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Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

What is multiple myeloma?

A

A haematological malignancy characterised by plasma cell proliferation.

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2
Q

What are the complications of multiple myeloma?

A 
Hypercalcaemia,
Renal damage,
Anaemia,
Thrombocytopenia,
Bone lesions,
Immune deficiency

(CRABBI)

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3
Q

How does multiple myeloma present?

A

Hypercalcaemia: constipation, nausea, confusion.
Renal damage: dehydration, thirst.
Anaemia: fatigue, pallor.
Thrombocytopenia: bleeding, bruising.
Bone lesions: back pain, fragility fractures.
Immune deficiency: freq. infections.

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4
Q

What investigations are performed in multiple myeloma?

A

FBC, U&E, blood film, imaging, protein electrophoresis, bone marrow biopsy.

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5
Q

What does FBC show in multiple myeloma?

A

Anaemia.

Thrombocytopenia.

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6
Q

What do U&Es show in multiple myeloma?

A

Raised urea.

Raised creatinine.

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7
Q

What does peripheral blood film show in multiple myeloma?

A

Rouleaux formation.

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8
Q

What is a common X-ray finding in patients with multiple myeloma?

A

Rain-drop skull (dark spots on skull due to bone lysis).

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9
Q

What does serum/urine protein electrophoresis show in patients with multiple myeloma?

A

Raised concentrations of monoclonal antibody proteins.

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10
Q

What does bone marrow biopsy show in patients with multiple myeloma?

A

Raised monoclonal plasma cells (>10%).

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11
Q

What is the management of multiple myeloma?

A

Stem cell transplantation and rigorous chemotherapy regimes.

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12
Q

What is myelofibrosis?

A

Myeloproliferative disorder thought to be caused by hyperplasia of abnormal megakaryocytes.

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13
Q

How does myelofibrosis present?

A

In an elderly person with fatigue, massive hepatosplenomegaly… as well as weight loss and night sweats.

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14
Q

What investigations are performed in myelofibrosis?

A

FBC, blood film, bone barrow biopsy.

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15
Q

What does FBC show in patients with myelofibrosis?

A

Anaemia, thrombocytopenia, raised WCC.

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16
Q

What does blood film show in patients with myelofibrosis?

A

Tear-drop poikilocytes.

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17
Q

What does bone marrow aspiration show in patients with myelofibrosis?

A

Bone marrow aspiration may result in a dry tap - no sample is collected because the bone marrow is replaced by collagen.

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18
Q

What are thalassaemias?

A

A group of inherited disorders characterised by abnormal haemoglobin production.

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19
Q

What is the inheritance pattern of alpha-/beta-thalassaemia?

A

Autosomal recessive.

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20
Q

Beta-thalassaemia trait is characterised by what findings on investigation?

A

Hypochromic, microcytic anaemia. As well as raised reticulocytes and raised bilirubin.

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21
Q

The clinical severity of alpha-thalassaemia is dependent on what?

A

The number of alpha globulin alleles affected.

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22
Q

In alpha-thalassaemia: how does 1 or 2 affected alleles present clinically?

A

Hypochromic, microcytic anaemia but normal haemoglobin. Rarely symptomatic.

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23
Q

In alpha-thalassaemia: how does 3 affected alleles present clinically?

A

Hypochromic, microcytic anaemia with splenomegaly.

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24
Q

In alpha-thalassaemia: how does 4 affected alleles present clinically?

A

Death in utero (incompatible with life).

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25
Q

What is raised HbA2 a sign of?

A

Beta-thalassaemia.

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26
Q

What is factor V Leiden?

A

The most common cause of inherited thrombophilia.

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27
Q

What is antiphospholipid syndrome?

A

An acquired, autoimmune, hypercoagulable state.

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28
Q

How may antiphospholipid syndrome present?

A

Venous/arterial thrombosis, recurrent foetal loss (in women) and livedo reticularis.

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29
Q

What does FBC show in antiphospholipid syndrome?

A

Thrombocytopenia.

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30
Q

What does APTT show in antiphospholipid syndrome?

A

Prolonged APTT.

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31
Q

What prophylaxis is provided for individuals with antiphospholipid syndrome?

A

Primary: low-dose aspirin.
Secondary: life-long warfarin.

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32
Q

What is the target INR for an individual with antiphospholipid syndrome after an initial episode of VTE?

A

2-3.

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33
Q

What is the target INR for an individual with antiphospholipid syndrome after recurrent episodes of VTE?

