This document provides an overview of pathology. It defines pathology as the study of structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease. A pathologist examines cells and tissues removed from the body to identify diseases. The core areas of pathology include studying the etiology, pathogenesis, and morphological and functional changes that result from disease. Pathology aids in the diagnosis and management of disease processes by examining biopsied tissue samples microscopically, as seen in the example case of a woman diagnosed with follicular lymphoma following biopsy of an enlarged lymph node.
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
This document discusses cell injury, adaptation, and death. It explains that cells can undergo adaptation to physiologic or pathologic stresses to maintain homeostasis. Adaptation allows cells to modify their structure and function to avoid injury. If stresses exceed a cell's adaptive capacity, injury occurs. Adaptations include hypertrophy, where cells increase in size rather than number. Hypertrophy can be physiologic, like uterine enlargement during pregnancy, or pathologic, like cardiac enlargement from hypertension. The document then focuses on hypertrophy in more detail.
This document summarizes the key aspects of inflammation. It begins by defining inflammation and describing the cardinal signs. It then discusses the etiological factors, types of inflammation (acute vs chronic), and the haemodynamic and cellular events in acute inflammation. Specifically, it outlines the vascular changes, increased permeability, exudation of leukocytes, and process of phagocytosis. It also discusses the chemical mediators of inflammation like histamine, kinins, cytokines, prostaglandins, and the resolution of inflammation. Finally, it concludes that inflammation is an important immune response but better understanding its pathways could aid in treating diseases.
Cells can adapt to changes in their environment through various processes including hyperplasia, hypertrophy, atrophy, metaplasia, and dysplasia. Hyperplasia is an increase in cell number, hypertrophy is an increase in cell size, and atrophy is a decrease in cell size or number. Metaplasia is a reversible change where one adult cell type replaces another. Dysplasia involves disordered cellular development and proliferation with cytological abnormalities. These adaptations allow cells to survive stresses and ensure tissue homeostasis.
Cell injury, adaptation, and death can occur through various stimuli and stresses. Cells may undergo reversible or irreversible changes. Reversible changes include cellular adaptation through hypertrophy, hyperplasia, and metaplasia to stressors. Irreversible changes result in cellular atrophy and eventually cell death through necrosis or apoptosis. The morphology of reversible injury includes cellular swelling, fatty change, and changes to organelles. Necrosis is the degradative process of cell death where cellular contents are digested by enzymes.
This document discusses cell injury and cell death. It defines cell injury as a change in cell structure, metabolism or function that impairs its vital activity. Causes of cell injury include internal stresses like metabolic imbalances and external stresses such as physical agents, toxins, and chemicals. Cell injury can be reversible or irreversible and lead to cell death through mechanisms like necrosis, autolysis, or apoptosis. Signs of cell injury include morphological changes, functional impairments, and metabolic derangements. Specific types of cell injury discussed include fatty change, pigmentation, calcification, amyloidosis, and various forms of necrosis.
Cell injury: causes, pathogenesis, Morphology of reversible cell injuryVijay Shankar
The document discusses cell injury and its mechanisms. It describes how cells can become injured through various stressors like hypoxia, physical/chemical agents, infections, etc. This causes damage to key cellular components like membranes, respiration, and DNA. The injury can be reversible through mild changes like hydropic swelling, or progress to irreversible necrosis or apoptosis if the cell cannot adapt. Free radicals are also discussed as a mediator of injury through lipid peroxidation, protein/DNA oxidation, and cytoskeletal damage. Examples of reversible changes include hydropic swelling seen as cloudy vacuoles, while irreversible injury leads to cell death.
This document provides an overview of pathology. It defines pathology as the study of structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease. A pathologist examines cells and tissues removed from the body to identify diseases. The core areas of pathology include studying the etiology, pathogenesis, and morphological and functional changes that result from disease. Pathology aids in the diagnosis and management of disease processes by examining biopsied tissue samples microscopically, as seen in the example case of a woman diagnosed with follicular lymphoma following biopsy of an enlarged lymph node.
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
This document discusses cell injury, adaptation, and death. It explains that cells can undergo adaptation to physiologic or pathologic stresses to maintain homeostasis. Adaptation allows cells to modify their structure and function to avoid injury. If stresses exceed a cell's adaptive capacity, injury occurs. Adaptations include hypertrophy, where cells increase in size rather than number. Hypertrophy can be physiologic, like uterine enlargement during pregnancy, or pathologic, like cardiac enlargement from hypertension. The document then focuses on hypertrophy in more detail.
This document summarizes the key aspects of inflammation. It begins by defining inflammation and describing the cardinal signs. It then discusses the etiological factors, types of inflammation (acute vs chronic), and the haemodynamic and cellular events in acute inflammation. Specifically, it outlines the vascular changes, increased permeability, exudation of leukocytes, and process of phagocytosis. It also discusses the chemical mediators of inflammation like histamine, kinins, cytokines, prostaglandins, and the resolution of inflammation. Finally, it concludes that inflammation is an important immune response but better understanding its pathways could aid in treating diseases.
Cells can adapt to changes in their environment through various processes including hyperplasia, hypertrophy, atrophy, metaplasia, and dysplasia. Hyperplasia is an increase in cell number, hypertrophy is an increase in cell size, and atrophy is a decrease in cell size or number. Metaplasia is a reversible change where one adult cell type replaces another. Dysplasia involves disordered cellular development and proliferation with cytological abnormalities. These adaptations allow cells to survive stresses and ensure tissue homeostasis.
