This document discusses cell injury and pathology. It begins by defining pathology and noting that Rudolf Virchow is considered the father of modern pathology. It then discusses various types of cell injury including reversible and irreversible injury. The main causes of cell injury are genetic factors and acquired factors such as hypoxia/ischemia, physical agents, chemicals/drugs, microbes, immunological factors, nutritional imbalances, and psychological stress. The document explores the pathogenesis of cell injury in detail for different causes. It notes that free radicals also play an important role in several types of cell injury processes.
This document discusses the etiology of cell injury, which can be genetic or acquired. Genetic causes include developmental defects, cytogenetic abnormalities like aneuploidy and structural defects, and single gene defects. Acquired causes include hypoxia, physical agents, chemicals/drugs, microbial agents, immunological factors, nutritional imbalances, aging, psychogenic factors, iatrogenic causes, and idiopathic diseases of unknown etiology. Specific examples are provided for each category of genetic and acquired causes of cell injury.
Covid -19 informations you have to knowfathi neana
With Corona worldwide pandemic the people who exposed to the virus show different reactions some did not catch the virus and among those who catch the virus most of them did not show any symptoms or mild unnoticeable symptoms but some of them show sever manifestations and are killed by this virulent virus. Luckily enough this last group are the minority. The question is not why some people is affected by the virus but th question should be why most of the people are not affected or even those who are affected can defeat the virus and escape its fatal outcome?. To answer this question we have to know some basic facts.
This document discusses the etiology and causes of cell injury, which can be genetic or acquired. Genetic causes include developmental defects, chromosomal abnormalities like aneuploidy and structural defects. Acquired causes include hypoxia, physical agents, chemicals/drugs, microbial agents, immunological reactions, nutritional imbalances, aging, psychogenic factors, iatrogenic medical errors, and some idiopathic diseases of unknown cause. Overall, the document provides a comprehensive overview of the various genetic and acquired factors that can lead to cell injury.
This document discusses cell injury, including its definition, types, causes, and pathogenesis. It defines cell injury as a change that occurs in a cell due to external or internal factors in its environment. There are two types of cell injury - reversible and irreversible. Reversible injury is when the cell is damaged but viable, while irreversible injury means the cell is nonviable. Common causes of cell injury include hypoxia, chemicals, infections, physical factors, and genetic factors. The pathogenesis of cell injury involves mitochondrial damage, disturbances in calcium metabolism, damage to cellular membranes, DNA and proteins. Reversible injury can progress to irreversible injury when ATP production ceases, cell membranes lyse, vital proteins are absent, and vital
This document discusses cell injury, cellular adaptations, and cellular aging. It covers various causes of cell injury including hypoxia, physical agents, chemicals, microbes, immunologic factors, nutritional imbalances, and aging. It describes the pathogenesis of injury from these various sources and the cellular responses, which can be reversible or irreversible. Reversible changes include hydropic swelling, hyaline changes, mucoid changes, and fatty changes. The document outlines various morphologic features of reversible cell injury and discusses cellular adaptations like stress protein production in response to injury.
Cell injury – cell injury and cell deathaanchal puri
Most forms of disease begin with cell injury and loss of function. Cell injury is defined as stresses that disrupt a cell's internal and external environment. The response to injury depends on the cell/tissue type, extent, and type of injury.
Cells are classified by proliferative potential as labile, stable, or permanent. Labile cells continuously divide with a short lifespan in skin and gastrointestinal epithelia. Stable cells undergo limited postnatal division and can regenerate injured tissues like liver and kidney. Permanent cells cannot divide postnatally, like neurons, and cannot regenerate once destroyed. Prolonged hypoxia can lead to irreversible cell injury characterized by mitochondrial and membrane damage, ultimately resulting in cell death
This document discusses cellular injury. It defines cell injury as changes to a cell's internal and external environment caused by various stresses from etiological agents. Short term, mild stresses can lead to reversible cell injury through adaptations, while long term, severe stresses can cause irreversible injury and cell death. Reversible injury involves things like decreased ATP and protein synthesis, while irreversible injury includes nuclear damage, lysosomal enzyme release, and cell digestion. The document outlines various causes of cell injury and the morphological changes seen in reversible versus irreversible injury states.
This document summarizes causes and mechanisms of reversible and irreversible cell injury. It discusses how cells attempt to adapt to stressors but can experience reversible or irreversible injury depending on severity and duration of the stressor. Hypoxia is a major cause of cell injury, initially resulting in reversible changes like swelling as ATP is depleted, but leading to irreversible injury if hypoxia persists due to damage to cell membranes and mitochondria. The four main systems vulnerable to injury are the cell membrane, mitochondria, Golgi apparatus, and nucleus.
This document discusses the etiology of cell injury, which can be genetic or acquired. Genetic causes include developmental defects, cytogenetic abnormalities like aneuploidy and structural defects, and single gene defects. Acquired causes include hypoxia, physical agents, chemicals/drugs, microbial agents, immunological factors, nutritional imbalances, aging, psychogenic factors, iatrogenic causes, and idiopathic diseases of unknown etiology. Specific examples are provided for each category of genetic and acquired causes of cell injury.
Covid -19 informations you have to knowfathi neana
With Corona worldwide pandemic the people who exposed to the virus show different reactions some did not catch the virus and among those who catch the virus most of them did not show any symptoms or mild unnoticeable symptoms but some of them show sever manifestations and are killed by this virulent virus. Luckily enough this last group are the minority. The question is not why some people is affected by the virus but th question should be why most of the people are not affected or even those who are affected can defeat the virus and escape its fatal outcome?. To answer this question we have to know some basic facts.
This document discusses the etiology and causes of cell injury, which can be genetic or acquired. Genetic causes include developmental defects, chromosomal abnormalities like aneuploidy and structural defects. Acquired causes include hypoxia, physical agents, chemicals/drugs, microbial agents, immunological reactions, nutritional imbalances, aging, psychogenic factors, iatrogenic medical errors, and some idiopathic diseases of unknown cause. Overall, the document provides a comprehensive overview of the various genetic and acquired factors that can lead to cell injury.
This document discusses cell injury, including its definition, types, causes, and pathogenesis. It defines cell injury as a change that occurs in a cell due to external or internal factors in its environment. There are two types of cell injury - reversible and irreversible. Reversible injury is when the cell is damaged but viable, while irreversible injury means the cell is nonviable. Common causes of cell injury include hypoxia, chemicals, infections, physical factors, and genetic factors. The pathogenesis of cell injury involves mitochondrial damage, disturbances in calcium metabolism, damage to cellular membranes, DNA and proteins. Reversible injury can progress to irreversible injury when ATP production ceases, cell membranes lyse, vital proteins are absent, and vital
This document discusses cell injury, cellular adaptations, and cellular aging. It covers various causes of cell injury including hypoxia, physical agents, chemicals, microbes, immunologic factors, nutritional imbalances, and aging. It describes the pathogenesis of injury from these various sources and the cellular responses, which can be reversible or irreversible. Reversible changes include hydropic swelling, hyaline changes, mucoid changes, and fatty changes. The document outlines various morphologic features of reversible cell injury and discusses cellular adaptations like stress protein production in response to injury.
Cell injury – cell injury and cell deathaanchal puri
Most forms of disease begin with cell injury and loss of function. Cell injury is defined as stresses that disrupt a cell's internal and external environment. The response to injury depends on the cell/tissue type, extent, and type of injury.
Cells are classified by proliferative potential as labile, stable, or permanent. Labile cells continuously divide with a short lifespan in skin and gastrointestinal epithelia. Stable cells undergo limited postnatal division and can regenerate injured tissues like liver and kidney. Permanent cells cannot divide postnatally, like neurons, and cannot regenerate once destroyed. Prolonged hypoxia can lead to irreversible cell injury characterized by mitochondrial and membrane damage, ultimately resulting in cell death
This document discusses cellular injury. It defines cell injury as changes to a cell's internal and external environment caused by various stresses from etiological agents. Short term, mild stresses can lead to reversible cell injury through adaptations, while long term, severe stresses can cause irreversible injury and cell death. Reversible injury involves things like decreased ATP and protein synthesis, while irreversible injury includes nuclear damage, lysosomal enzyme release, and cell digestion. The document outlines various causes of cell injury and the morphological changes seen in reversible versus irreversible injury states.
This document summarizes causes and mechanisms of reversible and irreversible cell injury. It discusses how cells attempt to adapt to stressors but can experience reversible or irreversible injury depending on severity and duration of the stressor. Hypoxia is a major cause of cell injury, initially resulting in reversible changes like swelling as ATP is depleted, but leading to irreversible injury if hypoxia persists due to damage to cell membranes and mitochondria. The four main systems vulnerable to injury are the cell membrane, mitochondria, Golgi apparatus, and nucleus.
This document discusses cell injury and homeostasis. It defines cell injury as occurring when adaptive responses are exceeded or the cell is exposed to an injurious stimulus. There are two types of cell injury: reversible and irreversible. Free radicals can cause cell injury by reacting with lipids, DNA and proteins. Free radicals are generated through normal metabolic processes, radiation exposure, and chemical metabolism, and can be neutralized by antioxidants. Increased calcium levels and decreased ATP can also occur during cell injury.
