Respiratory Flashcards
Asthma
Chronic inflammatory disorder of the airways characterised by reversible airflow limitation, airway hyperresponsiveness & inflammation of the bronchi
Asthma aetiology
Atopy - genetic predisposition to IgE-mediated allergen sensitivity
Hygiene hypothesis - reduced exposure to infectious pathogens at a young age predisposes individuals to such diseases
Aspirin-induced asthma - asthma, aspirin sensitivity & nasal polyps (Samter’s triad)
Occupational asthma
Exercise-induced asthma
Asthma pathophysiology
Early phase - inhalation of allergens results in an immediate (type 1) hypersensitivity reaction in the airways, sensitisation occurs causing release of IgE antibodies from plasma cells -> bind to mast cells, subsequent exposure to antigens cause mast cell degranulation -> smooth muscle contraction & bronchoconstriction
Late phase - recruitment of a variety of inflammatory cells
Chronicity - airways lay down fibrous tissue due to persistent chronic inflammation, airway remodelling occurs and manifests as fixed airway obstruction
Asthma symptoms
Cough (worse at night)
Dyspnoea
Chest tightness
Poor sleep
Asthma signs
Expiratory wheeze
Prolonged expiratory phase
Tachypnoea
Harrison’s sulcus: groove at the inferior border of the rib cage that may be seen in children with chronic severe asthma (seen in rickets too)
Asthma grading
Moderate - increasing symptoms of asthma, O2 >/= 92%, PEFR >/= 50-70%
Severe - can’t complete sentences, HR >/= 110, RR >/= 25, O2 >/= 92%, PEFR 33-50%
Life-threatening - silent chest, cyanosis, exhaustion, confusion, poor respiratory effort, PaO2 < 8kPa, O2 < 92%, PEFR < 33%
Near-fatal - raised PaCO2 or requires mechanical ventilation with raised inflation pressures
Asthma investigations
Spirometry - measures the flow and volume of air during inhalation and exhalation
-FVC may be normal but often reduced
-FEV1 is reduced
-FEV1/FVC < 70%
-Reversibilty after the administration of a bronchodilator
PEFR
-Demonstrates characteristic variability on PEFR diaries
FeNO - typically offered same time as spirometry, newer way of testing for eosinophilic airway inflammation
-FeNO > 40ppb = supports asthma diagnosis
-FeNO 25-39ppb = suggestive of asthma
-FeNO < 25ppb = does not support asthma diagnosis
Asthma management
1) SABA PRN (if doses > 3 week, step up treatment)
2) ICS - fluticasone and beclomethasone
3) + LABA - MART is a combined inhaler eg. fostair which contained formoterol/beclometasone, should be used daily as maintenance (should not be prescribed a SABA with this)
4) increase ICS/LTRA - consider increasing ICS to medium dose/adding a leukotriene receptor antagonist
5) consider specialist referral
Acute asthma management
Initial management
-Salbutamol nebulisers - 2.5-5mg driven by oxygen & may be repeated every 15 to 30 minutes
-Oxygen - should be started immediately in severe attacks & titrated to saturations of 94-98%, ABG considered if sats < 92% or life-threatening features
-Steroids - PO with prednisolone 40-50mg daily/IV hydrocortisone 100mg six hourly, continued for at least 5 days
-Ipratropium bromide - nebulisers, 0.5mg 4-6 hourly, are given to most patients with acute asthma attack
Second line therapies
-Magnesium sulphate
-Beta 2 agonist infusion
-Aminophylline
Asthma follow-up
All patients with a peak flow <50% of best/predicted on admission require prednisolone 40-50mg/day until recovery
Check inhaler technique & will need GP follow-up within two days of discharge and referral to asthma specialist nurse clinic
If admitted to hospital, they will require a respiratory clinic appt. within four weeks
COPD
Progressive, obstructive airway disease that is not fully reversible, results from disease of the airways and parenchyma in the form of chronic bronchitis and emphysema
Chronic bronchitis and emphysema
Chronic bronchitis - clinical term relating to a chronic productive cough for at least 3 months over two consecutive years
Emphysema - structural lung changes, abnormal airspace enlargement distal to terminal bronchioles with evidence of alveoli destruction & no obvious fibrosis
COPD aetiology
Smoking
Alpha-1 antitrypsin deficiency - autosomal recessive disorder
A1A is a protease inhibitor (made in the liver) and acts in the lung parenchyma to oppose the action of elastase
Elastase is a protease that causes the breakdown of elastin, a protein important to the structural integrity of alveoli -> causes emphysema
COPD chronic bronchitis aetiology
Chronic bronchitis - inflammation of the bronchi, defined as a chronic productive cough for 3 or more months in two consecutive years
