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Phase 3A Revision > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

What is the presentation of pneumonia?

A

Wet and productive cough
High fever
Tachypnoea
Tachycardia
Increased work of breathing
Lethargy
Delirium

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2
Q

What are the characteristic chest signs of pneumonia?

A

Bronchial breath sounds
Focal course crackles
Dullness to percussion

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3
Q

What is the most common bacterial cause of pneumonia in children?

A

Streptococcus pneumoniae

Also:
Group A/B strep
Staphylococcus aureus
Haemophilus influenzae (pre-/unvaccinated)

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4
Q

What is the most common viral cause of pneumonia in children?

A

Respiratory syncytial virus (RSV)

Also:
Parainfluenza
Influenza

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5
Q

What is the first line management of bacterial pneumonia in children?

A

Amoxicillin

Adding a macrolide (erythromycin, clarithromycin, azithromycin) will cover atypical pneumonia, or if penicillin allergy

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6
Q

What is the typical age for croup?

A

6 months to 2 years

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7
Q

What is the cause of croup?

A

Parainfluenza
Influenza
Adenovirus
RSV
Diphtheria (if unvaccinated)

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8
Q

What is the presentation of croup?

A

Barking cough
Increased work of breathing
Hoarseness
Stridor
Low grade fever

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9
Q

What is the management of mild croup?

A

Simple supportive management at home (fluids and rest)
Measures to avoid spread

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10
Q

What is the management of severe croup?

A

Oral dexamethasone
Oxygen
Nebulised budesonide
Nebulised adrenalin
Intubation and ventilation

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11
Q

Why is viral-induced wheeze more common in children?

A

Smaller airways

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12
Q

How can viral-induced wheeze be distinguished from asthma?

A

Presenting before 5 years of age
No atopic history
Only occurs during viral infection

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13
Q

What is the presentation of viral induced wheeze?

A

Evidence of viral illness (cough, fever)
Shortness of breath
Signs of respiratory disease
Expiratory wheeze throughout the chest

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14
Q

What does a focal wheeze suggest?

A

Foreign body or tumour

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15
Q

What is the presentation of an acute exacerbation of asthma?

A

Progressively worsening shortness of breath
Use of accessory muscles
Fast respiratory rate
Symmetrical expiratory wheeze
Reduced air entry

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16
Q

What is the grading system for acute asthma?

A

Moderate

PEFR = 50-75% predicted

Severe

PEFR 33-50% predicted
RR >25
HR>110
Unable to complete sentences

Life-threatening

PEFR<33%
Sats<92%
Tiredness
Silent chest
Signs of shock

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17
Q

What is the management of a moderate acute asthma exacerbation?

A

Nebulised beta-2 agonists (salbutamol as required)
Nebulised ipratropium bromide
Steroids
Antibiotics if suspected bacterial infection

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18
Q

What is the management of a severe acute asthma exacerbation?

A

Oxygen to maintain sats 94-98%
Aminophylline infusion
Consider IV salbutamol

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19
Q

What is the management of a life-threatening acute asthma exacerbation?

A

IV magnesium sulphate infusion
Admission to HDU/ICU
Intubation

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20
Q

What presentations suggest asthma?

A

Episodic symptoms
Diurnal variation
Dry cough, wheeze, shortness of breath
Typical triggers
PMH of other atopic conditions
Family history
Bilateral, widespread, polyphonic wheeze
Symptoms improve with bronchodilators

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21
Q

What are typical triggers of asthma?

A

Dust
Animals
Cold air
Exercise
Smoke
Food allergens

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22
Q

What is the asthma management protocol in children under 5?

A
  1. Short-acting beta-2 agonist (salbutamol) inhaler as required
  2. Add low dose corticosteroid inhaler or leukotriene antagonist (eg oral montelukast)
  3. Add the other option from step 2
  4. Refer to specialist
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23
Q

What is the asthma management protocol in children aged 5-12?

A
  1. Short-acting beta-2 agonist (salbutamol) inhaler as required
  2. Add low dose corticosteroid inhaler
  3. Add long-acting beta-2 agonist (salmeterol)
  4. Titrate corticosteroid to medium dose and consider adding oral montelukast or theophylline
  5. Increase corticosteroid to high dose
  6. Refer to specialist
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24
Q

What is the asthma management protocol in children over 12?

A

Same as adults
1. Short-acting beta-2 agonist (salbutamol) inhaler as required
2. Add low dose corticosteroid inhaler
3. Add long-acting beta-2 agonist (salmeterol)
4. Titrate corticosteroid to medium dose and consider adding oral montelukast, oral theophylline or inhaled LAMA (tiotropium)
5. Titrate corticosteroid to high dose and consider combining treatments from step 4, including oral salbutamol
6. Add oral steroids at lowest possible dose

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25
Q

What is the most common cause of bronchiolitis?

A

RSV

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26
Q

At what age can bronchiolitis be diagnosed?

A

Generally under 1
Most commonly under 6 months
Rarely up to 2 years old

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27
Q

What is the presentation of bronchiolitis?

A

Coryzal symptoms
Signs of respiratory distress
Dyspnoea
Tachypnoea
Poor feeding
Mild fever
Wheeze and crackles

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28
Q

What is the management of bronchiolitis?

A

Supportive
Manage at home
Give advice about when to seek further medical attention

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29
Q

What factors are reasons for admission with bronchiolitis?

A

Aged under 3 months
Pre-existing conditions (prematurity, Down’s, CF)
Dehydration
RR>70
O2<92%
Moderate to severe respiratory distress (deep recessions, head bobbing)
Apnoeas

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30
Q

What factors are reasons for admission with bronchiolitis?

A

Aged under 3 months
Pre-existing conditions (prematurity, Down’s, CF)
Dehydration
RR>70
O2<92%
Moderate to severe respiratory distress (deep recessions, head bobbing)

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31
Q

What presentations suggest possible epiglottitis?

A

Sore throat/stridor
Drooling
Sat forward with a hand on each knee (tripod position)
Difficulty/painful swallowing
Muffled voice
Unwell/septic

Three Ds –> Dysphagia, Drooling Distress

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32
Q

What is the management of epiglottitis?

A

Not distressing the patient
Ensure airway is secure
Be ready to intubate if required
IV antibiotics (ceftriaxone)
Steroids (dexamethasone)

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33
Q

What is the inheritance pattern of cystic fibrosis?

A

Autosomal recessive

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34
Q

What is the initial presentation of cystic fibrosis?

A

Screened for at birth
Meconium ileus –> first stool passed is thick and sticky, causing bowel obstruction
If developed later in childhood –> recurrent LRTIs, failure to thrive, pancreatitis

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35
Q

What are the symptoms of cystic fibrosis?

A

Chronic cough
Thick sputum
Recurrent LRTIs
Steatorrhoea
Abdominal pain/bloating
Salty sweat
Failure to thrive
Diabetes –> Blocking of pancreatic duct

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36
Q

What is the gold standard test for cystic fibrosis?

A

Sweat test

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37
Q

What is the management of cystic fibrosis?

A

Chest physiotherapy
Exercise
High calorie diet
Treat symptoms
Bronchodilators

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38
Q

What organism causes whooping cough?

A

Bordetella pertussis

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39
Q

What is the presentation of whooping cough?

A

Starts as mild coryzal symptoms, low grade fever and mild dry cough
After 1 week, more severe cough –> Paroxysmal cough so severe that the patient is completely out of breath, and can faint, vomit or develop pneumothorax

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40
Q

What is the management of whooping cough?

A

Notify PHE
Simple supportive care
Macrolide Abx (erythromycin, clarithromycin, azithromycin) can be beneficial in first 21 days or vulnerable patients

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41
Q

What is the most common bacterial cause of otitis media?

A

Streptococcus pneumoniae

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42
Q

What is the presentation of otitis media?

A

Ear pain
Reduced hearing
General symptoms of upper airway infection (fever, coryzal symptoms etc)
Discharge if tympanic membrane ruptured

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43
Q

What is the management of otitis media?

A

Simple analgesia to help with pain and fever
Avoid antibiotics unless bilateral or discharge, or if symptoms not improved after 1 week
Then prescribe 5 days of amoxicillin

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44
Q

What is the management of persistent glue ear?

A

Grommets

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45
Q

What are congenital causes of deafness?

A

Maternal rubella or cytomegalovirus during pregnancy
Genetic deafness
Down’s syndrome

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46
Q

What are perinatal causes of deafness?

A

Prematurity
Hypoxia during or after birth

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47
Q

What is the name of the hole in the atrial septum that normally closes after birth?

