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Year 3 - TCD > Case 11 - Anaemia > Flashcards

Case 11 - Anaemia Flashcards

1
Q

What is anaemia?

A

Decrease in the quantity of circulating red blood cells represented by a reduction in haemoglobin concentration (Hb), haematocrit (Hct), or RBC count.

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2
Q
  • What determines if anaemia is microcytic, normocytic, and macrocytic?
  • What are the normal values?
A

MCV - average volume of RBC

- 80–100 fL

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3
Q
  • What is microcytic anaemia?

- What is the mechanism?

A
  • RBC too small
  • MCV: <80fL
  • Insufficient haemoglobin production
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4
Q
  • What is normocytic anaemia?

- What is the mechanism?

A
  • RBC normal
  • MCV: 80-100fL
  • Decreased blood volume and/or decreased erythropoiesis
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5
Q
  • What is macrocytic anaemia?

- What is the mechanism?

A
  • RBC too big
  • MCV: >100fL
  • Insufficient cell production and/or maturation
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6
Q

What are the symptoms of anaemia

A
  • Tiredness
  • Shortness of breath
  • Headaches
  • Dizziness
  • Fatigue
  • Loss of appetite
  • Muscle cramps
  • Worsening of angina pectoris
  • Weight loss
  • Conjunctival pallor (also lips, nail beds)
  • Koilonychia
  • Brittle nails, hair loss
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7
Q
  • What type of anaemia is iron deficiency?

- What are the causes?

A
  • Microcytic
  • Menorrhagia, pregnancy, low birth weight (neonates), cow’s milk (infants), GI bleeds (due to GI tract cancer, oesophagitis and gastritis), IBD,
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8
Q

What are the symptoms of iron deficiency?

A
  • Signs and symptoms of anaemia
  • Koilonychia: specific for IDA
  • Sore or smooth tongue – glossitis
  • Angular cheilitis
  • Pica: specific for IDA
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9
Q

What are the investigations for iron deficiency anaemia?

A
  • Decreased haemoglobin and MCH
  • Decreased haematocrit
  • Lower MCV – microcytic
  • Lower mean corpuscular haemoglobin – hypochromic
  • Increased red cell distribution width – differentiates IDA from anaemia of chronic disease and thalassemia where RDW is normal
  • Decreased serum ferritin
  • OGD: GI malignancy
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10
Q

What are the causes of microcytic anaemia?

A

TAILS -

  • T: Thalassaemia
  • A: Anaemia of chronic disease (later phase)
  • I: Iron deficiency anaemia
  • L: Lead poisoning
  • S: Sideroblastic anaemia
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11
Q

What differentiates IDA from anaemia of chronic disease and thalassemia?

A

RDW -

  • Increased in IDA
  • Normal in anaemia of chronic disease and thalassemia
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12
Q

How to treat IDA?

A
  • Dietary modification: increase consumption of iron rich diets
  • Ferrous sulphate - 200mg, 3 TDS: 3-6 months (65 mg iron)
  • Blood transfusion: severe anaemia
  • Treat underlying cause:OCPs for menorrhagia
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13
Q

What are the SE for ferrous sulphate tablets?

A
  • GI discomfort
  • Nausea
  • Constipation
  • Black discolouration of stool
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14
Q

What confirms IDA?

A

Serrum ferritin <15 micrograms/L

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15
Q

What does IDA blood film show?

A

Small (microcytic) and pale (hypochromic) cells.

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16
Q

What is sideroblastic anaemia?

A

Iron trapping inside the mitochondria due to increasdi iron absorption or inefficient erythropoiesis.

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17
Q

When to consider sideroblastic anaemia?

A

Microcytic anaemia not responding to iron

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18
Q

What are the causes of sideroblastic anaemia?

A
  • Congenital (rare and X-linked)
  • Myeloproliferative/myelodysplastic disease – caused by bone marrow failure
  • Chemotherapy, anti-TB drugs,
  • Irradiation
  • Alcohol use disorder
  • Lead poisoning
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19
Q

What are the investigations of sideroblastic anaemia?

