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Phase 2A > Haematology > Flashcards

Haematology Flashcards

1
Q

What causes increased reticulocytes on an FBC?

A

Bleeding, haemolysis

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2
Q

What causes neutrophils to be raised?

A

Acute inflammatory process e.g. infection, acute illness, steroid therapy, myeloid cancer

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3
Q

What type of infection raises eosinophils?

A

A parasitic infection

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4
Q

What are platelets derived from?

A

Megakaryocytes

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5
Q

What leukaemia typically affects children?

A

Acute lymphoblastic leukaemia

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6
Q

What investigations would you do for ?leukaemia?

A

FBC, blood film, U&Es, LFTs, clotting and a bone marrow biopsy

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7
Q

What are the basics of the treatment of acute leukaemia?

A

Induction - aims to remove 99% of leukaemic cells
Consolidation- lower intensity therapy
Maintenance
CNS prophylaxis - intrathecal

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8
Q

What chromosomal abnormality do CML patients tend to have?

A

The philadelphia chromosome

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9
Q

How is CML treated?

A

Imatinib

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10
Q

What is the most common leukaemia?

A

Chronic lymphocytic leukaemia

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11
Q

What makes a Hodgkin’s lymphoma different from non-Hodgkin’s lymphoma?

A

Reed-Steinberg cells

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12
Q

What is the common age range for Hodgkin’s lymphoma?

A

20-40

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13
Q

What system is used to class Hodgkin’s lymphoma?

A

Ann Arbor system

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14
Q

What is multiple myeloma?

A

A malignant proliferation of plasma cells

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15
Q

What are the emergencies in haematology?

A 
Spinal cord compression
SVC obstruction
Neutropenic sepsis
Tumour lysis syndrome
Hypercalcaemia
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16
Q

What are the general signs and symptoms of anaemia?

A

Lethargy, SOB, reduced exercise tolerance, headache, pallor of the palmar creases and conjunctiva
Severe: angina, tachycardia

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17
Q

What are the different causes of anaemia?

A

Decreased RBC production
Increased RBC destruction
Increased RBC loss

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18
Q

What anaemias are microcytic?

A

Iron deficiency
Thalassaemia
Haemaglobinopathies
(Sideroblastic anaemia)

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19
Q

What anaemias are normocytic?

A 
Acute blood loss
Haemolysis
Renal failure
Chronic disease
Cancer
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20
Q

What anaemias are macrocytic?

A 
B12 deficiency
Folate deficiency
Alcohol excess
Liver/thyroid disease
Anti-folate medication (anti-epileptics, trimethoprim and methotrexate)
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21
Q

What are the specific signs of iron deficiency anaemia?

A

Kolionychia
Glossitis
Angular stomitis (sores in the corners of the mouth)

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22
Q

What investigations would you do for anaemia?

A

FBCs, blood film

Investigate for underlying cause e.g. malignancy

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23
Q

What is the management for iron-deficiency anaemia?

A

Treat underlying condition
Iron replacement
Transfuse if very flow
Prescribe laxatives as iron salts constipate patients

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24
Q

What types of crises occur is sickle cell anaemia?

A

Haemolytic, occlusive, aplastic and sequestration

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25
Q

How do you investigate sickle cell anaemia?

A

FBC, blood film, Hb electrophoresis, G&S

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26
Q

What is the management for sickle cell anaemia?

A

Supportive e.g. aggressive analgesia, treat underlying cause, folic acid, transfuse with falling Hb
Chronic e.g. hydroxycarbamide

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27
Q

What are the causes of B12 deficiency?

A

Pernicious anaemia, malabsorption (e.g. in Crohn’s), dietary

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28
Q

What is pernicious anaemia?

A

An autoimmune condition where antibodies are produced against parietal cells, associated with other autoimmune conditions e.g. Addison’s.
Parietal cells produce intrinsic factor which is necessary for B12 absorption.

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29
Q

What are the causes of folate deficiency?

A

Dietary, malabsorption, increased requirements (e.g. pregnancy), folate antagonists

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30
Q

Where is folate absorbed?

A

Duodenum/upper small anaemia

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31
Q

What are the congenital causes of haemolytic anaemia?

A

Hereditary spherocytosis/elliptocytosis, thalassaemia, sickle cell anaemia, G6P deficiency

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32
Q

What are the symptoms of haemolytic anaemia?

