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Alice's finals cards > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Give 3 signs of respiratory distress in a child.

A
  1. Tachypnoea, RR 40-60.
  2. Subcostal and intercostal recession.
  3. Stridor.
  4. Tracheal tug.
  5. Cyanosis.
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2
Q

Describe the epidemiology of ADHD.

A

5% school aged children.

M:F = 4:1

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3
Q

Describe the aetiology of ADHD.

A
  • Genetic and environmental.
  • Neuroanatomical and neurochemical factors too.
  • CNS insults e.g. FAS or premature.
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4
Q

What are the 3 core behaviours of ADHD?

A
  1. Hyperactivity.
  2. Inattention.
  3. Impulsivity.
    (HII)
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5
Q

ADHD core behaviours: give 3 signs of hyperactivity.

A
  1. Fidgety.
  2. Talkative.
  3. Noisy.
  4. Can’t remain seated.
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6
Q

ADHD core behaviours: give 3 signs of impulsivity.

A
  1. Blurts out answers.
  2. Interrupts.
  3. Difficulty waiting turns.
  4. When older, pregnancy and drug use.
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7
Q

ADHD core behaviours: give 3 signs of inattention.

A
  1. Easily distracted.
  2. Not listening.
  3. Mind wandering.
  4. Struggling at school.
  5. Forgetful.
  6. Organisational problems.
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8
Q

What is the diagnostic criteria for ADHD?

A

6/9 inattentive symptoms and 6/9 hyperactivity/impulsivity.

The symptoms are present before 12 years and occur in more than one place and in a primary setting. There is clear evidence that symptoms interfere with social/academic function.

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9
Q

What tools can be used in order to diagnose ADHD?

A
  1. Clinical interview - are there any RF’s for ADHD?
  2. ADHD nurse classroom observation.
  3. Questionnaires (SNAP).
  4. Quantitative behavioural (QB) analysis.
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10
Q

Describe the treatment for ADHD.

A
  1. Education.
  2. Parenting programmes and school support.
  3. Medications e.g. methylphenidate.
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11
Q

Why is it important to do a cardiac assessment before prescribing medications to help treat a child with ADHD.

A

Some ADHD medications can affect HR and BP and so it is important to do a cardiac assessment first.

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12
Q

Describe the epidemiology of ASD.

A

1% prevalence.

Boys>girls.

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13
Q

Give 4 signs of ASD.

A
  1. Communication problems.
  2. Social interaction difficulties.
  3. Social imagination difficulties.
  4. Sensory issues.
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14
Q

ASD signs: what communication problems might a child with ASD show?

A
  • They may find non-verbal communication very challenging.
  • Lack of desire to communicate.
  • Tendency to communicate needs only.
  • No understanding of jokes, very literal.
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15
Q

ASD signs: what social interaction problems might a child with ASD show?

A
  • Overly friendly or overly shy.
  • Struggles to understand social roles.
  • Often no desire to interact with others.
  • Touches inappropriately, plays alone, poor eye contact, finds it hard to take turns.
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16
Q

ASD signs: what social imagination problems might a child with ASD show?

A
  • Struggles with change.
  • Obsessions/rituals.
  • Repetitive with play.
  • Unable to play or write imaginatively.
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17
Q

Describe the treatment for ASD.

A
  • Education and games to encourage social communication.
  • Visual aids and timetables.
  • Parenting workshops and school liaison.

There are no medications available for ASD.

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18
Q

What are the liver dependent clotting factors?

A

2, 7, 9 and 10.

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19
Q

Name 2 coagulopathies.

A
  1. Von Willebrand disease.

2. Haemophilia.

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20
Q

Briefly describe the pathophysiology behind Von Willebrand disease.

A

Bleeding disorder due to an abnormality of vWF. vWF acts as an adhesive bridge between platelets and the damaged sub-endothelium. Without it it takes longer for bleeding to stop.

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21
Q

Describe the treatment for VWD.

A

There is no cure.

But desmopressin can be used to try increase vWF levels
| Pressure should be applied to try and minimise bleeding and tranexamic acid can be taken.

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22
Q

Describe the inheritance pattern seen in haemophilia.

A

X linked recessive.

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23
Q

Haemophilia A is due to a deficiency in which clotting factor?

A

Factor VIII.

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24
Q

Haemophilia B is due to a deficiency in which clotting factor?

A

Factor IX.

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25
Q

Give 3 signs of haemophilia.

A
  1. Easy bruising.
  2. Haematomas.
  3. Mouth bleeds.
  4. Joint bleeds - prophylaxis should be given to prevent this.
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26
Q

Give 2 causes of thrombocytopenia in children.

A
  1. ITP.

2. Marrow failure.

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27
Q

Give 3 signs of thrombocytopenia.

A
  1. Petechial rash.
  2. Bruising.
  3. Bleeding.
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28
Q

What diagnosis would you suspect in a child with a single figure platelet count but is otherwise well?

A

ITP.

They would have a normal blood film and clotting, just very low platelets.

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29
Q

What can trigger acute ITP?

A

Viral infection.

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30
Q

What is the most common cause of anaemia in children?

A

Iron deficiency.

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31
Q

Give 3 signs of anaemia in children.

A
  1. Pallor.
  2. Irritable.
  3. Lethargy.
  4. SOB.
  5. Tachycardic.
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32
Q

What is the treatment for iron deficiency anaemia?

A

Ferrous sulphate tablets.

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33
Q

Why does the treatment for iron deficiency anaemia sometimes fail?

A

Treatment can often fail due to non-compliance.

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34
Q

Give 3 signs of beta thalassaemia major.

A
  1. Severe anaemia.
  2. Jaundice.
  3. Splenomegaly.
  4. Failure to thrive.
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35
Q

Describe the management of beta thalassaemia major.

A
  • Genetic counselling.
  • Blood transfusions.
  • Iron chelation.
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36
Q

What does a low reticulocyte count indicate?

A

A production problem e.g. infection, renal disease, drugs, marrow failure/infiltration.

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37
Q

What does a high reticulocyte count indicate?

A

A degradation problem e.g. bleeding or haemolysis.

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38
Q

Give 3 consequences of sickle cell disease.

A
  1. Anaemia.
  2. Infection.
  3. Painful crises.
  4. Stroke.
  5. Acute chest infection/infarction.
  6. Splenic sequestration.
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39
Q

Describe the inheritance pattern seen in sickle cell disease.

A

Autosomal Recessive.

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40
Q

What is the affect of sickle cell disease on Hb and reticulocyte count?

A

Low Hb.

Raised reticulocyte count.

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41
Q

Describe the treatment for sickle cell disease.

A
  • Hydroxyurea - for prevention of crisis
  • Transfusions.
  • Stem cell transplants.
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42
Q

What can trigger spherocytosis?

A

Parvovirus infection.

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43
Q

Describe the inheritance pattern seen in hereditary spherocytosis.

A

Autosomal Dominant.

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44
Q

How can spherocytosis be treated?

A

Folate replacement & Splenectomy - can increase RBC survival.

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45
Q

What type of leukaemia is most common in children?

A

ALL.

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46
Q

Give 3 symptoms of ALL.

A
  1. Anaemia.
  2. Bleeding.
  3. Bruising.
  4. Bone/limb pain.
  5. Infections.
  6. Tired.
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47
Q

Describe the treatment for ALL.

A

2 years combination chemotherapy.

CNS directed therapy.

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48
Q

Give an example of a live, attenuated vaccine.

A

MMR.
BCG.
Rotavirus (oral vaccine).

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49
Q

Give an example of an inactivated vaccine.

A

Influenza.

Diphtheria.

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50
Q

Name 5 vaccine preventable diseases.

A
  1. Tetanus.
  2. Diphtheria.
  3. Whooping cough.
  4. Polio.
  5. Measles.
  6. Mumps.
  7. Rubella.
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51
Q

What virus can cause croup?

A

Parainfluenza virus.

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52
Q

Name 2 respiratory infections that are common in paediatrics.

A
  1. Croup.

2. Bronchiolitis.

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53
Q

Give 3 signs of bronchiolitis.

A
  1. Recurrent cough.
  2. Noisy breathing.
  3. Crackles and wheeze.
  4. Use of respiratory muscles.
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54
Q

What viruses can cause bronchiolitis.

A
  1. RSV = main causative organism!

Also: rhinovirus, influenza, adenovirus, parainfluenza virus.

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55
Q

What is croup?

A

Acute larygnotracheobronchitis - trachea, bronchi and larynx are all affected.

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56
Q

You do a lumbar puncture and find raised proteins and low glucose. Is this likely to be due to a bacterial or a viral infection?

A

Bacterial.

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57
Q

Give 3 signs of immune deficiency.

A
  1. Frequent infections.
  2. Infection with unusual organisms.
  3. Severe infections.
  4. Failure to thrive.
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58
Q

How much should you feed to a neonate?

A

150ml/Kg/day.

Day 1: 60ml/kg/day Day 2: 90ml/kg/day Day 3: 120ml/kg/day Day 4: 150ml/kg/day

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59
Q

What fluid would you give to a neonate?

A

0.9% Sodium Chloride + 5% glucose +/- KCl

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60
Q

How do you calculate the rate at which to give maintenance fluids to a child?

A

100ml/Kg/day for first 10Kg.
50ml/Kg/day for the next 10Kg.
20ml/Kg/day for every Kg after that.

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61
Q

When taking a history from a teenager, the HEADDS framework can be used. Describe this framework.

A 
Home.
Education.
Activity.
Drugs/alcohol.
Depression/suicide.
Sexuality.
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62
Q

Radiology: give 5 ways in which imaging a child differs to imaging an adult?

A
  1. Size.
  2. Growth plates.
  3. Skill sutures.
  4. Ossification.
  5. Congenital problems e.g. dextrocardia and osteogenesis imperfecta.
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63
Q

When might an abdominal XR be indicated on a child?

A
  1. Abdominal distension e.g. obstruction.
  2. Abdominal pain of unknown cause.
  3. Constipation.
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64
Q

What are the 3 main differentials for a limping child?

A
  1. Infection e.g. sepsis/osteomyelitis.
  2. Trauma e.g. NAI, fracture.
  3. Tumour.
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65
Q

What is the likely cause of a limp in a child aged 0-3?

A
  1. NAI.
  2. Osteomyelitis/septic arthritis.
  3. DDH.
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66
Q

What is the likely cause of a limp in a child aged 3-10?

A
  1. Trauma.
  2. Transient synovitis.
  3. Osteomyelitis.
  4. Perthe’s disease.
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67
Q

What is the likely cause of a limp in a child aged 10-15?

A
  1. Trauma.
  2. Osteomyelitis.
  3. SCFE.
  4. Perthe’s disease.
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68
Q

What must you remember to consider as a differential in a limping child?

A

Intra-abdominal pathology e.g. hernia, testicular torsion.

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69
Q

Why might you want to ask about socioeconomic class and smoking status in a child presenting with a limp?

A

Social deprivation and passive smoking are RF’s for Perthe’s disease.

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70
Q

What investigations might you want to do on a child presenting with a limp?

A
  1. General observations e.g. HR, BP, T, RR, O2 sats.
  2. FBC, BM, ESR and CRP.
  3. XR - AP and lateral views of the the joint and the joints above and below.
  4. USS - effusion in joints?
  5. CT/MRI.
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71
Q

Describe Kocher’s criteria.

A

Criteria for septic joint
~~~
T>38.5
CRP>20
ESR>40
WCC>12
Cannot weight bear
~~~

3/4 = septic joint.

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72
Q

Give 3 signs of septic arthritis.

A
  1. Systemically very unwell.
  2. Pain at rest.
  3. Raised WCC and CRP.
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73
Q

What is transient synovitis?

A

Acute onset joint inflammation following illness often respiratory.

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74
Q

How does transient synovitis differ from septic arthritis?

