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Phase 3a Jemima > Paediatrics - Haematology, oncology and immunology > Flashcards

Paediatrics - Haematology, oncology and immunology Flashcards

1
Q

what are causes of anaemia in infancy

A

physiologic anaemia of infancy
anaemia of prematurity
blood loss
haemolysis
twin twin transfusion
haemolytic disease of the newborn
hereditary spherocytosis
G6PD deficiency

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2
Q

what is physiological anaemia of infancy

A

there is a normal dip in a hemoglobin around 6 to 9 weeks of age in healthy term babies
this is caused by high oxygen delivery due to high haemoglobin at birth causing negative feedback and reduced production of EPO by the kidneys, reducing haemoglobin production

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3
Q

what are causes of anaemia of prematurity

A

less time in utero receiving iron from the mother
red blood cell creation cannot keep up with rapid growth in the first few weeks
reduced erythropoietin levels
blood tests remove a significant portion of their circulating volume

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4
Q

what is haemolytic disease of the newborn

A

haemolysis and jaundice in the neonate due to incompatibility between the rhesus antigens on the surface of the red blood cells of the mother and fetus

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5
Q

what test can be done to check for immune haemolytic anaemia

A

a direct Coombs test - will be positive

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6
Q

what are key causes of anaemia in older children

A

iron deficiency anemia - normally secondary to dietary insufficiency
blood loss - mentruation in older girls

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7
Q

what are rarer causes on anaemia in children

A

sickle cell anaemia
thalassemia
leukaemia
hereditary spherocytosis
hereditary elliptocytosis
sideroblastic anaemia

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8
Q

what is a common cause of blood loss causing chronic anaemia particularly in developing countries

A

helminth infection - roundworms, hookworms and whipworms

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9
Q

what are causes of microcytic anaemia

A

TAILS
thalassemia
anaemia of chronic disease
iron deficiency anemia
lead poisoning
sideroblastic anaemia

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10
Q

what are causes of normocytic anaemia

A

3 As and 2 Hs
Acute blood loss
Anaemia of chronic disease
aplastic anaemia
Haemolytic anaemia
hypothyroidism

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11
Q

what are causes of megaloblastic macrocytic anaemia

A

B12 deficiency
folate deficiency

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12
Q

what are causes of normoblastic macrocytic anaemia

A

alcohol
reticulocytosis
hypothyroidism
liver disease
drugs such as azathioprine

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13
Q

what are symptoms of anaemia

A

tiredness
shortness of breath
headaches
dizziness
palpitations
worsening of other conditions

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14
Q

what are symptoms specific of iron deficiency anemia

A

Pica - dietary craving of non food items
hair loss

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15
Q

what are signs of anaemia

A

pale skin
conjunctival pallor
tachycardia
raised respiratory rate

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16
Q

what are signs specific to iron deficiency anaemia

A

koilonychia - spoon shaped nails
angular chelitis
atrophic glossitis - atrophy of papillae
brittle hair and nails

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17
Q

what investigations are done for anaemia

A

full blood count
blood film
reticulocyte count - high level indicates active production of RBC w
ferritin
B12 and folate
bilirubin
direct coombs test
haemoglobin electrophoresis

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18
Q

what does a high reticulocyte count infer about the type of anaemia present

A

if there is a high reticulocyte count it shows that there is active production of red blood cells to replace lost cells, which normally indicates the anaemia is due to haemolysis or blood loss

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19
Q

what type of leukaemia is most common in children

A

acute lymphoblastic leukaemia

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20
Q

what age is the peak of ALL development

A

2-3 years

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21
Q

what are risk factors for developing leukaemia in childhood

A

radiation exposure
downs syndrome
kleinfelter syndrome
nonnan syndrome
fanconis anaemia

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22
Q

how does leukaemia present

A

persistent fatigue
unexplained fever
failure to thrive
weight loss
night sweats
pallor
petechiae and abnormal bruising
unexplained bleeding
abdominal pain
generalised lymphadenopathy
unexplained or persistent bone or joint pain
hepatosplenomegaly

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23
Q

how is leukaemia diagnosed in children

A

NICE recommends referral of any child with unexplained petechiae or hepatomegaly
urgent full blood count within 48 hours
blood film - shows blast cells
bone marrow biopsy
lymph node biopsy
chest XR
CT
genetic analysis and immunophenotyping

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24
Q

how is leukaemia managed in childhood

A

paediatric oncology and MDT
- chemotherapy
- radiotherapy
- bone marrow transplant
- surgery

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25
Q

what are complications of chemotherapy

A

failure to treat the leukaemia
stunted growth and development
immunodeficiency and infections
neurotoxicity
infertility
secondary malignancy
cardiotoxicity

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26
Q

what is the prognosis of ALL in children

A

overall cure rate is around 80%

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27
Q

what is immune thrombocytopenia (ITP)

A

condition characterised by spontaneous low platelet count causing a purpuric rash due to immune dysregulation

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28
Q

what type of immune reaction is ITP

A

type II hypersensitivity reaction - production of antibodies that target and destroy platelets

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29
Q

how does ITP present

A

usually presents in children under 10
often there is history of a recent viral illness
bleeding - from gums, epistaxis or menorrhagia
bruising
petechial or purpuric rash caused by bleeding under the skin (non blanching)

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30
Q

how is ITP diagnosed

A

condition is diagnosed by doing an urgent full blood count for the platelet count
exclude other causes of low platelet count

