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Flashcards in Respiratory Deck (124)
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What is aspergillus lung disease?

Lung disease associated with Aspergillus fungal infection


What is the aetiology of aspergillus lung disease?

Inhalation of the ubquitous Aspergillus spores can produce three different clinical pictures:
1) Aspergiolloma: Growth of an A. fumigatus mycetoma ball in a preexisting lung cavity (e.g. post-TB old infarct or abscess)
2) Allergic bronchopulmonary aspergillosis (ABPA): Aspergillus colonisation of the airways (usually in asthmatics) leads to IgE- and IgG- mediated immune responses. Proteolytic enzymes and mycotoxins released by fungi, CD4/Th2 cells producing IL-4 and IL_5 and mediating eosinophilic inflammation, and IL-8 mediated neutrophilic inflammation result in airway damage and central bronchiectasis


What is invasive aspergillosis?

Invasion of Aspergillus into lung tissue and fungal dissemination.
Secondary to immunosuppression (e.g. neutropaenia, steroids, haematopoietic stem cell/ solid organ transplantation, AIDS)


What is the epidemiology of aspergillosis?

- Uncommon
- Most common in elderly and immunocompromised


What are presenting symptoms of aspergillus lung disease?

- Aspergilloma: Asymptomatic, haemoptysis, which may be massive
- ABPA: Difficult to control asthma, recurrent episodes of pneumonia with wheeze, cough, fever and malaise
- Invasive aspergillosis: Dyspnoea, rapid deterioration, septic picture


What are the signs of aspergillus lung disease on examination??

- Tracheal deviation in large aspergillomas
- Dullness in affected lung, reduced breath sounds, wheeze in ABPA
- Cyanosis may develop in invasive aspergillosis


What are the investigations for aspergilloma?

- Aspergilloma: CXR: Round opacity may be seen with a crescent of air around it (usually in the upper lobes)
- CT or MR imaging if CXR does not clearly delineate a cavity
- Cultures of the sputum may be negative if there is no communication between the cavity and the bronchial tree. Also Aspergillus is a common common coloniser of an abnormal respiratory tract


What are the investigations for Allergic bronchopulmonary aspergillosis (ABPA)?

- Immediate skin test reactivity to Aspergillus antigens
- Eosinophilia
- Increased serum total IgE
- Increased serum specific IgE and IgG to A. fumigatus or precipitating antibodies to A. fumigates
- CXR: Transient patchy shadows, collapse, distended mucus-filled bronchi producing tubular shadows
- CT: Lung infilitrates
- LFT: reversible airflow limitation


What are the investigations for invasive aspergillosis?

- Detection of Aspergillus in cultures or by histological examinations
- Chest CT scan may show nodules surrounded by a ground-glass appearance (halo sign)


What is asthma?

Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation


What is the aetiology of asthma?

- Genetic factors: Positive family history, twin studies. Almost all asthmatic patients show some atopy.
- Environmental factors: House dust mite, pollen, pets (e.g. urinary proteins, furs), cigarette smoke, viral respiratory tract infection, Aspergillus fumigatus spores, occupational allergens


What is the pathogenesis of asthma with regards to the early phase??

Early phase (up to 1 hour): Exposure in inhaled allergens in a presensitised individual results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These induce bronchoconstriction, mucous hypersecretion, oedema and airway obstruction


What is the pathogenesis of asthma with regards to the late phase?

- After 6-12 hours
- Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness
- Structural cells may also release cytokines, profibrogenic and proliferative growth factors and contibute to the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts ('airway remodelling')


What is the epidemiology of asthma?

- Affects 10% of children and 5% of adults
- Prevalence is increasing
- Male=Female


What are the presenting symptoms of asthma?

- Episodes of wheeze, breathlessness, cough, worse in the morning and at night
- Ask about interference with exercise, sleeping, days off school and work
- In an acute attack it is important to ask whether the patient has been admitted to hospital because of his/her asthma, or to ITU, as a gauge of potential severity
- Precipitating factors: Cold, viral infection, drugs (B-blockers, NSAIDs), exercise, emotions
- May have a history of allergic rhinits, uticaria, eczema, nasal polyps, acid reflux and family history


What are the signs of asthma on examination?

- Tachypnoea, use of accessory muscles, prolonged expiratory phase, polyphonic wheeze, hyperinflated chest
- Severe attack: PEFR less than 50% predicted, pulse more than 110/min, respiratory rate more than 25/min, inability to complete sentences
- Life threatening attack: PEFR less than 33%, silent chest, cyanosis, bradycardia,, hypotension, confusion, coma


What are the investigations for acute asthma?

