Praktikum Patologi Sistem Respirasi

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  • PRAKTIKUM PATOLOGI SISTEM RESPIRASI

  • Pulmonary embolus and infarctGeneral descriptionPulmonary embolism refers to blockage of pulmonary arteries by blood clot from another site. Clots are almost always embolic in origin if they occur in pulmonary arteries. PE usually has its source in the deep veins of legs (95% of cases) when a DVT (deep vein thrombosis) embolizes.

  • Incidence1.6% of general surgical patients 10% of acute hospital deaths 50,000 deaths in US each year Symptoms and clinical signsSudden chest pain, dyspnea, loss of consciousness Blood on coughing PathophysiologyDVT embolism occurs in most cases. Sudden death often ensues after blockage of blood flow thru lungs (bronchial circulation MAY sustain patient) Acute cor pulmonaleif patient survives 10% of cases result in infarction.

  • Histopathology Embolus appears laminated (this shows it has TRAVELLED, i.e. it is not of local origin and is not a primary thrombi) Alveoli are necrotic in infarcted area Hemorrhage is noticeable in alveolar spaces (because vast amount of collateral circulation, i.e. bronchial circulation, means blood continues to pump into the necrotic areas but cells are obviously too damaged to use the blood).

  • Alv:alveoliT:trombusH:haemorhage

  • Alv:alveoliH:haemorhage

  • General DescriptionBronchopneumoniarefers toa type of pneumonia that is localized, often to the bronchioles and surrounding alveoli. (Compare to lobar pneumonia below) Clinical SignsOne or more of the following symptoms: coughing, chest pains, fever, blood-streaked sputum, chills, and difficulty in breathing. Signs of pulmonary congestion

    Bronchopneumonia

  • Pathophysiology- Inhalation of organisms. - Scarring if alveoli destroyed.

    Histopathology Patchy distribution in and around small airways Dense acute inflammatory exudate of PMNs, fibrin and blood in bronchi, bronchioles and adjacent alveoli. FOCAL destruction of alveolar walls (you can see normal parenchyma in other areas adjacent)

    Lanj.Bronchopneumonia

  • Infiltrasi PMN yang padat

  • General DescriptionBronchiectasis is a chronic nerotizing infection of the bronchi and bronchioles leading to abnormal dilation of these airways. Dilation must be permanent as reversible dilation often accompanies pneumonia.

    Clinical Signs Severe, persistent cough. Fever if pathogens are present. Dyspnea if severe. Expectoration of copious amounts of foul-smelling, purulent sputum

    Bronchiectasis

  • Pathophysiology Either infection or obstruction are major influences associated with disease. Early changes are reversible. If 1) obstruction persists or 2) if there is added infection, especially during periods of growth, airways develop abnormally. Infection causes inflammation of bronchial wall, bronchial damage, weakening and further dilation. Lower lobes affected bilaterally, most severly in most distal bronchi. Airways become dilated up to 4x normal size. A severe form is associated with cystic fibrosis. Lanj.Bronchiectasis

  • Histopathology

    Intense inflammatory exudate is visible in bronchioles. Desquamation of lining epithelium. Necrotizing ulceration of lining also possible. Possible squamous metaplasia of remaining epithelium. Destruction of bronchial walls may lead to lung absess.

  • General Description Adenocarcinoma is the most common type of lung cancer in women and non-smokers (only 75% vs. 98% with squamous/small cell carcinoma).Incidence 30-35% of all lung cancers.

    Adenocarcinoma

  • Clinical Signs Lesions are peripheral, pigmented, and puckered: lesions are found near pleural surfaces, have black pigment and may glisten if mucin is present, and cause the pleural surface to retract (pucker) over the tumor site. Symptoms common to all lung cancers include: Cough Hemoptysis (coughing up of blood) Wheezing Shortness of breath Discomfort during breathing Chest pain Symptoms of pneumonia (fever and a mucus-producing cough) Discomfort during swallowing Hoarseness Weight loss and poor appetite Lanj. Adenocarcinoma

  • PathophysiologyArise in peripheral areas (as opposed to central origin of other 2 types of lung cancer). 80% will contain mucin. Slower growth compared with squamous cell carcinoma. HistopathologyAcinar pattern: predominance of glandular structures . Single layer of large cells with basally located nuclei (since they are glandular).

    Lanj. Adenocarcinoma

  • General Description Absestos refers to a family of fiber types linked to tumor formation. It is an example of "pneumoconiosis," a descrip- tion of any fibrotic diseasecaused by inhaled dust. AsbestosisIncidence Approximately 4 in 10,000 people. Clinical Signs Dyspnea (shortness of breath) is the first symptom, intially via exertion and then present at rest as well. Takes commonly 20 years to manifest itself. Associated cough includes production of sputum.

  • Pathophysiology Depends on interaction of lung macrophages and other parenchymal cells. Still fibers land and penetrate small airways and cuts. Macrosphages attempt to ingest and clear fibers and activate fibrogenic mediators as an immune response. Chronic deposition of fibers and persistent release of mediators leads to generalized pulmonary inflammation and interstitial fibrosis. Asbestos bodies arise when macrophages attempt to phagocytose asbestos fibers using ferritin (they may exist as "ferruginous bodies" lacking an absestos core in normal lungs.in these cases there is no accompanying scarring and fibrosis). Progression of disease to congestive heart failure, cor pulmonale, and death. May be complicated by presence of lung or pleural cancer (very bad prognosis).

  • Histopathology Fibrosis and scarring are visible. Macrophages and inflammatory cells may also be prominent. Distinguishing feature (from other causes of diffuse interstitial fibrosis) is present of asbestos bodies. Asbestos bodies are golden brown beaded rods with a translucent center (consist of asbestos fibers coated with an iron-containing proteinaceous material)

  • Nasopharyngeal CarcinomaSynonyms: Lymphoepithelioma-Like Carcinoma, Lymphoepithelioma, Regaud's-Type

  • Lanj. Nasopharyngeal CarcinomaHistopathologyCrucial distinction is between: (keratinizing) squamous cell carcinomas: show clearcut evidence of keratinizationless marked association with EBVolder age group28,29nonkeratinizing carcinomas: most common typedo not show clearcut evidence of keratinization30subdivided into: differentiated: stratified or tiled arrangementwell-defined cell marginsundifferentiated31,32 syncytial appearanceindistinct cell marginssome tumor cells may be spindle-shapedhigh proportion, particularly if undifferentiated, accompanied by prominent inflammatory infiltrate: rich in lymphocytesmay be other inflammatory cells such as: plasma cellseosinophils33rarely, epithelioid and multinucleated giant cells

  • Two patterns of growth, sometimes in combination: Regaud's-type: inaccurate designationwell-defined aggregates of epithelial cells surrounded by fibrous tissue and lymphoid cellsSchmincke-type: inaccurate designationneoplastic epithelial cells: grow diffusely Lanj. Nasopharyngeal Carcinoma

  • closely intermingled with inflammatory cellsnuclei tend to be: vesicularsmooth outlinenucleolus: singlelargesharply etchedeosinophilic34Occasionally oval or spindle shaped tumor cells Lanj.Nasopharyngeal Carcinoma

  • Undifferentiated nasopharyngeal adenocarcinoma composed of cells growing in a diffuse syncytial pattern (Schmincke type).

  • Undifferentiated nasopharyngeal carcinoma composed of oval and spindle tumor cells.