Pathological calcification involves the abnormal deposition of calcium salts in tissues other than bone. There are two main types: dystrophic calcification occurs in dead or damaged tissue with normal calcium levels, while metastatic calcification affects normal tissues and results from disorders that increase calcium levels in the blood (hypercalcemia). Dystrophic calcification is seen in areas of necrosis, atherosclerotic plaques, and infarcts. Metastatic calcification commonly involves the kidneys, lungs, blood vessels, and stomach, and is caused by hyperparathyroidism, bone destruction, or excessive vitamin D intake.
Intracellular accumulations can occur through the buildup of various cellular constituents, including fat, proteins, carbohydrates, and pigments. Fatty change is the accumulation of triglycerides in cells, commonly seen in liver cells due to alcohol abuse, obesity, or other metabolic derangements. Proteins can accumulate intracellularly in conditions like myeloma or nephrotic syndrome. Glycogen storage diseases result in glycogen accumulation in cells. Pigment accumulations include lipofuscin, melanin, hemosiderin, and exogenous pigments like carbon. These accumulations can be transient or permanent and range from harmless to toxic.
Haemodynamic disorders , thromboembolism and shock by Dr Nadeem (RMC)Hassan Ahmad
The document discusses various haemodynamic disorders including thrombosis, embolism, shock, hyperemia, congestion, and edema. It provides details on the pathophysiology and morphological changes seen in these conditions.
Hyperemia is an active process resulting from increased blood flow due to arteriolar dilation, causing engorged tissue that appears red. Congestion is a passive process resulting from impaired outflow, causing tissue to appear bluish-red due to accumulation of deoxygenated blood.
Pulmonary congestion microscopically shows engorged alveolar capillaries and edema, while chronic pulmonary congestion shows thickened fibrotic septa and hemosiderin
Intracellular accumulations of substances can occur in the cytoplasm or nucleus of cells. Mild accumulations cause reversible cell injury, while severe accumulations result in irreversible injury. Abnormal intracellular accumulations fall into three categories: accumulations of normal cell constituents like lipids and proteins; accumulations of abnormal substances from abnormal metabolism; and accumulations of pigments, both endogenous like melanin and lipofuscin, and exogenous pigments. Fatty liver is a common site of fat accumulation and can range from mild and reversible to severe and irreversible. The pathogenesis of fatty liver involves defects in the normal processes of fat transport and metabolism in the liver.
This is a presentation on the topic of Adaptations, Cell injury and cell death, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
This document provides information about myocardial infarction including:
- Myocardial infarction is caused by interruption of blood supply to the heart muscle, usually due to blockage of a coronary artery.
- Risk factors that can lead to coronary artery blockage include hypertension, hyperlipidemia, diabetes, and smoking.
- A thrombus or embolism in a coronary artery cuts off the blood supply, causing cell death in the affected heart muscle area.
- The location and size of the infarction depends on which coronary artery is blocked. Transmural infarcts that penetrate the full heart wall thickness are more likely to cause complications than smaller subendocardial infarcts.
Hyperaemia and congestion both refer to an increased volume of blood in vessels. Hyperaemia is an active process involving arteriolar dilation that brings more blood to an area, while congestion is passive with impaired drainage causing blood accumulation. There are physiological and pathological forms. Pathological hyperaemia can be acute or chronic, localized or generalized, and active via increased arterial flow or passive due to impaired venous drainage. Chronic passive hyperaemia develops slowly over time from obstructions like tumors or abscesses blocking venous drainage. Congestive heart failure is an example of chronic generalized passive hyperaemia. Hyperaemia is identifiable by tissue color changes and swelling due to increased blood volume.
This document provides an overview of shock, including its definition, types, etiology, pathogenesis, stages, and pathophysiological changes. It discusses the classification of shock into types such as hypovolemic, septic, traumatic, neurogenic, and distributive shock. For septic shock specifically, it covers the etiology as severe infection, pathophysiology involving the immune response and release of toxins, and key features including hypotension, tissue hypoperfusion, and high mortality rates. Treatment focuses on fluid resuscitation and source control for hypovolemic and septic shock.
Pathological calcification involves the abnormal deposition of calcium salts in tissues other than bone. There are two main types: dystrophic calcification occurs in dead or damaged tissue with normal calcium levels, while metastatic calcification affects normal tissues and results from disorders that increase calcium levels in the blood (hypercalcemia). Dystrophic calcification is seen in areas of necrosis, atherosclerotic plaques, and infarcts. Metastatic calcification commonly involves the kidneys, lungs, blood vessels, and stomach, and is caused by hyperparathyroidism, bone destruction, or excessive vitamin D intake.