A
  • Iron studies: ↑ferritin and iron and transferrin saturation
  • Blood film: hypochromic, microcytic anaemia,
  • Bone marrow staining - sideroblasts
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20
Q

How to treat sideroblastic anaemia?

A
  • Treat the cause.

- Pyridoxine (vitamin B6) ± repeated blood transfusions for severe anaemia.

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21
Q
  • What is thalassemia?

- What are the 2 different types?

A
  • Faulty globin chain synthesis resulting in defective haemoglobin, which can lead to anaemia.
  • Normal haemoglobin consists of 2 alpha and 2 beta globin chains, therefore Alpha and beta
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22
Q
  • Which thalassemia is more common in Mediterranean descent?

- Which thalassemia is more common in Asian and African descent?

A
  • Beta

- Alpha

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23
Q
  • Which chromosome is affected in beta thalassemia?

- What are the 2 different types of beta thalassemia?

A
  • Chromosome 11
  • Beta thalassemia minor (trait): one defective allele: Heterozygous carrier state.
  • Beta thalassemia major (Cooley’s anaemia): two defective alleles: Homozygous carrier state
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24
Q

What are the signs and symptoms of thalassemia?

A
  • Skeletal deformities – high forehead, prominent zygomatic bones and maxilla
  • Hepatosplenomegaly
  • Growth retardation
  • Jaundice
  • Fatigue
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25
Q

What are the 4 different types of alpha thalassemia?

A
  • All 4 genes are deleted, death is in utero (Bart’s hydrops fetalis)
  • HbH occurs if 3 genes are deleted, with moderate anaemia and features of haemolysis.
  • 2 genes deleted: asymptomatic carrier state
  • 1 gene deleted: normal clinical state.
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26
Q

What are the investigations for thalassemia?

A
  • Blood sample: Microcytic anaemia, low RBC count and high RDW
  • Increased indirect bilirubin and reticulocytes
  • Blood smear
  • Confirmatory tests: Hb -electrophoresis, abnormal pattern
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27
Q

What is the treatment for thalassemia?

A
  • Healthy diet + folate supplement

- Life-long erythrocyte transfusions: can lead to iron overload

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28
Q
  • What iron overload lead to?
  • What is the treatment?
  • What are the SE of treatment?
A
  • Cardiac iron overload, hypothyroidism, hypocalcaemia, and hypogonadism.
  • Iron-chelators: desferasirox and desferrioxamine
  • SE: deafness, retinal damage
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29
Q

What are the different causes of normocytic anaemia?

A
  • Sickle cell anaemia
  • Infections
  • Blood loss
  • Haemolytic anaemia
  • Iron deficiency anaemia (early phase)
  • Anaemia of chronic disease (early phase)
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30
Q

What are the signs of acute blood loss?

A

Clinical signs of hypovolaemic shock, e.g. pale and clammy, weak pulse, hypotensive, decreased level of consciousness

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31
Q

What are the causes of acute blood loss for women of child-bearing age?

A

Menorrhagia

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32
Q

What is anaemia of chronic disease?

A
  • Anaemia due to chronic inflammation
33
Q

What are the causes of anaemia of chronic disease?

A
  • Inflammation: rheumatoid arthritis, lupus
  • Malignancy: lung cancer, breast cancer
  • Infection: TB
34
Q

What investigations are done anaemia of chronic disease?

A
  • FBC: normocytic anaemia (early phase), microcytic anaemia (late phase)
  • Iron studies: elevated serum ferritin
35
Q

What is the treatment for anaemia of chronic disease?

A

Treat underlying cause

36
Q

What are the causes of macrocytic anaemia?

A
  • Vitamin B12 deficiency
  • Folate deficiency
  • Fanconi anaemia
  • Diamond-Black fan anaemia
  • Haemolytic anaemia: elevated reticulocytes count (>2%)
37
Q

What is the role of vitamin B12 (cobalamin)?

A

Essential role in enzymatic reactions responsible for red blood cell (RBC) formation

38
Q

What are the causes of vitamin B12 deficiency anaemia?