Cell injury, adaptation, and death can occur through various stimuli and stresses. Cells may undergo reversible or irreversible changes. Reversible changes include cellular adaptation through hypertrophy, hyperplasia, and metaplasia to stressors. Irreversible changes result in cellular atrophy and eventually cell death through necrosis or apoptosis. The morphology of reversible injury includes cellular swelling, fatty change, and changes to organelles. Necrosis is the degradative process of cell death where cellular contents are digested by enzymes.
This document discusses cell injury and cell death. It defines cell injury as a change in cell structure, metabolism or function that impairs its vital activity. Causes of cell injury include internal stresses like metabolic imbalances and external stresses such as physical agents, toxins, and chemicals. Cell injury can be reversible or irreversible and lead to cell death through mechanisms like necrosis, autolysis, or apoptosis. Signs of cell injury include morphological changes, functional impairments, and metabolic derangements. Specific types of cell injury discussed include fatty change, pigmentation, calcification, amyloidosis, and various forms of necrosis.
Cell injury: causes, pathogenesis, Morphology of reversible cell injuryVijay Shankar
The document discusses cell injury and its mechanisms. It describes how cells can become injured through various stressors like hypoxia, physical/chemical agents, infections, etc. This causes damage to key cellular components like membranes, respiration, and DNA. The injury can be reversible through mild changes like hydropic swelling, or progress to irreversible necrosis or apoptosis if the cell cannot adapt. Free radicals are also discussed as a mediator of injury through lipid peroxidation, protein/DNA oxidation, and cytoskeletal damage. Examples of reversible changes include hydropic swelling seen as cloudy vacuoles, while irreversible injury leads to cell death.
Pathology is the study of disease and involves examining organs, tissues, cells, and bodily fluids to diagnose disease and understand disease mechanisms. The main subfields of pathology include anatomical pathology, clinical pathology, surgical pathology, cytopathology, and forensic pathology. Pathology uses various techniques including microscopic examination, biochemical analysis, microbiology, and cell/tissue culture to make diagnoses and advance understanding of disease causes, processes, and outcomes.
This document defines and describes various pathological processes including degeneration, necrosis, apoptosis, gangrene, and calcification. It discusses four main types of degenerative cell changes: cellular swelling, fatty change, hyaline change, and mucoid change. It also describes five types of necrosis: coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Apoptosis is defined as a genetically programmed form of cell death. Gangrene is described as necrosis with superadded putrefaction. Pathologic calcification can be either dystrophic or metastatic.
Principles of cell injury and cellular adaptation .pptMirza Anwar Baig
This document provides an overview of cell injury and adaptation. It discusses various causes of cell injury including hypoxia, infections, physical and chemical agents. The pathogenesis and morphology of reversible and irreversible cell injury is explained. Cellular adaptations such as atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia are defined. Necrosis and apoptosis are compared as two types of cell death. Specific examples of cell injuries and adaptations in different organ systems are also presented.
Acute inflammation is the immediate and early response to harmful stimuli, characterized by vascular changes that increase blood flow and permeability, allowing plasma proteins and cells to enter tissues. This forms an exudate containing antibodies, leukocytes, and other factors that work to dilute, destroy, and remove the cause of injury. The cardinal signs of inflammation - heat, redness, swelling, pain, and loss of function - result. Acute inflammation is usually short-lived and resolves once the stimulus has been dealt with.
Cellular adaptations allow cells to survive stress by changing their environment through physiologic or pathologic means. Cells can adapt by decreasing or increasing in size (atrophy and hypertrophy), increasing in number (hyperplasia), or changing phenotype (metaplasia and dysplasia). Common cellular adaptations include atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia, which allow cells to respond to various stresses or stimuli.
Cellular response to injury can include adaptation, injury, or disease. Adaptation represents a new abnormal state where cells maintain viability and homeostasis in response to stress. Key types of cellular adaptation include hyperplasia (increased cell number), hypertrophy (increased cell size), atrophy (decreased cell size and number), and metaplasia (one cell type replaces another). While adaptation allows cell survival, the underlying stresses that cause adaptation could also promote cancer if persistent over time.
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.
MBBS 2nd Year Pathology - Neoplasia : IntroductionNida Us Sahr
Chapter 7 (Neoplasia) from Robbins and Cotran Pathologic Basis of Disease (9th Edition) for MBBS 2nd Year.
After going through this presentation, it will be easy to understand Neoplasia from Robbins.
General pathology lecture 1 introduction & cell injuryHuang Yu-Wen
This document provides an overview of pathology and cell injury. It begins with definitions of pathology and discusses its focus on etiology, pathogenesis, morphology, and manifestations of disease. It then covers cell injury, describing the process from normal cell to reversible and irreversible injury. Specific types of cell injury are outlined like cloudy swelling, fatty change, and hyaline degeneration. The document concludes with examples of intracellular accumulations seen in various disease states.
An embolism is the obstruction of blood vessels by a mass or clot that has detached from its origin and traveled through the bloodstream. Embolisms can be classified based on the material causing the obstruction and the source and direction of blood flow. Common types of embolisms include pulmonary, fat, air, amniotic fluid, and tumor embolisms. Pulmonary embolisms originate in the lower leg veins and are caused by stasis, hypercoagulability, or a saddle embolism. Fat embolisms result from trauma or medical conditions and obstruct arterioles and capillaries. Decompression sickness is a form of gas embolism that affects scuba divers or caisson workers
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.
