1) Arterial blood pressure is regulated by the balance of cardiac output and peripheral resistance, with regulatory systems including baroreceptors and the renin-angiotensin system maintaining homeostasis.
2) Primary hypertension has an unknown cause but may involve defects in regulatory mechanisms or membrane ion pumps, while secondary hypertension can result from renal, endocrine, neurogenic, drug or other causes that increase blood volume or activate vasoconstriction.
3) Uncontrolled hypertension can lead to organ damage over time through mechanisms such as left ventricular hypertrophy, atherosclerosis, stroke and renal failure.
This document discusses drugs affecting the renin-angiotensin system and cardiac electrophysiology. It begins by providing an overview of the renin-angiotensin system (RAS), including that renin cleaves angiotensinogen to form angiotensin I which is converted to angiotensin II by ACE. Angiotensin II causes vasoconstriction, sodium retention, and increased blood pressure. The document then focuses on ACE inhibitors, describing their mechanism of blocking angiotensin II formation, uses in hypertension and heart conditions, and examples such as captopril, enalapril, and lisinopril.
This document discusses various aspects of hypertension and its treatment. It begins by defining hypertension as a blood pressure higher than 140/90 mmHg. It then explains factors that determine blood pressure like cardiac output and peripheral resistance. It discusses the renin-angiotensin system and how beta blockers, ACE inhibitors, calcium channel blockers, and diuretics are used to treat hypertension by various mechanisms like reducing cardiac output or blocking angiotensin II formation. Common side effects and considerations for different drug classes are also outlined.
This document discusses the pathophysiology of cardiovascular system arterial hypertension. It begins by outlining the relevance and prevalence of hypertension as a major health problem. It then describes the main mechanisms that regulate arterial pressure in the immediate, middle, and late term, including baroreceptor and chemoreceptor responses, the renin-angiotensin system, vasopressin secretion, and renal control of fluid volume. Secondary forms of hypertension are discussed which are caused by renal, endocrine, or neurogenic factors. Primary or essential hypertension is described as being caused by genetic and environmental risk factors that disrupt the balance of pressor and depressor influences on the cardiovascular system. Several theories of its pathogenesis are mentioned involving the brain, kid
Heart as a pump, heart failure & its treatmentChirantan MD
This document discusses cardiac physiology and heart failure. It begins by introducing the authors and location. It then discusses normal cardiac physiology parameters such as preload, afterload, heart rate, and ionotropic state. It explores these parameters in depth including how they are altered in heart failure. The document also examines factors that can lead to heart failure like cardiomyopathy or arrhythmias. In summary, it provides a comprehensive overview of cardiac function and the pathophysiology of heart failure.
Heart as a pump, heart failure & its treatmentChirantan MD
This document discusses cardiac physiology and heart failure. It begins by introducing the authors and location. It then discusses normal cardiac physiology parameters such as preload, afterload, heart rate, and ionotropic state. It explores these parameters in depth including how they are altered in heart failure. The document also examines factors that can lead to heart failure like cardiomyopathy or arrhythmias. In summary, it provides a comprehensive overview of cardiac function and the pathophysiology of heart failure.
Heart as a pump, heart failure & its treatmentChirantan MD
The document discusses normal cardiac physiology and heart failure. It describes how cardiac function depends on preload, afterload, heart rate, and ionotropic state. It then discusses the pathophysiology of systolic heart failure, including activation of neurohormonal systems and changes at the molecular level in contractile proteins and calcium homeostasis. Compensatory mechanisms in heart failure and the progression to decompensated heart failure are also summarized.
Short-term control of blood pressure is mediated by the nervous system and chemicals that regulate peripheral resistance within seconds or minutes. The baroreceptor reflex detects changes in blood pressure and regulates heart rate, stroke volume, and vascular tone to maintain pressure. Chemoreceptors sense oxygen and carbon dioxide levels and stimulate the vasomotor center. If blood flow to the brain decreases severely, the CNS ischemic response triggers powerful vasoconstriction to increase pressure.
This document provides an overview of the pathophysiology of heart failure. It discusses the essential functions of the heart in maintaining adequate blood supply and receiving returning blood from tissues. When the heart can no longer meet the metabolic demands of tissues, heart failure occurs. This can be due to disorders of preload, contractility, afterload, or the heart's electrical and mechanical functions. Compensatory mechanisms initially help but eventually maladapt. Neurohormonal changes further exacerbate heart failure over time. The document details causes and mechanisms of both systolic and diastolic heart failure.
This document discusses drugs affecting the renin-angiotensin system and cardiac electrophysiology. It begins by providing an overview of the renin-angiotensin system (RAS), including that renin cleaves angiotensinogen to form angiotensin I which is converted to angiotensin II by ACE. Angiotensin II causes vasoconstriction, sodium retention, and increased blood pressure. The document then focuses on ACE inhibitors, describing their mechanism of blocking angiotensin II formation, uses in hypertension and heart conditions, and examples such as captopril, enalapril, and lisinopril.
This document discusses various aspects of hypertension and its treatment. It begins by defining hypertension as a blood pressure higher than 140/90 mmHg. It then explains factors that determine blood pressure like cardiac output and peripheral resistance. It discusses the renin-angiotensin system and how beta blockers, ACE inhibitors, calcium channel blockers, and diuretics are used to treat hypertension by various mechanisms like reducing cardiac output or blocking angiotensin II formation. Common side effects and considerations for different drug classes are also outlined.