A

Foramen ovale

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48
Q

In an atrial septal defect, which way does the blood move initially?

A

Left atrium –> right atrium due to higher pressure in LA (no cyanosis)
Eventually, extra blood flow in RA increases the pressure, causing pulmonary hypertension, and the blood then flows right to left, bypassing the lungs (cyanosis) –> Eisenmenger syndrome

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49
Q

What are the complications of an atrial septum defect?

A

Stroke (in the context of DVT) –> Embolus would normally return to right atrium and cause PE, however, in ASD, the clot can travel to the left atrium and enter the peripheral circulation

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50
Q

What would be heard on auscultation in a patient with an atrial septal defect?

A

Mid-systolic, crescendo-decrescendo murmur loudest at upper left sternal edge

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51
Q

What are typical symptoms of atrial septal defects in children?

A

Shortness of breath
Difficulty feeding
Poor weight gain
LRTIs
May be asymptomatic

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52
Q

What is the management of an atrial septal defect?

A

If small and asymptomatic –> watch and wait
Transvenous catheter closure
Open heart surgery
Anticoagulants to reduce risk of clots and stroke

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53
Q

What is Einsenmenger syndrome?

A

When blood flows from the right side to the left side of the heart, bypassing the lungs

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54
Q

What are the underlying lesions that can cause Einsenmerger syndrome?

A

ASD
VSD
Patent ductus arteriosus

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55
Q

What are the examination findings in a patient with Eisenmenger syndrome?

A

Signs of pulmonary oedema:
Right ventricular heave
Loud second heart sound (due to forceful shutting of the pulmonary valve)
Raised JVP
Peripheral oedema

Signs of septal defect:
Mid-systolic crescendo-decrescendo murmer at left upper sternal edge –> ASD
Pan-systolic murmer at left lower sternal edge –> VSD
Continuous crescendo-decrescendo “machinery” murmur –> Patent ductus arteriosus

Signs of right-left shunt:
Cyanosis
Clubbing
Dyspnoea

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56
Q

What is the management of Eisenmenger syndrome?

A

Ideally should have underlying defect surgically corrected before it develops
Once developed, not possible to reverse condition without heart-lung transplant

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57
Q

What genetic conditions are ventricle septal defects associated with?

A

Down’s syndrome
Turner’s syndrome

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58
Q

What is the presentation of ventricle septal defects?

A

Initially asymptomatic
Poor feeding
Dyspnoea
Tachypnoea
Failure to thrive

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59
Q

What would be heard on auscultation in a patient with a ventricle septal defect?

A

Pan-systolic murmur heard loudest at lower left sternal edge and in third and fourth intercostal spaces

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60
Q

What is the management of a ventricle septal defect?

A

Watch and wait if asymptomatic –> open close spontaneously
Transvenous catheter closure/open heart surgery
Prophylactic antibiotics to protect against infective endocarditis

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61
Q

What underlying genetic condition is linked to coarctation of the aorta?

A

Turner’s syndrome

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62
Q

What is the main presentation of coarctation of the aorta in neonates?

A

Weak femoral pulses

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63
Q

What are the findings in four limb blood pressure monitoring in coarctation?

A

High blood pressure in limbs supplied before the narrowing (normally upper limbs) and low pressure in limbs after the narrowing (lower limbs)

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64
Q

What is the management of coarctation?

A

Removal of the narrowing and reconnection of the aorta –> Can be in adulthood in mild cases or emergency after birth in severe cases
Prostaglandin E –> used in emergency cases to keep the ductus arteriosus open whilst awaiting surgery to prevent heart failure and death

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65
Q

What are the features of a patent ductus arteriosus on examination of the chest?

A

Left subclavicular thrill
Continuous machinery murmur
Large volume bounding and collapsing pulse
Wide pulse pressure
Heaving apex beat

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66
Q

What pathologies exist in Tetralogy of Fallot?

A

Pulmonary valve stenosis
Right ventricular hypertrophy
Overriding aorta
VSD

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67
Q

What are risk factors for Tetralogy of Fallot?

A

Rubella infection
Increased maternal age
Alcohol consumption in pregnancy
Diabetic mother

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68
Q

What are the signs and symptoms of a patient with Tetralogy of Fallot?

A

Cyanosis
Clubbing
Poor feeding
Poor weight gain
Ejection systolic murmur

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69
Q

What is the management of Tetralogy of Fallot?

A

Open heart surgery
Prostaglandin infusion to maintain the ductus arteriosus and maintain blood flow to the pulmonary arteries

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70
Q

What is the significance of GORD in babies?

A

Immaturity of the lower oesophageal sphincter means that GORD is common and is not problematic

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71
Q

What are the signs of a problematic reflux?

A

Chronic cough
Hoarse cry
Distress/crying after feeding
Reluctance to feed
Pneumonia
Poor weight gain

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72
Q

What is the management of mild cases of GORD?

A

Reassurance
Small, frequent meals
Burping to help milk settle
Not over-feeding
Keep the baby upright after feeding

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73
Q

What is the management of more problematic GORD?

A

Gaviscon mixed with feeds
Thickened milk/formula
PPIs

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74
Q

What is the initial presentation of pyloric stenosis?

A

Hungry baby
Thin, pale, failure to thrive
Projectile vomiting
Firm mass felt in upper abdomen

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75
Q

What is the standard investigation for diagnosing pyloric stenosis?

A

Abdominal ultrasound

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76
Q

What is the treatment of pyloric stenosis?

A

Laparoscopic pyloromyotomy

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77
Q

What are the most common viral causes of gastroenteritis?

A

Rotavirus
Norovirus

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78
Q

What are the common causes of bacterial gastroenteritis?

A

E.coli
Campylobacter jejuni (Traveller’s diarrhoea)
Shigella
Salmonella
Bacillus cereus (Typically occurs after eating leftover fried rice)
Yersinia enterocolitica (Pork)
S.aureus
G.lamblia

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79
Q

What are the symptoms of gastroenteritis?

A

Vomiting and nausea (gastritis)
Diarrhoea (enteritis)

If bacterial/more severe:
Abdominal cramps
Blood/mucus in stool
Fever

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80
Q

What are the principles of gastroenteritis management?

A

Good hygiene
Isolation
Hydration
Antibiotics ONLY IF causative organism confirmed (bacterial but not E.coli)

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81
Q

What are possible post-infection complications of gastroenteritis?

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain-Barre syndrome

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82
Q

What are typical features that suggest constipation?

A

Less than 3 stools per week
Hard stools
Straining when passing
Abdominal pain
Rectal bleeding

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83
Q

What is encopresis?

A

Faecal incontinence, only pathological after 4 years old, due to constipation causing stretching of the rectum and loss of sensation

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84
Q

What lifestyle factors can be associated with constipation?

A

Habit of not opening bowels
Low fibre diet
Poor fluid intake
Sedentary lifestyle
Psychosocial problems

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85
Q

What are some secondary causes of constipation?

A

Hirschsprung’s disease
Cystic fibrosis
Hypothyroidism
Spinal cord lesions
Sexual abuse
Intestinal obstruction
Cows milk intolerance

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86
Q

What is the management of idiopathic/functional constipation?

A

High fibre diet and hydration
Laxatives (movicol first line) –> wean off once normal bowel habits established
Encourage and praise going to the toilet
(Star charts etc)

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87
Q

What antibodies are associated with coeliac disease?

A

Anti-tissue transglutaminase (anti-TTG)
Anti-endomysial (anti-EMA)

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88
Q

What are common symptoms of coeliac disease?

A

Failure to thrive
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia –> iron/B12/folate deficiency

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89
Q

What non-intestinal symptoms can be associated with coeliac disease?

A

Dermatitis herpetiformis
Gluten ataxia

Big up TG3 and TG6!!!

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90
Q

What is the management of coeliac disease?

A

Lifelong gluten free diet

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91
Q

What are the characteristic features of Crohn’s disease?

A

No blood or mucus
Entire GI tract affected
Skip lesions
Transmural/Termial ileum most affected
Smoking is a risk factor

(crows NESTS)

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92
Q

What are the characteristic features of ulcerative colitis?

A

Continuous inflammation (no skip lesions)
Limited to colon and rectum
Only superficial mucosa
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis

(U-C-CLOSEUP)

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93
Q

What tests can be performed to diagnose IBD?

A

FBC –> anaemia
WCC –> Infection
CRP –> active inflammation
Faecal calprotectin –> released by intestines when inflamed

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94
Q

What is the management for inducing remission in Crohn’s disease?

