Home > Documents > Obstructive Pulmonary Diseases

Obstructive Pulmonary Diseases

Date post: 19-Jan-2016
Author: zaza
View: 71 times
Download: 2 times
Share this document with a friend
Obstructive Pulmonary Diseases. Obstructive Pulmonary Diseases. Chronic Obstructive Pulmonary Diseases. COPD is defined as a disease state characterized by the presence of airflow obstruction due to Chronic bronchitis Bronchiectasis Emphysema A sthma - PowerPoint PPT Presentation
Embed Size (px)
Popular Tags:
of 51 /51
Obstructive Obstructive Pulmonary Diseases Pulmonary Diseases
  • Obstructive Pulmonary Diseases

  • Obstructive Pulmonary Diseases

    1. Localised (Mechanical Obstruction) - AcuteTumor Trauma Foreign body2. Diffuse - Distal airway disease (COPD) - ChronicChronic bronchitisBronchiectasisEmphysema Asthma

  • Chronic Obstructive Pulmonary Diseases

  • COPD is defined as a disease state characterized by the presence of airflow obstruction due to Chronic bronchitisBronchiectasisEmphysemaAsthma The airflow obstruction generally is progressive, may be accompanied by airway hyperreactivity, and may be partially reversible.

  • The term chronic obstructive pulmonary disease (COPD) refers to a group of conditions;They are accompanied by chronic or recurrent obstruction to air flow within the lung,They share a major symptom: dyspnea.

  • PathophysiologyPathological changes in COPD occur in: the large (central) airways, the small (peripheral) bronchioles,the lung parenchyma.

    The increased number of activated polymorphonuclear leukocytes and macrophages release elastases lung destructionIncreased oxidative stress free radicals (released by phagocytes, and polymorphonuclear leukocytes) apoptosis or necrosis of exposed cells

  • Factors in COPDSmoking Air pollution and COPDOther factorsAirway hyperresponsivenessAlpha1-antitrypsin (a 1-AT) deficiency

  • SMOKINGThe primary cause of COPD is exposure to tobacco smoke. Chronic bronchitis is primarily a disease of cigarette smokers: 90% of cases occur in smokers. Chronic bronchitis occurs in less than 5% of nonsmokers, 10% to 15% of moderate smokers, and more than 25% of heavy smokers.

  • SmokeThe primary cause of COPDClinically significant COPDchronic bronchitisemphysemaAlmost 4000 chemicals, 43 carcinogens

    Neoplastic and Non-neoplastic diseases

  • Neoplastic diseases (cancers): Lung Bladder Stomach Pancreas Oral cavityLarynx Cervix

    Non-neoplastic diseases: Lung diseasesGastritisAtherosclerosis Ischemic heart diseaseHypertension Brgers disease

  • Pathophysiology of COPD in smokersSmokers have greater numbers of neutrophils and macrophages in their alveoliSmoking Stimulates release of elastase from neutrophilsEnhances elastolytic protease(s) activity in macrophagesInhibition of antielastase activityoxidants in cigarette smoke oxygen free radicals secreted by neutrophils inhibit a1-AT.

  • AIR POLLUTIONThe use of solid fuels for cooking and heating may result in high levels of indoor air pollution and the development of COPDsulfur dioxidenitrogen dioxide

  • OTHER FACTORS IN COPDAirway hyperresponsivenessSmokers with airway hyperresponsiveness are at increased risk of developing COPD with an accelerated decline in lung function a1-antitrypsin deficiencya1-antitrypsin deficiency is the only known genetic risk factor for developing COPD (panacinar emphysema) and accounts for less than 1% of all cases (a1-antitrypsin is a protease inhibitor produced by the liver that acts predominantly by inhibiting neutrophil elastase in the lungs)

  • Chronic BronchitisBronchiectasisEmphysemaAsthma

  • Chronic bronchitis is four to ten times more common in heavy smokers irrespective of age, sex, and occupation.When persistent for years, it may (1) lead to cor pulmonale and heart failure, (2) cause atypical metaplasia and dysplasia of the respiratory epithelium (cancerous transformation). Chronic Bronchitis