This document discusses the pathophysiology of cardiovascular system arterial hypertension. It begins by outlining the relevance and prevalence of hypertension as a major health problem. It then describes the main mechanisms that regulate arterial pressure in the immediate, middle, and late term, including baroreceptor and chemoreceptor responses, the renin-angiotensin system, vasopressin secretion, and renal control of fluid volume. Secondary forms of hypertension are discussed which are caused by renal, endocrine, or neurogenic factors. Primary or essential hypertension is described as being caused by genetic and environmental risk factors that disrupt the balance of pressor and depressor influences on the cardiovascular system. Several theories of its pathogenesis are mentioned involving the brain, kid
Heart as a pump, heart failure & its treatmentChirantan MD
This document discusses cardiac physiology and heart failure. It begins by introducing the authors and location. It then discusses normal cardiac physiology parameters such as preload, afterload, heart rate, and ionotropic state. It explores these parameters in depth including how they are altered in heart failure. The document also examines factors that can lead to heart failure like cardiomyopathy or arrhythmias. In summary, it provides a comprehensive overview of cardiac function and the pathophysiology of heart failure.
Heart as a pump, heart failure & its treatmentChirantan MD
This document discusses cardiac physiology and heart failure. It begins by introducing the authors and location. It then discusses normal cardiac physiology parameters such as preload, afterload, heart rate, and ionotropic state. It explores these parameters in depth including how they are altered in heart failure. The document also examines factors that can lead to heart failure like cardiomyopathy or arrhythmias. In summary, it provides a comprehensive overview of cardiac function and the pathophysiology of heart failure.
Heart as a pump, heart failure & its treatmentChirantan MD
The document discusses normal cardiac physiology and heart failure. It describes how cardiac function depends on preload, afterload, heart rate, and ionotropic state. It then discusses the pathophysiology of systolic heart failure, including activation of neurohormonal systems and changes at the molecular level in contractile proteins and calcium homeostasis. Compensatory mechanisms in heart failure and the progression to decompensated heart failure are also summarized.
Short-term control of blood pressure is mediated by the nervous system and chemicals that regulate peripheral resistance within seconds or minutes. The baroreceptor reflex detects changes in blood pressure and regulates heart rate, stroke volume, and vascular tone to maintain pressure. Chemoreceptors sense oxygen and carbon dioxide levels and stimulate the vasomotor center. If blood flow to the brain decreases severely, the CNS ischemic response triggers powerful vasoconstriction to increase pressure.
This document provides an overview of the pathophysiology of heart failure. It discusses the essential functions of the heart in maintaining adequate blood supply and receiving returning blood from tissues. When the heart can no longer meet the metabolic demands of tissues, heart failure occurs. This can be due to disorders of preload, contractility, afterload, or the heart's electrical and mechanical functions. Compensatory mechanisms initially help but eventually maladapt. Neurohormonal changes further exacerbate heart failure over time. The document details causes and mechanisms of both systolic and diastolic heart failure.
The PATH program is a multi-year U.S. initiative focused on global health that works in over 50 countries. It aims to save lives and ensure self-sufficiency by providing vaccines, preventative treatments, and training for healthcare workers. The goal is to cut deaths from HIV/AIDS, tuberculosis, and malaria in half by 2020.
The PATH program aims to help homeless individuals and families in Los Angeles County access stable housing and supportive services to achieve long-term stability. It provides short-term rental assistance and case management to quickly rehouse homeless people and connect them to resources to address challenges like lack of income, untreated mental illness or substance abuse issues. The goal is to transition participants into permanent housing within a few months through this intensive temporary support and help acquiring job skills or public benefits.
The PATH program aims to improve global health and development through partnerships that accelerate innovation. It brings together experts from government, academia, non-profit, and industry to address major health challenges. The goal is to develop affordable, accessible tools like vaccines, drugs, diagnostics and devices that can have the greatest impact on improving lives in developing countries.
This document discusses types of hypertension, treatment of hypertension, and antihypertensive drugs. It describes the two main types of hypertension as essential and secondary. Treatment is necessary to prevent damage to blood vessels and the heart from high blood pressure. Several classes of antihypertensive drugs are discussed in detail, including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. The mechanisms of action and important effects of specific drugs like captopril, enalapril, lisinopril, and losartan are summarized as well.
Hypertension is defined as persistently elevated blood pressure. It can be primary (essential) hypertension which accounts for 95% of cases and has no known cause, or secondary hypertension which is caused by other diseases or drugs. Primary hypertension risk factors include sedentary lifestyle, obesity, salt sensitivity, smoking, alcohol, and family history. The renin-angiotensin-aldosterone system plays a key role in regulating blood pressure through mechanisms like vasoconstriction and sodium retention. Autonomic nervous system imbalances and defects in local vascular regulation and endothelial function can also contribute to the development of hypertension.
This document discusses hypertension and its treatment. It defines hypertension and describes the types as essential or secondary. It explains how factors like stress, sodium intake, obesity, and smoking can cause environmental hypertension. The document outlines the need for treatment to prevent damage to blood vessels and organs. It then details various classes of antihypertensive drugs like diuretics, ACE inhibitors, calcium channel blockers, and others. It focuses on the renin-angiotensin system and how ACE inhibitors work to inhibit angiotensin II production and lower blood pressure.
This document discusses hypertension (high blood pressure) and its causes and classifications. It defines hypertension as a sustained elevation of systemic arterial pressure and notes it can be caused by increased cardiac output or peripheral resistance. The document then classifies blood pressure levels and states 90-95% of hypertension has unknown origin but is linked to excess weight, sedentary lifestyle, and heredity. It proceeds to describe various types and causes of hypertension including those related to obesity, kidney function, pregnancy, neurogenic factors, and experimental procedures. Overall it provides a comprehensive overview of hypertension definitions, mechanisms, classifications and etiologies.