-Characterised by chronic inflammation with neutrophilic infiltration, CD8+ T lymphocytes & macrophages
-Leads to
–Goblet cell hyperplasia
–Mucus hypersecretion
–Chronic inflammation and fibrosis
–Narrowing of small airways
COPD emphysema aetiology
Emphysema - permanent enlargement of airspaces distal to the terminal bronchiole when interstitial pneumonias are excluded, destruction of the lung parenchyma results in a reduced area for gas exchange and chronic hypoxia
-Loss of elastin has two effects
–Collapse - alveoli are prone to collapse
–Dilation & bullae formation - alveoli dilate and may eventually join with neighbouring alveoli forming bullae
COPD cor pulmonale aetiology
Cor pulmonale - refers to right ventricular impairment secondary to pulmonary disease (COPD is most common cause)
-Chronic hypoxia causes vasoconstriction of pulmonary arteries -> elevated pulmonary arterial pressure
-Chronic elevation of pulmonary arterial pressure -> right heart failure
COPD symptoms
Chronic cough
Sputum production
Breathlessness
Frequent episodes of bronchitis
Wheeze
COPD signs
Dyspnoea
Pursed lip breathing
Wheeze
Coarse crackles
Loss of cardiac dullness
Downward displacement of liver
Signs of CO2 retention - drowsy, asterixis, confusion
Signs of cor pulmonale - peripheral oedema, left parasternal heave, raised JVP, hepatomegaly
COPD investigations
Spirometry - confirm diagnosis
Bedside - observations, BMI, sputum cultures, ABG, ECG
Bloods - FBC, alpha-1 antitrypsin levels
Imaging - CXR, CT scan, ECHO
CXR - hyperexpanded, flattened hemidiaphragms, hypodense, saber-sheath trachea
MRC dyspnoea scale
1) breathlessness on strenuous exercise
2) breathlessness on hurrying/slight hill
3) walks slower than contemporaries on ground level due to breathlessness OR have to stop to catch breath when walking at own pace
4) stops to catch breath after 100 metres OR a few minutes of walking
5) breathlessness on minimal activity/unable to leave the house due to breathlessness
COPD severity
Mild - >/= 80
Moderate - 50-79
Severe - 30-49
Very severe - < 30
(based on predicted FEV1 %)
COPD management (non-pharmacological)
Education
Smoking cessation
Vaccination - seasonal influenza vaccine & pneumococcal vaccine
Pulmonary rehab - multidisciplinary programme that aims to optimise the physical and social performance of patients
Self-management plans - helping patients manage their symptoms including how to manage acute exacerbations
Management of comorbidities
COPD management pharmacological
1) offer a SABA/SAMA to use on PRN basis
2) offer LABA+LAMA if no evidence of steroid responsiveness or asthma features OR offer LABA+ICS if evidence of steroid responsiveness/asthmatic features
3) offer escalation to triple therapy (LABA+LAMA+ICS)
-If already on LABA+LAMA:
–Struggling with quality of life - add ICS (3 month trial)
–1 severe/2 moderate acute exacerbations within one year - add ICS
-If already on LABA+ICS:
–Add LAMA if struggling with QoL/exacerbations
Oral pharmacological options
-Corticosteroids - mainstay of treatment in acute exacerbations
-Theophylline - (some bronchodilator action through inhibition of phosphodiesterase): used in difficult to treat COPD
-Mucolytics - used in patients with a chronic productive cough to reduce frequency & sputum production
-Antibiotics - used for acute exacerbations & prophylactically in certain situations
COPD acute management
Oxygen - any known/new evidence of CO2 retention then a sats target of 88-92% should be used
-NIV for patients who require high levels of O2 to prevent hypoxia but are at high risk of hypercapnic respiratory failure
-Venturi masks - allow an exact fraction of inspired oxygen to be administered
Bronchodilators - usually given as nebulisers
-Salbultamol 2.5mg nebulised
-Ipratropium 500mcg nebulised
Corticosteroids - prednisolone 30mg once daily should be given for 5 days
Antibiotics - doxycycline/co-amoxiclav
IV theophylline may be considered in severe cases
LTOT
Arterial PaO2 < 7.3kPa
Arterial PaO2 < 8kPa with any of
-Pulmonary hypertension
-Peripheral oedema
-Secondary polycythaemia
COPD complications
Respiratory failure
Pneumonia
Pneumothorax
Polycythaemia/anaemia
Depression
PE aetiology
One or more emboli usually arising from a thrombus break off and obstruct within the pulmonary arteries
Usually arises from a DVT
PE pathophysiology
Predominant therapy of development of VTE is Virchow’s triad
-Venous stasis
-Endothelial injury
-Hypercoagulable state
Occlusion of one or more of the pulmonary arteries leads to absence of perfusion to that area of the lung