  • Productive coughAcute & Chronic inflammation of mucosaSecondary Pulmonary Infections (Haemophilus influenzae and Streptococcus pneumoniae)Inflammation retention infection obstructioninflammation....... (circulus viciosus).Acute respiratory failure in patients with advanced chronic bronchitis Clinical observations: Chronic bronchitis

  • Pathology: Chronic bronchitisMucous gland enlargement is the histologic hallmark of chronic bronchitisIncreased ratio of mucous cells to serous ones Excess mucus in airwaysIncrease in the number of goblet cells (hyperplasia)Lack of ciliaThickening of the bronchial wall Mucous gland enlargement and edema (which leads to encroachment on the bronchial lumen)Increased smooth muscle (which may indicate bronchial hyperreactivity)Squamous metaplasia of the bronchial epithelium (epithelial damage from tobacco smoke)

  • HistologyEarliest features of chronic bronchitis are hypersecretion of mucus in the large airways, hypertrophy of the submucosal glands in the trachea and bronchi. As chronic bronchitis persists, marked increase in goblet cells of small airways (small bronchi and bronchioles)excessive mucus production that contributes to airway obstruction.

  • Chronic Bronchitis: Histology

  • BronchiectasisBronchiectasis is a chronic necrotizing infection of the bronchi and bronchioles leading to or associated with abnormal dilation of these airways. It is manifested clinically by cough, fever, the expectoration of copious amounts of foul-smelling, purulent sputum. To be considered bronchiectasis, the dilation should be permanent;reversible bronchial dilation often accompanies viral and bacterial pneumonia

  • Etiology: Bronchial obstructionLocalized (to the obstructed lung segment): tumor foreign bodies mucous impaction Diffuse (obstructive airway diseases):asthmachronic bronchitis

  • Pathogenesis

    Smoking irritation of mucosaMucus hypersecretion Obstruction, CoughAtelectasisMetaplasia loss of ciliated epitheliumRetention of secretionSecondary infectionRecurrent Inflammation and FibrosisDestruction of bronchial wallDilated bronchus filled with pus

  • The dilatation ("-ectasis") results from recurrent inflammations, and contraction of scar surrounding the bronchus.

  • Gross PathologyGeneralized bronchiectasis is usually bilateral and is most common in the lower lobes The left more commonly involved than the rightBronchi are dilated and have white or yellow thickened walls Bronchial lumens frequently contain thick, mucopurulent secretions

  • Gross PathologyOn gross examination, bronchial dilation is saccular, cylindrical or varicose (they may produce cystic pattern):Saccular bronchiectasis: bronchi are severely dilated and end blindly in dilated sacs, with collapse and fibrosis of the distal lung parenchyma.Cylindrical bronchiectasis shows uniform, moderate dilation. It is a milder disease than saccular bronchiectasis and leads to fewer clinical symptoms.Varicose bronchiectasis: bronchi resemble varicose veins when visualized by radiologic bronchography, with irregular dilations and constrictions. Bronchiolar obliteration is not as severe, and parenchymal abnormalities are variable.

  • Bronchiectasis

  • Bronchiectasis

  • Pleural adhesions

  • MicroscopySevere inflammation of bronchi and bronchiolesDestruction of all components of the bronchial wallCollapse of distal lung parenchyma, the damaged bronchi dilateHypersecretion of mucus Abnormalities of the surface epitheliumsquamous metaplasiaincreased goblet cellsLymphoid follicles are often seen in the bronchial wallsScarred and often obliterated bronchi and bronchioles (distal ones)The bronchial arteries increase in size to supply the inflamed bronchial wall and fibrous tissue

  • In the full-blown, active case: Intense acute and chronic inflammatory exudation within the walls of the bronchi and bronchioles, A vicious circlepool of mucus is liable to further infection, which leads to progressive destruction of the bronchial walls more mucus new infection .......Desquamation of the lining epithelium and extensive areas of ulceration (necrosis), Pseudostratification of the columnar cells or squamous metaplasia of the remaining epithelium, Necrosis (destroys the bronchial or bronchiolar walls and forms a lung abscess),

    In chronic cases: Fibrosis of the bronchial and bronchiolar walls.

  • Bronchiectasisintense acute and chronic inflammatory exudationdesquamation of the lining epithelium

  • BronchiectasisNecrosis (destroys the bronchial or bronchiolar walls and forms a lung abscess).

