introduction disease of the respiratory system are some of the leading causes of mortality and...

Introduction Disease of the respiratory system are some of the leading causes of mortality and morbidity in animal and a major source of economic losses

Structure and function Conducting, transitional and gas exchange system Conducting include nasal cavity,paranasal sinuses,pharynx,larynx,trachea and extra and intra pulmonary bronchi All of which are largely lined by pseudo stratified columnar cells plus variable secretory goblet cells and serous cell Transitional system composed of bronchioles save as transition zone between the conducting system (ciliated )and the gas exchange alveolar system

Normal bronchiole lack goblet cell but instate have other type of secretory cells(Clara and neuroendocrine cells) Clara cells contain numerous biosynthetic organelles that play role in detoxification of xenobiotics (foreign body) The gas exchange system of respiratory tract in all mammals is formed by alveolar duct and million of alveoli. Alveoli are superficially lined by two distinct type of epithelial cells,known as the 1 pneumonocytes (membrane ) and type 2 pnemonocyes (granular)

Vulnerability of respiratory system to aerogenous (air borne ) injury is primarily because of 1-extensive area of alveoli 2-the large volume of the air passing continuously in to lung 3-the high consternation of noxious element that can present in the air

Surface of pulmonary alveoli is approximately 2000 m2 in equine,in human 200 m2,9000 liter \day, 9% of total blood volume within pulmonary vasculature right ventricle of cardiac goes in to lung, so lungs are also susceptible to blood borne microbes,toxin and emboli. capillary bed of the lung surface area of 70 m2 equal to 2400 km of capillaries with 1 ml of blood occupying up to 16 km of capillary bed.

Normal bacterial flora of respiratory system The respiratory system has its own normal bacterial flora. Many spices of bacteria are found such as Mannheimia (pasteurella) heamolytica in cattle,pasteurella multocida in cat,cattle and pigs, bordetella bronchiseptica in dogs and pigs. The organism that consist the normal flora of respiratory tract are restricted to proximal region (nasal cavity,pharynx and larynx). The thoracic portion of trachea,bronchi,lung are sterile. Type of bacteria in nasal flora very considerable among animal species and geographic region.

Portal of entry in to respiratory system Microbe, toxin and pneumotoxicants can gain access in to respiratory system by the following routes 1-airoginous The most common route in transmission of most respiratory infection in domestic animals, bacteria,mycoplasma and viruses along with toxic gas and foreign particles include food can gain access to the respiratory system via inspired air. 2- hematogenous via circulating blood, some viruses,bacteria parasites and toxin can inter the respiratory system 3-directed extension, pathogenic organism can also reach the pleura and lung through penetrating injury or rupture esophagus or perforated diaphragm.

Defense mechanism of respiratory tract Particles,microbe,toxic gas most be gain entry to a vulnerable region of the respiratory system before it can have a pathologic effect. Size,shape,dispersal,and deposition of particles Clearance is process by which deposited particles are destroyed,neutralized and removed from the mucosal surface Removal by sneezing,coughing,mucocilliary transport and phagocytosis Difference between deposit and clearance is referred to as retention

The anatomic configuration of the nasal cavity and bronchi in the upper respiratory tract plays a unique role in preventing or reducing the penetration of noxious material in to the lung specially in to alveolar region.the narrow nasal meatuses and the coiled arrangement of the nasal generate enormous turbulences of air flow, slow Velocity, reduce centrifugal force. and as result physical forces are created that forcefully impact particles larger than 10 um on to the surface of nasal mucosa 10 um and more in nasal mucosa 2-10 um in bronchial mucosa 2 um and smaller by gravitation o.1-2 um (bacteria,virus)

shape,length,electrical charge,humidity 200 um may reach lower region,asbestos Defense mechanism of conducting system Nose, trachea,bronchi Mucocilliary clearance (the main defense ) Mucus is complex mixture of (water,glycoprotein,immunoglobulin,lipid,electrolyte) produce by goblet cell, serous cells,submucosal gland and fluid from transepithelial ion and water transport Mucus (thin double layer film of mucous is formed,)outer layer is in a viscous gel phase,inner layer is in fluid or solution phase.100 ml of mucous daily,250 cilia in each cell (each cilia 6 um long). 1000 strokes / minute,Mucus move 20 mm /minute

