Cardiac glycosides, antiarrhythemic drugs-Dr.Jibachha Sah,M.V.Sc,Lecturer
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Dr. Jibachha Sah,M.V.Sc( Veterinary pharmacology, TU,Nepal),posted lecturer notes on AUTONOMIC AND SYSTEMIC PHARMACOLOGY for B.V.Sc & A.H. 6 th semester veterinary students of College of veterinary science,Nepal Polytechnique Institute, Bharatpur, Bhojard, Chitwan, Nepal.I hope this lecture notes may be beneficial for other Nepalese veterinary students. Please send your comment and suggestion .Email:jibachhashah@gmail.com,moble,00977-9845024121
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Cardiac glycosides
Cardiac glycosides like digoxin are derived from plants like Digitalis lanata and act on the heart by increasing the force of contraction. They work by increasing intracellular calcium levels in heart muscle cells through multiple mechanisms - increasing calcium influx, releasing calcium from intracellular stores, and blocking calcium efflux from cells. This makes the heart muscle contract with more force, increasing cardiac output which benefits patients with heart failure. Digoxin is commonly used for heart failure, atrial fibrillation, and other arrhythmias but has a narrow therapeutic window. Its toxicity can be managed with electrolyte supplementation, drugs to control arrhythmias, and antibodies in severe cases. Drug interactions and dose adjustments based on kidney function are important considerations with
Congestive heart failure
Congestive heart failure occurs when the heart cannot pump enough blood to meet the body's needs. It is caused by problems with factors that determine cardiac performance like preload, afterload, contractility, and heart rate. Common treatments aim to reduce symptoms by decreasing preload and afterload through drugs like ACE inhibitors, beta blockers, diuretics, and vasodilators. Digoxin and other inotropic drugs are used to improve contractility but have side effects risking toxicity. Managing comorbidities, sodium intake, and activity levels also helps treatment.
Pharmacology of Cardiovascular System 2
Cardiac glycosides are a class of organic compounds that increase the force of heart contractions and decrease heart rate. They act on the sodium-potassium ATPase pump. Digitalis is a genus of plant that contains cardiac glycosides used medicinally to treat heart failure and arrhythmias. Cardenolides contain an enolide ring and are more commonly used than bufadienolides, which contain a dienolide ring. Cardenolides increase intracellular sodium levels, inhibiting calcium export and increasing calcium levels inside cardiac muscle cells for more forceful contractions.
Antihypertensives acting on RAAS
- A 48-year-old male presented with essential hypertension and was prescribed captopril. He returned with a persistent brassy cough.
- Captopril is an ACE inhibitor that works by inhibiting the renin-angiotensin-aldosterone system to lower blood pressure. However, it can cause cough as a side effect by inhibiting the breakdown of bradykinin.
- The patient's cough was likely caused by captopril as a side effect. His blood pressure was now under control, so the doctor would need to consider changing him to an alternative antihypertensive like an ARB that is less likely to cause cough.
Aldersterone
1) Conn syndrome is caused by excessive aldosterone production independent of renin, often due to an adrenal tumor.
2) This leads to sodium retention and expansion of extracellular fluid volume, increasing blood pressure and causing hypertension.
3) Despite volume expansion, edema is absent because increased atrial natriuretic peptide secretion inhibits aldosterone's effects and sodium retention.
4) The pathophysiology involves hypertension from increased cardiac output and blood volume, while ANP prevents further sodium retention and edema formation.
ACUTE MANAGEMENT OF Hyperkalemia
This document discusses hyperkalemia, or high levels of potassium in the blood. It begins by listing the normal potassium range and then describes some common causes of hyperkalemia, including the release of potassium from cells due to conditions like rhabdomyolysis or tumor lysis syndrome, and decreased renal excretion of potassium due to renal failure or medications. Clinical manifestations of hyperkalemia are then outlined, such as weakness, paralysis, arrhythmias, and ECG changes including peaked T waves. The document concludes by presenting two case histories of patients with hyperkalemia and CKD and recommends treatment approaches starting with calcium gluconate for cardiac instability and then other options to increase potassium excretion or remove it through dialysis if
cardiac glycosides
This document provides information on the treatment of congestive heart failure (CHF). It begins by defining CHF as a condition where the heart is unable to pump enough blood to meet the body's needs. It then discusses various contributing diseases and clinical features of CHF. The treatment of CHF involves restoring cardiac performance and arresting disease progression. Positive inotropic drugs discussed include cardiac glycosides like digitalis, beta-adrenergic agonists, phosphodiesterase inhibitors, and calcium sensitizers. Other treatments include diuretics, vasodilators, RAS inhibitors, and beta-blockers. The mechanisms of action and effects of cardiac glycosides like digitalis are explained in detail.
Vasodilators
This document discusses various vasodilators used to treat conditions like hypertension, heart failure, and peripheral vascular disease. It describes different classes of vasodilators including direct-acting vasodilators like calcium channel blockers and drugs that increase cyclic nucleotides, and indirect vasodilators that interfere with the sympathetic nervous system or renin-angiotensin system. Specific vasodilators discussed in detail include nitroglycerin, hydralazine, minoxidil, diazoxide, nitric oxide, and natriuretic peptides. Their mechanisms of action, pharmacological effects, uses, and adverse effect profiles are summarized.
Recommended
Cardiac glycosides
Cardiac glycosides like digoxin are derived from plants like Digitalis lanata and act on the heart by increasing the force of contraction. They work by increasing intracellular calcium levels in heart muscle cells through multiple mechanisms - increasing calcium influx, releasing calcium from intracellular stores, and blocking calcium efflux from cells. This makes the heart muscle contract with more force, increasing cardiac output which benefits patients with heart failure. Digoxin is commonly used for heart failure, atrial fibrillation, and other arrhythmias but has a narrow therapeutic window. Its toxicity can be managed with electrolyte supplementation, drugs to control arrhythmias, and antibodies in severe cases. Drug interactions and dose adjustments based on kidney function are important considerations with
Congestive heart failure
Congestive heart failure occurs when the heart cannot pump enough blood to meet the body's needs. It is caused by problems with factors that determine cardiac performance like preload, afterload, contractility, and heart rate. Common treatments aim to reduce symptoms by decreasing preload and afterload through drugs like ACE inhibitors, beta blockers, diuretics, and vasodilators. Digoxin and other inotropic drugs are used to improve contractility but have side effects risking toxicity. Managing comorbidities, sodium intake, and activity levels also helps treatment.
Pharmacology of Cardiovascular System 2
Cardiac glycosides are a class of organic compounds that increase the force of heart contractions and decrease heart rate. They act on the sodium-potassium ATPase pump. Digitalis is a genus of plant that contains cardiac glycosides used medicinally to treat heart failure and arrhythmias. Cardenolides contain an enolide ring and are more commonly used than bufadienolides, which contain a dienolide ring. Cardenolides increase intracellular sodium levels, inhibiting calcium export and increasing calcium levels inside cardiac muscle cells for more forceful contractions.
Antihypertensives acting on RAAS
- A 48-year-old male presented with essential hypertension and was prescribed captopril. He returned with a persistent brassy cough.
- Captopril is an ACE inhibitor that works by inhibiting the renin-angiotensin-aldosterone system to lower blood pressure. However, it can cause cough as a side effect by inhibiting the breakdown of bradykinin.
- The patient's cough was likely caused by captopril as a side effect. His blood pressure was now under control, so the doctor would need to consider changing him to an alternative antihypertensive like an ARB that is less likely to cause cough.
Aldersterone
1) Conn syndrome is caused by excessive aldosterone production independent of renin, often due to an adrenal tumor.
2) This leads to sodium retention and expansion of extracellular fluid volume, increasing blood pressure and causing hypertension.
3) Despite volume expansion, edema is absent because increased atrial natriuretic peptide secretion inhibits aldosterone's effects and sodium retention.
4) The pathophysiology involves hypertension from increased cardiac output and blood volume, while ANP prevents further sodium retention and edema formation.