Intracellular accumulations can occur through the buildup of various cellular constituents, including fat, proteins, carbohydrates, and pigments. Fatty change is the accumulation of triglycerides in cells, commonly seen in liver cells due to alcohol abuse, obesity, or other metabolic derangements. Proteins can accumulate intracellularly in conditions like myeloma or nephrotic syndrome. Glycogen storage diseases result in glycogen accumulation in cells. Pigment accumulations include lipofuscin, melanin, hemosiderin, and exogenous pigments like carbon. These accumulations can be transient or permanent and range from harmless to toxic.
Haemodynamic disorders , thromboembolism and shock by Dr Nadeem (RMC)Hassan Ahmad
The document discusses various haemodynamic disorders including thrombosis, embolism, shock, hyperemia, congestion, and edema. It provides details on the pathophysiology and morphological changes seen in these conditions.
Hyperemia is an active process resulting from increased blood flow due to arteriolar dilation, causing engorged tissue that appears red. Congestion is a passive process resulting from impaired outflow, causing tissue to appear bluish-red due to accumulation of deoxygenated blood.
Pulmonary congestion microscopically shows engorged alveolar capillaries and edema, while chronic pulmonary congestion shows thickened fibrotic septa and hemosiderin
Intracellular accumulations of substances can occur in the cytoplasm or nucleus of cells. Mild accumulations cause reversible cell injury, while severe accumulations result in irreversible injury. Abnormal intracellular accumulations fall into three categories: accumulations of normal cell constituents like lipids and proteins; accumulations of abnormal substances from abnormal metabolism; and accumulations of pigments, both endogenous like melanin and lipofuscin, and exogenous pigments. Fatty liver is a common site of fat accumulation and can range from mild and reversible to severe and irreversible. The pathogenesis of fatty liver involves defects in the normal processes of fat transport and metabolism in the liver.
This is a presentation on the topic of Adaptations, Cell injury and cell death, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
This document provides information about myocardial infarction including:
- Myocardial infarction is caused by interruption of blood supply to the heart muscle, usually due to blockage of a coronary artery.
- Risk factors that can lead to coronary artery blockage include hypertension, hyperlipidemia, diabetes, and smoking.
- A thrombus or embolism in a coronary artery cuts off the blood supply, causing cell death in the affected heart muscle area.
- The location and size of the infarction depends on which coronary artery is blocked. Transmural infarcts that penetrate the full heart wall thickness are more likely to cause complications than smaller subendocardial infarcts.
Hyperaemia and congestion both refer to an increased volume of blood in vessels. Hyperaemia is an active process involving arteriolar dilation that brings more blood to an area, while congestion is passive with impaired drainage causing blood accumulation. There are physiological and pathological forms. Pathological hyperaemia can be acute or chronic, localized or generalized, and active via increased arterial flow or passive due to impaired venous drainage. Chronic passive hyperaemia develops slowly over time from obstructions like tumors or abscesses blocking venous drainage. Congestive heart failure is an example of chronic generalized passive hyperaemia. Hyperaemia is identifiable by tissue color changes and swelling due to increased blood volume.
This document provides an overview of shock, including its definition, types, etiology, pathogenesis, stages, and pathophysiological changes. It discusses the classification of shock into types such as hypovolemic, septic, traumatic, neurogenic, and distributive shock. For septic shock specifically, it covers the etiology as severe infection, pathophysiology involving the immune response and release of toxins, and key features including hypotension, tissue hypoperfusion, and high mortality rates. Treatment focuses on fluid resuscitation and source control for hypovolemic and septic shock.
Pathologic calcification occurs when calcium salts abnormally deposit in tissues. There are two types: dystrophic calcification occurs in dead or dying tissues with normal calcium levels, while metastatic calcification deposits calcium in healthy tissues due to problems that cause high blood calcium levels. Dystrophic calcification is seen in areas of tissue damage like atherosclerosis or valve stenosis. Metastatic calcification's main causes include parathyroid hormone increases, bone destruction, vitamin D disorders, and kidney failure, and it notably affects lungs, kidneys, and blood vessels. Both types appear as basophilic calcium deposits that can impact organ function.
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.
1. The document discusses various hemodynamic disorders including edema, hyperemia, congestion, hemorrhage, thrombosis, embolism, infarction, and shock.
2. Edema results from fluid movement into tissues and can affect subcutaneous tissues, lungs, and brain. Congestion is the passive filling of tissues with blood due to impaired outflow.
