COPD

1. Acute tracheobronchitis
• Etiology:
– Viruses
• Influenza A & B, para influenza
• Respiratory syncytial virus
• Adenovirus & Rhinovirus
• Acute & chronic bronchitis, dusts, chemical irritants
• Weakness
– Chronic sinusitis and Rhinitis

2. Pathology and Pathophysiology
• Congestion of mucus membrane, edema,
leukocytes cause sputum production
• Cilia, Phagocyte & Lymphocyte are disturbed
• Bactries attack normal bronchus and mucopurulent
exudate and necrotic cell collections
• Bronchospasm
– Dueto edema and mucus secreation

3. Clinical finding
• First day
• Retrosternal irritation
• Weakness and sweat
• Cough
– Dry and worse, later with sputum
• Fever 38.5-39.5c 3-5 days
• Dyspnea
– Airway obstruction
• Tachypnea

4. Physical exam
• Inspection, Palpation & Percussion are normal
• Auscultation:
– Ronchi
– Sometime crickles
– One side local finding (Bronchopneumonia)

5. Lab exam
• Inflammation stage:
– Leukocytosis 10000-12000
– ESR ↑
– Culture pneumoccoc & H. influenza
– Chest-X-Ray Normal

6. • 2-3 weeks
• If partially treated Bronchopneumonia
• Chronic obstructive pulmonary disease

7. Treatment
• Control of symptoms
– Cough, chest discomfort & fever
• If wheezing
– Bronchodilators
• Metoproterenol & Albuterol
– Culture, antibiogram & empirical antibiotic
is not indicated
– COPD is exceptional

8. Case study
‫مردی‬
55
‫سابقه‬ ‫که‬ ‫ساله‬
15
‫دارد‬ ‫کشیدن‬ ‫سگرت‬ ‫ساله‬
)
‫با‬
pack-year
‫به‬ ‫مساوی‬
22.5
)
‫شکایات‬ ‫با‬
‫سرفه‬
.
‫تقشع‬
‫و‬
‫جهدی‬ ‫تنفس‬ ‫عسرت‬
‫ب‬
‫ه‬
‫است‬ ‫نموده‬ ‫مراجعه‬ ‫عاجل‬ ‫شعبه‬
.
‫وی‬ ‫مریض‬ ‫گفتار‬ ‫طبق‬
‫ازمدت‬
5
‫سال‬
‫در‬ ‫معموال‬ ‫که‬ ‫میبرد‬ ‫رنج‬ ‫شده‬ ‫ذکر‬ ‫تنفسی‬ ‫شکایات‬ ‫از‬ ‫اینطرف‬ ‫به‬
‫م‬
‫وسم‬
‫سرما‬
‫میگردند‬ ‫تشدید‬ ‫اززکام‬ ‫بعد‬ ‫و‬
.
‫شده‬ ‫تشدید‬ ‫اینطرف‬ ‫به‬ ‫روز‬ ‫دو‬ ‫مدت‬ ‫از‬ ‫وی‬ ‫سرفه‬ ‫مریض‬ ‫حکایه‬ ‫قرار‬
.
‫مق‬
‫دار‬
‫است‬ ‫شده‬ ‫زرد‬ ‫ان‬ ‫رنگ‬ ‫و‬ ‫گردیده‬ ‫زیاد‬ ‫ان‬ ‫تقشع‬
.
‫ن‬ ‫وی‬ ‫تنفس‬ ‫عسرت‬
‫یز‬
‫است‬ ‫گردیده‬ ‫شدید‬
.

9. ‫ادامه‬
...
‫دارد‬ ‫وجود‬ ‫ذیل‬ ‫های‬ ‫یافته‬ ‫فزیکی‬ ‫معایه‬ ‫در‬
:
•
BP=125/80
•
Pulse rate =110b/min
•
Respiratory rate=30 cycle/min
•
Temperature=38.5 C
•
Cyanosis on lips
•
Diffuse ronchi throughout the lung field

10. ‫ادامه‬
...
‫معاینات‬ ‫در‬
:
•
‫اکسیجن‬ ‫اشباع‬ ‫درجه‬
=
%
85
•
‫هیموگلوبین‬
=
19 gr/dl
•
‫سفید‬ ‫کریوات‬ ‫تعداد‬
=
13500
•
‫صدری‬ ‫دراکسری‬
=
dierty lung