If cilliary transport is reduced (Loss of cilia) or mucous production is excessive,coughing becomes an important mechanism for clearance the air way M cell( microfold cells ) modified epithelial cells covering the (BALT) By M cell,macrophage,dendritic cell (APCs) and B,T cell, IgA and less IgG and IgM Defense mechanism of alveoli Lack ciliated and mucus Phagocytosis by alveolar macrophages,capillary macrophages Transferrin,anionic peptide,pulmonary surfactant

Defense mechanism of alveoli Lack ciliated and mucus Phagocytosis by alveolar macrophages,capillary macrophages Innate immunity :Transferrin,anionic peptide,pulmonary surfactant. Humeral immunity :IgA in the nasal and tracheal secretion,IgG and lesser IgE and IgM in alveolar surface. Cellular immunity :Pulmonary alveolar macrophage,pnemocyte,endothelial cell,lymphocyte, plasma cell,Dentric cell,(macrophage receptor,Fc,C3b,C3a,C5a,TNF,CD40,TLR, FAS)

Defense mechanism against blood borne pathogens (intra vascular space ) In ruminant,cat, horse,pigs,pulmonary intra vascular macrophage are the cell responsible for the removable of circulating particles, pathogen bacteria and endotoxin from the blood Defense mechanism against oxidant induced lung injury Existing in an oxygen rich in environment and being site of numerous metabolic reaction This form of damage is caused by inhaled oxidant gases example nitrogen dioxide,ozon,sulfur di oxide,tobacco smoking,and by xenobiotic toxic metabolite produced locally or by reaching the lung via the blood stream,example (paraquat),or by free radical (reactive oxygen species ) released by phagocytic cells during inflammation.

Oxygen and free radical scavengers such as catalase,superoxide dismutase,and vitamin E are largely responsible for production pulmonary cells against peroxidation,these scavenger are present in alveolar and bronchiolar epithelial and in the extra cellular space of the lung. The defense mechanism are so effective in trapping, destroying and removal bacteria that under normal condition,animal can be exposed to aerosol containing massive number of bacteria without any ill effect. If defense mechanism are impaired,inhaled bacteria colonized and multiply in bronchi, bronchiole and alveoli and produce infection, similarly when air born and blood born pathogen,inhaled toxicant or free radicals impairment the protective defense mechanism of respiratory system and causing injury and serious respiratory disease

Impairment of defense mechanism in the respiratory system 1-viral infection: viral agent are notorious in predisposing animal to secondary bacterial pneumonia by what in known as viral -bacterial synergism.e.g. influenza virus. The mechanism of the synergistic effect of viral- bacterial infection by destruction of the mucociliary blanket and reduction of mucociliary clearance. Also the phagocytic function of pulmonary alveolar macrophage is notably impaired. 2-Toxic Gases Hydrogen sulfide and ammonia,poor ventilation,polluted cities,impaired respiratory defense mechanism and increase susceptibility to bacterial pneumonia

Immunodeficiency: Immunodeficiency disorder whether acquired or congenital are often associated with increased susceptibility to viral- bacterial and protozoal pneumonia. Large dose of chemotherapeutic agents such as steroids and alkylating agent causes immunosuppression. Other condition that predispose to secondary bacterial pneumonia Uremia,endotoxemia, dehydration,starvation, hypoxia,acidosis,pulmonary edema,anesthesia,ciliary dyskinesia,and stress

Hypoxia and pulmonary edema decrease phagocytic function of pulmonary alveolar macrophages and alter the production of surfactant by type 11 pneumonocytes. Dehydration is thought to increase the viscosity of mucous,reducing or stopping mucocillary movement. Anesthesia induced cilliostasis with concurrent loss of mucocilliary function. Cilliary dyskinesia,an inherited defect in cilia causes abnormal mucus transport Starvation,hypothermia and stress can reduce humeral and cellular immune response.