3. Thrombosis is the formation of clots within vessels, which can then embolize and travel to other sites (embolism), potentially causing ischemic tissue damage or infarction if blood flow is not restored.
4. Shock represents a failure of circulation to maintain adequate tissue perfusion and oxygenation.
Cell injury and alterations can occur through various causes and result in reversible or irreversible changes to cells. Reversible cell injury may allow the cell to return to normal, while irreversible injury leads to cell death through necrosis or apoptosis. Specific patterns of acute cell injury include cellular swelling and fatty change. Long-term or persistent stimuli can also result in subcellular alterations and intracellular accumulations of substances such as lipids, proteins, pigments, and more. Extracellular accumulations may involve changes to collagen, elastic fibers, proteoglycans, and basement membranes in connective tissue.
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.
Intracellular accumulations ppt by dr usman nasirUsman Nasir
This document discusses intracellular accumulations, which occur due to metabolic derangements within cells. It defines intracellular accumulations and categorizes them as normal cellular constituents or abnormal endogenous or exogenous substances. Accumulations can occur in the cytoplasm or nucleus. The document then discusses the processes and sites of accumulations, including accumulation of lipids (resulting in steatosis), cholesterol, proteins, glycogen, and pigments. Specific diseases associated with accumulations of these substances are provided as examples.
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.
This document discusses hemodynamic disorders and their classification. It covers topics like hyperemia, hemorrhages, thrombosis, and edema. Hyperemia can be arterial from vasodilation or venous from impaired outflow. Hemorrhages are blood loss classified by size and site. Thrombosis involves inappropriate clotting within vessels. Edema is fluid accumulation in tissues. Organ-specific effects of disorders are also described.
This document discusses different types of cell death known as necrosis. It defines necrosis as irreversible damage to cells that cannot be corrected and involves failure of ATP generation, membrane damage, and damage from reactive oxygen species. The document outlines several patterns of necrosis including coagulative necrosis where tissue architecture is preserved, liquefactive necrosis where tissue turns into a viscous liquid, and caseous necrosis where tissue has a cheesy, yellow-white appearance. It also discusses specific forms of necrosis that can occur in conditions like infections, gangrene, acute pancreatitis, and immune reactions.
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 intracellular accumulation of lipids, carbohydrates, and proteins. It describes how accumulation can occur due to excess production or inadequate breakdown of normal substances, or buildup of abnormal endogenous or exogenous materials. Specific types of accumulation are then discussed in more detail, including lipid accumulation seen in fatty liver, cholesterol accumulation in atherosclerosis and xanthomas, protein accumulation in renal disease, and glycogen accumulation in diabetes mellitus and glycogen storage disorders. Causes and morphological features of each type are provided.
Pathologic calcification involves the abnormal deposition of calcium salts in tissues. There are two main types: dystrophic calcification occurs in dead or damaged tissues and is associated with normal calcium levels, while metastatic calcification occurs in normal living tissues and is associated with high calcium levels. Dystrophic calcification results from calcium deposition in areas of tissue damage or necrosis. Metastatic calcification is usually caused by hypercalcemia from conditions like hyperparathyroidism or certain cancers. The lungs, kidneys, and gastric mucosa are especially susceptible to metastatic calcification.
Neoplasia refers to new abnormal growth of tissue. A neoplasm is an abnormal mass of tissue that grows in an uncontrolled manner. Neoplasms can be benign (non-cancerous) or malignant (cancerous). The growth of neoplasms is driven by genetic changes that allow the cells to proliferate autonomously. Tumors are monoclonal in origin, arising from a single cell. The hallmarks of neoplasms include persistent and purposeless proliferation, a parasitic nature, progression, and clonal expansion. Tumors are classified based on their tissue of origin and behavior. Malignant tumors can invade surrounding tissues and metastasize to distant sites. The development of neoplasms involves genetic and environmental factors
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 chronic venous congestion (CVC) and its effects on various organs. It describes how CVC results in localized blood volume increase within dilated vessels. It then summarizes the gross and microscopic findings of CVC in the lungs, liver, spleen, and kidneys. The lungs show brown induration and thickened alveolar septa. The liver has a nutmeg appearance and centrilobular necrosis. The spleen exhibits congestion and fibrosis. The kidneys demonstrate mild degenerative changes. Hemorrhage and its causes, effects based on amount/speed of blood loss are also outlined.
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 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.
Thrombosis is the formation of a blood clot within a blood vessel or cavity of the heart. Virchow identified three main factors that contribute to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Thrombi can propagate or embolize, becoming lodged in another vessel and resulting in infarction of downstream tissue. Infarctions appear pale/white in solid organs and red/hemorrhagic in lungs/other tissues. Over time, infarcted tissue progresses from coagulative necrosis to phagocytosis and scar formation.
