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Clinical Management Respiratory Diseases. Judith Coombes University of Queensland Brisbane, Australia. Pathology. major international cause of morbidity and mortality In Australia single biggest cause of days lost from work generate largest number of GP visits. Objectives.

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clinical management respiratory diseases

Clinical Management Respiratory Diseases

Judith Coombes

University of Queensland

Brisbane, Australia

pathology
Pathology

major international cause of morbidity and mortality

In Australia single biggest cause of days lost from work

generate largest number of GP visits

Judith Coombes UQ and PAH

objectives
Objectives

Be able to interpret Spirometry as a lung function test and monitoring tool

Be able to interpret Peake Expiratory Flow rate (PEFR) as a monitoring tool

Understand goals of treatment and be able to communicate pharmaceutical care plan in asthma

Understand goals of treatment of and be able to communicate pharmaceutical care plan in COPD

Not discussing infections, neoplasms or TB

the lungs
The Lungs

Trachea

Bronchus(L&R)

Bronchi

Bronchiole

Alveoli

Trachea

respiratory symptoms
Respiratory Symptoms

cough

sputum production/haemoptysis

dyspnoea

wheezing

chest/lung pain

measurement of ventilatory function
Measurement of ventilatory function

Spirometry

PEFR

Blood Gas

Exercise test-6 min

chest Xray- normal is asthma and COPD

spirometry
Spirometry

Spirometer

FVC = Forced Vital Capacity

FEV1= Forced Expiratory Volume over 1 second

FEV1/FVC is forced expiratory ratio

should be >75%

useful for diagnosis

accurately measures degree of impairment

slide10
PEFR

Peak Flow Meter

maximum flow rate which can be forced during an expiration

may differ between meters

Submaximal effort invalidates reading

Not a substitute for spirometry

most useful for regular monitoring to detect variation

warning signs

sustained reduction

>20-25% diurnal variation

monitoring

chest x ray
Chest X ray

Diagnosis is uncertain (PE, pneumonia, heart failure)

symptoms may not be explained by asthma or COPD

physical evidence of complications-pneumothorax, atelectasis (lung collapse)

failure to respond to treatment

blood gas arterial
Blood Gas (arterial)

H+ rises with Pco2

In acute hypoventilation CO2 rises and so does H+ causing respiratory acidosis

In acute hyperventilation CO2 drops as does H+ causing respiratory alkalosis

(in acute no time for metabolic process so bicarbonate is not changed)

oximetry
Oximetry

Measure oxygen saturation

Non invasive

Light emiting diodes

Expressed as % where normal is 100%

asthma
Asthma

a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils and epithelial cells. In susceptible individuals this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly, at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli. USA97

airflow obstruction excessive airway narrowing
Airflow obstruction (Excessive airway Narrowing)

Smooth muscle hypertrophy and hyperplasia

Inflammatory cell infiltration

Oedema

Goblet cell and mucous gland hyperplasia

Mucus hypersecretion

Protein deposition

Epithelial desquamation

asthma diagnosis 1
Asthma Diagnosis-1

No Gold Standard

Consensus of respiratory physicians

History, physical examination, supportive diagnostic testing

History

Wheeze

Chest tightness

Shortness of breath

cough

asthma diagnosis 2
Asthma Diagnosis-2
  • Physical examination
    • Expiratory wheeze suggests asthma (not pathonomonic)
    • Absence of physical signs doesn’t exclude asthma
    • Crackles indicate concurrent or alternate diagnosis
asthma diagnosis 3
Asthma diagnosis -3
  • Diagnostic testing –Spirometry
  • Pay Attention to technique
    • Pre and post bronchodilator
    • Baseline FEV1>1.7L and increase of 12% post bronchodilator is significant
    • Or 200ml greater than baseline
    • Or same rules for FVC
      • Also % predicted from tables in the Asthma guidelines
spirometry for asthma management
Spirometry for asthma management

