This document discusses hypoxia, or low oxygen levels. It begins by classifying hypoxia based on its causes, such as respiratory hypoxia from issues with oxygen diffusion or ventilation. It then describes the urgent reactions in response to hypoxia, including increased heart rate and blood flow. Finally, it outlines the permanent compensations that develop over time to hypoxia, such as increased capillaries and mitochondria, more efficient oxygen use, and adaptations in metabolic and cardiovascular systems to optimize function with low oxygen.
Pathology is the study of diseases through identifying changes in tissues and cells. It examines the patterns, causes, mechanisms, and effects of diseases. Pathology bridges clinical practice and basic science. Cell injury can result from physical, chemical, infectious, or environmental factors and causes damage through mechanisms like ATP depletion, oxygen deprivation, calcium dysregulation, and mitochondrial dysfunction. Cells respond to injury through reversible or irreversible changes, repair, or death by necrosis or apoptosis.
This document discusses various types of cell injury and cellular adaptations. It defines cell injury as stress encountered by cells due to changes in their internal or external environment. Virchow's cellular theory of disease proposed that diseases occur due to abnormalities at the cellular level. The document then discusses various genetic and acquired causes of cell injury, including physical, chemical, microbial, immunological, nutritional, aging, and iatrogenic factors. It also describes different types of cellular responses to stress like hypoxia, as well as cellular adaptations such as hyperplasia, hypertrophy, atrophy, metaplasia, and dysplasia. Finally, it discusses reversible cell injuries including edema, fatty change, hyaline change, amyloidosis, mu
Cell injury and death can occur through various mechanisms including hypoxia, physical or chemical insults, and microbial or immunological agents. The cellular response to injury depends on the cell type, extent, and type of injury. Initial responses include cellular adaptation, subcellular changes, or intracellular accumulations. Injury may result in reversible or irreversible cell damage and cell death. Irreversible injury is characterized by mitochondrial dysfunction and membrane damage, leading to necrosis or apoptosis. Different patterns of necrosis include coagulative, liquefactive, caseous, and gangrenous necrosis.
Infective Endocarditis(IE)
Is due to bacterial or fungal infection of the heart valves (endocardium).
Characterized by:
Formation of bulky, friable,easily detached and infected vegetations.
Damage to heart Valves and Chorda tendinae
perforation, ulceration, destruction (causes valve dysfunction)
This document provides an overview of necrosis and apoptosis. It defines necrosis as cell death resulting from external injury to cells, characterized by swelling and organelle breakdown. Apoptosis is defined as tightly regulated programmed cell suicide. The document discusses the morphology of necrosis under light microscopy and different types of necrosis. It then covers the mechanism, morphology, and triggers of apoptosis. Key differences between necrosis and apoptosis are that necrosis elicits inflammation while apoptosis does not and apoptosis is a tightly regulated process.
This document discusses inflammation, including its definition, causes, signs, types (acute vs chronic), vascular and cellular events in acute inflammation, chemical mediators (cell-derived like histamine and prostaglandins, plasma-derived like complement), roles of inflammatory cells, and features of acute and chronic inflammation. It provides detailed descriptions of the pathogenesis and mechanisms of acute and chronic inflammation.
Cellular adaptations, injury and death.. Lecture 1Ashish Jawarkar
This is a series of lectures on general pathology useful for undergraduate and postgraduate pathology students. The ppts here have are enriched with explanatory pictures as well as useful video links.. hope you find them useful
Pathology is the study of diseases through identifying changes in tissues and cells. It examines the patterns, causes, mechanisms, and effects of diseases. Pathology bridges clinical practice and basic science. Cell injury can result from physical, chemical, infectious, or environmental factors and causes damage through mechanisms like ATP depletion, oxygen deprivation, calcium dysregulation, and mitochondrial dysfunction. Cells respond to injury through reversible or irreversible changes, repair, or death by necrosis or apoptosis.
This document discusses various types of cell injury and cellular adaptations. It defines cell injury as stress encountered by cells due to changes in their internal or external environment. Virchow's cellular theory of disease proposed that diseases occur due to abnormalities at the cellular level. The document then discusses various genetic and acquired causes of cell injury, including physical, chemical, microbial, immunological, nutritional, aging, and iatrogenic factors. It also describes different types of cellular responses to stress like hypoxia, as well as cellular adaptations such as hyperplasia, hypertrophy, atrophy, metaplasia, and dysplasia. Finally, it discusses reversible cell injuries including edema, fatty change, hyaline change, amyloidosis, mu
Cell injury and death can occur through various mechanisms including hypoxia, physical or chemical insults, and microbial or immunological agents. The cellular response to injury depends on the cell type, extent, and type of injury. Initial responses include cellular adaptation, subcellular changes, or intracellular accumulations. Injury may result in reversible or irreversible cell damage and cell death. Irreversible injury is characterized by mitochondrial dysfunction and membrane damage, leading to necrosis or apoptosis. Different patterns of necrosis include coagulative, liquefactive, caseous, and gangrenous necrosis.
Infective Endocarditis(IE)
Is due to bacterial or fungal infection of the heart valves (endocardium).
Characterized by:
Formation of bulky, friable,easily detached and infected vegetations.
Damage to heart Valves and Chorda tendinae
perforation, ulceration, destruction (causes valve dysfunction)
This document provides an overview of necrosis and apoptosis. It defines necrosis as cell death resulting from external injury to cells, characterized by swelling and organelle breakdown. Apoptosis is defined as tightly regulated programmed cell suicide. The document discusses the morphology of necrosis under light microscopy and different types of necrosis. It then covers the mechanism, morphology, and triggers of apoptosis. Key differences between necrosis and apoptosis are that necrosis elicits inflammation while apoptosis does not and apoptosis is a tightly regulated process.
This document discusses inflammation, including its definition, causes, signs, types (acute vs chronic), vascular and cellular events in acute inflammation, chemical mediators (cell-derived like histamine and prostaglandins, plasma-derived like complement), roles of inflammatory cells, and features of acute and chronic inflammation. It provides detailed descriptions of the pathogenesis and mechanisms of acute and chronic inflammation.
Cellular adaptations, injury and death.. Lecture 1Ashish Jawarkar
This is a series of lectures on general pathology useful for undergraduate and postgraduate pathology students. The ppts here have are enriched with explanatory pictures as well as useful video links.. hope you find them useful
Tissue repair occurs through regeneration, replacing damaged cells with the same cell type, or fibrosis, replacing tissue with scar tissue. During fibrosis, blood vessels bleed and mast cells release histamine to promote vasodilation. A clot forms while macrophages remove damaged tissue. Fibroblasts migrate in and produce collagen, forming scar tissue through angiogenesis, fibroblast migration and proliferation, extracellular matrix deposition, and remodeling. Vascular endothelial growth factor is important for angiogenesis and permeability while transforming growth factor promotes fibroblast migration.
The document discusses cellular responses and adaptations to stress and injury. It provides an overview of how normal cells require specific environmental conditions to function properly and will try to adapt to changes through processes like hypertrophy, hyperplasia, atrophy and metaplasia. If cells cannot adapt to stress, either reversible or irreversible injury can occur, potentially leading to cell death through necrosis or apoptosis. The mechanisms of cellular injury include oxidative stress, depletion of ATP, calcium dysregulation, and damage to organelles like mitochondria and lysosomes.
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.
Cellular adaptations include reversible changes in cells' size, number, phenotype, or functions in response to environmental changes. Physiologic adaptations represent responses to normal stimulation, while pathologic adaptations allow cells to avoid injury but compromise normal function. Common cellular adaptations include:
- Atrophy, a shrinkage in cell size from loss of substance.
- Hypertrophy, an increase in cell size from increased organelles and proteins.
- Hyperplasia, an increase in cell number through cell division.
- Metaplasia, replacement of one adult cell type with another better suited to stresses.
