Medicine Phase 3a > PAEDIATRICS - 2 > Flashcards

PAEDIATRICS - 2 Flashcards

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1
Q

Define acute lymphoblastic leukaemia (ALL)

A

Malignancy of lymphoid cells, affecting B + T lymphocytes

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2
Q

ALL: pathology

A

• Uncontrolled proliferation of immature blast cells

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3
Q

ALL: clinical presentation

A 
Marrow failure:
•	Anaemia (low Hb)
•	Neutropenia (low WCC)
•	Bleeding (low platelets)
Infiltration:
•	Hepatomegaly
•	Splenomegaly
•	Lymphadenopathy
•	Cranial nerve palsies
•	Meningism
•	Enlarged salivary glands
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4
Q

ALL: investigations

A
  1. ) Blood film
    - Blast cells
    - High WCC
  2. ) CXR/ CT
    - Mediastinal and abdominal lymphadenopathy
  3. ) LP
    - To look for CNS involvement
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5
Q

ALL: supportive management

A
  1. ) Blood/ platelet transfusion
  2. ) IV fluids
  3. ) Allopurinol (prevents tumour lysis syndrome)
  4. ) Insertion of Hickman line
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6
Q

ALL: management of infection

A
  1. ) Neutropenic antibiotic regime

2. ) Prophylactic antivirals, antifungals and antibiotics

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7
Q

ALL: chemotherapy regimes

A
  1. ) To induce remission: Vincristine + prednisolone + L-asparaginase + daunorubicin
  2. ) CNS prophylaxis: Intrathecal methotrexate
  3. ) Maintenance: Mercaptopurine (daily), methotrexate (weekly), vincristine + prednisolone (monthly
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8
Q

ALL: eventual management

A

Bone marrow transplant

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9
Q

Define acute myeloid leukaemia (AML)

A

Neoplastic proliferation of blast cells derived from marrow myeloid elements

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10
Q

ALL: epidemiology

A
  • Commonest childhood malignancy

* Rare in adults

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11
Q

AML: epidemiology

A

• Most common acute leukaemia of adults

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12
Q

AML: clinical presentation

A 
Marrow failure:
•	Anaemia
•	Infection
•	DIC (promyelocytic leukaemia)
Infiltration:
•	Hepatomegaly
•	Splenomegaly
•	Gum hypertrophy
•	Skin involvement
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13
Q

AML: investigations

A
  1. ) Blood film
    - Few blast cells, not diagnostic
  2. ) FBC
    - Low WCC
  3. ) Bone marrow biopsy
    - Presence of Auer rods
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14
Q

AML: management

A

Supportive:
1.) Walking exercises to relieve fatigue
Chemotherapy:
1.) Daunorubicin + cytarabine
Bone marrow transplant:
1.) Pluripotent haematopoietic stem cells
2.) Allogeneic transplants from HLA-matched donors

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15
Q

Chronic lymphocytic leukaemia (CLL): epidemiology

A

• Most common leukaemia

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16
Q

CLL: pathology

A
  • Often asymptomatic
  • Can be anaemic
  • May have weight loss or sweats if severe
  • Enlarged, rubbery, non-tender nodes
  • Bilateral cervical lymphadenopathy
  • Splenomegaly
  • Hepatomegaly
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17
Q

CLL: staging

A

Rai stage:
0 = lymphocytosis
I = lymphocytosis + lymphadenopathy
II = lymphocytosis + splenomegaly or hepatomegaly
III = lymphocytosis + anaemia
IV = lymphocytosis + platelets <100 x109/L

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18
Q

CLL: investigations

A
  1. ) FBC
    - Significantly raised lymphocytes
    - Low Hb
    - Low neutrophils
    - Low platelets
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19
Q

CLL: management

A
  1. ) Fludarabine + rituximab + cyclophosphamide

2. ) Stem cell transplant

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20
Q

Define chronic myeloid leukaemia (CML)

A

Uncontrolled clonal proliferation of myeloid cells

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21
Q

CML: epidemiology

A
  • Peak incidence between 40-60
  • More common in males
  • Rare in childhood
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22
Q