This document provides an overview of neoplasia and tumor characteristics and classification. It defines neoplasia as new abnormal cell growth that can be benign or malignant. Benign tumors remain localized, while malignant tumors invade surrounding tissues and metastasize to distant sites. Tumors are classified based on tissue of origin, degree of differentiation, growth patterns, and whether they are benign or malignant. Malignant tumors are generally less differentiated, grow and spread more rapidly, and invade locally and metastasize, making them more difficult to treat. The document also discusses cellular adaptations, causes of cancer, tumor properties, grading, staging, and nomenclature used in tumor classification.
This document provides an overview of neoplasia (tumors), including definitions, nomenclature used to classify benign and malignant tumors, the biology of tumor growth, epidemiology, molecular basis of cancer and carcinogenesis. It discusses the natural history of malignant tumors from malignant change to growth, invasion and metastasis. Key concepts covered include differentiation, dysplasia, tumor growth rates, features that distinguish benign from malignant tumors, predisposing geographic, environmental and genetic factors for cancer development.
Pathologic calcification occurs when calcium salts abnormally deposit in tissues. There are two types: dystrophic calcification occurs in dead or dying tissues with normal calcium levels, while metastatic calcification deposits calcium in healthy tissues due to problems that cause high blood calcium levels. Dystrophic calcification is seen in areas of tissue damage like atherosclerosis or valve stenosis. Metastatic calcification's main causes include parathyroid hormone increases, bone destruction, vitamin D disorders, and kidney failure, and it notably affects lungs, kidneys, and blood vessels. Both types appear as basophilic calcium deposits that can impact organ function.
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.
1. The document discusses various hemodynamic disorders including edema, hyperemia, congestion, hemorrhage, thrombosis, embolism, infarction, and shock.
2. Edema results from fluid movement into tissues and can affect subcutaneous tissues, lungs, and brain. Congestion is the passive filling of tissues with blood due to impaired outflow.
3. Thrombosis is the formation of clots within vessels, which can then embolize and travel to other sites (embolism), potentially causing ischemic tissue damage or infarction if blood flow is not restored.
4. Shock represents a failure of circulation to maintain adequate tissue perfusion and oxygenation.
Cell injury and alterations can occur through various causes and result in reversible or irreversible changes to cells. Reversible cell injury may allow the cell to return to normal, while irreversible injury leads to cell death through necrosis or apoptosis. Specific patterns of acute cell injury include cellular swelling and fatty change. Long-term or persistent stimuli can also result in subcellular alterations and intracellular accumulations of substances such as lipids, proteins, pigments, and more. Extracellular accumulations may involve changes to collagen, elastic fibers, proteoglycans, and basement membranes in connective tissue.
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.
Intracellular accumulations ppt by dr usman nasirUsman Nasir
This document discusses intracellular accumulations, which occur due to metabolic derangements within cells. It defines intracellular accumulations and categorizes them as normal cellular constituents or abnormal endogenous or exogenous substances. Accumulations can occur in the cytoplasm or nucleus. The document then discusses the processes and sites of accumulations, including accumulation of lipids (resulting in steatosis), cholesterol, proteins, glycogen, and pigments. Specific diseases associated with accumulations of these substances are provided as examples.
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.
This document discusses hemodynamic disorders and their classification. It covers topics like hyperemia, hemorrhages, thrombosis, and edema. Hyperemia can be arterial from vasodilation or venous from impaired outflow. Hemorrhages are blood loss classified by size and site. Thrombosis involves inappropriate clotting within vessels. Edema is fluid accumulation in tissues. Organ-specific effects of disorders are also described.
This document discusses different types of cell death known as necrosis. It defines necrosis as irreversible damage to cells that cannot be corrected and involves failure of ATP generation, membrane damage, and damage from reactive oxygen species. The document outlines several patterns of necrosis including coagulative necrosis where tissue architecture is preserved, liquefactive necrosis where tissue turns into a viscous liquid, and caseous necrosis where tissue has a cheesy, yellow-white appearance. It also discusses specific forms of necrosis that can occur in conditions like infections, gangrene, acute pancreatitis, and immune reactions.
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 intracellular accumulation of lipids, carbohydrates, and proteins. It describes how accumulation can occur due to excess production or inadequate breakdown of normal substances, or buildup of abnormal endogenous or exogenous materials. Specific types of accumulation are then discussed in more detail, including lipid accumulation seen in fatty liver, cholesterol accumulation in atherosclerosis and xanthomas, protein accumulation in renal disease, and glycogen accumulation in diabetes mellitus and glycogen storage disorders. Causes and morphological features of each type are provided.
