Respiratory Flashcards

1
Q

What is bronchiolitis?

A

Inflammation and infection in the bronchioles, generally considered to occur in children under 1 year.

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2
Q

Aetiology of bronchiolitis?

A

Respiratory syncytial virus (RSV).

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3
Q

Presentation of bronchiolitis.

A
  • coryzal symptoms
  • signs of respiratory distress
  • dyspnoea
  • tachypnoea
  • poor feeding
  • mild fever
  • apnoeas
  • wheeze and crackles on auscultation
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4
Q

Signs of respiratory distress.

A
  • tachypnoea
  • use of accessory muscles
  • intercostal and subcostal recession
  • nasal flaring
  • head bobbing
  • tracheal tugging
  • cyanosis
  • abnormal airway noises
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5
Q

Define the characteristics of:

a) wheezing

b) grunting

c) stridor

A

a) whistling sound caused by narrowed airways, typically heard during expiration.

b) exhalation with the glottis partially closed, increasing positive end-expiratory pressure.

c) high pitched inspiratory noise caused by obstruction of the upper airway, for example in croup.

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6
Q

Typical RSV course.

A
  1. URTI with coryzal symptoms.
  2. Spontaneous resolution within a few days OR:
  3. Chest symptoms

Symptoms usually last 7-10 days, and patients fully recover within 2-3 weeks.

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7
Q

When to admit a child with bronchiolitis.

A
  • aged <3 months
  • prematurity
  • Downs syndrome
  • CF
  • <75% normal milk intake
  • clinical dehydration
  • RR >70
  • SpO2 <92%
  • moderate to severe respiratory distress
  • apnoeas
  • parents not confident in their ability to manage at home
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8
Q

Management of bronchiolitis.

A

Patients typically only require supportive management:
- ensuring adequate food and fluid intake (e.g. NG / IV tube)
- saline nasal drops and nasal suctioning to clear nasal secretions
- supplementary oxygen
- ventilatory support if required

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9
Q

What are the types of ventilatory support available for children?

A
  1. High-flow humidified oxygen via a tight nasal cannula. This delivers air and oxygen continuously with some added pressure.
  2. Continuous positive airway pressure (CPAP). This delivers oxygen continuously with high pressure added.
  3. Intubation and ventilation. This involves inserting an endotracheal tube into the trachea to fully control ventilation.
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10
Q

How is ventilation assessed in children?

A

Capillary blood gas monitoring.

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11
Q

What are the signs of poor ventilation on capillary blood gas in children?

A

Rising pCO2 - showing the airways have collapsed and can’t clear waste carbon dioxide.

Falling pH - showing CO2 is building up and causing a respiratory acidosis.

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12
Q

What can be used to prevent bronchiolitis in high-risk babies.

A

For babies who are ex-premature and those with congenital heart disease, administer Palivizumab.

It is a monoclonal antibody that provides passive immunity to RSV, therefore a monthly injection is required.

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13
Q

Acute asthma presentation.

A
  • progressive shortness of breath
  • signs of respiratory distress
  • tachypnoea
  • expiratory wheeze on ausculation heard throughout the chest
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14
Q

BTS (2016) criteria for moderate asthma exacerbation.

A
  • PEFR >50% predicted
  • normal speech
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15
Q

BTS (2016) criteria for severe asthma exacerbation.

A
  • PEFR <50% predicted
  • SpO2 <92%
  • unable to complete sentences in one breath
  • signs of respiratory distress
  • tachypnoea
  • tachycardia
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16
Q

BTS (2016) criteria for life threatening asthma exacerbation.

A
  • PEFR <33% predicted
  • saturations <92%
  • exhaustion and poor respiratory effort
  • hypotension
  • silent chest
  • cyanosis
  • altered consciousness / confusion
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17
Q

General management of acute asthma exacerbation.

A
  • supplementary oxygen
  • bronchodilators
  • steroids
  • antibiotics if bacterial cause is suspcected
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18
Q

Management of mild asthma exacerbation.

A

Manage as an outpatient with regular salbutamol inhalers via a spacer (4-6 puffs every 4 hours).

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19
Q

Management of moderate / severe asthma exacerbation.

