histopathologic tissues

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Study of Pathologic Tissues Cellular Damage and Injury

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Overview of pathologic tissues.

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Page 1: Histopathologic tissues

Study of Pathologic Tissues

Cellular Damage and Injury

Page 2: Histopathologic tissues

DEGENERATION AND INFILTRATION

• Degeneration– Injury accumulation of metabolites

• Infiltration– Accumulation of metabolites injury

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Page 4: Histopathologic tissues

Hyaline Degeneration-regressive change in cells in which the cytoplasm takes on a homogenous, glassy appearance.-the term HYALINE is used in a purely descriptive sense to characterize the physical appearance of the alteration in the cell. It is a form of protein coagulation, usually an indication of severe cell damage.

Substances responsible for producing hyaline degeneration may be classified, according to their chemical reactions and gross and microscopic appearance of tissues, into:a. Mucinb. Colloidc. Amyloidd. Glycogen

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Zenker’s Degeneration of Musculus rectus-hyaline degeneration-accumulation of lactic acid due to bacterial toxins-striations become loose

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Parenchymatous and fatty degeneration of liver

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Parenchymatous degeneration of kidney

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Hemorrhagic infarct of lung-caused by an embolus which damages the endothelium

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Hemorrhagic necrosis of the liver – usually caused by a lung problem

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Atrophy

• “wasting”• Physiologic Atrophy– Atrophy of thymus

and lymphoid tissues during puberty

– Sexual organs and brain

– Senile atrophy

• Pathologic Atrophy– Vascular– Pressure– Starvation or Hunger– Atrophy of disuse– Exhaustion atrophy– Endocrine atrophy

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Granular Atrophy of Kidney-caused by chronic interstitial disease

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Brown atrophy of the liver; accumulation of lipofucsin

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Infiltration

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Fat accumulation

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Glycogen storage disease I; Von Gierke’s; absence of G6Phosphatase

\PAS stains the cells bright orange

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Accumulation of Carbon

Anthracosis of the Lung

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Hemosiderosis of liver

Hemosiderin in Kupffer cells

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Malarial melanemia of spleen

Hemozoin crystals

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HYPERTROPHY/ HYPERPLASIA

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Normal versus Hypertrophic Prostate

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Hyperplasia of Leydig cells