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Phase 3A Sam Harper > Paediatrics 1 > Flashcards

Paediatrics 1 Flashcards

1
Q

Shunt direction for Ventricular Septal Defect

A

Left to Right

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2
Q

Effects of a moderate VSD

A

Enlarged atria and ventricles leads to pulmonary HTN and Congestive heart failure

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3
Q

Effects of Severe VSD

A

Severe pulmonary HTN and early onset heart failure

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4
Q

RF for VSD

A

Prematurity
Genetic Conditions - Downs, Edwards, Patau
Family Hx

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5
Q

Upper vs Lower RTI’s

A

Upper - rhintis, otitis media, pharyngitis, tonsilitis, Laryngitis

Lower - Bronchitis, croup, epiglottitis, Tracheitis, bronchiolitis, pneumonia

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6
Q

Clinical presentation of VSD

A

Often asymptomatic
Pansystolic murmur at lower left sternal border
Poor feeding
Tachypnoea
Dyspnoea
Failure to thrive

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7
Q

Diagnosing VSD

A

ECHO, ECG, XR

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8
Q

XR finding for VSD

A

Cardiomegaly

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9
Q

Tx for VSD

A

Diuretics for pulmonary congestion
ACE-i
Surgical repair

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10
Q

Complications of VSD

A

Eisenmengers, Endocarditis, Heart Failure

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11
Q

Shunt in ASD

A

Left to right

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12
Q

RF for ASD

A

Maternal smoking, FHx of CHD, Maternal diabetes, Maternal Rubella

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13
Q

Clinical Presentation of ASD

A

Tachypnoea, Poor weight gain, Recurrent Chest infections, Soft systolic ejection murmur in 2nd intercostal space, Wide flexed split S2 sound

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14
Q

Ix for ASD

A

ECG and Echo

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15
Q

Tx for ASD

A

Small - conservative, wait and weight it may close
Surgical closure if larger than 1cm

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16
Q

Complications of ASD

A

Stroke from DVT, AF, Pul Htn, Eisenmengers

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17
Q

Croup summarise

A

Viral - para flu
Spring/autumn
Self limiting
Worse at night
Barking sound
Stridor
Recession
Steroids help

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18
Q

Most common cyanotic congenital heart disease

A

Overriding aorta
Large VSD
Pulmonary stenosis
RVH

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19
Q

Epidemiology of ToF

A

More common in males
Rubella
Increased maternal age

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20
Q

Pathophysiology of ToF

A

Decreased right ventricular outflow. Dilated and displaced aorta.

Mild - asymptomatic but as heart grows they become cyanotic at 1-3 years
Moderate - Cyanosis and resp distress in first few months
Extreme - seen on antenatal scan, cyanosis quickly

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21
Q

Clinical Presentation of ToF

A

Irritability, Cyanosis, Clubbing, Poor feeding, Poor weight gain, Ejection systolic murmur in pul region and tet spells

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22
Q

What is a tet spell

A

Baby suddenly turns bluish and faints

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23
Q

Ix for ToF

A

CXR - boot shaped heart
MRI,Cardiac catheter
Echo

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24
Q

Tx for ToF

A

Prostaglandin infusion PGE1 to maintain ductus arteriosus
Beta blockers
Morphine to reduce resp drive
Surgical repair under bypass 3mo-4y but needs ICU

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25
Q

Why do you maintain the ductus arteriosus in ToF

A

To provide additional pulmonary blood flow to improve oxygen sats

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26
Q

Complications of ToF

A

Pulmonary regurg, Lifelong follow up

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27
Q

RF for ToF

A

Downs, Digeorge

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28
Q

What is Transposition of the Great Arteries (TGA)

A

Aorta rises from the right ventricle and pulmonary artery from the left ventricle

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29
Q

Epidemiology of TGA

A

More common in males
Maternal age over 40
Rubella
Maternal Diabetes
Alcohol consumption

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30
Q

Pathophysiology of TGA

A

Deox blood is delivered systemically
Mixing needs to be present to sustain life so a patent foramen ovale, VSD or patent ductus arteriosus must be present

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31
Q

Clinical presentation of TGA

A

Cyanosis in first 24 hours, Right ventricular heave, Loud S2 heart sound, Systolic murmur if VSD present,

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32
Q

Dx of TGA

A

Low SATS, ECHO, CXR shows egg on a string due to narrowed mediastinum and cardiomegaly, metabolic acidosis

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33
Q

Tx for TGA

A

PGE1 to ensure PDA
Surgical repair

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34
Q

What is a PDA

A

Persistent connection between the aorta and pulmonary artery

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35
Q

Shunt in PDA

A

Left to right

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36
Q

RF for PDA

A

Female and premature

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37
Q

Clinical presentation of PDA

A

Resp distress, Apnoea, Tachypnoea, Tachycardia, Continuous machinery murmur at left sternal edge

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38
Q

Dx of PDA

A

Echo, ECG/CXR

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39
Q

Tx for PDA

A

Cardiac catheterisation to close around 1 years old or sooner in more severe cases

Premature - Indomethacin or ibuprofen will inhibit prostaglandin and stimulate closure

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40
Q

What is croup

A

Acute laryngotracheobronchitis

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41
Q

Epidemiology of croup

A

Children ages 6mo-3yo
Common in autumn and spring
More common in boys

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42
Q

Pathophysiology of croup

A

Mucosal inflammation anywhere between nose and trachea
Caused by parainfluenza mainly but also Adenovirus, Rhinovirus, Enterovirus

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43
Q

Clinical features of corup

A

Mild: Barking cough with no stridor, no recession, child happy to eat or drink
Moderate: Frequent barking cough with audible stridor at rest, suprasternal recession, no agitated
Severe: Frequent barking cough, Prominent stridor, Sternal recession, agitated and distressed potentially tachy

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44
Q

Exam and Hx for Croup

A

1-4 days of non specific rhinorrhea, fever and barking cough
Worse at night
Stridor
Decreased bilateral air entry
Tachypnoea
Costal recession