Disease of respiratory system Rhinitis :Inflammation of nasal cavity Rhinitis,Sinusitis.these conditions usually occur together. Disturbance in the balance of the normal and pathogenic flora,caused by viruses,fungi,bacteria,gases,environmental changes and immunosuppression,local trauma,stress,prolong antibacterial therapy, lead to inflammation of the nasal cavity. -Based on nature of exudate,Rhinitis classified as serous,catarrhal,purulent,fibrinous, or granulomatous, this type of inflammatory reaction can progress from one to another. Acute, subacute or chronic according to the age of the lesion,mild, moderate, severe according to the severity. Other types are hemorrhage, ulcers, mucosal hyperplasia.

Serous Rhinitis is the mildest form of inflammation characterized by hyperemia and increased production of a clear fluid, caused by mild irritants or cold air or it occurs during early stages of viral infection. Catarrhal Rhinitis is slightly more sever process increase in mucous production by increase activity of goblet cells and mucous glands. Mucous exudate is a thick translucent slightly turbid viscous fluids.some time containing a few exfoliated cells, leucocyte and cellular debris. In chronic case hyperplasia of goblet cell,infiltrated with neutrophil giving the exudate a cloudy mucopurulent appearance. Purulent Rhinitis :this inflammation characterized by a neutrophilic exudate.sever injury that is accompanied by mucosal necrosis and secondary bacterial infection. Cytokine leukotrienes, complement activation,and bacterial product cause exudation of leukocyte specially neutrophil.

Grossly the exudate is thick and opaque and vary from white to green to brown depending on the types of bacteria and type of leukocytes(neutrophils or eosinophils) present in the exudate. Fibrinous Rhinitis :this reaction occur when nasal injury and sever increase in vascular permeability,resulting in abundant exudation of plasma fibrinogen which coagulates into fibrin (yellow or gray ). Some times forms pseudomembrane. Granulomatous Rhinitis :this reaction in the nasal mucosa and sub mucosa is characterized by infiltration of numerous activated macrophages mixed with few lymphocyte and plasma cells. In some cases lead to the formation of polypoid nodules. Granulomatous Rhinitis is generally associated with chronic allergic or with systemic mycosis,tuberculosis or foreign bodies.

Acute Rhinitis lead to chronic and destruction of nasal conchae - deviation of the septum and craniofacial deformation -, otitis media and interna,and vestibular syndrome (abnormal head tilt and abnormal gait which may lead to emaciation. Sinusitis Sinusitis occur frequently accompanied with Rhinitis or as sequel to penetrating or septic wound of the cranium improper dehorning in cattle, or tooth infection. Para nasal sinuous have poor drainage,there for exudate tends to accumulate causing mucocele or empyema,sinusitis osteomyelitis meningitis. Specific disease of the nasal Cavity and sinuous : equine viral infection (equine viral Rhino pneumonitis,equine Influenza, equine bacterial infection (strangles and glanders ). Infectious Bovine Rhinotrichitis.

Pharyngitis,laryngitis and tracheitis Pharynx, larynx and trachea are important because of their potential to obstructed air flow and lead to aspiration pneumonia The pharynx is effected by disease of the upper respiratory tract and upper digestive tract. Obstruction of pharynx can be caused by masses in surrounding tissues such as neoplasm of thyroid gland,thymus and Parathyroid gland. Eg. Calf diphtheria Trachea can be involved by extension from both the lung and larynx.the most common causes of tracheitis are viral infection. According to the exudate tracheitis is classified as catarrhal,purulent,fibrinous or granulomatous

Lungs Each lung is subdivided into various number of pulmonary lobe. Left lung is composed of cranial and caudal lobe. Right lung is composed of cranial,middle (absent in horse), caudal and accessory lobe. In dog,cat,cattle and pigs,the lung are well lobated and well lobulated Goat, sheep are well lobated and poorly lobulated. Horse and human have both poorly lobated and lobulated. Pores of kohn :this pore between lobule and adjacent alveoli,poor in cattle and pigs and good in dog.