A

Lethargy, SOB, reduced exercise tolerance, headache, pallor of the palmar creases and conjunctiva, jaundice, splenomegaly

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33
Q

What is prothrombin time a marker for?

A

The extrinsic pathway

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34
Q

What is the activated Prothrombin time a marker for?

A

The intrinsic pathway

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35
Q

What is the mechanism of action of warfarin?

A

It is antagonises vitamin K dependant clotting factors e.g. 2, 7, 9, 10

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36
Q

How does heparin work?

A

It inactivates factor Xa

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37
Q

What are the causes of DIC?

A

Sepsis, haematological cancers, eclampsia, anaphylaxis, severe trauma/burns, severe liver disease

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38
Q

What is DIC?

A

A pathological activation of the coagulation cascade. There is formation of microvascular thrombi and multi-organ failure.

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39
Q

What causes thrombophilia?

A

Primary: Factor V Leiden, Protein C deficiency, protein S deficiency, anti-thombin III deficiency
Secondary: Virchow’s triad

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40
Q

What are the risk factors for DVT?

A

Increased age, pregnancy, malignancy, trauma, past DVT, smoking, immobility, infection, thrombophilia, HRT

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41
Q

What are the symptoms of a DVT?

A

Pain/ache, unilateral swelling, calf warmth, pitting oedema below the DVT, erythema, Homan’s sign (pain on foot dorsiflexion)

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42
Q

What is the Well’s score?

A

The diagnostic score for a DVT

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43
Q

What investigations would you do for a DVT?

A

D-dimer, USS doppler, CTPA with a PE

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44
Q

What is the management of a DVT?

A

Anticoagulate with treatment dose dalteparin or LMWH
Warfarin/NOAC
Exclude underlying cause - IVC filters may be used

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45
Q

What is the cause of iron deficiency anaemia?

A

Excessive blood loss e.g. from the GI tract or menorrhagia, dietary inadequacy e.g. in children, failure of iron absorption e.g. coeliac disease or excessive requirements for iron e.g. pregnancy

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46
Q

What is the pathophysiology behind iron deficiency anaemia?

A

Iron is required for haemoglobin synthesis therefore inadequate iron means haemoglobin can’t be synthesised properly and the patient becomes anaemic

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47
Q

What are the symptoms of iron deficiency anaemia?

A

Fatigue, shortness of breath on exertion, palpitations, brittle hair, headache, tinnitus, angina (if there’s pre-existing coronary heart disease)

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48
Q

What are the signs of iron deficiency anaemia?

A

Spoon shaped nails (koilonychia)

Angular stomatitis, brittle nails, pallor

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49
Q

What tests are used to diagnose iron deficiency anaemia?

A

FBC - decreased Hb, decreased MCV, decreased MCH (mean corpuscular Hb)
Serum iron (low)
Total iron binding capacity (high)
Serum ferritin (low)
Serum soluble transferrin receptors (high)
OGD in all males and post menopausal females to look for GI causes of bleeding

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50
Q

What is the treatment for iron deficiency anaemia?

A

Find and treat the underlying cause

Give iron supplements to treat the anaemia and replace stores - oral iron is usually sufficient

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51
Q

What type of anaemia is iron deficiency anaemia?

A

Microcytic

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52
Q

What is the aetiology of vitamin B12-deficiency anaemia?

A

Impaired absorption of vitamin B12 e.g. gastrectomy, ileal resection
Inadequate intake e.g. vegan diet
Drugs e.g. colchicine

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53
Q

What is the pathophysiology of pernicious anaemia?

A

Absorption of vitamin B12 occurs in the terminal ileum and needs intrinsic factor (produced in the stomach). Pernicious anaemia is an autoimmune process causing gastritis which leads to atrophy of all layers of the body and fundus of the stomach leading to a lack of intrinsic factor

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54
Q

What is the peak age at diagnosis for pernicious anaemia?

A

60

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55
Q

What are the symptoms of pernicious anaemia?

A

Fatigue, lethargy, dyspnoea, faintness, palpitations, headache, paraesthesia, numbness, visual disturbances

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56
Q

What are the signs of pernicious anaemia?

A

Pallor, lemon tinge to the skin, glossitis, oral ulceration, angular stomatitis, reflex loss, mild to moderate ataxia

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57
Q

What tests are used to diagnose pernicious anaemia?

