1. Extrinsic (extracurpuscular)
1.1. Immune mediated
1.1.1. Iso-Abs
1.1.1.1. ABO incompatibility
1.1.1.2. Rh incompatibility
1.1.2. Auto-Abs
1.1.2.1. Idiopathic
1.1.2.2. Infection
1.1.2.2.1. When the antigen of the microbe is similar to an protein (antigen) in the RBCs. Or if the microbe release an antigen and change the protein (antigen) of the RBCs, this also might happen with malignancy and some drugs.
1.1.2.3. Malignancy
1.1.2.4. Drugs
1.2. Non-Immune mediated
1.2.1. Mechanical causes
1.2.1.1. Cardiac mechanical valve
1.2.1.1.1. When RBCs touch the mechanical valve it ruptures..!
1.2.1.2. D.I.C
1.2.1.2.1. Disseminated intravascular coagulation. Fibrin forms biological knife..!! Due to wide spread damage to the endothelium.
1.2.1.3. T.T.P
1.2.1.3.1. Thrombotic thrompocytopenic purpura. Thrompocytopenia due to thrombosis.
1.2.1.4. March Hemoglubinuria
1.2.2. Infections
1.2.2.1. Malaria
1.2.2.2. Clustredial infection
1.2.3. Chemical
1.2.3.1. Lead
1.2.3.1.1. Lead poisoning (lead thrombus).
1.2.4. Splenomegaly (splenic sequestration)
1.2.4.1. Infection
1.2.4.1.1. Infectious mononucleosis
1.2.4.2. Malignancy
1.2.4.2.1. Lymphoma
1.2.4.2.2. Leukemia
1.2.4.3. Portal hypertension
1.2.4.3.1. portal hypertnesion may result from liver cirrhosis
2. Intrinsic (intracurpucular)
2.1. Inherited
2.1.1. Membrane
2.1.1.1. H.Spherocytosis
2.1.1.2. H.Elliptocytosis
2.1.2. Enzymes
2.1.2.1. Glycolysis
2.1.2.1.1. Hexokinase
2.1.2.1.2. Pyruvate kinase
2.1.2.2. HMP-S
2.1.2.2.1. G6PD
2.1.2.2.2. Glutathione synthase
2.1.2.2.3. Hexose Monophosphate Shunt pathway. This protects the RBCs against oxidative crisis, how? 2 molecules of (GSH) will react with H2O2 to give 2 H2O.. So it is a problem when it is deficient..!
2.1.3. Hb synthysis
2.1.3.1. Glubin chain synthysis defect
2.1.3.1.1. Quantitative defect
2.1.3.1.2. Qualitative defect
2.2. Acquired
2.2.1. Paroxysmal nocturnal hemoglubinuria
2.2.1.1. They discovered the whole name is wrong..! Paroxysmal: it might be chronic.. Nocturnal: it might be in the daytime.. Hemoglobinuria: it might cause also leukuria and platelet in the urine.. - It happens due to absence of complement cutters which supposed to be found in the surface of RBCs, to fight the complement system, when its absence the complement system will attack the RBCs and destroy them > Hemolysis It is a membrane defect..!