A

Transient synovitis: no pain at rest, XR normal, USS may show effusion, rest, physiotherapy and NSAIDs often help.

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75
Q

What is DDH?

A

DDH - developmental dysplasia of the hip.

Abnormal relationship of the femoral head to the acetabulum -> aberrant development of the hip.

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76
Q

Give 3 risk factors for DDH.

A
  1. Female (M:F - 1:8).
  2. First born.
  3. Breech birth.
  4. Family history.
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77
Q

What tests can be done on clinical examination in the neonatal period to pick up DDH?

A
  1. Ortolani test.
  2. Barlow manoeuvre.

Can be confirmed with USS.

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78
Q

What 3 lines can be drawn to aid diagnosis of DDH?

A
  1. Hilgenreiner line
  2. Perkin line – perpendicular to Hilgenreiner line.
  3. Shenton line.
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79
Q

Describe the management of DDH.

A
  1. Pavlik harness.

2. Surgical reduction.

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80
Q

What are the 2 main risks associated with the surgical management of DDH.

A
  1. Avascular necrosis.

2. Re-dislocation.

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81
Q

What is Perthe’s disease?

A

A self-limiting idiopathic disease characterised by avascular necrosis of the femoral head.

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82
Q

Describe the management of Perthe’s disease.

A

Contain the hip, either on their own or with the aid of plasters, brace, physiotherapy or surgery.

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83
Q

Give 3 risk factors for Perthe’s disease.

A
  1. ADHD.
  2. Deprivation.
  3. Passive smoking.
  4. LBW.
  5. Short stature.
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84
Q

What is SCFE?

A

Slipped capital femoral epiphysis - a fracture through the growth plate leads to slippage of the femoral head through the zone of hypertrophy.

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85
Q

Through what zone of the physeal cartilage does the femoral head slip through in SCFE?

A

The zone of hypertrophy.

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86
Q

Who is likely to be affected by SCFE?

A

A pre-pubescent obese male.

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87
Q

How does SCFE present?

A

The patient may complain of a several week history of vague groin or thigh discomfort. In 40% this will be bilateral. They may have a waddling gait and a decreased range of motion.

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88
Q

What is the treatment for SCFE?

A

internal fixation with a screw

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89
Q

What is chondrosarcoma?

A

A malignant neoplasm of cartilage.

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90
Q

What is the criteria for making a clinical diagnosis of juvenile idiopathic arthritis?

A

Joint swelling/stiffness >6 weeks in children <16 and no other cause is identified.

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91
Q

What symptoms are associated with JIA?

A
  1. Fever.
  2. Salmon-pink rash.
  3. Uveitis.
  4. Pain.
  5. Morning stiffness.
  6. Swelling.
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92
Q

Describe the non-medical treatment for JIA.

A
  1. Information.
  2. Education.
  3. Support.
  4. Liaison with school.
  5. Physiotherapy.
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93
Q

Describe the medical treatment for JIA.

A
  1. Steroid joint injections.
  2. NSAIDS.
  3. Methotrexate.
  4. Systemic steroids.
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94
Q

Give 5 potential consequences that can occur if you fail to treat JIA.

A
  1. Damage.
  2. Deformity.
  3. Disability.
  4. Pain.
  5. Bony overgrowth.
  6. Uveitis.
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95
Q

Define child development.

A

The biological, psychological and emotional changes that occur between birth and adolescence as the individual progresses from dependency to increasing autonomy. It is a continuous process with a predictable sequence however each child’s development is unique.

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96
Q

Give 5 influences on a child’s development.

A
  1. Genetic factors.
  2. Stimulating environment.
  3. Pregnancy factors e.g. premature? Mums health?
  4. Healthy attachment.
  5. Medical conditions.
  6. Abuse/neglect/domestic violence.
  7. Healthy peer relationships.
  8. Education.
  9. Nutrition.
  10. Parenting style.
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97
Q

What are the 4 domains of child development?

A
  1. Gross motor.
  2. Fine motor and vision.
  3. Speech, language and hearing.
  4. Social interaction and self care skills.
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98
Q

What are the developmental milestones for gross motor function?

A
  • 3m: lifts head on tummy.
  • 6m: chest up with arm support, can sit unsupported.
  • 8m: crawling.
  • 9m: pulls to stand.
  • 12m: walking.
  • 2 years: walking up stairs.
  • 3 years: jumping.
  • 4 years: hopping.
  • 5 years: rides a bike.
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99
Q

With regards to gross motor development, at what age would you expect a child to do the following:

a) walking.
b) jumping.
c) crawling.
d) walking up stairs.

A

a) Walking - 12 months.
b) Jumping - 3 years.
c) Crawling - 8 months.
d) Walking up stairs - 2 years.

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100
Q

What are the developmental milestones for fine motor and visual function?

A
  • 4m: grabs an object using both hands.
  • 8m: takes objects in each hand.
  • 12m: scribbles with crayons e.g. circle, cross, square.
  • 18m: builds a tower of 2 cubes.
  • 3 years: builds a tower of 8 cubes.
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101
Q

With regards to fine motor and visual development, at what age would you expect a child to do the following:

a) drawing with crayons.
b) building a tower of 8 cubes.
c) takes an object in each hand.
d) builds a tower of 2 cubes.

A

a) Drawing with crayons - 12m.
b) Building a tower of 8 cubes - 3 years.
c) Takes an object in each hand - 8m.
d) Builds a tower of 2 cubes - 18m.

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102
Q

What are the developmental milestones for speech, language and hearing?

A
  • 3m: laughs and squeals.
  • 9m: can make sounds such as ‘dada’ and ‘mama’.
  • 12m: can say one word.
  • 2 years: can form short sentences and name body parts.
  • 3 years: speech is mainly understandable.
  • 4 years: knows colours and can count.
  • 5 years: knows the meaning of words.
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103
Q

With regards to speech, language and hearing, at what age would you expect a child to do the following:

a) form short sentences and name body parts.
b) knows colours and can count.
c) laughs and squeals.
d) has mainly understandable speech.

A

a) Forms short sentences and name body parts - 2 years.
b) Knows colours and can count - 4 years.
c) Laughs and squeals - 3 months.
d) Has mainly understandable speech - 3 years.

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104
Q

What are the developmental milestones for social interaction and self-care skills?

A
  • 6 weeks: smiles.
  • 6 months: finger feeds.
  • 9m: waves bye-bye.
  • 12m: uses cutlery.
  • 2 years: undresses, feeds toys.
  • 3 years: plays with others, names a friend.
  • 4 years: dresses with no help, plays a board game.
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105
Q

With regards to social interaction and self-care skills, at what age would you expect a child to do the following:

a) uses cutlery.
b) plays with others, names a friend.
c) smiles.
d) waves bye-bye.

A

a) Uses cutlery - 12 months.
b) Plays with others, names a friend - 3 years.
c) Smiles - 6 weeks.
d) Waves bye-bye - 9 months.

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106
Q

What does ‘The healthy child programme’ encourage?

A
  1. Encourages care to keep children healthy and safe.
  2. Promotes healthy eating and activity.
  3. Identifies problems in children’s development.
  4. Identifies ‘at risk’ families for more support.
  5. Ensures children are prepared for school.
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107
Q

Give two examples of concerning child development with regards to gross motor function.

A
  1. Not sitting by 12 months.

2. Not walking by 18 months.

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108
Q

Give an example of concerning child development with regards to fine motor function.

A

Hand preference before 18 months.

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109
Q

Give two speech and language examples that may suggest concerning child development.

A
  1. Not smiling by 3 months - blindness? ASD?

2. No clear words by 18 months - ASD? Language problems?

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110
Q

Give two examples of concerning child development with regards to social development.

A
  1. No response to carers interactions by 8 weeks.

2. No interest in playing by 3 years.

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111
Q

Give 5 causes of developmental delay.

A
  1. Genetics.
  2. Pregnancy.
  3. Factors around birth.
  4. Factors in childhood.
  5. Environmental.
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112
Q

Causes of developmental delay: give examples of genetic causes.

A
  1. Chromosomal disorders e.g. Down’s syndrome.
  2. Single gene disorders e.g. Duchenne.
  3. Polygenic e.g. ASD, ADHD.
  4. Micro-deletions or micro-duplications.
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113
Q

Causes of developmental delay: give examples of pregnancy related causes.

A
  1. Congenital infections e.g. CMV, HIV.
  2. Exposure to drugs/alcohol e.g. FAS.
  3. MCA infarct.
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114
Q

Causes of developmental delay: give examples of birth related causes.

A
  1. Prematurity.

2. Birth asphyxia (due to hypoxia).

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115
Q

Causes of developmental delay: give examples of medical causes that may occur during childhood.

A
  1. Infections e.g. meningitis.
  2. Chronic illness.
  3. Hearing or visual impairment.
  4. Acquired brain injury.
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116
Q

Causes of developmental delay: give examples of environmental causes.

A
  1. Abuse and neglect.

2. Low stimulation.

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117
Q

How might you investigate someone’s child development if you suspected that there was something wrong?

A

Thorough history and examination. Tailor any investigations to the child e.g.

  • Boys not walking by 18m check creatinine kinase for Duchenne.
  • Focal neurological signs -> MRI brain.
  • Genetic testing.
  • Unwell, failure to thrive -> metabolic investigations.

There is no ‘developmental screen’, investigations need to be tailored towards to the child.

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118
Q

Define childhood disability.

A

Someone who has a physical or mental impairment that results in a marked, pervasive limitation on activity. For example, Down’s syndrome and Cerebral Palsy.

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119
Q

Give 3 factors that influence childhood disability.

A
  1. Environment.
  2. Social background.
  3. Impairment.
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120
Q

Give 3 signs of down’s syndrome.

A
  1. Learning/developmental delay.
  2. Hypotonia.
  3. Short stature.
  4. CHD.
  5. Brushfield spots.
  6. upslanting palpebral fissures
  7. flat occiput
  8. Single palmar crease
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121
Q

What is cerebral palsy?

A

A permanent, non-progressive cerebral pathology that leads to handicap and disability in children.

A non progressive developmental disorder of movement and posture.

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122
Q

Give 3 causes of cerebral palsy.

A

80% antenatal - hypoxia, infection, haemorrhage, ischaemia.

10% peri-natal - hypoxia, infection, haemorrhage.

10% postnatal - hypoxia, infection e.g. meningitis, haemorrhage, encephalopathy, trauma.

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123
Q

Describe the support that is offered to someone with cerebral palsy.

A
  1. Physiotherapists for mobility and hand function.
  2. SALT for communication.
  3. Feeding support.
  4. Sleeping support.

Support for children with disabilities needs to be holistic, child focused and with an MDT approach.

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124
Q

Name 3 embryonal tumours.

A
  1. Wilm’s tumour.
  2. Neuroblastoma.
  3. Rhabdomyosarcoma.
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125
Q

Give examples of children who are at increased risk of cancer.

A
  1. Down’s syndrome children are at increased risk of leukaemia.
  2. Immunocompromised children are at increased risk of lymphoma.
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126
Q

An abnormal red reflex in a child may be a sign of what paediatric malignancy?

A

Retinoblastoma.

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127
Q

Give 5 signs of ALL.

A
  1. Fever.
  2. Fatigue.
  3. frequent infections.
  4. Bruising.
  5. Bone pain - not wanting to weight bear.
  6. Anaemia.
  7. Lymphadenopathy.
  8. Hepatosplenomegaly.
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128
Q

What investigations might you do in a child to determine whether they have ALL?

A
  1. Blood film.
  2. Serum chemistry.
  3. CXR.
  4. BM aspirate.
  5. Lumbar puncture - see if disease is in the CSF.
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129
Q

Describe the treatment for ALL.

A

5 phase chemotherapy.
A stem cell transplant may be needed for high risk or relapsed patients.

The treatment is 2 years for girls and 3 years for boys.

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130
Q

Treatment of ALL: what are the 5 phases of chemotherapy?

