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Phase 3a > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

What are the most common causes of pneumonia?

A
  • Neonates = group B strep
  • Infants = strep pneumoniae
  • Children = strep pneumoniae/staph aureus/group A strep
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2
Q

What is the investigation/finding and management for pneumonia?

A
  • CXR = consolidation
  • Supportive management
  • Oxygen (if severe)
  • Abx (amoxicillin/co-amoxiclav/erythromycin)
  • Mycoplasma pneumonia = macrolides (azithromycin/erythromycin)
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3
Q

Describe croup

A
  • 6 months - 3 years
  • Peak incidence at 2 years
  • More common in males
  • Parainfluenza virus
  • 1-4 day history
  • Sx worse at night
  • Barking cough
  • Hoarse voice
  • Stridor
  • Fever/rhinorrhoea
  • Single oral dose of dexamethasone or prednisolone
  • Nebulised adrenaline
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4
Q

Describe roseola infantum

A
  • Self limiting
  • Human herpes virus type 6
  • Febrile illness followed by rash with blanching papules
  • Patient is well
  • No exclusion from school
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5
Q

What are red flag sx in respiratory?

A
  • Drowsiness/decreased consciousness
  • Tachypnoea (>60)
  • Intercostal recession
  • Cyanosis
  • Laboured breathing
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6
Q

How is croup severity calculated?

A

Westley Croup Score
- Mild = 0-2
- Moderate = 3-5
- Severe = 6-11
- Impending respiratory failure = 12-17

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7
Q

What criteria is included in the Westley Croup Score?

A
  • SaO2 <92%
  • Stridor
  • Retractions
  • Air entry
  • Consciousness
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8
Q

What is a common differential diagnosis for croup?

A

Epiglottitis (shorter time course and more severe)

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9
Q

Describe acute epiglottitis

A
  • Haemophilus influenzae type B (Hib)
  • Acute onset (hours)
  • Tripoding (lean forward with mouth open and tongue out)
  • Sore throat/SOB/fever
  • Drooling
  • Stridor
  • DON’T EXAMINE THROAT
  • CXR (thumb sign)
  • O2
  • Nebulised adrenaline
  • Secure airway/tracheostomy
  • Fluids
  • Abx (if underlying infection) e.g. ceftriaxone
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10
Q

What is an important preventative measure for acute epiglottitis?

A
  • 6-in-1 DTaP/IPV/Hib vaccination
  • At 8/12/16 weeks
  • Booster at 1 year
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11
Q

Describe asthma

A
  • Risk factors = genetics (atopy)/prematurity/low birth weight/not breastfed/exposure to allergens
  • Episodic wheeze
  • Dry cough (often worse at night)
  • Chest tightness
  • SOB
  • Reduced peak flow
  • Diurnal variability
  • FEV1 reduced
  • FVC normal
  • FEV1:FVC <70%
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12
Q

What is the long-term management for asthma in children?

A
  1. SABA PRN (salbutamol)
  2. ICS (beclomethasone)
  3. LRTA (montelukast)
  4. Stop LRTA and add LABA (salmeterol)
  5. Switch ICS/LABA for ICS MART (formoterol and ICS)
  6. Add separate LABA
  7. Increase ICS dose and refer
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13
Q

What is the long-term amanagement for asthma in children <5?

A
  1. SABA PRN (salbutamol)
  2. SABA + 8 week trial of ICS (restart if sx reoccur within 4 weeks)
  3. Refer
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14
Q

What is the management for acute asthma?

A

Acute - O SHIT ME
1. Oxygen
2. Salbutamol nebulisers (SABA)
3. Hydrocortisone IV or oral prednisolone (steroids)
4. Ipratropium bromide nebulisers (SAMA)
5. Theophylline/aminophylline
6. IV magnesium sulphate
7. Escalate

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15
Q

What is the criteria for life threatening asthma?

A
  • SpO2 <92%
  • PEFR <33% predicted
  • Silent chest
  • Poor respiratory effort
  • Altered consciousness
  • Agitation/confusion
  • Exhaustion
  • Cyanosis
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16
Q

Describe viral induced wheeze

A
  • RSV/rhinovirus
  • Evidence of viral illness (fever/cough/coryzal sx 1-2 days prior)
  • SOB
  • Signs of respiratory distress
  • Expiratory wheeze throughout chest
  • Manage same as asthma
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17
Q

Describe bronchiolitis

A
  • Children <2 (3-6 months)
  • Very common
  • Peaks in winter/spring
  • RSV
  • Risk factors = breastfeeding <2 months/smoke exposure/older siblings who attend nursery/school/chronic lung disease of prematurity
  • 2-5 day history
  • Coryzal symptoms (fever/nasal congestion/rhinorrhoea)
  • Cough
  • Reduced feeding
  • Bilateral wheeze
  • Bilateral crepitations
  • Nasopharyngeal aspirate/throat swab
  • Supportive management/Palivizumab
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18
Q

What is cystic fibrosis?

A

Autosomal recessive genetic condition caused by mutation of CFTR gene on chromosome 7

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19
Q

What are common microbial colonisers in CF?

A
  • Staph aureus
  • Pseudomonas aeruginosa
  • Haemophilus influenzae
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20
Q

How does CF affect the respiratory tract?

A
  • Recurrent LRTIs
  • Chronic cough
  • Thick sputum
  • Crackles and wheeze
  • Nasal polyps
  • Chest hyperinflation
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21
Q

How does CF affect the pancreas?

A
  • Pancreatitis
  • Pancreatic insufficiency (steatorrhoea due to lack of fat digesting enzymes)
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22
Q

How does CF affect the GI tract?

A
  • Bowel obstruction in-utero (meconium ileus)
  • Cholestasis in-utero (neonatal jaundice)
  • Distal intestinal obstruction syndrome
  • Steatorrhoea (due to lack of fat digesting enzymes)
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23
Q

How does CF affect the reproductive tract?

A

Congenital bilateral absence of vas deferens = male infertility

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24
Q

What are investigations for CF?

A
  • Genetic testing for CFTR gene (amniocentesis/CVS/blood test)
  • Meconium ileus + abdominal distension + vomiting
  • Newborn heel prick test
  • Bloods = immunoreactive trypsinogen (high)
  • Sweat test (cause skin to sweat and test Cl- conc)
  • CXR (hyperinflation)
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25
Q

What is the lifestyle management for CF?

A
  • Patient/family education
  • Avoid other CF px
  • Chest physiotherapy
  • Vitamin A/D/E supplements
  • High calorie and high fat diet
  • CREON tablets (pancreatic enzyme supplementation)
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26
Q

What is the cause of whooping cough?

A

Bacterium Bordetella Pertussis (gram -ve bacillus)

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27
Q

What are the clinical features of whooping cough?

A
  • Rhinitis/conjunctivitis
  • Irritability/sore throat/fever/dry cough
  • Severe paroxysms of coughing followed by inspiratory gasp (whoop) often followed by going blue and vomiting
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28
Q

What are investigations for whooping cough?

A
  • Culture of nasopharyngeal aspiration/swab
  • Anti-pertussis toxin IgG serology
  • Anti-pertussis toxin detection in oral fluid
  • FBC (lymphocytosis)
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29
Q

What is the management for whooping cough?

A
  • Macrolide abx (clarithromycin <1 month, azithromycin/clarithromycin >1 month, co-trimoxazole 2nd line)
  • Isolation for 21 days after sx onset or 2 days after abx
  • Supportive management
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30
Q

What are important preventative measures for whooping cough?

A
  • Vaccinations given at 2/3/4 months (8/12/16 weeks) = 6-in-1
  • Booster at 3 years and 4 months = 4-in-1
  • Prophylactic abx for close contacts at high risk
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31
Q

What is otitis media and what are common causes of it?

A

Infection of middle ear

Bacterial:
- Strep pneumoniae

Viral:
- RSV
- Rhinovirus

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32
Q

What are the clinical features of otitis media?

A
  • Ear pain
  • Reduced hearing
  • Bulging tympanic membrane
  • General sx of URTI
  • Balance issues/vertigo
  • Discharge (if tympanic membrane perforated)
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33
Q

What are the investigations for otitis media?

A
  • Examine ears and throat
  • Otoscope - to visualise tympanic membrane (normal = pearly-grey/translucent/slightly shiny; otitis media = bulging/red/inflamed looking membrane)
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34
Q

What is the management for otitis media?

A
  • Analgesia
  • Most cases resolve without abx within 3 days but can last up to 1 week
  • Abx (amoxicillin 1st line then erythromycin/clarithromycin)
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35
Q

What are complications of otitis media?

A
  • Otitis media with effusion (glue ear)
  • Hearing loss
  • Perforated eardrum
  • Recurrent infection
  • Mastoiditis
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36
Q

What are the clinical features of glue ear?

A
  • Difficulty hearing
  • Retracted eardrum
  • Sensation of pressure inside ear (accompanied by popping/crackling noises)
  • Disequilibrium/vertigo
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37
Q

What is the investigation for glue ear?

A

Otoscopy:
- Tympanic membrane appears dull
- Light reflex lost (indicates fluid in middle ear)
- Bubble seen behind TM

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38
Q

What is the management for glue ear?

A
  • Some cases resolve within 3 months
  • Hearing aid insertion
  • Surgery - myringotomy and grommet insertion
  • Surgery - adenoidectomy
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39
Q

What are grommets?

A

Small tubes inserted into the tympanic membrane to allow fluid from the middle ear to drain through the tympanic membrane to the ear canal - usually fall out within a year

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40
Q

What type of hearing loss is more common in children?

A

Conductive - recurrent ear infections or insertion of foreign objects into ear canal

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41
Q

What are some causes of congenital deafness?

A
  • Maternal rubella/CMV infection during pregnancy
  • Genetic deafness
  • Associated conditions e.g. Down’s syndrome
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42
Q

What are some causes of perinatal deafness?

A
  • Prematurity
  • Hypoxia during/after birth
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43
Q

What are some causes of deafness after birth?

A
  • Jaundice
  • Meningitis/encephalitis
  • Otitis media/glue ear
  • Chemotherapy
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44
Q

What are some causes of sensorineural deafness?

A
  • Exposure to loud noise
  • Injury
  • Disease
  • Drugs
  • Inherited condition
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45
Q

What are some causes of conductive deafness?

A
  • Ear wax/foreign object
  • Fluid/infection/bone abnormality/eardrum
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46
Q

What are the investigations for hearing loss?

A
  • UK newborn hearing screening programme (NHSP)
  • Audiometry
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47
Q

What is periorbital cellulitis and what are common causes of it?

A

Eyelid/skin infection of periorbital soft tissue superficial to orbital septum
- Staph aureus (most common)
- Strep pneumoniae/haemophilus influenzae

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48
Q

What are risk factors for periorbital cellulitis?

A
  • Male
  • Previous sinus infection
  • Lack of Hib infection
  • Recent eyelid injury
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49
Q

What are the clinical features of periorbital cellulitis?

A
  • Eyelid erythema
  • Eyelid oedema
  • Hot skin around eyelids/eye
  • Normal vision
  • Normal ocular motility with no pain
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50
Q

What are the investigations for periorbital cellulitis?

A
  • CT sinus and orbits with contrast
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51
Q

What is the management for periorbital cellulitis?

A

Empirical abx e.g. cefotaxime/clindamycin

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52
Q

What is a common differential diagnosis for periorbital cellulitis?

A

Orbital cellulitis - muscles of orbit affected usually due to bacterial sinusitis - LIFE-THREATENING

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53
Q

What is a squint and what are some common causes of it?

A

Misalignment of the eye a.k.a strabismus
- Hydrocephalus
- Cerebral palsy
- Space-occupying lesions e.g. retinoblastoma
- Trauma

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54
Q

What is amblyopia?

A

In squint, lazy eye becomes progressively more passive and has reduced function

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55
Q

What is the main feature of a squint and what is the management?

A
  • Diplopia
  • Occlusive patch over good eye
  • Atropine drops in dominant eye (causes blurred vision)
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56
Q

What does the foramen ovale connect?

A

Left and right atria in foetuses - can bypass pulmonary circulation

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57
Q

What does the ductus arteriosus connect?

A

Pulmonary artery and aorta in foetuses - can bypass pulmonary circulation

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58
Q

What is the most common septal defect?

A

Ventricular septal defect

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59
Q

What are risk factors for VSD?

A
  • Prematurity
  • Genetic conditions e.g. Down’s syndrome/Edward’s/Patau
  • Fhx
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60
Q

What are the clinical features specific to VSD?

A
  • Asx
  • Pansystolic murmur in LLSE –> transmits to USE and axillae
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61
Q

What are the investigations for VSD?

A
  • Echo
  • CXR (large pulmonary arteries/cardiomegaly)
  • ECG
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62
Q

What is the management for VSD?

A
  • Many close spontaneously
  • Surgery
  • Diuretics (to relieve pulmonary congestion)
  • ACEi (to reduce systemic pressure)
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63
Q

What are complications of VSD?

A
  • Eisenmenger’s
  • Endocarditis
  • HF
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64
Q

What are risk factors for ASD?

A
  • Maternal smoking in 1st trimester
  • Fhx
  • Maternal diabetes/rubella
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65
Q

What are the types of ASD?

A
  • Ostium primum (AV valve)
  • Ostium secundum (centre of atrial septum)
  • Sinus venosus (superior/inferior vena with right atrium connection)
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66
Q

What are the clinical features specific to ASD?

A
  • Asx
  • Fixed, widely split S2 sound
  • Ejection systolic murmur in pulmonary area
  • Recurrent chest infections
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67
Q

What are the investigations for ASD?

A
  • CXR (large pulmonary arteries/cardiomegaly)
  • Echo
  • ECG
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68
Q

What is the management for ASD?

