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Year 2 - MCD Haem > Anaemia > Flashcards

Anaemia Flashcards

1
Q

Define anaemia

A

Reduction in amount of Hb in a given volume of blood
BELOW
what would be expected in comparison with a healthy subject of the same age and gender

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2
Q

What is normally reduced in anaemia?

A

Hb

RBC and Hct/PCV are also usually reduced

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3
Q

What can often lead to anaemia but is NOT the case in a healthy person?

A

o reduction is ABSOLUTE amount of Hb in the blood stream

Could also occasionally result from an INCREASE in PLASMA VOLUME (rather than a decrease in Hb)
- this would NOT persist however because the body would be able to remove excess fluid

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4
Q

Mechanisms of anaemia?

A

o Reduced production of RBC/Hb in the bone marrow

o Loss of blood from the body

o Reduced survival of RBCs in circulation

o Pooling of RBCs in the spleen (splenomegaly)

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5
Q

In regards to the MECHANISM of anaemia, how is this different to the CAUSES of anaemia

A

MECHANISM:
- might be due to reduced synthesis of Hb in the bone marrow

CAUSE:
- could be due to a condition causing:
o reduced synthesis of haem (iron deficiency)
o reduced synthesis of globin (beta-thalassaemia)

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6
Q

Classification of anaemia based on cell size?

A

Microcytic (usually also hypochromic)

Normocytic (usually also normochromic)

Macrocytic (usually normochromic)

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7
Q

Common causes of microcytic anaemia?

A

o Defect in haem synthesis

  • iron deficiency
  • anaemia of chronic disease

o Defect in globin synthesis (thalassaemia)

  • defect in alpha-chain synthesis (alpha thalassaemia)
  • defect in beta-chain (beta thalassaemia)
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8
Q

Why does macrocytic anaemia usually occur?

A

Due to abnormal haemopoiesis:
- RBC precursors continue to synthesise Hb and other cellular proteins
BUT
- fail to divide normally

Therefore RBC end up larger than normal

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9
Q

2 causes of macrocytic?

A
  1. Megaloblastic erythropoiesis

2. Premature release of cells

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10
Q

Explain megaloblastic erythropoiesis

A

One of the causes of MACROcytic anaemia

Delay in the maturation of the nucleus
BUT
the cytoplasm continues to mature = cell continues to grow

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11
Q

What is a megaloblast?

A

Abnormal bone marrow erythrocyte - it is:
o larger than normal
o shows nucleocytoplasmic dissociation

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12
Q

What is required to reach a diagnosis of megablastic erythropoiesis?

A

Possible from peripheral blood features
BUT
requires bone marrow examination

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13
Q

Explain premature release of cells from the bone marrow

A

One of the causes of macrocytic anaemia

Young RBCs are 20% larger than normal RBCs so more young cells = MCV will be increased

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14
Q

Common causes of macrocytic anaemia?

A

o Megaloblastic anaemia - as a result of lack of:
- vitamin B12
OR
- folic acid

o DNA synthesis interfering drugs

o Liver disease & ethanol toxicity

o Recent major blood loss with adequate iron stores (reticulocyte no. increases as bone marrow tries to compensate)

o haemolytic anaemia (reticulocytes no. increase as RBCs lost (lyse in blood stream)

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15
Q

Mechanisms that cause normocytic (normochromic) anaemia?

A

o Recent blood loss

o Failure of production RBCs

o Pooling of RBCs in the spleen

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16
Q

Causes of normocytic (normochromic) anaemia?

A

o Peptic ulcers, oseophageal varices, trauma ( for blood loss)

o Early stages of iron deficiency, renal failure, bone marrow failure (for failure of RBC production)

o Hypersplenism e.g. portal cirrhosis (for pooling of RBC in the spleen)

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17
Q

What is haemolytic anaemia and what can it arise from?

A

Shortened survival of RBCs in the circulation

Can result from either:
o INTRINSIC abnormality of the RBCs
o EXTRINSIC factors acting on the normal RBCs

EXTRINSIC factors can also interact with RBCs that have an intrinsic abnormality

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18
Q

Haemolytic anaemia can be further classified - explain this (i.e. I & A)

A

Can be classified as either:
o INHERITED
o ACQUIRED

INHERITED:
- arise due to abnormalities in the cell membrane, Hb OR enzymes in the RBC

ACQUIRED:
- arise due to extrinsic factors such as micro-organisms, chemicals or drugs that damage the RBC

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19
Q

Haemolytic anaemia can be further classified - explain this (i.e. I & E)

A

Can be classified as either:
o INTRAvascular haemolysis
o EXTRAvascular haemolysis

INTRAvascular:
- occurs if there is acute damage to the RBC

EXTRSvascular:
- occurs when defective RBCs are removed by the spleen

Haemolysis is often partly both of these!

20
Q

Examples of INHERITED factors resulting in Haemolytic anaemia?

A

ONENOTE!!

o abnormal RB cell membrane e.g. spherocytosis

o abnormal Hb e.g. sickle cell anaemia

o defect in glycolytic pathway e.g. pyruvate kinase deficiency

21
Q

Examples of ACQUIRED factors resulting in Haemolytic anaemia?