ACUTE MANAGEMENT OF Hyperkalemia
This document discusses hyperkalemia, or high levels of potassium in the blood. It begins by listing the normal potassium range and then describes some common causes of hyperkalemia, including the release of potassium from cells due to conditions like rhabdomyolysis or tumor lysis syndrome, and decreased renal excretion of potassium due to renal failure or medications. Clinical manifestations of hyperkalemia are then outlined, such as weakness, paralysis, arrhythmias, and ECG changes including peaked T waves. The document concludes by presenting two case histories of patients with hyperkalemia and CKD and recommends treatment approaches starting with calcium gluconate for cardiac instability and then other options to increase potassium excretion or remove it through dialysis if
cardiac glycosides
This document provides information on the treatment of congestive heart failure (CHF). It begins by defining CHF as a condition where the heart is unable to pump enough blood to meet the body's needs. It then discusses various contributing diseases and clinical features of CHF. The treatment of CHF involves restoring cardiac performance and arresting disease progression. Positive inotropic drugs discussed include cardiac glycosides like digitalis, beta-adrenergic agonists, phosphodiesterase inhibitors, and calcium sensitizers. Other treatments include diuretics, vasodilators, RAS inhibitors, and beta-blockers. The mechanisms of action and effects of cardiac glycosides like digitalis are explained in detail.
Vasodilators
This document discusses various vasodilators used to treat conditions like hypertension, heart failure, and peripheral vascular disease. It describes different classes of vasodilators including direct-acting vasodilators like calcium channel blockers and drugs that increase cyclic nucleotides, and indirect vasodilators that interfere with the sympathetic nervous system or renin-angiotensin system. Specific vasodilators discussed in detail include nitroglycerin, hydralazine, minoxidil, diazoxide, nitric oxide, and natriuretic peptides. Their mechanisms of action, pharmacological effects, uses, and adverse effect profiles are summarized.
Aldosterone
This document discusses aldosterone, a steroid hormone that regulates electrolyte and fluid balance. It is synthesized in the adrenal cortex and works by increasing sodium absorption and potassium secretion in the kidneys, salivary glands, and gastrointestinal tract. Aldosterone secretion is primarily regulated by angiotensin II through the renin-angiotensin-aldosterone system. This system controls blood pressure by stimulating aldosterone release in response to decreases in blood volume or pressure. Aldosterone antagonists and ACE inhibitors are used to treat hypertension by blocking the effects of aldosterone or inhibiting angiotensin II formation, respectively.
Vasodilators and vasoconstrictors
Vasoactive drugs act on vascular smooth muscle to cause vasoconstriction or vasodilation. Vasoconstrictors such as endothelin, angiotensin II, and ADH cause contraction through increasing calcium levels or sensitivity. Vasodilators such as calcium channel blockers, ACE inhibitors, and nitrates cause relaxation through decreasing calcium, increasing cGMP/cAMP, or inhibiting phosphodiesterases. The vascular endothelium releases various mediators like prostanoids, nitric oxide, and C-type natriuretic peptide that regulate vascular tone. RAAS activation leads to vasoconstriction and sodium retention through angiotensin II, while drugs blocking RAAS cause indirect vasodilation.
Aldosterone by M.Pandian
Introduction
HORMONES OF ADRENAL CORTEX
MINERALOCORTICOIDS
Aldosterone
Life-saving Hormone
Actions of aldosterone
Aldosterone escape or escape phenomenon
Regulation of aldosterone secretion
Renin–angiotensin system
Applied
TISSUE RENIN ANGIOTENSIN SYSTEM
This document discusses newer concepts in the renin-angiotensin-aldosterone system (RAAS), including tissue and cardiac RAAS. It describes how the RAAS was traditionally viewed as circulating in the bloodstream, but is now understood to also exist locally in tissues. Local tissue RAAS can generate angiotensin II independently of circulating RAAS through local synthesis of angiotensinogen and renin. Inhibition of tissue RAAS provides benefits like reducing endothelial dysfunction, vascular damage, and organ damage in the heart and kidneys.
RAAS mbbs
The renin-angiotensin system (RAS) plays a key role in hypertension and other cardiovascular diseases. It involves renin cleaving angiotensinogen to form angiotensin I, which is then cleaved by ACE to form the active peptide angiotensin II. Angiotensin II causes vasoconstriction and sodium retention. RAS inhibitors like ACE inhibitors, ARBs, and direct renin inhibitors are used to treat hypertension and related conditions by blocking the formation or effects of angiotensin II. These drugs effectively lower blood pressure and protect organs but can cause side effects like cough, hypotension, and hyperkalemia.
Hyperkalemia in children
This document discusses hyperkalemia, or high levels of potassium in the blood. It covers the normal physiology of potassium balance in the body, including intake through foods, absorption in the intestines, and excretion primarily through the kidneys under regulation of the hormone aldosterone. Causes of hyperkalemia include reduced kidney function, medications that interfere with potassium excretion, and conditions that cause a shift of potassium out of cells. The document provides details on evaluating, diagnosing, and classifying different severities of hyperkalemia based on serum potassium levels.
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This document discusses potassium levels in the blood and factors that can cause hypokalemia (low potassium) or hyperkalemia (high potassium). It begins by stating the normal range for potassium in blood is 3.5-5 mEq/L. It then provides multiple potential causes for abnormal potassium levels including medications, diet, vomiting/diarrhea, kidney disease, and cellular shifts of potassium between extracellular and intracellular fluid. Mnemonics are also presented to help remember key points. Assessment findings and complications associated with hypo- and hyperkalemia like arrhythmias and muscle weakness are described.
Drugs acting on Renin Angiotensin Aldosterone system
This document discusses drugs that act on the renin-angiotensin-aldosterone system (RAA system). It describes the RAA system and lists the main drug classes: renin inhibitors, ACE inhibitors, angiotensin receptor blockers, and aldosterone antagonists. For each drug class, it covers the mechanism of action, pharmacological effects, clinical uses, and adverse effects. The key drugs discussed are aliskiren, various ACE inhibitors like enalapril and lisinopril, angiotensin receptor blockers like losartan and valsartan, and aldosterone antagonists spironolactone and eplerenone.
Hypokalemia and hyperkalemia indore pedicon 2014 final
This document discusses two case studies of pediatric patients presenting with electrolyte abnormalities. Case 1 involves a 2-year-old boy named Rahul who was brought to the emergency department with diarrhea and dehydration. His lab work showed sodium of 131 mEq/L and potassium of 2 mEq/L, indicating hypokalemia. Case 2 involves a 7-year-old girl named Vinita who was admitted to the PICU for severe diabetic ketoacidosis. Her initial potassium was 4.4 mEq/L but the resident was concerned about potential hyperkalemia with further potassium supplementation. The document then reviews the causes, clinical manifestations, diagnosis, and management of hypo- and hyperkalemia in
Cardiac glycosides
Cardiac glycosides like digoxin are used to treat heart failure and cardiac arrhythmias. They work by inhibiting sodium-potassium ATPase, increasing intracellular calcium levels, and enhancing cardiac contractility. Common side effects include nausea, arrhythmias, and toxicity at high levels. While they were once a standard treatment, newer heart failure drugs like ACE inhibitors, ARBs, beta blockers, and diuretics are now preferred due to their better safety profiles. Digitalis remains an option when symptoms are not adequately controlled by other treatments.
Dihydropyridines effect on Ca Channels
Dihydropyridines can act as both agonists and antagonists of calcium channels. As antagonists, compounds like amlodipine bind to L-type calcium channels in the closed mode 0, preventing opening and thereby decreasing calcium influx, cardiac contractility, and blood pressure. In contrast, the agonist Bay K8644 binds channels in the prolonged open mode 2, increasing calcium influx and having a positive ionotropic effect by enhancing contractility. Thus dihydropyridines demonstrate the ability to modulate calcium channels in both inhibitory and stimulatory fashions depending on the specific compound and its binding properties.
A new perspective on metabolic alkalosis
The document discusses metabolic alkalosis, outlining causes such as hypokalemia, hypomagnesemia, corticosteroid excess, and gastrointestinal or renal hydrogen ion loss. It explains the mechanisms by which these factors can lead to enhanced bicarbonate reabsorption and reduced hydrogen ion secretion in the kidney. Treatment focuses on increasing renal bicarbonate excretion through volume depletion, chloride replacement, and medications like acetazolamide or potassium-sparing diuretics.