A
  1. Induction.
  2. Consolidation.
  3. Interim maintenance.
  4. Intensification.
  5. Maintenance.
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131
Q

Give 5 signs of CNS malignancy in children.

A
  1. Early morning headache.
  2. Headache that is worse on lying down.
  3. Vomiting - especially in the morning.
  4. Papilloedema.
  5. Squint.
  6. Nystagmus.
  7. Ataxia.
  8. Personality or behavioural change.
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132
Q

Describe the general treatment for CNS malignancies.

A
  1. Surgical resection + VP shunt (reduces the risk of coning).
  2. Chemotherapy.
  3. Radiotherapy.
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133
Q

Why are there fewer chemotherapy options available for children with CNS malignancies?

A

Because there are fewer chemotherapy drugs able to penetrate the BBB.

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134
Q

Give 5 signs that lymphadenopathy may be due to malignancy rather than a benign cause e.g. infection.

A
  1. Enlarging node without infective cause.
  2. Persistently enlarged.
  3. Unusual site e.g. supra-clavicular.
  4. B symptoms e.g. fever, weight loss.
  5. Abnormal CXR.
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135
Q

What is the treatment for lymphoma?

A

Combination chemotherapy.

High dose therapy and stem cell transplantation is offered to those who have relapsed.

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136
Q

Give 5 differential’s for abdominal mass in children.

A
  1. Hepatoblastoma.
  2. Wilm’s tumour.
  3. Neuroblastoma.
  4. Lymphoma/leukaemia.
  5. Constipation/bowel obstruction.
  6. Enlarged kidneys - polycystic.
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137
Q

What investigations might you do on a child with an abdominal mass?

A
  • USS.
  • CT.
  • Biopsy.
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138
Q

What is are neuroblastoma tumours?

A

Tumours arising from neural crest tissue in the adrenal medulla and sympathetic nervous system.

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139
Q

Give 2 signs of a neuroblastoma tumour.

A
  1. Abdominal mass - often crosses the midline and envelopes major vessels and lymph nodes.
  2. Symptoms of metastases e.g. bone pain, weight loss, pallor, limp, hepatomegaly.
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140
Q

Describe the treatment for a neuroblastoma malignancy.

A
  • Surgery - localised primaries can often be cured with surgery alone.
  • Chemotherapy - can be given before and/or after surgery to control disease.
  • Radiotherapy for high risk groups.
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141
Q

What is Wilm’s tumour?

A

Nephroblastoma, malignancy arising from embryonal renal tissue.

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142
Q

Give 3 signs of Wilm’s tumour.

A
  1. Abdominal mass.
  2. Haematuria.
  3. Abdominal pain.
  4. Anorexia.
  5. Anaemia.
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143
Q

Describe the treatment for Wilm’s tumour.

A
  • Chemotherapy - before and after surgery.
  • Nephrectomy.
  • Radiotherapy for higher stage disease.
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144
Q

Describe the aetiology of retinoblastoma.

A
  1. Mutations in RB1 (tumour suppressor gene) located on chromosome 13.
  2. Familial (AD).
  3. Sporadic.
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145
Q

Give 3 signs of retinoblastoma.

A
  1. Loss of red reflex.
  2. Pain around the eye.
  3. Poor vision.
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146
Q

Describe the treatment for retinoblastoma.

A

Laser therapy is 1st line!

Chemotherapy and radiotherapy may also be indicated.

Phototherapy.
Surgical repair/removal.

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147
Q

Give 3 late effects of cancer treatment in children.

A
  1. Endocrine related e.g. growth and development problems.
  2. Intellectual.
  3. Fertility problems.
  4. Psychological issues.
  5. Cardiac and renal toxicity.
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148
Q

Define osteoporosis in children.

A

> 1 vertebral crush fracture OR

Bone density 2 long bone fractures (before age 10) or >3 fractures (age 19).

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149
Q

Describe the aetiology of osteoporosis in children.

A
  1. Inherited/congenital e.g. osteogenesis imperfecta, inborn errors, idiopathic.
  2. Acquired e.g. drug induced, malabsorption, immobilisation.
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150
Q

What investigation might you do to determine if a child has osteoporosis?

A

DEXA scan.

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151
Q

What is osteogenesis imperfecta and what causes it?

A

An AD inherited osteoporotic condition that leads to bone weakness in children. It is due to a defect in type 1 collagen genes.

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152
Q

Describe the aetiology of osteogenesis imperfecta.

A

AD inheritance in 90%.

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153
Q

Give 5 signs of osteogenesis imperfecta.

A
  1. Bone fragility.
  2. Fractures.
  3. Deformity.
  4. Pain.
  5. Impaired mobility.
  6. Poor growth.
  7. Deafness.
  8. Blue sclera.
  9. Bruises.
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154
Q

What classification is used in osteogenesis imperfecta?

A

The Sillence classification.

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155
Q

Describe the treatment of osteogenesis imperfecta.

A

MDT approach - physicians, surgeons, physiotherapists, OT’s.

Bisphosphonates e.g. pamidronate.

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156
Q

What is Rickets?

A

A disorder of bone mineralisation, it leads to bone weakness.

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157
Q

What is the main cause of Rickets?

A

Vitamin D deficiency.

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158
Q

Give 4 signs of Rickets.

A

aching bones and joints
lower limb abnormalities: in toddlers genu varum (bow legs,) in older children - genu valgum (knock knees)
‘rickety rosary’ - swelling at the costochondral junction (where rib joins the sternum)
kyphoscoliosis

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159
Q

What might you find when examining a child with Rickets?

A
  • Metaphyseal swelling.
  • Bone deformity e.g. bowed legs.
  • Motor delay.
  • Hypotonia.
  • Fractures.
  • Cupping and spraying seen on XR.
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160
Q

What investigations might you do to determine if a child has Rickets?

A
  1. Serum biochemistry e.g. ALP, PTH.
  2. Bone profile.
  3. Measure vitamin D levels.
  4. XR.
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161
Q

Describe the treatment for Rickets.

A

Treat the underlying problem.

If vitamin D deficiency, give Adcal D3.

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162
Q

What is the role of vitamin D?

A

It acts to increase Ca absorption at the gut and Ca reabsorption at the kidneys.

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163
Q

Give 3 sources of vitamin D.

A
  1. Sunlight!
  2. Cereals.
  3. Egg yolk.
  4. Oily fish.
  5. Spreads.
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164
Q

Secretion of which hormone will increase in response to low calcium?

A

PTH.

Increased PTH = bone resorption, Ca reabsorption at kidneys and Ca absorption at gut.

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165
Q

Give 5 differentials for a painful joint.

A

Life-threatening differentials:

  • Leukaemia.
  • Septic arthritis.
  • NAI.

Pain and swelling:

  • Trauma.
  • Infection.
  • Reactive arthritis.
  • JIA.

Pain and no swelling:

  • Hypermobile joint syndrome.
  • Perthe’s disease.
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166
Q

What investigations might you do on a child who you suspect may have JIA?

A
  • Thorough history and examination.
  • Lab tests/imaging in order to exclude other causes.
  • Ophthalmology review.
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167
Q

Name 5 types of JIA.

A
  1. Oligoarticular.
  2. Polyarticular.
  3. Psoriatic.
  4. Enthesitis related.
  5. Systemic onset JIA.
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168
Q

Define pauciarticular JIA.

A

<4 joints involved, often asymmetrical. Normally ANA+ and associated with a high risk of developing uveitis.

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169
Q

Define polyarticular JIA.

A

> 4 joints involved, often symmetrical and more destructive.

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170
Q

What extra-articular features might you see in someone with JIA?

A

pyrexia
salmon-pink rash
lymphadenopathy
arthritis
uveitis
anorexia and weight loss

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171
Q

Which type of JIA is most similar to ankylosing spondylitis?

A

Enthesitis related arthritis.

The point where the tendon joins a bone is inflamed.

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172
Q

Which antigen is closely associated with enthesitis related arthritis?

A

HLAB27.

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173
Q

What signs might you see in someone with systemic onset JIA?

A
  • Rash.
  • Lymphadenopathy/organomegaly.
  • Fever.
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174
Q

Name a severe, potentially life-threatening complication of systemic onset JIA.

A

Macrophage-activation syndrome (MAS).

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175
Q

What signs might you see in someone with macrophage-activation syndrome (MAS)?

A
  • High fever.
  • Hepatosplenomegaly.
  • CNS dysfunction.
  • Purpuric rash.
  • Cytopaenia.
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176
Q

What is the treatment for macrophage-activation syndrome (MAS)?

A
  • Supportive treatment.

- Steroids.

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177
Q

Give 5 signs of SLE.

A
  1. Malar rash.
  2. Discoid rash.
  3. Photosensitivity.
  4. Oral ulcers.
  5. Arthritis.
  6. Pleuritis.
  7. Pericarditis.
  8. Renal failure.
  9. Seizures.
  10. Thrombocytopenia.
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178
Q

What is the most common causative organism of UTI in children?

A

E.coli.

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179
Q

Give 3 signs of UTI in children.

A
  1. Fever.
  2. Miserable.
  3. Vomiting.
  4. Dysuria.
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180
Q

What investigations might you do on a child who you suspect has a UTI?

A
  1. Urine dip.
  2. MCS on clean catch urine. A sample can also be obtained using an in-out catheter.
  3. USS KUB.
  4. DMSA - renal scarring.
  5. MCUG - reflux.
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181
Q

What is the treatment for UTI in children?

A

IV cefuroxime.

Switch to PO trimethoprim if stable.

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182
Q

How would you treat a UTI that has been caused by ESBL e.coli?

A

You would give meropenem.

ESBL bacteria are resistant to all penicillins and cephalosporins.

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183
Q

Name an organism that commonly causes osteomyelitis in children.

A

Staphylococcus aureus.

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184
Q

Give 3 signs of osteomyelitis in children.

A
  1. Joint pain.
  2. Lethargy.
  3. Fever.
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185
Q

What investigations might you do on a child who you suspect has an infected joint?

A
  • XR.
  • MRI.
  • Blood cultures.
  • Joint aspirate.
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186
Q

How would you treat a child with osteomyelitis?

A

Flucloxacillin for 6 weeks. Clindamycin if allergic

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187
Q

What bacteria commonly causes meningitis in children?

A
  • Neonates: Group B strep, E.coli, lysteria monocytogenes.
  • 1m -> 6 years: Neisseria meningitidis, S.pneumoniae, H.influenzae.
  • > 6 years: Neisseria meningitidis.
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188
Q

What investigations might you do on a child who you suspect has meningitis?

A
  • Thorough history and examination.
  • Blood cultures.
  • Lumbar puncture.
  • EDTA blood for PCR.
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189
Q

Describe the treatment for a child with meningitis.

A

IV ceftriaxone (80mg/kg/od) or cefotaxime (50mg/kg/tds).

Prophylaxis is needed to prevent further spread.
Dexamethasone is given to reduce swelling.

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190
Q

Who must you notify when you diagnose a child with meningitis?

A

Public Health England.

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191
Q

Give 3 bacterial organisms that commonly cause pneumonia in children.

A
  1. Group B strep in neonates.
  2. S.pneumoniae.
  3. H.influenzae.
  4. K.pneumoniae.
  5. M.pnuemoniae.
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192
Q

Give 5 signs of pneumonia in children.

A
  1. Fever.
  2. Miserable.
  3. Rapid breathing.
  4. Cough.
  5. Poor feeding.
  6. Lethargy.
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193
Q

What investigations might you do in a child who you suspect has pneumonia?

A
  • CXR: look for consolidation.
  • Blood cultures.

It is often difficult to get a sputum sample.

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194
Q

Briefly describe the treatment for a child with pneumonia.

A

Amoxicillin first line for all children presenting with pneumonia

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195
Q

What is the difference between wheeze and stridor?

A

Wheeze: polyphonic noise heard on expiration.