- Dysplasia, disordered cell development with proliferation and cytologic changes that can progress to carcinoma
This document discusses hemodynamic disorders and disturbances in blood flow. It describes two broad categories of circulatory disturbances: 1) disturbances in blood volume, such as hyperemia, congestion, hemorrhage, and shock, and 2) obstructive disturbances like thrombosis, embolism, ischemia, and infarction. Specific organ manifestations of chronic venous congestion are described, including changes seen in the lungs (brown induration), liver (nutmeg appearance), spleen (enlarged with grey-tan coloring), and kidneys (enlarged medulla). Causes, effects, and histopathological findings of hemorrhage are also outlined.
Cell growth and differentiation are normally controlled processes that maintain tissue structure. Disorders can occur when these processes are deregulated. Key disorders include hypertrophy (enlarged cells), hyperplasia (increased cell number), atrophy (decreased cell size and number), metaplasia (one cell type replaces another), dysplasia (abnormal cell growth), and neoplasia (uncontrolled cell growth, i.e. cancer). These disorders are caused by various stimuli and involve molecular pathways regulating cell growth and protein synthesis. Disorders can progress from early changes like metaplasia and dysplasia to late stage cancers if deregulation persists over time.
This document summarizes acute inflammation and the key chemical mediators involved. It describes how injury causes vasodilation, increased vascular permeability, and leukocyte emigration through the actions of histamine, bradykinin, prostaglandins, leukotrienes, cytokines, and other mediators. These chemical mediators cause effects like vasodilation, increased vascular permeability, chemotaxis, fever, pain, and tissue damage during acute inflammatory responses.
Acute inflammation is an immediate response to injury that involves vasodilation, increased vascular permeability, and leukocyte migration. This leads to redness, swelling, heat, and pain at the site of injury. Chronic inflammation is a prolonged response that involves lymphocytes, macrophages and plasma cells. It can lead to tissue destruction and attempts at repair through fibrosis and new blood vessel formation. The response involves many chemical mediators like histamine, kinins, cytokines, and eicosanoids that regulate vascular permeability and leukocyte behavior. Defects in leukocyte function can impair inflammatory response. Acute inflammation may resolve with repair or progress to chronic inflammation and tissue damage.
A condition in which the blood doesn't have enough healthy red blood cells.
Anaemia results from a lack of red blood cells or dysfunctional red blood cells in the body. This leads to reduced oxygen flow to the body's organs.
Arteriosclerosis is the hardening and narrowing of arteries due to plaque buildup. The three main types are arteriolosclerosis (small arteries), Monckeberg medial sclerosis (calcification of muscular arteries), and atherosclerosis (most common). Atherosclerosis features atheromas that protrude into the vessel lumen. Risk factors like age, gender, genetics, hyperlipidemia, hypertension, smoking, and diabetes accelerate atherosclerosis. Inflammation and infection also contribute to plaque formation and rupture, which can cause acute issues like heart attack or stroke.
Describes the process of ageing in cells, factors affecting cells like telomere, free radicals, oxidative stress, DNA damage, environmental factors, proteostasis, mitochondrial disfunction etc are described
Adaptations of cellular growth and diffrentiationrashree-singh
This document discusses various types of cellular adaptation in response to environmental changes. It defines key adaptations like hypertrophy, hyperplasia, atrophy, and metaplasia. Hypertrophy involves cell enlargement while hyperplasia is an increase in cell number. Atrophy is a decrease in cell size and number. Metaplasia is the reversible replacement of one cell type with another. Adaptations can be physiological from things like exercise or pathological from issues like hypertension. The mechanisms of adaptations involve growth factors, hormones, and changes in protein expression levels. Cellular adaptations allow tissues to survive stresses but can sometimes progress to disease if the stressors remain.
This document discusses cellular adaptation, injury, and death. It covers topics like hyperplasia, hypertrophy, atrophy, metaplasia, causes of cell injury including hypoxia and free radicals, necrosis and apoptosis. It provides detailed descriptions of the morphological changes that occur during cellular injury and the mechanisms of necrosis, apoptosis and intracellular accumulation.
Cell injury occurs when cells can no longer maintain homeostasis or adapt to stress. There are two types of cell injury: reversible and irreversible. Reversible injury allows cells to return to normal after stress is removed, while irreversible injury leads to cell death through necrosis or apoptosis. Causes of cell injury include hypoxia, chemicals, physical agents, infections, immunologic reactions, genetics, and nutrition. Mechanisms of injury involve depletion of ATP, mitochondrial damage, calcium dysregulation, oxidative stress, and membrane damage.
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
This document discusses cell injury, adaptation, and death. It explains that cells can undergo adaptation to physiologic or pathologic stresses to maintain homeostasis. Adaptation allows cells to modify their structure and function to avoid injury. If stresses exceed a cell's adaptive capacity, injury occurs. Adaptations include hypertrophy, where cells increase in size rather than number. Hypertrophy can be physiologic, like uterine enlargement during pregnancy, or pathologic, like cardiac enlargement from hypertension. The document then focuses on hypertrophy in more detail.
Necrosis is the death of cells and living tissue. There are several types of necrosis including coagulative, liquefactive, and caseous necrosis. Coagulative necrosis involves the preservation of the basic cellular structure but loss of cellular details. Liquefactive necrosis results in the transformation of tissue into a liquid mass where all cellular and architectural details are lost. Caseous necrosis converts dead tissue into a cheesy-like granular mass where no cellular or architectural details remain. The document further describes the characteristics, causes, and microscopic appearance of each type of necrosis.
This document discusses inflammatory mediators, which are messengers that contribute to the inflammatory response by acting on blood vessels, immune cells, or other cells. Inflammatory mediators can be classified as either cell-derived or plasma-derived. Cell-derived mediators include histamine, serotonin, lysosomal enzymes, eicosanoids such as prostaglandins and leukotrienes, platelet-activating factor, reactive oxygen species, nitric oxide, and cytokines. Plasma-derived mediators include components of the complement, coagulation, kinin, and fibrinolytic systems. Many of these mediators stimulate the release of other mediators and have effects like increasing vascular permeability and chemotaxis. Cytokines and
Cell injury can result from depletion of ATP, mitochondrial damage, calcium influx, oxidative stress, and defects in membrane permeability. The main cellular adaptations to injury are hyperplasia, hypertrophy, atrophy, and metaplasia. ATP depletion affects energy-dependent functions, potentially leading to necrosis. Mitochondrial damage causes further ATP loss and leakage of proteins involved in apoptosis. Calcium influx activates enzymes that damage cell components and may trigger apoptosis. Oxidative stress modifies proteins, lipids, and nucleic acids. Increased membrane permeability affects organelle and plasma membranes, usually culminating in necrosis or triggering of apoptosis pathways.
Cellular swelling or cloudy swelling is a reversible degeneration where cells swell due to metabolic disturbances. Mild irritants like bacteria or temperature changes can cause swelling. Swollen cells appear cloudy under microscopy. Hydropic degeneration involves cellular swelling with fluid accumulation that can cause blistering. Mucinous degeneration is the excessive mucin production in epithelial cells due to irritants. Mucoid degeneration involves the appearance of mucin-like glycoprotein in connective tissue. Hyaline change results in a glassy, translucent appearance as cells or tissues lose structure and fuse. It can involve keratin, cells, or connective tissues.
The splanchnic circulation provides blood flow to the gastrointestinal tract and liver. Approximately 1450 ml of blood flows through the splanchnic circulation per minute, accounting for 29% of total blood flow. The splanchnic circulation regulates blood volume and pressure and can reduce its flow during hemorrhage to prioritize more vital organs. Blood flow to the intestinal mucosa increases after eating to support metabolic activity. Splanchnic blood flow is regulated intrinsically through local metabolic and myogenic controls and extrinsically through the sympathetic nervous system and circulating hormones. Sympathetic stimulation causes vasoconstriction that redirects blood flow away from the splanchnic circulation during exercise.