Renin angiotensin system
This document discusses drugs that inhibit the renin-angiotensin system for treating hypertension and other conditions. It describes how ACE inhibitors work by inhibiting the angiotensin converting enzyme and decreasing angiotensin II formation, while also increasing bradykinin levels. Angiotensin receptor blockers competitively block the angiotensin II receptor. Both classes lower blood pressure by vasodilation and reduced sodium retention. They are used to treat hypertension, heart failure, diabetic nephropathy, and myocardial infarction. Adverse effects include hypotension, hyperkalemia, and cough with ACE inhibitors.
Renin angiotensin aldosterone- Updates
The document provides an overview of the renin-angiotensin-aldosterone system (RAAS). It discusses the classical components of RAAS including renin, angiotensinogen, angiotensin peptides, angiotensin receptors, and angiotensin converting enzyme. It also covers newer concepts such as local tissue RAAS, intracellular RAAS, receptor heterodimerization, and the roles of angiotensin converting enzyme 2 and angiotensin (1-7). The document highlights functions of RAAS in various organs and pathophysiological processes.
Hyperkalemia
This document discusses hyperkalemia, defined as a plasma potassium level above 5.5 mM. Causes include a shift of potassium from cells to plasma due to factors like acidosis, medications, or tissue breakdown. Symptoms range from cardiac arrhythmias to paralysis. Diagnosis involves blood tests. Treatment involves calcium to stabilize the heart, insulin or beta-agonists to shift potassium into cells, and resins, diuretics or dialysis to remove potassium from the body. The document provides details on treatment options, their mechanisms of action, dosages and cautions.
Drug therapy for Hyperlipoproteinemia
This PPT covers Drug therapy for Hyperlipoproteinemia/ hyperlipidemia. It includes the basic concepts of Lipoproteins like LDL,HDL,VLDL, LDL and Chylomicron. Pharmacotherapy of all hyperlipidemic drugs are covered.
Potassium disorders , comprehensive & practical approach .
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
Ace inhibitors hf
This document discusses the use of ACE inhibitors like lisinopril for the treatment of heart failure. It covers types of heart failure, how the renin-angiotensin-aldosterone system is activated in heart failure and contributes to disease progression, how ACE inhibitors work to inhibit this system, potential drug interactions with medications like Entresto and rifampin, side effects like cough and angioedema, pharmacokinetics of lisinopril, and the importance of monitoring for adverse reactions and assessing other medications when using ACE inhibitors.
Directly acting vasodilators
Directly acting vasodilators include oral and parenteral drugs that act to dilate arteries and veins. Oral vasodilators include hydralazine and minoxidil which increase blood pressure by activating the renin-angiotensin system and sympathetic nervous system. Parenteral vasodilators such as sodium nitroprusside are used for hypertensive emergencies and directly cause vasodilation. These vasodilators are often used with beta blockers and diuretics to prevent reflex tachycardia and fluid retention respectively. Common side effects include headache, flushing, and tachycardia due to increased sympathetic activity.
Duane phchem ppt
The document describes the renin-angiotensin system and its role in regulating blood pressure and cardiovascular function. It discusses key components of the system, such as renin, angiotensin I and II, and angiotensin converting enzyme. It also describes how therapeutic agents have been developed that act on enzymes and receptors in the renin-angiotensin system to treat hypertension and heart failure.
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Drugs used in Heart Failure
1. Heart failure occurs when the heart cannot pump enough blood to meet the body's needs due to issues like hypertension, valve disease, or cardiomyopathy which decrease cardiac output.
2. Therapies for heart failure include diuretics to remove excess salt and water, ACE inhibitors to reduce afterload and fluid retention, and beta blockers to decrease sympathetic stimulation.
3. Digitalis works by inhibiting the sodium-potassium pump, increasing intracellular calcium levels and contractility, but can cause arrhythmias with toxicity. It is used for congestive heart failure and atrial fibrillation.
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This document discusses aldosterone, a steroid hormone that regulates electrolyte and fluid balance. It is synthesized in the adrenal cortex and works by increasing sodium absorption and potassium secretion in the kidneys, salivary glands, and gastrointestinal tract. Aldosterone secretion is primarily regulated by angiotensin II through the renin-angiotensin-aldosterone system. This system controls blood pressure by stimulating aldosterone release in response to decreases in blood volume or pressure. Aldosterone antagonists and ACE inhibitors are used to treat hypertension by blocking the effects of aldosterone or inhibiting angiotensin II formation, respectively.
Vasodilators and vasoconstrictors
Vasoactive drugs act on vascular smooth muscle to cause vasoconstriction or vasodilation. Vasoconstrictors such as endothelin, angiotensin II, and ADH cause contraction through increasing calcium levels or sensitivity. Vasodilators such as calcium channel blockers, ACE inhibitors, and nitrates cause relaxation through decreasing calcium, increasing cGMP/cAMP, or inhibiting phosphodiesterases. The vascular endothelium releases various mediators like prostanoids, nitric oxide, and C-type natriuretic peptide that regulate vascular tone. RAAS activation leads to vasoconstriction and sodium retention through angiotensin II, while drugs blocking RAAS cause indirect vasodilation.
Aldosterone by M.Pandian
Introduction
HORMONES OF ADRENAL CORTEX
MINERALOCORTICOIDS
Aldosterone
Life-saving Hormone
Actions of aldosterone
Aldosterone escape or escape phenomenon
Regulation of aldosterone secretion
Renin–angiotensin system
Applied
TISSUE RENIN ANGIOTENSIN SYSTEM
This document discusses newer concepts in the renin-angiotensin-aldosterone system (RAAS), including tissue and cardiac RAAS. It describes how the RAAS was traditionally viewed as circulating in the bloodstream, but is now understood to also exist locally in tissues. Local tissue RAAS can generate angiotensin II independently of circulating RAAS through local synthesis of angiotensinogen and renin. Inhibition of tissue RAAS provides benefits like reducing endothelial dysfunction, vascular damage, and organ damage in the heart and kidneys.
RAAS mbbs
The renin-angiotensin system (RAS) plays a key role in hypertension and other cardiovascular diseases. It involves renin cleaving angiotensinogen to form angiotensin I, which is then cleaved by ACE to form the active peptide angiotensin II. Angiotensin II causes vasoconstriction and sodium retention. RAS inhibitors like ACE inhibitors, ARBs, and direct renin inhibitors are used to treat hypertension and related conditions by blocking the formation or effects of angiotensin II. These drugs effectively lower blood pressure and protect organs but can cause side effects like cough, hypotension, and hyperkalemia.
Hyperkalemia in children
This document discusses hyperkalemia, or high levels of potassium in the blood. It covers the normal physiology of potassium balance in the body, including intake through foods, absorption in the intestines, and excretion primarily through the kidneys under regulation of the hormone aldosterone. Causes of hyperkalemia include reduced kidney function, medications that interfere with potassium excretion, and conditions that cause a shift of potassium out of cells. The document provides details on evaluating, diagnosing, and classifying different severities of hyperkalemia based on serum potassium levels.
Hypokalemia & Hyperkalemia PPT (2)
This document discusses potassium levels in the blood and factors that can cause hypokalemia (low potassium) or hyperkalemia (high potassium). It begins by stating the normal range for potassium in blood is 3.5-5 mEq/L. It then provides multiple potential causes for abnormal potassium levels including medications, diet, vomiting/diarrhea, kidney disease, and cellular shifts of potassium between extracellular and intracellular fluid. Mnemonics are also presented to help remember key points. Assessment findings and complications associated with hypo- and hyperkalemia like arrhythmias and muscle weakness are described.
Drugs acting on Renin Angiotensin Aldosterone system
This document discusses drugs that act on the renin-angiotensin-aldosterone system (RAA system). It describes the RAA system and lists the main drug classes: renin inhibitors, ACE inhibitors, angiotensin receptor blockers, and aldosterone antagonists. For each drug class, it covers the mechanism of action, pharmacological effects, clinical uses, and adverse effects. The key drugs discussed are aliskiren, various ACE inhibitors like enalapril and lisinopril, angiotensin receptor blockers like losartan and valsartan, and aldosterone antagonists spironolactone and eplerenone.
