Cell injury can occur through various causes like ischemia, toxins, infections, radiation, and genetic defects. The cellular response depends on the severity and duration of the injury. Mild or short injuries may result in reversible cell injury through intracellular accumulation of waste products. Strong or persistent injuries can lead to irreversible cell injury and cell death through necrosis. Cells can also undergo programmed cell death through apoptosis. When faced with stress or injury, cells can adapt through processes like atrophy, hypertrophy, hyperplasia, and metaplasia to achieve a new steady state and preserve viability between the normal and injured states.
Antioxidants are compounds that can act as reducing agents and prevent oxidation reactions. They are used in pharmaceuticals to maintain easily oxidized substances in their reduced form. Oxidation causes damage to cells through free radicals but living organisms contain antioxidant systems like glutathione and vitamins C and E to prevent oxidative damage. Antioxidants prevent reactive oxygen species from being formed or remove them before they can harm cells. Hypophosphorous acid, sulfur dioxide, and sodium thiosulfate are official antioxidants used pharmaceutically to prevent oxidation.
Cell injury can be reversible or irreversible and result from genetic or acquired causes like hypoxia, toxins, microbes. Cells adapt through hypertrophy, hyperplasia, atrophy or metaplasia. Reversible injury causes swelling or fatty change while irreversible injury involves autolysis, heterolysis or necrosis. Necrosis is characterized by loss of membrane integrity, organelle damage and nuclear changes like pyknosis, karyorrhexis and karyolysis. Apoptosis is programmed cell death where intact cells are targeted for phagocytosis.
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.
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
The document summarizes information about various oxygen compounds and anesthetic gases including their production, purity testing, and assay methods. It discusses the manufacture of oxygen through fractional distillation of liquid air or electrolysis of water. Tests for purity of oxygen include checking for carbon dioxide and oxidizing substances. Assay requires at least 99% oxygen by volume. Methods are provided for the production, purity testing involving indicators, and assay of other substances like carbon dioxide, nitrous oxide, diethyl ether, and hydrogen peroxide.
This document summarizes different mediators of inflammation. It describes cell-derived mediators like vasoactive amines (histamine, serotonin), arachidonic acid metabolites from cyclooxygenase and lipoxygenase pathways, lysosomal components, platelet activating factor, cytokines, and nitric oxide. It also discusses plasma-derived mediators including the kinin system, clotting system, fibrinolytic system, and complement system. These mediators cause effects like vasodilation, increased vascular permeability, adhesion of leukocytes, and chemotaxis during inflammation.
This document discusses various hormone therapies and antagonists used to treat cancers like breast cancer and prostate cancer. It describes several classes of drugs including glucocorticoids, estrogens, selective estrogen receptor modulators, aromatase inhibitors, antiandrogens, 5-α reductase inhibitors, and GnRH analogues. For each drug class or individual drug, it provides information on mechanism of action, pharmacokinetics, uses, and adverse effects. The goal of these hormone therapies is to block the effects of hormones like estrogen and androgen that can promote the growth of hormone-sensitive cancers.
This document discusses astringents and their properties. It provides information on zinc sulfate and potash alum, including their formulas, preparation methods, properties, assay methods, and common uses. Zinc sulfate and potash alum are both used as astringents to constrict tissues and stop bleeding from minor wounds. They are also used as nutritional supplements or in water treatment processes.
Antioxidants are compounds that can act as reducing agents and prevent oxidation reactions. They are used in pharmaceuticals to maintain easily oxidized substances in their reduced form. Oxidation causes damage to cells through free radicals but living organisms contain antioxidant systems like glutathione and vitamins C and E to prevent oxidative damage. Antioxidants prevent reactive oxygen species from being formed or remove them before they can harm cells. Hypophosphorous acid, sulfur dioxide, and sodium thiosulfate are official antioxidants used pharmaceutically to prevent oxidation.
Cell injury can be reversible or irreversible and result from genetic or acquired causes like hypoxia, toxins, microbes. Cells adapt through hypertrophy, hyperplasia, atrophy or metaplasia. Reversible injury causes swelling or fatty change while irreversible injury involves autolysis, heterolysis or necrosis. Necrosis is characterized by loss of membrane integrity, organelle damage and nuclear changes like pyknosis, karyorrhexis and karyolysis. Apoptosis is programmed cell death where intact cells are targeted for phagocytosis.
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.
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
The document summarizes information about various oxygen compounds and anesthetic gases including their production, purity testing, and assay methods. It discusses the manufacture of oxygen through fractional distillation of liquid air or electrolysis of water. Tests for purity of oxygen include checking for carbon dioxide and oxidizing substances. Assay requires at least 99% oxygen by volume. Methods are provided for the production, purity testing involving indicators, and assay of other substances like carbon dioxide, nitrous oxide, diethyl ether, and hydrogen peroxide.
This document summarizes different mediators of inflammation. It describes cell-derived mediators like vasoactive amines (histamine, serotonin), arachidonic acid metabolites from cyclooxygenase and lipoxygenase pathways, lysosomal components, platelet activating factor, cytokines, and nitric oxide. It also discusses plasma-derived mediators including the kinin system, clotting system, fibrinolytic system, and complement system. These mediators cause effects like vasodilation, increased vascular permeability, adhesion of leukocytes, and chemotaxis during inflammation.
This document discusses various hormone therapies and antagonists used to treat cancers like breast cancer and prostate cancer. It describes several classes of drugs including glucocorticoids, estrogens, selective estrogen receptor modulators, aromatase inhibitors, antiandrogens, 5-α reductase inhibitors, and GnRH analogues. For each drug class or individual drug, it provides information on mechanism of action, pharmacokinetics, uses, and adverse effects. The goal of these hormone therapies is to block the effects of hormones like estrogen and androgen that can promote the growth of hormone-sensitive cancers.
