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Paediatrics > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Signs of moderate respiratory distress

A

Tachypnoea
Tachycardia
Nasal Flaring
Use of accessory rest muscles
Intercostal and subcostal recession
Head retraction
Inability to feed

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2
Q

Signs of severe respiratory distress

A

Cyanosis
Tiring because of inc work of breathing
Reduced consciousness
Oxygen sat <92 despite O2 therapy

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3
Q

Stridor

A

Harsh musical sound due to partial obstruction of the lower portion of the upper airway including the upper trachea and larynx.

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4
Q

Wheeze

A

Partial obstruction of the intrathoracic airways from mucosal inflammation and swelling.

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5
Q

Physiology of inspiration

A

Contraction and downward movement of the diaphragm + upward and outward movement of ribcage to generate negative pressure - sucks air into lungs

Airway walls are pulled outwards due to negative intrathoracic pressure.

Recoil pressure of chest creates a positive intrathoracic pressure to air is forcibly expelled.

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6
Q

Difference between stridor and stertor

A

Stridor is harsh but musical whilst snoring (stertor) is rough and lacks a single note.

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7
Q

Most common resp infection

A

Upper resp tract infection - average of 5 in first few years of life.

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8
Q

URTI categories

A

Common cold - coryza
Sore throat - pharyngitis, inc tonsillitis
Acute otitis media
Sinusitis

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9
Q

URTI complications in infant

A

Difficulty in feeding in infants as their noses are blocked and obstructs breathing
Febrile seizures
Acute exacerbations of asthma.

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10
Q

Coryza features

A

Clear or mucopurluent nasal discharge and nasal blockage.

Most common - rhinoviruses, coronaviruses and respiratory syncytial virus (RSV)

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11
Q

Treatment coryza

A

Parents are told colds self limiting and have no specific curative treatment.

Paracetamol or ibuprofen for pain PTN

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12
Q

How long does cough persist after common cold

A

4 weeks

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13
Q

Most common cause of stridor

A

Viral laryngotracheobronchitis (croup)

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14
Q

Most common causes of croup

A

Parainfluenza viruses

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15
Q

Age range of croup

A

6 months to 6 years but peak is 2nd year of life.

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16
Q

Typical features of croup

A

Hoarseness due to inflammation of vocal cords

Barking cough - due to tracheal oedema and collapse

Harsh stridor

Variable degree of difficulty breathing with chest retraction

Symptoms start and are worse at night.

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17
Q

Factors influencing admission from croup

A

Time of day
Ease of access to hospital
Childs age (most likely <12 months)
Parental understanding and confidence about the disorder.

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18
Q

Treatment of mild to moderate croup

A

Oral dexomethasone, prednisolone or nebulised steroids (budesonide) reduce severity and need for hospitalisation.

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19
Q

Treatment for severe croup

A

Nebulised epinephrine (adrenaline) with oxygen by face mask.
Observed closely for 2-3 hours.

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20
Q

Acute Epiglossitis

A

Intense swelling of the epiglottis and surrounding tissues associated with septicaemia

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21
Q

Why is acute epiglossitis life threatening

A

High risk of respiratory obstruction

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22
Q

Cause of acute epiglossitis

A

H.influenzae type B

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23
Q

Onset of epiglossitis

A

High fever in a very ill toxic looking child

Intensely painful throat that prevents child swallowing or speaking and saliva drools down the chin

Soft inspiratory stridor and rapidly increasing rest difficulty over hours

The child sitting immobile, upright with an open mouth to optimise airway.

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24
Q

Contrast of epiglossitis to croup

A

Epiglossitis - cough is minimal or absent, and examination of throat reveals swollen epiglottis.

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25
Q

What should happen when acute epiglossitis is queried

A

ENT surgeon
ICU admission incase of respiratory obstruction
Paediatrician and senior anaesthetist
Child intubated.
Iv abx - cefuroxime

Tracheal tube removed after 24 hours and abx given for 3-5 days.

