Paediatrics Flashcards

1
Q

Triggers for viral induced wheeze?

A

Viral infections - RSV, rhinovirus

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2
Q

What age do children grow out of virally induced wheeze?

A

3-4 years

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3
Q

Presentation of VIW:

A

SOB, signs of resp distress, expiratory wheeze

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4
Q

Signs of respiratory distress:

A

Raised respect rate
Use of accessory muscles
Intercostal recessions
Subcostal recessions
Nasal flaring
Head bobbing
Tracheal tugging
Cyanosis
Abnormal airway noises

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5
Q

Management of VIW?

A

Bronchodilators in acute episodes
(usually salbutamol)

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6
Q

Cystic fibrosis inheritance, gene defect, chromosome?

A

Autosomal recessive, due to defect in CFTR gene on chromosome 7

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7
Q

What does CF affect?

A

Chloride channels
Pancreases, lungs, liver, gonads

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8
Q

Presentation of CF

A

Newborn - bloodspot positive, meconium ileus

Recurrent LRTIs, failure to thrive, pancreatitis
Chronic cough with thick sputum
Steatorrhoea, abdominal pain, bloating
Low height and weight
Finger clubbing
Crackles and wheeze on auscultation
Male infertility

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9
Q

Investigations for CF:

A

Newborn blood spot test
Sweat test - Cl 60-120mmol/L compared to 10-14
Raised immunoreactive trypsin
Genetic testing

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10
Q

Management of CF:

A

Chest physio BD
Prophylactic ABx for staph aureus - fluclox
Daily nebuliser anti-pseudomonas abx

High calorie diet
CREON tablet for pancreatic insufficiency
Nebulised hypertonic saline or DNAase
Vaccination - pneumococcal, influenza, varicella

Bilateral lung transplant

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11
Q

What does nebuliser hypertonic saline or DNAase do in CF treatment?

A

Decreases viscosity to increase clearance

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12
Q

What is the causative agent of croup?

A

Parainfluenza, RSV

Metapneumovirus, influenza

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13
Q

What age group get croup and when?

A

6 months - 3 years (up to 6)

Autumn time

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14
Q

Croup presentation:

A

Barking cough (foehn worse at night)
Preceded by low-grade fever and coryza
Stridor, hoarseness, recession

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15
Q

Treatment for croup?

A

Can be self-limiting

Oral dexamethasone 150mcg/kg, repeat after 12 hours if needed

Oxygen –> nebulised budesonide –> nebuliser adrenaline –> intubation

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16
Q

What is the causative agent of epiglottitis?

A

Haemophilus influenza type B (HiB)

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17
Q

Who gets epiglottitis?

A

1-6 years

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18
Q

Presentation of epiglottitis:

A

Pyrexial (>39)
Stridor - soft inspiratory
Drooling
Muffled voice
No/minimal cough
Tripod position

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19
Q

Investigations for epiglottitis:

A

Blood cultures
DO NOT EXAMINE
Lateral XR neck = thumb sign

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20
Q

Treatment for epiglottitis:

A

Intubation
IV ceftriaxone for 2-5 days
Prophylaxis with rifampicin for close contacts

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21
Q

Causative agent of bronchiolitis?

A

RSV

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22
Q

What age group gets bronchiolitis?

A

1-9 months (rare after 1 year)

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23
Q

Presentation of bronchiolitis?

A

Coryzal symptoms, respiratory distress, feeding difficulties, tachypnoea, apnoea episodes, wheeze and fine end inspiratory crackles on auscultation

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24
Q

Investigations for bronchiolitis?

A

Nasopharyngeal aspirate rapid testing (PCR)

CXR not necessary but = hyper inflating, air trapping, focal atelectasis

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25
Q

Treatment for bronchiolitis:

A

Self-limiting

Admission if < 3 months, pre-existing condition =
Supportive management - NG/IV fluids, saline nasal drops, O2, ventilation support if severe (high flow, CPAP or intubation)

CF patients = broad spec abx for 2-3 weeks

Palivizumab month injections - high risk

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26
Q

What is palivizumab? Who is it used for?

A

Monoclonal antibody used to prevent bronchiolitis

High risk for bronchiolitis - ex-prem, chronic lung disease, pulmonary hypoplasia, congenital heart disease, immune deficiency, CF

Monthly IM injections in winter months

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27
Q

Most common bacterial cause of pneumonia in children?

A

Strep pneumoniae - most common
Group A strep - pyogenes
Group B strep - newborns

Staph aureus - infrewuent

HiB - unvaccinated

Mycoplasma pneumoniae - extrapulmonary manifestation

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28
Q

Most common viral cause of pneumonia in children?

A

RSV

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29
Q

Pneumonia presentation in children:

A

Productive cough
High fever >38.5
Tachypnoea, tachycardia
Lethargy
Hypoxia, hypotension
Bronchial breathing
Focal coarse crackles, dullness to percussion

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30
Q

Investigations for pneumonia in children?

A

CXR, sputum cultures, viral PCR, blood cultures if septic

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31
Q

Antibiotics for pneumonia treatment in children?

A

First line - amoxicillin

Atypical - Amoxicillin +/- macrolide (eryth/clarith,azithromycin)

Complicated or influenza associated - co-amoxiclav

^5 days

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32
Q

Causative agent of whooping cough?

