anaemia Flashcards
define anaemia, what values are raised
reduction in haemoglobin concentration compared to healthy person of same age and gender
thus, Hb reduced, but also RBC and HCT usually-
temporary cause of anaemia
usually due to lower absolute haemoglobin, but can be due to increase in plasma volume- in healthy person this is temporary as excess fluid excreted
mechanisms of anaemia, NOT causes
lower production of RBC/haemoglobin in bone marrow
loss of blood
reduced lifespan of RBC
large spleen may cause pooling of RBC rather than in blood
cause of lower haemoglobin production in bone marrow
either reduced synthesis of haem (due to lack of iron) or globin ( due to thalassemia
classifying anaemia
based on cell size
microcytic, normocytic or macrocytic
causes of microcytic anaemia
lower haem synthesis (due to iron deficiency, or anaemia of chronic disease, where chronic inflammation occurs)
defect in globin synthesis (thalassemia), either alpha (lower alpha chain) or beta (lower beta chain) thalassemia
macrocytic anaemia
abnormal erythropoeisis where precursors of RBC produce haemoglobin but they don’t divide, so become large
macrocytic vs megaloblastic
macrocytic= increased cell size
one cause is megaloblastic erythropoeisis, where nucleus maturation delayed (DNA synthesis impaired), but cytoplasm keeps growing, so cell becomes large- thus megaloblast is an abnormal erythroblast (red blood cell precursor with nucleus)
another MECHANISM of macrocytic anaemia
premature release of cells from bone marrow- reticulocytes are larger than RBC, so if there are more of them, average cell size increases
causes of macrocytic anaemia
megoblastic anaemia due to B12/folic acid deficiency
drugs affecting DNA synthesis
liver disease/alcohol toxicity
recent major blood loss (loads of reticulocytes produced to combat blood loss)
haemolytic anaemia (increases reticulocytes)
mechanisms of normocytic anaemia
recent blood loss (body hasn’t responded yet)
failure of stem cells to produce red cells
pooling of red cells in spleen
causes of normocytic anaemia/ normochromic (ie normal synthesis of haem)
blood loss- peptic ulcer, esophageal varices and trauma due to accident
failure of production- renal failure (less erythropoetin), bone marrow failure or early stages of iron deficiency/anaemia of chronic disease
pooling- hypersplenism eg in cirrhosis where spleen enlarges
what is haemolytic anaemia and 2 causes
anaemia due to shorter lifespan of RBC (greater haemolysis= more RBC broken down), either due to intrinsic abnormality (issue with RBC itself) or extrinsic abnormality (something acting on normal RBC)
inherited vs acquired haemolytic anaemia and causes of each
inherited anaemia due to abnormalities in cell membrane (eg hereditary spherocytosis), haemoglobin (sickle cell) or enzymes (defect in glycolysis due to pyruvate kinase deficiency, G6P dehydrogenase deficiency)
acquired due to extrinsic factors- can be autoimmune (macrophages damage membrane), drugs can cause oxidant damage, and malaria can damage whole cell as well
intravascular vs extravascular haemolytic anaemia
intravascular occurs in circulation- acute damage to RBC
extravascular occurs when RBC removed by spleen
when to suspect haemolytic anaemia
abnormal red cells (eg more fragments, spherocytes)
more RBC breakdown (high bilrubin- can lead to gallstones/yellow eyes)
more bone marrow activity (more reticulocytes)
anaemia can’t be explained otherwise and is normochormic and normocytic/macrocytic
hereditary spherocytosis and effect
inherited intrinsic defect of membrane- cells lose membrane in spleen so become like a sphere
these RBC are more rigid so are removed by spleen (extravascular haemolysis)- bone marrow responds by reticulocytosis: leads to haemolytic anaemia and bilrubin production= jaundice
treatment of hereditary spherocytosis
splenectomy- only done in severe cases
because bone marrow very active, folic acid deficiency can occur, so diet is important, and folic acid supplementation given as well
G6P dehydrogenase importance
needed for pentose phosphate shunt- protects RBC from oxidant damage (oxidants either intrinsic from blood or extrinsic due to broad beans, chemicals and drugs)
effect of G6P dehydrogenase deficiency and who usually vulnerable
gene for G6PD is on X chromosome, so usually occurs in males
causes intravascular haemolysis due to oxidants- forms irregularly contracted cells, and also denatured haemoglobin called heinz bodies
treatment of someone with G6PD deficiency
blood transfusion may be needed- then diet restriciton, awareness of harmful drugs/chemicals important
autoimmune haemolytic anaemia
autoantibodies bind to red cell antigens, which is recognised by splenic macrophages (complement often present as well), which remove bits of cell membrane= spherocytosis
combination of rigidity of spherocytes and recognition by macrophages leads to removal by spleen
diagnosing autoimmune haemolytic anaemia
spherocytes and increased reticulocytes
detection of autoanitbodies to red cell antigens
treatment of autoimmune haemolytic anaemia
immunosuppressive drugs like corticosteroids
splenectomy for severe cases
microangiopathic haemolytic anaemia causes and treatment
hypertension- treat this
antibody in plasma that causes fibrin deposition in small blood vessels- treat by plasma exchange
