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YR2: MCD Haematology > Anaemia and Polycythaemia > Flashcards

Anaemia and Polycythaemia Flashcards

1
Q

What is anaemia?

A

A reduction in the amount of Hb in a given volume of blood below what would be expected in comparison with a healthy subject of the same age + gender
RBC + Hct usually also reduced

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2
Q

Other than a reduction in the absolute amount of haemoglobin in the blood stream, what else could cause anaemia?

A

Increase in plasma volume (decreases the Hb concentration)

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3
Q

Why would anaemia from an increase in plasma volume only be transient in a healthy individual?

A

Excess fluid would be excreted

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4
Q

State 4 mechanisms of anaemia.

A

Reduced production of RBC’s/Hb in the bone marrow
Loss of blood from the body (haemorrhage)
Reduced survival of RBC’s (haemolytic)
Pooling of RBC’s in a very large spleen

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5
Q

For each type of anaemia, state whether they are usually hypochromic, normochromic or hyperchromic.

A

Microcytic: hypochromic
Normocytic: normochromic
Macrocytic: normochromic

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6
Q

State 2 common causes of microcytic anaemia.

A

Defect in Haem synthesis: Iron deficiency, Anaemia of chronic disease
Problem with globin synthesis: Alpha thalassemia, Beta thalassemia

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7
Q

What mechanism usually causes macrocytic anaemia?

A

Abnormal haemopoiesis- red cell precursors continue to synthesise Hb + other proteins but fail to divide
Thus, cells end up larger than normal

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8
Q

What is megaloblastic erythropoiesis? Describe the appearance of a megaloblast.

A

A delay in the maturation of the nucleus while the cytoplasm continues to mature + the cell continues to grow
= a cause of macrocytic anaemia
Large + show nucleo-cytoplasmic dissociation

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9
Q

What is an alternative mechanism of macrocytosis?

A

Premature release of cells from the bone marrow

Reticulocytes are ~ 20% larger than mature red cells so reticulocytosis would increase the MCV

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10
Q

State the 2 most common causes of megaloblastic anaemia.

A

B12 deficiency

Folate deficiency

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11
Q

State 5 common causes of macrocytic anaemia.

A

Drugs that interfere with DNA synthesis (e.g. chemotherapy)
Liver disease
Ethanol toxicity
Recent major blood loss with adequate iron stores (reticulocytes increased)
Haemolytic anaemia (reticulocytes increased)

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12
Q

State 3 mechanisms of normocytic normochromic anaemia.

A

Recent blood loss
Failure to produce RBCs
Pooling of RBCs in the spleen

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13
Q

State 5 causes of normocytic normochromic anaemia.

A 
Peptic ulcer  
Oesophageal varices  
Trauma 
Failure of production of RBC's: Early stages of iron deficiency, ACD, Renal failure, Bone marrow failure/ infiltration 
Hypersplenism
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14
Q

Define haemolytic anaemia.

A

Anaemia resulting from shortened survival of RBC’s in the circulation
Can result from intrinsic abnormality of cells or extrinsic factors acting on normal cells

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15
Q

State 2 different classifications of haemolytic anaemia.

A

Inherited: abnormalities of the cell membrane, Hb or the enzymes in the RBC
Acquired: extrinsic factors e.g. micro-organisms, chemicals or drugs

Intravascular: if there is very acute damage to the red cell
Extravascular: when the spleen removes defective red cells

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16
Q

State 4 inherited abnormalities that can cause haemolytic anaemia.

A

Abnormal red cell membrane
Abnormal Hb
Defect in the glycolytic pathway e.g. pyruvate kinase deficiency
Defect in enzymes of the pentose shuttle e.g. G6PD deficiency

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17
Q

State 3 acquired abnormalities that cause haemolytic anaemia.

A

Damage to the red cell membrane e.g. AIHA
Damage to the whole red cell
Oxidant exposure

18
Q

Explain how G6PD Deficiency can cause haemolytic anaemia.

A

Oxygen-carrying role of RBC’s means they are at constant risk of oxidant damage
G6PD is part of the pentose phosphate pathway
G6PD deficiency is very susceptible to oxidant damage + thus HA, as lacking enzyme needed to protect the cell

19
Q

When would you suspect haemolytic anaemia?

A

Otherwise unexplained anaemia that is normochromic + usually normocytic or macrocytic
Morphologically abnormal red cells
Increased RBC turnover e.g. high BR
Increased bone marrow activity

20
Q

What does the presence of fragments in the blood film suggest? What condition can cause this?

