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anti-protazoan parasitic drugs Flashcards

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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
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

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