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Blood > Haem 3 > Flashcards

Haem 3 Flashcards

1
Q

Define anaemia

A

reduction in the amount of haemoglobin in a given volume of blood, below what would be expected in comparison with a healthy subject of the same age and gender

Hb reduced, The RBC and the PCV/Hct are usually also reduced

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2
Q

2 conceptual causes of anaemia

A

usually due to a reduction of the absolute amount of haemoglobin in the blood stream

Occasionally it results from an increase in the volume of plasma rather than a decrease in the amount of haemoglobin

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3
Q

In healthy person, can anaemia be from an increase in plasma volume?

A

NO- increase in plasma volume cannot persist because the excess fluid in the circulation is excreted

(anaemia can therefore be regarded as a resulting from a decrease of the absolute amount of haemoglobin in the circulation)

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4
Q

4 Mechanisms of anaemia

A

Reduced production of red cells/haemoglobin in the bone marrow

Loss of blood from the body

Reduced survival of red cells in the circulation

Pooling of red cells in a very large spleen

This is really critical for framework... think 
Production reduces
Pooling in spleen
Blood loss
Lifespan reduces
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5
Q

Differentiate mechanism and cause

A

The mechanism of the anaemia might be reduced synthesis of haemoglobin in the bone marrow

The cause of this could be either a condition causing reduced synthesis of haem or one causing reduced synthesis of globin

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6
Q

Classification of anaemia on cell size, and whether each type is hyperchromic or hypochromic or normochromic

A

Microcytic (usually also hypochromic)
Normocytic (usually also normochromic)
Macrocytic (usually also normochromic)

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7
Q

Common cause of microcytic anaemia

A
  1. Defect in haem synthesis
    (Iron deficiency or
    Anaemia of chronic disease)
  2. Defect in globin synthesis (thalassaemia)

Defect in α chain synthesis (α thalassaemia)
Defect in β chain synthesis (β thalassaemia)

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8
Q

2 mechanisms of macrocytic anaemia

A
  1. usually result from abnormal haemopoiesis so that the red cell precursors continue to synthesize haemoglobin and other cellular proteins but fail to divide normally
    e. g. megaloblastic erythropoiesis
  2. premature release of cells from the bone marrow
    Young red cells are about 20% larger than mature red cells so if there is an increased proportion of young red cells (reticulocytes) in the circulation, the average cell size (MCV) will be increased
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9
Q

What is megaloblastic erythropoiesis

A

A specific type of macrocytic anaemia, in which there is delay in maturation of the nucleus while the cytoplasm continues to mature and the cell continues to grow (nothing wrong with ribosomes but DNA synthesis wrong) shows nucleo-cytoplasmic dissociation

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10
Q

What might imply megaloblastic anaemia without needing to do bone marrow test

A

Hypersegmented neutrophil and oval macrophages in perpheral blood

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11
Q

Outline premature release of cells from bone marrow as a cause of macrocytic anaemia

A

premature release of cells from the bone marrow

Young red cells are about 20% larger than mature red cells so if there is an increased proportion of young red cells (reticulocytes) in the circulation, the average cell size (MCV) will be increased

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12
Q

List common causes of macrocytic anaemia

A
  • Megaloblastic anaemia as a result of lack of vitamin B12 or folic acid
  • Use of drugs interfering with DNA synthesis
  • Liver disease and ethanol toxicity
  • Recent major blood loss with adequate iron stores (reticulocytes increased)
  • Haemolytic anaemia (reticulocytes increased)
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13
Q

Mechanism of normocytic normochromic anaemia

A

Recent blood loss
Failure of production of red cells
Pooling of red cells in the spleen

(note… soon after lots of blood loss you’ll get macrocytic anaemia)

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14
Q

Causes of normochromic anamia (distinct from mechanism)

A

Blood loss (mech): Peptic ulcer, oesophageal varices, trauma

Failure of production: 
Early stages of iron deficiency or anaemia of chronic disease
Renal failure
Bone marrow failure or suppression
Bone marrow infiltration

Hypersplenism: e.g. portal cirrhosis

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15
Q

What is haemolytic anaemia

A

anaemia resulting from shortened survival of red cells in the circulation

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16
Q

2 causes of haemolytic anaemia

A

intrinsic abnormality of the red cells

extrinsic factors acting on normal red cells

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17
Q

Inherited and acquired cause of haemolytic anaemia

A

inherited:
1. abnormalities in the cell membrane (e.g hereditary spherocytosis),

  1. abnormalities in the Hb (e.g. sickle cell)
  2. enzyme defect (G6PD deficiency) in the red cell
  3. defect in glycolytic pathway (pyruvate kinase deficiency)

Acquired:

  1. Damage to whole red cell
    - microangiopathic haemolytic anaemia, see end
  2. Oxidant exposure (such as?), damage to red cell membrane and Hb this will lead to episodic haemolysis in inviduals with G6PD deficiency
  3. Damage to cell membrane (autoimmune haemolytic anaemia or snake bite)

EXTRINSIC FACTORS can interact with INHERENTLY ABNORMAL RED CELLS TOO

18
Q

How else can haemolytic anamia be classified

A

Intravascular haemolysis occurs if there is very acute damage to the red cell

Extravascular haemolysis occurs when defective red cells are removed by the spleen
Often haemolysis is partly intravascular and partly extravascular

19
Q

When to suspect haemolytic anaemia

A

Otherwise unexplained anaemia, which is normochromic and usually either normocytic or macrocytic (reticulocytes increased in haemolysis)

Evidence of increased bone marrow activity increased reticulocte count/polychromasia)

Evidence of morphologically abnormal red cells

Evidence of increased red cell breakdown (unconjgated bilirubin)

20
Q

Why would jaundice in child imply haemolytic anaemia?

