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Year 3 > Anaemia (CH) > Flashcards

Anaemia (CH) Flashcards

1
Q

Define anaemia.

A

Anaemia is a Hb level two standard deviations below the mean for the age and sex of the patient

A decrease in the [Hb] in circulating blood

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2
Q

What are the general blood results for anaemia?

A

Reduced RBC, reduced Hct, reduced PCV (packed cell volume)

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3
Q

What can be used to distinguish the mechanism of anaemia?

A

Reticulocyte count

  • increased = haemolytic anaemia, recent blood loss, recent treatment with iron, B12/folate
  • decreased = reduced output of RBC from bone marrow
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4
Q

What are the causes of anaemia? (4 types + examples of each)

A
  • reduced production of RBC by bone marrow
    • iron deficiency anaemia
    • anaemia of chronic disease
    • megaloblastic anaemia (B12 deficiency)
  • blood loss from body (normocytic)
  • reduced survival of RBC in circulation
    • hereditary spherocytosis
    • autoimmune haemolytic anaemia
    • G6PD deficiency
  • increased pooling of RBC in enlarged spleen (sickle cell anaemia)
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5
Q

What are the general symptoms of anaemia? (5)

A
  • tiredness
  • lethargy
  • malaise
  • dyspnoea
  • pallor
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6
Q

What are some general investigations for anaemia?

A
  • FBC - low Hb
  • iron studies - IDA
  • blood film - reticulocytes, abnormalities
  • electrophoresis - haemoglobinopathies
  • DAT/Coomb’s Test
  • LFTs, bilirubin - haemolytic anaemia
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7
Q

What are the three types of anaemia?

A
  • microcytic
  • normocytic
  • macrocytic
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8
Q

Define microcytic anaemia.

A
  • insufficient Hb production
  • MCV < 80 fL
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9
Q

What are the types of causes of microcytic anaemia?

A
  • defective haem synthesis
    • iron deficiency anaemia
    • anaemia of chronic disease (may also be normocytic)
  • defective globin synthesis
    • thalassaemia
  • sideroblastic anaemia
  • lead poisoning
  • anaemia of chronic disease
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10
Q

How does microcytic anaemia present?

A
  • brittle hair and nails
  • pallor
  • koilonychia (spoon-shaped nails in IDA)
  • glossitis
  • angular stomatitis (red patches in corner of mouth in IDA)
  • signs of thalassaemia
  • ankle swelling
  • palpitations
  • tachycardia
  • post-cricoid webs
  • exacerbation of ischaemic conditions
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11
Q

What investigations are done for microcytic anaemia?

A
  • FBC - MCV<80, reticulocytes
  • blood film - microcytes, increased area of central pallor, hypochromic, basophilic stippling
  • iron studies
  • CRP, ESR - elevated in ACD
  • serum lead - elevated in lead poisoning
  • Hb electrophoresis - thalassaemia, SCA
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12
Q

Iron studies - what would be suggestive of iron deficiency anaemia?

A
  • low iron and ferritin
  • raised transferrin
  • increased TIBC (total iron binding capacity)
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13
Q

Iron studies - what would be suggestive of anaemia of chronic disease?

A
  • low/normal iron and ferritin
  • low transferrin
  • low TIBC
  • increased hepcidin
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14
Q

Iron studies - what would be suggestive of sideroblastic anaemia?

A
  • high iron
  • high ferritin
  • high transferrin saturation
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15
Q

Iron studies - what would be suggestive of thalassaemia?

A

Mentzer index (MCV/RBC) <13

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16
Q

What is the difference in blood count results between iron deficiency anaemia vs anaemia of chronic disease?

A
  • MCV: low vs low/normal
  • ferritin: low vs high
  • transferrin: high vs low/normal
  • transferrin saturation: low vs normal
  • ESR: may be high (due to low Hct) vs high
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17
Q

What are the causes of iron deficiency anaemia?

