You are on page 1of 8

PATHOLOGY Respiratory system

Tuberculosis is one of the leading cause of death. The WHO currently estimates that 6% of all deaths is occurred due to TB. Definition: Tuberculosis is an infectious disease caused by M.Tuberculosis, usually involves the lungs, but it also occurs in the larynx, kidneys, bones, adrenal glands, lymph nodes, and meninges and can be disseminated throughout the body. Low immunity M.Tuberculi enter Some are phagocytized by macrophages Many of bacilli may survive within blood cells and reach hilar lymph node Necrotic degeneration occur at the site of infection Form cavities filled with a cheese like mass of tubercle bacilli, dead WBC& necrotic lung tissue. Material liquefies, drain into tracheobronchial tree. Form scars and then calcified lesion (ghon tubercles)

Most primary tubercles heal over a period of months by forming scare and then calcified lesions, also known as GHON TUBERCLES. It contains living bacilli that can be reactivated, even after many years, and cause secondary infection.
Secondary Infection

Primary site of infection containing TB bacilli may remain latent for years and then may be reactivated if the clients resistance is lowered. Most of the secondary infections are due to reactivation of dormant bacilli in the primary lesions. Occasionally, it is caused by re-infection with exogenous tubercle bacilli. Secondary tuberculosis is generally found in the apices of the lungs, where oxygen tension is high and M. tuberculosis grows in high oxygen. Chronic Bronchitis
Inflammation of the bronchi (chronic obstructive bronchitis) causes increased mucous production and chronic cough. Definition Acute Bronchitis: Acute bronchitis is an inflammation of the bronchi in the lower respiratory tract usually due to infection.

Chronic Bronchitis: Chronic bronchitis, a disease of the airway, is defined as the presence of cough and sputum production for at least 3 months in each of two consecutive years in a patient in whom other causes of chronic cough have been excluded. Damaged surface ciliated epithelium. This is followed by their differentiation to mucussecreting goblet cells. In severe cases, there is hyperplasia and hypertrophy of the mucussecreting cells. As a result, both the individual acini and the glands become larger. The increase in size has been measured in a number of ways, but the usual measure is the Reid index. Reid index is the ratio of gland to wall. The bronchial wall is thickened, mainly by mucous glands enlargement, but also as a result of edema of the bronchi. Clusters of pigmented macrophages are present in the alveoli.

Infection Increased mucous production Bronchial wall become thickened and inflamed Airway obstruction, especially during expiration Airway collapse Air trapped in distal portion of the lung Decreased alveolar ventilation Abnormal V/Q ratio Hypoxemia. PLEURAL EFFUSION Pleural fluid normally seeps continually into the pleural space from the capillaries lining the parietal pleura and is reabsorbed by the visceral pleural capillaries and lymphatic system. Any condition that interferes with either secretion or drainage of this fluid leads to pleural effusion. Normally, only a small amount of fluid in the pleural cavity lubricates the space between the lung and the chest wall. This fluid is not more than 15 ml, serous, more or less acellular and clear. Pleural effusion is the accumulation of fluid in the pleural cavity and is named according to the appearance of the effusion. This is detected radiologically only, as obliteration of the costophrenic angle to a massive accumulation of fluid that shifts the mediastinum and the trachea to the opposite side.

PNEUMONIA Definition: Pneumonia is an acute inflammation of the lung parenchyma caused by a microbial agent. Pneumonia (pneumonitis) is an inflammatory process in lung parenchyma usually associated with a marked increase in interstitial and alveolar fluid. It is one of the most common cause of death in older adults. Among all nosocomial infections, pneumonia is the second most common but has the highest mortality. Aspiration of S.Pneumoniae Release of bacterial endotoxin Inflammatory response: Attraction of neutrophils Release of inflammatory mediators Accumulation of fibrinous exudates RBC and bacteria. Red hepatization and consolidation of lung parenchyma (neutrophils & macrophages) Leukocyte infiltration Gray hepatization & deposition of fibrin on pleural surface; phagocytosis in alveoli Resolution of infection Macrophages in alveoli ingest and remove degenerated neutrophils, fibrin & bacteria Pneumococcal pneumonia is the most common cause of bacterial pneumonia. There are 4 characteristic stages in the disease process: 1.CONGESTION:- After the pneumococcus organism reach the alveoli via droplets or saliva, there is an outpouring of fluid into the alveoli. The organisms multiply in the serous fluid, $ the infection is spread. The pneumococci damage the host by their overwhelming growth and interference with lung function. 2.RED HEPATIZATION:- There is massive dilation of the capillaries, and alveoli are filled with organisms, neutrophils, RBCs and fibrin. The lung appears red and granular, similar to the liver, which is why the process is called hepatization. 3.GRAY HEPATIZATION:- Blood flow decreases, and leukocytes and fibrin consolidate in the affected part of the lung. 4.RESOLUTION:- Complete resolution and healing occur if there are no complication. The exudates become lysed and is processed by the macrophages. The normal lung tissue is restored, and the persons gas-exchange ability returns to normal.

