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POM PERSONAL > Anaemia microcytic Part 2 Cell Abnormalities > Flashcards

Anaemia microcytic Part 2 Cell Abnormalities Flashcards

1
Q

Describe anaemia

A

Reduction in haemoglobin circulating blood below what is normal for healthy person of same age and gender of an individual.

Reduction on red blood cell count RBC
And haematocrit Hct

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2
Q

Mechanisms that result in anaemia 4

A
  • reduced production of red blood cells by bone marrow
  • loss of blood from the body
  • reduced survival of red cells in circulation (haemolysis)
  • increased pooling of red cells in an enlarged spleen
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3
Q

Classified by mechanism and by size. Describe the sizes….

A

Microcytic
Macrocytic
Normocytic

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4
Q

What are microcytic cells?

A

They are small

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5
Q

How do we measure size of red cells

A

By measuring the mean cell volume of automated blood counter

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6
Q

What are microcytic cells like

What their cells present

A

They are hypochromic, very pale under the microscope.

Occasional target cells and elliptocytes

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7
Q

Common causes of microcytosis?

A

Iron deficiency anaemia
Anaemia of chronic disease
Thalassaemia

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8
Q

What can microcytosis be caused by?

A

Reduced synthesis of haemoglobin

  • reduction of haem, (iron deficiency or anaemia of disease)
  • reduced synthesis of globin (thalassaemia)
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9
Q

What are the causes of iron deficiency?

A

Increased blood loss

  • menstrual cycle
  • hookworm commonest cause worldwide
  • gastrointestinal

Insufficient intake

  • dietary veggie
  • malabsorption- coeliac disease
  • h. Pylori

Increased requirements
- pregnancy, infancy

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10
Q

What are the stages of iron depletion

A

Iron depletion
- storage iron reduced or absent

Iron deficiency
- low serum iron and transferrin saturation

Iron deficiency anaemia
- low haemoglobin and haematocrit

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11
Q

Clinical features of iron deficiency

A

Palor, fatigue and breathlessness
Failure to thrive, impaired intelectual development in children
Koilonychia, glotitis, inflammation of corners of mouth, angular dermatitis

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12
Q

Causes of anaemia of chronic disease? 5

A

Usually inflammation aspect

Rheumatoid arthiritis 
Autoimmune disease 
Malignancy 
Kidney disease 
Infections of TB or HIV
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13
Q

How is iron best absorbed in what form?

A

The Fe 2+ (animal products) ferrous is better than the 3+ (veggies) ferric

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14
Q

Why do we need iron homeostasis ?

A

No way to excrete iron by ourselves. (Little lost on skin and GI tract.

1-2mg per day
Excess is toxic to the heart and the liver

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15
Q

What is and what is the purpose of hepcerin?

A

Released by the liver
Controls absorption of iron
If amount of iron increases then so does hepcerin.

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16
Q

How is iron absorbed - get ready for many steps

A

Iron enters duodenal enterocytes
It turns into ferritin which is a storage molecule
The it passes through a transmembrane protein called Ferroportin which transports from inside to outside
This then binds to transferrin and can be transferred around the blood

Hepcedin binds here and causes internalisation - prevents influx of iron from entire site
Absorbed iron bound to ferritin and lost from body when enterocyte dies

17
Q

When does hepcedin increase

A

In inflammation leads to low iron supply and the. Anaemia of chronic disease
Actually it leads to increased iron storage but not released into the blood and not transferred as transferrin so to be moved to erythroblasts.
Caused by increase in inflammation of interleukin 6

18
Q

Lab clues for anaemia of chronic disease

A 
C reactive protein is higher
Erythrocyte sedimentation rate is high ESF (time taken for anti coagulated whole blood descend in a standardised tube over a period of time, red blood cells fall in a period of time). Increase occurs with inflammation, anaemia, pregnancy and aging 
Ferritin is high 
Transferrin is low 
Acute phase proteins increase
19
Q

What decreases erythropoietin and pore vents normal flow of iron from the duodenum into the red blood cells

A

Cytokines such as TNF alpha and interleukins in chronic disease IL6 IL1 and IFN γ

This increases hepcidin and decreases iron absorption, and transport and availability

20
Q

Treatment for anaemia of chronic disease

A

Not useful to give iron replacement therapy

Usually treat the illness by reducing inflammation but some patients benefit from erythropoietin treatment.

21
Q 
Compare haemoglobin 
MCV, 
Serum iron 
Ferritin 
Transferrin
A 
Iron deficiency 
Low 
Low 
Low 
Low 
High 
ACD 
Low 
Low 
Low 
High 
Low
22
Q

What are the thalassaemias

A

Mutation or deletion of a gene encoding one of the globin chain results in reduced rate of synthesis.
Reduces rate of synthesis of haemoglobin and therefore microcytosis.

23
Q

What happens in milder forms and in more advanced?

A

Milder forms - the bone marrow can compensate by producing more red cells so microcytosis without anaemia
In more advance cases - fatal or sustained by blood transfusion

24
Q

What are the types of thalassaemias

A

Alpha a deletion and beta a mutation (in this we can see in electrophoresis that there is more hb A2 and more foetal hb because there is no beta globin to compensate) which affect us

25
Q

Some key features in blood count

Plus some other links to the cells present in a blood film

A

More cells so blood count is larger
Increased RBC and normal Hb and Hct
Reduced MCV and MCH (absolute amount of haemoglobin in an individual red cell)
BUT THE MCHC (concentration of haemoglobin in a red cell- relates to shape) which is usually low is iron deficiency is normal (links to hypochromia) in thalassaemia.
The blood film may show only microcytes, or poikilocytes including target cells.

26
Q 
Comparison of iron deficiency and thalassaemia trait 
Hb
MCV
MCH
MCHC
RBC
Hb electrophoresis
A 
Iron deficiency 
 Normal or lower 
Low in proportion to Hb
Low in proportion to Hb
Low 
Low 
Normal 
Thalassaemia 
Normal or mildly lower 
Lower for same Hb 
Lower for same Hb 
Relatively preserved 
Increased 
HbA2 raised in beta thalassaemia trait but normal in alpha trait
27
Q

Why is it important to distinguish thalassaemias and iron deficiency?

A

To replacement in iron in thallasemia has no effect

Need to advise individuals in future of potential risks in offspring (genetic counselling)

28
Q

What other tests can help you distinguish these?

A

One is the iron stores, serum ferritin

POM PERSONAL (13 decks)

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