This document discusses the local and humoral regulation of tissue blood flow. It begins by outlining the specific needs of tissues for blood flow, including delivery of oxygen and nutrients and removal of waste. It then describes the mechanisms by which changes in tissue metabolism or oxygen availability alter blood flow, including the vasodilator and oxygen demand theories. The document also discusses acute responses like active and reactive hyperemia, as well as long-term regulation through changes in vascularity and remodeling of blood vessels. Finally, it outlines various humoral factors that can cause vasoconstriction or vasodilation, such as sympathetic nerves, angiotensin, bradykinin, and ions like calcium, potassium, and hydrogen ions
Tissue repair occurs through regeneration, replacing damaged cells with the same cell type, or fibrosis, replacing tissue with scar tissue. During fibrosis, blood vessels bleed and mast cells release histamine to promote vasodilation. A clot forms while macrophages remove damaged tissue. Fibroblasts migrate in and produce collagen, forming scar tissue through angiogenesis, fibroblast migration and proliferation, extracellular matrix deposition, and remodeling. Vascular endothelial growth factor is important for angiogenesis and permeability while transforming growth factor promotes fibroblast migration.
The document discusses cellular responses and adaptations to stress and injury. It provides an overview of how normal cells require specific environmental conditions to function properly and will try to adapt to changes through processes like hypertrophy, hyperplasia, atrophy and metaplasia. If cells cannot adapt to stress, either reversible or irreversible injury can occur, potentially leading to cell death through necrosis or apoptosis. The mechanisms of cellular injury include oxidative stress, depletion of ATP, calcium dysregulation, and damage to organelles like mitochondria and lysosomes.
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.
Cellular adaptations include reversible changes in cells' size, number, phenotype, or functions in response to environmental changes. Physiologic adaptations represent responses to normal stimulation, while pathologic adaptations allow cells to avoid injury but compromise normal function. Common cellular adaptations include:
- Atrophy, a shrinkage in cell size from loss of substance.
- Hypertrophy, an increase in cell size from increased organelles and proteins.
- Hyperplasia, an increase in cell number through cell division.
- Metaplasia, replacement of one adult cell type with another better suited to stresses.
- Dysplasia, disordered cell development with proliferation and cytologic changes that can progress to carcinoma
This document discusses hemodynamic disorders and disturbances in blood flow. It describes two broad categories of circulatory disturbances: 1) disturbances in blood volume, such as hyperemia, congestion, hemorrhage, and shock, and 2) obstructive disturbances like thrombosis, embolism, ischemia, and infarction. Specific organ manifestations of chronic venous congestion are described, including changes seen in the lungs (brown induration), liver (nutmeg appearance), spleen (enlarged with grey-tan coloring), and kidneys (enlarged medulla). Causes, effects, and histopathological findings of hemorrhage are also outlined.
Cell growth and differentiation are normally controlled processes that maintain tissue structure. Disorders can occur when these processes are deregulated. Key disorders include hypertrophy (enlarged cells), hyperplasia (increased cell number), atrophy (decreased cell size and number), metaplasia (one cell type replaces another), dysplasia (abnormal cell growth), and neoplasia (uncontrolled cell growth, i.e. cancer). These disorders are caused by various stimuli and involve molecular pathways regulating cell growth and protein synthesis. Disorders can progress from early changes like metaplasia and dysplasia to late stage cancers if deregulation persists over time.
This document summarizes acute inflammation and the key chemical mediators involved. It describes how injury causes vasodilation, increased vascular permeability, and leukocyte emigration through the actions of histamine, bradykinin, prostaglandins, leukotrienes, cytokines, and other mediators. These chemical mediators cause effects like vasodilation, increased vascular permeability, chemotaxis, fever, pain, and tissue damage during acute inflammatory responses.
Acute inflammation is an immediate response to injury that involves vasodilation, increased vascular permeability, and leukocyte migration. This leads to redness, swelling, heat, and pain at the site of injury. Chronic inflammation is a prolonged response that involves lymphocytes, macrophages and plasma cells. It can lead to tissue destruction and attempts at repair through fibrosis and new blood vessel formation. The response involves many chemical mediators like histamine, kinins, cytokines, and eicosanoids that regulate vascular permeability and leukocyte behavior. Defects in leukocyte function can impair inflammatory response. Acute inflammation may resolve with repair or progress to chronic inflammation and tissue damage.
A condition in which the blood doesn't have enough healthy red blood cells.
Anaemia results from a lack of red blood cells or dysfunctional red blood cells in the body. This leads to reduced oxygen flow to the body's organs.
Arteriosclerosis is the hardening and narrowing of arteries due to plaque buildup. The three main types are arteriolosclerosis (small arteries), Monckeberg medial sclerosis (calcification of muscular arteries), and atherosclerosis (most common). Atherosclerosis features atheromas that protrude into the vessel lumen. Risk factors like age, gender, genetics, hyperlipidemia, hypertension, smoking, and diabetes accelerate atherosclerosis. Inflammation and infection also contribute to plaque formation and rupture, which can cause acute issues like heart attack or stroke.
Describes the process of ageing in cells, factors affecting cells like telomere, free radicals, oxidative stress, DNA damage, environmental factors, proteostasis, mitochondrial disfunction etc are described
Adaptations of cellular growth and diffrentiationrashree-singh
This document discusses various types of cellular adaptation in response to environmental changes. It defines key adaptations like hypertrophy, hyperplasia, atrophy, and metaplasia. Hypertrophy involves cell enlargement while hyperplasia is an increase in cell number. Atrophy is a decrease in cell size and number. Metaplasia is the reversible replacement of one cell type with another. Adaptations can be physiological from things like exercise or pathological from issues like hypertension. The mechanisms of adaptations involve growth factors, hormones, and changes in protein expression levels. Cellular adaptations allow tissues to survive stresses but can sometimes progress to disease if the stressors remain.
This document discusses cellular adaptation, injury, and death. It covers topics like hyperplasia, hypertrophy, atrophy, metaplasia, causes of cell injury including hypoxia and free radicals, necrosis and apoptosis. It provides detailed descriptions of the morphological changes that occur during cellular injury and the mechanisms of necrosis, apoptosis and intracellular accumulation.
Cell injury occurs when cells can no longer maintain homeostasis or adapt to stress. There are two types of cell injury: reversible and irreversible. Reversible injury allows cells to return to normal after stress is removed, while irreversible injury leads to cell death through necrosis or apoptosis. Causes of cell injury include hypoxia, chemicals, physical agents, infections, immunologic reactions, genetics, and nutrition. Mechanisms of injury involve depletion of ATP, mitochondrial damage, calcium dysregulation, oxidative stress, and membrane damage.
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
This document discusses cell injury, adaptation, and death. It explains that cells can undergo adaptation to physiologic or pathologic stresses to maintain homeostasis. Adaptation allows cells to modify their structure and function to avoid injury. If stresses exceed a cell's adaptive capacity, injury occurs. Adaptations include hypertrophy, where cells increase in size rather than number. Hypertrophy can be physiologic, like uterine enlargement during pregnancy, or pathologic, like cardiac enlargement from hypertension. The document then focuses on hypertrophy in more detail.
Necrosis is the death of cells and living tissue. There are several types of necrosis including coagulative, liquefactive, and caseous necrosis. Coagulative necrosis involves the preservation of the basic cellular structure but loss of cellular details. Liquefactive necrosis results in the transformation of tissue into a liquid mass where all cellular and architectural details are lost. Caseous necrosis converts dead tissue into a cheesy-like granular mass where no cellular or architectural details remain. The document further describes the characteristics, causes, and microscopic appearance of each type of necrosis.
This document discusses inflammatory mediators, which are messengers that contribute to the inflammatory response by acting on blood vessels, immune cells, or other cells. Inflammatory mediators can be classified as either cell-derived or plasma-derived. Cell-derived mediators include histamine, serotonin, lysosomal enzymes, eicosanoids such as prostaglandins and leukotrienes, platelet-activating factor, reactive oxygen species, nitric oxide, and cytokines. Plasma-derived mediators include components of the complement, coagulation, kinin, and fibrinolytic systems. Many of these mediators stimulate the release of other mediators and have effects like increasing vascular permeability and chemotaxis. Cytokines and
Cell injury can result from depletion of ATP, mitochondrial damage, calcium influx, oxidative stress, and defects in membrane permeability. The main cellular adaptations to injury are hyperplasia, hypertrophy, atrophy, and metaplasia. ATP depletion affects energy-dependent functions, potentially leading to necrosis. Mitochondrial damage causes further ATP loss and leakage of proteins involved in apoptosis. Calcium influx activates enzymes that damage cell components and may trigger apoptosis. Oxidative stress modifies proteins, lipids, and nucleic acids. Increased membrane permeability affects organelle and plasma membranes, usually culminating in necrosis or triggering of apoptosis pathways.