LUNG ABSCESS A lung abscess is a localized necrotic lesion of the lung parenchyma containing purulent material that collapses and form a cavity. Definition: Lung abscess is a collection of pus within lung tissue. Most lung abscesses are a complication of bacterial pneumonia or are caused by aspiration of oral anaerobes into the lung. The site of lung abscess is related to gravity and is determined by position. Commonly affected areas are, the posterior segment of an upper lobe and the superior segment of the lower lobe are the most common areas. Initially, the cavity in the lung may or may not extend directly into the bronchus. Eventually, the abscess becomes surrounded, or encapsulated, by a wall of fibrous tissue. The necrotic process may extend until it reaches the lumen of a bronchus or the pleural space and estimates communication with the respiratory tract, the pleural cavity, or the both. If the bronchus is involved, the purulent contents are expectorated continuously in the form of sputum. If the pleura is involved empyema results. Aspiration of an anaerobes in the lung Puss collection (abscess formation) Encapsulated by fibrous tissue, necrotic process Bronchus involvement Purulent contents are expectorated EMPHYSEMA Emphysema is a disorder in which the alveolar walls are destroyed. This destruction leads to permanent over distention of the air spaces. Air passes are obstructed as a result of these changes, rather than from mucus production, as in chronic bronchitis. Definition: It is defined pathologically as an increased beyond normal in size of the air spaces distal to the terminal bronchiole with destructive changes in their walls Structural changes in emphysema include: a) Hyperinflation of alveoli. b) Destruction of alveolar walls. c) Destruction of alveolar capillary walls. d) Narrowed, tortuous, small airways e) Loss of lung elasticity.

Alpha-1 Antitrypsin Deficiency(AAT) Collapse Of Bronchial Wall Inelastic Structure With Decreased Surface Area Blebs/Bullae Forms Increased Dead Space Increase Work Of Respiratory System Destruction Of The Pulmonary Capillaries Hypoxemia In a healthy person there is a balance between elastases and proteases and antiproteases in the lung. In smokers the numbers of neutrophils and macrophages are increased. Release of their elastases and proteases may overwhelm the normal antiprotease defense. In addition, smoking inactivates AAT. In AAT-related emphysema, AAT activity is greatly diminished and may be overwhelmed by normal protease activity. In emphysema, elastin and collagen, the supporting structures of the lung, are destroyed. As a result there is no pull or traction on the wall of the bronchioles. Like air being blown into a paper bag, air goes into the lungs easily but is unable to come out on its own and remains in the lung. Thus the bronchioles tend to collapse (especially on expiration) and air is trapped in the distal alveoli, resulting in hyperinflation and overdistention of the alveoli. This trapped air in the lungs gives the patient the typical barral-chested appearance. In emphysema the lungs can be inflated easily but can deflate only partially. As more alveoli are destroyed and alveoli coalesce, larger air spaces called bleb (in the visceral pleura) and bullae (in the lung parenchyma) may develop. Because of the loss of alveolar walls and the capillaries surrounding them, the amount of surface area that is available for diffusion of O2 in the blood decreases. The patient with emphysema compensates fot this problem by increasing the respiratory rate to increase alveolar ventilation.