A
  • Most close spontaneously
  • Surgery
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69
Q

What are complications of ASD?

A
  • Eisenmenger’s
  • AF
  • Stroke from DVT
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70
Q

What are the risk factors for patent ductus arteriosus?

A
  • Female
  • Prematurity
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71
Q

What are the clinical features for patent ductus arteriosus?

A
  • Continuous machinery murmur in pulmonary area
  • Collapsing pulse
  • Heaving apex beat
  • Left subclavicular thrill
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72
Q

What are the investigations for patent ductus arteriosus?

A
  • CXR (cardiomegaly)
  • Echo
  • ECG
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73
Q

What is the management for patent ductus arteriosus?

A
  • Surgery (cardiac catheterisation)
  • Indomethacin/ibuprofen (inhibits prostaglandins and stimulates closure)
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74
Q

What are complications of patent ductus arteriosus?

A
  • Eisenmenger’s
  • Differential cyanosis
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75
Q

What are generic clinical features of septal defects?

A
  • Poor feeding/failure to thrive
  • Tachypnoea/dyspnoea
  • Active precordium
  • Thrill
  • Gallop rhythm
  • Hepatomegaly
  • Oedema
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76
Q

What are the clinical features specific to AVSD?

A

Murmur arises from valvular regurgitation

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77
Q

What are the investigations for AVSD?

A
  • Echo
  • Screen children for Down’s syndrome
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78
Q

What is the management for AVSD?

A

Surgery

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79
Q

What is a complication of AVSD?

A

Pulmonary vascular disease

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80
Q

Briefly describe the pathophysiology of coarctation of aorta

A
  • Collateral circulation forms to increase flow to lower part of body
  • Intercostal arteries become dilated and tortuous
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81
Q

What are the clinical features of coarctation of aorta?

A
  • Weak femoral pulses
  • Pre and post ductal difference in saturations
  • Murmur over back
  • Collapse/acidosis
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82
Q

What are the investigations for coarctation of aorta?

A
  • 4 limb BP (discrepancy between upper and lower limbs)
  • CXR (rib notching)
  • CT/MRI
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83
Q

What is the management for coarctation of aorta?

A

Surgery - angioplasty and stent insertion

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84
Q

What are complications of coarctation of aorta?

A
  • HTN
  • Re-coarctation
  • CHF
  • Intracerebral haemorrhage
  • Bacterial endocarditis
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85
Q

What are the clinical features of aortic stenosis?

A
  • Weak pulses
  • Thrill palpable in suprasternal region and carotid area
  • Ejection systolic murmur in aorta area
  • Collapse/acidosis
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86
Q

What is the management for aortic stenosis?

A

Aortic valve replacement surgery

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87
Q

What are the clinical features of pulmonary stenosis?

A
  • Ejection systolic murmur in LUSE (often radiates to back)
  • Right ventricular heave
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88
Q

What is the management for pulmonary stenosis?

A

Balloon valvuloplasty

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89
Q

What are the 3 main cyanotic heart conditions?

A
  • Transposition of the great arteries
  • Tetralogy of Fallot
  • Ebstein’s anomaly
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90
Q

What is transposition of the great arteries?

A

Heart defect in which the aorta and pulmonary artery have swapped over

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91
Q

What are risk factors for transposition of the great arteries?

A
  • Maternal diabetes
  • Males
  • Increased maternal age
  • Maternal rubella
  • Alcohol consumption
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92
Q

What are clinical features of transposition of the great arteries?

A
  • Cyanosis/acidosis/collapse/death
  • Right ventricular heave
  • Loud S2 sound
  • Systolic murmur
  • Respiratory distress/tachycardia/poor feeding/poor weight gain/sweating
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93
Q

What are the investigations for transposition of the great arteries?

A
  • Antenatal USS
  • CXR (‘egg on a string’ due to narrowed mediastinum and cardiomegaly)
  • Low SATS
  • Metabolic acidosis
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94
Q

What is the management for transposition of the great arteries?

A
  • Prostaglandin infusion (to maintain ductus arteriosus)
  • Surgery
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95
Q

What conditions make up tetralogy of fallot?

A
  • Pulmonary stenosis
  • Overriding aorta
  • Ventricular septal defect
  • Right ventricular hypertrophy
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96
Q

What are risk factors for tetralogy of fallot?

A
  • Male
  • Maternal diabetes/rubella
  • Alcohol consumption
  • Increased maternal age
  • Associated with 22q11 deletion
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97
Q

What are the clinical features of tetralogy of fallot?

A
  • Cyanosis
  • Acidosis
  • Collapse/death
  • Irritability
  • Clubbing
  • Poor feeding/weight gain
  • Ejection systolic murmur in pulmonary area
  • Tet spells
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98
Q

What are tet spells?

A

Intermittent symptomatic periods where right to left shunt becomes temporarily worsened –> irritability/cyanosis/SOB/reduced consciousness/seizures/death

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99
Q

What are the investigations for tetralogy of fallot?

A
  • Check for 22q deletion
  • Echo
  • CXR (boot-shaped heart due to right ventricular thickening)
  • MRI/cardiac catheter
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100
Q

What is the management for tetralogy of fallot?

A
  • Surgery
  • Prostaglandin infusion (to maintain ductus arteriosus)
  • Morphine (to reduce respiratory drive)
  • Tet spells (O2/beta blockers/fluids/morphine/sodium bicarbonate/phenylephrine infusion)
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101
Q

What are complications of tetralogy of fallot?

A
  • Pulmonary regurgitation
  • Right HF
  • Death
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102
Q

What is Ebstein’s anomaly?

A

Congenital heart condition in which tricuspid valve is set lower in the right side of the heart causing a bigger right atrium and smaller right ventricle

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103
Q

What are the causes of Ebstein’s anomaly?

A
  • Genetics
  • Lithium (teratogenic)
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104
Q

What conditions are associated with Ebstein’s anomaly?

A
  • ASD
  • Wolff-Parkinson-White Syndrome
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105
Q

What are the clinical features of Ebstein’s anomaly?

A
  • Evidence of HF (e.g. oedema)
  • Gallop rhythm
  • 3rd and 4th heart sounds
  • Cyanosis
  • SOB/tachypnoea
  • Poor feeding
  • Collapse/cardiac arrest
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106
Q

What is the investigation for Ebstein’s anomaly?

A

Echo

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107
Q

What is the management of Ebstein’s anomaly?

A
  • Treat arrhythmia/HF
  • Prophylactic abx (prevent IE)
  • Surgical correction
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108
Q

What are risk factors for rheumatic fever?

A
  • Female
  • Children
  • Poverty
  • Overcrowding/poor hygiene
  • Fhx
  • D8/17B cell antigen positivity
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109
Q

What is the cause of rheumatic fever?

A

Strep pyogenes - systemic infection that occurs 2-4 weeks after pharyngitis due to cross-reactivity to strep pyogenes

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110
Q

What are the clinical features of rheumatic fever?

A
  • Tachycardia
  • Murmur
  • Pericardial rub
  • Erythema marginatum
  • Prolonged PR interval
  • Fever/fatigue
  • Arthritis
  • Chest pain/SOB
  • Chorea
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111
Q

What criteria is used to diagnose rheumatic fever?

A

Jones diagnostic criteria - 1 positive test + 2 major criteria (or 1 major + 1 minor criteria)

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112
Q

What are the investigations for rheumatic fever?

A
  • Throat culture for group A beta-haemolytic strep (strep pyogenes) = positive
  • Anti-streptolysin O (ASO) = elevated
  • Anti-deoxyribonuclease B (anti-DNASE B) titre = elevated
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113
Q

What are the major criteria for rheumatic fever?

A
  • Carditis (tachycardia/murmur/pericardial rub/cardiomegaly)
  • Polyarthritis
  • Erythema marginatum (red rash with raised edges and clear centre)
  • Sydenham’s chorea
  • Subcut nodules
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114
Q

What are the minor criteria of rheumatic fever?

A
  • Fever
  • Raised CRP/ESR
  • Arthralgia
  • Prolonged PR interval
  • Previous rheumatic fever
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115
Q

What are common differential diagnoses for rheumatic fever?

A
  • Septic arthritis
  • Reactive arthropathy
  • Infective endocarditis
  • Myocarditis
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116
Q

What is the management for rheumatic fever?

A
  • Bed rest until CRP is normal for 2 weeks consistently
  • Abx = benzylpenicillin/phenoxymethylpenicillin/amoxicillin
  • Aspirin/NSAIDs
  • Assess for emergency valve replacement
  • Glucocorticoids/diuretics (if severe carditis)
  • Haloperidol/diazepam (for chorea)
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117
Q

What is the long-term management for rheumatic fever?

A

Secondary prophylaxis with:
- IM benzylpenicillin every 3-4 weeks
- Oral phenoxymethylpenicillin BD
- Oral sulfadiazine or azithromycin

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118
Q

What are risk factors for IE?

A
  • Male
  • IVDU
  • Immunocompromised
  • Congenital/acquired heart disease
  • Abnormal valves (e.g. regurgitant/prosthetic)
  • Poor dental hygeine
  • Pacemaker
  • IV cannula
  • Previous IE
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119
Q

What are the most common cause of IE?

A
  • Staph aureus (IVDU/diabetes/surgery) = MOST COMMON
  • Strep viridans (poor dental health)
  • Staph epidermis (prosthetic valves)
  • Pseudomonas aeruginosa
  • Strep bovis
  • Enterococci
  • Coxiella burnetii
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120
Q

What are the clinical features of IE?

A
  • Anaemia
  • Splenomegaly
  • Clubbing
  • New murmur
  • Sepsis
  • Generic sx (fever/fatigue/loss of appetite/rigors/night sweats/malaise/weight loss)
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121
Q

What are the clinical features more specific to IE?

A
  • Embolic skin lesions
  • Petechiae
  • Splinter haemorrhages
  • Osler nodes
  • Janeway lesions
  • Roth spots
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122
Q

What are the investigations for IE?

A
  • Fever + new murmur = suspect IE
  • Echo (gold standard) = vegetation
  • Blood cultures
  • Bloods
  • ECG
  • CXR
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123
Q

What criteria is used to diagnose IE?

A

Modified Duke’s Criteria (2 major criteria/1 major + 3 minor criteria/5 minor criteria)

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124
Q

What are the major criteria for IE?

A
  • Pathogen grown from blood cultures
  • Evidence of endocarditis on echo or new valve leak
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125
Q

What are the minor criteria for IE?

A
  • Predisposing heart condition/IVDU
  • Fever
  • Vascular phenomena (Janeway lesions/major arterial emboli/intracranial haemorrhage)
  • Immune phenomena (Osler’s nodes/Roth spots/glomerulonephritis)
  • Positive blood cultures that don’t meet major criteria
  • Echo findings consistent with IE but don’t meet major criteria
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126
Q

What is the management for IE?

A

Abx
- First line = flucloxacillin, ampicillin (rifampicin if staph) and gentamicin
- MRSA = vancomycin, rifampicin and gentamicin
- Benzylpenicillin and gentamicin

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127
Q

When would surgery be required in IE?

A
  • Valve replacement
  • Remove/replace infected devices
  • Remove large vegetation at risk of embolising
  • If complications e.g. severe valve damage
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128
Q

What are the most common causes of UTIs in children?

A
  • E Coli (most common)
  • Klebsiella
  • Staph saprophyticus
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129
Q

What are the risk factors for UTIs?

A
  • Age <1 year
  • Females
  • Caucasian
  • Previous UTI
  • Voiding dysfunction
  • Vesicoureteral reflux
  • Sexual abuse
  • Spinal abnormalities
  • Constipation
  • Immunosuppression
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130
Q

What is the difference between cystitis and pyelonephritis?

A
  • Cystitis - lower renal tract (bladder/urethra)
  • Pyelonephritis - upper renal tract (renal pelvis/kidneys)
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131
Q

What are common clinical features of UTIs in children <3 months?

A
  • Fever
  • Vomiting
  • Lethargy
  • Irritability
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132
Q

What are common clinical features of UTIs in preverbal children >3 months?

A
  • Fever
  • Abdominal pain/loin tenderness
  • Vomiting
  • Poor feeding
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133
Q

What are common clinical features of UTIs in verbal children >3 months?

A
  • Frequency/dysuria
  • Dysfunctional voiding
  • Changes to continence
  • Abdominal pain/loin tenderness
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134
Q

What are the investigations for UTIs?

A
  • Urine microscopy
  • Urine culture
  • Urine dipstick (leucocytes/nitrites)
  • Imaging (USS/dimercaptosuccinic acid/micturating cystourethrogram)
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135
Q

What is the management for UTIs in infants <3 months?

A
  • Minimum 2-4 days IV abx followed by oral
  • Trimethoprim/nitrofurantoin/cephalosporin/amoxicillin
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136
Q

What is the management for UTIs in systematically well children?

A
  • 3 days oral/IV abx
  • Return if no better after 24-48 hours for reassessment
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137
Q

What is the management for UTIs in systematically unwell children (fever >38 +/- loin pain/tenderness)?

A
  • 7-10 days oral/IV abx
  • Ciprofloxacin/co-amoxiclav
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138
Q

What are complications of UTIs?

A
  • Renal scarring/damage
  • HTN
  • Renal insufficiency/failure
  • Recurrence
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139
Q

Who is vesicoureteral reflux most common in?

A

Girls

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140
Q

What are the clinical features of vesicoureteral reflux?

A

Usually only becomes apparent following UTI:
- Fever
- Vomiting
- Reduced appetite
- Foul smelling urine
- Abdominal pain whilst voiding
- Urgency/frequency

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141
Q

What are the investigations for vesicoureteral reflux?

A
  • Antenatal scan = dilated ureter
  • Micturating cystography (a.k.a voiding cystourethrogram)
  • USS KUB
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142
Q

What is the management for vesicoureteral reflux?

