Tissue renewal
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GENERAL PATHOLOGY
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Repair 2017
Tissue repair occurs through two main processes: regeneration and scar formation. Regeneration involves the proliferation of residual cells to replace damaged tissue. Some tissues like skin and liver can regenerate fully. Scar formation involves the deposition of connective tissue when regeneration is not possible. This involves granulation tissue formation, fibronectin production, collagenization, and scar maturation. Cell proliferation in repair is regulated by growth factors and the extracellular matrix plays a key role in wound healing and scar formation.
Repair 2
This document discusses the process of wound healing through first and second intention. It begins by outlining the steps of healing by first intention for clean surgical incisions, including clot formation, re-epithelialization across the wound by day 3, and collagen deposition and scar maturation over subsequent weeks. Healing by second intention for wounds with separated edges involves more granulation tissue formation and wound contraction to reduce the gap between tissue edges. Complications can arise from deficient or excessive scar formation, including dehiscence, ulceration, hypertrophic scarring, and contractures.
Repair and healing_1
Tissue repair occurs through two main processes: regeneration and scar formation. Regeneration involves the proliferation of residual cells to replace damaged tissue. Some tissues like skin and liver can regenerate fully. Scar formation involves the deposition of connective tissue when regeneration is not possible. This involves granulation tissue formation, fibronectin production, collagenization, and scar maturation. Cell proliferation in repair is regulated by growth factors and the extracellular matrix plays a key role in wound healing and scar formation.
Infarction
Infarction is defined as an area of necrosis due to decreased blood flow. It can be hemorrhagic or anemic, red or white. Cardiac biomarkers such as troponin T and I, creatine kinase (CK-MB), and myoglobin are released from damaged heart muscle and can help evaluate myocardial injury. These biomarkers have characteristic rise and fall patterns. Renal failure can alter the diagnostic accuracy of cardiac biomarkers. Treatment of acute myocardial infarction focuses on restoring normal blood flow and salvaging heart muscle.
Neoplasia 120107095645-phpapp01
Cancer arises from uncontrolled cell growth and spread of abnormal cells. It is not a single disease but many disorders that differ in causes and responses to treatment. Some cancers like Hodgkin's lymphoma are curable, while others like pancreatic cancer are usually fatal. Understanding the molecular basis and causes of cancer has led to declines in cancer mortality in recent decades. Neoplasia refers to abnormal cell growth, and tumors can be benign or malignant. Benign tumors are self-limited and do not spread, while malignant tumors invade nearby tissue and metastasize. Cancers are classified based on the cell type of origin, such as carcinomas arising from epithelial cells and sarcomas from connective tissue cells.
Cell injury dec 2019 lecture 1
This document discusses cellular responses to stress and noxious stimuli. It describes how cells maintain homeostasis through adaptations like hypertrophy, hyperplasia, and atrophy in response to physiological changes. If stresses exceed adaptive responses, cells undergo injury which can initially be reversible but lead to irreversible injury and cell death if the stress persists. The document outlines different types of cell death including necrosis, apoptosis, and autophagy, and discusses how cellular derangements and metabolic issues can also contribute to cell injury over time.
Cell injury reversible injury lecture 5
Cells can become rapidly nonfunctional after injury, though the damage may be reversible. Prolonged injury can lead to irreversible damage and cell death. Under the microscope, reversible injury shows cellular swelling and fatty change, while necrosis appears glassy and homogeneous as proteins and RNA denature. Necrotic cells release enzymes and can be detected in blood earlier than microscopic changes appear.
Cell injury metaplasia l autosaved]
Metaplasia is a reversible change where one differentiated cell type is replaced by another. The most common epithelial metaplasia is the replacement of columnar cells with squamous cells. Stones in excretory ducts can lead to squamous metaplasia by replacing the normal columnar epithelium with stratified squamous epithelium. Prolonged influences that cause metaplasia can initiate cancer if the metaplastic epithelium undergoes malignant transformation.
Recommended
Repair 2017
Tissue repair occurs through two main processes: regeneration and scar formation. Regeneration involves the proliferation of residual cells to replace damaged tissue. Some tissues like skin and liver can regenerate fully. Scar formation involves the deposition of connective tissue when regeneration is not possible. This involves granulation tissue formation, fibronectin production, collagenization, and scar maturation. Cell proliferation in repair is regulated by growth factors and the extracellular matrix plays a key role in wound healing and scar formation.
Repair 2
This document discusses the process of wound healing through first and second intention. It begins by outlining the steps of healing by first intention for clean surgical incisions, including clot formation, re-epithelialization across the wound by day 3, and collagen deposition and scar maturation over subsequent weeks. Healing by second intention for wounds with separated edges involves more granulation tissue formation and wound contraction to reduce the gap between tissue edges. Complications can arise from deficient or excessive scar formation, including dehiscence, ulceration, hypertrophic scarring, and contractures.