This document discusses astringents and their properties. It provides information on zinc sulfate and potash alum, including their formulas, preparation methods, properties, assay methods, and common uses. Zinc sulfate and potash alum are both used as astringents to constrict tissues and stop bleeding from minor wounds. They are also used as nutritional supplements or in water treatment processes.
The document discusses homeostasis and cell injury. It defines homeostasis as the body's ability to maintain stable internal conditions despite external changes. It provides examples of homeostasis systems like temperature regulation and blood sugar levels. The document also discusses feedback mechanisms that help regulate homeostasis. It then covers causes of cell injury like hypoxia, chemicals, infections, and genetics. It explains the process of cell injury, including damage to mitochondria, membranes, ribosomes and the nucleus. Overall, the document provides an overview of homeostasis and the pathways involved in cell injury.
Complexometric titration involves the formation of a soluble complex between the analyte metal ion and the titrant. EDTA is commonly used as the chelating agent in the titrant. EDTA forms stable 1:1 complexes with metal ions, allowing for accurate determination of the equivalence point. Metallochromic indicators are used to signal the endpoint, changing color as the metal ion is removed from solution by complexation with EDTA. Selectivity can be improved through methods like masking interfering ions with reagents before titration or controlling the pH.
Cell injury can be reversible or irreversible. Reversible cell injury involves cell swelling and changes to organelles. Irreversible injury leads to cytoplasmic and nuclear changes, as well as damage to mitochondria and plasma membranes. Failure of ATP production in mitochondria during ischemia or hypoxia can cause failure of the sodium-potassium pump, leading to intracellular sodium and calcium accumulation and cellular swelling. There are several types of cell necrosis characterized by different morphological features, including coagulative, liquefactive, caseous, fat and fibrinoid necrosis.
This document describes giant cell tumor, a rare bone tumor. It typically affects people between 20-40 years old and is more common in females. Giant cell tumor originates from primitive stromal cells that promote the proliferation and differentiation of osteoclasts. Common sites are the distal femur, proximal tibia, and lower radius. On x-ray, it appears lytic and expands the bone. Microscopically, it contains multinucleated giant cells and mononuclear stromal cells. Symptoms include pain and arthritis-like symptoms near the affected joint.
The document discusses various dental products including anticaries agents, cleaning agents, and desensitizing agents. It describes the roles of calcium carbonate, sodium fluoride, and stannous fluoride as anticaries agents. It explains the mechanisms of dental caries/plaque formation and how fluoride prevents caries by forming fluorapatite. It also discusses the administration and potential side effects of fluoride overdose. Zinc chloride and strontium chloride are provided as examples of desensitizing agents.
This document discusses the mechanisms of inflammation. It defines inflammation as a protective response against injury from various causes. The cardinal signs of acute inflammation are redness, swelling, heat, pain, and loss of function. The components of the inflammatory response include plasma proteins, circulating cells, connective tissue, and the extracellular matrix. Acute inflammation involves vascular changes like increased permeability and cellular changes like chemotaxis and phagocytosis by neutrophils and macrophages. Chronic inflammation is prolonged and involves mononuclear cell infiltration and tissue destruction and repair.
This document discusses redox titrations. It begins by defining oxidation and reduction reactions. It then discusses different types of redox titrations including cerimetry, iodimetry, iodometry, bromatometry, dichrometry, and titration with potassium iodate. For each type of titration, the document describes the basic principles and provides some examples of applications. The document is presented by Miss Harshada R. Bafna and contains information on concepts, types, and specific techniques for various redox titration methods.
Nonsteroidal anti-inflammatory drugs (usually abbreviated to NSAIDs /ˈɛnsɛd/ en-sed), also called nonsteroidal anti-inflammatory agents/analgesics (NSAIAs) or nonsteroidal anti-inflammatory medicines (NSAIMs), are a drug class that groups together drugs that provide analgesic (pain-killing) and antipyretic (fever-reducing) effects, and, in higher doses, anti-inflammatory effects.
DEFINATION
TYPES OF COUGH
CLASSIFICATION OF EXPECTORANT AND MECHANISM OF ACTION
DEFINATION OF EMETICS
MECHANISM OF ACTION OF EMETICS
COMPOUND RELATED TO EXPECTORANT.
Methods of minimizing errors in chemical analysis involve careful calibration of apparatus, running blanks to account for impurities, using control determinations with standard substances, employing independent analytical methods for comparison, and performing parallel or duplicate determinations. Accuracy refers to how close a measurement is to the true value, while precision describes the agreement between repeated measurements of the same quantity. Significant figures indicate the certainty of measured values and help to properly calculate and report results.
This document describes the limit test for iron according to the Indian Pharmacopoeia. The test involves comparing the color produced by reacting a sample with thioglycolic acid in an ammonical citrate buffer to the color produced by a standard iron solution under the same conditions. If the color produced by the sample is less than the standard, it passes the limit test for iron. If the color is greater than the standard, it fails the limit test. The test is sensitive and uses citric acid to eliminate interference from other metal cations.
This document provides information about various gravimetric analysis techniques including precipitation gravimetry, volatilization gravimetry, electrogravimetry, and thermogravimetry. It explains that gravimetric analysis involves determining the mass of a compound or element through a chemical reaction such as precipitation or volatilization. Key steps like precipitation, filtration, drying and calculation are outlined for the common example of chloride analysis via silver chloride precipitation. Advantages and disadvantages of gravimetric analysis are also summarized.
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.
Zinc toxicity is summarized in 3 sentences:
Zinc is an essential mineral but can be toxic in high amounts. Acute zinc toxicity from ingestion causes nausea, vomiting, and stomach cramps, while chronic high intake over months can lead to copper deficiency, decreased immune function, and fatigue. Inhalation of zinc oxide fumes can cause metal fume fever, a temporary flu-like illness.