A

1st line = Steroids eg. oral prednisolone, IV hydrocortisone
Consider adding immunosuppressant eg. azathioprine, methotrexate, infliximab

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95
Q

What is the management for inducing remission in Crohn’s disease?

A

1st line = Steroids eg. oral prednisolone, IV hydrocortisone
Consider adding immunosuppressant eg. azathioprine, methotrexate, infliximab

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96
Q

What is the management for maintaining remission in Crohn’s disease?

A

1st line = Azathioprine/mercaptopurine
Alternatives = Methotrexate/inflixumab

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97
Q

What is the management for inducing remission in mild/moderate and severe UC?

A

Mild/moderate
1st line = Aminosalicylates eg. mesalazine
2nd line = Prednisolone

Severe
1st line = IV hydrocortisone
2nd line = IV ciclosporin

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98
Q

What is the management for maintaining remission in UC?

A

Mesalazine
Azathioprine
Mercaptopurine

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99
Q

What conditions have an association with Hirschsprung’s disease?

A

Down’s syndrome
Neurofibromatosis

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100
Q

What is Hirschsprung’s disease?

A

A congenital condition where parasympathetic ganglia in the bowel wall are absent, causing bowel constriction and loss of movement of faeces and bowel obstruction, and bowel distension proximal to the pathology

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101
Q

What is the presentation of Hirschsprung’s disease?

A

Delay in passing meconium (>24hours)
Chronic constipation
Abdominal pain/distension
Vomiting
Poor weight gain/failure to thrive

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102
Q

What is the gold standard investigation to diagnose Hirschsprung’s disease?

A

Suction rectal biopsy

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103
Q

What is the management of Hirschsprung’s disease?

A

Resection of the aganglionic section of bowel (Swenson procedure)

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104
Q

What are the signs and symptoms of appendicitis?

A

Central abdominal pain that moves to right iliac fossa (McBurney’s point)
Loss of appetite
Nausea/vomiting
Guarding
Rebound tenderness –> Suggests rupture causing peritonitis
Rovsing’s sign –> Palpation of LIF causes pain in RIF

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105
Q

What is the management of appendicitis?

A

Immediate emergency admission
Appendicectomy

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106
Q

What is biliary atresia?

A

Narrowing or absence of the bile duct, resulting in cholestasis

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107
Q

What is the presentation of biliary atresia?

A

Significant jaundice

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108
Q

What is the investigation of biliary atresia?

A

Conjugated and unconjugated bilirubin –> High proportion of conjugated suggests biliary atresia as the liver has conjugated the bilirubin but is unable to excrete it as the bile duct is faulty

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109
Q

What is the management of biliary atresia?

A

Surgery

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110
Q

What are the possible causes of intestinal obstruction?

A

Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Intussusception
Volvulus
Strangulated hernia

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111
Q

What is the presentation of an intestinal obstruction?

A

Persistent vomiting –> may be bilious (bright green)
Abdominal pain/distension
Failure to pass stool/wind
Abnormal bowel sounds –> initially high pitched, later absent

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112
Q

What is the management of an intestinal obstruction?

A

Nasogastric tube to drain the stomach
IV fluids and electrolytes
Manage underlying condition

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113
Q

What is intussusception?

A

When the bowel “telescopes” into itself

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114
Q

What is the presentation of intususception?

A

Severe colicky abdominal pain
Pale, lethargic and unwell
“Redcurrant jelly stool”
RUQ mass (“sausage-shaped”)
Vomiting
Intestinal obstruction

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115
Q

What typically precedes a intussusception?

A

Viral URTI

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116
Q

What is the initial investigation for intususception?

A

Ultrasound

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117
Q

What is the management of intussusception?

A

Therapeutic enema with water, air or contrast
Surgical reduction
Surgical resection

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118
Q

What are the complications of intussusception?

A

Obstruction
Gangrenous bowel
Perforation
Death

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119
Q

What are the symptoms of UTI in babies?

A

Fever
Lethargy
Irritability
Vomiting
Poor feeding
Frequency

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120
Q

What are the symptoms of UTI is older infants and children?

A

Fever
Abdominal pain
Vomiting
Dysuria
Frequency
Incontinence

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121
Q

What features indicate that a UTI is acute pyelonephritis?

A

Temperature > 38oC
Loin pain/tenderness

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122
Q

What is the management of a child under 3 months with UTI and fever?

A

Urgently refer to specialist
IV antibiotics

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123
Q

What is the management for pyelonephritis/upper UTI in children over 3 months?

A

Oral cefalexin or co-amoxiclav

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124
Q

What is the management for cystitis/lower UTI in children over 3 months?

A

1st line = Oral trimethoprim or nitrofurantoin (if eGFR > 45)
2nd line = Oral nitrofurantoin/amoxicillin/cefalexin

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125
Q

What are the definitions of recurrent UTI?

A

2 or more episodes of pyelonephritis/upper UTI
1 episode of upper UTI + 1 or more episodes of lower UTI
3 or more episodes of cystitis/lower UTI

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126
Q

What is the management of recurrent UTI?

A

Treat current UTI
Prescribe prophylactic antibiotics (trimethoprim or nitrofurantoin)

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127
Q

What is the classic triad of nephrotic syndrome?

A

Low serum albumin
High proteinuria
Oedema

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128
Q

What are the causes of nephrotic syndrome?

A

Minimal change disease (MOST COMMON)
Intrinsic kidney disease (focal segmental glomerulosclerosis/membranoproliferative glomerulonephritis)
Underlying systemic illness (Henoch schonlein purpura, diabetes, infection)

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129
Q

What is the pathophysiology of nephrotic syndrome?

A

The basement membrane of the glomerulus becomes highly permeable to protein

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130
Q

What is the presentation of nephrotic syndrome?

A

2-5 years old
Frothy urine
Generalised oedema
Pallor

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131
Q

What is the management of minimal change disease?

A

Corticosteroids eg prednisolone

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132
Q

What is the management of nephrotic syndrome?

A

High dose prednisolone
Low salt diet
Diuretics to treat oedema
Albumin infusion if severe hypoalbuminaemia
Antibiotic prophylaxis in severe cases

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133
Q

What are the two most common causes of nephritis in children?

A

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

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134
Q

What is the presentation of nephritis?

A

Reduction in kidney function
Haematuria –> visible or invisible
Proteinuria (although less than nephrotic syndrome)

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135
Q

What is the pathophysiology of post-streptococcal glomerulonephritis?

A

Following B-haemolytic streptococcus infection, eg. tonsillitis, streptococcal antigens and antibodies become stuck in the glomeruli of the kidney and cause inflammation

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136
Q

What is the management of post-streptococcal glomerulonephritis?

A

Supportive (80% of cases)
May need antihypertensive medication and diuretics if hypertensive or has oedema

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137
Q

What is the pathophysiology of IgA nephropathy (Berger’s disease)?

A

IgA deposits in the nephrons causing inflammation
Related to Henoch-Schonlein Purpura (IgA vasculitis)

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138
Q

What is the management of IgA nephropathy?

A

Supportive
Immunosuppressant medication (steroids and cyclophosphamide)

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139
Q

What is haemolytic uraemic syndrome?

A

Thrombosis in small blood vessels throughout the body, caused by shiga toxin from bacteria (E.coli and shigella)
Use of antibiotics and anti-motility medications following gastroenteritis increases the risk of HUS

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140
Q

What is the classic triad haemolytic uraemic syndrome?

A

Haemolytic anaemia –> destruction of RBCs
Acute kidney injury –> failure of kidneys to remove waste eg. urea
Thrombocytopenia –> Low platelets

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141
Q

What is the presentation of haemolytic uraemic syndrome?

A

Symptoms develop 5 days after diarrhoea from gastroenteritis
Reduced urine output
Haematuria
Abdominal pain
Lethargy and irritability
Confusion
Oedema
Hypertension

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142
Q

What is the management of haemolytic uraemic syndrome?

A

Medical emergency
Urgent referral
Antihypertensives if required
Fluid maintenance
Blood transfusions if required

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143
Q

What is enuresis?

A

Involuntary urination

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144
Q

At what age do most children get the ability to control urination?

A

Daytime urination (diurnal enuresis) = 2 years old
Night-time urination (nocturnal enuresis) = 3-4 years

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145
Q

What are causes of primary nocturnal enuresis?

A

Variation on normal development
Overactive bladder
Increased fluid intake
Failure to wake
Psychological distress

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146
Q

What is the management of primary nocturnal enuresis?