Cellular swelling or cloudy swelling is a reversible degeneration where cells swell due to metabolic disturbances. Mild irritants like bacteria or temperature changes can cause swelling. Swollen cells appear cloudy under microscopy. Hydropic degeneration involves cellular swelling with fluid accumulation that can cause blistering. Mucinous degeneration is the excessive mucin production in epithelial cells due to irritants. Mucoid degeneration involves the appearance of mucin-like glycoprotein in connective tissue. Hyaline change results in a glassy, translucent appearance as cells or tissues lose structure and fuse. It can involve keratin, cells, or connective tissues.
The splanchnic circulation provides blood flow to the gastrointestinal tract and liver. Approximately 1450 ml of blood flows through the splanchnic circulation per minute, accounting for 29% of total blood flow. The splanchnic circulation regulates blood volume and pressure and can reduce its flow during hemorrhage to prioritize more vital organs. Blood flow to the intestinal mucosa increases after eating to support metabolic activity. Splanchnic blood flow is regulated intrinsically through local metabolic and myogenic controls and extrinsically through the sympathetic nervous system and circulating hormones. Sympathetic stimulation causes vasoconstriction that redirects blood flow away from the splanchnic circulation during exercise.
This document discusses the local and humoral regulation of tissue blood flow. It begins by outlining the specific needs of tissues for blood flow, including delivery of oxygen and nutrients and removal of waste. It then describes the mechanisms by which changes in tissue metabolism or oxygen availability alter blood flow, including the vasodilator and oxygen demand theories. The document also discusses acute responses like active and reactive hyperemia, as well as long-term regulation through changes in vascularity and remodeling of blood vessels. Finally, it outlines various humoral factors that can cause vasoconstriction or vasodilation, such as sympathetic nerves, angiotensin, bradykinin, and ions like calcium, potassium, and hydrogen ions
The document discusses cardiogenic shock, which occurs when the heart is unable to generate sufficient cardiac output to maintain tissue perfusion. Myocardial infarction is a frequent cause, due to valve disease, cardiomyopathy, or direct contusion. This leads to compensatory tachycardia but eventually decreased organ perfusion and hypotension, exacerbating the mismatch between coronary blood flow and oxygen demand. Management goals are to enhance ventricular performance, improve hypoperfusion, limit infarct size, and minimize myocardial oxygen demand. Initial treatment includes supplemental oxygen, pain relief, sedation, and monitoring. In critically ill patients, measurements from a Swan-Ganz catheter are crucial, as cardiogenic shock presents with low cardiac output but normal or slightly
Shock is the failure of the cardiovascular system to provide sufficient oxygen to tissues due to systemic hypoperfusion. It can result from reduced blood volume, cardiac dysfunction, obstruction of circulation, or distributive disorders. Severe hemorrhage, trauma, burns, myocardial infarction, pulmonary embolism, or sepsis can cause shock by damaging the cardiovascular system or reducing intravascular volume. Persistent shock leads to cellular hypoxia, tissue injury, organ failure, and death if not treated.
The document discusses different types of shock and their pathophysiology. It defines shock and describes classifications proposed by Blalock and others. Types include hemorrhagic, cardiogenic, obstructive, distributive, and endocrine shock. The body responds to shock through neuroendocrine and physiological changes aimed at maintaining perfusion. These include activation of the sympathetic nervous system, renin-angiotensin-aldosterone system, and antidiuretic hormone among others. Clinical assessment and management of shock are also covered.
This document discusses various factors that regulate blood flow locally and systemically. It covers topics such as local blood flow regulation including reactive and active hyperemia. It also discusses humoral regulation by various vasoconstrictors like epinephrine, vasopressin, angiotensin, and endothelin as well as vasodilators like bradykinin, serotonin, prostaglandins, and histamine. Finally, it mentions regulation by ions and chemicals in the blood as well as long-term regulation through angiogenesis and collateral circulation development.
Nervous control of blood vessels regulation of arterial pressureAmen Ullah
The main function of the circulatory system is to give local blood flow to the tissue. There arespecial need of the tissue which is:
delivery of oxygen to the tissue
delivery of nutrients to the tissue
removal of carbon dioxide from tissue
maintaining of normal concentration of ions
transform of hormones and other substance to tissue
This document discusses the anatomy, physiology, and functions of the liver as they relate to anesthesia. It begins with an overview of hepatic anatomy including gross and microscopic structure, blood supply, and drainage. It then covers hepatic blood flow regulation by intrinsic and extrinsic factors and how anesthesia can affect blood flow. The major sections discuss hepatic functions such as metabolism, synthesis, and detoxification. In particular, it notes the liver's roles in glucose regulation, protein and lipid metabolism, coagulation factor production, and bilirubin metabolism.
This document provides an overview of shock and its management. It defines shock as the body's response to poor perfusion and discusses the significance of fluids and electrolytes. It describes the roles of the cardiovascular and nervous systems in maintaining perfusion. The stages of shock are outlined as compensated, decompensated, and irreversible. Signs and symptoms are provided for each stage. Finally, it briefly mentions the types and management of shock.
The document discusses the regulation of blood flow to tissues and organs. It describes acute control which occurs rapidly through vasoconstriction or vasodilation and long term control which involves changes to blood vessel structure over days or weeks. Key mechanisms of acute control include autoregulation to maintain constant blood flow despite pressure changes, active hyperemia to increase flow during increased activity, and reactive hyperemia providing a temporary surge in flow after ischemia. Long term control involves angiogenesis and developing collateral blood vessels. Regulation also occurs through vasoactive hormones, ions, and other chemicals that cause vasoconstriction or vasodilation.
This document provides information about homeostasis. It begins by defining homeostasis as the regulation of physical and chemical factors within the internal environment to maintain optimal conditions for cell function. It describes the importance of homeostasis in enabling biochemical reactions to occur at their maximum rate. It then discusses the key components of control systems that detect changes and trigger responses to maintain homeostasis, including sensors, control centers, and effectors. Several examples of homeostatic control of body temperature, blood sugar levels, carbon dioxide levels, and blood pressure are examined in more detail.
Shock is a state of low tissue perfusion that can be fatal if not treated promptly. There are several types of shock based on the underlying pathophysiology, including hypovolaemic shock (from blood or fluid loss), cardiogenic shock (from heart failure), distributive shock (from sepsis or anaphylaxis), and obstructive shock (from embolism or pulmonary hypertension). Early resuscitation is crucial and involves restoring circulating volume through intravenous fluids while also identifying and treating the underlying cause of shock. Outcomes depend on limiting the duration of tissue hypoperfusion to prevent multiple organ failure.
This document discusses hypovolemic shock and hypothermia. It defines hypovolemic shock as a systemic state of low perfusion caused by inadequate fluid volume. It describes the pathophysiology as reduced perfusion leading to cellular hypoxia, microvascular injury, and systemic responses like tachycardia and vasoconstriction. The document outlines methods for assessing fluid status, such as the modified shock index and fluid challenge tests. It also discusses the risks of hypothermia for trauma patients, like coagulopathy, and different techniques for warming patients, with active internal warming through conduction seen as most effective.
This document provides an overview of shock, including:
1. Definitions of shock and classifications according to etiology and pathophysiology. Shock results from inadequate oxygen delivery to tissues.
2. Descriptions of the pathophysiology of shock at the cellular, microvascular, and systemic levels, including metabolic changes, inflammation, and compensatory responses.
3. Clinical features of shock ranging from mild to severe based on degree of blood or fluid loss. Monitoring includes vital signs, urine output, and invasive monitoring like Swan-Ganz catheter.