This document provides an overview of cellular injury and cell death. It discusses the concepts of pathology, adaptation through hypertrophy, atrophy, hyperplasia and metaplasia. Cell injury occurs when stress exceeds a cell's adaptive capacity and can result from hypoxia, toxins, infections or genetic factors. Mitochondrial dysfunction reduces ATP and causes cell swelling. Reversible injuries include cloudy swelling and fatty change. Irreversible injuries include necrosis, which involves membrane rupture and organelle damage, and apoptosis, which is programmed single-cell death. Necrosis causes inflammation while apoptosis does not. The document also covers pathologic calcification and its dystrophic and metastatic forms.
Cell injury can occur through a variety of mechanisms and may be either reversible or irreversible. The key targets of injury are the plasma and mitochondrial membranes. Early injury is often reversible through restoration of oxygen and nutrients, but prolonged injury can lead to a "point of no return" characterized by a drop in pH, rise in calcium, and cell death through necrosis or apoptosis. A variety of factors can cause cell injury, ranging from physical trauma to genetic defects to chemical or microbial agents.
1. Reversible cell injury involves mild damage that is reversible if the stimulus is removed and causes changes like swelling, fatty changes, and pigment accumulation.
2. Irreversible injury leads to cell death through apoptosis or necrosis. Apoptosis is programmed cell death without inflammation while necrosis is unregulated cell death that triggers inflammation.
3. The document describes the patterns of cellular changes seen in reversible injury including swelling, fatty changes, and pigment accumulation as well as the differences between apoptosis and necrosis.
Basic principles of Cell injury and AdaptationAkshayYadav176
Basic principles of Cell injury and Adaptation:
(As per new syllabus of PCI)
Introduction, definitions, Homeostasis, Components and Types of Feedback systems, Causes of cellular injury,Pathogenesis (Cell membrane damage, Mitochondrial damage, Ribosome damage, Nuclear damage),Morphology of cell injury – Adaptive changes (Atrophy, Hypertrophy, hyperplasia, Metaplasia, Dysplasia),Cell swelling, Intra cellular accumulation, Calcification, Enzyme leakage and Cell Death Acidosis & Alkalosis,Electrolyte imbalance.
Cell injury can be caused by a variety of factors that disrupt homeostasis, including oxygen deprivation, chemicals, infectious agents, immunological reactions, genetic defects, nutritional imbalances, physical trauma, and aging. Specifically, the document outlines how hypoxia, chemicals, viruses, bacteria, fungi, protozoa, autoimmune reactions, genetic mutations, vitamin deficiencies, physical trauma like temperature extremes, and cellular senescence can all damage cells through various biochemical mechanisms.
This document is an undergraduate thesis that examines the effects of ethanol-induced oxidative stress on antioxidant enzyme expression levels in three tissues of the zebrafish Danio rerio. The student measured expression levels of the antioxidant enzymes CuZnSOD, MnSOD, and CAT in the brain, liver, and gonads of zebrafish after acute ethanol exposure. The results showed that different tissues exhibited distinct expression patterns, with the highest levels found in gonad tissue and no significant changes in brain tissue. The study provides insight into how antioxidant enzymes may protect against oxidative DNA damage caused by excess reactive oxygen species produced during ethanol metabolism.
Mitochondria are organelles found in cells that are involved in biochemical processes like respiration and energy production. Mitochondrial dysfunction increases during aging and age-related disorders. The crosstalk between mitochondrial biogenesis, which generates new mitochondria, and mitophagy, which eliminates damaged mitochondria, is important for maintaining mitochondrial health and cellular homeostasis in response to physiological and environmental cues. Exercise can stimulate mitochondrial biogenesis and mitophagy through activation of AMPK signaling pathways, and may help treat various diseases by modulating mitochondrial dynamics proteins.
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
Cell injury occurs when stresses exceed a cell's adaptive capacity. Reversible injury involves loss of function but not death, while irreversible injury leads to cell death. The key mechanisms of injury include ATP depletion, oxidative stress from free radicals, loss of calcium homeostasis, and mitochondrial and genetic damage. Morphological changes range from swelling in reversible injury to lysosomal rupture and inflammation in irreversible injury and death.
Cell injury causes and overview of cell injury and cell death lect 4 jan 2020DrAbdulAzizShaikh
Cell injury occurs when cells are stressed beyond their ability to adapt or are exposed to damaging agents. Injury can progress from a reversible to an irreversible stage, ultimately leading to cell death. The hallmarks of reversible injury include reduced ATP production, cellular swelling, and alterations to organelles. With continued damage, injury becomes irreversible and the cell dies through necrosis or apoptosis. Hypoxia is the most common cause of cell injury, as it reduces aerobic respiration. Other causes include physical and chemical agents, infections, immunological reactions, genetic factors, and nutritional imbalances.
Pathology is the study of diseases through identifying changes in tissues and cells. It examines the patterns, causes, mechanisms, and effects of diseases. Pathology bridges clinical practice and basic science. Cell injury can result from physical, chemical, infectious, or environmental factors and causes damage through mechanisms like ATP depletion, oxygen deprivation, calcium dysregulation, and mitochondrial dysfunction. Cells respond to injury through reversible or irreversible changes, repair, or death by necrosis or apoptosis.
This document discusses metals in medicine and their importance in biological systems. It covers topics such as medicinal bioinorganic chemistry, classification of metal elements, the role of metal ions in critical biological functions, and examples of metal deficiencies that can lead to disease. The document also addresses how some metals can be toxic in excess and cause conditions like Wilson's disease from copper overload or hemochromatosis from iron poisoning. Finally, it mentions how some metals like plutonium, mercury, and others are used for diagnosis and treatment of diseases.
Role of antioxidants in neurologic diseasesNeurologyKota
This document discusses oxidative stress and various neurological conditions where free radicals may play a role, such as Alzheimer's disease, Parkinson's disease, and stroke. It then summarizes several antioxidants that have been studied for treating these conditions, including vitamin E, tirilazad, ebselen, coenzyme Q10, idebenone, and combinations of antioxidants for ALS and mitochondrial diseases. While some studies showed benefits, the evidence is limited and more research is still needed on dosing schedules. Cocktail antioxidant regimes may not be cost-effective options.
Cell injury can be reversible or irreversible depending on the severity and duration of the stress. Reversible cell injury involves changes like swelling that can be repaired when the stress is removed, while irreversible injury leads to cell death. Causes of cell injury include hypoxia, radiation, toxins and free radicals. Cells have adaptations like atrophy, hypertrophy, hyperplasia and metaplasia in response to stresses. Neoplasms are abnormal masses of tissue that are benign (non-cancerous) or malignant (cancerous).
Cellular adaptation
Adjustments which the cells make in response to stresses.
Adjustments may be for physiologic need or response to non-lethal pathogenic injury (Pathologic adaptation).
Adaptive responses are reversible on withdrawal of stimulus.
If the irritant stimulus persists for longer duration or is more lethal, the cell may not be able to survive.
“Survival of the Adaptable”
TYPES OF CELLULAR ADAPTATION:
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
The document discusses cellular structure and function. It describes that cells are the basic living units of the body, with each organ composed of many different cell types. The two main types of fluid in the body are intracellular fluid within cells and extracellular fluid outside cells, which provides nutrients to cells. A normal cell maintains homeostasis through adaptations like atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia in response to stress or increased demand. The main mechanisms of cellular injury are free radical injury, which damages lipids, proteins and DNA, and hypoxic injury caused by lack of oxygen leading to energy depletion and calcium overload within cells.
This document discusses cellular injury and adaptation. It notes that cells exist in a state of homeostasis but can become injured by various stressors like hypoxia or toxins. Injuries can be reversible or irreversible. Initial injuries disrupt ATP production and increase intracellular calcium levels, activating damaging enzymes. This can lead to further damage of mitochondria and lysosomes as well as increased reactive oxygen species. Depending on the severity and duration of injury, cells may undergo apoptosis, necrosis, or adaptational changes in an attempt to survive.
Oxidative Stress in Aging and Human Diseases - Exploring the MechanismsQIAGEN
Many modern diseases, including cancer, cardiovascular disease, diabetes, liver disease, arthritis and neurodegenerative disease are related to aging, and aging is closely linked to oxidative stress. Intensive research is being conducted to understand the antioxidant defense mechanism, the mechanisms of aging itself, as well as their roles in human diseases. This slidedeck provides an update on how oxidative stress is linked to aging and how inflammation leads to aging through DNA damage, telomere dysfunction, cellular senescence and oxidative stress. Recent progress on the health benefits of antioxidants and examination of their potential mechanisms in the prevention and treatment of chronic diseases are also covered. Various assay technologies to tackle the complex signaling pathways in this process will be introduced. Learn how you can apply these advanced tools to your research!
