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
Laboratory features of iron overload (4)
Increased serum iron and ferritin and transferrin. Increased liver iron.
26
What are the treatment methods for iron overload? (2)
-For genetic haemochromatosis- regular venesections to reduce iron levels. -For transfusional siderosi- iron chelation