phase 2 kirsty mclauchlan and vicky cox

Phase 2

Kirsty McLauchlan and Vicky Cox

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

• Asthma• COPD• Pulmonary Fibrosis


Aims


Introduction

• A chronic relapsing/episodic inflammatory condition of the airways

• Characterised by 1. Airflow limitation2. Airway hyper-responsiveness3. Bronchial inflammation


Asthma

• 15 % of population• 5.2 million people in UK – 1.1million children

• Prevalence is increasing

• More in developed counties eg. UK, NZ, Australia


Asthma - Epidemiology

Asthma

Extrinsic Intrinsic

Childhood – atopic Middle-aged Late onset – occupational

- NSAID-intolerance- β-adrenoreceptor blocking agents


Asthma – Aetiology (cause)Not

immunologically mediated

Type I hypersensitivity

reactions


Asthma - triggersALLERGENS (atopy)

Viral infection

Cold air

Emotion

Irritant dusts, vapor, fumes(cigarette smoke)

Occupationalsensitizers

Atmospheric pollution

Exercise

Drugs – NSAIDs, β-adrenoreceptor blocking agents

• Type of hypersensitivity – (Type 1)• Runs in families• Have increased IgE antibodies – allergen

specific• Can be caused by environmental factors

– Early exposure to allergens– Maternal smoking– Hygiene hypothesis


Asthma – what is Atopy?


Occupational Asthma

animals latex dyes

bleachWood dustAntibioticsFlour

paints


Asthma - Pathogenesis

InflammationMucus and oedemaBronchoconstriction

AIRWAY OBSTRUCTION REMODELING

EpitheliumSmooth muscle

Basement membrane


Asthma 1. INFLAMMATION

• IgE = bronchoconstriction• By blocking β-adrenoreceptor in smooth

muscle surrounding airways


Asthma – 2. Bronchoconstriction

This is why β-adrenoreceptor blockers (e.g propranolol) can trigger asthmatic response!


Asthma 3. oedema + mucus


Asthma - remodeling• Hypertrophy• Contractility

• Loss of cilia• Goblet cells= more infection+ more mucus

Deposition of collagen = thickened basement membrane

• Episodes/attack of shortness of breath and wheezing

• Bilateral, polyphonic, expiratory, widespread• Worse at night• Cough


Asthma – Clinical Features

• Spirometry – reduced FEV1 • PEF – reduced


Asthma – investigations

• 15% improvement in either after a bronchodilator indicates asthma

• Exercise tests• Blood count – eosinophils• Exhaled nitric oxide - eosinophils

• Controlling extrinsic factors

• Long term treatment

• Treatment of acute attack


Asthma - Treatment


Asthma - Pathogenesis

InflammationMucus and oedemaBronchoconstriction

AIRWAY OBSTRUCTION REMODELING

EpitheliumSmooth muscle

Basement membraneB2-agonistB2-agonist

corticosteroidcorticosteroid


Step-wise management

salbutamol

budesonide

salmeterol

monteleukast

prednisolone


Management of Acute Attack

IV aminophylline

Practice Questions

• ‘A common progressive disorder characterized by airway obstruction with little or no reversibility’

– Chronic bronchitis– Empyhsema


Chronic Obstructive Pulmonary Disease

Obstructive:

- FEV1 (<80% predicted)- FEV1/FVC (<0.7 predicted)


COPD

•Prevalence: 10-20% of over-40s

•2.5 x 106 deaths worldwide


COPD - epidemiology

•caused by long-term exposure to toxic particles

– (cigarette smoking >90% of cases)


COPD - aetiology


COPD - pathophysiology

Neutrophils & CD8 lymphocytes

Inactivation of α1-antitrypsin by cigarette smoke

Columnar cells are replaced by squamous cells

Widespread narrowing of small ariways



Early disease, predominantly in the small airways, is reversible.



With mucous gland hypertrophy


Chronic Bronchitis - pathophysiology

.

