficient in this oxidative activity?
    CYP2C; Asians and Kenyans
  37. Why is proguanil usually given in combination with
    atovaquone?
    Due to rapid resistance development
  38. What are the mainstay anti-malarial agents for the past 400 years?
    Quinolines (chloroquine and hydroxycholroquine more widely used)
  39. Chloroquine is very effective against _______ forms of all species of Plasmodium except for some strains of __________. They are the agents of choice for both prophylaxis and treatment of these infections.
    Erythrocytic; P. falciparum
  40. Describe the mechanism of action for chloroquine.
    Plasmodium use hemoglobin as primary source of amino acids. Acts by concentrating in parasite food vacuoles, preventing the polymerization of heme (Ferriprotoporphyrin IX) into hemozoin and thus eliciting parasite toxicity due to buildup of free heme.
  41. What is Crt?
    • Chloroquine resistance transporter. It may code for
    • a vacule transporter by which chloroquine enters.
  42. What are the two active metabolites of chloroquine?
    Desethylchloroquine and bisdesethlychloroquine
  43. Chloroquine is used for prophylaxis and treatment for ________, _____, and ________ in non-resistant areas.
    P. malariae, ovale and vivax
  44. Chloroquine is used with primaquine because
    chloroquine has no activity against what?
    Liver plasmoidial forms
  45. Other than malaria, what else is chloroquine indicated for?
    Rheumatoid arthritis
  46. When is toxicity seen with chloroquine and what results?
    • Too rapid IV infusion; extensive CNS toxicity
    • including convulsions and coma. Can also have cardiovascular toxicity.
  47. Chloroquine is an inhibitor of CYP___.
    2D6
  48. The mechanism of action of quinine is the same as _________.
    Chloroquine
  49. Quinine is _____ toxic and _____ effective than chloroquine.
    More; less
  50. Why can quinine be used for symptomatic relief of myotonia congenita?
    It can antagonize tetanic stimulation of skeletal muscle.
  51. Quinine is extensively metabolized by CYP____.
    3A4
  52. The active metabolite of quinine is ________ which can cause toxicity in ______________ patients.
    3-hydroxyquinine; renally impaired.
  53. Quinine is the treatment of choice for _________.
    Drug-resistant P. falciparum
  54. Quinine is available in the U.S. as _______ and, prior to 1995, was marketed to treat ________.
    Quinidine; nocturnal leg cramps
  55. Primaquine is effective against ______ forms of the
    plasmoidial organisms.
    Hepatic
  56. Primaquine is used for ___________ and _____ for P. vivax and P. ovale.
    Terminal prophylaxis; cure
  57. At high doses, primaquine can cause ________________ because it is an analog of methylene blue.
    Methmoglobinemia
  58. In patients with _____________________, primaquine can cause acute hemolysis and hemolytic anemia.
    G6P dehydrogenase deficiency
  59. ____________ are slow-acting blood schizontocides used as monotherapy.
    Tetracyclines
  60. Tetracylcines are used for travelers going to which two
    resistant endemic areas?
    Chloroquine and methoquine
  61. _________________ is equivalent to tetracycline action.
    Doxycycline
  62. Malarial resistance to ___________/___________, ___________ and ________ has been found in Southeast Asia.
    Sulfadoxine/pyrimethamine, mefloquine and halofantrine

What would you like to do?

Home > Flashcards > Print Preview