A
  1. Salbutamol inhalers via a spacer device.
  2. Nebulisers with salbutamol / ipratropium bromide
  3. Oral prednisolone
  4. IV hydrocortisone
  5. IV magnesium sulphate
  6. IV salbutamol
  7. IV aminophylline

Use a stepwise approach and escalate after each step; escalate for anaesthetics to consider intubation and ventilation.

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20
Q

Monitoring when using salbutamol inhalers.

A

Monitoring of U&Es required as salbutamol causes potassium to be absorbed from the blood into the cells (hypokalaemia).

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21
Q

When is discharge for an acute asthma exacerbation considered?

A

When the child is well on 6 puffs every 4 hours of salbutamol. They can be prescribed a reducing regime of salbutamol to continue at home.

Consider:
- finish the course of steroids if they were started
- provide safety-net information about when to return to hospital or seek help
- provide an individualised asthma action plan

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22
Q

What is chronic asthma?

A

A chronic inflammatory airway disease leading to variable airway obstruction.

The smooth muscle in the airways is hypersensitive, and bronchoconstricts when responding to stimuli.

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23
Q

Presentation suggesting chronic asthma.

A
  • episodic symptoms with intermittent exacerbations
  • diurnal variability
  • dry cough with wheeze and shortness of breath
  • typical triggers
  • family history / personal history of atopy
  • bilateral wheeze
  • symptoms improve with bronchodilators
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24
Q

What features in the presentation would indicate a diagnosis other than asthma?

A
  • wheeze only related to coughs and colds
  • isolated or productive cough
  • normal investigations
  • no response to treatment
  • unilateral wheeze
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25
Q

What does unilateral wheeze suggest?

A
  • focal lesion
  • inhaled foreign body
  • infection
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26
Q

Typical triggers for asthma.

A
  • dust
  • animals
  • cold air
  • exercise
  • smoke
  • food allergens
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27
Q

How is asthma diagnosed?

A
  • spirometry with reversibility testing (age >5 years)
  • direct bronchial challenge test with histamine
  • FeNO
  • peak flow variability
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28
Q

BTS (2016) for chronic asthma management in children aged under 5 years.

A
  1. SABA inhaler prn
  2. Add low dose corticosteroid inhaler
  3. Add LTRA (e.g. montelukast)
  4. Refer to a specialist
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29
Q

BTS (2016) for chronic asthma management in children aged 5 to 12 years.

A
  1. SABA inhaler prn
  2. Add regular low dose corticosteroid inhaler
  3. Add LABA inhaler; continue if response good
  4. Titrate up corticosteroid inhaler to a medium dose
  5. Add LTRA or theophylline
  6. Titrate up corticosteroid inhaler to a high dose
  7. Refer to a specialist
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30
Q

BTS (2016) for chronic asthma management in children aged over 12 years.

A

Same as adults:

  1. SABA inhaler prn
  2. Add regular low dose corticosteroid inhaler
  3. Add LABA inhaler; continue if good response
  4. Titrate up the corticosteroid inhaler to a medium dose
  5. Add LTRA or LAMA
  6. Titrate up the corticosteroid inhaler to a high dose
  7. Refer to specialist
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31
Q

What is the effect of inhaled corticosteroids in children?

A

Evidence that inhaled steroids can cause a small reduction in final adult height of up to 1cm when used long-term. This is dose dependent, and the child will have regular asthma reviews to ensure they are growing well.

Inhaled corticosteroids are effective medications that work to prevent poorly controlled asthma and asthma attacks, which could lead to higher doses of oral steroids being given. Poorly controlled asthma can lead to a more significant impact on growth and development.

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32
Q

How is inhaler technique optimised in children?

A

Use with a spacer device to maximise the effectiveness.

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33
Q

MDI technique without a spacer.

A
  1. Remove the cap
  2. Shake the inhaler (depending on the type)
  3. Sit or stand up straight
  4. Lift the chin slightly
  5. Fully exhale
  6. Make a tight seal around the inhaler between the lips
  7. Take a steady breath in whilst pressing the canister
  8. Continue breathing for 3 – 4 seconds after pressing the canister
  9. Hold the breath for 10 seconds or as long as comfortably possible
  10. Wait 30 seconds before giving a further dose
  11. Rinse the mouth after using a steroid inhaler
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34
Q

MDI technique with a spacer.