A

Bordetella pertussis = gram -ve

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33
Q

Presentation of whooping cough:

A

Low grade fever
Paroxysmal cough
Loud inspiratory whoop
Apnoeas

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34
Q

Investigations for whooping coughing?

A

Nasopharyngeal or nasal swab for PCR and cultures

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35
Q

What are the school attendance recommendations for whooping cough?

A

No school for 48 hours once abx started

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36
Q

Treatment for whooping cough

A

Supportive macrolide - azithromycin, erythromycin, clarithromycin within first 21 days (no longer contagious after this)

Vaccination as baby

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37
Q

Causes of heart failure in neonates?

A

Obstructed (duct-dependent) systemic circulation
- Hypoplastic left heart syndrome
- Critical aortic valve stenosis
- Severe coarctation of aorta
- Interruption of aortic arch

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38
Q

Causes of heart failure in infants?

A

High pulmonary blood flow:
- VSD
- AVSD
- Large PDA

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39
Q

Causes of heart failure in older children and adolescents?

A

Right or left heart failure:
- Eisenmenger syndrome (RHF only)
- Rheumatic heart disease
- Cardiomyopathy

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40
Q

Causes of heart failure in children - circulation failure?

A

Reduced oxygen carrying capacity - anaemia
Increased tissue demands - sepsis
Iatrogenic - fluid overload

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41
Q

Signs of innocent heart murmurs (s)

A

aSymptomatic
Soft blowing murmur
Systolic murmur only
left Sternal edge
+
Normal HS with no added sounds, no parasternal thrill, no radiation

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42
Q

Acyanotic heart defects:

A

VSD
ASD
AVSD
PDA
Coarctation of the aorta
Aortic stenosis
Pulmonary stenosis

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43
Q

Cyanotic hearts defects:

A

ToF
TGA
Truncus arteriosus
Tricuspid atresia
Total anomalous pulmonary venous return

Eisenmenger’s
Ebstein’s

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44
Q

Which way is the shunt in acynanotic defects?

A

L –> R

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45
Q

Which way is the shunt in cyanotic defects?

A

R –> L

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46
Q

What conditions are associated with ASD?

A

Fetal alcohol syndrome, Downs, TORCH, Trisomy 13, Trisomy 18

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47
Q

What conditions are associated with VSD?

A

Downs, TORCH, fetal alcohol syndrome, trisomy 13, trisomy 18

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48
Q

What is associative with AVSD?

A

Trisomy 21

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49
Q

What is associated with PDA?

A

Maternal rubella
Prematurity
Females

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50
Q

What is associated with coarctation of the aorta?

A

Turner’s, berry aneurysms, males, bicuspid aortic valve

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51
Q

What condition is associated with aortic stenosis?

A

Turner’s

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52
Q

What conditions are associated with pulmonary stenosis?

A

Noonan’s, William’s, rubella

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53
Q

Which heart defects make up ToF?

A

VSD
Pulmonary stenosis
Overriding aorta
RVH

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54
Q

What conditions are associated with ToF?

A

DiGeorge syndrome (22q deletion)
Downs
Rubella

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55
Q

What causes Eisenmenger’s syndrome?

A

LT complication of unrepared L –> R shunt (ASD, VSD, PDA) –> pulmonary hypertension –> reversal of shunt

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56
Q

What is Ebstein’s anomaly associated with?

A

ASD, WPW, lithium use in pregnancy

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57
Q

Describe the murmur in ASD

A

Ejection systolic, upper left sternal border

Wide fixed split S2

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58
Q

Describe the murmur in VSD

A

Pansystolic lower left sternal border

Quiet pulmonary second sound
Systolic thrill

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59
Q

Describe the murmur in AVSD

A

Thrill, gallop rhythm

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60
Q

Describe the murmur in PDA

A

Continuous crescendo-decrescendo machinery, 2nd left intercostal space

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61
Q

Describe the murmur in coarctation of the aorta

A

Systolic murmur in left axilla or left infraclavicular area

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62
Q

Describe the murmur in aortic stenosis

A

Ejection systolic murmur in aortic area (RUSE)

Carotid thrill
Delayed and soft aortic 2nd sound

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63
Q

Describe the murmur in pulmonary stenosis

A

Ejection systolic murmur in LUSE (can radiate to back)

Ejection click
Right ventricular heave

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64
Q

Describe the murmur in ToF

A

Harsh ejection systolic murmur at left upper sternal border

(+/- at left mid-sternal border)

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65
Q

Describe the murmur in ToGA

A

No murmur

Can get loud, single 2nd heart sound

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66
Q

Describe the murmur in Eisenmenger’s

A

No murmur or can be due to underlying septal defect

Loud P2

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67
Q

Presentation of ASD:

A

Asymptomatic
Resp infections, difficulty breathing, feeding difficulties, SOB, palpitations, HF, stroke

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68
Q

Presentation of VSD:

A

Asymptomatic
SOB, tachypnoea, sweating, feeding difficulties, poor weight gain, failure to thrive

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69
Q

Presentation of AVSD:

A

Poor feeding, failure to thrive, tachypnoea, hepatomegaly, oedema

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70
Q

Presentation of PDA:

A

Failure to thrive, SOB, poor feeding, tachycardia, tachypnoea

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71
Q

Presentation of coarctation of the aorta:

A

Weak femoral, pale, irritable, sweating, difficult breathing, higher BP in arms than legs, bounding pulses in arms and weak in legs

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72
Q

Presentation of aortic stenosis:

A

Asymptomatic
Weak pulses, reduced exercise tolerance, chest pain on exertion, syncope, dizziness

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73
Q

Investigations and findings for aortic stenosis:

A

CXR - post stenotic dilation of ascending aorta

ECG - LVH

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74
Q

Presentation of pulmonary stenosis:

A

Asymptomatic
Fatigue on exertion, SOBm dizziness, fainting

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75
Q

ECG findings for pulmonary stenosis:

A

RVH (upright T wave in V1)

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76
Q

Presentation of ToF?

