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MSRA > Haematology > Flashcards

Haematology Flashcards

1
Q

What is the mnemonic for the causes of microcytic anaemia?

A

T: Thalassaemia
A: Anaemia of chronic disease
I: Iron deficiency anaemia
L: Lead poisoning
S: Sideroblastic anaemia

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2
Q

What conditions cause normocytic anaemia? (Mnemonic: 3 As and 2 Hs)

A

A: Acute blood loss
A: Anaemia of chronic disease
A: Aplastic anaemia
H: Haemolytic anaemia
H: Hypothyroidism

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3
Q

What are the causes of macrocytic anaemia?

A

Megaloblastic macrocytic anaemia: B12 and folate deficiency

Normoblastic macrocytic anaemia: Alcohol, reticulocytosis, hypothyroidism, liver disease, drugs (e.g., azathioprine)

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4
Q

What are symptoms specific to iron deficiency anaemia?

A

Pica: Cravings for unusual substances like dirt or soil
Hair loss

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5
Q

What signs indicate iron deficiency anaemia specifically?

A

Koilonychia (spoon-shaped nails)
Angular cheilitis (inflammation around the mouth)
Atrophic glossitis (smooth tongue)
Brittle hair and nails

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6
Q

What specific signs might suggest haemolytic anaemia or thalassaemia?

A

Jaundice suggests haemolytic anaemia

Bone deformities may indicate thalassaemia

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7
Q

What investigations are typically done for anaemia?

A
  • Full blood count for haemoglobin and MCV
  • Reticulocyte count (indicates red blood cell production)
  • Blood film for abnormal cells
  • Ferritin, B12, and folate for iron and vitamin deficiencies
  • Intrinsic factor antibodies for pernicious anaemia
  • Thyroid function tests for hypothyroidism
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8
Q

What are the key causes of iron deficiency anaemia?

A
  • Insufficient dietary iron
  • Reduced iron absorption (e.g., coeliac disease)
  • Increased iron requirements (e.g., pregnancy)
  • Blood loss (e.g., peptic ulcers, cancer)
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9
Q

What are common sources of gastrointestinal blood loss leading to iron deficiency?

A
  • Cancer (stomach or bowel)
  • Oesophagitis, gastritis, peptic ulcers
  • Inflammatory bowel disease
  • Angiodysplasia
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10
Q

How do proton pump inhibitors (e.g., omeprazole) affect iron absorption?

A

They reduce stomach acid, making iron less soluble and harder to absorb.

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11
Q

What is transferrin, and how is it related to iron deficiency?

A

Transferrin is a carrier protein for iron in the blood. In iron deficiency, transferrin levels and total iron-binding capacity (TIBC) increase, while transferrin saturation decreases.

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12
Q

What does ferritin indicate, and why is it an important marker for iron deficiency?

A

Ferritin stores iron in cells. Low ferritin suggests iron deficiency, but it may be elevated during inflammation, liver disease, or iron supplementation, making it less reliable in those conditions.

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13
Q

What conditions lead to iron overload, indicated by high serum iron and transferrin saturation?

A
  • Haemochromatosis
  • Iron supplements
  • Acute liver damage
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14
Q

Why should iron infusions be avoided during infections?

A

There is a risk that iron could “feed” bacteria, potentially worsening the infection.

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15
Q

What are the key causes of vitamin B12 deficiency?

A
  • Pernicious anaemia (autoimmune condition)
  • Insufficient dietary B12 (e.g., vegan diet)
  • Medications that reduce B12 absorption (e.g., proton pump inhibitors, metformin)
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16
Q

What is pernicious anaemia?

A

An autoimmune condition where antibodies target parietal cells or intrinsic factor, leading to reduced absorption of vitamin B12 in the distal ileum.

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17
Q

What role does intrinsic factor play in vitamin B12 absorption?

A

Intrinsic factor, produced by the parietal cells in the stomach, is essential for the absorption of vitamin B12 in the distal ileum.

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18
Q

What are the neurological symptoms associated with vitamin B12 deficiency?

A
  • Peripheral neuropathy (numbness, paraesthesia)
  • Loss of vibration sense
  • Loss of proprioception
  • Visual changes
  • Mood and cognitive changes
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19
Q

What is the first-line antibody test for diagnosing pernicious anaemia?

A

Intrinsic factor antibodies are the first-line investigation for diagnosing pernicious anaemia

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20
Q

How is vitamin B12 deficiency treated when there are no neurological symptoms?

A

Intramuscular hydroxocobalamin is given 3 times weekly for two weeks.

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21
Q

How is vitamin B12 deficiency treated when there are neurological symptoms?

