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Flashcards in anti-protazoan parasitic drugs Deck (83):
1

what are some protazoal infections of the blood and tissue

plasmodium (malaria)
babesia (babesiosis)
leishmania (chronic ulcers/viceral)
trypanosoma
toxoplasma gondii

2

what are some protozoal infections of the intestines

etamoeba histolytica (liver abcess, dysentery)
giardia lamblia (chronic diarrhea)
cryptosporidium parvum (OI, diarrhea)

3

what are some urogenital protozoal infections

trichomaonas vaginalis (STD)

4

what are the key characteristics of plasmodium falciparum

can infect all RBCs
causes agglutination, blood gets stuck in microcirculation
sleeping form occurs for 6-12 months
causes more severe disease (more RBC able to be infected)
associated with drug resistance
only early ring form trophozoites found in blood smears
banana shaped gametocytes
high parasitemia index involving all ages of RBC

5

what are the key characteristics of plasmodium vivax

persistant exoerythrocytic stage - can relapse up to 40 years after initial infection
ca't infect all peripheral RBCs

6

tinidazole - mechainsm

forms free radical that leads to cell destruction by inhibition of acetyl coA synthesis

7

tinidazole - metabolsm

p450, 3a4
can induce and inhibit

8

tinidazole - use

trichomoniasis, giardiasis, systemic E histolytica infection

9

drug of choice for trichomonas vaginalis

tinidazole

10

drug of choice for giardiasis

tinidazole

11

metonidazole - mechanism

same as tinidazole, more GI distress

form free radical that leads to cell destruction by inhibition of acetyl coA synthesis

12

giardiasis symptoms

sometimes asymptomatic
symptoms are mild diarrhea to abdominal pain to severe malabsorption syndrome

ingestion of cyst

13

trichomoniasis symptoms

persistant vaginal imflammation, discharge, itching and burning
infection in males is generally asymptomatic

14

sometimes asymptomatic
symptoms are mild diarrhea to abdominal pain to severe malabsorption syndrome

giardiasis

15

persistant vaginal imflammation, discharge, itching and burning
infection in males is generally asymptomatic

trichomoniasis

16

amoebiasis symptoms

majority are asymptomatic
vague non-specific abdominal symptoms to dystentery, abdominal pain, anorexia, weight loss, chronic fatigue

sometimes can produce abscesses of the liver and lungs

17

majority are asymptomatic
vague non-specific abdominal symptoms to dystentery, abdominal pain, anorexia, weight loss, chronic fatigue

sometimes can produce abscesses of the liver and lungs

amoebiasis

18

amoebiasis is caused by

Entamoeba histolytica

ingesting cyst

19

treatment of amoebiasis is with:

luminal drugs - paromomycin
systemic drugs - tinidazole (followed by paromomycin)

20

paromomycin - mechanism

binds 30S ribosome and prevents protein synthesis

21

paromomycin - clinical uses

drug of choice for asymptomatic luminal amebiasis

- iodoquinol used to be drug of choice for amebiasis but studies have shown association with optic atrophy and blindness

22

drug of choice for asymptomatic luminal amebiasis (e histolytica, extracellular)

paromomycin

23

paromomycin - drug interactions

decreases digoxin serum concentration by 30-80 percent

24

drug of choice for active intestianl and systemic infection

tinidazole
followed by course of paromomycin due to how much is absorbed in upper GI tract; T alone fails to eradicate trophozoites in lower GI tract

25

sleeping sickness is caused by:

african trypanosomiasis

26

what are the two subspecies that are human parasites

trypanosoma brucei gambiense
t. b. rhodesiense

27

infection by t b gamiense causes what symptoms?

fever, lymph node enlargement, generalized pain, muscle weakness
parasitic invasion of CNS leads to sleepiness
---> apathy, prgressive loss of coordiantion, tremor, paralysis, coma, finally death

