Hameotology - RBC Flashcards
What produces all types of blood cells?
Bone marrow
What is the production of new blood cells called?
Haemopoiesis
Multipotent haematopoietic stem cells have three fates
Self renewal
Common myeloid progenitor
Common lymphoid progenitor
What is the process of RBC production called?
What is required for the proper functioning of this process?
Erythropoiesis
Erythropoietin, Folic acid, vitamin B12, iron
Where is iron absorbed? What inhibits this?
How much?
Duodenum (phytates in food reduce iron absorption. Further fe 3+ must be reduced further for absorption. Both are found in veg making iron absorptioless efficient than meat
1-2 mg of Fe a day (as high iron levels in blood are toxic and excess iron can only be secreted by 1-2 mg a day through the skin)
What transports iron in plasma?
Where and how is iron stored?
Fe-transferrin
Liver, bound ferritin
What is the function of hepcidin?
Liver makes hepcidin in response to high fe stores triggering inflammation. Hepcidin degrades ferroportin so any iron trapped in the enterocyte is lost when the cell dies and is shed
Role of B12 and folate in RBC
To make dTTP (precursor to thymidine) requires B12 and folate. Without cell can’t divide properly.
How is B12 absorbed?
Parietal cells of stomach make intrinsic factor which binds to B12 in ileum and are absorbed
RBC lifespan
120 days
Microcytic
Small RBCs (often hypochromatic as well)
Normocytic
Normal sized RBCs
Macrocyctic
Large RBCs (often polychromatic)
Polychromasia
Immature increased blue tinge of RBC cytoplasm (sign of immaturity)
Hypochromia
Larger area of central pallor (often accompanies microcytosis)
Hyperchromia
Cells lack central pallor (abnormal shape)
Reticulocytes
Immature RBCs
Reticulocystosis
Increased presence of reticulocytes due to bleeding or increased RBC destruction
Anisocytosis
More variation in RBC size
Poikilocytosis
More variation in shape
Spherocyte
Round RBC most often due inheritance of a faulty gene(s) coding for protein(s) of the cytoskeleton
Target cells
Increased Hb in centre of central pallor
Sickle cell
HbSS has tendency to polymerise especially when deoxygenated
Anaemia
Reduced Hb conc
Microcytic anaemia
Usually also hypochromic
Often caused by defect in haem synthesis (Fe deficiency, anaemia of chronic disease) or globin synthesis (thalassemia)
Causes of Fe deficiency
Increased blood loss, insufficient intake, increased requirements (pregnancy, infancy, physiological)
Microcytic anaemia
Megaloblastic erythropoiesis → delay in maturation of nucleus while cytoplasm continues to
mature and cell continues to grow, megaloblasts generally seen in bone marrow not on blood
film
▪ Causes → lack of B12 or folate, use of drugs interfering w/DNA synthesis, liver disease +
ethanol toxicity, recent major blood loss w/adequate iron stores (increased reticulocytes),
haemolytic anaemia (increased reticulocytes)
Normocytic anaemia
Recent blood loss → GI haemorrhage, trauma
▪ Failure of production of red cells → early stages of iron deficiency, bone marrow failure or
suppression, bone marrow infiltration e.g. leukaemia
▪ Pooling of red cells in spleen → hypersplenism e.g. liver cirrhosis, splenic sequestration in
sickle cell anaemia
Polycythaemia
POLYCYTHAEMIA → too many red cells in circulation, Hb, RBC and Hct are all increased
o Blood doping or over transfusion
o Appropriately increased erythropoietin → e.g. as result of hypoxia
o Inappropriate erythropoietin synthesis or use → e.g. from renal tumour secretions
o Independent of erythropoietin → polycythaemia vera – intrinsic bone marrow disorder
(myeloproliferative neoplasm) leading to hyper viscosity (thick blood) – drugs given to reduce bone
marrow production of red cells