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45
Q

Resp failure red flags

A

Drowsiness, Lethargy, Cyanosis, Tachycardia, Laboured breathing

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46
Q

Dx of Croup

A

FBC, CRP, U+E, CXR to exclude a foreign body

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47
Q

Tx of Croup

A

Symptoms from 48 hours-week
Paracetamol or Ibuprofen for sore throat
Admission if moderate/severe and if dehydrated
Single dose of dexamethasone 0.15mg/kg or prednisolone
Nebulised adrenaline for relief of severe symptoms
Oxygen if needed
Monitor for needed ENT intervention if suspected airway blockage

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48
Q

Complications of Croup

A

Otitis Media, Dehydration due to reduced fluids, Superinfection such as pneumonia

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49
Q

Define Bronchiolitis

A

Viral infection of the bronchioles

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50
Q

Epidemiology of Bronchiolitis

A

under 2’s
Common
Winter and spring peak
Caused by RSV

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51
Q

RF for Bronchiolitis

A

Breastfeeding for less than 2 mo
Smoke
Older siblings who could spread
Chronic lung disease of prematurity

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52
Q

Clinical features of Bronchiolitis

A

Symptoms onset 2-5 days
Low grade fever
Rhinorrhoea
Cough
Reduced feeding
Signs of resp distress: nasal flaring, tracheal tug, head bobbing, grunting, recession
Inspiratory crackles

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53
Q

Ix for Bronchiolitis

A

Nasopharyngeal aspirate for RSV culture
FBC, Urine, Blood gas

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54
Q

Home Tx for Bronchiolitis and prevention

A

Supportive at home
Palvizumab vaccine considered if child under 9 mo with chronic lung or child under 2 with severe immunodeficiency require long term vent

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55
Q

When to admit urgently in bronchiolitis

A

Apnoea
- Resp Rate > 70
- Central cyanosis
- SpO2 < 92%

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56
Q

When to do a non urgent admission in bronchiolitis

A
  • Resp Rate > 60
  • Clinical dehydration
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57
Q

Inpatient management for bronchiolitis

A

O2
Fluids
CPAP if in resp failure
Suctioning of secretions
Ribavirin for severe

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58
Q

What treatment has no evidence for use in bronchiolitis

A

Bronchodilation, Abx and steroids

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59
Q

What is Pneumonia

A

Infection of the LRT and lung parenchyma leading to consolidation

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60
Q

Epidemiology of Pneumonia

A

Highest incidence in infants
Viral cause more common in younger infants
Bacterial more common in older infants
Viral disease more common in winter

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61
Q

Aetiology of Pneumonia

A

Neonates: Group B strep, E.coli, Klebsiella, S.Aureus

Infants: Strep pnuem, Chlamydia

School age: Strep pneum, S.Aureus, Group a strep, Mycoplasma pneum

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62
Q

Clinical presentation of Pneumonia

A

Usually precede a URTI, Fever, SOB, Lethargy, Signs of resp distress, wheeze and hyperinflation when viral

Auscultation: dullness to percuss, crackles, Decreased breathing sounds, Bronchial breathing

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63
Q

Ix for Pneumonia

A

Clinical mainly

CXR - fluids in lungs

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64
Q

Tx for Pneumonia

A

Manage at home with analgesia

Admitted: O2 and Iv fluids

Abx:
Neonates: Broad spectrum
Infants: amox/co-amox
Over 5: Amox/Erythromycin

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65
Q

Complications of Pneumonia

A

Risk of parapneumonic collapse and empyema

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66
Q

Is whooping cough a URTI or LRTI

A

URTI

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67
Q

Whooping cough causative organsism

A

Bordatella Pertussis - Gram -ve bacillus

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68
Q

Epidemiology of Whooping Cough

A

Less common now due to vax
Impacts infants worse

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69
Q

Clinical presentation of Whooping cough

A

Catarrhal phase: 1-2w with coryzal Sx
Paroxysmal phase: week 3-6, inspiratory whoop
Cough worse at night
Spasmodic coughing episodes
Low grade fever
Sore throat
Convalescent phase - downgrade to cough and can last 3 mo

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70
Q

Dx for Whooping cough

A

Naso-pharyngeal swab with pertussis
FBC
Antibody test

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71
Q

Tx for Whooping cough

A

Macrolide
Prophylactic Abx for contacts
Isolate for 21 days after symptom onset or for 5 days after Abx

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72
Q

Complications of Whooping cough

A

Seizures, Pneumonia, Bronchiectasis, Encephalopathy, Otitis Media

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73
Q

What is Asthma

A

Reversible paroxysmal contriction of the airways with inflammatory exudate and followed by airway remodelling

Most common chronic condition in children

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74
Q

Aetiology of Asthma

A

Genetic, Premature, Low birth weight, Smoking, Early viral bronciolitis, Cold air, allergen exposure

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75
Q

Clinical presentation of asthma

A

Episodic wheeze, dry cough, SOB, Reduced peak flow

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76
Q

Ix for Asthma

A
  • FEV1 significantly reduced
  • FVC normal
  • FEV1:FVC may be <70% if poorly controlled
  • Reversible spirometry is highly suggestive of asthma
  • ENO levels of nitric oxide correlate to inflammation
  • Baseline chest x ray
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77
Q

Management of Asthma

A

Step 1: SABA PRN - Salbutamol
Step 2: ICS Preventer therapy - Beclomethasone
Step 3: LTRA Montelukast
Step 4: Strop LTRA if hasn’t helped and add LABA - Salmeterol
Step 5: Switch ICS/LABA for ICS MART: Formoterol and ICS
Step 6: Add a separate LABA
Step 7: High dose ICS (>400mcg), referral

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78
Q

Management of Asthma in under 5

A

Step 1: SABA PRN - Salbutamol
Step 2: SABA + 8 week trial of ICS if symptoms reoccur within 4 weeks, restart ICS
Step 3: Refer to specialist