4. Treatment principles for different types of shock including fluid resuscitation and management of underlying causes like bleeding control or cardiac dysfunction. Outcomes can include
This document provides an overview of fluid and electrolyte balance in the human body. It discusses the regulation of body fluid compartments through mechanisms like osmosis, diffusion, and the sodium-potassium pump. Gains and losses of fluids occur through drinking, eating, urination, sweating, breathing, and digestion. Homeostatic organs like the kidneys, heart, lungs, and endocrine glands help regulate fluid volume and composition. Imbalances can cause fluid volume deficits or excesses, leading to conditions like dehydration or edema. Diagnostic tests and nursing care aim to restore normal fluid status.
The document summarizes key aspects of the respiratory system, including:
1) The respiratory system facilitates gas exchange between an organism and the environment, taking in oxygen and removing carbon dioxide.
2) The main functions of the respiratory system are intake of oxygen, removal of carbon dioxide, and maintaining pH and acid-base balance of the blood.
3) Respiration requires the coordinated efforts of the respiratory muscles, airways, and alveoli where gas exchange takes place.
Shock is the state of not enough blood flow to the tissues of the body as a result of problems with the circulatory system.Initial symptoms may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest as complications worsen.
Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. Low volume shock may be from bleeding, diarrhea, vomiting, or pancreatitis. Cardiogenic shock may be due to a heart attack or cardiac contusion. Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. Distributed shock may be due to sepsis, spinal cord injury, or certain overdoses.
The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation.
Treatment of shock is based on the likely underlying cause.[2] An open airway and sufficient breathing should be established.[2] Any ongoing bleeding should be stopped, which may require surgery or embolization.[2] Intravenous fluid, such as Ringer's lactate or packed red blood cells, is often given.[2] Efforts to maintain a normal body temperature are also important.[2] Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%
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Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
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it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
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You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
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Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
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1. Hypoxia
Compiled by Associate Professor of Pathophysiology Department
Arsenteva Ekaterina Vladimirovna
Ev.arsenteva@yandex.ru
Lecturer: Professor of Pathophysiology Department
Vlasova Tatyana Ivanovna
v.t.i@bk.ru
11. Respiratory hypoxia
due to:
• alveolar hypoventilation,
• impaired oxygen diffusion through the air-
blood barrier,
• dissociation of the ventilation-perfusion ratio,
• reduced perfusion with blood of the lungs.
11
24. Urgent reaction.
Cardiovascular system
Heart (by activation of sympathetic system):
• Tachycardia.
• Increased shock release of blood from the heart.
• Increase in the minute volume of blood circulation (cardiac blood
flow).
• Increased linear and volumetric blood flow velocity in the vessels.
Vascular system (by activation of sympathetic system and release of
catecholamines; by accumulation in the myocardium and brain tissue
of metabolites with a vasodilator effect):
• centralization of the blood flow (due to expansion of arterioles and
increased blood supply to the brain and heart, narrowing of the lumen
of arterioles and reduction of the blood supply in other organs and
tissues)
24
25. Urgent reaction.
Blood system
• Activation of the release of red blood cells from the bone
marrow and blood depot;
• Increased degree of Hb02 dissociation in tissues;
• An increase in the affinity of Hb for oxygen in the
capillaries of the lungs.
25
26. Urgent reaction.
Biological oxidation cell’s system
•Improving the efficiency of the processes of assimilation of oxygen and
oxidation substrates by the tissues of the body and their delivery to
mitochondria;
•Activation of oxidation and phosphorylation enzymes;
•Increasing the degree of conjugation of the oxidation and
phosphorylation of adenine nucleotides: ADP, AMP, and creatine;
• Activation of the glycolytic oxidation pathway.
26
27. Permanent compensation.
Biological oxidation systems.
Providing optimal energy supply of functioning structures and the level
of plastic processes by:
- Increase in the number of mitochondria and the number of
mitochondrial cristae.
- An increase in the number of enzyme molecules of tissue respiration in
each mitochondria, as well as the activity of enzymes, especially
cytochrome oxidase.
- Improving the efficiency of biological oxidation and its conjugation
with phosphorylation.
- Improving the efficiency of the mechanisms of anaerobic resynthesis
of ATP in cells.
27
28. Permanent compensation.
Biological oxidation systems.
Providing optimal energy supply of functioning structures and the level
of plastic processes by:
- Increase in the number of mitochondria and the number of
mitochondrial cristae.
- An increase in the number of enzyme molecules of tissue respiration in
each mitochondria, as well as the activity of enzymes, especially
cytochrome oxidase.
- Improving the efficiency of biological oxidation and its conjugation
with phosphorylation.
- Improving the efficiency of the mechanisms of anaerobic resynthesis
of ATP in cells.
28
29. Permanent compensation.
Respiration systems.
The system regulates a level of gas exchange by:
- Hypertrophy of the lungs and an increase in the area of the alveoli,
in the capillaries in the interalveolar septa, in the level of blood flow
in these capillaries.
- Increase the diffusion ability of the air-blood barrier of the lungs.
- Improving the efficiency of the ventilation-perfusion ratio.
-Hypertrophy and increase in the power of the respiratory muscles.
- Ascending the vital capacity of the lungs
29
30. Permanent compensation.
Cardiovascular system.
Heart:
- Moderate balanced hypertrophy of all structural elements of the
heart: myocardium, vascular bed, nerve fibers.
- Increase in the number of functioning capillaries in the heart.
- Reducing the distance between the capillary wall and the sarcolemma
of the cardiomyocyte.
- Increasing the number of mitochondria in cardiomyocytes and the
effectiveness of biological oxidation reactions. In this regard, the heart
spends 30-35% less oxygen and metabolic substrates than in a state that
is not adapted to hypoxia.
- Improving the efficiency of transmembrane processes (ion transport,
substrates and metabolic products, oxygen, etc.).
- Increase in the power and speed of interaction of actin and myosin in
cardiomyocyte myofibrils.
- Improving the efficiency of adrenal and cholinergic systems of heart
regulation.
30
31. Permanent compensation.
Cardiovascular system.
Vascular system:
Reduction of myogenic arteriole tone and
reduction of the reactive properties of the walls
of resistive vessels to vasoconstrictors/
-Increasing the number of functioning capillaries
in tissues and organs.
31
33. Permanent compensation.
Blood system.
1. Increase in the affinity of deoxyhemoglobin for
oxygen in the capillaries of the lungs significantly.
2. Activation under the influence of ischemia and
hypoxia
education in the kidney erythropoietin
stimulating erythropoiesis
The increase in blood oxygen capacity
33
35. Permanent compensation.
Metabolic processes
- High efficiency and lability of the reactions of anaerobic
resynthesis of ATP.
-The economical use of oxygen and metabolism substrates in
the reactions of biological oxidation and plastic processes.
-Reducing intensity of metabolic processes
-The dominance of anabolic processes in tissues compared with
catabolic.
-High power and mobility of transmembrane ion transfer
mechanisms.
35
36. Permanent compensation.
Nervous and endocrine systems.
Nervous system:
- Increased resistance of neurons to hypoxia and ATP
deficiency, as well as to some other factors/
- Hypertrophy of neurons and an increase in the number
of nerve endings in tissues and organs.
- Increased sensitivity of receptor structures to
neurotransmitters.
Endocrine system :
- A lesser degree of stimulation of the adrenal medulla,
hypothalamic-pituitary-adrenal and other systems.
- Increased sensitivity of cell receptors to hormones.
36
38. Thank you for your
attention!
To your success!
Send me your question
v.t.i@bk.ru
Editor's Notes
Hypoxia is a typical pathological process that develops as a result of insufficiency of biological oxidation. It leads to a violation of the energy supply of functions and plastic processes in the body.
Hypoxia is often combined with hypoxemia (a decrease in the oxygen content in the blood)
Due to the severity of hypoxia
Normobaric exogenous hypoxia (restriction of oxygen in the body with air at normal barometric pressure)
The causes:
finding people in small and / or poorly ventilated spaces
Violations of air regeneration and / or oxygen mixture supply for breathing in flying and deep-seated vehicles, etc.
