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Flashcards in Haematology Anaemia Deck (70):
1

WHO definition of anaemia

Anaemia is a condition in which the number of red blood cells (and consequently their oxygen-carrying capacity) is insufficient to meet the body’s physiological need

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Anemia Varies by

Age – older lower hb
Gender – more in males
Altitude – higher hb from hypoxic dribe
Smoking behaviour
Stage of pregnancy – haemodilute (although RBC is raised despite increased fluid)

3

Most useful parameter when assessing anaemia

Mean cell volume (MCV) is the most useful parameter when considering the cause of anaemia

4

Hb (g/L)

F:115-155
M:130-170

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RBC volumes

F:3.8-5.3
M:4.5-6.0

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Haematocrit ranges

F:0.37-0.45
M:0.40-0.52

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MCV ranges

F:83-96
M:83-96

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Mean cell haemoglobin

F:27-32
M:27-32

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MCV <83 fL

Microcytic

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MCV 83-96 fL

Normocytic

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MCV >96 fL

Macrocytic

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Microcytic

Iron defiency
Thalassemia
Anaemia of chronic disorder

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Normocytic

Acute blood loss
Haemolysis
Anaemia of chronic disorder
Bone marrow infiltration
Combined haematinic deficiency

14

Macrocytic

B12/folate deficiency
Haemolysis
Hypothyroidism
Liver disease
Alcohol excess
Myelodysplasia

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Microcytic Anaemia: types

• Iron deficiency (covering this)
• Thalassaemia – covered elsewhere
• Anaemia of chronic disease

16

Iron deficiency Epi

Most common cause worldwide

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Iron deficiency Causes (most common)

1. Dietary insufficiency (80% from meat, 20% from vegetables) -
2. Physiological (infancy, adolescence, pregnancy)
3. Blood loss (GI, mennorhagia)
4. Malabsorption e.g. coeliac disease

18

Iron deficiency Total body iron

4g:
1. Hb 3g
2. Reticuloendothelial system 1g

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Iron deficiency Normal diet

Absorption = loss

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Iron deficiency Clinical Features

1. Angular stomatitis
2. Glossitis
3. Koilonchia
4. Pharyngeal and oesophageal webs

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Iron deficiency Laboratory Features

Microcytic hypochronic anaemia (Greater central pallor)
Low serum ferritin (beware: acute phase protein) *
Absent iron stores in bone marrow (rare late stage)

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Further investigations: Physiological

Treat with oral iron

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Further investigations: Females: pre-menopausal

Localising GI symptoms or signs
• Treat with oral iron
• Colonoscopy/Barium Enema OGD (Smal bowel study)

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Further investigations: Males and post-menopausal women

Investigate:
Colonoscopy/Barium Enema OGD (Smal bowel study)

25

Normocytic Anaemias: types

• Acute blood loss
• Anaemia of chronic disease – insufficient production
• Bone marrow infiltration
• Combined haemotinic deficiency
• Haemolysis (exam favourite) - augmented destruction

26

Anaemia of Chronic disease: Definition




Depression of erythropoiesis of multifactorial aetiology seen as a secondary manifestation in a wide variety of disorders:
• Mild to moderate (hb 90-110 g/L)
• Normochromic/microcytic hypochromic
• Serum ferritin normal or increased

27

Anaemia of Chronic disease: Mechanisms

Main defect is failure of transport of iron from RE system to developing red cells
→ Proteins in liver/spleen/ bone marrow defect and therefore preventing transport to red cells

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Anaemia of Chronic disease: Common causes

Chronic infection/inflammation – RA/SLE
Malignancy – nutritionally deficient and malignancy supresses erythropoiesis
Uraemia – high concentrations suppress erythropoiesis (kidney disease double hit)
Endocrine disorders – poorly controlled (hypothyroidism/diabetes)

29

Anaemia of Chronic disease: Treatment

Correction of underlying causes
Erythropoietin (+iron Iv) – potentially in inflammatory conditions. Floods bone marrow with iron readily available to ue and doesn’t rely on transport from elsewhere.

30

Haemolytic Anaemia: Definition

Increased destruction of red cells; reduced life span.
Compensation: expansion of erythropoiesis can increase red cell production 7x without anaemia presenting (will see haemolysis)
Decompensating: due to infection, folate deficiency or other stressors – when the anaemia presents

31

Haemolytic Anaemia:Haemolysis categorisation

Intravascular
Extravascular
Congenital (can be intra or extra vascular)
Acquired (can be intra or extra vascular)

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Haemolytic Anaemia: Intravascular

Red cells lyse in circulation, release Hb into plasma (toxic)

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Haemolytic Anaemia: Extravascular

Red cells phagocytised by macrophages In liver and spleen – no free Hb in plasma.

