MALARIA

Question 1

 P. vivax and P. ovale – fever spikes _______ apart (_______ ________ )

 P. malariae – spikes at ________ intervals (________ ________)

 P. falciparum –spikes often at ________ intervals (________ ________)

Answer 1

48hrs ; benign tertian

72 hrs ; benign quartan

48hrs malignant tertian

Question 2

Falciparum –________ _________ (_________ hrs)

Ovale & Vivax – _________ _________ (____)

Malariae– _________ _________ (____ hrs)

Answer 2

malignant tertian (12-24/48 hrs)

benign tertian (48 hrs)

benign quartan (72 hrs)

Question 3

Pathogenesis

Red cell destruction causes ________
 Malarial pigment produced by ______________________ is released
 Damaged red cells and malarial pigment are removed from the blood by the __________________________ system inducing _________ and _________

 P. falciparum parasitizes all red cells with _________ receptors
 Induces __________q in erythrocyte membranes resulting in ________ of small vessels and tissue ________ and _______________

Answer 3

anemia

parasite’s digestion of heme

monocyte- phagocyte reticulo-endothelial

splenomegaly ; hepato-megaly

glycophorin ; sticky knobs

plugging ; hypoxemia

ischemic necrosis

Question 4

________ blood group factor is necessary for P.vivax red cell penetration, and black persons without that red cell receptor are refractory to ________________ malaria

Answer 4

Duffy

benign tertian malaria

Question 5

Transmission ?

The malaria parasite life cycle involves _______ hosts.

During a blood meal, a malaria-infected female Anopheles mosquito inoculates ____________ into the human host (1).
These infect _______ cells (2) and mature into ________ (3), which _________ and release _________ 4.

Answer 5

sporozoites ; liver cells

schizonts ; rupture

merozoites

Question 6

(Of note, in P. vivax and P. ovale a dormant stage [ ___________ ] can persist in the _______ and cause relapses by invading the bloodstream weeks, or even years later.?

Answer 6

hypnozoites

liver

Question 7

After this initial replication in the liver (exo- erythrocytic __________ A), the parasites undergo _______ multiplication in the erythrocytes (erythrocytic _________ B).

__________ infect red blood cells 5.

The ring stage ___________ mature into _________ , which rupture releasing _________ 6.

Some parasites differentiate into sexual erythrocytic stages (________) 7.
_________ stage parasites are responsible for the clinical manifestations of the disease.

Answer 7

schizogony ; asexual

schizogony ; Merozoites

trophozoites ; schizonts

merozoites ; gametocytes

Blood

Question 8

The gametocytes, male (_______gametocytes) and female (_________gametocytes), are ingested by an _______________ during a blood meal 8.

The parasites’ multiplication in the mosquito is known as the ___________ cycle C.
While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating __________ 9.

Answer 8

micro gametocytes

macrogametocytes

Anopheles mosquito

sporogonic ; zygotes

Question 9

In the mosquitoe

The zygotes, in turn, become _______ and __________ (ookinetes) 10 which invade the ________ wall of the mosquito where they develop into ________ 11. These grow, rupture, and release ________ 12, which make their way to the mosquito’s ________. Inoculation of the sporozoites 1 into a new human host perpetuates the malaria life cycle.

Answer 9

motile ; elongated

midgut ; oocysts

sporozoites ; salivary glands.

Question 10

Epidemiology

There are about 300-500 million cases of malaria yearly.
 1 million children die annually from the effects of malaria. About 90% occur in children under five (5) in Africa.
 It kills one child every __________ .
 It is probably the commonest cause of childhood morbidity and ranks among the top three killers of children after ________ and _________ diseases.

Answer 10

30 seconds.

ARI

diarrhea diseases.

Question 11

It is estimated one out of _______ cases of malaria in children will become complicated

Answer 11

100

Question 12

The direct and indirect economic implications of malaria cannot be overemphasized. It has been estimated to be __________

Answer 12

$2 billion

Question 13

it is believed that _________ deficient individuals are protected from the severe forms of malaria. There is ___________________ of ring infected _______ deficient red cells

Answer 13

G6PD ; early phagocytosis

G6PD

Question 14

Diet and Nutrition: there exists an antagonism between malaria and malnutrition such that severe (cerebral) malaria is _______ in the presence of severe malnutrition. This is due to the ???

Answer 14

rare

deficiency of macro- and micronutrients like iron, folic acid, para-amino benzoic acid etc.

Question 15

Symptoms of uncomplicated malaria

 ________ activity, poor appetite
 Periodic _______,_______, and ______
 Headaches
 Nausea, vomiting and poor appetite (“_______” taste)
 Generalized aches and pains (arthalgia and myalgia)
 Weakness (tiredness with or without anaemia)
 Frequent, often loose stools, sometimes ________
 ________ and mild ______

Answer 15

Reduced

chills, fever and sweating

bitter; bloody

Cough; URTI

Question 16

Complicated malaria

 Impaired __________,
____________ ,
 Respiratory distress,
 ____________ ,
 Severe ________,
_______________________(Algid)

Answer 16

consciousness; Prostration

Convulsions; anaemia

Hypothermic circulatory collapse

Question 17

Presence of parasitaemia does not prove that malaria is the main or only cause of the patient’s illness

T/F

Answer 17

T

Question 18

In practical treatment of malaria

Avoidance of harmful ancillary treatment e.g. _________ and other _________, _________, _________, osmotic/diuretic agents for cerebral oedema.
 Anticipate complications arising from pre-hospital interventions e.g administration of _______________

Answer 18

dexamethasone ; corticosteroids

heparin ; sodium bicarbonate

native concoctions.

Question 19

Urgent management of severe malaria

 ______ and maintain _________
 Position _________ or on the _________
 _________ patient and calculate _________
 Start ___________________
 Make rapid clinical assessment
 Exclude or treat ________
 Assess state of _________

Answer 19

Clear and maintain airway

semi-prone ; side

Weigh ; dosage

anti-malaria chemotherapy

hypoglycaemia ; hydration

Question 20

Interpretation of test

+ —–____/___________
++ —- > _____/ __________
+++ —_____/_________
++++ – > ____/_________

________________ are classified as severe malaria

Answer 20

1-10/100 thick field

10/100 thick field

1-10/thick field

10/thick field

+++ and ++++

Question 21

Still managing severe malaria

 Measure and monitor ___________
 Take blood for diagnostic smear (serially), monitor _________ , PCV and other laboratory tests
 Plan first _________ of fluids (diluents of drugs, glucose and blood transfusions)
 Consider CVP line in anticipation of _________.
 Antipyretics if core temperature exceeds _________
 _________ to exclude meningitis. Consider other infections.
 Anticonvulsants and other drugs as indicated

Answer 21

urine output ; blood sugar

8 hours ; shock.

39oc ; Lumbar puncture

Question 22

 Vaccines to reduce morbidity and mortality. In endemic areas, it is suggested that vaccines based on the _________ stages of the parasites would be more useful than vaccines based on the ____________ stage specific antigens.

Answer 22

blood

sporozoite/liver

Question 23

Effective chemotherapy. This has played a major role in the prevention of mortality. The development of new drugs such as the artemisinin related compounds ,___________ have been shown to have the potential for treating drug-resistance malaria.

Answer 23

atovaquone

Question 24

Chemoprophylaxis. The general recommendation is that this option is not used in children except among _________ and __________ children who are visiting endemic areas. Reasons for this include cost, unsustainability, impairment of development of resistance and the emergence of drug resistance.

Answer 24

sicklers and non-immune