This document discusses shock, which occurs when oxygen delivery does not meet tissue oxygen demand. It defines shock as a clinical condition commonly seen in practice but not well understood. The document outlines multiple factors that can cause imbalances in oxygen delivery, such as decreased cardiac output, increased oxygen demand from infection, and abnormal tissue perfusion. It also describes the body's compensatory mechanisms for shock at the acute, moderate, and chronic stages, including responses from the sympathetic nervous system, renin-angiotensin-aldosterone system, and antidiuretic hormone. Overall, the document provides an overview of shock by defining it, outlining causes of oxygen delivery-demand imbalances, and explaining the body's physiological responses.
Electrophysiology of Heart & Drugs Affecting Renin Angiotensin System Monika Bhardwaj
The document discusses cardiac electrophysiology and the renin-angiotensin system. It describes how cardiac myocytes in the sinoatrial and atrioventricular nodes can generate impulses, and how these impulses propagate through specialized conducting tissue. It also details the actions of angiotensin II, including its effects on vasoconstriction, sodium reabsorption, and aldosterone secretion. Common drugs for manipulating the renin-angiotensin system are also summarized, such as ACE inhibitors like lisinopril and angiotensin receptor blockers like losartan.
This document discusses renal failure and renal parenchymal disease. It defines acute renal failure as a rapid deterioration in renal function characterized by azotemia and a decline in GFR, which may or may not be accompanied by oliguria. Chronic renal failure is defined as kidney damage or decreased function for 3 or more months resulting in a GFR of less than 60 mL/min/1.17m2. The causes of acute and chronic renal failure are discussed under prerenal, intrarenal and postrenal categories. Imaging findings of various renal parenchymal diseases on ultrasound, CT and MRI are also summarized. Morphological criteria to categorize different renal abnormalities based on ultrasound findings are provided.
The adrenal glands consist of an outer cortex and inner medulla. The cortex produces mineralocorticoids like aldosterone and glucocorticoids like cortisol. Cortisol regulates metabolism and immune function. Aldosterone regulates sodium and potassium levels. Their release is controlled by the HPA axis and renin-angiotensin system. The medulla produces catecholamines like epinephrine and norepinephrine which increase heart rate and blood pressure through adrenergic receptors. Together these hormones help regulate vital processes and the stress response.
This document discusses hypertension and its treatment. It begins by defining hypertension and describing the types. It then discusses the normal blood pressure regulation system and how this is disrupted in hypertension. The remainder of the document focuses on the treatment of hypertension, describing various classes of antihypertensive drugs including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. It provides details on specific drugs in each class, their mechanisms of action, uses, and side effects.
This document discusses hypertension and its treatment. It defines hypertension as a blood pressure higher than 140/90 mmHg. It describes the types of hypertension and risk factors like stress, sodium intake, obesity, and smoking. Treatment is important to prevent damage to blood vessels and organs. Antihypertensive drugs lower blood pressure by interfering with normal blood pressure regulating mechanisms like the renin-angiotensin system and sympathetic nervous system. Common antihypertensive classes discussed include diuretics, ACE inhibitors, calcium channel blockers, and beta blockers.
Hypertension, or high blood pressure, is a disorder where blood pressure is consistently above 140/90 mmHg. It can be caused by unknown factors (essential hypertension) or other diseases (secondary hypertension). Untreated hypertension can damage blood vessels and organs over time.
The document discusses various types of medications used to treat hypertension, including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and alpha blockers. It provides details on specific drugs, their mechanisms of action, effects, uses, and potential side effects in the treatment of hypertension.
Hypertension results from an interplay of peripheral, neuronal, and humoral mechanisms. The renin-angiotensin-aldosterone system (RAAS) plays a key role in regulating blood pressure via sodium and fluid balance. Angiotensin II causes vasoconstriction and sodium retention, increasing blood volume and pressure. Baroreceptor reflexes and local autoregulation work to maintain tissue oxygenation when pressure increases. Endothelial dysfunction and imbalances in vasoactive substances like nitric oxide can also contribute to hypertension.
Hypertension results from an interplay of peripheral, neuronal, and humoral mechanisms. The renin-angiotensin-aldosterone system (RAAS) plays a key role in regulating blood pressure via sodium and fluid balance. Angiotensin II causes vasoconstriction and sodium retention, increasing blood volume and pressure. Baroreceptor reflexes and local autoregulation work to maintain tissue oxygenation when pressure increases. Endothelial dysfunction and imbalances in vasoactive substances like nitric oxide can also contribute to hypertension.
The document discusses the renin-angiotensin system (RAS) and drugs that affect it. RAS regulates blood pressure and electrolyte balance through the actions of angiotensin II, which is produced from renin and angiotensin converting enzyme. Angiotensin II causes vasoconstriction, sodium retention, and other effects. Drugs like ACE inhibitors and angiotensin receptor blockers inhibit parts of the RAS pathway to lower blood pressure. Captopril is an ACE inhibitor that blocks the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and sodium retention.
This document summarizes the pathophysiology of heart failure (HF). It discusses how HF results from abnormalities in cardiac structure/function that limit oxygen delivery to tissues, despite normal filling pressures. The progression of HF is driven by neurohumoral activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, which initially help compensate but eventually exacerbate cardiac remodeling and dysfunction. The document outlines the effects of various neurohormones involved in HF, including their normal and maladaptive roles in the progression of disease. Management of HF focuses on interrupting the harmful effects of long-term neurohumoral activation.