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79
Q

What is viral indued wheeze

A

Episodic wheeze - symptom of viral URTI and symptom free between events

Multiple trigger wheeze - URTI and other factors trigger wheeze

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80
Q

Management of Viral induced wheeze

A

Symptomatic - Saba with spacer max of 4 hourly up to ten puffs
LTRA and ICS via spacer
Multiple trigger: trial ICS or LTRA for 4-8 weeks

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81
Q

What is Respiratory Distress syndrome

A

Affects premature neonates, before the lungs start producing adequate surfactant, common in below 32 w babies

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82
Q

Pathophysiology of Resp distress syndrome

A

Inadequate surfactant leads to high surface tension in alveoli leading to atelectasis as it more difficult for the alveoli to expand so inadequate gas exchange and hypoxia, hypercapnia and resp distress

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83
Q

Management of Resp distress syndrome

A

Dexamethasone to mothers with suspected preterm labour to increase surfactant production, Intubation and ventilation may be needed to fully assist breathing if distress is severe, Endotracheal surfactant via tube, CPAP, O2

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84
Q

Complications of resp distress syndrome

A

Short term - Pneumothorax, Infection, Apnoea, Intraventricular haemorrhage, Pul Haemorrhage, Necrotising Enterocolitis

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85
Q

Long term complications of resp distress syndrome

A

Chronic lung disease of prematurity, Retinopathy of prematurity, Nuerological, hearing, visual impairment

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86
Q

What is Bronchopulmonary dysplasia

A

Infants who still require oxygen at postnatal age of 36 weeks are described as having BPD

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87
Q

Bronchopulmonary Dysplasia aetiology

A

lung samage from pressure and vilume trauma of artificial ventilation, oxygen toxicity and infection

CXR - widespread opacification and sometimes cystic changes, fibrosis and even lung collpase

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88
Q

Tx for Bronchopulmonary dysplasia

A

Weaned onto CPAP followed by additional oxygen where needed and sometimes corticosteroids to facilitate weaning however there is a risk of neurodevelopmental issues with these

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89
Q

What is epiglottitis

A

inflammation and swelling of the epiglottis caused by infection. Life threatening emergency

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90
Q

Epiglottitis causative organism

A

Haemophilus influenzae B

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91
Q

Typical presentation of epiglottitis

A

Drooling, Tripod position, unvaxed, fever, sore throat, difficulty swallowing, muffled voice, scared and quiet child, septic and unwell

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92
Q

Ix for epiglottitis

A

If acutely unwell and obvious then dont investigate just treat them. Dont scare the child.

Can do a Xr of neck - thumb sign due to swollen epiglottis, can exclude a foreign body

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93
Q

Management of epiglottitis

A

Alert the most senior paediatrician available and anaesthetics.

Ensure airway is secure, prep for intubation and prep ICU

Tx once airway is secure: IV AbX (Ceftriaxone) and steroids (dexamethasone)

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94
Q

Prognosis for Epiglottitis

A

Most recover without intubation

Epiglottic abscess - pus around the epiglottis - similar tx to epiglottitis

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95
Q

Briefly summarise Laryngomalacia

A

Where part of the larynx above the vocals cords is structured in a way that partially blocks the airway

Chronic stridor

Omega shaped epiglottis

In infants peaking at 6 mo. intermittent stridor that is worse during feeding, upset, lying on back and during infection

Usually self resolving. Rarely surgery or a tracheostomy is needed

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96
Q

Define Cystic Fibrosis

A

Autosomal reccessive condition affecting mucus glands

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97
Q

Genetic mutation in CF

A

Mutation of the cystic fibrosis transmembrane conductance regulatory gene on chromosome 7 - lots of variants with the most common being delta-F508 which codes for a chloride channel

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98
Q

CF incidence

A

1/2500

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99
Q

Key consequences on physiology of CF

A

Thick pancreatic and biliary secretions that blocks ducts resulting in lack of digestive enzymes

Low volume thick airway secretions - reduce airway clearance resulting in bacterial colonisation and increased infection

Congenital bilateral absence of vas deferens - male infertility

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100
Q

Presentation of CF

A

Screened for in bloodspot test

Meconium ileus is the first sign - not passing meconium in 24 hours with abdo distension and vomiting

Recurrent LRTI, Failure to thrive and pancreatitis

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101
Q

Symptoms of CF

A

Chronic cough, Thick sputum production, Recurrent RTI, Loose greasy stools, Salty child, Poor weight and height gain

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102
Q

Signs of CF

A

Low weight or height on chart, Nasal polyps, Clubbing, Crackles and wheeze, Abdo distension

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103
Q

Causes of clubbing in children

A

Hereditary clubbing, Cyanotic heart disease, IE, CF, Tuberculosis, IBD, Liver Cirrhosis

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104
Q

Dx of CF

A

Newborn blood spot, sweat test, Genetic testing

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105
Q

What is the sweat test

A

Gold standard for CF

Patch of skin chosen, Pilocarpine is applied, Electrodes next to patch, current causes sweating, lab is sent sweat to look for a chloride concentration of over 60 mmol/L

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106
Q

Microbial colonisers in CF

A

S. Aurues, Hib, Klebsiella, E.coli, Burkhoderia cepacia, Psedomonas aeruginosa

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107
Q

Pseudomonas Aeruginosa in CF

A

Hard to clear, resistant, reccomend isolating those infected. Keep away from other children with CF.

