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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
Other than physiological and prematurity, give three other causes of Anaemia in Infancy
Blood loss Twin to twin transfusion Haemolysis
26
Name the two common causes of Anaemia in Older Children
``` Dietary Insufficiency Blood loss (ie through menstruation) ```
27
Name the causes of Microcytic Anaemia (TAILS)
``` Thalassaemia Anaemia of Chronic Disease Iron Deficiency Lead Poisoning Sideroblastic ```
28
Name the causes of Normocytic Anaemia (3As and 2Hs)
``` Acute Blood Loss Anaemia of Chronic Disease Aplastic Anaemia Haemolytic Anaemia Hypothyroidism ```
29
Macrocytic Anaemia can be megaloblastic or normoblastic. Give examples of each.
Megaloblastic - Vit B12 and Folate | Normoblastic - Alcohol, Hypothyroidism, Liver Disease
30
Describe some classical features of Iron Deficiency Anaemia
``` Glossitis Angular Cheilitis Koilonychia Pica Hair loss ```
31
Name five investigations for Anaemia
``` FBC and Haematinics Blood film Bilirubin Direct Coombs Haemoglobin Electrophoresis ```
32
Other than dietary insufficiency and blood loss, what are other causes for Iron Deficiency Anaemia?
Inadequate absorption (eg Crohns) Reduced Stomach Acid (eg from PPIs) (required to keep iron in soluble form)
33
There are many specific tests for Iron Deficiency. What is TIBC?
Total space available on transferrin to bind
34
There are many specific tests for Iron Deficiency. What is Ferritin?
Form iron takes when it is stored/deposited Increase seen in infection/malignancy
35
There are many specific tests for Iron Deficiency. What is Transferrin Saturation?
Serum Iron/TIBC
36
There are many specific tests for Iron Deficiency. What would you expect in Iron Deficiency?
Increased TIBC
37
Define DIC
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
38
What are the causes of DIC in Neonates?
Severe Asphyxia Sepsis RDS NEC
39
What are the causes of DIC in older children?
Sepsis Severe Trauma Burns
40
How does DIC present?
Bleeding from mucosal surfaces, tracts, wounds Microthrombi leading to renal impairment, cerebral dysfunction ARDS Haemolytic Anaemia
41
What is the classical blood pattern for DIC?
Low platelets Low fibrinogen Increased PT/APTT/TT
42
How should DIC be managed?
A to E IV and Blood transfusions Only transfuse platelets if uncontrolled bleeding If fibrinogen <500 then give FFP and Cryoprecipitate
43
What is the difference between Asplenia and Hyposplenia?
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
44
Why is the spleen particularly important in under 4s?
Clears encapsulated bacteria and at this age, few other alternative routes exist
45
There are many causes of hyposplenism. Give two vascular and two haematological.
Haematological - Sequestration Crises, Sickle Cell | Vascular - Splenic Artery Occlusion, Splenic Vein Thrombosis
46
Name four things you would see on a blood film of Asplenism/Hyposplenism
Howell Jolly Bodies (Nuclear Remnants) Heinz Bodies (Denatured Haemoglobin) Pappenheimer Bodies (Iron Deposits) Target Cells
47
How can a Doppler be used to investigate Hyposplenism/Asplenism?
Assesses spleen size Assesses direction of flow in splenic vein and portal vessels
48
How is Hyposplenism managed?
Immunised with pneumococcal, meningococcal and haemophilus vaccines Antimicrobial prophylaxis Medic Alert Bracelet
49
Define Sickle Cell
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
How is Sickle Cell screened?
Pregnant women who are at risk are screened in pregnancy | Newborn screening heel prick at 5 days
51
Give 5 complications of Sickle Cell
``` Anaemia Crises Priapism Avascular Necrosis of Hip etc Pulmonary Hypertension ```
52
What can you give Sickle Cell patients to prevent complications?