Poisons are substances that cause illness and death when absorbed by the body. Antidotes counteract or oppose the effects of poisons and are used to treat poisoning. There are three types of antidotes - physiological antidotes counteract poison effects chemically, mechanical antidotes prevent poison absorption, and chemical antidotes convert poisons to non-toxic compounds. Sodium thiosulfate and sodium nitrite are antidotes used to treat cyanide poisoning.
This document discusses the principles and methods of gravimetric analysis. Gravimetric analysis involves quantitatively estimating an element or compound based on weighing it after isolation. The key steps are: 1) converting the analyte into an insoluble precipitate of known composition, 2) purifying it by washing, 3) weighing the dried residue to calculate the amount of analyte based on its composition. Common gravimetric methods include precipitation, volatilization, electrogravimetry, and particulate methods. Considerations for choosing appropriate precipitates and weighed forms include solubility, structure, and composition.
Major intra and extra cellular electrolyteskalyaniGopale1
This document discusses the major intracellular and extracellular electrolytes in the body. It begins by defining electrolytes as ions that dissociate in body fluids. The main electrolytes discussed are sodium, calcium, chloride, potassium, magnesium, sulfate, bicarbonate, and phosphate. For each electrolyte, the normal levels, locations, and functions in the body are described. Potential deficiencies or excesses of each electrolyte are also summarized, along with their symptoms and treatment.
This document discusses the epidemiology, pathogenesis, and histopathology of fatty liver disease. It covers both non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). For NAFLD, key points include its increasing prevalence due to the rise in obesity and diabetes. The pathogenesis involves insulin resistance leading to lipid accumulation in the liver. Histologically, NAFLD is graded based on steatosis, lobular inflammation, and hepatocyte ballooning. For ALD, heavy drinking can lead to steatosis in most people, while a subset develop alcoholic steatohepatitis. The pathogenesis of ALD also involves oxidative stress and cytokine pathways. Liver biopsy remains the gold standard
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.
Cells are constantly adjusting to their environment and stresses to maintain homeostasis. Adaptive responses include atrophy, hypertrophy, hyperplasia and metaplasia. If stresses exceed adaptive capabilities, reversible or irreversible cell injury occurs. Causes of injury include oxygen deprivation, chemicals, infections, immune reactions, genetics, nutrition and physical agents. Injuries include ischemic, free radical and toxic injuries. Cells adapt through changes in size, number or cell type to withstand stresses or return to viability.
The document discusses homeostasis and cell injury. It defines homeostasis as the body's ability to maintain stable internal conditions despite external changes. It provides examples of homeostasis systems like temperature regulation and blood sugar levels. The document also discusses feedback mechanisms that help regulate homeostasis. It then covers causes of cell injury like hypoxia, chemicals, infections, and genetics. It explains the process of cell injury, including damage to mitochondria, membranes, ribosomes and the nucleus. Overall, the document provides an overview of homeostasis and the pathways involved in cell injury.
Complexometric titration involves the formation of a soluble complex between the analyte metal ion and the titrant. EDTA is commonly used as the chelating agent in the titrant. EDTA forms stable 1:1 complexes with metal ions, allowing for accurate determination of the equivalence point. Metallochromic indicators are used to signal the endpoint, changing color as the metal ion is removed from solution by complexation with EDTA. Selectivity can be improved through methods like masking interfering ions with reagents before titration or controlling the pH.
Cell injury can be reversible or irreversible. Reversible cell injury involves cell swelling and changes to organelles. Irreversible injury leads to cytoplasmic and nuclear changes, as well as damage to mitochondria and plasma membranes. Failure of ATP production in mitochondria during ischemia or hypoxia can cause failure of the sodium-potassium pump, leading to intracellular sodium and calcium accumulation and cellular swelling. There are several types of cell necrosis characterized by different morphological features, including coagulative, liquefactive, caseous, fat and fibrinoid necrosis.
This document describes giant cell tumor, a rare bone tumor. It typically affects people between 20-40 years old and is more common in females. Giant cell tumor originates from primitive stromal cells that promote the proliferation and differentiation of osteoclasts. Common sites are the distal femur, proximal tibia, and lower radius. On x-ray, it appears lytic and expands the bone. Microscopically, it contains multinucleated giant cells and mononuclear stromal cells. Symptoms include pain and arthritis-like symptoms near the affected joint.
The document discusses various dental products including anticaries agents, cleaning agents, and desensitizing agents. It describes the roles of calcium carbonate, sodium fluoride, and stannous fluoride as anticaries agents. It explains the mechanisms of dental caries/plaque formation and how fluoride prevents caries by forming fluorapatite. It also discusses the administration and potential side effects of fluoride overdose. Zinc chloride and strontium chloride are provided as examples of desensitizing agents.
This document discusses the mechanisms of inflammation. It defines inflammation as a protective response against injury from various causes. The cardinal signs of acute inflammation are redness, swelling, heat, pain, and loss of function. The components of the inflammatory response include plasma proteins, circulating cells, connective tissue, and the extracellular matrix. Acute inflammation involves vascular changes like increased permeability and cellular changes like chemotaxis and phagocytosis by neutrophils and macrophages. Chronic inflammation is prolonged and involves mononuclear cell infiltration and tissue destruction and repair.
This document discusses redox titrations. It begins by defining oxidation and reduction reactions. It then discusses different types of redox titrations including cerimetry, iodimetry, iodometry, bromatometry, dichrometry, and titration with potassium iodate. For each type of titration, the document describes the basic principles and provides some examples of applications. The document is presented by Miss Harshada R. Bafna and contains information on concepts, types, and specific techniques for various redox titration methods.