28

fever, lymph node enlargement, generalized pain, muscle weakness
parasitic invasion of CNS leads to sleepiness --> apathy, prgressive loss of coordiantion, tremor, paralysis, coma, finally death
intense itching in late stage disease

usually greater than 2 years for full progression

t b gamiense

29

fever, lymph node enlargement, generalized pain, muscle weakness
parasitic invasion of CNS leads to sleepiness --> apathy, prgressive loss of coordiantion, tremor, paralysis, coma, finally death
intense itching in late stage disease

all occuring within the first few months of infection

t b rhodesiense

30

the non CNS stage of tryptanosomiasis is called

hemolymphatic stage

31

treatment of hemolymphatic stage of tryptanosomiasis is

suramin

32

suramin - mechanism

inhibits energy metabolism
mechanism isnt quite clear

33

suramin - resistance

no resistance after 80 years of usage

34

suramin - admin

IV only, no oral

35

suramin - use

drug of choice for tryptanosomiasis (t b gambiense, t b rhodeiense) in early stages before CNS involvement
rarely used on its own for tb gambia - often give with pentamidine

36

drug of choice for tryptanosomiasis in early stages before CNS involvement
rarely used on its own - often give with pentamidine

suramin

37

pentamidine - use

non CNS t b gambia with suramin
not useful against t b rhodeiense
doesnt cross the BBB so not useful for infections inbrain or spinal cord

38

pentamidine - mechanism

binds/causes DNA deletion via topoisomerase II

39

pentamidine - side effects

adverse effects in about half patients
-headaches, dizziness, breathlessness, tachycardia
impaired renal function in about a quarter of patients
damages pancreatic islet cells - can cause hypoglycemia and diabetes

40

what drugs are used to treat t. b. rhodeiense/gambia when there is CNS involvement (late stages)

melarsoprol
eflornithine

41

melarsoprol - mechanism

thought to inactivate many enzymes by reactive sulfhydryl groups
mammalian cells can deactivate drug faster than trypanosomas
also selective permeability of the parasite membrane

42

melarsoprol - use

t b rhodeiense and t b gambia

if t b rhodeiense relapse, use eflornithine
if t b gambia are not cured by melarsoprol, they rarely will respond to a second treatment

43

melarsoprol - side effects

ver toxic
encephalopathy
phlebitis
peripheral neuritis
anemia in patients with G6P deficiency

44

eflornithine - mechanism

irreversible inhibition of ornithine decarboxylase - interferes in production of necessary macromolecules (polyamines, putrescine, spermine, spermidine)

45

eflornithine - use

for treatment of late stage trypanosomiasis with CNS involvement caused by t b gambiense
not effective against t b rhodesience

46

what drug would be used to treat trypanosomiasis with CNS involvement caused by t b gambiense

elfornthine

47

what drug would be used to treat trypanosomiasis with CNS involvement caused by t b rhodesience

melarsoprol

48

America trypanosomiasis is also called

chagas disease

49

american trypanosomiasis is caused by:

the flagellate trypanosoma truzi transmitted by the reduviid bug (kissing bug)

50

describe how a person is infected with america trypanosomiasis

deposition of bug feces containing trypomastigotes (trypanosomes) onto skin
the trypanosomes get transmitted into skin, into blood by the bite or itching, or scratching skin with fingers contaminated with bug feces
trypanosomes then become amastigote (loss of flagella)
replication
then turn back to trypanosomes which lyse the cell and emerge to invade other cells or reinfect reduviid bug
-exhibit preference for cardiac, smooth, skeletal muscle and nerve cells

51

what is the presentation of chagas disease

acute phase - anemia, weakness, nervous disorders, chills, muscle and bone pain, variable heart failure
-most severe in children, death might result in a matter of weeks

chronic phase - more common in adults
-central and peripheral nervous system dysfunction and damage to heart and maybe esophagus, colon

