The document summarizes cellular adaptation and injury. It states that cells can undergo adaptation to achieve a new steady state and preserve viability when faced with physiological stresses, but severe or persistent stress can lead to reversible or irreversible injury. It describes different types of cellular adaptation like atrophy, hypertrophy, hyperplasia and metaplasia. It also discusses various causes of cellular injury like hypoxia, chemicals, infections and genetic factors. The key mechanisms of injury involve defects in membranes, ATP production and protein/DNA integrity.
This is a presentation on the topic of Adaptations, Cell injury and cell death, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
This is a presentation on the topic of Adaptations, Cell injury and cell death, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Cellular adaptations, injury and death.. Lecture 1Ashish Jawarkar
This is a series of lectures on general pathology useful for undergraduate and postgraduate pathology students. The ppts here have are enriched with explanatory pictures as well as useful video links.. hope you find them useful
Cellular adaptations, injury and death.. Lecture 1Ashish Jawarkar
This is a series of lectures on general pathology useful for undergraduate and postgraduate pathology students. The ppts here have are enriched with explanatory pictures as well as useful video links.. hope you find them useful
Cellular Adaptation
as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis.
Injury - altered homeostasis
if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs.
Reversible Cell Injury
removal of stress results in complete restoration of structural & functional integrity.
b) Irreversible Cell Injury / Cell Death
if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death.
2 main morphologic patterns: necrosis & apoptosis.
Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediators
Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy refers to an increase in the size of cells, that results in an increase in the size of the affected organ
The hypertrophied organ has no new cells, just larger cells.
Types:
a) physiologic b) pathologic
Causes:
a) increased functional demand b) hormonal stimulation
Information about how cell get injured from different stimuli. Mechanism of cellular injury. Different types of cellular injury. Different examples of cellular injury with images which makes it easy to understand.
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3. Irreversible Injury (cell death) Reversible Injury adaptation normal When cells encounter physiological stresses or pathological stimuli, they undergo adaptation, achieving a new a steady state and preserving viability. If the adaptive capacity is exceeded, cell injury develops. Within certain limits, injury is reversible. with severe and persistent stress, irreversible injury results.
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6. Incomplete occlusion of coronary artery Complete or prolonged occlusion hypertesion Prolonged starvation
101. Chemical nature of amyloid fibrils Two major forms: AL (amyloid light chain protein) AA (amyloid-associated protein): Derived from serum AA (12kd) synthesized in liver and elevated in inflammatory states.
102. Minor forms of amyloid fibrils: Transthyretin (TTR): A mutant form of a serum protein in familial amyloid polyneuropathy. A variant of TTR in aging. Beta-2-microglobulin (the component of class I MHC molecules) in long-term hemidialysis.
103. Minor forms of amyloid fibrils: Beta-2-amyloid protein forms the core of cerebral plaques and deposits within cerebral vessel walls in Alzheimer disease, deriving from a transmembrane glycoprotein precursor.
104. Minor forms of amyloid fibrils: Transthyretin (TTR): A mutant form of a serum protein in familial amyloid polyneuropathy. A variant of TTR in aging. Beta-2-microglobulin (the component of class I MHC molecules) in long-term hemidialysis.
105. Minor forms of amyloid fibrils: Beta-2-amyloid protein forms the core of cerebral plaques and deposits within cerebral vessel walls in Alzheimer disease, deriving from a transmembrane glycoprotein precursor.
171. Necrosis Apoptosis Stimuli Hypoxia Physical Toxins Pathological Histology Cell swelling Single cell Coagulation N Chromatin Disruption of condensation organelles Apoptotic bodies DNA Random Internucleosomal breakdown Diffuse
172. Necrosis Apoptosis Mechanism ATP depletion Gene activation Membrane Endonuclease injury Free radicals Tissue Inflammation No inflammation reaction Phagocytosis of apoptotic bodies
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175. Biochemical features of apoptosis 1.PROTEIN CLEAVAGE: Caspases (cysteine protease) Nuclear scaffold Cytoskeletal protein 2.PROTEIN CROSS-LINKING: Transglutaminase Cytoplasmic protein shrunken shalls apoptotic bodies Biochemical features of apoptosis
176. 3. DNA breakdown: 50-300 kb pieces Ca2+, Mg2+ dependent endonucleases DNA oligonucleosomes DNA ladders (also seen in necrosis) 4. PHAGOCYTIC RECOGNITION Receptors on macrophages for the surface components (phosphatidylserine, thrombospondin) on apoptotic bodies.
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183. normalcell Cellular swelling, chromatin cluping Membrane damage Nuclear chromatin condensation and fragmentation Cytoplasmic budding and apoptosisi body Phagocytosisi of apoptosis body The sequential ultrastructual changes in necrosis and apoptosis
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