Summary
Summary Pathology of Haemolytic Anaemia
- Module
- Medicine (A100)
- Institution
- Imperial College London (ICL)
Summary notes of everything you need to do to answer questions on this topic in medical school exams.
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Haemolytic AnaemiaIntroduction
Normal red cell life span 120 days
Haemolysis defined as shortened red cell survival
Classified as intravascular and extravascular
Intravascular: Within circulation
Extravascular: Removal/destruction by reticuloendothelial (RE) system
They can be further categorised by if they are inherited or acquired
Extravascular Causes
Autoimmune
Alloimmune
Hereditary Spherocytosis (Autosomal Dominant)
Intravascular Causes
Malaria (Globally most common cause)
G6PD deficiency (Protection against Malaria)
Mismatched blood transfusion (ABO)
Cold antibody haemolytic syndrome
Drugs
Microangiopathic Haemolytic Anaemia (MAHA) e.g., Haemolytic Uraemic syndrome
(HUS), Thrombotic Thrombocytopenic Purpura (TTP)
Paroxysmal Nocturnal Haemoglobinuria
Hereditary Haemolytic Anaemias
Disorders of Membrane
Cytoskeletal Proteins
Cation Permeability
Haemoglobin
Thalassaemia
Sickle Cell Syndromes
Unstable Hb variants
Other
Red cell metabolism
Consequences of Haemolysis
Anaemia (+/-)
Erythroid hyperplasia with increased rate of red cell production and circulating reticulocytes
Increased folate demand
Susceptibility to effect of parvovirus B19 (Can lead early red cell arrest)
Cholelithiasis -> Gilbert’s Syndrome increases risk in chronic HA (UGT 1A1 and TA7/TA7)
Increased risk of iron overload (increased intestinal absorption +/- transfusions)
Increased risk of osteoporosis
Clinical Features of Haemolysis
Pallor
Jaundice
Splenomegaly (Extravascular and Extra-medullary haemopoiesis)
Pigmenturia
Family History
Laboratory Features
Anaemia
, Increased reticulocytes
Polychromasia
Hyperbilirubinaemia
Increased LDH
Reduced/absent haptoglobins
Haemoglobinuria
Haemosiderinuria
Band 3 is the major transport anion transporter
Paroxysmal nocturnal haemoglobinuria-> Lack GPI anchor->Attachment of biomolecules to
cell surface-> i.e., Complement regulatory proteins-> Complement destruction
Defects in Red Cell Membrane Disorders
Hereditary Spherocytosis
Vertical interaction-> Proteins that link the cytoskeleton and the lipid bilayer
Band 3
Protein 4.2
Ankyrin
β Spectrin
Hereditary Elliptocytosis
Horizontal interaction
α Spectrin
β Spectrin
Protein 4.1
Hereditary Spherocytosis
Genetic defect of red cell cytoskeleton
Family history in 75%- typically autosomal dominant
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