A

Hypercyanotic ‘tet’ spells - irritability, inconsolable crying, cyanotic
Tissue acidosis - breathlessness, pallor
Clubbing

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77
Q

CXR findings for ToF:

A

Small heart
Uptilted apex (RVH) –> boot shaped

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78
Q

Presentation of ToGA:

A

Neonatal cyanosis and acidosis if closing/closed
Usually 2nd day of life

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79
Q

CXR findings for ToGA:

A

Egg on side

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80
Q

Presentation of Eisenmenger’s:

A

Peripheral oedema, raised JVP, dyspnoea, cyanosis, clubbing, plethoric complexion (due to polycythaemia)

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81
Q

Describe the murmur in Ebstein’s anomaly

A

Gallop rhythm

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82
Q

Presentation of Ebstein’s anomaly:

A

HF
Gallop rhythm
Cyanosis, SOB, tachypnoea, poor feeding, collapse
Present when ductus arteriosus shuts (day 2)

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83
Q

Management of ASD:

A

Monitor
Surgery if symptomatic

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84
Q

Management of VSD:

A

Monitor
Surgery if symptoms persistent - transvenous catheter closure or open heart surgery
Diuretics, captopril, calories if large and HF

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85
Q

Management of AVSD:

A

Surgery at 3-5 years

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86
Q

Management of PDA:

A

Premature - NSAIDs or indomethacin

Prostaglandin E1 - keep open

Watchful waiting

Surgical ligation if > 1 y/o

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87
Q

Management of coarctation of the aorta:

A

Prostaglandin E1 - keep ductus open
Surgical repair between 2-4 y/o

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88
Q

Management of aortic stenosis:

A

Regular clinic appointments and ECHOs
Balloon valvotomy - if high pressure gradient across aortic valve (>64mmHg)

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89
Q

Management of pulmonary stenosis:

A

Monitoring
Transcatheter balloon dilation if pressure gradient across pulmonary valve > 64mmHG

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90
Q

Management of ToF:

A

Tet spells > 15 mins - sedation, pain relief, IV propranolol, bicard

Very cyanosed infants - Blalock Taussig shunt surgery at 6-9 months

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91
Q

ToGA management:

A

Prostaglandin infusion - maintains latency of foramen ovale

Balloon atrial septostomy

Arterial switch operation in neonatal period - 1 week

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92
Q

Management of Eisenmenger’s syndrome:

A

Heart-lung transplant
Symptomatic treatment

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93
Q

Management of Ebstein’s anomaly:

A

Prophylactic abx for IE
Surgical correction

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94
Q

Complications of ASD:

A

Right-sided HF
Pulmonary HTN –> Eisenmenger
AF
Stroke in context of VTE

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95
Q

Complications of VSD:

A

HF
Pulmonary HTN
Arrhythmias
Stroke

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96
Q

Complications of AVSD:

A

Pulmonary vascular disease

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97
Q

Complications of PDA:

A

Congestive HF
Recurrent pneumonia

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98
Q

Complications of coarctation of the aorta:

A

Heart failure
Duct closure - babies collapsed and acidotic its HF (2nd day of life)

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99
Q

Complications of aortic stenosis:

A

Left ventricular outflow obstruction –> LVH –> HF

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100
Q

Complications of pulmonary stenosis:

A

RVH

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101
Q

Complications of ToF:

A

RVH

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102
Q

Complications of Eisenmenger’s:

A

HF
Infection
Thromboembolism
Haemorrhage

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103
Q

What is the definition of GORD in children?

A

Passage of gastric contents into oesophagus with or without regurgitation or vomiting due to immaturity of the LOS, mostly liquid diet and horizontal position

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104
Q

Risk factors for GORD:

A

Prematurity
Parental history of heartburn or acid regurgitation
Hx of congenital diaphragmatic hernia or congenital oesophageal atresia
Neurodisability –> cerebral palsy

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105
Q

GORD presentation red flags in paeds:

A

Projectile vomiting –> pyloric stenosis (up to 2 months)
Bile-stained vomit –> intestinal obstruction
Abdominal distension, tenderness, palpable mass
Blood in vomit or stool
Bulging fontanelle, altered responsiveness, increased head circumference

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106
Q

Presentation of GORD:

A

Distressed behaviour –> crying while feeding, unusual neck posture, change in crying, reluctance to feed
Hoarseness and/or chronic cough
Episode of pneumonia
Faltering growth
Severe signs = oesophagitis, apnoea, aspiration, IDA

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107
Q

Management of GORD:

A

Positioning and changing feeds - smaller, more frequent, sit upright after feeds

Thicken feeds - carobel

Drugs:
- 1-2 weeks of gaviscon –> if improves, continue for 2 weeks
- 4 weeks PPI (omeprazole) or histamine-2 receptor antagonist (ranitidine)
- surgery - fundoplication (>1y/o)

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108
Q

What is used to thicken milk for paediatric GORD?