CML: pathology

A

• Philadelphia chromosome present in >80%

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23
Q

CML: clinical presentation

A
  • Weight loss
  • Tiredness
  • Fatigue
  • Fever
  • Sweats
  • Gout (purine breakdown)
  • Bleeding (platelet dysfunction)
  • Abdominal discomfort (splenomegaly)
  • Splenomegaly
  • Hepatomegaly
  • Signs of anaemia
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24
Q

CML: investigations

A
  1. ) FBC
    - Very raised WBC
    - Increased neutrophils, monocytes, basophils, eosinophils
    - Low Hb
  2. ) U&E’s
    - Increased urate
    - Increased B12
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25
CML: management
1. ) Imatinib (tyrosine kinase inhibitor) (1st generation) 2. ) Dasatinib (2nd generation, more potent) 3. ) Stem cell transplant - Allogeneic transplantation from HLA-matched sibling or unrelated donor
26
Side effects of Imatinib
- Nausea - Oedema - Rash - Headache
27
Define myelodysplastic conditions
Heterogenous group of disorders that manifest as marrow failure
28
Myelodysplastic conditions: pathology
Marrow failure --> risk of life-threatening infection and bleeding
29
Myelodysplastic conditions: clinical presentation
Marrow failure: • Anaemia (low Hb) • Neutropenia (low WCC) • Bleeding (low platelets)
30
Myelodysplastic conditions: investigations
1. ) Pancytopenia 2. ) Low reticulocyte count 3. ) Blood film - Ring sideroblasts
31
Myelodysplastic conditions: management
1. ) Multiple transfusions of red cells or platelets 2. ) Erythropoietin 3. ) Allogenic stem cell transplant
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Types of brain tumour
1. ) Astrocytoma (40%) 2. ) Medulloblastoma (20%) 3. ) Ependymoma 4. ) Brainstem glioma 5. ) Craniopharyngioma
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Astrocytoma/ glioblastoma multiforme: site of tumour and clinical presentation
Supratentorial cortex - Seizures - Hemiplegia - Focal neurological signs
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Craniopharyngioma: site of tumour and clinical presentation
Midline - Visual field loss (bitemporal hemianopia) - Pituitary failure (growth failure, diabetes insidious, weight gain)
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Medulloblastoma: site of tumour and clinical presentation
Cerebellar/ IVth ventricle - Truncal ataxia - Coordination difficulties - Abnormal eye movements
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Brainstem glioma: site of tumour and clinical presentation
Brainstem - Cranial nerve defects - Pyramidal tract signs - Cerebellar signs (ataxia)
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Brain tumour: investigations
MRI | LP
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Management of brain tumours (except brainstem glioma)
1. ) Surgical resection 2. ) Radiotherapy 3. ) Chemotherapy
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Management of brainstem glioma
Palliative radiotherapy
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Define lymphoma
Malignancy of cells of immune system
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Classification of lymphoma
Hodgkins and non-hodgkins
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Hodgkins lymphoma: clinical features
``` Painless lymphadenopathy - neck - large and firm lymph nodes Gradual onset (months) Uncommon to have B symptoms ```
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B symptoms
Sweating Pruritis Weight loss Fever
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Hodgkins lymphoma: investigations
1. ) Lymph node biopsy 2. ) CT or MRI to assess all nodes 3. ) Bone marrow biopsy (staging)
45
Hodgkins lymphoma: management
Chemotherapy ± radiotherapy
46
Hodgkins lymphoma: investigation used to monitor treatment response
PET scan
47
Define non-hodgkin lymphoma
Malignancy of T cells or B cells
48
Non-hodgkin lymphoma: clinical features
T cell malignancy: Mediastinal mass --> SVC obstruction (dyspnoea, facial swelling, flushing) Bone marrow infiltration B cell malignancy: Lymphadenopathy in head and neck or abdomen
49
Non-hodgkins lymphoma: investigations
1. ) Lymph node biopsy 2. ) CT or MRI 3. ) Bone marrow biopsy 4. ) LP - CSF
50
Non-hodgkins lymphoma: management
Multiagent chemotherapy
51
Define neuroblastoma
Tumour that arises from neural crest tissue in adrenal medulla and sympathetic nervous system
