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3a > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

What is a VSD? How big are they?

A

A congenital hole in the septum between the two ventricles.
Can vary in size from small hole to entire septum.

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2
Q

What conditions are VSDs associated with?

A

Down’s syndrome and Turner’s syndrome.

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3
Q

What type of shunt does a VSD cause and why?

A

Left to right shunt.
Due to increased left ventricular pressure compared to right.

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4
Q

What are the cyanotic and acyanotic heart defects?

A

Cyanotic - Tetralogy of Fallot, TGA, TAPVR.
Acyanotic - ASD, VSD, PDA.

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5
Q

How do VSDs present?

A

Can be asymptomatic until adulthood.
-Poor feeding, dyspnoea, tachypnoea, failure to thrive.

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6
Q

What are the risk factors of VSDs?

A

Prematurity, genetic disorders, family history.

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7
Q

Is a murmur heard in VSDs?

A

Yes:
Left lower sternal edge - pan-systolic murmur.
Thrill may be palpated too.

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8
Q

How are congenital heart defects diagnosed?

A

ECHO scans.

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9
Q

What are the differences between a small and large VSD?

A

Small - May be asymptomatic and cause no complications.
Large - May cause pulmonary hypertension, Eisenmenger’s syndrome and heart failure.

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10
Q

How are VSDs treated?

A

Corrective - Transcatheter closure or open heart surgery.
Medications - Diuretics and ACEi.

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11
Q

Give three complications of VSDs.

A

Eisenmenger’s, endocarditis, heart failure.

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12
Q

What is Eisenmenger’s syndrome?

A

When blood flows from the right side of the heart to the left across a structural heart lesion, bypassing the lungs.

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13
Q

What causes Eisenmenger’s syndrome?

A

ASD, VSD, PDA.

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14
Q

Describe the pathophysiology of Eisenmenger’s syndrome.

A

1) Septal defects allow left to right shunting.
2) Over time, this shunt causes higher pulmonary pressure and eventually pulmonary hypertension.
3) When pulmonary pressure exceeds systemic pressure, the shunt reverses to right-left (bypassing lungs and sending deoxygenated blood to body).
4) This causes cyanosis.

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15
Q

What is cyanosis?

A

The blue discolouration of skin relating to a low level of oxygen saturation in the blood.

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16
Q

Give four examination findings of pulmonary hypertension.

A

1) Raised JVP.
2) Peripheral oedema.
3) Right ventricular heave.
4) Loud P2.

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17
Q

Give four features of right to left shunts and chronic hypoxia.

A

1) Cyanosis.
2) Clubbing.
3) Dyspnoea.
4) Plethoric complexion.

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18
Q

Why does cyanosis cause a plethoric complexion?

A

Bone marrow responds to cyanosis by producing more RBCs, causing polycythaemia and a plethoric complexion.

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19
Q

What is the prognosis of Eisenmenger’s syndrome?

A

Reduces life expectancy by approximately 20 years.
Causes death by heart failure, infection and thromboembolism.

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20
Q

What is the management of Eisenmenger’s syndrome?

A

Non-reversible - heart and lung transplant is the only definitive treatment.
-Oxygen.
-Treat pul. hypertension with sildenafil.
-Treat arrhythmias.
-Treat polycythaemia with venesection.
-Prevent thrombi with anticoagulants.
-Prevent infective endocarditis with prophylactic antibiotics.

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21
Q

What condition is associated with AV septal defect?

A

Down’s syndrome.

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22
Q

What is an ASD?

A

A hole in the septum between the two atria. This connects the right and left atria allowing blood to flow between them.

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23
Q

What are the three types of ASDs?

A

-Ostium secondum - Where septum secondum fails to fully close.
-Patent foramen ovale - Where foramen ovale fails to close.
-Ostium primum - Where the septum primum fails to close (tends to lead to AV septal defects).

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24
Q

What are four causes of ASDs?

A

Family history, maternal smoking, maternal diabetes, maternal rubella.

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25
Q

What are four complications of ASDs?

A

Stroke from DVT, AF, pulmonary hypertension, Eisenmenger.

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26
Q

What is the management on ASDs?

A

Asymptomatic - watch and wait.
Symptomatic - Transcatheter correction, open heart surgery.

Anticoagulation to reduce risk of DVT.

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27
Q

How do ASDs present?

A

Dyspnoea, poor weight gain, difficulty feeding, recurrent LRTIs.
-Murmur.

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28
Q

What murmur does an ASD cause?

A

Mid-systolic, crescendo-decrescendo murmur heard loudest at upper left sternal border.

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29
Q

Are the heart sounds normal in an ASD?

A

No, there is a wide fixed split S2 sound.

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30
Q

Why is there a wide fixed split S2 sound in an ASD?

A

Blood flows from left to right atrium across the ASD, increasing volume of blood in the right ventricle has to empty before the pulmonary valve closes.

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31
Q

What is Tetralogy of Fallot?

A

Congenital condition with four co-existing conditions:
-Pulmonary stenosis.
-Right ventricular hypertrophy.
-Overriding aorta.
-VSD.

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32
Q

What is the most common cyanotic congenital heart condition?

A

Tetralogy of Fallot

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33
Q

Give four risk factors of Tetralogy of Fallot.

A

Rubella infection, increased maternal age, alcohol in pregnancy, diabetic mother.

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34
Q

Describe the pathophysiology of Tetralogy of Fallot.

A

The overriding aorta describes the aortic valve being further right and is closer to the VSD.
Pulmonary stenosis means greater resistance so blood flows through VSD, encouraging blood to go from right to left - cyanosis.

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35
Q

What is shown on a chest x-ray of Tetralogy of Fallot?

A

Boot shaped heart due to right ventricular hypertrophy.

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36
Q

When does Tetralogy of Fallot usually present?

A

Usually picked up on the antenatal scans.
-Newborn check - ejection systolic murmur.

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37
Q

How do babies with Tetralogy of Fallot present?

A

Cyanosis, clubbing, poor feeding, poor weight gain and tet spells.

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38
Q

What are tet spells?

A

Intermittent symptomatic periods where right to left shunts usually worsens causing a cyanotic episode.

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39
Q

What usually causes tet spells?

A

Precipitated by waking, physical exertion or crying.

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40
Q

How are tet spells usually treated?

A

Older children may squat (increase systemic vascular resistance).
-Oxygen, beta-blockers, IV fluids, morphine, phenylephrine.

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41
Q

What is the management of Tetralogy of Fallot?

A

Total surgical repair by open heart surgery.
-Neonates: Prostaglandin infusion to maintain ductus arteriosus.

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42
Q

What is coarctation of the aorta?

A

Narrowing of the aortic arch, usually around the ductus arteriosus.

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43
Q

What is coarctation of the aorta associated with?

A

Turner’s syndrome.

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44
Q

Describe the pathophysiology of coarctation of the aorta?

A

Narrowing of the aorta reduces blood flow to arteries that are distal to the narrowing and increases pressure proximally (heart and three branches).

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45
Q

What is often the only sign of aortic coarctation in a neonate?

A

Weak femoral pulses.

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46
Q

What can be performed if you suspect aortic coarctation and what are the results?

A

Perform a four limb blood pressure:

-Higher in arms and lower in legs usually.

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47
Q

What signs may there be of aortic coarctation?

A

Tachypnoea, poor feeding, floppy baby.

Over time: Left parasternal heave (LVH), underdevelopment of legs.

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48
Q

How is severe aortic coarctation managed?

A

Prostaglandin E to maintain ductus arteriosus and await for surgery to stent the aorta open.

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49
Q

What is transposition of the greater arteries?

A

The attachments of the aorta and pulmonary trunk are swapped.
-Right ventricle pumps blood to the aorta and the left ventricle pumps blood to the pulmonary artery.

