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Phase 3A Revision > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Presentation of left to right shunt

A

Dyspnoea
Acyanotic

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2
Q

Causes of left to right shunt

A

Ventricular septal defect
Patent ductus arteriosus
Atrial septal defect

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3
Q

Presentation of right to left shunts

A

Cyanotic (blue)

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4
Q

Causes of right to left shunts

A

6Ts:
Tetralogy of Fallot
Transposition of great arteries
Truncus arteriosus
Total anomalous pulmonary venous connection
Tricuspid valve abnormalities
Ton of others: hypoplastic left heart, double outlet right ventricle, pulmonary atresia

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5
Q

Causes of cardiac outflow obstruction in a well child (asymptomatic with murmur)

A

Pulmonary stenosis
Aortic stenosis

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6
Q

Cause of outflow obstruction in a sick neonate (collapsed with shock)

A

Coarctation of the aorta

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7
Q

Presentation of VSD

A

Poor feeding
Failure to thrive
Dyspnoea/SOB
Tachycardia
Tachypnoea
Heart failure - may have hepatomegaly
Pansystolic murmur at lower left sternal edge
Systolic thrill on palpation

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8
Q

Conditions associated with VSD

A

Down’s syndrome
Turner’s syndrome
Foetal alcohol syndrome

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9
Q

Circulation in the foetus

A

Low left atrial pressure, as little blood returns from lungs
Right atrium > as receives systemic venous return, including from placenta
Foramen ovale open: blood flows right atrium –> left atrium –> left ventricle –> body
Ductus arteriosus connects pulmonary artery and aorta

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10
Q

Changes in circulation at birth

A

Breathing –> resistance to pulmonary blood falls –> increased volume of blood through lungs
–> increased left atrial pressure
Loss of placenta –> decreased venous return to right atrium –> decreased right atrial pressure
–> closure of foramen ovale
Ductus arteriosus closes in first few hours or days (1-2 days usually)

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11
Q

What is duct-dependent circulation

A

Where babies with congenital heart lesions rely on blood flow through the ductus arteriosus (connecting pulmonary artery to aorta)
When the duct closes, condition deteriorates rapidly

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12
Q

What features of a murmur lead you to believe it is not concerning

A

Innocent –> 5Ss
InnoSent = Soft, Systolic, aSymptomatic, left Sternal edge

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13
Q

Management of VSD

A

Small: will close spontaneously
Moderate: diuretic therapy (furosemide and spironolactone), feeding with high caloric feeds
Large: as for moderate lesion, surgery before 12 months

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14
Q

Findings on CXR for VSD

A

Severe VSD (heart failure): cardiomegaly, pulmonary oedema (increased pulmonary vascular markings)
Enlarged pulmonary artery

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15
Q

Why should a large VSD be corrected before 12 months

A

Prevent persistent pulmonary hypertension of the newborn

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16
Q

Why might a murmur be heard during febrile illness or anaemia

A

Increased cardiac output
Flow murmur

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17
Q

What causes Eisenmenger syndrome

A

When pulmonary pressure increases so much in a left to right shunt lesion, that the shunt becomes right to left, and the patient becomes cyanotic

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18
Q

Lesions that may result in Eisenmenger syndrome

A

Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus

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19
Q

Time of presentation of VSD

A

Antenatal diagnosis: 16-18 weeks
Presentation at 6-8 weeks old
Congestive heart failure typically presents after 4-6 weeks

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20
Q

Presentation of ASD in childhood

A

Typically asymptomatic
Recurrent chest infections
SOB
Difficulty feeding
Poor weight gain

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21
Q

Three types of ASD

A

Ostium secondum
Patent foramen ovale
Ostium primum

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22
Q

What is ostium secondum

A

Type of ASD where the septum secondum fails to close fully, leaving a hole

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23
Q

What is patent foramen ovale

A

Foramen ovale fails to close (not strictly an ASD)

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24
Q

What is ostium primum

A

Septum primum fails to close fully, leaving a hole in the wall
Leads to AV valve defects –> atrioventricular septal defect

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25
Q

Causes of pansystolic murmurs

A

Ventricular septal defect
Mitral regurgitation
Tricuspid regurgitation

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26
Q

Complications of ASD

A

Stroke in venous thromoboembolism (e.g. patient with DVT)
Atrial fibrillation/flutter
Pulmonary hypertension
Right sided heart failure
Eisenmenger syndrome

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27
Q

Murmur of ASD

A

Mid-systolic
Crescendo-decrescendo murmur
Loudest at upper left sternal border
Fixed split second heart sound (does not change with inspiration or expiration)

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28
Q

Presentation of ASD in adults

A

Dyspnoea
Heart failure
Stroke
Arrhythmia

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29
Q

Why is there a fixed split of second heart sound in ASD?

A

Left to right shunt increases right ventricle filling
–> RV ejection time is increased –> pulmonary valve closure is delayed

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30
Q

Management of ASD

A

Small + asymptomatic –> watch and wait
Surgical management: transvenous catheter closure, or open heart surgery
Anticoagulants in adults

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31
Q

Causes of PDA

A

Rubella infection
Maternal warfarin therapy
Prematurity - very common
Born at high altitude

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32
Q

Presentation of PDA

A

SOB
Difficulty feeding
Poor weight gain
Lower respiratory tract infections
Usually presents 3-5 days after birth, when duct begins to close

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33
Q

Murmur/cardiac signs of PDA

A

Continuous crescendo-decrescendo, machinery murmur
Heard at upper-left sternal border - best heard below left clavicle
May have thrill
Second heart sound difficult to hear
Large volume, bounding, collapsing pulse
Heaving apex beat
Wide pulse pressure

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34
Q

Main investigations in congential cardiac conditions in neonate

A

Echocardiogram
ECG
CXR

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35
Q

Management of PDA

A

Typically monitored until 1 year of age
Preterm: likely to close spontaneously
Term: less likely to close spontaneously
Medical - indomethacin/ibuprofen (not effective in term infants) –> stimulates closure of PDA
Surgical - catheter closure or PDA ligation, weight >5kg

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36
Q

Components of Tetralogy of Fallot

A

Pulmonary stenosis
VSD
Overriding aorta
Right ventricular hypertrophy

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37
Q

Risk factors/causes of Tetralogy of Fallot

A

Foetal alcohol syndrome
Chromosome 22q11.2 deletion
Rubella infection
Increased age of mother (>40)
Diabetic mother

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38
Q

What is an overriding aorta in ToF?

A

Aortic valve placed further right than normal, above the VSD
Right ventricle contracts –> blood up into aorta –> deoxygenated blood enters aorta

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39
Q

Presentation of ToF

A

Presenting when patent ductus arteriosus begins to close
Cyanosis
Clubbing
Poor feeding
Sweating during feeds
Poor weight gain
Tet spells

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40
Q

What are ‘tet spells’

A

Intermittent symptomatic periods where R to L shunt is worsened –> cyanotic episode
Occurs when pulmonary resistance increases, or systemic resistance decreases

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41
Q

What may cause a ‘tet spell’

A

Waking
Physical exertion: CO2 vasodilator –> systemic vasodilation
Crying

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42
Q

Presentation of ‘tet spell’

A

Irritable
Cyanotic
SOB
May squat/bring knees to chest –> increase systemic vascular resistance
Severe –> reduced consciousness, seizures, potential death

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43
Q

Murmur of ToF

A

Crescendo-decrescendo
Harsh ejection systolic quality
Loudest over upper-left sternal angle
Posterior radiation
Due to right ventricular outflow obstruction (pulmonary stenosis), not VSD

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44
Q

Management of ‘tet spell’

A

Knees to chest position
Oxygen: for hypoxia
Morphine: decrease respiratory drive
Beta-blockers: relax RV
IV fluids: increase pre-load
Sodium bicarbonate: for metabolic acidosis
Phenylephrine infusion: increase SVR

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45
Q

Management of ToF

A

Neonates: prostaglandin infusion to maintain ductus arteriosus
Surgery: Blalock-Taussig shunt

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46
Q

What is Transposition of the great arteries?