La Unión Europea ha acordado un paquete de sanciones contra Rusia por su invasión de Ucrania. Las sanciones incluyen restricciones a las transacciones con bancos rusos clave y la prohibición de la venta de aviones y equipos a Rusia. Los líderes de la UE esperan que las sanciones aumenten la presión económica sobre Rusia y la disuadan de continuar su agresión contra Ucrania.
This document discusses cell injury and homeostasis. It defines cell injury as occurring when adaptive responses are exceeded or the cell is exposed to an injurious stimulus. There are two types of cell injury: reversible and irreversible. Free radicals can cause cell injury by reacting with lipids, DNA and proteins. Free radicals are generated through normal metabolic processes, radiation exposure, and chemical metabolism, and can be neutralized by antioxidants. Increased calcium levels and decreased ATP can also occur during cell injury.
This document provides an overview of cellular injury and cell death. It discusses the concepts of pathology, adaptation through hypertrophy, atrophy, hyperplasia and metaplasia. Cell injury occurs when stress exceeds a cell's adaptive capacity and can result from hypoxia, toxins, infections or genetic factors. Mitochondrial dysfunction reduces ATP and causes cell swelling. Reversible injuries include cloudy swelling and fatty change. Irreversible injuries include necrosis, which involves membrane rupture and organelle damage, and apoptosis, which is programmed single-cell death. Necrosis causes inflammation while apoptosis does not. The document also covers pathologic calcification and its dystrophic and metastatic forms.
Cell injury can occur through a variety of mechanisms and may be either reversible or irreversible. The key targets of injury are the plasma and mitochondrial membranes. Early injury is often reversible through restoration of oxygen and nutrients, but prolonged injury can lead to a "point of no return" characterized by a drop in pH, rise in calcium, and cell death through necrosis or apoptosis. A variety of factors can cause cell injury, ranging from physical trauma to genetic defects to chemical or microbial agents.
1. Reversible cell injury involves mild damage that is reversible if the stimulus is removed and causes changes like swelling, fatty changes, and pigment accumulation.
2. Irreversible injury leads to cell death through apoptosis or necrosis. Apoptosis is programmed cell death without inflammation while necrosis is unregulated cell death that triggers inflammation.
3. The document describes the patterns of cellular changes seen in reversible injury including swelling, fatty changes, and pigment accumulation as well as the differences between apoptosis and necrosis.
Basic principles of Cell injury and AdaptationAkshayYadav176
Basic principles of Cell injury and Adaptation:
(As per new syllabus of PCI)
Introduction, definitions, Homeostasis, Components and Types of Feedback systems, Causes of cellular injury,Pathogenesis (Cell membrane damage, Mitochondrial damage, Ribosome damage, Nuclear damage),Morphology of cell injury – Adaptive changes (Atrophy, Hypertrophy, hyperplasia, Metaplasia, Dysplasia),Cell swelling, Intra cellular accumulation, Calcification, Enzyme leakage and Cell Death Acidosis & Alkalosis,Electrolyte imbalance.
Cell injury can be caused by a variety of factors that disrupt homeostasis, including oxygen deprivation, chemicals, infectious agents, immunological reactions, genetic defects, nutritional imbalances, physical trauma, and aging. Specifically, the document outlines how hypoxia, chemicals, viruses, bacteria, fungi, protozoa, autoimmune reactions, genetic mutations, vitamin deficiencies, physical trauma like temperature extremes, and cellular senescence can all damage cells through various biochemical mechanisms.
This document is an undergraduate thesis that examines the effects of ethanol-induced oxidative stress on antioxidant enzyme expression levels in three tissues of the zebrafish Danio rerio. The student measured expression levels of the antioxidant enzymes CuZnSOD, MnSOD, and CAT in the brain, liver, and gonads of zebrafish after acute ethanol exposure. The results showed that different tissues exhibited distinct expression patterns, with the highest levels found in gonad tissue and no significant changes in brain tissue. The study provides insight into how antioxidant enzymes may protect against oxidative DNA damage caused by excess reactive oxygen species produced during ethanol metabolism.
Mitochondria are organelles found in cells that are involved in biochemical processes like respiration and energy production. Mitochondrial dysfunction increases during aging and age-related disorders. The crosstalk between mitochondrial biogenesis, which generates new mitochondria, and mitophagy, which eliminates damaged mitochondria, is important for maintaining mitochondrial health and cellular homeostasis in response to physiological and environmental cues. Exercise can stimulate mitochondrial biogenesis and mitophagy through activation of AMPK signaling pathways, and may help treat various diseases by modulating mitochondrial dynamics proteins.
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
Cell injury occurs when stresses exceed a cell's adaptive capacity. Reversible injury involves loss of function but not death, while irreversible injury leads to cell death. The key mechanisms of injury include ATP depletion, oxidative stress from free radicals, loss of calcium homeostasis, and mitochondrial and genetic damage. Morphological changes range from swelling in reversible injury to lysosomal rupture and inflammation in irreversible injury and death.
Cell injury causes and overview of cell injury and cell death lect 4 jan 2020DrAbdulAzizShaikh
Cell injury occurs when cells are stressed beyond their ability to adapt or are exposed to damaging agents. Injury can progress from a reversible to an irreversible stage, ultimately leading to cell death. The hallmarks of reversible injury include reduced ATP production, cellular swelling, and alterations to organelles. With continued damage, injury becomes irreversible and the cell dies through necrosis or apoptosis. Hypoxia is the most common cause of cell injury, as it reduces aerobic respiration. Other causes include physical and chemical agents, infections, immunological reactions, genetic factors, and nutritional imbalances.
Pathology is the study of diseases through identifying changes in tissues and cells. It examines the patterns, causes, mechanisms, and effects of diseases. Pathology bridges clinical practice and basic science. Cell injury can result from physical, chemical, infectious, or environmental factors and causes damage through mechanisms like ATP depletion, oxygen deprivation, calcium dysregulation, and mitochondrial dysfunction. Cells respond to injury through reversible or irreversible changes, repair, or death by necrosis or apoptosis.
This document discusses metals in medicine and their importance in biological systems. It covers topics such as medicinal bioinorganic chemistry, classification of metal elements, the role of metal ions in critical biological functions, and examples of metal deficiencies that can lead to disease. The document also addresses how some metals can be toxic in excess and cause conditions like Wilson's disease from copper overload or hemochromatosis from iron poisoning. Finally, it mentions how some metals like plutonium, mercury, and others are used for diagnosis and treatment of diseases.
Role of antioxidants in neurologic diseasesNeurologyKota
This document discusses oxidative stress and various neurological conditions where free radicals may play a role, such as Alzheimer's disease, Parkinson's disease, and stroke. It then summarizes several antioxidants that have been studied for treating these conditions, including vitamin E, tirilazad, ebselen, coenzyme Q10, idebenone, and combinations of antioxidants for ALS and mitochondrial diseases. While some studies showed benefits, the evidence is limited and more research is still needed on dosing schedules. Cocktail antioxidant regimes may not be cost-effective options.
Cell injury can be reversible or irreversible depending on the severity and duration of the stress. Reversible cell injury involves changes like swelling that can be repaired when the stress is removed, while irreversible injury leads to cell death. Causes of cell injury include hypoxia, radiation, toxins and free radicals. Cells have adaptations like atrophy, hypertrophy, hyperplasia and metaplasia in response to stresses. Neoplasms are abnormal masses of tissue that are benign (non-cancerous) or malignant (cancerous).
Cellular adaptation
Adjustments which the cells make in response to stresses.
Adjustments may be for physiologic need or response to non-lethal pathogenic injury (Pathologic adaptation).
Adaptive responses are reversible on withdrawal of stimulus.
If the irritant stimulus persists for longer duration or is more lethal, the cell may not be able to survive.
“Survival of the Adaptable”
TYPES OF CELLULAR ADAPTATION:
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
The document discusses cellular structure and function. It describes that cells are the basic living units of the body, with each organ composed of many different cell types. The two main types of fluid in the body are intracellular fluid within cells and extracellular fluid outside cells, which provides nutrients to cells. A normal cell maintains homeostasis through adaptations like atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia in response to stress or increased demand. The main mechanisms of cellular injury are free radical injury, which damages lipids, proteins and DNA, and hypoxic injury caused by lack of oxygen leading to energy depletion and calcium overload within cells.
This document discusses cellular injury and adaptation. It notes that cells exist in a state of homeostasis but can become injured by various stressors like hypoxia or toxins. Injuries can be reversible or irreversible. Initial injuries disrupt ATP production and increase intracellular calcium levels, activating damaging enzymes. This can lead to further damage of mitochondria and lysosomes as well as increased reactive oxygen species. Depending on the severity and duration of injury, cells may undergo apoptosis, necrosis, or adaptational changes in an attempt to survive.
