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Patofisiologi on malaria has not been known. Various theoretical and hypothetical had been presented. Changes patofisiologi on malaria, especially related to the disruption of blood flow as a result of local melekatnya eritrosit containing parasites in endotelium capillary. This change in the fast reversibel they can live (survive). The role of some humoral mediators are still debatable, but patogenesis may be involved in the occurrence of fever and inflammation. Skizogoni eksoeritrositik may cause reaski leukosit and fagosit, while sporozoit and gametosit not cause changes patofisiologik.

Patofisiologi malaria is multifaktorial and may be related to the following:

a. Eritrosit devastation. Eritrosit eradication is not only with the outbreak eritrosit that contain parasites, but also by fagositosis eritrosit containing parasites and no parasites, causing anemia and anoksia network. With hemolisis intra vaskular the weight, may occur hemoglobinuria (blackwater fever) and can lead to kidney failure.

b. Mediator endotoksin-makrofag. At the time skizogoni, eirtosit containing parasites makrofag trigger sensitive endotoksin to release various mediators that play a role in the changes patofisiologi malaria. Endotoksin not found in the malaria parasite, may be derived from the channel cavity digested. Malaria parasite itself can deliver neksoris tumor factor (TNF). TNF is a monokin, found in the blood of animals and humans with malaria parasites. TNF and other related sitokin, cause fever, hipoglimeia and respiratory disease syndrome in adults (ARDS = adult respiratory distress syndrome) with sekuestrasi cells in the blood vessel neutrofil tuberculosis. TNF can also destroy plasmodium falciparum in vitro and can increase perlekatan eritrosit the dihinggapi parasites on endotelium capillary. Concentration of TNF in serum in children with acute falciparum malaria in touch directly with mortality, hipoglikemia, and the weight hiperparasitemia disease.

c. Sekuestrasi eritrosit infected. Eritrosit of plasmodium falciparum infected stadium information can form the bulge-bulge (knobs) on the surface. Bulge in the malaria antigen and antibody react with the malaria-related and afinitas eritrosit containing endotelium against plasmodium falciparum in the blood capillary in the instrument, so that progress in skizogoni tools in circulation, not in circulation perifer. Eritrosit infected, stick to the capillary blood and endotelium tablet form (sludge) in the capillary stem-tool in the nature.

Protein and fluid leak through the membrane of capillary leak (permeabel a) and edema cause anoksia and network. Anoksia network is extensive enough to cause death. Protein-rich histidin P. falciparum found in the bulge-bulge, and there are at least four types of protein for the infected sitoaherens eritrosit P. plasmodium falciparum.