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COPD
(chronic
bronchitis,emphysema,s
mall airway disease)
1
Definition of COPD
“A disease state characterized by
airflow limitation that is not
fully reversible..”
2
New Definition
• Chronic obstructive pulmonary disease (COPD) is
a preventable and treatable disease state
characterized by airflow limitation that is not fully
reversible.
• The airflow limitation is usually progressive and is
associated with an abnormal inflammatory
response of the lungs to noxious particles or
gases, primarily caused by cigarette smoking.
• COPD produces significant systemic
consequences.
3
Risk Factors for COPD
1.Host Factors Genes (e.g. alpha1antitrypsin
deficiency)
Hyperresponsiveness
Lung growth
2.Exposure
Tobacco smoke
Occupational dusts and chemicals
Infections
4
Pathogenesis of COPD
1.NOXIOUS AGENT (tobacco smoke, pollutants,
occupational agent)
2.Genetic factors
3.Respiratory infection,Other
5
Pathophysiology of COPD
• Increased mucus production and reduced
mucociliary clearance - cough and sputum production
• Loss of elastic recoil - airway collapse
• Increase smooth muscle tone
• Pulmonary hyperinflation
• Gas exchange abnormalities - hypoxemia
and/or hypercapnia
6
SYMPTOMS
cough
sputum
dyspnea
EXPOSURE TO RISK FACTORS
tobacco
occupational dusts
indoor/outdoor pollutannts
SPIROMETRY 7
Key Indicators for COPD Diagnosis
A.Chronic cough Present intermittently or every day
B.Chronic sputum production Present for many yea
C.Dyspnoea that is Progressive
D.Acute bronchitis Repeated episodes
E.History of exposure to risks
8
 Diagnosis
1.hx
2.spirometry
3.CXR
9
Spirometry in COPD
Normal FEV1 > 80% of predicted value
Predicted value varies with age, height and sex
Normal FEV1% > 70%
Consider spirometry in past and present smokers
over age 45, and patients with chronic
cough, dyspnea or wheezing
10
Classification of COPD
• Stage 0 = At Risk(Sx i.e cough…)
• Stage I= Mild COPD(FEV1>80%)
• Stage II= Moderate COPD(FEV1 50-80%)
• Stage III= Severe COPD(FEV1 30-50%)
• Stage IV =Very Severe COPD(FEV1<30%)
11
MX
Objectives of COPD Management
• Prevent Progression
• Relieve symptoms
• Improve exercise tolerance and general health
status
• Prevent and treat exacerbations and
complications
• Minimize treatment side effects
12
Management of COPD
Smoking cessation
Pulmonary rehabilitation(exercise..)
Pharmacologic(salbutamol,salmetrol…)
Supplemental oxygen
Surgical remedies
13
• Reducing exposure to tobacco smoke, occupational
dusts, and chemicals, and indoor and outdoor air
pollutants
• Smoking cessation is the single most
effective
14
• None of the existing medications for COPD affects
long-term decline in lung function that is the hallmark
of this disease
15
• The long-term O2 with chronic respiratory failure
increases survival
• Improves exercise tolerance
16
• All COPD patients benefit from exercise
training program
• Improves both exercise tolerance and
symptoms of dyspnea and fatigue
17
 What is the difference between asthma&COPD ?
18
COPD
• Onset in mid-life
• Symptoms slowly progressive
• Long smoking history
• Dyspnea during exercise
• Largely irreversible airflow limitation
19
Asthma
• Onset early in life (often childhood)
• Symptoms vary from day to day
• Symptoms at night/early morning
• Allergy, rhinitis, and/or eczema also present
• Family history of asthma
• Largely reversible airflow limitation
20
Interstitial Lung
Diseases
(Restrictive lung
disease)
21
Introduction
• ILDs represent a large and heterogeneous
group of lower respiratory tract disorders.
• >180 diseases are know to primarily involve the
interstitium.
• An acute phase may occur but onset is usually
insidious, leading to chronic progressive
disease.