Stridor: monophonic high pitched noise heard on inspiration.

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196
Q

list the differentials of recurrent wheeze.

A
  1. Persistent infantile wheeze.
  2. Viral episodic wheeze.
  3. Asthma.
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197
Q

What is persistent infantile wheeze normally associated with/exacerbated by?

A

Persistent infantile wheeze tends to affect the small airways. It is associated with parental smoking or post-viral infection.

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198
Q

Are inhalers likely to help a child with persistent infantile wheeze?

A

No. Inhalers are unlikely to help; symptoms will improve as the child gets older.

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199
Q

What is viral episodic wheeze normally associated with/exacerbated by?

A

It normally follows a URTI. The child will have no interval symptoms.

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200
Q

Are inhalers likely to help a child with viral episodic wheeze?

A

Bronchodilators may help but there is no benefit from inhaled steroids.

Symptoms are likely to improve with age.

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201
Q

How would you manage an acute exacerbation of asthma in a child?

A
  • O2.
  • Beta agonist nebulised.
  • Prednisolone 1mg/kg.

If still not improving…

  • IV salbutamol bolus.
  • Aminophylline/MgSO4/salbutamol infusion.
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202
Q

Inhalers: name 2 ‘preventers’.

A

ICS act as ‘preventers’ e.g. beclamethasone, budenoside.

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203
Q

Inhalers: name 2 ‘relievers’.

A

Beta agonists e.g. salbutamol.

Muscarinic antagonists e.g. ipratropium bromide.

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204
Q

Describe the step-wise approach to asthma management.

A

SABA -> SABA + ICS -> LABA + ICS -> LABA + increased dose of ICS -> LABA + daily PO steroids.

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205
Q

Give 3 long term risks of systemic steroids.

A
  1. Adrenal suppression.
  2. Growth suppression.
  3. Osteoporosis.
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206
Q

Why might asthma treatment fail in children?

A
  1. Adherence.
  2. Wrong diagnosis.
  3. Environmental factors.
  4. Choice of drug.
  5. Bad disease.
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207
Q

Name 3 URTI.

A
  1. Rhinitis.
  2. Otitis media.
  3. Pharyngitis.
  4. Tonsillitis.
  5. Laryngitis.
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208
Q

Name 3 LRTI.

A
  1. Bronchitis.
  2. Croup.
  3. Epiglottitis (bacterial).
  4. Tracheitis.
  5. Bronchiolitis.
  6. Pneumonia.
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209
Q

Would you expect a patient with bronchitis or with bronchiolitis to be hypoxic and tachypnoeic? Explain why.

A

Bronchiolitis.

Bronchiolitis affects the respiratory portion of the airway, where gas exchange takes place therefore you may see hypoxia and tachypnoea.

Bronchitis affects the conducting portion of the airway and so is unlikely to have these effects.

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210
Q

Give 3 signs of bronchitis in children.

A
  1. Chronic cough.
  2. Cough worst at night.
  3. No fever.
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211
Q

Name 4 LRTI that could be caused by RSV.

A
  1. Acute bronchiolitis.
  2. Wheezy bronchitis.
  3. Asthma exacerbation.
  4. Pneumonia.
  5. Croup.
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212
Q

Why are infants more susceptible to descending infection?

A

Infants have a poor innate immune response and so are more susceptible to descending infections.

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213
Q

What virus commonly causes croup?

A

Parainfluenza virus.

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214
Q

What is croup?

A

Acute larngotracheobronchitis.

215
Q

Describe the cough that is associated with croup.

A

A barking seal like cough - often worse at night.

216
Q

How do you treat croup?

A

single dose of oral dexamethasone

217
Q

Name a bacteria that causes acute epiglottitis.

A

H.influenzae B.

Acute epiglottitis is a severe acute illness.

218
Q

Give 5 signs of acute epiglottitis.

A
  1. Pyrexial.
  2. Septic.
  3. Dribbling.
  4. Stridor.
  5. Huge inflamed epiglottis that blocks the oesophagus -> quiet stridor.
219
Q

Name 2 respiratory illnesses that can present with stridor.

A
  1. Croup - often a louder stridor.

2. Acute epiglottitis - often a quieter stridor due to inflamed epiglottis blocking oesophagus and trachea.

220
Q

Describe the immediate management for acute epiglottitis.

A

Secure the airway - anaesthetist, ENT surgeon.

221
Q

What is pneumonia?

A

Inflammation of the lung parenchyma with congestion.

222
Q

Describe the diagnostic criteria for pneumonia in children.

A
  • If <3: pyrexial, chest recession and RR>50 = pneumonia.

- If older and the child has a history of breathing difficulties, cough and increased RR = pneumonia.

223
Q

Describe the treatment of pneumonia.

A

PO amoxicillin.
Co-amoxiclav if complicated or unresponsive.

O2, analgesia, IV fluids if indicated.

224
Q

What antibiotics might you use in a child with pneumonia caused by mycoplasma pneumoniae?

A

Mycoplasma pneumoniae is intracellular and so amoxicillin won’t work therefore give macrolides e.g. clindamycin, erythromyocin, azithromycin OR doxycycline

225
Q

Name the 4 broad categories of child abuse.

A
  1. Physical injury -> bruises, scratches, burns, fractures.
  2. Sexual abuse -> behaviour change, physical symptoms e.g. bleeding, STI, pregnancy.
  3. Emotional abuse -> relationships high in criticism and low in warmth.
  4. Neglect -> care that does not meet the needs of a child.
226
Q

How does child abuse present?

A
  • Disclosure.
  • Injury observed e.g. at school.
  • Incidental findings.
227
Q

How would you manage a child whom you suspect is a victim of child abuse?

A
  • Thorough history - ensure good documentation, are there any discrepancies?
  • Examination - use body charts.
  • FBC, clotting, swabs, bone profile, skeletal survey.
  • Social services assessment +/- police input.
228
Q

Give 5 symptoms of depression.

A
  1. Loss of interest.
  2. Fatigue.
  3. Poor sleep.
  4. Reduced appetite.
  5. Low concentration.
  6. Feelings of guilt and self blame.
  7. Low confidence.
  8. Agitated.
  9. Hopeless.
229
Q

Describe the non-medical and medical treatment of depression.

A

Non-medical: Education, CBT, IPT and family therapy.

Medical: fluoxetine 1st line in children

230
Q

Give 3 predisposing factors for a child developing depression.

A
  1. Family history.
  2. Stress in pregnancy.
  3. Poor attachment.
  4. Poverty.
  5. Isolation.
231
Q

Give 3 precipitating factors for a child developing depression.

A
  1. Trauma.
  2. Drugs.
  3. Infections.
  4. Puberty.
  5. Exam stress.
  6. Sexual abuse.
  7. Bullying.
232
Q

Give 3 perpetuating factors for a child developing depression.

A
  1. Chronic illness.
  2. Malnutrition.
  3. Ongoing neglect.
  4. Ongoing poverty.
233
Q

Define anorexia and what is the BMI

A

A restriction of energy intake relative to requirements. The person has an intense fear of gaining weight.
BMI <17.5.

234
Q

Give 5 RF’s for developing anorexia.

A
  1. Social pressure.
  2. Perfectionist traits.
  3. Family attitudes to food.
  4. Low self esteem.
  5. Occupation/interests.
  6. Family history.
235
Q

Name the screening tool that can be used for investigating eating problems.

A

SCOFF.

236
Q

Describe the treatment for anorexia.

A
  1. Family therapy - this is NICE recommended
  2. IPT.
  3. CBT.

Weight restoration at 0.5kg/week - monitor for re-feeding syndrome.

237
Q

What is a septic screen?

A

A septic screen is used to check for infection, in particular meningitis:

  1. Urine sample.
  2. Blood tests.
  3. Lumbar puncture.
238
Q

Why does a child with meningococcal septicaemia develop a rash?

A

The purpuric rash is due to bacterial endotoxins damaging blood vessels -> vasculitis -> bleeding into SC tissue -> thrombosis and DIC.

239
Q

Name 2 drugs that can be given as meningitis prophylaxis.

A

Ciprofloxacin - this is not preferred over rifampicin

240
Q

2-years-old, 2m history of malaise, pallor and reduced appetite. Occasional febrile episodes associated with a pink rash and soreness in her left thigh. Now reluctant to weight bear despite walking at 13 months. All immunisations are up to date and developmental history shows no concerns.
O/E: low grade fever and cervical lymphadenopathy.

ESR is significantly raised.

Give 3 differentials.

A
  1. JIA.
  2. ALL.
  3. Transient synovitis.
  4. Septic arthritis.
241
Q

3-year-old, 7-day history of high fevers. Now developed red eyes, a rash, sore mouth and throat. Miserable and unwell with a diffuse maculopapular rash on his torso. He has bilateral injected conjunctiva, red cracked lips and a strawberry tongue. 3x2cm cervical swelling and swollen reddened palms.

Give 3 differentials.

A
  1. Kawasaki disease.
  2. Scarlet fever.
  3. Shingles/chickenpox.
  4. Measles - ask about immunisation history.
242
Q

What is the diagnostic criteria for Kawasaki disease?

A 
>5 days fever.
And 4/5 of the following:
- Conjunctivitis.
- Cracked lips/strawberry tongue.
- Cervical lymphadenopathy.
- Rash.
- Swollen and red extremities.
243
Q

What is Kawasaki disease?

A

A systemic vasculitis that affects children.

244
Q

Describe the treatment for Kawasaki disease.

A

IV immunoglobulin and high dose PO aspirin.

245
Q

What might you see on the blood results in a patient with Kawasaki disease?

A

High CRP/WCC/ESR.

High platelet count.

246
Q

Why do you give high dose aspirin to children with Kawasaki disease?

A

To prevent thrombosis.

These children have thrombocytosis and so are at risk of thrombosis.

247
Q

Give a potential complication that may develop in children with Kawasaki disease.

A

Coronary artery aneurysm.

248
Q

Why is it important to avoid rapid rehydration?

A

Rapid rehydration can lead to cerebral oedema.

249
Q

Describe the management of DKA in children.

A
  1. Fluid resuscitation: 0.9% NaCl. Dehydration should be corrected gradually over 48 hours.
  2. Insulin infusion: 0.1units/kg/h. + 10% dextrose when <14mmol
    Blood glucose should be monitored hourly.
  3. Potassium replacement and cardiac monitoring.
250
Q

Name the test that can pick-up congenital hypothyroidism.

A

Guthrie test, heel-prick.

251
Q

What is the most common cause of hypothyroidism:

a) worldwide.
b) In the UK.
c) in a consanguineous pedigree.

A

a) iodine deficiency.
b) maldescent of the thyroid.
c) dyshormonogenesis.

252
Q

What is the treatment for a baby with congenital hypothyroidism?

A

Levothyroxine.

Neonatal dose: 10-15 micrograms/kg/od.

253
Q

Give 3 signs of congenital hypothyroidism.

A
  1. Feeding problems.
  2. Prolonged jaundice.
  3. Constipation.
  4. Hoarse cry.
  5. Goitre.
254
Q

A 10-day-old baby presents with collapse and shock. They have low sodium, high potassium and are found to be in metabolic acidosis.

What is the most likely diagnosis?

A

Congenital adrenal hyperplasia.

The baby is having a salt-losing adrenal crisis.

255
Q

What is CAH?

A

An autosomal recessive disease that is the most common cause of insufficient cortisol and mineralocorticoid secretion.

256
Q

Why might someone with CAH have low sodium and high potassium?

A

They are unable to produce aldosterone.

257
Q

How can CAH be diagnosed biochemically.

A

The result is a patient with low aldosterone, low cortisol and abnormally high testosterone

258
Q

What is the most common cause of CAH

A

21-hydroxylase deficiency. 21-hydroxylase is responsible for converting progesterone to cortisol and aldosterone.

259
Q

Describe the treatment for CAH.