A

Reassure parents of children under 5
Lifestyle changes –> Reduced fluid intake in evenings, going to toilet before bed etc
Encouragement and positive reinforcement
Treatment of underlying cause
Pharmacological –> Desmopressin, oxybutinin, imipramine

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147
Q

What is the definition of primary nocturnal enuresis?

A

Where the child wets the bed and has never managed to be consistently dry at night

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148
Q

What is the definition of secondary nocturnal enuresis?

A

Where the child wets the bed despite being consistently dry for at least 6 months

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149
Q

What are the causes of secondary nocturnal enuresis?

A

UTI
Constipation

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150
Q

What are the causes of secondary nocturnal enuresis?

A

UTI
Constipation
Type 1 Diabetes
New psychosocial problems
Maltreatment

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151
Q

What factors can exacerbate vulvovaginitis?

A

Wet nappies
Use of chemicals or soaps
Tight clothing
Poor toilet hygiene
Constipation
Threadworms
Pressure eg. horse riding/cycling

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152
Q

What is the presentation of vulvovaginitis?

A

Soreness/itching
Erythema
Vaginal discharge
Dysuria
Constipation

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153
Q

What is the management of vulvovaginitis?

A

Avoid soap/chemicals
Good toilet hygiene –> Wiping front to back
Keeping area dry
Emollients
Loose clothing
Treatment of constipation/worms
Oestrogen cream in severe cases

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154
Q

What is a Wilms tumour?

A

A specific kidney tumour, typically affecting children under 5

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155
Q

What is the presentation of a Wilms tumour?

A

Abdominal mass
Abdominal pain
Haematuria
Lethargy
Fever
Hypertension
Weight loss

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156
Q

What is the treatment of a Wilms tumour?

A

Surgical excision
May require adjuvant chemo/radiotherapy

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157
Q

What is the presentation of eczema?

A

Dry, red, itchy, sore patches on skin over the flexor region (inside elbows and knees) and on face and neck
Flaring of symptoms

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158
Q

What is the management of eczema?

A

Maintenance using emollients as often as possible
Avoiding triggers or factors that damage the skin barrier such as hot water and scratching
Treatment of flare-ups using thicker emollients, topical steroids and antibiotics in very severe cases

159
Q

What are the medications on the steroid cream ladder?

A

Mild = Hydrocortisone
Moderate = Eumovate (clobetasone butyrate)
Potent = Betnovate (betamethasone)
Very potent = Dermovate (clobetasol)

160
Q

What is eczema herpeticum?

A

A viral skin infection in patients with eczema

161
Q

What are the most common causes of eczema herpeticum?

A

HSV
VZV

162
Q

What is the presentation of eczema herpeticum?

A

Widespread, painful, vesicular rash
Fever, lethargy
Lymphadenopathy

163
Q

What is the treatment of eczema herpeticum?

A

Aciclovir

164
Q

What is the pathophysiology of psoriasis?

A

Rapid generation of new skin cells causes abnormal buildup and thickening of the skin in certain areas

165
Q

What is the presentation of psoriasis?

A

Dry, flaky, scaly, erythematous skin in raised rough patches, commonly over elbows, knees and scalp

166
Q

What is the management of psoriasis?

A

Topical steroids
Topical vitamin D analogues
Phototherapy

167
Q

What is the presentation of acne vulgaris?

A

Red, inflamed, sore spots
Typically on face, upper chest and upper back

168
Q

What is the management of acne vulgaris?

A

No treatment if mild
Topical benzoyl peroxide
Topical retinoids
Topical/oral antibiotics

169
Q

What drugs can cause Stevens-Johnson syndrome?

A

Allopurinol
Lamotrigine
Penicillin
Phenytoin

170
Q

What is the presentation of Stevens-Johnson syndrome?

A

Initially non-specific eg. fever, cough, sore throat, itchy skin
After, the skin starts to blister and break away, causing pain, erythema

171
Q

What is the management of Stevens-Johnson syndrome?

A

Medical emergency admission to dermatology or burns unit
Good supportive care
Steroids
Immunoglobulins
Immunosuppressant medication

172
Q

What are the causes of acute urticaria?

A

Allergies to food/medication/animals
Contact with chemicals/stinging nettles/latex etc
Medications
Viral infection
Insect bites
Rubbing of the skin

173
Q

What is chronic urticaria?

A

An autoimmune condition where autoantibodies target mast cells and cause them to release histamines

174
Q

What is the management of urticaria?

A

Antihistamines –> Fexofenadine
Oral steroids short course for severe flares
Anti-leukotrienes eg. montelukast
Omalizumab
Cyclosporin

175
Q

What is the presentation of urticaria?

A

Small itchy lumps on the skin
Patchy erythematous rash
Association with angioedema and flushing

176
Q

What is the most common causative organism for impetigo?

A

Staphylococcus aureas

Also streptococcus pyogenes

177
Q

What is non-bullous impetigo?

A

Typically occurs around nose and mouth
Forms a golden crust
Do not usually cause systemic symptoms

178
Q

What is the management of non-bullous impetigo?

A

Topical fusidic acid
Antiseptic cream
Control the spread
Oral flucloxacillin to treat more widespread or severe disease

179
Q

What is bullous impetigo?

A

Always caused by S.aureus
Painful and itchy lesions that grow in size and then burst, leaving golden crusts
Can cause patient to be more feverish and unwell
Severe infection with widespread lesion = staphylococcus scalded skin syndrome

180
Q

What vaccines are given after 8 weeks?

A

6-in-1 vaccine (1/3) (diphtheria, tetanus, pertussis, polio, haemophilus influenzae type B, hepatitis B)
Meningococcal type B (1/3)
Rotavirus (1/2)

181
Q

What vaccines are given after 12 weeks?

A

6-in-1 vaccine (2/3) (diphtheria, tetanus, pertussis, polio, haemophilus influenzae type B, hepatitis B)
Pneumococcal (1/2)
Rotavirus (2/2)

182
Q

What vaccines are given after 16 weeks?

A

6-in-1 vaccine (3/3) (diphtheria, tetanus, pertussis, polio, haemophilus influenzae type B, hepatitis B)
Meningococcal type B (2/3)

183
Q

What vaccines are given after 1 year?

A

Haemophilus influenza type B + meningococcal type C
Pneumococcal (2/2)
MMR (1/2)
Meningococcal type B (3/3)

184
Q

What vaccines are given after 3 years and 4 months (40 months)?

A

4-in-1 (diphtheria, tetanus, pertussis, polio)
MMR (2/2)

185
Q

What vaccines are given at 12-13 years old?

A

HPV –> 2 doses given 6-24 months apart

186
Q

What vaccines are given at 14 years?

A

3-in-1 (tetanus, diphtheria and polio)
MenACWY

187
Q

What is the most common cause of encephalitis in children in the UK?

A

HSV-1 from coldsores

Also:
VZV from chickenpox
CMV
EBV from infectious mononucleosis
Adenovirus
Influenza virus
Polio
MMR

188
Q

What is the most common cause of encephalitis in neonates in the UK?

A

HSV-2 from genital herpes contracted during birth

189
Q

What is the presentation of encephalitis?

A

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

190
Q

What is the management of encephalitis?

A

Aciclovir if HSV or VZV
Ganciclovir if CMV

191
Q

What is the causative organism of infectious mononucleosis?

A

EBV (glandular fever)

192
Q

What are typical symptoms of infectious mononucleosis?

A

Fever
Sore throat
Fatigue
Lymphadenopathy
Tonsillar enlargement
Splenomegaly

193
Q

What can cause a rash in infective mononucleosis?

A

Amoxicillin

194
Q

What is the management of infectious mononucleosis?

A

Usually self-limiting
Supportive

195
Q

What is the presentation of mumps?

A

Prodrome:
Fever
Muscle aches
Lethargy
Headache

Parotid gland swelling with pain

196
Q

What is the management of mumps?

A

Supportive with rest fluids and analgesia
Notify PHE

197
Q

What are risk factors for undescended testes?

A

Family history
Low birth weight
Small for gestational age
Prematurity
Maternal smoking during pregnancy

198
Q

What is the management for undescended testes?

A

Watching and waiting
Surgical correction considered if not descended by 6 months

199
Q

During what period of life can neonatal sepsis occur?

A

First 28 days

Early onset = within first 72 hours
Late onset = 7-28 days

200
Q

What are the most common causal organisms of neonatal sepsis?

A

Group B streptococcus
E.coli

201
Q

What are the risk factors for neonatal sepsis?

A

Mother with previous baby with group B strep infection/current GBS colonisation/bacteriuria
Membrane rupture >18 hours
<37 weeks
Low birth weight (<2.5kg)

202
Q

What is the presentation of neonatal sepsis?

