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A TO REVISE - PHASE 3A > PAEDS ONCOLOGY/HAEMATOLOGY TO DO > Flashcards

PAEDS ONCOLOGY/HAEMATOLOGY TO DO Flashcards

1
Q

ALL
What is acute lymphoblastic leukaemia (ALL)?

A
  • Affects precursors to B + T cells
  • It leads to uncontrolled proliferation of immature blast cells affecting both the blood + bone marrow (lymphoid progenitor cells and lymphoblasts)
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2
Q

ALL
What are the broad categories of clinical presentation in ALL?

A
  • General = anorexia, fever, weight loss, night sweats
  • Bone marrow infiltration = pancytopenia
  • Reticuloendothelial infiltration = hepatmospenolmegaly, lymphadenopathy
  • Other organ infiltration (more common at relapse) = headache, testicular enlargement, bone pain
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3
Q

ALL
What are some good prognostic factors in ALL?

A
  • Age 2-10
  • Female
  • WCC <20
  • No CNS disease
  • Caucasian
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4
Q

ALL
What is the management for ALL?

A
  • Blood and platelet transfusion
  • Chemotherapy
  • Steroids
  • Allopurinol to prevent tumour lysis syndrome
  • Intrathecal drugs, e.g. methotrexate
  • Acute control of infections with IV antibiotics
  • Neutropenia makes this high risk
  • Stem cell transplant
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5
Q

HODGKINS LYMPHOMA
What is the clinical presentation of Hodgkin’s lymphoma?

A

Fever and sweating
Enlarged rubbery non-tender nodes
Systemic ‘B’ symptoms, e.g. fever
Painful nodes on drinking alcohol
some patients (commonly young women) have disease localised to the mediastinum

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6
Q

HODGKINS LYMPHOMA
What is the management of Hodgkin’s lymphoma?

A
  • Combination chemo ± radiotherapy (overall 80% cured)
  • ABVD
    • Adriamycin
    • Bleomycin
    • Vinblastine
    • Decarbazine
  • autologous marrow transplant
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7
Q

NON-HODGKINS LYMPHOMA
What are the 3 broad presentations of Non-Hodgkin’s lymphoma?

A
  • T-cell malignancies
  • B-cell malignancies
  • Extra-nodal disease
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8
Q

NON-HODGKINS LYMPHOMA
How do T-cell malignancies present?

A
  • May present as ALL or non-Hodgkin lymphoma both being characterised by a mediastinal mass with bone marrow infiltration
  • Mediastinal mass may cause SVC obstruction
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9
Q

NON-HODGKINS LYMPHOMA
How do B-cell malignancies present?

A
  • Present as non-Hodgkin lymphoma with localised lymph node disease, usually in head + neck or abdomen
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10
Q

NON-HODGKINS LYMPHOMA
How does extra-nodal disease present?

A
  • Often GI > pain from obstruction, a palpable mass or even intussusception
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11
Q

NON-HODGKINS LYMPHOMA
What is the management of Non-Hodgkin’s lymphoma?

A

Steroids

R-CHOP
- Monoclonal antibodies to CD20 -> Rituximab
- CHOP regimen:
- Cyclophosphamide
- Hydroxy-daunorubicin
- Vincristine
- Prednisolone

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12
Q

BRAIN TUMOURS
What is a craniopharyngioma?
How does it present?

A
  • Developmental tumour arising from squamous remnant of Rathke pouch
  • Not truly malignant but locally invasive (bitemporal hemianopia often lower quadrant as superior chiasmal compression)
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13
Q

BRAIN TUMOURS
What are some signs of raised ICP?

A
  • Headache worse in morning
  • Papilloedema
  • Vomiting, esp. in the morning
  • Behaviour or personality change
  • Visual disturbance (squint secondary to 6th nerve palsy, nystagmus)
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14
Q

BRAIN TUMOURS
What are some focal neurological signs?

A
  • Spinal tumours = back pain, peripheral weakness of arms/legs or bladder + bowel dysfunction depending on level of lesion
  • Ataxia, seizures
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15
Q

NEUROBLASTOMA
What is a neuroblastoma? Epidemiology?

A
  • Arise from neural crest tissue in the adrenal medulla + sympathetic nervous system,
  • most common <5y,
  • NOT brain tumour
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16
Q

NEUROBLASTOMA
What is the clinical presentation of neuroblastoma?