A

3-4.

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34
Q

Neutropenic sepsis is often a complication of what?

A

Cancer therapy (e.g. chemotherapy).

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35
Q

When does neutropenic sepsis typically develop after chemotherapy?

A

7-14 days post chemotherapy.

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36
Q

What are the features of neutropenic sepsis?

A

Temperature (>38C) or other signs consistent with sepsis.

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37
Q

What is the treatment for neutropenic sepsis?

A

Tazocin (Piperacillin with Tazobactam).

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38
Q

What is haemophilia?

A

A disorder of coagulation that predisposes to bleeding.

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39
Q

What is the inheritance pattern of haemophilia?

A

X-linked recessive.

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40
Q

What are the main features of haemophilia?

A

Haemoarthroses (bleeding into a joint).
Haematomas (bleeding outside of vessels).
Prolonged bleeding.

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41
Q

What investigations are performed in the investigation of haemophilia?

A

Clotting screen.

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42
Q

What does clotting screen show in patients with haemophilia?

A

Prolonged APTT.
Normal PT.
Normal bleeding time.

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43
Q

Of haemophilia A and B, which is more common?

A

Haemophilia A accounts for 90% of cases.

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44
Q

Haemophilia A is marked by deficiency of which clotting factor?

A

Factor VIII.

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45
Q

Haemophilia B is marked by deficiency of which clotting factor?

A

Factor IX.

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46
Q

What is Hodgkin’s lymphoma?

A

A malignant proliferation of lymphocytes and their subsequent accumulation in the lymph nodes, blood and organs.

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47
Q

What ages does Hodgkin’s lymphoma typically affect?

A

Large peak in 20-30y age group and a smaller peak in older age (>55y).

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48
Q

Hodgkin’s lymphoma is associated with infection with what virus?

A

Epstein Barr Virus (EBV).

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49
Q

What is the characteristic presentation of Hodgkin’s lymphoma?

A

Painless, rubbery lymphadenopathy (affecting the cervical nodes especially) and B symptoms.

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50
Q

What are the B symptoms associated with Hodgkin’s and non-Hodgkin’s lymphoma?

A

Systemic symptoms that include fever, night sweats and weight loss (>10% in 6mo).

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51
Q

Other than B symptoms… what other systemic symptoms may be associated with HL?

A

Itch. Alcohol-induced pain in lymph nodes (rare).

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52
Q

What is the investigation of choice for diagnosing Hodgkin’s lymphoma?

A

Lymph node biopsy.

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53
Q

What does lymph node biopsy show in patients with Hodgkin’s lymphoma?

A

Reed-Sternberg cells (large multinucleate cells with eosinophilic nucleoli).

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54
Q

Why is extensive radiotherapy relied on less than previously in the management of Hodgkin’s lymphoma?

A

Risk of secondary malignancy (especially as HL predominantly affects young adults).

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55
Q

What is the management of Hodgkin’s lymphoma?

A

Two-eight cycles of ABVD chemotherapy (depends on severity of disease). ABVD = adriamycin, bleomycin, vinblastine, dacarbazine.

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56
Q

What is the Ann Arbor staging system?

A

Staging system for Hodgkin’s lymphoma and non-Hodgkin’s lymphoma.

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57
Q

Interpret the Ann Arbor staging classification (I, II, III and IV).

A

I - single lymph node region.
II - two or more regions on same side of diaphragm.
III - two or more regions on both sides of diaphragm.
IV - diffuse disease in extra-lymphatic sites.

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58
Q

What is non-Hodgkin’s lymphoma?

A

A group of malignant diseases arising from lymphocytes and their precursors. There is a wide spectrum of disease.

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59
Q

Give risk factors for non-Hodgkin’s lymphoma.

A

Longevity, prolonged immunosuppression, EBV infection, H. pylori infection, HIV infection.

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60
Q

How does non-Hodgkin’s lymphoma present?

A

Superficial, painless lymphadenopathy with B symptoms and hepatosplenomegaly.

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61
Q

What is the investigation of choice regarding diagnosis of non-Hodgkin’s lymphoma?

A

Lymph node biopsy.

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62
Q

What is follicular lymphoma?

A

Low-grade B-cell NHL. The most common subtype of indolent NHL.

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63
Q

Who does follicular lymphoma typically affect?

A

Those in older as late-stage disease.

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64
Q

What is Burkitt’s lymphoma?

A

Highly aggressive B-cell malignancy with two main variants.