  • Complications

    amyloidosismeningitisbrain abscessescor pulmonalepneumoniaempyemasepticemia

  • Emphysema Emphysema is a chronic lung disease characterized by enlargement of airspaces distal to the terminal bronchioles, with destruction of their walls but without fibrosis. Loss of elasticity of the lung with some destruction of the alveoli. Emphysema is a condition of the lung characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls, and without obvious fibrosis.Emphysema causes obstruction to air flow.

  • Classification of Emphysema

    (1) Centrilobular (centriacinar)(2) Panacinar (panlobular)(3) Localised (paraseptal)(4) SenileOf these, the first two are the most important clinically

  • 1. Centrilobular emphysema Most frequentUsually associated with cigarette smoking (often in association with chronic bronchitis)Destruction of the cluster of terminal bronchioles near the end of the bronchiolar tree in the central part of the pulmonary lobule Dilated respiratory bronchioles form enlarged airspaces that are separated from each other and from the lobular septa by normal alveolar ducts and alveoliDistal structures also may be involved Bronchioles proximal to the emphysematous spaces are inflamed and narrowed Centrilobular emphysema is most severe in the upper zones of the lung, the upper lobe, and the superior segment of the lower lobe

  • The walls of the emphysematous spaces often contain large amounts of black pigment. Inflammation around bronchi and bronchioles and in the septa is common. Focal dust emphysema, a disease of coal miners, resembles centrilobular emphysema but differs in that the enlarged spaces are smaller and more regular and inflammation of the bronchioles is not apparent.

  • Smokers lung Normal Lung

  • Smokers lung Emphysema

  • Centrilobular Emphysema

  • Severe Centrilobular Emphysema

  • Microscopy

  • 2. Panacinar (Panlobular) Emphysema The acinus is uniformly involved, with destruction of the alveolar septa from the center to the periphery of the acinus (entire alveolus distal to the terminal bronchiole) In the final stage, panacinar emphysema leaves behind a lacy network of supporting tissue (cotton-candy lung)This variant occurs in several situations

  • Diffuse panacinar emphysema is typically associated with a 1-AT deficiency [a congenital disease caused by a1-protease inhibitor ("antitrypsin") deficiency]It is also often found in cigarette smokers in association with centrilobular emphysema In such cases, the panacinar pattern tends to occur in the lower zones of the lung, whereas centrilobular emphysema is seen in the upper regions

  • Grossly, cut surface of the lung shows diffuse enlargement of airspaces in the affected parenchyma. Often the enlarged spaces are traversed by delicate, spider-web-like strands representing the residual alveolar walls. As in centrilobular emphysema, fibrosis is not seen.

  • Panacinar (Panlobular) Emphysema

  • 3. Localised (Paraseptal) Emphysema Characterized by destruction of alveoli and resulting emphysema in only one or at most a few locationsThe remainder of the lungs is normalThe lesion is usually found at the apex of an upper lobe, although it may occur anywhere in the pulmonary parenchyma, such as in a subpleural location. Progression of localized emphysema can result in a large area of destruction, termed a bulla, which ranges in size from as small as 2 cm to a large lesion (Bullous Emphysema).Although it is of no clinical significance itself, rupture of an area of localized emphysema produces spontaneous pneumothorax (sudden death).

  • Bullous Emphysema

  • Bullous Emphysema

  • 4. Senile emphysema

    This form of emphysema is usually associated with "old ageIt may occur anywhere in the pulmonary parenchyma

  • PathophysiologyTOBACCO: The major cause of emphysemaEmphysema results when elastolytic activity increases or antielastolytic activity is reduced.Increased numbers of neutrophils, which contain serine elastase and other proteases, are found in the bronchoalveolar lavage fluid of smokers. Smoking also interferes with alpha1-antitrypsin (a1-AT) activity.a1-AT DEFICIENCY: A hereditary deficiency a1-AT: a circulating glycoprotein produced in the liverMajor inhibitor of a variety of proteases, including elastase, trypsin, chymotrypsin, thrombin, and bacterial proteasesIts most important action to inhibit neutrophil elastase, an enzyme that digests elastin and other structural components of the alveolar septa