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Spectrum of disease in neuroblastoma
Ganglioneuroma --> neuroblastoma
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Neuroblastoma: clinical features
``` Common: Pallor Weight loss Abdominal mass Hepatomegaly Bone pain Limp ``` ``` Uncommon: Paraplegia Cervical lymphadenopathy Proptosis Periorbital brusing Skin nodules ```
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Neuroblastoma: investigations
1. ) CT/ MRI 2. ) Raised urinary catecholamine metabolite (VMA/ HVA) 3. ) Biopsy 4. ) Bone marrow sampling 5. ) MIBG scan (maps metastatic tumour marrow)
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Neuroblastoma: management
1. ) Surgical resection | 2. ) Chemotherapy (for metastases)
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Neuroblastoma: gene associated with aggressive tumour
Amplification of the MYCN oncogenic gene
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Define Wilms tumour
Nephroblastoma - originates from embryonal renal tissue
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Wilms tumour: clinical features
Large abdo mass Haematuria ``` Less common: Abdo pain Anorexia Anaemia HTN ```
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Wilms tumour: investigations
1.) US/ CT/ MRI
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Wilms tumour: management
1. ) Initial chemotherapy | 2. ) Delayed nephrectomy
61
Define soft tissue sarcoma
Cancer of the connective tissue e.g. muscle or bone
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Most common type of soft tissue sarcoma
Rhabdomyosarcoma
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Rhabdomyosarcoma origin
Primitive mesenchymal tissue
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Rhabdomyosarcoma: clinical features
Head and neck: Proptosis Nasal obstruction Blood stained nasal discharge GU: Dysuria Urinary obstruction Scrotal mass
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Rhabdomyosarcoma: investigations
1. ) Biopsy | 2. ) CT/ MRI
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Rhabdomyosarcoma: management
Surgery, chemotherapy and radiotherapy, depending on extent of disease
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Most common bone tumours
Osteosarcoma | Ewing sarcoma
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Bone tumour: clinical features
Persistent localised bone pain | Usually otherwise fit and well
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Bone tumour: investigations
1. ) Plan x-ray 2. ) MRI 3. ) Bone scan 4. ) Chest CT (to exclude lung mets) 5. ) Bone marrow biopsy (to exclude marrow mets)
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Clinical feutres of bone tumour on X-ray
Destruction and variable periosteal new bone formation
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Bone tumour: management
1. ) Chemotherapy 2. ) En bloc surgical resection with endoprosthetic resection 3. ) Radiotherapy (Ewing sarcoma)
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Define retinoblastoma
Malignant tumour of retinal cells
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Aetiology of retinoblastoma
If bilateral --> hereditary - retinoblastoma susceptibility gene on chromosome 13 - dominant inheritance with incomplete penetrance
74
Retinoblastoma: clinical features
White pupillary reflex (instead of red) | Squint
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Retinoblastoma: investigations
1. ) MRI | 2. ) Examination under anaesthetic
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Retinoblastoma: treatment
1. ) Chemotherapy 2. ) Radiotherapy 3. ) Enucleation as last resort
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Virus that triggers Kaposi sarcoma
Human herpesvirus-8
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Disease associated with Kaposi sarcoma
HIV
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Kaposi sarcoma: origin
Blood or lymph cells
80
Kaposi sarcoma: clinical features
Generalised lymphadenopathy
81
Kaposi sarcoma: investigations
Lymph node biopsy
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Kaposi sarcoma: treatment
Chemotherapy + antiretroviral therapy
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Most common liver tumours
``` Hepatoblastoma (65%) Hepatocellular carcinoma (25%) ```
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Liver tumours: clinical features