A
  • Abdominal mass
  • Sx of metastatic = weight loss, hepatomegaly, pallor, bone pain + limp
  • Uncommon = paraplegia, cervical lymphadenopathy, proptosis, periorbital bruising, skin nodules
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17
Q

NEUROBLASTOMA
How does the abdominal mass present?

A
  • Often crosses midline + envelopes major vessels + lymph nodes
  • Can grow very large
  • Classically abdo primary is of adrenal origin
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18
Q

NEUROBLASTOMA
What are the investigations for neuroblastoma?

A
  • Raised urinary catecholamine levels
  • CT/MRI + confirmatory biopsy
  • Evidence of metastatic disease = bone marrow sampling, MIBG scan ±bone scan
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19
Q

NEUROBLASTOMA
What is the management of neuroblastoma?

A
  • Localised primaries + no mets can often be cured with surgery
  • Metastatic = chemo, autologous stem cell rescue, surgery + radio
  • Immunotherapy may be used for long-term maintenance
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20
Q

BONE TUMOURS
What is the clinical presentation of bone tumours?

A
  • Limbs most common site (particularly femur, tibia + humerus)
  • Persistent localised bone pain often precedes mass, otherwise well
  • May be worse at night + cause disrupted sleep
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21
Q

BONE TUMOURS
What are some investigations for bone tumours?

A
  • Raised ALP on bloods
  • Plain XR followed by MRI + bone scan, ?PET scan + bone biopsy
  • CT chest for lung mets + bone marrow sampling to exclude involvement
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22
Q

BONE TUMOURS
How might bone tumours present on radiographs?

A
  • XR = destruction + variable periosteal new bone formation
  • Periosteal reaction leads to classic “sunburst” appearance
  • Ewing sarcoma often shows substantial soft tissue mass
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23
Q

RETINOBLASTOMA
What is a genetic cause of retinoblastoma?
How might it present?

A
  • Retinoblastoma susceptibility gene on chromosome 13 = AD but incomplete penetrance > offer genetic screening
  • All bilateral tumours are hereditary, 20% of unilateral are
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24
Q

RETINOBLASTOMA
What are some complications of retinoblastoma?