Hypokalemia and hyperkalemia indore pedicon 2014 final
This document discusses two case studies of pediatric patients presenting with electrolyte abnormalities. Case 1 involves a 2-year-old boy named Rahul who was brought to the emergency department with diarrhea and dehydration. His lab work showed sodium of 131 mEq/L and potassium of 2 mEq/L, indicating hypokalemia. Case 2 involves a 7-year-old girl named Vinita who was admitted to the PICU for severe diabetic ketoacidosis. Her initial potassium was 4.4 mEq/L but the resident was concerned about potential hyperkalemia with further potassium supplementation. The document then reviews the causes, clinical manifestations, diagnosis, and management of hypo- and hyperkalemia in
Cardiac glycosides
Cardiac glycosides like digoxin are used to treat heart failure and cardiac arrhythmias. They work by inhibiting sodium-potassium ATPase, increasing intracellular calcium levels, and enhancing cardiac contractility. Common side effects include nausea, arrhythmias, and toxicity at high levels. While they were once a standard treatment, newer heart failure drugs like ACE inhibitors, ARBs, beta blockers, and diuretics are now preferred due to their better safety profiles. Digitalis remains an option when symptoms are not adequately controlled by other treatments.
Dihydropyridines effect on Ca Channels
Dihydropyridines can act as both agonists and antagonists of calcium channels. As antagonists, compounds like amlodipine bind to L-type calcium channels in the closed mode 0, preventing opening and thereby decreasing calcium influx, cardiac contractility, and blood pressure. In contrast, the agonist Bay K8644 binds channels in the prolonged open mode 2, increasing calcium influx and having a positive ionotropic effect by enhancing contractility. Thus dihydropyridines demonstrate the ability to modulate calcium channels in both inhibitory and stimulatory fashions depending on the specific compound and its binding properties.
A new perspective on metabolic alkalosis
The document discusses metabolic alkalosis, outlining causes such as hypokalemia, hypomagnesemia, corticosteroid excess, and gastrointestinal or renal hydrogen ion loss. It explains the mechanisms by which these factors can lead to enhanced bicarbonate reabsorption and reduced hydrogen ion secretion in the kidney. Treatment focuses on increasing renal bicarbonate excretion through volume depletion, chloride replacement, and medications like acetazolamide or potassium-sparing diuretics.
Renin angiotensin system
This document discusses drugs that inhibit the renin-angiotensin system for treating hypertension and other conditions. It describes how ACE inhibitors work by inhibiting the angiotensin converting enzyme and decreasing angiotensin II formation, while also increasing bradykinin levels. Angiotensin receptor blockers competitively block the angiotensin II receptor. Both classes lower blood pressure by vasodilation and reduced sodium retention. They are used to treat hypertension, heart failure, diabetic nephropathy, and myocardial infarction. Adverse effects include hypotension, hyperkalemia, and cough with ACE inhibitors.
Renin angiotensin aldosterone- Updates
The document provides an overview of the renin-angiotensin-aldosterone system (RAAS). It discusses the classical components of RAAS including renin, angiotensinogen, angiotensin peptides, angiotensin receptors, and angiotensin converting enzyme. It also covers newer concepts such as local tissue RAAS, intracellular RAAS, receptor heterodimerization, and the roles of angiotensin converting enzyme 2 and angiotensin (1-7). The document highlights functions of RAAS in various organs and pathophysiological processes.
Hyperkalemia
This document discusses hyperkalemia, defined as a plasma potassium level above 5.5 mM. Causes include a shift of potassium from cells to plasma due to factors like acidosis, medications, or tissue breakdown. Symptoms range from cardiac arrhythmias to paralysis. Diagnosis involves blood tests. Treatment involves calcium to stabilize the heart, insulin or beta-agonists to shift potassium into cells, and resins, diuretics or dialysis to remove potassium from the body. The document provides details on treatment options, their mechanisms of action, dosages and cautions.
Drug therapy for Hyperlipoproteinemia
This PPT covers Drug therapy for Hyperlipoproteinemia/ hyperlipidemia. It includes the basic concepts of Lipoproteins like LDL,HDL,VLDL, LDL and Chylomicron. Pharmacotherapy of all hyperlipidemic drugs are covered.
Potassium disorders , comprehensive & practical approach .
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
Ace inhibitors hf
This document discusses the use of ACE inhibitors like lisinopril for the treatment of heart failure. It covers types of heart failure, how the renin-angiotensin-aldosterone system is activated in heart failure and contributes to disease progression, how ACE inhibitors work to inhibit this system, potential drug interactions with medications like Entresto and rifampin, side effects like cough and angioedema, pharmacokinetics of lisinopril, and the importance of monitoring for adverse reactions and assessing other medications when using ACE inhibitors.
Directly acting vasodilators
Directly acting vasodilators include oral and parenteral drugs that act to dilate arteries and veins. Oral vasodilators include hydralazine and minoxidil which increase blood pressure by activating the renin-angiotensin system and sympathetic nervous system. Parenteral vasodilators such as sodium nitroprusside are used for hypertensive emergencies and directly cause vasodilation. These vasodilators are often used with beta blockers and diuretics to prevent reflex tachycardia and fluid retention respectively. Common side effects include headache, flushing, and tachycardia due to increased sympathetic activity.
Duane phchem ppt
The document describes the renin-angiotensin system and its role in regulating blood pressure and cardiovascular function. It discusses key components of the system, such as renin, angiotensin I and II, and angiotensin converting enzyme. It also describes how therapeutic agents have been developed that act on enzymes and receptors in the renin-angiotensin system to treat hypertension and heart failure.
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CHF.pptx
Heart failure is a complex clinical syndrome characterized by impaired ventricular performance and exercise intolerance. The primary goals of treatment are to improve symptoms and decrease mortality. There are three categories of drugs used: positively inotropic drugs which increase cardiac contractility, vasodilators which decrease preload and afterload, and diuretics which reduce fluid retention. Antiarrhythmic drugs are also important for treatment and are classified based on their effects on sodium, potassium, or calcium ion channels.
TARGETS THAT CONTROL SPONTANEOUS ACTIVITY.pptx
This document outlines potential new targets for anti-arrhythmic drug therapy that control spontaneous cardiac activity. It discusses ion channels such as hyperpolarization-activated non-selective cation channels and stretch-activated ion channels, as well as calcium handling mechanisms like calcium-calmodulin dependent protein kinase II, the sodium-calcium exchanger, and ryanodine receptors. Specific drugs that target these channels and proteins are also reviewed, including ivabradine for hyperpolarization-activated channels and potential inhibitors of calcium handling targets.
Pharmacologycal approaches of Heart Failure
This document discusses pharmacological approaches for treating heart failure. It describes how heart failure progresses and the sites where drugs can act. The main treatment approaches are positive inotropes like cardiac glycosides to improve contractility, diuretics to reduce edema, and ACE inhibitors to reduce preload and afterload. It then provides details on the mechanisms of action, pharmacokinetics, indications, interactions and side effects of various drug classes used to treat heart failure, including cardiac glycosides, beta agonists, phosphodiesterase inhibitors, diuretics and ACE inhibitors. It also discusses how drugs can modulate cardiac contractility dysfunction at the cellular level.
Cardiac Glycosides and it's side affecte
The document discusses cardiac glycosides, specifically digoxin. It describes digoxin's mechanisms of action, including increasing cardiac contractility and decreasing heart rate. Therapeutic uses include heart failure and arrhythmias. Signs of digoxin toxicity are described. Treatment of digoxin toxicity may include administration of Digibind antibody fragments. Nursing care focuses on monitoring for toxicity and maintaining appropriate electrolyte levels.
Chf
Cardiac glycosides like digoxin are used to treat heart failure. They work by inhibiting the sodium-potassium ATPase pump, increasing intracellular calcium levels and improving cardiac contractility. At therapeutic doses, they have positive inotropic and chronotropic effects as well as autonomic effects like sensitizing baroreceptors. At toxic doses, they can cause arrhythmias by prolonging action potentials and causing delayed afterdepolarizations due to calcium overload. They are beneficial in both acute and chronic heart failure by improving cardiac function and efficiency without increasing oxygen demand.
Recent advances in management of heart failure
Recent advances in management of heart failure
This document discusses recent advances in the management of acute heart failure (AHF), including new drugs that target different pathways. It describes several new drugs that directly activate guanylate cyclase or are natriuretic peptides, such as cinaciguat and chimeric natriuretic peptides, to reduce preload and afterload. It also discusses new drugs that inhibit the renin-angiotensin-aldosterone system pathway or are cardiac myosin activators. Several new inotropes are mentioned, such as istaroxime and stresscopin, that have beneficial effects on both systolic and diastolic function without increasing oxygen demand.