Nonsteroidal anti-inflammatory drugs (usually abbreviated to NSAIDs /ˈɛnsɛd/ en-sed), also called nonsteroidal anti-inflammatory agents/analgesics (NSAIAs) or nonsteroidal anti-inflammatory medicines (NSAIMs), are a drug class that groups together drugs that provide analgesic (pain-killing) and antipyretic (fever-reducing) effects, and, in higher doses, anti-inflammatory effects.
DEFINATION
TYPES OF COUGH
CLASSIFICATION OF EXPECTORANT AND MECHANISM OF ACTION
DEFINATION OF EMETICS
MECHANISM OF ACTION OF EMETICS
COMPOUND RELATED TO EXPECTORANT.
Methods of minimizing errors in chemical analysis involve careful calibration of apparatus, running blanks to account for impurities, using control determinations with standard substances, employing independent analytical methods for comparison, and performing parallel or duplicate determinations. Accuracy refers to how close a measurement is to the true value, while precision describes the agreement between repeated measurements of the same quantity. Significant figures indicate the certainty of measured values and help to properly calculate and report results.
This document describes the limit test for iron according to the Indian Pharmacopoeia. The test involves comparing the color produced by reacting a sample with thioglycolic acid in an ammonical citrate buffer to the color produced by a standard iron solution under the same conditions. If the color produced by the sample is less than the standard, it passes the limit test for iron. If the color is greater than the standard, it fails the limit test. The test is sensitive and uses citric acid to eliminate interference from other metal cations.
This document provides information about various gravimetric analysis techniques including precipitation gravimetry, volatilization gravimetry, electrogravimetry, and thermogravimetry. It explains that gravimetric analysis involves determining the mass of a compound or element through a chemical reaction such as precipitation or volatilization. Key steps like precipitation, filtration, drying and calculation are outlined for the common example of chloride analysis via silver chloride precipitation. Advantages and disadvantages of gravimetric analysis are also summarized.
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.
Zinc toxicity is summarized in 3 sentences:
Zinc is an essential mineral but can be toxic in high amounts. Acute zinc toxicity from ingestion causes nausea, vomiting, and stomach cramps, while chronic high intake over months can lead to copper deficiency, decreased immune function, and fatigue. Inhalation of zinc oxide fumes can cause metal fume fever, a temporary flu-like illness.
Poisons are substances that cause illness and death when absorbed by the body. Antidotes counteract or oppose the effects of poisons and are used to treat poisoning. There are three types of antidotes - physiological antidotes counteract poison effects chemically, mechanical antidotes prevent poison absorption, and chemical antidotes convert poisons to non-toxic compounds. Sodium thiosulfate and sodium nitrite are antidotes used to treat cyanide poisoning.
This document discusses the principles and methods of gravimetric analysis. Gravimetric analysis involves quantitatively estimating an element or compound based on weighing it after isolation. The key steps are: 1) converting the analyte into an insoluble precipitate of known composition, 2) purifying it by washing, 3) weighing the dried residue to calculate the amount of analyte based on its composition. Common gravimetric methods include precipitation, volatilization, electrogravimetry, and particulate methods. Considerations for choosing appropriate precipitates and weighed forms include solubility, structure, and composition.
Major intra and extra cellular electrolyteskalyaniGopale1
This document discusses the major intracellular and extracellular electrolytes in the body. It begins by defining electrolytes as ions that dissociate in body fluids. The main electrolytes discussed are sodium, calcium, chloride, potassium, magnesium, sulfate, bicarbonate, and phosphate. For each electrolyte, the normal levels, locations, and functions in the body are described. Potential deficiencies or excesses of each electrolyte are also summarized, along with their symptoms and treatment.
This document discusses the epidemiology, pathogenesis, and histopathology of fatty liver disease. It covers both non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). For NAFLD, key points include its increasing prevalence due to the rise in obesity and diabetes. The pathogenesis involves insulin resistance leading to lipid accumulation in the liver. Histologically, NAFLD is graded based on steatosis, lobular inflammation, and hepatocyte ballooning. For ALD, heavy drinking can lead to steatosis in most people, while a subset develop alcoholic steatohepatitis. The pathogenesis of ALD also involves oxidative stress and cytokine pathways. Liver biopsy remains the gold standard
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.
Cells are constantly adjusting to their environment and stresses to maintain homeostasis. Adaptive responses include atrophy, hypertrophy, hyperplasia and metaplasia. If stresses exceed adaptive capabilities, reversible or irreversible cell injury occurs. Causes of injury include oxygen deprivation, chemicals, infections, immune reactions, genetics, nutrition and physical agents. Injuries include ischemic, free radical and toxic injuries. Cells adapt through changes in size, number or cell type to withstand stresses or return to viability.
This document outlines the various causes and mechanisms of cell injury. It discusses how oxygen deprivation, physical and chemical agents, infections, immune reactions, and nutritional imbalances can all lead to cell injury through mechanisms like ATP depletion, mitochondrial damage, calcium dysregulation, and oxidative stress. These mechanisms disrupt critical cellular processes and structures like membranes, ultimately leading cells to die through necrosis or apoptosis.
1.1 Basic principles of Cell injury.pptxMUNEZEROEvase
This document provides an overview of basic principles of cell injury and adaptation. It defines key terms like homeostasis, feedback systems, and causes of cellular injury. The main mechanisms of cellular injury include damage to the cell membrane, mitochondria, ribosomes, and nucleus. Cells can adapt to injury through processes like atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia, which refer to changes in cell size and number. The document also discusses examples of homeostasis maintenance through negative and positive feedback systems.
This document summarizes the key biochemistry processes involved in aging. It discusses how aging leads to a decline in biological functions over time due to factors like mitochondrial damage and free radicals. This causes changes in organs such as reduced immunity and loss of muscle strength. The document also examines specific aging-related processes like telomere shortening, apoptosis, protein and DNA modification from free radical damage, and diseases that affect the elderly like progeria. Gerontology focuses on studying these age-related changes while geriatrics aims to promote health in older adults.
