Respiratory Flashcards
What are these:
- FEV1
- FVC
- KCO
- TLCO
What is obstuctive and restrictive pattern involving FEV1 and FVC?
-
FEV1 = forced expiratory volume
- Volume that has been exhaled at the end of the first second of forced expiration
-
FVC = focred vital capacity
- Volume that has been exhaled after a maximal expiration following a full inspiration
- KCO = Diffusion capacity of the lung per unit area for CO
- TLCO = Diffusion capacity of the total lung capacity for CO
Obstructive pattern:
- Normal (or increased) FVC, reduced FEV1:FVC ratio
- Reduced FVC, normal (or increased) FEV1:FVC ratio
Define the classical features of asthma
(symptoms and signs)
Ashthma is a chronic inflammation condition of the airways, charactised by airway hypersensitivity to a number of factor.
Symptoms variable but recurring:
- Reverisible bronchospasm resulting in airway obstruction:
- Wheezing & SOB
- Classically worse during night or upon exercise
- Symptoms are typically worse in the morning (peak flow worse - ‘morning dipping’)
- Subjective feeling of chest tightness
- Cough, again classically nocturnal
Signs:
- Widespread expiratory wheeze
- Pulmonary function testing reveals a decreased FEV1 (peak flow) relieved by ß2 agonists
How may the symptoms of asthma be differentiated from those of COPD?
In asthma airflow limitation is often fully reversible, either spontaneously or with treatment whereas COPD is a disease of progressive airflow limitation that is not fully reversible.
Classify asthma into early and late onset and discuss the likely presenting characteristics of a typical patient who is likely to get each
Extrinsic asthma
- Type I hypersensitivity reaction
- ay occur in young patients with atopy (alergic diseases)
- Elevated IgE may be present, alongside eczema and/or rhinitis
- May disappear at age 15 but may recur.
Intrinsic asthma
- Non-immune mechanisms
- occurs in middle aged, with no causative agent can be identifie (no history of atopy - allergies)
- Skin tests are usually negative and IgE normal, remission is rare.
- They may present with shortness of breath and tight chest - more severe symptoms and associated with quicker deterioations in lung function
Outline common precipitants of an asthma attack
Common precipitants:
- Environmental allergens: pets, grass pollen, dust mites
- Viral infections
- Cold air
- Emotion
- Drugs: NSAIDs particularly aspirin. Beta-blockers
- Atmospheric pollution
- Occupational pollutants: e.g. flour or chemicals
What occupations may predispose to developing asthma?
Vehicle spray painting, woodworking, baking, soldering, healthcare workers, working with animals, working in agriculture, engineering, hairdressing
Describe the clinical features of an acute asthma attack
Features of acute severe asthma:
- Tachycardia (HR > 110)
- Marked SOB (RR>25)
- Peak expiratory flow (PEF) 33-50% of best
- Cant complete sentences in one breath
May have pulsus paradoxus (abnormally large decrease in systolic BP during inspiration)
- Widespread bilateral expiratory wheeze in a hyper inflated chest
- Accessory muscle of respiration are often used
Describe the blood gas abnormalities associated with severe asthma and highlight other clinical indices of severity
- In a mild attack, there may be low pCO2
- Due to hyperventilation
- A normal pCO2 with hypoxaemia suggests current deterioration (life threatening attack)
- In life threatening exacerbations there will be a high pCO2, severe hypoxia and low pH.
- PEF<50% indicates severity, and <33% life-threat.
Describe how to use inhaler devices and other aids appropriately
Shake the inhaler, take a normal breath out, place the inhaler in your mouth and simultaneously breathe in and press the button to release the aerosol.
Hold the breath in for 10 seconds if possible.
Important not to just spray the inhaler into the mouth!
With the steroid inhaler, the patient should be counselled to rinse the mouth out after use.
Describe the clinical features of life threatening asthma attack
-PEF less than 33% of best -SpO2 <92% -Silent chest, cyanosis or feeble respiratory effort -Bradycardia, hypotension or dysrhythmia -Exhaustion or confusion
Describe the morphology and pathological consequences of acute asthma
Asthma is an inflammatory condition with both acute and chronic elements.
Acute asthma:
- Acute episodes of bronchospasm that are triggered by recognised triggers
- These triggers activate mast cells, which lead to two phases;
-
An early phase of bronchospasm due to spasmogen production (histamine, prostaglandin D2 and leukotrienes)
- smooth muscle contraction narrows the airway
-
A late phase due to chemotaxins attracting eosinophils and mononuclear cells
- cells infiltrates and muscosal oedema narrow the airway.
- There will also be airway hyper-reactivity in the late phase, which can lead to further acute deteriorations
-
An early phase of bronchospasm due to spasmogen production (histamine, prostaglandin D2 and leukotrienes)
Describe the morphology and pathological consequences of chronic asthma
Asthma is an inflammatory condition with both acute and chronic elements.