Crush syndrome is caused by prolonged pressure on muscle tissue, leading to rhabdomyolysis. This releases myoglobin and other intracellular contents into the bloodstream, which can cause kidney damage, metabolic abnormalities, and complications affecting other organs. Treatment involves aggressive fluid resuscitation, dialysis if needed to manage kidney dysfunction, and surgery such as fasciotomy to release pressure in compartments. Early medical management is important to prevent further complications from crush syndrome.
This document discusses the class Cestoidea and two tapeworm species, Taenia saginata and Taenia solium. It provides details on the general characteristics, life cycles, transmission, and pathogenic significance of T. saginata and T. solium. It also covers the clinical manifestation and diagnosis of teniasis and cysticercosis, as well as prevention methods. Students are assigned tasks to examine slides of the proglottides and draw the key features of T. saginata and T. solium under magnification.
The PATH program is a multi-year U.S. initiative focused on global health that works in over 50 countries. It aims to save lives and ensure self-sufficiency by providing vaccines, preventative treatments, and training for healthcare workers. The goal is to cut deaths from HIV/AIDS, tuberculosis, and malaria in half by 2020.
The PATH program aims to help homeless individuals and families in Los Angeles County access stable housing and supportive services to achieve long-term stability. It provides short-term rental assistance and case management to quickly rehouse homeless people and connect them to resources to address challenges like lack of income, untreated mental illness or substance abuse issues. The goal is to transition participants into permanent housing within a few months through this intensive temporary support and help acquiring job skills or public benefits.
The PATH program aims to improve global health and development through partnerships that accelerate innovation. It brings together experts from government, academia, non-profit, and industry to address major health challenges. The goal is to develop affordable, accessible tools like vaccines, drugs, diagnostics and devices that can have the greatest impact on improving lives in developing countries.
This document discusses types of hypertension, treatment of hypertension, and antihypertensive drugs. It describes the two main types of hypertension as essential and secondary. Treatment is necessary to prevent damage to blood vessels and the heart from high blood pressure. Several classes of antihypertensive drugs are discussed in detail, including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. The mechanisms of action and important effects of specific drugs like captopril, enalapril, lisinopril, and losartan are summarized as well.
Hypertension is defined as persistently elevated blood pressure. It can be primary (essential) hypertension which accounts for 95% of cases and has no known cause, or secondary hypertension which is caused by other diseases or drugs. Primary hypertension risk factors include sedentary lifestyle, obesity, salt sensitivity, smoking, alcohol, and family history. The renin-angiotensin-aldosterone system plays a key role in regulating blood pressure through mechanisms like vasoconstriction and sodium retention. Autonomic nervous system imbalances and defects in local vascular regulation and endothelial function can also contribute to the development of hypertension.
This document discusses hypertension and its treatment. It defines hypertension and describes the types as essential or secondary. It explains how factors like stress, sodium intake, obesity, and smoking can cause environmental hypertension. The document outlines the need for treatment to prevent damage to blood vessels and organs. It then details various classes of antihypertensive drugs like diuretics, ACE inhibitors, calcium channel blockers, and others. It focuses on the renin-angiotensin system and how ACE inhibitors work to inhibit angiotensin II production and lower blood pressure.
This document discusses hypertension (high blood pressure) and its causes and classifications. It defines hypertension as a sustained elevation of systemic arterial pressure and notes it can be caused by increased cardiac output or peripheral resistance. The document then classifies blood pressure levels and states 90-95% of hypertension has unknown origin but is linked to excess weight, sedentary lifestyle, and heredity. It proceeds to describe various types and causes of hypertension including those related to obesity, kidney function, pregnancy, neurogenic factors, and experimental procedures. Overall it provides a comprehensive overview of hypertension definitions, mechanisms, classifications and etiologies.
This document discusses shock, which occurs when oxygen delivery does not meet tissue oxygen demand. It defines shock as a clinical condition commonly seen in practice but not well understood. The document outlines multiple factors that can cause imbalances in oxygen delivery, such as decreased cardiac output, increased oxygen demand from infection, and abnormal tissue perfusion. It also describes the body's compensatory mechanisms for shock at the acute, moderate, and chronic stages, including responses from the sympathetic nervous system, renin-angiotensin-aldosterone system, and antidiuretic hormone. Overall, the document provides an overview of shock by defining it, outlining causes of oxygen delivery-demand imbalances, and explaining the body's physiological responses.
Electrophysiology of Heart & Drugs Affecting Renin Angiotensin System Monika Bhardwaj
The document discusses cardiac electrophysiology and the renin-angiotensin system. It describes how cardiac myocytes in the sinoatrial and atrioventricular nodes can generate impulses, and how these impulses propagate through specialized conducting tissue. It also details the actions of angiotensin II, including its effects on vasoconstriction, sodium reabsorption, and aldosterone secretion. Common drugs for manipulating the renin-angiotensin system are also summarized, such as ACE inhibitors like lisinopril and angiotensin receptor blockers like losartan.
This document discusses renal failure and renal parenchymal disease. It defines acute renal failure as a rapid deterioration in renal function characterized by azotemia and a decline in GFR, which may or may not be accompanied by oliguria. Chronic renal failure is defined as kidney damage or decreased function for 3 or more months resulting in a GFR of less than 60 mL/min/1.17m2. The causes of acute and chronic renal failure are discussed under prerenal, intrarenal and postrenal categories. Imaging findings of various renal parenchymal diseases on ultrasound, CT and MRI are also summarized. Morphological criteria to categorize different renal abnormalities based on ultrasound findings are provided.