A 
FBC - increased MCV
Blood film - hypersegmented neutrophils
Serum vitamin B12 - low
Plasma total homocysteine - high
Serum folate
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58
Q

What is the treatment for pernicious anaemia?

A

Find the underlying cause of low vitamin B12
IM hydroxocobalamin 1mg for 3 times a week for 2 weeks then 1 mg every 3 months
Refer to gastro if the patient has malabsorption or GI symptoms

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59
Q

What type of anaemia is pernicious anaemia?

A

Macrocytic

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60
Q

What is the aetiology of folate deficiency?

A

Dietary deficiency e.g. malabsorption, alcohol excess
Excessive requirements e.g. pregnancy, malignancy, inflammation
Excessive excretion
Drugs e.g. methotrexate

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61
Q

What is the pathophysiology of folate deficiency?

A

Folate is involved in adenosine, guanine and thymidine synthesis so it’s required for DNA synthesis. Reduced DNA synthesis results in anaemia

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62
Q

What are the symptoms of folate deficiency?

A

Fatigue, lethargy, dyspnoea, faintness, palpitations, headache, leg cramps

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63
Q

What are the signs of folate deficiency?

A

Pallor, glossitis, angular stomatitis, tachycardia, systolic flow murmur, pale mucus membranes and palmar creases

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64
Q

What tests are used to diagnose folate deficiency?

A

FBC - increased MCV, low Hb
Serum folate - low
RBC folate level - low (more specific than serum folate level)

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65
Q

What is the treatment for folate deficiency?

A

Folic acid 5mg OD
Don’t give alone in megaloblastic anaemia of unknown cause as it makes neuropathy of B12 deficiency worse
Treat the underlying cause

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66
Q

What type of anaemia does folate deficiency cause?

A

Macrocytic

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67
Q

What causes anaemia of chronic disease?

A

Chronic infection e.g. TB
Chronic inflammation e.g. Crohn’s disease, RA, SLE, malignancy
CKD

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68
Q

What is the pathophysiology of anaemia of chronic disease?

A

Different causes contribute to anaemia in chronic diseases including diversion of iron, reduced erythropoiesis and reduced response to erythropoeitin

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69
Q

What are the symptoms of anaemia of chronic disease?

A

Fatigue, lethargy, dyspnoea, faintness, palpitations, headache, angina, intermittent claudication

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70
Q

What are the signs of anaemia of chronic disease?

A

Pallor, tachycardia, systolic flow murmur, cardiac failure, pale mucus membranes and palmar creases

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71
Q

What tests are used to diagnose anaemia of chronic disease?

A

FBC - low MCV, low Hb
Serum iron - low
Total iron binding capacity - low
Serum ferritin - high (increases due to the inflammatory process)

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72
Q

What is the treatment for anaemia of chronic disease?

A

Treatment and management of the underlying cause
Iron should only be given to patients with established iron deficiency
Consider erythropoiesis-stimulating agents in RA, HF and cancer

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73
Q

What type of anaemia is anaemia of chronic disease?

A

Microcytic

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74
Q

What is the aetiology of beta-thalassaemia?

A

It is an autosomal recessive condition with defects in transcription, RNA splicing & modification and translation leading to unstable and unusable beta-globin chains.

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75
Q

What is the pathophysiology of beta-thalassaemia?

A

There is little or no normal beta-globin and therefore there is excess alpha-globin. Alpha-globin combines with whatever beta, delta or gamma chains are available are there is an increased production of HbA2 and HbF leading to ineffective erythropoiesis and haemolysis.

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76
Q

Where is beta-thalassaemia prevalent?

A

The mediterranean, middle east and Africa

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77
Q

What are the symptoms of beta-thalassaemia?

A

Asymptomatic - minor/trait
Bone abnormalities and recurrent leg ulcers - intermedia
Chronic infections, failure to thrive - major (homozygous)

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78
Q

What are the signs of beta-thalassaemia?

A

Mild/absent anaemia - minor/trait
Moderate anaemia, splenomegaly and gallstones - intermedia
Severe anaemia, skull bossing, thalassaemia facies, hepatosplenomegaly (presents in the first year of life) - major (homozygous)

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79
Q

What tests are used to diagnose beta-thalassaemia?

A

FBC and blood film - hypochromic and microcytic anaemia, irregular and pale RBCS, increased reticulocytes and nucleated RBCs.
Hb electrophoresis - HbA2 >3.5%

80
Q

What is the treatment for beta-thalassaemia?