A

Attachments of the aorta and the pulmonary trunk to the heart are swapped
RV pumps blood into aorta, LV pumps blood into pulmonary arteries

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47
Q

Conditions associated with ToGA

A

VSD
Coarctation of aorta
Pulmonary stenosis

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48
Q

Presentation of ToGA

A

Present as ductus arteriosus closes
Severe, life-threatening cyanosis
Poor feeding
Sweating during feeds
Tachypnoea
Single loud S2 audible
Prominent right ventricular impulse

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49
Q

Management of ToGA

A

VSD or PDA can allow some time for definitive treatment
Prostaglandin infusion to maintan ductus arteriosus
Balloon septostomy: catheter into foramen ovale, inflate balloon –> create large ASD
Arterial switch surgery

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50
Q

Finding of ToGA on CXR

A

‘Egg on a string’ appearance

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51
Q

Conditions associated with pulmonary valve stenosis

A

Tetralogy of Fallot
William syndrome
Noonan syndrome
Congenital rubella syndrome

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52
Q

Presentation of pulmonary valve stenosis

A

Often asymptomatic
If significant: symptoms of fatigue on exertion, SOB, dizziness + fainting

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53
Q

Signs of pulmonary valve stenosis

A

Ejection systolic murmur, loudest at pulmonary area
Palpable thrill in pulmonary area
Right ventricular heave (due to RVH)
Raised JVP with giant A waves

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54
Q

Management of pulmonary valve stenosis

A

Mild, asymptomatic –> watch and wait
Symptomatic or more significant –> ballon valvuloplasty, or open heart surgery

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55
Q

Presentation of aortic valve obstruction

A

Often asymptomatic
More significant: fatigue, SOB, dizziness, fainting, symptoms worse on exertion

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56
Q

Signs of aortic valve stenosis

A

Ejection systolic murmur, loudest at aortic area
Crescendo-descrendo, radiating to carotids
Ejection click, just before murmur
Palpable systolic thrill
Slow rising pulse, narrow pulse pressure

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57
Q

Management of aortic valve stenosis

A

Exercise testing, echo + ECG to monitor progression
More significant stenosis, may need to restrict physical activities
Percutaneous balloon aortic valvuloplasty
Surgical aortic valvotomy
Valve replacement

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58
Q

Complications of aortic valve stenosis

A

Left ventricular outflow tract obstruction
Heart failure
Ventricular arrhythmia
Bacterial endocarditis
Sudden death (often on exertion)

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59
Q

What genetic condition is Coarctation of the Aorta associated with

A

Turner syndrome

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60
Q

Pathophysiology of Coarctation of aorta

A

Left ventricular outflow obstruction –> increased LV afterload –> LVH
Narrowing of aorta reduces pressure of blood in arteries distal to narrowing, and increases pressure of blood proximally (e.g. first three branches of aorta)

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61
Q

Presentation of coarctation of aorta

A

Typically presents as ductus arteriosus begins to close
Weak/absent femoral pulses
4 limb BP measurement: high BP in arms, low in legs
Radial:femoral delay/radial:radial delay
Tachypnoea/increased work of breathing
Poor feeding
Grey + floppy baby
Cold extremities

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62
Q

Murmur in coarctation of the aorta

A

Potential systolic murmur in left infraclavicular area/below left scapula

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63
Q

Management of coarctation of the aorta

A

Prostaglandin infusion to keep duct open
Surgery: correct coarctation, ligate ductus arteriosus

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64
Q

Investigation of cardiac conditions antenatally

A

Echocardiogram

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65
Q

Causes of heart failure in neonate

A

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

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66
Q

Causes of heart failure in infants

A

High pulmonary blood flow
VSD
Atrioventricular septal defect
Large PDA

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67
Q

Causes of heart failure in older children and adolescents

A

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

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68
Q

Symptoms of heart failure

A

Breathlessness: particularly on feeding, or exertion
Sweating
Poor feeding
Recurrent chest infections

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69
Q

Signs of heart failure

A

Poor weight gain, or faltering growth
Tachypnoea
Tachycardia
Heart murmur, gallop rhythm
Enlarged heart
Hepatomegaly
Cool peripheries

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70
Q

What is hypoplastic left heart syndrome

A

Underdevelopment of entire left side of the heart
Mitral valve is small or atretic
LV small
Aortic valve atresia
Ascending aorta very small
Coarctation of the aorta nearly always

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71
Q

Presentation of hypoplastic left heart syndrome

A

May be detected antenatally
Duct-dependent systemic circulation
No flow through Left side of heart: ductal constriction –> profound acidosis, rapid CVS collapse
Weakness/absence of peripheral pulses

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72
Q

Management of hypoplastic left heart syndrome

A

Surgery: norwood procedure
Followed by Glenn or hemi-Fontant at 6 months
Another Fontan at about 3 years

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73
Q

What is rheumatic fever

A

Autoimmune condition
Triggered by streptococcus bacteria (group A, beta-haemolytic streptococci e.g. strep pyogenes)
Type 2 hypersensitivity reaction

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74
Q

Presentation of rheumatic fever

A

Presents 2-4 weeks following streptococcal infection e.g. tonsilitis or pharyngeal infection
Polyarthritis
Mild fever
Malaise
Rash
SOB
Chorea
Nodules

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75
Q

Cardiac involvement in rheumatic fever

A

Inflammation –> pericarditis, myocarditis, endocarditis –>
Tachycardia/bradycardia
Murmur (from valvular heart disease, mitral valve normally)
Pericardial rub
Heart failure

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76
Q

Skin findings with rheumatic fever

A

Subcutaneous nodules: on extensor surfaces, firm and painless
Erythema marginatum rash: pink rings of varying size, on torso and proximal limbs, pink border with fading centre, borders may unite to give ‘map-like’ appearance

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77
Q

Investigations in rheumatic fever

A

Throat swab for bacterial culture
Antistreptococcal antibodies titres
Echo, ECG and CXR for heart involvement

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78
Q

What is the Jones criteria for rheumatic fever

A

Diagnostic criteria: evidence of recent streptococcal infection plus two major criteria, or one major + two minor

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79
Q

Major criteria for rheumatic fever

A

JONES
Joint arthritis
Organ inflammation e.g. carditis
Nodules
Erythema marginatum rash
Sydenham chorea

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80
Q

Minor criteria for rheumatic fever

A

FEAR
Fever
ECG changes (prolonged PR interval) without carditis
Arthralgia without arthritis
Raised inflammatory markers (CRP, ESR)

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81
Q

Management of rheumatic fever

A

Antibiotics for streptococcal infection to prevent development: e.g. 10 days phenoxymethylpenicillin for streptococcal tonsilitis
NSAIDs for joint pain
Aspirin + steroids for carditis
Prophylactic abx to prevent further infections + recurrence
Monitoring + management of complications

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82
Q

Complications of rheumatic fever

A

Recurrence
Valvular heart disease (mitral stenosis)
Chronic heart failure

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83
Q

Which children are at risk of infective endocarditis?

A

All children of any age with congenital heart diease, except secundum ASD
Risk particularly high with turbulent jet of blood e.g. VSD, coarctation of aorta, or PDA; or prosthetic material
Previous rheumatic fever

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84
Q

Clinical signs of infective endocarditis?