A

Respiratory distress
Tachycardia
Apnoea
Lethargy
Jaundice
Seizures
Reduced feeding
Symptoms related to source of infection (eg. respiratory with pneumonia, neurology with meningitis)

203
Q

What investigations are done for neonatal sepsis?

A

Blood culture
FBC
CRP
Blood gases
Urine tests
LP

204
Q

What is the management of neonatal sepsis?

A

First line = IV benzylpenicillin with gentamycin
Maintain oxygen/fluids/electrolytes

205
Q

What is Meckel’s diverticulum

A

A congenital diverticulum of the small intestine

206
Q

What is the rule of 2s for Meckel’s diverticulum?

A

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

207
Q

What is the presentation of Meckel’s diverticulum?

A

Usually asymptomatic
Rectal bleeding
Abdominal pain mimicking appendicitis
Intestinal obstruction

208
Q

What is the management of Meckel’s diverticulum?

A

Removal if symptomatic

209
Q

What is the first line management of a patent ductus arteriosus?

A

Indomethacin –> Ductus arteriosus kept open by prostaglandins so indomethacin (an NSAID) reduces the prostaglandin levels and allows the duct to close

210
Q

What is the presentation of chickenpox?

A

Initial fever
Itchy rash starting on head/trunk before spreading
Rash initially macular then papular then vesicular
Mild systemic upset

211
Q

What are complications of chickenpox?

A

Bacterial superinfection
Cerebellitis
Disseminated intravascular coagulation
Progressive disseminated disease

212
Q

What is the presentation of measles?

A

Prodrome - Iriitable, conjunctivitis, fever
Koplik spots on buccal mucosa
Rash starting behind ears before spreading to whole body
Rash is discrete and maculopapular before becoming blotchy and confluent

213
Q

What is the presentation of rubella?

A

Pink maculopapular rash initially on the face before spreading to whole body
Rash usually fades on day 3-5
Suboccipital/postauricular lymphadenopathy

214
Q

What is the causative organism of slapped-cheek syndrome (erythema infectiosum)?

A

Parvovirus B19

215
Q

What are the symptoms of slapped-cheek syndrome?

A

Lethargy
Fever
Headache
Slapped-cheek rash that spreads to proxial arms and extensor surfaces

216
Q

What is the presentation of Scarlet fever?

A

Fever
Malaise
Tonsillitis
Strawberry tongue
Fine punctate erythema that spares the mouth

217
Q

What is the causative organism of hand, foot and mouth disease?

A

Coxsackie A16 virus

218
Q

What are the symptoms of hand, foot and mouth disease?

A

Sore throat
Fever
Vesicles in mouth, palms and soles

219
Q

What causes Roseola Infantum?

A

HHV-6

220
Q

What is toddler’s diarrhoea?

A

A benign cause of diarrhoea in children due to the fast transit of food through the digestive tract
Can present with undigested food in stool
No treatment required

221
Q

What are the causes of cerebral palsy?

A

Antenatal (80%) - eg. cerebral malformation, infection
Intrapartum (10%) - eg. birth asphyxia/trauma
Postnatal (10%) - eg. intraventricular haemorrhage, meningitis, head trauma

222
Q

What are possible manifestations of cerebral palsy?

A

Abnormal tone in early infancy
Delayed motor milestones
Abnormal gait
Feeding difficulties
Learning difficulties
Epilepsy
Squints
Hearing impairment

223
Q

What are the 4 main subtypes of cerebral palsy?

A

Spastic (70%)
Dyskinetic
Ataxic
Mixed

224
Q

What are the subtypes of spastic cerebral palsy?

A

Hemiplegia
Diplegia
Quadriplegia

225
Q

What are the presentations of spastic cerebral palsy?

A

Increased tone due to UMN damage

226
Q

What are the presentations of dyskinetic cerebral palsy?

A

Athetoid movements (involuntary writhing movements)
Oro-motor problems (eg. drooling)

227
Q

What causes dyskinetic cerebral palsy?

A

Damage to the basal ganglia and substantia nigra

228
Q

What is the presentation of ataxic cerebral palsy?

A

Typical cerebellar signs (DANISH) due to cerebellar damage

229
Q

What is the inheritance pattern of congenital adrenal hyperplasia?

A

Autosomal recessive

230
Q

What is the pathophysiology of congenital adrenal hyperplasia?

A

Defective 21-hydroxylase enzyme
Means that progesterone cannot be converted to aldosterone and cortisol –> presents with low aldosterone and low cortisol
Excess progesterone is converted to testosterone as this conversion does not rely on 21-hydroxylase –> Also presents with abnormally high testosterone

231
Q

What are the likely biochemistry signs in congenital adrenal hyperplasia?

A

Hyponatraemia
Hyperkalaemia
Metabolic acidosis

232
Q

What is the presentation in mild cases of congenital adrenal hyperplasia?

A

Present during childhood or after puberty

Females:
Tall for age
Facial hair
Absent periods
Deep voice
Early puberty
Skin hyperpigmentation (due to increased amounts of ACTH due to low cortisol)

Males:
Tall for age
Deep voice
Large penis
Small testes
Early puberty
Skin hyperpigmentation (due to increased amounts of ACTH due to low cortisol)

233
Q

What is the presentation in severe cases of congenital adrenal hyperplasia?

A

Female patients = Ambiguous genitalia + enlarged clitoris
Hyponatraemia, hyperkalaemia, hypoglycaemia
Poor feeding
Vomiting
Dehydration
Arrhythmias

234
Q

What is the management of congenital adrenal hyperplasia?

A

Cortisol replacement with hydrocortisone
Aldosterone replacement with fludrocortisone
May require surgery for ambiguous genitalia

235
Q

What is hypospadias?

A

Where the urethral meatus in males is abnormally displaced to the ventral side of the penis towards the scrotum

236
Q

What is epispadias?

A

Where the urethral meatus in males is abnormally displaced to the dorsal side of the penis

237
Q

What is the management of hypospadias?

A

Mild cases may not require treatment
Surgery performed after 3-4 months of age to correct the position

238
Q

What conditions are associated with hypospadias?

A

Cryptorchidism
Inguinal hernia

239
Q

What are the presentations of congenital hypothyroidism?

A

Prolonged neonatal jaundice
Poor feeding
Constipation
Increased sleeping
Reduced activity
Slow growth and development

240
Q

What is the most common cause of acquired hypothyroidism?

A

Autoimmune (Hashimoto’s) thyroiditis

241
Q

What are the symptoms of autoimmune thyroiditis?

A

Fatigue and low energy
Poor growth
Weight gain
Poor school performance
Constipation
Dry skin and hair loss

242
Q

What is the management of hypothyroidism?

A

Levothyroxine

243
Q

Where is growth hormone produced?

A

Anterior pituitary gland

244
Q

What is the presentation of growth hormone deficiency?

A

Neonates:
Micropenis
Hypoglycaemia
Severe jaundice

Older infants/children:
Poor growth
Short stature
Slow development of movement and strength
Delayed puberty

245
Q

What is the management of growth hormone deficiency?

A

Daily subcutaneous GH (somatropin)
Close monitoring of height and development

246
Q

What are the causes of anaemia in infancy?

A

Physiological
Prematurity
Blood loss
Haemolysis (eg haemolytic disease of the newborn)
Twin-twin transfusion

247
Q

What investigation is done to check for haemolytic disease of the newborn?

A

Direct Coombs test

248
Q

What is the pathophysiology of haemolytic disease of the newborn?

A

Happens if mother is rhesus D negative and fetus is rhesus D positive
Fetal blood that enters the mother will present rhesus D antigen, which is recognised by mother’s immune system and produce antibodies to the rhesus D antigen
This does not usually cause problems in the first pregnancy
During subsequent pregnancies, the mother’s anti-D antibodies can cross the placenta into the fetus and, if the fetus is rhesus positive, these antibodies attach to fetal red blood cells, causing the fetal immune system to attack the red blood cells, causing haemolysisi and anaemia

249
Q

What are the causes of anaemia in older children?

A

Iron deficiency anaemia (due to dietary insufficiency)
Blood loss i.e. in menstruation
Sickle cell anaemia
Thalassaemia
Leukaemia
Hereditary spherocytosis
Hereditary eliptocytosis
Sideroblastic anaemia
Helminth infection (roundworms, hookworms, whipworms)

250
Q

What are the causes of microcytic anaemia?

A

Thalassaemia
Anaemia of chronic disease
Iron deficiency
Lead poisoning
Sideroblastic anaemia

TAILS

251
Q

What are the causes of normocytic anaemia?

