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Oncology & Haematology Flashcards

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1
Q

What are the age incidences in cancers?

A

ALL - 2-6yo
Non-Hodgkin lymphoma - childhood
Hodgkin lymphoma - adolescence

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2
Q

What is acute lymphoblastic leukaemia?

A

Excessive proliferation of lymphocytes –> many immature lymphocytes
Presents in 2-6yo
Presents insidiously over several weeks

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3
Q

How does ALL present?

A 
Malaise and anorexia
Bone marrow infiltration
- anaemia (lethargy)
- neutropenia (infection)
- thrombocytopenia (bruising, petechiae, nose bleeds)
- bone pain
Reticule-endothelial infiltration
- hepatosplenomegaly
- lymphadenopathy
Other organs
- CNS (nerve pansies, headache, vomiting)
- testes (enlargement)
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4
Q

How is ALL investigated?

A

FBC - low haemolytic, thrombocytopenia, circulating leukaemic blast cells
Bone marrow - indicates prognosis
CXR - mediastinal mass

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5
Q

How is ALL treated?

A

0-4 weeks - induction

  • steroids
  • IV vincristine
  • IT methotrexate
  • L-asparaginase

5-8 weeks - consolidation

  • steroid
  • vincristine
  • IT methotrexate
  • thiopurine

Maintenance treatment (2yrs girls, 3yrs boys)

  • methotrexate (oral and IT)
  • prophylactic co-trimoxazole (prevent pneumonia)
  • vincristine

Blood transfusions (platelets and whole red cells) - reduce symptoms

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6
Q

What is tumour lysis syndrome?

A

Systemic and rapid release of intracellular contents as chemotherapy destroys blast cells

  • Increased urea
  • Increased phosphate
  • Increased potassium
  • Decreased calcium

Can give allopurinol

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7
Q

What are negative prognostic factors for ALL?

A

10yo
>50 WBC
Male gender
CNS involvement

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8
Q

What is lymphoma?

A

Proliferation of cells in lymphatic system (nodes, spleen and liver)

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9
Q

How does non-Hodgkin’s lymphoma present, how is it investigated and treated?

A

Affects lymph nodes and younger children

Lymphoblastic (mainly T-cell)

  • anterior mediastinal mass
  • bone marrow, bone, skin, CNS, liver, kidneys, spleen

B cell malignancy (Burkitt)
- lymph nodes in head, neck or abdomen –> pain, intussusception

Ix: bone marrow aspirate, LP, CT, PET scan
Tx: chemotherapy
Px: >80%

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10
Q

How does Hodgkin’s lymphoma present, how is it investigated and treated?

A

Previous EBV infection, adolescents
Reed-Sternberg cells

Painless lymphadenopathy (neck or mediastinal)

Ix: CT neck, chest, abdo and pelvis, PET scan, bone marrow aspirate, EBV serology
Tx: radiotherapy +/- chemo
Px: >90%

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11
Q

How does NHL and HL differ?

A

HL

  • Reed-Sternburg cells
  • upper body
  • spreads slowly and receptive to Tx
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12
Q

What are the side effects of chemotherapy?

A 
Hair loss
Anaemia
Infection
Bruising
Sore mouth
N+V
Weight gain
Delayed puberty
Reduced fertility and growth
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13
Q

What is neuroblastoma?

A

Arise from neural crest tissue in adrenal medulla and sympathetic nervous tissue

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14
Q

What are the most common cancers in children?

A 
Leukaemia
CNS tumours
Lymphoma
Neuroblastoma
Soft tissue sarcoma
Wilms tumour
Bone tumour
Retinoblastoma
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15
Q

Where does haemopoiesis occur?

A

Fetal - liver

Postnatal - bone marrow

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16
Q

What are the physiological changes in blood count from neonate to adolescence?

A

Hb - starts high, falls due to increased RBC production and then levels off at adult levels

WBC - starts high and decreases

Platelet - similar to adult

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17
Q

How does iron deficiency arise and how does it present?

A

Common - sourced from breast milk, formula, cow’s milk or solids
May be due to delay in weaning

Child will tire easily and feed slowly

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18
Q

What does folate deficiency cause?

