Resp/ENT/Sleep Flashcards
Definition of chronic cough
Ddx
persistence of cough >4 weeks
Most common 3:
- Protracted bacterial bronchitis
- Bronchiectasis
- Asthma
Aspiration
Atypical infx
Inhaled foreign body
Post viral
ILD
Cardiac disease
Ear disease
Oesophageal disease
Medications
Somatic/habit cough
- What is protracted bacterial bronchitis
- What are the most common bacteria found in these cases?
- What should you be suspicious of if the cough doesn’t respond to 4 weeks abx?
- Cough lasting >4 weeks that is WET in nature with response to 2 weeks abx tx (ADF) with no other features to indicate another cause
- H. influenzae, Moraxella catarralis, Strep pneumonia
- Bronchiectasis
Asthma management step wise approach
- Reliever (salbutamol) PRN
- low dose ICS preventer (eg fluticasone, budesonide, ciclesonide) or montelukast or cromeo
- higher dose ICS OR low dose ICS plus montelukast OR LABA plus low dose ICS
- Refer resp physician
Wait 4 weeks after starting ICS or cromones to assess for sx resolution and 2 weeks after montelukast before stepping up
Bronchiectasis
Definition
Adults vs children
ADULT DEFINITION
Irreversible dilatation of one or more bronchi (bronchi larger than accompanying blood vessel) w failure of bronchi to taper in periphery of lung
Bronchoarterial ratio >1
Radiological diagnosis - seen on CT.
CHILDREN
- Reversible with early treatment
- Bronchoarterial ratio >0.8
- Bronchiole normal tubular -> cyclindrical/follicular (dilated) = ‘tree in bud appearance’ on CT -> varicose -> cystic
- Up to cylindrical point it is reversible in children but beyond this it is not.
FEATURES
- CT changes + chronic wet/productive cough
- Frequent resp exacerbations
Spectrum of chronic suppurative lung disease
Underlying pathogenesis
Mildest end of spectrum
Protracted bacterial bronchitis (can occur in healthy well children)
-> repeated infections ->
Chronic suppurative lung disease (CT scans normal)
->
Radiological bronchiectasis
Pathophys:
- Insult to lung (infection) -> inflammatory response with cytokines, nests, elastase and bacterial byproducts -> impairs lungs normal mucociliary clearance -> incr mucus production/decr clearance -> blocks small airways -> incr propensity for microbial colonisation -> bacteria cause more inflammation -> cycle continues
Treatment bronchiectasis
Antibiotics
Maximise airway clearance (chest PT)
Diet optimisation/nutrition
Minimise environmental pollutants (smoking)
Exercise
Classic bugs that cause infection in children with CF bronchiectasis
PSA
Staph aureus
Non typable haemophilis influenza
- what is its mode of pathogenicity?
- what condition has increased susceptibility to this bug?
Secretes biofilm (ECM protecting against host immune response and abx, helping to prolong existence in airways)
Incr susceptibility in PBB and CF
Worsens inflammation cycle
Abx therapy (abx + duration) in exacerbation of bronchiectasis
- mild-mod
- vs mod-severe
Initial empiric tx
Mild-mod: PO Augmentin DF (amoxicillin) or Azithromycin. Cipro if PSA in recent culture.
Mod-Severe: IV ampicillin, cefotazime, ceftriaxone. Tazocin or ceftaz and tobra if PSA in recent cultures.