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65
Q

What are the two main variants of Burkitt’s lymphoma?

A

Endemic.

Sporadic.

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66
Q

Describe the endemic subtype of Burkitt’s lymphoma.

A

Occurs most commonly in Africa, is strongly associated with infection with EBV and mainly affects children who present with head/neck tumours.

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67
Q

Describe the sporadic subtype of Burkitt’s lymphoma.

A

Less associated with EBV and abdominal disease is more common.

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68
Q

Under what circumstances does acute haemolytic transfusion reaction occur?

A

Results from a mismatch of blood group which causes massive intravascular haemolysis.

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69
Q

What pathophysiological mechanism causes the development of acute haemolytic transfusion reaction?

A

Red blood cell destruction by IgM-type antibodies.

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70
Q

When does acute haemolytic transfusion reaction begin following transfusion and what are the features?

A

Features begin minutes after transfusion begins… includes fever, abdominal pain, chest pain, agitation and hypotension.

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71
Q

What is the management of acute haemolytic transfusion reaction?

A

Immediate transfusion termination and generous fluid resuscitation (saline solution).

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72
Q

What mechanism causes the development of non-haemolytic febrile transfusion reaction?

A

Antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storage.

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73
Q

What are the features of non-haemolytic febrile transfusion reaction?

A

Fever.

Chills.

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74
Q

What is the management of non-haemolytic febrile transfusion reaction?

A

Slow or stop the transfusion. Give paracetamol.

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75
Q

What mechanism causes the development of a minor allergic transfusion reaction?

A

Foreign plasma proteins seen as allergens.

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76
Q

What are the features of a minor allergic transfusion reaction?

A

Pruritus.

Urticaria.

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77
Q

What mechanism leads to anaphylaxis post transfusion?

A

Patients with IgA deficiency who have anti-IgA antibodies.

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78
Q

What are the features of transfusion-related anaphylaxis?

A

Hypotension, dyspnoea, wheezing and angioedema.

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79
Q

What is the management of transfusion-related anaphylaxis?

A

Stop the transfusion. Give intramuscular adrenaline followed by antihistamines, bronchodilators and corticosteroids.

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80
Q

What is transfusion-related acute lung injury (TRALI)?

A

TRALI is a rare but potentially fatal complication of blood transfusion characterised by hypoxaemia/acute respiratory distress syndrome within six hours of transfusion.

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81
Q

What are the features of transfusion-related acute lung injury?

A

Hypoxia, pulmonary infiltrates on CXR, fever and hypotension.

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82
Q

What is transfusion-associated circulatory overload (TACO)?

A

TACO is a common reaction due to fluid overload resulting in pulmonary oedema.

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83
Q

What are the features of transfusion-associated circulatory overload?

A

Dyspnoea, raised JVP, fine crackles on chest auscultation, hypertension, afebrile.

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84
Q

What is the characteristic finding on lymph node biopsy of Burkitt’s lymphoma?

A

Starry sky appearance.

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85
Q

What is polycythaemia vera?

A

A myeloproliferative disorder caused by clonal proliferation of a marrow stem cell leading to an increase in blood cells (particularly red blood cells).

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86
Q

What mutation is present in 95% of patients with polycythaemia vera?

A

Mutation in JAK2 enzyme.

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87
Q

In which age group does polycythaemia vera peak in incidence?

A

60s

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88
Q

What is the definition of polycythaemia?

A

High concentration of red blood cells in the blood.

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89
Q

What are the presenting features of polycythaemia vera?

A

Pruritus (typically after hot bath), headache, splenomegaly, plethoric appearance and hypertension.

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90
Q

Polycythaemia vera carries an increased risk of what?

A

Thrombotic events such as myocardial infarction and stroke.

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91
Q

What investigations are required in the diagnosis of polycythaemia vera?

A

Full blood count. Positive JAK2 mutation.

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92
Q

What does FBC show in patients with polycythaemia vera?

A

Raised haematocrit, raised neutrophils, raised basophils and (in half of patients) raised platelets.

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93
Q

What is the management of polycythaemia vera?

A

Low dose aspirin (to reduce the risk of thrombotic events). Provide venesection (to maintain a normal range of haemoglobin). Some patients may require chemotherapy - hydroxyurea.

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94
Q

What is the inheritance pattern off sickle cell anaemia?

A

Autosomal recessive.

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95
Q

What is sickle cell anaemia?

