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Paediatrics > Haematology/ Oncology > Flashcards

Haematology/ Oncology Flashcards

1
Q

Name some iron rich foods

A
  • Red meat, liver and kidney
  • Beans and lentils
  • Eggs
  • Oily fish
  • Apricots, prunes and raisins
  • Leafy green vegetables
  • Oatmeal
  • Tuna
  • Fortified cereals
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2
Q

What is the most common cause of iron deficiency anaemia?

A

Diet lacking in iron rich foods, especially If it contains a large amount of cow’s milk. Inadequate intake of iron is common in infants because additional iron is required for the increase in blood volume accompanying growth and to build up the child’s iron stores.

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3
Q

What is the secondary causes of iron deficiency anaemia?

A
  • Blood loss
  • Malabsorption- coeliac?
  • Delay in weaning past 6 months and breastfed
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4
Q

Risk factors for iron def anaemia

A
  • High intake of fruit juice (late weaning)
  • Early intro of cows milk (late weaning -high iron content but only 10% is absorbed)
  • predominantly breastfed (low iron content but 50% of the iron is absorbed)
  • Disadvantaged community, inner city
  • Asian race
  • Poor food intake
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5
Q

Iron deficiency anaemia symptoms:

A
  • May be asymptomatic.
  • Fatigue.
  • Shortness of breath.
  • Failure to thrive.
  • Symptoms related to underlying disease pathology - eg, chronic/recurrent diarrhoea, which can suggest a malabsorption syndrome such as coeliac disease.
  • Some children have ‘pica’- inappropriate eating of non-food materials such as soil, chalk, gravel.
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6
Q

Iron deficiency anaemia signs:

A
  • Cardiovascular system - look for exertional tachycardia, a systolic flow murmur. Gallop rhythm, cardiomegaly and hepatomegaly are signs of congestive cardiac failure.
  • Plot weight, height and head circumference - in chronic anaemia, growth can be affected, usually with preservation of head circumference.
  • Pallor - examine conjunctivae, nail beds, palmar creases.
  • Evidence of blood loss
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7
Q

Mechanism of iron deficiency anaemia:

A

Reduction in Hb due to ineffective erythropoiesis due to lack of iron needed to make RBC.

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8
Q

In which condition are several mechanisms of anaemia combined (ineffective erythropoiesis, haemolytic, blood loss)

A

Anaemia of prematurity

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9
Q

Investigations needed in suspected Iron def anaemia:

A
  • FBC (low Hb, low MCV, normal reticulocyte). Microcytic, hypo chromic picture.
  • Iron, ferritin and total iron binding capacity levels

Can do many other tests if suspecting a different type of anaemia e.g. folate, B12, Coomb’s test, blood film etc.

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10
Q

Side effects of iron supplementation:

A
  • Nausea- can take with some food and vit c (e.g. orange juice) to help
  • Can cause black stool
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11
Q

Side effects of iron supplementation:

A
  • Nausea- can take with some food and vit c (e.g. orange juice) to help
  • Can cause black stool

Anaphylactic reactions can occur in IV iron

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12
Q

Treatment of iron deficiency anaemia:

A

Exclude serious cause e.g. blood loss (can be menorrhagia in early teens), consider thalassaemia in Indian subcontinent/ African/ Mediterranean patients

Primary prevention through dietary advice!

  • If clinical need, give an oral course for a few months. Can give slightly longer than necessary to build up stores. Recheck with blood test.
  • IV iron only given if oral therapy is unsuccessful/not tolerated or in continuing blood loss or malabsorption. Some with chronic renal failure will need this.

-Neonatal anaemia due to continuous blood sampling does not need iron or if due to changes in haematocrit and Hb levels at birth

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13
Q

Normal iron ranges iron deficiency anaemia:

A

For children aged 6 months to 5 years, current WHO guidelines (2001) recommend a cut-off value for anaemia as haemoglobin concentration of 110 g/L, while depleted iron stores are de ned as a ferritin value below 12 μg/L.

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14
Q

What is henoch schonlein purpura (HSP)?

A

Henoch-Schönlein purpura (HSP) is an IgA-mediated, autoimmune hypersensitivity vasculitis of childhood. It’s rare.

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15
Q

What is the epidemiology of HSP?

A

Henoch-Schönlein purpura (HSP) is the most common form of systemic vasculitis in children; 90% of cases occur in childhood.

The peak prevalence is in children aged 4-6 years. It is rare in infants and young children.

The male-to-female ratio is 1.5-2:1. Caucasians are more often affected than other ethnic groups.