34

Haemolytic Anaemia: Congenital (present during childhood)

1. Abnormal haemoglobulin e.g. sickle cell anaemia, thalassemia (contributes to anaemia)
2. Abnormal membrane e.g. hereditary spherocytosis – circular cells destroyed faster
3. Metabolic defect e.g. enzyme deficiency in glycolytic deficiency in glycolytic pathway (e.g. G6PD) or pentose phosphate shunt (e.g. pyruvate kinase

35

Haemolytic Anaemia: Acquired

1. Immune e.g. autoimmune haemolytic anaemia (auto antigens on RBCs), incompatible blood transfusion
2. Traumatic: cardiac valve replacement (abnormal flow), microangiopathic haemolytic anaemia (MAHA) – intravascular *
3. Infection e.g. malaria, mycoplasma pneumonia
4. Drugs/chemicals through a variety of mechanisms (penicillin- causes immune response)

36

Haemolytic Anaemia: Clinical features

• Anaemia
• Jaundice
• Splenomegaly – common in RE (extravascular)
• Skeletal abnormalities (chronic haemolytic conditions – bone marrow) - thalessaemia
• Gallstones – intravascular due to increased excretion
• Haemoglobinuria – overwhelmed capacity

37

Haemolytic Anaemia: Laboratory findings

• Anaemia
• Reticulocytosis – (Immature - large) up-regulated bone marrow action
• Unconjugated hyperbilirubinaemia
• Elevated LDH – marker of cell breakdown
• Absent/reduced haptoglobins – chaperone products of Hb in plasma
• Polychromasia, spherocytes, fragments of sickle cells – depending on cause
• Hyperplastic bone marrow

38

Autoimmune Haemolytic anaemia two types

Warm AIHI
Cold AIHI

39

Warm AIHA

IgG autoantibodies active at 37oCq

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Warm AIHA Type

Extravascular Haemolysis – RBC with autoantigens taken up by macrophages and destroyed in spleen

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Warm AIHA Causes

Idiopathic or Associated with Lymphoma
CLL
SLE
Drugs

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Warm AIHI Treatment

Steroids: suppression of immune system
Rituximab (anti CD20 on B cells): suppression of immune system
Splenectomy: remove site where destruction is occuring
Fix causes: Chemotherapy for CLL/Lymphoma

43

Cold AIHA:

IgM autoantibodies active at <30oC – cross linking

44

Cold AIHA: Type of Haemolysis

RBC agglutination
Intravascular haemolysis in extremities (temp lower and poor ciruclation)

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Cold AIHA: Causes

Idiopathic or associated with lymphoma
Mycoplasma and infectious mononucleosis (glandular fever)

46

Cold AIHA: Treatment

Keep Warm
Steroids
Rituximab
Chlorambucil

47

Macrocytic Anaemias: types

• Folate deficiency (most common)
• Vitamin B12 deficiency (Most common)
• Myelodysplasia (common in elderly)
• Hypothyroidism (macrocytes but normal Hb)
• Alcohol excess
• Liver disease (macrocytes but normal Hb)
• (Haemolysis)

48

Macrocytic definition

Red cells in peripheral blood are large. Erythropoiesis may or may not be megaloblastic.

49

Megaloblastic –

It is an assessment of bone marrow
• Red cell precursors are abnormally large because of impaired DNA synthesis. The cell continues to grow but does not divide, as it is incapable of replicating DNA.
• RNA synthesis of replicating DNA. RNA synthesis and translation not affected.

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Vitamin B12 Deficiency: Type

Megaloblastic anaemia

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Vitamin B12 Deficiency:Daily requirement of vitamin B12

1-2 ug.

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Vitamin B12 Deficiency: Body stores

2-3 mg; mainly in the liver

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Vitamin B12 Deficiency: Synthesised by

Micro-organisms: only present naturally in animal produce

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Vitamin B12 Deficiency: Absorption

Combines with intrinsic factor secreted by gastric parietal cells and absorbed in terminal ileum.

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Vitamin B12 Deficiency: Causes

Dietary: veganisms, rare
IF deficiency:
• Pernicious anaemia (Ab against parietal or IF)
• Gastrectomy
• Congenital
Intestinal malabsorption – disease in terminal ileum e.g. Crohns, blind loops and small bowel diverticulae.

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Vitamin B12 Deficiency: Clinical features

Anaemia
Jaundice
Glossitis
Neurological deficit

57

Vitamin B12 Deficiency: Laboratory findings

• Anaemia, neutropenia, thrombocytopenia
• Lower serum vitamin B12
• Antibodies against peripheral cells or IF
• Megaloblastic change in bone marrow
• Features of Haemolysis

58

Vitamin B12 Deficiency: Historical B12 test

B12 absorption test – schilling test

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Folic Acid deficiency: Anaemia Type

Megaloblastic anaemia

60

Folic Acid deficiency: Daily requirement

100-200 ug

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Folic Acid deficiency: Body stores

10-15 mg (low therefore easier to require)

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Folic Acid deficiency: Dietary sources

Green vegetables
Liver
Nuts
Cereal

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Folic Acid deficiency: Absorbed in

Jejunum

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Folic Acid deficiency: Close link with

Vitamin B12

65

Folic Acid deficiency: Causes

1. Dietary – common in elderly, poor diet related to alcohol misuse
2. Increased utilisation – e.g. in pregnancy, malignancy, haematological disorders with rapid ell turnover
3. Malabsorption e.g. coeliac disease
4. Drugs e.g. anticonvulsants
5. Excessive loss e.g. renal dialysis

66

Folic Acid deficiency: Clinical Featured

Similar to Vitamin B12 Deficiency but neurological problems don’t occur

67

Folic Acid deficiency:Lab features

Peripheral blood and bone marrow features identical to Vitamin B12 Deficiency

68

Folic Acid deficiency:Diagosis made by

Measuring low serum (and sometimes red cel) folate levels.

69

Folic Acid deficiency:Treatment

• Address underlying causes
• Vitamin B12 replacement as IM injection most common – 3x per week for 2 weeks then maintenance phase( patients usually have malabsorption therefore bypass)
• Oral folic acid replacement

70

Folic Acid deficiency: Care:

Risk subacute combined degeneration of the cord (with permanent neurological sequel) if folic acid replace in absence of Vitamin B12. Replace B before F.

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