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50
Q

When is TGA threatening and why?

A

After birth.
In the fetus, gas exchange occurs in the fetus so the lungs aren’t required.

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51
Q

Give four risk factors of TGA.

A

Increased maternal age, alcohol consumption in pregnancy, rubella and maternal diabetes.

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52
Q

What does immediate survival for TGA rely on?

A

A shunt to allow the mixing of blood:

-Patent ductus arteriosus, patent foramen ovale or VSD.

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53
Q

How does TGA present?

A

Cyanosis in the first 24hr/days of life.
-PDA, PFO or VSD may allow some mixing for a few weeks.

-Poor feeding, right ventricular heave, tachycardia, poor weight gain.

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54
Q

How is TGA diagnosed?

A

Usually on antenatal scans.

-ECHO, X-RAY and low sats.

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55
Q

How does TGA appear on an x-ray?

A

‘Egg on a string’ - Narrowed mediastinum and cardiomegaly.

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56
Q

How is TGA managed?

A

-Prostaglandins to maintain ductus arteriosus.
-Balloon septostomy to create large ASD.
-Open heart surgery and correction before 4 weeks.

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57
Q

What is a patent ductus arteriosus?

A

When the ductus arteriosus fails to close and there is a persistent connection between the aorta and pulmonary artery.

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58
Q

When does the ductus arteriosus usually close?

A

Stops functioning after 1-3 days and closes completely after 2-3 weeks.

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59
Q

What are risk factors for a PDA?

A

Prematurity, maternal rubella infection.

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60
Q

How does a PDA present?

A

Can be asymptomatic.

-Dyspnoea, tachypnoea, difficulty feeding, poor weight gain, recurrent LRTIs.

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61
Q

Is there a murmur in a PDA?

A

Yes but not always:

Continuous ‘crescendo decrescendo’ machinery murmur.

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62
Q

What is the management of PDAs?

A

ECHO monitoring until 1 year old. If not closed by itself then very unlikely by 1 year old so referral for transcatheter or open surgery to be done.
-If symptomatic then treat earlier.

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63
Q

What is Ebstein’s anomaly?

A

A congenital heart condition where the tricuspid valve is lower (towards the apex) meaning there is a larger right atrium and smaller right ventricle.

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64
Q

Describe the pathophysiology of Ebstein’s anomaly.

A

Low tricuspid valve means poor flow from the right atrium to ventricle and poor flow to pulmonary artery.

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65
Q

What is Ebstein’s anomaly associated with?

A

Wolff-Parkinson-White syndrome and ASD.

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66
Q

What is croup?

A

Acute laryngotracheobronchitis (upper) that causes oedema of the larynx.

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67
Q

Who does croup affect?

A

Children between 6 months and 2 years.

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68
Q

What causes croup?

A

Usually parainfluenza virus.
-Also, RSV, influenza and adenovirus.

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69
Q

How do children with croup present?

A

Increased work of breathing.
Barking cough.
Stridor (may be biphasic).
Hoarse voice and low grade fever.

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70
Q

Why shouldn’t you upset children with croup?

A

Crying will further narrow the airways which may be dangerous.

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71
Q

How is croup treated?

A

1) Oral dexamethasone.
2) Oxygen.
3) Nebulised budesonide.
4) Nebulised adrenaline.
5) Intubation and ventilation.

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72
Q

What is bronchiolitis?

A

Viral infection and inflammation of the bronchioles.

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73
Q

What usually causes bronchiolitis?

A

RSV.

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74
Q

Describe the epidemiology of bronchiolitis.

A

Generally affects children under 2. Most common in infants under 6 months.
-Very common in the winter.

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75
Q

Give four risk factors of bronchiolitis.

A

Breastfeeding for less than 2 months.
Chronic lung disease of prematurity.
Smoke siblings.
Older siblings who attend nursery/school.

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76
Q

How does bronchiolitis present?

A

-Coryzal symptoms (runny nose, sore throat).
-Dyspnoea and tachypnoea.
-Signs of respiratory distress.
-Reduced feeding.
-Mild fever (under 39).

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77
Q

How is bronchiolitis investigated?

A

Nasal swab for RSV.
-FBC, urine and blood gas if unwell.

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78
Q

How is bronchiolitis managed?

A

Supportive management from home - adequate intake, nasal drops, oxygen, ventilation

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79
Q

Describe the course of RSV bronchiolitis.

A

Starts as URTI with coryza.
-Half get better.
-Half get chest symptoms 1-2 days after with peak symptoms 3-4 days after with symptoms lasting 7-10 days.

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80
Q

Which infants are considered high risk in bronchiolitis?

A

Ex-premature babies and those with congenital heart defects.

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81
Q

What is given to high risk babies with bronchiolitis?

A

Palivizumab - monoclonal antibody against RSV that reduces the severity of the infection.

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82
Q

What are the signs of respiratory distress?

A

1) Raised respiratory rate.
2) Use of accessory muscles (sternocleidomastoid, abdominal and intercostal muscles).
3) Intercostal and subcostal recessions.
4) Nasal flaring.
5) head bobbing.
6) Tracheal tugging.
7) Cyanosis.
8) Abnormal breathing noises.

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83
Q

Give three abnormal breathing noises.

A

Wheezing, stridor and grunting.

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84
Q

What is wheezing?

A

An abnormal breathing sound caused by narrowing of the airways (whistling during expiration).

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85
Q

What is stridor?

A

High pitched inspiratory noise caused by obstruction of the airways (can be expiratory and biphasic).

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86
Q

What is grunting?

A

Abnormal breathing noise caused by exhaling with the glottis partially closed due to increase positive end-expiratory pressure.

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87
Q

Give seven criteria for hospital admission with bronchiolitis.

A

1) Aged under 3 months or any pre-existing condition (Down’s, prematurity, CF).
2) Resp rate above 60.
3) Clinical dehydration.
4) 50-75% reduced milk intake.
5) O2 sats below 92%.
6) Moderate to severe respiratory distress.
7) Apnoeas.

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88
Q

What is the difference between mild, moderate and severe respiratory distress?

A

Mild: Normal behaviour, normal talking, normal/slight increase of RR, HR, no signs of respiratory distress.

Moderate: Slight irritability, some talking limitation, increased RR, moderate recessions/accessory muscle use, mildly increased HR.

Severe: Increased irritability, marked limitation of talking, increased of markedly reduced RR, marked increase of accessory muscles with prominent recessions, sats less than 92%, significant tachycardia/bradycardia, cyanosis.

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89
Q

What is pneumonia?

A

Infection of the lung parenchyma which leads to inflammation and consolidation.

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90
Q

Describe the epidemiology of pneumonia in children.

A
  1. Viral pneumonia more common in winter.
    2) Viral pneumonia more common in younger children.
    3) Bacterial pneumonia more common in older children.
    4) Highest incidence in infants.
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91
Q

Give the viral causes of pneumonia.

A

RSV (mc), parainfluenza and influenza.

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92
Q

Give the bacterial causes of pneumonia.

A

Strep. pnuemoniae - most common.
Group B strep - most common in neonates.
H. influenzae - affects pre or unvaccinated children.
Mycoplasma - atypical bacteria on the rise.

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93
Q

How does pneumonia usually present?

A

Wet, productive cough with a high fever.
-Tachypnoea, tachycardia, increased work of breathing and lethargy.

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94
Q

Give six signs that may be present in pneumonia that indicate underlying sepsis.

A

Tachypnoea, tachycardia, hypoxia, hypotension, fever, confusion.

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95
Q

Give four characteristic chest findings of pneumonia.

A

1) Bronchial breath sounds (equally loud on inspiration and expiration).
2) Focal coarse crackles.
3) Dullness to percussion.
4) Reduced focal air entry.