Ascites (abdominal distension) Abdominal mass RARE to have pain and jaundice
85
Liver tumours: investigations
1. ) Elevated serum alpha fetoprotein (hepatoblastoma) | 2. ) CT abdomen
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Liver tumours: management
1. ) Chemotherapy 2. ) Surgical resection 3. ) Liver transplant as last resort
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Germ cell tumours: origin
Primitive germ cells which migrate from yolk sac endoderm --> gonads in embryo
88
Germ cell tumours: investigations
1. ) Alpha fetoprotein | 2. ) Beta-hCG
89
Germ cell tumours: management
Chemotherapy
90
Define langerhans cell histiocytosis
Abnormal proliferation of histiocytes
91
Define histiocyte
Type of dendritic antigen presenting cell
92
Langerhans cell histiocytosis: manifestations
Bone - Pain, swelling, fracture - X-ray: lytic lesion with well-defined border Diabetes insipidus Systemic - seborrheic rash - gum, ears, lungs, liver, lymph node involvement
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Langerhans cell histiocytosis: management
Chemotherapy
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Main site of haemopoiesis in fetus
Liver
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Main site of haemopoiesis in infant
Bone marrow
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Composition of fetal haemoglobin (HbF)
2x alpha | 2x gamma
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Compare fetal Hb to adult Hb
Fetal Hb has higher affinity for O2
98
Composition of adult haemoglobin (HbA)
2x alpha | 2x beta
99
Composition of adult haemoglobin (HbA2)
2x alpha | 2x theta
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Newborn ratio of types of Hb
HbF 74% HbA 25% HbA2 1%
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Child >1 ratio of types of Hb
HbA 97% | HbA2 2%
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Average blood volume in newborn
80ml/kg
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Hb concentration at birth
High at >140g/L
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Hb concentration at 2 months
Falls to its lowest level at >100g/L
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Define anaemia
Hb below the normal range
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3 mechanisms that can lead to anaemia
1. ) Reduced red cell production 2. ) Increased red cell destruction (haemolysis) 3. ) Blood loss
107
Aetiology of reduced red cell production
Red cell aplasia: - Parvovirus B19 - Diamond-Blackfan anaemia (congenital) - Transient erythroblastopenia of childhood Ineffective erythropoiesis: - Iron deficiency - Folic acid deficiency - Chronic inflammation (arthritis) - Chronic renal failure
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Aetiology of increased red cell destruction
``` Hereditary spherocytosis Glucose-6-phosphate dehydrogenase deficiency Thalassaemia Sickle cell disease Haemolytic disease of the newborn Autoimmune haemolytic disease ```
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Aetiology of blood loss
Meckel diverticulum --> chronic GI blood loss | Von Willebrand disease --> inherited
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Diagnostic results suggestive of ineffective erythopoeisis
Normal reticulocyte count Abnormal MCV Abnormal ferritin
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Iron deficiency anaemia: aetiology
1. ) Inadequate intake 2. ) Malabsorption 3. ) Blood loss
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Causes of anaemia: low reticulocytes
Reduced red cell production: - Parvovirus B19 - Diamond-Blackfan anaemia
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Causes of anaemia: normal/ high reticulocytes + high bilirubin
Haemolysis: - Hereditary spherocytosis - Thalassaemia - Sickle cell disease
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Causes of anaemia: normal/ high reticulocytes + normal bilirubin
Iron deficiency | Folic acid deficiency
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Red cell aplasia (reduced red cell production): investigations
1. ) Low reticulocyte count 2. ) Low Hb 3. ) Normal bilirubin 4. ) Negative direct antiglobulin test (Coombs test) 5. ) Parvovirus serology 6. ) Bone marrow aspirate - absent red cell precursors
116
Haemolysis: investigations
1. ) Blood film | 2. ) Hb HPLC/ Hb electrophoresis
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Hb HPLC results: sickle cell disease