Non-compliance with the method of artificial ventilation.
Causes of hypobaric exogenous hypoxia: a decrease in barometric pressure when climbing to a height (more than 3,000–3,500 m, where the p02 of air is reduced to about 100 mm Hg) or in a pressure chamber.
Under these conditions, development of either mountain or altitude or decompression sickness is possible.
• Mountain sickness is observed when climbing into the mountains, where the body is exposed to not only low oxygen content in the air and low barometric pressure, but also more or less pronounced physical exertion, cooling, increased insolation and other factors of the middle and high mountains.
Altitude sickness develops in people who are raised to a greater height in open aircraft, on lift chairs, and also when pressure in the pressure chamber decreases. In these cases, mainly reduced p02 in the inhaled air and barometric pressure affect the body.
Decompression sickness occurs with a sharp decrease in barometric pressure (for example, as a result of depressurization of aircraft at altitudes above 10,000–11,000 m). At the same time, a life-threatening condition is formed, which differs from an acute mountain or altitude sickness disease by acute or even fulminant course.
Endogenous hypoxia in most cases are the result of pathological processes and diseases leading to inadequate transport of oxygen to organs, metabolism substrates and / or their use by tissues. Hypoxia of varying severity and duration may also develop as a result of a sharp increase in the body's need for energy due to significantly increased loads (for example, with a sharp increase in physical activity). At the same time, even the maximum activation of oxygen-transport and energy-producing systems is not capable of eliminating energy deficiency (overloading hypoxia).
Substrate hypoxia due to decrease content of substanses which need to produce ATP except oxigen (for ex. Decrease in content of glucose)
The main parts of the pathogenesis of exogenous hypoxia include arterial hypoxemia, hypocapnia, gas alkalosis, alternating with acidosis; arterial hypotension, combined with the hypoperfusion of organs and tissues.
• Decrease in oxygen tension in arterial blood plasma (arterial hypoxemia) is the initial and main link of exogenous hypoxia. Hypoxemia leads to a decrease in the oxygen saturation of Hb, the total oxygen content in the blood and, as a result, to impaired gas exchange and metabolism in the tissues.
• Reduced blood pressure in hypocapnia. It occurs as a result of compensatory hyperventilation of the lungs (due to hypoxemia).
• Gas alkalosis is the result of hypocapnia. However, it should be remembered that if there is a high content of carbon dioxide in the inhaled air (for example, when breathing in a confined space or under production conditions), exogenous hypoxemia can be combined with hypercapnia and acidosis.
• Decreased systemic blood pressure (hypotension), combined with tissue hypoperfusion, is largely a consequence of hypocapnia. C02 is one of the main factors regulating the vascular tone of the brain. A significant decrease in pC02 is a signal to the narrowing of the lumen of the arterioles of the brain, heart, and reduction of their blood supply. These changes cause significant bodily disorders, including the development of syncope and coronary insufficiency (manifested by angina, and sometimes myocardial infarction).
In parallel with these abnormalities, impaired ionic balance is detected both in cells and in biological fluids: extracellular, blood plasma (hypernatremia, hypokalemia and hypocalcemia), lymph, cerebrospinal fluid.
Respiratory hypoxia The cause of respiratory (respiratory) hypoxia is a lack of gas exchange in the lungs is respiratory failure.
Pathogenesis of respiratory hypoxia The development of respiratory failure may be due to alveolar hypoventilation, reduced perfusion with blood of the lungs, impaired oxygen diffusion through the air-blood barrier, dissociation of the ventilation-perfusion ratio.
Regardless of the origin of respiratory hypoxia, the initial pathogenetic link is arterial hypoxemia, usually combined with hypercapnia and acidosis.
• Alveolar hypoventilation is characterized by the fact that the volume of ventilation of the lungs per unit of time is lower than the body's need for gas exchange during the same time. This condition is the result of a violation of the biomechanical properties of the breathing apparatus and a disorder in the regulation of ventilation of the lungs.
Violations of the alveolar ventilation can be obstructive and restrictive.
- Causes of obstructive disorders: edema of the walls of the bronchi and bronchioles, tumors, foreign bodies in the lumen of the airways.
- Causes of disorders of the restrictive type (due to a decrease in the elastic properties of the lungs and their elasticity): extensive pneumonia, atelectasis, edema and pulmonary fibrosis, pneumo- or hemothorax, rigidity of the bone and cartilage apparatus of the chest, significant volume of exudate in the pleural cavity.
- Disorders of respiratory regulation mechanisms.
Causes of disorders: direct effect of damaging factors on the neurons of the respiratory center (for example, hemorrhage, swelling, edema, inflammation in the medulla oblongata or areas of the bridge) and reflex effects in the form of:
- afferential deficit that excites the neurons of the respiratory center (for example, during drug poisoning);
- an excess of stimulating impulses, leading to frequent shallow breathing (for example, during stress, neurosis, encephalitis);
- an excess of inhibitory afferentation (for example, during irritation of the mucous membrane of the nasal passages and trachea by chemicals or mechanically, in acute tracheitis and bronchitis).
• Violation of oxygen diffusion through the air-blood barrier
Causes: Thickening and / or compaction of the components of the alveolocapillary membrane. This leads to a more or less pronounced alveolocapillary separation of the gas environment of the alveoli and the blood of the capillaries. This phenomenon is observed in interstitial pulmonary edema, diffuse fibrosis of the interstitium of the lungs (for example, in fibrosing alveolitis), pneumoconiosis (conditions characterized by focal and diffuse hyperproduction of connective tissue in the lungs, for example, in silicosis, asbestosis, sarcoidosis).
• Dissociation of the ventilation-perfusion ratio
Causes:
- Violation of the patency of the bronchi and / or bronchioles.
- Reduced tensile properties of the alveoli.
- Local decrease in blood flow in the lungs. Such changes are observed, for example, in bronchospasm and pneumosclerosis of various origins, pulmonary emphysema, embolism or thrombosis of the branches of their vascular bed. This leads to the fact that some regions of the lungs are normally ventilated, but not sufficiently perfused with blood, some, on the contrary, are well supplied with blood, but insufficiently ventilated. In this regard, hypoxemia is detected in the blood flowing from the lungs.
• Reduction of blood perfusion of lung. Causes:
- Reduction of BCC (hypovolemia).
- Lack of contractile function of the heart.
- Increased resistance to blood flow in the vascular bed of the lungs (pre- and / or postcapillary hypertension).
- Increased air pressure in the alveoli and / or airways.
-
Opening of arteriovenous anastomoses and discharge of blood through intra- and extrapulmonary shunts from right to left, by passing the capillaries of the alveoli.
Circulatory (cardiovascular, hemodynamic) hypoxia develops with local, regional and systemic hemodynamic disturbances. Depending on the mechanisms of development of circulatory hypoxia, ischemic and stagnant forms can be distinguished. The basis of circulatory hypoxia may lie absolute circulatory failure or relative with a sharp increase in tissue oxygen demand (in stress situations).
Generalized circulatory hypoxia occurs in heart failure, shock, collapse, dehydration, DIC syndrom, etc., moreover, if hemodynamic disorders occur in the pulmonary circulation, the oxygenation of the blood in the lungs can be normal and its delivery is disturbed to tissues in connection with the development of venous hyperemia and stagnation in the pulmonary circulation. When violations of hemodynamics in the vessels of the pulmonary circulation, arterial blood oxygenation suffers.
Local circulatory hypoxia occurs in the zone of thrombosis, embolism, ischemia, and venous hyperemia in various organs and tissues.
The hemic (blood) type of hypoxia arises as a result of a decrease in the effective oxygen capacity of the blood and its oxygen transporting function. The transport of oxygen from the lungs to the tissues is almost completely accomplished with the participation of Hb.
The main links to reduce the oxygen capacity of the blood are:
1) the reduction of Hb in a unit of blood volume and in full, for example, with pronounced anemia caused by impaired bone marrow hematopoiesis of various origins, with post-hemorrhagic and hemolytic anemia.