A

Lifelong hydrocortisone to suppress ACTH levels.
Fludrocortisone replacement therapy.

Growth, biochemistry and bone age need to be monitored frequently.
Psychological support may also be offered.

260
Q

What would you expect the fasting plasma glucose level to be in the following:

a) Diabetes.
b) Impaired glucose tolerance.
c) Euglycaemia.

A

a) Diabetes: >7mmol/l.
b) Impaired glucose tolerance: 5.7-7mmol/l.
c) Euglycaemia: 3.5-5.6mmol/l.

261
Q

What would you expect the post OGTT plasma glucose level to be in the following:

a) Diabetes.
b) Impaired glucose tolerance.

A

a) Diabetes: >11.1mmol/l.

b) Impaired glucose tolerance: 7.8-11mmol/l.

262
Q

What would you expect the HbA1c (%) to be in the following:

a) Diabetes.
b) Impaired glucose tolerance.
c) Euglycaemia.

A

a) Diabetes: >6.5%.
b) Impaired glucose tolerance: 5.7-6.4%.
c) Euglycaemia: 4-5.6%.

263
Q

20 genes have been identified in causing T1DM. Name two.

A
  1. HLADR3.

2. HLADR4.

264
Q

Which type of DM has a higher risk of transmission?

A

T2DM shows more of a genetic association and so a higher risk of transmission.

265
Q

Briefly describe the pathophysiology of T1DM.

A

Insulin deficiency -> glycogenolysis, gluconeogenesis, ketogenesis -> increased ketone and glucose production -> vomiting, osmotic diuresis, acidosis -> fluid and electrolyte depletion -> cellular dysfunction, cerebral oedema, shock.

266
Q

Give 3 symptoms of T1DM.

A
  1. Weight loss.
  2. Polyuria.
  3. Thirst (polydipsia).
267
Q

Give 3 signs seen in DKA.

A
  1. Acidosis, pH <7.3.
  2. Ketonaemia.
  3. Hyperglycaemia.
268
Q

Give 3 life-threatening complications of DKA.

A
  1. Cerebral oedema.
  2. Hypokalaemia -> arrhythmias.
  3. Aspiration pneumonia.
  4. Hypoglycaemia.
269
Q

Briefly describe the pathophysiology behind DKA.

A

No insulin -> lipolysis -> FFA’s -> oxidised in liver -> ketone bodies -> ketoacidosis.

Glucose is not metabolised or stored so the body goes into a ‘starvation state’.

Vomiting is common -> further dehydration and worsening acidosis.

270
Q

Why might a child with known T1DM have DKA?

A
  1. Non-compliance.
  2. Illness.
  3. Rapidly changing insulin requirements e.g. puberty.
271
Q

Give 3 symptoms of DKA.

A
  1. Unwell.
  2. Lethargic.
  3. Nausea.
  4. Vomiting.
  5. Abdominal pain.
272
Q

Give 3 signs of DKA.

A
  1. Kussmaul breathing.
  2. Subcostal and intercostal recessions.
  3. Tachycardia.
  4. Hypotension.
  5. Dry mucous membranes.
  6. Ketotic breath.
273
Q

Describe the management of DKA.

A
  1. ABCDE.
  2. IV fluid replacement.
  3. Insulin infusion.

Fluid should be corrected over 48 hours at an even hourly rate. Glucose, electrolytes and neurological status should also be monitored hourly.

274
Q

Why is it important to correct fluid balance slowly over 48 hours in someone with DKA?

A

Rapid fluid resuscitation can lead to cerebral oedema.

275
Q

Define hypoglycaemia.

A

Someone with a blood glucose less than 2mmol/l.

276
Q

Give 5 hypoglycaemic symptoms.

A
  1. Irritable.
  2. Hungry.
  3. Nauseous.
  4. Shakey.
  5. Anxious.
  6. Sweaty.
  7. Pallor.
  8. Dizzy.
  9. Headache.
  10. Confused.
277
Q

How would you offer support to a child who was newly diagnosed with diabetes?

A
  1. Education - diet and importance of monitoring
  2. MDT input.
  3. Liaison with school.
  4. Refer to support groups.
278
Q

Give 5 determinants of growth.

A
  1. Parental phenotype and genotype.
  2. Pregnancy factors.
  3. Nutrition.
  4. Psychosocial deprivation.
  5. Hormones.
279
Q

When is growth velocity fastest?

A

In utero and in infancy.

280
Q

When does growth end?

A

When the epiphyses fuse.

281
Q

What is hypochondroplasia?

A

A developmental disorder resulting in short limbs.

282
Q

What is the main factor driving infant growth?

A

Nutrition!

283
Q

Give 5 differentials for short stature.

A
  1. Constitutional delay.
  2. Slow maturation.
  3. Delayed puberty.
  4. Idiopathic.
  5. Environmental.
  6. Nutrition.
  7. Skeletal disease.
  8. Physical disease e.g. coeliac, IBD, CHD.
  9. Turner syndrome.
  10. Endocrine pathology.
284
Q

What can cause an increased final height?

A
  1. Androgen/oestrogen deficiency.
  2. GH excess.
  3. Marfan’s.
  4. Klinefelter’s.
285
Q

Name the scale that is used to describe physical development based on external sex characteristics.

A

Tanner scale.

286
Q

Define thelarche.

A

Breast development.

287
Q

Define adrenarche.

A

Maturation of the adrenal gland -> androgen production -> body odour and mild acne.

288
Q

Define pubarche.

A

Growth of pubic hair.

289
Q

What is the first sign of puberty in boys?

A

First ejaculation and testicular size >3ml.

290
Q

Define delayed puberty.

A

The absence of secondary sexual characteristics by age 14 or 16.

291
Q

What is the likely cause of delayed puberty in boys?

A

Constitutional delay - runs in the family.

292
Q

What must you rule out as a cause of delayed puberty in girls?

A

Turner syndrome (45X0).

293
Q

Give 3 potential consequences of delayed puberty.

A
  1. Psychological problems.
  2. Reproduction defects.
  3. Reduced bone mass.
294
Q

How might you investigate delayed puberty?

A

FBC, U+E, TFT’s, LH/FSH, karyotyping.

295
Q

Define precocious puberty.

A

The onset of secondary sexual characteristics before 8 or 9

296
Q

What must you rule out as a cause of precocious puberty in boys?

A

Brain tumour.

297
Q

How would you treat precocious puberty?

A

GnRH super-agonists can be given to suppress pulsatility of GnRH secretion.

298
Q

What is hypergonadotropic hypogonadism?

A

Primary gonadal failure e.g. testes/ovarian failure.

299
Q

What is the affect of hypergonadotropic hypogonadism on the following:

a) FSH/LH.
b) Oestrogen/testosterone.

A

a) High FSH/LH.

b) Low oestrogen/testosterone.

300
Q

Name 2 diseases that are examples of hypergonadotropic hypogonadism.

A
  1. Turner syndrome (45X0).

2. Klinefelter syndrome (47XXY).

301
Q

What is hypogonadotropic hypogonadism?

A

Secondary gonadal failure e.g. hypopituitary or hypothalamic problem.

302
Q

What is the affect of hypogonadotropic hypogonadism on the following:

a) FSH/LH.
b) Oestrogen/testosterone.

A

a) Low FSH/LH.

b) low oestrogen/testosterone.

303
Q

Name a disease that is an example of hypogonadotropic hypogonadism.

A

Kallman syndrome.

304
Q

Give 5 signs of Turner syndrome.

A
  1. Delayed puberty.
  2. Short stature
  3. Recurrent otitis media.
  4. CV and renal malformations.
  5. Webbed neck.
  6. Low posterior hairline.
305
Q

Give 3 signs of Klinefelter syndrome.

A

XXY
1. Azoospermia - semen contains no sperm.
2. Gynaecomastia - enlargement of male breast tissue.
3. Testicular size <5ml.
4. Reduced pubic hair.
5. Tall stature.

306
Q

Briefly describe the pathophysiology behind Kallman syndrome.

A

There is a congenital deficiency of GnRH meaning the pituitary isn’t stimulated to release FSH and LH this leads to secondary gonadal failure.

307
Q

What inheritance pattern is seen in Kallman syndrome?

A

X linked recessive or dominant.

308
Q

75% of people with which syndrome may have anosmia?

A

Kallman syndrome.

309
Q

Define faltering growth.

A

The failure to gain adequate weight or achieve adequate growth during infancy and childhood.

NICE defines faltering growth as weight that has fallen down 2 centile lines.

310
Q

Give 5 broad causes of poor growth.

A
  1. Inadequate calorie intake.
  2. Malabsorption.
  3. Inadequate retention.
  4. Increased calorie requirements.
  5. Inflammatory disease.
311
Q

Causes of faltering growth: give examples of inadequate calorie intake.

A
  1. Impaired suck/swallow.
  2. Inadequate availability of food.
  3. Psychosocial deprivation.
  4. Exclusion diets e.g. veganism
  5. Cleft palate.
312
Q

Causes of faltering growth: give examples of malabsorption.

A
  1. Coeliac disease.
  2. Pancreatic disease e.g. CF.
  3. Liver disease.
  4. Enteropathy e.g. infective causes - giardia.
  5. Cows milk protein intolerance.
313
Q

Causes of faltering growth: give an example of inadequate retention.

A

Vomiting e.g. severe GORD, pyloric stenosis.

314
Q

Causes of faltering growth: give example increased calorie requirements.

A
  1. Chronic illness e.g. CHD, CKD, CF.
  2. Thyrotoxicosis.
  3. Malignancy.
315
Q

Name 3 members of the MDT who would be involved in the management of a child with faltering growth.

A
  1. Health visitor.
  2. Dietitian.
  3. Community paediatrician.
316
Q

Why is prompt intervention important when managing a child with faltering growth?

A

Prompt intervention can avoid problems such as cognitive delay, feeding and behavioural problems and low maternal self-esteem.

317
Q

Describe the foetal circulation.

A

Placenta -> umbilical vein -> IVC -> RV -> foramen ovale -> LA -> aorta -> umbilical arteries -> placenta.

OR: … RV -> pulmonary artery -> ductus arteriosus -> aorta …

318
Q

What is the function of the foramen ovale and the ductus arteriosus in the foetal circulation?

A

They are used to bypass the non-functiong lungs.

319
Q

Name 4 congenital heart problems that can cause a L -> R shunt.

A
  1. VSD.
  2. ASD.
  3. AVSD.
  4. PDA.
320
Q

Give 5 signs of a VSD.

A
  1. Poor feeding and FTT.
  2. Tachypnoea.
  3. Thrill.
  4. Pan-systolic murmur.
  5. Hepatomegaly.
321
Q

You request a CXR for a patient with a VSD. What would you expect to see?

A
  1. Cardiomegaly.
  2. Pulmonary oedema.
  3. Enlarged pulmonary arteries.
322
Q

Why are ASD’s often asymptomatic?

A

ASD’s are often asymptomatic because the blood flow in the atria is low pressure and so breathlessness etc is uncommon.

323
Q

Give 3 signs of an ASD.

A
  1. S2 sound.
  2. Ejection systolic murmur in the pulmonary region.
  3. Palpitations.
324
Q

AVSD is a common defect in people with which chromosomal abnormality?

A

Trisomy 21 (Down’s syndrome).

325
Q

Give 5 signs of a PDA.

A
  1. Poor feeding, FTT.
  2. Tachypnoea.
  3. Active precordium.
  4. Left subclavicular Thrill.
  5. Continuous machinery murmur.
326
Q

Describe the management for congenital health defects that cause a L->R shunt.

A
  1. Stabilise the patient.
  2. Increase calorie intake.
  3. NG tube.
  4. Diuretics and ACEi to prevent HF symptoms.
  5. Surgical repair.
327
Q

Would a patient with a L->R shunt or a R->L shunt appear cyanotic?

A

A patient with a R -> L shunt would appear cyanotic.