A
  1. Assemble the spacer
  2. Shake the inhaler (depending on the type)
  3. Attach the inhaler to the correct end
  4. Sit or stand up straight
  5. Lift the chin slightly
  6. Make a seal around the spacer mouthpiece or place the mask over the face
  7. Spray the dose into the spacer
  8. Take steady breaths in and out 5 times until the mist is fully inhaled
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35
Q

Presentation of pneumonia.

A
  • cough (wet and productive)
  • fever
  • tachypnoea
  • tachycardia
  • increased work of breathing
  • lethargy
  • delirium
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36
Q

Signs of pneumonia.

A
  • tachypnoea
  • tachycardia
  • hypoxia
  • hypotension
  • fever
  • confusion
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37
Q

Chest signs of pneumonia.

A
  • bronchial breath sounds
  • focal coarse crackles
  • dullness to percussion
38
Q

Aetiology of pneumonia.

A

Bacterial:
- streptococcus pneumonia is most common bacterial cause
- Staphylococcus aureus
- Haemophilus influenza

Viral:
- RSV is most common viral cause
- parainfluenza virus
- influenza virus

39
Q

Investigations for pneumonia in children.

A
  • CXR
  • sputum cultures
  • throat swabs for bacterial cultures and viral PCR
  • blood cultures if ?sepsis
  • capillary blood gas analysis
40
Q

Management of pneumonia in children.

A

Amoxicillin used first line.

Add macrolide (e.g. erythromycin, clarithromycin) to cover for atypical pneumonia.

Oxygen if SpO2 <92%

41
Q

How are recurrent respiratory tract infections investigated?

A
  • FBC to check levels of WCC
  • CXR for structural abnormality
  • serum immunoglobulins
  • IgG to previous vaccines
  • sweat test for CF
  • HIV test
42
Q

What is croup?

A

An upper respiratory tract infection causing oedema in the larynx, most commonly affecting children aged 6 months to 2 years.

43
Q

Aetiology of croup.

A
  • parainfluenza
  • influenza
  • adenovirus
  • RSV
44
Q

Presentation of croup.

A
  • increased work of breathing
  • barking cough
  • hoarse voice
  • stridor
  • low-grade fever
45
Q

Management of croup.

A

Mostly managed at home with simple supportive management (fluids and rest).

In severe croup:
- oral dexamethasone
- oxygen
- nebulised budesonide
- nebulised adrenalin
- intubation and ventilation

46
Q

Prognosis of croup.

A

Usually improves spontaneously in less than 48 hours.

Responds well to steroids, particularly dexamethasone, in severe infection.

47
Q

What is epiglottitis?

A

The inflammation and swelling of the epiglottis caused by infection.

The epiglottis can swell to the point of completely obscuring the airway within hours of symptoms developing.

48
Q

Aetiology of epiglottis.

A

Haemophilus influenza type B.

Epiglottis is now rare due to the routine vaccination program.

49
Q

Presentation of epiglottitis.

A
  • sore throat
  • stridor
  • drooling
  • high fever
  • difficulty or painful swallowing
  • muffled voice
  • scared and quiet child
  • septic and unwell appearance
50
Q

Epiglottitis investigations.

A

If the patient is acutely unwell and epiglottitis is suspected then investigations should not be performed.

Neck xrays are useful in excluding a foreign body.

51
Q

Management of epiglottitis.

A

Life-threatening emergency.

Stay calm and involve senior paediatrician and anaesthetics immediately to secure the airway.

Additional treatment includes:
- IV abx (e.g. ceftriaxone)
- steroids (i.e. dexamethasone)

52
Q

Prognosis of epiglottitis.

A

Most children recover without requiring intubation.

Most patients that are intubated can be extubated after a few days, and make a full recovery.

Death is rare, but possible if not diagnosed or managed in time.

53
Q

Complications of epiglottitis.

A

Epiglottic abscess - a collection of pus around the epiglottis.