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96
Q

How is pneumonia investigated?

A

Mainly clinical.
-Chest XR and sputum cultures.

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97
Q

What is the management of pneumonia?

A

Home: Analgesia and supportive management.
Hospital: IV fluids and antibiotics.

-Usually amoxicillin +/- a macrolide (clarythromycin/erythromycin).
-Penicillin allergy -> Monotherapy with macrolide.

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98
Q

What six tests can be done for children with recurrent LTRIs?

A
  1. Chest X-RAY.
  2. FBC for WCC.
  3. Serum Ig for antibody deficiency.
  4. Test IgG to previous vaccines.
  5. Sweat test for CF.
  6. HIV test.
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99
Q

What is whooping cough?

A

An URTI caused by the Bordetella pertussis bacteria (gram -ve).

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100
Q

Why is whooping cough called whooping cough?

A

The coughing sounds like ‘whooping’ as the coughing fits are so severe the child is unable to take in any air between coughs so there is a sharp suck of air (whoop).

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101
Q

How is whooping cough prevented?

A

There is a vaccination programme for children and pregnant women.

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102
Q

How does whooping cough present?

A

-Catarrhal phase (1-2w): Coryzal symptoms, low grade fever.
-Paroxysmal phase (3-6w): Inspiratory whooping cough.
-Convalescent phase: Downgrade of cough (up to 3m).

Cough is worse at night and can be so severe it causes vomiting, faint or even pneumothorax.

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103
Q

How is whooping cough diagnosed?

A

Nasopharyngeal/nasal swab for pertussis.
Anti-pertussis toxin IgG.

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104
Q

Who needs to be notified of whooping cough cases?

A

Public health England.

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105
Q

What is the management of whooping cough?

A

Macrolides can be beneficial in the early stages.
Alternative: Co-trimoxazole.

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106
Q

What is given to close contacts of those with whooping cough?

A

Prophylactic antibiotics IF vulnerable (pregnant, unvaccinated children, health workers).

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107
Q

What is a key complication of whooping cough?

A

Bronchiectasis.

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108
Q

What is asthma?

A

Chronic inflammatory airway disease with reversible paroxysmal constriction of the airways with inflammatory exudate.

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109
Q

What is atopy?

A

The conditions asthma, eczema and hay fever. These are hypersensitive conditions where a patient with one of them are more likely to have another one of them.

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110
Q

What are the causes of asthma?

A

Genetic, premature, low birth weight, parental smoking, allergen exposure.

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111
Q

Describe a presentation suggesting asthma.

A

Episodic wheeze with intermittent exacerbations with diurnal variability (worse at night/early morning).
-Dry cough with SOB.

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112
Q

Give six typical triggers of asthma.

A

Dust, animals, cold air, exercise, smoke and food allergens.

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113
Q

Do bronchodilators help asthma?

A

Yes, asthma is reversible with salbutamol.

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114
Q

How is asthma diagnosed?

A

Spirometry:
-FEV1 reduced, FVC normal, ratio may be <0.7 with reversibility.
Peak flow variability.

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115
Q

State the long term management of asthma of children under 5.

A

1) SAB2A PRN.
2) Add a low dose ICS or monteleuksat.
3) Use all three.

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116
Q

State the long term management of asthma in children between age 5 and 12.

A

1) SAB2A PRN.
2) Add low dose ICS (beclomethasone).
3) Add LAB2A (salmeterol).
4) Titrate ICS up. Consider adding LTRA (montelukast).
5) Increase ICS dose.

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117
Q

State the long term management of asthma in children over 12 (same as adults).

A

1) SAB2A PRN.
2) Add ICS.
3) Add LAB2A.
4) Titrate ICS up to medium dose and consider adding LTRA.
5) Titrate ICS to high dose.
6) Add oral steroids.

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118
Q

What is a side effect of inhaled corticosteroids in children?

A

Stunting growth and reduce adult height. Dose-dependent so is less of a problem with smaller doses.

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119
Q

How does an acute exacerbation of asthma present?

A

Progressively worsening SOB, signs of respiratory distress, tachypnoea.
-Widespread expiratory wheeze.
-Reduced air entry.

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120
Q

What is an ominous sign of asthma?

A

A silent chest.

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121
Q

What are the features of moderate asthma exacerbation?

A

Peak flow above 50% predicted.
Normal speech and no other features.

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122
Q

What are the severe features of asthma exacerbation?

A
  1. Peak flow less than 50% predicted.
  2. Saturations less than 92%.
  3. Unable to complete sentences.
  4. Signs of respiratory distress.
  5. Tachypnoea and tachycardia.
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123
Q

What are the features of life threatening asthma exacerbation?

A
  1. Peak flow less than 33% predicted.
  2. Saturations less than 92%.
  3. Exhaustion, poor respiratory effort.
  4. Hypotension.
  5. Silent chest.
  6. Cyanosis.
  7. Confusion/altered consciousness.
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124
Q

How are mild asthma exacerbations managed?

A

Outpatient regular salbutamol inhaler.

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125
Q

How are moderate to severe asthma exacerbations managed?

A
  1. Salbutamol inhalers regular.
  2. Nebulisers with salbutamol/ipratropium bromide.
  3. Oral prednisolone.
  4. IV hydrocortisone.
  5. IV magnesium sulphate.
  6. IV salbutamol.
  7. IV aminophylline.
  8. Intubation and ventilation.
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126
Q

What is a viral-induced wheeze?

A

An acute wheezy illness caused by a viral infection.
-Small children have narrow airways that are further narrowed when a virus is encountered which causes a wheeze.

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127
Q

What is the difference between viral induced wheeze and asthma?

A

Generally, viral wheeze:
-Presents before age 3.
-No atopic history.
-Only occurs during viral infections.

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128
Q

How does a viral induced wheeze present?

A

Evidence of viral illness (fever, cough, coryza) which precedes:
-SOB, resp distress and expiratory wheeze throughout the chest.

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129
Q

Does asthma or viral induced wheeze cause a focal wheeze?

A

Neither - both cause widespread.
Focal will be caused by foreign body or tumour.

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130
Q

How is viral induced wheeze managed?

A

Same as acute asthma:
-SABA inhaler, ICS and LTRA.

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131
Q

What is respiratory distress syndrome?

A

Affects premature neonates (below 32w) before the lungs start producing surfactant.

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132
Q

Describe the the pathophysiology of respiratory distress syndrome?

A

Inadequate surfactant leads to high surface tension within alveoli leading to atelectasis as it is more difficult for the alveoli and lungs to expand.
-Leads to inadequate gaseous exchange and hypoxia, hypercapnia and respiratory distress.

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133
Q

How is respiratory distress syndrome managed?

A

-Dexamethasone given to mothers.
-Intubation and ventilation.
-Endotracheal surfactant (delivered to lungs).
-CPAP via nasal mask.
-Supplementary oxygen.

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134
Q

Give six short term complications of RDS.

A

Pneumothorax, infection, apnoea, pulmonary haemorrhage, intraventricular haemorrhage, necrotising enterocolitis.

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135
Q

Give three long term complications of RDS.

A

Chronic lung disease of prematurity.
Retinopathy of prematurity.
Neurological, hearing and visual impairment.

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136
Q

What is chronic lung disease of prematurity?

A

Infants of 36 weeks gestational age who still require oxygen after having RDS.

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137
Q

How is CLDP diagnosed?

A

Based on chest x-ray changes (widespread opacification, fibrosis and lung collapse.
-Lung damage comes from oxygen toxicity and artificial ventilation.

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138
Q

Give five features of CLDP.

