Shock occurs when arterial blood flow is inadequate to meet metabolic needs, resulting from cardiovascular collapse. The main types are hypovolemic, cardiogenic, and distributive shock. Hypovolemic shock results from decreased intravascular volume due to blood, plasma, or fluid loss. Cardiogenic shock is caused by pump failure from myocardial damage or obstruction. Distributive shock reduces vascular resistance from sepsis, anaphylaxis, or SIRS. The body initially compensates for shock but decompensation occurs when mechanisms fail, potentially progressing to irreversible shock without treatment.
Inflammation is the body's protective response to eliminate the initial cause of cell injury and initiate repair. It can be classified as acute or chronic based on duration, and by the type of exudate or cause. The classic signs of inflammation are redness, pain, swelling, heat, and loss of function. Acute appendicitis shows a swollen, reddish appendix on gross examination. Acute meningitis presents as a grayish-white exudate over the brain surface and prominent blood vessels on gross examination. Microscopy shows extensive necrosis surrounded by inflammatory cells in pyemic abscesses of the lung, kidney, and other organs. Pericarditis appears as an irregular, shaggy fibrinous ex
Shock is caused by inadequate systemic oxygen delivery that activates autonomic responses to maintain circulation. The main types of shock are hypovolemic, septic, cardiogenic, anaphylactic, neurogenic, and obstructive. Treatment focuses on airway control, oxygen delivery, circulation optimization through fluid resuscitation, and achieving hemodynamic goals to restore tissue perfusion. Early goal directed therapy for septic shock involving aggressive fluid administration and inotropes improves outcomes.
Shock is a circulatory disturbance characterized by reduced blood flow and oxygen delivery to tissues. There are two main types - primary (neurogenic) shock caused by sudden vasodilation and secondary (true) shock caused by decreased cardiac output, blood volume, or widespread vasodilation. Secondary shock includes cardiogenic (decreased cardiac function), hypovolemic (reduced blood volume), and septic (overwhelming infection) types. The pathogenesis involves an initial compensatory response followed by tissue hypoxia if not corrected. Shock progresses from a reversible to irreversible stage with widespread cellular injury and organ failure. Autopsy findings depend on the shock etiology but may include hemorrhage, infarction, acute tubular necrosis, and shock
This document discusses hemodynamic disorders including thromboembolic disease and shock. It defines shock and classifies it into four main types: hypovolemic, cardiogenic, septic, and traumatic shock. The pathogenesis of each type is described. Morphologic features in organs during shock like the brain, heart, lungs, kidneys, adrenals, gastrointestinal tract, and liver are outlined. The clinical features and complications of shock are also summarized.
This document discusses various haemodynamic disorders including hyperemia, congestion, hemorrhage, shock, thrombosis, embolism, and infarction. It defines these terms and describes their underlying mechanisms, examples, classifications, and importance. Hyperemia involves increased blood flow due to arteriolar dilation while congestion is the accumulation of deoxygenated blood due to impaired venous return. Thrombosis is the formation of a blood clot within vessels, which can embolize and occlude other vessels. Embolism is when a detached mass like a thrombus travels through the bloodstream. Infarction refers to the death of tissue from interrupted blood supply.
this presentation includes all the parts of shock. its definition classisfication, types of shock, pathophysiology, and additiionaly also includes clinical emergencies such as anaphylactic shock and syncope. hope this helps everyone.
Dr satyaki Verma
Dept of perio
This document discusses etiology and pathogenesis of cell injury. It defines cell injury as changes in a cell's internal and external environment due to various stresses from etiological agents. The cellular response depends on host factors like cell type and extent of injury. Injury can result in reversible or irreversible cell injury depending on factors like agent type/duration and cell adaptability. Common causes of cell injury include hypoxia, ischemia, toxins, microbes, nutrition imbalances, and aging. Ischemia and hypoxia are the most frequent causes of cell injury in humans. Reversible injury involves ATP depletion and membrane changes, while irreversible injury brings further damage including to mitochondria and nuclei, leading to cell death.
Shock occurs when arterial blood flow is inadequate to meet metabolic needs, resulting from cardiovascular collapse. The main types are hypovolemic, cardiogenic, and distributive shock. Hypovolemic shock results from decreased intravascular volume due to blood, plasma, or fluid loss. Cardiogenic shock is caused by pump failure from myocardial damage or obstruction. Distributive shock reduces vascular resistance from sepsis, anaphylaxis, or SIRS. The body initially compensates for shock but decompensation occurs when mechanisms fail, potentially progressing to irreversible shock without treatment.
