Classification of Anaemia and Iron (haematology) Flashcards

1
Q

What characterises anaemia?

A

Low haemoglobin levels below normal.

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2
Q

What are the normal values of Hb for:
1. Children(6mnths-5yrs)
2. Children (5-11yrs)
3. Children (12-14 yrs)
4. Pregnant women
5. Non-pregnant women
6. Men

A
  1. 11g/dL
  2. 11.5 g/dL
  3. 12 g/dL
  4. 11g/dL
  5. 12 g/dL
  6. 13 g/dL
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3
Q

What are the symptoms of anaemia? (8)

A

-Confusion, weakness, lethargy, palpitations, headaches, symptoms of heart failure and angina pectoris, difficulty in breathing.

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4
Q

What are the clinical signs of anaemia? (4)

A

General- hyperdynamic circulation with tachycardia, pallor of mucous membrane or nail beds, systolic flow murmur.
Specific- are associated with particular types of anaemia.

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5
Q

What determine the clinical features of anaemia? (4)

A

-Age, severity, speed of onset and haemoglobin O2 dissociation curve.

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6
Q

Is anaemia a syndrome or disease?

A

Syndrome

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7
Q

Two classifications of anaemia with regards to bone marrow response? (4)

A

-Regenerative anaemia (RPI>3)- bone marrow did try to compensate by producing more RBCs.
-Hypo-regenerative anaemia (RPI<2)- bone marrow did not succeed in compensating for the low RBCs.

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8
Q

What are the causes of microcytic hypochromic anaemia? (2)

A
  • Iron deficiency and chronic inflammation or malignancy.
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9
Q

What is the next step to be taken in normocytic anaemia?

A

Reticulocyte count

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10
Q

What type of normocytic anaemia has a high reticulocyte count

A

Haemolysis or blood loss

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11
Q

What are the dietary factors that affect the bioavailability or iron? (2)

A

Inhibitors such as calcium, oxalic acid, polyphenols and phytates.
Enhancers such as presence of heme iron and ascorbic acid.

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12
Q

What are the factors that regulate hepcidin, and what is hepcidin? (4)

A

Hepcidin is an iron inhibitor.
Factors affecting the synthesis of hepcidin are:
-Increased transferrin saturation (increases synthesis)
-Decreased transferrin saturation (inhibits synthesis)- IL6, EPO, increased erythropoiesis.

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13
Q

How does hepcidin affect iron? (2)

A

-It inhibits iron release from macrophages.
-It inhibits iron absorption in small intestines.

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14
Q

What are the five principles of iron deficiency anaemia management? (5)

A

-Confirm the diagnosis
-Find the cause
-Correct or manage the primary cause.
-Provide iron therapy, either orally or parenterally.
- Check whether the therapy was successful.

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15
Q

What causes iron deficiency? (4)

A

-Inadequate diet
-Increased demands due to prematurity, pregnancy, adolescence.
- Malabsorption
-Chronic blood loss such as menorrhagia.

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16
Q

What are the clinical features of iron deficiency anaemia, besides the ones for anaemia generally?

A

Koilonychia (spoon shaped nails), glossitis, pica and hair thinning.

17
Q

Laboratory features of iron deficiency

A

Peripheral blood smear
-Hypochromic, microcytic red cells, thrombocytosis is usually present, pencil-shaped poikilocytes, reticulocytopenia.

Bone marrow (not essential to do that)
-Absent iron stores and sideroblasts, small erythroblasts with ragged cytoplasm.

18
Q

What are the laboratory findings in IDA? (3)

A

Low serum iron.
Raised transferrin.
Low serum ferritin.

19
Q

How do we treat absolute iron deficiency? (6)

A

So in absolute it means that we have body iron stores are low.
It can be due to pregnancy, malabsorption, blood loss or inadequate intake.
-First line of treatment is oral iron.
-Parenteral iron.
Helps with:
-Controlling blood loss
-Malabsorption
-Iron intake

20
Q

How do we treat functional iron deficiency? (5)

A

-In functional the blood iron stores are normal, problem is with the mobilisation of iron (immobalisation).
-It can be due to infection, cancer, CKD and autoimmune diseases.
Treatment:
-Parenteral iron
-Consider erythropoiesis stimulating agents if erythropoietin is low.
Helps with:
Controlling the underlying disease.

21
Q

Describe the pathogenesis of anaemia of chronic diseases (ACD) (4)

A

-Iron transfer blockage (reduced iron release from the macrophages)
-Decreased erythrocyte survival.
-Decreased EPO in response to the anaemia.
-Impaired response to ERO by red cell precursors.

22
Q

Describe the laboratory findings of anaemia of chronic disease (3)

A
  • Initially normocytic then become microcytic.
    -Low serum iron and raised serum ferritin.
    -Absent sideroblast in bone marrow.
23
Q

What are the causes of iron overload? (3)

A

Increased iron absorption such as in haemochromatosis and chronic liver disease.
Increased iron intake
Repeated red cell transfusions.

24
Q

Clinical features of iron overload (6)

A

-Hypoparathyroidism, hypothyroidism, Hypopituitarism.
-Cardiomyopathy
-Cirrhosis
-Diabetes mellitus
-Excessive melanin skin pigmentation

25
Q

Laboratory features of iron overload (4)

A

Increased serum iron and ferritin and transferrin.
Increased liver iron.

26
Q

What are the treatment methods for iron overload? (2)

A

-For genetic haemochromatosis- regular venesections to reduce iron levels.
-For transfusional siderosi- iron chelation