Transcript Intracellular Accumulation

Intracellular
Accumulation-2
Pigments
Dr Shoaib Raza
Pigments
 They
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are colored substances
Normal constituents of the cell
 Melanin
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Abnormal and accumulate only under
special circumstances
 Endogenous
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Synthesize within the body
 Exogenous
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Coming from outside of the body
Exogenous Pigments
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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
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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
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Endogenous, non hemoglobin derived brown
black pigment
Tyrosinase catalyzes oxidation of tyrosine in
melanocytes
It is the only endogenous brown black
pigment
Ochronosis
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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)
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Hyaline Change
 The
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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
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Abnormal tissue deposition of calcium salts
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Dystrophic calcification:
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Deposition occur in the dead or injured tissue
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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
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Pathogenesis of Dystrophic
Calcification
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Ca is concentrated in the cells
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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
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Occur in normal tissue whenever there is
hypercalcemia
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Hyperparathyroidism
Destruction of bone tissue
Primary tumor of bone
 Metastatic tumors to bone
 Increase bone turnover
 Immobilization
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Vitamin D related disorders (Vitamin D
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Renal failure
intoxication)
Metastatic Calcification
 May
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occur widely throughout the body
Interstitial tissue of gastric mucosa
Kidney
Lung
Systemic arteries
Pulmonary veins
 Morphology
calcification
is similar to that of dystrophic
Aging
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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
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Genetic factors
Diet
Social condition
Occurrence of age related disorders
Contribution to Cell Aging
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Known changes that contribute to cell aging
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Decreased cellular replication
Non-dividing state of cell, the senescence
 Telomere shortening
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Accumulation of metabolic and genetic
damage
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Cell life span is determined by a balance
between oxidative damage and molecular
response for repair
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Ionizing radiation
Mitochondrial dysfunction
Reduction of antioxidant defense mechanism