A

Synthesis of an abnormal haemoglobin chain (HbS) which causes a rigid sickle-like shape of red blood cell.s

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96
Q

Which screening test includes screening for sickle cell anaemia?

A

The newborn heel-prick test at five days old.

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97
Q

When does a child begin to show signs/symptoms of sickle cell anaemia?

A

Five-to-six months old.

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98
Q

Why do signs/symptoms of sickle cell anaemia develop around six months old?

A

Foetal haemoglobin is protective in the first few months of life until levels begin to reduce.

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99
Q

Describe the pathophysiology of sickle cell disease.

A

Sickle cells cause increase blood viscosity, reducing blood flow through the small vessels and leading to tissue infarction.
Sickle cells are prematurely destroyed resulting in haemolytic anaemia.

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100
Q

What investigation is used for the definitive diagnosis of sickle cell anaemia?

A

Haemoglobin electrophoresis.

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101
Q

Maintenance therapy for sickle cell anaemia includes what?

A

Vaccinations, folic acid and hydroxyurea/hydroxycarbamide.

102
Q

What advice should be given to the patient and family of sickle cell patients to avoid sickle cell crises?

A

Avoid hypoxia (air travel), the cold and dehydration.

103
Q

Sequestration crisis (sickle cell crises) is associated with what findings on investigation?

A

Worsening anaemia.

Raised reticulocyte count.

104
Q

Acute chest syndrome (sickle cell crises) is associated with what features?

A

Dyspnoea, chest pain, pulmonary infiltrates and low partial pressure of oxygen.

105
Q

Aplastic crisis (sickle cell crisis) is associated with what findings on investigation?

A

Sudden fall in haemoglobin and reduced reticulocyte count.

106
Q

What is the most common inherited bleeding disorder?

A

von Willebrand’s disease.

107
Q

What is the most common inherited clotting disorder?

A

Factor V Leiden.

108
Q

What is the inheritance pattern of von Willebrand’s disease?

A

Autosomal dominant.

109
Q

What is the pathophysiology behind von Willebrand disease?

A

Deficiency in von Willebrand factor, a large glycoprotein which promotes platelet adhesion to damaged endothelium and a carrier molecule for factor VIII.

110
Q

What are the features of von Willebrand disease?

A

Epistaxis.

Menorrhagia.

111
Q

What investigations are performed in suspected von Willebrand disease and what are the results?

A 
Bleeding time (prolonged). 
APTT (prolonged).
112
Q

How is von Willebrand disease managed?

A

Give tranexamic acid for mild bleeding. Can give desmopressin.

113
Q

By what mechanism is desmopressin useful in the treatment of von Willebrand disease?

A

Raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells.

114
Q

What is idiopathic thrombocytopenic purpura (ITP)?

A

An isolated low platelet count with normal bone marrow in the absence of other causes of low platelets.

115
Q

Idiopathic thrombocytopenic purpura typically follows what?

A

A viral illness.

116
Q

How does idiopathic thrombocytopenic purpura present?

A

Characteristic red or purple bruise-like rash and an increased tendency to bleed.

117
Q

In patients with idiopathic thrombocytopenic purpura what are the results of a full blood count?

A

Low platelets.

118
Q

What is the prognosis of idiopathic thrombocytopenic purpura?

A

Typically self-limiting course between one and two weeks.

119
Q

How should significant bleeding in patients with idiopathic thrombocytopenic purpura be treated?

A

Oral prednisolone.

120
Q

What is a deep vein thrombosis (DVT)?

A

The formation of a thrombus in a deep vein, usually in the legs, which partially or completely obstructs blood flow.

121
Q

What is the most serious complication of DVT?

A

Pulmonary embolism.

122
Q

What scoring system can be used to assess an individual’s risk of DVT?

A

Well’s score.

123
Q

What presenting features are included in Well’s score for the assessment of DVT?

A

Localised tenderness along distribution of the venous system.
Entire leg swollen.
Calf swelling ≥ 3 cm larger than the asymptomatic side.
Pitting oedema confined to the asymptomatic leg.
Collateral superficial veins.

124
Q

Other than presenting features, what factors are included in Well’s score for the assessment of DVT?

A

Active cancer.
Paralysis, paresis or recent immobilisation of leg.
Recently bedridden for ≥ 3 days or major surgery within the prev. 12 weeks.
Previous DVT.

125
Q

How is Well’s score interpreted?

A

Score < 2 = DVT unlikely.

Score ≥ 2 = DVT likely and requires further investigation.

126
Q

What is the next step in management if Well’s score indicates DVT is unlikely?