Prophylaxis with rifampicin is offered to close household contacts.

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26
Q

Pseudomenbranous croup

A

Bacterial Tracheitis
High fever, appears ill and paisley progressive airway obstruction.

S.aureus
IV abx and intubation and ventilation.

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27
Q

Ddx for acute stridor that happened suddenly

A

Anaphylaxis or inhaled foreign body

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28
Q

What causes chronic stridor

A

Structural problem either from intrinsic narrowing or collapse of the laryngo-tracheal airway.

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29
Q

Conditions involving stridor

A

Croup
Acute Epiglottitis
Bacterial Tracheitis
Anaphylaxis
Inhaled foreign body

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30
Q

Bronchiolitis and pathogen

A

Most common serious resp infection.

RSV pathogen in 80%.

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31
Q

Symptoms of bronchiolitis

A

Coryzal symptoms precede dry cough and increasing breathlessness
Feeding difficulty
Inc dyspnoea
Recurrent apnoea

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32
Q

RF of severe bronchiolitis

A

Prematurity
Bronchopulmonary dysplasia
Often underlying lung disease
Cystic fibrosis or congenital heart disease.

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33
Q

Finding on examination bronchiolitis

A

Dry wheezy cough
Tachypnoea and tachycardia
Subcostal and intercostal recession
Hyperinflation of the chest
Fine end-inspiratory crackles
High pitched wheezes - expiratory > inspiratory.

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34
Q

Ix bronchiolitis

A

Pulse oximetry
No other routinely recommended.
Cxr and Blood gases only if resp failure suspected.

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35
Q

Hospital admission bronchiolitis

A

Apnoea
Persistent o2 sat of <90% on air
Inadequate oral fluid intake 50-75% normal.
Severe resp distress - grunting, marked chest recession, resp rate over 70 breaths pm

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36
Q

Management bronchiolitis

A

Humidified o2 either nasal cannulae or head box.
Fluids may be needed by nasogastric tube or IV
Assisted ventilation.
Infection control measures.
Most recover in 2 weeks.
However over half will have recurrent episodes of cough and wheeze.

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37
Q

Prevention of bronchiolitis

A

monoclonal antibody - palivizumab IM monthly - reduces number of hospital admissions in high risk preterm infants.

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38
Q

Patterns of wheezing

A
  • Viral episodic wheezing
  • Multiple trigger wheeze
  • Asthma
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39
Q

What causes viral episodic wheeze

A

small airways being more likely to narrow and obstruct due to inflammation and aberrant immune responses to viral infection.

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40
Q

RF of VEW

A

maternal smoking during and or after pregnancy
prematurity
FHx - not a rf but is common

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41
Q

VEW epidemiology

A

more common in males and usually resolves by 5 years of age

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42
Q

Causes of recurrent or persistent childhood wheeze

A

VEW
Multiple trigger wheeze
Asthma
Recurrent anaphylaxis
Chronic aspiration
CF
Bronchopulmonary dysplasia
Bronchiolitis obliterans
Tracheo-bronchomalacia.

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43
Q

Atopic asthma

A

when recurrent wheezing is associated with symptoms between viral infections, and evidence of allergy to one or more inhaled allergens

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44
Q

Allergens causing atopic asthma

A

house dust mite, pollen, pets

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45
Q

Associated conditions with atopic asthma

A

eczema, rhino conjunctivitis, and food allergy

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46
Q

Pathophysiology of asthma

A

Genetic predisposition, atopy or environmental triggers

Bronchial inflammation

Bronchial hyper responsiveness

Airway narrowing

Symptoms

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47
Q

Environmental triggers of asthma

A

URTI
Allergens
Smoking
Cold air
Exercise
Emotional upset or anxiety
Chemical irritants

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48
Q

What does asthmatic wheeze sound like

A

polyphonic noise coming from airways and represents many airways of different sizes vibrating from abnormal narrowing.