Inflammation is the body's protective response to eliminate the initial cause of cell injury and initiate repair. It can be classified as acute or chronic based on duration, and by the type of exudate or cause. The classic signs of inflammation are redness, pain, swelling, heat, and loss of function. Acute appendicitis shows a swollen, reddish appendix on gross examination. Acute meningitis presents as a grayish-white exudate over the brain surface and prominent blood vessels on gross examination. Microscopy shows extensive necrosis surrounded by inflammatory cells in pyemic abscesses of the lung, kidney, and other organs. Pericarditis appears as an irregular, shaggy fibrinous ex
Shock is caused by inadequate systemic oxygen delivery that activates autonomic responses to maintain circulation. The main types of shock are hypovolemic, septic, cardiogenic, anaphylactic, neurogenic, and obstructive. Treatment focuses on airway control, oxygen delivery, circulation optimization through fluid resuscitation, and achieving hemodynamic goals to restore tissue perfusion. Early goal directed therapy for septic shock involving aggressive fluid administration and inotropes improves outcomes.
Shock is a circulatory disturbance characterized by reduced blood flow and oxygen delivery to tissues. There are two main types - primary (neurogenic) shock caused by sudden vasodilation and secondary (true) shock caused by decreased cardiac output, blood volume, or widespread vasodilation. Secondary shock includes cardiogenic (decreased cardiac function), hypovolemic (reduced blood volume), and septic (overwhelming infection) types. The pathogenesis involves an initial compensatory response followed by tissue hypoxia if not corrected. Shock progresses from a reversible to irreversible stage with widespread cellular injury and organ failure. Autopsy findings depend on the shock etiology but may include hemorrhage, infarction, acute tubular necrosis, and shock
This document discusses hemodynamic disorders including thromboembolic disease and shock. It defines shock and classifies it into four main types: hypovolemic, cardiogenic, septic, and traumatic shock. The pathogenesis of each type is described. Morphologic features in organs during shock like the brain, heart, lungs, kidneys, adrenals, gastrointestinal tract, and liver are outlined. The clinical features and complications of shock are also summarized.
This document discusses various haemodynamic disorders including hyperemia, congestion, hemorrhage, shock, thrombosis, embolism, and infarction. It defines these terms and describes their underlying mechanisms, examples, classifications, and importance. Hyperemia involves increased blood flow due to arteriolar dilation while congestion is the accumulation of deoxygenated blood due to impaired venous return. Thrombosis is the formation of a blood clot within vessels, which can embolize and occlude other vessels. Embolism is when a detached mass like a thrombus travels through the bloodstream. Infarction refers to the death of tissue from interrupted blood supply.
this presentation includes all the parts of shock. its definition classisfication, types of shock, pathophysiology, and additiionaly also includes clinical emergencies such as anaphylactic shock and syncope. hope this helps everyone.
Dr satyaki Verma
Dept of perio
This document discusses etiology and pathogenesis of cell injury. It defines cell injury as changes in a cell's internal and external environment due to various stresses from etiological agents. The cellular response depends on host factors like cell type and extent of injury. Injury can result in reversible or irreversible cell injury depending on factors like agent type/duration and cell adaptability. Common causes of cell injury include hypoxia, ischemia, toxins, microbes, nutrition imbalances, and aging. Ischemia and hypoxia are the most frequent causes of cell injury in humans. Reversible injury involves ATP depletion and membrane changes, while irreversible injury brings further damage including to mitochondria and nuclei, leading to cell death.
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.
1) Chronic inflammation is inflammation of prolonged duration that can occur following acute inflammation or persistently as active inflammation, often resulting in tissue destruction and repair processes.
2) Causes of chronic inflammation include persistent infections, prolonged exposure to toxic agents, and autoimmunity.
3) Morphological features of chronic inflammation are characterized by infiltration of mononuclear cells like macrophages and lymphocytes, tissue destruction by these inflammatory cells, and attempts at repair through fibrosis and new blood vessel formation.
1. Hyperemia and congestion refer to localized increases in blood volume within dilated vessels and are associated with edema.
2. Edema occurs when hydrostatic pressure is increased or oncotic pressure is decreased, overwhelming the lymphatic system and causing fluid accumulation in tissues.
