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CP2 PAEDS > Oncology and Haematology > Flashcards

Oncology and Haematology Flashcards

1
Q

Most common type of paediatric cancer

A

Leukaemia (32%)

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2
Q

Which cancer is down’s syndrome associated with?

A

Leukaemia

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3
Q

What cancer is associated NFM?

A

Glioma

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4
Q

4 most common types of cancer (4)

A

Leukaemia (NHL)
Neuroblastoma
Wilms
Retinoblastoma

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5
Q

Presentation brain tumours in children (2)

A

Incr ICP

Neurological signs

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6
Q

Presentation retinoblastoma

A

White pupillary reflex

Squint

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7
Q

Presentation lymphomas

A

Enlarged LN in head, neck or abdomen

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8
Q

Presentation of Wilms tumour (4)

A

Large abdominal mass in well child

? Anorexia, abdo pain, haematuria

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9
Q

Langerhans cell histiocytosis presentation (4)

A

Seborrhoeic rash
Widespread soft tissue infiltration
Bone pain, swellnig, fracture
Diabetes insipidus

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10
Q

Neuroblastoma presentation (5)

A 
SC mass crossing midline 
SC compression 
W loss + malaise 
Pallor, bruising 
Bone pain
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11
Q

What % of leukaemia in children is ALL?

A

80%

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12
Q

When does clinical presentation of ALL peak?

A

2-5years

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13
Q

S+S ALL

A

Malaise + anorexia
BM infiltration - anaemia + neutropaenia (infection), thrombocytompaenia (brusing, bleeding petechiae) + bone pain
HPmegaly
Organ infiltration - CNS - nn palsy, headaches, vomiting, Testes enlargement

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14
Q

Ix ALL (3)

A

FBC
BM exam
CXR - mediastinal mass

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15
Q

What would you find on a FBC for ALL?

A

Decr Hb
Decr platelets
Evidence of leukaemic blast cells

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16
Q

What are the 2 subclassifications of ALL?

A 
Common subtype (75%)
T-Cell subtype (25%)
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17
Q

What stage of treatment is initiated at diagnosis ALL?

A

Remission induction

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18
Q

Tx - remission induction ALL

A

Vincristine
Steroids
Methotrexate
L-asparginase

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19
Q

What should you do before starting Tx for ALL?

A

Correct anaemia w/ blood + platelet transfusion

Tx infection

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20
Q

Tx weeks 5-8 ALL (Consolidation + CNS protection)

A

Methotrexate
Vincristine
Steroids
Thiopurine

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21
Q

What type of chemo in ALL is required for CNS penetration?

A

Intrathecal chemo

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22
Q

Tx w8-16 ALL (interim maintenance)

A

Prophylactic co-trimox
Monthly vincristine
5 day steroid daily, 6-mercaptopurine
Weekly PO methotrexate

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23
Q

Tx ALL week 16-23 (Delayed intensification)

A

Vincristine
Methotrexate
Dexamethasone

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24
Q

Tx ALL week 23 –> 2+years

A

Same as interim maintenance

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25
Q

What is TUmour lysis syndrome?

A

Metabolic derangement due to release of intracellular contents from chemotherapy destroying leukaemic blast cells

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26
Q

Features of tumour lysis syndrome (4)

A

Hyperuricaemia
Hypophosphatemia
Hypocalcaemia
Hyperkalaemia

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27
Q

Mx Tumour lysis syndrome

A

IV fl

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28
Q

ALL -Poor prognostic factors - age

A

<1 or >10

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29
Q

ALL -Poor prognostic factors - tumour load

A

> 50x109/L

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30
Q

ALL- Poor prognostic factors - cytogenic abnormalities

A

MLL rearrangement

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31
Q

ALL -Poor prognostic factors - speed of response to initial chemo

A

Persistance of leukaemia blasts in BM

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32
Q

ALL Poor prognostic factors - Minimal residual disease assessment

A

High

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33
Q

ALL -Poor prognostic factors - gender

A

Male

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34
Q

ALL -Poor prognostic factors - spread

A

CNS involvement

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35
Q

ALL - Tumour cells L1

A

Small uniform cells

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36
Q

ALL - Tumour cells L2

A

Large varied cells

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37
Q

ALL - Tumour cells L3

A

Large varied cells + vacuole

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38
Q

Anaemia - neonate

A

<140

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39
Q

Anaemia - 1-12months

40
Q

Anaemia - 1-12years

41
Q

What are the 3 main mechanisms leading to anaemia?

A

Decr RBC production
Incr RBC destruction/haemolysis
Blood loss

42
Q

E.g.s of Decr RBC production in anaemia (5)

A 
IDA (most common) 
Folic defic
Chronic inflamm 
Chronic renal failure 
Red cell aplasia
43
Q

What infection is red cell aplasia associated with?

A

Parovirus B19

44
Q

E.g.s of Haemolysis causing anaemia (4)

A

Membrane disorder - spherocytosis
Enzyme disorder - G6PD def
Haemoglobinopathies (SC, Thal)
Immune - haemolytic disease

45
Q

E.g.s of blood losses causing anaemia (v uncommon) (2)

A

Chronic GI bleed - Meckels

Inherited - vWD

46
Q

Causes of microcytic anaemia (TICS - 3)

A

Thalassaemia
IDA
Chronic disease/renal failure
Sideroblastic anaemia

47
Q

Causes normocytic anaemia (6)

A 
Acute blood loss 
Anaemia chronic disease 
BM failure 
Renal failure 
Hypoothyroid 
Haemolysis
48
Q

Causes macrocytic anaemia (3)

A

B12
Folate
Reticulocytosis

49
Q

What would make you suspect a haemolytic anaemia?