Biochemistry of Aging
Presented by Shanzay Annum Malik
Aging
Gradual change in an organism that leads to increased risk of weakness, disease, and death over the entire adult life span of any living thing.
There is a decline in biological functions and in ability to adapt to metabolic stress.
Changes in organs include
reduced immunity,
loss of muscle strength,
decline in memory and cognition,
loss of colour in the hair
elasticity in the skin.
Gerontology and Geriatrics
Gerontology is concerned with the changes that occur between maturity and death along with factors that influence these changes.
Geriatrics focuses on health care of elderly people and promote health by preventing and treating diseases and disabilities in older adults.
Factors of Aging
Mitochondria: main unit of chemical power supply
During the synthesis of macroergical bio-molecules(high energy releasing potentials e.g. ATP) free radicals are being produced as the by-product.
Free radicals released in large quantities cause intercellular oxidative stress (e.g. oxidative damage of mitochondria)
damaging mitochondria and cause early apoptosis
Free radical
A molecule that contains one or more unpaired electrons &is capable of independent existence.
Eg : Superoxide H2O2,
hydroperoxy radical (HOO+2 )
lipid peroxideradical (ROO)
Nitric oxide (NO)
Harmful effect of free radicals
Because of their reactive nature, free radical can provoke inflammation or altered cellular function through
Lipid peroxidation
Protein modification
DNA modification
Lipid peroxidation product:
React with amino acid mainly CYS, HIS,LYS to modify protein structure & function.
Can crosslink lipid in cell membrane interrupting structure & fluidity.
Protein modification
DNA modification :
Free radical induced DNA damage includes
strand break.
DNA protein crosslink.
large range of base & sugar modification.
Telomeres
Repetitive DNA sequences at the ends of all human chromosomes
aging cells have shorter telomeres
length differs between species
in humans 8-14kb long
Telomeres are thought to be the "clock" that regulates how many times an individual cell can divide.
Telomeric sequences shorten each time the DNA replicates.
Once the telomere shrinks to a certain level, the cell can no longer divide. Its metabolism slows down, it ages, and dies
Apoptosis and Necrosis
There are two ways that a cell can die:
Necrosis occurs when a cell is damaged by an external force, such as poison, a bodily injury, an infection or getting cut off from the blood supply (which might occur during a heart attack or stroke). When cells die from necrosis, it's a rather messy affair. The death causes inflammation that can cause further distress or injury within the body.
Apoptosis or programmed cell death
When a cell is compelled to commit suicide proteins called caspases go into action.
They break down the cellular components needed for surviva
Mechanism of cell injury
Types of cell injury
Reversible and irreversible cell injury
Etiology of cell injury
Apoptosis, it's types and mechanism
Necrosis, it's types and mechanism
This document provides an introduction to general pathology, which is concerned with the study of cellular and tissue-level changes that underlie disease. It discusses the causes of cell injury, including physical, chemical, infectious, immunological, nutritional, and genetic factors. Reversible cell injury features swelling and changes to organelles that are repairable, while irreversible injury leads to cell death through necrosis or apoptosis. Necrosis is characterized by loss of membrane integrity and digestion of cellular contents, resulting in increased eosinophilia and nuclear changes like karyolysis, pyknosis, and karyorrhexis. Different types of necrosis include coagulative, liquefactive, caseous, and fibrinoid.
This document provides an overview of cell injury, adaptation, and death. It discusses how cells maintain homeostasis but can undergo injury from various stressors like hypoxia, chemicals, physical trauma, infections, etc. If the injury is too severe, the cells die. The mechanisms of injury involve loss of energy, mitochondrial damage, loss of calcium homeostasis, defects in membrane permeability, and generation of reactive oxygen species. Cells can adapt to injury through atrophy, hypertrophy, hyperplasia, or metaplasia. Reperfusion after ischemia can paradoxically cause more damage through calcium overload and free radical production.
Aging is characterized by a declining ability to respond to stress and increased risk of disease. Differences in maximum lifespan between species correspond to different rates of aging, affected by genetic factors. Cells lose the ability to divide and function through the process of senescence. Traditional theories of aging include programmed and stochastic theories. More recent theories include molecular, cellular, and system-level theories. The free radical theory proposes that oxidative damage from free radicals produced during metabolism accumulates over time and causes aging. Telomere shortening leads to cell senescence.
Cell aging is characterized by a declining ability to respond to stress and increased homeostatic imbalance. Aging theories include programmed and stochastic theories. More recently, theories are categorized as molecular, cellular, and system-level. The free radical theory of aging proposes that reactive oxygen species generated during metabolism cause cumulative oxidative damage, resulting in structural degeneration, apoptosis, functional decline, and age-related diseases. Some believe oxidative stress is the predominant cause of age-associated degenerative changes. Telomere shortening causes cell senescence as telomeres reach a critical length after repeated cell division.
This document discusses cell injury, adaptations, and degenerations in pathology. It begins by defining key terms like etiology, pathogenesis, and morphology. It then explains the causes of cell injury including hypoxia, physical agents, chemicals, microbes, and immune reactions. The document delves into the pathogenesis of cell injury, noting factors like the type, duration, and severity of the injurious agent and target cell characteristics. It also describes the mechanisms of cell injury such as ATP depletion, mitochondrial damage, calcium influx, oxidative stress, and membrane permeability defects. Finally, it distinguishes between reversible and irreversible cell injury.
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.
