Intracellular Accumulation-2 Pigments

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Presentation transcript:

Intracellular Accumulation-2 Pigments Dr Shoaib Raza

Pigments They are colored substances Endogenous Exogenous Normal constituents of the cell Melanin Abnormal and accumulate only under special circumstances Endogenous Synthesize within the body Exogenous Coming from outside of the body

Exogenous Pigments Carbon is the ubiquitous air pollutant of urban life Picked up by alveolar macrophages Through lymphatic channels to regional (Hilar) lymph nodes Causes blackening of the tissues of lung (Anthracosis) Anthracosis + fibroblastic reaction = Coal workers pneumoconiosis Tattooing is another exogenous pigment

Endogenous Pigments Lipofuscin An insoluble pigment Wear-and-tear pigment Lipochrome Polymer of lipids & phospholipids Complex with protein Derive through lipid peroxidation of polyunsaturated lipids of subcellular membrane Yellowish brown, finely granular, cytoplasmic (perinuclear) pigment Seen in cells undergoing slow regressive changes Liver & heart of aging patients

Melanin Endogenous, non hemoglobin derived brown black pigment Tyrosinase catalyzes oxidation of tyrosine in melanocytes It is the only endogenous brown black pigment Ochronosis Rare disorder seen in alkaptonuria, Black pigment deposit in skin, connective tissues, cartilage, etc.

Hemosiderin Hb-derived golden yellow to brown, granular or crystalline pigment A major storage form of iron Iron transport via transferrin Iron + apoferritin = Ferritin micelles Excess of iron Hemosiderin Local excess (Common Bruises) Heme Biliverdin Bilirubin Systemic excess (Hemosiderosis)

Hyaline Change The term usually refers to: Intracellular or intercellular alteration that gives a homogenous, glassy, pink appearance in routine H&E staining Histological term rather than a specific form of injury Intracellular accumulation of proteins Collagenous fibrous tissue in old scars Vessel wall in long standing hypertension

Pathologic Calcification Abnormal tissue deposition of calcium salts Dystrophic calcification: Deposition occur in the dead or injured tissue Necrosis, (Coagulative, liquefactive, caseous, fat) Atheroma and atherosclerosis Thrombus Aging or damaged heart valves Basophilic amorphous granular, sometimes clumped appearance Intracellular, extracellular or both Lamellated configuration = psammoma bodies

Pathogenesis of Dystrophic Calcification Ca is concentrated in the cells Ca binds to phospholipids of vesicle membrane Phosphate is added to the calcium Repeated cycle Structural change generate microvesicle of calcium and phosphate groups Dystrophic calcification is a sign of previous injury Often cause organ dysfunction

Metastatic Calcification Occur in normal tissue whenever there is hypercalcemia Hyperparathyroidism Destruction of bone tissue Primary tumor of bone Metastatic tumors to bone Increase bone turnover Immobilization Vitamin D related disorders (Vitamin D intoxication) Renal failure

Metastatic Calcification May occur widely throughout the body Interstitial tissue of gastric mucosa Kidney Lung Systemic arteries Pulmonary veins Morphology is similar to that of dystrophic calcification

Aging Result of a progressive decline in cellular function and viability caused by genetic abnormalities, & accumulation of cellular and molecular damage due to the effects of exposure to exogenous influences Genetic factors Diet Social condition Occurrence of age related disorders

Contribution to Cell Aging Known changes that contribute to cell aging Decreased cellular replication Non-dividing state of cell, the senescence Telomere shortening Accumulation of metabolic and genetic damage Cell life span is determined by a balance between oxidative damage and molecular response for repair Ionizing radiation Mitochondrial dysfunction Reduction of antioxidant defense mechanism