The document discusses cell injury and cell death. It explains that cells have a normal steady state of homeostasis but stress can force cells to adapt or become injured if the stress exceeds their capacity. Cell injury can be reversible or irreversible and leads to cell death if irreversible. Key systems vulnerable to injury are membranes, respiration, protein synthesis and the genetic apparatus. Causes of injury include hypoxia, toxins, infections and more. Reversible injury disrupts mitochondria while irreversible injury causes mitochondrial and lysosomal damage leading to cell death.
Pathology is the study and diagnosis of disease. It has four main components: the cause or etiology, the mechanism of development/pathogenesis, structural alterations to cells (morphological changes), and the consequences of these changes (clinical manifestations). Pathology has evolved from autopsy and organ-based examination to cellular pathology and now utilizes various techniques including molecular pathology, genetics, immunology, and quantitative analysis. Key techniques used in pathology include autopsy, biopsy, cytology, animal experimentation, tissue/cell culture, histology, immunohistochemistry, electron microscopy, flow cytometry, image analysis, and molecular biology techniques like PCR and DNA sequencing.
Cell growth and differentiation are normally controlled processes that maintain tissue structure. Disorders can occur when these processes are deregulated. Key disorders include hypertrophy (enlarged cells), hyperplasia (increased cell number), atrophy (decreased cell size and number), metaplasia (one cell type replaces another), dysplasia (abnormal cell growth), and neoplasia (uncontrolled cell growth, i.e. cancer). These disorders are caused by various stimuli and involve molecular pathways regulating cell growth and protein synthesis. Disorders can progress from early changes like metaplasia and dysplasia to late stage cancers if deregulation persists over time.
This document provides an introduction to pathology. It defines pathology as the scientific study of disease and discusses its main branches of general pathology and systemic pathology. It also outlines several key techniques used in pathology like microbiologic, molecular, immunologic, and morphologic analysis. The document then discusses key aspects of the disease process including etiology, pathogenesis, clinical manifestations, and molecular and morphologic changes. It provides examples of different types of etiologies and explains key pathology concepts such as reversible and irreversible cell injury, necrosis, apoptosis, and intracellular accumulations.
Atrophy is the shrinkage of cells and tissues due to loss of cell substance. There are two types of atrophy: physiologic and pathologic. Physiologic atrophy occurs normally, such as the uterus after childbirth. Pathologic atrophy is caused by factors like decreased blood supply, nutrition, or innervation. At the cellular level, atrophy occurs through decreased protein synthesis and increased protein degradation via the ubiquitin-proteasome pathway and autophagy. While cells may have reduced function during atrophy, they are not dead, and atrophy can sometimes be reversed.
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
Cellular adaptations like hyperplasia, hypertrophy, atrophy, metaplasia, and apoptosis allow cells to respond to physiological and pathological stimuli in their environment. These adaptations preserve cell viability by allowing cells to modify their growth patterns or metabolism. Certain adaptations like sustained hyperplasia can increase cancer risk by providing fertile ground for neoplastic changes if the stimuli are persistent. Clinical terminology around cellular adaptations is important for understanding disease processes and responses.
Cellular adaptation involves alterations in cell structure and function in response to sublethal stimuli. There are several types of morphologic adaptation:
Hypertrophy is an increase in cell size without cell division. Hyperplasia is an increase in cell number. Atrophy is a decrease in cell size and number. Metaplasia is the replacement of one differentiated cell type with another. Dysplasia involves abnormal cell growth and maturation. These adaptive responses allow cells to withstand sublethal stimuli but may progress to more severe injury if the stimuli persist.
Hyperplasia is an increase in the number of cells in an organ or tissue. It can be physiologic, such as during pregnancy, or pathologic, such as with excessive hormone stimulation. Hypertrophy is an increase in cell size within an organ or tissue, often due to increased functional demands. Atrophy is a decrease in cell and organ size due to loss of cell substance from factors like disuse or inadequate nutrition. Metaplasia is a reversible change where one adult cell type replaces another, such as squamous replacing columnar epithelium from chronic irritation. These changes can sometimes progress to cancer if the predisposing stimuli persist long-term.
Pathology is the study of disease and involves examining organs, tissues, cells, and bodily fluids to diagnose disease and understand disease mechanisms. The main subfields of pathology include anatomical pathology, clinical pathology, surgical pathology, cytopathology, and forensic pathology. Pathology uses various techniques including microscopic examination, biochemical analysis, microbiology, and cell/tissue culture to make diagnoses and advance understanding of disease causes, processes, and outcomes.
This document defines and describes various pathological processes including degeneration, necrosis, apoptosis, gangrene, and calcification. It discusses four main types of degenerative cell changes: cellular swelling, fatty change, hyaline change, and mucoid change. It also describes five types of necrosis: coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Apoptosis is defined as a genetically programmed form of cell death. Gangrene is described as necrosis with superadded putrefaction. Pathologic calcification can be either dystrophic or metastatic.
Principles of cell injury and cellular adaptation .pptMirza Anwar Baig
This document provides an overview of cell injury and adaptation. It discusses various causes of cell injury including hypoxia, infections, physical and chemical agents. The pathogenesis and morphology of reversible and irreversible cell injury is explained. Cellular adaptations such as atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia are defined. Necrosis and apoptosis are compared as two types of cell death. Specific examples of cell injuries and adaptations in different organ systems are also presented.