3. Common causes of edema include increased venous pressure from heart failure, decreased plasma proteins, lymphatic obstruction, sodium retention, and inflammation.
This document discusses heart failure, including its definition, causes, types, and compensatory mechanisms. Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by intrinsic pump failure, an increased workload on the heart, or impaired filling of the cardiac chambers. The types of heart failure include acute or chronic, right-sided or left-sided, and forward or backward failure. When the heart begins to fail, compensatory mechanisms such as cardiac hypertrophy, dilation, and increased heart rate attempt to maintain adequate blood circulation.
The document discusses various types of embolism and thrombosis. It describes the Virschow triad of factors that can lead to thrombosis - endothelial injury, changes in blood flow, and hypercoagulability. It then examines different causes and outcomes of thrombosis and embolism in various parts of the body, such as pulmonary embolism from deep vein thrombosis, systemic embolism from cardiac sources, and amniotic fluid embolism during childbirth.
CONTENTS:
GENERAL
NORMAL FLUID CIRCULATION
EDEMA- INTRODUCTION
CAUSES
CLASSIFICATION
MAJOR TYPES
NOTE- Fonts may appear weird because the original fonts are different from the ones visible here.
This document defines and describes different types of embolism. The most common type is thromboembolism, which occurs when a thrombus or part of a thrombus breaks off and is carried by the bloodstream. Pulmonary thromboembolism is a significant type that occurs when thrombi travel to the lungs and obstruct the pulmonary arteries. Other types include fat, air, gas and paradoxical embolisms. Air embolism can be venous, entering systemic veins during surgery or trauma, or arterial, entering the lungs during procedures like angiography. Decompression sickness is a form of gas embolism that affects divers or those exposed to changes in atmospheric pressure.
This document provides information on the pathophysiology of shock. It defines shock and describes the main types: primary/initial shock, secondary/true shock. It then discusses the mechanisms and stages of shock, including compensated/non-progressive shock, decompensated progressive shock, and decompensated/irreversible shock. The management of different types of shock such as hypovolaemic shock and septic shock is also summarized.
Cell injury can be reversible or irreversible. Reversible injury is caused by decreased ATP and acidosis within cells. Irreversible injury occurs when mitochondrial and cell membrane dysfunction cannot be reversed, leading to calcium influx, membrane damage, and cell death. Free radicals generated during ischemia-reperfusion can also cause irreversible injury through lipid peroxidation, protein and DNA oxidation, and cytoskeletal damage. Stress proteins help cells cope with injury by moving molecules within the cell.
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injuryGovernment Medical College
Irreversible cell injury can occur through necrosis or apoptosis. Necrosis is unprogrammed cell death due to intracellular protein denaturation and lysosomal enzyme digestion, resulting in cell membrane rupture and content leakage. Apoptosis is genetically programmed cell death where cells activate enzymes to degrade their own DNA and proteins. Key differences are that apoptotic cells shrink while necrotic cells swell, and apoptotic cells remain intact while necrotic cells lyse. Free radicals can also cause cell injury by attacking cell components and structures like membranes, proteins, and DNA, resulting in lipid peroxidation, protein damage, and DNA lesions.
This document defines and classifies shock, discussing its pathogenesis and clinical features. It describes shock as a life-threatening condition characterized by reduced circulating blood volume and tissue perfusion. The document classifies shock into four main types - hypovolemic, cardiogenic, septic, and anaphylactic - and discusses their specific causes and pathophysiology. It also outlines the potential morbidities of shock including acute lung injury, kidney failure, liver dysfunction, and multi-organ failure.
It consists of basic detail about hemorrhage and shock.
In hemorrhage, there is classification of hemorrhage on various basis, it's sign and symptoms and treatment modalities.
The treatment consist of methods to control bleeding and substitutes use for restoration of blood.
It also explain the hemorrhagic shock.
Shock consist of its pathophysiology, classification and description of types of shock.
Each type consist of its general feature, pathogenesis and treatment.
Oedema, also called hydrops, results from an accumulation of excess fluid in the interstitial spaces or body cavities due to diseases rather than being a disease itself. It can be generalized affecting the entire body or localized to certain areas. The causes of oedema include problems with the veins, heart, liver, kidneys, lymphatics, hormones, nutrition, and inflammation which increase hydrostatic pressure, decrease plasma oncotic pressure, obstruct lymphatic drainage, or cause sodium and water retention leading to excess fluid build up.