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49
Q

Features associated with a high probability of asthma

A

Symptoms worse at night and early morning
Nonviral triggers
Interval symptoms
Personal or fhx of an atopic disease
Positive response to asthma therapy

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50
Q

Signs of longstanding asthma

A

Hyperinflation of the chest
generalised polyphonic expiratory wheeze with prolonged expiratory phase

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51
Q

Ddx asthma

A

CF
Allergic rhinitis
Bronchiectasis

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52
Q

Ix asthma

A

Examination and history - usually diagnostic
Skin prick - in cases of atopy
Cxr - normal
Peak flow or spirometry.
Response to a bronchodilator

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53
Q

Treatment asthma

A

B2 agonists - salbutamol, terbutaline,

Anticholinergic bronchodilator - ipratropium bromide

Inhaled steroids - budenoside, beclometasone, fluticasone, mometasone

Long acting B2 agonists - Salmeterol, formoterol

Methylxanthines - theophylline

LTRA - Montelukast

Oral steroid - prednisolone

Anti-ige monoclonal antibody - omalizumab

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54
Q

Pathways for asthma treatment

A

SABA
Low dose ICS
LTRA
Stop LTRA and add LABA
Change ICS and LABA to MART regime (steroid and laba)

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55
Q

S/E of ICS

A

Height velocity reduced but comes back and catches up in late childhood.

Impaired growth, adrenal suppression and altered bone metabolism.

56
Q

Difference in treatment for asthma in children over 5 and under 5

A

over 5 - Laba is next
under 5 - LTRA

57
Q

S/E of theophylline

A

vomiting,
insomnia
headache
poor conc

58
Q

Prednisolone S/E asthma

A

Adverse effect on growth

59
Q

Criteria for admission to hospital for asthma

A

Have not responded adequately clinically
Becoming exhausted
still have marked reduction in their predicted peak flow or FEV1
Have reduced O2 sat on air <92%

60
Q

Symptoms of asthma attack

A

Tachypnoea
Chest recession
Auscultation - silent chest or wheeze.
Tachycardia
Arrhythmia, hypotension
Exhaustion
Altered consciousness
Tongue cyanosis

61
Q

Peak flow measures and severity of asthma

A

Moderate >50%
Severe 33-50%
Life threatening <33%

62
Q

Trigger for asthma attacks

A

URTI or other viral illness
Allergen
Exercise
Cold air

63
Q

Causes of acute breathlessness in older children

A

Asthma
Pneumonia
Foreign body
Anaphylaxis
Pneumothorax or pleural effusion
Metabolic acidosis
Severe anaemia
HF
Panic attacks

64
Q

Management moderate asthma attacks

A

SABA
Oral prednisolone
Continue bronchodilators for 1-4 hours pre
Discharge when stable on 4h treatment.
Oral prednisolone 3-7 days.

65
Q

Management severe asthma attack

A

High flow oxygen
SABA
Oral prednisolone or IV hydrocortisone
Consider: Inhaled ipratropium, IV SABA or aminophylline or magnesium

66
Q

Treatment life threatening asthma

A

High flow oxygen
SABA
Oral prednisolone or IV hydrocortisone
Nebulised ipratropium
Consider IV B2 agonist
Discuss with PICU

67
Q

If not responding to asthma attack treatment

A

Transfer for HDU / PICU
Ensure medical senior review
IV therapies not already used
CXR - pneumothorax and check blood gases
Mechanical ventilation consideration

68
Q

Features of moderate acute asthma

A

Able to talk in sentences;
Arterial oxygen saturation (SpO2) ≥ 92%;
Peak flow ≥ 50% best or predicted;
Heart rate ≤ 140/minute in children aged 1–5 years; heart rate ≤ 125/minute in children aged over 5 years;
Respiratory rate ≤ 40/minute in children aged 1–5 years; respiratory rate ≤ 30/minute in children aged over 5 years.

