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Year 4 Paediatrics > Haematology And Oncology > Flashcards

Haematology And Oncology Flashcards

1
Q

If a child presents with abnormal bleeding/bruising, what broad aetiologies could be considered?

A

Coagulation factor deficiencies

Platelet deficiency/dysfunction

Microvascular abnormalities

Trauma (Accidental/Non Accidental)

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2
Q

How would a coagulation factor deficiency present?

A

Excess blood loss following surgery/dentistry
Recurrent bruises >1cm
Muscle haematomas
Joint haemarthroses

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3
Q

How could Platelet Deficiencies present?

A

Purpura
Petichiae
Mucosal Bleeding

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4
Q

How would microvascular abnormalities present?

A

Palpable purpura suggestive of vasculitis

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5
Q

What would make you think bruising/bleeding from trauma was NAI?

A

Immobile child
Disproportionate to injury sustained
Multiple sites/clusters
Shape of hand/ligatures

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6
Q

State four associated features in bruising/bleeding that could point to an underlying cause

A

Hepatosplenomegaly (Haemolysis)
Anaemia
Lower Limb bruising (HSP)
Arthritis (HSP)

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7
Q

In abnormal bleeding/bruising then a range of bloods would be done, including PT and APTT. If APTT was prolonged, what would be done next and why?

A

50:50 dilution with normal plasma

If the value fails to return to normal then its suggestive of an inhibitor (heparin, or antibodies)

If the value returns to normal then it suggests a deficiency

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8
Q

If the first line bloods for abnormal bleeding/bruising were normal, what further investigations could be done?

A

Platelet function assay
Von Willebrands Disease Screen
Autoantibody screen
Bone marrow aspirate

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9
Q

If abnormal bleeding/bruising, IM injections, ABG and NSAIDs should be avoided. When should you urgently assess for leukaemia?

A

Unexplained Petichiae
Hepatosplenomegaly
Suggestive FBC

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10
Q

If abnormal bleeding/bruising, IM injections, ABG and NSAIDs should be avoided. When should you urgently assess for Neuroblastoma?

A

Periorbital bleeding

Palpable abdominal mass

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11
Q

What would a normal PT/APTT in a bruising/bleeding child suggest?

A

Platelet abnormality

Vasculitis

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12
Q

What would an increased PT in a bruising/bleeding child suggest?

A

Deficiency of Factor VII or Vitamin K

Liver Disease

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13
Q

What would an increased APTT in a bruising/bleeding child suggest?

A

Deficiency of factors VIII, IX, XI or XII

AKA Haemophilia A/B, Von Willebrands Disease

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14
Q

What would an increased PT AND APTT in a bruising/bleeding child suggest?

A

Deficiency in in factors II/V/X/Fibrinogen

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15
Q

What would a decreased fibrinogen in a bruising/bleeding child suggest?

A

DIC

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16
Q

Define lymphadenopathy

A

Generalised lymphadenopathy is an enlargement of >2 non contiguous lymph node groups

NOTE: Most children have palpable lymph nodes, increasing in size until 8-12, then atrophy

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17
Q

Name four specific things you would want to ask about in a lymphadenopathy history

A

TB Contact
Recent travel
Contact with Pets/Livestock
Family history

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18
Q

Give 5 red flags for lymphadenopathy

A 
Sever pallor
Fever
Unexplained bruising
Unexplained bleeding
Mediastinal Mass (eg audible on auscultation)
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19
Q

Name four infective causes of lymphadenopathy

A

Infectious Mononucleosis
TB
Toxoplasmosis
CMV

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20
Q

Give four non infective causes of lymphadenopathy

A

SLE
Lymphoma
Leukaemia
Neuroblastoma

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21
Q

How would you manage lymphadenopathy?

A

Simple reassurance

If still enlarging, review after 2-3 weeks

If red/tender then suggests Bacterial Lymphadenitis so give 10d Co-Amoxiclav and review

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22
Q

Children should be referred as an emergency if they are not responding to antibiotics in bacterial lymphadenitis. When should children be referred via 2 week wait?