A

Intramuscular hydroxocobalamin is given on alternate days until there is no further improvement in symptoms.

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22
Q

What is the maintenance treatment for pernicious anaemia?

A

2-3 monthly intramuscular hydroxocobalamin injections are given for life.

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23
Q

What is the maintenance treatment for diet-related vitamin B12 deficiency?

A

Oral cyanocobalamin or twice-yearly intramuscular injections are used for maintenance.

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24
Q

Why must B12 deficiency be treated before folate deficiency if both are present?

A

Treating folate deficiency first can cause subacute combined degeneration of the spinal cord, leading to severe neurological damage.

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25
Q

Name some inherited conditions that cause chronic haemolytic anaemia.

A
  • Hereditary spherocytosis
  • Hereditary elliptocytosis
  • Thalassaemia
  • Sickle cell anaemia
  • G6PD deficiency
26
Q

What are some acquired conditions that cause haemolytic anaemia?

A
  • Autoimmune haemolytic anaemia
  • Alloimmune haemolytic anaemia
  • Paroxysmal nocturnal haemoglobinuria
  • Microangiopathic haemolytic anaemia
  • Prosthetic valve-related haemolysis
27
Q

What are the key features of haemolytic anaemia?

A
  • Anaemia
  • Splenomegaly (enlarged spleen)
  • Jaundice (due to bilirubin release from RBC destruction)
28
Q

What investigation findings indicate haemolytic anaemia?

A
  • Normocytic anaemia on a full blood count
  • Schistocytes (RBC fragments) on a blood film
  • Positive direct Coombs test in autoimmune haemolytic anaemia
29
Q

What is hereditary spherocytosis, and what are the key findings?

A

Hereditary spherocytosis is an autosomal dominant condition where red blood cells are sphere-shaped and fragile. Findings include:

  • Raised MCHC
  • Raised reticulocyte count
  • Spherocytes on a blood film
30
Q

What is the management of hereditary spherocytosis?

A
  • Folate supplementation
  • Blood transfusions when necessary
  • Splenectomy (removal of the spleen)
  • Cholecystectomy (if gallstones develop)
31
Q

What is G6PD deficiency, and what triggers its episodes of haemolysis?

A

G6PD deficiency is an X-linked recessive condition that makes RBCs more susceptible to oxidative damage. Triggers include:

  • Infections
  • Drugs (e.g., ciprofloxacin, sulfonylureas, sulfasalazine)
  • Fava beans
32
Q

What are key blood film findings in G6PD deficiency?

A

Heinz bodies, which are clumps of denatured haemoglobin, are seen on the blood film

33
Q

What are the two types of autoimmune haemolytic anaemia (AIHA)?

A

Warm AIHA: Haemolysis occurs at normal or above-normal temperatures.

Cold AIHA: Haemolysis occurs at temperatures below 10ºC, causing red cells to agglutinate.

34
Q

What are the key management strategies for autoimmune haemolytic anaemia (AIHA)?

A
  • Blood transfusions
  • Prednisolone (a corticosteroid)
  • Rituximab (monoclonal antibody)
  • Splenectomy
35
Q

What causes alloimmune haemolytic anaemia, and what are the two key scenarios?

A
  • Transfusion reactions: Antibodies target foreign red blood cells.
  • Haemolytic disease of the newborn: Maternal antibodies destroy fetal red blood cells.
36
Q

What is paroxysmal nocturnal haemoglobinuria, and what is a key presenting symptom?

A

A condition caused by a genetic mutation in haematopoietic stem cells, leading to RBC destruction by the complement system. The key symptom is red urine in the morning (containing haemoglobin and haemosiderin).

37
Q

How is paroxysmal nocturnal haemoglobinuria managed?

A
  • Eculizumab (a monoclonal antibody against complement C5)
  • Bone marrow transplantation
38
Q

What is microangiopathic haemolytic anaemia (MAHA), and what causes it?

A

MAHA is the destruction of red blood cells as they pass through small blood vessels obstructed by blood clots (thrombi).

Causes include:
- Haemolytic uraemic syndrome (HUS)
- Disseminated intravascular coagulation (DIC)
- Thrombotic thrombocytopenic purpura (TTP)
- Systemic lupus erythematosus (SLE)

39
Q

What key finding is seen on a blood film in microangiopathic haemolytic anaemia?

A

Schistocytes (fragmented red blood cells).

40
Q

What causes thalassaemia?

A

Thalassaemia is caused by genetic defects in the alpha- or beta-globin chains that make up haemoglobin, leading to haemolytic anaemia.

