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Yr 5 - Haematology > Anaemia Revision > Flashcards

Anaemia Revision Flashcards

1
Q

What is Hb?

A

Protein in RBCs –> binds O2 and carries it around body

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2
Q

What is essential for creating Hb?

A

Iron

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3
Q

Causes of microcytic anaemia?

Mneumonic: TAILS

A

T - thalassaemia
A - anaemia of chronic disease
I - iron deficiency
L - lead poisoning
S - sideroblastic anaemia

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4
Q

What is the difference between macrocytic and megaloblastic anaemia?

A

Megaloblastic anaemia is a type of macrocytic anaemia.

Macrocytes are enlarged RBCs (raised MCV).

Megaloblasts are large RBC precursors due to impaired DNA synthesis, preventing the cells from dividing normally. Rather than dividing, they grow into large, abnormal cells.

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5
Q

What is the cause of production of megaloblasts?

A

Impaired synthesis of RBC DNA e.g. folate deficiency

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6
Q

What hormone is responsible for production of RBCs?

A

EPO

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7
Q

Treatment of anaemia caused by CKD?

A

EPO

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8
Q

What type of anaemia does CKD cause?

A

Typically normocytic

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9
Q

What is sideroblastic anaemia ?

A

Body produces enough iron but is unable to put it into Hb (iron levels will be normal/high).

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10
Q

What is the main cause of sideroblastic anaemia?

A

Alcohol

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11
Q

Mechanism of iron absorption?

A

1) Mainly absorbed in duodenum & jejunum

2) Requires the acid from the stomach to keep the iron in the soluble ferrous (Fe2+) form

3) When the stomach contents are less acidic, it changes to the insoluble ferric (Fe3+) form.

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12
Q

How can PPIs result in iron deficiency?

A

Reduces stomach acid - iron stays in Fe3+ form (insoluble)

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13
Q

How can coeliac disease or Crohn’s disease cause iron deficiency?

A

Inflammation of duodenum or jejunum can reduce iron absorption.

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14
Q

What is the formula for transferrin saturation?

A

Transferrin saturation = serum iron / total iron-binding capacity

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15
Q

What is low ferritin highly suggestive of?

A

Iron deficiency

N.B. Normal ferritin does not exclude iron deficiency.

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16
Q

Raised ferritin is difficult to interpret.

What may it be caused by (i.e. what can cause iron overload)?

A
  • Inflammation (e.g., infection or cancer)
  • Acute liver damage (the liver contains lots of iron)
  • Iron supplements
  • Haemochromatosis
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17
Q

Why should iron infusions be avoided during infections?

A

there is potential for it to “feed” the bacteria.

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18
Q

What is the most common cause of B12 deficiency?

A

Pernicious anaemia

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19
Q

What is the role of intrinsic factor?

A

Produced by gastric parietal cells

It is a protein that is essential for the absorption of vitamin B12 in the distal ileum.

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20
Q

Pathophysiology of pernicious anaemia?1

A

1) Autoantibodies target parietal cells and/or intrinsic factor:

a) intrinsic factor antibodies: bind to intrinsic factor blocking the vitamin B12 binding site

b) gastric parietal cell antibodies: reduced acid production and atrophic gastritis as well as reduced intrinsic factor production

2) Lack of intrinsic factor and a lack of absorption of vitamin B12.

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21
Q

What are the 2 major roles of vitamin B12?

A

1) Myelination of nerves

2) Production of RBCs

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22
Q

What should you always test for in patients presenting with peripheral neuropathy, particularly with pins and needles?

A

vitamin B12 deficiency and pernicious anaemia

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23
Q

What is subacute degeneration of the spinal cord?

A

Vit B12 deficiency results in impairment of dorsal columns, lateral corticospinal tracts and spinocerebellar tracts.

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24
Q

Features of subacute combined degeneration of the spinal cord?

A

1) dorsal column involvement
- distal tingling/burning/sensory loss is symmetrical and tends to affect the legs more than the arms
- impaired proprioception and vibration sense

2) lateral corticospinal tract involvement
- muscle weakness, hyperreflexia, and spasticity
- upper motor neuron signs typically develop in the legs first
- brisk knee reflexes
- absent ankle jerks
- extensor plantars

3) spinocerebellar tract involvement
- sensory ataxia –> gait abnormalities
- positive Romberg’s sign

25
Q

What 2 autoantibodies can be used to diagnose pernicious anaemia?