A
  • Improving bladder function and infection monitoring
  • Abx
  • Surgery (rare)
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143
Q

What are causes/risk factors of primary nocturnal enuresis?

A
  • Variation of normal development
  • Fhx of delayed dry nights
  • Overactive bladder
  • Fluid intake
  • Failure to wake
  • Psychological distress
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144
Q

What are causes/risk factors of secondary nocturnal enuresis?

A

More indicative of underlying illness
- UTI
- Constipation
- T1DM
- New psychosocial problems
- Maltreatment

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145
Q

What is the management for nocturnal enuresis?

A
  • Reassurance that it is likely to resolve
  • Lifestyle changes (reduce fluid intake in evenings/pass urine before bed/etc.)
  • Encouragement/positive reinforcement
  • Treat underlying cause
  • Enuresis alarms
  • Medication
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146
Q

What medication can be given for nocturnal enuresis?

A
  • Desmopressin (ADH - reduces volume of urine produced by kidneys)
  • Oxybutynin (anticholinergic - reduces contractility of bladder - helpful in urge incontinence)
  • Imipramine (TCA - may relax bladder and lighten sleep)
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147
Q

What is nephrotic syndrome and who is it most common in?

A
  • Increased permeability of GBM
  • Most common in males
  • Most common between ages 2-5
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148
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease
- May be secondary to intrinsic kidney disease (focal segmental glomerulosclerosis/membranoproliferative glomerulonephritis)
- May be secondary to underlying systemic illness (HSP/diabetes/infection e.g. HIV/hepatitis/malaria)

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149
Q

What are the clinical features of nephrotic syndrome?

A
  • *Proteinuria (frothy urine)
  • *Hypoalbuminemia
  • *Oedema (pitting)
  • Hyperlipidaemia
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150
Q

What are the investigations for nephrotic syndrome?

A
  • Bloods (renal function/elevated lipids/low serum albumin)
  • Urine dipstick (proteinuria)
  • Urine protein:creatinine ratio
  • Renal biopsy
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151
Q

What is the management for nephrotic syndrome?

A
  • Prednisolone (if steroid sensitive)
  • Fluid/salt restriction
  • Loop diuretics
  • Treat cause
  • ACEis/ARBs (to reduce protein loss)
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152
Q

What are complications of nephrotic syndrome?

A
  • Hyperlipidaemia (give statins)
  • VTE (give heparin)
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153
Q

What is nephritic syndrome and what are the most common causes of it in children?

A
  • Inflammation within kidney
  • Post-streptococcal glomerulonephritis
  • IgA nephropathy (a.k.a Buerger’s disease)
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154
Q

What are the main clinical features of nephritic sydrome?

A
  • Haematuria
  • Oliguria
  • Proteinuria
  • HTN
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155
Q

What are the investigations for nephritic syndrome?

A
  • Urine dipstick = haematuria
  • Bloods = elevated ESR/CRP
  • Renal biopsy
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156
Q

What is the management for nephritic syndrome?

A
  • Treat cause
  • BP control (ACEis/ARBs)
  • Corticosteroids
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157
Q

What are complications of nephritic syndrome?

A
  • AKI
  • Decreased resistance to infection
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158
Q

What is hypospadias and what is it commonly associated with?

A
  • Condition in which urethral meatus is abnormally displaced to the ventral side of the penis (towards scrotum)
  • Often associated with chordee (head of penis bends downwards) and abnormally formed foreskin
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159
Q

What is the management for hypospadias?

A

Surgery to correct position of meatus and straighten penis

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160
Q

What are the complications of hypospadias?

A
  • Difficulty directing urination
  • Cosmetic/psychological concerns
  • Sexual dysfunction
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161
Q

What is haemolytic uraemic syndrome and what is the most common cause/risk factor?

A
  • Condition in which there is thrombosis in small blood vessels throughout the body
  • Usually triggered by shiga toxins from either E coli or shigella
  • Most often affects children following an episode of gastroenteritis (loperamide increases risk)
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162
Q

What are the clinical features of haemolytic uraemic syndrome?

A
  • Diarrhoea that turns bloody
  • Fever
  • Abdominal pain
  • Lethargy
  • Pallor
  • Oliguria
  • Haematuria
  • HTN
  • Bruising
  • Jaundice
  • Confusion
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163
Q

What are the investigations and treatment for haemolytic uraemic syndrome?

A
  • Stool culture
  • Self-limiting
  • Supportive treatment (IV fluids/treat HTN/blood transfusion/haemodialysis)
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164
Q

What is global developmental delay indicative of?

A
  • Down’s syndrome
  • Fragile X syndrome
  • Foetal alcohol syndrome
  • Rett syndrome
  • Metabolic disorders
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165
Q

What is gross motor delay indicative of?

A
  • Cerebral palsy
  • Ataxia
  • Myopathy
  • Spinal bifida
  • Visual impairment
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166
Q

What is fine motor delay indicative of?

A
  • Dyspraxia
  • Cerebral palsy
  • Muscular dystrophy
  • Visual impairment
  • Congenital ataxia
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167
Q

What is language delay indicative of?

A
  • Social circumstances (e.g. exposure to multiple languages)
  • Hearing impairment
  • Learning disability
  • Neglect
  • Autism
  • Cerebral palsy
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168
Q

What is personal/social delay indicative of?

A
  • Emotional/social neglect
  • Parenting issues
  • Autism
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169
Q

Which seizures are most common in children?

A

Absence seizures

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170
Q

What are the clinical features of generalised tonic-clonic seizures?

A
  • Loss of consciousness
  • Tonic (rigidity) and clonic (rhythmic jerking) phase
  • Tongue biting/incontinence/groaning/irregular breathing
  • Post-ictal period (confusion/drowsiness/irritability)
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171
Q

What are the clinical features of focal seizures?

A
  • Hallucinations
  • Memory flashbacks
  • Deja vu
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172
Q

What are the clinical features of absence seizures?

A
  • Blank/stare into space
  • Abruptly back to normal
  • Unaware of surroundings and unresponsive
  • Last 10-20 seconds
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173
Q

What are the clinical features of myoclonic seizures?

A
  • Remain conscious
  • Sudden brief muscle contractions
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174
Q

What are the clinical features of tonic/atonic seizures?

A
  • Sudden tension/stiffness
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175
Q

What are the investigations for epilepsy?

A
  • EEG
  • MRI
  • Blood electrolytes/glucose/cultures/LP
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176
Q

What is the criteria required for a diagnosis of epilepsy?

A
  • At least 2 unprovoked seizures occurring more than 24 hours apart
  • 1 unprovoked seizure and a probability of further seizures
  • At least 2 seizures in a setting of reflex epilepsy
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177
Q

What is the management for an acute seizure?

A
  • Recovery position
  • Place something soft under head
  • Remove anything that could cause injury
  • Note start and end time of seizures
  • Call ambulance if seizures lasts >5 minutes
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178
Q

What medication is used for generalised tonic-clonic seizures?

A
  • Sodium valproate
  • Lamotrigine
  • Carbamazepine
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179
Q

What medication is used for focal seizures?

A
  • Lamotrigine
  • Levetiracetam
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180
Q

What medication is used for absence seizures?

A

Ethosuximide

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181
Q

What medication is used for myoclonic seizures?

A
  • Sodium valproate
  • Levetiracetam
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182
Q

What medication is used for tonic/atonic seizures?

A
  • Sodium valproate
  • Lamotrigine
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183
Q

When is something diagnosed with epilepsy remission?

A
  • Individuals who had an age-dependent epilepsy syndrome but are now past the applicable age
  • Individuals have remained seizure-free for at least 10 years off anti-seizure medications
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184
Q

What are side effects of sodium valproate?

A
  • Teratogenic
  • Liver damage
  • Hair loss
  • Tremors
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185
Q

What are side effects of carbamazepine?

A
  • Agranulocytosis
  • Aplastic anaemia
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186
Q

What are side effects of ethosuximide?

A
  • Night tremors
  • Rashes
  • N+V
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187
Q

What are side effects of lamotrigine?

A
  • DRESS syndrome (drug reaction with eosinophilia and systemic symptoms)
  • Leukopenia
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188
Q

What is status epilepticus?

A
  • Medical emergency
  • Seizures last >5 minutes or 2+ seizures without regaining consciousness
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189
Q

What is the management for status epilepticus?

A
  • Secure airway
  • O2
  • Assess cardiac/respiratory function
  • IV lorazepam
  • Buccal midazolam/rectal diazepam (community)
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190
Q

By definition, when can febrile convulsions occur?

A

Only in children between the ages of 6 months and 5 years

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191
Q

What are risk factors for febrile convulsions?

A
  • Fhx
  • Socio-economic class
  • Winter season
  • Zinc/iron deficiency
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192
Q

What are the clinical features of simple febrile convulsions?

A
  • Generalised tonic-clonic seizures
  • Last <15 minutes
  • Only occur once during single febrile illness
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193
Q

What are the clinical features of complex febrile convulsions?

A
  • Focal seizures
  • Last >15 minutes
  • Occur multiple times during same febrile illness
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194
Q

What is the management for febrile convulsions (and a complication)?

A
  • Identify/manage source of infection
  • Simple analgesia
  • Parental education

*increased risk of developing epilepsy in future

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195
Q

What is eczema?

A

Chronic atopic condition caused by defects in the normal continuity of the skin barrier leading to inflammation in the skin

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196
Q

What are risk factors for eczema?

A
  • Genetics/fhx
  • Environmental triggers (changes in temperature/dietary products/washing powders/cleaning products/emotional events/stress)
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197
Q

What are the clinical features of eczema?

A
  • Dry, red, itchy, sore patches of skin over flexor surfaces and on face/neck
  • Episodic with flares
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198
Q

What is the management of eczema?

A
  • Emollients (E45/diprobase)
  • Thicker emollients (cetraben/topical steroids e.g. hydrocortisone/betnovate)
  • Avoid hot baths/scratching/scrubbing skin
  • Topical tacrolimus/methotrexate
  • IV abx
  • Oral steroids
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199
Q

What is Stevens-Johnson Syndrome?

A

Disproportional immune response causing epidermal necrosis resulting in blistering and shedding of the top layer of the skin

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200
Q

What is the difference between Stevens-Johnson Syndrome and toxic epidermal necrolysis?

A
  • Stevens-Johnson syndrome (SJS) - affects <10% of body surface area
  • Toxic epidermal necrolysis (TEN) - affects >10% of body surface area
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201
Q

What medications can cause SJS?

A
  • Anti-epileptics
  • Abx
  • Allopurinol
  • NSAIDs
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202
Q

What infections can cause SJS?

A
  • HSV
  • Mycoplasma pneumoniae
  • CMV
  • HIV
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203
Q

What are the clinical features of SJS?

A
  • Purple/red rash that blisters and breaks away to leave raw tissue underneath
  • Pain/blistering/shedding to lips/mucous membranes
  • Inflammation/ulceration of eyes
  • Fever/cough/sore throat/itchy skin
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204
Q

What is the management for SJS?

A
  • Supportive care
  • Steroids/immunoglobulins/immunosuppressants
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205
Q

What are the complications of SJS?

A
  • Secondary infections e.g. cellulitis/sepsis
  • Permanent skin damage
  • Visual complications
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206
Q

What is the management for allergic rhinitis (IgE mediated type I hypersensitivity reaction)?

A
  • Avoid triggers
  • Oral antihistamines (cetirizine/loratadine/fexofenadine/chlorphenamine/promethazine)
  • Nasal corticosteroids sprays (fluticasone/mometasone)
  • Nasal antihistamines
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207
Q

What is urticaria/angioedema?

A
  • Urticaria - swelling of surface of skin (hives/welts)
  • Angioedema - swelling of deeper layers of skin caused by build-up of fluid
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208
Q

What is the management for urticaria?

A
  • Antihistamines (fexofenadine)
  • Oral steroids
    Severe:
  • Antileukotrienes (montelukast)
  • Omalizumab (targets IgE)
  • Cyclosporin
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209
Q

What are the clinical features of anaphylaxis?

A
  • Rapid onset
  • ABC compromise
  • Urticaria
  • Itching
  • SOB/wheeze
  • Swelling of larynx –> stridor
  • Tachycardia
  • Collapse
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210
Q

How is anaphylaxis confirmed?

A

Serum mast cell tryptase (highest within 6 hours of event)

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211
Q

What is the management for anaphylaxis?

A
  • ABCDE
  • IM adrenaline
  • Antihistamines
  • Steroids
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212
Q

What are the most common types of birthmarks?

A
  • Pigmented = cells containing melanin collected together in one area (brown/black)
  • Vascular = vessels that have not formed properly (red/blue)
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213
Q

What are causes/risk factors for nappy rash?

A

Friction between skin and nappy and contact with urine/faces (most common between 9-12 months)
- Delayed changing of nappies
- Irritant soap products/vigorous cleaning
- Diarrhoea
- Oral abx
- Prematurity

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214
Q

What is the difference between petechiae and purpura?

A
  • Petechiae = small/non-blanching/red spots on skin caused by burst capillaries
  • Purpura = large/non-blanching/red/purple macules/papules caused by leaking of blood from vessels under skin
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215
Q

What are the most common causes of a rash?

A
  • Candida
  • Meningococcal septicaemia
  • HSP
  • ITP
  • Leukaemia
  • HUS
  • Mechanical (strong coughing/vomiting/breath holding)
  • Trauma
  • Viral illness
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216
Q

What are risk factors for GORD in infants?

A

Common in infants
- Prematurity
- Fhx
- Obesity
- Hiatus hernia
- Neurodisability e.g. cerebral palsy

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217
Q

What are risk factors for pyloric stenosis?

A
  • Male
  • First born
  • Fhx
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218
Q

What are the clinical features of pyloric stenosis?