Oxidative Stress in Aging and Human Diseases - Exploring the MechanismsQIAGEN
Many modern diseases, including cancer, cardiovascular disease, diabetes, liver disease, arthritis and neurodegenerative disease are related to aging, and aging is closely linked to oxidative stress. Intensive research is being conducted to understand the antioxidant defense mechanism, the mechanisms of aging itself, as well as their roles in human diseases. This slidedeck provides an update on how oxidative stress is linked to aging and how inflammation leads to aging through DNA damage, telomere dysfunction, cellular senescence and oxidative stress. Recent progress on the health benefits of antioxidants and examination of their potential mechanisms in the prevention and treatment of chronic diseases are also covered. Various assay technologies to tackle the complex signaling pathways in this process will be introduced. Learn how you can apply these advanced tools to your research!
La Unión Europea ha acordado un paquete de sanciones contra Rusia por su invasión de Ucrania. Las sanciones incluyen restricciones a las transacciones con bancos rusos clave y la prohibición de la venta de aviones y equipos a Rusia. Los líderes de la UE esperan que las sanciones aumenten la presión económica sobre Rusia y la disuadan de continuar su agresión contra Ucrania.
The document provides definitions and explanations of key genetics vocabulary terms like genes, alleles, dominant, recessive, genotypes, phenotypes, Punnett squares, and more. It discusses Gregor Mendel's pioneering experiments with pea plants that laid the foundations of modern genetics, including his conclusions that heredity factors are inherited individually as discrete units (genes) and that some gene forms may be dominant over others. Sample genetics problems applying these concepts to hypothetical crosses are also included.
The document summarizes the planning and production process for a graphic narrative book for children. Key points include:
- Flat plans were used as templates to layout scenes before adding details. Text placement was also planned.
- Characters were created using rotoscoping photos to make them simple shapes that are still recognizable. Backgrounds used gradients and textures.
- Text is placed clearly to be readable by young audiences. Speech bubbles identify the speaking character.
- The style aims to appeal to both children and adults interested in cars through simple, realistic graphics without being overly cartoon-like.
- Future improvements would fill empty white space and complete more pages to meet deadlines.
This document lists the attendance percentages for classes at Layton Primary School from November 23rd to 27th. Year 6 class 6R had the highest attendance at 99.2% while Foundation class FW had the lowest at 90.3%. Overall attendance was highest in upper school year groups with Year 5, Year 6 and Year 3 classes having the highest percentages.
El documento trata sobre fuentes de alimentación y describe sus dos tipos principales: fuentes conmutadas y fuentes reguladas. Explica los componentes básicos de una fuente convencional como el transformador, rectificador y filtro, y cómo convierten la tensión alterna de la red eléctrica en una tensión continua para alimentar dispositivos electrónicos. También enumera y define los diferentes tipos de configuraciones para fuentes conmutadas y reguladas, así como sus ventajas y usos comunes.
The proposal outlines adapting the classic story of "The Tortoise and the Hare" by replacing the characters with cars. Specifically, a Land Rover and a Bentley vehicle. The story would follow a similar plot, but end with the Bentley crashing due to rushing, and the Land Rover towing it to finish. The strengths identified are that it is a well-researched adaptation of a popular story. Areas for improvement include providing more character to the vehicle characters.
The idea generation includes mood boards outlining the adapted story concept. The clear outline of the story is identified as a strength. Developing more detail in the mind maps and story elements is suggested to further strengthen the idea generation process.
The document discusses the author's children's story and compares it to other linear and non-linear narratives. The author's story is linear, with a clear beginning, middle, and end that follows Barry and Lenny in a race through the desert. In contrast, Deadpool uses flashbacks to provide backstory and help audiences understand the plot. The author's story also has a single narrative thread, closed ending, and is meant for children, while shows like Coronation Street have multiple ongoing storylines.
This document provides instructions for an activity comparing renewable and non-renewable energy sources. Students will create an interactive notebook with sections defining key terms like energy, renewable energy, and non-renewable energy. They will then research and identify different types of renewable and non-renewable energy sources, including watching explanatory videos. Groups will read articles on the topics and answer questions to present their findings to the class. Websites are provided for additional research information.
New Age Cleaning Solutions, Kolkata, Cleaning Machine and Garden Equipmentindiamartsupplier
We bring to our clients a range of super grade Cleaning Machines and Gardening Equipment which eases the task of clean the garden and therefore we have been involved in the manufacturing, supplying, trading and wholesaling of these products. Our product range comprises of Professional Vacuum Cleaner, Single Disc Machine and Auto Scrubber Drier Floor Cleaners. Being used widely in hotels, hospitals, club and other places, we are capable of meeting the demand.
INDIAN ECONOMY- ECONOMIC GROWTH.
ECONOMIC DEVELOPMENT.
ECONOMIC GROWTH VS ECONOMIC DEVELOPMENT
INDICATORS OF ECONOMIC GROWTH
INDICATORS OF ECONOMIC DEVELOPMENT
FACTORS IN ECONOMIC DEVELOPMENT
Record-keeping and Budgeting Workbook for Organic Crop Producers (draft version)ElisaMendelsohn
This document provides templates and guidance for organic crop producers to keep records required for organic certification. It includes forms for recording farming activities and practices, inputs, harvests and sales, monitoring practices, and documentation to prevent commingling and contamination. The forms are designed to help producers meet organic certification requirements while also improving farm management and developing budgets. Producers are encouraged to modify the forms to best suit their individual operations. Keeping thorough and organized records supports both organic compliance and business planning.
Dokumen ini membahas tentang pelestarian hewan dan tumbuhan yang terancam punah di Indonesia, seperti orangutan, komodo, anoa, harimau sumatra, burung-burung langka, serta tumbuhan langka seperti raflesia dan amorphophallus. Hewan dan tumbuhan tersebut dilestarikan secara in situ di taman nasional dan ex situ di kebun binatang. Dokumen ini juga berisi diagram perbandingan jenis hewan dan tumbuhan yang terancam punah.
This document provides information on various manual cleaning equipment for floors, glass, and restrooms. It lists products like dry mops, wet mops, mop buckets, wringer trolleys, microfiber cloths, dust pans, brooms, and garbage bins along with product codes, descriptions, images, quantities, and prices. The equipment is intended to manually clean floors, glass, and restroom areas and includes options for dry sweeping, wet mopping, dusting, and waste collection.
This document discusses different types of letter writing. It describes business letters, which are used for professional correspondence between organizations or businesses, and personal letters, which are more informal and used for personal correspondence. The document outlines the typical format and style of business letters, including full block and semi-block formats, and notes that personal letters can take various formats and a more casual tone.
This document provides information to farmers about new markets for selling their crops beyond local farmers' markets. It discusses opportunities to sell to local institutions like schools, hospitals, and colleges, and the advantages and disadvantages of cooperative marketing through a nonprofit organization. Key details include requirements for consistent quality, quantity, and delivery from buyers; lower typical prices from institutions of 30-40% less than retail; and the benefits of combining resources and volumes through cooperation between multiple farms.
Pathology is the study of disease through examination of organs, tissues, fluids, and sometimes whole bodies. It involves studying the causes, mechanisms, structural changes, and clinical implications of disease. The main goals are to determine etiology, pathogenesis, morphological changes, and clinical significance. Cellular changes in disease include adaptation, reversible injury like hydropic and fatty change, and irreversible injury leading to necrosis or apoptosis. Necrosis can be coagulative, liquefactive, caseous, or gangrenous. Adaptive changes include atrophy, hypoplasia, hyperplasia, hypertrophy, and metaplasia.
Pathology is the study of disease through examination of organs, tissues, fluids, and whole bodies. It involves studying the cause, development, structural changes, and clinical significance of disease. When cells are injured, they may adapt, undergo reversible injury, or irreversible injury and death through necrosis or apoptosis. Necrosis results in cell contents spilling out while apoptosis is programmed cell death. At the cellular level, injury can be caused by lack of oxygen, toxins, radiation, and more. Cells attempt to adapt through changes in size, number, or type to cope with stressors.
The document discusses cell injury and its causes. It defines cell injury as damage to cells from changes in their internal or external environment. There are two main types of causes of cell injury - genetic and acquired. Acquired causes are more common and include hypoxia/ischemia, physical agents, chemicals/drugs, microbes, immunological factors, nutritional imbalances, aging, and psychological stress. The severity and reversibility of cell injury depends on factors like the injurious agent, duration of exposure, cell type, and underlying intracellular changes. Reversible cell injury from short-term hypoxia/ischemia involves decreased ATP production, lactic acidosis, and damage to membrane pumps causing swelling.
1. Cell injury refers to changes in a cell's internal and external environment due to stresses like lack of oxygen, toxins, or infections.
2. Causes of cell injury include hypoxia, physical and chemical agents, microbes, immunological reactions, nutritional imbalances, and genetic factors.
3. Cellular responses to injury include reversible changes like fatty change and swelling, or irreversible cell death through necrosis or apoptosis. Adaptive changes like hypertrophy and hyperplasia can also occur.