A

ONENOTE!!

o damage to RB cell membrane e.g. AHA or snake bite

o Damage to WHOLE RBC e.g. MAHA

o Oxidant exposure damages RBC membrane and Hb e.g. dapsone or primaquine

22
Q

Example of where an extrinsic factor can interact with RBCs that have an intrinsic abnormality?

A

(ONENOTE!!)

So people with G6PD deficiency are at risk of haemolytic anaemia in states of oxidative stress (LAZ!)

Defect in enzymes of the pentose shunt e.g. G6PD deficiency links with
Oxidant exposure damages RBC membrane
AS
causes precipitation of episodic haemolysis in individuals with enzyme deficiency

23
Q

When to suspect haemolytic anaemia?

A

o when otherwise unexplainable anaemia which is normochromic and usually either normocytic OR macrocytic

Evidence of:
o morphologically abnormal RBCs
o increased RBC breakdown
o increased bone marrow activity

24
Q

Certain conditions that the patient may have hence why would suspect haemolytic anaemia?

A

o Irregularly contracted cells

o Hereditary elliptocytosis (leads to haemolysis)

o Poikilocytosis

o Sickle cell disease

o Fragments - as not being broken down in spleen BUT within circulation (in small capillaries)
= MICROANGIOPATHIC HAEMOLYTIC ANAEMIA

o Gall stones - chronic HA means high excretion of bilirubin SO get higher incidence of gall stones

o Jaundice - sickle cell, RBC broken down quickly

25
Q

Define Hereditary Spherocytosis

A

H.A or chronic compensated haemolysis

resulting from an

INHERITED INTRINSIC defect of the RB CELL MEMBRANE

26
Q

What is the resulting end due to Hereditary Spherocytosis?

A

RBCs become less flexible SO are removed by the spleen prematurely

Known as EXTRAVASCULAR HAEMOLYSIS

27
Q

What happens to the RBCs in Hereditary spherocytosis?

A

After entering the circulation, the RBCs lose their membrane in spleen = spherocytic

28
Q

What often follows hereditary spherocytosis?

A

Extravascular haemolysis

The bone marrow responds by INCREASING output of RBCs. This leads to:

o polychromasia (immature RBCs in blood)

o reticulocytosis (premature cells)

Haemolysis also leads to increased bilirubin production = jaundice = gallstones

29
Q

What are spherocytes prone to?

A

Haemolysis WHEN osmotic pressure is REDUCED

30
Q

Treatment for hereditary spherocytosis?

A

o Splenectomy - ONLY effective treatment

o Good diet
- so that a 2o folic acid deficiency does not occur

31
Q

G6PD?

A

Glucose-6-phosphate dehydrogenase

32
Q

Why is G6PD important?

A

Important enzyme in the PENTOSE PHOSPHATE SHUNT - essential for:

o protection of RBCs from oxidant damage

33
Q

What can G6PDD lead to?

A

Oxidants may be generated in the BS so G6PDD may intrinsically affect the RBCs leading to

HA (haemolysis anaemia)

34
Q

Where do oxidants come from?

A

May be generated in the BS e.g.
o during infection

May be exogenous
o broad beans
o chemicals (mothballs/naphthalene)
o drugs (dapsone/primaquine)

35
Q

Who is normally affected by G6PDD?

A

Gene for G6PD is on the X chromosome

SO normally males BUT females as well is homozygous

36
Q

What does G6PDD usually end up causing?

A

Intermittent, severe INTRAvascular haemolysis

due to an exogenous oxidant

37
Q

G6PDD ends up causing severe intravascular haemolysis - what are these associated with and what does it lead to the formation of?

A

The appearance of IRREGULARLY CONTRACTED CELLS

Hb is denatured and so forms round-balls knows as HEINZ BODIES

38
Q

Can Heinz bodies be removed?

A

YES - by the spleen

BUT it leaves a defect in the RBC

39
Q

Howell-Jolly Bodies vs. Heinz Bodies?

A

Can get MORE THAN ONE Heinz Body in a cell

40
Q

Why does Autoimmune HA arise?

A

Due to the production of autoantibodies directed at RC antigens

41
Q

What does AI HA lead to?

A

Recognised by splenic macrophages = removes parts of RBC membrane = spherocytosis

Complement components can also be bound to Ig molecule which can also be recognised by receptors on the splenic macrophages

42
Q

Why are the RBCs formed in AI HA removed?

A

Form spherocytes which are less flexible - so combined with:
o cell rigidity
o recognition of Abs + complement on RB surface by splenic macrophages

LEADS to removal of these cells from the circulation by the spleen

43
Q

How can AI HA be diagnosed?

A

o Finding spherocytes & an INCREASED reticulocyte count

o Detecting Ig +/- complement of RB surface

o Detecting Abs to RB antigens OR autoAbs in the plasma

44
Q

Treatment for AI HA?

A

o Use CORTICOSTEROIDS and other immunosuppressive agents

o Splenectomy for severe cases

45
Q

Treatment for Microangiopathic HA?

A

o Remove cause e.g. treat severe hypertension OR stopping causative drug

o Plasma exchange when it is caused by an Ab in the plasma (as this leads indirectly to fibrin deposition - i.e. the FRAGMENTS!)

Year 2 - MCD Haem (11 decks)

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