Acute inflammation is the immediate and early response to harmful stimuli, characterized by vascular changes that increase blood flow and permeability, allowing plasma proteins and cells to enter tissues. This forms an exudate containing antibodies, leukocytes, and other factors that work to dilute, destroy, and remove the cause of injury. The cardinal signs of inflammation - heat, redness, swelling, pain, and loss of function - result. Acute inflammation is usually short-lived and resolves once the stimulus has been dealt with.
Cellular adaptations allow cells to survive stress by changing their environment through physiologic or pathologic means. Cells can adapt by decreasing or increasing in size (atrophy and hypertrophy), increasing in number (hyperplasia), or changing phenotype (metaplasia and dysplasia). Common cellular adaptations include atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia, which allow cells to respond to various stresses or stimuli.
Cellular response to injury can include adaptation, injury, or disease. Adaptation represents a new abnormal state where cells maintain viability and homeostasis in response to stress. Key types of cellular adaptation include hyperplasia (increased cell number), hypertrophy (increased cell size), atrophy (decreased cell size and number), and metaplasia (one cell type replaces another). While adaptation allows cell survival, the underlying stresses that cause adaptation could also promote cancer if persistent over time.
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.
MBBS 2nd Year Pathology - Neoplasia : IntroductionNida Us Sahr
Chapter 7 (Neoplasia) from Robbins and Cotran Pathologic Basis of Disease (9th Edition) for MBBS 2nd Year.
After going through this presentation, it will be easy to understand Neoplasia from Robbins.
General pathology lecture 1 introduction & cell injuryHuang Yu-Wen
This document provides an overview of pathology and cell injury. It begins with definitions of pathology and discusses its focus on etiology, pathogenesis, morphology, and manifestations of disease. It then covers cell injury, describing the process from normal cell to reversible and irreversible injury. Specific types of cell injury are outlined like cloudy swelling, fatty change, and hyaline degeneration. The document concludes with examples of intracellular accumulations seen in various disease states.
An embolism is the obstruction of blood vessels by a mass or clot that has detached from its origin and traveled through the bloodstream. Embolisms can be classified based on the material causing the obstruction and the source and direction of blood flow. Common types of embolisms include pulmonary, fat, air, amniotic fluid, and tumor embolisms. Pulmonary embolisms originate in the lower leg veins and are caused by stasis, hypercoagulability, or a saddle embolism. Fat embolisms result from trauma or medical conditions and obstruct arterioles and capillaries. Decompression sickness is a form of gas embolism that affects scuba divers or caisson workers
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.
The document discusses cell injury and cell death. It explains that cells have a normal steady state of homeostasis but stress can force cells to adapt or become injured if the stress exceeds their capacity. Cell injury can be reversible or irreversible and leads to cell death if irreversible. Key systems vulnerable to injury are membranes, respiration, protein synthesis and the genetic apparatus. Causes of injury include hypoxia, toxins, infections and more. Reversible injury disrupts mitochondria while irreversible injury causes mitochondrial and lysosomal damage leading to cell death.
Pathology is the study and diagnosis of disease. It has four main components: the cause or etiology, the mechanism of development/pathogenesis, structural alterations to cells (morphological changes), and the consequences of these changes (clinical manifestations). Pathology has evolved from autopsy and organ-based examination to cellular pathology and now utilizes various techniques including molecular pathology, genetics, immunology, and quantitative analysis. Key techniques used in pathology include autopsy, biopsy, cytology, animal experimentation, tissue/cell culture, histology, immunohistochemistry, electron microscopy, flow cytometry, image analysis, and molecular biology techniques like PCR and DNA sequencing.
Cell growth and differentiation are normally controlled processes that maintain tissue structure. Disorders can occur when these processes are deregulated. Key disorders include hypertrophy (enlarged cells), hyperplasia (increased cell number), atrophy (decreased cell size and number), metaplasia (one cell type replaces another), dysplasia (abnormal cell growth), and neoplasia (uncontrolled cell growth, i.e. cancer). These disorders are caused by various stimuli and involve molecular pathways regulating cell growth and protein synthesis. Disorders can progress from early changes like metaplasia and dysplasia to late stage cancers if deregulation persists over time.
This document provides an introduction to pathology. It defines pathology as the scientific study of disease and discusses its main branches of general pathology and systemic pathology. It also outlines several key techniques used in pathology like microbiologic, molecular, immunologic, and morphologic analysis. The document then discusses key aspects of the disease process including etiology, pathogenesis, clinical manifestations, and molecular and morphologic changes. It provides examples of different types of etiologies and explains key pathology concepts such as reversible and irreversible cell injury, necrosis, apoptosis, and intracellular accumulations.
Atrophy is the shrinkage of cells and tissues due to loss of cell substance. There are two types of atrophy: physiologic and pathologic. Physiologic atrophy occurs normally, such as the uterus after childbirth. Pathologic atrophy is caused by factors like decreased blood supply, nutrition, or innervation. At the cellular level, atrophy occurs through decreased protein synthesis and increased protein degradation via the ubiquitin-proteasome pathway and autophagy. While cells may have reduced function during atrophy, they are not dead, and atrophy can sometimes be reversed.