Pathologic calcification involves the abnormal deposition of calcium salts in tissues. There are two main types: dystrophic calcification occurs in dead or damaged tissues and is associated with normal calcium levels, while metastatic calcification occurs in normal living tissues and is associated with high calcium levels. Dystrophic calcification results from calcium deposition in areas of tissue damage or necrosis. Metastatic calcification is usually caused by hypercalcemia from conditions like hyperparathyroidism or certain cancers. The lungs, kidneys, and gastric mucosa are especially susceptible to metastatic calcification.
Neoplasia refers to new abnormal growth of tissue. A neoplasm is an abnormal mass of tissue that grows in an uncontrolled manner. Neoplasms can be benign (non-cancerous) or malignant (cancerous). The growth of neoplasms is driven by genetic changes that allow the cells to proliferate autonomously. Tumors are monoclonal in origin, arising from a single cell. The hallmarks of neoplasms include persistent and purposeless proliferation, a parasitic nature, progression, and clonal expansion. Tumors are classified based on their tissue of origin and behavior. Malignant tumors can invade surrounding tissues and metastasize to distant sites. The development of neoplasms involves genetic and environmental factors
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 chronic venous congestion (CVC) and its effects on various organs. It describes how CVC results in localized blood volume increase within dilated vessels. It then summarizes the gross and microscopic findings of CVC in the lungs, liver, spleen, and kidneys. The lungs show brown induration and thickened alveolar septa. The liver has a nutmeg appearance and centrilobular necrosis. The spleen exhibits congestion and fibrosis. The kidneys demonstrate mild degenerative changes. Hemorrhage and its causes, effects based on amount/speed of blood loss are also outlined.
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 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.
Thrombosis is the formation of a blood clot within a blood vessel or cavity of the heart. Virchow identified three main factors that contribute to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Thrombi can propagate or embolize, becoming lodged in another vessel and resulting in infarction of downstream tissue. Infarctions appear pale/white in solid organs and red/hemorrhagic in lungs/other tissues. Over time, infarcted tissue progresses from coagulative necrosis to phagocytosis and scar formation.
This document provides an overview of neoplasia and tumor characteristics and classification. It defines neoplasia as new abnormal cell growth that can be benign or malignant. Benign tumors remain localized, while malignant tumors invade surrounding tissues and metastasize to distant sites. Tumors are classified based on tissue of origin, degree of differentiation, growth patterns, and whether they are benign or malignant. Malignant tumors are generally less differentiated, grow and spread more rapidly, and invade locally and metastasize, making them more difficult to treat. The document also discusses cellular adaptations, causes of cancer, tumor properties, grading, staging, and nomenclature used in tumor classification.
This document provides an overview of neoplasia (tumors), including definitions, nomenclature used to classify benign and malignant tumors, the biology of tumor growth, epidemiology, molecular basis of cancer and carcinogenesis. It discusses the natural history of malignant tumors from malignant change to growth, invasion and metastasis. Key concepts covered include differentiation, dysplasia, tumor growth rates, features that distinguish benign from malignant tumors, predisposing geographic, environmental and genetic factors for cancer development.
Radiographic Features of Soft Tissue CalcificationsHadi Munib
The document discusses soft tissue calcifications, including:
1. Dystrophic calcifications form in degenerating or damaged tissue and can be localized. Idiopathic calcifications form in normal tissue. Metastatic calcifications result from high calcium/phosphate levels.
2. Common sites of dystrophic calcification include lymph nodes, tonsils, and muscles. Calcified lymph nodes appear irregular on radiographs. Tonsilloliths appear as clusters in the tonsillar region.
3. Cysticercosis larvae can cause calcifications throughout the body, including the oral region, appearing on examination as palpable nodules in muscles.
Pathologic calcification is the abnormal deposition of calcium salts in tissues. There are two types: dystrophic calcification occurs in dead or damaged tissues despite normal calcium levels, while metastatic calcification occurs in healthy tissues due to high calcium levels in the blood. Dystrophic calcification is often seen in areas of tissue necrosis, atherosclerotic vessels, and aging heart valves. Metastatic calcification results from hypercalcemia caused by disorders like hyperparathyroidism or bone marrow tumors, and affects tissues like the kidneys, lungs, and blood vessels. Both types microscopically appear as amorphous calcium deposits that can impair organ function if severe.
