Hameotology - RBC

Question 1

What produces all types of blood cells?

Answer 1

Bone marrow

Question 2

What is the production of new blood cells called?

Answer 2

Haemopoiesis

Question 3

Multipotent haematopoietic stem cells have three fates

Answer 3

Self renewal
Common myeloid progenitor
Common lymphoid progenitor

Question 4

What is the process of RBC production called?

What is required for the proper functioning of this process?

Answer 4

Erythropoiesis

Erythropoietin, Folic acid, vitamin B12, iron

Question 5

Where is iron absorbed? What inhibits this?

How much?

Answer 5

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)

Question 6

What transports iron in plasma?

Where and how is iron stored?

Answer 6

Fe-transferrin

Liver, bound ferritin

Question 7

What is the function of hepcidin?

Answer 7

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

Question 8

Role of B12 and folate in RBC

Answer 8

To make dTTP (precursor to thymidine) requires B12 and folate. Without cell can’t divide properly.

Question 9

How is B12 absorbed?

Answer 9

Parietal cells of stomach make intrinsic factor which binds to B12 in ileum and are absorbed

Question 10

RBC lifespan

Answer 10

120 days

Question 11

Microcytic

Answer 11

Small RBCs (often hypochromatic as well)

Question 12

Normocytic

Answer 12

Normal sized RBCs

Question 13

Macrocyctic

Answer 13

Large RBCs (often polychromatic)

Question 14

Polychromasia

Answer 14

Immature increased blue tinge of RBC cytoplasm (sign of immaturity)

Question 15

Hypochromia

Answer 15

Larger area of central pallor (often accompanies microcytosis)

Question 16

Hyperchromia

Answer 16

Cells lack central pallor (abnormal shape)

Question 17

Reticulocytes

Answer 17

Immature RBCs

Question 18

Reticulocystosis

Answer 18

Increased presence of reticulocytes due to bleeding or increased RBC destruction

Question 19

Anisocytosis

Answer 19

More variation in RBC size

Question 20

Poikilocytosis

Answer 20

More variation in shape

Question 21

Spherocyte

Answer 21

Round RBC most often due inheritance of a faulty gene(s) coding for protein(s) of the cytoskeleton

Question 22

Target cells

Answer 22

Increased Hb in centre of central pallor

Question 23

Sickle cell

Answer 23

HbSS has tendency to polymerise especially when deoxygenated

Question 24

Anaemia

Answer 24

Reduced Hb conc

Question 25

Microcytic anaemia

Answer 25

Usually also hypochromic | Often caused by defect in haem synthesis (Fe deficiency, anaemia of chronic disease) or globin synthesis (thalassemia)

Question 26

Causes of Fe deficiency

Answer 26

Increased blood loss, insufficient intake, increased requirements (pregnancy, infancy, physiological)

Question 27

Microcytic anaemia

Answer 27

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)

Question 28

Normocytic anaemia

Answer 28

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

Question 29

Polycythaemia

Answer 29

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