A
  • First few weeks of life
  • Projectile vomiting
  • Poor weight gain/failure to thrive
  • Dehydration/constipation
  • Firm, round, ‘olive sized’ mass in upper abdomen (hypertrophic pyloric muscle)
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219
Q

What are the investigations for pyloric stenosis?

A
  • Abdominal USS (thickened pylorus)
  • Blood gas (hypochloremic, hypokalemic, metabolic alkalosis )
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220
Q

What is the management for pyloric stenosis?

A
  • Correct metabolic imbalances (NaCl)
  • Fluids
  • NG tube and aspiration of stomach
  • Laparoscopic pyloromyotomy (Ramstedt’s operation) - incision made in smooth muscle of pylorus to widen canal
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221
Q

What are common causes of gastroenteritis?

A
  • Viral (most common) - rotavirus/norovirus/adenovirus
  • Bacterial - c. jejuni/e. coli
  • Parasitic
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222
Q

What are the clinical features of gastroenteritis?

A
  • Sudden onset diarrhoea with/without vomiting (risk of dehydration)
  • Abdominal pain/cramps
  • Mild fever
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223
Q

When does appendicitis peak?

A

Peak incidence at age 10-20 years

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224
Q

What type of hernia is most common in children?

A

Indirect inguinal hernias (more common in boys/prematurity)

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225
Q

What are the clinical features of an inguinal/inguino-scrotal hernia?

A
  • Cannot ‘get above’ mass
  • Reducible when lying flat
  • Does not transilluminate
  • Positive cough reflex
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226
Q

What are the main complications of a hernia?

A
  • Recurrence
  • Strangulation
  • Incarceration
  • Bowel obstruction
227
Q

Which IBD is more common in children?

A

Crohn’s disease

228
Q

What are the clinical features of UC?

A

CLOSE UP:
- Continuous inflammation
- Limited to colon/rectum
- Only superficial mucosa affected
- Smoking protective
- Excrete blood/mucus
- Use aminosalicylates
- PSC

229
Q

What are the clinical features of Crohn’s?

A

NESTS:
- No blood/mucus
- Entire GI tract
- Skip lesions
- Terminal ileum most affected/transmural inflammation
- Smoking is a RF

230
Q

What are the investigations for IBD?

A
  • GOLD STANDARD = Endoscopy with biopsy
  • Raised faecal calprotectin
  • Raised CRP
231
Q

What medications are used for Crohn’s?

A
  • Steroids (oral prednisolone/IV hydrocortisone)
  • Immunosuppressant (azathioprine/methotrexate/infliximab/adalimumab/mercaptopurine)
232
Q

What medications are used for UC?

A
  • Aminosalicylates (mesalazine)
  • Steroids (prednisolone/hydrocortisone)
  • IV ciclosporin
  • Azathioprine/mercaptopurine
233
Q

What are the investigations for coeliac disease?

A
  • Must be carried out whilst patient remains on gluten-containing diet
  • Antibodies (anti-TTG and anti-EMA)
  • Endoscopy and biopsy (crypt hypertrophy/villous atrophy)
234
Q

What are common causes of poor weight gain/failure to thrive?

A
  • Inadequate nutritional intake (maternal malabsorption/neglect/poverty)
  • Difficulty feeding (cleft lip/palate/pyloric stenosis)
  • Malabsorption (CF/coeliac/IBD)
  • Increased energy requirements (hyperthyroidism/malignancy/HIV)
  • Inability to process nutrition (T1DM)
235
Q

What is the difference between marasmus and kwashiorkor?

A
  • Marasmus = result of diet with total calorie insufficiency
  • Kwashiorkor = result of diet with sufficient calorie intake but insufficient protein intake (worse prognosis)
236
Q

What are the clinical features marasmus/kwashiorkor?

A
  • Wasting
  • Loss of body fat/muscle
  • Stunted growth
  • Kwashiorkor = bilateral pitting oedema/ascites
  • Marasmus = inadequate weight relative to height
237
Q

What is Hirschsprung’s?

A

Congenital condition in which nerve cells (parasympathetic ganglion cells) of the myenteric plexus (a.k.a Auerbach’s plexus) are absent in the distal bowel and rectum

238
Q

What are risk factors for Hirschsprung’s?

A
  • Male
  • Fhx
  • Other conditions (Down’s/neurofibromatosis/etc.)
239
Q

What are the clinical features of Hirschsprung’s?

A
  • Failure to pass meconium
  • Empty rectal vault
  • Palpable faecal mass in left lower abdomen (DRE may ease sx)
  • Abdominal pain/distension
  • Vomiting
  • Poor weight gain/failure to thrive
240
Q

What is Hirschsprung-associated enterocolitis?

A

Life threatening condition - inflammation/obstruction of intestine
- Presents with 2-4 weeks of birth
- Fever
- Abdominal distension
- Diarrhoea with blood
- Features of sepsis

241
Q

What are the investigations for Hirschsprung’s?

A
  • AXR
  • Rectal suction biopsy (absence of ganglionic cells)
  • Contrast enema (short transition zone between proximal/distal colon and small rectal diameter)
242
Q

What is the management for Hirschsprung’s?

A
  • Fluid resus
  • Bowel decompression
  • NG tube
  • IV abx
  • Surgery (Swenson, Soave, Dunhamel pull through surgery - remove aganglionic section of bowel)
243
Q

What is the difference between intussusception and malrotation/volvulus?

A

Intussusception - one piece of bowel telescopes inside another leading to ischaemia and bowel obstruction

Malrotation and volvulus - twisting loop of bowel leading to intestinal obstruction

244
Q

What are risk factors for intussusception?

A
  • CF
  • Meckel’s diverticulum
  • HSP
  • Rotavirus vaccine >23 weeks
245
Q

Who is intussusception most common in?

A
  • Most common cause of obstruction in neonates
  • 3 months-3 years (most commonly <1)
  • Most common in distal ileum at ileocecal junction
246
Q

What are the clinical features of intussusception?

A
  • Colic abdominal pain/distension
  • Pallor
  • Sausage-shaped mass palpable in RUQ
  • Redcurrant jelly stools
  • Shock
  • Peritonitis (guarding/rigidity/pyrexia)
247
Q

What are the investigations for intussusception?

A
  • USS (target-shaped mass)
  • AXR (distended small bowel/absence of gas in large bowel)
248
Q

What are the clinical features of malrotation/volvulus?

A
  • Abdominal pain
  • Bilious vomiting
  • Caecum at midline
  • Reflux sx
249
Q

What are the investigations for malrotation/volvulus?

A
  • Barium enema
  • AXR with contrast (double bubble sign - dilated stomach and proximal small bowel)
250
Q

What is the management for intussusception/malrotation/volvulus?

A
  • IV fluids
  • Air insufflation/air enema (intussusception)
  • Surgery - Ladd’s procedure (malrotation)
  • Broad spectrum abx e.g. gentamicin
251
Q

What is Meckel’s Diverticulum?

A

Congenital diverticulum of small intestine containing ilea/gastric/pancreatic mucosa

252
Q

What are the clinical features of Meckel’s Diverticulum?

A
  • Abdominal pain
  • Rectal bleeding
253
Q

What are the investigations for Meckel’s Diverticulum?

A
  • X-ray
  • USS
  • Laparoscopy
254
Q

What is the management of Meckel’s Diverticulum?

A
  • Surgical removal/resection
255
Q

What are complications of Meckel’s Diverticulum?

A
  • Risk of peptic ulceration
  • Obstruction due to intussusception/volvulus
256
Q

What is colic?

A

Frequent, prolonged and intense crying or fussiness in a healthy infant (usually worst between 4-6 weeks)

257
Q

What are the clinical features of colic?

A
  • Hard to soothe/settle baby
  • Clenched fists
  • Red in face
  • Curling up legs/arching back
258
Q

Who is biliary atresia more common in?

A
  • Females
  • Associated with CMV
259
Q

What are the clinical features of biliary atresia?

A
  • Jaundice
  • Dark urine/pale stools
  • Disturbed appetite
  • Hepatosplenomegaly
  • Abnormal growth
260
Q

What are the investigations for biliary atresia?

A
  • Serum bilirubin = high conjugated bilirubin
  • Raised LFTs
  • Alpha 1 antitrypsin (rule out)
  • Sweat test (rule out CF)
  • USS
261
Q

What is the management for biliary atresia?

A

Surgery (Kasai Portoenterostomy) - section of SI attached to opening of liver (where bile duct normally attaches)

262
Q

What is Kawasaki’s disease?

A

Mucocutaneous lymph node syndrome - systemic medium-sized vessel vasculitis

263
Q

Who is Kawasaki’s disease most common in?

A
  • Typically <5 years
  • Asian children, particularly Korean/Japanese
  • Males
264
Q

What are the clinical features of Kawasaki’s disease?

A
  • Persistent high fever >39 C for >5 days
  • Widespread erythematous maculopapular rash
  • Desquamation on palms/soles
  • Strawberry tongue
  • Cracked lips
  • Cervical lymphadenopathy
  • Bilateral conjunctivitis
265
Q

What are the investigations for Kawasaki’s disease?

A
  • Bloods (FBC/LFTs/ESR/CRP)
  • Urinalysis (raised WCC without infection)
  • Echo
266
Q

What is the management for Kawasaki’s disease?

A
  • High dose aspirin (usually avoided in children but Kawasaki’s is one of exceptions)
  • IV immunoglobulins
267
Q

What is the most common complication of Kawasaki’s disease?

A

Coronary artery aneurysm

268
Q

What are the clinical features of measles?

A
  • Sx start 10-12 days after exposure
  • Fever/coryzal sx
  • Conjunctivitis
  • Koplik spots (blue/white spots on inside of cheek)
  • Maculopapular rash
269
Q

What is the management for measles?

A
  • Self-resolving
  • Supportive treatment
  • Avoid school
  • Notify public health
  • Vaccination
270
Q

What is the cause of chickenpox and what is the incubation period?

A
  • Varicella zoster virus (VZV)
  • 21 days
271
Q

What are the clinical features of chickenpox?

A
  • Widespread, erythematous, raised, vesicular, blistering lesions
  • Fever
  • Itch
  • General fatigue/malaise
272
Q

What is the management for chickenpox?

A
  • Self-limiting
  • Calamine lotion
  • Avoid school until lesions have crusted over
273
Q

What are the clinical features of rubella?

A
  • Low grade fever
  • Erythematous maculopapular rash
  • Joint pain
  • Sore throat
  • Lymphadenopathy
274
Q

What is the management for rubella?

A
  • Self-limiting
  • Avoid school
  • Notify public health
275
Q

What is a complication of rubella in pregnancy?

A

Congenital rubella syndrome:
- Deafness
- Blindness
- Congenital heart disease

276
Q

What is scalded skin syndrome?

A

Condition caused by a type of staph aureus that produces epidermolytic toxins (enzymes that break down proteins that hold skin cells together)

277
Q

Who is scalded skin syndrome most common in?

A

Children <5 years

278
Q

What are the clinical features of scalded skin syndrome?

A
  • Generalised patches of erythema on skin
  • Skin looks thin/wrinkled
  • Formation of bullae
  • Fever
  • Irritability
  • Lethargy
  • Dehydration
  • Nikolsky sign (areas of epidermis separate on gentle pressure leaving denuded areas of skin which dry and heal without scarring)
279
Q

What is the management for scalded skin syndrome?

A
  • IV abx
  • Analgesia
  • Fluid and electrolyte balance
280
Q

What are the clinical features of TB?

A
  • Asx
  • Lethargy
  • Fever/night sweats
  • Weight loss
  • Cough with/without haemoptysis
  • Hilar lymphadenopathy
281
Q

What are the investigations for TB?

A
  • Ziehl-Neelsen stain (bright red)
  • Mantoux test (tuberculin injected)
  • CXR (patchy consolidation/pleural effusions/hilar lymphadenopathy)
  • Bacterial cultures
  • IGRA (blood test)
282
Q

What are the complications of TB medication?

A
  • Rifampicin = red/orange discolouration of secretions
  • Isoniazid = peripheral neuropathy
  • Pyrazinamide = hyperuciaemia –> gout
    ^ all associated with hepatotoxicity
  • Ethambutol = colour blindness/reduced visual acuity
283
Q

What is the management for TB?

A
  • BCG vaccine
  • Contact tracing
    RIPE:
  • Rifampicin for 6 months
  • Isoniazid for 6 months
  • Pyrazinamide for 2 months
  • Ethambutol for 2 months
284
Q

What are the clinical features of HIV?

A
  • Most remain asx
  • Lymphadenopathy (mild)
  • Recurrent bacterial infections (moderate)
  • Chronic diarrhoea (moderate)
  • Lymphocytic interstitial pneumonitis (moderate)
  • Pneumocystis jirovecii pneumonia (severe)
  • Severe faltering growth (severe)
  • Encephalopathy (severe)
285
Q

What are the investigations for HIV?

A
  • Antibody screen
  • Viral load
286
Q

What is the management for HIV?

A
  • Antiretroviral therapy
  • Normal childhood vaccines
  • Prophylactic co-trimoxazole
  • Prophylactic zidovudine/lamivudine/nevirapine
287
Q

What are the common causes of bacterial meningitis in children?

A
  • Neonates = group B strep
  • Children <2 = strep pneumoniae
288
Q

What are the common causes of viral meningitis in children?

A
  • Enteroviruses (echovirus/coxsackie)
  • HSV
  • VZV
289
Q

What are the common causes of fungal meningitis in children?

A
  • Cryptococcus
  • Candida
290
Q

What are the clinical features of meningitis?

A
  • Non-blanching rash (meningococcal septicaemia)
  • Fever
  • Neck stiffness
  • Vomiting
  • Headache
  • Photophobia
  • Altered consciousness
  • Seizures
291
Q

What are the investigations for meningitis?