- Peak flow
- Pulse oximetry
- CXR (to exclude other diagnoses e.g. pneumothorax, pneumonia), FBC (increased WCC if infective exacerbation), CRP, U&E, blood and sputum cultures


What are the investigations for chronic asthma?

- PEFR monitoring: often diurnal variation with morning 'dip'
- Pulmonary function test: Obstructive defect, with improvement after a trial of B2-agonist.
- Blood: Eosinophilia, IgE level, Aspergillus antibody titres ( see allergic Aspergillus lung disease)
- Skin prick tests: May help in identification of allergens


How is acute asthma managed?

- Resuscitate, monitor 02 sats, ABG and PEFR
- High flow oxygen
- Nebulized B2-agonist bronchodilator salbutamol, ipatropium
- Steroid therapy
- If no improvement: IV Mg sulphate. Consider IV salbutamol
- Summon anaesthetic help if pt is getting exhausted (PC02 increasing). Treat any underlying cause (infection, pneumothorax). Give antibiotics if there is evidence of chest infection (purulent sputum, abnormal CXR, increased WCC, fever). Monitor electrolytes closely
- May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early


How is asthma managed on discharge?

- When PEF more than 75% predicted or pts best, diurnal variation less than 25%, inhaler technique checked, stable on discharge medication for 25h, pt own a PEF meter and has steroid and bronchodilator therapy. Arrange follow-up


What is chronic 'stepwise' therapy for asthma?

Start on step appropriate to initial severity and step up or down to control symptoms. Treatment should be reviewed every 3-6 months
1) Inhaled short acting B2-agonist as needed. If used more than 1/day move to step 2
2) As step 1 plus regular inhaled low dose steroids
3) As step 2 plus long acting B2 agonist (LABA) . If inadequate control with LABA, increase steroid dose. If no response to LABA, stop and increase steroid dose
4) Increase inhaled steroid dose, add a 4th drug e.g. leukotriene receptor antagonist, SR theophylline or B2 agonist tablet
5) Addition of regular oral steroids. Maintain high-dose inhaled steroid. consider other treatments to minimise the use of oral steroids. Refer for specialist care


What advice should be given to pts with asthma?

Educate on proper inhaler technique and routine monitoring of peak flow
Develop an individualised management plan, with emphasis on avoidance of provoking factors


What are the possible complications of asthma?

- Growth retardation
- Chest wall deformity (e.g. pigeon chest)
- Recurrent infections
- Pneumothorax
- Respiratory failure
- Death


What is the prognosis of asthma?

- Many children improve as they grow older
- Adult-onset asthma is usually chronic


What is bronchiectasis?

Lung airway disease characterised by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections


What is the aetiology of bronchiectasis?

Severe inflammation in the lung causes fibrosis and dilation of the bronchi.This is followed by pooling of mucous, predisposing to further cycles of infection, damage, and fibrosis to bronchial walls
- Can be idiopathic and post-infectious (after severe pneumonia, whooping cough, tuberculosis)
Host defence defects e.g. Kartagener's syndrome, cystic fibrosis, immunoglobulin deficiency, yellow nail syndrome
- Obstruction of bronchi: foreign body, enlarged lymph nodes
- Gastric reflux disease
- Inflammatory disorders e.g. rheumatoid arthritis


What is the epidemiology of bronchiectasis?

- Most often arises initially in childhood
- Incidence has reduced with use of antibiotics


What are the presenting symptoms of bronchoiectasis?

- Productive cough with purulent sputum or haemoptysis
- Breathlessness, chest pain, malaise, fever, weight loss
- Symptoms usually begin after an acute respiratory illness


What are the signs of bronchiectasis on examination?

- Finger clubbing
- Coarse crepitations (usually at the bases) which shift with coughing
- Wheeze


What are the investigations for bronchiectasis?

- Sputum: Culture and sensitivity, common organisms in acute exacerbations. P. auruginosa, H. influenzae, S. aureus, S. pneumoniae, Klebsiella, M. catarrhalis, Mycobacteria
- CXR: Dilated bronchi may be seen as parallel line radiating from hilum to diaphragm (tramline shadows). May show fibrosis, atelactasis, pneumonic consolidations or may be normal
- High res CT: Dilated bronchi with thickened walls. Best diagnostic method
- Bronchography: Determine extent of disease before surgery - Other: sweat electrolytes, serum immunoglobulins, sinus X-ray, mucociliary clearance study