Soft tissue calcifications of the oral cavityNarmathaN2
This document discusses various types of soft tissue calcifications that can occur in the oral cavity and neck region. It describes dystrophic calcification, idiopathic calcification, and metastatic calcification. Specific examples of dystrophic calcification discussed include calcified lymph nodes, tonsilloliths, cysticercosis, arterial calcification. Idiopathic calcifications discussed include sialoliths, phleboliths, laryngeal cartilage calcifications, rhinoliths, and antroliths. Metastatic calcifications described include ossification of the styloid ligament and myositis ossificans. For each condition, the causes, clinical features, imaging appearance, differential diagnosis and management are provided
Pathological calcification of implantsBabin Khanal
Calcification refers to the abnormal deposition of calcium salts in soft tissues. There are two main types: dystrophic calcification occurs in dead or damaged tissues, while metastatic calcification results from abnormalities in calcium metabolism. Calcification can occur in various implants like heart valves, contact lenses, and IUDs, reducing their effectiveness over time. It is typically diagnosed through x-rays and addressed through treatments like surgery or medications, though prevention remains difficult as calcification stems from biological processes.
Shock is a clinical syndrome resulting from poor tissue perfusion that impairs cellular metabolism and causes serious abnormalities. There are four main types: hypovolemic, cardiogenic, obstructive, and distributive. Treatment focuses on fluid resuscitation regardless of the underlying cause, with vasopressor medications like norepinephrine, dopamine, and epinephrine also used. Prolonged shock can lead to organ damage through hypoxia, acidosis, and inflammation as cellular metabolism switches to anaerobic pathways.
This document provides information about performing and interpreting a peripheral blood smear. It discusses examining red blood cells for morphology, abnormalities in shape and distribution, and inclusions. White blood cell morphology of neutrophils, eosinophils, basophils, monocytes, and lymphocytes is also described. Platelet morphology and abnormalities in platelet count are briefly covered. The preparation, staining, and examination process for a peripheral blood smear is outlined.
Pathological calcification involves the abnormal deposition of calcium salts in tissues other than bone. There are two main types: dystrophic calcification occurs in dead or damaged tissue with normal calcium levels, while metastatic calcification affects normal tissues and is caused by high calcium levels in the blood (hypercalcemia). Dystrophic calcification is seen in areas of necrosis, atherosclerosis, and infarcts. Metastatic calcification is associated with disorders that cause hypercalcemia like hyperparathyroidism and bone destruction. The deposits appear histologically as basophilic intracellular and extracellular calcium salt accumulations.
Corneal Degenerations - Dr Arnav SaroyaDrArnavSaroya
Corneal degeneration refers to conditions where the normal corneal cells undergo degenerative changes due to age or pathology. There are many types of corneal degeneration classified based on etiology and location. Common types include arcus senilis, band keratopathy, lipid depositions, crocodile shagreen, and Terrien's marginal degeneration. Corneal degenerations can cause visual symptoms but often do not require treatment for mild cases. Severe degenerations may be treated with procedures like excimer laser, lamellar keratoplasty, or penetrating keratoplasty to improve vision or relieve discomfort.
Soft tissue calcifications and ossifications / oral surgery courses Indian dental academy
This document discusses various types of soft tissue calcification and ossification that can occur in the oral cavity. It describes two main types of pathologic calcification: dystrophic calcification, which occurs in dead or degenerated tissues with normal calcium metabolism, and metastatic calcification, which occurs in normal tissues associated with abnormal calcium metabolism. Specific examples of soft tissue calcifications discussed in detail include calcified lymph nodes, tonsilloliths, cysticercosis lesions, arterial calcification, sialoliths, and phleboliths. The document also covers heterotopic ossification and provides examples such as osteoma cutis and myositis ossificans.
Calciphylaxis, also known as calcific uremic arteriolopathy, is a rare disorder characterized by calcification of the small blood vessels of the skin and subcutaneous fat. It most commonly occurs in patients with end-stage renal disease on dialysis. The calcification leads to reduced blood flow and painful skin lesions. Risk factors include hyperparathyroidism, vitamin D use, and warfarin use. Diagnosis is made clinically and confirmed with biopsy showing vessel calcification. Treatment involves sodium thiosulfate, hyperbaric oxygen, bisphosphonates, and wound care. Prognosis is poor with high mortality rates due to complications like infection and organ failure.
This document discusses various types of crystal-associated arthropathies including:
- Monosodium urate monohydrate crystals which cause gout. Gout typically affects middle-aged males and causes painful inflammation in joints.