A

Perform D-dimer within four hours.

127
Q

What is the next step in management if Well’s score indicates DVT is unlikely and subsequent D-dimer is negative?

A

DVT is unlikely and an alternative diagnosis should be considered.

128
Q

What is the next step in management if Well’s score indicates DVT is unlikely and subsequent D-dimer is positive?

A

Offer a proximal leg vein ultrasound within four hours.

129
Q

What is the next step in management if Well’s score indicates DVT is likely?

A

Proximal leg vein ultrasound within four hours.

130
Q

What is the next step in management of DVT if proximal leg vein ultrasound is positive?

A

Diagnosis confirmed - commence treatment.

131
Q

What is the treatment for DVT?

A

Anticoagulant therapy (rivaroxaban or apixaban).

132
Q

What is the treatment for DVT if DOACs are contraindicated?

A

Low molecular weight heparin.

133
Q

How should suspected DVT be managed if proximal leg vein ultrasound cannot be obtained within the required four hours?

A

Interim therapeutic anticoagulation should be given.

134
Q

The length of anticoagulant therapy following DVT depends on what?

A

Whether the DVT was provoked or unprovoked.

135
Q

How long should anticoagulant therapy last following an unprovoked DVT?

A

Six months.

136
Q

How long should anticoagulant therapy last following a provoked DVT?

A

Three months.

137
Q

What disease(s) should be considered in patients following unprovoked DVT?

A

Undiagnosed active cancer.

Thrombophilia (antiphospholipid syndrome or a hereditary cause).

138
Q

What is the most common cause of anaemia worldwide?

A

Iron deficiency anaemia.

139
Q

Why does iron deficiency cause anaemia?

A

Iron is required to produce haemoglobin in red blood cells.

140
Q

Give four causes of iron deficiency anaemia.

A 
Excessive bleeding (menorrhagia, gastrointestinal bleeding).
Inadequate dietary intake (vegans, vegetarians).
Poor intestinal absorption (coeliac disease).
Increased iron requirements (children, pregnant women).
141
Q

What does a blood film show in patients with iron deficiency anaemia?

A

Hypochromic, microcytic anaemia.

142
Q

What do investigations of ferritin, TIBC and transferrin levels show in iron deficiency anaemia?

A

Low serum ferritin.
Raised TIBC.
Raised transferrin.

143
Q

How does iron deficiency anaemia present?

A

Fatigue, shortness of breath on exertion, palpitations, pallor, koilonychia, hair loss, atrophic glossitis.

144
Q

What is the management of iron deficiency anaemia?

A

Give oral ferrous sulphate.

145
Q

How long should oral ferrous sulphate be given for the treatment of iron deficiency anaemia?

A

At least three months after the iron deficiency has been corrected.

146
Q

What are side effects of oral ferrous sulphate?

A

Nausea, abdominal pain, constipation and diarrhoea.

147
Q

What is vitamin B12 used for in the body?

A

Red blood cell development and myelination of neurones.

148
Q

Where is vitamin B12 absorbed?

A

The terminal ileum.

149
Q

Vitamin B12 is absorbed in the terminal ileum after binding to which protein?

A

Intrinsic factor.

150
Q

Intrinsic factor is secreted by which cells?

A

Parietal cells.

151
Q

Vitamin B12 is found in what foods?

A

Animal-sourced foods such as meat, fish, milk and eggs.

152
Q

What are causes of vitamin B12 deficiency anaemia?

A

Pernicious anaemia, post-gastrectomy, vegan or poor diet, disorders of the terminal ileum

153
Q

What does a blood film show in patients with vitamin B12 deficiency anaemia?

A

Macrocytic anaemia.

154
Q

What does a blood film show in patients with vitamin B12 deficiency anaemia?

A

Macrocytic, megaloblastic anaemia.

155
Q

How is vitamin B12 deficiency anaemia treated?

A

1mg intramuscular hydroxocobalamin three times per week for two weeks… then once every three months for life.

156
Q

What is the most common cause of vitamin B12 deficiency anaemia?

A

Pernicious anaemia.

157
Q

What is pernicious anaemia?

A

An autoimmune condition that attacks parietal cells.

158
Q

What test may be used in the investigation of pernicious anaemia?

A

Anti-intrinsic factor antibodies (highly specific but 50% sensitive).

159
Q

What test may be used in the investigation of pernicious anaemia?

A

Anti-intrinsic factor antibodies (highly specific but 50% sensitive).