A
  • Significant risk of second malignancy (especially sarcoma) amongst survivors of hereditary retinoblastoma
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25
LIVER TUMOURS What are liver tumours? In neonates?
- Mostly hepatoblastoma or hepatocellular carcinoma - Primary liver tumours in neonates = haemangioma
26
LIVER TUMOURS What are the investigations for liver tumours?
- Elevated serum alpha fetoprotein in nearly all cases - USS/CT/MRI to visualise the tumour + extent of disease
27
FANCONI SYNDROME What is fanconi syndrome?
- Generalised reabsorptive disorder of renal tubular transport in the PCT resulting in... – Type 2 (proximal) renal tubular acidosis – Polydipsia, polyuria, aminoaciduria + glycosuria – Osteomalacia/rickets
28
FANCONI SYNDROME What are some causes of fanconi syndrome?
- Usually secondary to inborn errors of metabolism – Cystinosis (AR > intracellular accumulation of cysteine, most common) – Wilson's disease, galactosaemia, glycogen storage disorders
29
FOETAL HAEMOGLOBIN What is the main difference between HbF + HbA?
- HbF has greater affinity to oxygen than adult so oxygen binds more easily + is more reluctant to let go = crucial for oxygen to transport from maternal to foetal Hb
30
FOETAL HAEMOGLOBIN When is Hb concentration highest? When does the shift from HbF to HbA occur?
- At birth to compensate for low oxygen concentration in the foetus - By 6m of age very little HbF produced so HbA predominates
31
ANAEMIA OVERVIEW What is anaemia? How is it defined in paeds?
- Hb level below the normal range - Neonate = <14g/dL - 1–12m = <10g/dL - 1–12y = <11g/dL
32
ANAEMIA OVERVIEW What are some causes of decreased red cell production? What are some clues?
- Ineffective erythropoiesis (Fe, folate deficiency, CKD) - Red cell aplasia - Normal reticulocytes, abnormal MCV in nutrient deficiencies
33
ANAEMIA OVERVIEW What are some causes of haemolysis? What are some clues?
- G6PD deficiency, haemoglobinopathies, hereditary spherocytosis - Raised reticulocytes, abnormal appearance on blood films, +ve direct antiglobulin test if immune cause
34
ANAEMIA OVERVIEW What is haemolytic anaemia? What is the normal lifespan of RBC?
- Characterised by reduced red cell lifespan due to increased red cell destruction in the circulation (intravascular haemolysis) or liver/spleen (extravascular) - 120d
35
ANAEMIA OVERVIEW How does haemolysis cause anaemia? What is the difference in haemolytic anaemias in neonates + children?
- Red cell survival reduced significantly but bone marrow production increases too, anaemia = bone marrow cannot compensate - Neonates = immune haemolytic anaemias, children = instrinsic abnormalities (G6PD)
36
ANAEMIA OVERVIEW List 4 features of haemolytic anaemias
- Anaemia - Hepatosplenomegaly - Unconjugated bilirubinaemia - Excess urinary urobilinogen
37
ANAEMIA OVERVIEW What are some causes of anaemia in the neonate?
- Reduced RBC production = congenital red cell aplasia + congenital parvovirus infection > red cell aplasia - Haemolytic anaemia = immune (haemolytic disease of newborn) or hereditary (G6PD etc)
38
ANAEMIA OVERVIEW What are the main causes of anaemia of prematurity?
- Inadequate erythropoietin production - Reduced red cell lifespan - Frequent blood sampling whilst in hospital - Iron + folic acid deficiency after 2-3m.
39
IRON DEF ANAEMIA What are some causes of iron deficiency anaemia?
- Inadequate intake = common as infants require additional iron for increasing blood volume - Malabsorption = Crohn's + coeliac - Blood loss = common in menstruating females
40
IRON DEF ANAEMIA What are some sources of iron? What can affect iron absorption?
- Breast milk, formula, cow's milk or weaning (cereals) - Markedly increased when eaten with food rich in vitamin C + inhibited by tannin in tea
41
IRON DEF ANAEMIA What are some signs of iron deficiency anaemia?
- Generic = pallor (inc. conjunctival), tachycardia, tachypnoea - Pica = consumption of non-food materials - Koilonychia, angular cheilitis, brittle hair + nails
42
IRON DEF ANAEMIA What are some investigations for iron deficiency anaemia and what would you see?
- FBC = low Hb, microcytic (low MCV + MCH), normal reticulocytes - Blood film = hypochromic microcytic red cells - Iron studies: – Low = serum ferritin, iron + transferrin saturation – High = total iron binding capacity
43
IRON DEF ANAEMIA What is... i) transferrin saturation? ii) total iron binding capacity?
i) Proportion of transferrin bound to iron ii) Total space on transferrin for Fe to bind
44
IRON DEF ANAEMIA What are some side effects of treatment with oral iron supplementation?
- Constipation - Black coloured stools - Nausea
45
SICKLE CELL DISEASE What is the genetics behind sickle cell disease?
- Autosomal recessive - Abnormal gene for beta-globin on C11 - Heterozygous = sickle-cell trait - Homozygous = sickle cell disease (HbSS)