A
  1. Low oxygen saturations.
  2. Increased work of breathing.
  3. Poor feeding and poor weight gain.
  4. Crackles and wheeze.
  5. Increased susceptibility to infection.
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139
Q

How is CLDP prevented before childbirth?

A

Mothers are given corticosteroids that show signs of premature labour which speeds up the development of the fetal lungs to reduce the risk of CLPD.

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140
Q

How is the risk of CLDP reduced in a neonate?

A
  1. Using CPAP rather than intubation and ventilation.
  2. Using caffeine to stimulate respiratory effort.
  3. Not over-oxygenating.
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141
Q

What do babies with CLDP need protection from and how is it achieved?

A

RSV and bronchiolitis.
-Palivizumab injections monthly.

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142
Q

What usually kills babies with CLDP?

A

Severe cases may be fatal due to recurrent infections or pulmonary hypertension.

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143
Q

What is primary ciliary dyskinesia?

A

Autosomal recessive condition affecting the cilia of various cells in the body.
-Most commonly motile cilia of the respiratory tract.

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144
Q

Describe the pathophysiology of primary ciliary dyskinesia.

A

Leads to a buildup of mucus in the lungs that provides an easy area for infection leading to recurrent infections, poor growth and bronchiectasis.
-Also affects cilia of fallopian tubes and flagella of sperm - infertility.

145
Q

Which populations is primary ciliary dyskinesia more common in?

A

Populations with greater consanguinity.

146
Q

What is strongly linked to primary ciliary dyskinesia?

A

Situs inversus.

25% with situs inversus have PCD and 50% with PCD have situs inversus.

147
Q

How is PCD diagnosed and managed?

A

Diagnosis - Sample of ciliated epithelium.
-Consanguinity, CXR, semen analysis.

Management - Similar to CF and bronchiectasis (daily physio, high calorie diet, antibiotics).

148
Q

What is laryngomalacia?

A

A condition affecting infants where the supraglottic larynx is structured so that is allows partial airway obstruction and causes stridor.
-The supraglottic larynx is ‘floppy’ and is more floppy during inspiration.

149
Q

How does laryngomalacia present?

A

Occurs in infants at around 6 months with an inspiratory stridor.
-May cause difficulty feeding but isn’t associated with respiratory distress.

150
Q

What is the management of laryngomalacia?

A

The problem usually resolves by itself as the larynx matures and grows.
-Tracheostomy is rarely required.

151
Q

What is cystic fibrosis?

A

Autosomal recessive condition that affects the mucous glands of the body.

152
Q

Describe the pathophysiology of cystic fibrosis.

A

Auto rec condition of the CFTR gene on chromosome 7. Most commonly mutations in the chloride channels.
Results in:
1. Thick pancreatic and biliary secretions.
2. Low volume thick airway secretions.
3. Congenital bilateral absence of the vas deferens.

152
Q

How does CF present?

A

Newborn blood spot test.
-Meconium ileus is often the first sign (meconium doesn’t pass in 24h).
-If not diagnosed at birth then children will present with recurrent LRTIs, failure to thrive or pancreatitis.

153
Q

What are the symptoms of CF?

A

Chronic cough with thick sputum and recurrent LRTIs.
Abdominal pain, bloating and steatorrhoea.
Salty skin.

154
Q

Give five signs of CF.

A

Low weight/height, nasal polyps, clubbing, crackles/wheeze, abdominal distension.

155
Q

How is CF diagnosed?

A

-Sweat test is gold standard.
-Newborn blood spot test.
-CFTR genetic testing (amniocentesis or chorionic villous sampling).

156
Q

Describe the sweat test for CF.

A

Pilocarpine applied to skin and electrodes attach to make the skin sweat - Sweat absorbed with gauze and sent for testing.
Positive - >60mmol/L.

157
Q

What are the two key colonisers in people with CF?

A

Staph aureus and pseudomonas.

158
Q

Why is pseudomonas colonisation in patients with CF bad? How is it prevented and managed?

A

Difficult to get rid of as often resistant to antibiotics, will increase morbidity and mortality.
-Prevented by not allowing children with CF to mix.
-Treated with nebulised tobramycin and oral ciprofloxacin.

159
Q

How is CF managed?

A
  1. Chest physio.
  2. Exercise.
  3. High calorie diet.
  4. Pancreatic enzyme replacement.
  5. Prophylactic flucloxacillin.
  6. Bronchodilators.
  7. Nebulised DNase to break down secretions.
  8. Vaccinations.
160
Q

What monitoring is required in patients with CF?

A

Sputum cultures for pseudomonas, screening for diabetes, osteoporosis, vitD deficiency and liver failure.

161
Q

Describe the prognosis of patients with CF.

A

Life expectancy - 47.
-90% develop pancreatic insufficiency.
-50% develop diabetes.
-30% develop liver disease.
-Most males infertile.

162
Q

What is pyloric stenosis?

A

When there is hypertrophy of the pyloric sphincter which leads to narrowing (between stomach and duodenum).
-There is increased peristalsis of the stomach to push the stomach contents through the tighter gap and eventually food will go into the oesophagus and will cause projectile vomiting.

163
Q

How does pyloric stenosis present?

A

A thin baby that is failing to thrive with projectile vomiting in the first few weeks of life.

164
Q

What may be felt on examination in a baby with pyloric stenosis?

A

An olive shaped mass in the upper abdomen caused by hypertrophy of the pylorus.

165
Q

What is seen on a blood gas in pyloric stenosis?

A

Hypochloric metabolic alkalosis as the baby is vomiting HCl.

166
Q

What is the management of pyloric stenosis?

A

-Diagnosis is made by abdominal ultrasound.
-Treatment: Laparoscopic pylorotomy (Ramstedt’s operation).

167
Q

Describe the vomiting in pyloric stenosis.

A

Non bilious, forceful projectile vomiting 30 mins after eating,

168
Q

What is Hirschsprung’s disease?

A

A congenital condition where the nerve cells of the myenteric plexus are absent in the distal bowel and ileum.

169
Q

What is the pathophysiology of Hirschsprung’s disease?

A

The absent myenteric plexus in the bowel and ileum means that peristalsis cannot be stimulated where it is absent.
-Absence of parasympathetic ganglion cells.
-No peristalsis and always constricted - leads to loss of movement of faeces and causes obstruction.

170
Q

When Hirschsprung’s disease affects the entire colon what is it called?

A

Total ganglionic aganglionosis.

171
Q

What four syndromes is Hirschsprung’s disease associated with?

A

Down’s, neurofibromatosis, Waardenburg syndrome, MEN2.

172
Q

How does Hirschsprung’s disease present?

A

Delayed passing of meconium (24hr), abdominal pain and distention, bilious vomiting, constipation, poor feeding and failure to thrive.

173
Q

What is Hirschsprung’s-associated enterocolitis?

A

HAEC is inflammation and obstruction that occurs in 20% of neonates with Hirschsprung’s. It is life threatening and can lead to toxic megacolon and bowel perforation.

174
Q

How does HAEC present?

A

It typically presents 2-4 weeks after birth with fever, abdominal distension, diarrhoea and sepsis features.

175
Q

How is HAEC managed?

A

Urgent fluid resuscitation, antibiotics and bowel decompression.

176
Q

What is the management of Hirschsprung’s disease?

A

Rectal biopsy - confirms diagnosis by demonstrating the absence of parasympathetic ganglia.
Abdominal xray - helpful at looking for HAEC.

177
Q

What is definitive management of Hirschsprung’s disease?

A

Surgical removal of the aganglionic section of the bowel.

178
Q

What is intussusception?

A

When one piece of bowel telescopes inside itself, thickening the size of the bowel and narrowing the lumen. This leads to bowel ischaemia and infarction.

179
Q

What is the most common site for intussusception to occur?