9 cardiac glycosides
This document discusses treatments for congestive heart failure (CHF), focusing on digitalis glycosides and other positive inotropic agents. It provides details on:
- The mechanisms of action and molecular effects of digitalis glycosides, which increase cardiac contractility and output, lowering venous pressure and edema.
- Other positive inotropic drugs used in acute CHF like dobutamine and phosphodiesterase inhibitors.
- Drugs that reduce cardiac preload and edema like diuretics and angiotensin converting enzyme inhibitors, which lower blood pressure and sympathetic tone.
The document explains the benefits, side effects and clinical uses of various CHF drugs in detail through multiple sections and diagrams.
Antianginal drugs.pptx
Define Angina pectoris, its type and causes
Explain mechanism of action of Nitrates, calcium channel blockers and
Beta Blockers?
3. Describe the clinical uses and adverse effects of anti Anginal drugs
4. Explain why the combination of a nitrate with a beta blocker or a calcium blocker may be more effective than either alone
Pharmacological Management of Congestive Heart Failure.pptx
This document summarizes the pharmacological management of congestive heart failure. It describes the major drug classes used including diuretics to reduce fluid retention, ACE inhibitors and beta blockers to improve cardiac function, and inotropic drugs like digoxin to increase contractility. The mechanisms of action and clinical implications of each drug class are explained.
Drugs used in Congestive heart failure
This document provides an overview of drugs used to treat congestive heart failure (CHF). It begins with definitions and classifications of CHF, then describes diagnostic methods. The main treatment strategies and drugs are discussed, including inotropic drugs like digoxin, dobutamine, and dopamine. Renin-angiotensin system inhibitors like ACE inhibitors are also covered. The document provides details on mechanisms of action, pharmacokinetics, uses, interactions, and side effects of common CHF drugs.
Cardiac drugs
The document discusses drugs that affect the cardiovascular system, including their classification and mechanisms of action. Antihypertensive drugs include diuretics, beta blockers, ACE inhibitors, calcium channel blockers, and vasodilators. Antiarrhythmic drugs are classified by the Vaughn-Williams system and work by blocking ion channels involved in cardiac conduction and rhythms. Anticoagulants and antiplatelet drugs help prevent thrombosis.
Renin-Angiotensin Aldeaterone System RAAS
The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system that regulates blood pressure and fluid balance. It involves the release of renin from the kidneys in response to low blood pressure, sodium levels, or sympathetic stimulation. Renin then cleaves angiotensinogen to form angiotensin I and eventually angiotensin II with ACE. Angiotensin II causes vasoconstriction, sodium retention, and aldosterone release to increase blood pressure. ACE inhibitors are used to treat hypertension and heart failure by inhibiting the formation of angiotensin II and reducing RAAS activity.
Cardiac Drugs
The document discusses cardiovascular pharmacology, including drugs that affect the cardiovascular system. It covers topics like electrophysiology, antihypertensives, and hemostatic agents. It describes how the heart requires adequate ATP and calcium to function properly and coordinate electrical stimulation for contractions. It also summarizes the cardiac conduction cycle and discusses drugs that can treat cardiac dysrhythmias and hypertension.
Cardiac drugs
The document discusses drugs that affect the cardiovascular system, including their classification and mechanisms of action. It covers antiarrhythmic drugs classified by the Vaughn-Williams system as well as drugs that affect blood pressure like diuretics, beta blockers, ACE inhibitors, calcium channel blockers, and vasodilators. It also summarizes platelet inhibitors, anticoagulants, and how they interrupt steps in the coagulation cascade.
Cardiac drugs
The document discusses drugs that affect the cardiovascular system, including their classification and mechanisms of action. It covers antihypertensive drugs, drugs for cardiac function and electrophysiology, as well as antiplatelet and anticoagulant drugs. Key topics include the Vaughn-Williams classification system for antiarrhythmics, calcium channel blockers, beta blockers, ACE inhibitors, diuretics, and drugs for hemostasis including aspirin, heparin, warfarin, and thrombolytics.
Similar to Cardiac glycosides, antiarrhythemic drugs-Dr.Jibachha Sah,M.V.Sc,Lecturer (20)
Lecture 9. Cardiotonic and antiarrhythmic drugs.pdf
Lecture 9. Cardiotonic and antiarrhythmic drugs.pdf
Anti-Arrythmic Drugs, (Glycosides, CCBs, B-blockers) by Baqir Naqvi.pptx
Anti-Arrythmic Drugs, (Glycosides, CCBs, B-blockers) by Baqir Naqvi.pptx
Pharmacological Management of Congestive Heart Failure.pptx
Pharmacological Management of Congestive Heart Failure.pptx
More from Dr. Jibachha Sah
The use of fenbendazole in animals
Fenbendazole is a de-wormer medication used in animals. It is available as tablets, boluses, suspensions, powder, and paste. Fenbendazole is used to treat roundworms, pinworms, hookworms, tapeworms, and other parasites in various animals like cattle, horses, pigs, dogs, and cats. The recommended dosages vary depending on the type of parasite and animal. Fenbendazole is generally safe to use but may cause side effects like salivation, vomiting, and diarrhea if an overly high dose is administered. Pregnant animals also require special consideration for fenbendazole treatment.
जनावरहरूमा फेनबेन्डाजोलको प्रयोग (Use of Fenbendazole in animals )
The use of Fenbendazole in animals is an informational document for veterinary practitioner and farmers by Dr.Jibachha Sah
Heart worm disease in dog
Heartworm disease in dogs is caused by a parasite called Dirofilaria immitis transmitted through mosquito bites. Common signs include persistent coughing, reluctance to exercise, fatigue after moderate activity, decreased appetite, weight loss, and swollen belly. Diagnosis involves x-rays to check for enlarged heart, blood tests to detect the parasite, and antigen tests. Treatment consists of medications to kill the parasites along with antibiotics, rest, fluids and supportive care. Regular preventive medication is effective in preventing heartworm infection.
Tick paralysis in dog-Dr.jibachha Sah,M.V.SC
Tick paralysis is a parasitic disease of dogs, neurotoxin causes ascending paralysis. An inspirational note for dog lovers and veterinarians.Also available video on youtube.
Glaucoma in dog a case study-Dr.Jibachha Sah
Glaucoma is a condition that causes a build-up of fluid and pressure in the eye. If too much fluid (called aqueous humor fluid) is made or too little fluid is drained, the pressure of the eye increases and causes damage to the retina and the optic nerve, which ultimately leads to blindness
veterinary laboratory and clinical practice training-Dr.Jibachha Sah
The document provides information about veterinary training programs offered at the Jibachha Veterinary Hospital Research & Training Centre(P)Ltd in Nepal. The training programs include a one-week laboratory training course for NPR 35,000, a one-week poultry disease diagnostic training for NPR 25,000, and a one-week veterinary clinical practice training for NPR 30,000. It also lists contact information for Dr. Jibachha Sah to inquire about the programs.
Anaphylaxis shock due to penicillin-DR.Jibachha Sah
Anaphylaxis shock due to penicillin is a case study for practicing veterinarians and students, who will able to describe the mode of action of prescribing drugs.
The lack of aspiration value in veterinary profession-Dr.Jibachha Sah
The document summarizes research on suicide rates among veterinarians in the United States from 1979 to 2015. A few key points:
- A study found 398 suicide deaths among over 11,000 veterinarians, with 79% of suicides occurring among clinical practitioners. Male veterinarians were 2.1 times and female veterinarians 3.5 times more likely to die by suicide than the general population.
- Clinical practitioners experience approximately double the rates of anxiety, depression, and suicidal thoughts compared to veterinarians in non-clinical roles.
- High debt loads, long work hours, practice management responsibilities, and poor work-life balance are suggested as contributing factors to stress in the profession.
The day never come in your life - Dr.Jibachha Sah
Sachin Tendulkar was dismissed for 43 runs by Australian spinner Brad Hogg during an India-Australia ODI match. After celebrating the wicket of the iconic Indian batsman, Hogg approached Tendulkar for his autograph, thinking it was a career-defining moment. However, in their subsequent 21 matches against each other, Tendulkar committed to improving and dominated Hogg, showing that landmark moments can inspire growth and commitment to excellence.