• Lumen occlusion by mucus plugging• Goblet cell metaplasia• Smooth muscle hyperplasia• Distortion due to fibrosis

Airway narrowing


Emphysema - pathophysiology

.

• permanent enlargement of airspaces

• loss of alveolar walls reduced elastic recoil• loss of alveolar supporting structure

Reduced surface for gas exchange

Airflow limitation

• “cough and sputum production on most days for 3 months of 2 successive years”


Chronic Bronchitis

• “ enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls”


Emphysema

• Productive cough •White or clear sputum•Wheeze•Dyspnoea


Symptoms of COPD

COPD:- age of onset > 35 years- smoking (active or passive)- chronic dyspnoea- sputum production- minimal diurnal or day-to-day FEV1 variation


COPD vs. Asthma

Mild disease: no signs or quiet wheeze Severe disease: - tachypnoea

- prolonged expiration- use of accessory muscles- intercostal indrawing- lip-pursed expiration- poor chest expansion- hyperinflated lungs


Signs of COPD

Normally respiratory drive is largely initiated by PaCO2.


Pink Puffers/Blue Bloaters

-PaO2 < 8kPa

-PaCO2 > 7kPa


Respiratory Failure

“heart disease secondary to respiratory disease”

•Pulmonary hypertension•Right ventricular hypertrophy•Right heart failure


Cor Pulmonale

• Dyspnoea• Fatigue• Syncope• Cyanosis• Tachycardia• Raised JVP• RV Heave • Loud P2

•Pansystolic Murmur– tricuspic regurgitation


Cor Pulmonale – clinical features

• Lung Function tests (↓FEV1:FVC, ↓ PEFR)

• Chest X-ray (often normal)

• High-resolution CT (to show bullae in empyhsema)

• Blood gases (often normal)The Peer Teaching Society is not liable for false or misleading information…

COPD - Investigations

• British Thoracic Society/NICE COPD guidelines

– Mild: FEV1 50-80% of predicted

– Moderate: FEV1 30-49% of predicted

–Severe: FEV1 <30% of predicted


COPD – Assessing Severity

• General Treatments– stop smoking– encourage exercise– treat poor nutrition or obesity– influenza and pneumococcal vaccinations


COPD – Treatment

Initial Treatment

Antimuscarinic (e.g. Ipratropium) or β2 agonist (e.g. Salbutamol) inhaled PRN


COPD - Treatment


COPD - Treatment

Severe Disease

LABA + Inhaled Steroid + Anticholinergic

+ Refer to specialist

+ Consider steroid trial


COPD - Treatment

Long Term Oxygen Therapy

Consider LTOT if PaO2 <7.3kPa


COPD - Treatment


COPD – Acute Management

• Also known as diffuse parenchymal lung disorders

• Collection of disorders affecting – Alveoli– Alveolar epithelium– Capillary endothelium– And the spaces in-between


Pulmonary Fibrosis – (interstitial lung disease)


Acute and Chronic


ACEPT A - Ankylosing spondylitisC – CancerE – Extrinsic allergic alveolitisP – PneumoconiosisT - TB


SARCOIDOSIS

• Multisystem granulomatous disorder• Affects age 30-40• Pulmonary infiltration• Often no symptoms• If persists over 6 months treat with prednisolone


123

1 – primary pulmonary fibrosis2 – secondary pulmonary fibrosis

3 - asbestosis


DiffuseChemotherapy

DrugsRadiation

And progression of disease

• Scarred lungs • Breathlessness• Dry cough• Fatigue• Clubbing

• RESTRICTIVE


Clinical Picture

• Remove offending agent• Suppress inflammation (glucocorticosteroids)• Manage hypoxemia


Treatment depends on cause

Practice Questions

phase 2 kirsty mclauchlan and vicky cox

Documents

misleading informationasthma15

adrenoreceptor blockers

mucusdeposition of collagen

kirsty mclauchlan

asthmatic response

g propranolol

ciliagoblet cells

developed counties