This document discusses various drug classes used in the treatment of heart failure, including their mechanisms and effects. Diuretics such as loop diuretics are used to reduce preload on the heart by reducing extracellular fluid volume. Vasodilators such as nitroglycerin and ACE inhibitors reduce afterload by dilating blood vessels. Beta-blockers improve outcomes by inhibiting the deleterious effects of sympathetic activation on the heart. Other discussed drug classes include renin inhibitors, aldosterone antagonists, vasopressin antagonists, and the cardiac peptide nesiritide.
This document discusses various classes of antihypertensive agents used to treat hypertension. It defines hypertension and describes the renin-angiotensin-aldosterone system which is important in regulating blood pressure. Common classes of antihypertensive agents discussed include diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, alpha blockers, and central sympatholytics. Lifestyle modifications including weight loss, exercise, diet changes, and avoiding tobacco are also recommended for managing hypertension.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be treated through lifestyle modifications and medications. Common antihypertensive drug classes include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, calcium channel blockers, and vasodilators. Treatment involves reducing factors that increase blood pressure such as stress, weight, sodium intake, and sympathetic tone through both non-pharmacological and pharmacological approaches. Certain drugs should be avoided in patients with comorbidities like diabetes, gout, renal disease, etc. to prevent adverse effects.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be essential or secondary. Treatment approaches aim to reduce sympathetic tone, circulating angiotensin II levels, cardiac force, and increase peripheral vessel dilation. Common drug classes used include diuretics, sympatholytics, beta blockers, alpha blockers, ACE inhibitors, ARBs, CCBs, and vasodilators. Lifestyle changes such as weight control, reduced sodium intake, and exercise can help control early stage 1 hypertension alone or with pharmacological treatment.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be treated through lifestyle modifications like weight loss, reduced sodium intake, and exercise. Medications used include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, CCBs, and vasodilators. Treatment depends on the individual's medical history and any underlying conditions.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be treated through lifestyle modifications and medications. Common antihypertensive drug classes include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, calcium channel blockers, and vasodilators. Treatment involves reducing factors that increase blood pressure such as stress, weight, sodium intake, and sympathetic tone through both non-pharmacological and pharmacological approaches. Certain drugs should be avoided in patients with comorbidities like diabetes, gout, renal disease, etc. to prevent adverse effects.
Vk gmailcomcom and care Educate the ‘at the hell is not known meaning in 12 hindi meaning of the positive thought ke liye liye mana kiya hai maine us se baat karunga to delay ho gya h kya mere se baat
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be treated through lifestyle modifications like weight loss, reduced sodium intake, and exercise. Medications used include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, CCBs, and vasodilators. Treatment depends on the type and severity of hypertension as well as any underlying conditions, with some drugs contraindicated in certain diseases.
This document discusses heart failure and its treatment. Heart failure results from reduced cardiac output and activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, leading to sodium and water retention. Beta-blockers are beneficial for treating heart failure despite initially reducing cardiac function, as they prevent ischemia, induce remodeling, reduce toxicity, and apoptosis. Inotropic drugs like cardiac glycosides and beta-adrenergic agonists increase contractility but their long term use increases mortality.
This document discusses various classes of antihypertensive agents used to treat hypertension. It defines hypertension and describes the renin-angiotensin-aldosterone system which is important in regulating blood pressure. Common classes of antihypertensive agents discussed include diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, alpha blockers, and central sympatholytics. Lifestyle modifications including weight loss, exercise, diet changes, and avoiding tobacco are also recommended for managing hypertension.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be treated through lifestyle modifications and medications. Common antihypertensive drug classes include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, calcium channel blockers, and vasodilators. Treatment involves reducing factors that increase blood pressure such as stress, weight, sodium intake, and sympathetic tone through both non-pharmacological and pharmacological approaches. Certain drugs should be avoided in patients with comorbidities like diabetes, gout, renal disease, etc. to prevent adverse effects.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be essential or secondary. Treatment approaches aim to reduce sympathetic tone, circulating angiotensin II levels, cardiac force, and increase peripheral vessel dilation. Common drug classes used include diuretics, sympatholytics, beta blockers, alpha blockers, ACE inhibitors, ARBs, CCBs, and vasodilators. Lifestyle changes such as weight control, reduced sodium intake, and exercise can help control early stage 1 hypertension alone or with pharmacological treatment.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be treated through lifestyle modifications like weight loss, reduced sodium intake, and exercise. Medications used include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, CCBs, and vasodilators. Treatment depends on the individual's medical history and any underlying conditions.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be treated through lifestyle modifications and medications. Common antihypertensive drug classes include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, calcium channel blockers, and vasodilators. Treatment involves reducing factors that increase blood pressure such as stress, weight, sodium intake, and sympathetic tone through both non-pharmacological and pharmacological approaches. Certain drugs should be avoided in patients with comorbidities like diabetes, gout, renal disease, etc. to prevent adverse effects.