A

1) Intrinsic factor antibodies (the first-line investigation)

2) Parietal cell antibodies

26
Q

Are IF antibodies or gastric parietal cell antibodies more useful in the diagnosis of pernicious anaemia?

A

IF antibodies

27
Q

How often is IM hydroxocobalamin given in pernicious anaemia if there are NO neuro symptoms?

A

3 times weekly for 2 weeks

28
Q

How often is IM hydroxocobalamin given in pernicious anaemia if there are neuro symptoms?

A

alternate days until there is no further improvement in symptoms

29
Q

Long term management of pernicious anaemia?

A

2-3 monthly injections of IM hydroxocobalamin for life.

30
Q

Long term management of diet related B12 deficiency?

A

Oral cyanocobalamin or twice-yearly injections

31
Q

What cancer does pernicious anaemia increase risk of?

A

Gastric cancer

32
Q

Why is there splenomegaly in haemolytic anaemia?

A

Spleen becomes filled with destroyed RBCs

33
Q

What will a blood film show in haemolytic anaemia?

A

Schistocytes (fragments of RBCs)

34
Q

Inheritance of spherocytosis?

A

Autosomal dominant

35
Q

What is the most common inherited haemolytic anaemia in northern Europeans?

A

Hereditary spherocytosis

36
Q

What happens in hereditary spherocytosis?

A

It causes fragile, sphere-shaped RBCs that easily break down when passing through the spleen.

37
Q

What is seen on a blood film in spherocytosis?

A

Spherocytes

38
Q

Treatment of hereditary spherocytosis?

A

1) folate supplementations
2) blood transfusions when required
3) splenectomy

39
Q

Why can hereditary spherocytosis predispose to gallstones?

A

Higher bilirubin = gallstones

40
Q

What is hereditary elliptocytosis?

A

Hereditary elliptocytosis is similar to hereditary spherocytosis except that the red blood cells are ellipse-shaped.

The presentation and management are the same as hereditary spherocytosis.

41
Q

Inheritance of hereditary elliptocytosis?

A

Autosomal dominant

42
Q

Role of G6PD?

A

It is an enzyme responsible for protecting the cells from oxidative damage.

43
Q

What 3 drugs are most commonly implicated in acute episodes of haemolytic anaemia in G6PD deficiency?

A

1) Ciprofloxacin
2) Sulfalazine
3) Sulfonylureas (e.g. gliclazide)

44
Q

Why can haemolytic anaemias predispose to gallstones?

A

Due to raised bilirubin

45
Q

How can a diagnosis of G6PD deficiency be made?

A

G6PD enzyme assay.

46
Q

What is seen on a blood film in G6PD deficiency?

A

Heinz bodies

47
Q

What type of anaemia can methotrexate cause?

A

Megaloblastic macrocytic anaemia 2ary to folate deficiency

48
Q

What should be corrected before prescribing erythropoiesis-stimulating agents (ESA)?

A

Correct any iron deficiency

49
Q

What can trigger an aplastic crisis in hereditary spherocytosis?

A

Parvovirus B19 infection

50
Q

Why is calcium low in CKD?

A

Kidneys cannot activate vitamin D

51
Q

What is pellagra?

A

Deficiency of vitamin B3 (niacin)

52
Q

What features are seen in pellagra?

A

1) dermatitis
2) diarrhoea
3) dementia/delusions

53
Q

1st line mx of autoimmune haemolytic anaemia?

A

Steroids

54
Q

What condition are bite cells & blister cells on a blood film seen in?

A

G6PD deficiency

55
Q

What is haptoglobin?

A

Produced by the liver.

1ary function is to bind free Hb.

56
Q

Haptoglobin level in haemolysis?

A

LOW (as bound to free Hb)

57
Q

What type of anaemia can anti-TB meds cause?

A

Sideroblastic anaemia

58
Q
A

Yr 5 - Haematology (10 decks)

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