Prognosis Patients with G6PD enzyme deficiency get fewer illnesses as compared to other people and the possible outcome is general recovery from disease.
Proxymal Nocturnal Hemoglobinuria Pathogenesis
Morphology Microscopic Hypercellular marrow with erythroid hyperplasia .
Morphology Gross Flushing of skin due to pancytonpenia
Symptoms
Prognosis Death results after 10-11 years of diagnosis with decreased cell number
Autoimmune Hemolytic Anemia Some people develop antibodies -interact with determinants on RBCs - causing hemolytic anemia. C lassified according to nature of the antibody presence of predisposing conditions. Warm Antibody Immunohemolytic Anemia: It is caused by the IgG or IgA (rarely) immunoglobulins which are active at room temperature ( 37 C ) that attach to RBCs membranes making their Fc portion exposed which get attached to Fc receptors on monocytes and macrophages. This will allow them to phagocytize the RBC membranes changing them to spherocytes . Spherocytes are not flexible as normal RBCs and are, therefore, erythrophagocytosed in Spleen leading to hemolysis.
Autoimmune Hemolytic Anemia Cold Antibody Immunohemolytic Anemia: C irculating antibodies esp. IgM causes the destruction of RBCs T heir concentration in normal being is too low to trigger disease Patients with CAIA have higher concentrations of IgM At low temperatures i.e. below 30 C, IgM antibodies bind to glycoproteins on the surface of RBCs activating the complement system which then damages the RBCs by forming Membrane Attack Complex injecting proteins into the RBCs forming pores leading to membrane instability causing intravascular hemolysis. If the complement response is insufficient, then extravascular hemolysis occurs due to deposition of MAC proteins viz. C3b and C4b on RBCs activating opsonization process and their destruction by phagocytosis in spleen.
Etiology Warm AIHA Cold AIHA
Diagnosis
Malaria Pathogenesis
Morphology Microscopic B lood smear showing red blood cells that contain developing P. vivax parasites