Tx - Tobramycin or ciprofloxacin

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108
Q

Management of CF

A

Chest Physio - several times a day to clear mucus and reduce infection and colonisation risk

Exercise - clears mucus and improves resp reserve

High calorie diet - due to malabsorption, increased resp effort and coughing

CREON - digests fats

Prophylactic fluloxicillin

Treat infections

Bronchodilators like salbutamol

Nebulised DNase

Nebulised hypertonic saline

Vax - pneumococcal, influenza and varicella

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109
Q

Monitoring for CF

A

Specialist clinics typically every six months, regular sputum monitoring, screening for diabetes, osteoporosis, vit d def, liver failure

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110
Q

Prognosis for CF

A

Median life expectancy of 47

  • 90% develop pancreatic insufficiency
  • 50% develop diabetes
  • 30% develop liver disease
  • Most males are infertile
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111
Q

What is Primary Ciliary Dyskinesia

A

Aka Kartagners syndrome. Autosomal recessive affecting the cilia. More common when there is consanguinity

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112
Q

PCD pathophysiology

A

dysfunction of motile cilia most notably in resp tract. build up of mucus in lungs which increases risk of infection

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113
Q

Sx for PCD

A

Similar to CF, lots of infection, poor growth and bronchiectasis, also affects fallopian tubes and flagella of sperm so reduced or absent fertility

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114
Q

What is PCD strongly linked with

A

Situs Inversus

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115
Q

What is Kartagners Triad

A

Three features of PCD:

  • Paranasal Sinusitis
  • Bronchiectasis
  • Situs Inversus
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116
Q

What is Situs Inversus

A

All internal organs are mirrored in the body

25% of those with situs inversus have PCD

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117
Q

Dx of PCD

A

Recurrent infection. Family history looking for consanguinity. Imaging to look for situs inversus. Semen analysis, key test is to take a sample of ciliated epithelium

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118
Q

Management of PCD

A

Similar to CF and bronchiectasis

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119
Q

What is Pyloric Stenosis

A

Progressive hypertrophy of the pyloric sphincter causing gastric outlet obstruction

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120
Q

Epidemiology of Pyloric Stenosis

A

More common in boys, 1/500, Family Hx, First borns

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121
Q

Clinical presentation of Pyloric Stenosis

A

Presents at 4-6 weeks
Non bilious, forceful, projectile vomiting after feed
Will continue to feed despite vomiting
Weight loss
Dehydration
Constipation
Visible Peristalsis
Palpable olive sized pyloric mass felt

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122
Q

Ix for Pyloric Stenosis

A

Test feed with NG tube and empty stomach and feel for visible peristalsis and mass
USS - Hypertrophy of the muscle
Blood gas - Hypochloremic, Hypokalaemic Metabolic Alkalosis

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123
Q

Management of Pyloric Stenosis

A

Correct mentabolic imbalances - NaCl
Fluid bolus for hypovolemia
NG tube feed
Ramsteds Pyloromyotomy - feeding can commence after 6 hours

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124
Q

What is Hirschsprungs disease

A

Nerve cells of the myenteric plexus are absent in the distal bowel and rectum, specifically the parasympathetic ganglionic cells resulting in a lack of peristalsis

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125
Q

Epidemiology of Hirschprungs

A

90% present in neonates. Average age of presentation is 2 days. Males. Downs

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126
Q

Pathophysiology of Hirschprungs

A

Short segment is most common where it is confined to rectosigmoid section. Ganglion cells of submucosal plexus not present, failure of peristalisis and bowel movements causing obstruction, can lead to bacterial build up and enterocolitis and sepsis

127
Q

Clinical Features of Hirschsprungs

A

Failure to pass meconium, Abdo distended, Bilious vomiting, palpable faecal mass, Empty rectal vault

128
Q

Ix for Hirschsprungs

A

Rectal suction biopsy to test for ganglionic cells in anyone who has:
- delayed meconium, constipation early, family hx, distension, Faltering growth

Contrast enema

129
Q

Management of Hirshsprungs

A

Iv Ibx, decompress, NG tube and surgery

130
Q

What is malrotation and volvulus

A

Twisting loop of bowel leading to intestinal obstruction

131
Q

When does malrotation and volvulus present

A

First month of life

132
Q

Clinical presentation of malrotation and volvulus

A

Abdo pain, bilious vomiting, caecum in midline, reflux

133
Q

Ix for volvulus

A

Barium enema, Abdo XR with contrast to look for obstruction (double bubble sign)

134
Q

Tx for volvulus

A

Surgery

135
Q

What is intussusception

A

One piece of the bowel telescopes inside another leading to ischaemia and bowel obstruction

136
Q

Where is intussusception most common

A

distal ileum and ileocecal junction

137
Q

Epidemiology of intussusception

A

3 mo to 3 years
Most common under 1 yo
most common cause of obstruction in neonates

138
Q

RF for Intussusception

A

CF, Meckels, HSP, Rotavirus vaccine > 23 weeks

139
Q

Clinical presentation of intussusception

A

Colic abdo pain, Pallor, sausage shape mass palpable RUQ, Redcurrant jelly stools, abdo distension, shock, peritonitis (Guarding, rigidity, pyrexia)

140
Q

Ix for intussusception

A

USS: target shapes mass
Abdo XR: distended small bowel, absence of gas in bowel

141
Q

Tx for intussusception

A

Medical emergency, IV fluids, Air enema using USS to stretch the walls of the bowel and reduce the intussusception and if this is unsuccessful then operate. If perforation then broad spectrum Abx e.g. Gentamicin

142
Q

What is necrotising enterocolitis

A

Acute inflammatory disease affecting preterm neonates leading to bowel necrosis and multi system organ failure

143
Q

Epidemiology of NEC

A

Low birth weight, Most common surgical emergency, presents in first 2 weeks, prematurity, Abx therapy > 10 days, genetic

144
Q

Clinical presentation of NEC

A

New feed intolerance, vomiting with bile, Fresh blood in stool, Abdo distension, Reduced bowel sounds, Palpable abdo mass, Visible intestinal loops, sepsis

145
Q

Ix for NEC

A

Bloods: Thrombocytopenia, neutropenia
Cultures
Blood gas: acidotic
USS: air in portal system, ascites, perforation
XR: riglers sign: both sides of bowel are visible due to gas in peritoneal cavity, dilated bowel loops, distended bowel, thickened bowel wall, air outlining falciform ligament

