Lecture 5 - Haem 2

Question 1

What is the common causes of secondary erythroid hypoplasia/aplasia?

Answer 1

1. EPO deficiency
2. Anaemia of inflammatory disease
3. Immune-mediated anaemia
4. Pure red cell aplasia (PRCA)
5. Abnormalities in heme synthesis
6. Disorders of nucleic acid synthesis

Question 2

Briefly describe blood results that you would see with an EPO deficiency and a potential cause of it:

Answer 2

A potential cause could be chronic kidney disease - this results in decreased oxygen consumption and oxygen supply. This then leads to an EPO deficiency. This is seen as mild to moderate, non-regenerative, normocytic, normochromic anaemia

Question 3

Briefly describe the factors that often contribute to anaemia of inflammatory disease and state how this would be seen on a blood test:

Answer 3

1. Iron deficiency - total body iron is reduced as the body moves it into storage sites so that the parasites are not able to use
2. Shortened erythrocyte life span - secondary to membrane damage caused by exogenous oxidants generated during inflammation
3. Inhibition of erythropoiesis - secondary to inflammatory mediators

Mild to moderate, non regenerative, normocytic (rarely microcytic), normochromic anaemia (after 3-10 days & inflammatory leukocytosis)

Question 4

Briefly explain how immune mediated anaemia can lead to maturation arrest and/or marrow hyperplasia:

Answer 4

Nucleated erythrocyte precursors = maturation arrest. Reticulocytes = marrow hyperplasia (this is because we would expect large amounts of erythropoietin produced making prorubricytes and rubricytes). As a result we would see moderate to severe, non regenerative, normocytic, normochromic anaemia

Question 5

Briefly explain the process of pure red cell aplasia (with some potential causes) and state what you would see on a blood test:

Answer 5

Selective erythroid aplasia - DOG - immune mediated immune response to recombinant human EPO. FeLV subgroup C infections causes suppression of erythroid burst-forming units. This will be seen as severe, non regenerative, normocytic, normochromic anaemia

Question 6

Provide an example of a cause of abnormalities in heme synthesis (lead poisoning) and state what would be seen on blood results:

Answer 6

Lead toxicity –> porphyrias = accumulation of porphyrin compounds in cells, tissues and body fluids (seen as mild to moderate, non regenerative, normocytic, normochromic anaemia with basophilic stippling and nucleated RBCs

Question 7

Briefly state the nutrient requirements for erythropoiesis and common on the frequency of a deficiency:

Answer 7

Iron = required for the synthesis of heme (deficiency is common)

Copper = release of iron from tissue (deficiency is uncommon)

Folate and cobalamin (Vitamin B12) –> nucleic acid metabolism (deficiency is uncommon)

Question 8

What is the function of transferrin?

Answer 8

plasma protein involved in iron transport

Question 9

What is the function of ferritin (and haemosiderin)?

Answer 9

storage of iron into macrophages (spleen, liver, BM)

Question 10

Where is hepcidin secreted from and what is the function of it?

Answer 10

Hepcidin is a protein secreted by hepatocytes and is the main systemic regulator of iron metabolism. Hepcidin is decreased with iron deficiency and increased erythropoiesis leads to increased demand for iron.

Question 11

Provide three examples that could lead to iron (and copper) deficiencies:

Answer 11

1. Inadequete dietary Fe intake (e.g. piglets and calves)
2. Chronic external blood loss (GI ulcers, blood sucking parasites, fleas or ticks)
3. Anaemia of inflammatory (chronic) disease = due to over secretion of hepcidin

Question 12

What blood results would be observed as a result of iron (and copper) deficiency?

Answer 12

Moderate, non regenerative, microcytic, hypochromic, anaemia

Question 13

Why are folate and cobalamin (Vit B12) deficiencies rare? What is the exception? What would the blood results look like?

Answer 13

Cobalamin and folate are present in food and also produced by intestinal bacteria. No deficiency is seen in domestic animals. The exception is inherited selective malabsorption of cobalamin in Giant Schnauzers. This is seen as non regenerative anaemia, normocytic, normochromic

Question 14

Briefly explain the changes that are seen in acute blood loss anaemia:

Answer 14

1. Rapid loss of more than 20-30% of blood volume causes hypovolemic shock and death

Rapid loss of up to 20% of the blood volume:

1. Immediately after = hypovolemia w/out anaemia, thrombocytopenia and hypoproteinemia (erthrocytes and plasma)
2. After several hours = normovolemia - pre-regenerative + normocytic + normochromic anaemia + thrombocytosis + hypoproteinemia (the plasma protein concentration will return to normal within a few days
3. After 3-4 days = regenerative, macrocytic, hypochromic anaemia

Question 15

What does a low plasma protein concentration along with anaemia mean?

Answer 15

Recent or ongoing haemorrhage

Question 16

What factors could lead to chronic blood loss anaemia?

Answer 16

1. Parasites (hookworms, fleas)
2. GI ulcers (NSAID, glucocorticoids, mast cell tumours etc.)
3. Neoplasia (bleeding into body cavities and tissues)