Minimum 10-14 days or cough free for 2 days
Start with oral abx, if not effective then will need IV abx
Indication for long term abx in bronchectasis
3+ exacerbations in previous 12 months
Aims for suppression rather than eradication
Decr exac and hospitalisation rate BUT risk of resistance
Benefits of macrolides in CF
Risks
Example of a macrolide
ex: Azithromycin
BENEFITS
Antimicrobial and anti-inflammatory
Routinely used in CF
Inhibits biofilms (PSA, NTHI)
Decr exac rate
RISKS
1. BUT macrolide resistance (staph aureus specifically) and risk of GI side effects
Exclude NTM prior to starting tx to avoid induction of resistance to macrolides
2. QTc prolongation (need to perform baseline ECG prior to starting tx)
What conditions have evidence for inhaled abx
CF
Non-CF BE with PSA only
Features of salbutamol toxicity
what do u see on blood gas
Tremor, tachycardia, tachypnoea Metabolic acidosis (lactate high)
Pathophys of asthma
Two major components to airway obstruction
i. Chronic Airway inflammation
ii. Reactive airways = bronchoconstriction and airway hyperresponsivness
Pathology
i. Smooth muscle hyperplasia of bronchial and bronchiolar walls
ii. Thick tenacious mucous plugs
iii. Thickened BM
iv. Mucosal edema
v. Eosinophilia of the submucosa and secretions
vi. Increased mast cells in smooth muscle
Results in
Mucosal edema, bronchospasm and mucus plugging -> airflow obstruction -> increased resistance to airflow -> decreased ability to expel air -> hyperinflation
Explain VQ mismatch in asthma
Explain how ventolin can affect this
Airway inflammation and resulting airflow obstruction is NOT uniform throughout the tracheobronchial tree – distribution of inspired air is uneven, uneven circulation to the alveoli, uneven ventilation (VQ mismatch)
Ventolin
Can cause a paradoxical worsening in VQ mismatch (and thus spO2) early in treatment (first 30min). May need supplemental O2 for this short period of time.
Innervation of bronchial smooth muscle
Parasympathetic nervous system -> bronchoconstriction (M3 receptors) = cholinergic
Sympathetic nervous system -> bronchodilation (B2 receptors) = beta adrenergic
Spirometry findings in asthma
Define the values of abnormality for each
Airway obstruction defined as
- FEV1 <80% (predicted)
- FEV1/FVC <75% (varies with age)
- MMEF 25-75 <67% (predicted)
Bronchodilator reversibility = improvement of FEV1 of 12% in absolute values
How many actuations in a ventolin inhaler?
200
Asthma severity levels
Infrequent intermittent asthma (Symptom-free for at least 6 weeks at a time (flare-ups up to once every 6 weeks on average but no symptoms between flare-ups)
Frequent intermittent asthma (Flare-ups more than once every 6 weeks on average but no symptoms between flare-ups, normal exam and PFT between flares)
Persistent asthma
• Daytime symptoms >2 days/week
• Nocturnal symptoms >1 night/week
• Attacks <6 weeks apart
• May have abnormal lung function
• Multiple presentations to ED
Montelukast
Mechanism of action
Age cut off
Indication
Mechanism of action = LT receptor antagonist
Can be used in children >= 2 years of age
Main indication = alternative to ICS in children with Frequent intermittent asthma or Mild persistent asthma
Trialed first IF:
- The child is unable to use inhaled therapy
- The child also has significant allergic rhinitis
- The parents have strong concerns about adverse effects of ICS
Risk of LABA use and limitations of use in asthma
LABA also results in phosphorylation and internalisation of beta 2 receptor – results in increased mortality
No evidence for children <5 years
Should not be started when child is clinically unwell and should not be used as monotherpay (always with ICS)
Mepolizumab
Omalizumab
Mepo
i. Humanised anti-IgE Monoclonal Ab
ii. Prevents binding of free IgE to high affinity receptors on basophils and mast cells
iii. Approved for moderate to severe allergic asthma in children 12 years or older
iv. Delivered by SC every 2-4 weeks
Omal
i. An add-on maintenance therapy for severe asthma with an eosinophilic phenotype in patients age 12 years and older
ii. Anti-IL-5 Mab injected SC every 4 weeks
iii. Decreases the production an survival of eosinophils, a major inflammatory cell involved in asthma pathogenesis
Diagnosis of CF
New born screening test looks for elevated IRT (‘immunoreactive trypsinogen’ produced by stressed pancreas)
- screens for the most common 12 genotypes in the state although over 900 exist
Gold standard is the ‘Sweat Test’ (elevated Cl, Na, sweat weight)
However there is a risk of false negatives
Any child w evidence of pancreatic insufficiency (Steattorrhoea, fat globules or crystals in stool) +/- FTT should be considered for CF
CF gene (most common)
Delta 508 most common (90% of patients in australia)



