2) a violation of the transport properties of Hb, which may be due either to a decrease in the ability of Hb of erythrocytes to bind oxygen in the capillaries of the lungs, or to transport and deliver the optimal amount of it in the tissues, which is observed in hereditary and acquired hemoglobinopathies.
Quite often, hemic hypoxia occurs when carbon monoxide poisoning ("carbon monoxide"), since carbon monoxide has an extremely high affinity for hemoglobin, almost 300 times greater than the affinity for oxygen to it. When carbon monoxide interacts with blood hemoglobin, carboxyhemoglobin is formed, which lacks the ability to transport and release oxygen.
Carbon monoxide is found in high concentrations in the exhaust gases of internal combustion engines, in domestic gas, etc.
Pronounced impairment of the body's activity develops with an increase in the blood HbCO up to 50% (of the total concentration of hemoglobin). Increasing its level to 70-75% leads to severe hypoxemia and death.
Carboxyhemoglobin has a bright red color, so when it is excessively formed in the body, the skin and mucous membranes become red. Elimination of CO from inhaled air leads to HbCO dissociation, but this process proceeds slowly and takes several hours.
Impact on the body of a number of chemical compounds (nitrates, nitrites, nitric oxide, benzene, some toxins of infectious origin, drugs: phenazepam, amidopirin, sulfonamides, LPO products, etc.) leads to the formation of methemoglobin, which is not capable of carrying oxygen, as it contains the iron oxide form (Fe3 +).
The oxide form of Fe3 + is usually in association with hydroxyl (OH-). MetHb has a dark brown color and it is this shade that the blood and tissues of the body acquire. The formation of metHb is reversible, however, its recovery to normal hemoglobin occurs relatively slowly (within a few hours), when iron Hb again goes into the acidic form. The formation of methemoglobin not only reduces the oxygen capacity of the blood, but also reduces the ability of the active oxyhemoglobin to dissociate with the release of oxygen to the tissues.
Tissue (histotoxic) hypoxia develops due to a violation of the ability of cells to absorb oxygen (during normal delivery to the cell) or due to a decrease in the efficiency of biological oxidation as a result of separation of oxidation and phosphorylation.
The development of tissue hypoxia is associated with the following pathogenetic factors:
1. Violation of the activity of enzymes of biological oxidation in the process:
a) specific binding of the active sites of the enzyme, for example, cyanides and some antibiotics;
b) the binding of the SH groups of the protein part of the enzyme by heavy metal ions (Ag2 +, Hg2 +, Cu2 +), resulting in the formation of inactive forms of the enzyme;
c) competitive blocking of the active center of the enzyme by substances having a structural analogy with the natural substrate of the reaction (oxalates, malonates).
2. Violation of the synthesis of enzymes, which can occur with a deficiency of vitamins B1 (thiamine), VZ (PP), nicotinic acid, etc., as well as cachexia of various origin.
3. Deviations from the optimum physicochemical parameters of the internal environment of the body: pH, temperature, electrolyte concentrations, etc. These changes occur in a variety of diseases and pathological conditions (hypothermia and hyperthermia, kidney, heart and liver failure, anemia) and reduce the effectiveness of biological oxidation .
4. Disintegration of biological membranes, caused by the influence of pathogenic factors of infectious and non-infectious nature, accompanied by a decrease in the degree of conjugation of oxidation and phosphorylation, suppression of the formation of high-energy compounds in the respiratory chain. The ability to dissociate oxidative phosphorylation and respiration in mitochondria has: an excess of H + and Ca2 + ions, free fatty acids, adrenaline, thyroxine and triiodothyronine, some drugs (dicoumarin, gramicidin, etc.). Under these conditions, oxygen consumption by the tissues increases. In cases of mitochondrial swelling, separation of oxidative phosphorylation and respiration, most of the energy is transformed into heat and is not used for the resynthesis of macroergs. The effectiveness of biological oxidation is reduced.
With repeated short-term or gradually developing and long-existing moderate hypoxia, the process of adaptation develops.
Adaptation to hypoxia is a gradual increase in the body's resistance to hypoxia, as a result of which it acquires the ability to exist with a lack of oxygen, which was previously incompatible with normal life activity.
There are 4 stages of the adaptation process:
ROS - reactive oxigen species (mediators) – free radicals
The first is the emergency stage (urgent adaptation) —the early stage of hypoxia. There is a cider mobilization of transport systems (hyperventilation of the lungs, an increase in cardiac output, an increase in blood pressure), aimed at maintaining sufficient efficiency of biological oxidation in the tissues.
In response to hypoxia, the sympathetic-adrenal system and the ACTH system are activated — glucocorticoids, mobile energy and plastic resources “in favor” of organs and systems providing urgent adaptation.
At this stage, the activity of the organism proceeds with the full mobilization of functional reserves at the limit of physiological possibilities, but the adaptation effect is not complete. This is combined with the phenomena of functional insufficiency - anemia, a violation of the higher nervous activity, and a drop in weight.
If the actions of the agent that caused the reactions of urgent adaptation to hypoxia continue or periodically repeated for a long time, there is a gradual transition from urgent to long-term adaptation (the second is a transitional stage) during which the body begins to acquire increased resistance to hypoxia.
In case of continuation or repetition of the training action of hypoxia, the third stage is formed - the stage of economical and fairly effective sustainable long-term adaptation.
At this stage, adaptive shifts occurring at the cellular level are realized. With prolonged adaptation to hypoxia:
1. Activation of the hypothalamic-pituitary system and the adrenal cortex;
.
2. Increasing the power of oxygen capture and transport systems (these changes are based on DNA activation and a change in the protein synthesis system):
a) hypertrophy and hyperplasia of the neurons of the respiratory center, which improves the regulation of oxygen supply systems;
b) hypertrophy of the lungs, an increase in their respiratory surface, an increase in the power of the respiratory muscles, hyperfunction of the lungs;
c) cardiac hypertrophy, increase in myocardial contractility, increase in the power of the heart energy supply systems, hyperfunction of the heart;
d) polycythemia, an increase in the oxygen capacity of the blood, the formation of new capillaries in the brain and heart;
e) aerobic cell transformation - fixed by cell inheritance, increased ability to absorb oxygen, based on increasing the number of mitochondria per cell, increasing the active surface of each mitochondria, increasing the chemical affinity of mitochondria to oxygen, increasing oxygen transport from the blood into the cells (epigenome variability of somatic cells );
e) an increase in antioxidant activity to the deoxidation systems;
These mechanisms provide a sufficient supply of oxygen to the body, despite its deficiency in the environment, and the supply of oxygen to tissues.
Adaptation is considered complete if the alkaline reserve is reduced to such a value that the pH of the blood is established within the normal range.
If the training hypoxic exposure ceases, adaptation to it is lost, and maladaptation develops. When this occurs, the "reverse development" of those structural changes that ensured increased stability of the organism occurs.
In the case of a long-lasting and growing action of the hypoxic factor, the adaptive capacity of the organism gradually depletes, long-term adaptation (disadaptation) may occur and decompensation occurs, which is accompanied by an increase in destructive changes in organs and a number of functional disorders (fourth stage, which may manifest itself as chronic mountain syndrome).
Urgent reaction
Heart when adapting to hypoxia
In acute hypoxia, cardiac function is significantly intensified. Reason: activation of the sympathetic-adrenal system.
Mechanisms of adaptation to hypoxia
• Tachycardia.
• Increased shock release of blood from the heart.
• Increase in the minute volume of blood circulation (cardiac blood flow).
• Increased linear and volumetric blood flow velocity in the vessels.
Vascular system when adapting to hypoxia
Under hypoxic conditions, the phenomenon of redistribution, or centralization, of the blood flow develops.
The causes and mechanisms of the phenomenon of centralization of blood flow during adaptation to hypoxia:
• Activation in conditions of hypoxia of the sympathetic-adrenal system and release of catecholamines. The latter cause a narrowing of arterioles and a decrease in blood flow through them to most tissues and organs (muscles, abdominal organs, kidneys, hypoderm, etc.).