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31
Q

what is the management of ITP

A

dependent on how low the platelet count is
usually no treatment is required and patients are monitored until platelets return to normal
if severe thrombocytopenia or the patient is actively bleeding then give: prednisolone, IV immunoglobulins, blood transfusions and platelet transfusions (temporary)

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32
Q

why do platelet transfusions only work temporarily in ITP

A

because the antibodies against platelets will begin destroying the transfused platelets as soon as they are infused

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33
Q

what advice should be given to someone with a diagnoses of ITP

A

Avoid contact sports
Avoid intramuscular injections and procedures such as lumbar punctures
Avoid NSAIDs, aspirin and blood thinning medications
Advice on managing nosebleeds
Seek help after any injury that may cause internal bleeding, for example car accidents or head injuries

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34
Q

what are complications of ITP

A

Chronic ITP
Anaemia
Intracranial and subarachnoid haemorrhage
Gastrointestinal bleeding

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35
Q

what is the pathophysiology of sickle cell anaemia

A

during foetal development fetal haemoglobin production decreases around 32-36 weeks and adult haemoglobin increases. There is a transition from HbF to HbA, and by 6 months of age there is very little HbF.
Patients with sickle cell disease have an abnormal variant called HbS which results in the sickling of red blood cells

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36
Q

what is the inheritance pattern of sickle cell disease and the genetic mutation that causes it

A

autosomal recessive
caused by a point mutation in the beta haemoglobin gene on chromosome 11

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37
Q

what is the link between sickle cell and malaria

A

sickle cell disease is more common in areas traditionally affected by malaria such as Africa, India, the Middle east and the Caribbean.
having sickle cell trait reduces the severity of malaria

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38
Q

when is sickle cell screened for in the UK

A

newborn spot test at around 5 days old
pregnant women at a higher risk of being carriers are offered testing

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39
Q

what are complications of sickle cell disease

A

anaemia
increased risk of infection
chronic kidney disease
sickle cell crisis
stroke
avascular necrosis in large joints
pulmonary hypertension
gall stones
priapism (painful and persistent penile erections)

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40
Q

what is sickle cell crisis

A

refers to a spectrum of acute exacerbations caused by sickle cell disease which range from mild to life threatening
they can occur spontaneously or triggered by dehydration, infection, stress or cold weather

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41
Q

what is a vaso-occlusive crisis

A

known as a painful crisis - caused by the sickle shaped red cells blocking capillaries causing distal ischaemia

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41
Q

how is sickle cell crisis managed

A

low threshold for admission to hospital
treating infections that may have triggered the crisis
keep warm
good hydration (IV fluids may be required)
analgesia (NSAIDS should be avoided if there is renal impairment)

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42
Q

how does vaso-occlusive crisis

A

pain and swelling in the hands and feet
can affect the chest, back or other areas
fever
can causing priapism in men

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43
Q

what is splenic sequestration crisis

A

caused by red blood cells blocking blood flow within the spleen. It causes an acutely enlarged and painful spleen
blood pooling in the spleen can lead to severe anaemia and hypovolaemic shock

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44
Q

what is the management of splenic sequestration crisis

A

considered an emergency
management is supportive with blood transfusions, and fluid resuscitation to treat anaemia and shock

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45
Q

what can splenic sequestration crisis lead to

A

splenic infarction - leads to hyposplenism and susceptibility to infections particularly to encapsulated bacteria (strep. pneumoniae and Haem. influenzae

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46
Q

what can be done to prevent sequestration crises

A

splenectomy - used in recurrent cases

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47
Q

what is aplastic crisis

A

it is a temporary absence in the creation of new red blood cells in sickle cell

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48
Q

what can trigger aplastic crisis in sickle cell disease

A

parvovirus B19

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49
Q

what are affects of aplastic crisis

A

significant anaemia

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50
Q

what is the treatment of aplastic crisis

A

blood transfusions
supportive management

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51
Q

how long does it take aplastic crisis to resolve

A

usually resolves spontaneously within a week

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52
Q

what is acute chest syndrome

A

this is when vessels supplying the lungs become clogged with red blood cells

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53
Q

what can trigger an acute chest syndrome

A

vaso-occlusive crisis
fat embolism
infection

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54
Q

how does acute chest syndrome present

A

presents with fever
shortness of breath
chest pain
cough
hypoxia

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55
Q

what will a chest Xray show in acute chest syndrome

A

pulmonary infiltrates

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56
Q

how is acute chest syndrome managed

A

medical emergency
analgesia
good hydration - IV fluids
antibiotics or antivirals for infection
blood transfusions
incentive spirometry using a machine that encourages effective and deep breathing
respiratory support with oxygen, non invasive ventilation or mechanical ventilation

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57
Q

what is the general management for sickle cell disease

A

specialist MDT
avoid triggers or crisis such as dehydration
up to date vaccines
antibiotic prophylaxis typically with penicillin V
hydroxycarbamide - stimulates HbF
crizanlizumab
blood transfusions
bone marrow transplant

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58
Q

how does hydroxycarbamide work

A

works by stimulating the production of fetal haemoglobin which doesnt lead to sickling of red blood cells
- reduces frequency of vaso-occlusive crises improves anaemia and may extend lifespan

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59
Q

what is crizanlizumab

A

it is a monoclonal antibody that targets P-selectin
P-selectin is an adhesion molecule found on endothelial cells on the inside walls of blood vessels and platelets
it prevents red blood cells from sticking to the blood vessel wall

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60
Q

what is thalassaemia

A

it is a genetic defect in the protein chains that make up haemoglobin
- defects in the alpha globin chains leads to alpha thalasaemia
- defects in the beta globin chains leads to beta thalassaemia

