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Haematology and Oncology Flashcards

1
Q

What is the most common type of anaemia?

A

Iron deficiency anaemia (IDA)

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2
Q

List some risk factors for IDA

A

Pregnancy:

  • Preterm
  • LBW infants
  • Multiple births

Nutrition:

  • After exclusive breast feeding for >6mnths
  • Delayed introduction of iron-containing solids
  • Children fed mostly cows milk (low in iron)

Adolescent females:

  • Growth spurt
  • Menstruation

Low iron in diet:

  • Poverty
  • Veganism

Malabsorption:

  • Coeliac disuse
  • IBD
Blood loss (rare): 
(NB 1ml blood loss = 0.5mg iron)
- Mickel's diverticulum
- Oesophagitis
- Cysts
- Tumours
- NSAIDs

Intestinal parasites:
- Hookworms

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3
Q

What is pica?

A

Associated with IDA

A disorder characterised by appetite for non-nutritive substances eg ice, hair, paper, stones, soil etc

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4
Q

How should IDA be prevented in the newborn?

A

Newborns have approx 4 months of iron stores

From 4 months exogenous iron should be given of 1mg/kg/day (if exclusively breastfed)

From 6 months should be started on iron containing foods

Avoid non-modified cows milk

Supplemented formula milk given to 24 months in high risk groups

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5
Q

How may IDA present in a child?

A

Most cases are subclinical. Symptoms only develop in severe IDA

1) Fatigue
2) Irritability
3) Failure to thrive
4) Exertional dyspnoea
5) Anaemic signs eg pallor, koilonychia
6) Jaundice (if haemolysis)
7) Reduced cognitive and psychomotor performance
8) Pica (rare)

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6
Q

What investigations can be done for IDA and what do they show?

A

1) FBC:
- Hb <11g/dL
- Decreased MCV
- Increased platelets

2) Blood film
- Hypochromic, microcytic RBCs

3) Serum ferritin
- Decreased = 99% positive predictive value

4) Serum iron
- Low in IDA
- Normal in thalassaemia

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7
Q

What are some ddx for hypochromic, microcytic anaemia? (5)

A

Microcytic anaemia = MCV <80fL

From insufficient haemoglobin production

Defective haem synthesis:

1) Iron deficiency anaemia (most common)
2) Lead poisoning
3) Anaemia of chronic disease (late phase)
4) Sideroblastic anaemia

Defective globin chain:
5) Thalassemia

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8
Q

What can cause normocytic anaemia? (7)

A

Normocytic anaemia = MCV 80-100 fL

Decreased volume and/or decreased erythropoiesis

Haemoglobinopathies:

1) Sickle cell anaemia
2) Haemoglobin C disease

Enzyme deficiencies:

3) Pyruvate kinase deficiency
4) G6PD deficiency

5) Blood loss
6) Aplastic anaemia
7) Anaemia of CKD

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9
Q

What can cause macrocytic anaemia?

A

Macrocytic anaemia = MCV >100fL

Insufficient cell production and / or maturation

Megaloblastic:

1) Vit B12 def
2) Folate def
3) Medications:
- Phenytoin
- Sulfa drugs
- Trimethoprim
- Hydroxyurea
- Methotrexate

Non-megaloblastic:

4) Liver disease
5) Alcohol use
6) Myelodysplastic syndrome
7) Hypothyroidism
8) Multiple myeloma

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10
Q

What is the treatment of IDA in children?

A

Diet correction: 2mg/kg/day oral ferrous salt, continue until 3 months after normal Hb

NB failure to respond to iron supplements = malabsorption

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11
Q

How common are brain tumours in children?

A

Brain = most common site for solid tumours in childhood

5/100,000 between ages 5-9yrs

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12
Q

What structures may be involved in brain tumours?

A

Intracranial tumour affecting brain, meninges, pituitary gland, pineal gland and/or cranial nerves

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13
Q

Where are brain tumours in children most commonly?

A

Most (70-80%) = infratentorial
= Below tentorium - cerebellum
(supratentorium = cerebrum)

eg Glial tumours or medulloblastomas

Also midline = germ cell tumours, craniopharyngiomas

(unlike adults where most are secondary and supratentorial)

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14
Q

What proportion of childhood cancers are brain and CNS?

A

One quarter

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15
Q

How are brain tumours classified?