A
  • Lumbar puncture for CSF
  • Blood cultured
  • Meningococcal PCR
  • Kernig’s test
  • Brudzinski’s test
292
Q

What is the difference between CSF in bacterial vs viral meningitis?

A
  • Bacterial = cloudy/high protein/low glucose/neutrophils/culture
  • Viral = clear/normal protein/normal glucose/lymphocytes
293
Q

What is the management for meningitis?

A
  • Bacterial (community) = stat IM injection of benzylpenicillin
  • Bacterial (hospital) = IV cefotaxime + IV amoxicillin
  • Post exposure prophylaxis = ciprofloxacin
  • Viral = aciclovir
  • Notify public health
294
Q

What are common causes of encephalitis in children?

A
  • HSV1 (children - cold sores)
  • HSV2 (neonates - genital herpes contracted during birth)
  • VZV
  • CMV
295
Q

What are the investigations for encephalitis?

A
  • LP for CSF
  • CT
  • MRI
  • HIV testing
296
Q

What is the management for encephalitis?

A
  • Aciclovir (HSV/VZV)
  • Ganciclovir (CMV)
297
Q

What is the cause and risk factors for slapped cheek syndrome?

A
  • Parvovirus B19 virus
  • Immunocompromised
  • Pregnant
  • Haematological conditions (sickle cell anaemia/thalassaemia)
298
Q

What are the clinical features of slapped cheek syndrome?

A
  • Asx
  • Mild fever
  • Coryza
  • Non specific sx e.g. muscle aches/lethargy
  • Rash after 2-5 days (diffuse bright red on both cheeks followed by reticular mildly erythematous rash)
299
Q

What are the investigations for slapped cheek syndrome?

A
  • Serology testing for parvovirus
  • FBC/reticulocyte count
300
Q

What is the management for slapped cheek syndrome?

A
  • Self-limiting
  • Supportive treatment
301
Q

What are common causes of impetigo?

A
  • Staph aureus (most common) - causes bullous impetigo which is most common in neonates and children <2
  • Strep pyogenes
302
Q

What are the clinical features of impetigo?

A

Golden crust = characteristic
Non-bullous:
- Typically around nose/mouth
- Exudate from lesions dries to form golden crust
- Few/non systemic sx
Bullous:
- Fluid-filled vesicles
- Vesicles grow and burst to form golden crust
- Painful/itchy
- Systemic sx (fever)

303
Q

What are the investigations for impetigo?

A

Swabs

304
Q

What is the management for impetigo?

A
  • Topical fusidic acid
  • Antiseptic cream
  • Oral flucloxacillin
  • Avoid school
305
Q

What is the main complication of impetigo?

A

Scalded skin syndrome

306
Q

What is toxic shock syndrome?

A

Life-threatening condition caused by an infection (toxin producing staph aureus and group A strep)

307
Q

What are the clinical features of toxic shock syndrome?

A
  • Fever >39 C
  • Hypotension
  • Diffuse erythematous macular rash
  • Mucositis (conjunctivae/oral mucosa/genital mucosa)
  • Vomiting and diarrhoea
308
Q

What is the management for toxic shock syndrome?

A
  • Intensive care support
  • Abx (e.g. ceftriaxone + clindamycin)
309
Q

What is the cause of scarlet fever and who is it most common in?

A
  • Toxic producing strains of strep pyogenes
  • Common in those between 2-8 years
  • Higher risk in neonates/immunocompromised/concurrent chickenpox/influenza
310
Q

What are the clinical features of scarlet fever?

A
  • Sore throat/fever/fatigue/headache
  • N+V
  • Pinpoint, sandpiper-like, blanching rash
  • Strawberry tongue
  • Cervical lymphadenopathy
311
Q

What is the management for scarlet fever?

A
  • Oral abx e.g. benzylpenicillin for 10 days
  • Notify public health
312
Q

What is Coxsackie’s disease?

A

a.k.a hand, foot and mouth disease - caused by Coxsackie A virus

313
Q

What are the clinical features of hand, foot and mouth disease?

A
  • Typical viral URTI sx (sore throat/fever/cough)
  • Small mouth ulcers
  • Blistering red spots across body
  • Itchy
314
Q

What is the management for hand, foot and mouth disease?

A
  • Self-limiting
  • Supportive management
315
Q

What are risk factors for undescended testes (cryptorchidism)?

A
  • Fhx
  • Low birth weight
  • Small for gestational age
  • Prematurity
  • Maternal smoking
316
Q

What is the management for undescended testes?

A
  • Watch and wait (will usually descend in first 3-6 months)
  • Surgical orchidopexy
317
Q

What are complications of undescended testes?

A

Higher risk of:
- Testicular torsion
- Infertility
- Testicular cancer

318
Q

What is a risk factor for testicular torsion?

A

Bell-Clapper deformity:
- Absence of fixation between testicle and tunica vaginalis
- Testicle hangs in horizontal position
- Able to rotate within tunica vaginalis, twisting at spermatic cord

319
Q

What are the clinical features of testicular torsion?

A
  • Rapid onset unilateral testicular pain
  • Abdominal pain
  • Vomiting
  • Firm, swollen testicle
  • Elevated/retracted testicle
  • Absent cremasteric reflex
  • Abnormal testicular lie
  • Prehn’s sign negative
320
Q

What is the investigation for testicular torsion?

A

Scrotal USS - whirlpool sign (spiral appearance of spermatic cord and blood vessels)

321
Q

What is the management for testicular torsion?

A
  • NBM
  • Analgesia
  • Orchiopexy (within 6 hours)
  • Orchidectomy if delayed surgery/necrosis
322
Q

What is pica?

A

Eating disorder in which patients eat things not usually considered food e.g. dirt/clay/rocks/paper/crayons/hair/chalk

323
Q

Who is pica more common in?

A
  • ASD
  • Intellectual disabilities
  • OCD
  • Schizophrenia
  • Malnutrition/hunger
  • Stress (i.e. due to abuse/neglect)
324
Q

What is the criteria for pica?

A
  • Eating non-food items
  • Doing so for >1 month
  • Abnormal behaviour for child’s age/developmental stage
  • Has risk factor
325
Q

What are complications of pica?

A
  • Iron deficiency anaemia
  • Lead poisoning
  • Constipation/diarrhoea
  • Intestinal obstruction
  • Mouth/teeth injuries
326
Q

What are common causes of hypothyroidism?

A

Congenital:
- Dysgenesis (underdeveloped thyroid gland)
- Dyshormonogenesis (thyroid gland not producing enough hormone)
Acquired:
- Hashimoto’s thyroiditis

327
Q

What are the clinical features of hypothyroidism?

A
  • Prolonged neonatal jaundice
  • Poor feeding/growth
  • Constipation
  • Increased sleeping/fatigue
  • Weight gain
328
Q

What are the investigations for hypothyroidism?

A
  • Newborn blood spot screening test
  • TFTs
  • Thyroid USS
  • Thyroid antibodies (anti-TPO/anti-thyroglobulin)
329
Q

What is the management for hypothyroidism?

A

Levothyroxine

330
Q

What is the most common cause of congenital adrenal hyperplasia?

A

Congenital deficiency of 21-hydroxylase enzyme (autosomal recessive)

331
Q

Describe the pathophysiology of congenital adrenal hyperplasia?

A
  • Deficiency of 21-hydroxylase (enzyme responsible for converting progesterone into aldosterone/cortisol)
  • Progesterone unable to become aldosterone/cortisol so more converted into testosterone
332
Q

What are the clinical features of congenital adrenal hyperplasia in females?

A
  • Tall for age
  • Facial hair
  • Absent periods
  • Deep voice
  • Early puberty
  • Virilised (ambigious) genitalia and enlarged clitoris
333
Q

What are the clinical features of congenital adrenal hyperplasia in males?

A
  • Tall for age
  • Deep voice
  • Large penis
  • Small testicles
  • Early puberty
334
Q

What are the investigations/management for congenital adrenal hyperplasia?

A
  • Low aldosterone –> replacement (fludrocortisone)
  • Low cortisol –> replacement (hydrocortisone)
  • High testosterone
  • Corrective surgery for virilised genitalia
335
Q

What is Kallmann syndrome?

A

Genetic condition causing hypogonadotropic hypogonadism resulting in failure to start puberty

336
Q

What are the clinical features of Kallmann syndrome?

A
  • Anosmia
  • Delayed/incomplete puberty
  • Undescended/partially descended testicles
  • Small penile size
  • Facial defects e.g. cleft lip/palate
  • Short fingers/toes
337
Q

What are the investigations and management for Kallmann syndrome?

A
  • Bloods/MRI hypothalamus/pituitary gland
  • Hormone replacement therapy
338
Q

Who does androgen insensitivity syndrome affected and how?

A
  • Only affects genetically male people
  • X-linked recessive
  • Mutation in androgen receptor gene
  • Cells unable to respond to androgen hormone so converted into oestrogen –> female characteristics
339
Q

What are the clinical features of androgen insensitivity syndrome?

A
  • Female phenotype (breast tissue/female external genitalia)
  • Testes in abdomen/inguinal canal –> inguinal hernias
  • Absence of uterus/upper vagina/cervix/fallopian tubes/ovaries
  • Lack of pubic/facial hair
  • Taller than female average
  • Infertile
  • Primary amenorrhoea
340
Q

What are the investigations for androgen insensitivity syndrome?

A
  • Raised LH
  • Normal/raised FSH
  • Normal/raised testosterone
  • Raised oestrogen
341
Q

What is the management for androgen insensitivity syndrome?

A
  • Bilateral orchidectomy (increased risk of testicular cancer if not removed)
  • Oestrogen therapy
  • Vaginal dilators/vaginal surgery
  • Patients generally raised as female
342
Q

What bone tumours are most common in children?

A
  • Osteogenic sarcoma (osteosarcoma)
  • Ewing’s sarcoma more common in younger children
343
Q

What are the clinical features of bone tumours?

A
  • Patients generally well
  • Persistent/localised bone pain
  • Bone swelling
  • Palpable mass
  • Restricted joint movements
344
Q

What are the investigations for bone tumours?

A
  • XRAY (poorly defined lesions in bone with destruction of normal bone and ‘fluffy’ appearance)
  • XRAY (periosteal reaction - irritation of lining of bone - ‘sun burst’ appearance)
  • Bloods (raised ALP)
  • CT/MRI/PET
  • Bone scan
  • Bone biopsy
345
Q

What is the management/complications for bone tumours?

A
  • Surgery (resection/amputation)
  • Chemotherapy/radiotherapy
  • Pathological bone fractures
  • Metastasis
346
Q

What are risk factors for brain tumours in children and how common are they?

A
  • Fhx
  • Neurofibromatosis
  • Tuberous sclerosis
  • Leading cause of childhood cancer deaths in UK - almost always primary tumour
347
Q

What are the 5 main types of brain tumours in children?

A
  • Astrocytoma
  • Medulloblastoma
  • Ependymoma
  • Craniopharyngioma
  • Brainstem glioma
348
Q

What are the clinical features of brain tumours?

A
  • Raised ICP (headache/coughing/papilloedema)
  • Focal neurological signs
  • Behavioural changes/altered GCS
  • Back pain
  • Peripheral weakness of arms/legs
  • Bladder/bowel dysfunction
349
Q

What are the investigations/management/complications of brain tumours?

A
  • MRI
  • Surgery (+/- chemotherapy/radiotherapy)
  • Metastasis
350
Q

What are the clinical features of hepatoblastomas?

A
  • Abdominal distension/mass
  • Pain
  • Jaundice
351
Q

What are the investigations and management for hepatoblastomas?

A
  • Elevated a-fetoprotein
  • Good prognosis
  • Surgery/chemotherapy/liver transplant
352
Q

Which types of leukaemia are most common in children?

A
  • Acute lymphoblastic leukaemia (ALL) - peaks in ages 2-3 years
  • Acute myeloid leukaemia (AML) - peaks ages <2
353
Q

What are the clinical features of leukaemia?

A
  • Cancer sx (fatigue/weight loss/night sweats/etc.)
  • Petechiae/abnormal bruising/bleeding
  • Hepatosplenomegaly
  • Lymphadenopathy
354
Q

What are the investigations for leukaemia?

A
  • FBC (anaemia/leukopenia/thrombocytopenia/high WCC)
  • Blood film (blast cells)
  • BM biopsy
  • Lymph node biopsy
  • CXT/CT/LB (staging)
355
Q

What is the management for leukaemia?

A
  • Chemotherapy/radiotherapy
  • Surgery/BM transplant
356
Q

What is a neuroblastoma and when does it usually present?

A
  • Tumour arising from neural crest tissue in adrenal medulla and sympathetic nervous system
  • Usually occurs before 5 years of age
357
Q

What are the clinical features of neuroblastomas?

A
  • Abdominal mass
  • Weight loss
  • Pallor
  • Hepatomegaly
  • Lymphadenopathy
  • Periorbital bruising
  • Skin nodules
358
Q

What are the investigations/management/complications of neuroblastomas?

A
  • Raised urinary catecholamine levels
  • Biopsy/BM sampling
  • Generally good prognosis
  • Surgery (+/- chemotherapy/radiotherapy)
  • Metastasis
359
Q

When do retinoblastomas usually present and what are the clinical features?

A
  • Most cases present in first 3 years of life
  • White pupillary reflex replaces red one
  • Squint
360
Q

What are the investigations/management/complications of retinoblastomas?

A
  • MRI
  • Preserve vision/chemotherapy/laser treatment
  • Visual impairment/secondary malignancy
361
Q

What is Wilms tumour and who is it most common in?

A
  • Nephroblastoma (renal tumour)
  • Most common renal tumour in children
  • Often presents before 5 years
362
Q

What are the clinical features of Wilms tumours?