69
Q

Features of severe acute asthma

A

Can’t complete sentences in one breath or too breathless to talk or feed;
SpO2 < 92%;
Peak flow 33–50% best or predicted;
Heart rate > 140/minute in children aged 1–5 years; heart rate > 125/minute in children aged over 5 years;
Respiratory rate > 40/minute in children aged 1–5 years; respiratory rate > 30/minute in children aged over 5 years.

70
Q

Features life threatening asthma

A

SpO2 < 92%;
Peak flow < 33% best or predicted;
Silent chest;
Cyanosis;
Poor respiratory effort;
Hypotension;
Exhaustion;
Confusion.

71
Q

Types of inhaler

A

Pressurised metered dose inhaler and spacer (age 0-2)
Breath-acutated metered dose inhaler - 6+
Dry powder inhaler - 4+
Nebuliser - any age

72
Q

Why is a spacer recommended for all children

A

increases drug deposition to the lungs and reduced oropharyngeal deposition reducing steroidal side effects.

73
Q

Asthma review

A

growth and nutrition
Peak flow
Chest - hyperinflation, harrisons sulcus or wheeze
Allergic disorders comorbid?
Atypical features - sputum, finger clubbing, growth failure.
Triggers
Check - vaccinations, asthma management plan, medication stock.

Inhaler technique, lung function tests, peak flow diary, exercise tolerance, sleep, school attendance.

74
Q

Other causes of acute wheezing

A

Atypical pneumonia
Foreign body inhalation
Anaphylaxis

75
Q

What does dry cough suggest

A

with prolonged expiratory phase suggests narrowing of the small sized to moderate airways

76
Q

Barking cough suggests

A

a degree of tracheal inflammation, narrowing or collapse

77
Q

Moist cough suggests

A

mucus secretion or infection of airway.

78
Q

What bacteria causes whooping cough

A

bordetella pertussis.

79
Q

Symptoms whooping cough

A

after a week of coryza (catarrhal phase) ,

Characteristic paroxysmal or spasmodic cough followed by inspiratory whoop (paroxysmal phase) .
Spasms of cough are worse at night and may culminate in vomiting.

80
Q

Signs of paroxysm

A

child goes red or blue in the face and mucus flows from the nose and mouth.

81
Q

How long does paroxysmal phase last

A

3 months.
Symptoms gradually decrease (convalescent phase) but can persist for many months.

82
Q

Ix whooping cough

A

Pernasal swab
PCR
Blood test - lymphocytosis

83
Q

Prophylaxis whooping cough

A

macrolide prophylaxis.
Unimmunised infant contacts should be vaccinated.
Reimmunisation of mothers during pregnancy

84
Q

Abx for whooping cough

A

Macrolide but only effective if started in catarrhal phase.

85
Q

What is difference in symptoms between children and infants

A

apnoea rather than whoop in infants which is potentially dangerous.

86
Q

Complications of pertussis

A

Epistaxis
Subconjunctival haemorrhages
pneumonia
seizures
and bronchiectasis.

87
Q

Most common reasons for persistent cough.

A

Series of respiratory tract infections

Some infection - pertussis and RS and mycoplasma can cause a cough that persists for weeks or months.

88
Q

Persistent cough after an acute infection suggests

A

Indicate unresolved lobar collapse, persistent bacterial bronchitis, or suppurative lung disease.

89
Q

Causes of persistent cough

A

GORD
Asthma
Inhaled foreign body
Parental smoking
Recurrent rest infections
Persistent lobar collapse following pneumonia
TB

90
Q

Most common pathogen causing pneumonia in a newborn

A

Organisms from mothers genital tract - Group B streptococcus, and also gram negative enterococci and bacilli

91
Q

Most common pathogen causing pneumonia in an infant

A

resp viruses, RSV are most common,

but bacterial infections
S.pneumoniae
H.influenzae
B.pertussis
Chlamydia trachoma’s.