11. ‫ادامه‬
...
‫شماچیست‬ ‫احتمالی‬ ‫تشخیص‬
:
•
Chronic bronchitis
•
Bronchial asthma
•
Pneumonia
•
Pulmonary TB
•
Lung abscess

12. DRDDJJJ
‫الرحیم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
Dr.Nawshirwan Safi

13. COPD
• Definition:
• COPD = COLD
– Chronic bronchitis
– Emphysema
– Small airway disease
• 4th leading cause of death
• 10 million people in the USA

14. Types of COPD
• Type A COPD = emphysemia.
• Type B COPD = chronic bronchitis.
• Predominanat chronic bronchitis.
• Predominant emphysemia.

16. Chronic bronchitis
• Definition:
– Chronic inflammation of the bronchus
– 2 years, 3 months/a year cough & sputum
– types. Of chronic bronchitis.

17. • Age over 35 years, current or ex
smokers plus at least one of the
following:
1.Breathlessness
2.Cough
3.Sputum
4.Wheezing
5.Winter bronchitis

21. Risk factors:
– Cigarette smoking
– Airway reaction
– Respiratory system infection
– Occupation
– Air pollution
– Second hand smoking
– Genetic considerations

22. • Smoking :
 Decline of FEV1 proportional to smoking.
 Pack- year = packs of cigarette used in a day
multiply by years of smoking.
 Effects of smoking :
1.Hyperplasia of mucus glands.
2.Hypomotility of cillia.
3.Reduced alveolar macrophage activity.
4.Muscular spasm .

23. • Airways reaction :
 Character of asthma.
 Also seen in COPD.
 Dutch theory ( asthma , ch bronchitis ,
emphysemia are variant of the same
pathologic process).
 British theory ( COPD and asthma are
different , asthma is mainly allergic process,
COPD results from damage and
inflammation due to smoking)

24. • Air pollution ( indoor , outdoor).
• Passive smoking ( children exposure to
smoke of cigarette decreases lung maturity ,
smoking during pregnancy decreases lung
function of children after delivery).

25. Pathology:
– Mucus glands hypertrophy and hyperplasia
– Increased goblet cells
– Decreased ciliated cells (decrease mucus
clearance)
– Squamous metaplasia
• Carcinogenesis
• Mucuciliary clearance interrupt
• Goblet metaplasia
– Clara cell (surfactant producer) to mucus recreated cell

26. Cout…
• mucusal edema .
• Smooth muscle thickening.
• Bronchial fibrosis.
• These change cause airflow limitation.

31. Clinical finding
• Symptoms:
– Cough
– Sputum (mucoid , mucopurulent)
– Chest tightness(morning due to secretion
accumulation).
– Hand grip physical exercise decrease
– Dyspnea
• Bronchospasm & expectoration
– Headache & Fever
– Right side failure
• Lower limb edema

33. • Sign:
– Smokers
– Blue bloaters
• Cyanosis & edema
• Weight loss
– Temporal & loss of subcutaneous lipid
» ↓ nuitrition
» Increased TNF-α

35. • Inspection:
– Paradoxical inwards movements (Hoover's Sign)
• Palpation:
– Normal, suprasternal notch more than 3 fingers
• Percussion:
– If combined with emphysema hyper resonance
• Auscultation:
– Coarse crepitation & Ronchi, FET more than 6 seconds
• Corpulmonale

39. CHEST X-RAY
– Diaphragm is normal
– Broncho vascular marking increased
– Right failure
• Pul. Artery promenent
• Cardiomegaly

42. Pulmonary function tests
• FEV1 & vital capacity decreased
• Total Lung Capacity & Residual Volume &
• RV/TLC increased
• Hypoxemia & Hypercapnea
• FEV1/FVC less than 70%
• Reversibility test: done after salbutamol
inhalation or 2 weeks course of 30 mg
prednisolone per day. An increase of 400ml or
greater in FEV1 indicates reversible
bronchospasm( asthma)

43. • ABG: Pco2 increased, Po2 decreased,
chronic respiratory acidosis
• Pulse oximetry: decreased o2
saturation
• FBC: leukocytosis, increased HCT
• ECG
• Echocardiography
• Culture:
– H. influenza
– Streptococcal pneumonia
– Moraxella catarrhalis

44. • Diagnosis :
1.Prolonged (several years) history of cough
and sputum.
2.Cyanosis.
3.Coarse crepitation.
4.Radiographic findings.

