Transcript Clinical Pathology of Respiratory Diseases

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
Judith Coombes UQ and PAH
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
Trachea
Trachea
Bronchus(L&R)
Bronchi
Bronchiole
Alveoli
Respiratory Symptoms
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cough
sputum production/haemoptysis
dyspnoea
wheezing
chest/lung pain
Measurement of
ventilatory function
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Spirometry
PEFR
Blood Gas
Exercise test-6 min
chest Xray- normal is asthma and COPD
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
Normal
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
Chest X ray
• Diagnosis is uncertain (PE, pneumonia,
heart failure)
• symptoms may not be explained by
asthma or COPD
• physical evidence of complicationspneumothorax, atelectasis (lung collapse)
• failure to respond to treatment
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
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Measure oxygen saturation
Non invasive
Light emiting diodes
Expressed as % where normal is 100%
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)
• Smooth muscle hypertrophy and
hyperplasia
• Inflammatory cell infiltration
• Oedema
• Goblet cell and mucous gland hyperplasia
• Mucus hypersecretion
• Protein deposition
• Epithelial desquamation
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
• 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
• 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
Assessment of severity
• Severe acute attack <50% predicted or < 1litre
• Back titration of medication
• Check symptomatic assessment
• Maintain best lung function
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
National Asthma Council in Australia
– www.nationalasthma.org.au/cms/index.php
– Reduce mortality &morbidity of asthma
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Education
Patient self monitoring
Appropriate drug therapy
Regular medical review
Written asthma action plan
Asthma management
• Acute asthma management
– Treatment depends on severity
• Mild, moderate, life threatening
• Requires emergency care
• Hospital admission
• Long term asthma management-chronic
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Minimise symptoms and need for reliever
No exacerbations
No limitation on physical activity
Normal Lung Function
Asthma Management
• Medications to treat bronchospasm
– ACUTE
– RELEIVERS
• Short acting ß2-adrenergic agonists eg salbutamol
terbutaline
• Anticholinergic eg ipratropium
Relievers
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 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
Beclomethasone dipropionate
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
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.
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
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
COPD = shaded bit
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
Show ceases smoking figure
Progression
Severity
Symptoms
Treatment
Mild
FEV1<80
Smokers cough
Little breathlessness
Not known to GP
Moderate
FEV1<60
Breathlessness on
moderate exertion,
hypoxaemic, sputum,
known to GP
Breathlessness on any
exertion, some
hypercapnic, known to
hospital
Cease smoking,
Antibiotics,
Occasional
bronchodilator
Bronchodilators, trial of
steroids
Severe
FEV1<50
Flu vaccine, pulmonary
rehabilitation, assess
for LTOT
COPD Management
– Acute exacerbations
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Bronchodilators
Oxygen
Corticosteroids
Antibiotics
– Long term treatment- chronic
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Stop smoking
Bronchodilators
Corticosteroids
Immunisation-Pneumonia and flu
Pulmonary rehabilitation
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
• dysfunction of exocrine glands -abnormal
mucus production
– recurrent bronchopulmonary infection
– finger clubbing
– haemoptysis
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
Restrictive
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