A

Distal ileum and the ileocaecal junction.

180
Q

What is the most common cause of bowel obstruction in neonates?

A

Intussusception.

181
Q

What is the epidemiology of intussusception?

A

Occurs in children from 3 months to 3 years, most commonly under 1 year old.

182
Q

What five conditions are associated with intussusception?

A

Concurrent viral illnesses, HSP, CF, Meckel’s diverticulum and interstitial polyps.

183
Q

How does intussusception present?

A

Redcurrant jelly stools with a sausage shaped mass in the RUQ.
-Severe colicky abdo pain, vomiting, obstruction.
-Pale, lethargic unwell child.

184
Q

How is intussusception diagnosed?

A

Ultrasound or contrast enema.

185
Q

How is intussusception managed?

A

-Therapeutic enemas to try and reduce the intussusception.
-Corrective surgery if enema is unsuccessful.
-If gangrenous then surgical resection.

186
Q

What are four complications of intussusception?

A

Obstruction, gangrenous bowel, perforation and death.

187
Q

What is necrotising enterocolitis?

A

A life threatening disease affecting neonates where the bowel becomes necrotic.
-This may lead to perforation, peritonitis and shock.

188
Q

What are five risk factors for necrotising enterocolitis?

A

Very premature/low birth weight.
Formula feeds.
Respiratory distress and ventilation.
Sepsis.
PDA and congenital heart disease.

189
Q

How does necrotising enterocolitis present?

A

-Vomiting with bile, bloody stools.
Food intolerance, distended abdomen with absent bowel sounds.

190
Q

What investigations are there for necrotising enterocolitis?

A

Bloods - FBC, CRP, gas and cultures.
Abdominal x-ray:
-Pneumoperitoneum and pneumatosis intestinalis.
-Rigler’s sign, dilated and distended bowel.

191
Q

What is the management of necrotising enterocolitis?

A

Nil by mouth, IV fluids, antibiotics.
NG tube to drain fluid and gas from bowel.
-May have to remove necrotic portion of bowel.

192
Q

Give complications of necrotising enterocolitis.

A

Short bowel syndrome, peritonitis, shock and death.

193
Q

What is biliary atresia?

A

Congenital condition where the bile duct is narrowed or absent which results in cholestasis.

194
Q

What are the different types of biliary atresia?

A

Type 1 - Bile duct is gone.
Type 2 - Atresia of cystic duct in porta hepatis.
Type 3 - MC. Atresia of right and lefts ducts at level of porta hepatis.

195
Q

How does biliary atresia present?

A

Significant persistant jaundice after 2 weeks (term, 3 weeks in preterm).
-Dark urine and pale stools

196
Q

How is biliary atresia investigated?

A

Measuring both conjugated and unconjugated bilirubin levels.
-In biliary atresia, a high proportion of the bilirubin tends to be conjugated.

197
Q

What is the management of biliary atresia?

A

Kasai portoenterostomy - attaching a section of small intestine to liver opening.
Often a liver transplant is required.

198
Q

What is constipation in children?

A

Very common problem that is ‘functional’ with reduced stools, increased hardness and painful defecation.

199
Q

How does constipation present?

A

Less than 3 stools per week that are hard, ‘rabbit droppings’, abdominal pain, rectal bleeding, overflow soiling.

200
Q

What is encopresis?

A

Faecal incontinence - not pathological until age 4.
-Sign of chronic constipation where rectum becomes stretched and loses sensation.

201
Q

Give five lifestyle factors for constipation.

A

Habitually not opening bowels.
Low fibre diet.
Poor fluid intake and dehydration.
Sedentary lifestyle.
Psychosocial factors.

202
Q

Why does ignoring bowel habit cause constipation?

A

Over time, they lose the sensation of a full rectum, defecate less frequently and retain faeces in rectum which causes impaction, further worsening the constipation.

203
Q

What are some secondary causes of constipation?

A

Hirschsprung’s
Cystic fibrosis
Obstructions
Sexual abuse
Hypothyroidism

204
Q

Give eight red flags of constipation.

A

Not passing meconium within 48 hours of birth.
Neurological signs or symptoms.
Vomiting.
Acute severe abdominal pain and bloating.
Abnormal anus.
Abnormal back or buttocks.
Ribbon stool.
Failure to thrive.

205
Q

Give five complications of constipation.

A

Pain
Reduced sensation
Anal fissures
Haemorrhoids
Overflow soiling

206
Q

What is the management of constipation?

A

Idiopathic constipation can be diagnosed clinically - correct reversible risk factors.
-Start laxatives (Movicol).
-May need disimpactation regime (high dose laxatives).
-Encourage visiting toilet.

207
Q

What is epiglossitis?

A

Inflammation and swelling of the epiglottis caused by an infection, usually H. influenzae B.
-Can be life threatening as throat may close.

208
Q

How does epiglossitis present?

A

Tripod position with drooling, stridor and sore throat.
-Fever, muffled voice, painful swallowing.
-Scared and unwell child.
-Septic and unwell appearance.

209
Q

What are the investigations for epiglossitis?

A

Lateral CXR - Thumb sign.
-Don’t examine throat.

210
Q

What is the management on epiglossitis?

A

Ensure airway is secure, don’t upset child.
-Oxygen, nebulised adrenaline, steroids.
-Antibiotics (ceftriaxone) - 3rd gen cephalosporins.

211
Q

What is the prognosis of epiglossitis?

A

Most children don’t require intubation, those who are extubated fully recover.

212
Q

What is a key complication of epiglossitis?

A

Epiglottic abscess.

213
Q

What is otitis media? How is it caused?

A

An infection of the middle ear.
-Bacteria usually enter via eustachian tube and is usually preceded by viral URTI.

214
Q

What are the common causes of otitis media?

A

MC - Strep pneumoniae.
Others - H. influenzae, S. aureus.

215
Q

How does otitis media present?

A

Ear pain, reduced hearing.
-Fever, cough, coryzal symptoms and sore throat.

-May be vertigo and ear discharge.

216
Q

How does otitis media present in young children and infants?

A

Very non-specific:
-Fever, vomiting, irritability, lethargy and poor feeding.

217
Q

In otitis media, what does an ENT examination show?

A

Bulging, red, inflamed membrane.
-If perforated you may see discharge and a hole in the tympanic membrane.

218
Q

What is the management of otitis media?

A

Analgesia and antibiotics:
-5 days amoxicillin or erythromycin/clarythromycin.

219
Q

What are some complications of otitis media?

A

Recurrence, perforation, hearing loss, glue ear.

220
Q

What is glue ear?

A

Otitis media with effusion. The middle ear is full of fluid and there is hearing loss.

221
Q

How is glue ear treated?

A

Grommets - allow fluid to drain out of ear canal.

222
Q

What is a squint?

A

Misalignment of the eyes - strabismus.
-As they are misaligned, the images on the retina will not match and the patient will experience double vision.

223
Q

What is the pathophysiology of a squint?

A

When a squint occurs in childhood, the connections to the brain aren’t fully established so the brain will reduce the signal from the less dominant eye.
-This results in one dominant eye and a lazy eye. If this isn’t treated, it will progressively worsen - amblyopia.

224
Q

What is a concomitant squint?

A

Due to differences in control of the extraocular muscles.

225
Q

What is a paralytic squint?

A

A rare squint where there is paralysis in one or more of the extra ocular muscles.

226
Q

Define esotropia and exotropia.

A

Esotropia - Inward positioned squint.
Exotropia - Outward positioned squint.

227
Q

Define hypertropia and hypotropia.

A

Hypertropia - Upward moving affected eye.
Hypotonia - Downward moving affected eye.

228
Q

What are the causes of squint?