Vk gmailcomcom and care Educate the ‘at the hell is not known meaning in 12 hindi meaning of the positive thought ke liye liye mana kiya hai maine us se baat karunga to delay ho gya h kya mere se baat
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be treated through lifestyle modifications like weight loss, reduced sodium intake, and exercise. Medications used include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, CCBs, and vasodilators. Treatment depends on the type and severity of hypertension as well as any underlying conditions, with some drugs contraindicated in certain diseases.
This document discusses heart failure and its treatment. Heart failure results from reduced cardiac output and activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, leading to sodium and water retention. Beta-blockers are beneficial for treating heart failure despite initially reducing cardiac function, as they prevent ischemia, induce remodeling, reduce toxicity, and apoptosis. Inotropic drugs like cardiac glycosides and beta-adrenergic agonists increase contractility but their long term use increases mortality.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be essential or secondary hypertension. Treatment involves lifestyle modifications and medications. Common drug classes used to treat hypertension include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, calcium channel blockers, and vasodilators. Drug choice depends on the individual patient's condition and needs to avoid medications that could worsen other diseases.
Hypertension is defined as a systolic blood pressure above 140 mmHg or a diastolic blood pressure above 90 mmHg. It can be essential (of unknown cause) or secondary to other diseases. Normal blood pressure is regulated by the kidney which controls blood volume via the renin-angiotensin-aldosterone system (RAAS). RAAS is activated when blood pressure or sodium levels drop, causing vasoconstriction and sodium retention. Antihypertensive drugs target different parts of this system, like ACE inhibitors which block the conversion of angiotensin I to angiotensin II, reducing peripheral resistance and blood volume. Captopril is an ACE inhibitor that lowers blood pressure by
This document discusses various vasoactive drugs used to treat low blood pressure and cardiac issues in critically ill patients. It begins by explaining the immature heart's limited responsiveness to medications and calcium regulation. It then describes different types of effects that agents can have including increasing blood pressure, contractility, heart rate, and relaxation. The remainder of the document delves into specific drugs, outlining their mechanisms, indications, dosages, and side effects. These include catecholamines like epinephrine, norepinephrine, and dopamine, as well as dobutamine, milrinone, vasopressin, nitroprusside, and nesiritide.
Calcium channel blockers (CCBs) block voltage-gated calcium channels, reducing calcium influx into cells. They are used to treat hypertension, angina, and arrhythmias. In myocardial infarction, CCBs may reduce infarct size and arrhythmias but their use is not generally recommended due to risk of heart failure. Aspirin inhibits platelet aggregation to prevent clotting and is used long-term after myocardial infarction.
Calcium channel blockers work by blocking voltage-gated calcium channels, thereby reducing calcium influx into cells. They are used to treat hypertension, angina, and arrhythmias. There are several classes of calcium channel blockers that differ in their selectivity for specific calcium channel subtypes and durations of action. Nifedipine primarily dilates arterioles while verapamil and diltiazem also affect heart rate and conduction.
This document summarizes the properties and uses of drugs with cardiac inotropic effects for treating heart failure. It discusses how these drugs increase the force of cardiac contraction without proportionally increasing oxygen consumption. The document outlines the mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects of digitalis glycosides, which are commonly used inotropic drugs that work by inhibiting the sodium-potassium ATPase pump. Digitalis glycosides are used to treat both congestive heart failure and cardiac arrhythmias.
This document provides information on antihypertensive drugs. It begins by listing the specific learning objectives, which include defining hypertension, discussing types and drugs for treatment, mechanisms of action, adverse effects, and considerations for use in various conditions. It then covers primary and secondary hypertension, urgency vs emergency, and mnemonics for drug classes. Individual drug classes are discussed in detail, including diuretics, ACE inhibitors, ARBs, calcium channel blockers, arteriolar vasodilators, and beta blockers. Mechanisms, advantages, disadvantages, and special considerations are provided for each class.
The document discusses antihypertensive drugs. It describes how hypertension results from increased vascular resistance and defines normal and elevated blood pressure readings. It explains the two main mechanisms that control blood pressure - the baroreflex system and the renin-angiotensin-aldosterone system. The rest of the document summarizes several classes of antihypertensive drugs, including diuretics, beta-blockers, ACE inhibitors, ARBs, and calcium channel blockers. It provides details on their mechanisms of action, therapeutic uses, and side effects in treating hypertension.
Basic must know things about Anti Hypertensive drugs including the recent JNC-8 classification and protocols for treating Hypertension with various co-morbid condition.
Basic must know things about Anti-Hypertensives including the latest JNC-8 Classification and protocol for managing hypertension in various co-morbid conditions.