The document discusses shock, including its definition, types, pathophysiology, and stages. Shock is defined as a state of low tissue perfusion that is inadequate for normal cellular respiration, leading to hypotension and cellular hypoxia if left uncompensated. The types of shock discussed include hypovolaemic, cardiogenic, obstructive, distributive (septic, anaphylactic, neurogenic), and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. Shock is divided into three stages: non-progressive/compensated, progressive decompensated, and decompensated/irreversible shock. Compensatory mechanisms in the initial
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.
Reversible cell injury occurs when cells are exposed to a brief period of ischemia or hypoxia. This causes 1) decreased ATP generation, 2) intracellular lactic acidosis and nuclear clumping, 3) damage to plasma membrane pumps causing sodium accumulation and calcium influx, and 4) reduced protein synthesis. If the stressor is removed quickly, the cell injury may be reversible and the cell can return to normal functioning.
Cellular injury occurs when stress exceeds a cell's ability to adapt and can be caused by factors like oxygen deprivation, toxins, infections, or genetic mutations. The main mechanisms of cellular injury include ATP depletion, mitochondrial damage, loss of calcium homeostasis, accumulation of reactive oxygen species, defects in membrane permeability, and damage to DNA and proteins. Without adequate response to injury, irreversible damage occurs through mechanisms like lipid peroxidation, DNA fragmentation, and protein cross-linking, ultimately leading to cell necrosis.
This document discusses infarction, which is localized ischemic necrosis of tissue due to decreased blood supply. Infarction can be caused by thrombi, emboli, vasospasm, expansion of atheroma, extrinsic compression of vessels, vessel twisting, or traumatic vessel rupture. There are three main types of infarction: red (hemorrhagic), white (anemic), and septic. Factors that influence infarction development include vulnerability to hypoxia, blood oxygen content, rate of occlusion, and blood supply. Myocardial, pulmonary, and cerebral infarctions are provided as examples and their characteristics and outcomes described.
Hemodynamic disorders affect the heart and blood vessels and include conditions like edema, hyperemia, congestion, hemorrhage and thrombosis. Thrombosis involves blood clot formation within intact vessels and can develop due to endothelial injury, alterations in normal blood flow like stasis and turbulence, and hypercoagulability of the blood, as described by Virchow's triad. Endothelial injury, turbulence and stasis promote activation and dysfunction of endothelial cells, while hypercoagulability refers to genetic or acquired alterations that increase coagulation and the risk of clots.
shock is a Life threatening clinical syndrome of cardio-vascular collapse characterized by Hypotension and Hypoperfusion. If uncompensated, these mechanisms may lead to impaired cellular metabolism and death.
The document discusses the pathophysiology of shock. It defines shock and describes the types and stages of shock. The types of shock include hypovolemic, septic, cardiogenic, neurogenic, and anaphylactic shock. The stages are initial compensated shock, progressive decompensated shock, and decompensated irreversible shock. The mechanisms of shock involve reduced circulating volume and tissue anoxia. Management involves treating the underlying cause, restoring perfusion and oxygen delivery, and supportive care.
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.
1) Chronic inflammation is inflammation of prolonged duration that can occur following acute inflammation or persistently as active inflammation, often resulting in tissue destruction and repair processes.
2) Causes of chronic inflammation include persistent infections, prolonged exposure to toxic agents, and autoimmunity.
3) Morphological features of chronic inflammation are characterized by infiltration of mononuclear cells like macrophages and lymphocytes, tissue destruction by these inflammatory cells, and attempts at repair through fibrosis and new blood vessel formation.
1. Hyperemia and congestion refer to localized increases in blood volume within dilated vessels and are associated with edema.
2. Edema occurs when hydrostatic pressure is increased or oncotic pressure is decreased, overwhelming the lymphatic system and causing fluid accumulation in tissues.
3. Common causes of edema include increased venous pressure from heart failure, decreased plasma proteins, lymphatic obstruction, sodium retention, and inflammation.
This document discusses heart failure, including its definition, causes, types, and compensatory mechanisms. Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by intrinsic pump failure, an increased workload on the heart, or impaired filling of the cardiac chambers. The types of heart failure include acute or chronic, right-sided or left-sided, and forward or backward failure. When the heart begins to fail, compensatory mechanisms such as cardiac hypertrophy, dilation, and increased heart rate attempt to maintain adequate blood circulation.