22
The characteristic of clinical signs
including:
• Dyspnea after exercising
• chest X-ray shows diffuse abnormality of pulmonary
parenchymal, including nodules, linear(reticular)
infiltrates
• pulmonary function tests shows restrictive
hypoventilation reduced diffusing capacity
• tissue biopsy shows a variety pulmonary fibrosis
and
aveolar inflammation
23
Clinical Classification of ILD
• Etiological
Known
Unknown
• Disease onset
Acute
1.cryptogenic fibrosing alveolitis (CFA)
2.usual interstitial pneumonia (UIP)
Chronic
24
Chronic Interstitial Disease
• Idiopathic pulmonary fibrosis (IPF)
• Sarcoidosis
• Extrinsic allergic alveolitis (hypersensitivity
pneumonitis)
• Pneumoconiosis
• Connective tissue diseases
25
Pathogenesis
The pathogenesis of ILDs is unknown.
immune cells and their cytokines play an important
role in the course of ILDs.
26
Clinical manifestations
• Breathlessness, Progressive respiratory
insuffiency
• cough without sputum.
• Some patients may have fatigue, weight loss,
joint pain.
27
Physical examinations
• Bilateral basilar, crepitant velcro-like rale are found
in most patients
• wheezing, rhonchi
• tachypnea and tachycardia
• clubbing
• At last, pulmonary hypertention and cor-pulmonale
may be exist
28
Chest radiography
It is important method to diagnose the ILDs.
The majority of ILDs cause infiltrates in the
lower lung zones.
29
Pulmonary Function
• Pulmonary function tests of ILDs shows restrictive
hypoventilation.
•Spirometry reveals a restrictive pattern. FVC is
reduced, but FEV1/FVC supernormal.
• All lung volumes – TLC, FRC, RV – are reduced.
30
1.IDIOPATHIC PULMONARY FIBROSIS
• It is the prototype ILD
• IPF is an unknown chronic interstitial lung disease.
• clinically : non-productive cough and progressive
dyspnea on effort
• Radiology: reticulonodular/reticular veiling of lower
lung zones on XR chest
• Physiology: restrictive lung function
31
2.SARCOIDOSIS
Definition
Sarcoidosis is a disease of unknown cause and is
characterized by the presence of non-caseating
granulomas in one or more organ, system. It is
considered a systemic disease
Usually lungs and the lymph nodes in the
mediastinum and hilar regions are the most site of
involvement
The clinical course is quite variable asymptomatic
32
The cause of sarcoidosis is unknown.
But many researchers have suggested that
immune mechanisms are important in
disease pathogenesis.Genetic factor may
also play an important role.
33
The basic pathogenesis includes three
main stages:
 Pulmonary alveolus inflammation
 formation of non-caseating granulomas
 the stage of interstitial fibrosis
34
Clinical manifestations
The clinical course is variable
the respiratory system is the most commonly
affected(90% of patients)
sometime with or without extrathoracic disease
35
Clinical manifestations
Mainly no symptoms at the time of presentation
sometimes the disease is identified because of
abnormalities on a chest radiograph
some patients present with respiratory symptoms
such as dyspnea and cough
36
Specific signs and symptoms depend on the
particular organ system(s) involved
Respiratory system disease
Intrathoracic nodal involvement and parenchymal lung
disease are the most common ways in which sarcoidosis
affeccts the respiratory system
The pulmonary parenchyma demonstrates well
defined,non-caseating granulomas with the pulmonary
interstitium
Usually upper lobes of the lung tend to be more involved
37
Extrapulmonary sarcoidosis
Including:
skin disease: papules, plaques,nodules
eye disease and neurologic disease, liver and
spleen, peripheral lymph nodes, bone lesions
and myopathy
38
Experimental examinations and some specific
examinations
1.elevations in the level of angiotensinconverting
enzyme(ACE) The measurement of serum ACE might
be a useful diagnostic and prognostic test in
sarcoidosis
2.hypercalcemia:important complication of
sarcoidosis
3.BALF
39
LUNG CANCER
40
Lung Cancer: Defined
Uncontrolled growth of malignant cells in
one or both lungs and tracheo-bronchial
tree
A result of repeated carcinogenic irritation
causing increased rates of cell replication
Proliferation of abnormal cells leads to
hyperplasia, dysplasia or carcinoma in situ
41
Where Does it Come From?
Radiation Exposure
Smoking
Environmental/ Occupational
Exposure
Asbestos
Radon
Passive smoke
42
Smoking Facts
Tobacco use is the leading cause of lung cancer 87%
of lung cancers are related to smoking
Risk related to:
age of smoking onset
amount smoked (pack yrs)
gender
product smoked
depth of inhalation
43
Lung cancer is the most preventable form of cancer
Quitting tobacco use significantly reduces risk
of all cancers.