A

Fever
Anaemia + pallor
Splinter haemorrhages
Tender nodules on fingers/toes (Osler’s nodes)
Erythematous palms/soles of feet (Janeway lesions)
Clubbing (late)
Necrotic skin lesions
Splenomegaly
Retinal infarcts (Roth spots)
Arthritis/arthralgia
Haematuria (microscopic)
Heart murmurs (changing)

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85
Q

Mnemonic for signs of endocarditis (adults)

A

FROM JANE
Fever
Roth spots
Osler’s nodes
Murmur
Janeway lesions
Anaemi
Nail haemorrhage
Emboilism

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86
Q

Investigation of infective endocarditis

A

Blood cultures before antibiotics
Transthoracic Echocardiogrphy
Blood tests: acute-phase reactants (CRP/ESR), FBC, U+Es
Urine dipstick

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87
Q

Causative organisms of infective endocarditis

A

alpha-haemolytic streptococcus (streptococcus viridans)
Others: strep bovis, staph aureus, HACEK group (haemophilus species etc)

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88
Q

Management of infective endocarditis

A

IV antibioics
High-dose penicillin + an aminoglycoside e.g. gentamicin or vancomycin
Minimum 6 weeks
Surgery to remove infected prosthetic material

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89
Q

Prophylaxis of infective endocarditis

A

Good dental hygiene

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90
Q

What is croup

A

Laryngeotracheobronchitis
Viral infection causing upper airway obstruction

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91
Q

Common causative agent of croup

A

Parainfluenza viruses
Others: rhinovirus, RSV, influenza, adenovirus

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92
Q

Age of presentation of croup

A

6 months - 6 years
Peak in 2nd year of life

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93
Q

Presentation of croup

A

Common in autumn
Hoarseness (inflamed vocal cords)
Barking cough (tracheal oedema and collapse)
Harsh stridor (inspiratory)
Difficulty breathing - with chest retraction
Symptoms start/worse at night
Low grade fever

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94
Q

Onset of croup

A

Over days
With preceding coryza

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95
Q

Management of croup

A

Supportive treatment - get child to sit up when coughing, comfort, fluids and rest
?Inhalation of warm moist air
Oral dexamethasone - single dose given to all children regardless of severity (Oral prednisolone if not available)
Nebulised steroids (budenoside)
Nebulised adrenaline if more severe, with oxygen
Intubation + ventilation if necessary

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96
Q

Indications for admission with croup

A

Moderate or severe croup e.g. frequent cough, easily audible stridor at rest, obvious signs of increased work of breathing, may be agitated/distressed etc
<6 months of age
Known upper airway abnormalities
Uncertainty of diagnosis

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97
Q

Causative agent of acute epiglottitis

A

Haemophilus influenza type b (Hib)
Prevented by vaccination in many children

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98
Q

Life-threatening differential diagnosis of croup

A

Acute epiglottitis - more rapid onset

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99
Q

Presentation of acute epiglottitis

A

Sore throat
Stridor (soft)
Drooling
Tripod position - sat forward with hand on each knee
High fever
Difficulty/painful swallowing
Increasing respiratory difficulty
Muffled voice
Scared + quiet child
Septic and unwell appearance

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100
Q

Description of cough in acute epiglottitis

A

Minimal or absent

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101
Q

Most important point in investigation/management of acute epiglottitis

A

Do not lie the child down or examine the throat with a spatula
Do not perform an X-ray
Any of thse can cause total airway obstruction

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102
Q

Lateral X-ray sign for acute epiglottitis

A

Thumb sign/thumbprint sign: soft tissue shadow looks like a thumb is pressed into the trachea

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103
Q

Management of acute epiglottitis

A

Call for senior paediatrician + anaesthetist + ENT surgeon
Anaesthetist to secure airway
Intubation performed under controlled conditions if required
Urgent tracheostomy may be performed
Once airway is secure –> blood for cultures
IV antibiotics e.g. cefuroxime for 3-5 days (tube removed before this)
Rifampicin to close household contacts

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104
Q

Another name for whooping cough

A

Pertussis

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105
Q

Causative agent of whooping cough

A

Bordatella pertussis

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106
Q

Presentation of whooping cough

A

Preceding week of coryzal symptoms: low grade fever, mild cough (cattarhal phase)
Then a paroxysmal/sporadic cough: severe fits, keep building until out of breath
Child goes red or blue in face, mucus from nose and mouth
Followed by inspiratory whoop (inhalation against closed glottis). May be apnoea in infants
Can cough so hard –> fainting, vomiting, epistaxis, subconjunctival haemorrhage, pneumothorax

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107
Q

Duration of whooping cough

A

Paroxysmal phase (severe coughing fits +/- whoop) lasts up to 3 months
Symptoms then gradually decrease (convalescent phase) but may persist for many more months

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108
Q

Complications of whooping cough

A

Pneumothorax
Seizures
Bronchiectasis

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109
Q

Diagnosis of whooping cough

A

Nasopharyngeal or nasal swab with PCR testing or bacterial culture if cough present for 2-3 weeks
If cough >2 weeks, oral fluid tested for anti-pertussis toxin immunoglobulin G (blood if >17)
Lymphocytosis on blood count

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110
Q

Management of whooping cough

A

Supportive care
Antibiotics can be started in first 21 days of symptoms: macrolide e.g. azithromycin, erythromycin etc. Also used in vulnerable patients
Close contacts receive prophylactic antibiotics
Notifiable disease

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111
Q

What is the most common LRTI in children?

A

Bronchiolitis - inflammation and infection in the bronchioles

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112
Q

Commonest age for bronchiolitis

A

1-9 months

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113
Q

When might bronchiolitis be more likely in older infants?

A

Ex-premature infants with chronic lung disease

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114
Q

Causative pathogen(s) of bronchiolitis?

A

Respiratory syncitial virus (RSV)
Others: parainfluenza virus, rhinovirus, adenovirus, influenza virus, human metapneumovirus

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115
Q

Symptoms of bronchiolitis

A

Preceding coryzal symptoms
Dry cough
Increasing breathlessness
Feeding difficulty (due to increased dyspnoea)
Mild fever
Apnoeas are common

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116
Q

Findings on examination in bronchiolitis

A

Dry, wheezy cough
Tachycardia + tachypnoea
Subcostal + intercostal recession
Hyperinflation of the chest
Find end-inspiratory crackles (crepitations)
High-pitched wheeze (expiratory > inspiratory)

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117
Q

Signs of repiratory distress in an infant

A

Raised resp rate
Use of acessory muscles of breathing e.g. sternocleidomastoid, abdominal + intercostal
Intercostal + subcostal recessions
Nasal flaring
Head bobbing
Tracheal tugging
Cyanosis
Abnormal airway noises

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118
Q

What is wheezing?

A

A whistling sound caused by narrowed airways, typically heard during expiration

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119
Q

What is grunting?

A

Caused by exhaling with the glottis partially closed to increase positive end-expiratory pressure

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120
Q

What is stridor?

A

A high pitched, inspiratory noise cause by obstruction of the upper airway

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121
Q

When would a child with bronchiolitis be admitted to hospital?

A

Reported or observed apnoea
Persistent O2 <90% on air
Inadequate oral fluid intake (50-75% of usual volume)
Severe respiratory distress e.g. grunting, marked chest recession, resp rate >70

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122
Q

Management of bronchiolitis

A

Supportive
Humidified oxygen: nasal cannulae or head box
Monitoring
NG feeds
Fluids

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123
Q

Prevention of bronchiolitis

A

IM Palivizumab monthly (MAB against RSV)
Given to high-risk individuals e.g. CF, congenital heart disease, immunocompromised, Down’s syndrome, premature infants

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124
Q

What is asthma?