Possibility within you- Dr.Jibachha Sah
The document discusses Dr. Jibachha Sah's career journey establishing veterinary clinics and hospitals in Nepal over 28 years. It begins with his first private clinic in 1992 after working as a junior technician. Through hard work and dedication, he transformed that clinic into the largest mixed practice private veterinary hospital in Chitwan in 2008. In 2018, he opened a second large hospital in Kathmandu. The document compares his success to John Osteen who converted a feed store into the world's largest church, Lakewood Church in Houston, over 46 years.
Advantage of goal setting-Dr.Jibachha Sah
The advantage of goal setting is an inspirational matter to the young generation. Teach how to goal setting in his life, a case study of Yale University 1952.
Six steps in success -Dr. Jibachha Sah
Six steps of success are my real-life story, that inspire people to how cant get achieved success in life.
You are the self problem - Dr.Jibachha Sah
This document discusses the history of puerperal fever, a bacterial infection that was a major cause of maternal death in Europe in the 1800s. It describes how in 1843, Dr. Oliver Wendell Holmes suggested that physicians were unwittingly spreading the disease between patients due to a lack of hygiene. However, physicians at the time disagreed with this idea. It was not until 1847 when Dr. Ignaz Semmelweis mandated handwashing with chlorinated lime water before patient examinations that the rate of puerperal fever dropped dramatically, demonstrating that physicians were indeed the vector of transmission. The document compares this historical event to the current COVID-19 pandemic and emphasizes the importance of hand washing and other
Future of veterinary profession-Dr.Jibachha Sah
Veterinary professions have a promising future with opportunities in veterinary hospitals and clinics, animal feed and meat industries, poultry and feed industries, and farm animal and dairy industries. There is also potential to create new "blue ocean industries" in veterinary fields. The document promotes a YouTube channel by Dr. Jibachha Sah about the case study of his veterinary hospital.
Five regrets of dying- Dr.Jibachha Sah
This document summarizes the top five regrets of the dying as reported by Bronnie Ware, an Australian nurse. The five regrets are: 1) Not living a life true to oneself and doing what others expected instead. 2) Working too hard and not spending enough time with family. 3) Not expressing feelings to family and letting unhealthy relationships form. 4) Losing touch with family and friends. 5) Not allowing oneself to be happy and following what brings happiness instead of what others think should make one happy. The document encourages living consciously and choosing happiness.
The miracle morning-Dr.Jibachha Sah
Hal Elrod was in a serious car accident in 1999 where his heart stopped for 6 minutes and he fell into a coma. When he awoke 7 days later with 11 fractures, doctors said he would never walk again. However, Hal went on to make a full recovery and become an author and success coach. He developed 6 habits called SAVERS that transformed his life - Silence, Affirmation, Visualization, Exercise, Reading, and Scribing/Writing. These habits are meant to be done every morning before 7am.
Veterinary indigenous medicine-Dr.Jibachha Sah,M.V.Sc,Lecturer
Ethno veterinary medicine or traditional animal health care is based on folk beliefs, traditional knowledge, skills, methods and practices used for curing diseases and maintaining health of animals.
Canine ehrlichiosis - Dr. Jibachha Sah,M.V.Sc,Lecturer
Ehrlichiosis is a tick-borne disease of dogs usually caused by the organism Ehrlichia canis. A lecturer note for B.V. Sc & A.H. Students
Jibachha veterinary case study video-Dr.Jibachha Sah
This document promotes a veterinary educational video posted on a YouTube channel for Jibachha Veterinary Hospital. The video can be freely downloaded for educational purposes and appears to be the first of its kind in Nepal. It focuses on a case study related to veterinary medicine.
Antiseptic and disinfectant-Dr.Jibachha Sah,M.V.Sc,Lecturer,NPI
Antiseptics• These are chemical substances which inhibit the growth or kill micro- organisms on living surfaces such as skin & mucous membrane .Disinfectants are used to kill or eliminate microorganisms and/or inactivate viruses on inanimate objects and surfaces (medical devices, instruments, equipment, walls, floors).
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6快递给客户（国内顺丰国外DHLUPS等快读邮寄）。
教育部文凭学历认证认证的用途：
如果您计划在国内发展那么办理国内教育部认证是必不可少的。事业性用人单位如银行国企公务员在您应聘时都会需要您提供这个认证。其他私营 #外企企业无需提供！办理教育部认证所需资料众多且烦琐所有材料您都必须提供原件我们凭借丰富的经验帮您快速整合材料让您少走弯路。
实体公司专业为您服务如有需要请联系我: 微信176555708
存档可查的(USC毕业证)南加利福尼亚大学毕业证成绩单制做办理
精仿办理南加利福尼亚大学毕业证成绩单（【微信176555708】）毕业证学历认证OFFER专卖国外文凭学历学位证书办理澳洲文凭|澳洲毕业证,澳洲学历认证,澳洲成绩单【微信176555708】 澳洲offer,教育部学历认证及使馆认证永久可查 ,国外毕业证|国外学历认证,国外学历文凭证书 USC毕业证，USC毕业证，USC毕业证，USC毕业证，USC毕业证，USC毕业证【微信176555708】，USC毕业证，专业为留学生办理毕业证、成绩单、使馆留学回国人员证明、教育部学历学位认证、录取通知书、Offer、（留信学历认证永久存档查询）采用学校原版纸张、特殊工艺完全按照原版一比一制作（包括：隐形水印，阴影底纹，钢印LOGO烫金烫银，LOGO烫金烫银复合重叠，文字图案浮雕，激光镭射，紫外荧光，温感，复印防伪）行业标杆！精益求精，诚心合作，真诚制作！多年品质 ,按需精细制作，24小时接单,全套进口原装设备，十五年致力于帮助留学生解决难题，业务范围有加拿大、英国、澳洲、韩国、美国、新加坡，新西兰等学历材料，包您满意。