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
Cellular adaptations like hyperplasia, hypertrophy, atrophy, metaplasia, and apoptosis allow cells to respond to physiological and pathological stimuli in their environment. These adaptations preserve cell viability by allowing cells to modify their growth patterns or metabolism. Certain adaptations like sustained hyperplasia can increase cancer risk by providing fertile ground for neoplastic changes if the stimuli are persistent. Clinical terminology around cellular adaptations is important for understanding disease processes and responses.
Cellular adaptation involves alterations in cell structure and function in response to sublethal stimuli. There are several types of morphologic adaptation:
Hypertrophy is an increase in cell size without cell division. Hyperplasia is an increase in cell number. Atrophy is a decrease in cell size and number. Metaplasia is the replacement of one differentiated cell type with another. Dysplasia involves abnormal cell growth and maturation. These adaptive responses allow cells to withstand sublethal stimuli but may progress to more severe injury if the stimuli persist.
Hyperplasia is an increase in the number of cells in an organ or tissue. It can be physiologic, such as during pregnancy, or pathologic, such as with excessive hormone stimulation. Hypertrophy is an increase in cell size within an organ or tissue, often due to increased functional demands. Atrophy is a decrease in cell and organ size due to loss of cell substance from factors like disuse or inadequate nutrition. Metaplasia is a reversible change where one adult cell type replaces another, such as squamous replacing columnar epithelium from chronic irritation. These changes can sometimes progress to cancer if the predisposing stimuli persist long-term.
Adaptation of cellular growth and differentiationradhigapravin
This document summarizes various cellular adaptations including atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia. Atrophy is a shrinkage in cell size due to loss of cell substance. Hypertrophy is an increase in cell size without a change in cell number. Hyperplasia is an increase in cell number leading to tissue enlargement. Metaplasia is a reversible change where one cell type transforms into another. Dysplasia is a disordered cellular development accompanied by metaplasia and hyperplasia, characterized by proliferating cells with cytological changes. These adaptations can occur physiologically or pathologically in response to environmental changes or stimuli.
CELLULAR ADAPTATION AND ABERRANT CELL GROWTH [Autosaved].pptxzeexhi1122
Cellular structures and functions can change through normal adaptive processes like hypertrophy, hyperplasia, atrophy, and metaplasia in response to environmental changes. However, dysplasia and neoplastic growth represent aberrant cell growth. Dysplasia involves disordered cellular development and proliferation with cytological changes. Neoplastic growth is distinguished from normal adaptation by being non-reversible and having the potential for invasion and metastasis. Cancer development is influenced by proto-oncogenes and tumor suppressor genes, with characteristics like uncontrolled growth, invasion and metastasis.
This document discusses various cellular adaptations including physiological and pathological adaptations. It describes physiological adaptations like hypertrophy and hyperplasia that occur in response to increased needs. Pathological adaptations include atrophy, metaplasia, dysplasia, and cancerous changes. Atrophy is a reduction in cell size and number. Hypertrophy is an increased cell size while hyperplasia is an increased cell number. Metaplasia is the change of one cell type to another. Dysplasia shows disordered cellular development with potentially pre-cancerous changes. Examples and causes of each adaptation are provided along with morphological features.
This document discusses various cellular adaptations and injury. It defines atrophy, hypertrophy, hyperplasia, and metaplasia. Atrophy is a decrease in cell size and number. Hypertrophy is an increase in cell size. Hyperplasia is an increase in cell number. Metaplasia is the replacement of one cell type with another. Examples of each type of adaptation are given, including how squamous cell metaplasia in smokers replaces normal trachea and bronchial cells, and how warts represent skin hyperplasia.
Adaptation of cellular growth & differentiationHrudi Sahoo
This document discusses the adaptation of cellular growth and differentiation in response to environmental stressors. It describes several mechanisms of adaptation, including altered cell surface receptor binding and protein synthesis. Adaptive disorders that can occur include atrophy (shrinkage), hypertrophy (enlargement), hyperplasia (increased cell number), metaplasia (cell type transformation), and dysplasia (abnormal cell development). Metaplasia can be epithelial or mesenchymal, and dysplasia can progress to carcinoma if the stimulus is not removed. Overall, the document outlines how cells can adapt their size, number, and type in response to physiological or pathological stimuli.
This document discusses various types of cellular adaptations: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia. Atrophy is a reduction in cell size and number. Hypertrophy is an increase in cell size but not number. Hyperplasia is an increase in cell number. Metaplasia is a change from one adult cell type to another. Dysplasia refers to abnormal cell shapes and sizes that can progress to cancer. Cellular adaptations provide clues for pathologists to diagnose disease.
This document discusses various types of adaptive changes that cells undergo, including hypertrophy, hyperplasia, hypoplasia, atrophy, metaplasia, and dysplasia. It defines each term and provides examples. Hypertrophy is an increase in cell or organ size without cell multiplication. Hyperplasia is an increase due to cell proliferation. Hypoplasia is incomplete organ development. Atrophy is a decrease in cell or organ size due to cell loss. Metaplasia is the transformation of one cell type into another. Dysplasia refers to abnormal cell growth and differentiation where cells look abnormal but are not yet cancerous.
Cellular adaptations and growth disturbancesZaid Wani
cellular adaptations and growth disturbances and their mechanisms. please refer the books given in reference section of this presentation for further understandings and examples of subtypes.
nursing class cellularadaptation and apoptosis.pptxvandana thakur
The document discusses various types of cellular adaptations:
1. Adaptations are reversible changes in cells that allow them to respond to environmental changes through alterations in size, number, function or metabolism. This includes physiological adaptations to hormones and pathological adaptations that help cells survive.