A

Idiopathic.
Others - Hydrocephalus, cerebral palsy, trauma, space occupying lesions.

229
Q

How is a squint examined?

A

General inspection, eye movements, fundoscopy and visual acuity.

230
Q

What are two special tests for a squint?

A

Hirschberg’s test - Shine pen torch from 1m. Observe reflection on cornea which should be central and symmetrical. Deviation - squint.

Cover test - Cover one eye and focus on an object. Move cover across to opposite eye and watch movement on previously covered eye. Drifts inwards (esotropia) or exotropia (outwards).

231
Q

How is a squint managed?

A

The treatment must begin before age 8 as the visual fields are still developing - earlier is better.
-Occlusive patch used to cover good eye and force weak eye to develop.
-Atropine drops may be used in good eye to blur the vision so the bad eye is forced to develop.

232
Q

What is periorbital cellulitis and how does it present?

A

An eyelid and skin infection in front of the orbital septum.
Presents with swollen, hot and red skin around the eyelid and eye.

233
Q

What must be differentiated from periorbital cellulitis?

A

Orbital cellulitis as this is a sight and life threatening emergency.

234
Q

How is periorbital cellulitis diagnosed and treated?

A

CT sinus and orbits with contrast will differentiate periorbital and orbital cellulitis.
-Treated with systemic antibiotics.

235
Q

What is orbital cellulitis, how does it present and how is it treated?

A

An infection around the eyeball involving the muscles and tissues behind the orbital septum.
Presents with pain on eye movement, reduced eye movement, vision changes and proptosis.
Treated via IV antibiotics and may require drainage.

236
Q

What is a febrile convulsion?

A

Seizures that occur in children with a high fever between age 6m and 5y.

237
Q

What is the difference between a simple and complex febrile convulsion?

A

Simple - Generalised tonic-clonic seizures that are less than 15 minutes and in a single febrile illness.

Complex - When they consist of partial or focal seizures, last more than 15 minutes or occur multiple times during the same febrile illness.

238
Q

How is a febrile convulsion diagnosed?

A

Exclude other neurological pathology:
-Epilepsy, meningitis, encephalitis, space occupying lesions, syncope, electrolyte abnormalities, trauma.

239
Q

How are febrile convulsions managed?

A

Identify source of infection and and control fever with paracetamol.
-Reassure parents and educate, stay with the child in a safe place, call ambulance if concerned.

240
Q

What is the prognosis after a febrile convulsion?

A

A higher risk of developing epilepsy in the future.

241
Q

What is epilepsy? What are seizures?

A

Umbrella term for a condition where there is a tendency to have seizures.
-A seizure are transient episodes of abnormal electrical activity in the brain.

242
Q

What is a generalised tonic clonic seizure?

A

Loss of consciousness with muscle stiffness and jerking.
-Associated with incontinence, tongue biting, groaning and irregular breathing.
-Usually prolonged post-ictal period where they’re drowsy, irritable and low.

243
Q

What are focal seizures?

A

Seizures that begin in the temporal lobe that affect hearing, speech, memory and emotion.
-Present with hallucinations, memory flashbacks, deja vu and doing strange things.

244
Q

What are absence seizures? What is the prognosis?

A

Typically occur in children where the patient becomes blank, stare into space and then return to normal.
-Typically unaware of surroundings and won’t respond.
-Children typically outgrow this.

245
Q

What is an atonic seizure?

A

‘Drop attacks’ - Lapses in muscle tone.
-Don’t last more than 3 minutes.

246
Q

What condition may atonic seizures be a sign of?

A

Lennox-Gastaut syndrome.

247
Q

What is a myoclonic seizure?

A

Present as sudden muscle twitching like a sudden drop.
-Typically remain awake.

248
Q

What are infantile spasms? What is the prognosis and treatment?

A

West syndrome - rare condition that starts at around 6 months and has clusters of body spasms.
-1/3rd die by 25, 1/3rd seizure free.
-Prednisolone and vigabatrin.

249
Q

What is the management for generalised tonic clonic seizures?

A

1st - sodium valproate.
2nd - Lamotrigine or carbamazepine.

250
Q

What is the management for focal seizures?

A

1st - Carbamazepine or lamotrigine.
2nd - Sodium valproate.

251
Q

What are the investigations are used for epilepsy?

A

EEG and brain MRI - look at electrical activity and visualise brain.
-Other to exclude causes - ECG, electrolytes, glucose.

252
Q

What general advice is given to those with epilepsy?

A

Take showers instead of baths, be cautious with swimming, heights and traffic.

253
Q

How does sodium valproate work? What are the side effects?

A

Inhibiting GABA, relaxing brain.
-Teratogenic, liver damage, hair loss and tremor.

254
Q

How do you manage seizures?

A

Put patient in a safe position, in the recovery position, with a pillow, remove obstacles that would cause harm, time the seizure and call ambulance if it lasts longer than 5 minutes.

255
Q

What is status epilepticus?

A

A seizure lasting more than 5 minutes or 2 or more seizures without regaining consciousness.

256
Q

What is the management of status epilepticus?

A

ABCDE - Secure airway, give high concentration oxygen, assess cardiac and resp function.
-Check blood glucose, gain IV access.
-Give IV lorazepam. If it persists, give IV phenytoin/phenobarbital.

257
Q

What is cerebral palsy?

A

Permanent neurological problems resulting from damage to the brain around birth.
-It is not progressive and there is a huge variation in the severity of symptoms.

258
Q

What are the causes of cerebral palsy?

A

Antenatal - Maternal infections, trauma.
Perinatal - Asphyxia, prematurity.
Postnatal - Meningitis, severe neonatal jaundice, head injury.

259
Q

What are the types of cerebral palsy?

A

Spastic, dyskinetic, ataxic and mixed.

260
Q

What is spastic cerebral palsy?

A

Hypertonia and reduced function resulting from damage to UMN.

261
Q

What is dyskinetic cerebral palsy?

A

Problems controlling muscle tone with hypertonia and hypotonia causing athetoid and oro-motor problems due to damage to basal ganglia.

262
Q

What are athetoid movements?

A

Slow, continuous, involuntary writhing movements that prevents the maintenance of a stable posture.

263
Q

What is ataxic cerebral palsy?

A

Problems with coordinated movements due to damage in the cerebellum.

264
Q

What is mixed cerebral palsy?

A

A mix of spastic, dyskinetic and ataxic CP.

265
Q

What are the four patterns of cerebral palsy?

A

Monoplegia - One limb.
Hemiplegia - One side of body.
Diplegia - Four limbs affected but mostly legs.
Quadriplegia - Four limbs affected more severely often with seizures, speech disturbances and other impairments.

266
Q

How does cerebral palsy present?

A

Difficult to predict the extent of CP but will usually become more evident during development:
-Failure to meet milestones.
-Hypertonia/hypotonia.
-Hand preference below 18 months.
-Problems with speech, coordination or walking.
-Feeding or swallowing difficulties.
-Learning difficulties.

267
Q

What are the four signs of UMN lesions?

A

Muscle bulk preserved, hypertonia, slightly reduced power, brisk reflexes.

268
Q

What are the complications and associated conditions of CP?

A

Learning disability, epilepsy, kyphoscoliosis, muscle contractures, hearing/visual impairment and GORD.

268
Q

How is CP managed?

A

MDT approach: Physios, occupational therapy, SALT, dieticians, orthopaedics, paediatricians.

268
Q

What are the four signs of LMN lesions?

A

Reduced muscle bulk with fasciculations, hypotonia, dramatically reduced power with reduced reflexes.

269
Q

What is muscular dystrophy?

A

An umbrella term for conditions that cause gradual weakening and wasting of the muscles.

270
Q

What are the main types of muscular dystrophy?