A

Blood transfusions - risk of iron overload, give iron chelation (desferroxamine) or ascorbic acid (increases urinary excretion of iron)
Long term folic acid supplements
Promote fitness and a healthy diet

81
Q

What type of anaemia is beta-thalassaemia?

A

Microcytic anaemia

82
Q

What is the aetiology of sickle cell anaemia?

A

It is an autosomal recessive genetic disorder in the alpha globin gene

83
Q

What is the pathophysiology involved in sickle cell anaemia?

A

Substitution of valine for glutamic acid causes a conformational change producing HbS not HbA. Cells become rigid, sickle shaped and dehydrated leading to haemolysis (premature) and obstruction of the microcirculation leading to tissue infarction.

84
Q

What is sickling precipitated by?

A

Hypoxia, infection, dehydration and cold

85
Q

What are the symptoms of sickle cell anaemia?

A

Crisis: acute pain in the hands and feet in children, bone pain (ribs, spine and pelvis) in adults
Acute chest syndrome: chest pain, dyspnoea

86
Q

What are the signs of sickle cell anaemia?

A

Crisis: fever (+pain)
Acute chest syndrome: hypoxia and new CXR changes (consolidation) caused by infection, fat emboli and pulmonary infarction

87
Q

What tests are used to diagnose sickle cell anaemia?

A

FBC - low Hb, high reticulocytes
Blood film - sickled erythrocytes
Hb electrophoresis - HbS present

88
Q

What is the treatment for sickle cell anaemia?

A

Prophylactic antibiotics (daily penicillin) due to hyposplenism
Pneumococcal and influenza vaccine
Folic acid
Pain relief for crisis
Hydroxyurea to increase the concentration of HbF

89
Q

What are the complications of sickle cell anaemia?

A

Stunted growth, infections, leg ulcers, cholelithiasis, cardiac problems, avascular necrosis, spinal cord compression, CKD and pulmonary hypertension

90
Q

What causes haemolytic anaemias?

A

Genetic - G6PD deficiency, hereditary spherocytosis

Acquired - immune e.g. blood transfusion reaction or autoimmune e.g. SLE, CLL, DIC

91
Q

What is the pathophysiology involved in haemolytic anaemias?

A

There may be intravascular haemolysis due to complement fixation or trauma (e.g. heart valve) or it may be extravascular where RBCs are removed from the circulation

92
Q

What is the epidemiology of haemolytic anaemias?

A

Autoimmune: more common in females

93
Q

What are the symptoms of haemolytic anaemias?

A

Fatigue, lethargy, dyspnoea, faintness, palpitations, headache, dizziness, intermittent claudication

94
Q

What are the signs of haemolytic anaemias?

A

Pallor, tachycardia, systolic flow murmur, cardiac failure, pale mucus membranes and palmar creases, jaundice, gallstones, hepatosplenomegaly

95
Q

What tests are used to diagnose haemolytic anaemias?

A 
FBC - normal MCV and MCH, normal platelet count
Coombs test 
USS of spleen to asses size
CXR
ECG
96
Q

What is the treatment for haemolytic anaemias?

A

Give folic acid as active haemolysis can cause deficiency
Identify and treat the cause of haemolysis
Corticosteroids for autoimmune haemolytic anaemia
Splenectomy for hereditary spherocytosis

97
Q

What type of anaemia is sickle cell anaemia?

A

Microcytic

98
Q

What type of anaemia is haemolytic anaemia?

A

Normocytic

99
Q

What are some causes of aplastic anaemia?

A

Congenital e.g. Fanconi anaemia or Diamond-Blackfan syndrome

Acquired e.g. EBV, HIV, parvovirus, irradiation, pregnancy, drugs e.g. phenytoin

100
Q

What is the pathophysiology involved in aplastic anaemia?

A

Pancytopenia with hypocellularity (aplasia) of the bone marrow. The bone marrow is replaced with fat

101
Q

What are the symptoms of aplastic anaemia?

A

Fatigue, lethargy, dyspnoea, faintness, palpitations, headache, dizziness, skin or mucosal haemorrhages, visual disturbances, petechial rashes

102
Q

What are the signs of aplastic anaemia?

A

Pallor, bruising, bleeding gums, tachycardia, epistaxis, systolic flow murmur

103
Q

What tests are used to diagnose aplastic anaemia?