145
Q

Tx for NEC

A

Nil by mouth, Bowel decompression by NG, IV Cefotaxime, surgery

146
Q

What is Meckels Diverticulum

A

Congenital diverticulum of the SI containing ileal, gastric and pancreatic mucosa

147
Q

Meckels incidence

A

2%

148
Q

How far from the ileocaecal valve is Meckels

A

2cm

149
Q

Risks with Meckels

A

Peptic ulceration

150
Q

Clinical presentation of Meckels

A

Abdo pain, Rectal bleeding in children 1-2 yo, Obstruction due to intussusception and volvulus

151
Q

Management of Meckels

A

Removal if symptomatic

152
Q

What is biliary atresia

A

Obstruction of the biliary tree due to sclerosis of the bile duct, reducing bile duct flow

153
Q

Epidemiology of Biliary atresia

A

Females, Neonatal cholestasis 2-8 weeks, associated with CMV, congenital malformations

154
Q

Pathophysiology of Biliary atresia (types)

A

Type 1: Common bile duct obliterated
Type 2: Atresia of the cystic duct in the porta hepatis
Type 3: Most common atresia of the right and left ducts at level of porta hepatis

155
Q

Clinical presentation of Biliary atresia

A

Jaundice post 2 weeks, Dark urine, Pale stools, Appetite disturbance, hepatosplenomegaly, abnormal growth, duodenal atresia

156
Q

Ix for Biliary atresia

A

Serum bilirubin: Conjugated is high
LFT’s raised
Alpha 1 antitrypsin to rule out deficiency
Sweat test to rule out CF
USS to look for structural abnormalities

157
Q

Management of Biliary atresia

A

Surgical dissection of abnormalities: Kasai procedure
Abx

158
Q

Complications of Biliary atresia

A

Cirrhosis and HCC
Progressive liver disease

159
Q

What is neonatal jaundice

A

Hyperbilirubinaemia in the neonate

160
Q

Physiological vs pathological vs prologned jaundice

A

Physiological:
Breakdown of in utero Hb, immature liver cant break down bilirubin, starts 2-3 days of life

Pathological:
Onset less than 24 hours, G6PD def, Spherocytosis

Prolonged:
Jaunidce over 14 days, Biliary atresia, Hypothyroid, Breast milk jaundice resolves 1.5-4 months, UTI/infection

161
Q

Aetiology of neonatal jaundice

A

Prematurity, small for dates, previous sibling with it

162
Q

Clinical presentation of neonatal jaundice

A

Colour, Drowsiness, Signs of infection

163
Q

Ix for neonatal jaundice

A

TCB (transcutaneous bilirubinometry) for over 35 weeks gestation
Serum bilirubin if not TCB
Total and Conjugated bilirubin
Coombs test
Infection screen

164
Q

Management of Neonatal jaundice

A

Phototherapy, repeat tests, can do a transfusion

165
Q

Complications of neonatal jaundice

A

Kernicterus - bilirubin induced encephalopathy and irreversible neurological damage

166
Q

Secondary causes of constipation

A

Hirschprungs disease, CF, Hypothyroid, Spinal cord lesion, Sexual abuse, Intestinal obstruction, Cows milk intolerance

167
Q

Clinical presentation of constipation

A

Less than 3 stools per week, Hard and difficult to pass, Rabbit dropping stool, straining, abdo pain, overflow soiling, palpable hard stools in abdo

168
Q

Management of Constipation

A

Correct reversible factors e.g. diet, hydration
Laxatives: Movicol
Disimpaction regimen

169
Q

Red flags for constipation and their associated conditions

A

Failure to pass meconium - Hirschsprungs
Failure to thrive - hypothyroid, coeliac
Gross abdo distension - Hirschsprungs or other
Sacral dimple above natal cleft - Spina bifida
Abnormal anus - abnormal anorectal anatomy
Perianal bruising - sexual abuse
Perianal fistualae - perianal crohns

170
Q

What is otitis media

A

Infection of middle ear

171
Q

Aetiology of otitis media

A

Viral
Pneumococcus/Haemolytic Streptococcus/HiB

172
Q

Clinical presentation of otitis media

A

Ear pain, Fever, Bulging tympanic membrane, Discharge

173
Q

What is secondary otitis media

A

Glue ear
May have hearing loss
Retracted eardrum
If it goes on for over 3 months then refer for grommets and adenoidectomy

174
Q

Management of Otitis media

A

5 days Amox/Erythromycin

175
Q

What is squint

A

AKA strabismus, misalignment of the eyes, images on retina dont match do double vision

176
Q

Pathophysiology of squint

A

Bad connection of eyes to brain to brain reduces signal to one of the eyes so it becomes lazy and the problem worsens over time - amblyopia

177
Q

What is concomitant squint

A

Differences in control of extra ocular muscles

178
Q

What is esotropia

A

Inward position squint - affected eye deviated towards the nose

179
Q

What is exotropia

A

Outward position squint - deviated to ear

180
Q

What is hypertropia

A

Upward moving affected eye

181
Q

What is Hypotropia

A

Downward moving affected eye

182
Q

Aetiology of squint

A

Idiopathic, Hydrocephalus, Cerebral palsy, space occupying lesion, Trauma

183
Q

Ix for Squint

A

Eye movement and inspection, Fundoscopy, Visual acuity, Hrischbergs test and cover test

184
Q

Management of squint

A

start before age 8
Occlusive patch to force bad eye to develop
Atropine drops in good eye to cause blurring forcing good eye to develop

185
Q

What is periorbital cellulitis

A

eyelid and skin infection in front of the orbital septum confined to the soft tissue layer

186
Q

RF for orbital cellulitis

A

Boys
Previous sinus infection
Lack of Hib infection
Recent eyelid injury

187
Q

Clinical presentation of Periorbital cellulitis

A

Swelling, redness, hot skin around eyelid and eye

188
Q

Ix for periorbital cellulitis

A

Clinical
CT sinus with contrast to differentiate between orbital and periorbital

189
Q

Management of Periorbital Cellulitis

A

Abx empirical e.g. Cefotaxime/Clindamycin

190
Q

What is Epilepsy

A

Umbrella term for tendency to have seizures which are transient episodes of abnormal electrical activity in the brain

191
Q

What is a Generalised tonic-clonic seizure

A

Loss of consciousness with tonic (rigidity) and clonic (rhythmic jerking) phase with possible tongue biting, incontinence, groaning and irregular breathing. Postictal period of confusion, drowsiness and irritability

192
Q

Tx for generalised tonic clonic

A

Sodium valproate, lamotrigine or carbamazepine

193
Q

What are focal seizures

A

Begin in temporal lobes and affect speech, memory and emotions. Present with hallucinations, flashbacks and deja vu.