160
Q

What is folate (vitamin B9) used for in the body?

A

The synthesis of DNA and RNA.

161
Q

Folate is found in what foods?

A

Brocolli, brussel sprouts and leafy green vegetables.

162
Q

What does a blood film show in patients with folate deficiency anaemia?

A

Macrocytic, megaloblastic anaemia.

163
Q

Give four causes of folate deficiency.

A

Phenytoin use (treating tonic-clonic seizures).
Methotrexate use.
Pregnancy.
Alcohol excess.

164
Q

In patients with vit B12 deficiency and folate deficiency, which condition should be treated first?

A

Vitamin B12 deficiency.

165
Q

Why should vit B12 deficiency be treated before folate deficiency?

A

To prevent subacute combined degeneration of the spinal cord.

166
Q

There is an increased risk of which cancer in patients with pernicious anaemia?

A

Gastric cancer.

167
Q

Give three mechanisms by which chronic disease causes anaemia.

A

Reduced iron release from bone marrow.
Inadequate secretion of EPO for erythropoiesis.
Reduced red cell survival.

168
Q

What do investigations of iron, TIBC and ferritin levels show in anaemia of chronic disease?

A

Low iron, low TIBC and raised ferritin.

169
Q

On investigation, what is the differentiating factor between iron deficiency anaemia and anaemia of chronic disease?

A

Ferritin is raised in anaemia of chronic disease.

170
Q

Why is ferritin raised in anaemia of chronic disease?

A

Ferritin is an acute phase reactant and is raised in states of chronic inflammation.

171
Q

What is leukaemia?

A

A group of blood cancers that usually begin in the bone marrow.

172
Q

What are the four main types of leukaemia?

A

Acute lymphoblastic leukaemia.
Acute myeloid leukaemia.
Chronic lymphocytic leukaemia.
Chronic myeloid leukaemia.

173
Q

How does leukaemia generally present?

A

Fatigue, bruising, fever and infection with a feeling of general unwellness.

174
Q

What is acute lymphoblastic leukaemia?

A

A malignancy of lymphoid cells, affecting B- or T-lymphocyte cell lineages, arresting maturation and promoting uncontrolled proliferation of immature blast cells, with marrow failure and tissue infiltration.

175
Q

Is acute lymphoblastic leukaemia more common in children or adults?

A

ALL is the most common cancer in childhood and is rare in adults.

176
Q

Give two associations that may predispose to acute lymphoblastic leukaemia.

A

Down’s syndrome.

Foetal exposure to ionising radiation during pregnancy.

177
Q

In acute lymphoblastic leukaemia: presentation develops secondary to what two processes?

A

Bone marrow failure and tissue infiltration.

178
Q

In acute lymphoblastic leukaemia: what presentation occurs secondary to bone marrow failure?

A

Fatigue (anaemia), fever (infection), bleeding and bruising (thrombocytopenia).

179
Q

In acute lymphoblastic leukaemia: what presentation occurs secondary to tissue infiltration?

A

Hepatosplenomegaly, lymphadenopathy, orchidomegaly and CNS involvement (cranial nerve palsies, meningism).

180
Q

In acute lymphoblast leukaemia: what are six common infections?

A

Bacterial septicaemia, zoster, cytomegalovirus, measles, candidiasis, Pneumocystitis pneumonia.

181
Q

In acute lymphoblastic leukaemia: what investigations are performed?

A

FBC, blood film and bone marrow biopsy, imaging (CXR, CT scan).

182
Q

In acute lymphoblastic leukaemia: how would you provide supportive care?

A

Blood / platelet transfusions.
Intravenous fluids.
Allopurinol (to prevent tumour lysis syndrome),.

183
Q

In acute lymphoblastic leukaemia: what is the mainstay of treatment?

A

Chemotherapy.

184
Q

What is acute myeloid leukaemia?

A

A neoplastic proliferation of blast cells derived from marrow myeloid elements.

185
Q

What is the prognosis of acute myeloid leukaemia?

A

AML progresses rapidly and without treatment typically causes death within two months of onset.

186
Q

What is the most common acute leukaemia of adults?

A

Acute myeloid leukaemia.

187
Q

In acute myeloid leukaemia: presentation develops secondary to what two processes?

A

Bone marrow failure.

Tissue infiltration.

188
Q

In acute myeloid leukaemia: what presentation occurs secondary to bone marrow failure?

A

Fatigue (anaemia), fever (infection), bleeding and bruising (thrombocytopenia).