- Calcium pyrophosphate dihydrate crystals which cause pseudogout/chondrocalcinosis. This tends to affect the elderly and can mimic many other joint diseases.
- Calcium-containing crystals like hydroxyapatite which are associated with aging, osteoarthritis, and renal disease and can cause acute attacks of inflammation.
1. Muscle biopsy is used to diagnose neuromuscular diseases by examining muscle fiber histology and histochemistry under a microscope.
2. Indications for muscle biopsy include unexplained muscle weakness, elevated muscle enzymes, and suspected hereditary or inflammatory myopathies.
3. During the procedure, a small sample of muscle is removed using needle or open biopsy and processed with staining techniques to examine fiber characteristics.
4. Common findings include fiber necrosis, regeneration, inflammation, fatty or fibrotic changes which can help identify diseases like muscular dystrophies, myositis, or metabolic myopathies.
This document discusses tumor markers, which are biological substances that can indicate the presence of cancer. It provides an overview of the history and ideal characteristics of tumor markers, their clinical applications in screening, diagnosis, staging and monitoring cancer, and methods of detecting tumor markers. The document also discusses broad classifications of tumor markers like antigens, hormones and enzymes, and specific tumor markers implicated in head and neck cancers. It notes some drawbacks of tumor markers and new frontiers in their use, and concludes that tumor markers cannot be used alone for cancer diagnosis but are useful as laboratory tests to support diagnosis.
Atherosclerosis is a form of arteriosclerosis characterized by fatty streaks and atheromas that protrude into vessel lumens. Atheromas consist of a necrotic lipid core and fibrous cap. As atherosclerosis progresses, coronary fatty streaks form in adolescence and develop into atherosclerotic plaques composed of cells, extracellular matrix, and lipid that may calcify. Advanced plaques can rupture, hemorrhage, or form aneurysms. Complications of atherosclerosis include vessel weakness, thrombosis leading to myocardial infarction, stroke or bowel infarction, hypertension, and peripheral arterial disease.
This document discusses radicular cysts, which are the most common inflammatory cysts in the oral cavity. Radicular cysts arise from epithelial residues in the periodontal ligament as a result of periapical periodontitis following pulp necrosis. They are usually asymptomatic but can cause swelling and bone resorption as they expand. The cyst forms from the proliferation of epithelial cell rests in the granulation tissue surrounding the apex of an infected tooth. Histologically, they are lined by stratified squamous epithelium and surrounded by fibrous connective tissue that may contain cholesterol crystals. Treatment involves root canal therapy or extraction with curettage of the cyst lining.
The document provides information about tissue deposits (accumulations) from a pathology lecture. It defines intracellular and extracellular deposits and discusses various substances that can accumulate in tissues, including lipids, proteins, carbohydrates, pigments, calcium, and amyloid. Specific examples of each type of deposit are outlined. The case discusses a female patient with lower limb swelling and shortness of breath found to have kidney abnormalities.
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 discusses cell injury, including its definition, types, causes, and pathogenesis. It defines cell injury as a change that occurs in a cell due to external or internal factors in its environment. There are two types of cell injury - reversible and irreversible. Reversible injury is when the cell is damaged but viable, while irreversible injury means the cell is nonviable. Common causes of cell injury include hypoxia, chemicals, infections, physical factors, and genetic factors. The pathogenesis of cell injury involves mitochondrial damage, disturbances in calcium metabolism, damage to cellular membranes, DNA and proteins. Reversible injury can progress to irreversible injury when ATP production ceases, cell membranes lyse, vital proteins are absent, and vital
This document 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.
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.