A

Low-grade (1 and 2)

High-grade (3 and 4)

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16
Q

What does low-grade mean?

A

Grade 1 = doesn’t spread
Grade 2 sometimes spreads slowly and may recur if removed

Sometimes called ‘benign brain tumours’ but misleading as their mass effects mean they can still be harmful

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17
Q

What does high-grade mean?

A

Malignant tumours which spread to other tissues and tend to recur if removed

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18
Q

What is the lifetime risk of a primary brain tumour?

A

1/75

50% = malignant (high grade), risk of this is thus 1/150

Annual incidence = 1 / 10,000

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19
Q

How do brain tumours typically present? What % are diagnosed in ED?

A

Progressive and subacute

60% diagnosed in ED

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20
Q

Give some examples of low-grade brain tumours?

A

1) Meningioma
2) Pituitary adenoma
3) Acoustic neuroma
4) Craniopharyngioma

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21
Q

What is an acoustic neuroma?

A

Benign tumour of CN8 Schwann cells

aka vestibular schwannoma

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22
Q

What are acoustic neuromas associated with?

A

Neurofibromatosis type 2

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23
Q

How may an acoustic neuroma present?

A

Gradual onset of unilateral sensorineural deafness and pressure in one ear

Followed by unilateral face numbness and absent corneal reflex (due to CN5 compression), vertigo, n&v

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24
Q

How are acrostic neuromas managed?