2. Cells can adapt through hyperplasia (cell growth), hypertrophy (cell enlargement), atrophy (cell shrinkage), metaplasia (one cell type changing to another), and dysplasia (abnormal cell growth).
3. Apoptosis is a form of programmed cell death where cells activate an intrinsic suicide pathway in response to signals or stress, undergoing changes like chromatin condensation and blebbing before being phagocy
Adaptations of cellular growth and diffrentiationrashree-singh
This document discusses various types of cellular adaptation in response to environmental changes. It defines key adaptations like hypertrophy, hyperplasia, atrophy, and metaplasia. Hypertrophy involves cell enlargement while hyperplasia is an increase in cell number. Atrophy is a decrease in cell size and number. Metaplasia is the reversible replacement of one cell type with another. Adaptations can be physiological from things like exercise or pathological from issues like hypertension. The mechanisms of adaptations involve growth factors, hormones, and changes in protein expression levels. Cellular adaptations allow tissues to survive stresses but can sometimes progress to disease if the stressors remain.
Cell adaptation involves changes cells undergo in response to stimuli. Cells can adapt by changing size (atrophy and hypertrophy), number (hyperplasia and atrophy), or form (metaplasia). Atrophy is a decrease in cell size due to decreased protein synthesis. Hypertrophy is an increase in cell size due to increased protein synthesis. Hyperplasia is an increase in cell number. Metaplasia is the replacement of one cell type with another. Adaptations can be physiological or pathological responses. Dysplasia and anaplasia represent abnormal cellular changes that can precede cancer.
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
PATHOLOGY -Dr- Ammar Omar -Assistant professor of Histopathology -Departmen...ArfatAlmuallad
This document provides an overview of pathology and inflammation. It defines pathology as the scientific study of disease and outlines its main classifications. It also describes the core components of pathology including etiology, morphological changes, clinical significance, and pathogenesis. Different types of cell injuries, necrosis, and cellular adaptations such as atrophy, hypertrophy, hyperplasia, and metaplasia are discussed. The document concludes with a definition and causes of inflammation.
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).
This is the brief overview on the topic CELL INJURY. After reading this you will get to know about adaptations, types, etiology, pathogenesis of cell injury.
2- Pathology CELL INJURY L1 Medical Sept 2020.pptShady151977
This document outlines objectives and topics to be covered in three lectures on cell injury for first year medical students. The lectures will cover: cell adaptation to stress through hypertrophy, hyperplasia, atrophy and metaplasia; hypoxic cell injury and free radical injury; definitions of apoptosis, necrosis and their differentiation; and pathological accumulations and calcifications. The first lecture will focus on adaptation to stress, hypoxic injury, free radicals and reversible vs irreversible injury.
ROLE OF PATHOLOGIST IN DIAGNOSIS & MANAGEMENT OF DISEASEIra Bharadwaj
A pathologist plays two key roles in patient care: diagnosis of disease and management of disease. For diagnosis, the pathologist uses laboratory tests to confirm clinical diagnoses and determine the specific cause of disease. This informs evidence-based treatment. For management, the pathologist assesses treatment effectiveness through laboratory parameters and ensures safe blood transfusions when needed through the blood bank. As an example, a pathologist would diagnose and monitor the specific cause and treatment of a patient's anemia through hematological tests.
This document discusses primary immune deficiency diseases. It covers the general features, etiology, and types of congenital immune deficiencies including defects of B lymphocytes like X-linked agammaglobulinemia and common variable immunodeficiency. It also discusses defects of T lymphocytes including severe combined immunodeficiency. Other conditions mentioned include DiGeorge syndrome, Wiskott-Aldrich syndrome, and complement deficiencies. Multiple choice questions are provided to test understanding of these conditions.
Wet gangrene occurs due to venous obstruction leading to tissue ischemia and bacterial proliferation in moist tissues. It presents as soft, swollen, foul-smelling black tissue without a clear line of demarcation. Diabetic foot gangrene results from peripheral vascular disease, neuropathy, and infection facilitated by hyperglycemia. Dry gangrene occurs from arterial insufficiency and presents as a dry, shrunken black tissue with a well-demarcated border. Gas gangrene involves Clostridium bacteria producing tissue-damaging toxins and crepitus. Prompt surgical debridement and antibiotics are critical for treatment.
This document provides information about evaluating abnormalities in a semen analysis panel, including:
- The indications, sample collection/transport procedures, and normal ranges for semen volume, pH, motility, concentration, morphology, and other tests.
- How to interpret abnormalities in these parameters, such as low/high volume, pH, motility, oligospermia/azoospermia, teratozoospermia and their potential causes.
- Quality control procedures like repeat testing, and transient defects that could affect initial semen analysis results.
Four clinical cases are then presented to demonstrate applying this evaluation and interpretation of semen analysis results.