This threatens the airway, making it a life threatening emergency. Treatment is similar to epiglottitis.

54
Q

What is laryngomalacia?

A

A condition affecting infants, where the part of the larynx above the vocal cords is structured in a way to cause partial airway obstruction.

55
Q

Structural changes in laryngomalacia.

A

The aryepiglottic folds are shortened, pulling on the epiglottis and changing it to an ‘omega’ shape.

The tissue surrounding the supraglottic larynx is soft, meaning it can flop across the airway.

This causes an inspiratory stridor.

56
Q

Presentation of laryngomalacia.

A
  • inspiratory stridor
  • feeding difficulty
  • peaks at 6 months of age
57
Q

Management of laryngomalacia.

A

The problem usually resolves as the larynx matures and grows, preventing it from flopping of the airway.

Rarely tracheostomy may be necessary.

Surgery is also an option to alter the tissue in the larynx, and improve the symptoms.

58
Q

What is Whooping cough?

A

An URTI caused by Bordetella pertussis, a gram negative bacteria.

It causes severe coughing fits that prevent the child from taking in air between coughs, subsequently making a loud whooping sound as they forcefully suck in air after the coughing finishes.

59
Q

Presentation of Whooping cough.

A

Begins with mild coryzal symptoms, dry cough and low grade fever.

Severe coughing fits develop within around a week, following by a large inspiratory whoop.

60
Q

Diagnosis of Whooping cough.

A

Nasopharyngeal or nasal swab with PCR testing or bacterial culture can confirm the diagnosis.

61
Q

Management of Whooping cough.

A

Management typically involves supportive care.

Macrolide antibiotics (e.g. erythromycin, clarithromycin) can be useful in the early stages.

Whooping cough is a notifiable disease and close contacts are given prophylactic antibiotics if they are in a vulnerable group.

62
Q

Prognosis of Whooping cough.

A

Symptoms typically resolve within 8 weeks, but can last longer.

A key complication is bronchiectasis.

63
Q

What is bronchiectasis?

A

Permanent dilation of the bronchi as a result of damage to the airways:
- idiopathic
- pneumonia
- Whooping cough
- Tuberculosis
- cystic fibrosis

64
Q

Symptoms of bronchiectasis.

A
  • shortness of breath
  • chronic productive cough
  • recurrent chest infections
  • weight loss
65
Q

Signs of bronchiectasis.

A
  • cachexia
  • finger clubbing
  • scattered crackles
  • scattered wheezes and squeeks
66
Q

How is bronchiectasis investigated?

A

Sputum culture to identify any colonising organisms.

Chest X-ray.

HRCT showing signet ring sign.

67
Q

What are the most common infective organisms in bronchiectasis?

A
  • Haemophilus influenza
  • Pseudomonas aeruginosa
68
Q

Management of bronchiectasis.

A
  • vaccines
  • respiratory physiotherapy
  • pulmonary rehabilitation
  • long-term antibiotics
  • long acting bronchodilators
  • long-term oxygen therapy
  • surgical lung resection

Infective exacerbations require:
- sputum culture
- extended courses of antibiotics (7-14 days)

69
Q

What is chronic lung disease of prematurity (CLDP)?

A

Bronchopulmonary dysplasia occuring in premature babies, typically those born before 28 weeks gestation.

These babies suffer with respiratory distress syndrome and require oxygen therapy (CPAP), or intubation and ventilation.

70
Q

Features of CLDP.

A
  • low oxygen saturations
  • increased work of breathing
  • poor feeding and weight gain
  • crackles and wheezes on chest auscultation
  • increased susceptibility to infection
71
Q

How can CLDP be prevented?

A
  • maternal administration of corticosteroids if premature labour
  • CPAP preferentially used as NIV
  • caffeine used to stimulate respiratory effort in baby
72
Q

Management of CLDP.

A

A sleep study to assess oxygen saturations during sleep supports the diagnosis and guides management.

Babies can be discharged on low dose oxygen to continue at home. They are followed up to wean the oxygen level over the first year of life.

Babies with CLDP require protection against RSV; this involves monthly injections of palivizumab.