46
SICKLE CELL DISEASE When does sickle cell disease present? What do all sickle cell disease patients have?
- 6m as HbF unaffected so manifests as HbF reduces - All have moderate anaemia with detectable jaundice from chronic haemolysis - All have marked increase in infection susceptibility, esp. pneumococci + H. influenzae due to hyposplenism secondary to chronic sickling + microinfarction of the spleen
47
SICKLE CELL DISEASE What is a severe, classic feature of sickle cell disease? Common location? Presentation? Most severe?
- Vaso-occlusive (painful) crises - Bones of limbs + spine common (may lead to avascular necrosis e.g. femoral heads) - Pain, fever + often those of triggering infection - Acute chest syndrome
48
SICKLE CELL DISEASE What is acute chest syndrome? What can cause it? Management?
- Fever or resp Sx (CP, tachypnoea) with new infiltrates on CXR - Can be due to infection (pneumonia, bronchiolitis) or non-infective (pulmonary vaso-occlusion or fat emboli) - Emergency > Abx or antivirals, blood transfusions for anaemia, may need NIV or intubation
49
SICKLE CELL DISEASE Name 2 other vaso-occlusive crises
- 'Hand-foot syndrome' common leading to dactylitis - Priapism in men > urological emergency, aspiration
50
SICKLE CELL DISEASE Sickle cell disease may present with acute anaemia (sudden drop in Hb). What can cause this?
- Haemolytic crises (sometimes with associated infection) - Aplastic crises (parvovirus causes cessation of RBC production) - Sequestration crises
51
SICKLE CELL DISEASE What is a sequestration crisis? What is the management?
- Sudden hepatic or splenic enlargement, abdo pain + circulatory collapse from accumulation of sickled cells blocking blood flow - Supportive = blood transfusions, fluid resus, splenectomy can prevent this + used in recurrent crises as can lead to splenic infarction > increased infection susceptibility
52
SICKLE CELL DISEASE What are some investigations for sickle cell disease?
- Prenatal Dx via CVS - Detection via Guthrie test - FBC = low Hb, high reticulocytes - Blood film = sickled RBCs - Dx with Hb electrophoresis showing high amounts of HbSS + absent HbA
53
SICKLE CELL DISEASE What are some complications of sickle cell disease?
- Short stature + delayed puberty - Stroke + cognitive issues - Pulmonary HTN - Chronic renal failure - Psychosocial issues
54
SICKLE CELL DISEASE What is the general management for sickle cell disease?
- Fully immunised (PCV, HiB, meningococcus) - Avoid vaso-occlusive crisis triggers - PO phenoxymethylpenicillin prophylaxis - PO folic acid as increased demands due to haemolysis - Hydroxycarbamide + hydroxyurea can stimulate HbF production to prevent painful crises - Bone marrow transplant curative + offered if failed response
55
SICKLE CELL DISEASE What are some potential triggers of vaso-occlusive crises? How might these be prevented?
- Cold, dehydration, excessive exercise, stress + hypoxia - Dress warmly, plenty of drinks
56
SICKLE CELL DISEASE What is the management of an acute crisis?
- PO or IV analgesia according to need (?opiates) - IV fluids, oxygen - Infection treated with Abx, blood transfusion for severe anaemia - Exchange transfusion if severe (e.g. neuro complications)
57
THALASSAEMIA What is thalassaemia? Consequence? What are the 2 types?
- AR disorder arising from ≥1 gene defects, resulting in a reduced rate of production of ≥1 globin chains - RBCs more fragile + breakdown easily - Alpha = defect in alpha globin chains - Beta = defect in beta globin chains
58
THALASSAEMIA What happens if there is deletion of 1 or 2 alpha globin chains?
- Alpha thalassaemia trait - Often asymptomatic with mild or absent anaemia - Red cells hypochromic + microcytic
59
THALASSAEMIA What happens if there is deletion of 3 alpha globin chains?
- Mild-moderate hypochromic microcytic anaemia + splenomegaly - Few patients are transfusion dependent
60
THALASSAEMIA What happens if there is deletion of all 4 alpha globin chains?
- Alpha thalassaemia major - Death in utero with foetal hydrops from foetal anaemia - Occurs in families of South-East Asian origin, homozygotes
61
THALASSAEMIA What is the epidemiology of beta thalassaemia? What are the three types?
- Indian subcontinent, Mediterranean + Middle East - Beta thalassaemia minor (1 abnormal + 1 normal gene) - Beta thalassaemia intermedia (2 defective or 1 defective + 1 deletion genes) - Beta thalassaemia major (homozygous for deletion genes)
62
THALASSAEMIA What is beta thalassaemia minor? How does it present? Differentiate?
- Carriers of abnormally functioning beta-globin gene - Mild microcytic + hypochromic anaemia (monitor) - Differentiate from Fe deficiency by measuring serum ferritin (normal)
63
THALASSAEMIA What is beta thalassaemia intermedia? Management?
