phase 2 simon berry + liz stedman the peer teaching society is not liable for false or misleading...

Phase 2

Simon Berry + Liz Stedman

The Peer Teaching Society is not liable for false or misleading information…

• To give a brief overview of the following 3 topics:– COPD– Asthma– Pulmonary Fibrosis (Interstitial Lung Disease)

• Apply the knowledge to practice exam questions


Aims

Chronic Obstructive Pulmonary Disease made up of Chronic bronchitis vs Emphysema

•Chronic Bronchitis (Bronchi) – . Daily productive cough for at least 3 months over 2 years consecutive years. Pathology hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells. Bronchial wall thickening.

•Emphysema (alveoli) – permanent enlargement of airspaces distal to terminal bronchioles. Reduced SA for gas exchange. Reduced recoil, and loss of support = airway narrowing

•Mainly affects people over 35, more common with increasing age•Men >Women•Very common reason for hospitalisation (1 in 8 admissions)


Introduction

• Smoking / occupational exposure / air pollutants irritation and inflammation damage to the airways

• 1 in 10 (20/d) and 1 in 4 (40/d) will develop COPD

• Genetic alpha-1-antitryspin deficiency (affects the proteins in the lung, liver and blood disorder). 1 in100


Aetiology

• Defining feature irreversible airflow limitation during forced expiration. Result of loss of elastic recoil due to lung tissue destruction / increase in resistance of conducting airways (mucus)

• May develop HF reduced Ox. in blood and changes in lung tissue leading to increased pressure in pulmonary vasculature. increased strain on H. muscles = HF (worsening Breathlessness and fluid retention)

• Respiratory failure level of oxygen in blood too low, CO2 builds up in blood stream. May need palliative care


Pathophysiology

• Exertional breathlessness (PC) – MRC breathlessness scale

• Chronic productive Cough (PC) : may start of episodic persistent

• Wheeze• Frequent winter ‘bronchitis’ / exacerbations

– Bacteria 1 in 2/3 in COPD– Vrial 1 in3

• Symptoms all worsen with time if smoking not stopped!

Symptoms

• Physical examination in detecting mild – moderate COPD is poor.

• Severe disease may show– Tachypnea and respiratory

distress w/ simple activities– Accessory muscle usage and

indrawing of lower IC spaces (Hoover sign

– Cyanosis– Elevated JVP– Peripheral Oedema– Hyperinflation

• Thoracic signs may show

– Hyperinflation (barrel chest)

– Wheezing – forced+ unforced expiration

– Diffusely decreased breath sounds

– Hyperresonance on percussion

– Prolonged expiration

– Coarse crackles beginning with inspiration in some cases

Signs

• CB (blue bloaters)– alveolar ventilation– Low PaO2– High PaCO2– Cyanosed but not

Breathless– Rely on hypoxic drive– Oxygen sats: 88-92%– May progress to cor

pulmonale

• Emphysema (pink puffers)– alveolar ventilation– near normal PaO2– Normal / low PaCO2– Breathless, but NOT

cyanosed– May progress to Type

1 RF

Bronchitis vs Emphysema

http://www.medcomic.com/uploads/4/0/0/1/4001915/792407_orig.png

• Spirometry diagnostic. Check FEV1 - postbronchodilator– FEV1/FVC < 70% or 0.7 = COPD (compared to pred. value / matched control)– Mild (stage 1) FEV1 at least 80% predicted value– Moderate (stage 2) FEV1 50%-79% pv– Severe (stage 3) FEV1 30%-49% pv– Very Severe (stage 4) FEV1 <30% pv

• ABG– Best clues for acuteness an D. severity / exacerbation

• CXR – check for lung cancer– Hyperinflation (> 6 ant. Ribs seen above diaphragm and mid-clavicular line)– Flat hemidiaphragms, large central pulmonary arteries– in peripheral vasc markings, bullae (emphysema)

• High-res CT

Investigations

• FBC: anaemia can cause SOB, polycythemia secondary to COPD (RBC)

• Alpha—antitrypsin levels – if early onset, minimal smoking Hx, FHx presence

• Steroid trial – see if COPD responsive to steroids

• ECG/Echo – Monitor Cor Pulmonale

• TLCO – Ix symptoms disproportionate to spirometric impairment

Investigations (cont.)