A

FBC - normal MCV, pancytopenia, reticulocyte count low or absent, blood film, bone marrow biopsy (hypocellular)

104
Q

What is the treatment of aplastic anaemia?

A

Withdrawal of offending agent and supportive care
Blood and platelet transfusions
Prophylactic antibiotics or prompt treatment of infections
If <40 then a bone marrow transplant is curative
If >40 then immunosuppression with anti-thymocyte globulin and ciclosporin

105
Q

What is the aetiology of polycythaemia?

A

Primary - polycythaemia vera, mutations in Epo receptor

Secondary - high altitude, lung disease, dehydration, burns, RCC, Wilms’ tumour

106
Q

What is the pathophysiology of polycythaemia?

A

There is an increase in Hb, PCV and red cell count. It can be divided into absolute erythrocytosis (true increase in red cell volume) or relative erythrocytosis (red cell volume is normal but plasma volume is low)

107
Q

What are the symptoms of polycythaemia?

A

Polycythaemia vera - tiredness, depression, vertigo, tinnitus and visual disturbances, itching, hyperviscosity symptoms e.g. headache

108
Q

What are the signs of polycythaemia?

A

Thrombosis, splenomegaly, HTN, stroke/CVA, MI, PE, DVT

109
Q

What tests are used to diagnose polycythaemia?

A

FBC - primary: high Hb, PCV, WCC and platelets; secondary: increased RBCs
Bone marrow aspirate - tends to be hypercellular

110
Q

What is the treatment of polycythaemia?

A

Aspirin, venesection, bone marrow suppression with hydroxycarbamide

111
Q

What is the aetiology of myeloma?

A

Monoclonal gammopathy of undetermined significant (MGUS) increases the risk of developing myeloma, obesity is also a risk

112
Q

What is the pathophysiology of myeloma?

A

Clonal expansion of abnormal, proliferating plasma cells producing monoclonal paraprotein, malignant cells accumulate in the bone marrow leading to bone marrow failure.

113
Q

Who does myeloma affect predominantly?

A

Elderly males

114
Q

What are the symptoms of myeloma?

A

Bone pain, particularly backache, lethargy, anorexia, bleeding and/or bruising, recurrent bacterial infections, symptoms of hypercalcaemia e.g. thirst

115
Q

What are the signs of myeloma?

A

Hypercalcaemia, renal injury, anaemia, bone lesions, UMN muscle weakness, sensory level sensation loss, urinary incontinence - spinal cord compression

116
Q

What tests are used to diagnose myeloma?

A

FBC - low Hb, neutrophils and platelets
U&Es - high creatinine
Serum calcium - high
Urine electrophoresis - Bence Jones protein
Skeletal survey - pepper pot skull
Bone marrow aspirate - increased BM plasma cells

117
Q

What is the treatment for myeloma?

A

Anaemia - give transfusions and Epo
Infection prophylaxis - pneumococcal/influenza
Bone pain - radiotherapy and systemic chemotherapy or high dose dexamethasone, bisphosphonates
Kidney - dialysis
Stem cell transplant
Combination chemotherapy - steroid & melphalan & thalidomide

118
Q

What are some risks for developing Hodgkin’s lymphoma?

A

EBV, having had mononucleosis, HIV, immunosuppression, smoking

119
Q

What is the pathophysiology of Hodgkin’s lymphoma?

A

It is a malignant tumour of the lymphatic system characterised by Reed-Steinberg cells (multinucleated giant cells)

120
Q

What is the epidemiology of Hodgkin’s lymphoma?

A

Young patients: males > females

121
Q

What are the symptoms of Hodgkin’s lymphoma?

A

Enlarged but otherwise asymptomatic lymph node, typically in the lower neck/supraclavicular region
Night sweats, unexplained fever, weight loss, cough, dyspnoea

122
Q

What are the signs of Hodgkin’s lymphoma?

A

Lymphadenopathy, hepatomegaly, splenomegaly, SVC syndrome

123
Q

What tests are used to diagnose Hodgkin’s lymphoma?

A

FBC, U&E, ESR, LFTs, HIV (used to exclude DDx)
Lymph node biopsy - excisional is better than fine needle/core needle
CT scans for staging
CXR
Bone marrow aspiration
Ann Arbor Staging

124
Q

What is the treatment for Hodgkin’s lymphoma?

A

ABVD combination chemotherapy
Involved field radiotherapy
BEACOPP

125
Q

What are some problems associated with chemotherapy?