Repair and healing_1
Tissue repair occurs through two main processes: regeneration and scar formation. Regeneration involves the proliferation of residual cells to replace damaged tissue. Some tissues like skin and liver can regenerate fully. Scar formation involves the deposition of connective tissue when regeneration is not possible. This involves granulation tissue formation, fibronectin production, collagenization, and scar maturation. Cell proliferation in repair is regulated by growth factors and the extracellular matrix plays a key role in wound healing and scar formation.
Infarction
Infarction is defined as an area of necrosis due to decreased blood flow. It can be hemorrhagic or anemic, red or white. Cardiac biomarkers such as troponin T and I, creatine kinase (CK-MB), and myoglobin are released from damaged heart muscle and can help evaluate myocardial injury. These biomarkers have characteristic rise and fall patterns. Renal failure can alter the diagnostic accuracy of cardiac biomarkers. Treatment of acute myocardial infarction focuses on restoring normal blood flow and salvaging heart muscle.
Neoplasia 120107095645-phpapp01
Cancer arises from uncontrolled cell growth and spread of abnormal cells. It is not a single disease but many disorders that differ in causes and responses to treatment. Some cancers like Hodgkin's lymphoma are curable, while others like pancreatic cancer are usually fatal. Understanding the molecular basis and causes of cancer has led to declines in cancer mortality in recent decades. Neoplasia refers to abnormal cell growth, and tumors can be benign or malignant. Benign tumors are self-limited and do not spread, while malignant tumors invade nearby tissue and metastasize. Cancers are classified based on the cell type of origin, such as carcinomas arising from epithelial cells and sarcomas from connective tissue cells.
Cell injury dec 2019 lecture 1
This document discusses cellular responses to stress and noxious stimuli. It describes how cells maintain homeostasis through adaptations like hypertrophy, hyperplasia, and atrophy in response to physiological changes. If stresses exceed adaptive responses, cells undergo injury which can initially be reversible but lead to irreversible injury and cell death if the stress persists. The document outlines different types of cell death including necrosis, apoptosis, and autophagy, and discusses how cellular derangements and metabolic issues can also contribute to cell injury over time.
Cell injury reversible injury lecture 5
Cells can become rapidly nonfunctional after injury, though the damage may be reversible. Prolonged injury can lead to irreversible damage and cell death. Under the microscope, reversible injury shows cellular swelling and fatty change, while necrosis appears glassy and homogeneous as proteins and RNA denature. Necrotic cells release enzymes and can be detected in blood earlier than microscopic changes appear.
Cell injury metaplasia l autosaved]
Metaplasia is a reversible change where one differentiated cell type is replaced by another. The most common epithelial metaplasia is the replacement of columnar cells with squamous cells. Stones in excretory ducts can lead to squamous metaplasia by replacing the normal columnar epithelium with stratified squamous epithelium. Prolonged influences that cause metaplasia can initiate cancer if the metaplastic epithelium undergoes malignant transformation.
Cell injury causes and overview of cell injury and cell death lect 4 jan 2020
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.
Cell adaptations dec 2019 lect 2
Metaplasia is the replacement of one adult cell type with another adult cell type. It is typically irreversible (c) and describes the underlying pathology of Barrett's oesophagus (d), where the normal squamous epithelium of the lower esophagus is replaced by columnar epithelium resembling intestinal epithelium. Metaplasia is not an increase in cell number or size (e) and does not preserve mucus secretion or be caused by B12 deficiency (a,b).
Cell adaptation 31dec 2019 lect 3
1. Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferations may eventually arise. Patients with hyperplasia are at increased risk for developing cancer.
2. Hyperplasia is the result of growth factor-driven proliferation of mature cells and increased output of new cells from tissue stem cells.
3. Metaplasia is a reversible change where one cell type replaces another. It results from the reprogramming of stem cells or undifferentiated mesenchymal cells, causing them to differentiate along a new pathway in response to environmental signals.
Cell injury apoptosis lect 08jan 2020
Apoptosis is a tightly regulated and genetically programmed form of cell death where cells activate enzymes to degrade their own nuclear DNA and proteins. Cells undergoing apoptosis break into fragments called apoptotic bodies that are phagocytosed without eliciting inflammation. Apoptosis eliminates damaged or unneeded cells and plays an important role in development, tissue homeostasis, and the removal of infected or abnormal cells. It involves cell shrinkage, chromatin condensation, blebbing of the cell membrane, and the formation of apoptotic bodies that are phagocytosed without inflammatory response.
Cell injury necrosis lect 6 jan 2020
This document discusses various patterns of tissue necrosis seen microscopically:
- Coagulative necrosis preserves tissue architecture for days as cells are slowly removed by phagocytosis. It can result from ischemia.