Chronic asthma
- Many asthmatics will have normal respiratory function between attacks, but some will develop persistent airway obstruction that can become indistinguishable from COPD (more common in intrinsic asthma)
- There is bronchoconstriction due to increased responsiveness of bronchial smooth muscle, and hyper secretion of mucus that plugs the airways
- Mucosal oedema further narrows the airways
- The sputum will contain Charcot-Leyden crystals (from eosinophil granules) and Curschman spirals (mucus plugs from small airways)
- In long-standing disease, the can lead to pulmonary hypertension
How can you obtain an accurate peak flow rate (PEFR) from a patient
Stand tall, deep breath, encourage, and take the best of 3.
Define chronic obstructive pulmonary disease (COPD)
- COPD is a disease of progressive airflow limitation that is not fully reversible, associated with an abnormal inflammatory response of the lungs to noxious particles or gases, predeminantly inhaled cigarette smoke
- The airflow limitation is due to decreased outflow pressure (emphysema) plus increased airway resistance (chronic bronchitis/bronchiolitis)
Emyphysema causes COPD as causes decreased outflow pressure and therefore cause airflow limitation.
Describe the pathology of emphysema
Emphysema:
- Dilation of any part of the respiratory acinus (air spaces (air spaces distal to the terminal bronchioles) with destructive changes in the alvelor walls
- There is an absence of any scarring (fibrosis)
- Tissue destruction is caused by increased secretion and activation of extracellular proteases by inflammatory cells
- The inflammatory cells are stimulated by noxious particles e.g. smoking
- In centrilobular emphysema (most common cause) these changes are limited to the central part of the lobule directly around the terminal bronchiole, with normal aveoli elsewhere
- Panacinar emphysema leads to destruction and distension of the whole lobule, which can happen in smokers but is more common in a1-antitrypsin deficiency
- Dilated air spaces >1cm are termed bullae
- Loss of connective tissue in the alveolar walls leads to a loss of elastic recoil of the lungs, leading to air entrapment in the lungs and inadequate ventilation
- The reduction in the area available for gas exchange means there is reduced oxygen uptake
Chronic bronchitis and bronchiolitis causes COPD as causes increases airway resistance and therefore causes airflow limitation.
Describe the pathology of Chronic bronchitis and bronchiolitis
Chronic bronchitis:
- Daily cough with sputum for at least 3 months per year for two years
- The primary abnormality seen is abnormal amounts of mucus, which causes plugging of the airway lumen
- The hypersecretion is associated with hypertrophy and hyperplasia of brochial mucus-secreting glands
- Shown by Reid indec: the ratio of gland: wall thickness
- Inflammation not typically present, although frequent LRTIs develop with secondary inflammation and squamous metaplasia
Bronchiolitis
- Cigarette smokers also develop inflammation of the airways <2mm in diameter, i.e. the bronchioles, with macrophage and lymphoid cell infiltration
- This is actually the first pathological change in COPD
- It may lead to scarring and narrowing of the airways
Describe the typical history of a patient with COPD
(symptoms)
Clinical presentation:
- Productive morning morning cough, following many years of ‘smoker’s cough’
- Increased frequenced of lower respiratory tract infections
- Slowly progressive dyspnoea with wheezing
- Respiratory failure
- Chronic heart failure (cor pulmonale): occurs late
On examination what would you find with a patient with COPD?
Signs:
Mild disease:
- widespread disease
Severe disease:
- Observations:
- Tachypnoea
- Cyanosis
- Flapping tremor of outstretched hands (if CO2 retainer)
- Inspection
- Hyperinflation
- Intercostal recession on inspiration
- Lip pursing on expiration
- Signs of respiratory distress (tracheal tug, paradoxical breathing, accessory muscle use)
- Palpation:
- Poor chest expansion
- Percussion:
- Hyper-resonant throughout, loss of cardiac/hepatic dullness
- Auscultation:
- Decreased breath sounds, prolonged expiratory phase
- Polyphonic wheeze (many pitches)
What are complications of COPD?
- Acute exacerbations
- Polycthaemia (the bone marrow cells produces too many red blood cells)
- Respiratory failure
- Cor pulmonale (the enlargement and failure of the right ventricle of the heart)
- Pneumothorax
- Lung carcinoma
What are risk factors for COPD?
- Cigarette smoke exposure:
- Stimulates neutrophils to produce elastase
- Can inactivate a1-antitrypsin
- Directly causes mucous gland hypertrophy
- Occuptional exposure to dust
- a1-antitrysin deficiency
- Recurrent chest infections
- Low socioeconomic status
- Asthma/atopy (allergies)
Blue bloaters and Pink puffers are patients with COPD who exhibit specific phyical signs as a result of COPD
What are they? Why do they occur?
Blue bloaters:
- Patients with severe chronic bronchitis/COPD become insensitive to CO2 and thus rely on their hypoxic drive to stimulate respiratory effort
- These patients are not particularly breathless, but are cyanosed and oedematous
- Suggestive of cor pulmonale
- A blood gas will show type 2 respiratory failure (low oxygen, retaining CO2)
- Oxygen should be given with care in these patients
Pink puffers:
- These patients remain sensitive to CO2, thus keep a low CO2 and a near normal O2
- They are tachypnoeic and tachycardic, using accessory muscles to increase their ventilation and are breathless but not cyanosed
- The patients are very thin as large amounts f calories are used to breath
- This can progress to type 1 respiratory failure
Outline the investigation of a patient with suspected COPD
- Lung function tests will show evidence of airflow limitation – decrease in both FEV and FVC, and a reduction in the ratio, to below 70%.
