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Haematology Anaemia Flashcards

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1
Q

WHO definition of anaemia

A

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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2
Q

Anemia Varies by

A 
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)
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3
Q

Most useful parameter when assessing anaemia

A

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

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4
Q

Hb (g/L)

A

F:115-155
M:130-170

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5
Q

RBC volumes

A

F:3.8-5.3
M:4.5-6.0

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6
Q

Haematocrit ranges

A

F:0.37-0.45
M:0.40-0.52

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7
Q

MCV ranges

A

F:83-96
M:83-96

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8
Q

Mean cell haemoglobin

A

F:27-32
M:27-32

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9
Q

MCV <83 fL

A

Microcytic

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10
Q

MCV 83-96 fL

A

Normocytic

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11
Q

MCV >96 fL

A

Macrocytic

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12
Q

Microcytic

A

Iron defiency
Thalassemia
Anaemia of chronic disorder

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13
Q

Normocytic

A 
Acute blood loss
Haemolysis
Anaemia of chronic disorder
Bone marrow infiltration
Combined haematinic deficiency
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14
Q

Macrocytic

A 
B12/folate deficiency
Haemolysis
Hypothyroidism
Liver disease
Alcohol excess
Myelodysplasia
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15
Q

Microcytic Anaemia: types

A
  • Iron deficiency (covering this)
  • Thalassaemia – covered elsewhere
  • Anaemia of chronic disease
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16
Q

Iron deficiency Epi

A

Most common cause worldwide

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17
Q

Iron deficiency Causes (most common)

A
  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
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18
Q

Iron deficiency Total body iron

A

4g:

  1. Hb 3g
  2. Reticuloendothelial system 1g
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19
Q

Iron deficiency Normal diet

A

Absorption = loss

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20
Q

Iron deficiency Clinical Features

A
  1. Angular stomatitis
  2. Glossitis
  3. Koilonchia
  4. Pharyngeal and oesophageal webs
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21
Q

Iron deficiency Laboratory Features

A

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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22
Q

Further investigations: Physiological

A

Treat with oral iron

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23
Q

Further investigations: Females: pre-menopausal

A

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

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24
Q

Further investigations: Males and post-menopausal women

A

Investigate:

Colonoscopy/Barium Enema OGD (Smal bowel study)

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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
28
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)
32
Haemolytic Anaemia: Intravascular
Red cells lyse in circulation, release Hb into plasma (toxic)
33
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
40
Warm AIHA Type
Extravascular Haemolysis – RBC with autoantigens taken up by macrophages and destroyed in spleen
41
Warm AIHA Causes
Idiopathic or Associated with Lymphoma CLL SLE Drugs
42
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)
45
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.
50
Vitamin B12 Deficiency: Type
Megaloblastic anaemia
51
Vitamin B12 Deficiency:Daily requirement of vitamin B12
1-2 ug.
52
Vitamin B12 Deficiency: Body stores
2-3 mg; mainly in the liver
53
Vitamin B12 Deficiency: Synthesised by
Micro-organisms: only present naturally in animal produce
54
Vitamin B12 Deficiency: Absorption
Combines with intrinsic factor secreted by gastric parietal cells and absorbed in terminal ileum.
55
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.
56
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
59
Folic Acid deficiency: Anaemia Type
Megaloblastic anaemia
60
Folic Acid deficiency: Daily requirement
100-200 ug
61
Folic Acid deficiency: Body stores
10-15 mg (low therefore easier to require)
62
Folic Acid deficiency: Dietary sources
Green vegetables Liver Nuts Cereal
63
Folic Acid deficiency: Absorbed in
Jejunum
64
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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