Cardiac remodeling is an important compensatory mechanism in heart failure where the heart undergoes hypertrophy and changes shape to maintain function. Initially this is beneficial but eventually leads to worsening changes. Over time the compensatory mechanisms become exhausted and the heart enters a state of decompensated failure. Medications are aimed at reducing preload and afterload on the heart to improve function and symptoms. Diuretics reduce fluid overload while drugs like ACE inhibitors, beta blockers, and aldosterone antagonists inhibit pathological remodeling and improve outcomes in heart failure patients.
The document summarizes several classes of cardiovascular drugs used to treat conditions like hypertension and heart failure. It discusses the mechanisms of action, therapeutic effects, side effects and nursing considerations for drugs from classes like diuretics, beta blockers, calcium channel blockers, ACE inhibitors, ARBs, and cardiac glycosides like digoxin. The document provides an overview of how these drugs work and how they are used to treat various cardiac conditions.
This document discusses the classification and mechanisms of action of various classes of antihypertensive drugs used to treat hypertension. It describes beta blockers, diuretics, ACE inhibitors, angiotensin II receptor blockers, and calcium channel blockers. For each class, it provides details on their mechanisms of action in lowering blood pressure, medical uses for treating conditions like heart failure and hypertension, and potential side effects. The document aims to explain the pharmacology of antihypertensive drugs and help understand their different classifications and mechanisms of action.
This document discusses acute decompensated heart failure (ADHF), including definition, etiology, prognostic factors, signs and symptoms, treatment goals, monitoring, and management strategies. Key recommendations are that ADHF often requires hospitalization for intensive therapy like diuresis and vasodilators. Goals of treatment are to improve symptoms, optimize volume status, and identify precipitating factors. Initial therapies are often similar for systolic and diastolic dysfunction but some medications require caution in systolic HF. Atrial fibrillation may require rate control or cardioversion, and ventricular tachycardia needs prompt cardioversion.
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It has multiple causes and symptoms including shortness of breath, fatigue, fluid retention, and arrhythmias. Treatment focuses on controlling symptoms with diuretics, and improving the heart's function with ACE inhibitors, beta blockers, and other vasodilators. For severe cases, inotropic drugs or even advanced therapies like ventricular assist devices or transplant may be needed. The goals are to improve quality of life and survival through controlling risk factors and compensatory mechanisms that can worsen the condition over time.
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It has multiple causes and symptoms including shortness of breath, fatigue, swelling, and coughing up pink mucus. Treatment focuses on controlling symptoms with diuretics, and improving the heart's function with ACE inhibitors, beta blockers, and other medications. For severe cases, devices or surgery such as defibrillators, resynchronization therapy, or transplantation may be needed. The long-term goal is to improve quality of life through lifestyle changes and optimal medical management.
This document discusses cardiovascular pharmacology. It covers topics like diuretics and their indications for hypertension and fluid retention. It discusses treatment approaches for hypertension including lifestyle modifications and pharmacological therapies. The main antihypertensive drug classes covered are diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and alpha blockers. It also discusses heart failure pharmacology and angina management. The document provides details on the mechanisms and uses of different drug classes for cardiovascular conditions.
Ischemic heart disease occurs when coronary arteries become narrowed by atherosclerosis, reducing blood flow to the heart muscle. Angina, myocardial ischemia, and myocardial infarction can result. Myocardial infarction is caused by sudden blockage of a coronary artery and leads to cell death in the affected region. Treatment focuses on pain relief, oxygenation, volume maintenance, acidosis correction, and preventing/treating arrhythmias. Drugs like nitrates, beta blockers, and calcium channel blockers aim to reduce oxygen demand and increase supply.
This document discusses cardiovascular drugs used to treat hypertension and cardiac conditions. It covers major drug categories including diuretics, ACE inhibitors, ARBs, calcium channel blockers, and beta blockers. For each category, it describes the mechanism of action, therapeutic effects, potential adverse effects, examples of specific drugs, and important nursing considerations when administering these medications. The goal is to optimize blood flow and peripheral resistance to lower blood pressure and treat underlying cardiac issues.
Hypertension is classified based on blood pressure readings into normal, prehypertension, stage 1 hypertension, stage 2 hypertension, and hypertensive crisis. It can be essential or secondary hypertension. Treatment involves lifestyle modifications and medications. Common drug classes used to treat hypertension include diuretics, sympatholytics, beta-blockers, alpha-blockers, ACE inhibitors, ARBs, calcium channel blockers, and vasodilators. Drug choice depends on the individual patient's condition and needs to avoid medications that could worsen other diseases.