A
  • Pernicious anaemia
  • Atrophic gastritis
  • Surgical: ileal resection, gastric surgery
  • B12 deficient diet (without fish, eggs, meat, milk)
  • Pregnancy
  • Coeliacs, Crohns
39
Q

What are the symptoms of vitamin B12 deficiency anaemia?

A
  • Symptoms of anaemia
  • Neuropathy: peripheral (tingling and numbness, pins and needles, coldness),
  • Pre-hepatic jaundice
  • Glossitis – inflammation of tongue
  • Stomatitis (angular cheilosis)
40
Q

What autoantibodies cause pernicious anaemia?

A
  • Intrinsic factor antibody

- Gastric parietal cell antibody

41
Q

What investigations are done in vitamin B12 deficiency anaemia?

A
  • Decreased Hb
  • Raised MCV – macrocytic
  • Decreased reticulocytes
  • Serum B12 (↓),
  • Intrinsic factor antibodies and anti-parietal cells antibodies
42
Q

What is the treatment for vitamin B12 deficiency anaemia?

A
  • IM supplementation of vitamin B12

- Prevent future vitamin B12 deficiency

43
Q

Why might folate deficiency anaemia take 3 months to present?

A

The liver can store folate for up to three months

44
Q

What are the causes of folate deficiency anaemia?

A
  • Nutritional – poor diet (folate comes from leafy green vegetables, fruit), goats milk only
  • Chronic alcohol intake,
  • Coeliac disease, IBD, jejunal resection (folate is absorbed here)
  • Pregnancy
  • Drug related – methotrexate (folate antagonist), phenytoin, trimethoprim
45
Q

What are the symptoms of folate deficiency anaemia?

A
  • Signs of anaemia
  • Glossitis
  • Signs of B12 deficiency - but often only sensory peripheral neuropathy.
46
Q

What can be seen in investigation for folate deficiency anaemia?

A

Raised MCV

47
Q

What is the treatment for folate deficiency anaemia?

A
  • Oral folate for 4 months

- Nutritional counselling to increase folate intake

48
Q
  • What is haemolytic anaemia?

- Why type of anaemia is it?

A
  • Characterised by the breakdown of RBC

- Normocytic

49
Q

What are the 2 key features of haemolytic anaemia?

A
  • ↑(>2%) reticulocyte count

- Jaundice with unconjugated hyperbilirubinemia

50
Q

What do the investigations show for haemolytic anaemia?

A
  • Elevated indirect bilirubin
  • Elevated Lactate dehydrogenase
  • Elevated reticulocytosis
  • Decreased haemoglobin
  • Elevated WBC, LDH
51
Q
  • What is Coombs test?

- What do the results mean?

A
  • Detects antibodies on RBCs surface (direct test) or in patient’s serum (indirect test).
  • Autoimmune (positive Coombs test)
  • Non-autoimmune anaemia (negative Coombs test).
52
Q

What type of genetic disorder is thalassemia?

A

Autosomal recessive

53
Q

What is hereditary spherocytosis?

A

Haemolytic anaemia

54
Q

How does hereditary spherocytosis present?

A

Jaundice, anaemia, splenomegaly

55
Q

What type of genetic disorder is hereditary spherocytosis?

A

Autosomal dominant

56
Q

How to treat hereditary spherocytosis?

A
  • Folic acid

- Then try splenectomy

57
Q

What is sickle cell disease?

A

Autosomal recessive disease, from substitution of glu → val in the β-Hb chain

58
Q

How many sickle cell anaemia alleles do sickle-cell anaemia patients carry?

A
  • 2 alleles

- Homozygous

59
Q

How many sickle cell anaemia alleles do sickle-cell trait patients carry?

A
  • 1 allele

- Heterozygotes

60
Q

What is the pathophysiology of sickle cell anaemia?

A

HbS polymerises when deoxygenated, forming sickle RBCs which are fragile and haemolyse, as well as block small vessels. Triggered by certain events.

61
Q

What are the symptoms of sickle cell trait?

A

Asymptomatic

62
Q

What are the symptoms of sickle cell disease?