A

Infertility, lung damage, peripheral neuropathy, cardiomyopathy

126
Q

What are some risk factors associated with Non-Hodgkin’s lymphoma?

A

Chromosomal translocations, EBV, HTLV-1, Hepatitis C, environmental factors e.g. pesticides, autoimmune disorders

127
Q

What is the pathophysiology of Non-Hodgkin’s lymphoma?

A

A heterogenous group of lymphoproliferative malignancies with different patterns of behaviour and responses to treatment, can be low or high grade.
80% are of B cell origin

128
Q

What is the epidemiology of Non-Hodgkin’s lymphoma?

A

Adults >50

129
Q

What are the symptoms of Non-Hodgkin’s lymphoma?

A

Painless, peripheral lymphadenopathy, night sweats, fever, weight loss, testicular mass, bleeding, recurrent infections

130
Q

What are the signs of Non-Hodgkin’s lymphoma?

A

Pancytopenia, splenomegaly, hepatomegaly, skin lesions, SVC syndrome and an abdominal mass

131
Q

What tests are used to diagnose Non-Hodgkin’s lymphoma?

A 
FBC - anaemia, thrombocytopenia, neutropenia
U&amp;Es
Serum calcium - high
LFTs 
Serology 
CXR
CT head to pelvis
Lymph node biopsy
132
Q

What is the treatment of Non-Hodgkin’s lymphoma?

A

Depends on the type of lymphoma
Gastric lymphoma - eradicate H. pylori
Aggressive e.g. B cell lymphoma - rituximab and combination chemotherapy

133
Q

What are the risk factors for DVT and VTE?

A

Previous VTE, family history of VTE, having a cancer, age >60, immobilisation, smoking, BMI >30, being male, pregnancy, combined OCP and HRT

134
Q

What is the pathophysiology involved in DVT and VTE?

A

A thrombus occurs when Virchow’s triad is met - hypercoagulability, stasis and endothelial injury

135
Q

What are the symptoms of DVT/VTE?

A

Limb pain and tenderness, skin discolouration (erythema, purple or cyanosed), unilateral swelling of the calf/thigh

136
Q

What are the signs of a DVT/VTE?

A

Pitting oedema, distension of the superficial veins, increase in skin temperature, palpable cord

137
Q

What tests are used to diagnose DVT/VTE?

A

FBC, U&E, CRP (to rule out cellulitis), D-dimer

Imaging: USS of the leg with a colour doppler, CT or MRI venography

138
Q

What is the treatment for DVT/VTE?

A

Low molecular weight heparin or fondaparinux, novel oral anticoagulants e.g. rivaroxaban for 3 months (at least)
IVC filter
Catheter-directed thrombolytic therapy

139
Q

What is the aetiology of AML?

A

Most cases arise without apparent cause but some conditions predispose to it e.g. aplastic anaemia, myelofibrosis, polycythaemia rubra vera

140
Q

What is the pathophysiology of AML?

A

There is clonal expansion of myeloblasts in the bone marrow, blood and other tissues; failure of apoptosis leads to accumulation in various organs.

141
Q

What is the epidemiology of AML?

A

It is the most common leukaemia in adults

142
Q

What are the symptoms of AML?

A

Fatigue (over weeks/months), dizziness, dyspnoea on exertion, bleeding, recurrent infections, bone pain

143
Q

What are the signs of AML?

A

Pallor, gum hypertrophy and bleeding, fever, splenomegaly, hepatomegaly, signs of infection e.g. fever, petechiae

144
Q

What tests are used to diagnose AML?

A

FBC - anaemia, thrombocytopenia, increased WCC, decreased neutrophils
Clotting screen - DIC is common
LFTs and ECG - do before chemotherapy
Bone marrow aspiration - >20% blast cells, immunophenotyping
Blood film - Auer rods

145
Q

What is the treatment for AML?

A

Supportive treatment for infections etc
If <60: intense combination chemotherapy, consolidation and transplant
If >60: palliative chemotherapy

146
Q

What is the aetiology of ALL?

A

Genetic factors e.g. trisomy 21
Environmental factors e.g. high doses of radiation, infection - insulation from common infection in early life leads to abnormal immune responses later in life which increases the risk of ALL

147
Q

What is the pathophysiology of ALL?