A

Because break down of red blood cells exceeds the amount lliver can process

21
Q

Outline hereditary spherocytosis

A

Haemolytic anaemia or chronic compensated haemolysis resulting from an inherited intrinsic defect of the red cell membrane

AFTER ENTERING the circulation the cells lose membrane in the spleen and thus become spherocytic

22
Q

Consequences of hereditary spherocytosis and the type of anaemia this is

A

Red cells become less flexible and are removed prematurely by the spleen – extravascular haemolysis

bone marrow responds to haemolysis by an increased output of red cells leading to polychromasia and reticulocytosis

Haemolysis leads to increased bilirubin production, jaundice and gallstones

So haemolytic anaemia

OSMOTIC FRAGILITY TEST

23
Q

Treatment of Hereditary spherocytosis

A

only effective treatment is splenectomy (only in severe cases) due to the extravascular haemolysis

good diet is important so that a secondary folic acid deficiency does not occur (otherwise this can lead to megaloblastic crisis –> due to not enough vitamins)

or 1 folic acid tablet daily

24
Q

Function fo G6PD

A

essential for the protection of the red cell from oxidant damage

Oxidants may be generated in the blood stream, e.g. during infection, or may be exogenous

important enzyme in pentose phosphate shunt in normal carb metabolism

25
Q

Examples of extrinsic oxidants dangerous in G6PD deficiency

A

foodstuffs (e.g. broad beans), chemicals (e.g. naphthalene) or drugs (e.g. dapsone- leprosy, primaquine- malaria)

26
Q

Outline the genetics of G6PD deficiency

A

G6PD is on the X chromosome, so males are HEMIZYGOUS (i.e only have one gene for it- men are hemizygous for all genes on the x chromosome that are not also on the Y)….. (but occasionally homozygous females can get it or even hemizygous due to x inactivation)

27
Q

What type of haemolysis does G6PD cause and what kind of cells does this leave

A

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

this intravascular haemolysis leads to appearance of considerable numbers of irregularly contracted cells, with heinz bodies

28
Q

What are Heinz bodies

A

In irregularly contracted cells in G6PD, Haemoglobin is denatured due to oxidative stress and forms round inclusions WITHIN the cell known as Heinz bodies, which can be detected by a specific test

29
Q

How does the spleen deal with Heinz bodies

A

Heinz bodies are removed by the spleen, leaving a defect in the cell, this is also an irregularly contracted cell, known as a bite cell or a horn cell

30
Q

How can acute haemolysis be treated

A

blood transfusion

31
Q

What causes autoimmune haemolytic anaemia

A

production of autoantibodies directed at red cell antigens

The immunoglobulin bound to the red cell membrane is recognized by splenic macrophages, which remove parts of the red cell membrane, leading to spherocytosis

Complement components can also be bound to the immunoglobulin molecule, and they are also recognised by receptors on splenic macrophages

32
Q

What is the consequence of macrophage recognition of immunoiglobulins and compleme tin autoimmune haemolytic anaemia

A

The resulting spherocytes are less flexible than normal red cells

The combination of cell rigidity and recognition of antibody and complement on the red cell surface by splenic macrophages leads to removal of cells from the circulation by the spleen

33
Q

Diagnosis of autoimmune haemolytic anamia

A

Finding spherocytes and an increased reticulocyte count

Detecting immunoglobulin ± complement on the red cell surface

Detecting antibodies to red cell antigens or other autoantibodies in the plasma

34
Q

How can you treat Autoimmune haemolytic anaemia

A

Use of corticosteroids and other immunosuppressive agents

Splenectomy for severe cases

35
Q

Outline treatment for Microangiopathic haemolytic anaemia

A

Removing the cause, e.g. treating severe hypertension or stopping a causative drug

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

36
Q

What is a megaloblast….

A

An abnormal bone marrow erythroblast- larger than normal and shows nucleo-cytoplasmic dissociation.

You would have needed to do bone marrow test in past, but now can look for hypersegmented neutrophils, and oval macrocytes in the blood

37
Q

What is the osmotic fragility test and what can it prove

A

It measures resistance of a RBC to haemolysis at increasingly more dilute saline solutions. If it haemolyses early (i.e. when saline solution isnt that dilute yet), it’s fragile.

Fragility in hereditary spherocytosis and thalassamemia

38
Q

T/f spherocytes can only be hereditary

A

F! In autoimmune haemolytic anaemia (ACQUIRED), autoantibodies are recognised by splenic macophaes, and these macrophages remove part of red cell membrae, leading to spherocytosis….

39
Q

Why are cells removed by spleen in autoimmune haemolytic anaemia

A

spherocytes less flexible,
this rigidity + recognition of antobody and complement on red cell surface by splenic macrophages leads to removal of cells by spleen

40
Q

What is microangiopathic haemolytic anaemia

A

type of acquired haemolytic anaemia

formation of a fibrin mesh due to increased activation of the system of coagulation (pathological). The red blood cells are physically cut by these protein networks. The resulting fragments are the schistocytes

41
Q

Consequences with haemolytic anaemia

A

Bilirubin production, jaundice and gallstones

Blood (12 decks)

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