189
Q

Acute promyelocytic leukaemia (a subtype of AML) can result in what complication?

A

Disseminated intravascular coagulation.

190
Q

In acute myeloid leukaemia: what presentation occurs secondary to tissue infiltration?

A

Hepato-/splenomegaly, gum hypertrophy, skin involvement (purple deposits).

191
Q

In acute myeloid leukaemia: what investigations are performed?

A

Blood testing (FBC), bone marrow biopsy.

192
Q

In acute lymphoblastic leukaemia: what is the finding on blood film?

A

Characteristic blast cells.

193
Q

In acute myeloid leukaemia: what is the finding on bone marrow biopsy?

A

Myeloblasts present in > 20% of bone marrow.

Auer rods on biopsy.

194
Q

What is the normal myeloblast count in healthy bone marrow?

A

< 5%.

195
Q

How is acute lymphoblastic leukaemia differentiated from acute myeloid leukaemia on bone marrow biopsy?

A

The presence of Auer rods on biopsy of AML.

196
Q

In acute myeloid leukaemia: how would you provide supportive care?

A

Blood/platelet transfusions.
Intravenous fluids.
Allopurinol (to prevent tumour lysis syndrome).

197
Q

In acute myeloid leukaemia: what is the mainstay of treatment?

A

Intensive chemotherapy.

198
Q

What is a treatment option for individuals with acute myeloid leukaemia if chemotherapy fails or they have relapses?

A

Bone marrow transplant.

199
Q

What is a complication of bone marrow transplant for patients with acute myeloid leukaemia?

A

Graft-versus-host disease (GvHD).

200
Q

What is a graft-versus-host disease (following bone marrow transplant)?

A

New marrow attacks the patient’s body. The donor’s immune system white blood cells reject the recipient.

201
Q

How is graft-versus-host disease managed following bone marrow transplant?

A

Ciclosporin and methotrexate can be given to reduce the effect.

202
Q

What is chronic lymphocytic leukaemia?

A

CLL is characterised by a progressive accumulation of a malignant clone of functionally competent B-cells which effectively crowd out healthy blood cells.

203
Q

What is the most common leukaemia in those aged > 60 years?

A

Chronic lymphocytic leukaemia.

204
Q

Does chronic lymphocytic leukaemia develop slowly or quickly?

A

CLL develops slowly over several years.

205
Q

How does chronic lymphocytic leukaemia present in the early stages of disease?

A

CLL is typically asymptomatic in the early stages of the disease and may be an incidental finding on routine blood testing.

206
Q

How does chronic lymphocytic leukaemia present in later stages of the disease?

A

Later presentation may include non-painful lymph node swelling, hepatosplenomegaly, fatigue, fever, night sweats and/or weight loss.

207
Q

In chronic lymphocytic leukaemia: what is the finding on FBC?

A

Raised lymphocytes.

208
Q

In chronic lymphocytic leukaemia: what is the finding on blood film?

A

Smudge cells.

209
Q

How is chronic lymphocytic leukaemia managed if the patient is asymptomatic?

A

Watch and wait, monitoring FBC every three months.

210
Q

In chronic lymphocytic leukaemia: what is the first-line therapy for symptomatic individuals?

A

Fludarabine.
Rituximab.
Cyclophosphamide.

211
Q

What is the prognosis for individuals with chronic lymphocytic leukaemia?

A

1/3 never progress.
1/3 progress slowly.
1/3 progress actively.

212
Q

Give two complications of chronic lymphocytic leukaemia.

A

Warm autoimmune haemolytic anaemia.

Richter’s transformation.

213
Q

Describe the pathophysiology of warm autoimmune haemolytic anaemia (complication of CLL)?

A

IgG antibodies attach to red blood cells, which are transformed into spherocytes.

214
Q

What test is positive in patients with warm autoimmune haemolytic anaemia?

A

Coombs’ test.

215
Q

Describe the pathophysiology of Richter’s transformation (complication of CLL)?

A

Leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma.

216
Q

What is chronic myeloid leukaemia?

A

CML is characterised by an uncontrolled clonal proliferation of myeloid cells.

217
Q

In what age group does chronic myeloid leukaemia most commonly occur?

A

40-60 years.

218
Q

Chronic myeloid leukaemia is strongly associated with what genetic abnormality?

A

Philadelphia chromosome - present in over 80% of individuals with CML.

219
Q

How does chronic myeloid leukaemia present?