A

Carobel

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109
Q

What is the definition of faltering growth?

A

Failure to gain adequate weight for achieve adequate growth during infancy or early childhood?

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110
Q

What is the classification for faltering growth?

A
  • fall across 1 or more weight centile spaces, if birth weight was below 9th centile
  • fall across 2 or more weight centile spaces, if birth weight was between 9th and 91st gentile
  • fall across 3 or more weight gentile spaces, if birth weight was above the 91st centile
  • when current weight is below the 2nd gentile for age, whatever the birth weight
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111
Q

Non-organic causes of faltering growth?

A
  1. Inadequate availability of food
  2. Psychosocial
  3. Neglect or child abuse
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112
Q

Organic causes of faltering growth?

A
  1. Impaired suck/swallow
    - oro-motor dysfunction
    - neurological disorder - cerebral palsy
  2. Chronic illness leading to anorexia
    - Crohn’s
    - Chronic renal failure
    - CF
    - Liver disease
    - Congenital abnormalities
    - GORD, CMPA
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113
Q

Risk factors for CMPA:

A

Boys
Know food allergy or family history
Atopic conditions or family history

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114
Q

What re the 2 different types of CMPA?

A
  1. IgE
  2. Non-IgE
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115
Q

Presentation of IgE CMPA:

A

Rapid onset - within 2 hours
Urticaria, rash
Colicky abdo pain, vomiting, bloody stools
Rhinorrhoea, itching nose

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116
Q

Presentation of non-IgE CMPA:

A

2-72 hours
Loose frequent stool with blood and mucus
Colicky abdo pain

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117
Q

Diagnosis of CMPA:

A

Elimination diet
IgE - skin/allergy test

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118
Q

Management of CMPA:

A

If breastfed - mum to have lactose free diet
Extensively hydrolysed formula
Amino acid formula

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119
Q

Definition of constipation:

A

Infrequent passage of dry, hard stool associated with strain, pain and bleeding

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120
Q

Presentation of constipation (paeds):

A

< 3 stools per week
Abdo pain - waxes and wanes
Encopresis
PR superficial bleeding
Avoidance of eating due to fear of pain

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121
Q

What is encopresis?

A

Involuntary faecal soiling or incontinence secondary to chronic constipation

122
Q

What is encopresis?

A

Involuntary faecal soiling or incontinence secondary to chronic constipation

123
Q

Constipation red flags:

A

Delayed meconium passage
Fever/vomiting/blood in stool
Failure to thrive
Empty rectum with presence of palpable abdominal mass
Abnormal neuro exam

124
Q

Investigations for constipation (paeds):

A

Bloods - FBC, TFTs, anti-TTG
Abdominal XR

125
Q

What does anti-TTG test for?

A

Coeliac disease

126
Q

Management on constipation:

A

Reassurance, good hydration, good toilet habits, high fibre diet
Osmotic laxative - movicol
Softener - lactulose
Bulking agent - fybogel
Stimulant laxative - Senna

Treatment for 6 months
Can use disimpaction regime

127
Q

What is a disimpaction regime?

A

Build up laxatives over a course of time to clear out bowels

128
Q

Acute causes of diarrhoea:

A

Infection
Allergy/food hypersenisitivity reactions
Drugs
Haemolytic uraemia syndrome
Surgical
Toddler’s diarrhoea

129
Q

Causative agents of diarrhoea - viral:

A

Rotavirus
Norovirus
Adenovirus
Calicivirus
Astrovirus

130
Q

Causative agents of diarrhoea - bacterial

A

C. jejuni traveller’s diarrhoea
Salmonella
E. coli
Shigella
Bacillus cereus (eaten rice, recover in 24 hours)

131
Q

Causative agents of diarrhoea - parasites:

A

Giardia lamblia
Cryptosporidium

132
Q

What is toddler’s diarrhoea?

A

> 3 weeks
Well child
Usually cleared by school age

133
Q

Presentation of diarrhoea:

A

Diarrhoea +/- bloody stools
Fever +/- vomiting
Dehydration

134
Q

Investigations for serious/ongoing/bloody diarrhoea??

A

Stool microbiology
Blood tests

135
Q

Treatment for diarrhoea:

A

Antibiotics if bacterial gastroenteritis complicated by sepsis or immunocompromised

No anti-emetics or anti-motility drugs

136
Q

Definition of coeliac disease:

A

Autoimmune chronic gluten enteropathy causing inflammation of the bowel

137
Q

Presentation of coeliac disease:

A

Steatorrhea, diarrhoea
Weight loss

Neonatal failure to thrive, abdominal distension buttock wasting, irritability at 8-24 months

Non-classical:
IDA, osteoporosis, fatigue, dermatitis herpetiformis, short stature

138
Q

Investigations for coeliac disease:

A

Anti-TTG, anti-EMA, gliadin antibodies
Endoscopy and duodenal bipsy

139
Q

What does a duodenal biopsy show in coeliac disease?