The adrenal glands consist of an outer cortex and inner medulla. The cortex produces mineralocorticoids like aldosterone and glucocorticoids like cortisol. Cortisol regulates metabolism and immune function. Aldosterone regulates sodium and potassium levels. Their release is controlled by the HPA axis and renin-angiotensin system. The medulla produces catecholamines like epinephrine and norepinephrine which increase heart rate and blood pressure through adrenergic receptors. Together these hormones help regulate vital processes and the stress response.
This document discusses hypertension and its treatment. It begins by defining hypertension and describing the types. It then discusses the normal blood pressure regulation system and how this is disrupted in hypertension. The remainder of the document focuses on the treatment of hypertension, describing various classes of antihypertensive drugs including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. It provides details on specific drugs in each class, their mechanisms of action, uses, and side effects.
This document discusses hypertension and its treatment. It defines hypertension as a blood pressure higher than 140/90 mmHg. It describes the types of hypertension and risk factors like stress, sodium intake, obesity, and smoking. Treatment is important to prevent damage to blood vessels and organs. Antihypertensive drugs lower blood pressure by interfering with normal blood pressure regulating mechanisms like the renin-angiotensin system and sympathetic nervous system. Common antihypertensive classes discussed include diuretics, ACE inhibitors, calcium channel blockers, and beta blockers.
Hypertension, or high blood pressure, is a disorder where blood pressure is consistently above 140/90 mmHg. It can be caused by unknown factors (essential hypertension) or other diseases (secondary hypertension). Untreated hypertension can damage blood vessels and organs over time.
The document discusses various types of medications used to treat hypertension, including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and alpha blockers. It provides details on specific drugs, their mechanisms of action, effects, uses, and potential side effects in the treatment of hypertension.
Hypertension results from an interplay of peripheral, neuronal, and humoral mechanisms. The renin-angiotensin-aldosterone system (RAAS) plays a key role in regulating blood pressure via sodium and fluid balance. Angiotensin II causes vasoconstriction and sodium retention, increasing blood volume and pressure. Baroreceptor reflexes and local autoregulation work to maintain tissue oxygenation when pressure increases. Endothelial dysfunction and imbalances in vasoactive substances like nitric oxide can also contribute to hypertension.
Hypertension results from an interplay of peripheral, neuronal, and humoral mechanisms. The renin-angiotensin-aldosterone system (RAAS) plays a key role in regulating blood pressure via sodium and fluid balance. Angiotensin II causes vasoconstriction and sodium retention, increasing blood volume and pressure. Baroreceptor reflexes and local autoregulation work to maintain tissue oxygenation when pressure increases. Endothelial dysfunction and imbalances in vasoactive substances like nitric oxide can also contribute to hypertension.
The document discusses the renin-angiotensin system (RAS) and drugs that affect it. RAS regulates blood pressure and electrolyte balance through the actions of angiotensin II, which is produced from renin and angiotensin converting enzyme. Angiotensin II causes vasoconstriction, sodium retention, and other effects. Drugs like ACE inhibitors and angiotensin receptor blockers inhibit parts of the RAS pathway to lower blood pressure. Captopril is an ACE inhibitor that blocks the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and sodium retention.
This document summarizes the pathophysiology of heart failure (HF). It discusses how HF results from abnormalities in cardiac structure/function that limit oxygen delivery to tissues, despite normal filling pressures. The progression of HF is driven by neurohumoral activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, which initially help compensate but eventually exacerbate cardiac remodeling and dysfunction. The document outlines the effects of various neurohormones involved in HF, including their normal and maladaptive roles in the progression of disease. Management of HF focuses on interrupting the harmful effects of long-term neurohumoral activation.
Crush syndrome is caused by prolonged pressure on muscle tissue, leading to rhabdomyolysis. This releases myoglobin and other intracellular contents into the bloodstream, which can cause kidney damage, metabolic abnormalities, and complications affecting other organs. Treatment involves aggressive fluid resuscitation, dialysis if needed to manage kidney dysfunction, and surgery such as fasciotomy to release pressure in compartments. Early medical management is important to prevent further complications from crush syndrome.
This document discusses the class Cestoidea and two tapeworm species, Taenia saginata and Taenia solium. It provides details on the general characteristics, life cycles, transmission, and pathogenic significance of T. saginata and T. solium. It also covers the clinical manifestation and diagnosis of teniasis and cysticercosis, as well as prevention methods. Students are assigned tasks to examine slides of the proglottides and draw the key features of T. saginata and T. solium under magnification.
Design & functioning of an ultrasound therapy device.pptxSarvarshJanu
Ultrasound therapy uses high frequency sound waves to deliver thermal and non-thermal effects to tissues. It can be used to treat a variety of musculoskeletal conditions. The device generates frequencies between 1-3 MHz which determine treatment depth. Coupling methods like gel or immersion in water are required to transmit ultrasound to the body. Treatment parameters like duration, intensity and duty cycle are set based on the target tissue and therapeutic goals. Precautions must be taken when using ultrasound near the spine or growing bones. Proper maintenance ensures safe and effective use of these devices.
Biophysical action of Direct current on living tissues.pptxSarvarshJanu
Direct current (DC) therapy, also known as galvanization therapy, uses low voltage DC to treat tissues and reduce pain. DC is more likely than alternating current (AC) to cause muscle tetanus and "freeze" victims during electrical accidents. Galvanization therapy increases blood flow and promotes healing by improving tissue metabolism. It is applied using dry or moist electrodes in transverse, longitudinal, or dotted patterns. While it can treat conditions like pain and inflammation, galvanization therapy should not be used for acute issues, cancers, or in patients with poor heart health.