A
  • Large abdominal mass
  • Abdominal pain
  • Weight loss
  • Haematuria
  • HTN
  • Lethargy/fever
363
Q

What are the investigations/management/complications of Wilms tumours?

A
  • USS
  • CT/MRI
  • Biopsy
  • Chemotherapy/surgery (nephrectomy)
  • Metastasis
364
Q

What is Angelman syndrome?

A

Genetic condition caused by loss of function of UBE3A gene on chromosome 15

365
Q

What are the clinical features of Angelman syndrome?

A
  • Delayed development/learning disability
  • Severe delay/absence of speech development
  • Ataxia
  • Fascination with water
  • Happy demeanour/inappropriate laughter
  • Hand flapping
  • Wide mouth with widely space teeth
  • Microcephaly
  • ADHD/epilepsy
366
Q

What is Edward’s Syndrome and what are the clinical features?

A

Trisomy 18
- Low birthweight
- Small mouth/chin
- Short sternum
- Flexed/overlapping fingers
- Rocket-bottom feet
- Cardiac/renal malformations

367
Q

What is Klinefelter syndrome and who is affected?

A

Additional X chromosome ONLY IN MEN
- 47 XXY
- 48 XXXY (rare)
- 49 XXXXY (rare)

368
Q

What are the clinical features of Klinefelter syndrome?

A
  • Tall stature
  • Wide hips
  • Gynaecomastia
  • Weaker muscles
  • Small testicles
  • Reduced libido
  • Shyness
  • Subtle learning difficulties (particularly speech/language)
369
Q

What is the management for Klinefelter syndrome?

A
  • Testosterone injections
  • Breast reduction surgery
  • Speech and language therapy
  • Occupational therapy
  • Physiotherapy
370
Q

What are the complications of Klinefelter syndrome?

A
  • Infertility
  • Increased risk of breast cancer/osteoporosis/diabetes/anxiety and depression
371
Q

What is Turner syndrome and who is affected?

A

Single X chromosome ONLY IN WOMEN
- 45XO

372
Q

What are the clinical features of Turner syndrome?

A
  • Short stature
  • Webbed neck
  • High arching palate
  • Downward sloping eyes with ptosis
  • Broad chest with widely spaced nipples
  • Cubitus valgus
  • Overdeveloped ovaries
  • Late/incomplete puberty
  • Ejection systolic murmur
373
Q

What is the management of Turner syndrome?

A
  • Growth hormone therapy
  • Oestrogen/progesterone
374
Q

What are the complications of Turner syndrome?

A
  • Infertility
  • Associated with recurrent otitis media/UTIs/coarctation of aorta/aortic stenosis/hypothyroidism/HTN/obesity/diabetes/osteoporosis/learning disabilities
375
Q

What are the most common types of muscular dystrophy and when do they present?

A
  • Duchenne’s = 3-5 years
  • Becker’s = 8-12 years
  • Myotonic dystrophy
  • Facioscapulohumeral muscular dystrophy
  • Oculopharyngeal muscular dystrophy
  • Limb-girdle muscular dystrophy
  • Emery-Dreifuss muscular dystrophy
376
Q

Describe the pathophysiology of Duchenne’s/Becker’s muscular dystrophy

A
  • X linked recessive
  • Defective gene for dystrophin (protein that helps to hold muscles together)
  • Becker’s = gene less severely affected than Duchenne’s
377
Q

What are the clinical features of muscular dystrophy?

A
  • Gower’s sign (stand up from lying down using a specific technique)
  • Progressive weakness
  • Waddling gait
  • Language delay
  • Pseudohypertrophy of calves
  • Slow/clumsy
378
Q

What is the management for Duchenne’s/Becker’s muscular dystrophy?

A
  • Exercise
  • Night splints/passive stretching
  • Oral steroids
  • Creatinine supplementation
379
Q

What is the life expectancy of Duchenne’s muscular dystrophy?

A
  • 25-35 years
  • Usually due to cardiac/respiratory complications (dilated cardiomyopathy)
380
Q

What are the clinical features of Noonan syndrome?

A
  • Short stature
  • Broad forehead
  • Downward sloping eyes with ptosis
  • Wide space between eyes
  • Low set ears
  • Webbed neck
  • Widely spaced nipples
381
Q

What are the complications of Noonan syndrome?

A

Associated with:
- Congenital heart disease (pulmonary stenosis/HCM/ASD)
- Cryptorchidism –> infertility
- Learning disability
- Bleeding disorders
- Lymphoedema
- Increased risk of leukaemia/neuroblastoma

382
Q

What is Patau syndrome and what are the clinical features?

A

Trisomy 13
- Structural defects of brain
- Scalp defects
- Small eyes/eye defects
- Cleft lip/palate

383
Q

What is Prader Will Syndrome?

A

Genetic condition caused by loss of functional genes of proximal arm of chromosome 15

384
Q

What are the clinical features of Prader Willi Syndrome?

A
  • Constant insatiable hunger –> obesity
  • Hypotonia
  • Learning disability
  • Soft skin prone to bruising
  • Anxiety
  • Dysmorphic features
  • Narrow forehead
  • Almond shaped eyes
  • Squint
  • Thin upper lip
  • Hypogonadism
385
Q

What is Williams Syndrome?

A

Genetic condition caused by deletion of genetic material on one copy of chromosome 7

386
Q

What are the clinical features of Williams Syndrome?

A
  • Elfin facies
  • Broad forehead
  • Starburst eyes (star-like pattern on iris)
  • Flattened nasal bridge
  • Long philtrum
  • Wide mouth with widely spaced teeth
  • Small chin
  • Very social trusting personality
  • Mild learning disability
387
Q

What are complications of Williams Syndrome?

A

Associated with:
- Supravalvular aortic stenosis/pulmonary stenosis
- ADHD
- HTN
- Hypercalcaemia

388
Q

What are risk factors for developmental dysplasia of hip?

A
  • Fhx
  • Breech presentation
  • Multiple pregnancy
  • Oligohydramnios
389
Q

What are the clinical features of developmental dysplasia of hip?

A
  • Hip asymmetry
  • Reduced range of motion in hip
  • Limp/abnormal gait
  • Weakness
  • Recurrent subluxation/dislocation
  • Early degenerative changes
390
Q

What are the investigations for developmental dysplasia of hip?

A
  • Newborn examination
  • Leg length
  • Restricted hip abduction on one side
  • Difference in knee level when hips flexed
  • Ortolani and Barlow tests - clicking
  • USS
  • XRAY
391
Q

What is the management for developmental dysplasia of hip?

A
  • Pavlik harness
  • Surgery
392
Q

What is discoid meniscus and who is it most common in?

A
  • Congenital anatomical defect of menisci (2 pads of cartilage in knee joint)
  • Usually lateral meniscus affected
  • More common in Asian people
393
Q

What are the clinical features of discoid meniscus?

A
  • Can be asx
  • Activity related pain
  • Effusions
  • Joint line tenderness
  • Mechanical sx
  • Increased incidence of tears
  • Instability in meniscus –> snapping knee
394
Q

What are the investigations/management for discoid meniscus?

A
  • XRAY
  • MRI
  • Observation/conservative management
  • Surgery if tears/instability
395
Q

Which types of juvenile idiopathic arthritis are more common in children?

A
  • Oligoarticular JIA = more common in girls <6 years
  • Enthesitis related arthritis = more common in boys >6 years (can be caused by traumatic stress e.g. repetitive strain during sports)
396
Q

Briefly describe the main types of JIA

A
  • Systemic JIA
  • Polyarticular JIA = 5+ joints, inflammatory - tends to be more symmetrical
  • Oligoarticular JIA = 4 or less joints, usually only affects single joint, tends to affect larger joints e.g. knee/ankle
  • Enthesitis related arthritis = inflammatory arthritis and enthesitis (inflammation of point where tendon inserts into bone)
  • Juvenile psoriatic arthritis
397
Q

What are the clinical features of JIA?

A
  • Joint pain
  • Swelling
  • Stiffness
398
Q

What are the clinical features of systemic JIA?

A
  • Subtle pink rash
  • High swinging fevers
  • Enlarged lymph nodes
  • Weight loss
  • Joint inflammation/pain
  • Splenomegaly
  • Muscle pain
  • Pleuritis/pericarditis
399
Q

What are the clinical features of polyarticular JIA?

A
  • Mild fever
  • Anaemia
  • Reduced growth
400
Q

What are the clinical features of oligoarticular JIA?

A
  • Anterior uveitis
401
Q

What are the clinical features of enthesitis related arthritis?

A
  • Signs of psoriasis/IBD
  • Anterior uveitis
  • Tender to localised palpation of entheses
402
Q

What are the clinical features of juvenile psoriatic arthritis?

A
  • Associated with psoriasis
  • Plaques of psoriasis
  • Nail pitting
  • Onycholysis
  • Dactylitis
  • Enthesitis
403
Q

What criteria is required for a diagnosis of JIA?

A
  • Arthritis without any other cause
  • Lasts >6 weeks
  • Patient <16 years
404
Q

What are the investigations for systemic JIA?

A
  • ANA = -ve
  • RF = -ve
  • Raised CRP/ESR/platelets/serum ferritin
405
Q

What are the investigations for polyarticular JIA and juvenile psoriatic arthritis?

A

RF = -ve

406
Q

What are the investigations for oligoarticular JIA?

A
  • ANA = +ve
  • RF = -ve
  • Inflammatory markers normal/mildly elevated
407
Q

What are the investigations for enthesitis related arthritis?

A
  • MRI
  • Majority have HLA-B27 gene
408
Q

What is the management for JIA?

A
  • NSAIDs
  • Oral/IM/intra-articular steroids
  • DMARDs (methotrexate/sulfasalazine/leflunomide)
  • Biological therapy (etanercept/infliximab/adalimumab - TNF inhibitors)
409
Q

What is Osgood-Schlatter Disease and who is it most common in?

A
  • Inflammation at tibial tuberosity where patellar ligament inserts
  • Common cause of anterior knee pain in adolescents
  • Typically occurs in males aged 10-15
410
Q

What are the clinical features of Osgood-Schlatter Disease?

A
  • Visible/palpable lump below knee (initially tender due to inflammation but becomes hard/non-tender)
  • Gradual onset of sx
  • Pain in anterior aspect of knee
  • Pain exacerbated by physical activity/kneeling/extension of knee
411
Q

What is the management of Osgood-Schlatter Disease?

A
  • Sx usually resolve over time
  • Reduction in physical activity
  • Ice
  • NSAIDs
  • Stretching/physiotherapy
412
Q

What is osteogenesis imperfecta?

A

Autosomal dominant genetic condition resulting in brittle bones that are prone to fractures

413
Q

What are the clinical features of osteogenesis imperfecta?

A
  • Recurrent/inappropriate fractures
  • Joint/bone pain
  • Blue/grey sclera
  • Hypermobility
  • Triangular face
  • Deafness
  • Dental problems
  • Bone deformities e.g. bowed legs/scoliosis
414
Q

What are the investigations/management of osteogenesis imperfecta?

A
  • XRAY
  • Genetic testing
  • Bisphosphonates
  • Vit D supplementation
  • Physiotherapy/occupational therapy
  • Management of fractures
415
Q

What is osteomyelitis, what is the most common cause and who is it most common in?

A
  • Infection in bone and bone marrow
  • Staph aureus
  • More common in males <10 years/open bone fractures/orthopaedic surgery/immunocompromised/sickle cell anaemia/HIV/TB
416
Q

What are the clinical features of osteomyelitis?

A
  • Systemic sx
  • Refusal to use limb/weight bear
  • Pain
  • Swelling
  • Tenderness
417
Q

What are the investigations for osteomyelitis?

A
  • XRAY
  • MRI (gold standard)
  • Bone scan
  • Bloods (CRP/ESR/WCC)
  • Blood cultures
  • BM aspiration
418
Q

What is the management/complications of osteomyelitis?

A
  • Abx therapy
  • Surgery - drainage/debridement of infected bone
  • Complication = septic arthritis
419
Q

What is Perthes Disease and who is it most common in?

A
  • Disruption of blood flow to the femoral head causing avascular necrosis of the bone
  • Usually idiopathic
  • Most common in boys aged 5-8 years
420
Q

What are the clinical features of Perthes Disease?

A
  • Slow onset of pain in hip/groin
  • Limp
  • Restricted hip movements
  • Referred pain to knee
  • No history of trauma
  • Hyperactivity and short stature
421
Q

What are the investigations/management for Perthes Disease?

A
  • XRAY/bloods/MRI/technetium bone scan
  • Conservative management (bed rest/traction/crutches/analgesia/physiotherapy)
  • Surgery
422
Q

What is rickets?

A

Condition in which there is defective bone mineralisation causing soft and deformed bones

423
Q

What are the causes and risk factors for rickets?

A
  • Vit D/calcium deficiency
  • Hereditary hypophosphatemic rickets
  • RF = darker skin/low exposure to sunlight/colder climates/lack of time spent outdoors/malabsorption disorders
424
Q

What are the clinical features of rickets?

A
  • Lethargy
  • Bone pain
  • Poor growth
  • Dental problems
  • Muscle weakness
  • Bone deformities (bowed legs/knock knees/rachitis rosary/craniotabes/delayed teeth)
425
Q

What are the investigations for rickets?

A
  • Serum 25-hydroxyvitamin D
  • XRAY
  • Low serum calcium/phosphate
  • High serum ALP/PTH
  • Bloods (FBC/ESR/CRP/LFTs/TFTs)
  • Malabsorption screen
426
Q

What is the management for rickets?

A
  • Prevention (400IU supplements)
  • Ergocalciferol
  • Vitamin D/calcium supplementation
427
Q

What is scoliosis and what are the clinical features?