- More severe microcytic anaemia, beta-globin mutation allow a small amount of HbA and/or a large amount of HbF to be produced - Monitor + occasional blood transfusion
64
THALASSAEMIA What is beta thalassaemia major? How does it present?
- Most severe form with no HbA as abnormal beta globin gene - - Severe transfusion-dependent anaemia from 3-6m, jaundice, failure to thrive
65
THALASSAEMIA What is a complication of beta-thalassaemia major which isn't common in developed countries?
- Extramedullary haematopoiesis can occur if no regular blood transfusions - Leads to hepatosplenomegaly + bone marrow expansion leading to maxillary overgrowth + skull bossing
66
THALASSAEMIA What are some investigations for beta thalassaemia?
- FBC + blood film = hypochromic microcytic anaemia - HbA2 raised in beta-thalassaemia trait, HbA2 + HbF raised in major - Serum ferritin to differ between Fe anaemia + check iron overload - Hb electrophoresis for Dx - DNA testing via CVS before birth
67
THALASSAEMIA What is the main complication of thalassaemia? How might this present?
- Repeated + Regular blood transfusions can cause chronic iron overload - Heart (cardiomyopathy, heart failure) - Liver (cirrhosis) - Pancreas (diabetes) - Pituitary (delayed growth + sexual maturation) - Skin (hyperpigmentation) - Arthritis + joint pain
68
THALASSAEMIA What is the management of thalassaemia?
- Lifelong monthly blood transfusions for the most severe cases - Desferrioxamine for iron chelation to prevent overload - Bone marrow transplant can be curative, reserved for beta thalassaemia major
69
HAEMOPHILIA What are the 2 types of haemophilia? What causes it?
- Haemophilia A = factor VIII deficiency - Haemophilia B = factor IX deficiency - X-linked recessive (M>F), A>B, girls with Turner's increased risk as 1 X
70
HAEMOPHILIA When does haemophilia typically present? Important differential?
- Around 1y as children become more mobile - NAI
71
HAEMOPHILIA What are some investigations for haemophilia?
- FBC + blood film - Prothrombin time (factors 2, 5, 7, 10, extrinsic) normal - Activated partial thromboplastin time (intrinsic) = greatly increased - Severity dependent on amount of FVIII:C or FIX:C levels - Prenatal Dx with CVS
72
HAEMOPHILIA What is the management of haemophilia?
- IV infusion of recombinant FVIII or FIX concentrate if active bleeding (or prophylactic to reduce arthropathy risk) - Desmopressin stimulates vWF release for bleeding/prevention, TXA - AVOID aspirin, NSAIDs + IM injections (can worsen bleeding)
73
HAEMOPHILIA What is a complication of the treatment for haemophilia?
- Formation of antibodies against the clotting factor can render it ineffective
74
VON WILLEBRAND DISEASE What is the physiological role of von Willebrand factor?
- Facilitates platelet adhesion to damaged endothelium - Acts as carrier protein for FVIII:C, protecting it from inactivation + clearance
75
VON WILLEBRAND DISEASE What is von Willebrand disease (vWD)? What causes it? Types?
- Deficiency of vWF leading to defective platelet plug formation + deficient FVIII:C > most common inherited bleeding disorder - AD, type 1 most common + mildest - Severity increases with type 2, type 3 has very low or no vWF (AR)
76
VON WILLEBRAND DISEASE What is the clinical presentation of vWD?
- Bruising, excessive + prolonged bleeding after surgery, mucosal bleeding (epistaxis, menorrhagia, bleeding gums) - In contrast to haemophilia = spontaneous soft tissue bleeding like large haematomas uncommon
77
VON WILLEBRAND DISEASE What are some investigations for vWD?
- FBC (normal platelets) + blood film, biochemical screen including renal + liver function - Prolonged bleeding time - Prothrombin time normal - APTT = elevated or normal - vWF antigen decreased, vWF multimers variable
78
VON WILLEBRAND DISEASE What is the management of vWD?
- Pressure applied if active bleeding - Minimise bleeding with desmopressin or TXA - Severe = plasma derived FVIII concentrate or vWF infusion - AVOID aspirin, NSAIDs + IM injections as can worsen bleeding
79
VON WILLEBRAND DISEASE How is desmopressin given? What does it do?
- Nasal or s/c - Release of vWF + FVIII concentrate
80
COAGULATION DISORDERS What are acquired disorders of coagulation?
Secondary to - Haemorrhagic disease of the newborn due to vitamin K deficiency - Liver disease as location of clotting factor production - ITP + DIC
81
COAGULATION DISORDERS What can cause vitamin K deficiency?
- Inadequate intake = neonates, long-term chronic illness - Malabsorption = coeliac, cystic fibrosis - Vitamin K antagonists = warfarin
82
ITP What is immune thrombocytopenic purpura (ITP)?
- Commonest cause of thrombocytopenia in childhood - T2 hypersensitivity reaction with destruction of circulating platelets by anti-platelet IgGs
83
ITP What are the investigations for ITP?