This document discusses four parasitic tapeworms - Diphyllobotrium latum, Hymenolepis nana, Echinococcus granulosus, and Alveococcus multilocularis - that can cause human disease. It provides control questions about the morphological peculiarities, distribution, life cycle, transmission, and pathogenic significance of each parasite. It also discusses laboratory diagnostics and prevention of the diseases caused by each parasite. Finally, it lists tasks for examining specimens of Diphyllobotrium latum and hydatid cysts of E.multilocularis under microscopes.
This document outlines the topics and assignments for a practical lesson on cell morphology and membrane transport. The topics covered include the Cell Theory, organelle structures and functions, cell membrane composition and transport. Homework assignments include drawing the ultrastructure of an eukaryotic cell, drawing a chemical model of the plasma membrane, and classification of organelles. Class work includes observing chloroplast movement in plant cells under a microscope and observing the effects of a hypertonic solution on onion skin cells through plasmolysis.
This document discusses allergy and hypersensitivity. It defines allergy as a disorder of the immune system where allergic reactions occur to normally harmless environmental substances known as allergens. Hypersensitivity reactions are excessive, undesirable reactions produced by the normal immune system that require a pre-sensitized immune state. There are four types of hypersensitivity reactions classified by Gell and Coombs based on the mechanisms involved and time taken for the reaction: type I is immediate hypersensitivity mediated by IgE and mast cells; type II involves IgG or IgM; type III involves IgG, complement and immune complexes; and type IV is delayed hypersensitivity mediated by cell-mediated immune memory responses.
The document outlines 7 levels of evidence for medical research, with level 1 being the highest and consisting of systematic reviews and meta-analyses of randomized controlled trials (RCTs) or evidence-based guidelines based on RCTs, and level 7 being the lowest level based on expert opinions. Different clinical questions are best answered by different types of studies, and the highest levels of evidence may not always be available, so researchers should work their way down to the next highest available level of evidence.
Inflammation is characterized by cardinal signs such as redness, swelling, heat, and pain. It involves a complex series of events including increased blood flow, vascular permeability, and migration of leukocytes. Mediators like histamine, cytokines, prostaglandins, and leukotrienes are released from cells to induce and propagate the inflammatory response through effects on blood vessels and immune cells. Acute inflammation resolves within days while chronic inflammation persists long-term and can cause tissue damage.
This document discusses psychoactive drugs, also known as psychotropic or psychopharmaceutical drugs. It provides definitions and describes how these drugs affect the central nervous system and alter perceptions, moods, and behaviors. The document also summarizes key points about the history of psychoactive drug use, common classes of psychotropic drugs, their medical and non-medical uses, methods of administration, effects on neurochemistry, risks of addiction, and regulations around legality.
- Nociception is the transmission of noxious stimuli to the CNS, while pain is a subjective experience. Pain receptors transmit signals that result in pain perception.
- There are different types of pain including acute vs chronic, nociceptive vs neuropathic, somatic vs visceral, and referred pain.
- NSAIDs work by blocking cyclooxygenase (COX) enzymes and subsequent prostaglandin synthesis. COX-1 inhibition results in side effects while COX-2 inhibition provides pain relief.
- Opioid analgesics work in the CNS by binding to opioid receptors like mu and kappa receptors to reduce pain signal transmission.
This document provides information on adrenergic transmission, receptors, and drugs. It discusses the endogenous catecholamines epinephrine, norepinephrine, and dopamine, including their synthesis, storage, release, metabolism, and effects. It describes the different types of adrenergic receptors and their subtypes. The document also examines various adrenergic drugs, including direct-acting drugs like epinephrine, norepinephrine, phenylephrine, and indirect-acting drugs like amphetamines. It discusses the therapeutic uses, pharmacokinetics, mechanisms of action, and side effects of many commonly used adrenergic drugs.
This document provides an overview of the nervous system and autonomic nervous system, with a focus on the cholinergic system. It describes the organization and functions of the sympathetic and parasympathetic nervous systems. It discusses cholinergic transmission in detail, including the different types of cholinoceptors (muscarinic and nicotinic), the mechanism of cholinergic transmission, and cholinergic drugs. It summarizes the pharmacological actions and uses of cholinergic agonists like acetylcholine and cholinesterase inhibitors.
This document discusses levels of organization in living organisms and microscopy techniques. It begins by outlining 7 control questions on the topic, including the levels of organization (molecular genetic, cellular, tissue, organ, organismic, population-species, biogeocenotic). It then provides instructions for making temporary specimens of onion skin cells under a microscope, including placing a liquid drop on a slide, positioning the sample using tweezers, and lowering a cover slip to avoid bubbles. The document aims to teach biological organization and basic microscopy methods.
Unlocking the Secrets to Safe Patient Handling.pdfLift Ability
Furthermore, the time constraints and workload in healthcare settings can make it challenging for caregivers to prioritise safe patient handling Australia practices, leading to shortcuts and increased risks.
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Let's Talk About It: Breast Cancer (What is Mindset and Does it Really Matter?)bkling
Your mindset is the way you make sense of the world around you. This lens influences the way you think, the way you feel, and how you might behave in certain situations. Let's talk about mindset myths that can get us into trouble and ways to cultivate a mindset to support your cancer survivorship in authentic ways. Let’s Talk About It!
Michigan HealthTech Market Map 2024. Includes 7 categories: Policy Makers, Academic Innovation Centers, Digital Health Providers, Healthcare Providers, Payers / Insurance, Device Companies, Life Science Companies, Innovation Accelerators. Developed by the Michigan-Israel Business Accelerator
Trauma Outpatient Center is a comprehensive facility dedicated to addressing mental health challenges and providing medication-assisted treatment. We offer a diverse range of services aimed at assisting individuals in overcoming addiction, mental health disorders, and related obstacles. Our team consists of seasoned professionals who are both experienced and compassionate, committed to delivering the highest standard of care to our clients. By utilizing evidence-based treatment methods, we strive to help our clients achieve their goals and lead healthier, more fulfilling lives.
