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Pharm > anti-protazoan parasitic drugs > Flashcards

anti-protazoan parasitic drugs Flashcards

1
Q

what are some protazoal infections of the blood and tissue

A 
plasmodium (malaria)
babesia (babesiosis)
leishmania (chronic ulcers/viceral)
trypanosoma 
toxoplasma gondii
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2
Q

what are some protozoal infections of the intestines

A 
etamoeba histolytica (liver abcess, dysentery)
giardia lamblia (chronic diarrhea)
cryptosporidium parvum (OI, diarrhea)
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3
Q

what are some urogenital protozoal infections

A

trichomaonas vaginalis (STD)

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4
Q

what are the key characteristics of plasmodium falciparum

A

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

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5
Q

what are the key characteristics of plasmodium vivax

A

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

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6
Q

tinidazole - mechainsm

A

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

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7
Q

tinidazole - metabolsm

A

p450, 3a4

can induce and inhibit

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8
Q

tinidazole - use

A

trichomoniasis, giardiasis, systemic E histolytica infection

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9
Q

drug of choice for trichomonas vaginalis

A

tinidazole

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10
Q

drug of choice for giardiasis

A

tinidazole

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11
Q

metonidazole - mechanism

A

same as tinidazole, more GI distress

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

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12
Q

giardiasis symptoms

A

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

ingestion of cyst

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13
Q

trichomoniasis symptoms

A

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

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14
Q

sometimes asymptomatic

symptoms are mild diarrhea to abdominal pain to severe malabsorption syndrome

A

giardiasis

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15
Q

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

A

trichomoniasis

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16
Q

amoebiasis symptoms

A

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

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17
Q

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

A

amoebiasis

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18
Q

amoebiasis is caused by

A

Entamoeba histolytica

ingesting cyst

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19
Q

treatment of amoebiasis is with:

A

luminal drugs - paromomycin

systemic drugs - tinidazole (followed by paromomycin)

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20
Q

paromomycin - mechanism

A

binds 30S ribosome and prevents protein synthesis

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21
Q

paromomycin - clinical uses

A

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
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22
Q

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

A

paromomycin

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23
Q

paromomycin - drug interactions

A

decreases digoxin serum concentration by 30-80 percent

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24
Q

drug of choice for active intestianl and systemic infection

A

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

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25
Q

sleeping sickness is caused by:

A

african trypanosomiasis

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26
Q

what are the two subspecies that are human parasites

A

trypanosoma brucei gambiense

t. b. rhodesiense

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27
Q

infection by t b gamiense causes what symptoms?

A

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

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28
Q

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

A

t b gamiense

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29
Q

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

A

t b rhodesiense

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30
Q

the non CNS stage of tryptanosomiasis is called

A

hemolymphatic stage

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31
Q

treatment of hemolymphatic stage of tryptanosomiasis is

A

suramin

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32
Q

suramin - mechanism

A

inhibits energy metabolism

mechanism isnt quite clear

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33
Q

suramin - resistance

A

no resistance after 80 years of usage

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34
Q

suramin - admin

A

IV only, no oral

35
Q

suramin - use

A

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
Q

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

A

suramin

37
Q

pentamidine - use

A

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
Q

pentamidine - mechanism

A

binds/causes DNA deletion via topoisomerase II

39
Q

pentamidine - side effects

A

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
Q

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

A

melarsoprol

eflornithine

41
Q

melarsoprol - mechanism

A

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
Q

melarsoprol - use

A

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
Q

melarsoprol - side effects

A 
ver  toxic
encephalopathy
phlebitis
peripheral neuritis
anemia in patients with G6P deficiency
44
Q

eflornithine - mechanism

A

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

45
Q

eflornithine - use

A

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

46
Q

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

A

elfornthine

47
Q

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

A

melarsoprol

48
Q

America trypanosomiasis is also called

A

chagas disease

49
Q

american trypanosomiasis is caused by:

A

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

50
Q

describe how a person is infected with america trypanosomiasis

A

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
Q

what is the presentation of chagas disease

A

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
Q

what is the drug of choice for chagas disease

A

nifurtimox

53
Q

nifurtimox - use

A

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

54
Q

nifurtimox - mechanism

A

produces oxygen free radicals

parasite does not have enzymes to inactivate these ROS and is more sensitive to human host

55
Q

leishmania is trasmitted by:

A

promastigote through the pite of a sandfly

56
Q

the systemic form of leishmaniasis caused by leishmania donovani is called

A

kala azar - parasite gets into macrophages and lyses them

57
Q

the two cutaneous forms of leishmaniasis are:

A 
L tropica (old world cutaneous)
l braziliensis (new world cutaneous)
58
Q

the drug of choice for leishmaniaiss (cutaneous and systemic)

A

sodium stibogluconate

59
Q

sodium stibogluconate - mechanism

A

interferes with glycolysis and fatty acid oxidation, inhibiting energy production

60
Q

malaria is caused by

A

protozoa from plasmodiidae

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

61
Q

what is the alternative treatment for kala azar

A

pentamidine

62
Q

plasmodiidae - life cycle

A

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
Q

what drugs are used to treat malaria caused by plasmodiidae

A 
chloroquine
mefloquine
pyrimethamine and sufodoxine
atovaquone and proguanil
artemether and lumefantrine
primaquine
64
Q

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

A

primaquine

65
Q

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

A

chloroquine

mefloquine

66
Q

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

A

pyrimethamine + sulfadoxine

artemether + lumefantrine

67
Q

what drugs are used to treat the erythrocytic phase of malaria

A 
chloroquine
mefloquine
pyrimethamine + sulfadoxine
artemether + lumefantrine
atovaquone + proguanil
68
Q

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

A

tetracycline

doxycycline

69
Q

chloroquine - use

A

erythrocytic phase of p vivax, ovale, falciparum, malariae

70
Q

cloroquine, mefloquine - mechanism

A

blocks heme polymerization

71
Q

chloroquine, mefloquine - toxicity

A

hemolysis in patients with G6P deficiency

72
Q

mefloquine - use

A

erythrocytic phase of p vivax, ovale, falciparum, malariae

73
Q

pyrimethamine + sulfoxadine - use

A

erythrocytic phase of p falciparum

74
Q

pyrimethamine + sulfoxadine - mechanism

A

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

75
Q

pyrimethamine + sulfoxadine - side effects

A

bone marrow suppression

stevens johnsons syndrome

76
Q

atovaquone + proguanil - mechainsm

A

selective inhibitor of parasite mit ETC (atovaquone)

inhibition of dihydrofolate reductase (proguanil)

77
Q

atovaquone + proguanil - use

A

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

78
Q

artemether + lumefantrine - mechanism

A

free radicals and inhibition of heme polymerization

79
Q

primaquine - mechanism

A

interfers with pyrimidine synthesis and mitochondrial ETC

80
Q

primaquine - toxicity

A

hemolysis in patients with G6P deficiency

81
Q

primaquine - use

A

exo-erythrocytic phases of p vivax and p ovale

has ability to prevent drug relapses

82
Q

steven-johnson syndrome is also known as

A

exfoliative dermatitis

83
Q

hemolytic anemia occurs in patients with G6P DH mutation

many children play piano softly

A

melarsoprol chloroquine primaquine pyrimethamine sulfadoxine

Pharm (11 decks)

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