A

Presentation of CML includes weight loss, tiredness, fever and sweats. There may be features of gout, bleeding and abdominal discomfort.

220
Q

In chronic myeloid leukaemia: why may patients experience gout?

A

Increased cell turnover leads to excess purines… which are broken down to uric acid which accumulates and causes gout.

221
Q

In chronic myeloid leukaemia: what is found on FBC?

A

Raised WCC (raised neutrophils, monocytes, basophils, eosinophils).

222
Q

In chronic myeloid leukaemia: what is found on blood film?

A

All stages of granulocyte maturation.

223
Q

In chronic myeloid leukaemia: what is the management?

A

Intravenous fluids and allopurinol.
Imatinib.
Chemotherapy (in patients with lymphoblastic transformation).

224
Q

What is disseminated intravascular coagulation?

A

DIC is an inappropriate activation of the clotting cascade that results in an increased risk of bleeding.

225
Q

Describe the pathophysiology of disseminated intravascular coagulation?

A

Release of procoagulants into the circulation causes widespread activation of coagulation, consuming clotting factors and platelets.

226
Q

How does disseminated intravascular coagulation present?

A

Presentation may vary from no bleeding to severe epistaxis and gingival bleeds. Other features include bruising, petechiae, haematuria, fever, confusion and coma.

227
Q

In disseminated intravascular coagulation: what does a clotting screen show?

A

Reduced platelets.
Prolonged prothrombin time (PT).
Prolonged activated partial thromboplastin time (aPTT).
Fibrinogen reduced.

228
Q

In disseminated intravascular coagulation: what does a D-dimer show?

A

Markedly raised.

229
Q

In disseminated intravascular coagulation: what does a blood film show?

A

Schistocytes (broken RBCs).

230
Q

What is the presentation of autoimmune haemolytic anaemia?

A

Fatigue and shortness of breath.

231
Q

What tests are performed in autoimmune haemolytic anaemia (AIHA)?

A

Haemoglobin, lactate dehydrogenase, bilirubin and haptoglobin.

232
Q

What are the results of haemoglobin level in AIHA?

A

Anaemia.

233
Q

What are the results of bilirubin and haptoglobin level in AIHA?

A

Raised bilirubin and low haptoglobin.

234
Q

What is G6PD deficiency?

A

Inborn error of metabolism that predisposes to red blood cell breakdown (haemolytic anaemia).

235
Q

What is the inheritance pattern of G6PD deficiency?

A

X-linked recessive.

236
Q

What is the presentation of G6PD deficiency?

A

Jaundice, pallor, dark urine, shortness of breath and fatigue.

237
Q

G6PD deficiency presentation typically follows which triggers?

A

Infection, medication (ciprofloxacin) and stress.

238
Q

What investigations are performed in an individual suspected of having G6PD deficiency?

A

Full blood count and blood film.

239
Q

What does FBC reveal in an individual with G6PD deficiency?

A

Anaemia.

240
Q

What does blood film reveal in an individual with G6PD deficiency?

A

Heinz bodies and bite cells.

241
Q

In G6PD deficiency: how are bite cells formed?

A

Macrophage removal of Heinz body.

242
Q

How is G6PD deficiency managed?

A

Avoid triggers. Treat infection // stop offending medications.

243
Q

What is the most common hereditary haemolytic anaemia in people of Northern European descent?

A

Hereditary spherocytosis.

244
Q

What is the inheritance pattern of hereditary spherocytosis?

A

Autosomal dominant.

245
Q

What is the presentation of hereditary spherocytosis?

A

Failure to thrive (children), jaundice, gallstones, splenomegaly.

246
Q

What investigations are performed in an individual suspected of hereditary spherocytosis?

A

Reticulocyte count, blood film.

247
Q

What does reticulocyte count reveal in an individual with hereditary spherocytosis?

A

Raised reticulocytes.

248
Q

What does blood film reveal in an individual with hereditary spherocytosis?

A

Spherocytes on blood film.

249
Q

Post-thrombotic syndrome is a potential complication following what?

A

DVT.

250
Q

Describe the pathophysiology of post-thrombotic syndrome.

A

Venous outflow obstruction and venous insufficiency result in chronic venous hypertension.

251
Q

What are the features of post-thrombotic syndrome?

A

Heavy, painful calves, pruritus, swelling, varicose veins and venous ulceration.

252
Q

What is the management of post-thrombotic syndrome?

A

Graduated compression stockings and leg elevation.

Finals (11 decks)

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