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3. Regulation of arterial pressure (АP)
Formula: АP = CO · PR
CO – cardiac output
PR – peripheral resistance (depended to arterioles tone)
CO leads to PR and АP normalizes finally
PR leads to CO and АP normalizes finally
7. Depresors system
• Barroreceptors of aorta arch and
sinus caroticus
• PG A, E, I;
• Natriuretic peptide hormone
• Parasympathetic nervous system.
8. Regulative systems
1. Barroreceptors of aorta arch and sinus caroticus
Barroreceptors
of the vessels
Medulla oblongata
(vessel’s active center)
Afferent impulses
Heart (CO increase at
decreased АP)
Arterioles (spasm) Еfferent і impulses
9. Regulative systems
2. Renin–angiotensin system
АP
Activation of kidney
JGA (juxta glomerular
apparatus)
Excretion of the RENIN
(it is enzyme)
Conversation
angiotensin 1 into angiotensin 2
Conversation
angiotensinogen into
angiotensin 1
Angiotensin converting
enzyme (АCE)
10. Regulative systems
3. Renin–angiotensin-aldosteron system
Renin Actination of
suprarenal glangs
(cortical layer)
Na reabsorbtion
in kidney increase
Angiotensin 2
Aldosteron
excretion
Na concentration in
blood increase,
blood osmotic
pressure increase
Move of extravascular
fluid inside the
vessels
Increase of circulative
blood volume
(CBV)
CО increase
12. AP elevation
(value above 140/90 mm Hg), which
is resulted from rising of peripheral
vessels resistance
(one of the most common cardiovascular disorders)
Arterial hypertension (АH)
13. Classification of arterial hypertension
Category Systolic BP
(mm hg)
Diastolic BP
(mm hg)
Normal BP Below 130 Below 85
High-normal BP
(pre-hypertension)
130-139 85-89
Stage 1 (mild) hypertension 140-159 90-99
Stage 2 (moderate) hypertension 160-179 100-109
Stage 3 (severe) hypertension 180 or higher 110 or higher
15. Reason is unknown.
AH is polyetiological disease.
AH arises on the ground of genetically
peculiarities of metabolism.
That is possible to have genetically defect of the
systems, which control relaxation of the
smooth muscle cells of the arterioles.
Etiology (primary AH)
16. Contributing factors
Family history
Age-related changes in blood
pressure High salt intake
Stress
Hyperinsulinemia:
causes high activity sympathetic link of ANS and its
effect on cardiac output, peripheral vascular
resistance and renal sodium retention;
stimulates sodium and calcium transport across the
cell membrane of vascular smooth muscle,
thereby sensitizing blood vessels to vasopressor
stimuli
Obesity (because hyperinsulinemia)
Excess alcohol consumption
(mechanism in unclear)
17. Pathogenesis of primary (essential) hypertension
• Dysregulatory theory - violations of regulatory
mechanisms of arterial vessels tone.
There are two phases:
1. Hyperkinetic
1 stage: activation of the sympathetic and adrenal
system under the action of stress factors
2 stage: activation of the rennin-angiotensin-
aldosteron system
3 stage: activation of aldosteron and vasopressin
systems
18. Pathogenesis of primary (essential)
hypertension
2. Hypokinetic - is characterized by the irreversible
structural changes of compession and resistance
vessels, peripheral vascular resistance and arterial
vessels tone grows as a result constantly. The main
significance has following factors:
• constant spasm of arterioles;
• hypertrophy of smooth muscles;
• atherosclerosis and substitution of smooth
muscles by connective tissue.
19. Pathogenesis of primary (essential)
hypertension
• Membrane theory is the hereditarily conditioned
violation of ionic pumps of membranes of smooth
muscles fibers:
• defect of Ca2+- pump- this leads to the
development of permanent contraction and the
increase of peripheral vascular resistance.
• decrease work of Na -K –pump - the outcome is the
thickening of vessel’s wall and diminishing of
diameter of vessels increase of sensitization to the
action of catecholamine, damage and necrosis of
cells, atherosclerosis).
21. Renal
Renovascular
Reason of origin of renovascular AH is a reduced renal
blood flow :
a) compression of renal arteries by a tumor, scar;
b) narrowing of vessels by embolus, atherosclerotic
plaque;
c) hypovolemia ;
The decreased renal blood flow activates renin-
angiotensin-aldosterone mechanism.
22. 2. Renoprive
(arises after kidney remove)
Etiology
secondary АH
Reason of renoprive AH is a degradation of
structural components of kidneys which provide
hypotension effects, in particular:
1) angiotenzinazu, which destroys an angiotensin-II
2) Phospholipid inhibitir of renine;
3)Prostaglandin E
23. Depressive function of kidney – synthesis of the
substances for AP reduce
PG Е 2
Phospholipid Renin
Inhibitor
Angiotensinase
Phosphatydilcholin
alkali ethers
! ! !
