Respiratory (COPD, bronchiectasis, pulmonary fibrosis) Flashcards
COPD
a progressive lung disease characterised by airflow obstruction that is not fully reversible
Umbrella term
- Chronic bronhcitis
- Emphysema
COPD Risk Factors
- Cigarette smoking is associated with around 90% of cases
- Occupational exposure e.g. coal, grains, silica
- Air pollution
- Genetics e.g. alpha-1-antitrypsin deficiency
- Asthma
- Problems with lung growth and development
presentation of COOD
Cough – this is usually the initial presenting complaint
- This often starts off being worse in the morning but becomes constant as COPD gets worse
- Usually productive
Shortness of breath
- This is usually with exercise initially but can progress to shortness of breath at rest
Features of hyperinflation may be seen
- Hyperinflation occurs when air is trapped in the lungs due to blockages and reduced elasticity leading to the lungs overinflating.
- Hyper-resonance on percussion
- Barrel chest
- Distant breath sounds on auscultation
Wheeze on auscultation
Coarse crackles – often seen in exacerbations
Features of cor pulmonale:
* Distended neck veins
* Lower limb oedema
* Hepatosplenomegaly
what does COPD not cause
CLUBBING
investigations for COPD
- Spirometry <0.70
- FBC (secondary polycythaemia)
- CXR (rule out lung cancer, may show bullae, flattened diaphragm)
Other investigations
- Alpha-1-antitrypsin (if early onset)
- ECG and echocardiography (pulmonary hypertension)
- Sputum culture
- ABG
NICE classification of the severity of COPD
General management in all COPD patients
- Smoking cessation – the single most important measure to reduce progression
- Annual influenza vaccination and one-off pneumococcal vaccination
- Pulmonary rehabilitation – if COPD is limiting functional ability
medical therapy for COPD
First line
- short-acting beta2 agonist (SABA) or short-acting muscarinic antagonist (SAMA)
Second line determine if the patient has asthmatic/steroid-responsive features
- If asthmatic/steroid responsive features: add long-acting beta2 agonist (LABA) + inhaled corticosteroid (ICS):
- If non-asthmatic and no steroid-responsive features: LABA + long-acting muscarinic antagonist (LAMA)
- If the patient is already taking a SAMA, stop this and replace it with a SABA
Third line add whichever option was not added in the second-line step i.e. SABA + LABA + LAMA + ICS
- Consider adding theophylline
- Consider mucolytics in all patients
COPD atntibiotic prophylaxis
Antibiotic prophylaxis
In some patients, specialists may consider antibiotic prophylaxis. The antibiotic of choice is azithromycin.
Long-term oxygen therapy (LTOT) considered in COPD patients when
- PaO2 <7.3 kPa when stable or <8 kPa when stable + peripheral oedema
- Secondary polycythaemia
- Pulmonary hypertension
how can COPD cause heart failure
Cor pulmonale:
Chronic hypoxia can lead to vasoconstriction in the pulmonary arteries (in an attempt to increase oxygenation of the blood) leading to pulmonary hypertension. This leads to more strain on the right side of the heart leading to right ventricular hypertrophy and cor pulmonale.
single biggest factor which can reduce rate of decline
Smoking cessation can reduce the rate of decline
Alpha-1 Antitrypsin Deficiency
Alpha-1 antitrypsin (α1AT) is a glycoprotein produced in the liver and plays a role in inhibiting the action of protease enzymes released from neutrophils, such as neutrophil elastase released in inflammation, infection, or smoking.
pathophysiology of Alpha-1 antitrypsin (α1AT) deficiency
α1AT deficiency is an inherited condition in which the α1AT protein’s structure is modified.
- This can lead to excess elastin breakdown leading to the destruction of alveolar walls and COPD.