Up to date vaccinations Antibiotic prophylaxis with Pen V Avoid dehydration and other crises triggers
53
State three treatments of Sickle Cell
Hydroxycarbamide (stimulates production of foetal haemaglobin) Bone Marrow Transplant Blood Transfusion
54
State the four different types of Sickle Cell Crises
Vaso-Occlusive Sequestration Aplastic Acute Chest
55
What is a Vaso-Occlusive crisis?
Sickle cells clog capillaries, causing distal ischaemia | Associated with dehydration and raises haematocrit
56
What is a Sequestration Crisis?
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
What is an Aplastic Crisis?
Temporary loss of blood cell creation | Often triggered by Parvo 19
58
How would an Acute Chest present in Sickle Cell? How is it managed?
Fever/Respiratory symptoms with new infiltrates on CXR Antibiotics, Blood Transfusions, Ventilation
59
Thalassaemia is an autosomal recessive disease of protein chains making up Haemaglobin. Describe the pathophysiology.
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
Give five ways that Thalassaemias can present
``` Fatigue Pallor Jaundice Gallstones Splenomegaly ```
61
Name three investigations for Thalassaemia
FBC (Microcytic Anaemia) Haemaglobin Electrophoresis DNA Testing
62
Alpha Thalassaemia is a defect in alpha globin chains on chromosome 16. How is it managed?
Monitor FBC and complications | Blood transfusions
63
Beta Thalassaemia occurs due to a mutation on chromosome II. What are the three types?
``` 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
Hereditary Spherocytosis is an autosomal dominant cause of haemolytic anaemia. How can it present?
Jaundice/Anaemia/Gallstones Aplastic Crises (often triggered by Parvo 19) Haemolytic Crises (often triggered by infection)
65
What would the bloods of Hereditary Spherocytosis show?
Raised reticulocyte and raised MCHC
66
How would Hereditary Spherocytosis be managed?
Folate supplements Splenectomy Cholecystectomy In acute onset - transfusions
67
What is G6PD Deficiency?
X Linked abnormality common in Mediterranean/Middle Eastern/African populations Can have crises triggered by infections/medications/broad beans
68
How does G6PD Deficiency present?
Neonatal Jaundice Anaemia/Intermittent Jaundice/Gall Stones
69
Give 5 medications that trigger G6PD
``` Primaquine Ciprofloxacin Nitrofurantoin Trimethoprim Sulphonylurea ```
70
How can you diagnose G6PD?
Blood Films - Heinz Bodies | G6PD Enzyme Assay
71
Define Leukaemia
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
Describe the pathophysiology of Leukaemia
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
How does Leukaemia present?
``` Persistent fatigue Unexplained fever Failure to thrive Night sweats Bruising and Bleeding Bone/Joint Pain(Hyperplastic Marrow) Persistent Lymphadenopathy ```
74
If Leukaemia is suspected, a full blood count should be done within 48 hours. What would it show?
Anaemia Leukopenia Thrombocytopenia Increased Abnormal White Cells
75
Other than FBC, what investigations are required in Leukaemia?
Blood Films (Blast Cells) Bone Marrow/Lymph Node Biopsy CT Staging
76
Acute Lymphoblastic Leukaemia is the most common paediatric cancer. What other differentials could you consider?
Immunodeficiency NAI Reactive Lymphadenopthy
77
What factors indicate a better prognosis in ALL?
Aged between 1-10 WCC<50 at diagnosis Females No CNS involvement
78
How is ALL managed?
High WCC requires hydration to prevent hyperviscocity Treat coinciding infections Steroids if mediastinal mass Chemo (2y if Girl, 3y if Boy) 90% survival
79
What is Lymphoma?
Malignancy of lymphatic system, commonly divided into Hodgekins and Non Hodgekins More common in older children
80
Lymphoma aetiology is multifactorial, who is most at risk?
EBV | Immunosupressed (eg if solid organ transplant, or if treated for other infections in the past)
81
How would Lymphoma present?
B Symptoms (weight loss, night sweats, fever) Lethargy Anorexia Non Tender Lymphadenopathy
82
How does Lymphoma present differently to Leukaemia?