A

Villous atrophy and crypt hyperplasia

140
Q

Management of coeliac disease:

A

Lifelong gluten free diet

Complication prevention –> annual Ca and Vit D, DEXA scan when needed

141
Q

Pathophysiology of Chrohn’s:

A

Mouth to anus - terminal ileum mainly
Transmural inflammation
Skip lesions
Granuloma

142
Q

Pathophysiology of UC:

A

Only colon affected
Mucosal inflammation
Continuous
No granulomas

143
Q

Presentation of Chrohn’s:

A

Abdominal pain, malaise, dehydration
No blood or mucus
Weight loss
Fissures, fistula, abscesses, stricture
Perianal disease (rectal sparing)
Extra-intestinal - clubbing, erythema, gangrenous, episcleritis, arthritis

144
Q

Presentation of UC:

A

Abdominal pain, malaise, dehydration
Blood and mucus in stool

Extra-intestinal - clubbing, erythema, gangrenous, episcleritis, arthritis

145
Q

What is UC associated with?

A

Primary sclerosis cholangitis

146
Q

What is protective for ulcerative colitis?

A

Smoking

147
Q

Investigations for IBD:

A

Faecal calprotectin - 90% sensitive and specific
Endoscopy (OGD and colonoscopy) + biopsy = gold standard

148
Q

Treatment for Crohn’s:

A

Induction: steroids (Fred) +/- azathioprine, mercaptopurine, methotrexate, infliximab, adalimumab

Remission - azathioprine or mercaptopurine

Surgery if needed (distal ileum)

149
Q

Treatment for UC:

A

Induction (mild/mod): aminosalicylates (mesalazine) –> corticosteroids

Induction (severe): IV steroids –> IV ciclosporin

Remission - aminosalicylates –> azathioprine/mercaptopurine

Surgery if needed –> ileostomy

150
Q

Appendicitis presentation:

A

Central abdominal pain –> RIF pain (McBurney’s)
Loss of appetite, N&V
Rovsing’s sign
Guarding on abdominal palpation
Rebound and percussion tenderness –> ruptured

151
Q

What is Rovsing’s sign?

A

Palpation of LIF causes RIF pain

152
Q

Investigations for appendicitis:

A

Clinical presentation and raised inflammatory marker
CT scan
USS - often in women to rile out ovarian/gynae pathology

153
Q

Management for appendicitis:

A

Appendicectomy

154
Q

What is mesenteric adenitis?

A

Infamed abdominal lymph nodes

155
Q

Presentation of mesenteric adenitis:

A

Abdominal pain
Associated with tonsillitis or URTI

156
Q

Management of mesenteric adenitis:

A

Supportive

157
Q

What is pyloric stenosis?

A

Hypertrophy of the pylorus muscles –> causes gastric outlet obstruction

158
Q

What age group does pyloric stenosis usually affect?

A

2-8 weeks

More common in boys

159
Q

Presentation of pyloric stenosis:

A

Progressive projectile vomiting
Non bilious
Hungry after vomiting
Dehydration
Weight loss

160
Q

What is the electrolyte imbalance in pyloric stenosis?

A

Hypokalaemic, hypochloraemic metabolic alkalosis

161
Q

Examination findings in pyloric stenosis (test feed):

A

Olive size mass in RUQ
Visible peristalsis

162
Q

USS findings in pyloric stenosis:

A

Thickened pylorus

163
Q

Management of pyloric stenosis:

A

Fluid and electrolyte replacement
Non-urgent outpatient pyloromyotomy (Ramstedt’s)

164
Q

What is Meckel’s diverticulum?

A

Malformation of distal ileum

165
Q

When does Meckel’s diverticulum present?

A

Under 2 years if symptomatic

Present at birth but often asymptomatic for life

166
Q

Presentation of Meckel’s if symptomatic:

A

GI bleeding, obstipation, abdo pain, N+V

167
Q

Investigations for Meckel’s diverticulum:

A

Technetium-99m pertechnetate scan (Meckel’s scan)
USS
CT scan

168
Q

Management for Meckel’s diverticulum:

A

Surgical resection

169
Q

What is intussusception?

A

1 section of bowel telescopes into the other (ileum into caecum)

170
Q

At what age does intussusception usually present?

A

3 months to 2 years

171
Q

Name 4 conditions that intussusception is associated with:

A
  1. Meckel’s
  2. CF
  3. Lymphoma
  4. HSP
172
Q

Presentation of intussusception:

A

Preceded by viral infection
Colicky abdo pain - legs draw up
Lethargic between episodes
SBO signs
Sausage shaped mass
Red currant jelly stool

173
Q

USS and abdominal XR findings for intussusception:

A

USS - target/donut sign
AXR - dilated proximal bowel loop

174
Q

Management of intussusception:

A

Rectal insufflation (75% success)

Surgical correction - if air insufflation fails or signs of peritonism

175
Q

What is biliary atresia?

A

Narrow bile duct –> cholestasis

176
Q

Presentation of biliary atresia:

A

Jaundice > 14 days in newborns or > 21 days if premature

177
Q

Investigation findings for biliary atresia:

A

High conjugated bilirubin

178
Q

Management of biliary atresia:

A

Kasai portoenterostomy

179
Q

What is Hirschsprung’s?