73
Q

Inheritance pattern of cystic fibrosis.

A

Autosomal recessive

74
Q

Pathophysiology of cystic fibrosis.

A

Genetic mutation of the CFTR gene, which usually codes for cellular chloride channels:
- thick pancreatic and biliary secretions
- low volume thick airway secretions
- congenital bilateral absence of the vas deferens

75
Q

Presentation of cystic fibrosis.

A

Screened for on newborn blood spot test.

Meconium ileus: the meconium is thick and sticky, causing it to get stuck and obstruct the bowel. This presents as not passing meconium within 24 hours, abdominal distention and vomiting.

76
Q

Symptoms of cystic fibrosis.

A
  • chronic cough
  • thick sputum production
  • recurrent respiratory tract infections
  • steatorrhoea
  • abdominal pain and bloating
  • growth failure
77
Q

Signs of cystic fibrosis.

A
  • growth failure
  • nasal polyps
  • finger clubbing
  • crackles and wheezes
  • abdominal distention
78
Q

Causes of clubbing in children.

A
  • hereditary clubbing
  • cyanotic heart disease
  • infective endocarditis
  • cystic fibrosis
  • tuberculosis
  • inflammatory bowel disease
  • liver cirrhosis
79
Q

How can cystic fibrosis be diagnosed?

A

Newborn blood spot testing.

Sweat test is GOLD STANDARD.

Genetic testing for CFTR gene.

80
Q

What are the key microbial colonisers in cystic fibrosis?

A
  • Staphylococcus aureus
  • Psuedomonas aeruginosa
  • Haemophilus influenzae

Patients with cystic fibrosis take long term prophylactic flucloxacilin to prevent Staph. aureus infection.

81
Q

What is the risk of Psuedomonas in cystic fibrosis?

A

Psuedomonas aeruginosa is multi-drug resistant and difficult to clear.

It leads to significant increase in morbidity and mortality in patients with cystic fibrosis.

82
Q

Management of cystic fibrosis.

A

Manage by a specialist MDT:
- chest physiotherapy
- exercise
- high calorie diet
- CREON tablets
- prophylactic flucloxacillin
- bronchodilators
- vaccinations including pneumococcal, influenza and varicella

Other treatment options may include lung transplantation, fertility treatment and genetic counselling.

83
Q

Monitoring of patients with cystic fibrosis.

A
  • clinic appts every 6/12
  • sputum cultures regularly

Monitoring and screening for:
- diabetes
- osteoporosis
- vitamin D deficiency
- liver failure

84
Q

Prognosis of cystic fibrosis.

A

Life expectancy is improving and the cystic fibrosis trust gives a median life expectancy of 47 years.

85
Q

Complications of cystic fibrosis.

A
  • pancreatic insufficiency (90%)
  • cystic fibrosis-related diabetes
  • liver disease
  • infertility (M only)
86
Q

Inheritance pattern of primary ciliary dyskinesia (PCD).

A

Autosomal recessive

87
Q

Pathophysiology of PCD.

A

Genetic mutation causing dysfunction of motile cilia around the body, particularly the respiratory tract.

This leads to a build up of mucus within the lungs, providing a site of infection that is not easily cleared.

This allows for frequent and chronic chest infections, poor growth, and bronchiectasis.

88
Q

Link between PCD and infertility.

A

Cilia in the fallopian tubes of women, and flagella of sperm in men, are affected.

89
Q

What are the key features of PCD?

A

Kartagner’s triad:
1. Paranasal sinusitis
2. Bronchiectasis
3. Situs inversus

90
Q

What is Situs inversus?

A

A condition where all the internal organs are mirrored inside the body.

Situs inversus on its own does not cause any problems, and the patient can expect to live a normal life.

91
Q

Diagnosis of PCD.

A
  • recurrent respiratory tract infections
  • CXR to diagnose situs invertus
  • semen analysis for male infertility

Bronchoscopy with biopsy of ciliated epithelium required for GOLD STANDARD diagnosis.

92
Q

Management of PCD.

A

Managed by MDT:
- respiratory physiotherapy
- high calorie diet
- prophylactic antibiotics
- exercise
- vaccinations