• Rapid and significant accumulation in the myocardium and brain tissue of metabolites with a vasodilator effect: adenosine, prostacyclin, PgE, kinins, etc. They provide for the expansion of arterioles and an increase in the blood supply to the heart and brain in hypoxia.
Consequences when adapting to hypoxia
• Expansion of arterioles and increased blood supply to the brain and heart.
• Simultaneous narrowing of the lumen of arterioles and reduction of the blood supply in other organs and tissues: muscles, subcutaneous tissue, vessels of the abdominal cavity, kidneys.
Blood system when adapting to hypoxia
Acute hypoxia of any genesis is accompanied by adaptive changes in the blood system:
• Activation of the release of red blood cells from the bone marrow and blood depot (in the latter case, simultaneously with other blood cells).
Reason: high concentration in the blood of catecholamines, thyroid and corticosteroid hormones.
As a result, polycythemia develops in acute hypoxia.
Consequence: an increase in the oxygen capacity of the blood.
• Increased degree of Hb02 dissociation in tissues.
The reasons
- Hypoxemia, especially in capillary and venous blood. In this regard, it is in the capillaries and postcapillary venules that the degree of oxygen Hb02 recovers.
- Acidosis, regularly developing with any type of hypoxia. - Increased under hypoxic conditions, the concentration in erythrocytes of 2,3-diphosphoglycerate, as well as other organic phosphates: ADP, pyridoxal phosphate. These substances stimulate the removal of oxygen from Hb02.
• An increase in the affinity of Hb for oxygen in the capillaries of the lungs. This effect is realized with the participation of organic phosphates, mainly 2,3-diphos-phoglycerate. At the same time, the property of Hb to bind a significant amount of oxygen is important even under conditions of significantly reduced p02 in the capillaries of the lungs.
Biological oxidation systems when adapting to hypoxia
Activation of metabolism is an important link in the emergency adaptation of the organism to acute hypoxia.
It provides:
• Improving the efficiency of the processes of assimilation of oxygen and oxidation substrates by the tissues of the body and their delivery to mitochondria.
• Activation of oxidation and phosphorylation enzymes, which is observed with moderate damage to cells and their mitochondria.
• Increasing the degree of conjugation of the oxidation and phosphorylation of adenine nucleotides: ADP, AMP, and creatine.
• Activation of the glycolytic oxidation pathway. This phenomenon is recorded in all types of hypoxia, especially in its early stages.
The reason for the inclusion of mechanisms for long-term adaptation to hypoxia: repeated or ongoing failure of biological oxidation of moderate severity.
They cause repeated activation of urgent adaptation mechanisms. This ensures the formation of a structural-functional basis for the processes of long-term adaptation to hypoxia. In this case, it is essential that the interval between episodes of moderate hypoxia is not too large or small.
External respiration system when adapting to hypoxia
The system of external respiration provides a level of gas exchange, sufficient for the optimal flow of metabolism and plastic processes in the tissues.
This is achieved by:
- Hypertrophy of the lungs and an increase in this connection: - the area of the alveoli, - the capillaries in the interalveolar septa, - the level of blood flow in these capillaries.
- Increase the diffusion ability of the air-blood barrier of the lungs.
- Improving the efficiency of the ratio of ventilation of the alveoli and their perfusion with blood (ventilation-perfusion ratio).
- Hypertrophy and increase in the power of the respiratory muscles.
- Ascending the vital capacity of the lungs (YES).
Heart when adapting to hypoxia
With long-term adaptation to hypoxia, the strength and speed of the processes of contraction and relaxation of the myocardium increase. As a result, there is an increase in the volume and speed of blood ejected into the vascular bed - shock and heart (minute) emissions.
These effects are made possible by:
- Moderate balanced hypertrophy of all structural elements of the heart: myocardium, vascular bed, nerve fibers.
- Increase in the number of functioning capillaries in the heart.
- Reducing the distance between the capillary wall and the sarcolemma of the cardiomyocyte.
- Increasing the number of mitochondria in cardiomyocytes and the effectiveness of biological oxidation reactions. In this regard, the heart spends 30-35% less oxygen and metabolic substrates than in a state that is not adapted to hypoxia.
- Improving the efficiency of transmembrane processes (ion transport, substrates and metabolic products, oxygen, etc.).
- Increase in the power and speed of interaction of actin and myosin in cardiomyocyte myofibrils.
- Improving the efficiency of adrenal and cholinergic systems of heart regulation.
Vascular system when adapting to hypoxia
In an adapted organism, the vascular system is able to provide such a level of tissue perfusion with blood that is necessary for their function even in hypoxia.
The basis of this are the following mechanisms:
- Reduction of myogenic arteriole tone and reduction of the reactive properties of the walls of resistive vessels to vasoconstrictors: catecholamines, ADH, leukotrienes, individual PG, etc.
Increasing the number of functioning capillaries in tissues and organs.
This creates the conditions for the development of stable arterial hyperemia in functioning organs and tissues.
Blood system when adapting to hypoxia
With a stable adaptation of the organism to hypoxia, the oxygen capacity of the blood, the rate of Hb02 dissociation, and the affinity of deoxyhemoglobin for oxygen in the capillaries of the lungs increase significantly.
The increase in blood oxygen capacity is the result of stimulation of erythropoiesis and the development of erythrocytosis.
The mechanism of erythrocytosis: activation under the influence of ischemia and hypoxia education in the kidney erythropoietin, stimulating erythropoiesis.
Metabolism when adapting to hypoxia
Metabolic processes in tissues upon reaching a state of sustainable adaptability to hypoxia are characterized by:
- High efficiency and lability of the reactions of anaerobic resynthesis of ATP.
- Reducing their intensity.
- The economical use of oxygen and metabolism substrates in the reactions of biological oxidation and plastic processes.
- The dominance of anabolic processes in tissues compared with catabolic.
- High power and mobility of transmembrane ion transfer mechanisms. This is largely the result of an increase in the efficiency of membrane ATPases, which ensures the regulation of the transmembrane distribution of ions, myogenic arteriole tone, water-salt metabolism, and other important processes.
Regulation systems for adaptation to hypoxia
The systems of regulation of an organism adapted to hypoxia ensure sufficient efficiency, cost effectiveness and reliability of managing its life activity. This is achieved through the inclusion of the mechanisms of the nervous and humoral regulation of functions.
Nervous regulation during adaptation to hypoxia
Significant changes in the higher parts of the brain and in the autonomic nervous system of an organism adapted to hypoxia are characterized by:
- Increased resistance of neurons to hypoxia and ATP deficiency, as well as to some other factors (for example, toxins, lack of metabolism substrates).
- Hypertrophy of neurons and an increase in the number of nerve endings in tissues and organs.
- Increased sensitivity of receptor structures to neurotransmitters. The latter, as a rule, is combined with a decrease in the synthesis and release of neurotransmitters.
Humoral regulation during adaptation to hypoxia
The restructuring of the endocrine system during hypoxia causes:
- A lesser degree of stimulation of the adrenal medulla, hypothalamic-pituitary-adrenal and other systems. This limits the activation of stress response mechanisms and its possible pathogenic effects.
- Increased sensitivity of cell receptors to hormones, which helps to reduce the amount of their synthesis in the endocrine glands.
Changes in gas composition and blood pH (respiratory hypoxia):
• Decrease in p02a and p02v (arterial and venous hypoxemia).
• As a rule, an increase in pC02 (hypercapnia),
• Acidosis (at the early stage of acute respiratory failure - gas, and then non-gas).
• Decrease in Sa02 and Sv02 (saturation of Hb, respectively, of arterial and venous blood).
For circulatory hypoxia, the following are characteristic: a decrease in PaO2, an increase in the utilization of O2 by the tissues due to slower blood flow and activation of the cytochrome system, an increase in the level of hydrogen ions and carbon dioxide in the tissues. Violation of the gas composition of the blood leads to a reflex activation of the respiratory center, the development of hyperpnea, an increase in the rate of dissociation of oxyhemoglobin in the tissues.