Hypertension is defined as a systolic blood pressure above 140 mmHg or a diastolic blood pressure above 90 mmHg. It can be essential (of unknown cause) or secondary to other diseases. Normal blood pressure is regulated by the kidney which controls blood volume via the renin-angiotensin-aldosterone system (RAAS). RAAS is activated when blood pressure or sodium levels drop, causing vasoconstriction and sodium retention. Antihypertensive drugs target different parts of this system, like ACE inhibitors which block the conversion of angiotensin I to angiotensin II, reducing peripheral resistance and blood volume. Captopril is an ACE inhibitor that lowers blood pressure by
This document discusses various vasoactive drugs used to treat low blood pressure and cardiac issues in critically ill patients. It begins by explaining the immature heart's limited responsiveness to medications and calcium regulation. It then describes different types of effects that agents can have including increasing blood pressure, contractility, heart rate, and relaxation. The remainder of the document delves into specific drugs, outlining their mechanisms, indications, dosages, and side effects. These include catecholamines like epinephrine, norepinephrine, and dopamine, as well as dobutamine, milrinone, vasopressin, nitroprusside, and nesiritide.
Calcium channel blockers (CCBs) block voltage-gated calcium channels, reducing calcium influx into cells. They are used to treat hypertension, angina, and arrhythmias. In myocardial infarction, CCBs may reduce infarct size and arrhythmias but their use is not generally recommended due to risk of heart failure. Aspirin inhibits platelet aggregation to prevent clotting and is used long-term after myocardial infarction.
Calcium channel blockers work by blocking voltage-gated calcium channels, thereby reducing calcium influx into cells. They are used to treat hypertension, angina, and arrhythmias. There are several classes of calcium channel blockers that differ in their selectivity for specific calcium channel subtypes and durations of action. Nifedipine primarily dilates arterioles while verapamil and diltiazem also affect heart rate and conduction.
This document summarizes the properties and uses of drugs with cardiac inotropic effects for treating heart failure. It discusses how these drugs increase the force of cardiac contraction without proportionally increasing oxygen consumption. The document outlines the mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects of digitalis glycosides, which are commonly used inotropic drugs that work by inhibiting the sodium-potassium ATPase pump. Digitalis glycosides are used to treat both congestive heart failure and cardiac arrhythmias.
This document provides information on antihypertensive drugs. It begins by listing the specific learning objectives, which include defining hypertension, discussing types and drugs for treatment, mechanisms of action, adverse effects, and considerations for use in various conditions. It then covers primary and secondary hypertension, urgency vs emergency, and mnemonics for drug classes. Individual drug classes are discussed in detail, including diuretics, ACE inhibitors, ARBs, calcium channel blockers, arteriolar vasodilators, and beta blockers. Mechanisms, advantages, disadvantages, and special considerations are provided for each class.
The document discusses antihypertensive drugs. It describes how hypertension results from increased vascular resistance and defines normal and elevated blood pressure readings. It explains the two main mechanisms that control blood pressure - the baroreflex system and the renin-angiotensin-aldosterone system. The rest of the document summarizes several classes of antihypertensive drugs, including diuretics, beta-blockers, ACE inhibitors, ARBs, and calcium channel blockers. It provides details on their mechanisms of action, therapeutic uses, and side effects in treating hypertension.
Basic must know things about Anti Hypertensive drugs including the recent JNC-8 classification and protocols for treating Hypertension with various co-morbid condition.
Basic must know things about Anti-Hypertensives including the latest JNC-8 Classification and protocol for managing hypertension in various co-morbid conditions.
Cardiac remodeling is an important compensatory mechanism in heart failure where the heart undergoes hypertrophy and changes shape to maintain function. Initially this is beneficial but eventually leads to worsening changes. Over time the compensatory mechanisms become exhausted and the heart enters a state of decompensated failure. Medications are aimed at reducing preload and afterload on the heart to improve function and symptoms. Diuretics reduce fluid overload while drugs like ACE inhibitors, beta blockers, and aldosterone antagonists inhibit pathological remodeling and improve outcomes in heart failure patients.
The document summarizes several classes of cardiovascular drugs used to treat conditions like hypertension and heart failure. It discusses the mechanisms of action, therapeutic effects, side effects and nursing considerations for drugs from classes like diuretics, beta blockers, calcium channel blockers, ACE inhibitors, ARBs, and cardiac glycosides like digoxin. The document provides an overview of how these drugs work and how they are used to treat various cardiac conditions.
This document discusses the classification and mechanisms of action of various classes of antihypertensive drugs used to treat hypertension. It describes beta blockers, diuretics, ACE inhibitors, angiotensin II receptor blockers, and calcium channel blockers. For each class, it provides details on their mechanisms of action in lowering blood pressure, medical uses for treating conditions like heart failure and hypertension, and potential side effects. The document aims to explain the pharmacology of antihypertensive drugs and help understand their different classifications and mechanisms of action.
This document discusses acute decompensated heart failure (ADHF), including definition, etiology, prognostic factors, signs and symptoms, treatment goals, monitoring, and management strategies. Key recommendations are that ADHF often requires hospitalization for intensive therapy like diuresis and vasodilators. Goals of treatment are to improve symptoms, optimize volume status, and identify precipitating factors. Initial therapies are often similar for systolic and diastolic dysfunction but some medications require caution in systolic HF. Atrial fibrillation may require rate control or cardioversion, and ventricular tachycardia needs prompt cardioversion.