A

Acute blood loss
Anaemia of chronic disease
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism

3As + 2Hs

252
Q

What is megaloblastic anaemia?

A

Impaired DNA synthesis prevents the cell from dividing normally, instead growing into a large abnormal cell

253
Q

What are the causes of megaloblastic macrocytic anaemia?

A

B12 deficiency
Folate deficiency

254
Q

What are the causes of normoblastic macrocytic anaemia?

A

Alcohol
Reticulocytosis
Hypothyroidism
Liver disease
Drugs eg. azathioprine

255
Q

What are the symptoms of anaemia?

A

Tiredness
Shortness of breath
Headaches
Dizziness
Palpitations

256
Q

What are the generic signs of anaemia?

A

Pale skin
Conjunctival pallor
Tachycardia
Raised respiratory rate

257
Q

What is the management of anaemia?

A

Treat underlying cause
Iron supplementation if iron deficient
Blood transfusion if severe

258
Q

What are the main causes of iron deficiency?

A

Dietary insufficiency
Loss of iron eg. heavy menstruation
Inadequate iron absorption eg. Crohn’s disease

259
Q

How does iron travel around the body?

A

In the blood as ferric (Fe3+) ions bound to transferrin

260
Q

How is iron stored in cells?

A

Ferritin

261
Q

What can high ferritin suggest?

A

Inflammation rather than iron overload

262
Q

What is the inheritance pattern of sickle cell anaemia?

A

Autosomal recessive

263
Q

What condition is sickle cell disease protective against?

A

Malaria

264
Q

What is the general management of sickle cell anaemia?

A

Antibiotic prophylaxis to protect against infection
Hydroxycarbamide to stimulate production of fetal haemoglobin (normal)
Blood transfusion/bone marrow transplant if severe
Prophylactic penicillin due to possible splenectomy

265
Q

What is a vaso-occlusive crisis?

A

Caused by sickle red blood cells clogging capillaries, causing distal ischaemia
Symptoms = pain, fever
Associated with dehydration

266
Q

What is a splenic sequestration crisis?

A

Sickle red blood cells blocking blood flow in the spleen
Causes acutely enlarged and painful spleen, and can cause hypovolaemic shock

267
Q

What is an aplastic crisis?

A

Temporary loss of the creation of new blood cells
Triggered by parvovirus B19 infection

268
Q

What is thalassaemia?

A

A genetic defect in the protein chains that make haemoglobin, creating more fragile RBCs

269
Q

What are signs and symptoms of thalassaemia?

A

Microcytic anaemia
Fatigue
Pallor
Jaundice
Gallstones
Splenomegaly (due to increased uptake of destroyed RBCs due to them being more fragile and therefore destroyed more easily)
Poor growth and development
Pronounced forehead and malar eminences (due to expanded bone marrow to produce extra RBCs to compensate for anaemia0

270
Q

What are the causes of iron overload in thalassaemia?

A

Faulty creation of RBCs
Recurrent transfusion
Increased absorption in gut due to anaemia

271
Q

What are the effects of iron overload in thalassaemia?

A

Fatigue
Liver cirrhosis
Infertility
Impotence
Heart failure
Arthritis
Diabetes
Osteoporosis and joint pain

272
Q

What is the presentation of idiopathic thrombocytopenic purpura?

A

Children under 10
Bleeding
Bruising
Petechial or purpuric rash (non-blanching)

273
Q

What are the causes of idiopathic thrombocytopenia?

A

Spontaneous
Viral infection

274
Q

What is the management of idiopathic thrombocytopenic purpura?

A

Often no intervention and monitor until platelets return to normal
Prednisolone
IV immunoglobulins
Blood transfusion
Platelet transfusions

275
Q

What is the most common cause of leukaemia in children?

A

Acute lymphoblastic leukaemia

Also:
Acute myeloid leukaemia
Chronic myeloid leukaemia

276
Q

What is the classification of different leukaemias?

A

Acute or chronic (fast or slow progression)
Myeloid or lymphoid (depending on affected cell line)

277
Q

What is the presentation of leukaemia?

A

Persistent fatigue
Fever
Failure to thrive
Weight loss
Night sweats
Pallor
Petechiae/unexplained bleeding/bruising
Lymphadenopathy
Hepatosplenomegaly

278
Q

What are the investigations for leukaemia?

A

FBC –> Anaemia, leukopenia, thrombocytopenia
Blood film –> Blast cells
Bone marrow biopsy
Lymph node biopsy

279
Q

What chromosomal change is seen in Down’s syndrome?

A

Trisomy 21

280
Q

What are the dysmorphic features of Down’s syndrome?

A

Hypotonia
Bradycephaly (small head with flat back)
Short neck
Short stature
Flattened face and nose
Prominent epicanthic folds (folds on eyelid covering the inner corner)
Upward sloping palpebral fissures (gap between upper and lower eyelids)
Single palmar crease

281
Q

What are complications of Down’s syndrome?

A

Learning disability
Recurrent otitis media
Deafness
Visual problems
Hypothyroidism
Cardiac defects
Dementia

282
Q

What is the chromosomal change seen in Klinefelter syndrome?

A

Male has an extra X chromosome, so becomes 47XXY

283
Q

What are the features of Klinefelter syndrome?

A

Taller height
Wider hips
Gynaecomastia
Weaker muscles
Small testes
Reduced libido
Shyness
Infertility
Subtle learning difficulties

284
Q

What is the chromosomal change in Turner syndrome?

A

Female has only a single X chromosome, becoming 45XO

285
Q

What are the features of Turner syndrome?

A

Short stature
Webbed neck
High arching palate
Downward sloping eyes
Widely spaced nipples
Infertility
Bicuspid aortic valve

286
Q

What conditions are associated with Turner syndrome?

A

Recurrent otitis media/UTI
Coarctation of the aorta
Hypothyroidism
Hypertension
Obesity
Diabetes
Osteoporosis

287
Q

What is the inheritance pattern of Noonan syndrome?

A

Autosomal dominant

288
Q

What are the features of Noonan syndrome?

A

Short stature
Broad forehead
Downward sloping eyes with ptosis
Widely spaced eyes
Prominent nasal folds
Low set ears
Webbed neck
Widely spaced nipples
Pectus excavatum

289
Q

What conditions are associated with Noonan syndrome?

A

Congenital heart disease (ASD, pulmonary valve stenosis)
Undescended testes
Learning disability
Bleeding disorders
Lymphoedema
Leukaemia/neuroblastoma

290
Q

What is the genetic cause of Marfan syndrome?

A

Autosomal dominant condition affecting the gene responsible for fibrillin production (fibrillin is a component of connective tissue)

291
Q

What are the features of Marfan syndrome?

A

Tall stature
Long neck
Long limbs
Long fingers
High arch palate
Hypermobility

292
Q

What conditions are associated with Marfan syndrome?

A

Mitral/aortic regurgitation
Joint dislocations
Scoliosis
Aortic aneurysms

293
Q

What mutation is involved in fragile X syndrome?

A

FMR1 gene on X chromosome, responsible for cognitive development of the brain

294
Q

What are the features of fragile X syndrome?

A

Intellectual disability
Long, narrow face
Large ears
Large testes
Hypermobility
ADHD
Autism
Seizures

295
Q

What is the genetic cause of Prader-Willi syndrome?

A

Loss of functional genes on proximal arm of chromosome 15 inherited from father

296
Q

What are the features of Prader-Willi syndrome?

A

Constant insatiable hunger
Poor muscle tone
Learning disability
Hypogonadism
Narrow forehead

297
Q

What is the genetic cause of Angelman syndrome?

A

Loss of functional genes on chromosome 15 inherited from mother

298
Q

What are the features of Angelman syndrome?

A

Fascination with water
Happy demeanour
Learning disability
Ataxia
Microcephaly
Wide mouth with widely spaced teeth

299
Q

What is the genetic cause of William syndrome?

A

Deletion of genetic material on one copy of chromosome 7
Usually random deletion rather than inheritance

300
Q

What are the features of William syndrome?

A

Very sociable personality
Starburst eyes (star-shaped pattern on iris)
Wide mouth with widely spaced teeth
Broad forehead
Flattened nasal bridge

301
Q

What conditions are associated with William syndrome?

A

Supravalvular aortic stenosis
ADHD
Hypertension
Hypercalcaemia

302
Q

What is the presentation of osteogenesis imperfecta?

A

Hypermobility
Blue sclera
Short stature
Deafness
Dental problems
Bowed legs/scoliosis
Joint and bone pain

303
Q

What is the management of osteogenesis imperfecta?