A

Suggests RBC’s are being broken down within the circulation (in small vessels)
Microangiopathic haemolytic anaemia

21
Q

State 2 important signs of haemolytic anaemia.

A

Jaundice: due to increased break down of RBC’s there is an increase in BR
Increase in BR can also increase risk of gallstones

22
Q

State examples of inherited diseases causing haemolytic anaemia that have defects at the following sites:

a. Membrane
b. Haemoglobin
c. Glycolytic Pathway
d. Pentose Shunt

A

Membrane: Hereditary spherocytosis
Haemoglobin: Sickle cell anaemia
Glycolytic Pathway: Pyruvate kinase deficiency
Pentose Shunt: G6PD deficiency

23
Q

State examples of acquired disease causing haemolytic anaemia that have defects at the following sites:

a. Membrane - immune
b. Whole red cell - mechanical
c. Whole red cell - oxidant
d. Whole red cell - microbiological

A

Membrane – immune: AI haemolytic anaemia
Whole red cell –mechanical: Microangiopathic haemolytic anaemia
Whole red cell – oxidant: Drugs + chemicals
Whole red cell – microbiological: Malaria

24
Q

What is hereditary spherocytosis?

A

Haemolytic anaemia or chronic compensated haemolysis resulting from an intrinsic inherited defect of the red cell membrane
After entering the circulation, cells lose membrane in the spleen + become spherocytic

25
Q

What are the features of red cells in hereditary spherocytosis?

A

Become less flexible + are removed prematurely by the spleen
Are LARGE + ROUND
Have an increased MCHC

26
Q

How does the bone marrow respond to the increased extravascular haemolysis in hereditary spherocytosis?

A

It increases output of red cells leading to polychromasia + reticulocytosis

27
Q

What is an effective treatment for hereditary spherocytosis?

A

Splenectomy

28
Q

Why is a good diet important in patients with hereditary spherocytosis?

A

They have increased bone marrow activity + erythropoiesis so they need a supply of B12, folate + iron to keep producing RBC’s

29
Q

Describe the pattern of inheritance of G6PD deficiency.

A

X linked recessive

Those affected are usually hemizygous males

30
Q

What can G6PD deficiency cause?

A

Intermittent, severe intravascular haemolysis as a result of infection or exposure to an exogenous oxidant

31
Q

What tends to appear in blood films during episodes of severe intravascular haemolysis?

A

Irregularly contracted cells

32
Q

What happens to haemoglobin during episodes of severe intravascular haemolysis?

A

It becomes denatured + forms round inclusions called Heinz bodies
(can get >1 Heinz body per cell unlike Howell-Jolly bodies)

33
Q

What causes autoimmune haemolytic anaemia?

A

Results from production of autoantibodies against red cell antigens
Very sudden + dramatic

34
Q

Describe how autoimmune haemolytic anaemia can lead to spherocytosis.

A

Immunoglobulin bound to the red cell is recognised by splenic macrophages, which remove parts of the cell membrane leading to spherocytosis.
Complement components can also be bound to the immunoglobulin, + they are also recognised by receptors on splenic macrophages

35
Q

State 2 causes of spherocytosis.

A

Hereditary spherocytosis

Autoimmune haemolytic anaemia

36
Q

Describe the diagnosis of autoimmune haemolytic anaemia.

A

Finding spherocytes
Increased reticulocyte count
Detecting immunoglobulin on the red cell surface
Detecting antibodies to red cell antigens or other antibodies in the plasma

37
Q

What is the treatment for autoimmune haemolytic anaemia?

A

Corticosteroids /other immunosuppressive agents

Splenectomy in severe cases

38
Q

What is the difference between the mechanism and cause of anaemia? Give an example to illustrate

A 
Mechanism= reduced synthesis of Hb in bone marrow
Cause= a condition causing reduced synthesis of haem or globin
39
Q

What may cause G6PD deficiency?

A

Extrinsic oxidants in foodstuffs e.g. broad beans, chemicals e.g. naphthalene or drugs e.g. dapsone

40
Q

What happens to Heinz bodies?

A

Removed by spleen leaving a defect in the cell “bite cell”

41
Q

How is microangiopathic haemolytic anaemia treated?

A

Removing the cause e.g. treating severe hypertension

Plasma exchange when caused by an antibody in the plasma that is leading indirectly to fibrin deposition

YR2: MCD Haematology (11 decks)

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