biology : class12 Cerebral Malaria : Causative Organism, Plasmodium, Life Cycle, Symptoms, Prevention : Malaria MCQ Questions and Answers
Practice important
Cerebral Malaria
MCQ questions and answers.
Page 1
of
1
|
10
MCQ Questions
1. Which mechanism most directly explains the severe cerebral manifestations of Plasmodium falciparum malaria?
A.
Rupture of hepatocytes releases neurotoxins into the brain
B.
Infected erythrocytes adhere to cerebral capillary endothelium and obstruct microcirculation
C.
Merozoites invade neurons and multiply within the central nervous system
D.
Gametocytes directly destroy the blood-brain barrier
Correct Answer:
Infected erythrocytes adhere to cerebral capillary endothelium and obstruct microcirculation
Explanation:
In cerebral malaria, P. falciparum-infected erythrocytes undergo cytoadherence and sequestration in small cerebral vessels. This impairs microcirculatory blood flow and contributes to neurological dysfunction.
2. The erythrocyte-stage property of Plasmodium falciparum that is most closely associated with cerebral malaria is:
A.
Formation of dormant hypnozoites in liver cells
B.
Production of only female gametocytes
C.
Expression of surface proteins that promote adhesion to endothelial cells
D.
Invasion of red blood cells without causing haemolysis
Correct Answer:
Expression of surface proteins that promote adhesion to endothelial cells
Explanation:
P. falciparum-infected erythrocytes express parasite-derived adhesion proteins, especially PfEMP1, on their surfaces. These promote attachment to vascular endothelium and sequestration, particularly in cerebral microvessels.
3. A patient with falciparum malaria develops altered consciousness, repeated convulsions, and no alternative explanation for the neurological signs. Which interpretation is most appropriate?
A.
The patient has entered the mosquito stage of the parasite
B.
The findings are characteristic of cerebral malaria
C.
The parasite has formed hypnozoites in the brain
D.
The symptoms indicate only the incubation period of malaria
Correct Answer:
The findings are characteristic of cerebral malaria
Explanation:
Cerebral malaria is a severe complication of malaria, especially falciparum infection, characterized by impaired consciousness, seizures, or other neurological abnormalities after exclusion of other causes.
4. Why can cerebral malaria produce neurological symptoms even though Plasmodium falciparum usually does not multiply inside neurons?
A.
Sequestered infected erythrocytes disturb cerebral microvascular function without neuronal invasion
B.
Merozoites replace neurons during schizogony
C.
Gametocytes enter the cerebrospinal fluid and reproduce there
D.
Liver-stage schizonts release antibodies that paralyse neurons
Correct Answer:
Sequestered infected erythrocytes disturb cerebral microvascular function without neuronal invasion
Explanation:
The neurological injury in cerebral malaria is mainly associated with sequestration of infected erythrocytes, endothelial activation, impaired perfusion, and inflammatory effects rather than direct multiplication of parasites in neurons.
5. Which observation would most strongly support cerebral sequestration by P. falciparum in a patient with severe malaria?
A.
A high proportion of mature infected erythrocytes is absent from peripheral blood despite severe disease
B.
Only sporozoites are detected in circulating plasma
C.
Red blood cells contain dormant liver-stage hypnozoites
D.
Merozoites are found multiplying freely in cerebrospinal fluid
Correct Answer:
A high proportion of mature infected erythrocytes is absent from peripheral blood despite severe disease
Explanation:
Mature trophozoite- and schizont-infected erythrocytes of P. falciparum may sequester in deep vascular beds, including the brain. Consequently, peripheral blood may underestimate the total parasite burden.
6. Which combination most appropriately describes a major pathophysiological sequence in cerebral malaria?
Explanation:
After erythrocyte infection, P. falciparum-infected cells can adhere to endothelium and sequester in cerebral vessels. The resulting vascular and inflammatory disturbances may lead to coma and other neurological signs.
7. Which intervention is most important for preventing cerebral malaria at the community level?
A.
Preventing bites from infected female Anopheles mosquitoes
B.
Destroying gametocytes after they have entered the mosquito
C.
Increasing the number of erythrocytes available for parasite invasion
D.
Allowing untreated infections to proceed until natural immunity develops
Correct Answer:
Preventing bites from infected female Anopheles mosquitoes
Explanation:
Cerebral malaria begins with transmission of Plasmodium through the bite of an infected female Anopheles mosquito. Insecticide-treated bed nets, vector control, and avoiding mosquito bites reduce transmission and therefore prevent this complication.
8. Why is rapid diagnosis and treatment particularly critical when falciparum malaria is suspected to involve the brain?
A.
Falciparum parasites remain confined to the liver during cerebral disease
B.
Sequestration and microvascular obstruction can progress rapidly to coma, seizures, and death
C.
Treatment is effective only before the mosquito ingests gametocytes
D.
Neurological symptoms disappear permanently after the first fever spike
Correct Answer:
Sequestration and microvascular obstruction can progress rapidly to coma, seizures, and death
Explanation:
Cerebral malaria is a medical emergency because infected erythrocyte sequestration, impaired cerebral perfusion, inflammation, and metabolic disturbances can worsen rapidly. Prompt antimalarial treatment is essential.
9. A child with falciparum malaria has coma and recurrent seizures but no evidence that parasites have invaded brain tissue. Which conclusion is most scientifically accurate?
A.
Cerebral malaria is impossible without direct neuronal invasion
B.
The neurological condition can result from vascular sequestration and host-mediated cerebral dysfunction
C.
The symptoms must be caused by liver-stage schizonts entering neurons
D.
Only gametocytes can produce cerebral symptoms
Correct Answer:
The neurological condition can result from vascular sequestration and host-mediated cerebral dysfunction
Explanation:
Cerebral malaria does not require direct invasion of neurons. Sequestration of infected erythrocytes in cerebral microvessels, together with endothelial and inflammatory responses, can produce severe neurological dysfunction.
10. Which statement best distinguishes cerebral malaria from uncomplicated malaria?
A.
Cerebral malaria is defined by the presence of Plasmodium only in liver cells
B.
Cerebral malaria includes neurological impairment such as coma or repeated seizures in a patient with malaria
C.
Uncomplicated malaria always involves cerebral capillary sequestration, whereas cerebral malaria does not
D.
Cerebral malaria occurs only during the mosquito phase of the parasite
Correct Answer:
Cerebral malaria includes neurological impairment such as coma or repeated seizures in a patient with malaria
Explanation:
The defining clinical feature of cerebral malaria is severe neurological involvement, including impaired consciousness, coma, or repeated seizures, in association with malaria, most commonly falciparum infection.
Short Questions and Answers
Practice short questions and answers related to
Cerebral Malaria
.
Short questions are currently unavailable for this page.