A

Bisphosphonates
Vitamin D supplementation
Physio/OT
Multidisciplinary team

304
Q

What is the cause of Osgood-Schlatters disease?

A

Inflammation of the tibial tuberosity where the patella ligament inserts

305
Q

What is the presentation of Osgood-Schlatters disease?

A

Hard, tender lump at the tibial tuberosity
Anterior knee pain, exacerbated by physical activity, kneeling and extension

306
Q

What is the management of Osgood-Schlatters disease?

A

Reduction in physical activity
Ice
NSAIDs
Physiotherapy

307
Q

What are the causes of Rickets?

A

Vitamin D/calcium deficiency from diet and sunlight
Genetic

308
Q

What is the presentation of Rickets?

A

Lethargy
Bone pain
Swollen wrists
Poor growth
Dental problems
Bone deformities: Bowing, knock knees, soft skull

309
Q

What is the management of Rickets?

A

Prevention –> Vitamin D supplementation for mothers when breast feeding
Vitamin D/Calcium supplementation

310
Q

What is a common precursor to transient synovitis?

A

Recent viral upper respiratory tract infection

311
Q

What is the presentation of transient synovitis?

A

Limp
Refusal to weight bear
Groin/hip pain
Mild temperature
No signs of systemic illness –> other cause (eg. septic arthritis)

312
Q

What is the management of transient synovitis?

A

Analgesia
Safety net to avoid septic arthritis

313
Q

What is the presentation of septic arthritis?

A

Hot, red, painful, swollen joint
Refusal to weight bear
Stiffness and reduced range of motion
Systemic symptoms –> fever. lethargy, sepsis

314
Q

What is the most common causative organism of septic arthritis?

A

Staphylococcus aureus

315
Q

What is the management of septic arthritis?

A

Aspiration if possible
Aspirate culture/gram staining
Empirical IV antibiotics until organism and sensitivities found
May require surgical washout/drainage

316
Q

What is the most common causative organism of osteomyelitis?

A

Staphylococcus aureus

317
Q

What are the risk factors for osteomyelitis?

A

Open bone fracture
Orthopaedic surgery
Immunocompromised
Sickle cell anaemia
HIV
Tuberculosis

318
Q

What is the presentation of osteomyelitis?

A

Generally unwell
Refusing to weight bear
Pain
Swelling
Tenderness

319
Q

What is the treatment for osteomyelitis?

A

Flucloxacillin
May require drainage

320
Q

What is Perthes disease?

A

Disruption of blood flow to the femoral head causing avascular necrosis

321
Q

What is the presentation of Perthes disease?

A

Hip/groin pain
Limp
Restricted hip movement
Referred pain to the knee
No history of trauma

322
Q

In what age range is Perthes disease most common?

A

5-10 years old

323
Q

What is the management of Perthes disease?

A

Rest until the femoral head revascularises
Analgesia
Surgery in severe cases or in cases where it doesn’t heal

324
Q

What is the presentation of a slipped upper femoral epiphysis?

A

Hip, groin, thigh or knee pain
Restricted range of movement
Painful limp
History of minor trauma –> Pain disproportionate to trauma

325
Q

What is the management of a slipped upper femoral epiphysis?

A

Surgery

326
Q

What are the risk factors for developmental dysplasia of the hip?

A

Family history
Breech presentation
Multiple pregnancy
High birth weight
Oligohydramnios
Prematurity
Being female

327
Q

What tests are used to screen for developmental dysplasia of the hip?

A

Barlow’s and Ortolani tests

328
Q

What is the management of developmental dysplasia of the hip?

A

Pavlik harness (if under 6 months) to hold the femoral head in a correct position and allow the hip to grow normally
Surgery if older than 6 months

329
Q

What medications are used for pain in children?

A

Step 1 = Pracetamol/ibuprofen
Step 2 = Morphine

Codeine, aspirin and tramadol are contraindicated

330
Q

What is the genetic cause of Patau syndrome?

A

Trisomy 13

331
Q

What are the features of Patau syndrome?

A

Small eyes
Cleft lip/palate
Polydactyly
Scalp lesions

332
Q

What is the genetic cause of Edward’s syndrome?

A

Trisomy 18

333
Q

What are the features of Edward’s syndrome?

A

Micrognathia (overbite)
Low set ears
Rocker bottom feet
Overlapping fingers

334
Q

What is the presentation of Pierre-Robin syndrome?

A

Micrognathia
Posterior displacement of the tongue
Cleft palate

335
Q

What are the features of Kawasaki disease?

A

Fever for > 5 days
Widespread erythematous maculopapular rash
Skin peeling on hands and feet
Strawberry tongue
Cracked lips
Cervical lymphadenopathy
Bilateral conjunctivitis

CRASH & BURN (Conjunctivitis, Rash, Adenopathy, Strawberry tongue, Hands (red and swollen) & BURN (fever >5 days))

336
Q

What is the management of Kawasaki disease?

A

High dose aspirin –> Reduce thrombosis risk
IV immunoglobulins –> Reduce coronary artery aneurysm risk

337
Q

What is a key complication of Kawasaki disease?

A

Coronary artery aneurysm –> Echocardiogram

338
Q

What are the key features of juvenile idiopathic arthritis?

A

Joint pain
Swelling
Stiffness

339
Q

What is a complication of juvenile idiopathic arthritis?

A

Chronic anterior uveitis

340
Q

What is the management of juvenile idiopathic arthritis?

A

NSAIDs
Steroids
DMARDs eg. methotrexate, sulfasalazine
Biological therapy eg. infliximab, adalimumab

341
Q

What are the features of Ehlers-Danlos syndrome?

A

Joint hypermobility
Stretchy skin
Joint pain
Abnormal wound healing/easy bruising

342
Q

What is the Beighton score for hypermobility?

A

Palms flat on floor with straight legs (1 point)
Elbows hyperextended (1 point for each side)
Knees hyperextended (1 point for each side)
Thumb touches forearm (1 point for each side)
Little finger hyperextends past 90 degrees (1 point for each side)

Maximum score of 9

343
Q

What is the management of Ehlers-Danlos syndrome?

A

Exclude Marfan syndrome –> Examine for high palate, arachnodactyly, arm span
Physiotherapy/OT
Moderate activity to reduce flares

344
Q

What is the cause of rheumatic fever?

A

Autoimmune but triggered by streptococcus, typically streptococcus pyogenes causing tonsillitis
Antibodies against streptococcus target tissues

345
Q

What is the presentation of rheumatic fever?

A

Fever
Joint pain
Rash
Shortness of breath
Chorea
Nodules
Pericarditis/myocarditis/endocarditis –> tachy/bradycardia, murmurs, pericardial rub, heart failure

346
Q

What is the Jones criteria for diagnosis of Rheumatic fever?

A

2 major OR 1 major + 2 minor

Major:

Joint arthritis
Organ inflammation (eg carditis)
Nodules
Erythema marginatum rash
Sydenham chorea

Minor

Fever
ECG changes without carditis
Arthralgia without arthritis
Raised inflammatory markers

347
Q

What is the management of Rheumatic fever?

A

Antibiotics (penicillin V for 10 days) to treat the strep infection and prevent disease
NSAIDs –> joint pain
Aspirin and steroids –> carditis
Prophylactic antibiotics –> prevent further strep infection

348
Q

What are the categories on the APGAR score?

A

Appearance (skin colour)
Pulse (HR)
Grimace (reflex irritability)
Activity (tone)
Respiration

349
Q

What on the APGAR scores 0/2 for each category?

A

Appearance = Cyanotic/pale all over
Pulse = 0
Grimace = No response to stimuli
Activity = Floppy
Respiration = Apnoeic

350
Q

When should APGAR scores be assessed?

A

1 and 5 minutes after birth

351
Q

What is the ratio of chest compressions to rescue breaths in neonatal CPR?

A

15:2

352
Q

What is respiratory distress syndrome?

A

A condition affect premature (<32 weeks) neonates that are born before the lungs produce surfactant
Inadequate surfactant leads to increased surface tension on the lungs, which leads to lung collapse, and inadequate gas exchange, resulting in hypoxia, hypercapnia and respiratory distress

353
Q

What are the findings of respiratory distress syndrome on a chest xray?

A

Ground-glass appearance

354
Q

What is the management of respiratory distress syndrome?

A

Steroids (dexamethasone) given to mother antenatally if premature birth suspected
Intubation and ventilation to assist breathing
Endotracheal (artificial) surfactant
CPAP
Supplementary oxygen

355
Q

What is the most common cause of neonatal sepsis?