A

Duchenne muscular dystrophy and Becker’s muscular dystrophy.

271
Q

What is Gower’s sign?

A

A sign of proximal muscle weakness when a child standings from sitting down/squatting.
-Their pelvic muscles aren’t strong enough to allow them to stand from sitting.
-They get onto hands and knees, push their hips up and back, shift weight backwards with hands on knees then will keep their legs straight and walk their hands up their legs to stand.

272
Q

What is the management on muscular dystrophy?

A

No curative treatment - aim is to preserve quality of life for the longest time possible.
-Physio, occupational therapy and medical management.

273
Q

What is Duchenne muscular dystrophy?

A

X-linked recessive gene defect for dystrophin that leads to progressive muscle weakness in young boys aged 3-5y.
This affects skeletal muscles first then lungs, heart and diaphragm eventually.

274
Q

Describe the pathophysiology of DMD.

A

Dystrophin is a protein that holds muscles together on a muscular level. Without dystrophin, too much calcium enters myocytes and resulting in oxidative stress and cell death.

274
Q

What is the prognosis of DMD?

A

Usually in wheelchair by teen years and fatal by age 25-30.

275
Q

Why does DMD usually exclusively affect boys?

A

X-linked and males have only one X chromosome whereas females have two.
-If the mother is a carrier, there is a 50% chance of a girl being a carrier and a 50% chance of having the condition if male.

276
Q

What investigations are done in muscular dystrophy?

A

Raised CK in blood, genetic testing, muscle biopsy and positive Gower’s sign.

277
Q

Why are corticosteroids used in DMD?

A

Aggressively used below aged 10 as it can convert a Duchenne picture to a Becker’s picture.

278
Q

How does muscular dystrophy present?

A

Usually between aged 3-5 there is an abnormal gait with a positive Gower’s sign.
-Trouble getting upstairs and on chairs.
-Clumsiness and waddling gait.
-Difficulty with motor skills.

279
Q

What is eczema?

A

Chronic atopic condition caused by continuity of skin barrier , leading to inflammation in the skin.

280
Q

Can eczema be inherited?

A

There is a genetic component to eczema and it usually runs in families but there is no single inheritance pattern.

281
Q

What is the pathophysiology of eczema?

A

Defects in the barrier of the continuity of skin with gaps. This allows irritants, microbes and allergens in, creating an immune response and resulting in inflammation.

282
Q

How does eczema present?

A

In infancy with dry, red, itchy skin with sore patches over the flexor surfaces (inside of elbows and knees) and on face and neck.
Eczema is usually episodic and has flare ups.

283
Q

What is the management of eczema?

A

-Maintenance - emollients (E45).
-Flare ups - thicker emollients or topical steroids (hydrocortisone).
-Other specialist treatments - oral corticosteroids/methotrexate.

284
Q

What is eczema herpeticum?

A

Viral skin infection in patients with eczema caused by HSV or VZV.

285
Q

What is Stevens-Johnson syndrome?

A

A disproportional immune response causing epidermal necrosis resulting in blistering and shedding of the top layer of skin (less than 10% of body surface area).

286
Q

What causes SJS?

A

Medications: anti-epileptics, antibiotics, allopurinol, NSAIDs.

Infections: HSV, mycoplasma, CMV, HIV.

287
Q

What is a theory of the pathophysiology of SJS?

A

Altered drug metabolism in some patients triggers a T-cell-mediated cytotoxic reaction to drug antigens in keratinocytes.

288
Q

How does SJS present?

A

Ranges from mild to fatal:

-Non-specific symptoms initially with fever, cough, sore throat/mouth, sore eyes and itchy sin.
-Purple/red rash with spreads across skin and blisters which leaves the raw tissue underneath.
-Also happens to lips and mucous membranes.
-Inflammation and ulceration of eyes.
-It can also affect urinary tract, lungs and internal organs.

289
Q

What is the management of SJS?

A

Medical emergencies - supportive care (nutrition, antiseptics, analgesia, ophthalmology).

-Steroids, immunoglobulins, immunosuppressants.

290
Q

What are the complications of SJS?

A

Secondary infection - cellulitis/sepsis.
Permanent skin damage.
Visual complications.

291
Q

What is urticaria?

A

Hives - small itchy lumps on the skin.
-Can be localised or widespread.
-May be associated angioedema and flushing.
-Can be acute or chronic.

292
Q

What is the pathophysiology of urticaria?

A

Release of histamine and other inflammatory chemicals by mast cells in the skin.
May be part of allergic reaction in acute urticaria or autoimmune in chronic.

293
Q

What are the causes of acute urticaria?

A

Allergies to food, medications or animals.
Contact with chemicals, latex or nettles.
Medications.
Viral infections.
Insect bites.

294
Q

What is chronic urticaria?

A

Autoimmune condition where autoantibodies target mast cell and trigger them to release histamine and other chemicals.

295
Q

What is the management of urticaria?

A

Antihistamines.
-Fexofenadine is the choice for chronic urticaria.
-Oral steroids may be given for flare ups.
-Specialist treatment may be required.

296
Q

What is nappy rash?

A

Contact dermatitis in the nappy area, normally caused by friction between the skin and nappy and contact with the urine and faeces.
The breakdown of skin and warm environment in nappy can lead to infection with candida or bacteria.

297
Q

What is the most common age of nappy rash?

A

Between 9 and 12 months.

298
Q

What are the risk factors for nappy rash?

A

Delayed nappy changing.
Irritant soap products and vigorous cleaning.
Diarrhoea.
Oral antibiotics - candida.
Preterm infants.

299
Q

How does nappy rash present?

A

Sore, red and inflamed skin in nappy area.
Few red papules.
Tends to spare skin creases.
Nappy rash is uncomfortable, may be itchy.

Severe and longstanding nappy rash leads to erosions and ulceration.

300
Q

What is the difference between candida and nappy rash?

A

Candida:
-Extends into skin folds, large red macules, demarcated scaly border, circular rash pattern, satellite lesions.

301
Q

How is nappy rash managed?

A

Switch to highly absorbent nappies.
Change nappy clean as soon as used.
Use water to clean nappy area.
Ensure nappy is dry before replacing.
Maximise time not wearing nappy.

Infection: Anti-fungal cream or antibiotic.

302
Q

What are non-blanching rashes?

A

Rashes that don’t blanch caused by bleeding under the skin.
May be petechiae (small, red spots caused by burst capillaries).
Or purpura (larger, red-purple papules from leaking vessels).

303
Q

Why is immediate investigation needed in non-blanching rashes?

A

The risk of meningococcal septicaemia.

304
Q

Give 9 differentials of non-blanching rashes.

A

Meningococcal septicaemia.
Henoch-Schonlein purpura.
Idiopathic thrombocytopenic purpura (ITP).
Acute leukemias.
Haemolytic uraemic syndrome.
Mechanical (coughing, breath holding).
Traumatic.
Viral illness.

305
Q

What investigations should be used in non-blanching rashes?

A

FBC, U+Es, CRP/ESR, blood cultures, meningitis PCR, LP, BP and urine dipstick.

306
Q

What are viral exanthems?

A

Eruptive widespread rashes - originally 6 illnesses that cause this.
Measles, Scarlet fever, Rubella, Dukes’ disease, Parvovirus B19, Roseola Infantum.

307
Q

What is erythema multiforme?

A

Erythromatous rash caused by hypersensitivity reaction.
-Caused by viral infections and medications (most commonly HSV, mycoplasma).

308
Q

What is chickenpox?

A

Highly contagious infection caused by VZV.
-Causes a vesicular generalised rash.
-Common in children and once they develop immunity to VZV virus they will not be affected again.

309
Q

How does chickenpox present?

