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             Diagram showing common sites of

       Systemic Infarction from Arterial Emboli

 

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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

Bronchial Biopsy Specimen

Transbronchial Biopsy Specimen

Transbronchial biopsy in lung transplant recipients

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Histopathological reporting of pulmonary parenchymal biopsies

Histopathological reporting of pulmonary biopsies in cases  of Idiopathic Pulmonary Fibrosis

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Pathological Diagnosis of Granulomatous Lung Diseases

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Hemodynamic Disorder: Infarction

Pulmonary Infarction

Myocardial Infarction

Infarction in Specific Sites:

- Myocardial infarcts:  Visit: Myocardial Infarction: click here     

Myocardial infarcts are divided into two classes: transmural and subendocardial infarcts.

A transmural infarct results from complete occlusion of a major extramural coronary artery. A myocardial infarct is initially pale, but hemorrhage occurs with reflow into an injured vascular  bed.

Subendocardial infarction reflects prolonged ischemia caused by partially occluding stenotic lesions when the requirement for oxygen outstrips the supply.

- Cerebral infarcts:

Infarction of the brain may be the result of local ischemia or of a generalized reduction in blood flow.

A generalized reduction in blood flow resulting from systemic hypotension, as in shock, produces infarction in the border zones between the distributions of the major cerebral arteries.

If prolonged, severe hypotension can cause widespread brain necrosis. The occlusion of a single vessel in the brain - for example, after an embolus has lodged - causes ischemia and necrosis in a well defined area.

This type of cerebral infarct may be pale (non-hemorrhagic) or red (hemorrhagic), the latter being common with embolic occlusions.

Infarcts in the areas supplied by small penetrating arteries are referred to as "lacunar infarcts".

The occlusion of a large artery produces a wide area of necrosis that may ultimately resolve as a large fluid-filled cavity in the brain.

- Intestinal Infarct:    Visit: GI Path Online

The earliest tissue changes in intestinal ischemia are necrosis of the tips of the villi in the small intestine and necrosis of the superficial mucosa in the large intestine.

In either case more severe ischemia leads to hemorrhagic necrosis of the submucosa and muscularis, but not the serosa.

Small mucosal infarcts heal in a few days, but more severe injury leads to ulceration.

These ulcers can eventually re-epithelialize.

If the ulcers are large they are repaired by scar tissue, a process that may lead to strictures.

Severe transmural necrosis may be associated with massive bleeding or perforation, complications that often result in irreversible shock, sepsis, and death.

- Renal Infarct:

Renal infarcts are pyramidal in shape, with the base toward the capsule.

These pale infarcts acquire a hemorrhagic border as granulation tissue develops.

A gray rim in early infarcts is related to an exudate of polymorphonuclear leukocytes.

- Lung Infarct:     Visit: Pulmonary Infarction

Inspite of the dual blood supply, from bronchial and pulmonary vessels, pulmonary infarction is very common.

Embolus arising in any part of systemic circulation has to pass through the lungs.

Due to dual blood supply and free anastomosis between the pulmonary capillaries, small emboli fail to cause any infarction in a healthy lung. But when the circulation of the lung is slowed down associated with increased pulmonary circulatory pressure e.g. in chronic passive venous congestion, hypostatic congestion as seen in post-operative and post-natal period, infarction is common. Under such condition, when branch of pulmonary artery is blocked, force of the bronchial arteries is insufficient to supply the obstructed area due to increased pulmonary circulatory pressure. Blood drains into the area from all the connections and stagnate there.

Vessels in the alveolar walls give way and blood escapes into the alveolar space as a result  whole area becomes dead and coagulated into a firm blood-filled solid, airless mass i.e. a hemorrhagic infarct.

Big embolus blocking a big branch of pulmonary artery causes sudden death from shock,without infarction.

Cause: 

1. Embolism through pulmonary artery. Emboli come from deep veins of legs, usually in post-operative and post-natal period.

2. Pulmonary thrombosis, usually due to atherosclerosis of the pulmonary artery.

Gross:

1. Usually multiple, big or small, wedge-shaped and placed at the periphery of the lung, dark red in colour with clean cut outline. Feels firm and cut surface is dry.

2. Overlying pleura shows patches of fibrinous pleurisy due to irritation.

Microscopic features:

1. Alveoli are filled up with blood and their outline is indistinct due to coagulation necrosis.

2. Pleura is congested with deposition of fibrin.

Infarct spleen:

Cause:

1. Embolism-  Example: sub-acute bacterial endocarditis.

2. Thrombosis of splenic vessels in atherosclerosis, tropical splenomegaly, polyarteritis nodosa, myeloproliferative disorder.

Gross:

1. Spleen is enlarged.

2. Area of infarction is usually pale, wedge-shaped or irregular, surrounded by a zone of congestion.

3. Infarct extends up to the surface and involves the capsule causing peri-splenitis (differs from kidney).

4. In late stage healing by fibrosis (autosplenectomy) or abscess in case of septic thrombus.

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