Atelectasis The term atelectasis means incomplete distention of alveoli and lung that have failed to expand with air at the time of birth or lungs that have collapsed after inflation. 1. Acquired (Compressive and obstructive ) a. Compressive space occupying masses in plural cavity such as abscesses and tumor or bloat,hydrothorax,heamothorax and empyma, pneumothorax. b. Obstructive occur when there is reduction in the diameter of air ways caused by mucosal edema and inflammation or blocked by mucous plugs,exudate,aspirated foreign material or lung worm.

Atelectasis also occur when large animal are kept recumbent for prolonged period such as during anesthesia, milk fever. The lung with atelectasis appear depressed below the surface of the normally inflated lung.the color is generally dark, blue,and the texture is flabby or firm.

Pulmonary emphysema Abnormal permanent enlargement of air space distal to terminal bronchiole, accompanied by destruction of alveolar walls ((alveolar emphysema must separate from simple air space enlargement or hyper inflation in which there is no destruction of alveolar wall can occur congenitally (Down syndrome) or acquired with aged)). An imbalance between protease released by phagocytes and anti protease produce in the lung as a defense mechanism suggests that causes destruction of alveolar wall.

The destructive process is markedly accelerated by any factor such as cigarette smoking,pollution or defect in synthesis of anti protease. In animal,emphysema occur always secondary to abstraction of out flow of air by exudate plugging bronchi and bronchiole causes imbalance between the volume of air entering than leaving the lung. Classified of emphysema depending on effected area of the lung (alveolar emphysema and interstitial emphysema).

Circulating disturbance of the lung Lungs are extremely well vascularized organ,disturbance in pulmonary circulation have a notable effect on gases exchange result in hypoxemia and acidosis,also can have an impact on other organ such as the heart and liver. Hyperemia and congestion Hyperemia is an active process that is a part of acute inflammation. Congestion is the passive process,resulting from decreased outflow of venous blood.

Pulmonary congestion caused by heart failure result in stagnation of blood in pulmonary vessel lead to edema and egression of erythrocyte in to alveolar space lead to phagocytosed by pulmonary alveolar macrophage (erythrophagocytosis ). Brown cytoplasm,hemosiderin,iron pigment,siderophages,heart failure. Hypostatic congestion result from gravity and poor circulation,may be followed by hypostatic edema and hypostatic pneumonia.

Pulmonary hemorrhage Pulmonary hemorrhage can occur as a result of trauma,coagulopathies,pulmonary thromboembolism. Pulmonary edema in normal lung,fluid from the vascular space slowly but continuously passes into the interstitial tissue where it is rapidly drained by the pulmonary lymphatic vessel. Cardiogenic (hydrostatic,hemodynamic ) and non cardiogenic (permeability types ) Neurogenic pulmonary edema(head injury,brain edema,brain tumor,cerebral hemorrhage ) massive sympathetic stimulation released catecholamines, also in sever excitement,sever stress.

Pulmonary embolism With it is vast capillary bed and position in the circulation,the lung act as a safety net to catch emboli before they reach the brain and other tissue,septic bacterial emboli,fat emboli,tumor cell emboli,thromboemboli Pulmonary infarction Because of a dual arterial supply to the lung,pulmonary infarction is rare.

Bronchi The pattern of necrosis,inflammation and repair in intrapulmonary bronchi are similar to nasal and tracheal epithelium. Injury to ciliated bronchial epithelium may result in degeneration,detachment and exfoliation of necrotic cell. cellular exfoliation is promptly followed by inflammation. Mitosis,cell proliferation and cell differentiation and finally repair. Depending on the type of exudate,bronchitis can be fibrinous,catarrhal,purulent,fibrinonecrotic (diphtheritic) and some time granuloma.