• STOP SMOKING

• Exercise and weight loss

• Influenza and pneumococcal vaccination

• Cardiopulmonary rehabilitation

• Broncho-pulmonary exercises

• Caution with flying (increased risk of pneumothorax with altitude)

Management

Management (cont.)

Asthma

• Paroxysmal and reversible airways obstruction

– Airway hyperresponsiveness

– Inflammation of the bronchi

– Airway remodelling


Introduction

• Extrinsic– Atopic individuals– Often accompanied by eczema– Can be IgE related or non-IgE related

• Intrinsic– Middle age (‘late onset’)


Aetiology

• Occupational sensitizers• Cold symptoms – upper respiratory tract infection (URTI) • Cold air• Exercise (during or after)• Pollution eg cigarette smoke, car fumes• Infection• Drugs eg beta blockers, NSAIDs• Allergens – pollen exposure, exposure to animals, dust mites• Time of day: natural dip in peak flow overnight


Precipitants

• Intermittent dyspnoea• Wheeze• Cough (often nocturnal)• Sputum• Ask about:

– Triggers: at home, at work– Diurnal variation– Other atopic disease– Da


Symptoms

• RCP 3– Recent nocturnal waking?– Usual asthma symptoms in day?– Interference with ADLs?

• Asthma control test (out of 25)


Severity

• Tachypnoea• Hyperinflated chest• Hyperresonant percussion note• Diminished air entry• Widespread, polyphonic wheeze


Signs

• Respiratory Function Tests– Peak Expiratory Flow (PEF)

• diurnal variation of >20% on 3d a wk for 2wks

– Spirometry• obstructive defect (↓FEV1/FVC, ↑RV), >15% increase

improvement in FEV1 following beta2 agonists

• Other tests– Corticosteroid trial– Skin prick tests– CXR – exclude pneumothorax/ aspergillosis


Investigations

• 100% O2 via non-rebreathing bag

• Nebulized salbutamol + ipratropium bromide• Hydrocortisone IV or prednisolone PO• CXR to exclude pneumothorax• Magnesium sulphate if life-threatening


Management of Acute Attack

• Conservative Management– DON’T FORGET– Smoking cessation– Avoid Precipitants– Education: Inhaler technique, PEF monitoring,

self-management by altering medications in light symptoms, advise about oral prednisolone for rescue therapy

– Asthma action plan


Long-term Management

Long-term ManagementMedical Management

• COPD – permanent damage and constriction to airways

• Asthma – reversible constriction of the smooth muscle in the airways

• COPD more likely to cause productive cough than asthma

• Waking at night with SOB and wheeze asthma > COPD

• COPD rare <35, asthma common <35

• Asthma, allergies, eczema (atopic conditions)

Asthma vs COPD

Pulmonary Fibrosis

• Three main types:– Replacement fibrosis 2ry to lung damage

• Eg infarction, TB and pneumonia

– Focal fibrosis in response to irritants• Eg coal dust and silica

– Diffuse parenchymal lung disease• Occurs in idiopathic pulmonary fibrosis (IPF) and

extrinsic allergic alveolitis


Introduction

• Peak age 50-70 yrs. M=F• Common causes:

– Idiopathic pulmonary fibrosis– Replacement fibrosis– Pneumoconioses eg silicosis, asbestosis, CWP etc– Extrinsic allergic alveolitis– Granulomatous diseases eg sarcoidosis– Exposure to drugs eg amiodarone– Radiation exposure– Connective tissue diseases eg rheumatoid arthritis, SLE etc


Epidemiology + Aetiology

• Dependent on disease process• May be:

– Acute, with a fulminant, progressive, remitting or resolving course

– Subacute, with a resolving, remitting, relapsing or progressive course

– Chronic, insidious and slowly progressive• May be incidental findings on CXR, spirometry,

occupational risk assessment


Presentation

• Dyspnoea• Chronic cough• Wheezing• Haemoptysis• Chest pain


Symptoms

• Central cyanosis, fine end-inspiratory pulmonary crackles

• Nonspecific features eg low grade fever and myalgia

• Finger clubbing, esp with idiopathic pulmonary fibrosis and asbestosis

• Signs of pulmonary hypertension and cor pulmonale


Signs

• FBC - ?mild anaemia, ESR / CRP may ↑• Autoantibodies (antinuclear antibodies, rheumatoid factor)• ABGs: O2 desaturation is common

• Lung function tests– Restrictive pattern (but obstruction of airways may also

be present).– Reduced total lung capacity.– Reduced residual capacity.– Reduced residual volume.– Reduced gas transfer.


Investigations

• CXR– May show no abnormality– Reticular and/or nodular opacities– Honeycombing is a late finding = severe disease

• High resolution chest CT scanning – characteristic findings, extent and progression


Imaging

• Supportive measures– Smoking cessation, avoidance of cause, influenza

and pneumococcal vaccine, pulmonary rehabilitation

• Drug treatment– Immunosuppressive therapy

• Corticosteroids• Cytotoxic drugs (azathioprine)

• Lung transplantationThe Peer Teaching Society is not liable for false or misleading information…

Management

• Pulmonary hypertension• Coronary artery disease• Lung cancer


Complications

• Type 1 Respiratory Failure– PaO2 LOW < 8kPa

– *PaCO2 LOW/ NORMAL < 6.5kPa*

• Type 2 Respiratory Failure– PaO2 LOW < 8kPa

– *PaCO2 HIGH > 6.5kPa*


Respiratory Failure

• Type 1 Respiratory Failure– Ventilation-perfusion mismatch

• Under-ventilated alveoli eg pulmonary oedema, pneumonia, pneumothorax, pulmonary fibrosis

• Venous blood bypasses (eg R-L cardiac shunts, PE)

• Type 2 Respiratory Failure– Inadequate alveolar ventilation eg asthma, COPD


Respiratory Failure

Practice Questions

• What is the key pathological feature of asthma?a) Collapse of small airways on exhalationb) Increased connective tissue depositionc) Intermittent, inappropriate bronchoconstrictiond) Loss of alveolar surface areae) Smooth muscle hyperplasia and increased mucus


Practice Question

1. A young patient with a history of asthma arrives at the accident and emergency department with acute severe breathlessness, and is obviously wheezy and distressed. The doctors immediately give him a treatment which will rapidly improve his arterial oxygenation


Practice Question

Answer: C

2. The doctors then examine and investigate the same patient described in question 1 (above) and make a diagnosis of acute severe asthma. They decide to prescribe the bronchodilator treatment for initial therapy


Practice Question

Answer: I

3. Shortly after this the doctors then decide to administer anti-inflammatory treatment to the same patient. Which is the most appropriate treatment?


Practice Question

Answer: G

1. A 67 year old man is seen in outpatients with a 4 year history of progressive shortness of breath. He has worked for 12 years in a power station and was regularly exposed to all types of dust.


Practice Question

Answer: C

2. An 18-year-old hairdresser apprentice was seen by her GP with a 12 hour history of wheeze and shortness of breath. She was wheezy on examination with a pulse rate of 120 bpm, and had a recorded peak flow at 30% of her predicted value just prior to a nebuliser of salbutamol.


Practice Question

Answer: B

• For phase list:– Patient.co.uk/patientplus

• For OSCE– Geeky medics youtube channel


Hints and Tips

Thanks for listening!!

Please fill in feedback

Appendix

Asthma Control Test

phase 2 simon berry + liz stedman the peer teaching society is not liable for false or misleading...

Documents