Intracellular Accumulation
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Transcript Intracellular Accumulation
Intracellular
Accumulation-2
Pigments
Dr Shoaib Raza
Pigments
They
are colored substances
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
Renal failure
intoxication)
Metastatic Calcification
May
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
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