45. • ECG:
– P-pulmonal
– RBBB & RVH
– Supraventricular arrhythmias
• Atrial fibrillation
• Atrial flutter
– Echocardiography:
• Evaluation of Pulmonary hypertension

55. • Dx:
– Productive cough, cyanosis, coarse
cerpitation & X-ray changes
– DDx:
• Pulmonary TB(BK+ , radiographic findings)
• Bronchiectasis (character of sputum)
• Bronchial Asthma
• Emphysema
• Cystic fibrosis
• Mechanical obstruction of central way

57. Complications
• Secondary polycythemia
• Spontaneous Pneumothorax
• Acute Tracheobronchitis & other infections
• Pulmonary Emboli
• Emphysema
• Respiratory failure
• Right side heart failure

61. Treatment
• Prophylactic treatment:
– Quit smoking
• Nicotine patch, Nicotine or Bupropion gams
– Occupation & air pollution
– Vaccination
• Influenza
• Pneumoccoc
– Curative treatment:
• Control of symptoms, rehabilitation of pul.
Function

62. Continue
– Outpatient:
• O2 therapy
– Resting hypoxemia
– hypoxemic
» Pul. HTN, CPC, Erythrocytosis, Exercise intolerance,
Impaired cognitive function, inconvenience night &
morning headache
• 1-3lit/min, 15hour/day
• CPC & PaO2<55mmHg continuse

63. • Mobilization of sputum:
– Postural drainage
– Chest percussion
– Expectorants not effective

64. • Bronchodilator:
– Symptoms decreased
– Increased physical activity tolerance
– Anti cholinergic
• Ipratropium bromide ,.tiotropium
– β2 agonists
• Albuterol & Metaproterenol , salmeterol..
– Theophyllin

66. • Corticosteroid
– Asthmatic bronchitis
– Recurrent exacerbation or sever symptoms
– Resistant to bronchodilators
– Prednisolone 30mg/day trial :
• Before and 2-4 weaks after steroid therapy
spirometric evaluation to determine steroid
responsive COPD( 15-20% increase in FEV1 after
prednisolone trial).

67. • Antibiotics
– Acute exacerbation
– Acute bronchitis
– Prophylaxis of exacerbation
– 7-10 days from the folllowing antibiotics:
1:, amoxicillin –clavulanic acid
2:macroloides( azithromycin…)
3: fluroquinolones (levofloxacin…)
4:doxycyclin 100mg BID.

68. • Others therapies : fluid , steam inhalation , no
role to expectorant . Avoide sedatives.

69. Hospitalized patient
– Indication for hospitalization:
• Not responsive with outpatient treatment
• Acute Respiratory failure
• CPC (Corpulmonal)
• Pneumothorax
• Exacerbation of COPD( worsening dyspenia
,increased sputum purulence and volume) when
here are one of the following:
1. Cyanosis
2. So2 less than 90%
3. Ph less than 7,35
4. Po2 less than 7 KP
5. Worsening oedema
6. Acute confusion

70. Mx of exacerbation
• Short acting bronchodilators
• Oral corticosteroides( prednisolone 30
mg per day for 5 days)
• Antibiotics
• Supplemental oxygen therapy
• IV aminophylline NOT contraindicated,
no response with nebulizers
• Doxapram( res stimulant) in NIV not
available
• NIV; for hypercapnic repiratory failure

71. Hospitalized patient
–CPC(measures to reduce pul
pressure):
• Salt restriction
• bed rest
• Diuretics
• treatment of acidemia and O2
therapy

72. Hospitalized patient
–Arrhythmias
• Multi focal atrial tachycardia( COPD
therapy or verapamil).
• atrial flutter.
–Respiratory failure
• Mechanical ventilation

73. Phlebotomy
• Secondary polycythemia
– Erythrocytosis
• HTC > 55%
• Headache &

74. Surgical treatment
• Lung transplantation:
– Sever lung disease
– Restriction of daily works
– Failure to medical treatment