A

Chronic inflammatory airway disease, leading to variable airway obstruction (reversible)
Smooth muscle of airways is hypersensitive to stimuli –> constriction –> airflow obstruction
Atopic condition

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125
Q

Atopic conditions

A

Asthma
Eczema
Hay fever
Food allergies

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126
Q

What is viral-induced/episodic wheeze

A

Small airway obstruction due to inflammation in response to a viral infection
Diagnosed in children <5 years of age

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127
Q

Key features of asthma in a child

A

Diurnal variation of symptoms: worse at night and in early morning
Symptoms with nonviral triggers
Interval symptoms e.g. symptoms between acute exacerbations
Personal or family history of atopic disease
Positive response to asthma therapy

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128
Q

Examination findings in long-standing asthma

A

Hyperinflation of the chest
Generalised polyphonic expiratory wheeze
Prolonged expiratory phase
Harrison’s sulci: depression at base of thorax associated with muscular insertion of the diaphragm

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129
Q

Diagnosis of asthma

A

Clinical symptoms
FEV1:FVC <70%
Bronchodilator reversibility: FEV1 improved by 12% or more
FeNO >= 35ppb

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130
Q

Conditions screened for on newborn heel prick test

A

Congenital hypothyroidism
Sickle cell disorders
CF
Phenylketonuria
Medium-chain acyl-CoA dehyodrogenase deficiency (MCADD)
Maple syrup urine disease
Isolvaleric acidaemia
Glutaric aciduria type 1 (GA1)
Homocystinuria

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131
Q

First pubertal sign in females

A

Breast budding

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132
Q

First pubertal sign in males

A

Testicular enlargement

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133
Q

Paediatric sepsis 6 algorithm

A
  1. High flow O2
  2. IV or IO access - take blood cultures, blood glucose, blood lactate/gas
  3. Give IV or IO antibiotics
  4. Fluid resuscitation
  5. Consider inotropic support e.g. adrenaline
  6. Involve seniors/specialists early
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134
Q

What antibiotics should be used in suspected sepsis in children when causative organism is unknown

A

IV 3rd generation cephalosporins e.g. cefotaxime
IV amoxicillin in infants under 3 months to cover for Listeria

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135
Q

Features of glomerulonephritis

A

Proteinuria + haematuria
Oedema
Weight gain secondary to oedema

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136
Q

What is Henoch-Schonlein Purpura

A

Also known as IgA vasculitis
Produces non-blanching rash, general unwellness, fatigue and abdominal pain
Often triggered by URTI or gastroenteritis

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137
Q

Classic features of Henoch-Schonlein Purpura

A

Purpura - typically starting on legs and spreading to buttocks. Urticarial, then becomes maculopapular + purpuric
Joint pain - esp knees and ankles
Abdominal pain
Renal involvement (IgA nephritis)
(Fever can also occur_

138
Q

Complication of Henoch-Schonlein Purpura

A

IgA Nephropathy

139
Q

Difference between symptoms in IgE-mediated and non IgE-mediated CMPA?

A

IgE-mediated symptoms appear within minutes-2 hours of consuming cow’s milk
Non IgE-mediated develop 2-72 hours after consumption

140
Q

In which children does CMPA more commonly present?

A

<1 year age
More common in formula-fed babies, or when weaning, or when switched to formula milk
Can be present in breastfed babies when mother consumes dairy products
Family history of atopic conditions

141
Q

Symptoms of CMPA

A

Bloating + wind
Abdominal pain + Diarrhoea
Vomiting + regurgitation
Urticarial rash/atopic eczema
Angio-oedema
Cough or wheeze
Sneezing
Watery eyes

142
Q

Management of CMPA

A

Breast-feeding: avoid dairy products
Hydrloysed formulas designed for CMPA
In severe cases, elemental formulas made of basic amino acids (e.g. neocate)
Mostly outgrow by age 3
Start on milk ladder every 6 months or so

143
Q

Two most common causes of nephritis in children

A

Post-streptococcal glomerulonephritis
IgA nephropathy (Berger’s disease)

144
Q

How does nephritis/nephritic syndrome present

A

Reduction in kidney function
Haematuria
Proteinuria (less than nephrotic syndrome)

145
Q

Presentation of post-streptococcal glomerulonephritis

A

Occurs 1-3 weeks after a beta-haemolytic strep infection e.g. tonsilitis caused by strep pyogenes
Causes an acute kidney injury

146
Q

Management of post-strep glomerulonephritis

A

Throat swab + anti-streptolysin antibody titres to confirm diagnosis
Supportive
May need antihypertensives and diuretics if develop hypertension and oedema

147
Q

Management of IgA nephropathy

A

Supportive of renal failure
Immunosupressant medications e.g. steroids and cyclophosphamide to slow progression

148
Q

Renal biopsy findings in IgA nephropathy

A

IgA deposits
Glomerular mesangial proliferation

149
Q

What is slapped cheek syndrome

A

Erythema infectiosum
AKA fifth disease

150
Q

What causes erythema infectiosum

A

Parovirus B19

151
Q

Presentation of erythema infectiosum

A

Children aged 3-15 years
One week following exposure, mild prodromal illness e.g. headache, rhinitis, sore throat, low-grade fever, malaise
Symptom free for 7-10 days –> slapped cheek rash with eythematous cheeks
May also have arthropathy

152
Q

Description of rash in erythema infectiosum

A

Rash on cheeks, spares nose, perioral and periorbital regions
Develops on extremities after a few days (particularly extensor surfaces)
Not itchy in young children
Gradually fades (up to 3 weeks to resolve)

153
Q

Management of erythema infectiosum

A

Symptomatic
Avoid contact with pregnant women + immunocompromised individuals

154
Q

What is roseola infantum

A

Common disease of infanncy caused by human herpes virus 6 (and sometimes HHV-7)
Also known as roseola, or sixth disease

155
Q

Features of roseola infantum

A

High fever lasting a few days +/- coryzal symptom + swollen lymph nodes
Followed 1-2 weeks later by –>
Maculopapular rash (typically on chest, arms + legs; not itchy)
Nagayama spots: papular enanthem on uvula + soft palate
Febrile convulsions are relatively common
Diarrhoea + cough also commonly seen

156
Q

Presentation of haemophilia A

A

Joint bleeding
Deep muscular bleeds

157
Q

Geneology of haemophilia A

A

X-linked recessive disorder

158
Q

Coagulation findings in haemophilia A

A

Prolonged APTT
Normal PT

159
Q

Appropriate topical treatments for pseudomonas species

A

Ciprofloxacin and gentamicin

160
Q

What side effect needs to be monitored for with IV salbutamol?

A

Hypokalaemia

161
Q

Definition of moderate asthma attack <5 years old

A

Sats >92%, no clinical features

162
Q

First line management of asthma in children >5

A

Short-acting beta-agonist reliever therapy e.g. salbutamol only in children with infrequent, short-lived wheezze and normal lung function

163
Q

First line maintenance therapy for asthma in children >5

A

Low dose of an inhaled corticosteroid e.g. budesonide, beclometasone, fluticasone, mometasone

Used if symptoms at presentation clearly indicate maintenance therapy (symptoms 3x week, or waking at night), or if uncotrolled with SABA alone

164
Q

What medication regime should be used for asthma in children >5 where ICS does not control symptoms

A

Add a LABA e.g. salmeterol - only continue if there is a good response

165
Q

What medication regime should be used for asthma in children 5-12 where ICS + LABA does not control symptoms

A

Consider starting LTRA alongside ICS e.g. montelukast
Consider starting oral theophylline - side effects are strong

166
Q

If asthma uncontrolled on paediatric low dose ICS + LABA in children 5-12

A

Consider increasing ICS dose

167
Q

Initial management of suspected asthma in children <5

A

SABA for reliever therapy

168
Q

Initial prevention therapy for suspected asthma in children <5

A

Very low dose ICS or LTRA

169
Q

Therapy after initial prevention therapy in children <5 with suspected asthma

A

Very low dose ICS, plus LTRA

170
Q

Problems associated with long-term steroid use in children

A

Adverse effect on growth
Adrenal suppression
Altered bone metabolism

171
Q

Signs of moderate acute asthma attack in children

A

Peak flow >50% predicted
Normal speech
No clinical features

172
Q

What medication regime should be used for asthma in children >12 where ICS + LABA does not control symptoms

A

Titrate up ICS dosage
Consider adding oral LTRA, oral theophylline, or an inhaled long-acting muscarinic antagonist (LAMA) e.g. tiotropium