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16
Q

Associated preceding conditions in HSP:

A
  • Infections: for example, Group A streptococci, mycoplasma, Epstein-Barr virus.
  • Vaccinations.
  • Environmental exposures: for example, drug and food allergens, pesticides, cold exposure, insect bites
17
Q

Typical presentation of HSP:

A
  • The disease occurs mostly in the winter months. About 50-90% of patients have a preceding upper respiratory tract infection (URTI).
  • Generally, patients appear to be mildly ill, with low-grade fever.
  • There is a symmetrical, erythematous macular rash, especially on the back of the legs, buttocks and ulnar side of the arms.
  • Within 24 hours, the macules evolve into purpuric lesions, which may coalesce and resemble bruises. Typically the purpura are slightly raised and palpable.
  • Abdominal pain and bloody diarrhoea may precede the typical purpuric rash.
  • HSP may also cause nausea and vomiting.
  • Joint pain, especially in the knees and ankles. Joints may also be swollen and tender but permanent deformity does not occur.
  • Scrotal involvement may mimic testicular torsion.
  • Headaches may occur.
18
Q

What are the renal involvement risks in HSP?

A
  • Affects approximately 40% of children affected with HSP.
  • Only a small minority progresses to end-stage kidney disease.
  • Usually occurs within three months of disease onset.
  • There is usually no relationship between the severity of nephritis and the extent of the other manifestations of HSP.
  • Microscopic haematuria with mild-to-moderate proteinuria may occur.
  • Nephrotic syndrome may also occur.
  • Oliguria and hypertension are uncommon.
19
Q

Differential diagnosis when considering HSP:

A
  • SLE
  • Intussusception should be considered, even if the typical purpuric rash has evolved (intussusception occurs in 2-3% of HSP patients).
  • Other causes of purpuric rash - eg, thrombocytopenia.
  • Other causes of glomerulonephritis.
  • Acute haemorrhagic oedema of infancy: self-limiting condition presenting with fever, oedema and rosette-shaped, annular-shaped or targetoid-shaped purpura affecting the face, ears and extremities.
20
Q

Investigations in HSP:

A

Clinical diagnosis. Can also:

  • Urinalysis: haematuria and/or proteinuria are present in 20-40% of patients.[1, 4]
  • FBC: there may be raised white cell count with eosinophilia; normal or increased platelets.
  • Raised ESR.
  • Serum creatinine may be elevated in renal involvement.
  • Serum IgA levels are often increased.
  • Renal biopsy: if there is persistent nephrotic syndrome.
21
Q

Management of HSP:

A

-HSP is usually self-limiting. Therefore, treatment for most patients remains primarily supportive.

  • Non-steroidal anti-inflammatory drugs (NSAIDs) may help joint pain but should be used with caution in patients with renal insufficiency.
  • May require admission to hospital for monitoring of abdominal and renal complications.
  • Nephropathy: treated supportively.
  • Corticosteroids can ameliorate associated arthralgia and the symptoms associated with gastrointestinal dysfunction.
22
Q

Complications of HSP:

A

-Renal involvement occurs in 50% of older children but is only serious in approximately 10% of patients. Less than 1% of patients with HSP progress to end-stage kidney disease. The renal prognosis is worse in older children.

Other rare complications include myocardial infarction, pulmonary haemorrhage, pleural effusion, intussusception (in 2-3% of patients), gastrointestinal bleeding, bowel infarction, seizures and mononeuropathies.

23
Q

Prognosis of HSP, how long does it last for etc?

A

Initial attacks of HSP can last for several months. One in every four patients will have one or more recurrences.

  • Children younger than 3 years have a shorter, milder course and fewer recurrences.
  • Chronic kidney disease may progress, sometimes more than ten years after the initial flare.
  • The long-term prognosis of HSP is directly dependent on the severity of renal involvement.
24
Q

Monitoring for renal involvement in HSP:

A

Monitoring for renal involvement:

  • For those with no proteinuria, recommendations are for blood pressure checking and urinalysis at days 7 and 14 and at 1, 3, 6 and 12 months.
  • For those with proteinuria, follow-up is recommended at days 7 and 14, monthly from 1-6 months and then at 12 months.
25
Q

Presentation of a Wilm’s Tumour:

A
  • The most common presentation is an asymptomatic abdominal mass.
  • Abdominal pain.
  • Haematuria.
  • Urinary tract infection.
  • Hypertension, gross haematuria and fever may occur but are uncommon.
  • Advanced disease may rarely present with respiratory symptoms due to lung metastases.
26
Q

Age group affected by Wilm’s tumours:

A

Usually presents in the first five years of life but 3% of presentations are in adults. 2nd most common intra-abdominal cancer.

95% are unilateral. Only 1-2% have a positive family history.

27
Q

Associated syndromes of Wilm’s tumours:

A
  • Beckwith- Wiedemann
  • Edward’s Syndrome
  • WAGR
  • Can be familial

Extra screening recommended in these scenarios- refer to clinical geneticist.