75. Surgical treatment
– Critical illness
• Survival limitation without transplantation
– 2 year survival rate is 75%
– Complication after transplantation:
• Rejection
• opportunist infection
• Obliterative bronchiolitis

76. Prognosis
• Not good
• Survival rate
– 4 years (FEV1≤1L)

77. Emphysema
• Definition:
– Is characterized by destruction of alveolar
walls and permanent dilatation of gas-
exchanging air spaces(alveoli and terminal
bronchioles)

80. Pathology
• Distended ,large lung, decreased lung
retraction
• Pale, distended alveoli, thin alveolar
walls
• Destruction of alveoli causes bulla
• Bulla containing of:
– Fibrin, remmnant of alveolar walls &
atrophic vessels

83. Pathology
• Centro acinar emphysyma
– Distention and destruction in resp
Bronchiole & alveolar duct
– Less destruction in alveoli
– due to smoking
– Upper lob & upper segment of lower
lob

84. Pathology
• Pan acinus emphysema
– Distention and destruction in alveoli
– due to α1- antitrypsin deficiency
– Lower lob
• α1- antitrypsin is anti-elastase
• Elastase and anti-elastase
imbalance

86. Etiology
• Predisposing cause:(like chronic
bronchits)
– Old age , male prominent
– Air pollution, Smoking, occupation, genetic
and familial factors
– α1- antitrypsin
• 250mg/dl
• ZZ/SS homozygous = 0-50mg/dl

87. Etiology
• Stimulus cause:
– Obstructive disease of bronchioles‘
• Due to mucus aggregation & inflammation or allergy
– Bronchospasm
– Chronic bronchitis
– Pneumonia
– They cause easy air enterance but difficult air
exspulsion ( increased intra-alveolar pressure)
• Terminal bronchioles in ch bronchitis
– Valves structure easy air goes inside (inspiration) & difficult air
out (expiration), cause distention and destruction of alveolus

88. Clinical finding
• Symptoms:
– Dyspnea
• Exertional, rest
– Cough
– Sputum
• Mucoid, sometime mucoupurulent
– Due to hypoxia:
• Headache, weakness, anorexia

89. Sign (general)
• Cyanosis
• Pink puffers (
‫گالبی‬ ‫وجه‬
)
• Purse lip breathing
• Accessory respiratory muscle
– Scalen, Sternomastoid

90. Physical finding in chest
• Inspection: barrel chest , fullness of
supraclavicular fossa, chest movements
decreased, tracheal tug, PMI non-visible ‫و‬
, wide intercostal space , parallel ribs
• Palpation: Vocal fremitus & PMI is ↓
• Percussion: Hyper-resonance
• Auscultation:
– Respiratory and cardiac ↓
– Ronchi and fine crepitation

91. Lab exam
• Hematocrit Normal
• PaO2 65-75mmHg
• PCO2 35-40mmHg
• PFT MV, TLC & RV ↑ VC↓
• CT-scan Dx

92. Chest-X-Ray
• Hyperinflation of chest includes
the following
• Diaphragm is flate
• Wide intercostal space , parallel ribs
• Hypertranslucency
• bullae
• Due to decrease perfusion
– Absence of peripheral vascular
• Small and vertical heart

96. Dx
• History
• Sign and symptoms
• DDx:
– Bronchial asthma (episodes of
dyspenea and wheezing).
– Congestive heart failure
– Chronic bronchitis

98. Complications
• Spontaneous pneumothorax
– Open
– Close
– Valvular
• Acute infection
• Corpulmonal

99. Treatment
• Curative:
– Walking
– No treatment for alveolar restoration
– O2 therapy(PO2 is 40mmHg , no CO2
retention).
– Sputum mobilization
– Treatment for bronchospsam( inhaleres ,
theophylin)
– antibiotics
– Right Heart failure
– Same of chronic bronchitis
– α – 1 antitrypsin 60mg/kg/weak

100. Surgical treatment
• Lung Volume reduction surgery
– Dyspnea & recovery of physical exercise
– 20-30% both side of lung volume
– Mortality 4-10%
• Bullectomy
– Bulla resection
– Co2 Laser
• Thoracoscopy

101. Prognosis
• Progressive disease
– Due to disturbance of:
• PO2, PCO2 & PFT
– Poor prognosis