The document discusses various types of embolism and thrombosis. It describes the Virschow triad of factors that can lead to thrombosis - endothelial injury, changes in blood flow, and hypercoagulability. It then examines different causes and outcomes of thrombosis and embolism in various parts of the body, such as pulmonary embolism from deep vein thrombosis, systemic embolism from cardiac sources, and amniotic fluid embolism during childbirth.
CONTENTS:
GENERAL
NORMAL FLUID CIRCULATION
EDEMA- INTRODUCTION
CAUSES
CLASSIFICATION
MAJOR TYPES
NOTE- Fonts may appear weird because the original fonts are different from the ones visible here.
This document defines and describes different types of embolism. The most common type is thromboembolism, which occurs when a thrombus or part of a thrombus breaks off and is carried by the bloodstream. Pulmonary thromboembolism is a significant type that occurs when thrombi travel to the lungs and obstruct the pulmonary arteries. Other types include fat, air, gas and paradoxical embolisms. Air embolism can be venous, entering systemic veins during surgery or trauma, or arterial, entering the lungs during procedures like angiography. Decompression sickness is a form of gas embolism that affects divers or those exposed to changes in atmospheric pressure.
This document provides information on the pathophysiology of shock. It defines shock and describes the main types: primary/initial shock, secondary/true shock. It then discusses the mechanisms and stages of shock, including compensated/non-progressive shock, decompensated progressive shock, and decompensated/irreversible shock. The management of different types of shock such as hypovolaemic shock and septic shock is also summarized.
Cell injury can be reversible or irreversible. Reversible injury is caused by decreased ATP and acidosis within cells. Irreversible injury occurs when mitochondrial and cell membrane dysfunction cannot be reversed, leading to calcium influx, membrane damage, and cell death. Free radicals generated during ischemia-reperfusion can also cause irreversible injury through lipid peroxidation, protein and DNA oxidation, and cytoskeletal damage. Stress proteins help cells cope with injury by moving molecules within the cell.
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injuryGovernment Medical College
Irreversible cell injury can occur through necrosis or apoptosis. Necrosis is unprogrammed cell death due to intracellular protein denaturation and lysosomal enzyme digestion, resulting in cell membrane rupture and content leakage. Apoptosis is genetically programmed cell death where cells activate enzymes to degrade their own DNA and proteins. Key differences are that apoptotic cells shrink while necrotic cells swell, and apoptotic cells remain intact while necrotic cells lyse. Free radicals can also cause cell injury by attacking cell components and structures like membranes, proteins, and DNA, resulting in lipid peroxidation, protein damage, and DNA lesions.
This document defines and classifies shock, discussing its pathogenesis and clinical features. It describes shock as a life-threatening condition characterized by reduced circulating blood volume and tissue perfusion. The document classifies shock into four main types - hypovolemic, cardiogenic, septic, and anaphylactic - and discusses their specific causes and pathophysiology. It also outlines the potential morbidities of shock including acute lung injury, kidney failure, liver dysfunction, and multi-organ failure.
It consists of basic detail about hemorrhage and shock.
In hemorrhage, there is classification of hemorrhage on various basis, it's sign and symptoms and treatment modalities.
The treatment consist of methods to control bleeding and substitutes use for restoration of blood.
It also explain the hemorrhagic shock.
Shock consist of its pathophysiology, classification and description of types of shock.
Each type consist of its general feature, pathogenesis and treatment.
Oedema, also called hydrops, results from an accumulation of excess fluid in the interstitial spaces or body cavities due to diseases rather than being a disease itself. It can be generalized affecting the entire body or localized to certain areas. The causes of oedema include problems with the veins, heart, liver, kidneys, lymphatics, hormones, nutrition, and inflammation which increase hydrostatic pressure, decrease plasma oncotic pressure, obstruct lymphatic drainage, or cause sodium and water retention leading to excess fluid build up.
The document discusses shock, including its definition, types, pathophysiology, and stages. Shock is defined as a state of low tissue perfusion that is inadequate for normal cellular respiration, leading to hypotension and cellular hypoxia if left uncompensated. The types of shock discussed include hypovolaemic, cardiogenic, obstructive, distributive (septic, anaphylactic, neurogenic), and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. Shock is divided into three stages: non-progressive/compensated, progressive decompensated, and decompensated/irreversible shock. Compensatory mechanisms in the initial
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.