A

Body can’t make enough RBC so macrocytic megaloblastic anaemia

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19
Q

What is thrombocytopenia and what does it cause?

A

Platelet count bruising, petechiae, purpura, mucosal bleeding

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20
Q

What is immune thrombocytopenia?

A

Destruction of platelets by anti-platelet IgG autoantibodies

Usually post URTI

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21
Q

How does ITP present?

A

1-2 weeks post URTI
Petechiae, purpura or superficial bruising
Epistaxis, profuse and intracranial bleeding is rare

Mostly acute and self-limiting

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22
Q

How is ITP treated?

A

Oral prednisolone, IV anti-D or IVIG

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23
Q

What is Von Willebrand disease?

A

Deficiency in factor responsible for platelet adhesion and carrying factor VIII

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24
Q

How does pattern of bleeding help differentiate cause?

A

Into mucous membranes and skin - platelet disorder or vWD

Into muscles or joints - haemophilia

Scarring and delayed haemorrhage - disorders of connective tissue

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25
What is haemolytic anaemia?
Reduced RBC lifespan due to increased intra and extravacular destruction Leads to hepatosplenomegaly, increased unconjugated bilirubin and urinary urobilinogen
26
What are the causes of haemolysis?
Neonates - autoimmune | Childhood - hereditary spherocytosis, G6PD deficiency, PK deficiency, thalessaemia, sickle cell disease
27
What is hereditary spherocytosis?
Mutation in gene encoding RBC skeletal protein | RBC loses some of membrane going through spleen --> spheroidal and is destroyed
28
How does hereditary spherocytosis present and how is it treated?
Around birth Jaundice, anaemia, splenomegaly, gallstones Folate supplementation or splenectomy
29
What is G6PD deficiency?
Commonest RBC problem worldwide esp. central Aftrica X-linked but female carriers are clinically normal
30
How does G6PD deficiency present?
Neonatal jaundice | Acute haemolysis precipitated by infection, drugs, ?broad beans
31
What is pyruvate kinase deficiency?
Lack of enzyme which decreases ATP | Cell becomes rigid and is destroyed in spleen
32
What is haemophilia A?
Factor VIII deficiency | More common
33
What is haemophilia B?
Factor IX deficiency
34
How does haemophilia present?
Most present by 1yo when walking starts Recurrent spontaneous bleeding into joints and muscles --> arthritis In neonates - intracranial haemorrahge, oozing from heel prick or post circumcision
35
What do neuroblastoma arise from?
Neural crest tissue in adrenal medulla ad sympathetic nervous tissue
36
What is sickle cell disease?
Haemoglobinopathies in which HbS mutations are inherited | Change in amino acid from glutamine to valine
37
What is sickle cell anaemia?
HbSS (homozygous) | All Hb is HbS (small amount of fetal Hb)
38
What is sickle-cell haemoglobin C disease?
HbS and HbC from each parent HbC is different mutation in B-globlin, glutamine to lysine Not as severe as sickle cell anaemia (HbC doesn't polymerise as quickly)
39
What is sickle B-thalassaemia?
HbS and B-thalassaemia | No HbA so similar symptoms to sickle cell anaemia
40
What is sickle trait?
Inherit HbS and normal B-globin gene | Carriers and asymptomatic
41
What does HbS do?
Polymerises within RBC to form rigid tubular spiral bodies which deform cells into sickle cells Reduced life span and may be trapped in micro-circulation --> blood vessel occlusion and ischaemia Exacerbated by low oxygen tension, dehydration and cold
42
How does sickle cell disease present?
Anaemia - clinically detectable jaundice Infection - increased susceptibility to pneumococci and H. influenzae (hyposplenism secondary to microinfarction) Painful crises - vaso-occlusion in hands and feet, chest Splenomegaly Priapism (erectile dysfunction)
43
What are the long term complications of sickle cell disease?