- Liquefactive necrosis digests dead cells into a liquid mass due to bacterial or fungal infection stimulating leukocytes. Pus results.
- Specific types of necrosis include caseous, fat, fibrinoid, and those seen in conditions like gangrene and myocardial infarction.
Arteriosclerosis 5 5-2014 lect 3
This document discusses arteriosclerosis and atherosclerosis. It defines arteriosclerosis as hardening of the arteries, and identifies three patterns: small artery disease; calcification in aging muscular arteries; and atherosclerosis. Atherosclerosis is caused by fatty lesions called atheromas that protrude into arteries. Risk factors for atherosclerosis include age, gender, genetics, hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis involves endothelial injury, lipoprotein accumulation, monocyte recruitment, and smooth muscle cell proliferation. Morphologically, atherosclerosis begins as fatty streaks and progresses to atheromatous plaques containing lipids, cells, and extracellular matrix.
Aneurysms lect 4
This document defines and discusses different types of aneurysms. It begins by defining a true aneurysm as an abnormal dilation of a blood vessel or heart that involves an attenuated but intact arterial wall. It then discusses classifications of aneurysms by shape and size. The document goes on to explain the pathogenesis of aneurysms, focusing on processes that compromise the structure or function of vascular wall connective tissue. It provides details on abdominal aortic aneurysms, thoracic aortic aneurysms, and aortic dissection.
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Cell injury causes and overview of cell injury and cell death lect 4 jan 2020
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.
Cell adaptations dec 2019 lect 2
Metaplasia is the replacement of one adult cell type with another adult cell type. It is typically irreversible (c) and describes the underlying pathology of Barrett's oesophagus (d), where the normal squamous epithelium of the lower esophagus is replaced by columnar epithelium resembling intestinal epithelium. Metaplasia is not an increase in cell number or size (e) and does not preserve mucus secretion or be caused by B12 deficiency (a,b).
Cell adaptation 31dec 2019 lect 3
1. Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferations may eventually arise. Patients with hyperplasia are at increased risk for developing cancer.
2. Hyperplasia is the result of growth factor-driven proliferation of mature cells and increased output of new cells from tissue stem cells.
3. Metaplasia is a reversible change where one cell type replaces another. It results from the reprogramming of stem cells or undifferentiated mesenchymal cells, causing them to differentiate along a new pathway in response to environmental signals.
Cell injury apoptosis lect 08jan 2020
Apoptosis is a tightly regulated and genetically programmed form of cell death where cells activate enzymes to degrade their own nuclear DNA and proteins. Cells undergoing apoptosis break into fragments called apoptotic bodies that are phagocytosed without eliciting inflammation. Apoptosis eliminates damaged or unneeded cells and plays an important role in development, tissue homeostasis, and the removal of infected or abnormal cells. It involves cell shrinkage, chromatin condensation, blebbing of the cell membrane, and the formation of apoptotic bodies that are phagocytosed without inflammatory response.
Cell injury necrosis lect 6 jan 2020
This document discusses various patterns of tissue necrosis seen microscopically:
- Coagulative necrosis preserves tissue architecture for days as cells are slowly removed by phagocytosis. It can result from ischemia.
- Liquefactive necrosis digests dead cells into a liquid mass due to bacterial or fungal infection stimulating leukocytes. Pus results.
- Specific types of necrosis include caseous, fat, fibrinoid, and those seen in conditions like gangrene and myocardial infarction.
Arteriosclerosis 5 5-2014 lect 3
This document discusses arteriosclerosis and atherosclerosis. It defines arteriosclerosis as hardening of the arteries, and identifies three patterns: small artery disease; calcification in aging muscular arteries; and atherosclerosis. Atherosclerosis is caused by fatty lesions called atheromas that protrude into arteries. Risk factors for atherosclerosis include age, gender, genetics, hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis involves endothelial injury, lipoprotein accumulation, monocyte recruitment, and smooth muscle cell proliferation. Morphologically, atherosclerosis begins as fatty streaks and progresses to atheromatous plaques containing lipids, cells, and extracellular matrix.
Aneurysms lect 4
This document defines and discusses different types of aneurysms. It begins by defining a true aneurysm as an abnormal dilation of a blood vessel or heart that involves an attenuated but intact arterial wall. It then discusses classifications of aneurysms by shape and size. The document goes on to explain the pathogenesis of aneurysms, focusing on processes that compromise the structure or function of vascular wall connective tissue. It provides details on abdominal aortic aneurysms, thoracic aortic aneurysms, and aortic dissection.
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Cell injury causes and overview of cell injury and cell death lect 4 jan 2020
Cell injury causes and overview of cell injury and cell death lect 4 jan 2020
Tissue renewal
- 2. TISSUE RENEWAL,REPAIR AND REGENERATION BY DR ABDUL AZIZ SHAIKH