A

Axillary/Epitrochlear/Supraclavicular >1cm

Inguinal >1.5cm

Cervical >2cm and increasing in size/persistent

Over 10 years with any lymph node >1cm for >2 weeks

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23
Q

What is physiological anaemia in infancy?

A

Normal dip at 6-9 weeks

High oxygen delivery due to high haemoglobin at birth causes negative feedback and suppresses EPO

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24
Q

Describe the pathophysiology of Anaemia of Prematurity

A

Less time in utero receiving iron from mother
Reduced EPO
Blood tests remove significant circulating volume

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25
Q

Other than physiological and prematurity, give three other causes of Anaemia in Infancy

A

Blood loss
Twin to twin transfusion
Haemolysis

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26
Q

Name the two common causes of Anaemia in Older Children

A 
Dietary Insufficiency
Blood loss (ie through menstruation)
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27
Q

Name the causes of Microcytic Anaemia (TAILS)

A 
Thalassaemia
Anaemia of Chronic Disease
Iron Deficiency
Lead Poisoning
Sideroblastic
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28
Q

Name the causes of Normocytic Anaemia (3As and 2Hs)

A 
Acute Blood Loss
Anaemia of Chronic Disease
Aplastic Anaemia
Haemolytic Anaemia
Hypothyroidism
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29
Q

Macrocytic Anaemia can be megaloblastic or normoblastic. Give examples of each.

A

Megaloblastic - Vit B12 and Folate

Normoblastic - Alcohol, Hypothyroidism, Liver Disease

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30
Q

Describe some classical features of Iron Deficiency Anaemia

A 
Glossitis
Angular Cheilitis
Koilonychia 
Pica
Hair loss
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31
Q

Name five investigations for Anaemia

A 
FBC and Haematinics
Blood film
Bilirubin
Direct Coombs
Haemoglobin Electrophoresis
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32
Q

Other than dietary insufficiency and blood loss, what are other causes for Iron Deficiency Anaemia?

A

Inadequate absorption (eg Crohns)

Reduced Stomach Acid (eg from PPIs) (required to keep iron in soluble form)

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33
Q

There are many specific tests for Iron Deficiency. What is TIBC?

A

Total space available on transferrin to bind

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34
Q

There are many specific tests for Iron Deficiency. What is Ferritin?

A

Form iron takes when it is stored/deposited

Increase seen in infection/malignancy

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35
Q

There are many specific tests for Iron Deficiency. What is Transferrin Saturation?

A

Serum Iron/TIBC

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36
Q

There are many specific tests for Iron Deficiency. What would you expect in Iron Deficiency?

A

Increased TIBC

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37
Q

Define DIC

A

Coagulation pathway activation leading to diffuse fibrin deposition in micro vasculature and consumption of coagulation factors and platelets

Leads to abnormal bleeding, end organ damage, and haemolytic anaemia

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38
Q

What are the causes of DIC in Neonates?

A

Severe Asphyxia
Sepsis
RDS
NEC

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39
Q

What are the causes of DIC in older children?

A

Sepsis
Severe Trauma
Burns

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40
Q

How does DIC present?

A

Bleeding from mucosal surfaces, tracts, wounds
Microthrombi leading to renal impairment, cerebral dysfunction
ARDS
Haemolytic Anaemia

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41
Q

What is the classical blood pattern for DIC?

A

Low platelets
Low fibrinogen
Increased PT/APTT/TT

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42
Q

How should DIC be managed?

A

A to E
IV and Blood transfusions
Only transfuse platelets if uncontrolled bleeding

If fibrinogen <500 then give FFP and Cryoprecipitate

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43
Q

What is the difference between Asplenia and Hyposplenia?

A

Asplenia is the absence of the spleen due to either a congenital anomaly or surgical procedure

Hyposplenia is reduced or absent function of the spleen

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44
Q

Why is the spleen particularly important in under 4s?

A

Clears encapsulated bacteria and at this age, few other alternative routes exist

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45
Q

There are many causes of hyposplenism. Give two vascular and two haematological.