28
Q

Age group affected by Neuroblastoma:

A

90% of those diagnosed are under the age of 5, with a peak age of incidence of 2-3. It can even be diagnosed prenatally by US.

Fewer than 100 diagnosed every year but most common childhood brain cancer.

29
Q

Presenting symptoms of neuroblastoma:

A
  • Loss of appetite.
  • Occasionally watery diarrhoea due to vaso-active intestinal polypeptide (VIP) secretion.
  • Vomiting.
  • Weight loss.
  • Fatigue.
  • Bruising due to pancytopenia as a result of marrow infiltration.
  • Periorbital bruising - ‘racoon eyes’ (due to metastatic disease in the orbits).
  • Weakness, limping, paralysis and bladder and bowel dysfunction due to spinal cord compression from paraspinal sympathetic tumours.
  • Bone pain (due to bone metastases).
  • Permanent cognitive deficits - rare.
30
Q

Presenting signs of neuroblastoma:

A
  • Mild fever.
  • Abdominal distension due to enlarged liver.
  • Hypertension - due to pressure on the renal artery.
  • Horner’s syndrome due to thoracic lesion.
  • Primary cervical neuroblastoma is rare but may result in a mass in the neck.
  • ‘Blueberry muffin baby’ - occurs in neonates; metastases cause severe skin involvement, resulting in a characteristic appearance.
  • Opsoclonus myoclonus syndrome (dancing eye syndrome) is characterised by opsoclonus, myoclonus and ataxia, usually with behavioural difficulties. It is rare but is associated with neuroblastomas in children.
31
Q

Ddx for neuroblastoma

A 
Osteomyelitis
Rheumatoid arthritis
Disseminated bone disease
Primary neurological disease
Inflammatory bowel disease
Other cancers of childhood
32
Q

Ethnic groups and thalassaemia:

A

β thalassaemia is prevalent in areas around the Mediterranean, in the Middle East, in Central, South, and Southeast Asia, and in Southern China.
α thalassaemia is prevalent in Southeast Asia, Africa, and India.

33
Q

Presentation of alpha thalassaemia:

A

Severe homozygous α thalassaemia is usually lethal in utero. It should be considered when hydrops fetalis is diagnosed, as rhesus incompatibility has become a much rarer cause.

Silent carrier α thalassaemia is a fairly common type of subclinical thalassaemia, usually found incidentally. Patients are haematologically normal, except for occasional low RBC indices.

α-thalassaemia trait is characterised by mild anaemia and low red blood cell (RBC) indices.

Severe disease presents with with mildly to moderately severe haemolytic anaemia, pallor, hepatosplenomegaly, jaundice, and abnormal RBC indices at birth

34
Q

Presentation of beta thalassaemia:

A

In β thalassaemia, symptoms of anaemia start in the latter part of the first year of life but can be as late as 5 years old

Presentation of β thalassaemia major in infancy often includes failure to thrive, vomiting feeds, sleepiness, stunted growth and irritability. Ineffective erythropoiesis creates a hypermetabolic state with fever.

Symptoms are related to the severity of anaemia and vary along a spectrum. In untreated β thalassaemia major they tend to be extremely debilitating but may be mild or absent in those with milder forms of disease.

35
Q

Signs of thalassaemia:

A

In severe, untreated cases there may be:

  • Hepatosplenomegaly.
  • Bony deformities (frontal bossing, prominent facial bones, and dental malocclusion).
  • Marked pallor and slight to moderate jaundice.
  • Exercise intolerance, cardiac flow murmur or heart failure secondary to severe anaemia.

These features are absent in well-treated patients but there are often still problems:

  • Growth restriction is common even with well-controlled chelation therapy.
  • Iron overload can cause endocrinopathy with diabetes, thyroid, adrenal and pituitary disorders.
36
Q

What is thalassemia?

A

The thalassaemias are a group of recessively autosomal inherited conditions characterised by decreased or absence of synthesis of one of the two polypeptide chains in haemoglobin. (α or β).

37
Q

Ddx for thalassaemia

A
  • Other causes of microcytic anaemia - eg, iron-deficiency anaemia, sideroblastic anaemia and anaemia of chronic disease.
  • Acute leukaemia may require bone marrow aspiration to differentiate.
  • Rhesus incompatibility (rare)
  • Diamond-Blackfan syndrome is a rare congenital cause of erythroid aplasia. It causes a severe normochromic, macrocytic anaemia usually in infancy and is often associated with craniofacial or upper limb anomalies.
38
Q

Antenatal screening for thalassaemia:

A

Recommended for at risk groups/ family history.

39
Q

Type of anaemia that thalassaemia presents with:

A

If a patient, particularly a child, presents with microcytic, hypochromic anaemia and fails to respond to iron, consider haemoglobinopathies. Thalassaemia must be excluded, as giving more iron will only aggravate the condition.

Paediatrics (23 decks)

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