Pathophysiology Unit-I. Power PresentationSumedhGhodke
Mr. Chavan S.V. discusses pathophysiology and the causes, mechanisms, and consequences of cell injury. There are four main aspects of a disease process: (1) its cause, (2) how it develops, (3) structural changes to cells and organs, and (4) functional impacts. Cell injury can result from various genetic and acquired factors like hypoxia, toxins, microbes, and nutritional imbalances. Disruption of homeostasis through depletion of ATP, cell membrane damage, mitochondrial damage, and other processes can lead to reversible or irreversible cell injury and cell death. Understanding the pathogenesis or sequence of events from initial cause to ultimate disease expression is important in pathology.
Cell Injury in hindi
Cell injury is defined as the functional and morphologic effects of a variety of stresses on the cell from various etiologic agents which result in change in its internal and external environment.
The term cell injury is used to indicate a state in which the capacity for physiological adaptation is exceeded.
This may occur when the stimulus is excessive or when the cell is no longer capable to adapt without suffering some form of damage.
Cellular response to stress may vary depending upon following two factors:
Host Factors: Type of cell, Nutritional status of cell etc.
Factors pertaining to injurious agent: Its type, dose etc.
Etiology/Causes
Hypoxia and Ischaemia
Physical Agents
Chemicals and Drugs
Microbial Agents
Immunologic Causes
Nutritional Derangements
Ageing
Psychogenic Cause
Iatrogenic Cause
Idiopathic Disease
#rohitkumartrivedi
#cellinjury
#cellinjurypathology
This document provides an overview of cell injury, adaptation, and death from a pathology perspective. It defines pathology and discusses homeostasis, the types and mechanisms of cell injury including hypoxia, chemicals, infections, and genetics. It describes cellular adaptations like atrophy, hypertrophy, hyperplasia, and metaplasia that cells undergo in response to injury. It also discusses the types of cell death including necrosis, apoptosis, and gangrene.
This report, prepared by the student at the College of Dentistry, Hassan Atheed , in the third phase discusses scientific topics, but it maybe did not be 100% complete.
Cell injury (cell death): it is the variable changes in morphological and functional properties of cell occurs due to internal or external causes (ex. Chemical, physical, infectious and genetic agents), that obligate cell to respond for preserving normal hemostasis (adaptation) or death (necrosis) when the injury factors sever cell unable to adept, cell may also killed by another pathway even when it have the ability to adept for saving other cells and tissue by programed cell death (apoptosis).
حسن عضيد
This document provides information on cellular adaptation and injury. It discusses how cells can adapt through hypertrophy, atrophy, hyperplasia and metaplasia. Cellular adaptation aims to achieve a new steady state when faced with stress. If stresses exceed adaptive capacity, cell injury occurs which can be reversible or irreversible, caused by factors like hypoxia, toxins and pathogens. Mechanisms of injury include membrane damage, ATP depletion and genetic/metabolic alterations. The document also outlines different types of necrosis and intracellular pigment accumulation.
Cellular adaptations and injury can occur through various mechanisms:
(1) When cells are exposed to stressors, they may undergo reversible changes like atrophy, hypertrophy, hyperplasia, metaplasia, or dysplasia to adapt. (2) If the stressors are severe or persistent, irreversible cell injury and death through necrosis or apoptosis can result. (3) Cellular injury can be caused by free radicals, hypoxia, physical trauma, chemicals, radiation, or biological agents and can lead to tissue dysfunction or infection if necrosis occurs.
Cell injury can occur through various acquired and genetic causes and results in cellular adaptations or cell death. Reversible cell injury causes cellular swelling and fatty change, while irreversible injury leads to necrosis, apoptosis, or autolysis/heterolysis. Necrosis is characterized by loss of membrane integrity and cellular contents, resulting in nuclear changes like pyknosis, karyorrhexis, and karyolysis. In contrast, apoptosis is a programmed form of cell death where the cell activates enzymes to degrade its own DNA and proteins while keeping the plasma membrane intact.
This document discusses etiology and pathogenesis of cell injury. It defines cell injury as changes in a cell's internal and external environment due to various stresses from etiological agents. The cellular response depends on host factors like cell type and extent of injury. Injury can result in reversible or irreversible cell injury depending on factors like agent type/duration and cell adaptability. Common causes of cell injury include hypoxia, ischemia, toxins, microbes, nutrition imbalances, and aging. Ischemia and hypoxia are the most frequent causes of cell injury in humans. Reversible injury involves ATP depletion and membrane changes, while irreversible injury brings further damage including to mitochondria and nuclei, leading to cell death.
This document outlines objectives and content for a lecture on cell injury. The key points are:
1. Students should understand concepts of cellular adaptation to stress through hypertrophy, hyperplasia, atrophy, and metaplasia.
2. Hypoxic cell injury is a major cause of cell damage and can result from ischemia, anemia, or poor oxygenation.
3. Apoptosis and necrosis are the two main types of cell death, with necrosis occurring due to ischemia or chemicals and apoptosis through programmed suicide.
4. Causes of reversible and irreversible cell injury include hypoxia, physical agents, chemicals, infections, and genetic or nutritional factors.
(1,2) introduction of pathophysiology+ cell injury copyAlaa Radwan
This document provides an overview of pathophysiology concepts including biopsy, growth disorders, cell injury, and inflammation. It can be summarized as:
1) Biopsy is the use of diseased tissue or cells for diagnostic purposes, including different types of tissue and cell biopsies.
2) Growth disorders include increased growth like hypertrophy and hyperplasia, decreased growth like atrophy, and abnormal cell differentiation like metaplasia and dysplasia. Cell injury can be reversible or irreversible and cause cell death through necrosis or apoptosis.
3) Inflammation is characterized by redness, heat, pain, swelling, and loss of function, and involves processes like increased blood flow and the migration
This document discusses human pathology and cell injury. It defines pathology as the study of disease and notes that modern pathology studies cellular abnormalities. It explains that cell injury occurs through a limited set of basic biochemical processes, including plasma membrane damage, mitochondrial damage, ATP depletion, and nucleic acid damage. The document outlines various causes of cell injury like metabolic, chemical, free radical, immune, infectious, genetic, physical and iatrogenic insults. It describes different cellular responses to injury including recovery, cell death mechanisms like apoptosis, autophagy and necrosis, and subcellular changes or intracellular accumulations. The mechanisms of free radical generation and the role of reactive oxygen species in cell injury are explained. Methods of free radical removal like antioxidants
Cell injury occurs when homeostasis is disturbed and the limits of adaptive responses are exceeded. There are two main types of cell injury: reversible and irreversible. Reversible injury involves functional and morphological changes that can be reversed if the damaging stimulus is removed, such as reduced ATP and cellular swelling. Irreversible injury cannot be recovered from and leads to cell death, either through necrosis or apoptosis. Common causes of cell injury include oxygen deprivation, physical agents, chemical agents, infectious agents, immunological reactions, genetic defects, and nutritional imbalances. The initial manifestation of most injuries is cellular swelling. Mechanisms of injury involve ATP depletion, mitochondrial damage, calcium influx, reactive oxygen species accumulation, and increased membrane permeability, typically culminating in necrosis or
This document discusses various theories of disease causation and levels of prevention. It covers the germ theory, biomedical model, multi-causal theories including homeostasis and stress response theories, and psychosocial theories. It also defines the agent, host, environment triad and discusses the natural history of disease including prepathogenesis, pathogenesis, and levels of prevention such as primary, secondary, and tertiary prevention.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Dehradun #ℂall #gIRLS Oyo Hotel 8107221448 #ℂall #gIRL in Dehradun
CELL INJURY BY BISHNU ADHIKARI
1. Topics: Cell Injury by Bishnu Adhikari Gmail: rubdbishnu@gmail.com
Computerized by Bishnu Adhikari.
PATHOPHYSIOLOGY
Rudolf Virchow (1821-1902) the father of modern pathology.
Basic Principles of Cell Injury & Adaptation
Pathos means suffering
Logos means study
Thus “pathology” is derived from two Greek word pathos meaning suffering & logos meaning study.
Pathology is thus scientific study of structure & function of the body in disease. It deals with cause,
effect, mechanism & diseases.
Father of cellular pathology: Rudolf Virchow
Father of medicine: Hippocrates.
Some Termination used in pathology
Patient: patient is the person affected by the diseases.
Diseases: It is the condition of structural & functional abnormalities of the organ system called diseases.
In simple language diseases is opposite of health.
Lesions: lesions are the characteristic change in tissues & cells produced by diseases in an individual or
experimental animal.
Etiology: (why causes of diseases)
The casual factors responsible for lesions or included etiology of diseases. Why of diseases? E.g.:-
intrinsic or genetic & acquired.
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Pathogenesis: (How of diseases)
The mechanism by which the lesions are produced is term as pathogenesis of diseases.
Symptoms: The functional implication of the lesions felt by the patient is known as symptoms.
Diagnosis: To know what is wrong by morphological & functional changes together with results of other
investigation.
CELL INJURY
Cell injury is defined as variety of a stresses a cell encounter as a result of changes in its internal and
external environment.
If an injury exceeds the adaptive level of the cell, then only its effect can be seen. This condition is called
cell injury.