◆◆◆◆◆ — — — — — — — — 【留学教育】留学归国服务中心 — — — — — -◆◆◆◆◆
【主营项目】
一.毕业证【微信：176555708】成绩单、使馆认证、教育部认证、雅思托福成绩单、学生卡等！
二.真实使馆公证(即留学回国人员证明,不成功不收费)
三.真实教育部学历学位认证（教育部存档！教育部留服网站永久可查）
四.办理各国各大学文凭(一对一专业服务,可全程监控跟踪进度)
如果您处于以下几种情况：
◇在校期间，因各种原因未能顺利毕业……拿不到官方毕业证【微信：176555708】
◇面对父母的压力，希望尽快拿到；
◇不清楚认证流程以及材料该如何准备；
◇回国时间很长，忘记办理；
◇回国马上就要找工作，办给用人单位看；
◇企事业单位必须要求办理的
◇需要报考公务员、购买免税车、落转户口
◇申请留学生创业基金
留信网认证的作用:
1:该专业认证可证明留学生真实身份
2:同时对留学生所学专业登记给予评定
3:国家专业人才认证中心颁发入库证书
4:这个认证书并且可以归档倒地方
5:凡事获得留信网入网的信息将会逐步更新到个人身份内，将在公安局网内查询个人身份证信息后，同步读取人才网入库信息
6:个人职称评审加20分
7:个人信誉贷款加10分→ 【关于价格问题（保证一手价格）
8:在国家人才网主办的国家网络招聘大会中纳入资料，供国家高端企业选择人才
选择实体注册公司办理，更放心，更安全！我们的承诺：可来公司面谈，可签订合同，会陪同客户一起到教育部认证窗口递交认证材料，客户在教育部官方认证查询网站查询到认证通过结果后付款，不成功不收费！
我们所定的价格是非常合理的，而且我们现在做得单子大多数都是代理和回头客户介绍的所以一般现在有新的单子 我给客户的都是第一手的代理价格，因为我想坦诚对待大家 不想跟大家在价格方面浪费时间
对于老客户或者被老客户介绍过来的朋友，我们都会适当给一些优惠。
学历顾问：微信：176555708
重新申请毕业证书(RMIT毕业证)皇家墨尔本理工大学毕业证成绩单精仿办理
不能毕业办理【RMIT毕业证【微信176555708】皇家墨尔本理工大学文凭学历】【微信176555708】【皇家墨尔本理工大学文凭学历证书】【皇家墨尔本理工大学毕业证书与成绩单样本图片】毕业证书补办 Fake Degree做学费单【毕业证明信-推荐信】成绩单，录取通知书，Offer，在读证明，雅思托福成绩单，真实大使馆教育部认证，回国人员证明，留信网认证。网上存档永久可查！全套服务：皇家墨尔本理工大学皇家墨尔本理工大学本科学位证成绩单真实回国人员证明 #真实教育部认证。让您回国发展信心十足#铸就十年品质！信誉！实体公司！可以视频看办公环境样板如需办理真实可查可以先到公司面谈勿轻信小中介黑作坊！
可以提供皇家墨尔本理工大学钢印 #水印 #烫金 #激光防伪 #凹凸版 #最新版的毕业证 #百分之百让您绝对满意
印刷DHL快递毕业证 #成绩单7个工作日真实大使馆教育部认证1个月。为了达到高水准高效率
请您先以qq或微信的方式对我们的服务进行了解后如果有皇家墨尔本理工大学皇家墨尔本理工大学本科学位证成绩单帮助再进行电话咨询。
国外毕业证学位证成绩单如何办理：
1客户提供办理信息：姓名生日专业学位毕业时间等（如信息不确定可以咨询顾问：我们有专业老师帮你查询）；
2开始安排制作皇家墨尔本理工大学毕业证成绩单电子图；
3毕业证成绩单电子版做好以后发送给您确认；
4毕业证成绩单电子版您确认信息无误之后安排制作成品；
5成品做好拍照或者视频给您确认；
6快递给客户（国内顺丰国外DHLUPS等快读邮寄）。
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Discover the benefits of outsourcing SEO to India
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快速办理(新加坡SMU毕业证书)新加坡管理大学毕业证文凭证书一模一样
学校原件一模一样【微信：741003700 】《(新加坡SMU毕业证书)新加坡管理大学毕业证文凭证书》【微信：741003700 】学位证，留信认证（真实可查，永久存档）原件一模一样纸张工艺/offer、雅思、外壳等材料/诚信可靠,可直接看成品样本，帮您解决无法毕业带来的各种难题！外壳，原版制作，诚信可靠，可直接看成品样本。行业标杆！精益求精，诚心合作，真诚制作！多年品质 ,按需精细制作，24小时接单,全套进口原装设备。十五年致力于帮助留学生解决难题，包您满意。
本公司拥有海外各大学样板无数，能完美还原。
1:1完美还原海外各大学毕业材料上的工艺：水印，阴影底纹，钢印LOGO烫金烫银，LOGO烫金烫银复合重叠。文字图案浮雕、激光镭射、紫外荧光、温感、复印防伪等防伪工艺。材料咨询办理、认证咨询办理请加学历顾问Q/微741003700
【主营项目】
一.毕业证【q微741003700】成绩单、使馆认证、教育部认证、雅思托福成绩单、学生卡等！
二.真实使馆公证(即留学回国人员证明,不成功不收费)
三.真实教育部学历学位认证（教育部存档！教育部留服网站永久可查）
四.办理各国各大学文凭(一对一专业服务,可全程监控跟踪进度)
如果您处于以下几种情况：
◇在校期间，因各种原因未能顺利毕业……拿不到官方毕业证【q/微741003700】
◇面对父母的压力，希望尽快拿到；
◇不清楚认证流程以及材料该如何准备；
◇回国时间很长，忘记办理；
◇回国马上就要找工作，办给用人单位看；
◇企事业单位必须要求办理的
◇需要报考公务员、购买免税车、落转户口
◇申请留学生创业基金
留信网认证的作用:
1:该专业认证可证明留学生真实身份
2:同时对留学生所学专业登记给予评定
3:国家专业人才认证中心颁发入库证书
4:这个认证书并且可以归档倒地方
5:凡事获得留信网入网的信息将会逐步更新到个人身份内，将在公安局网内查询个人身份证信息后，同步读取人才网入库信息
6:个人职称评审加20分
7:个人信誉贷款加10分
8:在国家人才网主办的国家网络招聘大会中纳入资料，供国家高端企业选择人才
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假文凭国外(Adelaide毕业证)澳大利亚国立大学毕业证成绩单办理
购买澳大利亚国立大学毕业证>【微信176555708】办理澳大利亚国立大学毕业证成绩单【微信176555708】Adelaide毕业证成绩单Adelaide学历证书Adelaide文凭【Adelaide毕业套号文凭网认证澳大利亚国立大学毕业证成绩单】【哪里买澳大利亚国立大学毕业证文凭Adelaide成绩学校快递邮寄信封】【开版澳大利亚国立大学文凭】Adelaide留信认证本科硕士学历认证(诚招代理)微信：176555708办理国外高校毕业证成绩单文凭学位证,真实使馆公证（留学回国人员证明）真实留信网认证国外学历学位认证雅思代考国外学校代申请名校保录开请假条改GPA改成绩ID卡
1.高仿业务:【本科硕士】毕业证,成绩单（GPA修改）,学历认证（教育部认证）,大学Offer,,ID,留信认证,使馆认证,雅思,语言证书等高仿类证书；
2.认证服务: 学历认证（教育部认证）,大使馆认证（回国人员证明）,留信认证（可查有编号证书）,大学保录取,雅思保分成绩单。
3.技术服务：钢印水印烫金激光防伪凹凸版设计印刷激凸温感光标底纹镭射速度快。
办理澳大利亚国立大学澳大利亚国立大学毕业证成绩单流程：
1客户提供办理信息：姓名生日专业学位毕业时间等（如信息不确定可以咨询顾问：我们有专业老师帮你查询）；
2开始安排制作毕业证成绩单电子图；
3毕业证成绩单电子版做好以后发送给您确认；
4毕业证成绩单电子版您确认信息无误之后安排制作成品；
5成品做好拍照或者视频给您确认；
6快递给客户（国内顺丰国外DHLUPS等快读邮寄）
-办理真实使馆公证（即留学回国人员证明）
-办理各国各大学文凭（世界名校一对一专业服务,可全程监控跟踪进度）
-全套服务：毕业证成绩单真实使馆公证真实教育部认证。让您回国发展信心十足！
（详情请加一下 文凭顾问+微信:176555708）欢迎咨询！
可查真实(Monash毕业证)西澳大学毕业证成绩单退学买
办理假西澳大学毕业证【微信176555708】购买,办理Monash成绩单,Monash毕业证制作【微信176555708】【西澳大学毕业证】，Monash毕业证购买，Monash学位证，西澳大学学位证【Monash成绩单制作】【Monash毕业证文凭 Monash本科 澳洲学历认证原版制作【diploma certificate degree transcript 】【留信网认证，本科，硕士，海归，博士，排名，成绩单】代办国外（海外）澳洲、韩国、加拿大、新西兰等各大学毕业证。 ?我们对海外大学及学院的毕业证成绩单所使用的材料，尺寸大小，防伪结构（包括：水印，阴影底纹，钢印LOGO烫金烫银，LOGO烫金烫银复合重叠。 文字图案浮雕，激光镭射，紫外荧光，温感，复印防伪）都有原版本文凭对照。#一整套西澳大学文凭证件办理#—包含西澳大学西澳大学毕业证成绩单学历认证|使馆认证|归国人员证明|教育部认证|留信网认证永远存档教育部学历学位认证查询办理国外文凭国外学历学位认证#我们提供全套办理服务。
一整套留学文凭证件服务：
一：西澳大学西澳大学毕业证成绩单毕业证 #成绩单等全套材料从防伪到印刷水印底纹到钢印烫金
二：真实使馆认证（留学人员回国证明）使馆存档
三：真实教育部认证教育部存档教育部留服网站永久可查
四：留信认证留学生信息网站永久可查
国外毕业证学位证成绩单办理方法：
1客户提供办理西澳大学西澳大学毕业证成绩单信息：姓名生日专业学位毕业时间等（如信息不确定可以咨询顾问：我们有专业老师帮你查询）；
2开始安排制作毕业证成绩单电子图；
3毕业证成绩单电子版做好以后发送给您确认；
4毕业证成绩单电子版您确认信息无误之后安排制作成品；
5成品做好拍照或者视频给您确认；
6快递给客户（国内顺丰国外DHLUPS等快读邮寄）。
教育部文凭学历认证认证的用途：
如果您计划在国内发展那么办理国内教育部认证是必不可少的。事业性用人单位如银行国企公务员在您应聘时都会需要您提供这个认证。其他私营 #外企企业无需提供！办理教育部认证所需资料众多且烦琐所有材料您都必须提供原件我们凭借丰富的经验帮您快速整合材料让您少走弯路。
实体公司专业为您服务如有需要请联系我: 微信176555708
Gen Z and the marketplaces - let's translate their needs
The product workshop focused on exploring the requirements of Generation Z in relation to marketplace dynamics. We delved into their specific needs, examined the specifics in their shopping preferences, and analyzed their preferred methods for accessing information and making purchases within a marketplace. Through the study of real-life cases , we tried to gain valuable insights into enhancing the marketplace experience for Generation Z.