A

Haematological - Sequestration Crises, Sickle Cell

Vascular - Splenic Artery Occlusion, Splenic Vein Thrombosis

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46
Q

Name four things you would see on a blood film of Asplenism/Hyposplenism

A

Howell Jolly Bodies (Nuclear Remnants)
Heinz Bodies (Denatured Haemoglobin)
Pappenheimer Bodies (Iron Deposits)
Target Cells

47
Q

How can a Doppler be used to investigate Hyposplenism/Asplenism?

A

Assesses spleen size

Assesses direction of flow in splenic vein and portal vessels

48
Q

How is Hyposplenism managed?

A

Immunised with pneumococcal, meningococcal and haemophilus vaccines

Antimicrobial prophylaxis

Medic Alert Bracelet

49
Q

Define Sickle Cell

A

Autosomal recessive genetic mutation on chromosome 11, leading to sickle erythrocytes and subsequent haemolytic anaemia

Can be sickle trait with just one HbS (reduces severity of Malaria)

50
Q

How is Sickle Cell screened?

A

Pregnant women who are at risk are screened in pregnancy

Newborn screening heel prick at 5 days

51
Q

Give 5 complications of Sickle Cell

A 
Anaemia
Crises
Priapism
Avascular Necrosis of Hip etc
Pulmonary Hypertension
52
Q

What can you give Sickle Cell patients to prevent complications?

A

Up to date vaccinations
Antibiotic prophylaxis with Pen V

Avoid dehydration and other crises triggers

53
Q

State three treatments of Sickle Cell

A

Hydroxycarbamide (stimulates production of foetal haemaglobin)

Bone Marrow Transplant

Blood Transfusion

54
Q

State the four different types of Sickle Cell Crises

A

Vaso-Occlusive
Sequestration
Aplastic
Acute Chest

55
Q

What is a Vaso-Occlusive crisis?

A

Sickle cells clog capillaries, causing distal ischaemia

Associated with dehydration and raises haematocrit

56
Q

What is a Sequestration Crisis?

A

Red blood cells flow back into the spleen, causing an enlarged painful spleen, severe anaemia and circulatory collapse

If recurrent, will require a splenectomy

57
Q

What is an Aplastic Crisis?

A

Temporary loss of blood cell creation

Often triggered by Parvo 19

58
Q

How would an Acute Chest present in Sickle Cell? How is it managed?

A

Fever/Respiratory symptoms with new infiltrates on CXR

Antibiotics, Blood Transfusions, Ventilation

59
Q

Thalassaemia is an autosomal recessive disease of protein chains making up Haemaglobin. Describe the pathophysiology.

A

Red blood cells are fragile and break more easily, causing splenomegaly

Bone marrow expands to compensate for chronic anaemia, causing pronounced forehead and malar eminences

60
Q

Give five ways that Thalassaemias can present

A 
Fatigue
Pallor
Jaundice
Gallstones
Splenomegaly
61
Q

Name three investigations for Thalassaemia

A

FBC (Microcytic Anaemia)
Haemaglobin Electrophoresis
DNA Testing

62
Q

Alpha Thalassaemia is a defect in alpha globin chains on chromosome 16. How is it managed?

A

Monitor FBC and complications

Blood transfusions

63
Q

Beta Thalassaemia occurs due to a mutation on chromosome II. What are the three types?

A 
Thalassaemia Minor (one abnormal and one normal gene)
Thalassaemia Intermedia (two defective genes or one defective and one deleted)
Thalassaemia Major (both genes deleted, severe anaemia and failure to thrive)

Reliance on transfusions increases with more defect

64
Q

Hereditary Spherocytosis is an autosomal dominant cause of haemolytic anaemia. How can it present?

A

Jaundice/Anaemia/Gallstones

Aplastic Crises (often triggered by Parvo 19)

Haemolytic Crises (often triggered by infection)

65
Q

What would the bloods of Hereditary Spherocytosis show?

A

Raised reticulocyte and raised MCHC

66
Q

How would Hereditary Spherocytosis be managed?

A

Folate supplements
Splenectomy
Cholecystectomy

In acute onset - transfusions

67
Q

What is G6PD Deficiency?