Etiology of cell injury :
The causes of cell injury, reversible or irreversible, may be broadly classified in to two main groups.
1) Genetic causes 2) Acquired causes
Genetic causes:
a) Development defects ( errors in morphogenesis)(teratogenesis).
Eg: Thalidomide
b) Cytogenetic (karyotypic) abnormalities
c) Single gene defects
d) Storage diseases
2) Acquired:
These causes are gained during life time. It comprises of vast majority of common diseases afflicting
mankind. The acquired causes of cell injury on the basis of underlying agent are categorized as:
a) Hypoxia and ischemia
b) Physical agent
c) Chemical agent and drugs
d) Microbial agents
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Computerized by Bishnu Adhikari.
e) Immunological agent
f) Nutritional derangement
g) Psychological factors
a) Hypoxia and ischemia:
Reduced supply of oxygen to the cell (i.e. hypoxia) causes difficulty of cell to perform the metabolic
function and the cell cannot generate energy.
So hypoxia is major causes of cell injury, the causes of hypoxia are,
Ischemia (reduced supply of blood to cells) is a major cause of hypoxia.
Other causes like anemia, carbon monoxide poisoning, cardio respiratory insuffiency, increased
demand of tissue, defects in alveolar space of lungs e.t.c.
b) Physical agents: They include:
mechanical trauma (road accidents)
Thermal trauma (by heat and cold)
Radiation (ultra violet and ionizing (α, β, γ)
Rapid change in atmospheric pressure.
c) Chemical agents and drugs:
Chemical poison such as cyanide, arsenic, mercury.
Strong acids and alkali
Environmental pollutant.
Insecticide & pesticides
Oxygen at high concentration.
Hypertonic glucose and salt.
Social agents such as alcohol, narcotics drugs.
Therapeutic administration of drugs.
Endogenous toxins: uremia, jaundice, diabetes, ketosis.
d) Microbial agents:
Infection caused by, Bacteria, viruses, fungi, protozoa, metazoan and other parasites.
e) Immunological agents: They act like a double edge ‘sword’. Sometimes protects the hosts against
various infectious agents but sometime may also turn lethal and causes cell injury. E.g. Hypersensitivity
reaction, Anaphylactic reaction, Autoimmune diseases
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Computerized by Bishnu Adhikari.
f) Nutritional derangement:
Due to deficiency or an access of nutrients
Starvation
(Marasmus, kashwashiwork) deficiency
Anemia
Obesity
Atherosclerosis
Heart diseases
Hypertension
g) Psychological factors:
Common acquired mental diseases like
Mental stress
Mental strain
Anxiety (a feeling of worry, uneasiness)
Over work & frustration. (E.g. depression, schizophrenia)
In this condition there are no specific biochemical or morphological changes.
Drug addiction like alcoholism & smoking causes various organic diseases like
Liver damage
Chronic bronchitis
Lung cancer
Peptic ulcer
Hypertension
Ischemic heart diseases e.t.c
Pathogenesis of Cell Injury
The etiologic factors produce different underlying alteration in biochemical system of cell for reversible
& irreversible cell injury.
It is when environmental changes exceed the capacity of the cell to maintain normal homeostasis.
But in general, the following principles apply in pathogenesis of the most forms of cell injury by various
agents.
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1) Type durations & severity of injurious agent.
2) Type status & adaptability of target cells.
3) Underlying intracellular phenomena
1) Type duration and severity of injurious agent:
E.g.:- small dose of chemical or short duration of ischaemia cause reversible cell injury.
While large dose of the some chemical agents, persistent ischemia causes cell death.
2) Type, status & adaptability of target cell:-
The status of cell based on its nutritional & metabolic condition & adaptation of the cell to hostile
environment affects the susceptibility of the cell to injury.
Type of cell influence the with stand capacity in the following way.
e.g. skeletal muscle can with stand hypoxic injury for long time, while cardiac muscle suffers irreversible
cell injury after 30- 60 minutes of persistent ischemia.
3) Underlying intracellular phenomena :-
Irrespective of other factors, two essential biochemical phenomena underlie all forms of cell injury to
distinguish between reversible & irreversible cell injury.
a) Inability to reverse mitochondrial dysfunction by reperfusion or reoxygenation.
b) Disturbance in cell membrane functions in general & in plasma membrane in particular.
Pathogenesis of ischaemia and hypoxia injury:-
Ischemia & hypoxia are common causes of cell injury. The underlying intracellular process &
mechanism involved in reversible & irreversible cell injury by hypoxia and ischemia are as follows,
Types of cell injury :-
1) Reversible cell injury
2) Irreversible cell injury
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1) Reversible Cell Injury:-
If the ischaemia or hypoxia is of short duration, the effects are reversible on rapid restoration of
circulation.
E.g. coronary artery occlusion, myocardial contractility, metabolism and ultra structure is quickly
reversed if the circulation is quickly restored.
The sequential changes in reversible cell injury are as under,
1) Decreased ATP synthesis in cell :-
ATP’s which are essentially required for a variety of cellular functions such as,
a) Membrane transport
b) Protein synthesis
c) Lipid synthesis
d) Phospholipids metabolism
A. Fig: Normal Cell
7. Topics: Cell Injury by Bishnu Adhikari Gmail: rubdbishnu@gmail.com
Computerized by Bishnu Adhikari.
ATP in human cell derived from two sources:-
a) Aerobic respiration (in presence of o2), or (oxidative phosphorylation).
b) Anaerobic respiration (glycoltic pathway)
In ischemia & hypoxia both there is less supply of o2. So aerobic respiration is decreased & thus ATP
decreases.
Ischemia is more severe than hypoxia because here in ischemia along with reduction in o2 supply blood
supply is also reduced. So ATP synthesis is further decreased.
Thus cell injury is more severe than cell injury in hypoxia.
Highly specialized cells like myocardium, proximal tubular cells of the kidney & neurons of the CNS are
dependent only on aerobic respiration for ATP generation & thus those tissues suffer from ill effects of
ischaemia more rapidly and severely.
Fig:-REVERSIBLE CELL INJURY
2) Reduced intracellular PH:- Due to low oxygen supply to cell aerobic respiration by mitochondria
fails first. This is followed by switch on the glycolytic pathway for energy requirement for this result the
rapid depletion of glycogen & accommodation of lactic acid, lower in the intracellular PH. After reduced
intracellular PH (intracellular acidosis) resulting in clumping of nuclear chromatin.
3) Damage to plasma membrane sodium pump:- In plasma membrane ATP dependent on sodium
pump,(i.e. Na+, k+ ATPase) operates. This allows the transport of Na+ out of the cell & diffuse k+ inside
the cell when sufficient amount of ATP is present.
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Lowered ATP in the cell causes consequent increases in ATPase activity which interfere the membrane
regulated process. This result in intracellular accumulation of sodium & diffusion of potassium out of
cell. Sodium accumulation inside the cell leads to increase in intracellular water to maintain iso-osmotic
condition (hydropic swelling).
4) Reduced protein synthesis :- Due to hypoxia (prolonged) the ribosome gets detached from granular
endoplasmic reticulum & polysomes are degraded to monosomes, thus protein synthesis is reduced.
5) Functional consequences:- Due to all above causes it may result in the functional disturbance. E.g.
Myocardial contractility ceases within 60 seconds of occlusion but can be reversed if circulation is
restored.
6) Ultra structural changes:- The following ultra structural changes can be seen in reversible cell
injury.
a) Endoplasmic reticulum: - Distension of cisternae by fluid and detachment of membrane bound poly
ribosome from the surface of RER.
b) Mitochondria: - Mitochondrial swelling & phospholipids rich amorphous densities.
c) Plasma membrane: - loss of microvillus & focal projection of cytoplasm (blebs).
d)Myelin figures:- They appear in cytoplasm’s or outside the cell. They are derived from membrane
(plasma or organelles) enclosing water dissociated lipoproteins between the lamellae of injured
membranes.
e) Nucleolus: - there is segregation granular & fibrillar components of nucleus & reduced synthesis of
ribosomal RNA, up to this point, withdrawal of acute stress that resulted in reversible cell injury can
restore the cell to normal state.
Irreversible Cell Injury :-
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FIG:- IRREVERSIBLE CELL INJURY
When ischemia or hypoxia is persistent then cell may be irreversibly injured leading it to the death. This
injury is the continuation of sequence events of reversibly injured cell. Two essential phenomena always
distinguish irreversible cell injury from reversible cell injury.
a) Inability of the cell to reverse mitochondrial dysfunction by reperfusion or re-oxygenation.
b) Disturbance in cell membrane functions in general & plasma membrane in particular.
In addition, there is continued depletion of protein, leakage of lysosomal enzymes in to cytoplasm,
reduced intracellular PH & further reduction in ATP.
1) Mitochondrial dysfunction:-
Due to continued hypoxia, a large cytosolic influx of ca++ ion occurs, especially after reperfusion of
irreversibly injured cell, which is taken up by mitochondria & is morphologically the mitochondria gets
vacuoles deposits of amorphous calcium salts in the mitochondrial matrix takes place.