A

Lateral curvature of spine
- One shoulder higher than other
- One shoulder blade more prominent than other
- One hip more prominent than other (uneven waistline)
- Changed position of spine/chest/pelvis

428
Q

What are the investigations/management/complications of scoliosis?

A
  • Visible curvature/XRAY/MRI
  • Observation/bracing/surgery
  • Lung/heart problems
429
Q

What are common causes of septic arthritis and who is it most common in?

A
  • Staph aureus
  • N. gonorrhoea/group A strep/haemophilus influenzae/e. coli
  • Most common in children <4 years
430
Q

What are the clinical features of septic arthritis?

A
  • Usually one joint affected (knee/hip)
  • Rapid onset
  • Hot/red/swollen/painful joint
  • Refusal to weight bear
  • Stiffness/reduced ROM
  • Systemic sx (fever/lethargy/sepsis)
431
Q

What are the investigations/management of septic arthritis?

A
  • Joint aspiration sent for gram staining/crystal microscopy/culture/abx sensitivities
  • Aspirate joint + empiric IV abx + specific abx
  • Surgical drainage and washout
432
Q

What is slipped femoral epiphysis and who is it most common in?

A
  • Head of femur displaced along growth place
  • More common in males/obese children/ages 8-15 years
433
Q

What are the clinical features of slipped femoral epiphysis?

A
  • Adolescent, obese male undergoing a growth spurt
  • History of minor trauma which may trigger onset of sx
  • Hip/groin/thigh/knee pain
  • Restricted hip ROM/movement
  • Painful limp
434
Q

What are the investigations/management of slipped femoral epiphysis?

A
  • XRAY/bloods/CT/MRI/technetium bone scan
  • Surgery to return femoral head to correct position and fix in place
435
Q

What is torticollis?

A

Persistent tilting of the head to one side

436
Q

What are the causes of congenital torticollis?

A

Associated with birth trauma/antenatal complications
- Congenital muscular torticollis (caused by shortening and fibrosis of sternocleidomastoid)
- Cervical spine malformations
- Chiari malformations
- Spina bifida

437
Q

What are the causes of acquired torticollis?

A

Typically occurs after 4-6 months
- Usually results from SCM/trapezius muscle injury/inflammation
- Retropharyngeal abscess
- C-spine injury
- CNS tumour
- Spinal epidural haematoma

438
Q

What are the clinical features of torticollis?

A
  • Chin pointing towards opposite side/ear and head tilted to affected shoulder
    Red flag symptoms:
  • Neck stiffness
  • Fever/drooling/vomiting
  • Pain increasing/unremitting/disturbing sleep
  • Recent trauma
  • Repeated hospital attendances with persistence of sx
  • Gait disturbance
  • History of headaches/change in behaviour
439
Q

What are the investigations/management of torticollis?

A
  • XRAY/CT/MRI/USS neck
  • Physiotherapy/analgesia/treat underlying cause
440
Q

Why might resuscitation be necessary in neonates?

A
  • Large SA:weight ratio –> get cold easily
  • Babies are born wet –> lose heat rapidly
  • If born through meconium, may have it in mouth/airway
441
Q

What are the steps to resuscitation of babies?

A
  • Warm baby
  • Calculate APGAR score
  • Stimulate breathing
  • Inflation breaths
  • Chest compressions
  • Severe situations
  • Delayed umbilical cord clamping
442
Q

How are babies warmed in neonatal resuscitation?

A
  • Vigorous drying
  • Warm delivery room/heat lamp
  • Placed in plastic bag
443
Q

What is an APGAR score?

A

Used as an indicator of neonatal resuscitation progression - scored 0-2
- Appearance (skin colour)
- Pulse
- Grimmace (response to stimulation)
- Activity (muscle tone)
- Respiration

444
Q

How is breathing stimulated in neonatal resuscitation?

A
  • Dry vigorously
  • Place head in neutral position to keep airway open
  • Check for airway obstruction - consider aspiration
445
Q

How are chest compressions and inflation breaths given in neonatal resuscitation?

A
  • 2 cycle of 5 inflation breaths lasting 3 seconds each
  • Chest compression with ventilation breaths if no response - 3:1 ratio
446
Q

What severe situations may be required in neonatal resuscitation?

A
  • IV drugs
  • Intubation
  • Therapeutic hypothermia with active cooling
447
Q

What is the significance of delayed umbilical cord clamping in neonatal resuscitation?

A
  • Blood in placenta after birth
  • Delayed clamping allows time for blood to enter neonate’s circulation (placental transfusion)
448
Q

What are the effects of delayed umbilical cord clamping?

A
  • Improve Hb
  • Improved iron
  • Improved BP
  • Reduced intraventricular haemorrhage risk
  • reduced necrotising enterocolitis risk
  • Increased neonatal jaundice
449
Q

What are the main complications of slow neonatal resuscitation?

A
  • Hypoxic ischaemic encephalopathy (HIE)
  • Cerebral palsy
450
Q

Who does respiratory distress syndrome typically occur in?

A

Premature neonates (usually <32 weeks) due to insufficient surfactant

451
Q

What is the investigation and management for respiratory distress syndrome?

A
  • CXR (ground glass appearance)
  • Dexamethasone given to mothers (increases surfactant production)
  • Endotracheal surfactant
  • CPAP
  • Intubation/ventilation/oxygen
452
Q

What are the complications of respiratory distress syndrome?

A

Short term:
- Pneumothorax
- Infection
- Apnoea
Long term:
- Chronic lung disease of prematurity
- Retinopathy of prematurity
- Neurological/hearing/visual impairment

453
Q

What is bronchopulmonary dysplasia?

A

Lung damage due to pressure and volume trauma of artificial ventilation, O2 toxicity and infection

454
Q

What is the investigation and management for bronchopulmonary dysplasia?

A
  • CXR (widespread areas of opacification +/- lung collapse)
  • CPAP
  • O2
  • Corticosteroids
455
Q

What are the risk factors for meconium aspiration?

A
  • > 42 weeks
  • Foetal distress
  • Thick meconium
  • Maternal HTN/diabetes/pre-eclampsia/smoking/etc.
456
Q

What are the clinical features of meconium aspiration?

A
  • Tachypnoea
  • Tachycardia
  • Cyanosis
  • Grunting
  • Nasal flaring
  • Recession (intercostal/supraclavicular/tracheal tug)
  • Hypotension
457
Q

What are the investigations for meconium aspiration?

A
  • CXR (increased lung volumes/asymmetrical patchy pulmonary opacities/pleural effusions/pneumothorax/etc.)
  • Infection markers (FBC/CRP/blood cultures)
  • ABG
  • Oximetry
  • Echo
  • Cranial USS
458
Q

What is the management for meconium aspiration?

A
  • Observation
  • Routine care (warm/O2 monitoring/bloods/fluids)
  • Ventilation/O2 therapy
  • Abx
  • Surfactant
  • Inhaled nitric oxide
  • Corticosteroids
459
Q

What are the causes of hypoxic ischaemic encephalopathy?

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord
  • Nuchal cord
460
Q

How is hypoxic ischaemic encephalopathy graded?

A

Mild = poor feeding/general irritability/hyper-alert/resolves within 24 hours
Moderate = poor feeding/lethargic/hypotonic/seizures/takes weeks to resolve
Severe = reduced consciousness/apnoeas/flaccid/reduced/absent reflexes

461
Q

What is the management for hypoxic ischaemic encephalopathy?

A
  • Supportive care (resuscitation/ventilation/circulatory support/nutrition/acid base balance/treat seizures)
  • SEVERE = therapeutic hypothermia
462
Q

What is the main complication of hypoxic ischaemic encephalopathy?

A

Cerebral palsy

463
Q

What are the TORCH infections?

A
  • Toxoplasmosis
  • Other (syphilis/varicella/mumps/parvovirus/HIV)
  • Rubella
  • CMV
  • HSV
464
Q

What are the clinical features of a neonatal toxoplasmosis infection?

A
  • Intracranial calcification
  • Hydrocephalus
  • Chorioretinitis
465
Q

What are the clinical features of a neonatal varicella infection?

A
  • Foetal growth restriction
  • Microcephaly/hydrocephalus/learning disability
  • Scars/significant skin changes
  • Limb hypoplasia
  • Cataracts/chorioretinitis
466
Q

What are the clinical features of a neonatal rubella infection?

A
  • Congenital cataracts
  • Congenital heart disease (PDA/pulmonary stenosis)
  • Learning disability
  • Hearing loss
467
Q

What are the clinical features of a neonatal CMV infection?

A
  • Foetal growth restriction
  • Microcephaly
  • Hearing/vision loss
  • Learning disability/seizures
468
Q

How can varicella/rubella infections be prevented in neonates?

A
  • Vaccines before or after pregnancy
  • Varicella - oral aciclovir for mother if present within 24 hours and >20 weeks gestation
469
Q

Who is jaundice more common in?

A
  • Normal after birth (no access to placenta –> normal rise in bilirubin)
  • More common in breastfed babies
470
Q

What are some causes of jaundice due to increased bilirubin production?

A
  • Haemolytic disease of newborn
  • ABO incompatibility
  • Haemorrhage
  • Sepsis/DIC
  • Polycythaemia
  • G6PD deficiency
471
Q

What are some causes of jaundice due to decreased bilirubin clearance?

A
  • Prematurity
  • Breast milk jaundice (components of breast milk inhibit liver’s ability to process bilirubin)
  • Neonatal cholestasis
  • Extrahepatic biliary atresia
472
Q

What are the clinical features of jaundice and when does it become prolonged?

A
  • Mild yellowing of skin and sclera
  • Prolonged if lasts >14 days in full term babies or >21 days in premature babies
473
Q

What are the investigations for jaundice?

A
  • If presents in first 24 hours of life = urgent investigation/management required (indicates sepsis)
  • FBC/blood film
  • Conjugated bilirubin
  • Blood type testing
  • Direct coombs tets
  • TFTs
  • Blood/urine cultures
  • G6PD levels
474
Q

What is the management for jaundice?

A
  • Phototherapy (blue light - converts unconjugated bilirubin into isomers that can be excreted in bile/urine without conjugation)
  • Exchange transfusion
475
Q

What is the main complication of jaundice?

A

Kernicterus - brain damage due to high bilirubin levels (bilirubin can cross blood-brain barrier)

476
Q

What are the clinical features and complications of Kernicterus?

A
  • Floppy, drowsy baby with poor feeding
  • Cerebral palsy
  • Learning disability
  • Deafness
477
Q

When does necrotising enterocolitis commonly present and how common is it?

A
  • Commonly presents in first 2 weeks of life
  • Most common surgical emergency in neonates
478
Q

What are the risk factors for necrotising enterocolitis?

A
  • Low birth weight/premature
  • Formula feeding
  • Respiratory distress/assisted ventilation
  • Sepsis
  • Patent ductus arteriosus
479
Q

What are the clinical features of necrotising enterocolitis?

A
  • Intolerance to feeds
  • Vomiting (particularly with green bile)
  • Generally unwell
  • Distended/tender abdomen
  • Absent bowel sounds
  • Blood in stool
480
Q

What are the investigations for necrotising enterocolitis?

A
  • Bloods (FBC/CRP/blood gas/culture)
  • AXR (dilated bowel loos/bowel wall oedema/pneumatosis intestinalis (gas in bowel wall)/pneumoperitoneum (indicates perforation - Rigler’s sign (both sides of bowel visible)))
  • USS (air in portal system/ascites/perforation)
481
Q

What is the management for necrotising enterocolitis?

A
  • NBM + IV fluids + TPN + Abx (cefotaxime)
  • Bowel decompression (NG tube inserted to drain fluid/gas from GI tract)
  • Surgery (remove necrotic tissue)
482
Q

What are the complications of necrotising enterocolitis?

A
  • Perforation/peritonitis
  • Sepsis
  • Death
483
Q

What is gastroschisis?

A

Abdominal organs protrude outside abdomen without protective membrane

484
Q

What are the risk factors for gastroschisis?

A
  • Younger mothers (<20 years)
  • Maternal smoking
  • Environmental exposure (e.g. nitrosamines)
  • Maternal cyclooxygenase inhibitors use (e.g. aspirin/ibuprofen)
485
Q

What are the clinical features of gastroschisis?

A
  • Abdominal organs herniated outside of abdominal cavity (often to the right of the umbilical cord) and no membrane covering contents
  • Swollen/inflamed/thickened/short intestines
  • Thick fibrous peel seen over contents (secondary to inflammation from amniotic fluid exposure)
  • Small abdominal cavity
  • Associated with intestinal malrotation/intestinal atresia
  • Malabsorption/hypomotility
486
Q

What are the investigations for gastroschisis?

A
  • Prenatal USS (echogenic and dilated bowel loops freely floating in amniotic cavity)
  • Alpha-fetoprotein (typically elevated)
487
Q

What is the management for gastroschisis?

A
  • Sterile/clear covering over contents
  • Surgery (immediate)
488
Q

What is exomphalos/omphalocele and how is it managed?

A
  • Abdominal defect in which abdominal contents protrude through abdominal wall but are covered by an amniotic sac
  • Staged repair with completion at 6-12 months
489
Q

What is oesophageal atresia?

A

Birth defect in which the upper part of the oesophagus does not connect with the lower oesophagus/stomach

490
Q

What are the risk factors for oesophageal atresia?

A
  • Polyhydramnios (excess amniotic fluid in pregnancy)
  • Developmental problems regarding kidneys/heart/spine
  • Often happens alongside tracheo-oesophageal fistula
491
Q

What are the clinical features of oesophageal atresia?

A
  • Coughing
  • Choking
  • Turning blue
  • Inability to feed
492
Q

What are the investigations for oesophageal atresia?