- The α1AT can accumulate in the liver, leading to liver cell destruction and cirrhosis. In exams, α1AT deficiency classically causes COPD in young people and non-smokers.
presentation of α1AT deficiency
α1AT deficiency should be considered in any young patient presenting with features consistent with COPD, or any patient with severe and aggressive COPD. Features may be:
- Early presentation of COPD symptoms
- Imaging shows emphysema in the lower lobes of the lung
- Cirrhosis and hepatocellular carcinoma may be present, even in the absence of alcohol consumption
- Not every patient with α1AT deficiency will develop liver disease
investigations for a1AT deficiency
Serum α1AT levels:
- All patients with COPD, non-responsive asthmatic adults/adolescents, and people with liver disease of unknown aetiology should be screened using this test
Spirometry:
- FEV1: significantly reduced
- FVC: significantly reduced
- FEV1/FVC: significantly reduced
Chest x-ray:
- Usually shows emphysematous changes – particularly in the lower lobes
Liver function tests (LFTs):
- ALT, bilirubin, and ALP may be raised
management of a1AT def
- STOP smoking
- supportuve therapies such as bronchodilators and pulmonary rehab
- lung volume reduction surgery
An acute exacerbation of chronic obstructive pulmonary disease (COPD)
is a sudden worsening of COPD symptoms beyond normal day-to-day variations.
causes of COPD exacerbation
Bacterial causes
- Haemophilus influenzae – most common
- Streptococcus pneumoniae
- Moraxella catarrhalis
Other causes
- Pollution
- Viruses – rhinoviruses, influenza, parainfluenza etc.
- Swallowing dysfunction
- Gastro-oesophageal reflux disease (GORD)
presentation of acute COPD exacerbation
- Increased shortness of breath, cough, and wheezing
- Increased sputum production which may suggest an infection
- Purulent (green/pus-filled) sputum is suggestive of a bacterial infection
- Malaise
- Signs of respiratory failure
Signs of respiratory failure:
- Changes in mental status e.g. confusion
- Morning headaches and increased daytime sleepiness suggest worsening hypercapnia
- Accessory muscle use and pursed lip breathing
- Cyanosis
investigations for acute exacerbation of COPD
- CXR
- ABG Used to detect chronic hypercapnia and acute respiratory acidosis- guides oxygen therapy
- FBC - infections and anaemia
- U&Es
- ECGs
- Sputum culture - bacterial infection
- Blood culture
when pt with COPD should be referred to hospital
- Significantly worsened dyspnoea
- Tachypnoea
- Oxygen saturations <90%
- Pursed-lip breathing
- Use of accessory muscles
- Mental status changes e.g. confusion or impaired levels of consciousness
- New-onset cyanosis
- Worsening peripheral oedema
- Rapid onset
- Significant reduction in activities of daily living
- Inability to cope at home
- Poor or worsening general condition
- Already receiving home oxygen therapy
sarcoidosis presentation
The presentation can vary widely depending on what sites are affected.
Classical presentations in exams are:
- Cough + erythema nodosum (tender, erythematous nodules on the lower limbs)
- Bilateral hilar lymphadenopathy and hypercalcaemia
Some features seen may be:
- Cough – usually dry
- Dyspnoea – gradual in onset
- Wheeze on auscultation
- Lymphadenopathy – usually axillary, cervical, inguinal, and submandibular
- Symptoms of uveitis:
- Red, painful eye
- Blurred vision
- Photophobia
- Erythema nodosum
- Lupus pernio – hardened, raised, purple lesions on the nose, cheeks, lips, and ears
Other possible features can be:
- Arthralgia
- Hepato- and/or splenomegaly
- Heart failure
- Facial nerve palsy
- Arrhythmia
- Heart block
- Headaches
- Seizures
sarcoidosis investigations
Chest x-ray:
- Can be normal
- May show bilateral hilar lymphadenopathy
Serum calcium:
- Hypercalcaemia is often present due to the cells in the granulomas producing calcitriol
Serum ACE:
- Usually elevated
Urea and electrolytes (U&Es):
- May be deranged
Tuberculin skin test (Mantoux):
- Usually negative
Erythrocyte sedimentation rate (ESR):
- Usually raised
Tissue biopsy:
- Shows non-caseating granulomas