41
Q

What are the universal features of thalassaemia?

A

Microcytic anaemia (low MCV)
Fatigue
Pallor
Jaundice
Gallstones
Splenomegaly
Poor growth and development

42
Q

What investigations are used to diagnose thalassaemia?

A
  • Full blood count showing microcytic anaemia
  • Haemoglobin electrophoresis to identify globin abnormalities
  • DNA testing for genetic mutations
43
Q

What are the key causes of iron overload in thalassaemia?

A
  • Increased iron absorption in the GI tract
  • Frequent blood transfusions
44
Q

What are the management strategies for iron overload in thalassaemia?

A
  • Monitoring serum ferritin levels
  • Limiting blood transfusions
  • Iron chelation therapy
45
Q

What complications can arise from iron overload in thalassaemia?

A
  • Liver cirrhosis
  • Hypogonadism
  • Hypothyroidism
  • Heart failure
  • Diabetes
  • Osteoporosis
46
Q

What genetic abnormality causes alpha-thalassaemia, and what chromosome is affected?

A

Alpha-thalassaemia is caused by defects in the alpha-globin chains, coded on chromosome 16.

47
Q

What are the types of alpha-thalassaemia, and how do they differ in severity?

A
  • Carrier: Asymptomatic
  • Haemoglobin H disease: Moderate anaemia
  • Alpha-thalassaemia major: Severe fetal anaemia, often leading to intrauterine death
48
Q

What are the three types of beta-thalassaemia?

A
  • Thalassaemia minor: Mild microcytic anaemia
  • Thalassaemia intermedia: Moderate anaemia, may need occasional transfusions
  • Thalassaemia major: Severe anaemia, requiring regular transfusions
49
Q

What is beta-thalassaemia, and what chromosome is affected?

A

Beta-thalassaemia is caused by defects in the beta-globin chains, coded on chromosome 11.

50
Q

What abnormal skeletal features are associated with beta-thalassaemia major?

A
  • Frontal bossing (prominent forehead)
  • Enlarged maxilla (prominent cheekbones)
  • Depressed nasal bridge (flat nose)
  • Protruding upper teeth
51
Q

What causes the abnormal sickle shape of red blood cells in sickle cell disease?

A

The abnormal shape is due to the presence of haemoglobin S (HbS), an abnormal variant of haemoglobin.

52
Q

How is sickle cell anaemia inherited?

A

It is an autosomal recessive condition. One abnormal gene results in sickle-cell trait, while two abnormal genes result in sickle-cell disease.

53
Q

How is sickle cell disease screened in newborns?

A

It is included in the newborn blood spot screening test at around five days of age.

54
Q

What are common complications of sickle cell disease?

A
  • Anaemia
  • Increased risk of infection
  • Chronic kidney disease
  • Acute chest syndrome
  • Stroke
  • Avascular necrosis
  • Pulmonary hypertension
  • Gallstones
  • Priapism
55
Q

What is vaso-occlusive crisis, and how does it present?

A

Vaso-occlusive crisis (painful crisis) occurs when sickle cells block capillaries, causing distal ischaemia. It presents with pain, swelling, and sometimes fever, commonly affecting the hands, feet, chest, or back.

56
Q

How is priapism treated in a vaso-occlusive crisis?

A

Priapism, a painful and persistent erection, is treated by aspirating blood from the penis, which is considered a urological emergency.

57
Q

What is splenic sequestration crisis, and how is it managed?

A

It occurs when red blood cells block blood flow in the spleen, causing splenomegaly, severe anaemia, and hypovolaemic shock. Management includes blood transfusions and fluid resuscitation.

58
Q

What is aplastic crisis, and what commonly triggers it?

A

Aplastic crisis is a temporary cessation of red blood cell production, often triggered by parvovirus B19 (slapped cheek syndrome). It leads to significant anaemia and is managed supportively.

59
Q

What is acute chest syndrome in sickle cell disease, and why is it an emergency?

A

Acute chest syndrome occurs when vessels in the lungs are blocked by sickle cells, causing fever, shortness of breath, chest pain, and hypoxia. It is a medical emergency with high mortality.

60
Q

What is the role of hydroxycarbamide in managing sickle cell disease?

A

Hydroxycarbamide stimulates the production of fetal haemoglobin (HbF), which reduces the frequency of vaso-occlusive crises and improves anaemia.

61
Q

How does crizanlizumab work in sickle cell disease management?

A

Crizanlizumab is a monoclonal antibody targeting P-selectin, which prevents red blood cells from sticking to vessel walls, reducing the frequency of vaso-occlusive crises.

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