The document provides information on cerebrospinal fluid (CSF) examination including indications, collection, analysis, and findings in different conditions like meningitis. It discusses three clinical cases. For case 1, the diagnosis is bacterial meningitis based on cloudy CSF, low glucose, and high neutrophil count. Further tests would include cultures and sensitivity. For case 2, the diagnosis is viral meningitis (measles) based on clear CSF, normal glucose, and lymphocytic pleocytosis; complications include encephalitis. For case 3, the diagnosis is tuberculous meningitis based on low glucose, low chloride, and lymphocytic pleocytosis; confirmation requires microbiological tests.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
-------------------------------------------------------------------------------
Find out more about ISO training and certification services
Training: ISO/IEC 27001 Information Security Management System - EN | PECB
ISO/IEC 42001 Artificial Intelligence Management System - EN | PECB
General Data Protection Regulation (GDPR) - Training Courses - EN | PECB
Webinars: https://pecb.com/webinars
Article: https://pecb.com/article
-------------------------------------------------------------------------------
For more information about PECB:
Website: https://pecb.com/
LinkedIn: https://www.linkedin.com/company/pecb/
Facebook: https://www.facebook.com/PECBInternational/
Slideshare: http://www.slideshare.net/PECBCERTIFICATION
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
3. SLO
• DEFINITION OF ADAPTATION
• TYPES OF ADAPTATIONS
• ATROPHY
• HYPERTROPHY
• HYPERPLASIA
• METAPLASIA
• RELATED CONDITIONS
• DYSPLASIA
• REVISION WITH QUIZ
4. ADAPTATION
DEFINITION
Adaptation is a reversible change in
• size,
• number,
• phenotype,
• metabolic activity, or function of cell
in response to physiological changes or mild
injurious agents in their micro environment
resulting in new steady state preserving
structure and function of the cell.
5. ADAPTATIONS
TYPES
Various types of adaptations are -
• CHANGE IN SIZE OF CELLS - ATROPHY &
HYPERTROPHY –affect all types of cells eg labile,
stable & permanent cells
• CHANGE IN NUMBER OF CELLS - HYPERPLASIA –
affects only labile & stable cells
• CHANGE IN PHENOTYPE - METAPLASIA – affects
only labile & stable cells
6. ATROPHY
DEFINITION – decrease in cell size, may lead to
decreased organ size , depending on number of
cells affected
ETIOLOGY [CAUSE]
PHYSIOLOGICAL- (ka involution )
• notochord
• thyroglossal duct
• Many other embryonic / fetal structures
during embryogenesis or shortly after birth
9. ATROPHY
AUTOPHAGY
• It refers to lysosomal digestion of cell’s own
components
• Survival mechanism of starved cells to
recycle cell contents for nutrition & energy
• Multiprotein complex initiates formation of
autophagic vacuole (autophagosome) near
SER, which fuses with lysosome to form
phagolysosome, digested material is
released for cellular recycling
11. ATROPHY
AUTOPHAGY
PATHOLOGICAL CAUSES
• For clearing misfolded proteins in the cells, eg,
neurodegenerative disorders – Alzheimer,
Huntington
• Infectious organisms like mycobacteria,
shigella, HSV 1,
• Inflammatory bowel disease
• Cancer
12. ATROPHY
C/F & PROGNOSIS-
• Decrease in size of cells & organs,
• Decrease function of cell & organ
• Withdrawal of initiating cause is followed
by recover to normal
• Persistence of cause leads to cell death
14. HYPERTROPHY
PATHOGENESIS
• mechanical stretch,
• increase in growth factors & adrenergic
hormones
• increased protein synthesis,
• change to fetal or neonatal type eg,
alpha myosin of adult muscle replaced by
beta myosin as it is more energy efficient
15. HYPERTROPHY
MORPHOLOGY- increase size of cell &
organ, increase protein in each cell
CLINICAL FEATURES & PROGNOSIS –
• increase work done per cell,
• return to normal if stimulus is
withdrawn,
• degenerative changes or cell injury
occurs if cause persists
18. HYPERPLASIA
DEFINITION- increase in number of cells by
proliferation of cells [labile or stable]
ETIOLOGY
PHYSIOLOGICAL
• Hormonal eg lactation,
• Compensatory, following loss of tissue eg
nephrectomy
19. HYPERPLASIA
PATHOLOGICAL
• Excess hormones
• Excess growth factors,
• Some viral infections
PATHOGENESIS- growth factors are
increased leading to increase in mitotic
activity of cell
21. HYPERPLASIA
C/F & PROGNOSIS-
• Increase number of cells leads to
increase work done by the organ
• Returns to normal on withdrawal of
stimulus,
• If cause & increased mitotic activity
persist; it increases chances of
mutations & may lead to dysplasia &
neoplasia.
22. The normal microscopic appearance of female breast
tissue is shown here. There is a larger duct to the
right and lobules to the left. A collagenous stroma
extends between the structures. A variable amount
of adipose tissue can be admixed with these
elements.
23. The female breast during pregnancy undergoes
lobular hypertrophy & hyperplasia so that
following birth lactation can occur. Seen here are
lobules filled with pink secretions. The breast,
which histologically is a modified sweat gland,
secretes by budding off portions of cell cytoplasm.
24. These breast ducts demonstrate
pathological epithelial hyperplasia. The
epithelial cells are multilayered. There
is no atypia. Thus, there is no increased
risk for carcinoma
25. More florid ductal pathological epithelial
hyperplasia with dysplasia of the breast is
shown here. There is a slightly increased risk
(1.5 to 2 times normal) for breast carcinoma
when such changes are present.