Reversible cell injury occurs when cells are exposed to a brief period of ischemia or hypoxia. This causes 1) decreased ATP generation, 2) intracellular lactic acidosis and nuclear clumping, 3) damage to plasma membrane pumps causing sodium accumulation and calcium influx, and 4) reduced protein synthesis. If the stressor is removed quickly, the cell injury may be reversible and the cell can return to normal functioning.
Cellular injury occurs when stress exceeds a cell's ability to adapt and can be caused by factors like oxygen deprivation, toxins, infections, or genetic mutations. The main mechanisms of cellular injury include ATP depletion, mitochondrial damage, loss of calcium homeostasis, accumulation of reactive oxygen species, defects in membrane permeability, and damage to DNA and proteins. Without adequate response to injury, irreversible damage occurs through mechanisms like lipid peroxidation, DNA fragmentation, and protein cross-linking, ultimately leading to cell necrosis.
This document discusses infarction, which is localized ischemic necrosis of tissue due to decreased blood supply. Infarction can be caused by thrombi, emboli, vasospasm, expansion of atheroma, extrinsic compression of vessels, vessel twisting, or traumatic vessel rupture. There are three main types of infarction: red (hemorrhagic), white (anemic), and septic. Factors that influence infarction development include vulnerability to hypoxia, blood oxygen content, rate of occlusion, and blood supply. Myocardial, pulmonary, and cerebral infarctions are provided as examples and their characteristics and outcomes described.
Hemodynamic disorders affect the heart and blood vessels and include conditions like edema, hyperemia, congestion, hemorrhage and thrombosis. Thrombosis involves blood clot formation within intact vessels and can develop due to endothelial injury, alterations in normal blood flow like stasis and turbulence, and hypercoagulability of the blood, as described by Virchow's triad. Endothelial injury, turbulence and stasis promote activation and dysfunction of endothelial cells, while hypercoagulability refers to genetic or acquired alterations that increase coagulation and the risk of clots.
shock is a Life threatening clinical syndrome of cardio-vascular collapse characterized by Hypotension and Hypoperfusion. If uncompensated, these mechanisms may lead to impaired cellular metabolism and death.
The document discusses the pathophysiology of shock. It defines shock and describes the types and stages of shock. The types of shock include hypovolemic, septic, cardiogenic, neurogenic, and anaphylactic shock. The stages are initial compensated shock, progressive decompensated shock, and decompensated irreversible shock. The mechanisms of shock involve reduced circulating volume and tissue anoxia. Management involves treating the underlying cause, restoring perfusion and oxygen delivery, and supportive care.
Shock is defined as failure to meet the metabolic demands of tissues due to decreased systemic tissue perfusion. There are several stages and types of shock. The pathophysiology involves cellular hypoxia leading to metabolic acidosis, endothelial injury, and organ dysfunction. Management involves addressing airway, breathing, circulation, and the underlying cause of shock. Fluid resuscitation is initially used but vasopressors may be needed. Complications can include acute renal failure, acute respiratory distress syndrome, and multi-organ failure if shock is not promptly recognized and treated.
Shock and its management is summarized as follows:
1. Shock is a life-threatening condition characterized by inadequate tissue perfusion due to reduced circulating blood volume or cardiac output.
2. Shock is classified as hypovolemic, cardiogenic, septic, traumatic, neurogenic, or hypoadrenal based on etiology.
3. The pathophysiology involves reduced circulating volume, impaired tissue oxygenation, and release of inflammatory mediators, progressing from compensated to decompensated to irreversible stages if left untreated.
Shock is a life-threatening condition caused by insufficient blood flow to organs and tissues. There are three main types of shock: hypovolemic (due to blood or fluid loss), cardiogenic (due to heart failure), and septic (due to infection). Shock progresses through compensated, decompensated, and irreversible stages as mechanisms fail to maintain blood flow. Untreated, shock can lead to organ damage and failure as tissues become hypoxic. Rapid diagnosis and treatment are needed to prevent irreversible consequences.
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shock is the state of insufficient blood flow to the tissues of the body .it contains introduction, definition, stages of shock, types of shock, diagnostic evaluation, prognosis ,prevention, care for each stage.
1. Shock is defined as a state where the delivery of oxygen to tissues is inadequate to meet metabolic demands, resulting in cellular dysfunction.