A

Group B streptococcus from the vagina during delivery

356
Q

What are the risk factors of neonatal sepsis?

A

Vaginal Group B strep
GBS sepsis in previous pregnancy
Maternal sepsis
Prematurity
Premature rupture of membrane
Prolonged rupture of membrane

357
Q

What are the clinical features of neonatal sepsis?

A

Fever
Reduced tone and activity
Poor feeding
Respiratory distress
Vomiting
Tachy/bradycardia
Jaundice within 24 hours
Seizures

358
Q

What are the red flags in neonatal sepsis?

A

Maternal sepsis
Shock
Seizures
Respiratory distress starting more than 4 hours after birth

359
Q

What is the management of neonatal sepsis?

A

1 risk factor or clinical feature = monitor
2 or more risk factors/features = antibiotics (benzylpenicillin and gentamycin within 1 hour)
1 red flag = antibiotics (benzylpenicillin and gentamycin within 1 hour)
Blood cultures before antibiotics given

360
Q

What are the causes of hypoxic ischaemic encephalopathy?

A

Maternal shock
Intrapartum haemorrhage
Prolapsed cord
Nuchal cord (cord wrapped around neck)

361
Q

What is physiological jaundice in neonates?

A

High concentration of RBCs that are more fragile + reduced liver function
Fast break down of RBCs, releasing bilirubin, which was previously excreted via placenta
Neonate no longer has access to placenta, so bilirubin levels rise, causing 2-7 days of jaundice
Normally resolves by 10 days

362
Q

After how many days is neonatal jaundice pathological vs physiological?

A

Within first 24 hours = pathological
2-7 days = physiological

363
Q

What are the causes of pathological neonatal jaundice?

A

Increased bilirubin production:
Haemolytic disease of the newborn
Haemorrhage
Polycythaemia

Decreased bilirubin clearance:
Prematurity (immature liver)
Neonatal cholestasis
Extrahepatic biliary atresia
Gilbert syndrome

364
Q

What is the management of neonatal jaundice?

A

Total bilirubin levels monitored and plotted on treatment threshold charts
Phototherapy –> converts unconjugated bilirubin to isomers that can be excreted in bile and urine

365
Q

What is kernicterus?

A

Brain damage caused by excessive bilirubin levels
Bilirubin crosses BBB and causes direct damage to CNS
Damage is permanent
Important to treat once bilirubin passes threshold

366
Q

What are the risk factors for developing necrotising enterocolitis?

A

Very low birth weight
Prematurity
Formula feeds
Respiratory distress and assisted ventilation
Sepsis
Patent ductus arteriosus/other congenital heart disease

367
Q

What is the presentation of necrotising enterocolitis?

A

Intolerance to feeds
Vomiting with green bile
Generally unwell
Distended, tender abdomen
Absent bowel sounds
Blood in stools
Peritonitis/shock = Perforation

368
Q

What is the investigation of choice for necrotising enterocolitis?

A

Abdominal xray –> dilated loops of bowel, bowel wall oedema, gas in the bowel wall, free gas in the peritoneum

369
Q

What is the management of necrotising enterocolitis?

A

IV fluids and antibiotics to stabilise
Surgery to remove dead bowel

370
Q

What are the risk factors for sudden infant death syndrome?

A

Prematurity
Low birth weight
Smoking during pregnancy

371
Q

How do you minimise the risk of sudden infant death syndrome?

A

Put baby on their back when not directly supervised
Keep head uncovered
Keep cot clear of toys and blankets
Maintain comfortable room temperature
Avoid smoking
Avoid co-sleeping

372
Q

What is the classic triad of shaken baby syndrome?

A

Retinal haemorrhages, subdural haematoma and encephalopathy

373
Q

What are the gross motor milestones in development?

A

4 months = Support head
6 months = Maintain sitting position but don’t have balance
9 months = Sit unsupported and start crawling
12 months = Stand and begin cruising
15 months = Walk unaided
18 months = Squat and pick things up from floor
24 months = Run and kick a ball
36 months = Climb stairs one foot at a time, stand on one leg for a few seconds
48 months = Hop, climb stairs like an adult

374
Q

What are the fine motor early milestones in development?

A

8 weeks = Fixes eyes on object 30cm away, show preference for faces over inanimate objects
6 months = Palmar grasp
9 months = Scissor grasp
12 months = Pincer grasp
18 months = Use spoon clumsily to bring food to mouth

375
Q

What are the fine motor drawing milestones in development?

A

12 months = Hold crayon and scribble randomly
2 years = Copies vertical line
2.5 years = Copies horizontal line
3 years = Copies circle
4 years = Copies cross and square
5 years = Copies triangle

376
Q

What are the fine motor tower building milestones for development?

A

14 months = 2 bricks
18 months = 4 bricks
2 years = 8 bricks
2.5 years = 12 blocks
3 years = 3 block bridge or train
4 years = Can build steps

377
Q

What are the expressive language milestones for development?

A

3 months = Cooing
6 months = Makes noises with consonants
9 months = Babbles, sounds like talking but not recognisable words
12 months = Single words in context
18 months = 5-10 words
2 years = Combines 2 words
2.5 years = Combines 3-4 words
3 years = Basic sentences
4 years = Tells stories

378
Q

What are the receptive language milestones in development?

A

3 months = Recognise parents and familiar voices
6 months = Responds to tone of voice
9 months = Listens to speech
12 months = Follows very simple instructions
18 months = Understands nouns (eg. show me the spoon)
2 years = Understands verbs (eg. show me what you eat with)
2.5 years = Understands propositions (eg. put the spoon ON the table)
3 years = Understands adjectives
4 years = Follows complex instructions (more than one instruction at a time)

379
Q

What are the personal and social milestones for development?

A

6 weeks = Smiles
3 months = Communicates pleasure
6 months = Curious and engaged
9 months = Cautious and apprehensive with strangers
12 months = Points, hands objects, waves, claps
18 months = Imitates activities
24 months = Extends interest beyond parents, plays next to but not with other children
36 months = Seek out and play with other children, bowel control
48 months = Dresses self, has friends, imaginative play, dry by night

380
Q

What are the risk factors for meconium aspiration syndrome?

A

Post-date gestation
Small for gestational age

381
Q

What areas of the body can chemotherapy not reach and are therefore areas for relapse?

A

CNS –> due to BBB
Testes

382
Q

What is the common presentation of haemophilia?

A

Easy bruising
Bleeding into muscles/joints
Extensive bleeding after surgery etc

383
Q

What is the inheritance pattern of haemophilia?

A

X-linked recessive –> Only boys can get it (unless affected father and carrier/affected mother)

384
Q

What is the management of haemophilia?

A

IV infusion of clotting factors (either prophylactically or as a response to bleeding)

385
Q

Which clotting factor is deficient in Haemophilia A?

A

Factor VIII

386
Q

Which clotting factor is deficient in Haemophilia B?

A

Factor IX

387
Q

What is the presentation of Hodgkin’s lymphoma?

A

Lymphadenopathy –> Neck/axilla/inguinal, non-tender, rubbery, worse with alcohol
B symptoms –> Fever, weight loss, night sweats
Fatigue
Itching
Cough
SoB
Abdo pain
Recurrent infections

388
Q

What is the key test for diagnosing lymphoma?

A

Lymph node biopsy –> Reed-Sternberg cell

389
Q

What is the staging of lymphoma?

A

Stage 1 = Confined to one region of lymph nodes
Stage 2 = In more than one region but on the same side of the diaphragm (above or below)
Stage 3 = Affects lymph nodes above and below the diaphragm
Stage 4 = Widespread involvement including non-lymphatic organs such as lungs or liver

390
Q

What is the management of Diabetic Ketoacidosis in a patient who is vomiting?

A

IV fluids (0.9% NaCl 10ml/kg) and SC Insulin (0.1units/kg/hour)

391
Q

What is the management of DKA in a patient who is alert and not vomiting?

A

PO fluids and SC insulin

392
Q

What can be seen on a blood test in DKA?

A

Hyperglycaemia
Acidosis
Ketonaemia
Low bicarbonate (Ketones use up bicarbonate)
Mildly raised creatinine (sign of dehydration)
High potassium (Lack of insulin means potassium stays in the blood rather than being transferred to cells)

393
Q

What is the presentation of Henoch-Schonlein purpura?

A

Rash over buttocks, extensor surfaces of arms, legs and ankles (TRUNK IS SPARED)
Joint pain
Abdominal pain
Glomerulonephritis
Fever

Phase 3A Revision (23 decks)

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