A

Incr reticulocytes

Incr bilirubin

50
Q

What are reticulocytes?

A

Immature RBC

Circulate for 1 day –> RBC

51
Q

Where are blood cells prdoduced post-natally?

A

Bone marrow

52
Q

What type of Hb do newborns predominantly have (75%)

A

HbF (higher O2 affinity)

53
Q

What type of Hb do children >1 predominantly have (97%)

54
Q

What can incr HbF be a indicator of?

A

Inherited disorder of Hb prod (Sickle cell)

55
Q

WCC in neonates

A

10-25 x10 9/L

56
Q

Platelets in neonates

A

150-400x10 9/L (norm)

57
Q

How much iron intake does a newborn need /day?

58
Q

Where does a newborn get the majority of its iron from?

A

Breast milk

59
Q

Clinical features IDA (4)

Hb<70g/l

A

Fatigue
Slow feeding
Pallor
Innapprop eating non-food material

60
Q

Ix IDA (2)

A

Blood film

Low Se ferritin

61
Q

Mx IDA (2)

A

Diet

Supplement - iron-sytron/niferex 3 months

62
Q

What is folate vital for?

63
Q

What is B12 vital for?

64
Q

What is haemolytic anaemia?

A

Incr RBC destruction, BM compensates, then –> anaemia

65
Q

Signs haemolytic anaemia (2)

A

HSmegaly

Incr unconjugated bilirubin

66
Q

Causes of haemolytic anaemia (5)

A 
Hereditary spherocytosis 
G6PD deficiency 
Pyruvate Kinase deficiency 
Thalassaemia 
Sickle Cell
67
Q

What is Hereditary spherocytosis

A

Mutation in gene –> spheroidal shape –> spleen –> destroyed

68
Q

Sx Hereditary spherocytosis (5)

A 
Jaundice 
Anaemia 
Splenomegaly 
Aplastic crisis 
Gall stones
69
Q

G6PD features

A

Neonatal jaundice

Acute haemolysis

70
Q

What is the 2nd most common cause of haemolytic anaemia?

A

Pyruvate kinase deficiency

71
Q

When does Sickle Cell disease start to present?

A

After 6 months

72
Q

Where is Sickle cell common?

A

Africa or Carribean

73
Q

Homogenous HbS

A

Sickle cell mutation in both B-chains

74
Q

HbSC

A

1 HBs from one parents
1 HBc from other
No HbA - near normal Hb + fewer painful crises

75
Q

Sickle-B thalassemia

A

HbS from one parent

B-thalassaemia from other

76
Q

Sickle train

A

HbS from 1 parent, norm from other
40% Hb = HbS
Asymp

77
Q

Affect of HbS on life

A

Shorter life span

78
Q

Sx Sickle Cell (3)

A

Anaemia
Incr infection susceptibility
Priaprism

79
Q

What occurs in a Sickle Cell painful crises (5)

A 
Vaso-occlusive 
Pain + swelling in hands + feet 
Acute chest syndrome 
Severe hypoxia req ventilation 
Avascular necrosis of femoral heads
80
Q

Long term problems Sickle cell (7)

A 
Short stature + delayed puberty 
Stroke/cognitive issues 
Adenotonsilar hypertrophy - OSA
Cardiac enlargement 
Heart failure 
Renal dysfunction 
Pigment gallstones
81
Q

How is Sickle cell screened for?

A

Guthrie test

82
Q

What prophylaxis can be given for Sickle cell

A

Penicillin

83
Q

Prenatal diagnosis Sickle cell

A

CVS @ end trim1

84
Q

Mx Sickle Cell

A

Pen prophylaxis
Imms
Daily folic acid
Avoid cold, dehydration, excessive exercise, hypoxia

85
Q

Prognosis Sickle cell

A

50% Die before 40

86
Q

What is B-thalassaemia

A

Severe reduction prod B-globin chains hence reduction ni HbA prod

87
Q

Where is B-thalassaemia most common?

A

India
Mediterranean
Middle East

88
Q

What are the 3 types of B-thalassaemia

A

B-T major
B-T intermedia
Hb trait

89
Q

Which is the most severe type of B-thalassaemia

90
Q

B-T major - HbA

A

No HbA production

91
Q

B-T intermedia HbA

A

Small no’ HbA + HbF prod

92
Q

Which type is the B-thalassaemia is Asymp carrier?

93
Q

Features B-thalassaemia (4)

A

Severe anaemia
Jaundice
FTT
Bone deformity (maxillary overgrowth, skull bossing)

94
Q

Diagnosis B-thalassaemia

A

Prenatal

CVS + DNA analysis

95
Q

Mx B-thalassaemia

A

Montly blood transfusions
Iron chelation
BM transplant = cure

96
Q

What % patients w/ B-thalassaemia live to 40?

97
Q

What is repeated blood transfusions in B-thalassaemia associated with? (4)

A

Cardiac failure
Liver cirrhosis
DM
Infertility

CP2 PAEDS (18 decks)

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