328
Q

Name 2 congenital heart problems that can cause a R -> L shunt.

A
  1. Tetralogy of fallot.

2. Transposition of the great arteries.

329
Q

What 4 components make up Tetralogy of fallot?

A
  1. Pulmonary stenosis.
  2. RVH.
  3. Overriding aorta.
  4. VSD.
330
Q

Give 3 signs of Tetralogy of fallot.

A
  1. Cyanosis.
  2. Collapse.
  3. Acidosis.
331
Q

What is coarctation of the aorta?

A

Arterial duct tissue encircles the aorta at the point of insertion of the duct. When the duct closes, the aorta constricts, this causes severe obstruction to LV outflow.

332
Q

Give 3 signs of coarctation of the aorta.

A
  1. Radio-femoral delay.
  2. Weak femoral pulses.
  3. Difference in pre and post-ductal saturations.
333
Q

Give 3 signs of aortic stenosis.

A
  1. Palpable thrill.
  2. Ejection systolic murmur.
  3. LVH.
334
Q

Name 3 congenital heart problems that are often associated with Down’s syndrome.

A
  1. AVSD.
  2. Tetralogy of Fallot.
  3. VSD.
335
Q

Give 2 signs of pulmonary stenosis.

A
  1. Ejection systolic murmur, often radiates to the back.

2. RV heave if severe.

336
Q

Name 3 congenital heart problems that are often associated with Turner syndrome.

A
  1. Coarctation of the aorta.
  2. Aortic stenosis.
  3. Aortic dissection.
337
Q

What is a possible consequence of persistent pulmonary hypertension, like that seen in CHD associated with a L->R shunt?

A

Eisenmenger syndrome: high pressure pulm. blood flow damages pulmonary vasculature -> increased resistance (pulm. hypertension) -> RV pressure increase -> shunt direction reverses -> CYANOSIS!

338
Q

Describe the pathophysiology behind Eisenmenger syndrome.

A

Persistent pulmonary hypertension -> high pressure pulm. blood flow damages pulmonary vasculature -> increased resistance (pulm. hypertension) -> RV pressure increase -> shunt direction reverses -> CYANOSIS!

339
Q

What is a unilateral pleural effusion suggestive of?

A

Infection e.g. parapneumonic or empyema.

340
Q

What is a bilateral pleural effusion suggestive of?

A

Fluid overload e.g. HF or nephrotic syndrome.

341
Q

Give 3 potential consequences of hearing loss.

A
  1. Speech and language delay.
  2. Social problems e.g. behavioural issues.
  3. Academic underachievement.
342
Q

How does hearing loss in children often present?

A
  1. Parental concern.
  2. Speech, behavioural or educational problems.
  3. Incidentally on screening.
343
Q

What are the 3 types of hearing loss?

A
  1. Conductive hearing loss.
  2. Sensori-neural hearing loss.
  3. Mixed.
344
Q

Give 3 causes of conductive hearing loss.

A
  1. Glue ear.
  2. Ear wax.
  3. Otitis media.
  4. Perforated ear drum.
345
Q

Describe the management of conductive hearing loss.

A

Conductive hearing loss is usually ENT managed:

  • Wait and wait - most will resolve on their own.
  • Grommet insertion.
  • Temporary hearing aid.
346
Q

Give 3 risk factors for sensori-neural hearing loss.

A
  1. Family history.
  2. SCBU.
  3. Consanguinity.
347
Q

Describe the management of sensori-neural hearing loss.

A

Sensori-neural hearing loss is often managed by a paediatrician. Treatments involve hearing aids or cochlea implants.

348
Q

How would you manage mixed hearing loss?

A

You would address the conductive problem first and then offer a hearing aid.

349
Q

When is hearing tested in children?

A
  1. New-born hearing screen.
  2. School entry hearing test.
  3. Long term monitoring is done in high risk groups.
350
Q

Is the new-born hearing screen an objective or subjective test?

A

It is an objective test - response or no response.

If there are concerns, the patient is followed up with evoked response audiometry.

351
Q

What are the 3 aims of hearing testing in children?

A
  1. Measure hearing threshold (dB).
  2. To be frequency specific (Hz).
  3. Obtain single ear information if possible.
352
Q

Name 4 types of subjective hearing testing.

A
  1. Behavioural observational audiometry.
  2. Distraction testing.
  3. Visual reinforcement audiometry.
  4. Performance testing and play audiometry.
353
Q

Name 2 organisms that can cause acute otitis media.

A

S.pneumoniae.

H.influenzae.

354
Q

Give 3 symptoms of acute otitis media.

A
  1. Pain.
  2. Fever.
  3. Generally unwell.
  4. Otorrhoea.
355
Q

Give 2 potential complications of acute otitis media.

A
  1. Extra-cranial: mastoiditis, TM perforation.

2. Intra-cranial: meningitis, abscess.

356
Q

Describe the treatment for acute otitis media.

A

Watch and wait.
Analgesia.
If recurrent, offer antibiotics and consider a grommet.

357
Q

What is the function of a grommet?

A

A grommet keeps the middle ear aerated and prevents the accumulation of fluid in the middle ear.

358
Q

When might a grommet be indicated?

A
  1. Recurrent AOM.
  2. Chronic otitis media + effusion.
  3. ET dysfunction.
359
Q

What is the common name for otitis media + effusion?

A

Glue ear.

360
Q

What causes glue ear?

A

Infection!

45% follow AOM.

361
Q

Give 3 risk factors for glue ear.

A
  1. Older sibling.
  2. Male.
  3. Nursery attendance.
  4. Parental smoking.
  5. Allergies.
362
Q

What are the criteria for considering a tonsillectomy?

A
  1. > 7 episodes of acute tonsilitis in a year.

2. OSA or sleep-deprived breathing.

363
Q

A baby makes many adaptations to ex-utero life. Give 4 CV adaptations.

A
  1. Closure of foetal shunts e.g. foramen ovale and ductus arteriosus.
  2. Perfusion of lungs.
  3. Fall in pulmonary artery pressure and increase in systemic blood pressure.
  4. Increase in CO.
364
Q

A baby makes many adaptations to ex-utero life. Give 4 respiratory adaptations.

A
  1. Foetal lung fluid removed.
  2. Surfactant released.
  3. Gaseous exchange.
365
Q

A baby makes many adaptations to ex-utero life. Aside from CV and respiratory give 4 other adaptations.

A
  1. Control of own movements.
  2. Independent hormonal responses.
  3. Thermoregulation.
  4. Feeding.
  5. Immunocompetence.
366
Q

Give 3 functions of surfactant.

A
  1. Reduces surface tension.
  2. Prevents alveoli collapse.
  3. Allows homogenous aeration.
367
Q

When is surfactant produced?

A

From 34 weeks gestation. Production increases rapidly 2-weeks before birth.

368
Q

Where is surfactant produced?

A

Surfactant is produced by T2 pneumocytes.

369
Q

What can mothers be given antenatally to prevent surfactant deficiency?

A

Steroids can be given to the mother to encourage foetal surfactant release.

370
Q

Premature babies may have surfactant deficiency. Give 3 consequences of this.

A
  1. Respiratory distress syndrome.
  2. Chronic lung disease of prematurity.
  3. Non-compliant lungs.
  4. Unequal aeration.
  5. Reduced lung volume.
371
Q

Briefly describe the pathophysiology of chronic lung disease of prematurity.

A

There is reduced lung volume and reduced alveolar SA -> diffusion defect. This often leads to recurrent hospital admissions and increased mortality.

372
Q

Give 3 reasons why pre-term infants are particularly vulnerable to hypothermia.

A
  1. Large SA relative to mass.
  2. Thin and heat permeable skin.
  3. Little fat for insulation.

Temperatures can be maintained using incubators.

373
Q

The brain stem is not fully myelinated until 32/34w. What problem can this cause in preterm infants?

A

They are at risk of apnoea of prematurity.

They have no respiratory drive due to the lack of myelination and so ‘forget to breathe’. It is often associated with bradycardia.

374
Q

What is apnoea of prematurity?

A

When a preterm infant has no respiratory drive due to a lack of myelination around the brain stem -> they ‘forget to breathe’. It is often associated with bradycardia.

375
Q

Describe the treatment for apnoea of prematurity.

A
  1. Nasal CPAP.

2. Stimulation - caffeine.

376
Q

Why are high levels of unconjugated bilirubin concerning in a neonate?

A

Unconjugated bilirubin is fat soluble and can diffuse into brain tissue.

High levels of unconjugated bilirubin can lead to kernicterus and then cerebral palsy.

377
Q

What is kernicterus?

A

Brain damage due to high levels of bilirubin.

378
Q

Give 3 causes of high levels of unconjugated bilirubin.

A
  1. Haemolytic disease.
  2. Physiological.
  3. Infection/Sepsis.
  4. Breast milk jaundice.
  5. CF.
379
Q

How can you treat high levels of unconjugated bilirubin in a neonate?

A

Phototherapy.

380
Q

Why are pre-term babies at increased risk of infection?

A

Active IgG transfer happens in the last 3 months of pregnancy therefore pre term babies are at increased risk of infection; particularly with organisms that are not normally pathogenic.

381
Q

What is necrotising enterocolitis?

A

Inflammation and necrosis of a portion of the GI tract.

382
Q

What can increase the risk of necrotising enterocolitis?

A

prematurity

383
Q

What can decrease the risk of necrotising enterocolitis?

A

Breast feeding and probiotics.

384
Q

Give 3 signs of necrotising enterocolitis.

A
  1. Feed intolerance.
  2. Vomiting.
  3. Distended abdomen.
  4. Shock.
385
Q

How can you treat necrotising enterocolitis?

A

Broad spectrum antibiotics.

386
Q

Give a cause of retinopathy of prematurity.

A

Hyperoxic insult.

Retinopathy of prematurity can lead to blindness.

387
Q

Breast feeding has many benefits. Give 3 benefits for the infant.

A
  1. Reduces the risk of infection.
  2. Reduces the risk of allergic disease.
  3. Reduces the risk of GORD.
  4. Increased IQ and cognition.
388
Q

Breast feeding has many benefits. Give 3 benefits for the mother.

A
  1. Reduces the risk of some types of cancer.
  2. Reduces the risk of PPH and post-natal depression.
  3. Optimum child spacing.
  4. Less food/medical expense.
389
Q

Give 5 medical problems that preterm infants may suffer from.

A
  1. Respiratory distress syndrome.
  2. Apnoea and bradycardia.
  3. Patent ductus arteriosus.
  4. Infection.
  5. Jaundice.
  6. Intraventricular haemorrhage.
  7. Cystic periventricular leukomalacia.
  8. Necrotising enterocolitis.
  9. Retinopathy of prematurity.
  10. Hypothermia.
390
Q

Give 3 gastrointestinal causes of abdominal pain.

A
  1. IBS.
  2. Constipation.
  3. Gastritis.
  4. Peptic ulcer.
  5. Malrotation.
  6. Appendicitis.
  7. IBD.
  8. Abdominal migraine.
391
Q

Give 3 gynaecological causes of abdominal pain.

A
  1. Dysmenorrhoea.
  2. PID.
  3. Ectopic pregnancy.
  4. Ovarian torsion.
392
Q

Give 3 hepatobiliary/pancreatic causes of abdominal pain.

A
  1. Hepatitis.
  2. Gall stones.
  3. Pancreatitis.
393
Q

Give 2 urinary causes of abdominal pain.

A
  1. UTI.

2. PUJ obstruction.

394
Q

Give 3 signs of appendicitis.

A
  1. Anorexia.
  2. Pyrexia.
  3. Abdominal pain - initially central as the appendix is a mid gut structure but then localises to R side as the appendix irritates peritoneum.
  4. Vomiting.
  5. RIF rebound tenderness.
395
Q

Why is central trauma and bruising to the abdomen a concern?