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It has multiple causes and symptoms including shortness of breath, fatigue, fluid retention, and arrhythmias. Treatment focuses on controlling symptoms with diuretics, and improving the heart's function with ACE inhibitors, beta blockers, and other vasodilators. For severe cases, inotropic drugs or even advanced therapies like ventricular assist devices or transplant may be needed. The goals are to improve quality of life and survival through controlling risk factors and compensatory mechanisms that can worsen the condition over time.
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It has multiple causes and symptoms including shortness of breath, fatigue, swelling, and coughing up pink mucus. Treatment focuses on controlling symptoms with diuretics, and improving the heart's function with ACE inhibitors, beta blockers, and other medications. For severe cases, devices or surgery such as defibrillators, resynchronization therapy, or transplantation may be needed. The long-term goal is to improve quality of life through lifestyle changes and optimal medical management.
This document discusses cardiovascular pharmacology. It covers topics like diuretics and their indications for hypertension and fluid retention. It discusses treatment approaches for hypertension including lifestyle modifications and pharmacological therapies. The main antihypertensive drug classes covered are diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and alpha blockers. It also discusses heart failure pharmacology and angina management. The document provides details on the mechanisms and uses of different drug classes for cardiovascular conditions.
Ischemic heart disease occurs when coronary arteries become narrowed by atherosclerosis, reducing blood flow to the heart muscle. Angina, myocardial ischemia, and myocardial infarction can result. Myocardial infarction is caused by sudden blockage of a coronary artery and leads to cell death in the affected region. Treatment focuses on pain relief, oxygenation, volume maintenance, acidosis correction, and preventing/treating arrhythmias. Drugs like nitrates, beta blockers, and calcium channel blockers aim to reduce oxygen demand and increase supply.
This document discusses cardiovascular drugs used to treat hypertension and cardiac conditions. It covers major drug categories including diuretics, ACE inhibitors, ARBs, calcium channel blockers, and beta blockers. For each category, it describes the mechanism of action, therapeutic effects, potential adverse effects, examples of specific drugs, and important nursing considerations when administering these medications. The goal is to optimize blood flow and peripheral resistance to lower blood pressure and treat underlying cardiac issues.
This document summarizes the key aspects of communicable diseases and their transmission cycles. It discusses the epidemiological triad of agent, host, and environment. It explains the natural history of diseases and how they are transmitted from reservoirs to hosts through various routes of exit and entry. It also covers the incubation period, types of disease occurrence, and the importance of epidemiological investigations in outbreaks. The goal is to understand disease transmission and implement appropriate prevention and control measures.
This document discusses calcium homeostasis and hypercalcemia. It notes that approximately 1000-1200 mg of calcium is present in an adult, mostly in bone. It describes the distribution and protein binding of calcium in extracellular fluid and intracellular fluid. Factors that influence calcium absorption in the gut and renal handling of calcium are outlined. Mechanisms involved in response to changes in serum calcium levels, including the roles of TRPV5 calcium channels and calbindin D28k protein, are summarized. Causes, clinical features, pathophysiology, and treatment approaches for hypercalcemia and various hypercalcemic disorders like primary hyperparathyroidism and familial hypocalciuric hypercalcemia are described.
1. Anemia is defined as a low red blood cell count or low hemoglobin levels. It can be caused by blood loss, impaired red blood cell production, or increased red blood cell breakdown.
2. Common types of anemia include iron deficiency anemia, thalassemia, anemia of chronic disease, and sideroblastic anemia. Iron deficiency anemia is usually caused by blood loss or poor iron absorption. Thalassemia involves a genetic defect in hemoglobin production. Anemia of chronic disease occurs during chronic illnesses and involves trapped iron. Sideroblastic anemia has a genetic defect affecting iron utilization.
3. Diagnosis involves blood tests to measure red blood cell
Leptospirosis is a zoonotic disease caused by bacteria of the genus Leptospira. It is transmitted to humans through contact with water contaminated by the urine of infected animals like rats. It is most common in tropical and subtropical regions during the monsoon season. Occupations like farming, sewage work, and fishing are at high risk. Clinical features range from a mild flu-like illness to severe multi-organ involvement including jaundice, acute kidney injury, pulmonary hemorrhage and bleeding diathesis. Diagnosis involves culture, serology and PCR of blood, urine or CSF. Treatment consists of antibiotics and supportive care such as dialysis. Prevention focuses on health education, immunizing livestock
This document provides an overview of anemia, including its classification and causes. It discusses impaired red blood cell production, excessive destruction of RBCs, and blood loss as the main etiologic classifications. The morphologic classifications are macrocytic, microcytic hypochromic, and normochromic normocytic anemia. Causes of impaired RBC production include bone marrow abnormalities and deficiencies in essential factors or stimulation factors. Excessive destruction can be due to intracorpuscular or extracorpuscular defects. Blood loss can be acute or chronic. Specific causes are discussed under each classification.