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61
Q

what is the inheritance pattern of thalassaemia

A

autosomal recessive

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62
Q

why does thalassaemia cause splenomegaly

A

because in thalassaemia the red blood cells are more fragile and broken down easier, the spleen filters and removes the broken down red blood cells at a more rapid rate leading the splenomegaly

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63
Q

why does thalassaemia lead to prominent features such as a pronounced forehead and cheekbones

A

because the bone marrow expands to produce extra red blood cells to compensate for the chronic anaemia
this causes susceptibility to fractures and prominent features

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64
Q

what are potential signs and symptoms of thalassaemia

A

microcytic anaemia
fatigue
pallor
jaundice
gallstones
splenomegaly
poor growth and development
pronounced forehead and malar eminences

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65
Q

how is thalassaemia diagnosed

A

full blood count shows microcytic anaemia
haemoglobin electrophoresis is used to diagnose globin abnormalities
DNA testing
pregnant women in the UK are offered a screening test for thalassaemia at booking

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66
Q

why does iron overload happen in thalassaemia

A

it happens as a result of the faulty creation of ref blood cells, recurrent transfusions and increased absorption of irion in the gut in response to anaemia

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67
Q

how is iron overload managed in thalassaemia

A

patients have serum ferritin levels monitored to check for iron overload
limiting of transfusions
performing iron chelation

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68
Q

what are the symptoms of iron overload in thalassaemia

A

fatigue
liver cirrhosis
infertility
impotence
heart failure
arthritis
diabetes
osteoporosis and joint pain

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69
Q

what is the chromosomal abnormality in alpha thalassaemia

A

mutation on chromosome 16

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70
Q

what is the management of alpha thalassaemia

A

monitoring of full blood count
monitoring of complications
blood transfusions
splenectomy may be performed
bone marrow transplant may be curative

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71
Q

what is the genetic defect in beta thalassaemia

A

caused by mutation on chromosome 11

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72
Q

what are the different types of beta thalassemia

A

thalassaemia minor
thalassaemia intermedia
thalassaemia major

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73
Q

what is thalassaemia minor

A

this is when patients are carriers of an abnomally functioning beta globin gene
- one normal one abnormal
- causes a mind microcytic anaemia

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74
Q

what is thalassaemia intermedia

A

patients have two abnormal copies of the beta globin gene which can be either two defective or one defective and one deletion
- causes more significant microcytic anaemia
- require monitoring and some transfusions
- may require iron chelation

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75
Q

what is thaassaemia major

A

homozygous for the deletion genes meaning they have no functioning beta globin genes at all
the most severe form usually presents with severe aneamia and failure to thrive in early childhood

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76
Q

what does thalassaemia major cause

A

severe microcytic anaemia
splenomegaly
bone deformities

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77
Q

what is the management of thalassaemia major

A

regular transfusions
iron chelation
splenectomy
bine marrow transplant

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78
Q

what is hereditary spherocytosis

A

a condition where the red blood cells are sphere shaped making them fragile and easily destroyed when passing through the spleen

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79
Q

what is the inheritance pattern of hereditary spherocytosis

A

autosomal dominant

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80
Q

how does hereditary spherocytosis present

A

jaundice
anaemia
gallstones
splenomegaly
episodes of haemolytic crisis
aplastic crisis

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81
Q

what can cause haemlytic crisis in hereditary spherocytosis

A

infections

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82
Q

what can cause aplastic crisis in hereditary spherocytosis

A

infection with parvovirus
- presents with anaemia, haemolysis and jaundice

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83
Q

how is hereditary spherocytosis diagnosed

A

family history
clinical features
spherocytes on blood film
MCHC will be raised
reticulocytes will be raised

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84
Q

what is the management if hereditary spherocytosis

A

folate supplementation
splenectomy
removal of the gallbladder may be required
transfusions during acute crisis

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85
Q

what is G6PD deficiency

A

it is a defect in the G6PD enzyme in cells which is responsible for protecting cells from ROS damage

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86
Q

what is the inheritance pattern of G6PD deficiency

A

X linked recessive

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87
Q

what are triggers of G6PD crisis

A

infections
medications
fava beans

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88
Q

what is the pathophysiology of G6PD deficiency

A

G6PD prevents cell damage due to ROS, which are reactive molecules produced during normal cell metabolism and in higher quantities during cell stress
G6PD enzyme is particularly important in red blood cells and a deficiency in G6PD makes cells more vulnerable to ROS leading to haemolysis of red blood cells

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89
Q

what is the presentation of G6PD

A

neonatal jaundice
anaemia
intermittent jaundice - in response to triggers
gall stones
splenomegaly

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90
Q

what can be seen on a blood film in G6PD deficiency

A

Heinz bodies - denatured haemoglobin seen within red blood cells

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91
Q

how is G6PD deficiency diagnosed

A

by doing a G6PD enzyme assay

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92
Q

what is the management of G6PD deficiency

A

people should avoid triggers where possible

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93
Q

what medications should be avoided in G6PD deficiency

A

primaquine
ciprofloxacin
nitrofurantoin
trimethoprim
sulfonylureas
sulfasalazine and other sulphonamide drugs

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94
Q

what is haemolytic disease of the newborn

A

due to incompatibility between mother and babies resus group or ABO group causing the babies red blood cells to break up more quickly that usual

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95
Q

how does haemolytic disease of the newborn occur

A

when a small amount of babies blood is exposed to the mothers blood circulation during pregnancy, the mother produces antibodies to the babies blood. these antibodies are able to cross the placenta and enter the babies circulation causing red cell haemolysis