44
Symptoms
cough
dyspnea
hemoptysis
recurrent infections
chest pain
45
DX
 CXR
 HX
 Biopsy
Treatment=pallative
46
Wish you all the
best!
47

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5anesthesia 8 copd

  • 2. Definition of COPD “A disease state characterized by airflow limitation that is not fully reversible..” 2
  • 3. New Definition • Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. • The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking. • COPD produces significant systemic consequences. 3
  • 4. Risk Factors for COPD 1.Host Factors Genes (e.g. alpha1antitrypsin deficiency) Hyperresponsiveness Lung growth 2.Exposure Tobacco smoke Occupational dusts and chemicals Infections 4
  • 5. Pathogenesis of COPD 1.NOXIOUS AGENT (tobacco smoke, pollutants, occupational agent) 2.Genetic factors 3.Respiratory infection,Other 5
  • 6. Pathophysiology of COPD • Increased mucus production and reduced mucociliary clearance - cough and sputum production • Loss of elastic recoil - airway collapse • Increase smooth muscle tone • Pulmonary hyperinflation • Gas exchange abnormalities - hypoxemia and/or hypercapnia 6
  • 7. SYMPTOMS cough sputum dyspnea EXPOSURE TO RISK FACTORS tobacco occupational dusts indoor/outdoor pollutannts SPIROMETRY 7
  • 8. Key Indicators for COPD Diagnosis A.Chronic cough Present intermittently or every day B.Chronic sputum production Present for many yea C.Dyspnoea that is Progressive D.Acute bronchitis Repeated episodes E.History of exposure to risks 8
  • 10. Spirometry in COPD Normal FEV1 > 80% of predicted value Predicted value varies with age, height and sex Normal FEV1% > 70% Consider spirometry in past and present smokers over age 45, and patients with chronic cough, dyspnea or wheezing 10
  • 11. Classification of COPD • Stage 0 = At Risk(Sx i.e cough…) • Stage I= Mild COPD(FEV1>80%) • Stage II= Moderate COPD(FEV1 50-80%) • Stage III= Severe COPD(FEV1 30-50%) • Stage IV =Very Severe COPD(FEV1<30%) 11
  • 12. MX Objectives of COPD Management • Prevent Progression • Relieve symptoms • Improve exercise tolerance and general health status • Prevent and treat exacerbations and complications • Minimize treatment side effects 12
  • 13. Management of COPD Smoking cessation Pulmonary rehabilitation(exercise..) Pharmacologic(salbutamol,salmetrol…) Supplemental oxygen Surgical remedies 13
  • 14. • Reducing exposure to tobacco smoke, occupational dusts, and chemicals, and indoor and outdoor air pollutants • Smoking cessation is the single most effective 14
  • 15. • None of the existing medications for COPD affects long-term decline in lung function that is the hallmark of this disease 15
  • 16. • The long-term O2 with chronic respiratory failure increases survival • Improves exercise tolerance 16
  • 17. • All COPD patients benefit from exercise training program • Improves both exercise tolerance and symptoms of dyspnea and fatigue 17
  • 18.  What is the difference between asthma&COPD ? 18
  • 19. COPD • Onset in mid-life • Symptoms slowly progressive • Long smoking history • Dyspnea during exercise • Largely irreversible airflow limitation 19
  • 20. Asthma • Onset early in life (often childhood) • Symptoms vary from day to day • Symptoms at night/early morning • Allergy, rhinitis, and/or eczema also present • Family history of asthma • Largely reversible airflow limitation 20
  • 22. Introduction • ILDs represent a large and heterogeneous group of lower respiratory tract disorders. • >180 diseases are know to primarily involve the interstitium. • An acute phase may occur but onset is usually insidious, leading to chronic progressive disease. 22
  • 23. The characteristic of clinical signs including: • Dyspnea after exercising • chest X-ray shows diffuse abnormality of pulmonary parenchymal, including nodules, linear(reticular) infiltrates • pulmonary function tests shows restrictive hypoventilation reduced diffusing capacity • tissue biopsy shows a variety pulmonary fibrosis and aveolar inflammation 23
  • 24. Clinical Classification of ILD • Etiological Known Unknown • Disease onset Acute 1.cryptogenic fibrosing alveolitis (CFA) 2.usual interstitial pneumonia (UIP) Chronic 24