- FBC shows marked thrombocytopenia - May have compensatory megakaryocyte increase in bone marrow
84
ITP What is the management of ITP?
- Often acute + self-limiting - Severe bleeding may need prednisolone, IVIg, blood/platelet transfusions
85
HAEMOLYTIC DISEASE OF THE NEWBORN what is the clinical presentation?
- anti-D antibodies in mother detected by Coombe's test that all women have at 1st antenatal appointment - routine USS may detect hydrops fetalis or polyhydramnios - mild cases = jaundice, pallor + hepatosplenomegaly, hypoglycaemia - severe cases = oedema, petechiae + ascites
86
HAEMOLYTIC DISEASE OF THE NEWBORN what are the investigations?
- indirect coombe's test show antibodies - antenatal USS shows hydrops fetalis - fetal blood sample
87
HAEMOLYTIC DISEASE OF THE NEWBORN what is the management in utero?
- transfusion of O negative packed cells cross-matched with maternal blood at 16-18 weeks
88
HAEMOLYTIC DISEASE OF THE NEWBORN what is the management after delivery?
50% = normal haemoglobin + bilirubin but should be monitored for anaemia for 6-8 weeks 25% = require transfusion + may require phototherapy to avoid kernicterus 25% = stillborn or have hydrops fetalis
89
HAEMOLYTIC DISEASE OF THE NEWBORN what are the complications?
- kernicterus which can cause extrapyramidal, auditory and visual abnormalities and cognitive deficit - late-onset anaemia - graft-versus-host disease - portal vein thrombosis + portal hypertension
90
HAEMOLYTIC DISEASE OF THE NEWBORN how can it be prevented?
identify all women who have been sensitised by coombe's testing at first antenatal visit anti-D immunoglobulin should be given to all rhesus negative women at 28 + 34 weeks
91
ALL What are the risk factors for acute lymphoblastic leukaemia (ALL)?
- Trisomy 21, - immunocompromised (HIV, immunosuppressants)
92
ALL What do blood and bone marrow tests show in ALL?
FBC and blood film = WCC usually high Blast cells on film and in bone marrow
93
HODGKINS LYMPHOMA What blood results may you see in someone with Hodgkin's lymphoma?
- high ESR - FBC = anaemia (normochromic normocytic) - reed sternberg cells - low Hb - high serum lactase dehydrogenase
94
NON-HODGKINS LYMPHOMA What are the signs and symptoms of non-hodgkins lymphoma?
Fever and sweating Enlarged rubbery non-tender nodes Systemic ‘B’ symptoms, e.g. fever GI and skin involvement
95
AML What is acute myeloid leukaemia (AML)?
Neoplastic proliferation of blast cells (immature blood cells) affects myeloid progenitor cells and myeloblasts
96
AML What are the risk factors for AML?
Preceding haematological disorders Prior chemotherapy Exposure to ionising radiation Down’s syndrome
97
AML what are the clinical features of AML?
Anaemia -> breathlessness, fatigue, pallor Infection Hepatosplenomegaly Peripheral lymphadenopathy Gum hypertrophy Bone marrow failure and bone pain
98
AML What would you expect to see on an FBC and bone marrow biopsy in someone you suspect to have AML?
FBC = anaemia and thrombocytopenia and neutropenia BM biopsy = leukaemic blast cells (with Auer rods)
99
AML Describe the treatment for AML
Blood and platelet transfusions IV fluids Allopurinol to prevent tumour lysis Infection control with IV antibiotics Chemotherapy Steroids Sibling matched allogenic bone marrow transplant
100
CML What is chronic myeloid leukaemia (CML)?
Uncontrolled clonal proliferation of myeloid cells (basophils, eosinophils and neutrophils)
101
CML what are the clinical features of CML?
Insidious onset Symptomatic anaemia Abdominal pain - splenomegaly Weight loss, tiredness, palor Gout - due to purine breakdown Bleeding - due to platelet dysfunction
102
CML what are the investigations for CML?
FBC - anaemia, raised myeloid cells, high WCC (eosinophilia, basophilia, neutrophilia) Increased B12 Blood film - left shirt, basophilia Bone marrow biopsy - increased cellularity Philadelphia chromosome seen in 80+% of cases  t(9;2) - Stimulates cell division
103
CML What is the treatment for CML?
Chemotherapy Tyrosine kinase inhibitors, e.g. Imatinib - Given orally Stem cell transplant
104
CML Why does the Philadelphia chromosome cause CML?
FORMS fusion gene BCR/ABL on chromosome 22 –> tyrosine kinase activity –> stimulates cell division
105
CLL What is Chronic lymphoblastic leukaemia (CLL)?
Proliferation of mature B lymphocytes leads to accumulation of mature B cells that have escaped apoptosis Chronic malignant transformation of mature lymphoid cells
106
CLL what are the investigations for CLL?
● Normal or low Hb ● Raised WCC with very high lymphocytes ● Blood film – smudge cells may be seen in vitro
107
CLL What is the treatment for CLL?
Watch and wait Chemotherapy Monoclonal antibodies, e.g. rituximab Targeted therapy, e.g. bruton kinase inhibitors (ibrutinib)

A TO REVISE - PHASE 3A (16 decks)

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