173
Q

What medication regime should be used for asthma in children 5-12 where ICS + LTRA/LAMA etc does not control symptoms

A

Titrate ICS up to high dose
Combine treatments from step 4 e.g. LTRA + LAMA
Consider oral beta-2 agonist e.g. salbutamol

174
Q

Signs of severe asthma attack

A

Peak flow 33-50% predicted
Saturations <92%
Unable to complete sentences in one breath
Signs of respiratory distress
Resp rate >40 (1-5 years); >30 (5-12 years): >25 (12-18)
Heart rate >140 (1-5 years); >125 (5-12 years); >110 (12-18)

175
Q

Signs of life-threatening asthma attack

A

Peak flow <33% predicted
Saturations <92%
Exhuastion + poor resp effort
Hypotension
Silent chest
Cyanosis
Altered consciousness/confusion

176
Q

Management of moderate asthma attack

A

Keep calm + reassure
SABA via spacer (or face mask): 2-4 puffs, increasing by 2 puffs every 2 minutes to 10 puffs
Oral prednisolone
Monitor response for 15-30 minutes

177
Q

Principles of management in acute viral induced wheeze or asthma

A

Supplementary oxygen if required
Bronchodilator therapy
Steroids (oral prednisolone, or IV hydrocortisone)
Antibiotics if bacterial cause suspected

178
Q

Step-up pathway of bronchodilators in acute asthma

A

Inh or neb salbutamol
Inh or neb ipratropium bromide (anti-muscarinic)
IV magnesium sulphate
IV aminophylline

179
Q

Management of severe acute asthma attack

A

High-flow oxygen
SABA via spacer (10 puffs) or nebulised - assess response + repeat as required
Oral prednisolone or IV hydrocortisone
Consider: inhaled iptraopium, IV beta-2 agonist e.g. salbutamol, or aminophylline, or magnesium

180
Q

Management of life-threatening acute asthma attack

A

High-flow oxygen
SABA nebulised - assess response continuously and repeat a required (back to back)
Orl pred or IV hydrocortisone
Nebulised ipratropium
Consider: IV beta-2 agonist e.g. salbutamol, or aminophylline, or magnesium

181
Q

Management of acute asthma attack if responding to treatment

A

Continue bronchodilators for 1-4 hours PRN
Discharge when stable on 4h treatment
Continue oral prednisolone for 3-7 days
Arrange follow-up

182
Q

Management of asthma attack not responding to treatment

A

Transfer to HDU/PICU
Senior medical review
Consider IV therapies not already used
Consider CXR to check for pneumothorax, and blood gases
Consider need for mechanical ventilation

183
Q

Geneology of cystic fibrosis

A

Autosomal recessive defect in CFTR gene affecting mucus glands

184
Q

GI consequences of CF

A

Thick pancreatic + biliary secretions –> blockage of ducts –> lack of digestive enzymes in digestive tract e.g. pancreatic lipase

185
Q

Respiratory consequences of CF

A

Low volume thick airway secretions –> reduce airway clearance –> bacterial colonisation + susceptibility to infections

186
Q

Reproductive consequence of CF

A

Congenital bilateral absence of vas deferens in males
Healthy sperm, but cannot get to ejaculate –> male infertility

187
Q

First sign of CF (not bloodspot test)

A

Meconium ileus - mecoium thick + sticky, gets stuck and obstructs bowel
Meconium not passed within 24 hours, abdominal distension + vomiting

188
Q

If CF not diagnosed at birth, how does it present in childhood

A

Recurrent LTRI
Failure to thrive
Pancreatitis

189
Q

Symptoms of CF

A

Chronic cough
Thick sputum production
Recurrent resp infections
Steatorrhoea
Abdominal pain + bloating
Failure to thrive (poor weight + height gain)
May taste salty when kissed (concentrated salt in sweat)

190
Q

Signs of CF

A

Low weight or height on charts
Nasal polyps
Finger clubbing
Crackles + wheezes on auscultation
Abdominal distension

191
Q

Causes of clubbing in children

A

Hereditary
Cyanotic heart disease
Infective endocarditis
CF
Tuberculosis
IBD
Liver cirrhosis

192
Q

Diagnosis of CF (x3)

A

Newborn guthrie heel prick bloodspot testing
Sweat test (gold standard)
Genetic testing for CFTR gene (during pregnancy or after birth)

193
Q

Key colonisers seen in CF

A

Staphylococcus aureus
Pseudomonas aeruginosa

Haemophilus influenza
Klebsiella pneumoniae
Escherichia coli
Burkhodheria cepacia

194
Q

Management of pseudomonas colonisation in CF

A

Long-term nebulised antibiotics e.g. tobramycin
Oral ciprofloxacin

195
Q

Management of CF

A

Chest physio
Exercise
High calorie diet
CREON tablets if pancreatic insufficiency
Prophylactic flucloxacillin
Treat chest infection
Bronchodilators
Nebulised dornase alfa (reduce viscosity of secretions)
Nebulised hypertonic saline
Vaccinations

196
Q

Longer-term management of CF

A

Lung transplantation if end-stage resp failure
Liver transplant in liver failure
Fertility treatment
Genetic counselling

197
Q

What conditions do people with CF need to monitored/screened for?

A

Diabetes
Osteoporosis
Vit D deficiency
Liver failure

198
Q

Early features of meningococcal septicaemia in children

A

Leg pain
Diarrhoea
Abnormal skin colour
Breathing difficulty
Cold peripheries

199
Q

Triad of findings in Haemolytic Uraemic Syndrome

A

AKI
Thrombocytopenia (normal clotting time)
Normocytic anaemia (microangiopathic haemolytic anaemia)

200
Q

What triggers HUS?

A

Usually shiga toxin (bacterial toxin) typically produced by e.coli 0157, or Shigella

201
Q

Risk factors for HUS

A

Use of antibiotics and anti-motility medications e.g. loperamide to treate gastroenteritis caused by E.coli or Shigella

202
Q

Presentation of HUS

A

Gastroenteritis (caused by E.coli) with bloody diarrhoea
Symptoms start 5 days after diarrhoea

Reduced urine output
Haematuria
Abdominal pain
Lethargy and irritability
Confusion
Oedema
Hypertension
Bruising

203
Q

Management of HUS

A

Supportive
Renal dialysis if required
Antihypertensives if required
Fluid balance
Blood transfusions if required

204
Q

Complications of HUS

A

Abdominal pain
Myocarditis
Encephalitis-like features
Hepatitis
Pancreatitis
Retinal haemorrhages
Hypertension due to renal damage

205
Q

Causative agent of Infectious mononucleosis

A

Epstein Barr Virus

206
Q

Complication of amoxicillin in infectious mononucleosis

A

Maculopapular pruritic rash
Also happens with cephalosporins

207
Q

Features of infectious mononucleosis

A

Fever
Sore throat
Fatigue
Lymphadenopathy
Tonsillar enlargment
Splenomegaly (or rupture)

208
Q

Investigations in glandular fever

A

Monospot test - heterophile antibodies react to horse red blood cells
Paul-Bunnell test - similar, but uses blood cells from sheep

209
Q

Complications of glandular fever

A

Splenic rupture - advised to avoid contact sports
Glomerulonephritis
Haemolytic anaemia
Thrombocytopenia
Chronic fatigue

Avoid alcohol

210
Q

Cancer associated with EBV infection

A

Burkitt’s lymphoma

211
Q

Vaccinations in 6-in-1

A

Parents Will Immunise Toddlers Because Death
P - Polio
W - Whooping Cough (pertussis)
I - Influenza (haemophilus influenzae B)
T - Tetanus
B - hepatitis B
D - Diptheria

212
Q

Vaccinations at 8 weeks

A

6 in 1
MenB
Rotavirus (oral)