194
Q

Tx of focal seizure

A

Lamotrigine or levetiracetam

195
Q

What is an absent seizure

A

Most common in children. Become blank and stare into space then return to normal. Usually 10-20 seconds

196
Q

Tx for absent seizures

A

Ethosuximide

197
Q

What is a myoclonic seizure

A

Sudden brief muscle contractions where they remain awake. Often part of juvenile myoclonic epilepsy

198
Q

Tx for myoclonic seizures

A

Sodium valproate or levetiracetam

199
Q

What are tonic/atonic seizures

A

Sudden tension/stiffness affecting the body

200
Q

Tx for atonic seizures

A

Sodium Valproate or lamotrigine

201
Q

Ix for epilepsy

A

full history
EEG after second simple tonic clonic
MRI brain for abnormalities
Blood electrolytes, glucose, cultures and LP

202
Q

Management of acute seizures

A

Recovery position
Soft under head
Remove obstacles
Make a note of timings
Call an ambulance if longer than 5 mins

203
Q

Side effects of Sodium valproate

A

Teratogenic, Liver damage, Hair loss and tremors

204
Q

SE of Carbamazepine

A

Agrunlocytosis, Aplastic anaemia

205
Q

SE of Ethosuximide

A

Night tremors, rashes and N+V

206
Q

SE of Lamotrigine

A

DRESS syndrome, Leukopenia

207
Q

What is Status Epilepticus

A

Emergency where seizures last over 5 mins or 2 or more seizures without regaining consciousness

208
Q

Management of status epilepticus in community and hospital

A

Hospital - secure airway, high conc O2, Assess cardiac and resp function, IV lorazepam

Community - Buccal midazolam or rectal diazepam

209
Q

What are febrile convulsion

A

Occur in children with a high fever 6 mo - 5 yo

210
Q

Length of simple febrile seizure and type

A

less than 15 minute generalised tonic clonic

211
Q

Length and type of complex febrile convulsion

A

Focal and last more than 15 mins or multiple times

212
Q

Ix for febrile convulsion

A

Rule out other causes such as epilepsy, syncope, trauma, lesion and neuro infection

213
Q

Management of febrile convulsion

A

manage infection. control fever with analgesia. Parental education

214
Q

What is eczema

A

Chronic atopic condition caused by defects in the normal skin barrier, leading to gaps which let irritants, microbes and allergens to enter creating an immune response and inflammation

215
Q

Triggers of eczema

A

Temp change, Dietary products, washing powders, cleaning products, stress

216
Q

Clinical presentation of eczema

A

Infancy, dry red and itchy skin, sore patches over flexors, face and neck. Episodic flares

217
Q

Management of eczema

A

Maintenance: Emollients e.g. E45 or diprobase. Use as often as possible especially after washing and before bed

Flare ups: Thicker emollient e.g. Cetraben or can use topical steroids e.g. Hydrocort and beclomethasone

Other: Topical tacrolimus, oral steroids, methotrexate

218
Q

What is stevens-johnson syndrome

A

Disproportional immune response causing epidermal necrosis resulting in shedding of top layer of skin - less than 10% of body surface affected

219
Q

Aetiology of stevens-johnson

A

Meds - Anti-epileptics, Abx, Allopurinol, NSAIDs
Infections - HSV, Mycoplasma pneumonia, CMV, HIV

220
Q

Clinical presentation of stevens johnson

A

Non specific: fever, cough, sore throat, sore mouth, sore eyes, itchy skin
Purple/red rash which spreads and blisters
can affect urinary tract, lungs and internal organs

221
Q

Management of stevens johnson

A

Steroids, Immunoglobulins, immunosuppressant

222
Q

Complications of Stevens Johnson

A

Secondary infection: cellulitis, sepsis
Permanent skin damage

223
Q

What is urticaria

A

Also known as hives, small itchy lumps which appear on the skin

224
Q

What is urticaria associated with

A

angioedema

225
Q

Pathophysiology of Urticaria

A

Release of histamine and other pro-inflammatory chemicals by mast cells in skin. Could be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic uritcaria

226
Q

Aetiology of Urticaria

A

Allergies, Contact with chemicals/latex/nettles, Meds, Virus, Insect bites

227
Q

What is chronic urticaria

A

Autoimmune condition where autoantibodies target mast cells and trigger them to release histamines and other chemicals

228
Q

Tx of Urticaria

A

Antihistamines
For chronic - Fexofenadine
Steroids
Omalizumab - targets IgE

229
Q

What is Nappy rash

A

Contact dermatitis in nappy area caused by friction between skin and urine/faeces in nappy. common in 9-12 mo. Breakdown can lead to candida or bacterial infection

230
Q

RF for nappy rash

A

Delayed nappy change
Soaps
Diarrhoea
Oral Abx use -> candida
Preterm

231
Q

Clinical presentation of nappy rash

A

Sore, red or inflamed skin
No rash on creases of the groin
Itchy rash - distress
Severe and long standing rash -> erosion and ulceration

232
Q

Candida vs nappy rash

A

In nappy rash the flexures are spared, its patchy and red

Candida has beefy red papules and white scaling

233
Q

Management of nappy rash

A

Switch to absorbant nappies
Change nappy often and clean skin
Maximise time out of the nappy
Infection - antifungal or abx cream

234
Q

What are petechiae

A

Small, non blanching, red spots caused by burst capillaries

235
Q

What is purpura

A

Larger, non blanching, red-purple macules or papules caused by leaking of blood from vessels under the skin

236
Q

Urgency of child with non blanching rash?