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96
Q

how is haemolytic disease of the newborn diagnosed

A

direct antibody test - DAT
either on the cord blood or directly on babies blood

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97
Q

what are signs of haemolytic disease of the newborn in babies

A

high bilirubin levels causing jaundice
anaemia
respiratory distress
lethargy
increased effort of breathing
breathlessness

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98
Q

how is haemolytic disease of the newborn treated

A

jaundice - phototherapy
blood transfusions
folic acid
monitoring of baby - follow up clinic checking babies haemoglobin levels

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99
Q

what is fanconi anaemia

A

inherited disease caused by mutations in the FA genes (23 different genes) causing bone marrow failure, where the bone marrow doesnt create healthy blood cells and platelets

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100
Q

how many children born with fanconi anaemia have physical abnormalities

A

about 75%

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101
Q

how many people with fanconi anaemia have bone marrow failure or lack of function

A

about 90%

102
Q

how many people with fanconi anaemia develop certain cancers such as leukaemia

A

between 10-30%

103
Q

what are common cancers people with fanconi anaemia develop

A

acute myeloid leukaemia
skin cancer
cancer of the head and neck

104
Q

what are common fanconi anaemia symptoms

A

anaemia - fatigue, pallor, work of breathing, tachycardia, headaches
bone marrow failure - increased infections, excessive bleeding
cancer - common cancer sx
physical abnormalities

105
Q

what physical abnormalities are common in people with fanconi anaemia

A

odd shaped thumbs - two on one hand or none
microcephaly
hydrocephaly
hearing loss or difficulty
skin that has large light brown coloured patches called cafe-au-lait spots
scoliosis

106
Q

how is fanconi anaemia diagnosed

A

physical abnormalities
progressive bone marrow failure
cancer
bloods - complete blood count, reticulocyte count, basic metabolic panel
bone marrow biopsy
MRI
ultrasound

107
Q

by what age do most children with fanconi anaemia develop bone marrow failure symptoms

A

10

108
Q

what genetic tests may be used to diagnose fanconi anaemia

A

chromosome breakage test
genetic screening
in pregnancy may perform amniocentesis and chorionic villus sampling

109
Q

what is the management for fanconi anaemia

A

bone marrow transplant
androgen therapy - helps stimulate your red blood cell production
synthetic growth factors - stimulates bone marrow
surgery - correct physical abnormalities or repair damaged organs

110
Q

what causes haemophilia A

A

deficiency of factor 8

111
Q

what causes haemophilia B

A

deficiency in factor 9

112
Q

what is the inheritance pattern of haemophilia

A

both are X linked recessive diseases

113
Q

what are the features of haemophilia A/B

A

bleeding excessively in response to minor trauma
spontaneous bleeding without any trauma
in neonates can present with intercranial haemorrhage, haematomas and cord bleeding
haemarthrosis - ankle, knee, elbow
compartment syndrome
bleeding into the oral mucosa
epistaxis
GI bleeding
haematuria

114
Q

how is haemophilia diagnosed

A

bleeding scores
coagulation factor assays
genetic testing

115
Q

what is the management of haemophilia

A

IV replacement of affected clotting factors
- need to monitor this as there can be formation of antibodies against treatment

116
Q

what is von willebrand disease

A

bleeding disorder that keeps blood from clotting

117
Q

what are symptoms of von willebrand disease

A

epistaxis
prolonged bleeding from minor injury
unexplained bruising
iron deficiency anaemia
post surgical bleeding
heavy menstrual bleeding
post partum haemorrhage
blood in stool haematuria

118
Q

what causes von willebrand disease

A

deficiency of the pro-von willebrand factor which is a part of haemostasis

119
Q

what is the pathophysiology of von willebrand disease

A

normally pro-vWF undergoes cleavage and the propeptide and mature von willebrand factor are secreted into the lumen
it functions as a carrier for factor 8 to maintain its levels and help in platelet adhesion and binding to endothelial components post injury
with a deficiency in von willebrand factor will lead to increased bleeding tendency

120
Q

what are the types of von willebrand disease

A

type 1: autosomal dominant caused by a partial deficiency in von willebrand factor
type 2: autosomal dominant disease caused by a defect in von willebrand factor
type 3: autosomal recessive caused by a complete defect

121
Q

how is von willebrand disease diagnosed

A

complete blood count
platelet aggregation tests
activated partial thromboplastin time test (APTT)
prothrombin time
fibrinogen test
von villebrand factor antigen
ristocetin cofactor - evaluates von willebrand factor activity

122
Q

how is von willebrand disease treated

A

desmopressin - used to boost von willebrand levels
von willebrand factor infusions
antifibrinolytics
birth control pills - helps with menstrual bleeding

123
Q

what is microcytic anaemia

A

this happens with red blood cells are smaller than usual because they dont have enough haemoglobin

124
Q

what conditions can cause microcytic anaemia

A

iron deficiency
thalassaemia
sideroblastic anaemia
anaemia of chronic disease
lead poisoning

125
Q

what are symptoms of microcytic anaemia

A

fatigue and dizziness
pallor
tachycardia
shortness of breath
dry skin
skin that bruises easily

126
Q

how do healthcare providers diagnose microcytic anaemia

A

complete blood count
peripheral blood smear
reticulocyte count

127
Q

what is the most common type of leukaemia in children

A

ALL

128
Q

what can increase the chance of leukaemia in childhood

A

inherited disorders such as Li-fraumeni syndrome, down syndrome, klinefelter
inherited immune system issues
first generation family member with leukaemia
history of exposure to high levels of radiation, chemotherapy or chemicals
history of immune system suppression