213
Q

Vaccinations at 12 weeks old

A

6 in 1 booster
Pneumococcal
Rotavirus booster

214
Q

Vaccinations at 16 weeks

A

6 in 1 booster
MenB booster

215
Q

1 year old vaccinations

A

2 in 1: Hib and MenC
Pneumococcal booster
MenB booster
MMR dose 1

216
Q

How is the influenza vaccination given to children

A

Nasal spray
All children primary school –> year 7
Highr risk: from 6 months

217
Q

Vaccinations at 3 years 4 months

A

4 in 1: diptheria, tetanus, pertussis, polio
MMR dose 2

218
Q

Vaccination at 12-13 years old

A

HPV - two doses 6-24 months apart
Given before sexual activity

219
Q

Vaccinations at 14 years old

A

3 in 1: tetanus, diptheria, polio
Meningococcal groups A, C, W, Y (WACY)

220
Q

Types of leukaemia in children

A

Acute lymphoblastic leukaemia (ALL) - most common
Acute myeloid leukaemia (AML) - next most common
Chronic myeloid leukaemia (CML) - rare

221
Q

Age peak for ALL

A

2-3 years

222
Q

Age peak for AML

A

<2 years

223
Q

Risk factors for leukaemia

A

Radiation exposure e.g. abdo x-ray in pregnancy
Down’s syndrome
Kleinfelter syndrome
Noonan syndrome
Fanconi’s anaemia

224
Q

Presentation of leukaemia

A

Typically symptoms of anaemia e.g. fatigue
Unexplained fever
Weight loss
Night sweats
Pallor
Petechiae and abnormal bruising
Unexplained bleeding
Generalised lymphadenopathy
Bone or joint pain
Hepatosplenomegaly
Abdominal pain

225
Q

Diagnosis of leukaemia

A

FBC: pancytopenia e.g. anaemia, leukopenia and thrombocytopenia
Blood film: blast cells
Bone marrow biopsy
Lymph node biopsy

226
Q

Congenital adrenal hyperplasia inherited mechanism

A

Autosomal recessive
Deficiency of 21-hydroxylase enzyme –> underproduction of cortisol and aldosterone, overproduction of androgens
Can also be 11-beta-hydroxylase enzyme

227
Q

Consequences of congenital adrenal hyperplasia

A

Decreased sodium retention –> hyponatraemia
Decreased potassium excretion –> hyperkalaemia

228
Q

Presentation of CAH in females

A

Typically present at birth with virilised genitalia e.g. enlarged clitoris due to high testosterone

229
Q

Presentation of severe CAH

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia
May have metabolic acidosis

Poor feeding
Vomiting
Dehydration
Arrhythmias

230
Q

Presentation of mild CAH

A

Symptoms relate to high androgen levels
Females: tall for age, facial hair, absent periods, deep voice, early puberty
Males: tall for age, dep voice, large penis, small testicles, early puberty

231
Q

Hyperpigmentation in CAH

A

Anterior pituitary gland responds to low cortisol by producing ACTH –> melanocyte stimulating hormone –> melanin

232
Q

Management of CAH

A

Followed for growth and development
Cortisol replacement - hydrocortisone
Aldosterone replacement - fludrocortisone
Corrective surgery for genitals if required

233
Q

Typical presentation of febrile convulsion

A

18 months old
2-5 minute tonic-clonic seizure
During high fever usually caused by underlying viral illness or bacterial infection e.g. tonsilitis

234
Q

‘Sanctuary sites’ from chemotherapy

A

Central nervous system (BBB)
Testes

235
Q

Complications of sickle cell disease

A

Anaemia
Infection
Stroke
Avascular necrosis in large joints e.g. hip
Pulmonary hypertension
Priapism
CKD
Sickle cell crises
Acute chest syndrome

236
Q

Management of sickle cell disease

A

Antibiotic prophylaxis, usually with PenV
Hydroxycarbamide - stimulates production of HbF, prevents vaso-occlusive complications
Blood transfusion
Bone marrow transplant/stem cell transplant

237
Q

What conditions come under sickle cell crisis

A

Vaso-occlusive crisis (painful)
Splenic sequestration crisis
Aplastic crisis
Acute chest syndrome

238
Q

Vaso-occlusive crisis features

A

Distal ischaemia
Dehydration + raised haematocrit
Pain, fever, features of infection
Pripaism

239
Q

Features of splenic sequestration crisis

A

Acutely enlarged and painful spleen
Can lead to severe anaemia and hypovolaemic shock
Supportive management e.g. blood transfusion + fluid resuscitation
Splenectomy often used to prevent

240
Q

Aplastic crisis

A

Typically triggered by parovirus B19
Significant anaemia
Management is supportive (blood transfusions)
Usually resolves spontaneously

241
Q

Acute chest syndrome

A

Fevere/respiratory symptom with new infiltrates seen on CXR
Antibiotics/antivirials
Blood transfusion
Incentive spirometry to encourage effective breathing
Artifical ventilation

242
Q

Inheritance of haemophilia A/B

A

X-linked recessive –> almost exclusively affects males

243
Q

Deficiencies in haemophilia

A

A - factor VIII
B - factor IX

244
Q

Features of haemophilia

A

Excessive bleeding in response to minor trauma
Spontaneous haemorrhage
Neonates + children: intracranial haemorrhage, haematomas, cord bleeding
Spontaneous bleeding into joints + muscles (severe)

245
Q

Management of haemophilia

A

IV infusion of clotting factors - prophylactic or response to bleeding. Antibodies can form against these
In acute episodes: desmopressin (stimulate release of vWF), and antifibronlytics e.g. tranexamic acid

246
Q

What is kawasaki disease

A

Mucocutaneous lymph node syndrome
Systemic, medium-sized vessel vasculitis
Affects children usally <5, typically Asian

247
Q

Key complication of Kawasaki disease

A

Coronary artery aneurysm

248
Q

Presentation of Kawasaki disease

A

CRASH + Burn
Conjunctivitis (bilateral)
Rash (widespread erythematous maculopapular)
Adenopathy (cervical lymph nodes)
Strawberry tongue
Hands (palmar erythema, swelling, desquamation)

Burn = Persistent high fever >5 days (>39 degrees)

249
Q

Investigations in Kawasaki disease

A

FBC - anaemia, low WCC, low platelet
LFT - low albumin, elevated liver enzymes
Inflammatory markers - raised (especially ESR)
Urinalysis - white cells w/o infection
Echocardiogram - rule out coronary artery pathology

250
Q

Cardiac complications of kawasaki disease

A

Pericardial effusion
Myocardial disease
Valve damage
Coronary artery disease

251
Q

Common age of Perthes disease presentation

A

5-10 years
Males

252
Q

What is Perthes disease

A

Avascular necrosis of the capital femoral epiphysis

253
Q

Complication of Perthes disease

A

Soft and deformed femoral head –> early hip osteoarthritis
Premature fusion of growth plates

254
Q

Presentation of Perthes disease

A

Pain in hip or groin
Limp
Restricted hip movements
Potentiall referred knee pain
No history of trauma (if minor trauma, consider slipped upper femoral epiphysis)

255
Q

Management of Perthe’s disease

A

Age <6, no significant collapse of the femoral head or gross structural abnormalities :
- Observation including serial X-rays
- Physiotherapy
In severe cases (especially if >6), surgery may be required to improve alignment and function of femoral head + hip

256
Q

Risk factors for developmental dysplasia of the hip

A

First degree family history
Breech presentation from 36 weeks
Breech presentation at birth if 28 weeks onwards
Multiple pregnancy
Female
Oligohydramnios
High birth weight
Prematurity

257
Q

Screening for DDH

A

Barlows and Ortolani tests

258
Q

Which children require USS examination for DDH

A

First degree family history of hip problems in early life
Breech presentation at, or after, 6 weeks gestation (regardless of presentation at birth, or mode of delivery)
Multiple pregnancy

259
Q

Management of DDH

A

Most unstable hips will spontaneously stabilise by 3-6 weeks of age
Pavlik harness (dynamic flexion-abduction orthosis) in children <4-5 months
Older children may require surgery