2. Shock is classified into five main types: hypovolemic, cardiogenic, obstructive, distributive, and endocrine.
3. Treatment for shock involves rapid fluid resuscitation to restore circulating volume, with vasopressors or inotropes as needed depending on the type of shock. Ongoing monitoring of vital signs and urine output is also critical.
This document provides an overview of shock, including its pathophysiology, classification, and treatment. It defines shock as inadequate tissue perfusion for normal cellular respiration. The pathophysiology involves cellular, microvascular, and systemic effects that lead to tissue hypoxia and organ dysfunction. Shock is classified as hypovolemic, cardiogenic, obstructive, distributive, or endocrine. Resuscitation involves fluid resuscitation, vasopressors or inotropes as needed, and monitoring of vital signs and urine output. The goal is to restore adequate perfusion while identifying and treating the underlying cause of shock.
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Subject: Medical Surgical Nursing / Adult Health Nursing
Title: Shock
Prepared by: Misfa Khatun, Nursing tutor
Content:
- Introduction
- Definition of Shock
- Classify Shock
- Stages of Shock
- Enumerate the Causes of shock
- Pathophysiology of Shock
- Identify the Signs and symptoms of Shock
- First ais management of Shock
- Treatment of Shock
- Management of Shock
- Nursing management of Shock
Circulatory shock refers to inadequate blood flow throughout the body and is a life-threatening condition. The main manifestations are low blood pressure, weak pulse, pale and cold skin, increased respiratory rate, and reduced urinary output. There are different types of circulatory shock including hypovolemic, cardiogenic, vasogenic, and obstructive shock. Treatment focuses on restoring blood volume through blood or plasma transfusions, administering plasma substitutes, and using drugs to increase blood pressure.
Circulatory shock refers to inadequate blood flow throughout the body and is a life-threatening condition. The main causes are decreased blood volume, increased vascular capacity, cardiac disease, or obstruction of blood flow. Common manifestations include low blood pressure, pale and cold skin, fast breathing, and fainting. Treatment focuses on restoring blood volume through transfusions, medications to constrict blood vessels, oxygen therapy, and posture changes.
This document summarizes the key aspects of shock. Shock occurs when there is inadequate oxygen delivery to tissues, which can lead to cellular damage and death if left untreated. The main causes of shock discussed are hypovolaemic, septic, and cardiogenic shock. Signs and symptoms of shock include low blood pressure, fast heart rate, pale skin, confusion, and low urine output. Management involves identifying the type and stage of shock to guide fluid resuscitation and drug therapy aimed at restoring adequate circulation and oxygen delivery to tissues.
The document discusses the different types of shock: hypovolemic, cardiogenic, circulatory (septic, neurogenic, anaphylactic), and endocrine shock. It provides details on the causes, pathophysiology, clinical manifestations, medical management, and nursing management of each type of shock. The primary types covered are hypovolemic, cardiogenic, septic, neurogenic, and anaphylactic shock.
This document discusses shock, including its pathophysiology, classification, clinical features, consequences, and resuscitation. Shock is defined as inadequate tissue perfusion resulting in cellular changes from aerobic to anaerobic metabolism. The main types of shock are hypovolemic, cardiogenic, obstructive, distributive, and endocrine. Left untreated, shock can lead to multiple organ failure and death. Initial resuscitation focuses on airway, breathing, and restoring circulating volume through fluid administration. Ongoing monitoring and support of vital organs is needed until the underlying cause is addressed.
Shock is a state of low tissue perfusion that prevents normal cellular respiration. There are several classifications of shock including hypovolaemic, cardiogenic, obstructive, distributive, and endocrine shock. The key goals of resuscitation are to ensure adequate oxygenation, ventilation, and cardiovascular support through fluid administration and vasopressors if needed. Ongoing monitoring of vital signs, urine output, and markers of tissue perfusion like lactate levels are important to guide resuscitation efforts and avoid complications like multiple organ failure.
This document discusses various types of shock, their clinical features, management, and monitoring. It defines shock as a state of poor perfusion and tissue hypoxia. The main types discussed are hypovolemic, cardiogenic, obstructive, distributive (septic), and anaphylactic shock. For hypovolemic shock, the document covers clinical features, fluid resuscitation, vasopressors, and monitoring including central venous pressure and pulmonary capillary wedge pressure. Septic shock management includes antibiotics, source control, vasopressors, and steroids. The document provides details on assessing, investigating, and closely monitoring patients in shock.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
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.
