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IHO Week 3 (EH) > Malaria > Flashcards

Malaria Flashcards

1
Q

what mosquito carries plasmodia

A

anopheles

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2
Q

plasmodium is a _____

A

protozoan

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3
Q

species plasmodium

A

vivax, ovale, malariae, falciparum

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4
Q

which species have low parasite burden

A

vivax, ovale, malariae

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5
Q

which species have high parasite burden

A

falciparum

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6
Q

vivax, ovale, malariae cause

A

mild anemia

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7
Q

which species relapse

A

vivax, ovale

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8
Q

which species cause severe anemia

A

falciparum

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9
Q

what does falciparum cause

A

severe anemia
cerebral and multi-organ symptoms
high-fatality rate

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10
Q

Most common

A

vivax, falciparum

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11
Q

most deadly

A

falciparum

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12
Q

relapses

A

vivax, ovale

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13
Q

life cycle of plasmodium falciparum

A

mosquito digestive tract –> sporozoites in mouth –> hepatic cell in mammal –> schizonts which multiply –> merozoites burst out of cell –> ring form into RBC –> trophozoite –> schizonts –> merozoites, continue in that cycle

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14
Q

morphology: P. falciparum

A

lots of rings

crescent-shaped gametocytes

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15
Q

morphology: P. malariae

A

“rosette” arrangement of merozoites

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16
Q

morphology: P. ovale

A

enlarged red cells

Schuffner’s dots

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17
Q

morphology: P. vivax

A

Schuffner’s dots

enlarged red cells

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18
Q

P. falciparum is able to infect ____ (special)

A

red cells of any age

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19
Q

P. falciparum causes what kind of red blood cell pathology

A

“rosettes” – abnormal binding to endothelium
blood flow is impeded
main cause of death in children = cerebral ischemia

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20
Q

P. falciparum and cytokines

A

Stimulates high production of cytokines
TNF, INF-Υ, IL-1
suppress red cell production, cause fever, tissue damage, and red cell binding to endothelium

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21
Q

malaria: what happens in the patient

A

spleen becomes enlarged
liver enlarged/pigmented
brain vessels get plugged
heart/lungs maybe involved

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22
Q

spleen pathology

A

enlarged
parasites in red cells
super-active macrophages
if chronic: fibrosis, grayish color

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23
Q

brain vessels pathology

A

red cell rosettes
hypoxia around vessels
eventual, ischemia

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24
Q

incubation

A

1-2 weeks

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25
Q

prodrome

A

flu-like illness

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26
Q

paroxysms

A

fever/chills, sweating, myalgia

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27
Q

quotidian

A

daily

falciparum

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28
Q

tertian

A

every 48 hrs

vivax, ovale

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29
Q

quartan

A

every 72 hrs

malariae

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30
Q

host resistance (2 ways)

A

inherited red cell alterations

partial immune-mediated resistance

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31
Q

inherited red cell alterations

A

Hemoglobinopathies (e.g., sickle cell)
Thalassemias
G6PD deficiency
RBC antigens (ABO, Duffy)

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32
Q

partial immune-mediated resistance

A

Develops over time in patients in endemic areas
Reduces severity of disease
P. falciparum uses antigenic variation

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33
Q

blood type and binding

A

O - least adhesive (cannot bind to endothelium)

A and or B most

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34
Q

diagnosis

A

sxs and hx
ID plasmodia in red cells on regularly-stained blood smear (gold standard)
rapid immunochromatographic tests sometimes used (quicker but less accurate)

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35
Q

The science that deals with drugs, their sources, appearance, chemistry, actions, mechanism of action and use

A

pharmacology

36
Q

The practical branch of medicine dealing with the treatment of disease

A

therapeutics

37
Q

best plan for malaria

A

DON’T GET BIT
use of netting and insect repellents
avoid areas and exposure during high insect activity

38
Q

plan B

A

prophylaxis
treat active malaria
use radical cure if indicated

39
Q

considerations in treatment?

A

which area? resistance? persistent hepatic forms? clinical status of disease?

40
Q

which species have resistance?

A

falciparum, vivax

41
Q

which ones have latent forms

A

ovale, vivax

42
Q

what treats latent malaria

A

primaquine

43
Q

best choice suppressive prophylaxis - prevention of malaria

alternative?

A

chloroquine

atovaquone/proguanil

44
Q

best choice suppressive prophylaxis - prevention of malaria in CHLOROQUINE RESISTANT
alternative?