A

Absence of ganglia in colon

Congenital

180
Q

Name 4 conditions that Hirschsprung’s is associated with:

A
  1. Down’s
  2. Neurofibromatosis
  3. Waardenburg syndrome
  4. Multiple endocrine neoplasia type II
181
Q

Presentation of Hirschsprung’s:

A

Failure to pass meconium within 24-48 hours
Abdominal distension
Late bilious vomiting
Poor weight gain and failure to thrive

182
Q

Name a complication of Hirschsprung’s:

A

Enterocolitis (HAEC) - inflammation and obstruction can lead to toxic megacolon or perforation

183
Q

Investigations and findings for Hirschsprung’s:

A

PR - contracted distal segment followed by rush of liquid stool and temporary relief of symptoms

AXR - contracted distal segment + dilated proximal segment

Barium enema

Rectal suction biopsy - GOLD STANDARD

184
Q

Management of Hirschsprung’s:

A

Surgical removal of ganglionic section

185
Q

Management of HAEC:

A

Fluid resuscitation, IV Abx, treatment of obstruction

186
Q

When does duodenal atresia present?

A

0-2 days old

187
Q

What is duodenal atresia associated with?

A

Downs syndrome

188
Q

Presentation of duodenal atresia:

A

SCO symptoms
Bilious vomiting

189
Q

What does AXR show for duodenal atresia?

A

Double bubble sign

190
Q

Management of duodenal atresia:

A

Surgical correction

191
Q

What is malrotation?

A

Abnormality in the bowel, does not form and turn as it should

192
Q

What is intestinal volvulus?

A

Complication of malrotation

Bowel twist on itself and blood supply is cut off

193
Q

When does malrotation/volvulus present?

A

2-30 days old

194
Q

Presentation of volvulus:

A

Can pass meconium normally
SBO symptoms
Bilious vomiting

195
Q

AXR findings in volvulus:

A

Coffee bean sign

196
Q

Investigations for volvulus:

A

AXR
Upper GI contrast series

197
Q

What are the upper GI contrast series findings in volvulus:

A

Spiral appearance of distal duodenum and proximal jejunum

198
Q

Management of volvulus?

A

Ladd’s procedure

199
Q

What is meconium ileus?

A

Failure to pass meconium –> small bowel obstruction

200
Q

What is meconium ileus associated with?

A

CF

201
Q

Presentation of meconium ileus:

A

Failure to pass meconium
SBO symptoms
Bilious vomiting

202
Q

Investigations for meconium ileus:

A

Heel prick test to confirm CF

203
Q

Management for meconium ileus:

A

Therapeutic contrast enema

204
Q

3 bacterial causes of paediatric meningitis:

A
  1. Strep pneumoniae
  2. Neisseria meningitidis
  3. GBS
205
Q

What is the most common cause of bacterial meningitis in newborns?

A

Group B strep

206
Q

Name 4 viral causes of viral meningitis?

A
  1. HSV
  2. VSV
  3. Enterovirus
  4. Adenovirus
207
Q

Describe the rash in meningococcal septicaemia:

A

Non-blanching rash
Red/pruple
Petechial rash/purpura

208
Q

Presentation of meningitis:

A

Fever
Neck stiffness
Headache
Vomiting
Photophobia
Altered consciousness
Seizures
Kernig’s sign
Brudzinski’s sign

209
Q

What is Kernig’s sign?

A

Physical test used when meningitis is suspected

Patient supine with hip flexed to 90 degrees, knee can’t be fully extended

210
Q

What is Brudzinski’s sign?

A

Physical tested used when meningitis is suspected

Passive flexion of the neck causes flexion of both legs

211
Q

Investigations for meningitis:

A

LP
Blood cultures

212
Q

LP findings for:
1 - bacterial meningitis
2 - viral meningitis

A

1 - cloudy, high protein, low glucose, high neutrophils

2 - clear, normal protein, normal glucose, high lymphocytes

213
Q

Community treatment for meningitis:

A

IM benzylpenicillin

214
Q

Meningitis treatment:
1. < 3 months
2. > 3 months

A
  1. Cefotaxime + amoxicillin
  2. Ceftriaxone + dexamethasone
215
Q

What is given for prophylaxis of bacterial meningitis?

A

Single dose of ciprofloxacin or rifampicin

216
Q

Treatment for viral meningitis:

A

Self-resolving
Aciclovir if HSV/VZV

217
Q

Complication of meningitis:

A

Hearing loss
Epilepsy
Learning difficulties
Vision loss
Limb loss

Death

218
Q

Causative agent of chicken pox:

A

Varicella zoster virus

219
Q

Describe the 3 stages of rash in chicken pox:

A

Macular –> papular –> vesicles

Non-infectious after scabbing over

220
Q

Symptoms of chicken pox:

A

Rash
Fever

221
Q

Treatment for chicken pox:

A

Symptomatic - calamine lotion, antihistamine

Severe/ immunocompromised - IV acyclovir

If infection (staph aureus) - fluclox

222
Q

Causative agent of measles:

A

Morbillivirus of RNA paramyxovirus

223
Q

Describe the rash in measles:

A

Maculopapular and erythematous rash on face and ears –> descends down the body

224
Q

Presentation of measles:

A

Prodromal period
Fever > 39
Cough
Coryza
Conjunctivitis
Koplik spots

225
Q

What are Koplik spots?