A

Often present as complications (sickle cell crisis):

  • Acute symptom of vaso-cclusive/painful crises
  • Splenic sequestration crisis
  • Aplastic crisis
63
Q

What is splenic sequestration crisis in sickle cell anaemia?

A
  • RBC blocking blood flow within the spleen
  • Acute left upper quadrant pain
  • Can lead to a severe anaemia and circulation collapse (hypovolaemic shock)
64
Q

What is aplastic crisis in sickle cell anaemia?

A
  • Temporary loss of new RBC creation
  • Due to parvovirus B19
  • Usually self-limiting <2wks
  • Transfusion may be needed.
65
Q
  • What is vaso-cclusion/painful crisis?

- How does it present?

A
  • Sickle shaped blood cells clogging capillaries resulting in ischaemia
  • Episodes of severe deep bone pain
  • Dactylitis: swollen dorsa of hands and feet
  • Acute chest syndrome: chest pain, respiratory distress
  • Stroke
  • Infarctions of any organ
66
Q

What investigations are done in sickle cell disease?

A
  • FBC: ↑reticulocytes, ↑bilirubin
  • Film: sickle cells
  • Microcytic, low MCV: due to the very small diameter of the sickle shaped red blood cells.
  • Hb electrophoresis: Confirms diagnosis and differentiates between disease and trait.
67
Q

How to treat sickle cell disease?

A
  • Keep patient warm, hydrated, well-nourished and rested.
  • Hydroxycarbamide (hydroxyurea – turns on the production of foetal haemoglobin genes HbA and it should be above 15%)
  • Bone marrow transplant may be curative but controversial.
68
Q

What are other complications of sickle cell disease?

A
  • Increased vulnerability to infection (pneumonia and meningitis)
  • Lung: Pulmonary hypertension
  • Heart: MI, HF, cardiomegaly
  • Eye:retinal occlusion
  • Kidney: glomerulonephritis
  • Skeletal: osteoporosis
69
Q

Which 2 enzyme defects can led to haemolytic anaemia?

A
  • G6PD deficiency: X-linked recessive disease

- Pyruvate kinase deficiency: autosomal recessive disease

70
Q

What are the different acquired haemolytic condition?

A
  • Autoimmune haemolytic anaemia
  • Wilsons disease: Copper deficiency
  • Drugs, infections, toxins
71
Q

What are the 2 types of autoimmune haemolytic anaemia?

A

Warm and cold depending on the thermal range across which the antibody is active.

72
Q
  • What is cold AIHA?

- What are the causes?

A
  • IgM mediated, binds to RBCs at low temp

- Idiopathic or secondary to EBV infection, mycoplasma pneumonia, UC

73
Q

What are the signs of cold AIHA?

A
  • Pallor
  • Fatigue
  • Weakness
  • Acrocyanosis – cyanosis of the extremities
74
Q

What are the investigations of both AIHA?

A
  • Lab tests signs of haemolysis
  • Peripheral blood smear: spherocytes, polychromasia
  • Coombs test: positive
75
Q

How to treat cold AIHA?

A
  • Mild disease: avoid cold exposure

- Moderate disease: immunosuppressive therapy with rituximab

76
Q
  • What is warm AIHA?

- What are the causes?

A
  • IgG-mediated, binds to RBCs at body temperature (37deg)
  • Lymphoproliferative disease (chronic lymphocytic leukaemia, lymphoma)
  • Drugs – cephalosporins, penicillin’s
  • Autoimmune disease – SLE, ovarian teratoma
77
Q

What are the signs of warm AIHA?

A
  • Often more severe and more acute than cold AIHA

- Signs of anaemia (pallor, fatigue, weight loss)

78
Q

How to treat warm AIHA?

A
  • Initially glucocorticoids

- If glucocorticoids unsuccessful then splenectomy

79
Q
  • How to test for SLE?
  • When is it likely to develop?
  • What is a frequent complication of SLE?
A
  • Check for anti-DNA antibodies
  • After AIHA
  • Immune thrombocytopenia (ITP)

Year 3 - TCD (17 decks)

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