A

atovaquone/proguanil

doxycycline or mefloquine

45
Q

treatment of acute attack for all plasmodium except resistant

A

oral chloroquine

46
Q

treatment of acute attack for chloroquine resistant P. falciparum

A

quinine sulfate + doxycycline

alternative: atovaquone/proguanil OR artemether/lumefantrine or Mefloquine

47
Q

treatment of acute attack for chloroquine resistant P. vivax

A

Quinine sulfate + doxycycline

alternative: mefloquine

48
Q

treatment of severe disease

A

parenteral
quinidine gluconate + doxycycline

alternative: artesunate + oral drug when tolerated

49
Q

radical cure

A

primaquine phosphate

50
Q

which drugs act at primary liver stage

A

pyrimethamine/sulfadoxine
atovaquone/proguanil
primaquine

51
Q

what drugs act at hypnozoite stage

A

primaquine

52
Q

what drugs act RBC asexual stage

A

all (chloroquine, mefloquine, quinine, quinidine….) but primaquine

53
Q

what drugs act at RBC gametocyte

A

chloroquine
quinine, quinidine
artesunate
primaquine

54
Q

chloroquine basis for selectivity

A

The parasitized RBC concentrates Chloroquine at least 25 fold more than unparasitized RBC. Chloroquine accumulates in the acid pH of the food vacuole.

55
Q

chloroquine mechanism

A

parasite digest hgb and makes FPIX which is toxic - parasite heme polymerase turns it to hemozoin (not toxic)
chloroquine binds to FPIX and prevents conversion to hemozoin

56
Q

adverse effects chloroquine

A

low dose prophylaxis - no tox
acute attack doses:
dizziness, headache, itching, vomiting, skin rashes
difficulty in visual accommodation
large doses for prolonged periods can cause severe eye damage and even blindness

57
Q

main AE chloroquine

A

eye issues

58
Q

what is more toxic than chloroquine but no resistance yet

A

quinine, quinidine

59
Q

mechanism quinine/quinidine

A

parasite digest hgb and makes FPIX which is toxic - parasite heme polymerase turns it to hemozoin (not toxic)
chloroquine binds to FPIX and prevents conversion to hemozoin

60
Q

AE quinine

A

Acute attack doses – Cinchonism
tinnitus, blurred vision, nausea,
headache, decreased hearing acuity
permanent damage to vision, balance and hearing can result

61
Q

Anti-arrhythmic drug that blocks Na and K currents

A

quinidine

62
Q

quinine used in

A

Used in chloroquine resistant P. falciparum

63
Q

quinidine used in

A

Intravenous for severe malaria

64
Q

AE quinidine

A

Cardiac problems - so patients need cardiac monitoring

65
Q

mefloquine mechanism

A

Disrupts sequestration of heme as hemozoin (same as chloroquine)

66
Q

AE mefloquine

A

Sometimes nausea, vomiting, dizziness, visual or auditory disturbances
May cause disorientation, hallucinations and depression

67
Q

main AE mefloquine

A

neuropsychiatric reactions

68
Q

indications mefloquine

A

Indicated only for the treatment and prevention of Chloroquine resistant P. falciparum

69
Q

atovaquone given with

A

proguanil

70
Q

atovaquone MOA

A

unique

Depolarizes parasitic mitochondria and inhibits their electron transport

71
Q

proguanil given w/

A

atovaquone

72
Q

proguanil MOA

A

metabolite of proguanil inhibits dihydrofolate reductase
selective for the plasmodial enzyme
Enhances the mitochondrial toxicity of atovaquone
Reduces the frequency of atovaquone resistance

73
Q

proguanil not active against

A

hepatic stages of P. vivax or P. ovale

74
Q

A/P onset

A

slow

75
Q

A/P effectiveness against exo-erythrocytic forms

A

unclear

Proguanil concentrates in erythrocytes

76
Q

A/P use

A

replacing mefloquine for prophylaxis

77
Q

AE of A/P

A

GI disturbances

78
Q

Artemisinins and combinations

A

+mefloquine
+lumefantrine

don’t use alone (resistance)

79
Q

mechanism artemisinins

A

Heme iron in the malarial pigment acts on the drug to produce free radicals that damage parasite proteins
Inhibits a calcium ion ATPase in P. falciparum

80
Q

artemisinins onset and efficacy

A

rapid and potent activity against even multi-drug resistant organisms

81
Q

lumefantrine mechanism

A

unknown

82
Q

lumefantrine effective against

A

erythocytic stage

83
Q

give lumefantrine with

A

artemether
Rapid initial reduction in parasite biomass afforded by artemether and subsequent clearance of remaining viable parasites by the more slowly eliminated lumefantrine

84
Q

primaquine use

A

Drug of choice to eliminate hepatic forms of P. vivax and P. ovale
Eradicates hypnozoite forms dormant in liver
Some prefer to wait for the low risk of relapse rather than face potential side-effects of the drug.

85
Q

mechanism primaquine

A

Unknown

Possibly by generation of reactive oxygen species or by interfering with electron transport in the parasite

86
Q

AE primaquine

A

occasional GI distress, nausea, headache, pruritis, leukopenia
Hemolytic anemia in people with a glucose-6-phosphate dehydrogenase deficiency

IHO Week 3 (EH) (5 decks)

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