In chronic bronchitis,production of mucous is increased via goblet cell hyperplasia,chronic catarrhal inflammation in smoker who continuously coughing out excessive mucous secretion (sputum). Chronic bronchial irritation causes squamous metaplasia, in which highly functional ciliated epithelium is replaced by non functional. Bronchiectasis is one of the most devastating sequel that follows chronic bronchitis,permanent dilatation of bronchus as a result of accumulation of exudates in the lumen and partial rupture of bronchial wall.

Bronchioles The epithelial lining of bronchiolar region is susceptible to injury particularly respiratory viruses (A deno virus, Canine distemper ), and oxidant gases. The prone to injury may due to : 1. It is highly vulnerability to oxidant and free radical 2. Clara cells rich in oxidase which generate toxic metabolite. 3. The tendency for macrophage and leukocytes to accumulate in this region

Depending on the types of injury band inflammatory response,bronchiolitis is classified as catarrhal,supportive, necrotizing or granulomatous. In sever injury,exudate can not be removed from the basement membrane and the exudate become infiltrated by fibroblast which form small masses of fibrovascular tissues and developed in to polyps. Air way hyperresponsiveness following transient viral infection of the lower respiratory tract or exposure to certain allergens lead to increased number of mast cell,eosinophil's and T lymphocyte in air way mucosa. Clinically,air way hyperresponsiveness is characterized by an exaggerated bronchoconstriction following exposure to mild stimuli such as cold air or exposed to aerosols of histamine.

Alveoli Three layer composed of blood air barrier (vascular endothelium,basal lamina and alveolar interstitium Injury of type 1 pneumonocytes causes swelling and vacuolation.when cellular damage has become irreversible,type 1 cells detach,resulting in denudation of the basement membrane,increased alveolar permeability and edema. Alveolar repair is possible as long as the basement membrane remain intact.when alveolar injury is diffuse,proliferation of type 2 pneumonocytes, and interfere in gas exchange and causes hypoxemia. When sever injury, fibroblast proliferate in alveolar wall (alveolar interstitium )casing alveolar fibrosis. In more sever injury,fibroblast actively migrate from the interstitium to alveolar space causing intra alveolar fibrosis. These two types of fibrosis are most commonly seen in toxic and allergic pulmonary disease

General aspects of lung inflammation Pulmonary inflammation is highly regulated process that involve a complex interaction between cells important from the blood (neutrophil,eosinophil,mast cell and lymphocyte ) and pulmonary cells type 1 and type 2 pneumonocyte and endothelial, Clara and stromal interstitial cells). 1. Complement (c3a,c3b,c5a),Coagulation factor (v1,v2),Arachidonic acid,metabolites(leukotriene and prostaglandins),Cytokines(interleukin,monokines, chemokinase ),Enzymes and enzyme inhibiter (elastase, antitrypsin ),Oxygen metabolites(O2,OH,H2O2),Antioxidant,Nitric oxide 2. Pulmonary macrophage (alveolar,intravascular and interstitial ) which have an immense biologic armamentarium.

Feature of pulmonary injury: 1. Leukocyte can exit the vascular system through the alveolar capillaries unlike other tissues where post capillary venules are the site of leukocyte diapedesis (extravasation ). 2. The intact lung contain within alveolar capillaries a large pool of resident leukocyte 3. Additional neutrophil are sequestered within alveolar capillaries within minutes of local or systemic inflammatory response.

Nitric oxide has bee identified as a major regulatory molecules of inflammation in lung producing locally by macrophages,pulmonary endothelium and pneumonocytes. nitric oxide regulate the vascular and bronchial tone,modulate the production of cytokine,trafficking of neutrophil,switches on/off genes involved in inflammation and immunity. As alveolar injury is transient and there is no interference with the normal host response,the entire process of injury,,degeneration,necrosis,inflammation and repair can occur vin less than 1 week. When alveolar injury become persistent or when capacity of the host for repair is impaired,lesion can progress to an irreversible stage lesion progress to a stage of terminal alveolar fibrosis