The workshop was held on the DMA Conference in Vienna June 2024.
留学挂科(UofM毕业证)明尼苏达大学毕业证成绩单复刻办理
精仿办理明尼苏达大学学历证书＜176555708微信＞【毕业证明信-推荐信做学费单＞【微信176555708】【制作UofM毕业证文凭认证明尼苏达大学毕业证成绩单购买】【UofM毕业证书】{明尼苏达大学文凭购买}】成绩单，录取通知书，Offer，在读证明，雅思托福成绩单，真实大使馆教育部认证，回国人员证明，＞【制作UofM毕业证文凭认证明尼苏达大学毕业证成绩单购买】【UofM毕业证书】{明尼苏达大学文凭购买}留信网认证。
明尼苏达大学学历证书＜微信176555708（一对一服务包括毕业院长签字,专业课程,学位类型,专业或教育领域,以及毕业日期.不要忽视这些细节.这两份文件同样重要!毕业证成绩单文凭留信网学历认证！）（留信学历认证永久存档查询）采用学校原版纸张、特殊工艺完全按照原版一比一制作（包括：隐形水印，阴影底纹，钢印LOGO烫金烫银，LOGO烫金烫银复合重叠，文字图案浮雕，激光镭射，紫外荧光，温感，复印防伪）行业标杆！精益求精，诚心合作，真诚制作！多年品质 ,按需精细制作，24小时接单,全套进口原装设备，十五年致力于帮助留学生解决难题，业务范围有加拿大、英国、澳洲、韩国、美国、新加坡，新西兰等学历材料，包您满意。
◆◆◆◆◆ — — — — — — — — 【留学教育】留学归国服务中心 — — — — — -◆◆◆◆◆
【主营项目】
一.毕业证【微信：176555708】成绩单、使馆认证、教育部认证、雅思托福成绩单、学生卡等！
二.真实使馆公证(即留学回国人员证明,不成功不收费)
三.真实教育部学历学位认证（教育部存档！教育部留服网站永久可查）
四.办理各国各大学文凭(一对一专业服务,可全程监控跟踪进度)
如果您处于以下几种情况：
◇在校期间，因各种原因未能顺利毕业……拿不到官方毕业证【微信：176555708】
◇面对父母的压力，希望尽快拿到；
◇不清楚认证流程以及材料该如何准备；
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我们所定的价格是非常合理的，而且我们现在做得单子大多数都是代理和回头客户介绍的所以一般现在有新的单子 我给客户的都是第一手的代理价格，因为我想坦诚对待大家 不想跟大家在价格方面浪费时间
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留信网认证的作用:
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3:国家专业人才认证中心颁发入库证书
4:这个认证书并且可以归档倒地方
5:凡事获得留信网入网的信息将会逐步更新到个人身份内，将在公安局网内查询个人身份证信息后，同步读取人才网入库信息
6:个人职称评审加20分
7:个人信誉贷款加10分
8:在国家人才网主办的国家网络招聘大会中纳入资料，供国家高端企业选择人才
留学学历(UoA毕业证)奥克兰大学毕业证成绩单官方原版办理
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Gen Z and the marketplaces - let's translate their needs
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Cardiac glycosides, antiarrhythemic drugs-Dr.Jibachha Sah,M.V.Sc,Lecturer
- 1. Cardiac glycosides, antiarrhythemic drugs Dr.Jibachha Sah M.V.Sc (Pharmacology) College of veterinary Science,NPI, Bhojard,Chitwan
- 2. Introduction Cardiac glycosides are a class of organic compounds that increase the output force of the heart and increase its rate of contractions by acting on the cellular sodium-potassium ATPase pump Their beneficial medical uses are as treatments for congestive heart failure and cardiac arrhythmias.
- 3. Mechanism of action of cardiac glycosides Cellular mechanism of action of cardiac glycosides. It has long been known that cardiac glycosides can inhibit the membrane sodium-potassium (Na+-K+) pump, raising intracellular Na+. Digitalis and its derivatives such as digoxin and digitoxin are cardiac glycosides used typically in the therapy of congestive heart failure and atrial fibrillation. Cardiac glycosides are found in a diverse group of plants including Digitalis purpurea and Digitalis lanata (foxgloves), Nerium oleander ...
- 4. Biochemical Mechanism of Action The mechanism whereby cardiac glycosides cause a positive inotropic effect and electrophysiologic changes is still not completely clear. Several mechanisms have been proposed, but the most widely accepted involves the ability of cardiac glycosides to inhibit the membrane bound Na+-K+-ATPase pump responsible for Na+-K+ exchange.
- 5. The process of muscle contraction can be pictured as shown below.
- 6. The process of membrane depolarization / repolarization is controlled by the movement of three cations, Na+, Ca+2, and K+, in and out of the cell. the resting stage, the concentration of Na+ is high on the outside. On membrane depolarization sodium fluxes-in leading to an immediate elevation of the action potential. Elevated intracellular Na+ triggers the influx of free of Ca++ that occurs more slowly. The higher intracellular [Ca++] results in the efflux of K+. The reestablishment of the action potential occurs later by the reverse of the Na+-K+ exchange. The Na+ / K+ exchange requires energy which is provided by an enzyme Na+-K+-ATPase. Cardiac glycosides are proposed to inhibit this enzyme with a net result of reduced sodium exchange with potassium that leaves increased intracellular Na+. This results in increased intracellular [Ca++]. Elevated intracellular calcium concentration triggers a series of intracellular biochemical events that ultimately result in an increase in the force of the myocardial contraction or a positive inotropic effect.
- 12. Class IB antiarrhythmics •Weak blockade of Na+ channels (fast association/dissociation) •Shorten AP duration (left shift) → slow ERP •Strongest effect on ischemic myocardium •Lidocaine •Mexiletin Class Drug group •Main mechanism of action •Examples Class I antiarrhythmic drugs •Fast sodium channel blockers •Inhibit conduction velocity(negative dromotropy), part icularly in depolarized tissue (e.g., during tachycardia ) •Moderate blockade of Na+ channels(interme diate Quinidine Procainamide Disopyramide Ajmalin Antiarrhythemic drugs
- 13. Class IC antiarrhythmics •Strong blockade of Na+ channels (slow association/dissociation) → QRS prolongation •No to minimal effect on AP duration (no shift) → ERP unaffected •Flecainide •Propafenone Class II antiarrhythmic drugs •Beta blocker •Inhibit β- adrenergic activation of adenylate cyclase →↓ cAMP → ↓ Ca 2+ •Decrease slope of phase 4 in pacemaker cells, leading to a slower conduction velocity •Metoprolol •Esmolol •Propranolol •Atenolol •Timolol •Carvedilol •Sotalo
- 14. Class III antiarrhythmic drugs •Potassium channel blocker •Inhibit potassium delayed r ectifier currents •Prolongs AP duration (Reverse use-dependence) and effective refractory period (ERP) •No effect on conduction velocity •Amiodarone •Dronedarone •Sotalol •Bretylium •Ibutilide •Dofetilide lass IV antiarrhythmic drugs •Calcium channel blocker •Inhibit slow calcium channels •Decrease slope of phase 0 and 4 → slower conduction velocity •Prolong repolarization of AV node •Decreasing conduction velocity leads to •Verapamil •Diltiazem •Nifedipine
- 15. Class V antiarrhythmic drugs •Variable mechanisms •See section on “Other antiarrhythmic drugs” below for details. •Adenosine •Digoxin •Magnesium sulfate