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Pulmonary Pathology Online Anatomy and Histology of the Normal Lung and Airways Examination of pulmonary and pleural biopsies Useful chromatic and immunostains in pulmonary pathology Percutaneous Needle and Trucut Biopsy Specimen Transbronchial Biopsy Specimen Transbronchial biopsy in lung transplant recipients Lobectomy and pneumonectomy specimen Histopathological reporting of pulmonary parenchymal biopsies Histopathological reporting of pulmonary biopsies in cases of Idiopathic Pulmonary Fibrosis Closed pleural biopsy for neoplasm or inflammatory lesions ; Open pleural biopsy and pneumonectomy or pleural stripping Anatomical Distribution of Pulmonary Disease Congenital Cystic Adenomatoid Malformation Bronchopulmonary Sequestration Acute Respiratory Distress Syndrome Neonatal Respiratory Distress Syndrome Complications of Neonatal Respiratory Distress Syndrome Extrinsic Allergic Alveolitis (Hypersensitivity Pneumonitis) Pulmonary Eosinophilic Granuloma Pathological Diagnosis of Granulomatous Lung Diseases Infectious Granuloma of the Lung Non-necrotising Granulomatous Inflammation of the lung An approach to Histopathological Examination of Pulmonary Granulomatous Inflammation Chronic Obstructive Pulmonary Disease Emphysema Bronchiolitis Nodular Pulmonary Amyloid (Amyloidoma) Pulmonary Alveolar Proteinosis Other forms of Pulmonary Embolism Pulmonary Collapse (Atelectasis) and Pneumothorax Pulmonary Edema |
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Idiopathic Pulmonary Fibrosis Usual Interstitial Pneumonia (UIP) Non-specific interstitial pneumonia (NSIP) Desquamative interstitial pneumonia (DIP) Respiratory bronchiolitis-interstitial lung disease (RBILD) Acute interstitial pneumonia (AIP)/organizing diffuse alveolar damage DAD) Lymphocytic Interstitial Pneumonia / Follicular Bronchiolitis Wegener's Granulomatosis of the Lung Churg-Strauss Syndrome (allergic granulomatosis) Isolated Pulmonary Capillaritis Necrotizing Sarcoid Granulomatosis |
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Hemostasis and Thrombosis: Hemostasis is a normal physiologic process. It maintains blood in fluid condition and clot-free state in normal vessels by inducing a rapid and localized hemostatic plug at sites of vascular injury. Thrombosis represents a pathologic state in which there is formation of intra-vascular solid mass (thrombus) from the elements of circulating blood. The vessel may be uninjured or with minor injury. Thrombosis: Three primary factors influence thrombus formation (Virchow’s triad): 1. Endothelial injury. 2. Slowing of blood flow. 3. Hyper coagulability of blood. 1. Endothelial injury commonest cause, mainly in the heart and arterial circulation (e.g. Myocardial infarction, endocarditis, ulcerated atherosclerosis). Injury may occur from diverse causes e.g. hemodynamic stress (hypertension or turbulent flow in aneurysms), radiation, products absorbed from cigarette smoke, extensive burn etc. 2. Slowing of circulation (alteration in normal blood flow): Normal blood flow is laminar (i.e., the cellular elements flow centrally inside the vessel, separated from endothelium by a clear zone of plasma). Stasis and turbulence disrupt laminar flow and bring platelets into contact with the endothelium. They prevent dilution of activated clotting factors by fresh flowing blood, retard the inflow of clotting factor inhibitors and permit the build-up of thrombi. Stasis is important in causing thrombosis in veins, cardiac chambers and arterial aneurysms. Hyperviscosity syndrome - Example: In polycythemia or deformed RBC as in sickle cell anemia causes stasis in small blood vessels predisposing to thrombosis. 3. Hypercoagulability of blood may be due to heritable gene mutation or acquired. Example: Severe burn, shock, oral contraceptive, increased hepatic synthesis of coagulation factors and reduced synthesis of anti-thrombin III. Mechanism: Normally, in a blood vessel, cellular elements flow centrally, forming axial stream separated from endothelium by a clear, cell-free, plasmatic zone. Due to slowing of the circulation, platelets come in contact with endothelium and are activated to liberate tissue factors. Tissue factors recruit more platelets, which are deposited in the form of ridges at right angles to the blood flow forming corrugations, known as line of Zahn. Coming in contact with sub-endothelial collagen, platelets are activated to release ADP, Thromboxanes etc. ADP aggregate more platelets. Thromboplastin, liberated from platelets and injured endothelium initiate precipitation of fibrin on the surface of platelets. Fibrin network may entangle RBC and leucocytes. A thrombus is thus formed, on the basis of platelets and fibrin, with varying number of RBC and leucocytes. Thrombi may form anywhere in the cardiovascular system. Aortic and cardiac thrombi are typically nonocclusive (mural) as a result of rapid and high-volume flow. Smaller arterial thrombi may be occlusive. All these thrombi usually begin at sites of endothelial injury (e.g. atherosclerotic plaque) or turbulence (vessel bifurcation). Venous thrombi characteristically occur in sites of stasis and are occlusive. At sites of origin, thrombi are generally firmly attached. Arterial thrombi tend to extend retrograde from the attached point, where as venous thrombi extend on the direction of blood flow. The propagating tail may not be well attached and may fragment to create an embolus. Sites of thrombus formation: Cardiac and arterial thrombi are formed slowly in rapid circulation. They are pale-gray and tend to have gross and microscopic lamination (lines of Zahn) produced by pale layers of plates and fibrin alternating with darker red cell-rich layers. These are mostly seen in