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 cell death. It describes how cells can adapt through hyperplasia, hypertrophy, and atrophy in response to stimuli. Irreversibly injured cells may undergo necrosis or apoptosis. Necrosis is characterized by cellular swelling, fatty change, and nuclear changes like pyknosis and karyorrhexis. Oxidative stress from free radicals and mitochondrial damage are mechanisms of cell injury. Membrane damage can also occur through defects in permeability. Cellular accumulations provide signs of injury. Forensic pathologists commonly observe fat, iron, and calcification accumulations as well as coagulative necrosis.
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.
- Aging is characterized by a declining ability to respond to stress, increasing homeostatic imbalance, and higher risk of disease. It is a degenerative process with no positive features.
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1. The presentation discusses the pathogenesis of cell injury, outlining factors like the type, duration, and severity of injurious stimuli and the target cell's adaptability.
2. Common mechanisms of cell injury are discussed, including ATP depletion, mitochondrial damage, calcium influx, oxidative stress, and membrane permeability defects.
3. Specific causes of injury like ischemia and hypoxia can lead to ATP loss, pH changes, impaired sodium pumping, and decreased protein synthesis, ultimately causing reversible or irreversible cell injury.
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.
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2. Cell Injury, Adaptation and Death
• Overview of cell injury
• Causes of cell injury
• Mechanisms of cell injury
• Cellular adaptation to injury
• Reversible and irreversible cell injury
• Programmed cell death---- apoptosis
• Cellular aging
3. Overview of cell injury
• Cells in a living, health person participate
actively in their microenvironment.
• They must adjust their structure and function to
fit the dynamic changed demands and stress.
• There must be a homeostasis to keep the
harmonization between cells and extracellular
environment which requires functional
cooperation amongst widely distributed cells.
• If the demands or stress persist a long time, or
they are too strong to exceed the adjusting
range, the cells will be damaged.
5. Cell response to injury
• When the stimuli are mild and continuous, the
involved cells, tissue and organ can fit them
through adaptation.
• When the stimuli are strong or persisted, the
cells will be dead (necrosis).
• When the stimuli are intermediate, there is
reversible cell injury: intracellular accumulation
(so called degeneration).
• Note the reversibility of injured cells.
7. Hypoxia = deficiency in oxygen at cell Due to :
Decreased oxygen in air
Decreased hemoglobin or decreased oxygen
transported to cells
Diseases of the respiratory and/or cardiovascular
system
Oxygen is important to cell because of oxidative
phosphorylation, which results in the production
of ATP
8. Cellular response to hypoxia
Decreased mitochondrial reactions
decreased ATP produced
decreased energy
Ion pumps cease, so can't regulate ions
into/out of cell (ATP needed for this)
Can't pump Na+ and water out of cell, so get
cell swelling organelle swelling
cell death
9. Mechanisms of ischemic cell injury
• ATP depletion
• Oxygen deprivation and/or generation of
reactive oxygen species (Free radicals).
• Loss of calcium homeostasis
• Defects in plasma membrane permeability
• Mitochondria damage
• Cell death
10. Mechanism of ischemic and hypoxic injury
Reversible cell
injury . Diminished
oxidative
phosphorylation
and ATP levels
play a central role
in mediating
intracellular effects
(K+ ion, Ca++ ion).
Note: all changes
are potentially
reversible, if the
blood supply
restore in time.
Glycolysis:
anaerobic
glycolysis
11. Free radicals : are chemical species (Unstable atom/s)
with a single unpaired electron on their outer orbital.
Formed by: cell metabolism reactions, radiation,
chemicals (Ex. reduction-oxidation reaction inside
mitochondria which yield small amounts of toxic
intermediate species are generated.
Atom is unstable (needs to gain or lose an electron)
• can alter chemical bonds in proteins, lipids,
carbohydrates and nucleic acids
• can cause chain reaction in cell
Common free radicals: superoxide, hydrogen peroxide
(H2O2) and hydroxyl free (OH•), nitric oxide (NO) .
12. Neutralization of free radicals
• Normally, there are several enzymic and nonenzymic
systems to inactivate free radicals. Examples.
• Superoxide dismutases (SOD) catalyze the reaction
of 2 superoxide p+ 2 hydrogens (H+) to hydrogen
peroxide (H2O2) plus oxygen (O2).
• Catalase converts hydrogen peroxides to H2O & O2.
• Glutathione peroxidase catalyzes free radical
breakdown. In Fenton reaction 2 molecules of
hydroxyl radical plus 2 molecules of reduced
glutathione (GSH) give 2 molecules of water and one
molecule of oxidized glutathione (GSSH).
14. Cell mechanisms of injury due to Free Radicals
Free radicals/ reactive chemicals
Normal
metabolisms
O 2
OH•
H2O2
NO
Superoxide dismutases SOD/Catalase
Glutathiole peroxidase/GSSG
Vitamin E, C
Detoxification
Cell membrane
Mitochondria
Endo. Retic.
DNA
15. Effects of Free Radicals
• they attack & destroy the cell membrane,
nuclear acid, mitochondria and endoplasmic
reticulum and lead to cell damage.
• With ischemia, there will be Increased Ca++
concentration inside cells which activates
phospholipases, proteases, ATPases and
endonucleases.
• These activated enzymes lyse the structures of
cells and lead the cell death.
16. Intracellular accumulations/ Intoxication
• Substances that can’t used or disposed off & toxins inhaled or
introduced into cell. Effect on cell depends on toxin and on cell
• Normal body substances (wear & Tear)
• Abnormal products (errors of metabolism) – phenylketonuria
• Substances from outside Fe & Copper deposition
• Lead – CNS toxin – interferes with neurotransmitters causing
hyperactivity. Lead paints cause anemia & toxicity
• CO – binds irreversibly to Hb & deprives body of O2
• Ethanol – CNS toxic – liver toxin- interrupts protein transport –
can cause fetal alcohol syndrome
• Mercury – neurotoxin can cause bone deformities
• Social or street addictive drugs (Marijuana, heroin, hashish,
Tramal).