A

X Linked abnormality common in Mediterranean/Middle Eastern/African populations

Can have crises triggered by infections/medications/broad beans

68
Q

How does G6PD Deficiency present?

A

Neonatal Jaundice

Anaemia/Intermittent Jaundice/Gall Stones

69
Q

Give 5 medications that trigger G6PD

A 
Primaquine
Ciprofloxacin
Nitrofurantoin
Trimethoprim
Sulphonylurea
70
Q

How can you diagnose G6PD?

A

Blood Films - Heinz Bodies

G6PD Enzyme Assay

71
Q

Define Leukaemia

A

Cancer of a particular line of stem cells in bone marrow (can be myeloid or lymphoid, acute or chronic)

ALL peaks between 2 and 3, ALL peaks at 2

72
Q

Describe the pathophysiology of Leukaemia

A

Excess production of a single type of white cell, leading to suppression of other cell lines (resulting in Pancytopenia)

Risk Factors - Radiation exposure, Downs, Klinefelters, Noonans

73
Q

How does Leukaemia present?

A 
Persistent fatigue
Unexplained fever
Failure to thrive
Night sweats
Bruising and Bleeding
Bone/Joint Pain(Hyperplastic Marrow)
Persistent Lymphadenopathy
74
Q

If Leukaemia is suspected, a full blood count should be done within 48 hours. What would it show?

A

Anaemia
Leukopenia
Thrombocytopenia
Increased Abnormal White Cells

75
Q

Other than FBC, what investigations are required in Leukaemia?

A

Blood Films (Blast Cells)
Bone Marrow/Lymph Node Biopsy
CT Staging

76
Q

Acute Lymphoblastic Leukaemia is the most common paediatric cancer. What other differentials could you consider?

A

Immunodeficiency
NAI
Reactive Lymphadenopthy

77
Q

What factors indicate a better prognosis in ALL?

A

Aged between 1-10
WCC<50 at diagnosis
Females
No CNS involvement

78
Q

How is ALL managed?

A

High WCC requires hydration to prevent hyperviscocity
Treat coinciding infections
Steroids if mediastinal mass
Chemo (2y if Girl, 3y if Boy)

90% survival

79
Q

What is Lymphoma?

A

Malignancy of lymphatic system, commonly divided into Hodgekins and Non Hodgekins

More common in older children

80
Q

Lymphoma aetiology is multifactorial, who is most at risk?

A

EBV

Immunosupressed (eg if solid organ transplant, or if treated for other infections in the past)

81
Q

How would Lymphoma present?

A

B Symptoms (weight loss, night sweats, fever)
Lethargy
Anorexia
Non Tender Lymphadenopathy

82
Q

How does Lymphoma present differently to Leukaemia?

A

Leukaemia may have signs of anaemia or thrombocytopenia

83
Q

How is Lymphoma staged?

A

Ann Arbor for Hodgekins or St Judes for Non Hodgekins

1) Single group of lymph nodes/single organ
2) Disease in two or more lymph nodes/organs on same side of diaphragm
3) Disease in two or more lymph nodes/organs on both sides of diaphragm
4) Diffuse involvement

‘+B if any B symptoms’

84
Q

Lymphoma is definitively managed with Chemotherapy and Radiotherapy. How would you treat Tumour Lysis Syndrome?

A

Hyper hydration

Allopurinol

85
Q

What are the three different subtypes of Non Hodgekins Lymphoma?

A

Lymphoblastic
Mature B Cell
Large Cell

86
Q

What is characteristic of Hodgekins Lymphoma on blood film?

A

Reed Sternberg Cells

87
Q

Blood results are not used to diagnose Lymphoma. What is used?

A

Lymph Node Biopsy

88
Q

What is Idiopathic Thrombocytopenic Purpura?

A

Spontaneous Thrombocytopenia causing purpuric rash (key differential for non blanching) due to type II hypersensitivity reaction against platelets

Can be spontaneous or triggered by infection

89
Q

How does ITP normally present?

A

Children <10y with history of viral illness (typically)
Symptoms onset over 24-48h hours
Bleeding/Bruising/Petichial (<1mm)or Purpuric (3-10mm) Rash

90
Q

What main differential needs to be excluded in ITP?

