copd lecture

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RAHEEF ALATASSI Free syria

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Page 1: COPD  lecture

RAHEEF ALATASSIFree syria

Page 2: COPD  lecture

objectives chronic bronchitis :

definition causes path physiology morphology mechanism of obstruction management complication S/S Investigation

Emphysema: definition Causes path physiology morphology types management complication S/S Investigation

Pulmonary hypertension: Definition

Page 3: COPD  lecture

CHRONIC BRONCHITIS

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Definition

It is defined as a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years

forms features

Simple chronic bronchitis  the productive cough raises mucoid sputum, but airflow is not obstructed

Chronic asthmatic bronchitis  hyper-responsive airways with intermittent bronchospasm and wheezing

Chronic obstructive bronchitis develops chronic outflow obstructionAssociated with emphysema

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Causes

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Pathogenesis of Chronic Bronchitis

Pathogenesis of Chronic Bronchitis

Cigarette smoking or other air pollutants lead to:

1-Hypertrophy and hyper secretion of bronchial mucous glands

2-Metaplastic formation of goblet cells

3-Infiltration by CD+8 lymphocytes ,macrophages and neutrophils

mucous gland hyperplasia,

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morphology The trachea

in the mid-upper field is hyperemic

the bifurcation & bronchi contain mucopurulent exudate secretion.

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enlargement of the mucus-secreting glands

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management Stop smoking > inhaled

bronchodilator (anticholinergic agonist or b2 agonist) > combination > glucocorticosteroid > oxygen.

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Complications: Pulmonary hypertension and cardiac failure Recurrent infections Respiratory failure

S/S : cough , sputum ,frequent infections ,

intermittent dyspnea, wheeze. Some patients develop significant COPD with

outflow obstruction: hypercapnia, hypoxemia, cyanosis

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Investigation Spirometry

CXR > hyperinflation FBC > polycythemia ABG > hypoxemia or hypercapnia

Severity of COPD (GOLD scale)

FEV1 % predicted

Mild ≥80

Moderate 50–79

Severe 30–49

Very severe <30 or chronic respiratory failure symptoms

The severity of COPD also depends on the severity of dyspnea and exercise limitation. These and 

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Spirometry

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EMPHYSEMA

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definition

• It is permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of their walls.

• not associate with fibrosis

Causes:SmokingDeficinecy of a1 antitrypsin

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path physiology

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Pathogenesis of Emphysema

Emphysema arises as a consequence of two imbalances:Protease-antiprotease imbalanceOxidant-antioxidant imbalance * INCRESE elastase

The destructive effect of protease in subjects with low antiprotease activity leads to emphysema

Free radical → deplete the lung antioxidant mechanisms → tissue damage

Protease releasefree radical

Tobacco smoke

free radical

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morphology

The external surfaces of the upper lobes of both the right and left lungs have large bullae.

Distal type. bullaeCyst more than 1 cm.

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the permanent enlargement of the airspace, accompanied by destruction of the septa

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typestype features

Centriacinar It involve the central or proximal parts of the aciniThe lesions are more common and severe in the upper lobesThis type is seen as a result of cigarette smoking

Panacinar It occurs more commonly in the lower lung zonesThe type of emphysema occurs in α1-antitrypsin deficiency

Distal Acinar The distal part of the acinus is involved It is seen adjacent to the pleura, along the lobular

margins,scarring. Cystlike structures can be formed (bullae)

Irregular The acinus is irregularly involvedIt is associated with scarringClinically asymptomaticThe most common form of emphysema

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Management & Investigation

The same treatment & Investigation as the chronic bronchitis

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Chronic hypoxia

Pulmonary vasoconstriction

Muscularizati

on

Intimal hyperplasia

Fibrosis

Obliteration

Pulmonary hypertension

Cor pulmonale

Death

Edema

Pulmonary Hypertension in COPD

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complication

I. Pulmonary hypertension;hypoxia-induced pulmonary vascular spasm loss of capillary surface area due to alveolar wall

destructionII. Right side heart failureIII. Respiratory failure

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S/S Patients present with dyspnea, and

abnormal pulmonary function tests

Patients with underlying chronic bronchitis

They have less dyspnea and retain more CO2

They are always hypoxic and cyanotic (blue bloaters)

Patients with no bronchitis They have more severe dyspnea and hyperventilation

They have normal gas exchange and adequate oxygenation of hemoglobin (pink puffers)

Page 25: COPD  lecture

Pulmonary hypertension:

The pulmonary circulation is normally one of low resistance, with pulmonary blood pressures being only about one-eighth of systemic pressure. Pulmonary hypertension (when mean pulmonary pressures reach one-fourth or more of systemic levels) is most often secondary to a decrease in the cross-sectional area of the pulmonary vascular bed, or to increased pulmonary vascular blood flow

Page 26: COPD  lecture

morphology

 A, Gross photograph of atheroma formation, a finding usually limited to large vessels.

 B, Marked medial hypertrophy. 

C, Plexogenic lesion characteristic of advanced pulmonary hypertension seen in small arteries.