52

what is the drug of choice for chagas disease

nifurtimox

53

nifurtimox - use

useful for treating trypomastigote but not amastigote phase of chagas disease
(ineffective for treating chronic, intracellular t. cruzi)

54

nifurtimox - mechanism

produces oxygen free radicals
parasite does not have enzymes to inactivate these ROS and is more sensitive to human host

55

leishmania is trasmitted by:

promastigote through the pite of a sandfly

56

the systemic form of leishmaniasis caused by leishmania donovani is called

kala azar - parasite gets into macrophages and lyses them

57

the two cutaneous forms of leishmaniasis are:

L tropica (old world cutaneous)
l braziliensis (new world cutaneous)

58

the drug of choice for leishmaniaiss (cutaneous and systemic)

sodium stibogluconate

59

sodium stibogluconate - mechanism

interferes with glycolysis and fatty acid oxidation, inhibiting energy production

60

malaria is caused by

protozoa from plasmodiidae

falciparum (malignant tertian)
vivax (benign tertian)
malariae, ovale (mild)

61

what is the alternative treatment for kala azar

pentamidine

62

plasmodiidae - life cycle

sporozoites are injected into blood stream
form schizonts in the liver
asexual reproduction --> merozoites (pre-erythrocytic phase)
merozoites enter RBC, initiating erythrocytic phase
transforms back into schizont, asexual repro --> merozoites that invade other erythrocytes

63

what drugs are used to treat malaria caused by plasmodiidae

chloroquine
mefloquine
pyrimethamine and sufodoxine
atovaquone and proguanil
artemether and lumefantrine
primaquine

64

what drug is used to treat the exo-erythrocytic cycle (of p vivax, p ovale)

primaquine

65

what drugs can be used to treat the erythrocytic phase of p vivax, ovale, faciparum, and malariae

chloroquine
mefloquine

66

what drugs are used to treat the erythrocytic phase of p falciparum (resistant forms)

pyrimethamine + sulfadoxine
artemether + lumefantrine

67

what drugs are used to treat the erythrocytic phase of malaria

chloroquine
mefloquine
pyrimethamine + sulfadoxine
artemether + lumefantrine
atovaquone + proguanil

68

what other non-protozoan parasitic drugs are used to treat chloroquinon-resistant strains of malaria int he exo-erythrocytic phase

tetracycline
doxycycline

69

chloroquine - use

erythrocytic phase of p vivax, ovale, falciparum, malariae

70

cloroquine, mefloquine - mechanism

blocks heme polymerization

71

chloroquine, mefloquine - toxicity

hemolysis in patients with G6P deficiency

72

mefloquine - use

erythrocytic phase of p vivax, ovale, falciparum, malariae

73

pyrimethamine + sulfoxadine - use

erythrocytic phase of p falciparum

74

pyrimethamine + sulfoxadine - mechanism

blocks folic acid synthesis
pyrimethamine - inhibits reduction of FH2 to FH4
sulfoxadine - inhibits synthesis of precursor to FH2

75

pyrimethamine + sulfoxadine - side effects

bone marrow suppression
stevens johnsons syndrome

76

atovaquone + proguanil - mechainsm

selective inhibitor of parasite mit ETC (atovaquone)
inhibition of dihydrofolate reductase (proguanil)

77

atovaquone + proguanil - use

use of atovaquone alone = 30% faulure
use of the two together = 100% cure rate
against erythrocytic phase of

78

artemether + lumefantrine - mechanism

free radicals and inhibition of heme polymerization

79

primaquine - mechanism

interfers with pyrimidine synthesis and mitochondrial ETC

80

primaquine - toxicity

hemolysis in patients with G6P deficiency

81

primaquine - use

exo-erythrocytic phases of p vivax and p ovale
has ability to prevent drug relapses

82

steven-johnson syndrome is also known as

exfoliative dermatitis

83

hemolytic anemia occurs in patients with G6P DH mutation

many children play piano softly

melarsoprol chloroquine primaquine pyrimethamine sulfadoxine