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August 2008

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

Anatomical Distribution of Pulmonary Disease

Acute Respiratory Distress Syndrome

Neonatal Respiratory Distress Syndrome

Chronic Obstructive Pulmonary Disease

Bronchial Asthma

Bronchiectasis

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Pathologic accumulations of glycogen occur in the tissues of patients with diabetes mellitus in whom the normal cellular uptake of glucose is impaired.

Excessive storage of glycogen is also found in genetic diseases in which there is absence of one or another of the enzymes that constitute the Embden-Meyerhof glycolytic pathway, or when an abnormally structured glycogen that cannot be degraded by glycolytic enzymes is synthesized.

Intracellular accumulations of glycogen impart a vacuolated appearance to the cytoplasm.

Since accumulations of glycogen morphologically resemble those of water (hydropic swelling) and fat (triglyceride under the light microscope), one of the following tests is necessary to establish that the deposit is glycogen:

(1) application of the periodic acid-Schiff test in which glycogen is stained reddish purple (tissues previously digested with diastase serve as negative controls) or

(2) quantitative analysis of the glycogen content of affected tissues.

Massive intracellular deposits of glycogen occurring in glycogen storage disease cause affected organs such as the liver, kidney or heart to be greatly enlarged and their function to be ultimately compromised.

In diabetes mellitus, glycogen deposits are encountered in epithelium of the distal segment of the proximal convoluted renal tubules and the descending loop of Henle, hepaocytes, beta cells of pancreatic islets, and cardiac muscle. Accumulation in the kidney occurs when the degree of glycosuria leads to levels of glucose in the glomerular filtrate that exceed the rate at which glucose is reabsorbed by epithelial cells of the renal tubules (tubular mass).

Excessive intracellular deposits of glycogen lipids, glycolipids, mucolipids, and mucopolysaccharides develop in patients with genetic disorders characterized by lysosomes with specific enzyme deficiencies that render them incapable of hydrolyzing them.

Abnormal metabolites accumulate in neurons of the centrals nervous system, as well as parenchymal cells of the liver, kidney, and heart, and cells of the reticuloendothelial system such that massive enlargement of the spleen and to a lesser degree the lymph nodes and liver occurs.

As in the other storage diseases attributable to gene defects, involvement may become so severe that it is incompatible with life. These and similar diseases are considered in greater detail in a subsequent section dealing with inborn errors of metabolism.

                  

 

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Introduction of Pathology

An outline of Diagnostic Techniques available in Pathology

Cellular Injury

Diagram showing Structural Changes in Reversible and Irreversible Cell Injury

Autolysis

Heterolysis

Necrosis

Coagulation  necrosis

Caseative necrosis

Liquefaction necrosis

Fat necrosis

Fibrinoid necrosis

Apoptosis

Gangrene

Pathologic Calcification

Hyaline Change

Atrophy

Hypertrophy

Hyperplasia

Metaplasia

Aplasia

Hypoplasia

Circulatory Anatomy, Physiology and Regulation


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