A

There is clonal expansion of lymphoblasts, the majority of cases are B cell origin but can also arise from T cell precursors

148
Q

What is the epidemiology of ALL?

A

It is the most common cancer in children

149
Q

What are the symptoms of ALL?

A

Fatigue, dizziness, palpitations, bone and joint pain, dyspnoea, recurrent and severe infections (oral, throat and skin), headaches

150
Q

What are the signs of ALL?

A

Pallor, tachycardia and systolic flow murmur, hepatomegaly, splenomegaly, fever, petechiae, lymphadenopathy, testicular enlargement, gum hypertrophy

151
Q

What tests are used to diagnose ALL?

A

FBC - anaemia, thrombocytopenia, neutropenia, increased WCC
Blood film - increase in blasts
Bone marrow aspirate - lymphoblasts >20%

152
Q

What is the treatment of ALL?

A

Chemotherapy: induction then intense consolidation then maintenance
CNS therapy as patients can have meningeal leukaemia
Stem cell transplant
Allopurinol - prevents tumour lysis syndrome

153
Q

What factors affect the prognosis of ALL?

A

Age of the patient and whether or not they have the Philadelphia chromosome t(9;22)

154
Q

What is the aetiology of CML?

A

Unknown - there are no known hereditary, familial, geographic, ethnic or economic associations.

155
Q

What is the pathophysiology of CML?

A

It is characterised by the Philadelphia chromosome which produces a fusion protein - BCR-ABL which becomes a constitutively active tyrosine kinase. This increases cell division and affects basophils, neutrophils and eosinophils

156
Q

What is the epidemiology of CML?

A

It only affects adults (40-60)

157
Q

What are the symptoms of CML?

A

Fatigue, night sweats, weight loss, abdominal fullness/distension, left upper quadrant pain

158
Q

What are the signs of CML?

A

Splenomegaly, hepatomegaly, enlarged lymph nodes, anaemia, easy bruising, fever, gout

159
Q

What tests are used to diagnose CML?

A

FBC - leukocytosis, anaemia
U&Es, LFTs, blood film
Bone marrow aspirate - percentage of blasts and basophils
Cytogenetics - Philadelphia chromosome

160
Q

What is the treatment for CML?

A

Tyrosine kinase inhibitors e.g. imatinib, nilotinib, dasotinib
Stem cell transplant

161
Q

What are some risk factors for CLL?

A

Trisomies and pneumonia

162
Q

What is the pathophysiology of CLL?

A

There is malignant monoclonal expansion of B lymphocytes with accumulation of abnormal lymphocytes in the blood, bone marrow, spleen, lymph nodes and liver

163
Q

What is the mean age at diagnosis of CLL?

A

72

164
Q

What are the symptoms of CLL?

A

Susceptibility to infection, symmetrically enlarged lymph nodes, abdominal discomfort, bleeding, petechiae, fatigue

165
Q

What are the signs of CLL?

A

Local or generalised lymphadenopathy, splenomegaly, hepatomegaly, petechiae, pallor, skin infiltration, tonsillar enlargement

166
Q

What tests are used to diagnose CLL?

A

FBC - lymphocytosis and anaemia
Blood film - smudge cells
Bone marrow aspirate - lymphocytes
Lymph node biopsy

167
Q

What is the treatment for CLL?

A

Supportive treatment e.g. transfusions, Epo, infection prophylaxis
Watch and wait
Chemotherapy - only for patients with symptomatic disease
Purine analogues
Rituximab (anti-CD20 mAb)
Allogenic stem cell transplant

168
Q

What is the aetiology of immune thrombocytopenic purpura?

A

Primary - after a viral infection

Secondary - associated with malignancies e.g. CLL and infections e.g. HIV, hep C

169
Q

What is the pathophysiology of immune thrombocytopenic purpura?

A

There is immune destruction of platelets. IgG antibodies form to the platelet/megakaryocyte surface, they’re removed by the reticuloendothelial system

170
Q

What are the symptoms of immune thrombocytopenic purpura?

A

Can be asymptomatic to life threatening haemorrhage; petechiae, bruising, nose bleeds

171
Q

What is the epidemiology of immune thrombocytopenic purpura?

A

Mean age of onset is 5.7 years

172
Q

What are the signs of immune thrombocytopenic purpura?

A

Bleeding - GI bleeding and haematuria

173
Q

What tests are used to diagnose immune thrombocytopenic purpura?