129
Q

what are the types of childhood leukaemia

A

ALL - most common
AML - second most common
hybrid/mixed leukaemia
CML - rare in children
CLL - very rare in children
juvenile myelomonocytic leukaemia

130
Q

what are symptoms of leukaemia in children

A

fatigue
pallor
easy bruising or bleeding
extreme fatigue or weakness
shortness of breath
coughing
bone swelling or pain
swelling in the abdomen, face, arms, groin etc
swelling above collarbone
loss of appetite or weight loss
headaches, seizures
vomiting
rashes
gum recession

131
Q

how do you diagnose leukaemia

A

bloods - look at cell counts
bone marrow aspiration and biopsy
lumbar puncture
blood smear

132
Q

how is leukaemia treated in children

A

antibiotics if the child has any infections, blood transfusions
chemotherapy
targeted therapy - monoclonal antibodies
stem cell transplant
CAR-T

133
Q

what are the most common solid tumours affecting children and adolescents

A

brain tumours

134
Q

what are symptoms of brain tumours in children

A

signs of increased intercranial pressure
- headaches
- seizures
- nausea and vomiting
- irritability
- lethargy and drowsiness
- personality and mental activity changes
- brain tissue dysfunction depending on where the tumour is located
- macrocephaly in infants whos skull bones havent fully fused yet
- coma and death if left untreated

135
Q

how are brain tumours diagnosed in children

A

child experiencing brain tumour symptoms should be thoroughly evaluated by a paediatrician, paediatric neurologist
MRI
biopsy

136
Q

what are the types of brain tumours in children

A

primary
metastatic
benign
malignant

137
Q

what cancer accounts for about half a=of all childhood brain tumours

A

astrocytomas - most common in children between 5-8

138
Q

what are astrocytomas

A

they are tumours which develop from glial cells called astrocytes

139
Q

what are the four main types of astrocytomas in children

A

pilocytic astrocytoma (grade 1): slow growing, most common, Often cystic
diffuse astrocytoma (grade 2): infiltrates surrounding brain tissue making complete removal more difficult
anaplastic astrocytoma (grade 3): malignant
glioblastoma multiforme (grade 4): most malignant, grows rapidly and causes pressure

140
Q

what are other paediatric brain tumours

A

brain stem gliomas
choroid plexus tumours
craniopharyngiomas - benign near pituitary
ependymomas - brain and spinal cord in CSF
germ cell tumours
medulloblastomas - form in cerebellum, account for 15% of brain tumours in children
optic nerve gliomas

141
Q

what is the treatment for paediatric brain tumours

A

surgery - biopsy and removal
follow up care post surgery - physio, SALT
radiation therapy
chemotherapy

142
Q

what are signs of brain tumours in children

A

pronounced or swollen fontanelle in babies
changes in eye movement
confusion and irritability
balance issues
hearing issues
seizures
slurring of speech
walking issues
swallowing issues
weakness or drooping of one side of the face
weakness or sensation change in arm or leg

143
Q

what are risk factors for pardiatric brain tumours

A

younger age - younger than 5
exposure to radiation
weakened immune system
genetic syndromes that run in the family - neurofibromatosis 1 and 2, tuberous sclerosis, gorlin syndrome, turcot syndrome, cowden syndrome

144
Q

what is Wilms tumour

A

it is a specific type of tumour affecting the kidney in children, typically under the age of 5

145
Q

how does Wilms tumour present

A

mass in the abdomen
abdominal pain
haematuria
lethargy
fever
hypertension
weight loss

146
Q

how is wilms tumour diagnosed

A

ultrasound of the abdomen to visualise the kidneys
CT or MRI can be used to stage the tumour
biopsy to identify the histology

147
Q

how is Wilms tumour managed

A

surgical excision of the tumour along with the affected kidney - nephrectomy
adjuvant treatment - chemotherapy and radiotherapy

148
Q

what is neuroblastoma

A

it is a cancer that develops from immature nerve cells - commonly arise in and around the adrenal glands, however they can also develop in other areas of the abdomen and in the chest, neck and near the spine

149
Q

what age group do neuroblastomas commonly affect

A

children 5 or under

150
Q

what are symptoms of neuroblastoma in the abdomen

A

abdominal pain
a mass under the skin which isnt tender
changes in bowel habits such as diarrhoea and constipation

151
Q

what are symptoms of neuroblastoma in the chest

A

wheeze
chest pain
changes in the eyes - ptosis and unequal pupil size

152
Q

what are non specific signs of neuroblastoma

A

lumps of tissue under the skin
eyeballs that seem to protrude from the sockets - proptosis
dark circles similar to bruises around the eyes
back pain
fever
unexplained weight loss
bone pain

153
Q

what is the cause of neurofibromas

A

mutation in neuroblasts (immature nerve cells) causing a neuroblastoma

154
Q

what are complications of neuroblastomas

A

metastasis of the disease
spinal cord compression
signs and symptoms caused by tumour secretions - paraneoplastic syndrome

155
Q

how is neuroblastoma diagnosed

A

physical examination and history
urine and blood tests
imaging tests - X ray, CT, ultrasound, MRI
biopsy
bone marrow aspiration

156
Q

how is neuroblastoma staged

A

using CT/MRI (can also be done with other imaging tests)
stages range from 0-IV

157
Q

how is neuroblastoma treated

A

surgery
chemotherapy
radiation therapy
bone marrow transplant - autologous
immunotherapy
MIBG radiation therapy