Assessment of severity

Severe acute attack <50% predicted or < 1litre

Back titration of medication

Check symptomatic assessment

Maintain best lung function

pefr with asthma
PEFR with asthma

Diagnosis-not a substitute for spirometry

PEF increases >15% with bronchodilator

PEF in adult varies >20% for 3 days in a week over several weeks

Severe Acute

<50% predicted or < 100 L/min

Useful for daily home measurement

Useful in action plan

>80% OK, 60-80% increase preventer, 40-60% oral steroids, <40% no relief 000

asthma treatment
Asthma treatment

National Asthma Council in Australia

  • www.nationalasthma.org.au/cms/index.php
  • Reduce mortality &morbidity of asthma
    • Education
    • Patient self monitoring
    • Appropriate drug therapy
    • Regular medical review
    • Written asthma action plan
asthma management
Asthma management
  • Acute asthma management
    • Treatment depends on severity
      • Mild, moderate, life threatening
      • Requires emergency care
      • Hospital admission
  • Long term asthma management-chronic
      • Minimise symptoms and need for reliever
      • No exacerbations
      • No limitation on physical activity
      • Normal Lung Function
asthma management1
Asthma Management
  • Medications to treat bronchospasm
    • ACUTE
    • RELEIVERS
      • Short acting ß2-adrenergic agonists eg salbutamol

terbutaline

      • Anticholinergic eg ipratropium
asthma management2
Asthma Management
  • Medications to treat bronchospasm
    • Chronic
    • SYMPTOM CONTROLLER
      • Inhaled long acting ß2-adrenergic agonists eg salmeterol
      • Also use
        • Theophylline
        • Oral ß2-adrenergic agonists (salbutamol syrup)
asthma management3
Asthma Management
  • Medications to treat inflamation

PREVENTERS

Inhaled sodium cromoglycate

Inhaled nedocromil sodium

Inhaled cortocosteroids eg beclomethasone

Oral corticosteroids eg prednisolone

Leukotrienne receptor antagonists eg montelukast

asthma action plans
Asthma Action plans
  • Developed by doctor with patient
  • Added role for pharmacist to give advice to patient
  • Individualised Action for Deterioration in asthma
    • ↑ in frequency, severity of symptoms
    • ↑ use of bronchdilator
    • Drop in peak flow
slide30

Misuse of Home Nebulizers High Among Inner-City

Children with Asthma

October 25, 2006 (Salt Lake City)

A study of asthma-related deaths among inner-city children

and young adults shows that only about half use their home

nebulizers as prescribed and rarely have an asthma action

plan to manage disease exacerbations, or if they do have a

written plan in the home, they rarely use it.

The findings were presented here yesterday at CHEST 2006, the 72nd annual

meeting of the American College of Chest Physicians.

slide32
COPD

smoking is major cause but susceptibility is variable

directly related to exposure to tobacco smoke

pack years=cigarettes/day x years of smoking /20

relatively fixed airway obstruction with minimal reversibility from bronchodilators

slide33
COPD

Chronic bronchitis- productive cough for >3 months in 2 successive years

emphysema-abnormal permanent enlargement of air-spaces distal to terminal bronchioles caused by destruction of alveolar walls.

Most have a combination of both

Elderly with reversibility has all 3

diagnosis of copd
Diagnosis of COPD

symptoms

breathlessness doesn’t occur until obstruction is advanced (unless intercurrent infection)

physical examination

little until disease is severe-over inflated chest

chest x rays

over inflation, enlarged heart, bullae

spirometry

mild check FEV1/FVC<75%

moderate check FEV1 % of predicted

copd management
COPD Management
  • Acute exacerbations
      • Bronchodilators
      • Oxygen
      • Corticosteroids
      • Antibiotics
  • Long term treatment- chronic
      • Stop smoking
      • Bronchodilators
      • Corticosteroids
      • Immunisation-Pneumonia and flu
      • Pulmonary rehabilitation
bronchiectasis
Bronchiectasis

defined as dilation of the bronchi-

bronchial walls become inflamed, thickened and irreversibly damaged.

Mucociliary transport is impaired-bacterial infections

cough productive of sputum

cystic fibrosis
Cystic Fibrosis

dysfunction of exocrine glands -abnormal mucus production

recurrent bronchopulmonary infection

finger clubbing

haemoptysis

interstitial lung disease
Interstitial lung disease

heterogeneous group involving alveolar walls and peri alveolar tissue

insidious onset, chronic disease

inflammatory process probably initiated by an antigen

eventual interstitial fibrosis will cause a restrictive pattern

severe obstructive sleep apnoea
Severe Obstructive Sleep Apnoea

2% women , 4% men

Recurrent episodes of airway occlusion in sleep

Apnoea

Arousal

Daytime sleepiness

Increased CO2

Sleep lab

Weight loss, CPAP