``` Short stature and delayed puberty Stroke and cognitive problems Adeno-tonsillar hypertrophy Cardiac enlargement and heart failure - chronic anaemia Renal dysfunction Pigmented gallstones ```
44
How is sickle cell disease managed?
Prophylaxis - full immunisation and daily oral penicillin Daily folic acid Avoid vaso-occlusive crises - analgesia and hydration if occur
45
How is sickle cell disease screened for?
Guthrie test Chorionic villus sampling
46
What is B-thalassaemia and what are the different types?
Occur in people from Indian subcontinent, Mediterranean and Middle East Reduction of production of B-globin --> reduction in HbA B-thalassaemia major - most severe, HbA cannot be produced B-thalassaemia intermedia - milder, B-globin mutations allow small amount of HbA to be produced
47
How does B-thalassaemia present?
Severe anaemia and jaundice Failure to thrive Extramedullary haemopoiesis --> hepatosplenomegaly and bone marrow expansion (maxillary overgrowth and skull bossing)
48
What haematological disorder causes a change in facial structure?
B-thalassaemia | Bone marrow expansion in maxillary
49
How is B-thalassaemia managed?
Lifelong monthly blood transfusions - keep Hb above 100g/l to reduce growth failure and bone deformation This can cause chronic iron overload --> cardiac failure, liver cirrhosis, diabetes, infertility, growth failure Treated with iron chelation from 2 years old Bone marrow transplant will cure
50
What is the B-thalassaemia trait?
Heterozygotes are asymptomatic | RBC are hypochromic and microcytic
51
What is alpha-thalassaemia?
Healthy people have 4 alpha-globin genes No alpha-globin = alpha-thalassaemia major, fetal hydrops 1 alpha-globin = mild to moderate anaemia 2 or 3 alpha-globin = asymptomatic
52
What is a Wilm's tumour?
Nephroblastoma - originates from embryonic renal tissue Most present before 5 years old and it's very rare after 10 Associated with trisomy 18
53
How does a Wilm's tumour present?
Large abdominal mass in otherwise well child Usually metastasises to lung
54
How is Wilm's tumour treated?
Chemo plus delayed nephrectomy Prognosis is good >80% but recurrence has poor prognosis
55
What is rhabdomyosarcoma?
Soft tissue sarcoma Originates from primitive mesenchymal tissue - head and neck, GU
56
How does rhabdomyosarcoma present?
Head and neck - proptosis, nasal obstruction or bloody nasal discharge GU (bladder, paratesticular or urethra) - dysuria, urinary obstruction, blood stained vaginal discharge
57
What is the prognosis for rhabdomyosarcoma?
Metastasis is present in 15% and associated with poor prognosis
58
When and how do bone tumours present?
Uncommon before puberty Osteosarcomas are more common Ewings seen more often in younger children Persistant bone pain in otherwise well patient
59
How are bone tumours diagnosed and treated?
X-ray - destruction and new bone formation, Ewing's has soft tissue mass Chest CT - lung metastases Bone marrow sample - exclude marrow involvement
60
What is disseminated intravascular coagulation?
Disorder of coag pathway --> diffuse fibrin deposition in microvasculature and consumption of coag factors and platelets Tiny clots and severe bleeding
61
What are the causes of DIC and how does it present?
SEPSIS or SHOCK Meningococcal septicaemia Trauma and burns Bruising, purpura, haemorrhage Thrombocytopenia, prolonged prothrombin or APTT, low fibrinogen
62
How do retinoblastoma present?
Malignant tumour of retinal cells, may affect one or both (hereditary) eyes Most present within 3 years White pupillary reflex replaces red one
63
How are retinoblastomas treated?
Cure but preserve vision if possible | Chemotherapy to shrink tumour and then local laser treatment
64
What are the indications for splenectomy?
Hereditary spherocytosis, lymphoma, ITP | Trauma
65
What are the complications of splenectomy?
Low dose Abx needed for life | Malaria
66
What are side effects of chemotherapy?
Bone marrow suppression - anaemia, thrombocytopenia, bleeding Immunosuppression - infection Gut mucosal damage - infection and undernutrition N+V, anorexia - undernutrition Alopecia

Paediatrics (14 decks)

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