A

Bruising and trauma to the abdomen is a concern because mid-line structures such as the pancreas, spleen, bowel and liver may be damaged.

396
Q

If you suspect trauma and abdominal organ damage what investigation might you do?

A

CT.

397
Q

Give 5 differentials for abdominal pain + rectal bleeding.

A
  1. Anal fissures.
  2. Haemorrhoids.
  3. Polyps.
  4. Proplapse.
  5. Infective causes.
  6. Meckel diverticulum.

If melaena, suspect gastritis or duodenal ulcer.

398
Q

What is Meckel diverticulum a remnant of?

A

It is a remnant of the vitelline duct.

The vitelline duct joins the yolk sac to the midgut lumen in the foetus.

399
Q

Give 3 signs of Meckel diverticulum.

A
  1. Severe rectal bleeding.
  2. Intussusception.
  3. Volvulus.
400
Q

How would you treat Meckel diverticulum?

A

Surgical resection.

401
Q

Give 3 differentials for abdominal mass.

A
  1. Constipation.
  2. Appendicitis.
  3. Organomegaly.
  4. Nephroblastoma/Wilm’s tumour.
402
Q

Give 5 differentials for vomiting.

A
  1. GORD.
  2. Infection e.g. gastroenteritis.
  3. Food allergy/intolerance.
  4. Intestinal obstruction.
  5. Appendicitis.
  6. Coeliac disease.
  7. Over-feeding - common in bottle-fed infants.
  8. Necrotising enterocolitis.
  9. Malrotation - biliary vomit.
  10. DKA.
403
Q

Give 3 causes of intestinal obstruction that can cause vomiting.

A
  1. Pyloric stenosis.
  2. Duodenal atresia.
  3. Intussusception.
  4. Hirschsprung’s.
404
Q

What is pyloric stenosis?

A

A disease characterised by hypertrophy of the pyloric muscle causing gastric outlet obstruction.

405
Q

Give 3 signs of pyloric stenosis.

A
  1. Vomiting - projectile, milk, straight after feeding.
  2. Weight loss.
  3. Visible gastric peristalsis and palpable mass on test feed.
406
Q

You suspect pyloric stenosis in a neonate. What investigations might you do?

A
  1. U+E.
  2. Blood gas.
  3. USS - hypertrophy of pyloric sphincter.
407
Q

You do a blood gas on a neonate with pyloric stenosis. What would it show?

A

Metabolic Alkalosis - low K+ and Cl-.

The baby has vomited up all the HCl and the kidneys go into overdrive - increased K+ secretion.

408
Q

How would you treat a neonate with pyloric stenosis?

A
  • IV fluids.
  • Repeat gases to monitor alkalosis.
  • Stop feeding to stop vomiting.
  • Pyloromyotomy once stable.
409
Q

How might malrotation in a neonate present?

A

Obstruction with bilious vomiting. Abdominal pain and tenderness.

410
Q

Any child presenting with dark green vomiting needs what urgent investigation?

A

An urgent upper GI contrast study and USS to assess intestinal rotation.

411
Q

Give a potential consequence of malrotation.

A

SMA blood supply to the small intestine can be compromised -> infarction.

412
Q

What is duodenal atresia?

A

A congenital absence or complete closure of the duodenum. It causes intestinal obstruction in neonates.

413
Q

You do an AXR on a neonate with duodenal atresia. What would you expect to see?

A

A double bubble sign.

414
Q

What syndrome is associated with duodenal atresia?

A

20-40% have Down’s syndrome.

415
Q

What is intussusception?

A

Where proximal bowel telescopes into a distal segment -> obstruction, inflammation, bloody stools.

416
Q

Give 2 signs of intussusception.

A
  1. Colicky pain.
  2. Vomiting.
  3. Abdominal mass.
  4. Redcurrant jelly stool.
417
Q

What investigations might you do on a child who you suspect has an intussusception?

A

USS - ‘target sign’.

AXR.

418
Q

Describe the treatment for intussusception.

A
  1. reduction by air insufflation under radiological control
  2. Analgesia e.g. morphine.
  3. IV fluids if shocked.
419
Q

Define seizure.

A

A convulsion caused by a paroxysmal discharge of cerebral neurones.

420
Q

Define epileptic seizure.

A

Excessive, unsynchronised neuronal discharges in the brain cause paroxysmal changes in behaviour, sensation or cognitive processes.

421
Q

How long do epileptic seizures tend to last for?

A

30 - 120 seconds.

422
Q

Give 3 signs of epileptic seizures.

A
  1. Movement.
  2. Tongue biting.
  3. Head turning.
  4. Muscle pain.
423
Q

What are febrile convulsions?

A

Febrile convulsions are epileptic seizures accompanied by fever. They usually occur early in viral infection and tend to be brief generalised tonic-clonic seizures.

424
Q

How long do non-epileptic seizures tend to last for?

A

1 - 20 minutes.

425
Q

Give 3 signs of non-epileptic seizures.

A
  1. Eyes closed.
  2. Talking/crying.
  3. Pelvic thrusting.
426
Q

What is the first line AED offered to those suffering from focal seizures?

A

Carbamazepine or lamotrigine

Surgery may also be offered.

427
Q

Give 3 examples of generalised seizures.

A
  1. Absence.
  2. Myoclonic.
  3. Tonic.
  4. Atonic.
  5. Generalised tonic-clonic.
428
Q

What would you expect to see in a myoclonic seizure?

A

Isolated muscle jerking.

429
Q

What would you expect to see in a tonic seizure?

A

Generalised increase in tone.

430
Q

What would you expect to see in an atonic seizure?

A

Transient loss of muscle tone.

431
Q

What would you expect to see in a generalised tonic-clonic seizure?

A

Sudden onset rigid phase followed by a convulsion in which the muscles jerk rhythmically.

432
Q

What is the first line AED offered to those suffering from focal seizures?

A

Sodium valporate.

433
Q

Why must you do an ECG in those suffering from seizures?

A

To check for arrhythmia as the cause e.g. long-QT syndrome.

434
Q

What investigations might you want to do in someone presenting with seizures.

A
  1. Eye witness account/video is invaluable!
  2. ECG.
  3. EEG.
  4. MRI or CT.
435
Q

Give 3 potential side effects of AED’s.

A
  1. Cognitive disturbances
  2. Heart disease.
  3. Drug interactions.
  4. Teratogenic.
436
Q

Name 3 conditions hat are commonly diagnosed as being epilepsy.

A
  1. Sandifer syndrome.
  2. Benign neonatal sleep myoclonus.
  3. Syncope.
437
Q

What is syncope?

A

Insufficient blood or O2 supply to the brain causes paroxysmal changes in behaviour, sensation and cognitive processes.

438
Q

What non-neurological disease is sandifer syndrome associated with?

A

GORD.

Patients present with GORD and a characteristic neck movement disorder.

439
Q

Give 4 causes of diarhorrea.

A
  1. Spurious/over-flow diarrhoea due to constipation.
  2. Chronic non-specific diarrhoea.
  3. Malabsorption.
  4. Enteric infection.
  5. IBD.
  6. Drug induced.
  7. Non-intestinal e.g. hyperthyroid, neuroblastoma.
440
Q

Give 2 non-intestinal causes of diarrhoea.

A
  1. Hyperthyroid.

2. Neuroblastoma.

441
Q

Give 2 infective causes of diarrhoea.

A
  1. Adenovirus.
  2. Rotavirus.
  3. Protozoan: giardiasis.
442
Q

What is the diagnostic criteria for giardiasis?

A

Cysts in stool and motile forms in small intestine.

443
Q

How do you treat giardiasis?

A

3 days high dose metronidazole.

444
Q

What is lactose hydrolysed into?

A

Glucose and galactose.

445
Q

Briefly describe the pathophysiology behind lactose intolerance.

A

A deficiency of intestinal lactase prevents the hydrolysis of lactose. The osmotic load of the unabsorbed lactose causes secretion of fluid and electrolytes until osmotic equilibrium is reached -> diarrhoea.

446
Q

Give 3 causes of lactose intolerance.

A
  1. Primary: deficiency of lactase.
  2. Secondary causes e.g. due to small intestine injury from infection, coeliac, IBD.
  3. Post-infective lactose intolerance.
447
Q

What test can be done to check for lactose intolerance?

A

Hydrogen breath test.

448
Q

With what immunoglobulins is cow’s milk allergy associated with?

A

IgG or IgE.

449
Q

Give 3 symptoms of cow’s milk allergy.

A
  1. Vomiting.
  2. Abdominal pain.
  3. Diarrhoea.
  4. Malabsorption.
  5. Intestinal bleeding.
  6. Urticaria and lip swelling.
450
Q

What is the treatment for cow’s milk allergy?

A

Specialised formula feeds.

451
Q

A 6-month old breast fed infant developed widespread urticaria immediately after the first formula feed.

a) What investigation might you do?
b) What is the most likely diagnosis?

A

a) Skin-prick test for cow’s milk.

b) IgE mediated cow’s milk allergy.

452
Q

A 4-month-old infant, formula fed since birth, has loose stools and faltering growth. Skin prick test to cow’s milk is negative but elimination of cow’s milk results in resolution of symptoms which return on trial re-introduction. What is the most likely diagnosis?

A

Non-IgE mediated cow’s milk allergy.

453
Q

With which HLA molecules is Coeliac Disease often associated with?

A

DQ2 and DQ8.

454
Q

Give 3 risk factors for developing Coeliac Disease.

A
  1. Family history.
  2. T1 Diabetes Mellitus.
  3. Down Syndrome.
  4. IgA deficiency.
  5. Often associated with other autoimmune disease.
455
Q

Give 3 symptoms of Coeliac Disease.

A
  1. Bloating.
  2. Abdominal pain.
  3. Diarrhoea.
  4. Dermatitis herpetiformis.
  5. Dental enamel defects.
456
Q

Describe the diagnostic criteria for Coeliac Disease.

A
  1. Characteristic histology e.g. villous atrophy, crypt hyperplasia, increased lymphocytes.
  2. Positive serology.
  3. Symptom resolution with gluten exclusion.
  4. Resolution of antibodies.
457
Q

Describe Crohn’s disease.

A

A type of inflammatory bowel disease that affects anywhere from the mouth to the anus. It is characterised by patchy non-caseating granulomatous inflammation that can affect any layer of the bowel wall (transmural).

458
Q

Give 3 symptoms of Crohn’s Disease.

A
  1. Ulcer’s.
  2. General ill-health.
  3. Growth failure.
  4. Abdominal pain.
  5. Diarrhoea.
459
Q

Give 3 extra-intestinal signs of Crohn’s Disease.

A
  1. Oral ulcers.
  2. Uveitis.
  3. Arthralgia.
  4. Erythema nodosum.
460
Q

Describe Ulcerative Colitis.

A

A type of inflammatory bowel disease that starts at the rectum and spreads proximally but only affects the colon. There is continuous inflammation that is confined to the mucosa.

461
Q

Give 3 symptoms of Ulcerative Colitis.

A
  1. PR bleeding.
  2. Diarrhoea.
  3. Colicky pain.
  4. Weight loss.
  5. Growth failure.
462
Q

Give 2 extra-intestinal signs of Ulcerative Colitis.

A
  1. Erythema nodosum.
  2. Arthritis.
  3. Iritis and episcleritis.
463
Q

What investigations might you want to do on someone who you suspect has IBD?

A
  1. ESR and CRP.
  2. Measure Hb - will often have microcytic anaemia (IDA).
  3. Low serum albumin.
  4. Endoscopy.
  5. Biopsy.
464
Q

What histological findings would you see on a biopsy taken from someone with IBD?

A
  1. Mucosal inflammation.
  2. Crypt damage.
  3. Ulceration.
465
Q

Describe the treatment for IBD.

A
  1. Steroids.
  2. Dietary modifications.
  3. Immunosuppressants e.g. methotrexate and infliximab.
466
Q

Give 3 benefits of using immunosuppressants as opposed to steroids for the treatment of IBD.