A

Very urgent, immediate investigation due to risk of meningococcal sepsis

237
Q

Name the differentials for non blanching rash

A

Meningoccocal septicaemia, HSP, ITP, HUS, Leukaemia, Mechanical, Traumatic and Viral

238
Q

Explain the DDx for non blanching rash

A

Meningococcal septicaemia - fever, unwell manage with Abx
HSP - Purpuric rash on legs and buttocks, may also have joiny and abdo pain
ITP - rash over several days in an otherwise unwell child
Leukaemia - Gradual petechiae with other signs such anaemia, lymphadenopathy and hepatosplenomegaly
HUS - recent diarrhoea alongside oliguria and anaemia
Mechanical - coughing, vomiting, breath holding can produce petechiae
Traumatic - tight pressure on skin e.g. NAI
Viral illness can lead to rash

239
Q

Ix for non blanching rash

A

FBC, U+E, CRP, ESR, Blood cultures, Meningococcal PCR, LP, BP, urine dip

240
Q

Main cause of anaphylaxis

A

Food allergy with an IgE mediated reponse

241
Q

Other causes of Anaphylaxis

A

Drugs, stings, latex, exercise, idiopathic

242
Q

Management of Anaphylaxis

A

Adrenaline and long term management is avoiding allergens and prescribing epipen

243
Q

What is kawasaki disease

A

Mucocutaneous, lymph node syndrome - a systemic medium-sized vessel vasculitis

244
Q

Epidemiology of kawasaki

A

Young children under 5 with no clear cause or trigger, more common in boys of Japanese or Korean origin

245
Q

Clinical presentation of kawasaki

A

Persistent high fever for more than 5 days, unwell and unhappy, widespread erythematous maculopapular rash and desquamation of the palms and soles, strawberry tongue, cracked lips, Cervical lymphadenopathy, bilateral conjunctivits

246
Q

Ix for Kawasaki

A

FBC - Anameia, Leukocytosis, thrombocytosis
LFT - hypoalbuminaemia
Raised ESR
Urinalysis shows raised WBC
ECHO - rule out aneurysm

247
Q

Disease course of kawasaki

A

Acute phase - child will be unwell with fever, rash, lymphadenopathy
Subacute phase - acute symptoms will settle but the arthralgia and risk of aneurysm continues
Convalescent stage - remaining symptoms return to normal and blood tests return to normal 2-4 weeks

248
Q

Management of Kawasakis

A

High dose aspirin, IV Ig, inform public health

249
Q

What is meningitis

A

Inflammation of the meninges

250
Q

Meningitis causative agent

A

Gram negative diplococcus bacteria that occurs in pairs

251
Q

What is meningococcal meningitis

A

When bacteria infects the meninges and CSF

252
Q

What is most common cause of meningitis in neonates

A

Group B strep

253
Q

Clinical presentation of meningitis

A

Fever, neck stiffness, vomiting, headache, photophobia, altered consciousness and seizures

254
Q

Neonatal signs of meningitis

A

hypotonia, poor feeding, lethargy, hypothermia, bulging fontanelle

255
Q

Two tests for meningitis

A

Kernig’s: lay patient on back and flex one hip and knee then straighten knee while keeping hip flexed which will produce pain or resistance
Brudzinski’s: lay patient on back and lift their head and neck off bed and flex chin to the chest, causes involuntary flexion of hips and knees

256
Q

Criteria for an immediate LP

A

All children under 1 month with a fever
1-3 mo with a fever and unwell
Under 1 yo with fever and other signs of serious illness

257
Q

Ix for meningitis

A

LP to be sent for meningococcal PCR

258
Q

Community management for meningitis

A

Stat injection of Benzylpencillin then transfer to hospital

259
Q

Management for meningitis in under 3 mo

A

IV Cefotaxime plus IV amoxicillin

260
Q

Management for meningitis above 3 mo

A

IV Ceftriaxone

261
Q

Post exposure prophylaxis for meningitis

A

Ciprofloxacin

262
Q

Common causes of viral meningitis

A

HSV, VZV, enterovirus

263
Q

Management of viral meningitis

A

Supportive, sometimes use aciclovir

264
Q

Differences between Bacterial and viral meningitis CSF samples

A

Bacterial: Cloudy, High protein, Low glucose, High neutrophils, cultures bacteria

Viral: Clear, Mildly raised or normal protein, normal glucose, high lymphocytes, Negative culture

265
Q

Is measles a bacteria or virus

A

Virus

266
Q

Clinical presentation of measles

A

Fever, Koplik spots (blue/white spots on inside of cheeks), conjunctivitis, coryza, cough, rash that spreads downwards from behind ears to whole body - maculopapular

267
Q

Management of measles

A

Supportive, avoid school for at least 5 days, Public health

268
Q

Complications of measles

A

otitis media, pneumonia, febrile convulsions, encephalitis/subacute sclerosing panencephalitis

269
Q

Clinical presentation of chicken pox

A

Fever, Vesicular rash beginning on head and trunk which spreads to peripheries, itching can lead to secondary infection

270
Q

Management of chickenpox

A

Symptomatic, Immunocompromised given aciclovir, Avoid school until lesions have crusted over

271
Q

Complications of Chicken pox

A

Bacterial superinfection, pneumonitis, DIC

272
Q

What is rubella

A

mild disease in childhood that occurs in winter and spring
Incubation of 15-20 days
resp droplet spread

273
Q

Clinical presentation of Rubella

A

Low grade fever, Maculopapular rash on face that spread to body

274
Q

Rubella Tx

A

None needed, diagnosis made serologically if there is any risk of exposure for non immune pregnant women