A

Slow growing so can be monitored with annual MRI

Removed with surgery or Gamma knife radiosurgery

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25
What ages does craniopharyngiomas affect?
5-15 and 65-75yrs
26
Where do craniopharyngiomas arise? Where may they also affect?
Pituitary stalk May affect hypothalamus and pituitary
27
How may a craniopharyngioma present?
Signs of raised ICP Bitemporal menianopia Hydrocephalus Endocrine symptoms
28
List some examples of high-grade brain tumours?
1) Gliomas 2) Medulloblastomas 3) Primary CNS lymphoma
29
What is the most common type of glioma?
Astrocytoma
30
What are types of astrocytoma?
Glioblastoma aka glioblastoma multiforme (GBM) (most common malignant tumour in adults, life expectancy 1yr) Pilocytic astrocytoma (PCA) = commonest benign tumours in kids
31
What is the 5yr survival of pilocytic astrocytoma?
95%
32
Other than astrocystoma, what are other types of gliomas?
Ependymomas | Oligodendrogliomas
33
What are medulloblastomas?
Tumour of cerebellar neurons A type of primitive neuroectodermal tumour (PNET)
34
How common are medulloblastomas?
Most common malignant tumours in children
35
How may a medulloblastoma present?
Hydrocephalus | Cerebellar signs eg abnormal gait and coordination
36
What is the 5yr survival of medulloblastomas?
70%
37
What are primary CNS lymphomas most commonly?
Diffuse large B-cell lymphoma
38
Which population are more likely to have primary CNS lymphomas?
Those with HIV
39
What are the most common type of brain tumours in children?
Gliomas, either: 1) Astrocytomas (40%) - very variable prognosis 2) Medulloblastomas (20%) - most have spinal mets at diagnosis
41
How may brain tumours present in children?
Mostly cerebellar signs = DANISH Signs of raised ICP +/- focal neurological signs depending on site of tumour - eg squint from 6th nerve palsy, seizures, cerebellar signs, personality changes
43
What is are cerebellar signs - DANISH?
``` Dysdiadochokinesia Ataxia Nystagmus Intension tremor Scanning dysarthria Heel-shin test +ve ```
45
What are signs of raised ICP?
``` Papilloedema Altered LOC Headache Vomiting Behavioural changes Bulging fontanelle Raised BP Decreased HR ```
47
What has the best survival rates of brain tumours?
Astrocytomas
48
What is haemophilia?
Bleeding disorder caused by a deficiency of clotting factors No fibrin is formed in blood clots leading to easy clot breakdown
49
What are the two types of haemophilia?
Haemophilia A = Factor VIII deficiency Haemophilia B = Factor IX deficiency A8 B9
50
What is the mode of inheritance of haemophilia?
X-linked recessive Affects males born to carrier mothers
51
How is severity of factor VIII deficiency classified? - % FVIII activity - Age of presentation
1) Mild - >5% FVIII activity - Presents >2yrs of age 2) Moderate - 1-5% FVIII activity - Presents <2yrs 3) Severe (most) - <1% FVIII activity - Presents in infancy
52
What mutation causes haemophilia A?
``` Usually FH (2/3rd) But sporadic cases can occur due to novel mutations (1/3rd) ```
53
What is more common haemophilia A or B?
A is 5x more common than B
54
How may severe haemophilia A present?
1) Neonatal bleeding (1/3rd) eg following circumcision 2) Neonatal haemorrhage 3) Haematoma 4) Prolonged bleeding from cord or umbilical area 5) Hx of spontaneous bleeding into joints esp knees, ankles and elbows, without hx of significant trauma 6) IM haemorrhage 7) GI / mucosal haemorrhage - but more often haemophilia B/von Willibrand's disease 8) Haematuria
55
How may moderate haemophilia A present?
Bleeding after venepuncture
56
How may mild haemophilia A present?
Bleeding after major trauma
57
What may untreated cases of severe haemophilia A lead to? (4)
1) Athropothy and joint deformity - May require replacement of affected joints 2) Soft tissue haemorrhages - Can lead to compartment syndrome and neurological damage 3) Extensive retroperitoneal bleeds - Can cause haemodynamic compromise 4) Haematoma formation - May require fasciotomy
58
List some ddx for haemophilia A (7)
1) Haemophilia B 2) Von Willebrand's disease 3) Vit K deficinty / antagonism with antiogoagulants 4) Haemophilia C (factor XI deficiency) 5) Disorders of fibrinogen or fibrinolytic production 6) Platelet disorders 7) Blood vessel disorders
59
What investigations are performed for haemophilia A?
FBC - Low haematocrit and reduced Hb if recent bleeding PT, bleeding time, fibrinogen levels and VWF - Normal APTT - Usually prolonged but can be normal if mild - Mixed pt plasma 1:1 with donor plasma should normalise Factor VIII:C - Reduced - % activity shows severity of disease Imagine arthtopathies with MRI or US CT head if haemorrhage
60
What is the prophylactic management of haemophilia A?
Infusions of factor VIII minimum once weekly
61
What is a complication of haemophilia A?
Degenerative joint disease due to recurrent haemarthrosis
62
What tends to be more severe - haemophilia A or B?
A = more severe
63
What does the activated partial thromboplastin time (aPTT) measure?
The intrinsic and common pathways
64
What is the intrinsic pathway?
HMWK activates: FXII - XIIa XIIa activates: FXI to FXIa FXIa activates: FIX to FIXa 12 + 11 + 9 9trinsic FVIIIa (8 = Haemophilia A) then with FIXa activates FX
65
What does prothrombin time (PT) measure?
Extrinsic and common pathways
66
What is the extrinsic pathway?
Tissue factor activates factor FVII - FVIIa 7 = heaven = extrinsic
67
What is the common pathway?
Factor X is activated by FIXa (intrinsic) and FVIIa (extrinsic) Xa AND Va then activate: Prothrombin (FII) to thrombin (FIIa) Thrombin activates: Fibrinogen (FI) to Fibrin (FIa) 10 + 5 + thrombin + fibrin
68
What is protein C?
= autoprothrombin IIa A proenzyme that inactivates FVa and VIIIa Too little = clot too much
69
What % of haemophilia B are mild, moderate and severe?
Severe - 50% Moderate - 3-% Mild - 20%
70
In general, deficiencies in what cause: a) Petechial haemorrhages and ecchymoses (bruising) b) Haematomas and haemarthroses
a) Petechial haemorrhages and ecchymoses (bruising) - platelet deficiency b) Haematomas and haemarthroses - Clotting factor deficiency
71
What did haemophilia B used to be known as?
Christmas disease
72
What are signs/symptoms of haemophilia B?
Same as A May be slower to bleed
73
What investigations are done for haemophilia B?
aPTT - elevated % activity of FIX = reduced
74
What is the management of haemophilia B?
Recombinant FIX usually twice a week
75
What is the management of brain tumours?
Surgery = first line Not all operable eg brainstem not Chemo/radiotherapy
76
What should you do with a child presenting with persistent back pain?
Always do MRI with contrast
77
Why should a LP never be performed if suspected raised ICP?
High pressure gradient from within cranium can cause herniation of brainstem through foramen magnum
78
How should brain tumours in children be investigated?
MRI with contrast Never perform a LP if raised ICP

extra 1 (e) (19 decks)

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