- CXR often normal - useful in ruling out other pathology
- CT may outline bullae
- Hb, PCV and CRP may be raised
- ABG may be normal at rest
- Sputum examination normally not required.
- ECG and Echo useful if heart involvement suspected
- Alpha-1 antritrypsin investigation may be required in younger patients or non-smokers.
What spirometry data will show restrictive patterns?
obstructive patterns?
Restrictive pattern:
- Decrease in FEV and FVC but maintenance of normal ratio
Obstructive pattern:
- Decrease in FEV, normal FVC, and so decrease in ratio
What is bronchiectectasis?
Chronic dilatation of the airways, leading to chronic infection/inflammation
Describe history of a patient with bronchiectectasis
(symptoms and signs)
Symptoms:
- Recurrent cough, producing copious quantities of infected sputum
- Intermittent haemoptysis (can be only symptom)
- Persistant halitosis (bad breath)
- Dyspnoea
- Reccurent febrile episodes and episodes of pneumonia
Signs:
- Clubbing is common (unlike in COPD)
- Coarse inspiratory crackles over infected areas, typically bibasal
- Wheeze
- Often low body habitus due to high energy demands
How do the symptoms and signs of brochiectasis differ from COPD?
- Clubbing is common, unlike in COPD.
- Sputum in COPD is not of the same quantity.
- Unlike in COPD, there is no wheeze.
Outline the pathology of bronchiectasis
- Any bronchi may be involved, but most commonly at the lung bases
- Airways are dilated, with purulent secretions and chronic inflammation in the wall with inflammatory granulation tissue
- Granulation tissue can bleed leading to haemoptysis
- With repeated exacerbations there can be fibrous scarring leading to respiratory failure
What are complications of bronchiectasis?
- Pneumonia
- Pneumothorax
- Empyema
- Lung abcess
- Haematogenous spread of infection
- Severe life threatening haemoptysis: more severe in cystic fibrosis
List risk factors for bronchiectasis
Most commonly no cause found, ‘idiopathic bronchiectasis’, however anything that interferes with drainage of brochial secretions or causes recurrent/persistent infection can lead to bronchiectasis:
- Post-infective: TB, measles, pertussis, pneumonia
- Cystic fibrosis
- Bronchial-obstruction: tumour/foreign body
- Allergic broncho-pumonary aspergillosis
- Ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
- Immune deficiency: Specific IgA, hypoammaglobulinaemia
- Connective tissue diseases: 1/3rd of RA pts develop bronchiectasis
Elicit the physical signs of bronchiectasis
- Production of a khaki coloured, thick, foul-smelling sputum
- Haemoptysis may occur.
- Coarse inspiratory crackles can be heard over infected areas of the lung
- Halitosis (odorous breath) will persist
- Patients will often be febrile
- Clubbing is present.
What are the investigations required for a patient with suspected bronchiectasis?
- Sputum culture: atypical organisms
- CXR: cystic shadowing
- CT: to access distribution of disease, can see dilated airways with signet ring sign
- Spirometry: obstructive pattern, reversibility should be assessed
Describe the typical presentation of a patient with a community aquired pneumonia (CAP)
(symptoms and signs)
Symptoms:
- Acute systemic illness
- Fever
- Rigors
- Vomiting
- Cough
- Initally short, dry and painful progressing to a productive with mucopurulent sputum
- Dyspnoea
- Pleuritic chest pain - may be referred to shoulder or anterior abdominal wall
Signs:
- Tachypnoea
- Decreased chest expansion on the affected side
- Dullness to percussion over the affected area
- Coarse crackles and a pleural rub over the affected area, with bronchial breathing
- Increased vocal resonance
- ‘Blue balloons’ can be heard better: seen in consolidation, can’t hear as well in effusions, pneumothorax or collapse
- Upper abdominal tenderness: in lower lobe pneumonia
How is the severity of pneumonia assessed?
CURB-65
- Confusion: mini mental test score <8
- Urea >7mmol/l
- Respiratory rate >30 per minute
- Blood pressure: hypotensive <90/60
- 65 years or older
One point for each finding
0/1 = non-severe CAP
2 = moderately severe CAP \>2 = severe CAP
How is hospital acquired pneumonia defined?
- Pneumonia that develops at least 48 hours after admission to hospital, with no signs of incubation on adission or develops in somebody in hospital in the past 10 days
List the common pathogens causing community acquired pneumonia
- Conventional bacteria (60-80%)
- Streptococcus pneunomia (most common)
- Haemophilus influenzae
- Atypical bacteria (10-20%)
- mycoplasma pneumonia
- Chylamdia pneumonia
- Legionella pneumonia
- Viruses (10-20%)
- Influenza/parainfluenza
List the common pathogens causing community acquired pneumonia
- Gram –ve bacteria (E Coli, Pseudomonas, Klebsiella)
- Staph Aureus