  • 25. Chronic Interstitial Disease • Idiopathic pulmonary fibrosis (IPF) • Sarcoidosis • Extrinsic allergic alveolitis (hypersensitivity pneumonitis) • Pneumoconiosis • Connective tissue diseases 25
  • 26. Pathogenesis The pathogenesis of ILDs is unknown. immune cells and their cytokines play an important role in the course of ILDs. 26
  • 27. Clinical manifestations • Breathlessness, Progressive respiratory insuffiency • cough without sputum. • Some patients may have fatigue, weight loss, joint pain. 27
  • 28. Physical examinations • Bilateral basilar, crepitant velcro-like rale are found in most patients • wheezing, rhonchi • tachypnea and tachycardia • clubbing • At last, pulmonary hypertention and cor-pulmonale may be exist 28
  • 29. Chest radiography It is important method to diagnose the ILDs. The majority of ILDs cause infiltrates in the lower lung zones. 29
  • 30. Pulmonary Function • Pulmonary function tests of ILDs shows restrictive hypoventilation. •Spirometry reveals a restrictive pattern. FVC is reduced, but FEV1/FVC supernormal. • All lung volumes – TLC, FRC, RV – are reduced. 30
  • 31. 1.IDIOPATHIC PULMONARY FIBROSIS • It is the prototype ILD • IPF is an unknown chronic interstitial lung disease. • clinically : non-productive cough and progressive dyspnea on effort • Radiology: reticulonodular/reticular veiling of lower lung zones on XR chest • Physiology: restrictive lung function 31
  • 32. 2.SARCOIDOSIS Definition Sarcoidosis is a disease of unknown cause and is characterized by the presence of non-caseating granulomas in one or more organ, system. It is considered a systemic disease Usually lungs and the lymph nodes in the mediastinum and hilar regions are the most site of involvement The clinical course is quite variable asymptomatic 32
  • 33. The cause of sarcoidosis is unknown. But many researchers have suggested that immune mechanisms are important in disease pathogenesis.Genetic factor may also play an important role. 33
  • 34. The basic pathogenesis includes three main stages:  Pulmonary alveolus inflammation  formation of non-caseating granulomas  the stage of interstitial fibrosis 34
  • 35. Clinical manifestations The clinical course is variable the respiratory system is the most commonly affected(90% of patients) sometime with or without extrathoracic disease 35
  • 36. Clinical manifestations Mainly no symptoms at the time of presentation sometimes the disease is identified because of abnormalities on a chest radiograph some patients present with respiratory symptoms such as dyspnea and cough 36
  • 37. Specific signs and symptoms depend on the particular organ system(s) involved Respiratory system disease Intrathoracic nodal involvement and parenchymal lung disease are the most common ways in which sarcoidosis affeccts the respiratory system The pulmonary parenchyma demonstrates well defined,non-caseating granulomas with the pulmonary interstitium Usually upper lobes of the lung tend to be more involved 37
  • 38. Extrapulmonary sarcoidosis Including: skin disease: papules, plaques,nodules eye disease and neurologic disease, liver and spleen, peripheral lymph nodes, bone lesions and myopathy 38
  • 39. Experimental examinations and some specific examinations 1.elevations in the level of angiotensinconverting enzyme(ACE) The measurement of serum ACE might be a useful diagnostic and prognostic test in sarcoidosis 2.hypercalcemia:important complication of sarcoidosis 3.BALF 39
  • 41. Lung Cancer: Defined Uncontrolled growth of malignant cells in one or both lungs and tracheo-bronchial tree A result of repeated carcinogenic irritation causing increased rates of cell replication Proliferation of abnormal cells leads to hyperplasia, dysplasia or carcinoma in situ 41
  • 42. Where Does it Come From? Radiation Exposure Smoking Environmental/ Occupational Exposure Asbestos Radon Passive smoke 42
  • 43. Smoking Facts Tobacco use is the leading cause of lung cancer 87% of lung cancers are related to smoking Risk related to: age of smoking onset amount smoked (pack yrs) gender product smoked depth of inhalation 43
  • 44. Lung cancer is the most preventable form of cancer Quitting tobacco use significantly reduces risk of all cancers. 44
  • 46. DX  CXR  HX  Biopsy Treatment=pallative 46
  • 47. Wish you all the best! 47