A
  • Antenatal USS (excess amniotic fluid)
  • Attempt to pass NG tube
  • XRAY
493
Q

What is the management for oesophageal atresia?

A
  • Surgery
  • IV TPN + NG tube
494
Q

What are risk factors for bowel atresia?

A
  • Twin/multiple birth
  • Premature/low birth weight
495
Q

What are the clinical features for bowel atresia?

A
  • Appear well at birth
  • Vomiting when feeding
  • Soft, distended abdomen
  • Jaundice
  • May not pass meconium/small amount
496
Q

What are the investigations and management for bowel atresia?

A
  • Antenatal USS (polyhydramnios)
  • XRAY +/- contrast scan/enema (blockage)
  • Surgery
  • IV TPN + NG tube
497
Q

What are clinical features of hypoglycaemia?

A
  • Shaking/sweating
  • Irritability
  • Pale
  • Sudden behaviour changes
  • Clumsy/jerky movements
498
Q

What is the management for hypoglycaemia in neonates?

A
  • If asymptomatic, encourage normal feeding and monitor glucose
  • If symptomatic or very low, admit to neonatal unit and give IV infusion of 10% dextrose
499
Q

Who is hypoglycaemia most common in?

A
  • Newborns
  • Usually temporary
500
Q

What are risk factors for Group B Strep infection?

A
  • Premature
  • Previous baby with GBS infection
  • Fever during labour
  • Positive GBS urine/swab test during pregnancy
  • Waters broken >24 hours before birth
501
Q

What are the clinical features of Group B Strep infection?

A
  • Noisy breathing
  • Sleepy/unresponsive
  • Inconsolable crying
  • Being unusually floppy
  • Poor feeding
  • High/low temperature
  • Changes in skin colour
502
Q

What is the management for Group B Strep infection?

A
  • IV abx in labour
  • IV abx
503
Q

Describe listeria infection

A
  • Bacterial infection much more common in pregnancy
  • Typically transmitted by unpasteurised dairy products/processed meats/contaminated foods
  • Usually asx or flu-like symptoms
  • Pregnant women advised to avoid high risk foods e.g. blue cheese
  • Complications = pneumonia/meningoencephalitis/miscarriage/foetal death/neonatal infection
504
Q

What are the causes of HSV encephalitis?

A
  • HSV-1 (from cold sores) = more common in children
  • HSV-2 (from genital herpes) = more common in neonates
505
Q

What are the clinical features of HSV encephalitis?

A
  • Altered consciousness
  • Acute onset of focal neurological sx
  • Acute onset of focal seizures
  • Fever
506
Q

What are the investigations and management for HSV encephalitis?

A
  • LP and CSF sent for viral PCR testing
  • CT/MRI
  • EEG
  • Swabs to determine causative organism
  • HIV testing
  • Management = IV aciclovir
507
Q

What is cleft lip/palate?

A

Cleft lip - a split/open section of the upper lip

Cleft palate - defect in the hard/soft palate at the roof of the mouth, leaving an opening between the mouth and nasal cavity

508
Q

What is the management for cleft lip/palate?

A
  • Ensure baby can eat/drink (specifically shaped bottles/teats)
  • Surgery
509
Q

What are the causes of microcytic anaemia?

A

TAILS:
- Thalassaemia
- Anaemia of chronic disease
- Iron deficiency anaemia
- Lead poisoning
- Sideroblastic anaemia

510
Q

What are the causes of normocytic anaemia?

A

AAAHH:
- Acute blood loss
- Anaemia of chronic disease
- Aplastic anaemia
- Haemolytic anaemia
- Hypothyroidism

511
Q

What are the causes of megaloblastic macrocytic anaemia?

A

B12/folate deficiency

512
Q

What are the causes of normoblastic macrocytic anaemia?

A
  • Alcohol
  • Reticulocytosis
  • Hypothyroidism
  • Liver disease
  • Drugs e.g. azathioprine
513
Q

What are common causes of anaemia in infants?

A
  • Physiologic anaemia of infancy
  • Iron deficiency anaemia
  • Anaemia of prematurity
  • Haemolysis (haemolytic disease of newborn)
514
Q

What are the investigations and management for anaemia?

A
  • Blood film
  • MCV
  • Hb
  • Treat cause
515
Q

What is thalassaemia?

A

Genetic defect in protein chains that make up Hb (autosomal recessive)
- Alpha thalassaemia = defects in alpha globin chains (gene on chromosome 16)
- Beta thalassaemia - defects in beta globin chains (gene on chromosome 11 - minor/intermedia/major)

516
Q

What are the clinical features of thalassaemia?

A
  • Fatigue
  • Pallor
  • Jaundice
  • Gallstones
  • Bone deformities/poor growth
  • Splenomegaly
  • Pronounced forehead/malar eminences
517
Q

What are the investigations for thalassaemia?

A
  • FBC
  • Hb electrophoresis
  • DNA testing
  • Pregnancy screening test
518
Q

What is the management for thalassaemia?

A
  • Monitor FBC
  • Monitor for complications
  • Blood transfusions
  • Splenectomy
  • BM transplant
519
Q

What is a complication of thalassaemia?

A

Iron overload

520
Q

What is haemolytic disease of newborn?

A

Blood disorder in which a mother and baby’s blood types are incompatible (rhesus D negative)

521
Q

What are the clinical features of haemolytic disease of newborn?

A
  • Jaundice
  • Severe anaemia
  • Compensatory splenomegaly/hepatomegaly
522
Q

What is the investigation and management for haemolytic disease of newborn?

A
  • Direct Coombs test (DCT)
  • Prevention of sensitisation with Rh immune globulin
  • Intrauterine transfusion
523
Q

Who is sickle cell anaemia more common in?

A

Patients from areas traditionally affected by malaria - Africa/India/Middle East/Caribbean

524
Q

Describe the genetics of sickle cell anaemia

A

Autosomal recessive - affects gene for beta globin on chromosome 11
- Sickle cell trait = one copy (usually asx)
- Sickle cell disease - two copies

525
Q

What are the investigations for sickle cell anaemia?

A
  • Newborn blood spot screening (at around 5 days old)
  • High risk pregnant women offered testing
526
Q

What is the management for sickle cell anaemia?

A
  • Vaccinations
  • Abx prophylaxis (phenoxymethylpenicillin)
  • Hydroxycarbamide (stimulates HbF)
  • Crizanlizumab (monoclonal antibody that targets P-selectin to stop RBCs from sticking to blood vessel wall)
527
Q

What is the main complication of sickle cell anaemia?

A

Sickle cell crisis:
- Vaso-occlusive crisis (RBCs clog capillaries –> distal ischaemia)
- Splenic sequestration crisis (RBCs block flow within spleen)
- Aplastic crisis (temporary absence of creation of new RBCs)
- Acute chest syndrome (vessels supplying lungs become clogged with RBCs)

528
Q

What is Fanconi anaemia?

A
  • Rare genetic disease characterised by bone marrow failure syndromes
  • Mutations in FA genes (23 different FA genes)
  • BM failure –> aplastic anaemia
529
Q

What are the clinical features for Fanconi anaemia?

A
  • Failure to thrive/growth deficiency
  • Skeletal anomalies (no thumb/radius bone)
  • Abnormal skin pigmentation (cafe au lait spots)
  • Structural anomalies of kidneys/heart/GI tract/urinary tract/genitals/etc.
  • Small head/eyes
  • Unexplained fatigue
  • Frequent infections
  • Frequent nosebleeds
  • Easy bruising
  • Blood in stool/urine
530
Q

What are the investigations and management for Fanconi anaemia?

A
  • Bloods/BM testing
  • Blood/platelet transfusions
  • WCC support with growth factor (G-CSF = granulocyte colony stimulating factor)
  • Androgen
  • BM transplant = definitive treatment
531
Q

What are the complications of Fanconi anaemia?

A

Higher risk of:
- Myelodysplastic syndrome
- Leukaemia
- Tumours

532
Q

Who is haemophilia most common in?

A

Haemophilia A = factor VIII deficiency (more common)
Haemophilia B = factor IX deficiency

  • Mainly affects men (X linked recessive)
533
Q

What are the clinical features of haemophilia?

A
  • Haematoma
  • Hemarthrosis
  • Frequent spontaneous bleeding into muscles/joints
  • Bleeding following injury/spontaneous bleeding
  • Easy bruising
  • Haematuria
  • Epistaxis
534
Q

What are the investigations for haemophilia?

A
  • PTT (normal - not in extrinsic pathway)
  • vWF (normal)
  • APTT (prolonged - intrinsic pathway)
  • Reduced plasma factor VIII/IX
535
Q

What is the management for haemophilia?

A
  • IV factor VIII/IX
  • Fresh frozen plasma
  • Desmopressin (boosts activity)
  • Hep A/B vaccinations
  • Exercise/avoid contact sports/avoid aspirin
536
Q

What is a complication of haemophilia?

A

Joint deformities and arthritis from recurrent bleeding into joints

537
Q

Who is Von Willebrand Disease more common in?

A
  • Most common hereditary coagulopathy
  • More common in females
  • Poorer prognosis in blood type O
538
Q

What are the clinical features of Von Willebrand Disease?

A
  • Epistaxis
  • Menorrhagia
  • Spontaneous bleeding
539
Q

What are the investigations for Von Willebrand Disease?

A
  • FBC
  • Fibrinogen
  • Platelet count (normal)
  • Clotting screen
  • Plasma vWF (decreased)
  • Factor VIII levels (may be decreased)
540
Q

What is the management for Von Willebrand Disease?

A
  • Stop any antiplatelet drugs/NSAIDs
  • Tranexamic acid
  • COC
  • Desmopressin
  • Platelet transfusions
  • Family screening
541
Q

What are the clinical features of anaemia?

A
  • Tiredness
  • SOB
  • Headaches/dizziness/palpitations
  • Pale skin/conjunctival pallor
  • Tachyardia/rasied RR
542
Q

What are causes of iron deficiency anaemia?

A
  • Dietary insufficiency
  • Loss of iron e.g. menorrhagia
  • Inadequate absorption e.g. IBD
  • PPIs (stomach acid keeps it in soluble ferrous form)
543
Q

What are the clinical features of iron deficiency anaemia?

A
  • Pica
  • Hair loss
  • Koilonychia
  • Angular cheilitis
  • Atrophic glossitis
  • Brittle hair/nails
544
Q

What are the investigations for iron deficiency anaemia?

A
  • FBC
  • Blood film
  • Serum ferritin/iron/total iron binding capacity
545
Q

What is the management for iron deficiency anaemia?

A
  • Iron supplementation e.g. ferrous fumarate/sulphate (causes constipation/black stool)
  • Blood transfusion
546
Q

What is immune thrombocytopenic purpura?

A
  • Type II hypersensitivity reaction
  • Low platelet count causing a non-blanching purpuric rash
547
Q

What are the investigations of immune thrombocytopenic purpura?

A

Diagnosis of exclusion:
- Often preceded by viral illness
- Acute onset
- No other concerning features
- Normal examination except bruising/petechiae
- FBC/platelet count/blood film

548
Q

What is the management for immune thrombocytopenic purpura?

A
  • Treatment rarely required unless bleeding
  • Steroids
  • IVIG
  • TPO-RA (thrombopoietin receptor agonists)
549
Q

What are the most common birth injuries in neonates?

A
  • Caput succedaneum
  • Cephalohematoma
550
Q

Describe caput succedaneum

A
  • Caused by pressure on scalp during birth
  • Results in subcutaneous extraperiosteal collection of fluid
  • Presents as oedematous swelling/bruising over scalp that crosses suture lines
  • Usually reduces over a few days
551
Q

Describe cephalohematomas

A
  • Occurs after spontaneous vaginal delivery/following trauma from forceps/ventouse
  • Causes haemorrhage between skull and periosteum
  • Presents as swelling of scalp that doesn’t cross suture lines
  • Reduces over a few weeks/months
552
Q

Which intracranial haemorrhage is most common in neonates?

A
  • Subarachnoid haemorrhage
  • Intraventricular haemorrhages more common in pre-term infants
553
Q

What is the most common cause of a subdural haemorrhage in neonates?

A

Use of forceps

554
Q

What are the clinical features of intracranial haemorrhages in neonates?

A
  • No obvious head trauma/swelling
  • Irritability/convulsions over first 2 days of life
555
Q

At what ages are vaccinations given?

A
  • 8 weeks
  • 12 weeks
  • 16 weeks
  • 1 year
  • 2-15 years
  • 3 years 4 months
  • 12-13 years
  • 14 years
556
Q

What vaccinations are given at 8 weeks?

A
  • 6-in-1 (DTaP/IPV/Hib/HepB)
  • Rotavirus
  • MenB
557
Q

What vaccinations are given at 12 weeks?

A
  • 6-in-1 (DTaP/IPV/Hib/HepB)
  • Pneumococcal
  • Rotavirus
558
Q

What vaccinations are given at 16 weeks?

A
  • 6-in-1 (DTaP/IPV/Hib/HepB)
  • MenB
559
Q

What vaccinations are given at 1 year?

A
  • Hib/MenC
  • MMR
  • Pneumococcal
  • MenB
560
Q

What vaccinations are given at 2-15 years?

A

Flu vaccine

561
Q

What vaccinations are given at 3 years 4 months?

A
  • MMR
  • 4-in-1 pre-school booster (DTaP/IPV)
562
Q

What vaccinations are given at 12-13 years?

A

HPV

563
Q

What vaccinations are given at 14 years?

A
  • 3-in-1 teenage booster (Td/IPV)
  • MenACWY
564
Q

Describe paediatric IV fluid prescribing

A
  • Usually 0.9% sodium chloride + 5% glucose
  • 1000ml/kg for first 10kg
  • 500ml/kg for next 10kg
  • 20ml/kg for next 1kg

Phase 3a (21 decks)

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