2) Membrane damage:-
Defects in membrane function in general and plasma membrane in particular, is the most important event
in irreversible cell injury in ischemia. The mechanism involved is:-
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Computerized by Bishnu Adhikari.
a) Accelerated degradation of membrane phospholipids:-
Oxygen deprivation shifts calcium from mitochondria & endoplasmic reticulum in to the cytosol.
Increased level of cytosol activates endogenous phospholipases from ischemia tissue which degrade
membrane phospholipids which are the main constituents of the lipid bilayer membrane. An alternative
hypothesis is decreased replacement synthesis of membrane phospholipids due to reduced ATP.
b) Cytoskeleton damage:- cytoskeleton filaments (intermediate) in cell membrane are damaged due to
degradation by activated intracellular protease or physical effect of cell swelling producing irreversible
cell membrane injury.
c) Toxic oxygen radicals :-
Reactive oxygen derived species- superoxide(o2-), hydrogen peroxide (H2O2) & hydroxyl radicals (OHˉ)
are increased in ischaemia during reperfusion by incoming polymorphs.
Free radical injury is also operative in radiation injury, chemical injury, microbial, killing, aging,
atherosclerosis, carcinogenesis.
d) Breakdown products of lipid:-
lipid break down products & catabolic products which accumulates in the injured cell causes further
damage to various cell membrane.
e) Reperfusion damage:-
normal calcium ion concentrated is 10-3min, extracellular fluid & 10-7 in cytosol ( m for millimole).
Upon reperfusion of irreversibility injured cell calcium homeostasis is disturbed & there is large cytosolic
influx of calcium ions. Increased cytosolic calcium concentration may activate membrane phospholipases
leading phospholipid degradation.
3) Hydrolytic enzymes:-
Damage to lysosomal membrane is followed by liberation of hydrolytic enzymes (RNAase, DNAase,
Proteases, glycosidases,phosphateses & cathepsin), which on activation cause enzymatic digestion of
cellular components and induce the nuclear changes (pyknosis, karyolysis, & karyorrhexis) & hence cell
death.
Masses of phospholipids called myelin figures replace dead cell. These myelin figures are phagocytosed
by macrophages or there may be calcium soaps formulation.
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4) Serum estimation of liberated intracellular enzymes:-
The liberated enzymes leaks across the abnormally permeable cell membrane in to the serum, the
estimation of which may be used as clinical parameters for cell death.
e.g In myocardial infraction, estimation of elevated serum glutamic oxaloacetic transaminases (SGOT),
lactic dehydrogenase (LDH), isoenzymes of creatine kinase & cardiactroponins are useful guides for
death of heart muscle.
Free Radical –Mediated Cell Injury
For life oxygen is both a blessing & curse without its life is impossible, but its metabolism can produce
partially reduced oxygen species ( reactive oxygen intermediates) that reacts with virtually any molecule
they reach.
Free radical- mediated cell injury plays an important role in the following situations:
In ischemia reperfusion injury, by incoming inflammatory cells (WBC’s), by adhesion and
activation of neutrophils.
In chemical toxicity.
Hyperoxia (toxicity due to oxygen therapy)
cellular aging
killing of exogenous biologic agent.
inflammatory damage
Destruction of tumor cells.
Chemical carcinogenesis
Atherosclerosis
Generation Of Oxygen Free radicals
Generation of oxygen free radicals begin within mitochondrial inner membrane, when cytochrome
oxidases catalyses the four electron reduction of oxygen (o2) to water(H2O). Intermediate between
reaction of H20 to O2 three partially reduced species of oxygen are generated depending upon the
number of electrons transferred.
These are
Superoxide oxygen (O2) : one electron
Hydrogen peroxide (H2O2) : Two electron
Hydroxyl radical ( OHˉ) : Three electron
A few other oxygen radicals may be generated in reaction other than those during O2 to H2O are,
Hypochlorous acid (HOCL)
Peroxynitrate ion (ONOO)
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Nitric oxide (No)
Free radical generation (synthesis):- The three partially reduced oxygen intermediate species formed
during conversion of O2 to H2O are derived from enzymatic reaction as under:-
1) Superoxide (O2) :- superoxide anion(O2) may be generated by direct auto-oxidation of O2 during
mitochondrial electron transport reaction. Also enzymatic action of xanthine oxidase & cytochrome P450
overt O2 in mitochondrial or cytosol produces it. O2 so formed is catabolised to produce H2O2 by
superoxide dismutase (SOD).
2) Hydrogen peroxide (H2O2):
The H2O2 is reduced to water enzymatically by catalase ( in the peroxime) & glutathione peroxide
(GSH) (both in the cytosol & mitochondria).
3) Hydroxy radicals (OHˉ):-
OHˉ radicals is formed by 2 ways in biological process:-
a) By radidolysis of water (Dissociation of water by nuclear radiation)
b) By reaction of H2O2 with ferrous (Fe++) ions (Fenton reaction).
FREE RADICAL REACTIONS:-
FIG:- Mechanism of generation of free radicals by free radicals (SOD =
Superoxide Dismutase ; GSH = Glutathione peroxide
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a) Lipid peroxidation:-
poly unsaturated fatty acids (PUFA) of the membrane (phospholipids) are attack repeatedly & severily by
oxygen derived free radicals (O2, H2O2, OHˉ) & abstracts the hydrogen atom to yield highly destructive
PUFA radicals & lipid hydroxyperoxy radicals & lipid hypoperoxide. This reaction is termed as lipid
peroxidation.
The lipid radicals (hydroxyperoxy radicals) now reacts with molecular oxygen (O2) & forms a lipid
peroxide radical.
The peroxide radicals can in turn function as a initiator to remove another hydrogen atom from a second
unsaturated fatty acid. A lipid peroxide attacks another lipid radicals resulting a chain reaction of lipid
breaking finally collapse the membrane. The decomposition of lipid peroxidases is possible by transition
metal such as iron.
b)Oxidation of proteins:-
The OHˉ radicals may also attack the proteins the sulphur containing amino acids
(cistine,methinone,arginine,histidine,protine).
There OHˉ groups attack the sulphur (s) & abstract it. Due to this oxidative reaction the progein
undergoes fragmentation, cross linking of liable amino acids. Finally it leads to aggregation, degradation
of cytosolic neutral protease and eventually the cell destruction.
C) DNA damage:-
The nitrogen(N) present is the base of the DNA is an important target for hydroxyl radical. It causes the
breaking in the single strands of the nuclear & mitochondrial DNA.
A variety of structural alteration occurs which includes DNA stand breaking, modified base cross-linking
between strands, it may also cause malignant transformation.
d) Cytoskeletal damage:-
ROS are also known to interact with cytoskeleton elements & interfere in mitochondria aerobic
phosphorylation & thus cause ATP depletion.
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Fig:- Mechanism Of Generation of Free Radicals.
(SOD = superoxide dismutase; GSH ; glutathione peroxidase)
MORPHOLOGY OF IRREVERSIBLE CELL INJURY
(Cell death or cell sucide)
Cell death is state of irreversible injury. It may occur in the living body as local or focal changes.
TYPES OF CELL DEATH
1) Autolysis
2) Necrosis
3) Aptosis
4) Gangrene
1) Autolysis:-
Autolysis is disintegration of the cell by its own hydrolytic enzymes liberated from lysosomes. Autolysis
is rapid in some tissues rich in hydrolytic enzymes such as in the pancreases, GIT mucosa, intermediate
in tissue like heart, liver, & low in fibrous tissue.
Autolysis can occur in the living body when it is surrounded by inflammatory reaction.
2) Necrosis:-
It is defined as focal death along with degradation of tissue hydrolytic enzyme liberated by cell. It can be
caused by various agent such as hypoxia, chemical (ROS) physical (ROS) & microbial & immunological
injury. Changes in necrosis cell digestion by lytic enzyme & denaturation protein.
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TYPESS OF NECROSIS:- (C3F2)
a) Coagulative necrosis
b) Liquefaction (colliquaqtive) necrosis
c) Caseous necrosis
d) Fat necrosis
e) fibrinoid necrosis
a) Coagulative Necrosis:-
This is the most common types by irreversible cell injury mostly from sudden cessation of blood flow
(ischemia) and less often from bacterial & ischemia agents. The organs commonly affected are the heart,
kidney, and spleen, (pale from slightly swollen lead to yellow soft shrinkage)
b) Colliquative Necrosis:-
This type occurs due to ischemic injury & bacterial or fungal infections. It occurs due to degradation of
tissue by the action of powerful hydrolytic enzymes. E.g. Brain & abscess activity. Grossly the affected
area is soft’s with liquefied center containing necrotic debris & later a crystal wall is formed.
c) Caseous Necrosis:- caseous necrosis is found in centers of foci of tuberculosis infection. It’s is
combines features of both coagulative and liquifactive necrosis.
d) Fat Necrosis :-
Fat necrosis is a special form of cell death occurring at two anatomically different locations but
morphologically similar lesions.