BRONCHIECTASIS Definition: It is a chronic irreversible dilation of the bronchi or bronchioles. Chronic permanent dilation of one or more bronchi that will cause impairment in the drainage. This will leads to persistent infection. Impairment Of Bronchial Clearance Increased Bronchial Secretion Stasis Of Secretion Infection Further Weakening & Destruction Of Bronchial Wall Increased Bronchial Dilation Atelectasis Inflammatory Scaring Fibrosis Respiratory Insufficiency Ventilation & Perfusion Imbalance Hypoxemia There are 2 pathologic types of bornchiectasis: Saccular and Cylindric. Saccular bronchiectasis occurs mainly in large bronchi and is characterized by cavity-like dilations. The affected bronchi end in large sacs. Cylindric bronchiectasis involves medium-sized bronchi that are mildly to moderately dilated. It is mainly associated with bacterial infections. (Adenovirus, influenza virus, S.aureus, klebsiella and anaerobes). Infection causes the bronchial wall to weaken, and pockets of infection begin to form. When the walls of the bronchial system are injured, the mucocillary mechanism is damaged, allowing bacteria and mucus to accumulate within the pockets. The infection becomes worse and results in bronchiectasis. ASTHMA Definition: Asthma is a chronic inflammatory disease of the airways that causes airway hyper-responsiveness, mucosal edema, and mucous production

Triggers Infection, allergens Exercise, Irritants IgE-mast cell mediated response Release of mediators from mast cells, eosinophils, macrophages, lymphocytes Early phase Response Peaks in 30 to 60 Late phase response Peaks in 5 to 6 hr Infiltration with Eosinophils & neutrophils Inflammation Bronchial hyperreactivity Within 1 to 2 days Infiltration with monocytes $ lymphocytes

Bronchial smooth muscle Constriction Mucus secretion Vascular leakage Mucosal rdema

Obstruction of large and small airways Air trapping Respiratory acidosis Hypoxemia The hallmark of asthma are airway inflammation and nonspecific hypersensitivity or hyperresponsiveness of the tracheobronchial tree. It is due to physical, chemical, and pharmacologic agents. The early -phase of asthma is characterized by bronchospasm, which includes the inflammatory sequelae of the late response. The early-phase response is triggered when an allergen or irritant cross-links IgE receptors on mast cells found beneath the basement membrane of the bronchial wall. The mast cell become activated, with subsequent release of granules and disruption of the phospholipid cell membrane. Both processes result in the release of inflammatory mediators, including histamine, bradykinin, leukotrienes, prostaglandins, etc. They causes intense inflammation associated with the classic immediate reaction of asthma, which consists of bronchial smooth muscle constriction, increased vasodilation and permeability, and epithelial damage. This response peaks within 30 to 60 minutes of exposure to the trigger and subsides in another 30-90 minutes. Clkinically the patient has wheezing, chest tightness, dyspnea, and cough. The late-phase response in asthma peaks 5 to 6 hours after exposure and may last for several hours or days. It is characterized primarily by inflammation. Eosinophils and neutrophils infiltrate the airways. These cells can subsequently release mediators

that cause mast cell to release histamine and other mediators that eventually set up a self-sustaining cycle. In addition, lymphocytes and monocytes influx into the area. These events, which define the late-phase response, increase airway reactivity, which may worsen the symptoms of future asthma attacks. The prominent pathophysiologic features of asthma are a reduction in airway diameter and an increase in airway resistance related to mucosal inflammation, constriction of bronchial smooth muscle, and excess production of mucus. Accompanying these changes are bronchial smooth muscle hypertrophy, basement membrane thickening, mucus gland hypertrophy, thick and tenacious sputum, hyperinflation, and air trapping in the alveoli leading to an increased work of breathing. As a consequence of these events, alterations in respiratory muscle function, abnormal distribution of both ventilation and perfusion, and altered ABG occurs. CHRONIC OBSTRUCTIVE PULMONARY DISEASE Definition COPD refers to several disorders that affect the movement of air in and out of the lungs. Although the most important of these obstructive bronchitis, emphysema, and asthma. Tobacco smoke Air pollution Continual bronchial Irritation $ inflammation Chronic bronchitis Airway obstruction Air trapping Dyspnea,infections Abnormal ventilation perfusion ratio Hypoxemia; hypoventilation Cor-Pulmonale Alpha -1 antitrypsin deficiency Breakdown of elastin in connective tissue of lung Emphysema