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
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Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
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1. PA 2.5 B
DESCRIBE & DISCUSS
PATHOLOGICAL CALCIFICATION
Dr IRA BHARADWAJ
MCI TEACHER ID: PAT 2300569
KUHS FACULTY ID: M21512
2. REFRENCES
• ROBBINS BASIC PATHOLOGY
• HARSH MOHAN TEXTBOOK OF PATHOLOGY
• OTHER STANDARD REFRENCES
• PHOTOGRAPHS OF GROSS SPECIMEN
• MICROPHOTOGRAPHS OF HISTOPATHOLOGY SLIDE
• DIAGRAM
3. SLO
• DEFINITION OF PATHOLOGICAL CALCIFICATION
• TYPES OF PATHOLOGICAL CALCIFICATION
• MORPHOLOGY OF PATHOLOGICAL CALCIFICATION
• DYSTROPHIC CALCIFICATION – DEFINITION,
ETIOPATHOGENESIS, EXAMPLES
• METASTATIC CALCIFICATION – DEFINITION,
ETIOPATHOGENESIS, SITES
• CALCINOSIS CUTIS – DEFINITION, ETIOLOGY, MORPHOLOGY,
CLINICAL FEATURES & CASE
4. PATHOLOGICAL [HETEROTOPIC] CALCIFICATION
DEFINITION & TYPES
DEFINITION:
Deposition of Calcium salts in tissues other than osteoid &
enamel
TYPES [common]:
• DYSTROPHIC - deposition in dead & degenerated tissue
• METASTATIC– deposition in normal tissue
• CALCINOSIS CUTIS – deposition of calcium in skin
5. PATHOLOGICAL [HETEROTOPIC] CALCIFICATION
TYPES
TYPES [uncommon]
• In some cases it starts in a single cell, around which
concentric layers of calcium & minerals are deposited to give
lamellated sand like appearance – psammoma bodies
• In asbestosis, calcium & iron salts deposit along asbestos
spicules creating beaded dumbbell shapes
6. PATHOLOGICAL [HETEROTOPIC] CALCIFICATION
MORPHOLOGY
Irrespective of type of pathological calcification, the
morphology remains same
GROSS
• Presents as firm to hard whitish areas, which are gritty to
cut
MICROSCOPY
• Shows deep blue granular irregular material, may be
intra/extra cellular
SPECIAL STAIN – von Kossa – black color, alizarin red - red
7. DYSTROPHIC CALCIFICATION
DEFINITION & ETIOPATHOGENESIS
DEFINITION
• Deposition of calcium salts in dead & degenerating tissues
other than osteoid & enamel
ETIOLOGY& PATHOGENESIS
• Serum Ca & Ca metabolism are normal.
• Ca is deposited in dead & degenerated cells by process of
initiation & propagation
8. DYSTROPHIC CALCIFICATION
PATHOGENESIS: INITIATION & PROPAGATION
• Intracellular accumulation of Ca in mitochondria of dead &
dying cells, as well as in membrane bound vesicles (acidic
phospholipids in mitochondria & vesicles attract Ca)
• Phosphatases lead to accumulation of phosphates
• Ca and phosphates interact to form crystals [increased by
osteopontin, collagen & Decreased by mineral inhibitors]
• Cellular membranes rupture & release the crystals outside
the cells (extra cellular)
11. METASTATIC CALCIFICATION
DEFINITION
• Deposition of calcium salts in normal tissues other than
osteoid & enamel
ETIOPATHOGENESIS
• Serum Ca is increased & excess calcium is deposited in cells ,
which bind phosphates
Some causes are :
• Hyper parathyroid function
12. METASTATIC CALCIFICATION
• Increased resorption of bone as in Multiple Myeloma,
tumors, immobilization of bone due to any cause
• Increased absorption of Ca in hypervitaminosis D, milk alkali
syndrome
• Renal failure
SITES
Common sites of deposition are kidney, lung, gastric mucosa,
internal elastic lamina of blood vessels, cornea & synovium
13. CALCINOSIS CUTIS
DEFINITION
Calcification occurring in skin [dermis] & subcutaneous tissue
ETIOLOGY
• Idiopathic [most cases]
• Sometimes due to dystrophic calcification associated with
immunological connective tissue diseases, eg, systemic
sclerosis [CREST syndrome]
• Infrequently as part of metastatic calcification
14. CALCINOSIS CUTIS
GROSS:
• Most common in skin [dermis] & subcutaneous tissue of
scrotum and around iliac crests
• Skin appears nodular
• Seen as chalky white areas closely related to skin
• Cuts firm to hard with gritty sensation
17. CALCINOSIS CUTIS
MICROSCOPY:
• The epidermis appears normal.
• Focal irregular dark blue (calcium deposition) areas of
amorphous morphology are seen in dermis & subcutaneous
tissue.
• Usually there is no inflammation.
• Special stains for calcium are von Kossa & alizarin red
20. CALCINOSIS CUTIS
CLINICAL FEATURES
• Initially asymptomatic hard nodules [ D/D neoplasia]
• Later may ulcerate, discharge chalky white contents
• Other symptoms may be present according to etiology
21. SHORT ESSAY – CLINICAL CASE
A 60 yr old male presented with hard nodules in the scrotum.
On examination multiple small hard nodules were present in
the scrotal skin. Thick milky white fluid discharge was seen
from one nodule.
Answer the following:
• What is your diagnosis?, give two reasons.
• What is the etiopathogenesis of this condition?
• What microscopic features do you expect on biopsy
• Name one blood investigation which you will do