Leukaemia may have signs of anaemia or thrombocytopenia
83
How is Lymphoma staged?
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
Lymphoma is definitively managed with Chemotherapy and Radiotherapy. How would you treat Tumour Lysis Syndrome?
Hyper hydration | Allopurinol
85
What are the three different subtypes of Non Hodgekins Lymphoma?
Lymphoblastic Mature B Cell Large Cell
86
What is characteristic of Hodgekins Lymphoma on blood film?
Reed Sternberg Cells
87
Blood results are not used to diagnose Lymphoma. What is used?
Lymph Node Biopsy
88
What is Idiopathic Thrombocytopenic Purpura?
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
How does ITP normally present?
Children <10y with history of viral illness (typically) Symptoms onset over 24-48h hours Bleeding/Bruising/Petichial (<1mm)or Purpuric (3-10mm) Rash
90
What main differential needs to be excluded in ITP?
Leukaemia
91
ITP is normally self limiting and patients should avoid things which could cause them to bleed. How would active bleeding be managed?
Prednisolone IVIG Blood Transfusion if required Note: Platelet infusion would just be destroyed
92
Give four causes of Pancytopenia
Acute Leukaemias Bone Marrow Failure Syndromes Infections Megaloblastic Anaemias
93
Give four causes of Vitamin B12 deficiency
Vegan Diet Lack of IF Lack of Transcobalamin Malabsorption
94
Give five causes of folate deficiency
Malnutrition Malabsorption Increased requirements (eg chronic Haemolysis) Drugs (valproate, trimethoprim, phenytoin) Metabolic Disorders (Lesch Nyhan Syndrome)
95
How does severe B12/Folate deficiency present?
Subacute degeneration of Cord Ataxia Paraesthesia of Hands and Feet
96
Why is red cell folate more reliable than serum folate?
Serum folate reflects recent intake
97
How should B12 deficiency be treated?
IM Hydroxycobalamin three times weekly until Hb normalises
98
How is Folate Deficiency managed?
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
What is a Nephroblastoma/Wilms Tumour?
Most common childhood tumour of the kidney Tumour suppressor genes are strongly implicated Median age of diagnosis is 3.5y
100
How does a Nephroblastoma present?
Abdominal Mass Pain Fever Haematuria
101
One of the main differentials for a Nephroblastoma is a Neuroblastoma. How does this present differently?
Abdominal mass (crossing midline) Hypertension Bone marrow infiltration Periorbital Ecchymosis
102
Wilms Tumour requires a biopsy for definitive diagnosis and US and CT for staging. Describe the risk scoring.
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
How is Wilms Tumour managed?
Stage 1 and 2 with surgery (Nephrectomy) Further stages will require chemotherapy 85% cure
104
What is Haemophila 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
Haemophilia A commonly presents as child starts to mobilise (small lumpy pea sized bruises). What blood result is characteristic?
Increased APTT
106
What is Haemophilia B?
X linked deficiency in factor IX Indistinguishable clinically from Haemophilia A
107
How does Desmopressin work in Haemophilia A?
Stimulates release of VWF
108
What is Von Willebrands Factor?
Carrier protein for factor VIII | Protects it from degradation and facilitates platelet adhesion
109
What are the three subtypes of Von Willebrands Disease?
70% Autosomal Dominant 25% Dominant or Recessive 5% Recessive (near absence of VWF)
110
What bloods are characteristic of VWD?
Increased APTT Increased PFA Decreased factor VIII
111
How is VWD managed?
Avoid NSAIDs and IM injection Minor bleeding - pressure/Tranexamic acid Significant - Desmopressin Severe - FVIII concentrate, VWF
112
When would you treat ITP?
Generally if platelet counts <20
113
Would you still consider ITP if the child had splenomegaly?
No
114
What is the new developing treatment for ITP?
TPO agonists | Increasing production of platelets to compensate

Year 4 Paediatrics (15 decks)

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