260
Q

Causes of intestinal obstruction

A

Meconium ileus
Hirschsprung’s disease
Oesophageal or duodenal atresia
Intussusception
Imperforate anus
Volvulus
Strangulated hernia

261
Q

Presentation of intestinal obstruction

A

Persistent vomiting (may be bilious)
Abdominal pain + distension
Failure to pass stools or wind
Abnormal bowel sounds

262
Q

Investigation of intestinal obstruction

A

Abdominal X-ray: dilatedloops of bowel proximal to obstructions, collapsed loops distal. Absence of air in rectum

263
Q

Facial features of Down’s syndrome (x7)

A

Brushfield spots in the iris
Small ears
Upslanted palpebral features
Round face
Flat occiput
Epicanthic folds
Protruding tongue

264
Q

Non-facial features of Down’s syndrome (x4)

A

Short stature
Learning difficulties
Hypotonia
Delayed motor milestones

265
Q

Medical problems associated with Down’s syndrome

A

Congenital heart defects: Tetralogy of Fallot, AVSD, VSD, ASD
Hearing loss
Visual problems: cataracts, strabismus, keratoconus
GI problems: oesphageal/duodenal atresia, Hirschsprung’s disease, coeliac disease
Hypothyroidism
AML/ALL
Alzheimer’s disease

266
Q

When should an ambulance be called for a febrile convulsion

A

If the convulsions last longer than 5 minutes, or if recovery takes longer than 60 minutes

267
Q

Characteristic early signs of measles

A

High fever
Conjunctivitis
Koplik’s spots = white lesions on buccal mucosa (pathognomic), typically develop before rash
Irritable

268
Q

Description of the rash in measles

A

Starts behind ears –> whole body
Maculopapular rash
Flat lesions
Becomes blotchy and confluent
Desquamation typically sparing palms + soles may occur after a week

269
Q

Complications of measles

A

Otitis media - most common
Pneumonia - most common cause of death
Encephalitis - typically 1-2 weeks following onset
Subacute sclerosing panencephalitis - very rare, may present 5-10 years following illness
Febrile convulsions
Keratoconjunctivitis, corneal ulceration
Diarrhoea
Increased incidence of appendicitis
Myocarditis

270
Q

Risk factors for necrotising enterocolitis

A

Very low birth weight, or very premature
Formula feeding
Respiratory distress + assisted ventilation
Sepsis
PDA + other congenital heart disease

271
Q

Initial presentation of NEC

A

Feeding intolerance
Abdominal distension
Bloody stools
Vomiting (green bile)
Generally unwell
Absent bowel sounds

272
Q

Presentation of perforation in NEC

A

Peritonitis
Shock
Severely unwell

273
Q

Findings on AXR for NEC

A

Dilated bowel loops (often asymmetrical)
Bowel wall oedema
Intramural gas (pneumatosis intestinalis)
Pneumoperitoneum (due to perforation)
Gas in portal veins
Air both inside and outside of bowel wall (Rigler sign)
Air outlining falciform ligament (football sign)

274
Q

Management of NEC

A

Nil by mouth
IV fluids, TPN and antibiotics
NG tube may be used to drain fluid + gas
Surgical emergency (some require with medical treatment, some require removal of dead bowel tissue –> short bowel syndrome)

275
Q

What is Ebstein’s anomaly

A

‘Atrialisation’ of the right ventricle - low insertion of tricuspid valve –> large right atrium, small right ventricle –> tricuspid incompetence

276
Q

What causes Ebstein’s anomaly

A

Exposure to lithium in utero

277
Q

Features of Ebstein’s anomaly

A

Cyanosis
Prominent a-wave in distended JVP
Hepatomegaly
Tricuspid regurgitation - pansystolic murmur, worse on inspiration
RBBB (widely split S1 and S2)
May also have patent foramen ovale or atrial septal defect

278
Q

Features of pyloric stenosis

A

Hungry baby: thin, pale, failing to thrive
Projectile vomiting (strong peristalsis of stomach), typically 30 minutes after feed
Firm, round mass in upper abdomen (feels like a large olive)
Dehydration + constipation may also be present
Tends to present in first 2-4 weeks of life

279
Q

Blood gas analysis in pyloric stenosis

A

Metabolic alkalosis
Hypochloraemia
Elevated bicarbonate
Hypokalaemia

280
Q

Diagnosis of pyloric stenosis

A

Ultrasound - visualise thickened pylorus

281
Q

Management of pyloric stenosis

A

Laparoscopic pyloromyotomy = Ramstedt’s operation

282
Q

Key points of paediatric BLS

A

Open airway
Look, listen + feel for breathing: no breathing? –> give 5 rescue breaths (more likely to be resp cause)
Check for signs of circulation (brachial or femoral in infants, femoral in children)
Give chest compressions 15:2 ratio with rescue breaths
100-120/min

283
Q

Commonest causative organisms of neonatal sepsis

A

Group B streptococcus
Escherichia coli
Listeria
Klebsiella
Staphylococcus aureus

284
Q

Risk factors for neonatal sepsis

A

Vaginal GBS colonisation
GBS sepsis in previous baby
Maternal sepsis, chorioamnionitis, or fever >38
Prematurity, low birthweight
P-PROM
Prolonged rupture of membranes

285
Q

Presentation of neonatal sepsis

A

Non-specific (high degree of suspicion required)
Respiratory distress or apnoea
Tachycardia or bradycardia
Fever
Reduced tone + activity
Poor feeding
Vomiting
Hypoxia
Jaundice within 24 hours
Seizures
Hypoglycaemia

286
Q

Red flags concerning for neonatal sepsis

A

Confirmed or suspected sepsis in the mother
Signs of shock
Seizures
Term baby needing mechanical ventilation
Resp distress >4 hours after birth
Presumed sepsis in another baby (in multiple pregnancy)

287
Q

Management of neonatal sepsis

A

IV benzylpenicillin with gentamicin = first line
Monitor CRP levels (abx ceased at 48 hours if CRP <10mg/L, and negative BC at presentation and at 48 hours)
Ozygen
Normal fluid + electrolyte status

288
Q

Features of Prader-Willi syndrome

A

Constant, insatiable hunger –> obesity
Hypotonia as an infant
Learning disability
Hypogonadism
MH problems (anxiety)
Dysmorphic features: narrow forehead, almond shaped eyes, strabismus, thin upper lip, downturned mouth

289
Q

Management of Prader-Willi syndrome

A

Carefully limiting access to food/interaction with dietitians
Growth hormone - improve muscle development + body composition
MDT approach

290
Q

Causes of neonatal hypotonia

A

Neonatal sepsis
Werdnig-Hoffman disease (spinal muscular atrophy type 1)
Hypothyroidism
Prader-Willi
Maternal drugs e.g. benzodiazepines
Maternal myasthenia gravis

291
Q

Pathophysiology of Meckel’s diverticulum

A

Failure of vitelline duct to obliterate during fifth week of foetal development
Typically just proximal to ileocaecal valve –> mimics appendicitis pain
Haemodynamically unstable patient - due to substantial haemorrhage (rectal bleeding)

292
Q

Rule of 2s in Meckel’s diverticulum

A

Occurs in 2% of population
2 feet from ileocaecal valve
2 inches long

293
Q

Presentation of Meckel’s diverticulum

A

Often asymptomatic
Abdominal pain mimicking appendicitis
Rectal bleeding - most common cause of painless massive GI bleeding requiring a transfusion in children 1-2 years old
Intestinal obstruction

294
Q

Investigations of Meckel’s diverticulum

A

Investigation of choice for stable children with suspected Meckel’s –> technetium scan
Mesenteric arteriography may be used in more severe cases

295
Q

Management of Meckel’s diverticulum

A

Removal if narrow neck or symptomatic

296
Q

Presentation of laryngomalacia

A

Stridor - most common cause in infants - on inhalation
- Intermittent
- Worse when feeding, upset, lying on back, or during URTI
Peaks at arund 6 months