17. 17
Trauma: Unintentional and Intentional
Injuries
• Blunt force injuries
– Application of mechanical energy to the body
resulting in the tearing, shearing, or crushing of
tissues
– Contusion vs. hematoma – bleeding in skin &
underlying layers
– Abrasion – removal of superficial skin layers
– Laceration or puncture of skin & other layers
– Fractures – broken bones
19. 19
Unintentional & Intentional Injuries
• Unintentional injuries are harmful acts that occurred without
any intention of causing damage to oneself or others. It occur
in or around the home and many of these injuries occur as a
result of falls, streets, highways, and recreational areas.
• intentional injuries, which are injuries resulting from
purposeful harmful actions upon oneself or others.
• Gunshot wounds
– Entrance wounds (small)
• Close-Contact range entrance wound
• Intermediate range entrance wound (tattooing and
stippling)
– Exit wounds (Large) - Shored exit wound
22. 22
Infectious Injury
• Pathogenicity of a microorganism – gram (-) or (+) will
determine which antibiotics to use or anti viral agents
for viral infections
• Virulence: some strains are more dangerous than
others.
• Can affect entire body (fever, pain, increased heart
rate)
• Disease-producing potential
– Invasion and destruction
– Toxin production
– Production of hypersensitivity reactions
23. 23
Immunologic and Inflammatory Injury
• Phagocytic cells – immune cells that engulf and
destroy invading microbes and toxins
• Immune and inflammatory substances
– Histamine (released by injured or infected cells that
cause local vasodilation), antibodies (endogenous
proteins that combat and identify invading cells and
toxins), lymphokines (chemical produced by imune
cells), complement, and enzymes
• Membrane alterations – leakage of cell contents
due to the presence of antibodies and
histamines
24. 24
Injurious Genetic Factors
• Nuclear alterations: mutations & damage to
DNA
• Alterations in the plasma membrane structure,
shape, receptors, or transport mechanisms
• Examples of genetic diseases
– Down syndrome
– Sickle cell anemia
– muscular dystrophy
25. 25
Injurious Nutritional Imbalances
• Essential nutrients are required for cells to
function normally inadequate proteins,
carbohydrates, fats, vitamins, minerals
• Deficient intake – starvation and improper
diets – protein deficiency “kwashiokor” most
common, Vitamin B 12 deficiency leads to
pernicious anemia, Vit C DEF. --- SCURVY.
• Excessive intake - obesity
27. 27
Atmospheric Pressure Changes
• Sudden increases or decreases in
atmospheric pressure
–Blast injury
–Nitrogen Narcosis or rapture of the deep
Nitrogen gas has a narcotic effect (laughing
gas)
–Decompression sickness (caisson disease)
• “The bends”
28. 28
Ionizing Radiation
• Any form of radiation capable of removing
orbital electrons from atoms
–X-rays, gamma rays, alpha and beta particles
–Amount of exposure measured in RADS.
People working with X-rays must wear badge
that measures doses of exposure over time
• Mechanism of damage – ionization of
chemicals and breakage of chemical
bonds
30. 30
Light & sound cell injury
• Illumination injury
– Eyestrain, obscured vision, and cataract formation
– Caused by light modulation
• Mechanical stresses
– Physical impact or irritation
• Noise – sound can cause tisse and organ
trauma
– Acoustic trauma and noise-induced hearing loss –
tinnitus very common among performing rock band
members
31. Apoptosis
• Cells “fallen apart”
• Regulated cell death during development
• Worn out cells
• Diseased cells (tumor suppressor p53
gene, natural killer or Tc cells)
Cell aging
• Programmed cell change theories
• Developmental Error theories
• Telomerase errors
32. 32
Aging
• Cellular aging: all cells can replicate 40 –
60 times max and may be why clones do
not live as long as parents.
• Tissue and systemic aging: immune
function goes down with age and free
radicals damage cells speeding aging
–Frailty – wasting syndrome of aging due to
decreased protein synthesis and reduced
muscle mass and lowered bone density
33. Summary of cell injury
• Any stimuli and stresses can result in cell
injuries.
• The injurious consequences depend on not only
the type of injury, its duration, its severity, and
also the type, status, adaptability and genetic
makeup of the injured cell.
• Cell injury can be divided into reversible and
irreversible.
• The loss of cell function is far before the cell
death, but the morphological visible changes
appear far behind the cell death.
35. Cellular adaptation to injury
Adaptation: When cells encounter physiologic
stresses or pathologic stimuli from outside and
inside of body, they can alter themselves to
achieve a new steady state and preserve
viability.
• All kinds of adaptation may be considered as
disorders of growth and/or differentiation
• Cellular adaptation can be considered as a
state between the normal, unstressed cell and
injured, overstressed cell.
37. Cells Adaptive responses to injuries & Inflammation
• Atrophy, Aplasia, Agenesis
– a = without
– nourishment, form, begining
• Hypertrophy
– hyper = above, more
– trophe = nourishment, food
• Hyperplasia
– plastein = (v.) to form, to shape;
(n.) growth, development
• Hypoplasia
– hypo = below, less
• Metaplasia
– meta = change or beyond
• Dysplasia
– dys = bad or disordered
• Factors behind these
changes
• Altered demand (muscle
activity)
• Altered stimulation
(growth factors,
hormones)
• Altered nutrition &
Substances use
(including gas exchange)
38. Atrophy
• Definition: (briefly, decrease in cell size)
Shrinkage in the size of the parenchymal cells by
loss of cell substances in a well developed organ or
tissue is known as atrophy. Or acquired shrinkage of
cells, tissues or organs.