27. METAPLASIA
DEFINITION- reversible change of one type of
adult cell to other type of adult cell [seen in
epithelial (labile) & stable cells]
ETIOLOGY-always pathological-
• Chemicals -tobacco smoke, GI secretions in
inappropriate site eg gastric secretions in
esophagus
• Mechanical – calculi eg in gall bladder &
bladder
28. METAPLASIA
• Vitamin A deficiency,
• Chronic infection eg H pylori
PATHOGENESIS-
• Reprogramming of stem cells to
differentiate to cells better able to
withstand stress
• Accompanied by loss of specialized
cellular function
29. METAPLASIA
MORPHOLOGY-
• Ciliated columnar cells in bronchus
change to squamous cells due to tobacco
smoke
• Squamous epithelium in esophagus
changes to intestinal/gastric type due to
reflux of gastric secretions
30. METAPLASIA
MORPHOLOGY-
• Transitional urothelium of bladder
changes to squamous epithelium due to
mechanical trauma of calculus
• mesenchymal tissues also show features
of metaplasia, though less commonly
than epithelial tissues, eg fibrous tissue
may change to bony tissue, following
repeated mild trauma
31. METAPLASIA
C/F & PROGNOSIS-
• Loss of normal function with survival
advantage eg loss of ciliary function in
bronchial mucosa
• Returns to normal on withdrawal of stimulus
• Increase in incidence of malignancy
[premalignant change]
33. Metaplasia of laryngeal respiratory epithelium has
occurred in a smoker. The chronic irritation has led to
an exchanging of one type of epithelium the normal
respiratory epithelium for another, the more resilient
squamous epithelium. Metaplasia is not a normal
physiologic process and may be the first step toward
neoplasia [premalignant change]
34. RELATED TERMINOLOGY &
CONDITIONS
• DYSPLASIA [discussed in detail]
• HYPOLASIA/AGENESIS [decreased/absence of
formation of structure]
• MALFORMATION [ill formed structure]
35. DYSPLASIA
• Dysplasia also ka atypical hyperplasia is a
growth disorder, usually occurring in
background of hyperplasia & metaplasia
• Dysplasia is a growth disorder, characterized
by loss of uniformity of cells & loss of normal
cellular architecture
• It usually affects the epithelium
36. DYSPLASIA
ETIOLOGY - Chronic inflammation due to any cause
• Chemical - smoking
• Infection – Human Papilloma Virus
• Mechanical - calculi
PATHOGENESIS
Changes in basal cells, which promote mitosis with
decrease differentiation & maturation of cells
37. DYSPLASIA
MORPHOLOGY OF NORMAL EPITHELIUM
• Only basal layer shows mitosis
• Upper layers show features of maturation &
differentiation, with orderly arrangement of cells
• Top layer is that of mature keratinized cells
38. DYSPLASIA
MORPHOLOGY OF DYSPLASTIC EPITHELIUM
• Increased number of layers of epithelial cells
• There is disorientation of cells, the cells are
not arranged in orderly layers eg individual
cells in middle layers may show keratinization
• There is increased mitosis in basal layer
39. DYSPLASIA
MORPHOLOGY OF DYSPLASTIC EPITHELIUM
[continued]
• Cells in upper layers also show mitotic activity
• Pleomorphic cells (variation in size & shape) are
present in all layers of cells
• Hyperchromatic nuclei (large deeply staining
nuclei) are evident in many cells in all layers
40. DYSPLASIA
CLASSIFICATION OF DYSPLASIA:
• MILD dysplasia – affects lower 1/3 of epithelium
• MODERATE dysplasia– affects 2/3 of epithelium
• SEVERE dysplasia also known as carcinoma in situ
( CA-IN-SITU ) – affects all layers of epithelium,
however basement membrane is intact & there is
no invasion
43. MODERATE DYSPLASIA
Dysplastic basal cells occupy the lower two
thirds of the epithelium, characterized by:
• cuboidal shape,
• high nuclear cytoplasmic ratio,
• hyperchromatism,
• mitotic activity, and
• some loss of orientation to the basement
membrane
45. CARCINOMA IN SITU
( SEVERE DYSPLASIA)
• This section shows that the dysplastic basaloid
cells go all the way to the surface
• They never undergo significant differentiation
towards more differentiated flattened
squamous cells.
• Note however that the basement membrane
is still intact.
46. DYSPLASIA
CLINICAL FEATURES
• Dysplasia's are usually asymptomatic or may present
with non specific symptoms
CLINICAL APPLICATION
• It is widely used as a screening tool for neoplasia ,
especially in uterine cervix, a common site for
malignancy, by technique of cytology [pap smear]
PROGNOSIS
• It is reversible in the early, mild & moderate stages
• The later severe stage, if untreated, may progress to
invasive Ca
47. QUIZ 1
ONE OF THESE IS NOT A FEATURE OF
ADAPTATION:
• IRREVERSIBLE CHANGE
• CHANGE IN CELL STRUCTURE
• CHANGE IN CELL FUNCTION
• NEW STEADY STATE
48. QUIZ 2
WHICH OF THESE IS NOT AN ADAPTATION:
• HYPERPLASIA
• METAPLASIA
• HYPOPLASIA
• HYPERTROPHY
49. QUIZ 3
AUTOPHAGY IS:
• INGESTION OF SELF CELLS
• INGESTION OF CELLULAR ORGANELLES
• INGESTION OF INTRA CELLULAR
MULTIPROTEIN COMPLEXES
• PROCESS OF CELL DEATH