A

Leukaemia

91
Q

ITP is normally self limiting and patients should avoid things which could cause them to bleed. How would active bleeding be managed?

A

Prednisolone
IVIG
Blood Transfusion if required

Note: Platelet infusion would just be destroyed

92
Q

Give four causes of Pancytopenia

A

Acute Leukaemias
Bone Marrow Failure Syndromes
Infections
Megaloblastic Anaemias

93
Q

Give four causes of Vitamin B12 deficiency

A

Vegan Diet
Lack of IF
Lack of Transcobalamin
Malabsorption

94
Q

Give five causes of folate deficiency

A

Malnutrition
Malabsorption
Increased requirements (eg chronic Haemolysis)
Drugs (valproate, trimethoprim, phenytoin)
Metabolic Disorders (Lesch Nyhan Syndrome)

95
Q

How does severe B12/Folate deficiency present?

A

Subacute degeneration of Cord
Ataxia
Paraesthesia of Hands and Feet

96
Q

Why is red cell folate more reliable than serum folate?

A

Serum folate reflects recent intake

97
Q

How should B12 deficiency be treated?

A

IM Hydroxycobalamin three times weekly until Hb normalises

98
Q

How is Folate Deficiency managed?

A

Daily PO folic acid

Note:don’t treat with folate alone unless B12 is normal as it can precipitate subacute degeneration of the spinal cord

99
Q

What is a Nephroblastoma/Wilms Tumour?

A

Most common childhood tumour of the kidney
Tumour suppressor genes are strongly implicated
Median age of diagnosis is 3.5y

100
Q

How does a Nephroblastoma present?

A

Abdominal Mass
Pain
Fever
Haematuria

101
Q

One of the main differentials for a Nephroblastoma is a Neuroblastoma. How does this present differently?

A

Abdominal mass (crossing midline)
Hypertension
Bone marrow infiltration
Periorbital Ecchymosis

102
Q

Wilms Tumour requires a biopsy for definitive diagnosis and US and CT for staging. Describe the risk scoring.

A

1 - Only confined to kidney
2 - Begins to spread from kidney but can be completely removed with it
3 - Can’t be surgically respected due to LN spread
4 - Distant Metastases
5 - Bilateral tumours (can each have different stages)

103
Q

How is Wilms Tumour managed?

A

Stage 1 and 2 with surgery (Nephrectomy)

Further stages will require chemotherapy

85% cure

104
Q

What is Haemophila A?

A

X Linked Recessive deficiency in factor VIII

MILD - only requires desmopressin if surgery
MOD - bleeding is rare and normally involves soft tissue
SEV - Spontaneous Haemarthroses/most require FVIII prophylaxis

105
Q

Haemophilia A commonly presents as child starts to mobilise (small lumpy pea sized bruises). What blood result is characteristic?

A

Increased APTT

106
Q

What is Haemophilia B?

A

X linked deficiency in factor IX

Indistinguishable clinically from Haemophilia A

107
Q

How does Desmopressin work in Haemophilia A?

A

Stimulates release of VWF

108
Q

What is Von Willebrands Factor?

A

Carrier protein for factor VIII

Protects it from degradation and facilitates platelet adhesion

109
Q

What are the three subtypes of Von Willebrands Disease?

A

70% Autosomal Dominant
25% Dominant or Recessive
5% Recessive (near absence of VWF)

110
Q

What bloods are characteristic of VWD?

A

Increased APTT
Increased PFA
Decreased factor VIII

111
Q

How is VWD managed?

A

Avoid NSAIDs and IM injection
Minor bleeding - pressure/Tranexamic acid
Significant - Desmopressin
Severe - FVIII concentrate, VWF

112
Q

When would you treat ITP?

A

Generally if platelet counts <20

113
Q

Would you still consider ITP if the child had splenomegaly?

A

No

114
Q

What is the new developing treatment for ITP?

A

TPO agonists

Increasing production of platelets to compensate

Year 4 Paediatrics (15 decks)

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