A
  • increased blood loss
    • hookworm
    • menstrual
    • GI (aspirin/NSAIDs, cancers, ulcers, coeliac, gastrectomy, H.pylori, angiodysplasia)
  • insufficient intake
    • dietary
    • malabsorption - coeliac, gastritis
  • increased requirement
    • pregnancy
    • infancy
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18
Q

What investigations are done for iron deficiency anaemia?

A
  • FBC
  • iron studies (high transferrin/TIBC, low serum iron/ferritin)
  • blood film (poikilocytosis, anisocytosis, microcytosis hypochromia)
  • if >40yrs OR post-menopausal women OR male with unexplained IDA: upper GI endoscopy, colonoscopy
  • if Hb<10 - refer within two weeks
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19
Q

How do we manage iron deficiency anaemia?

A
  • iron supplements
    • oral ferrous sulfate/fumarate/gluconate, continue for 3 months after IDA correction to allow stores to replenish
    • if oral iron not tolerated, IV iron
  • iron-rich diet (dark leafy veg, meat, iron-fortified bread)
  • address underlying causes (e.g. treat menorrhagia, stop NSAIDs)
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20
Q

What are some causes of anaemia of chronic disease?

A
  • no unrelated cause except for a different unrelated pathology (hepcidin production increased in inflammation –> reduced iron supply by blocking absorption from gut/release of storage iron)
  • infections: TB and HIV
  • autoimmune disorders (inflammatory): RA, SLE, Crohn’s/UC, CKD
  • cancer, lymphomas/leukaemia
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21
Q

What investigations are done for anaemia of chronic disease?

A

FBC - increased ferritin, low/normal transferrin

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22
Q

What is the pathophysiology of anaemia of chronic disease?

A
  • involvement of pro-inflammatory cytokines
  • IL1, TNF-a, IL6
  • all decreased EPO production
  • increase hepcidin production = decreased release of storage iron
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23
Q

How do we manage anaemia of chronic disease?

A

Treat the underlying cause

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24
Q

What is sideroblastic anaemia?

A

Inability to form haem in mitochondria –> deposits of iron in mitochondria form a ring around nucleus called a ring sideroblast

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25
Q

What is a congenital cause of sideroblastic anaemia?

A

Delta-aminolevilinate synthase-2 deficiency

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26
Q

What are the acquired causes of sideroblastic anaemia?

A

MALA

  • myelodysplasia
  • alcohol
  • lead
  • anti-TB medications
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27
Q

What is seen on a blood film of sideroblastic anaemia? (3)

A
  • basophilic stippling of RBCs
  • dimorphic blood film
  • hypochromic microcytes
  • (bone marrow film: Prussian blue staining shows ring sideroblasts)
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28
Q

How do we manage sideroblastic anaemia?

A
  • supportive
  • if secondary - treat the cause
  • pyridoxine
  • iron chelation if not treatment
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29
Q

Define normocytic anaemia.

A
  • decreased blood volume or erythropoiesis
  • MCV 80-100 fL
30
Q

What are some causes of normocytic anaemia?

A
  • aplastic
  • bleeding (haemorrhage/trauma, BM failure or infiltration)
  • chronic disease (early stages)
  • CKD
  • destruction - haemolysis
  • endocrine disorders (hypothyroidism, hypoadrenalism)
  • splenic sequestration (hypersplenism, liver cirrhosis)
  • vitamin B2/B6 deficiency
  • uncompensated increase in plasma volume (pregnancy, fluid overload)
31
Q

What investigations are done for normocytic anaemia?

A
  • FBC - normal MCV, low Hb
  • check Hx for haemorrhage
  • if WCC or platelets low - suspect marrow failure
32
Q

How can we classify normocytic anaemia by reticulocyte count?

A
  • <2% (hypoproliferative) - leukaemias, aplastic anaemia, pure red cell aplasia, other marrow failure syndromes
  • > 2% (hyperproliferative) - haemorrhage, haemolytic anaemias
33
Q

What will ferritin be in normocytic anaemia?

A

Normal/high

34
Q

What is aplastic anaemia?