Exhaustion of kidney
depressive function
leads to arterial
hypertension
stabilization
dilates renal arteries, reduces renin
synthesis and reduces Na
reabsorbing in kidney
24. Endocrine
(develops in the result of endocrine glands pathology)
Etiology
secondary АH
Cushing's disease
(Adrenocorticotropin over production
by the pituitary gland anterior part)
Pheochromocytoma
(increase production of
catecholamines epinephrine and
norephinephrine )
Hyperaldosteronism –tumor of
glomerular zone of adrenal
Menopause
(age-depended decrease of female
gonads activity – estrogens
excretion decrease)
Possible mechanism – deficit of NO
synthesis by endotheliocytes
25. Neurogenic
(is accompanying to nerves system pathology)
Etiology
secondary АH
Brain hemorrhage
Encephalitis
Brain tumor
Brain trauma
Brain ischemia
30. 2. Cardiac output increase
SAS activation
Adrenalin excretion
Increase of cardiac
contractility force
Increase of cardiac
output
Increase of heart beats
AP elevation
Pathogenesis
Formula: АP = CO · PR
31. 3. SAS activation
Interaction adrenalin and
alpha-adrenoreceptors
Arterioles smooth
muscles spasm
Suprarenal glands
activation
Venues smooth
muscles spasm
Increase of circulative
blood in big blood
circle
adrenoreceptors of
heart
Аdrenalin
Noradrenalin
Increase of CBV
CO increase
Arterioles
narrowing
alpha-adrenoreceptors
of vessels
CO increase
AP increase
SAS activation
Arterioles narrowing
PR increase
Pathogenesis
Formula: АP = CO · PR
32. 4. Kidney functions violation
Long time spasm of
kidney’s arteries
AP increase
AP decrease in renal
capillaries
Activation of JGA
Renin excretion
Angiotensin 2
synthesis
Angiotensin 2 effects
• Smooth muscles contraction in the
vessels
• Stimulation of the vasoactive center
in brain
• Noradrenalin excretion increase
• Adrenalin excretion increase from
suprarenal glands
• Aldosteron excretion increase from
suprarenal glands (Na retention due
to kidney)
Pathogenesis
33. 1st period
functional violations
(heart hypertrophy)
2d period
Pathological changes in arteries and arterioles (dystrophy):
- Arterioles sclerosis
- Arteriole’s wall infiltration by plasma (leads to dystrophy)
- Arterioles necrosis (hypertonic crisis arises in clinic)
- Vein’s wall thickening
Arterial hypertension after-effects
34. 3d period
Secondary changes in organs and systems
Kidney
(nephrosclerosis and chronic
kidney insufficiency)
CNS
– brain hypoxia
– neurons destruction
– apoplexy (because vessels destruction and rupture
leads to brain hemorrhages and brain
destruction)
Heart
Decompensate heart failure
Organs of vision
- retinopathy (retina’s vessels injury)
- hemorrhages and separation (exfoliation) of
retina, that leads to blindness
Endocrine system
Glands atrophy and sclerosis
Arterial hypertension after-effects
45. Pathology and pathogenesis
The lesions associated with atherosclerosis are of
three types:
The fatty streak
The fibrous atheromatous plaque
Complicated lesion
The latter two are responsible for the clinically
significant manifestations of the disease.
46.
47.
48. Fatty streaks are thin, flat yellow intimal discolorations that
progressively enlarge by becoming thicker and slightly elevated as
they grow in length.
They consist of macrophages and smooth muscle cells that have
become distended with lipid to form foam cells.
They increase in number until about age 20 years, and then they
remain static or regress.
50. Atheromatous plaques are the basic
lesions within the intima, having a core of
lipid (cholesterol and cholesterol esters)
and covering fibrous cap.
APs are also called fibrous, fibrofatty, lipid,
or fibrolipid plaques which have white to
whitish yellow colour and rise intima
slightly into the lumen of the artery.
The centers of larger plaques may contain
a yellow debris, hence the term atheroma.
51. Atheromatous plaques have 3 principal
components:
1) cells, including smooth muscle calls,
macrophages, and other leukocytes,
2) connective tissue extracellular matrix,
including collagen, elastic fibers, and
proteoglycans,
3) intracellular and extracellular lipid
deposits.
In advanced atherosclerosis, the fatty
atheroma may be converted to a fibrous scar.
52.
53. As the lesions increase in size, they encroach on the
lumen of the artery and eventually may occlude the
vessel or predispose to thrombus formation, causing a
reduction of blood flow.
54. The more advanced complicated lesions are characterized by
Hemorrhage
Ulceration
Scar tissue deposits
Thrombosis is the most important complication of
atherosclerosis.
It is caused by slowing and turbulence of blood flow in the region
of the plaque and ulceration of the plaque.
63. Clinical Manifestations
The clinical manifestations of atherosclerosis depend on the
vessels involved and the extent of vessel obstruction.
Atherosclerotic lesions produce their effects through:
narrowing of the vessel and production of ischemia;
sudden vessel obstruction caused by plaque hemorrhage
or rupture;
thrombosis and formation of emboli resulting from
damage to the vessel endothelium;
In larger vessels such as the aorta, the important
complications are those of thrombus formation and
weakening of the vessel wall.
In medium-size arteries such as the coronary and cerebral
arteries, ischemia and infarction caused by vessel occlusion
are more common.
Although atherosclerosis can affect any organ or tissue, the
arteries supplying the heart, brain, kidneys, lower extremities,
and small intestine are most frequently involved.
64. Atherosclerosis symptoms
If the narrowing of an artery is less than 70% - asymptomatic
Symptoms occur due to the location of the narrowing
Coronary arteries – angina pectoris, heart attack
Carotid arteries - brain stroke.
Arteries in the legs - leg cramps (intermittent claudication).
Renal arteries - kidney failure or high blood pressure (malignant
hypertension).
65.
66. Prevention and Treatment
Prevention – to modify risk factors
smoking,
high blood cholesterol levels,
high blood pressure,
obesity,
physical inactivity.
When atherosclerosis becomes severe the complications
themselves must be treated.