Classification of pneumonia based on: 1-Causes :Viral pneumonia, Pasteurella pneumonia,Verminous pneumonia, chemical pneumonia,hypersensitivity pneumonia 2- Type of exudate :Suppurative pneumonia,Fibrinous pneumonia, Pyogranulomatous pneumonia 3-Morphologic feature :Gangerenous pneumonia, Proliferative pneumonia,Embolic pneumonia 4-Distribution of lesion :Focal pneumonia, cranioventral pneumonia,diffuse pneumonia, lobar pneumonia 5-Epidemiologic attributes :Enzootic pneumonia, contagious bovine pleuropnemonia 6-Geographic region,Montana pneumonia 7 -Miscellaneous attributes : a typical pneumonia,cuffing pneumonia, aspiration pneumonia,progressive pneumonia,farmers lung

Pneumonia in domestic animal can be classified on texture,distribution appearance and exudation in to 4 morphologically distinct type : 1-broncho pneumonia 2- interstitial pneumonia 3-embolic pneumonia 4- granulomatous pneumonia 1-Bronchopneumonia Bronchopneumonia refer to a particular type of pneumonia in which injury and the inflammatory process take place primarily in the bronchial,bronchiolar and alveolar lumens,and it is the most common type of pneumonia seen in domestic animal.

Factor contributing to topographic selectivity within the lungs include: 1. Gravitational sedimentation of the exudate 2. Greater deposition of infectious organism 3. Inadequate defence mechanism 4. Reduced vascular perfusion 5. Shortness and abrupt branching of airways 6. Regional differences in ventilation Bronchopneumonia are caused by bacteria and mycoplasma.the lesion tend to spread centripetally by kohn pores Consolidation is used when the texture of pneumonic lung becomes firmer or harder than normal because of exudation and atelectasis.

2-Fibrinous bronchopneumonia : are the result of more sever pulmonary injury and thus are more life threatening than suppurative bronchopneumonia. Early stage of fibrinous bronchopneumonia are characterized by severe congestion and hemorrhage. A few hours later,fibrin starts to accumulate on the plural surface,giving the pleura a ground glass appearance and forming plagues of fibrinous exudate over a red dark lung. Marbled appearance :the distention of intralobular septa by edema and dilation and thrombosis of lymphatic vessels. Pulmonary sequestra :pulmonary necrosis develop when isolated pieces of necrotic lung in capsulated by connective tissues caused by sever ischemia or necrotizing toxin released by pathogenic bacteria. Fibrin is chemotactic for neutrophil, these type of leukocyte are always present a few hours' after the onset of fibrinous inflammation.

3-Interstitial pneumonia The inflammatory process take place primarily in any of the three layer of the alveolar wall. Erogenous inhalation of toxic gases,toxic fumes (smoke inhalation ),and infectious agent (viruses). Fungal spore (antigen ) combine with antibody and deposits in alveolar wall, a cascade of inflammatory response occur (allergic alveolitis ). When the source of alveolar injury persist,the proliferative and infiltrative lesion progress to chronic interstitial pneumonia and the hallmark of chronic interstitial pneumonia is fibrosis of alveolar wall and accumulation of mononuclear inflammatory cells and lead to granuloma and hyperplasia of smooth muscles in air ways of pulmonary vasculature.

4-Embolic pneumonia The injury is hematogenous, and the inflammatory response is typically centered in pulmonary arterioles and alveolar capillaries.to caused pulmonary infection,circulating bacteria must first attached to the pulmonary endothelium with specific binding proteins or simply attach to intravascular fibrin and then evade phagocytosis by intravascular macrophage or leukocyte. Infected thrombi,because of there size facilitate entrapment of bacteria in the pulmonary vessels and provide a favorable environment to escape phagocytosis. Omphalophlebitis,skin or hoof infection,valvular or mural endocarditis.

5-Granulomatous pneumonia Granulomatous pneumonia refer to type of pneumonia in which aerogenous or hematogenous injury is caused by organism or particles that can not be normally eliminated by phagocytosis and that evoke a local inflammatory reaction with numerous alveolar and interstitial macrophage,lymophocyte, a few neutrophil and some time giant cell. systemic fungal disease,cryptococcus coccidioidimycosis,tuberculosis,inhalation starch,foreign bodies. Granulomatous pneumonia is characterized by the presence of variable number of caseous or non caseous granulomas randomly disturbed in the lung

Pleura and thoracic cavity The thoracic wall and mediastinum are lined by the parietal pleura. Hilus :where bronchi and blood vessels inter the lung. Pleural space :the space between the lung and chest.