A

Pancytopenia and hypoplastic bone marrow caused by diminished haematopoietic precursors –> normocytic anaemia

35
Q

What are some causes of aplastic anaemia?

A
  • acquired anaemia (at 30y)
  • autoimmune
  • congenital
    • Fanconi anaemia (AR) = increased risk of AML
    • dyskeratosis congenita
  • drugs (cytotoxics, chloramphenicol, sulphonamides, phenytoin, gold)
  • toxins (benzene)
  • infections (Parovirus, hepatitis)
  • paroxysmal nocturnal haemoglobinuria or myelodysplasia
36
Q

How does aplastic anaemia present?

A
  • thrombocytopenia
    • easy bruising
    • bleeding gums
    • epistaxis
  • leukopenia - infections
37
Q

How do we investigate aplastic anaemia?

A
  • FBC - leukopenia with lymphocytes spared, thrombocytopenia
  • bone marrow biopsy
38
Q

How can we manage aplastic anaemia?

A
  • haematopoietic stem cell (bone marrow) transplant
  • immunosuppressive therapy
  • androgens e.g. oxymetholone
39
Q

Define macrocytic anaemia.

A
  • defective DNA synthesis or repair
  • MCV > 100 fL
40
Q

What are the causes of macrocytic anaemia?

A

FAT RBC

  • foetus
  • alcohol excess
  • thyroid disorders
  • reticulocytosis
  • B12/folate deficiency (megaloblastic)
  • cirrhosis

Also:

  • drugs interfering with DNA synthesis - tyrosine kinase inhibitors
  • haemolytic anaemia
  • myelodysplasia, multiple myeloma, pregnancy
  • aplastic anaemia
41
Q

How does pernicious anaemia (macrocytic anaemia) present?

A
  • jaundice
  • glossitis
  • angular stomatitis
  • weight loss
42
Q

How does B12 deficiency (macrocytic anaemia) present?

A
  • peripheral neuropathy
  • ataxia
  • SACD
  • optic atrophy
  • dementia
  • positive Babinksi’s
  • absent ankle reflex
  • increased knee reflex
43
Q

What investigations do we do for macrocytic anaemia?

A
  • FBC - MCV>100fL, low Hb, pancytopenia in megaloblastic anaemia
  • LFTs - high BR in ineffective erythropoiesis or haemolysis
  • ESR
  • TFT
  • B12/folate
  • homocysteine and methylmalonic acid levels
  • anti-parietal cell and anti-IF antibodies
  • protein electrophoresis (dense band in myeloma)
  • blood film - large erythrocytes, megaloblasts, hypersegmented neutrophil nuclei, target cells (liver disease)
  • Schilling test (pernicious anaemia) - B12 absorbed with IF
44
Q

What is seen in a blood film of macrocytic anaemia?

A
  • large erythrocytes
  • megaloblasts
  • hypersegmented neutrophil nuclei
  • target cells (liver disease)
45
Q

What investigation is done for pernicious anaemia?

A

Schilling test - B12 absorbed with IF

46
Q

How can we treat pernicious anaemia?

A

IM hydroxycobalamin

47
Q

How can we treat anaemia caused by B12 deficiency?

A

Dietary supplements - PO cyanocobalamin

48
Q

How can we treat anaemia caused by folate deficiency?

A

Folic acid (B12 must be corrected first) - oral folic acid 5mg daily for 4 months

49
Q

What is a complication of pernicious anaemia?

A

Gastric cancer

50
Q

What is a complication of folate deficiency?

A

Neural tube defects

51
Q

What blood result may suggest macrocytic anaemia due to alcohol use?

A

Isolated GGT raise

52
Q

What are some inherited causes of haemolytic anaemia?

A
  • membrane integrity defects - hereditary spherocytosis/elliptocytosis
  • haemoglobinopathies - sickle cell anaemia, thalassaemia
  • defect in glycolytic pathway - pyruvate kinase deficiency
  • defect in pentose shunt pathway - G6PD deficiency
53
Q

What are some acquired causes of haemolytic anaemia?