HbS and no HbA
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Hb HPLC results: beta thalassaemia major
Only HbF
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Hb HPLC results: beta thalassaemia trait
Increased HbA2
120
Hb HPLC results: alpha thalassaemia trait
Normal
121
Blood film results: hereditary spherocytosis
Spherocytes
122
Blood film results: sickle cell disease
Sickle cells + target cells
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Blood film results: thalassaemia/ iron deficiency
Hypochromic microcytic
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Iron deficiency anaemia: clinical features
Tire more easily Feed slower than usual Pale Pallor of conjunctivae/ tongue or palmar creases Pica (inappropriate eating of non-food materials)
125
Iron deficiency anaemia: management
Increase dietary iron | Sytron or Niferex (iron supplements)
126
Diamond-Blackfan anaemia: clinical presentation
Anaemia Short stature Abnormal thumbs
127
Diamond-Blackfan anaemia: treatment
Oral steroids | Monthly red cell transfusions
128
Haemolytic anaemia: investigations
1. ) Raised reticulocyte count 2. ) Increased unconjugated bilirubin and increased urinary urobilinogen 3. ) Abnormal blood film 4. ) Positive direct anti globulin test (autoimmune caused) 5. ) Increased red cell precursors in bone marrow
129
Hereditary sphreocytosis: clinical features
Anaemia Jaundice Splenomegaly Gallstones
130
Hereditary sphreocytosis: management
1.) Folic acid
131
G6PD: inheritance pattern
X-linked
132
Glucose-6-phosphate dehydrogenase deficiency: pathology
Red cells that lack glucose-6-phosphate dehydrogenase are more susceptible to oxidant-induced haemolysis
133
Glucose-6-phosphate dehydrogenase deficiency: drugs that can cause anaemia in children with this condition
Antimalarials: - Primaquine - Quinine - Chloroquine Antibiotics: - Sulphonamides (co-trimoxazole) - Quinolones (ciprofloxacin) - Nitrofurantoin Analgesics: - aspirin
134
Glucose-6-phosphate dehydrogenase deficiency: chemicals that can cause anaemia in children with this condition
Naphthalene (moth balls) | Divine (broad beans)
135
Glucose-6-phosphate dehydrogenase deficiency: clinical features
1. ) Neonatal jaundice 2. ) Acute haemolysis presentation 3. ) Fever, malaise, abdo pain 4. ) Dark urine
136
Glucose-6-phosphate dehydrogenase deficiency: diagnosis
1.) Measure glucose-6-phosphate dehydrogenase levels
137
Glucose-6-phosphate dehydrogenase deficiency: management
1. ) Give parents advice about red flags for haemolytic crisis: - dark urine - jaundice - pallor 2. ) Provide list of foods/ chemicals to avoid
138
Aetiology of beta thalassaemia
Mutation in the beta-globin gene
139
Aetiology of alpha thalassaemia
Deletions in the alpha-globin gene
140
Sickle cell disease: inheritance
Autosomal recessive
141
Sickle cell disease: pathology
Point mutation in codon 6 of beta-globulin gene Changes glutamine --> valine HbS polymerises --> rigid, tubular, spinal bodies --> deforms RBC into sickle shape
142
Sickle cell disease: clinical features
Anaemia Infection Priapism Splenomegaly
143
Sickle cell disease: long-term problems
``` Short stature Delayed puberty Stroke and cognitive problems Adenotonsillar hypertrophy Cardiac enlargement Heart failure ```
144
Sickle cell disease: general management
1. ) Full immunisation 2. ) Daily oral penicillin (children) 3. ) Daily folic acid
145
Sickle cell disease acute crisis: treatment
1. ) Analgesia | 2. ) Hydration
146
Sickle cell disease chronic problems: treatment
Hydroxycarbamide | - increases HbF production
147
Beta-thalassaemia: management
1.) Lifelong monthly blood transfusions
148
Another term for bone marrow failure
Aplastic anaemia
149
Most common form of aplastic anaemia
Inherited aplastic anaemia
150
Inherited aplastic anaemia: inheritance and genes
Autosomal recessive | Mutations of FANC genes
151
Inherited aplastic anaemia: pathology
Mutations in FANC genes --> peripheral blood pancytopenia (low RBC, low WBC and low platelets)
152
Acquired aplastic anaemia: aetiology
Viruses: - hepatitis Drugs: - sulphonamides - chemo Toxins: - benzene - glue
153
Define haemostasis
Normal process of blood clotting
154
Components of haemostasis
1. ) Coagulation factors 2. ) Coagulation inhibitors 3. ) Fibrinolysis 4. ) Platelets 5. ) Blood vessels
155
Location of production of coagulation factors
Liver
156
Coagulation pathway
Prothrombin --> thrombin Fibrinogen --> fibrin (thrombin = enzyme) Fibrin --> fibrin cross-link (clot)