A

Sign of measles
Small white spots on buccal mucosa

226
Q

Investigations for measles:

A

Clinical diagnosis
Saliva swab for measles IgM to confirm

227
Q

Treatment for measles:

A

Self-limiting
Rest, isolation for 5 days after rash onset

228
Q

Complications of measles:

A

Otitis media, pneumonia, convulsions

229
Q

Causative agent of mumps:

A

RNA paramyxovirus

230
Q

What time of year is mumps most common?

A

Winter and spring months

231
Q

Presentation of mumps:

A

Parotid swelling - unilateral then bilateral
Fever
Malaise
Parotitis
Trismus (lockjaw)

232
Q

Blood test findings in mumps:

A

Raised plasma amylase

233
Q

Mumps treatment:

A

Self-limiting
No school for 7 days

234
Q

Complications of mumps:

A

Hearing loss
Orchitis
Meningitis

235
Q

Causative agent of rubella:

A

RNA paramyxovirus - rubivirus

236
Q

Describe the rash in rubella:

A

Non photogenic pink maculopapular rash –> starts on face

237
Q

Presentation of rubella (non-congenital):

A

Coryzal prodrome
Suboccipital and post auricular lymphadenopathy
Arthralgia

238
Q

Presentation of congenital rubella:

A

Sensorineural deafness
Cardiac and eye abnormalities

239
Q

Management of rubella:

A

Isolation for 5 days after rash appears

240
Q

What are the risks for pregnant women with rubella?

A

< 13 weeks - TOP, 80% risk of transmission, baby usually severely affected
> 13 weeks - 25% risk of transmission

241
Q

Causative agent of hand, foot and mouth disease:

A

Cocksackie (A16)

242
Q

Presentation of hand, foot and mouth disease:

A

Tender lumps of hand, feet and mouth
Sore throat
Dry cough
Fever

243
Q

Management of hand, foot and mouth disease:

A

Spontaenously resolves within 10 days
NO school exclusion

244
Q

Causative agent of slapped cheek syndrome?

A

Parvovirus B19

Also known as fifth disease

245
Q

Presentation of slapped cheek syndrome:

A

Bright red malaria rash (not contagious once rash appears)
Asymptomatic
Coryzal prodrome
Fever
Hydrops in babies

246
Q

Management of slapped cheek syndrome:

A

Spontaneously resolves within 10 days

247
Q

Complications of slapped cheek syndrome:

A

Hydrops in babies
Pure red cell aplasia
Transient aplastic crisis

248
Q

Cause of scalded skin syndrome?

A

Reaction to staph toxin from stat aureus infection

Usually in children < 5

249
Q

Presentation of scalded skin syndrome:

A

Extensive tender erythema with flaccid superficial blisters/bullae
Erosion
+ve Nikolsky sign (rubbing causes skin to peel away)
Fever, lethargy, dehydration

250
Q

Management of scalded skin syndrome:

A

IV anti-staph abx

251
Q

Cause of Scarlet fever:

A

Strep A
(Reaction to strep A toxins)

252
Q

What age group is mostly affected by Scarlet fever?

A

2-8 years old

253
Q

Presentation of Scarlet Fever:

A

Rash - fingered sandpaper rash on neck and chest –> spreading to flexor creases

Prodrome - fever, vomiting, abdo pain

Strawberry tongue
Flushed red face, pale around mouth

Anterior cervical lymphadenopathy

254
Q

Investigations for Scarlet fever:

A

Throat swab
Serum antistreptolysin O and and antiDNAase B titres

255
Q

Management of Scarlet Fever:

A

Pen V for 10 days
No school until after 24 hours on Abx

256
Q

Complications of Scarlet Fever:

A

Peritonsillar or retropharyngeal abscess, acute glomerulonephritis, rheumatic fever

257
Q

What is Kawasaki’s disease?

A

Medium sized vasculitis

258
Q

What age group does Kawasaki’s mainly effect?

A

6 months - 5 years

259
Q

Presentation of Kawasaki’s:

A

Widespread erythematous maculopapular rash and desquamation on palms and soles

Fever > 5 days
Bilateral conjunctivitis
Cracked lips
Cervical lymphadenopathy
Strawberry tongue

260
Q

Investigations for Scarlet Fever:

A

FBC - anaemia, leucocytosis, thrombocytosis

LFT - hypoalbuminaemia, elevated liver enzymes

ESR + CRP raised

Urinalysis - WBC without infection

ECHO

261
Q

Management of Kawasaki’s disease:

A

High dose aspirin –> reduce risk of thrombosis then reduce until echo

IVIG –> reduced risk of coronary artery aneurysms for 10/7

Echo 6-8 weeks after for coronary artery aneurysms

262
Q

Cause of Toxic Shock Syndrome:

A

Toxins produced by staph aureus and group A strep

263
Q

Presentation of toxic shock syndrome:

A

Diffuse erythematous, macular rash

Fever > 39
Hypotension
Mucositis
Renal and liver impairment
Clotting abnormalities + thrombocytopenia

264
Q

Toxic shock syndrome management:

A

Debridement
Abx - ceftriaxone + clindamycin
IVIG

265
Q

Causative agent of Impetigo:

A

Staph aureus or group B strep

266
Q

Which age group is impetigo most common in?

