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Y4 Paediatrics > Resp > Flashcards

Resp Flashcards

1
Q

what is asthma?

A

“Chronic respiratory condition associated with airway inflammation and hyper-responsiveness” leading to episodes of bronchoconstriction where airways narrow and obstruct airflow to lungs

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2
Q

what is the pathophysiology of asthma?

A

type 1 hypersensitivity reaction immediately where allergens react with IgE causing mast degranulation to release histamine leading to bronchoconstriction

then comes the type 4 hypersensitivity late phase where mediators and cytokines cause inflammation in airways

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2
Q

what are some risk factors for asthma?

A
  • genetics, low birth weight, parental smoking
  • personal or FHx
  • antenatal factors: maternal smoking, viral infection during pregnancy
  • exposure to high concentrations of allergens
  • hygiene hypothesis
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3
Q

what are some key points in the history of asthma?

A
  • env triggers: exercise, allergens, weather, infections, medications
  • dry cough, wheeze b/L, chest tightness, SOB
  • episodic, worse at night, family history
  • frequent hospital admissions
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4
Q

what are some key examination findings of asthma?

A

*normal inbetween attacks
- finger clubbing (not for asthma, CF or bronchiectasis)
- chest shape - hyperinflated chest
- chest symmetry
- breath sounds
- crepitations (not only asthma)
- wheeze!!
- tonsillar enlargement - infection

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5
Q

how is asthma investigated?

A
  • fractional inhaled NO
  • over 5y spirometry, bronchodilator with reversibility
  • bronchial challenge
  • CXR
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6
Q

what is the aim of asthma management?

A

good symptom control with full school attendance, no sleep disturbance, <2 a week of daytime sx, no limitation on daily activities, SABA <2/ week and normal lung function

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7
Q

how is asthma managed?

A
  • SABA —> ICS —> add on therapy like ICS+ LABA —> increase ICS —> stop LABA and add montelukast —> oral steroids and resp paediatrician
  • then potential monoclonal antibody therapy with Omalizumab for those with persistent poor control and raised IgE
  • general Mx
    • spacer use
    • question compliance
    • LABA given as combination inhaler with ICS
    • asthma management plan!
    • inhaler technique review with asthma or practice nurse
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8
Q

how do you define mild/ moderate asthma exacerbation?

A

SpO2 - >92%
talking in full sentences
wheeze audible
no accessory muscle use
RR <30

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9
Q

how do you define severe asthma exacerbation?

A

SpO2 <92%
PEFR 33-50%
too breathless to feed or talk
use of accessory muscles
audible wheeze
RR> 30

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10
Q

how do you define life threatening asthma?

A

SpO2 <92%
PEFR <33%
silent chest
altered consciousness
cyanosis

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11
Q

how is an asthma exacerbation managed?

A
  • Oxygen
  • salbutamol can be given with O2 *make sure it is asthma as salbutamol increases HR so could exacerbate conditions.
  • 3 day course of oral prednisolone (if vomiting or unwell IV hydrocortisone)
  • Ipatropium and reassess
  • Mg IV
  • Escalate!
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12
Q

how do you ensure a safe discharge post exacerbation of asthma?

A

bronchodilators taken with spacer every 4h, SATS over 94%, inhaler technique assessed and taught, asthma management plan updated and explained to parents, GP review within 2 days after discharge

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13
Q

what is the pathophysiology of bronchiectasis?

A
  • Abnormal dilatation of the airways with associated destruction of bronchial tissue
  • Inflammatory response to severe infection leads to structural damage within the bronchial walls, which causes dilatation, scarring as a result
  • This reduces the number of cilia within the bronchi which predisposes them to further infections
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14
Q

what are some common causes of bronchiectasis?

A
  • CF
  • post-infectious due to strep pneumonia
  • immunodeficiency
  • primary ciliary dyskinesia
  • post-obstructive foreign body
  • congenital syndromes
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15
Q

what are some key points in a history for bronchiectasis?