158
Q

what is retinoblastoma

A

eye cancer that starts off as a growth of the cells in the retina

159
Q

what are symptoms of retinoblastoma

A

white colour in the centre of the eye when light is shone in the eye
eye redness
eye swelling
eyes that seem to be looking in different directions
vision loss

160
Q

what are risk factors for developing retinoblastoma

A

young age - typically diagnosed by 2
DNA mutations that run in families - tend to get retinoblastoma younger and tend to get it in both eyes

161
Q

what are complications of retinoblastoma

A

cancer returns - need good follow up
increased risk of other cancers - bone, bladder, breast, hodgkin, lung, melanoma, pineoblastoma, soft tissue sarcoma

162
Q

can retinoblastoma be prevented

A

no but in those with an increased risk care can be planned to manage risk
- eye exams from birth
- regular screening

163
Q

how is retinoblastoma diagnosed

A

eye exam - testing vision and using an ophthalmoscope to look inside the eye
imaging tests - ultrasound and MRI
genetic testing - look at the RB1 gene

164
Q

how is retinoblastoma treated

A

chemotherapy - whole body, into an artery near the eye or injected into the eye
cryotherapy
laser therapy - transpupillary thermotherapy
radiation
surgery to remove the eye

165
Q

what is hepatoblastoma

A

it is a rare tumour that originates in cells in the liver. It is the most common cancerous liver tumour in early childhood (around 5)

166
Q

what is the most common side for hepatoblastoma metastasis

A

lungs

167
Q

what group of children in hepatoblastoma the most common in

A

caucasian
boys
under 5
in children who were born very prematurely with low birth weight

168
Q

what genetic conditions are associated with hepatoblastoma

A

Beckwith-wiedemann syndrome - Wilms, kidney failure, genitourinary malformations and gonad abnormalities
familial adenomatous polyposis
hemihypertrophy - where one limb on one side grows faster than on the other

169
Q

what are signs and symptoms of hepatoblastoma

A

A large mass in the abdomen
Swollen abdomen
Weight loss
Decreased appetite
Vomiting
Jaundice (yellowing of eyes and skin)
Itchy skin
Anemia
Back pain

170
Q

how is hepatoblastoma diagnosed

A

Alpha-fetoprotein test
CT or CAT scan
MRI
bloods - evaluate liver function
biopsy
bone scan

171
Q

how is hepatoblastoma treated

A

resection of the tumour
chemotherapy prior to surgery
continuous follow up care

172
Q

what is the most common type of bone cancer in children

A

osteosarcoma

173
Q

where do osteosarcomas occur most commonly

A

bones on either side of the knee (tibia or femur)
upper arm

174
Q

what age group is osteosarcoma most common in

A

2/3 of cases occur between the ages of 10-14
male excess emerges at around 15-16

175
Q

what is the survival rate of osteosarcoma

A

65% of children will survive of 5 years or more after the diagnosis
patients with localised disease have a higher survival rate at 60-78% (much lover in metastatic disease)

176
Q

what are the symptoms of osteosarcoma

A

bone pain - may come and go initially and then becomes persistent (unresponsive to NSAIDS)
pain that is worse at night
tenderness
redness
swelling
pathological fractures
palpation may reveal soft tissue mass

177
Q

how is osteosarcoma diagnosed

A

initial X ray
referral to oncologist
biopsy
bloods
scans - bone scan, CT, MRI

178
Q

what is the staging system of osteosarcoma

A

staged 1A, B, 2A, B or 3 depending on size, whether the tumour has spread from the starting site

179
Q

how is osteosarcoma treated

A

chemotherapy before and after therapy
radiotherapy
surgery - amputation, or limb sparing dependent on size and where it is
biological therapy - mifamurtide

180
Q

what are the short term side effects of treatment for osteosarcoma

A

pain
tenderness
nausea
vomiting
infections
hair loss
bruising
tenderness

181
Q

what are the long term side effects of treatment for osteosarcoma

A

abnormal bone growth
heart or lung effects
infertility
increased risk of developing another cancer

182
Q

what are different types of paediatric bone tumours

A

osteosarcoma
ewing sarcoma
nonossifying fibroma
osteochondroma
langerhans cell histiocytosis
unicameral bone cyst
aneurysmal bone cyst
osteoid osteoma

183
Q

what is Ewing sarcoma

A

second most common bone cancer in children and mainly affects the legs, pelvis, arms and ribs

184
Q

what are the different types of Ewings sarcoma

A

it is a group of 4 different types of cancer
- ewing sarcoma of the bone
- extraosseous ewing sarcoma (soft tissue round bone)
- peripheral primitive neuroectodermal tumour
- askin tumour (chest wall)

185
Q

what age group is Ewings sarcoma most common in
is it more common in males or females

A

10-14 yrs
more common in boys

186
Q

what are the symptoms of Ewing sarcoma

A

bone pain - initially comes and goes and then becomes persistent
tenderness
redness
swelling
pathological fractures

187
Q

what genetic disorders are sarcomas associated with

A

Li-Fraumeni syndrome (familial mutation of P53)
patients cured of familial retinoblastoma

188
Q

where does osteosarcoma commonly metastasise to

A

lung
bones

189
Q

how is Ewing sarcoma diagnosed

A

X ray
biopsy
lactate dehydrogenase and alkaline phosphatase
MRI
CT chest
isotope bone scan
bone marrow aspirates