A

Widespread, erythromatous, raised, vesicular, blistering lesions. Usually starts on trunk or face and spreads outwards affecting the whole body over 2-5 days.
-Fever, itch, general fatigue/malaise.

310
Q

How is chickenpox managed?

A

Self-limiting - usually doesn’t require treatment.
Acyclovir in immunocompromised patients, adults/adolescents, neonates and those at risk of complications.

311
Q

What is hand, foot and mouth disease?

A

Viral illness caused by coxsackie A virus with mouth ulcers and blistering red spots on feet and hands.

312
Q

How does hand, foot and mouth disease present?

A

Begins with typical viral URTI.
1-2 days later small mouth ulcers appear followed by blistering red spots across the body with them most notably on hands, feet and around mouth.
-Painful mouth ulcers with them particularly on the tongue.

313
Q

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

A

Diagnosis based on appearance of the rash.
-No treatment and management is supportive.
-Highly contagious so implement measures to avoid transmission.

314
Q

What is scabies?

A

Tiny mites called sarcoptes scabiei that burrow under skin causing infection and intense itching.
-They lay eggs in skin leading to further infection and symptoms.
-Can take up to 8 weeks for rash or symptoms to appear after initial infestation.

315
Q

How does scabies present?

A

Itchy small red spots with possible track marks where mites have burrowed.
-Classic rash is between finger webs but can spread to whole body.

316
Q

How is scabies managed?

A

Permethrin cream applied to entire body - left for 12 hours and washed off.
-Oral ivermectin for difficult to treat.
-Household contacts to be treated.

317
Q

What is impetigo?

A

Infectious superficial bacterial skin infection usually caused by staph aureus.

318
Q

What is characteristic of impetigo?

A

Golden crust.

319
Q

What are the two types of impetigo? How is it treated?

A

Bullous and non-bullous.
Antibiotics and antibiotic cream.

320
Q

What is Kawasaki disease? Who is it more common in?

A

Systemic medium sized vessel vasculitis commonly affecting children under 5y.
More common in boys and Asian children (Japan, Korea).

321
Q

What is a key complication of Kawasaki disease?

A

Coronary artery aneurysm.

322
Q

How does Kawasaki disease present?

A

Persistent high fever for more than 5 days. Unwell child.
-Widespread erythematous maculopapular rash and desquamation on palms and soles.
-Strawberry tongue.
-Cracked lips.
-Cervical lymphadenopathy.
-Bilateral conjunctivitis.

323
Q

What are the investigations for Kawasaki disease?

A

FBC - anaemia, leukocytosis, thrombocytosis.
LFTs - hypoalbuminemia.
Raised ESR.
Urinalysis - raised WBC.
ECHO to rule out coronary artery aneurysms.

324
Q

What is the disease course of Kawasaki disease?

A

Acute - Unwell with fever, rash, lymphadenopathy (1-2w).
Subacute phases - Acute symptoms settle but arthralgia and risk of coronary artery aneurysms form (2-4w).
Convalescent stage - Symptoms settle and blood tests normal (2-4w).

325
Q

What is the management of Kawasaki disease?

A

High dose aspirin to reduce risk of thrombosis
IV immunoglobulins
-Follow up with ECHOs.

326
Q

What is meningitis?

A

Inflammation of the meninges - can be viral or bacterial.

327
Q

What are the most common causes of meningitis?

A

N. meningitidis - gram negative diplococcus.
S. pneumoniae.
Neonates - group B strep from mothers vagina.

328
Q

How does meningitis present?

A

Fever, neck stiffness, vomiting, headache, photophobia, altered consciousness and seizures.
-Non-blanching rash (meningococcal septicaemia).

329
Q

How does meningitis present in neonates?

A

Very non-specific - hypotonia, poor feeding, lethargy, hypothermia.

330
Q

What investigations can be used in meningitis?

A

Lumbar puncture.
Kernig’s test - flexing hip and knee at 90, straighten knee (spinal pain).
Brudzinski’s test - lay flat, lift head off bed to chin the chest (positive is involuntary flexing hips and knees).

331
Q

How is meningitis managed? How is it managed under 3 months?

A

Community - stat IM benzylpenicillin.
Hospital - Blood culture, LP, meningococcal PCR, IV antibiotics.

-Under 3m: IV cefotaxime with IV amoxicillin.
-Above 3m: IV ceftriaxone.

332
Q

What is post-exposure prophylaxis for meningitis?

A

Single dose of ciprofloxacin.

333
Q

Viral meningitis - causes, investigation and management?

A

HSV, VZV, enterovirus.
Sample of CSF for PCR.
Only supportive, sometimes aciclovir.

334
Q

What is measles?

A

Highly contagious virus caused by measles virus and spread by respiratory droplets.

335
Q

How does measles present?

A

Initial - fever, coryza, cough and conjunctivitis.

-Koplik spots - grey/white spots on buccal mucosa (inside cheek).
Rash starts on face , classically behind ears then spreads to rest of body - erythematous macular rash.

336
Q

How is measles managed?

A

Supportive treatment.
Avoid school for at least 5 days after initial rash.
Notify public health.

337
Q

How common are measles complications and what are they?

A

30%:

Otitis media.
Pneumonia.
Febrile convulsions.
Encephalitis.
Death.

338
Q

Why is measles still prevalent?

A

Despite vaccination - anti-vax movements still allow transmission of the measles virus.

339
Q

What is rubella?

A

Highly contagious rubella virus that is spread via respiratory droplets.
-2-3w incubation period.

340
Q

How does rubella present?

A

General mild disease:
-Low grade fever and maculopapular rash on face that spreads to body (3 days).
-May have joint paint and a sore throat.

341
Q

What is the management of rubella?

A

Supportive as the condition is self-limiting.
-Notify public health.
-Avoid pregnant women.

342
Q

What are the complications of rubella?

A

Encephalitis, thrombocytopenia.
-Dangerous in pregnancy - can lead to congenital rubella syndrome (triad of deafness, blindness and congenital heart disease).

343
Q

What is scalded skin syndrome?

A

Condition caused by S. aureus that produces epidermolytic toxins - proteases that breaks down skin barrier - infection occurs and skin is damages and breaks down.

343
Q

How does scalded skin syndrome present?

A

General erythema patches with bullae - ‘skin/scald’.
Systemic symptoms - fever irritability, lethargy, dehydration.
Nikolsky sign - gentle rubbing causes skin to peel away.

344
Q

How is scalded skin syndrome managed?

A

Admit and treat with IV antibiotics.
Fluid and electrolyte balance.

345
Q

What is encephalitis? Most common type?

A

Inflammation of the brain which can be infective or non-infective.
-Viral - HSV1 and HSV2.

346
Q

What are the causes of encephalitis?

A

Viral, bacterial and fungal.
Viral - HSV, VZV, CMV, EBV, chickenpox.

347
Q

How does encephalitis present?

A

Altered consciousness/cognition.
Unusual behaviour.
Acute onset of focal neurological symptoms and seizures.
Fever.

348
Q

What investigations are used in encephalitis?

A

LP (CSF PCR) or CT if LP contraindicated.
MRI.
EEG.
HIV testing.

349
Q

What are four contraindications of LPs?

A

GCS below 9, haemodynamically unstable, active seizures, post-ictal.

350
Q

What is the management of encephalitis?

A

Aciclovir - HSV and VZV.
Ganciclovir - CMV.

Repeat LP before stopping antivirals.

351
Q

What are the complications of encephalitis?

A

Lasting fatigue, change in personality/mood/memory/cognition, headaches, seizures.

352
Q

What is slapped cheek syndrome?

A

Parvovirus B19 causing bright red erythema on both cheeks.

353
Q

How does slapped cheek syndrome present?

A

Begins with mild fever, coryza and

3a (8 decks)

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