92
Q

Most common pathogen causing pneumonia in children 5+

A

Mycoplasma pneumoniae
S.pneumoniae
Chlamydia pneumoniae

93
Q

Most common pathogen causing pneumonia in all ages

A

Mycobacterium TB

94
Q

Clinical symptoms pneumonia

A

Fever, cough and rapid breathing

Preceded by a URTI
Lethargy, poor feeding, and an unwell child.

95
Q

Examination of pneumonia

A

tachypnoea
Nasal flaring
chest undraping
inc resp rate
End inspiratory phase crackles over affected area.

(Consolidation with dullness on percussion
decreased breath sounds
bronchial breathing over affected area - NOT PRESENT IN CHILDREN)

96
Q

Ix of pneumonia

A

CXR
Nasopharyngeal aspirate may identify viral causes, but blood tests inc fbc.

If associated with pleural effusion, blunting of costophrenic angle on CXR.

97
Q

Hospital admission for pneumonia

A

O2 <92%
recurrent apnoea
grunting and or inability to maintain adequate fluid or feed

98
Q

Supportive care pneumonia

A

O2 for hypoxia,
Analgesia for pain
IV fluid to correct dehydration and maintain adequate hydration and sodium balance.

99
Q

Management pneumonia

A

Newborn - broad spectrum ABx

Older - amoxicillin - co-amoxiclav for complicated or unresponsive pneumonia.

Children 5+ - Macrolide such as erythromycin

100
Q

Complications of pneumonia

A

small parapneumonic effusions

Persistent fever >48 hours suggests pleural collection which requires drainage with a small chest drain and regular instillation of a fibrinolytic agent to break down fibrin strands.

101
Q

Follow up pneumonia

A

Those who have simple consolidation, none required
Those with evidence of lobar collapse, repeat CXR 4-6 weeks to check lung fields

102
Q

What is persistent bacterial bronchitis

A

Persistent inflammation of the Lower airways driven by chronic infection leading to chronic wet cough.

103
Q

Common organisms of persistent bacterial bronchitis

A

H.influenzae and m.catarrhalis.

104
Q

Treatment of persistent bacterial bronchitis

A

high dose abx, - co-amoxiclav coupled with physio therapy.

105
Q

Ddx of persistent bacterial bronchitis

A

Bronchiectasis

106
Q

Average life expectancy CF

A

40s

107
Q

CF dysfunction

A

defective protein called the CF transmembrane conductance regulator CFTR which is a Cyclic amp dependent chloride channel found in membrane of cells.

Located on chromosome 7 - ΔF508

108
Q

Mutation I CF

A

nonsense / frameshift mutation. no protein synthesised

109
Q

Mutation II CF

A

Incorrect folding - cannot traffic to membrane

110
Q

Mutation III CF

A

Channel opening defect.

111
Q

Mutation IV CF

A

Pore abnormalities cause decreased conductance

112
Q

Mutation V CF

A

Splicing abnormality - reduced protein synthesis

113
Q

Mutation VI CF

A

Shortened half life of protein.

114
Q

Pathophysiology CF

A

Abnormal ion transport across epithelial cells. Reduction in airway surface liquid layer and consequent impaired ciliary function and retention of mucopurulent secretions.

Defective CFTR causes dysregulation of inflammation and defence against infection. Thick viscid meconium in intestine can lead to meconium ileum

Pancreatic ducts become blocked by thick secretions leading to pancreatic enzyme deficiency and malabsorption

Abnormal function of sweat glands leads to excessive concentrations of sodium and chloride in sweat

115
Q

Clinical features of newborn CF

A

Diagnosed through newborn screening
Meconium ileus

116
Q

Clinical features of Infant CF

A

prolonged neonatal jaundice
Growth faltering
Recurrent chest infections
Malabsorption and steatorrhoea

117
Q

Clinical features of young child CF

A

Bronchiectasis
Rectal prolapse
Nasal polyp
Sinusitis

118
Q

Clinical features of older child and adolescent CF

A

Allergic bronchopulmonary aspergillosis
DM
Cirrhosis and portal hypertension
Distal intestinal obstruction
Sterility in males
Pneumothorax or recurrent haemoptysis

119
Q

General signs and symptoms of CF

A

Recurrent chest infections, faltering growth or malabsorption.