190
Q

how is Ewing sarcoma managed

A

chemotherapy followed by surgery followed by chemotherapy
limb preserving therapy were possible
radiotherapy as an adjuvant

191
Q

what is an adverse outlook with Ewings sarcoma associated with

A

large primaries
axial sites
poor response to chemotherapy
metastatic disease

192
Q

what is rhabdomyosarcoma

A

it is the most common soft tissue sarcoma in childhood
- most are either embryonic or alveolar

193
Q

what are the presenting features of rhabdomyosarcoma

A

mass, pain and obstruction of:
bladder
pelvis
nasopharynx
parameningeal
paratestis
extremity
orbit
intrathoracic

194
Q

how is rhabdomyosarcoma diagnosed and staged

A

imaging of the primary site: CT or MRI
biopsy
CT scan of the chest
bone marrow aspirates
isotope bone scan
lumbar puncture

195
Q

what is the treatment for rhabdomyosarcoma

A

chemotherapy - 6-9 courses
surgery reserved for accessible sites after 3-6 courses of chemotherapy
radiotherapy after surgery

196
Q

what is the definition of atopy

A

predisposition to having hypersensitivity reactions to allergens

197
Q

what is the skin sensitisation theory regarding allergies

A
  1. break in the infants skin (eczema or skin infection) that allows allergens to cross the skin and react with the immune system
  2. the child doesn’t have contact with the allergen from the GI tract and there is an absence of GI exposure to the allergen
198
Q

what is a type 1 hypersensitivity reaction

A

IgE antibodies to a specific allergen trigger mast cell and basophils to release histamines and other cytokines - immediate reaction

199
Q

what is a type 2 hypersensitivity reaction

A

IgG and IgM antibodies react to an allergen and activate the complement system leading to direct damage to the local cells.

200
Q

what is a type 3 sensitivity reaction

A

immune complexes accumulate and cause damage to local tissues

201
Q

what is a type 4 hypersentivity reaction

A

T lymphocyte mediated reaction where t cells are inappropriately activated causing local inflammation and damage

202
Q

what is an example of a type 2 hypersensitivity reaction

A

haemolytic disease of the newborn
transfusion reactions

203
Q

what is an example of a type 3 hypersensitivity reaction

A

SLE
rheumatoid arthritis
Henoch-Scholein purpura

204
Q

what is an example of a type 4 hypersensitivity reaction

A

organ transplant rejection
contact dermatitis

205
Q

what are three main ways to test for allergy

A

skin prick testing
RAST testing - blood tests for total and specific IgE antibodies
food challenge testing - gold standard

206
Q

how will anaphylaxis present

A

urticaria
itching
angio-oedema
abdominal pain
SOB
wheeze
swelling of larynx
tachycardia
lightheadedness
collapse

207
Q

what blood test can be done to confirm anaphylaxis

A

serum mast cell tryptase within 6 hours of the event

208
Q

what is allergic rhinitis

A

it is a condition caused by IgE mediated type 1 hypersensitivity reaction, due to environmental allergens causing an allergic inflammatory response in the nasal mucosa

209
Q

how does allergic rhinitis present

A

runny, blocked and itchy nose
sneezing
itchy, red and swollen eyes

210
Q

how is allergic rhinitis managed

A

history
skin prick testing

211
Q

what are some triggers for allergic rhinitis

A

tree pollen or grass
house dust mites
pets
mould

212
Q

what advice would you give to a parent of a child suffering with allergic rhinitis to help ease the symptoms

A

avoid trigger - hoover, change pillows, good ventilation, staying inside with high pollen count, showering after youve been outside
minimise contact with pets which are a known trigger

213
Q

How is allergic rhinitis treated

A

oral antihistamines - taken prior to allergen exposure
- non sedating: cetirizine, loratadine, fexofenadine
- sedating - chlorphenamine and promethazine
nasal corticosteroid sprays - fluticasone
nasal antihistamines

214
Q

what is cows milk protein allergy

A

it is a condition typically affecting infants under 3, involving hypersensitivity to the protein in cows milk

215
Q

what are the two types of cows milk protein allergy

A

IgE mediated - rapid reaction occurring within 2 hours of ingestion
non IgE mediated - reactions occurring slowly over several days

216
Q

how does cows milk protein allergy present

A

bloating and wind
abdominal pain
diarrhoea
vomiting
urticarial rash
angio-oedema
cough or wheeze
sneezing
watery eyes
eczema
rarely in severe cases anaphylaxis can occur

217
Q

how is cows milk protein allergy diagnosed

A

full history and examination
skin prick testing can help support the diagnosis

218
Q

how is cows milk protein allergy managed

A

avoiding cows milk:
breast feeding mothers should avoid dairy products
replace formula with special hydrolysed formulas
every 6 months or so infants are tried on the first step of the ‘milk ladder’ and slowly progress up to gradually progress towards a diet containing milk

219
Q

what is hydrolysed cows milk formula

A

Hydrolysed formulas contain cow’s milk, however the proteins have been broken down so that they no longer trigger an immune response.