• Simple atrophy (loss of cell size only)
• Numerous atrophy (loss of cell size and number
through apoptosis)
• Differentiation: aplasia, hypoplasia
40. kidneys & ureters of a one-year-old boy. The Rt Kidney is
hypoplastic and the LT one with a three-ureters abnormality.
41. The reasons of atrophy
Decreased workload ------disuse atrophy
Loss of innervation ------neuropathic atrophy
Diminished blood supply --ischemic atrophy
Absence of nutrition -----undernourished atrophy
Loss of hormone stimuli -- endocrine atrophy
Aging process --- senile atrophy
42. Brain atrophy in an old patient with arteriosclerosis. Note the
widened sulci and narrow convolutions.
43. Brain atrophy in a patient with Alzheimer’s disease. The gyri
are narrowed and the sulci widened toward to frontal pole.
44. some skeletal muscle fibers. The number of cells is the same as
before atrophy occurred, but the size of some fibers is reduced.
In this case, innervation of the small fibers in the center was lost.
This is a trichrome stain.
Muscle Atrophy
45. Atrophy
• The atrophied cells, tissue and organ have
the following caracteristics:
– Reduction of physiologic functions
– Decreased synthesis
– Increased catabolism—increased protein
degradation through
Lysosomes digest the senescent organelles
(autolysis)
– If the number of cells decrease, there is
apoptosis (cell suicide), or programmed cell
death
46. Hypertrophy
• Definition: (briefly: increase in cell size)
• an increase in the size of parenchymal cells
and consequently an increase in the size of
the organ.
No increase of cell
number in a purified
hypertrophy!
48. Physiologic hypertrophy of the uterus during pregnancy.
Left: gross appearance of a normal uterus and a gravid uterus.
Middle: small spindle-shaped uterine smooth muscle cells from
A normal uterus.
Right: large, plump hypertrophied smooth muscle cells from
a gravid uterus.
50. Hypertrophy of left ventricle (centripetal hypertrophy) in
a patient with essential hypertension. Note the marked
thickened wall of ventricle.
51. a. Hypertrophy of the left ventricle
b. Normal myocardial fibers
c. Hypertrophic myocardial fibers
52. Hypertrophy
Hypertrophic cells & organ are characterized with:
• Increased function
• Increased synthesis of structural protein
• Induced by two types of signals
– Mechanical triggers:-stretch
– Trophic triggers:-activation of alpha-adrenergic
receptors
Different from hyperplasia & pseudohypertrophy (a
pathologic situation . Ex.in myasthenia gravis, a type
of myopathy caused by hyperplastic thymus or
thymoma. In this condition the muscles in lower limbs
are atrophied and replaced by fat, so the legs of
patient look enlarged. It is actually real atrophy.
53. Hyperplasia
• Definition: (briefly, increase in cell number)
• An increase in the number of parenchymal
cells in an organ or tissue.
• Hyperplasia can occur with hypertrophy in
various tissue except muscles.
• Hyperplasia can be divided into
– Physiologic hyperplasia
• Hormonal: breast glandular epithelium at
pregnancy
– Pathologic hyperplasia
• Compensatory: liver after partial resection
54. Hyperplasia of endometrium in an adult woman with menorrhagia
(too much bleeding of menses in an adult woman )
58. Hyperplasia of
prostatic gland - The
reason of hyperplasia is
exceeding androgen
secretion which leads
hyperplasia of prostatic
gland and stroma cells
Note the prostate is
nodular enlarged
59. Hyperplasia
• Hyperplasia is induced by
stimulation of hormonal or growth
factors, cytokines and chemokines
through the signal transduction
pathway.
• Hyperplasia can turn off when the
organ restores or the stimulus
stops
• Continuous pathologic hyperplasia
constitutes a fertile soil for
cancerous proliferation
60. Metaplasia
• Definition: (briefly: change in cell type)
• A reversible change in which one adult cell type
is replaced by another adult cell type.
• This replacement is through hyperplasia of
“stem cell” or “undifferentiated cell”, so
metaplasia is actually an abnormal hyperplasia.
• The significances of metaplasia are
– To be able to withstand the stress better
– To be able to transform into a cancerous
proliferation
66. Dysplasia
• Dysplasia is considered as an abnormal
epithelial hyperplasia with the loss of the normal
cell architectural orientation and uniformity of
the individual cells.
• change in cell resulting in abnormal cell size,
shape or organization (Seen In mature cells only,
in respiratory tract, cervix w/ pathology)
– Immature cells are normally expected to
change in size, shape as they grow and
mature
• Considered a reversible change
68. Neoplasia
• Neoplasia (from Ancient Greek neo- "new" and plasma
"formation creation"), is an abnormal growth of tissue,
and when also forming a mass called tumor or tumour,
• The World Health Organization (WHO) classifies
neoplasms into four main groups: benign neoplasms, in
situ neoplasms, malignant neoplasms, and neoplasms of
uncertain or unknown behavior. Malignant neoplasms are
also simply known as cancers.
• Prior to the abnormal growth of tissue, as neoplasia, cells
often undergo an abnormal pattern of growth, such as
metaplasia or dysplasia. However, metaplasia or
dysplasia do not always progress to neoplasia.
69.
70. Summary of adaptation
• Shrinkage of an organ can result from
– Atrophy
– Aplasia and hypoplasia
• Hyperplasia persists only for so long as the
stimulus is applied. When it is removed, the
hyperplastic tissue tends to revert to its normal
size.
• Hyperplasia must be distinguished from
dysplasia and neoplastic proliferation.
71. Summary of adaptation
• Metaplasia is an abnormal hyperplasia.
• It can become a malignant neoplasm.
• All kind of adaptation can be considered as
abnormal growth and/or differentiation
• Adaptation is the result of long time persisted,
but mild stimuli
• Most adaptations are reversible when the
stimulus is removed