Degeneration and disturbance Pleural calcification In chronic uremia :lesion appear as white streaks in parietal pleura,mainly over the intercostal nephritic muscles of the cranial part of the thoracic cavity. The lesion are not functionally significant but indicate a severe underlying renal problem. Vitamin D toxicity(hypervitaminosis D) and ingestion of hypercalcemic substance,such as vitamin D analogs.

Pneumothorax Presence of air in the thoracic cavity where there should normally be negative pressure to facilitate inspiration. there are two types of Pneumothorax - In spontaneous Pneumothorax,air leaking into the pleural cavity occurs without any known underlying disease or trauma. - In secondary Pneumothorax,movement of air into pleural cavity results from an underlying pulmonary or thoracic wall disease most common causes of secondary Pneumothorax in veterinary medicine are penetrating wounds,ruptured esophagus, biopsy. Clinical signs of Pneumothorax include respiratory distress and the lesion is simply a collapsed,atelectasis lung. The air is readily reabsorbed from the cavity if the site of entry is sealed

Circulatory and lymphatic disturbance Pleural effusion General term is used to described accumulation of any fluid (transudate,modified transudate,exudate,blood,lymph,or chyle ) in the thoracic cavity. Cytological and biochemical evaluations of pleural effusions are some times helpful in suggesting possible pathogenesis. Based on protein concentration and total number of nucleated cells, pleural effusions are cytological divided into transudates, modified transudate and exudate

Hydrothorax When the fluid is serous,clear and odorless,and fails to coagulate when exposed to air,the condition is referred to as hydrothorax(transudates). Cause : Edema in other organs :increased hydrostatic pressure (heart failure),decreased oncotic pressure (hypoprotenima,as in liver disease ), alteration in vascular permeability, obstruction of lymph drainage (neoplasia ). In case where the leakage is corrected, if the fluid is a transudate,it is rapidly reabsorbed. if the fluid persist,it irritates pleura and causes mesothelial hyperplasia and fibrosis which thickens the pleura. Excessive fluid in the thorax causes compressive atelectasis,resulting in respiratory distress. Congestive heart failure, chronic hepatic disease, nephrotic syndrome.

Hemothorax Blood in the thoracic cavity (exudate with a sanguineous component ) Causes Rupture of major blood vessel as a result of severe thoracic trauma( hit by car ),erosion of a vascular wall by malignant cell or inflammation, rupture aortic aneurysms,clotting defects (warfarin toxicity ), thrombocytopenia bone marrow suppression. Hemothorax is generally acute and fatal.

Chylothorax The accumulation of chyle (lymph rich in triglycerides ) in thoracic cavity. Causes : Rupture of major lymph vessel (thoracic neoplasia ), trauma,fungal infection,congenital lymph vessel anomalies.

Pleuritis or pleurisy : Inflammation of pleura Pleural tissue is readily susceptible to injury caused by direct implantation of an organism through a penetrating thoracic or abdominal wounds, by hematogenous dissemination of infectious organism in septicemias, direct extension from an adjacent inflammatory process, such as in fibrinous bronchopneumonia or from perforated esophagus. Chronic injury typically results in serosal fibrosis and tight adhesions between visceral and parietal pleura. in severe case,these adhesion can obliterate the pleural space.

according to the type of exudate,can be fibrinous,suppurative,granulomatous,hemorrhagic or combination. Pyothorax (thoracic empyema ) accumulation of purulent exudate in the cavity in suppurative pleuritis. Clinical signs :pain,severe toxemia,interfere with inflation of the lungs. Pleurtitis can occur as an extenion of pneumonia (fibrinous bronchopnemonia

introduction disease of the respiratory system are some of the leading causes of mortality and...

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