220
Q

what is the difference between cows milk intolerance and cows milk allergy

A

intolerance will present with similar GI symptoms as cows milk allergy however it does not give the allergic features

221
Q

how is cows milk intolerance managed

A

they can be fed with breast milk, hydrolysed formular and weaned to foods not containing cow milk

222
Q

what features would make you refer a child with recurrent infections to a specialist for further investigations

A

chronic diarrhoea since infancy
failure to thrive
appearing unusually well for quite a severe infection
significantly more infections than expected particularly bacterial lower respiratory tract infections
unusual of persistent infections such as CMV, candida and pneumocystis jiroveci

223
Q

what investigations should be done in a child referred with recurrent infections

A

full blood count
immunoglobulins - b cell disorders
complement proteins
antibody responses to vaccines specifically pneumococcal and haemophilus vaccines
HIV test if clinically relevant
Chest Xray
sweat test
CT chest

224
Q

what is severe combined immunodeficiency (SCID)

A

most severe condition causing immunodeficiency, with children with SCID having almost no immunity to infections, due to a lack of or dysfunctioning of T and B cells

225
Q

how does SCID present

A

persistent severe diarrhoea
failure to thrive
opportunistic infections that are more frequent or severe than in healthy children
unwell after live vaccines such as BCG, MMR
Omenn syndrome

226
Q

what are causes of SCID

A

over 50% caused by mutations in the common gamma chain on the X chromosome which codes for interleukin receptors on T and B cells
- other mutations that can cause SCID are JAC3 mutations and mutations leading to adenosine deaminase deficiency

227
Q

what is omenn syndrome

A

it is a rare cause of SCID as a result of a mutation in the recombination-activating gene that codes for important proteins in T and B cells

228
Q

what are the features of Omenn syndrome

A

red scaly dry scalp
hair loss
diarrhoea
failure to thrive
lymphadenopathy
hepatosplenomegaly

229
Q

what causes the features of omenn syndrome

A

caused by the abnormally functioning and dysregulated T cells attacking the tissues i the fetus or neonate

230
Q

how is SCID treated

A

it is fatal unless treated
MTD approach
treat underlying infections
immunoglobulin therapy
sterile environment to minimise risk of new infections
avoid live vaccines
haematopoietic stem cell transplantation

231
Q

what is hypogammaglobulinemia

A

a deficiency in immunoglobulins

232
Q

what is the most common immunoglobulin deficiency

A

selective immunoglobulin A deficiency

233
Q

what is selective immunoglobulin A deficiency

A

where patients have low levels of IgA and normal levels of IgG and IgM

234
Q

what other condition are you likely to come across IgA deficiency

A

in coeliac disease

235
Q

what is common variable immunodeficiency

A

a deficiency in IgG and IgA with or without a deficiency in IgM, due to a genetic mutation in the genes coding for components of B cells

236
Q

what is the management of common variable immunodeficiency

A

regular immunoglobulin infusions
treating infections and complications as they occur

237
Q

what are symptoms of common variable immunodeficiency

A

recurrent respiratory tract infections
chronic lung disease
unable to develop immunity to infections or vaccinations
prone to immune disorders such as RA
prone to cancers such as non-Hodgkins lymphoma

238
Q

what is X linked agammaglobulinaemia

A

it is an X linked recessive condition that results in abnormal B cell development and deficiency in all classes of immunoglobulins

239
Q

what is DiGeorge syndrome

A

condition caused by a microdeletion on chromosome 22 resulting in a developmental defect in the third pharyngeal pouch and third brachial cleft

240
Q

what is one of the consequences of incomplete development in DiGeorge syndrome

A

an incomplete thymus gland resulting in the inability to create functional T cells

241
Q

what are the features of DiGeorge syndrome

A

CATCH-22
congenital heart disease
abnormal facies (characteristic facial appearance)
thymus gland incompletely developed
cleft palate
hypothyroidism and resulting hypocalcaemia
22 chromosome affected

242
Q

what is purine nucleoside phosphorylase deficiency

A

autosomal recessive condition where there is a deficiency in PNPase leading to a metabolite called dGTP builds up, which is toxic to T cells resulting in low levels of T lymphocytes

243
Q

what is the role of PNPase

A

it is an enzyme which helps to break down purines

244
Q

what is the presentation of purine nucleoside phosphorylase deficiency

A

immunity to infection gradually gets worse
increasingly susceptible to infections particularly viruses and live vaccines

245
Q

what is Wiskott-aldrich syndrome

A

it is an X linked condition with a mutation on the WAS gene causing abnormally functioning T cells

246
Q

what are features of Wiskott-aldrich syndrome

A

thrombocytopenia
immunodeficiency
neutropenia
eczema
recurrent infections
chronic bloody diarrhoea

247
Q

what is ataxic telangiectasia

A

an autosomal recessive condition affecting the genes coding for the ATM serine/threonine kinase protein on chromosome 11, required for several functions in DNA coding

248
Q

what are features of ataxic telangiectasia

A

low numbers of T cells and immunoglobulins, causing immunodeficiency and recurrent infections
ataxia
telangiectasia particularly in the sclera and damaged areas of the skin
predisposition to cancers
slow growth and delayed puberty
accelerated aging
liver failure

249
Q

what is the microscopic appearance of osteosarcoma

A

Poorly formed trabecular bone is seen with (in the typical high-grade conventional subtype) cellular pleomorphism and mitoses. Variable amounts of fibrocystic and chondroblastic appearing cells may also be encountered.

250
Q

what is seen on an X ray in osteosarcoma

A

medullary and cortical bone destruction
wide zone of transition, permeative or moth eaten appearance
sunburst look
soft tissue mass
fluffy or cloud like

251
Q

what is seen on Xray in Ewing sarcoma

A

large with wide zone or transition or poorly defined margins
80% extend into adjacent soft tissue
lamellated/onion skin appearance
sclerosis

252
Q

what type of organisms are complement proteins important in dealing with

A

encapsulated organisms
- haemophilus influenza B
- streptococcus pneumonia
- neisseria meningitidis

253
Q
A

Phase 3a Jemima (16 decks)

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