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
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In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
How to Add Chatter in the odoo 17 ERP ModuleCeline George
In Odoo, the chatter is like a chat tool that helps you work together on records. You can leave notes and track things, making it easier to talk with your team and partners. Inside chatter, all communication history, activity, and changes will be displayed.
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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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.
3. Definition
• An acute reduction of effective circulating
blood volume -hypotension
• An indequet perfusion of cells and tissues-
hyperfustion
Shock is a life- threating clinical
syndrome of cardiovascular collapse
characterised by
4. Two type of
shock
1.True or ( secondary) shock
• is a circulatory imbalance between oxygen supply
and oxygen requirements at the cellular level and
is also called as circulatory shock.
2. Intial or ( primary ) shock
• Is used for transient and usually a benign
vasovagal attack resulting from reduction of
venous retrun to the heart
5. Etiology
1.Hypovolemic shock
• This form of shock result form inadequate
circulatory blood volume by various etiologic factors
that may be either from the loss of whole blood ( i.e
red cell mass and plasma ) from haemorrhage or
from the loss of plasma volume alone
• The major effect in this are due to decreased cardiac
output and low intracardiac pressut
6. • The severity feature depends upon of blood
volume Los
• Type
1.Compensated : < 1000ml
2.Mild : 1000 – 1500ml
3.Moderate : 1500- 2000ml
4.Severe : > 2000 ml
• Major clinical feature are
1. Tachycardia- increased heart rate
2.Hypotension- low blood pressure
3.Oliguria to anuria – low urinary output
4.Aginated to confused to lethargic alternation in
mental state .
7. 2. Cardiogenic
shock
Result form
• . Severe left ventricular dysfunction_ cause
myocardial infarction from
• Leads to decrease tissue perfusion and movement
of fluid form pulmonary vascular bed into
pulmonary interstitial fluid leading to interstitial
pulmonary odema and later alvelar pulmonary
oedema
8. 3 Septic shock
• Septic shock result from bacteria or fungal
infection
• Microbes gain entry into the body from various
route most often via respiratory tract infection
May be a result oF 1. gram negative
septicaemia _ endotoxic shock
2. Gram positive septicaemia _ exotic shoch
9. Pathogenes
is
1.Reduced effective circulatory blood volume due
to
• Acute loss of blood as in _ hypovolemic shock
• Decreased cardiac output without actual loss of
blood as in _ cardiogenic and septic shock
• Leads to venous return to the heart leading
decreased cardiac output .
2. Reduced oxygen supply cause anoxia leading
cell injury leads to activation of body defence
mecanism
10. Stages
Shock is divided Into 3 types
1.Compensated shock ( non – progressive intial
reversible )
-In the early stages of shock an attempt is made to
maintain adequate cerebral and coronary blood
supply by redistribution of blood so that the vital
organ are adequately perfused and oxygenated
-This is achievd by activation of various
neurohormanal mechanism causing widespread
vosoconstriction and by fluid conservation by the
11. 1 ) widespread vosoconstriction
2) F)luid conservation by the kidney
3) Stimulation of adrenal medulla.
2. Progressive decompensated shock
_ This is a stage when patient suffer from
some other stress or risk factors besides
persistence of the shock condition that
cause progressive determiration
_ the effect of resultant tissue hyperfustion in
progressive decompensated shock are as
under
1)Pulmonary hypoperfustion
12. 3 Irreversible decompensated shock
_ when the shock is so severe that is inspite of
compensated mechanism and etiologic agent
which caused the shock no recovery takes place ,
it is called decompensated or Irreversible shock
_ it’s effect
1)Progressive vosodilation
2)Increased vascular permeability
3)Myocardial depressant factor ( MDF)
4)Worsening pulmonary hypoperfustion
5)Anoxic damage to heart , kideny , and brain
6)Hypercoagulability of blood
13. Clinical
features
The clinical features of decompensated
shock are characterised by depression of
four vital factors
1)Very low blood pressure
2)2) subnormal temperature
3) Feeble and irregular pulse
4)Shallow and sighing respiration cold and
clammy skin
14. _
_ shock may lead to
1. Acute respiratory distress
syndrome ( ARDS)
2.Disseminated intravascular
coagulation (DIC)
3.Acute renal failure (ARF)
4.Multiple oragan dysfunction
syndrome (MODS)