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Cardio > Haematology Anaemia > Flashcards

Haematology Anaemia Flashcards

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
Q

Normocytic Anaemias: types

A
  • Acute blood loss
  • Anaemia of chronic disease – insufficient production
  • Bone marrow infiltration
  • Combined haemotinic deficiency
  • Haemolysis (exam favourite) - augmented destruction
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26
Q

Anaemia of Chronic disease: Definition

A

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

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27
Q

Anaemia of Chronic disease: Mechanisms

A

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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28
Q

Anaemia of Chronic disease: Common causes

A

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)

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29
Q

Anaemia of Chronic disease: Treatment

A

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
Q

Haemolytic Anaemia: Definition

A

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
Q

Haemolytic Anaemia:Haemolysis categorisation

A

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

32
Q

Haemolytic Anaemia: Intravascular

A

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

33
Q

Haemolytic Anaemia: Extravascular

A

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

34
Q

Haemolytic Anaemia: Congenital (present during childhood)

A
  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
Q

Haemolytic Anaemia: Acquired

A
  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
Q

Haemolytic Anaemia: Clinical features

A
  • 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
Q

Haemolytic Anaemia: Laboratory findings

A
  • 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
Q

Autoimmune Haemolytic anaemia two types

A

Warm AIHI

Cold AIHI

39
Q

Warm AIHA

A

IgG autoantibodies active at 37oCq

40
Q

Warm AIHA Type

A

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

41
Q

Warm AIHA Causes

A

Idiopathic or Associated with Lymphoma
CLL
SLE
Drugs

42
Q

Warm AIHI Treatment

A

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
Q

Cold AIHA:

A

IgM autoantibodies active at <30oC – cross linking

44
Q

Cold AIHA: Type of Haemolysis

A

RBC agglutination

Intravascular haemolysis in extremities (temp lower and poor ciruclation)

45
Q

Cold AIHA: Causes

A

Idiopathic or associated with lymphoma

Mycoplasma and infectious mononucleosis (glandular fever)

46
Q

Cold AIHA: Treatment

A

Keep Warm
Steroids
Rituximab
Chlorambucil

47
Q

Macrocytic Anaemias: types

A
  • 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
Q

Macrocytic definition

A

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

49
Q

Megaloblastic –

A

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
Q

Vitamin B12 Deficiency: Type

A

Megaloblastic anaemia

51
Q

Vitamin B12 Deficiency:Daily requirement of vitamin B12

A

1-2 ug.

52
Q

Vitamin B12 Deficiency: Body stores

A

2-3 mg; mainly in the liver

53
Q

Vitamin B12 Deficiency: Synthesised by

A

Micro-organisms: only present naturally in animal produce

54
Q

Vitamin B12 Deficiency: Absorption

A

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

55
Q

Vitamin B12 Deficiency: Causes

A

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
Q

Vitamin B12 Deficiency: Clinical features

A

Anaemia
Jaundice
Glossitis
Neurological deficit

57
Q

Vitamin B12 Deficiency: Laboratory findings

A
  • Anaemia, neutropenia, thrombocytopenia
  • Lower serum vitamin B12
  • Antibodies against peripheral cells or IF
  • Megaloblastic change in bone marrow
  • Features of Haemolysis
58
Q

Vitamin B12 Deficiency: Historical B12 test

A

B12 absorption test – schilling test

59
Q

Folic Acid deficiency: Anaemia Type

A

Megaloblastic anaemia

60
Q

Folic Acid deficiency: Daily requirement

A

100-200 ug

61
Q

Folic Acid deficiency: Body stores

A

10-15 mg (low therefore easier to require)

62
Q

Folic Acid deficiency: Dietary sources

A

Green vegetables
Liver
Nuts
Cereal

63
Q

Folic Acid deficiency: Absorbed in

A

Jejunum

64
Q

Folic Acid deficiency: Close link with

A

Vitamin B12

65
Q

Folic Acid deficiency: Causes

A
  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
Q

Folic Acid deficiency: Clinical Featured

A

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

67
Q

Folic Acid deficiency:Lab features

A

Peripheral blood and bone marrow features identical to Vitamin B12 Deficiency

68
Q

Folic Acid deficiency:Diagosis made by

A

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

69
Q

Folic Acid deficiency:Treatment

A
  • 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
Q

Folic Acid deficiency: Care:

A

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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