157
Molecule that activates the coagulation factors
Tissue factor, released from vessel during endothelial injury
158
Function of plasmin
Limits fibrin deposition at site of injury
159
Vasodilator molecules secreted by endothelium
Nitric oxide | Prostaglandin I2
160
Function of nitric oxide and prostaglandin I2
Vasodilators | Inhibit platelet aggregation
161
Molecules secreted by endothelium that stimulate the coagulation pathway
Tissue factor vWF (von Willebrand factor) Collagen
162
Molecules secreted by endothelium that inhibit the coagulation pathway
Thrombomodulin Antithrombin Protein S
163
Bleeding disorders: initial screening tests
1. ) FBC and blood film 2. ) PT, factors II, V, VII and X 3. ) APTT 4. ) Thrombin time 5. ) Quantitative fibrinogen assay 6. ) D-dimers
164
Investigations and results: haemophilia A
``` PT: normal APTT: VERY raised Factor VIII:C : VERY low vWF antigen: normal RiCoF activity: normal Ristocetin-induced platelet aggregation: normal vWF multimers: normal ```
165
Investigations and results: von Willebrand disease
``` PT: normal APTT: raised or normal Factor VIII:C : low or normal vWF antigen: low RiCoF activity: low Ristocetin-induced platelet aggregation: abnormal vWF multimers: variable ```
166
Most common bleeding disorders
1. ) Haemophilia A | 2. ) Haemophilia B
167
Haemophilia: inheritance pattern
X-linked recessive
168
Haemophilia A: pathology
Factor VIII deficiency
169
Haemophilia B: pathology
Factor IX deficiency
170
Classification of severity of haemophilia
Mild: >5-40% of relavent factor (VIII in haemophilia A, IX in haemophilia B) Moderate: 1-5% Severe: <1%
171
Mild haemophilia: bleeding tendency
Bleed after surgery
172
Moderate haemophilia: bleeding tendency
Bleed after minor trauma
173
Severe haemophilia: bleeding tendency
Spontaneous joint/ muscle bleeds
174
Haemophilia A: management
IV recombinant factor VIII concentrate is given whenever there is any bleeding OR Desmopressin (DDAVP) can be given (stimulated FVIII:C and vWF release)
175
Haemophilia B: management
IV recombinant factor IX concentrate is given whenever there is any bleeding
176
Complications of treatment of haemophilia
F VIII or F IX antibodies can develop (20% of people) Transfusion-transmitted infections Establishing vascular access may be difficult
177
Functions of vWF (von Willebrand factor)
1. ) Facilitates platelet adhesion to damaged endothelium | 2. ) Carrier protein for FVIII
178
von Willebrand disease: inheritance
Autosomal dominant | Gene defect on chromosome 12
179
von Willebrand disease: clinical features
``` Bruising Excessive, prolonged bleeding after surgery Mucosal bleeding (epistaxis, menorrhagia) ```
180
von Willebrand disease: management
Type 1: 1.) Desmopressin (DDAVP) Other types: 1.) Plasma-derived FVIII concentrate
181
Factors dependent on vitamin K
II, VII, IX, X
182
Define thrombocytopenia
Platelet count less than 150 x10^9/L
183
Thrombocytopenia: clinical features
Bruising Petechiae Purpura Mucosal bleeding
184
Most common form of thrombocytopenia
ITP - immune thrombocytopenia
185
ITP: pathology
Destruction of circulating platelets by antiplatelet IgG autoantibodies
186
ITP: diagnosing
Diagnosis of exclusion
187
Acute ITP: management
``` Treatment is usually unnecessary If evidence of major bleed: 1.) Oral prednisolone 2.) IV anti-D 3.) IV Ig ```
188
Chronic ITP: management
Rituximab | Splenectomy
189
Define disseminated intravascular coagulation (DIC)
Activation of the coagulation pathway that leads to fibrin deposits in the microvasculature and consumes the platelets and factors
190
DIC: aetiology
Severe sepsis | Cardiogenic shock
191
DIC: clinical features
Bruising Purpura Haemorrhage
192
DIC: investigation results
``` Thrombocytopenia Prolonged PT Prolonged APTT Low fibrinogen Raised fibrinogen degradation products Reduction in protein C and S Reduction in antithrombin ```
193
DIC: management
1. ) Treat underlying cause 2. ) Fresh frozen plasma (to replenish factors) 3. ) Antithrombin and protein C concentrates
194
Define thrombophilia
Inherited abnormalities in coagulation and fibrinolytic pathways
195
Types of thrombophilia
Protein C deficiency Protein S deficiency Antithrombin deficiency Factor V leiden
196
Diagnosing thrombophilia
Screening: - Protein C and S assays - Antithrombin assay - Factor V leiden PCR - Prothrombin gene PCR
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