This document discusses various types of anemia. It defines anemia as a condition with fewer than normal red blood cells or hemoglobin. The types discussed include iron deficiency anemia, thalassemia, anemia of chronic disease, sideroblastic anemia, and hemolytic anemia. For each type, the document outlines causes, pathophysiology, clinical presentation, laboratory findings, and management. Key points like ringed sideroblasts, ineffective erythropoiesis, and hereditary spherocytosis are explained. Treatment involves addressing the underlying cause, iron supplementation, blood transfusions, or splenectomy in some cases.
This document discusses anemia, including its definition, classification, symptoms, evaluation and treatment. It defines anemia as a hemoglobin level below 130g/L for men and 120g/L for women. Anemia can be classified based on four critical elements of erythropoiesis: EPO production, iron availability, bone marrow proliferative capacity and red cell maturation. Evaluation involves history, physical exam, blood tests like complete blood count and iron studies, and bone marrow examination if needed. Causes of anemia include blood loss, hemolytic anemia, bone marrow disorders, chronic diseases and nutritional deficiencies. Treatment depends on the underlying cause.
Hepatology - 2018 - Terrault - Update on prevention diagnosis and treatment...Sheik4
This document provides an update to the 2018 AASLD Hepatitis B Guidance, summarizing key changes and interim data. It discusses the approval of tenofovir alafenamide (TAF) for treatment of chronic hepatitis B in adults, which joins entecavir, tenofovir disoproxil fumarate (TDF), and peginterferon as preferred therapies. Phase 3 trials found TAF had similar antiviral efficacy to TDF but significantly less negative impact on bone density and renal function. The guidance was updated to reflect TAF as a new preferred treatment and changes to screening and prevention recommendations.
The document discusses calcium homeostasis and hypercalcemia. It provides details on:
- Calcium distribution in the body, with 99% located in bones and teeth.
- Intestinal and renal handling of calcium and the roles of TRPV5 channel and calbindin D28k protein.
- Causes of hypercalcemia including primary hyperparathyroidism, malignancy, and vitamin D excess.
- Presentation of hypercalcemia ranging from asymptomatic to severe symptoms like confusion.
- Workup and treatment of hypercalcemia depending on its underlying cause and severity.
Dr. T.V. Rao provides an overview of Helicobacter pylori (H. pylori), the bacterium associated with peptic ulcer disease and gastric cancer. Some key points:
- H. pylori was discovered in 1983 by Warren and Marshall and linked to gastritis and ulcers. They received the 2005 Nobel Prize in Physiology or Medicine.
- H. pylori colonizes the stomach of about half of individuals worldwide. It is a gram-negative, spiral-shaped bacterium that lives in the mucus layer of the stomach.
- H. pylori infection can cause chronic gastritis, peptic ulcers, and in rare
Hyperkalemia is defined as a plasma potassium level above 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space due to acidosis or tissue damage. Other causes include reduced renal excretion due to medications like ACE inhibitors or renal failure. Symptoms range from none to muscle weakness to cardiac arrhythmias. Treatment involves calcium to antagonize cardiac effects, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins or dialysis to remove excess potassium.
This document discusses thyroid storm, which is a life-threatening exacerbation of hyperthyroidism. It can have a mortality rate of 20-30%. Causes include infections, discontinuing thyroid medications, and other systemic stresses. Patients experience high metabolism, tachycardia, hypertension, and other symptoms. Treatment involves medications to stop thyroid hormone synthesis and block peripheral effects, supportive care, treating any precipitating causes, and monitoring for complications. Early diagnosis and aggressive treatment are needed to reduce mortality from this medical emergency.
This document discusses thyroid storm, which is a life-threatening exacerbation of hyperthyroidism. It can have a mortality rate of 20-30%. Causes include infections, discontinuing thyroid medications, and other systemic stresses. Patients experience high metabolism, tachycardia, hypertension, and other symptoms. Treatment involves medications to stop thyroid hormone synthesis and block peripheral effects, supportive care, treating any precipitating causes, and monitoring for complications. Early diagnosis and treatment are important to reduce the high mortality risk associated with thyroid storm.
This document summarizes guidelines from the WHO on rabies post-exposure prophylaxis. It recommends modern cell-culture or embryonated egg-derived rabies vaccines over nerve tissue vaccines. It outlines considerations for wound treatment, administration of rabies immunoglobulin, and intramuscular vaccine regimens. It also discusses intradermal regimens, vaccination of immunosuppressed individuals, pre-exposure prophylaxis, and booster doses.