A
  1. Safe.
  2. Effective.
  3. Steroid sparing.
  4. Prevent relapse.
467
Q

Name 3 diseases with AD inheritance.

A
  1. ADPKD.
  2. HD.
  3. Marfan’s.
468
Q

Give 3 characteristics of AD inheritance.

A
  1. Vertical transmission.
  2. Male to male.
  3. Every generation affected.
  4. 50% chance of inheritance.
469
Q

Give 3 characteristics of AR inheritance.

A
  1. Both parents must be carriers.
  2. Often only one generation is affected.
  3. 2/3 carrier risk for unaffected siblings.
470
Q

Name 3 diseases with AR inheritance.

A
  1. CF.
  2. Sickle cell.
  3. Haemochromatosis.
471
Q

Give an example of an X linked disease.

A

Duchenne and Becker muscular dystrophy.

472
Q

Give 3 characteristics of X linked inheritance.

A
  1. Male > female affected.
  2. No male to male transmission.
  3. 50% of daughters are carriers and 50% of sons are affected.
473
Q

Give 4 examples of non-mendelian inheritance.

A
  1. Multifactorial e.g. neural tube defects.
  2. Mitochondrial.
  3. Genomic impriting.
  4. Gonadal mosaicism.
474
Q

What is gonadal mosaicism?

A

Gonadal mosaicism is when there are two different populations of cells in the gonads. One population is normal and the other is mutated. All gametes from the mutated line are effected.

475
Q

What are the two main types of strabismus?

A
  1. Manifest: esotropia, exotropia, hypertropia, hypotropia.

2. Latent: esophoria, exophoria, hyperphoria. hypophoria.

476
Q

Describe the aetiology of strabismus.

A

Multifactorial - hereditary and refractive errors.

There is also a higher incidence in infants with cerebral palsy.

Febrile illness can be a trigger.

477
Q

Name 2 ways in which strabismus can be investigates.

A
  1. Cover test: will determine presence and direction.
  2. Corneal reflections.

It is important to assess visual acuity too.

478
Q

What does the management of strabismus aim to achieve?

A
  1. Restore comfortable binocular single vision.
  2. Eliminate diplopia.
  3. Restore good alignment of the eyes.
479
Q

Give 3 conservative management techniques for strabismus.

A
  1. Glasses.
  2. Prisms for diplopia.
  3. Orthoptic exercises.
480
Q

Define ambylopia.

A

Defective acuity that persists after correction of refractive error and removal of any pathology.

481
Q

Describe the treatment for ambylopia.

A
  1. Refractive adaptation - wear appropriate glasses for 16w.
  2. Occlusion of better seeing eye.
  3. Atropine drops in better eye.
482
Q

Give 4 differentials for the acute scrotum.

A
  1. Testicular torsion.
  2. Epididymo-orchitis.
  3. Trauma.
  4. Acute hydrocele.
  5. Idiopathic scrotal oedema.
483
Q

Give 5 signs and symptoms of testicular torsion.

A
  1. Severe, constant pain.
  2. Sudden onset pain.
  3. Vomiting.
  4. Tenderness.
  5. Swelling.
  6. Redness.
484
Q

In what age groups is testicular torsion more common?

A

Neonates and peri-pubertal.

485
Q

What is hypospadias?

A

When the urethral opening is on the under side of the penis.

486
Q

Give 2 differentials for a groin swelling in children.

A
  1. Hernia.

2. Hydrocele.

487
Q

Give 3 signs of an inguinal hernia.

A
  1. Can’t get above it.
  2. Reducible.
  3. Often indirect in children.

Will need surgical repair.

488
Q

Give 3 signs of a hydrocele.

A
  1. Can get above it.
  2. Confined to scotrum.
  3. Non reducible.
  4. Should resolve by 2 years old.
489
Q

What is the hydatid?

A

The ‘appendix of the testicle’ - it is an embryological remnant of the Mullerian duct.

490
Q

Give 3 differentials for head and neck lumps in children.

A
  1. Lymphadenopathy.
  2. Thyroglossal cyst.
  3. Goitre.
  4. Malignancy.
  5. Branchial arch remnants.
  6. Dermoid cysts.
491
Q

What are the red flag signs for head/neck lumps in children?

A

> 2cm for >2w and enlarging.

492
Q

Give 5 causes of bilious vomiting in children.

A
  1. Volvulus.
  2. Hirschsprung’s.
  3. Necrotising enterocolitis.
  4. Intussusception.
  5. Bowel obstruction.
  6. Strangulated hernia.
  7. Adhesions.
493
Q

What analgesia is appropriate for a paediatric fracture?

A

Paracetamol.

Oromorph.

494
Q

Give 3 reasons why newborns become jaundiced.

A
  1. RBC lifespan is shorter -> increased bilirubin production.
  2. Hepatic bilirubin metabolism is less efficient -> hepatic immaturity.
  3. Absence of gut flora impedes elimination of bile pigment.
495
Q

What is the likely cause of jaundice in a neonate who is <24h old?

A
  1. Sepsis.

2. Haemolytic cause e.g. rhesus haemolytic disease, ABO incompatibility, GP6D deficiency.

496
Q

Why is it important to identify a neonate with a haemolytic cause of their jaundice?

A

The bilirubin is unconjugated and if allowed to reach high levels could cause kernicterus.

497
Q

Describe the treatment for haemolytic jaundice.

A
  1. Phototherapy.

2. Exchange transfusion.

498
Q

How does phototherapy work in treating jaundice?

A

Light converts unconjugated bilirubin into a water soluble pigment.

499
Q

When might exchange transfusion be used in the treatment of jaundice?

A

If bilirubin rises to very dangerous levels and phototherapy alone is not effective.

500
Q

What must you rule out as a cause of hyperbilirubinaemia in a child >2 weeks old who has jaundice?

A

Biliary atresia.

(Conjugated bilirubin and pale stools).

501
Q

24h - 2w old: give 3 causes of unconjugated hyperbilirubinaemia.

A
  1. Physiological jaundice.
  2. Breast milk jaundice.
  3. Infection e.g. UTI.
  4. Congenital hypothyroidism.
  5. Haemolytic cause.
502
Q

Give 2 causes of conjugated hyperbilirubinaemia.

A
  1. Biliary atresia (bile duct obstruction).

2. Neonatal hepatitis syndrome.

503
Q

What is biliary atresia?

A

When there is progressive fibrosis and obliteration of the extra-hepatic and intra-hepatic biliary tree. Chronic liver failure and death can occur within 2 years.

504
Q

What investigations might you do to determine whether a child has biliary atresia?

A
  1. Measure transcutaneous bilirubin - conjugated bilirubin would be raised.
  2. LFT’s would be abnormal.
  3. ERCP imaging would fail to outline a normal biliary tree.
505
Q

What is the treatment for biliary atresia?

A

Surgery to bypass fibrotic ducts.
Nutrition and vitamin supplementation.

If unsuccessful or late presentation = liver transplant.

506
Q

Give 5 signs of hepatic dysfunction in children.

A
  1. Encephalopathy.
  2. Jaundice.
  3. Epistaxis.
  4. Ascites.
  5. Varices.
  6. Spider naevi.
  7. Bruising.
  8. Palmar erythema.
    9 Clubbing.
  9. Malnutrition and faltering growth.
507
Q

How would you manage respiratory distress in a neonate?

A
  1. O2.
  2. Intubate.
  3. CO2 monitoring.
  4. Surfactant therapy.
  5. Nasal CPAP and mechanical ventilation.
  6. Fluids if indicated.
508
Q

What antibiotics would you prescribe empirically to reduce the risk of neonatal infections in a pre-term baby?

A

Benzylpenicillin (50mg/kg BD).

Gentamicin (5mg/Kg OD).

509
Q

How would you feed a baby born at 27 weeks?

A

NG tube feeds.

At 35 weeks you can start breast/bottle feeding as this when suckling reflex develops.

510
Q

What long term problems can a pre-term baby develop?

A
  1. Retinopathy of prematurity.
  2. Chronic lung disease.
  3. Osteopenic bones.
  4. Neurodevelopmental delays.
511
Q

What is the Moro reflex?

A

The Moro (startle) reflex is a primitive reflex that is a response due to a sudden loss of support. Sudden extension of the head causes symmetrical extension then flexion of the arms.

512
Q

Why should primitive reflexes disappear?

A

Primitive reflexes should gradually disappear as postural reflexes develop. This essential for good motor development.

513
Q

Why is it concerning if primitive reflexes persist?

A

There may be a sign of CNS dysfunction.

514
Q

Name 3 primitive reflexes.

A
  1. Palmar.
  2. Rooting.
  3. Moro.
  4. Tonic neck reflex.
  5. Parachute.
515
Q

How does cerebral palsy often present?

A

Abnormal limb/trunk posture and tone in infancy and delayed milestones. Feeding difficulties. Abnormal gait once walking is achieved. Asymmetric hand function before 12 months. Primitive reflexes may persist.

516
Q

Cerebral palsy is characterised according to neurological features. What are the categories?

A
  1. Spastic - hemiplegic, quadriplegic, diplegic.
  2. Dyskinetic.
  3. Ataxic.
517
Q

How might you investigate a child who is presenting with signs of cerebral palsy?

A
  1. Cytogenetic tests.
  2. Metabolic tests.
  3. Imagine e.g. MRI brain.
  4. Neurophysiological tests.
  5. Histopathology.
518
Q

Why might the clinical signs of cerebral palsy change over time?

A

The clinical signs may change over time as the brain matures but the underlying aetiology is not progressive.

519
Q

What drugs can be used to treat hypertonia in children with cerebral palsy?

A

treatments for spasticity include oral diazepam, oral and intrathecal baclofen, botox injection

520
Q

What are absence seizures?

A

Seizures where there is a transient loss of consciousness with an abrupt onset and termination. Momentary unresponsive stare with motor arrest, lasts <30s. Developmentally normal but can interfere with school.

521
Q

How might you investigate suspected absence seizures?

A
  1. Observe an episode - hyperventilation, ask the child to blow on a windmill.
  2. EEG - would show 3-second spike and wave discharges.
522
Q

What medications can be given to treat absence seizures?

A

Ethosuxamide or Sodium Valporate.

523
Q

Give some possible side effects of Ethosuxamide and Sodium Valporate.

A

Ethosuxamide - rash, nausea, D+V.

Sodium Valporate - weight gain, hair loss, teratogenic.

524
Q

What can absence seizures evolve into?

A

Juvenile myoclonic epilepsy (JME).

525
Q

What are the signs of juvenile myoclonic epilepsy?

A

Clumsiness and GTCS that occur shortly after waking and are often provoked by sleep deprivation.

526
Q

Which is more concerning: a paralytic or a non-paralytic squint?

A

Paralytic squints are more concerning.

527
Q

What type of squint may require neuro-imaging?

A

Paralytic squints. These may be due to a space occupying lesion e.g. brain tumour.

528
Q

What conditions does the new born blood spot (Guthrie test) screen for?

A
  1. CF.
  2. Congenital hypothyroidism.
  3. Sickle cell disease.

6 metabolic diseases e.g. MCADD, phenylketonuria and maple syrup disease etc.

529
Q

What biochemical derangement might you see in a patient with pyloric stenosis?

A

Metabolic alkalosis.

530
Q

What is the name of the surgery that can be used to treat pyloric stenosis?

A

Pyloromyotomy.

531
Q

What area of the brain does high levels of unconjugated bilirubin affect?

A

The basal ganglia.

532
Q

What is HSP?

A

A systemic vasculitis where there is deposition of IgA complexes. It is characterised by a palpable purpura and there is often renal involvement.

533
Q

Define sepsis.

A

Dysregulated host response leading to end organ dysfunction.

534
Q

How could you treat retinopathy of prematurity?

A

Laser therapy.

Alice's finals cards (23 decks)

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