the left ventricle overlying an infarct, ruptured atherosclerotic plaques, and aneurysmal sacs. Venous thrombosis (phlebothrombosis) often created a long red-blue cast of the vein lumen as it occurs in a relatively slow circulation. The thrombus contains more enmeshed erythrocytes among sparse fibrin strands (red or stasis thrombus). Fibrin and attachment to the vessel wall distinguish stasis thrombus from postmortem clot. Phlebothrombosis is most commonly (more than 90 %) seen in the veins of the lower extremities. Thrombi may also form on heart valves. In infective endocarditis, bacteria or fungi form large infected thrombi (vegetations), causing underlying valve damage and systemic infection. Sterile vegetations (nonbacterial thrombotic endocarditis) can also develop on noninfected valves in patients with hypercoagulable states, particularly in those with disseminated cancer. Noninfective, verrucous(Libman-Sacks) endocarditis is seen in patients of SLE due to circulating immune complex. Heart: i) Ball thrombus is seen in left atrium in mitral stenosis. It is large and spherical. ii) Mural thrombus is seen over the wall of heart in cardiac infarct, cardiomyopathy iii) Agonal thrombus is seen in right ventricle in case of death due to pneumonia. iv) Vegetations over the cardiac valves are seen in endocarditis. Artery: i) On the atheromatous patch in coronary, cerebral, spleen, and renal arteries. ii) Laminated thrombus is seen in aneurysmal sac. iii) Marasmic thrombus is seen in marasmic children, in mesenteric artery (stasis) Vein: Veins are the commonest sites of thrombus formation due to slow circulation. Other causes of venous thrombosis are: i) Trauma, burn, due to reduced physical activity, injury to vessels and release of pro-coagulants from tissue. ii) Puerperal and postpartum thrombosis occurs mainly due to amniotic fluid infusion into blood and hypercoagulability in late pregnancy and in postpartum period. . iii) Disseminated cancer, due to release of tumour-associated -procoagulants. iv) Advanced age, bed rest, immobilization, reduced physical activity diminishes milking action of muscle. v) Thrombophlebitis is the inflammation of the venous wall due to septic thrombus. Example: a) Pelvic veins in puerperal sepsis ; b) Portal vein in acute appendicitis ; c) Cavernous sinus in facial infection Fate of a thrombus: Septic thrombus causes abscess formation. Aseptic thrombus may show: i) Propagation causing complete vessel obstruction. ii) Dissolution by fibrinolytic action. iii) Detachment- with embolism. iv) Organization and recanalization, re-establishing vascular flow by in-growth of endothelial cells, smooth muscle cells and fibroblasts to create through-and through capillary channels or by incorporating the thrombus as a sub-endothelial swelling of the vessel wall. Effect of thrombosis: Septic: Forms abscess and may cause pyaemia. Aseptic: Effect will depend upon the vessel involved and efficiency of the collateral circulation of the area. 1. Arterial thrombus - in a small vessel is occlusive and usually causes infarction. This is particularly seen when it involves organs supplied with end-arteries (Example: cerebral, coronary, splenic, mesenteric and renal arteries). 2. Venous thrombosis - rarely causes infarction, as collateral channels soon enlarge to maintain the venous drainage. Superficial venous thrombosis, as in varicose saphenous veins, causes local edema and impaired venous drainage, predisposing to skin infection and varicose ulcer. Deep thrombi in larger leg veins above the knee (Example: popliteal, femoral and iliac veins), have good collateral circulation but commonly embolize (about 50 % cases). Occlusive venous thrombi with poor collateral channels cause increased venous and capillary pressure forming edema (Example: ascites in portal vein thrombosis). Beneficial effect of thrombosis: Thrombosis causes hemostasis and sealing of the vessel wall after erosion by malignant tumours and attempts to prevent hematogenous spread. Blood clot: Coagulation of dead blood (Example: in a test tube, in a blood vessel after death or after ligature). Types of clot: 1. Current jelly clot (soft and red) forms rapidly in great vessels or heart. All the elements of blood are involved. 2. Chicken fat clot (lower part dark, upper part yellow) forms slowly, RBC settles at the bottom and pale upper part consists of leucocytes and fibrin.
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Difference between Thrombus and clot: Thrombus- 1. A solid mass formed during life from the elements of circulating blood. 2. Platelet is the essential element, fibrin and corpuscles may or may not be present 3. Surface is corrugated and firmly attached to endothelium ; either pale, or alternate pale and red. Clot- 1. Coagulation of dead blood after death or in a test tube. 2. Fibrin is the essential element and corpuscles entangled in it are always present. 3. No surface corrugation, friable, the surface is roughened uniformly red , easily detachable from smooth endothelium. |
FUNCTIONAL ANATOMY OF THE HEARTANATOMY OF THE CORONARY ARTERIES AUTOPSY EXAM. OF CORONARY ARTERIES MITRAL, PULMONARY AND TRICUSPID VALVE LESIONS Myocardial infarctionhypertensive heart diseaseGIANT CELL MYOCARDITISpericardial diseaseHISTOPATHOLOGY REPORTING OF PERICARDIAL SPECIMEN HEART TRANSPLANTS - PATHOLOGICAL EXAMINATION ENDOMYOCARDIAL BIOPSY-(ALLOGRAFT REJECTION): ISHLT SYSTEM FOR GRADING REJECTION POST-OPERATIVE CARDIAC PATHOLOGY |
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Pneumoconiosis
Talcosis
Pulmonary Infections in immuno-compromised
patients Haemophilus influenza Infection Legionellosis (Legionnaires 'Disease) Atypical Mycobacterial Infection Mycobacterium Avium Intracellulare Mycobacterium Kansasii Infection |