A
  • Chronic productive cough
  • purulent sputum expectoration
  • chest pain
  • wheeze
  • SOB on exertion
  • haemoptysis
  • recurrent or persistent LRTI
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16
Q

what are some complications of bronchiectasis?

A
  • recurrent infection
  • life-threatening haemoptysis
  • lung abscess
  • pneumothorax
  • poor growth and development
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17
Q

how do you investigate bronchiectasis?

A

diagnose and find cause
- CXR: bronchial wall thickening, airway dilatation
- high resolution CT
- bronchoscopy
- lung function

  • underlying cause: chloride sweat test, FBC, immunoglobulin, HIV, microbiology
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18
Q

what is the gold standard of investigating bronchiectasis and what do you see?

A

high resolution CT gold standard

  • bronchial wall thickening
  • diameter of bronchus larger than accompanying bronchial artery (signet ring sign)
  • visible peripheral bronchi
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19
Q

what is bronchiolitis?

A

viral infection of bronchioles, smallest air passages in lungs, commonly caused by respiratory syncytial virus (RSV)

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20
Q

what is the pathophysiology of bronchiolitis and what physiological changes take place as a result?

A
  • RSV causes
  • proliferation of goblet cells causing excess mucus production
  • IgE-mediated type 1 allergic reaction causing inflammation
  • Bronchiolar constriction
  • Infiltration of lymphocytes causing submucosal oedema
  • Infiltration of cytokines and chemokines
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21
Q

what are some risk factors for bronchiolitis?

A

breast fed for less than 2 months
smoke exposure (parents smoke)
having siblings who attend nursery or school (increased virus exposure)
chronic lung disease due to prematurity

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22
Q

what are some key features of bronchiolitis?

A

*affects children under 2

  • winter and spring hospitalisations
  • increasing sx over 2-5 days
  • low grade fever
  • nasal congestion
  • rhinorrhoea
  • cough
  • feeding difficulty
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23
Q

what examination findings might you detect in bronchiolitis?

A
  • tachypnoea
  • grunting
  • nasal flaring
  • intercostal, subcostal or supraclavicular recessions
  • inspiratory crackles
  • expiratory wheeze
  • hyper-inflated chest
  • cyanosis or pallor
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24
Q

what red flags warrant an urgent referral?

A
  • apnoea
  • child looks seriously unwell
  • severe respiratory distress eg: grunting, marked recessions, respiratory rate over 70
  • central cyanosis
  • oxygen sats <92%
25
Q

what are some complications of bronchiolitis?

A

hypoxia, dehydration, fatigue, respiratory failure, persistent wheeze

26
Q

how might you investigate bronchiolitis?

A

*clinical!!

  • labs: nasopharyngeal aspirate or throat swab for RSV
  • septic screen
  • blood gas for resp failure
  • CXR: hyperinflation, focal atelectasis, air trapping, flattened diaphragm
27
Q

how is bronchiolitis managed?

A

*most can be managed at home with supportive measures like fluids, nutrition etc

  • referral if RR >60, inadequate fluid intake, clinical dehydration
  • give O2
  • fluids via NGT
  • consider CPAP
  • airway suctioning if required
28
Q

when would you consider discharge in bronchiolitis?

A

discharge when clinically stable, taking adequate oral fluids, maintaining sats over 92% for more than 4h

29
Q

what is the pathophysiology of CF?

A

autosomal recessive disease caused by mutation in CF transmembrane conductance regulator gene (CFTR) resulting in multisystem dysfunction

  • CFTR protein is a chloride channel which drives Cl against conc using ATP, present in airway
  • when defective disrupts this and affects sodium reabsorption reducing water in secretion, reduced airway surface liquid which has important immunological functions like mucus clearance. so bacteria growth and tissue damage
30
Q

what other complications may result as a result of CF?
*outside of the lung?