-V/Q mismatch because ventilation is unaffected
-May lead to hypoxia and clinical features of breathlessness
-Area of lung may undergo infarction (usually prevented by the bronchial circulation)
PE symptoms
Dyspnoea
Pleuritic chest pain
Cough
Haemoptysis
Dizziness
Syncope
Leg pain and swelling
PE signs
Tachycardia (> 100 bpm)
Low grade fever (>37.5)
Hypoxia (sats < 94%)
PE investigations
Routine bloods
D-dimer
ECG - sinus tachycardia, S1Q3T3 pattern
CXR, V/Q scan, lower limb USS, echo
CTPA
PE Wells score
PE - series of seven criteria are used that given a score between 0-12.5
Clinical signs and symptoms of DVT (+3)
PE is #1 diagnosis/equally likely (+3)
HR > 100 (1.5)
Immobilisation at least 3 days or surgery in the previous 4 weeks (+1.5)
Previous, objectively diagnosed PE/DVT (+1.5)
Haemoptysis (+1)
Malignancy with treatment within 6 months/palliative (+1)
PE likely (score > 4) = straight to CTPA, if not available, interim anticoagulation if safe
PE unlikely (score < 4) d-dimer blood test within 4 hours, if positive = CTPA
PE management anticoagulation
Stable - offer apixaban/rivaroxaban
Haemodynamic instability - consider thrombolysis & heparin-based anticoagulation according to local guidelines
Active cancer - consider DOAC (edoxaban)
Renal impairment - if CrCl 15-50ml/min, offer apixaban/rivaroxaban or LMWH for 5 days then edoxaban/warfarin, if CrCl <15ml/min, offer LMWH/UFH as per local guidance
PE management thrombolysis
Thrombolysis - use of recombinant tissue plasminogen activator (fibrinolytic drug that breaks down clots)
-Cardiac arrest with confirmed or suspected PE
-Confirmed PE with deterioration despite anticoagulation
-Haemodynamic instability & high clinical suspicion of PE/confirmed PE within 14 days
PE long-term management
Long-term management - patients are advised to continue anticoagulation for a minimum period of 3 months
After this patients should be referred to a specialist anticoagulation clinic & discuss whether to continue anticoagulation
PE complications
High mortality (20%) in patients with haemodynamic instability
Maternal death in pregnancy
Chronic thromboembolic pulmonary hypertension & associated right sided HF
TB (different types)
Caused by bacteria of the mycobacterium tuberculosis complex & is one of the world’s most common and deadly infective diseases
Latent TB - refers to individuals infected with TB, who suppressed the initial infection, have no active diseases & not infectious
Active TB - refers to symptomatic/progressive disease
Primary TB - initial infection, often subclinical, suppressed in the majority of individuals
Progressive-primary TB - primary infection is not suppressed & prolonged infection occurs
Post-primary TB - occurs in patients with latent TB, frequently due to immunocompromised (may be pulmonary/extra-pulmonary)
TB pathophysiology
Inhaled bacilli find their way into alveoli & begin dividing
In some individuals -> may be immediately cleared, in others primary TB develops
Once a critical mass is reached a host immune response is elicited with mycobacterium producing a strong immune response
Ghon complex may develop
-Ghon focus - small caseating granuloma
-Ipsilateral mediastinal lymph node
After 2-10 weeks a sufficient cell-mediated response halts the proliferation of the bacilli in the majority of individuals - these patients develop latent TB (may have a Ranke complex = calcified Ghon’s complex)
Small proportion of patients do not halt the primary infection & develop primary-progressive TB (linked to patients with inadequate T-cell immunity)
TB symptoms and signs
Pulmonary TB - cough, fever, weight loss
Lymph node - enlarged, firm, non-tender (most commonly affects cervical and supraclavicular nodes)
Genitourinary TB - sterile pyuria, salpingitis, epididymo-orchitis, renal abscess
Miliary TB - disseminated haematogenous spread of bacilli
CNS TB - TB meningitis: fever, malaise and headache
TB investigations
CXR - demonstrate consolidation, cavitation (typically upper lobe) & effusion
-Miliary TB - appearance of millet seeds throughout the lung fields
Latent TB
-Mantoux test - intradermal injection of tuberculin
-If patient has had exposure to TB they exhibit a delayed hypersensitivity reaction
-Previous BCG vaccination affects results
Interferon-gamma release assay - assays detect the bodies cellular immune response (tests for the T-cell interferon-gamma response to M. tuberculosis)
-Unaffected by previous BCG and non-tuberculous mycobacterium
Active TB
-Microbial - microscopy & culture, cytology & histology, nucleic acid amplification
-Imaging