A
  • *autoimmune haemolytic anaemia** - antibodies attach = intravascular + extravascular haemolysis
  • isoimmune (transfusion, haemolytic disease of the newborn)
  • drugs (penicillin, quinine)
  • trauma (microangiopathic haemolytic anaemia, haemolytic uraemic syndrome, DIC, malignant hypertension
  • infection - sepsis, malaria
  • paroxysmal nocturnal haemoglobinuria
  • snake venom, alloimmune (blood transfusion)
54
Q

What can precipitate haemolysis?

A

Drugs, infections or consumption of broad beans –> hypotension, tachycardia, petechiae, ecchymosis, altered conscious state

55
Q

What are some risk factors for haemolytic anaemia?

A
  • African-American
  • X-linked recessive (G6PD deficiency) = men more likely
  • Fx of hereditary spherocytosis (autosomal dominant)
56
Q

How does haemolytic anaemia present?

A
  • jaundice
  • hepatosplenomegaly
  • leg ulcers (poor flow)
  • haematuria
  • dark urine
57
Q

What investigations is diagnostic for haemolytic anaemia?

A

DAT test AKA Coomb’s test

58
Q

What are the blood results of someone with haemolytic anaemia?

A
  • increased: unconjugated bilirubin, LDH, reticulocytes
  • deranged LFTs
  • reduced haptoglobins
59
Q

What does a blood film of haemolytic anaemia show?

A
  • reticulocytosis
  • leucoerythroblastic (macrocytosis, polychromasia)
  • Heinz bodies (oxidised Hb in G6PD deficiency), bite cells, blister cells (G6PD)
  • spherocytes (hereditary spherocytosis)
60
Q

What investigation is done for hereditary spherocytosis?

A

Eosin-5-malemide (EMA) for binding

61
Q

What investigations are done for membrane abnormalities in haemolytic anaemia?

A

Osmotic fragility test or Spectrin mutation analysis

62
Q

What investigations are done for paroxysmal nocturnal haemoglobinuria?

A
  • Ham’s test - lysis of erythrocytes in acidified serum
  • flow cytometry
63
Q

How do we manage hereditary spherocytosis?

A

Folic acid, splenectomy

64
Q

How do we manage G6PD deficiency?

A

Patients should avoid oxidant drugs, should not eat broad beans (fava beans), avoid naphthalene and be aware that haemolysis can result from infection

65
Q

What is the aetiology of autoimmune haemolytic anaemia?

A

Mostly idiopathic, can be secondary to a lymphoproliferative disorder, infection or drugs

66
Q

What are the two types of autoimmune haemolytic anaemia?

A
  • warm AIHA (more common
  • cold AIHA
67
Q

Describe warm autoimmune haemolytic anaemia and how to manage it.

A
  • IgG causes haemolysis in extravascular sites (spleen)
  • caused by autoimmune disease (SLE), neoplasia (lymphoma, CML), drugs (methyldopa)
  • management: treat underlying disorder, steroids +/- rituximab (1st line)
68
Q

Describe cold autoimmune haemolytic anaemia.

A
  • IgM causes haemolysis mediated by complement in intravascular sites
  • caused by neoplasia (lymphoma), infections (mycoplasma, EBV)
  • Raynaud’s, acrocyanosis
  • less responsive to steroids
69
Q

What is haemolytic uraemic syndrome?

A
  • uraemia, thrombocytopenia, microangiopathic haemolytic anaemia
  • two forms: diarrhoea-associated, and no diarrhoea prodrome
  • overlap with thrombotic thrombocytopenia purpura: additional features of fever, fluctuating CNS signs
  • E.coli with bloody diarrhoea in children under 5
70
Q

How is haemolytic anaemia treated?

A

Steroids (prednisolone) +/- rituximab

71
Q

How is anaemia treated if severe?

A

Blood transfusion with RBCs

Year 3 (22 decks)

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