Damage to bronchial wall, bronchiectasis and abscess formation.

Persistent wet cough and productive purulent sputum.

Hyperinflation of the chest, coarse inspiratory crepitations and or expiratory wheeze.

120
Q

Ix CF

A

Sweat test - markedly elevated chloride

Stimulated by low voltage current to pilocarpine applied to skin.

Captured into a special capillary tube or absorbed onto a weighted piece of filter paper.

Testing for gene abnormality

121
Q

Management CF

A

Physio twice daily

Prophylactic oral Abx - flucloxacillin
Persisting symptoms or signs use PIC (peripherally inserted central line) IV

Nebulised DNase or hypertonic saline may be helpful to decrease viscosity of sputum and to increase clearance.

Pseudomonas infection - treated with nebulised antipseudomonal abx

Macrolide abx azithromycin - dec resp exacerbations

Bilateral sequential lung transplantation only option for end stage CF lung disease.

122
Q

Nutritional management CF

A

Pancreatic replacement therapy with all meals and snacks.
High calorie diet is essential and dietary intake 150% normal.
Overnight feeding via gastrostomy tube is used.

Fat soluble vitamin supplements,

123
Q

Periodic review of child with CF

A

Sweat
Central venous line?
Chest - hyper expansion, harrisons sulcus, coarse inspiratory crepitations, chest infection.
Monitor for potential complications
Sputum
Growth
Nutrition
Review of chest problems - spirometry, breathing exercises, nebulised antipseudomonal antibiotics and DNase.
General overview - school and specific problems.

124
Q

Later complications of CF

A

DM
Hepatomegaly and liver failure
Pneumothorax
Infertility

125
Q

Why are males infertile with CF

A

absence of vas deferens

Can be outdone with intracytoplasmic sperm injection.

126
Q

What is primary ciliary dyskinesia

A

Congenital abnormality in the structure of cilia lining of resp tract
Impaired mucociliary clearance

127
Q

Symptoms and signs of primary ciliary dyskinesia

A

recurrent infection of upper and lower respiratory tracts
Severe bronchiectasis
Recurrent productive cough
purulent nasal discharge
chronic ear infections

128
Q

Kartagener syndrome

A

major organs are in mirror position to normal

129
Q

Diagnosis of PCD

A

examination of the structure and function of cilia of nasal epithelial cells brushed from norse

130
Q

Management PCD

A

daily physio to clear secretions, proactive treatment of infections with abx and appropriate ENT intervention

131
Q

Pathophysiology sleep disordered breathing

A

During REM sleep control of breathing becomes unstable and there is relaxation of voluntary muscles in the upper airway and chest. Makes upper airway collapse more likely.

Either due to airway obstruction, dental hypoventilation or a combination

132
Q

History of sleep disordered breathing

A

loud snoring
witnessed pauses in breathing (apnoeas)
restlessness and disturbed sleep.

133
Q

Complications of obstructive sleep apnoea

A

excessive daytime sleepiness, hyperactivity, learning and behaviour problems, faltering growth, and in severe cases pulmonary hypertension.

134
Q

Cause of obstructive sleep apnoea

A

upper airway obstruction secondary to adenotonsillar hypertrophy

Duchenne muscular dystrophy

craniofacial abnormalities

dystonia of upper airway muscles

severe obesity

135
Q

Ix of sleep disordered apnoea

A

overnight pulse oximetry

normal does not exclude diagnosis but means severe physical consequences are unlikely.

sometimes assess neurological arousals and sleep staging

136
Q

Management sleep disordered breathing in pt with andenotonsillar hypertrophy

A
  • adenotonsillectomy
137
Q
A

Paediatrics (17 decks)

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