A

2-5 years old

267
Q

Presentation of impetigo:

A

Rapidly spreading clear blisters –> straw-coloured lesions with yellow crusting

268
Q

Management of impetigo:

A

Hydrogen [eroxide 1% or fusidic acid

Severe - oral fluclox

No school for 48 hours after abx or crusted over

269
Q

What is molluscum contagiosum:

A

Common pox viral infection

Warm, overcrowded environments

270
Q

Presentation of molluscum contagiosum:

A

Pink umbilicate papule with central dimple

271
Q

Management of molluscum contagiosum:

A

Resolves spontaneously

272
Q

Causative agent of pityriasis:

A

Human herpes virus 6 or 7

273
Q

Presentation of pityriasis rosea:

A

Herald patch - faint red scaly oval 2cm lesion –> widespread faint scaly oval rash

Low grade fever, headache, lethargy

274
Q

Management of pityriasis rosea:

A

Self-limiting
Non-contagious

275
Q

Causative agent of seborrhoeic dermatitis:

A

Malassezia yeast

276
Q

Presentation of seborrhoeic dermatitis:

A

Cradle cap flaky scalp, flaky itchy skin

277
Q

Management of seborrhoeic dermatitis:

A

Cradle cap - vaseline

Face/body - clotrimazole or miconazole ring

Scalp - shampoo ketoconazole

278
Q

What is JIA?

A

Autoimmune onset of persistent joint inflammation lasting > 6 weeks before age 16 with no identified underlying cause

279
Q

What is Still’s disease?

A

Systemic JIA

280
Q

Presentation of systemic JIA:

A

Subtle salmon-pink rash
Spiking daily fever
Joint pain
Lymphadenopathy
Splenomegaly
Arthritis
Polyserositis –> pericarditis, pleurites, sterile peritonitis

281
Q

Blood findings in systemic JIA:

A

Raised CRP, ESR, platelets and serum ferritin

ANA antibodies -ve, RF -ve

282
Q

What is the first line treatment for systemic JIA?

A

Methotrexate (DMARD)

283
Q

Treatment for systemic JIA:

A

NSAIDs
Steroids
DMARDs
Biological therapies

284
Q

Name a serious complication of JIA?

A

Macrophage activation syndrome

Life-threatening, low ESR

285
Q

Name the 5 subtypes of JIA:

A
  1. Systemic JIA
  2. Polyarticular JIA
  3. Oligoarticular JIA
  4. Enthesitis-related arthritis
  5. Juvenile psoriatic arthritis
286
Q

What is the inheritance pattern and genetic mutation in Osteogenesis Imperfecta?

A

AD (80% but can be AR)
Defect in type 1 collage genes (COL1A1, COL1A2)

287
Q

Presentation of OI:

A

Bone fragility, fracture, deformity
Bone ache/pain
Impaired mobility –> ligamentous laxity, sarcopenia
Poor growth
Deafness, hernias, valvular prolapse
Blue sclera

288
Q

What is the classification of OI?

A

Sillence Classification
I - Mild (AD)
II - Perinatally lethal (AR, AD)
III - Progressively deforming, severe (AR)
IV - moderate (AD, AR)

289
Q

Management of OI:

A

Education, PT/OT, analgesia

Vitamin D supplementation –> prevent deficiency

Bisphosphonate therapy - inhibits osteoclasts (stay on this until at least stopped growing)

Surgery –> long bones, spine, skull base, hearing, teeth

290
Q

What is Rickets?

A

Undermineralised bone (osteomalacia) usually due to vitamin D deficiency

291
Q

What causes Rickets?

A

Lack of sunlight
Poor nutrition
Intestinal malabsorption –> pancreatic insufficiency (CF), coeliac, IBD

292
Q

Presentation of Rickets:

A

Metaphyseal swellings
Bowing deformities
Slowing of linear growth
Motor delay, hypotonia
Fractures
Splayed/frayed metaphyses
Ping pong ball sensation of the skull (craniotabes)
Harrison sulcus - horizontal depression of lower chest

293
Q

Blood and XR findings in Rickets:

A

Low phosphate, normal or low Ca, raised serum AlkP

If vit D deficiency - raised PTH and low vit D

XR - cupping and fraying of metaphases, widened epiphyseal plate

294
Q

Management of Rickets:

A

Treat underlying cause
Vit D3 +/- calcium
Cod liver oil, sunlight

295
Q

What is Developmental Dysplasia of the Hip?

A

Abnormal development resulting in instability, dysplasia, subluxation and possible dislocation of the hip

296
Q

What are some risk factors for DDH?

A

Females
Breech
1st child
Prematurity
Oligohydramnios
FHx
Club feet
Spina bifida

297
Q

Presentation of DDH:

A

Painless limp
Delayed walking
Prone to falls
Asymmetrical thigh/buttock skin creases
Unequal leg length
Galeazzi sign (flex knees with feet together) - +ve is unequal length (-ve if bilateral DDH)

298
Q

What are the screening tests for DDH?

A

Barlow’s and Ortolani’s

299
Q

Management of DDH:

A

< 6 months - Pavlik harness (keeps hips flexed and abducted)
Cosed reduction or open reduction +/- femoral shortening

300
Q

What is the triad of presentations for haemolytic uraemic syndrome?

A
  1. AKI
  2. Microangipathic haemolytic anaemia
  3. Thrombocytopaenia
301
Q

What is the most common cause of haemolytic uraemic syndrome?

A

Shigatoxin producing E.coli O157:H7

302
Q
A