This document discusses various types of thyroiditis and thyrotoxicosis. It defines thyrotoxicosis as a hypermetabolic condition associated with elevated thyroid hormone levels. The causes of thyrotoxicosis include Graves' disease, toxic multinodular goiter, and toxic adenoma. Thyroiditis can be painful or painless and is caused by chronic autoimmune thyroiditis, postpartum thyroiditis, subacute thyroiditis, and other conditions. Subacute thyroiditis is often viral in origin and causes neck pain and signs of thyrotoxicosis. Postpartum thyroiditis can cause thyrotoxicosis, hypothyroidism, or a combination in the first postpartum year.
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
2. Diuretics:
•Reduce extracellular fluid volume
•Natriuresis and decrease in intravascular volume
•Reduce preload on heart
•Dietary sodium intake restriction
•Loop diuretics – furosemide, bumetanide, torsemide- inhibit
Na+-K+-2Cl- symporter in the ascending loop of Henle to
increase Na+ and water delivery to distal tubule
•Also increase K+ excretion
•Thiazide Diuretics- chlorthiazide, hydrochlorthiazide- limited
value in CHF
•Act on Na+Cl- co-transporter in distal convoluted tubule
3. •K+ loss occurs more than that with loop diuretics
•Often combined with loop diuretics when patient is refractory
to loop diuretics
•K+ Sparing Diuretics- Spironolactone, triamterene, amiloride
are weak diuretics-for achieving volume reduction with
minimal K+ loss
•Usually, treatment is started with loop diuretics either orally
(compensated) or i.v. (decompensated) patients
•Diuretic resistance- due to compensatory increase in renal
tubular reabsorption of Na+
•Diuretics do not improve upon the mortality rate in patients
4. Vasodilators:
•Nitrosovasodilators
•ACE inhibitors/ARBs
•Nitrosovasodilators:
NO donors which activate soluble guanylate cyclase in
vascular smooth muscle cells to relax them
Rapid acting nitroglycerine tablets or spray (sublingual)
Short acting oral agents like isosorbide dinitrate
Long acting oral agents like isosorbide mononitrate
Topical like transdermal patches, ointments of nitroglycerine
I.V. like nitroglycerine
5. How nitrates are helpful in CHF?
•Reduce preload due to peripheral pooling
•Reduction of pulmonary and systemic arterial resistance
•Epicardial coronary artery dilatation- reperfusion
•Given alone their efficacy is limited due to:
limited effect on systemic resistance
Nitrate tolerance
•Often combined with other vasodilators for better results
6. Na Nitroprusside: During biotransformation of nitroprusside,
cyanide is produced which is quickly converted to thiocynate in the
liver and excreted by the kidney
•ADR: Thiocynate or cyanide toxicity may occur following
prolonged drug administration
•Symptoms: unexplained abdominal pain, change in mental status,
convulsions, lactic acidosis
•Treatment:
Sodium nitrite: It oxidizes some iron of haemoglobin to ferric
state and converts it to methaemoglobin. Cyanide preferntially
binds to methaemoglobin to form cyanmethaemoglobin.
Administration of sodium thiosulphate converts
cyanmethaemoglobin to thiocyanate, sulfite and haemoglobin.
Thiocyanate is excreted by the kidney
7. Hydrocobalamin (B12): It binds to cyanide to form harmless
vitamin B12acyanacobalamin that is excreted by the kidney
4-Dimethylaminophenol: It forms methaemoglobin in the
body that binds to cyanide
Dicobalt adetate: It chelates cyanide
•ADR: Methaemoglobinemia: due to oxidation of haemoglobin
by NO-
•Treatment: Methylene blue: It acts as artificial electron
acceptor for NADPH-methaemoglobin reductase and allows the
enzyme to function again
8. Hydralazine:
•Direct acting vasodilator
•Mechanism of action not known
•Reduces both right and left ventricular afterload by reducing
pulmonary and systemic vascular resistance
•Results in increased cardiac output and decreased ventricular wall
stress during systole
•Also has moderate direct positive inotropic activity independent
of its afterload reducing effects
•Reduces renal vascular resistance and increases renal blood flow
•Increases renal blood flow more than any other vasodilator except
ACE inhibitors
•Preferred drug in CHF (ACE intolerant) with renal impairment
9. •Hydralazine is more often used in combination with isosorbide
dinitrate
•The combination is as effective in CHF as 1 blocker prazosin
•ACE inhibitors are superior to hydralazine in reducing mortality
in CHF
•ADRs: withdrawal effect, lupus like syndrome
•Oral/i.v. – oral is equally effective as i.v.
