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Showing posts from October, 2019

Necrosis

Necrosis • Is the spectrum of morphologic changes that follow cell death in a living tissue from the progressive degradation action of the enzymes on lethally injured cell. Cells immediately placed in a fixative are dead but not necrotic. Necrosis results from 2 processes: 1. Enzymatic digestion from auto enzymes (autolysis) or from leukocyte enzymes (heterolysis) 2. Protein denaturation. • The process of necrosis needs hours to develop (heart 4-12h) but enzymes showing cardiac cell death are found in the blood as early as 2 hours after the cell’s death. Morphology of cell necrosis: ü Cytoplasm • Increase of cyt, eosinophilie due to loss of cyt, RNA, more homogeneous glassy appearance of the cyt, due to loss of glycogen, cyt, vacuoles known as moth eaten from digested organelle. • TEM – Membrane discontinuity, marked mitochondrial dilatation, amorphous density in the mitochondria, myelin figures Nuclear changes in necrosis. Ø Karyolysis (DNAase a...

Cell aging

Cell aging   is due to genetic factors, diet, social conditions, and presence of age related disease like diabetes, atherosclerosis, osteoarthritis.       There are progressive accumulations of sub lethal injuries that lead cell death or reduced capacity to respond to injury.   The cell function decline progressively with age: reduction of ATP synthesis, nucleic acids, cytoskeleton and enzyme proteins, uptake of nutrients, DNA repair. Morphology:-   Nucleus is bilobed, mitochondria vacuolated distorted GA, ER reduced in number and accumulation of lipofucsins. There are advanced glycosylation end products due to non enzymatic glycosylation which facilitate the cross linking of adjacent proteins and abnormal folding of the proteins.   The mechanism of aging centers into 2 interrelated processes: 1.   Genetic determined clock. a)     Incomplete chromosome ends (telomere shortening.) The telomere, a...

CELL INJURY

CELL INJURY Ø   Normal cell has fairly narrow range of function and structure by its genetic program, by neighboring cells and availability of metabolites but handle normal physiologic demands (homeostasis.) If excessive physiologic stress or pathologic stimuli bring a physiologic and morphologic cellular adaptation, a new but altered steady state is achieved which preserve viability and functional change. When the limit of adaptive response is exceeded or adaptation is not possible a sequence of events follow known as cell injury.   Ø   The cell injury is reversible up to certain limit but if the pathological stimuli persist or severe enough at the beginning the cell reaches the point of no return: irreversible cell injury and cell death. Causes of cell injury 1.      Oxygen deprivation- due to hypoxia (lack of oxygen) or ischemia (lack of blood supply). 2.     Physical agents. 3.     Chemical a...