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1. Acquired hemolytic anaemia Dr. Fatma Al-Qahtani
2. Immune haemolytic anaemias A – Auto immune .H.A
Are caused by AB production by the body
against its own red cells.
C/BY apositive (DAT) / Coomb’s test.
Divided into ? 1) warm? 37c
2) cold ? 4 c
4. Warm AIHA IgG alone or with complement and take up by RE macrophages
More in spleen
Spherocytosis prominent
DAT is positive
Bind at 37c
5. Cold AIHA The AB ? monoclonal ? ICHS ,
lymphoproliferative disorder
? Polyclonal ? infection ? IM, MP
Usually IgM
Bind to red cell at 4c
Mild jaundice and splenomegaly
Spherocytosis is less marked
6. B. Alloimmune hemolytic anemias
Hemolytic transfusion reactions
Hemolytic disease of the newborn
Allograft associated
C. Drug-induced immune hemolytic anemia
Drug absorption mechanism
Membrane modification mechanism
Immune complex mechanism
7. Coombs TestAntiglobulin Test
8. Coombs TestAntiglobulin Test
9. Non-Immune Hemolytic Anemias Hemolytic anaemias due to mechanisms or agents
other than antibodies +/or complement e.g.:
Mechanical (traumatic) (fragmentation)
Toxins
Infections
Splenomegaly (hypersplenism)
Burn (physical)
Renal failure and liver failure
Chemical
10. Non-Immune Acquired Hemolytic Anemia
11. Non-Immune Acquired Hemolytic Anemia
12. Mechanical (Traumatic) (Fragmentation) This is due to direct trauma (stress) to the RBCs causing fragmentation of the RBCs & intra-vascular hemolysis. The fragmented cells can be seen on peripheral blood smears & are called (schistocytes).
Types:
Cardiac – most common
Due to:
Prosthetic valves
Patches
Valvular diseasse e.g., stenosis
13. Mechanical (Traumatic) (Fragmentation)(cont…) Microangiopathic: mechanical hemolysis due to contact between the RBCs & the abnormal intema of thrombosed, narrowed, necrotic small vessels or fibrin strand formation.
Caused by many diseases e.g., DIC (disseminated intravascular coagulation), malignant hypertension, disseminated malignancies especially mucin secreting adenocarcinomas, TTP (thrombocytopenic purpura), hemolytic uremic syndrome (HUS).
14. Causes of Microangiopathic Hemolytic Anemia
15. Causes of Microangiopathic Hemolytic Anemia(cont…)
16. Mechanical (Traumatic) (Fragmentation)(cont…) Causes intravascular hemolysis
Hemoglobinurea
Hemoglobinemia
Low haptoglobin
Fragmented RBCs (schistocytes) on peripheral blood film
Hemosidrinurea
18. Clostidium Perfringens:
Due to action of lipase and proteinase enzymes produced by the organism.
Meningococcal:
Due to DIC
19. Malaria due to:
Direct invasion causing intravascular lysis &/or extravascular lysis.
Immune complex formation.
Splenomegaly.
Black water fever:
Is an example of severe intravascular hemolysis due to falciparum sp.
20. Chemical:
e.g., some toxins e.g., spider venom, snake venom, bacterial toxins, arsenic (As), (Cu).
Physical:
Burn: characterized by the presence of many spherocytes in the peripheral blood.
Splenomegaly
Renal failure and liver failure
Due to change in the metabolic structure of the RBCs,
22. Hemolytic Uremic Syndrome Acquired-disorder affecting mainly infants and
children.
Characterized by:
Intravascular hemolysis
Renal failure
Thrombocytopenia
23. Classification Sporadic:
Occuring denovo with no preceeding disease. Believed to be due to an inherited defect in vascular hemostasis.
Epidemic, typical form:
Following a systemic illness of fever, diarrhea and vomiting. In many cases, no organisms are identified. However, in some cultures are positive e.g., for E. coli.
Mechanisms:
Endothelial swelling & disruption resulting in platelet deposition on the vessel wall.
24. Clinical Features Jaundice, hemoglobinuria, proteinuria.
Hypertension, uremia, oliguria.
Anemia, thrombocytopenia purpura.
CNS – unusual: convulsion, coma
25. Laboratory Findings(Cont…) Chemistry:
Elevated urea
Elevated creatinine
Elevated bilirubin
Proteinuria + hemoglobinuria
Coagulation:
Prolonged PT, PTT but not always
26. Laboratory Findings Blood film:
Fragmentation of RBCs
Thrombocytopenia
Polychromasia
CBC:
Anemia
Thrombocytopenia: usually <50,000
Bone marrow:
Hypercellular with increased erythropoiesis + increased megakaryopoiesis
27. Thank You For Your Attention!