297
Q

Shaken baby syndrome features

A

Retinal haemorrhages
Subdural haematoma
Encephalopathy

298
Q

Exanthemas in children

A

Eruptive widespread rashes:
- Measles
- Scarlet fever
- Rubella
- Dukes’ disease
- Parovirus B19
- Roseola infantum

299
Q

Is measles a notifiable disease

A

Yes

300
Q

Causative organism/s of Scarlet fever

A

Group A streptococcus (typically associated with tonsillitis) e.g. strep pyogenes

301
Q

Features of scarlet fever

A

Red-pink, blotchy, macular rash with rough skin
Starts on trunk and spreads outwards
Fever
Red, flushed cheeks
Sore throat
Strawberry tongue
Lethargy
Cervical lymphadenopathy

302
Q

Management of scarlet fever

A

Phenoxymethylpenicillin for 10 days
Notifiable disease
Kept off school until 24 hours after starting abx

303
Q

Causative organism for hand, foot + mouth disease

A

Coxsackie A virus

304
Q

Presentation of hand, foot + mouth disease

A

Starts with URTI symptoms - tiredness, sore throat, dry cough, raised temperature
1-2 days later: small mouth ulcers appear
Red, blistering spots across body (on hands, feet, and around mouth)
Painful mouth ulcers

305
Q

Features of benign rolandic epilepsy

A

4-12 years old
Seizures characteristically occur at night
Typically partial seizures e.g. paraesthesia affecting face
Secondary generalisation may occur
Child otherwise normal, although commonly sleep-deprived
EEG - shows centro-temporal spikes
Seizures stop by adolescence

306
Q

Complications post-gastroenteritis

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain-Barre syndrome

307
Q

Features of slipped upper femoral epiphysis

A

10-15 years old
More common if obese, and if male
Hip, groin, medial thigh or knee pain
Loss of internal rotation of leg in flexion
May present acutely following trauma, or with chronic, persistent symptoms
Biltateral slip in 20% cases

308
Q

Investigation of SUFE

A

AP + Lateral (frog-leg) x-rays of hips
Displacement of femoral head epiphysis postero-inferiorly

309
Q

Management of SUFE

A

Internal fixation - single cannulated screw placed in centre of epiphysis

310
Q

Pathophysiology of Hirschsprung’s disease

A

Parasympathetic neuroblasts fail to migrate from neural crest to distal colon
–> developmental failure of parasympathetic plexuses
–> uncoordinated peristalsis
–> functional obstruction
Aganglinic section does not relax –> becomes constricted

311
Q

Features of Hirschsprung’s disease

A

3x more common in males
Associated with Down’s syndrome
Neonatal period: failure or delay to pass meconium
Older children: constipation, abdominal distension
Bilious vomiting
Lethargy
Dehydration

312
Q

Investigations for Hirschsprung’s disease

A

Abdominal X-ray
Rectal biopsy = gold standard

313
Q

Management of Hirschsprung’s disease

A

Initial: rectal washouts/bowel irrigation
Definitive: surgery to affected segment (swenson procedure –> remove section of affected bowel and anastamose remaining bowel together)

314
Q

Management of nocturnal enuresis

A

Look for possible underlying causes
General advice: fluid intake, toileting patterns
Reward systems e.g. reward using toilet to pass urine before sleep
1st line = enuresis alarm
Desmospressin - used for short-term control, or if enuresis alarm not appropriate or working

315
Q

What is Osgood-Schlatters disease

A

Osteochondrosis characterised by inflammation at the tibial tuberosity where the patella ligament inserts

316
Q

Presentation of Osgood-Schlatters diseas

A

More common in males
10-15 years
Often unilateral (can be bilateral)
Gradual onset of symptoms
Visible or palpable hard and tender lump at tibial tuberosity
Pain in anterior aspect of the knee
Pain exacerbated by physical activity, kneeling, and on extension of the knee

317
Q

Management of Osgood-Schlatters disease

A

Reduce physical activity
Ice
NSAIDs for symptomatic relief
Once symptoms settle –> stretching + physiotherapy
Symptoms will fully resolve over time - may be left with a hard, boney lump on knee

318
Q

Rare complication of Osgood-Schlatters disease

A

Avulsion fracture - tibial tuberosity separated from rest of tibia
Requires surgery

319
Q

Investigations for intussusception

A

Abdominal ultrasound - target/bull’s eye sign
Safer + less invasive than barium enema

320
Q

Congenital diaphragmatic hernia pathophysiology

A

Usually represents a failure of the pleuroperitoneal canal to close completely

321
Q

Presentation of congenital diaphragmatic hernia

A

Evidence of bowel sounds in a neonate in respiratory distress

322
Q

Risk factors for GORD

A

Preterm delivery
Neurological disorders

323
Q

Features of GORD

A

Typically develops before 8 weeks
Vomiting/regurgitation following feeds

324
Q

Management of GORD

A

Positioning during feeds
Sleeping on backs
Ensure not being overfed - trial smaller + more frequent feeds
Trial of thickened formula
Trial of alginate therapy (not at same time as thickening agents)
Trial of PPI if: unexplained feeding difficulties, distressed behaviour, faltering growth
Prokinetic agents e.g. metoclopramide, only used with specialist advice

325
Q

Complications of GORD

A

Distress
Failure to thrive
Aspiration
Frequent otitis media
In older children, dental erosion may occur

326
Q

Presentation of neonatal hypoglycaemia

A

Autonomic features e.g. irritability, jitteriness, tachypnoea, pallor
Neuroglycopenic features e.g. drowsiness and poor feeding/sucking, weak cry, hypotonia, seizures
Apnoea
Hypothermia

327
Q

Causes of persistent/severe neonatal hypoglycaemia

A

Preterm birth
Maternal diabetes mellitus
IUGR
Hypothermia
Neonatal sepsis
Inborn errors of metabolism

328
Q

Management of neonatal hypoglycaemia

A

Asymptomatic: encourage normal feeding, monitor blood glucose
Symptomatic, or very low blood glucose: admit to neonatal unit, IV infusion of 10% dextrose

329
Q

6 weeks personal + social milestone

A

Social smile - refer at 10 weeks

330
Q

3 months personal + social milestones

A

Laughs - communicates pleasure
Enjoys friendly handling

331
Q

6 months personal + social milestones

A

Not shy - curious and engaged with people

332
Q

9 months personal + social milestones

A

Shy - become cautious and apprehensive with strangers

333
Q

12 months personal + social milestone

A

Engages with others by pointing + handing objects
Waves bye-bye
Claps hands

334
Q

18 months personal + social milestones

A

Imitates activities e.g. using a phone

335
Q

2 years personal + social milestones

A

Extends interest to others beyond parents e.g. waving at strangers
Parallel play with other children
Usually dry during day

336
Q

3 years personal + social milestones

A

Seek out other children + plays with them
Bowel control

337
Q

4 years personal + social milestones

A

Has best friend
Dry by night
Dresses self
Imaginative play

338
Q

What is William syndrome

A

Neurodevelopmental disorder
Caused by a microdeletion on chromosome 7

339
Q

Features of William syndrome

A

Elfin-like facies:
Broad forehead
Starburst eyes (star-like pattern on iris)
Flattened nasal bridge
Long philtrum
Wide mouth with widely spaced teeth
Small chin
Very sociable, trusting personality
Mild LD
Short stature

340
Q

Conditions associated with William syndrome

A

Supravavlular aortic stenosis
ADHD
Hypertension
Hypercalcaemia

341
Q

Features of meconium aspiration syndrome

A

Meconium-stained liquor
Respirtory distrss at or shortly following birth
Typical features on CXR: hyperinflation, patchy opacification, and consolidation
Increased O2 requirements

Phase 3A Revision (12 decks)

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