A 
Tends to be a diagnosis of exclusion. 
FBC - decreased platelets 
Blood film 
Bone marrow aspirate
Investigations for a cause if it's secondary e.g. serology for HIV and Hep C
174
Q

What is the treatment for immune thrombocytopenic purpura?

A

Treat the cause of ITP

Prednisolone, IV IG, IV anti-D IG (in rhesus +ve children)

175
Q

What are some risk factors for DIC?

A

Sepsis, trauma, surgery, burns, promyelocytic leukaemia, incompatible blood transfusion, dissecting aortic aneurysm

176
Q

What is the pathophysiology of DIC?

A

There is increased/exposed tissue factor on the endothelium which leads to activation of the clotting cascade. All the clotting factors are used up and so there is bleeding too.

177
Q

What are the symptoms of DIC?

A

Spontaneous bleeding at venepuncture sites, bleeding, confusion or disorientation, petechiae

178
Q

What are the signs of DIC?

A

Bleeding from at least 3 unrelated sites, fever, signs of haemorrhage, signs of ARDS, signs of thrombosis, localised infarction or gangrene

179
Q

What tests are used to diagnose DIC?

A

D-dimer
Prothrombin time - increased
Activated partial thromboplastin time - increased
FBC - decreased platelets and fibrinogen

180
Q

What is the treatment for DIC?

A

ABCDE
Treat the cause e.g. sepsis
Supportive treatment e.g. platelets, FFP, cryoprecipitate
Heparin where thrombosis predominates

181
Q

What is a complication of DIC?

A

Organ failure due to infarction

182
Q

What are the risk factors for heparin-induced thrombocytopenia?

A

Prolonged use of heparin for post-operative thromboprophylaxis
Heparin flushes for maintaining line patency

183
Q

What is the pathophysiology of heparin-induced thrombocytopenia?

A

IgG antibodies form against the platelet-heparin complex forming an IgG/platelet/heparin complex leading to platelet activation and thrombosis

184
Q

What are the symptoms of heparin-induced thrombocytopenia?

A

Symptoms of arterial thrombosis e.g. CVA, MI, acute leg ischaemia
Symptoms of venous thrombosis e.g. DVT, PE
Symptoms of a systemic reaction

185
Q

What are the signs of heparin-induced thrombocytopenia?

A

Enlargement or extension of a previously diagnosed blood clot, HTN, dyspnoea, tachycardia, skin necrosis

186
Q

What tests are used to diagnose heparin-induced thrombocytopenia?

A

FBC - sharp decrease in platelets 5-10 days after starting heparin
ELISA for anti-heparin antibodies

187
Q

What is the treatment for heparin-induced thrombocytopenia?

A

Immediately stop the heparin, give alternative anticoagulation, never expose the patient to heparin again

188
Q

What is the cause of malaria?

A

It is caused by infection by species of the genus Plasmodium e.g. Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale and Plasmodium malariae

189
Q

What is the pathophysiology of malaria?

A

Sporozites in mosquitos saliva infect the liver where they mature (or lie dormant), they then rupture and release merozites. The merozites then invade the red blood cells and undergo asexual reproduction

190
Q

What are the risk factors for developing malaria?

A

Lack of access to effective treatment e.g. the poor, young children and infants, pregnant women, the elderly and non-immune people

191
Q

Where is malaria common?

A

The tropics and subtropics

192
Q

What are the symptoms of malaria?

A

Fever (often recurring), chills, rigors, headache, cough, myalgia, GI upset

193
Q

What are the signs of malaria?

A

Fever, splenomegaly, hepatomegaly, jaundice, abdominal tenderness, bleeding, dyspnoea, fits, hypovolaemia, AKI, nephrotic syndrome

194
Q

What tests are used to diagnose malaria?

A

Thick and thin blood smears with Giemsa stain; PCR
FBC - thrombocytopenia, anaemia
LFTs - abnormal
U&Es - hyponatraemia, increased creatinine
Low blood glucose in severe disease
Ill patients: ABGs, CXR, LP, blood cultures, MC&S of the urine and stool, clotting screen

195
Q

What is the treatment of malaria?

A

Non-falciparum: chloroquine or quinine

Falciparum: Quinine sulfate and doxycycline

196
Q

What are some complications of malaria?

A

Cerebral malaria, ARDS, acidosis, DIC, anaemia, splenic rupture, renal impairment

Phase 2A (11 decks)

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