A
  • pancreas: duct occlusion
  • GI tract: viscous mucus causing bowel obstruction
  • biliary tract occlusions
  • reproductive: congenital lack of vas deferens, pregnancy complications for women
31
Q

what are some key features in a CF history and presentation?

A
  • neonates: meconium ileus, bilious vomiting, failure to thrive, prolonged jaundice
  • infancy: failure to thrive, recurrent chest infections, steatorrhoea
  • childhood: polyps, sinusitis
  • adolescence: pancreatic insufficiency, CLD, gall stones
32
Q

what are some complications of CF?

A
  • pancreatic insufficiency
  • CF related DM
  • liver disease - mucus buildup and blockage of ducts leading to inflammation and scarring
  • infertility
33
Q

how is CF diagnosed?

A

chloride sweat test
- >60mmol/L suggestive, second test or identification or mutations needed to confirm

34
Q

what other investigations are carried out for CF?

A
  • microbiology sputum cultures, swabs showing S.aureus and pseudomonas
  • glucose tolerance test
  • liver functions
  • bone profile
  • lung function testing
35
Q

how is CF managed?

A

MDT
- chest physio for clearance
- high calorie diet as malabsorption, increased resp effort, physio
- CREON to replace lipase enzymes
- prophylactic abx fluclox
- chest infection mx
- bronchodilators
- vaccinations

36
Q

what is the role of monitoring for CF?

A

specialist clinics every 6m

  • regular monitoring of sputum for colonisation
  • screening for DM, osteoporosis, vitamin D insufficiency and liver failure
  • prognosis - 47 year life expectancy
37
Q

what is the pathophysiology of croup?

A
  • acute infective URTI affecting young children aged 6m-2yrs
  • causes oedema in larynx - mucosal inflammation between nose and trachea
  • classically caused by parainfluenza virus
38
Q

what are some RF for croup?

A

male, autumn and spring months, genetic variants of certain genes have been seen to have lower prevalence

39
Q

how does croup present?

A
  • 1-4 day history of non-specific cough, rhinorrhoea and fever
  • progressing to barking cough which occurs in clusters and hoarseness
  • increased work of breathing
  • symptoms worse at night
  • fever (low grade)

*stridor, chest normal, reps distress sx

40
Q

how is croup investigated?

A

*westley croup done to categorise features

  • clinical diagnosis
  • FBC, U&E, CRP
  • CXR
  • laryngoscopy
  • pulse oximetry
41
Q

what are some complications of croup?

A

lymphadenitis, otitis media, dehydration, rarely bacterial superinfection and very rarely pulmonary oedema and pneumothorax

42
Q

how is croup managed?

A

*consider admission if previous history of severe obstruction, <6m, immunocompromised, inadequate fluids, diagnosis uncertain

  • home managed: resolves within 48h, may last upto 1w, no abx, supportive

hosp
- treatment - single dose of oral dexamethasone (or prednisolone)
- nebulised adrenaline for temporary relief
- keep child calm as crying increases oxygen demand
- oxygen therapy as required
- ENT and anaesthesia if airway support needed

43
Q

what is the pathophysiology of obstructive sleep apnoea?

A
  • condition that affects the airway and how we breath caused by natural relaxation is airways during sleep due to having large tonsils or adenoids
  • breathing is interrupted or reduced causing fall in level of oxygen in body which leads to bigger efforts to breathe hence causing brief waking up
44
Q

what could cause OSA?

A

adenoids!!
obesity, sickle cell disease and downs syndrome, neuromuscular disorders like duchenne, craniofacial abnormalities, dystonia of airways like CP

45
Q

how might OSA present?

A
  • snoring, unusual sleeping position, brief night arousals
  • daytime sleepiness, headache
  • children may be hyperactive and aggressive
  • craniofacial abnormalities, increased soft tissue volume, large neck circumference
46
Q

how might OSA be investigated?