E.g. acute pancreatic necrosis & in breasts.
In the case of pancreas, there is liberation of pancreatic lipases from injured or inflamed tissue that results
fat depots throughout the peritoneal cavity & sometimes, even affecting the extra abdominal adipose
tissue. Fat necrosis in either of the two instance results in hydrolysis of neutral fat present in adipose cells
in to glycerol & free fatty acids.
The damaged adipose cells assume cloudy appearance when only free fatty acids remain behind, after
glycerol leaks out.
e) Fibrinoid Necrosis:-
Fibrinoid necrosis or fibrinoid degeneration is characterized by deposition of fibrin like material which
has the staining properties of fibrin. It is encountered in various examples of immunological tissue injury.
e.g. in many complex vasculities autoimmune diseases e.t.c.
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*APOPTOSIS :- (degeneration mechanism)
Apoptosis is a form of “coordinated & internally programmed cell death”. Which is triggered by a variety
of extracellular & intracellular signals.
Apotosis is part of the balance between life and death of the cells and determines that a cell dies when it
is no longer useful or when it may be harmful to the organism. It is also a self defence mechanism.
(Apoptosis is a greek word meaning “falling off “ or “dropping off”. The term was first coined in 1972 as
distinct from necrosis.
*GANGRENE:-
Gangrene is a greek word. This name was came from the American football team in 1791. In that team
one player is suffer from the gangrene diseases.
Gang means group
Grene means green (so this diseases is look like as a green.)
Gangrene is a form of necrosis of a tissue superadded puterification due to bacteria and viral infection.
Here superadded means increasing. Puterification means degranulation of protein.
ETIOLOGY OF GANGRENE:-
The bacteria caused gangrene is costeridium perfingus.
Gangrene is caused by a viral attack, bacteria.
It is a maximum caused by Diabeties patient.
Due to the ischaemia condition also.
Due to some chemical also.
TYPES OF GANGRENE:-
1) Dry gangrene
2) Wet gangrene
3) Gas gangrene
1) DRY GANGRENE:-
It is in the external part of the body, where it is less supply of blood.
e.g. in toes, leg e.t.c
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2) WET GANGRENE:-
It is in the internal part of the body where bacteria growth easily. Fig: wet gangrene
e.g. in mouth
3) GAS GANGRENE:-
It caused in the muscle of the body due to the increase of bacteria and release of gas.
5.9% of hydrogen, 3.4% of carbon dioxide, 74.5% of nitrogen, 16.2% of oxygen.
Very bad smell comes from the gas gangrene due to the more nitrogen present.
CELLULAR ADAPTATION
Cellular Adaptation:-
For the sake of survival on expose to stress, the cells make adjustment with the changes in this
environment (i.e. adapt) to the physiologic needs (physiologic adaptation) & to non lethal pathologic
injury (pathologic adaptation). The common forms of cellular adaptive process are:-
1) Atrophy 2) Hyper atrophy 3) Hyperplasia 4) Metaplasia 5) Dysplasia
1) Atrophy :- Reduction of the number and size of parenchymal cells of an organ or it’s parts which was
once normal is called atrophy.
Here, aplasia means extreme failuire of development.
Causes:- Atrophy may occur from physiologic or pathologic causes.
A. Physiologic atrophy:- Atrophy is a normal process of aging in some tissues which could be due to
loss of endocrine stimulation or arteriosclerosis.
e.g. Atrophy of breast after menopause, Atrophy of brain.
B. Pathologic Atrophy:- The causes are as under:-
a) Starvation atrophy:- In starvation, there is first depletion of carbohydrates & fat stores followed by
protein catabolism.
e.g. weakness, anaemia
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b) Ischaemic atrophy:- Gradual diminution of blood supply due to atherosclerosis may result in shrinkage
of affected organ.
e.g. Atrophy of brain in cerebral atherosclerosis.
c) Disuse atrophy :- prolonged diminished functional activity is associated with disuse atrophy of the
organ.
e.g. wasting of muscle of limb immoblised in cast.
d) Neuropathic atrophy:- interruption in nerve supply leads to wasting of muscles.
e.g. poliomyelitis, nerve section, motor neuron ddiseases.
2) Hypertrophy :- It is an increase in size of parenchymal cells resulting in enlargement of the organ or
tissue, without any change in the number of cells.
CAUSES:- It may be physiologic and pathologic. In both case, it is caused either by increased functional
demand or by hormonal situation. [ in non dividing cells too, only hypertrophy occurs.
A) physiologic hypertrophy:- Enlarged size of thr ulcers in pregnancy is an excellent example of
physiologic hypertrophy as well as hyperplasia. Greater muscle size and strength following repeated
exercise.
B) Pathologic hypertrophy:- Example of certain diseases associated with hypertrophy are as under.
1) Hypertrophy of cardiac muscle may occurring number of cardiovascular diseases. A few examples
producing left ventricular hypertrophy are:-
a) systemic hypertension
b) Aortic valve diseases
c) Mitral insuffiency
2) Hypertrophy of smooth muscle:- Examples :
a) cardiac achalasia ( in oesophagus)
b) Pyloric stenosis ( in stomach)
c) Muscular arteries ( in hypertension)
3) Hypertrophy of skeletal muscle:-
e.g. Hypertrophied muscles in athelets and manual labourers.
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3) Hyperplasia:- it is an increase in the number of parenchymal cells resulting in enlargement of the
organ or tissue. Quite of an, both hyperplasia and hypertrophy occur together. It occurs due to increased
recruitment of cells from G. (resting) phase of the cycle to undergo mitosis, when stimulated.
e.g. Increased estrogen level at puberty and during the early stage of menstrual cycle leads to an
increased number of both endometrial and uterine stromal cells.
Causes:- As with other non- neoplastic disorders of growth, hyperplasia as also being divided in to
physiologic and pathologic.
A) physiologic hyperplasia :- The two most common types are as follows:
a) Hormonal hyperplasia :- I.e hyperplasia occurring under the influence of hormonal stimulation. E.g.
hyperplasia of female breast at puberty during pregnancy and lactation.
b) hyperplasia of pregnant uterus .
c) Prostatic hyperplasia in old age.
B) compensatory hyperplasia :- I.e. Hyperplasia occurring following removal of part of an organ , or a
contralateral organ in paired organ.
e.g. a) Regeneration of the liver following partial hepatectomy.
b) Regeneration of epiderm is after skin abrasion.
B) Pathologic Hyperplasia :- Most example of pathologic hyperplasia are due to excessive stimulation
of hormons or growth factor.
e.g. a) endometrial hyperplasia following estrogen excess.
b) In wound healing, there is a formation of granulation tissue due to proliferation of fibroblast and
endometrial cells.
c) pseudocarcinimateous hyperplasia of the skin.
4) Metaplasia:-
Meta means transformation
Plasia means growth
It is defined as a reversible change of one type of epithelial or mesenchymal cells, usually in response to
abnormal stimuli, & often reverts back to normal on removal of stimulus. Metaplasia is broadly divided
in to 2 types:-
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A) Epithelial metaplasia:- This is the more common type. The metaplasia change may be patchy or
diffuse and usually results in replacement by stronger but less well specialized epithelial. How ever, the
metaplastic epithelial being less well specialized such as squamous type, results in deprivation of
protective mucus secretion and hence more prone to infection
1) Squamous metaplasia :- various type of epithelial are capable of undergoing squamous metaplastic
changes due to chronic irritation that may be mechanical, chemical or infective in origin. E.g. In
bronchous (normally) lined by pseudo stratified columnar ciliated epithelial in chronic smokers.
2) columnar metaplasia :- There are some condition in which there is transformamtion to columnar
epithelium. E.g.
a) Intestinal metaplasia in healed chronic gastric ulcer.
b) Conversion of pseudostartified columnar epithelium in chronic bronchitis & bronchiectasis to
columnar type.
B) Mesenchymal metaplasia:- Less often, there is a conformation of one adult type of mesencdhymal
tissue to another. E.g.
a) Osseous metaplasia:- osseous metaplasia is a formation of bone in fibrous tissue, cartilage and myxoid
tussue. E.g.
In arterial wall in old age
In soft tissue in myositis ossificans.
In cartilage of larynx and bronchi in a elderly people.
2) Cartilaginous metaplasia:- In healing of fracture cartilaginous metaplasia may occur where there is un
due mobility.
5) Dysplasia:- ( disordered of growth)
The cells that compose an epithelium normally exihibit uniformity of size, shape and nucleus or
organized.
More over they are arranged in a regular fashion. Dysplasia mean disordered cellular development,
variation in the size & shape of the cell enlarged.
Disorderly arrangement of the cell within the epithelium, increase nucleo-cytoplasmic ratio (1:4),
increased mitotic activity.
Dysplasia occurs most often in an epithelial cell. It occurs due to chronic irritation or prolonged
inflammation. Some time dysplasia progresses in to carcinoma (cancer). The two most common
examples of dysplastic changes are the uterine cervix and respiratory tract.