• Has to be taken 3-4 times a day- patient compliance
•I.V. hydralazine is used for its immediate effect only- urgency
•10-25 mg/day orally increased gradually; maximum dose 100 mg
3-4 times a day
10. ACE Inhibitors:
•Effects of angiotensin II:
Potent vasoconstrictor
Na+ and water reabsorption from renal tubule (effect on filtration
pressure and secretion of aldosterone)
Modulation of neural and medullary catecholamine release
Arrhythmogenic
Promotes vascular and myocardial hyperplasia
Induces myocyte death
Reduction of RAS leads to beneficial effects in CHF
11. •ACE inhibitors:
Suppress angiotensin II and aldosterone production
Decrease sympathetic activity
Potentiate effects of diuretics in CHF
•Angiotensin II escape: After chronic therapy with ACE inhibitors,
angiotensin II levels return to normal but effect of ACE inhibitors
persists- the normalization of angiotensin II is called “escape”
•Suggests that other mechanisms besides ACE inhibition also play a
role in their effects
•Bradykinin and other kinins- stimulate production of NO, cyclic
GMP, vasoactive eicosanoids that dilate the blood vessels, oppose
angiotensin II effect on smooth muscle cells of blood vessels and
fibroblasts proliferation & extracellular matrix deposition in heart
12. •ACE inhibitors are preferential arterial vasodilators
• Left ventricular afterload by PVR & cardiac output
•HR remains unchanged probably due to sympathetic activity
•Acts via AT1 receptors so ARBs are more effective than ACE
inhibitors
•Both beneficial and deleterious effects are due to activation of
AT1 receptors
•AT2 receptor activation appears to counterbalance deleterious
effects of AT1 activation
•Increase in circulating levels of angiotensin II in response to
ARBs results in relative increase in AT2 receptor activation
•Combination therapy with ACE inhibitors and ARBs is under
trial
13. •ACE inhibition alone is not sufficient for optimal attenuation of
angiotensin II induced CV dysfunction in patients of CHF
•Reasons:
ACE independent pathways that convert Ang I to Ang II
Activation of ACE homologs like ACE2 occurs that are insensitive
to conventional ACE therapy
Suppression of negative feed back effect on renin secretion
•Thus, some amount of angiotensin like activity persists that is
deleterious to CV functions
•Inhibition of renin secretion prevents conversion of angiotensinogen
to angiotensin I due to which angiotensin II formation does not occur,
directly or through alternate routes
•Under trial
14. Nesiritide:
•Introduced recently for treatment of CHF
•Recombinant form of human natriuretic peptide
•Naturally secreted by the ventricles, increases cGMP in vascular
smooth muscles and reduces arteriolar and venous tone
•Causes natriuresis
•Short t½ of 18 min
•Administered as bolus dose 2 µg/kg i.v. followed by continuous
i.v.infusion of 0.01 to 0.03 µg/kg/min
•Used in acute decompensated heart failure associated with
dyspnoea at rest
•ADR: hypotension
15. Vasopressin receptor antagonists:
•Vasopressin or ADH is released in response to:
Increased plasma osmolality
Decreased arterial pressure
Reduced cardiac filling
•Two types of vasopressin receptors- V1 and V2
•V1 mediate vasoconstrictor while V2 mediate antidiuretic action
•Conivaptan is mixed V1 and V2 antagonists and Tolvaptan is V2
antagonist
•Conivaptan is given i.v. while tolvaptan is given orally
•Though beneficial, they donot reduce mortality so long term
usefullness is doubtful
16. Role of sympathetic activation in CHF
CHF
Sympathetic activation
Inotropy
( contractility)
Lusitropy
( Ventricular relaxation & filling)
Chronotropy
( Heart rate)
17. -Adrenoceptor antagonists:
• agonists dobutamine as also dopamine provide relief in CHF but
their long term use increases mortality
•Long term administration of -antagonists reduce mortality rate in
CHF
•Initially the systolic function decreases but over 2-4 months it
recovers and improvement beyond baseline occurs
•Mechanism of beneficial effects in CHF not clear
By preventing myocardial ischemia without significantly
influencing serum electrolytes, they may decrease frequency of
unstable tachyarrhythmias
Betterment of left ventricular morphology by decreasing left
ventricular size and increasing ejection fraction
18. By inhibiting sustained sympathetic discharge, they reduce
catecholamine induced cardiomyote toxicity and prevent or delay
myocardial contractile dysfunction
Decrease cardiomyocyte apoptosis
May induce positive myocardial remodeling by decreasing
oxidative stress on myocardium
•Drugs used: metoprolol, carvedilol, bisoprolol- other -blockers
are not effective
•Combined and blocker is preferred
•Carvedilol has additional advantages that it reduces free radical
induced lipid peroxidation and prevents cardiac and vascular
smooth muscle mitogenesis independent of its or receptor
blocking activity
19. • Adrenoceptor blockers have proven utility in improving
symptoms, hospitalization and mortality in patients of CHF
•They are recommended for use in patients along with ACE
inhibitors or ARBs
•Recommended only when the ejection fraction of heart is
<35% to counter the deleterious effects of circulating
catecholamines
•They are usually given in small doses initially, less than 1/10th
of the final dose and gradually titration of dose is done
•Not recommended for use in patients with severe, new onset
or acutely decompensated CHF