A
  • overnight pulse oximetry
  • polysomnography
  • EEG
47
Q

how is OSA managed?

A
  • adenotonsillectomy for those with adenotonsillar hypertrophy
  • CPAP and BiPAP
  • weight loss
  • nasopharyngeal airway as a splint to keep airway open and keep tongue from falling back
  • orthodontics? to bring jaw forwards
48
Q

what are some types of LRTI?

A

community acquired pneumonia: RSV, influenza, strep.pneumoinae etc

pleural: empyema strep penumoinae

aspiration: contents of pharynx or oesophagus spill over into larynx and bronchial tree

49
Q

how might an LRTI present?

A
  • fever
  • coryza, cough
  • wheeze, breathing difficulty and increased work of breathing
  • feeding problems
  • lethargy
  • confusion
  • aspiration pneumonia - coughs and choked during feeds and now breathless and fever
50
Q

what are some key examination findings in LRTI?

A
  • bronchial breathing sounds
  • focal coarse crackles
  • dullness to percussion
51
Q

how might you investigate LRTI?

A
  • CXR:
  • sputum culture
  • swabs, PCR
  • blood cultures
  • CBG
52
Q

what might your thought process be if a child is presenting with recurrent infections?

A

if requiring frequent antibiotics and admission investigate underlying lung or immune system pathology

  • Assess reflux, aspiration, neurological disease, heart disease, asthma, CF, primary ciliary dyskinesia, immune deficiency
53
Q

how is LRTI managed?

A
  • viral - mostly manages at home, anti-pyretics and small feeds, usually 1-2 weeks
    • admission when significant breathing difficulties, dehydration, apnoea, needing oxygen
  • antibiotics - Amoxicillin first line, macrolide will cover atypical or in pen allergy
  • supportive
54
Q

how would you manage a pleural collection?

A
  • Pleural collections - drainage via chest drain under GA, fluid sent for cultures with IV Abx
    • intrapleural fibrinolytic to breakdown any adhesions in pleural fluid
    • 6w CXR after discharge to ensure resolution
    • consider malignancy potential like lymphoma and leukaemia so CT!
55
Q

what conditions may require home ventilation?

A
  • extreme prem birth
  • neuromuscular disorders
  • spinal cord injuries
  • neuro disorders
  • severe tracheal and bronchomalacia
  • chest wall disroders
  • chronic lung disease
56
Q

what are some benefits of a ventilator?

A
  • By blowing air into the lungs, the ventilator keeps the airway open
    and helps the lung expand to avoid compression or collapse of the
    lung tissue (atelectasis) and improve clearing secretions
  • The ventilator can help bring more oxygen into the body and
    remove carbon dioxide.
  • The ventilator can help reduce the child’s work of breathing
57
Q

what must be in order before going on home ventilation?

A
  • medically stable
  • settings working
  • atleast 2 family caregivers fully trained in care and CPR
  • clear plan and equipment
  • caregivers given help to quit smoke or vape
58
Q

how do you diagnose chronic respiratory failure?

A
  • worsening of accompanying symptoms of the underlying disease such as weight loss, dyspnea, and decreased exercise capacity
  • polycythaemia
  • signs of carbon dioxide-associated vasodilation, such as conjunctival injection, leg oedema, and morning headache
  • tachypnea
  • tachycardia
  • anxiety or personality change
59
Q

what are some complications of a tracheostomy?

A
  • Tracheostomies may result in significant complications, such as granuloma, infection, obstruction of the cannulae, and accidental decannulations
    • impaired language development and negatively impact the body image of children
60
Q

when is ventilation considered?

A
  • daytime hypercapnia
  • nocturnal hypoventilation
    • Symptoms of nocturnal hypoventilation may include sleep
      fragmentation, morning headaches, hypersomnolence and cognitive dysfunction
  • progressive respiratory muscle weakness where future respiratory failure is expected

Y4 Paediatrics (16 decks)

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