275
Q

Complications of rubella

A

Arthritis, Encephalitis, Myocarditis

276
Q

Summarise diphtheria

A

Infection which causes local disease with membrane formation affecting the nose, pharynx, larynx or systemic with myocarditis and neuro manifestations
Generally been eradicated in UK

277
Q

What is scalded skin syndrome

A

Caused by exfoliative staphylococcal toxin which causes separation of epidermal skin through the granular cell layers

278
Q

Clinical presentation of scalded skin syndrome

A

Fever, Malaise, Purulent crusting localised infection around eyes,nose,mouth with widespread erythema and tenderness

279
Q

What is the Nikolsky sign

A

Areas of epidermis seperate on gentle pressure leaving denuded areas of skin which then dry and heal without scarring

280
Q

Management of scalded skin syndrome

A

IV Fluclox, Analgesia and fluids

281
Q

Clinical presentation of Tuberculosis

A

Asymptomatic children have minimal signs of infection
If it spreads through lymphatic system - fever, anorexia, weight loss, cough and CXR changes such as hilar lymphadenopathy
Enlargement of peribronchial lymph nodes which can cause consolidation, obstruction and effusions

282
Q

What is post-primary TB

A

infection can be local or spread across systems such as bones, joints, kidneys and CNS

283
Q

Ix for TB

A

Gastric washing for 3 days to culture acid-fact bacilli through NG
Mantoux - however can be positive due to vax
IGRA - T cell response

284
Q

Management of TB

A

RIPE therapy initially and then reduce to Rifampicin and Isoniazid after 2 mo - last 6 mo
After puberty - give pyridoxine to reduce peripheral neuropathy SE of Isoniazid
Contact trace

285
Q

HIV Epidemiology

A

Affects 2 million children a year
Main transmission is during pregnancy, at delivery or breastfeeding

286
Q

Ix for HIV

A

Over 18 mo - presence of antibodies
Under 18 mo - HIV DNA PCR

287
Q

Clinical presentation of HIV

A

Most remain asymptomatic for years
Lymphadenopathy, recurrent bacterial infection, chronic diarrhoea, lymphocytic interstitial pneumonitis

288
Q

What does a severe AIDS diagnosis often present with

A

Pneomocystis jirovecii pneumonia, severe faltering growth and encephalopathy

289
Q

Tx for HIV

A

ART based on HIV load and CD4 count
Avoid breast feeding and active management of labour and delivery

290
Q

What is encephalitis

A

Inflammation of the brain - can be infective or not

291
Q

Most common cause of encephalitis

A

Viral, however bacterial and fungal are possible

292
Q

Most common virus causing encephalitis

A

HSV 1 from cold sores in children
HSV 2 for neonates from genital herpes following birth

293
Q

Clinical presentation of Encephalitis

A

Altered consciousness, Altered cognition, Unusual behaviour, Acute onset focal neurological symptoms, acute onset focal seizures, Fever

294
Q

Ix for encephalitis

A

LP to send CSF for PCR
CT if LP is contraindicated
MRI after LP for visualisation
HIV testing is recommended

295
Q

Management of Encephalitis

A

Herpes and VZV - Aciclovir
CMV - Ganciclovir
Repeat LP to ensure success before ending antivirals

296
Q

Complications of encephalitis

A

Lasting fatigue, change in personality/mood/memory/cognition, headaches and chronic pain, Sensory disturbance, Seizures

297
Q

Slapped cheek causative agent

A

Parvovirus B19

298
Q

Slapped cheek pathophysiology

A

Virus infects erythroblastosis red cell precusors in bone marrow

299
Q

Clinical presentation of slapped cheek

A

Erythema infectiosum - fever, headache, myalgia, rash on face which progresses to maculopapular rash on trunk and limbs

300
Q

Complications of slapped cheek

A

Aplastic crisis: in children with haemolytic anaemia where there is increased red cell turnover and immunodeficiency
Foetal disease which can lead to death due to severe anaemia

301
Q

Management of Slapped cheek

A

Supportive

302
Q

What is impetigo

A

Superficial bacterial skin infection caused by S.aureus

303
Q

Characteristic sign in impetigo

A

Golden crust

304
Q

What are the two types of impetigo, explain them

A

Non bullous - around nose and mouth and exudate from lesions causes golden crust, no systemic symptoms and wont be unwell

Bullous - 1-2 cm fluid filled vesicles which then burst to cause golden crust, more common in neonates and under 2’s, will have systemic Sx such as fever and malaise

305
Q

Tx for impetigo

A

Non-bullous - topical fusidic acid or antiseptic cream or fluclox if its widespread

Bullous - Fluclox

306
Q

Complications of impetigo

A

Sepsis, Scarring, Post strep glomerulonephritis, scarlet fever, Staphylococcal scaled skin syndrome

307
Q

Toxic shock syndrome causative agent

A

S.Aureus and Group A strep

308
Q

Clinical presentation of toxic shock syndrome

A

Fever over 39
Hypotension
Diffuse erythematous, macular rash
Organ dysfunction: Mucositis, D/V, Renal impairment, Liver impairment, Clotting abnormalities and thrombocytopenia

309
Q

Tx for toxic shock syndrome

A

Intensive care to manage the shock and areas of infection should be debrided
Abx such as Ceftriaxone and Clindamycin
After 1-2 weeks there is desquamation of the palms, soles, fingers and toes
Risk of recurrent infections

310
Q

Scarlet fever causative bacteria

A

Strep pyogenes

311
Q

RF for scarlet fever

A

Neonate, Immunocompromised, Concurrent chickenpox or flue

312
Q

Clinical presentation of scarlet fever

A

Sore throat, fever, headache, fatigue, nausea and vom
Pinpoint, sandpaper like blanching rash initially on trunk which then spreads
Strawberry tongue
Cervical lymphadenopathy

313
Q

Management of scarlet fever

A

Oral Abx such as benzylpenicillin for 10 days
tell public health

Phase 3A Sam Harper (4 decks)

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