This is a comprehensive approach to a hypertensive patient presenting to the emergency department.
Discussing:-
- Hypertensive emergency
- Hypertensive Urgency
- Hypertensive Crisis
- Hypertensive encephalopathy and retinopathy
- Accelerated Hypertension
- Malignant hypertension
Hepatic encephalopathy occurs when the liver fails to detoxify toxic substances, such as ammonia, which are then able to pass into the brain. This causes neurological symptoms ranging from mild confusion to coma. Precipitating factors include gastrointestinal bleeding, infections, and certain drugs. Treatment focuses on reducing ammonia production in the gut through lactulose, antibiotics, and low-protein diets. Correcting electrolyte imbalances and removing precipitating medications or infections are also important for management of hepatic encephalopathy.
This document discusses hypertensive crises, including definitions, epidemiology, pathophysiology, assessment, diagnosis, and management. It defines hypertensive emergencies as elevated blood pressure with acute end-organ damage, while hypertensive urgencies involve impending end-organ damage. The typical patient presenting with crisis is middle-aged, noncompliant with medications, and may use substances. Treatment of emergencies requires immediate blood pressure reduction in the ICU to prevent further damage, while urgencies can be treated gradually as uncontrolled hypertension. Nitroprusside is very effective but has limitations like toxicity risks with prolonged use.
This document provides an overview of the management of hypertensive crisis. It begins with definitions of hypertensive urgency and emergency. It then covers etiology, pathophysiology, clinical evaluation, workup, and management. The goals of management are to lower blood pressure gradually in hypertensive urgencies, and more rapidly in emergencies to prevent end organ damage, while avoiding too rapid a drop in pressure. Drugs discussed for acute treatment include sodium nitroprusside, nicardipine, clevidipine, labetalol, and esmolol. Special scenarios like myocardial ischemia and aortic dissection are also addressed.
This document discusses hemorrhagic stroke, including intracerebral and subarachnoid hemorrhage. Intracerebral hemorrhage is caused by bleeding into the brain tissue and accounts for 10-15% of strokes. It has high mortality, especially if the patient is in a coma. Subarachnoid hemorrhage is caused by bleeding into the subarachnoid space, often due to ruptured aneurysms. Both require imaging like CT or MRI to diagnose and determine treatment, which may include surgery to remove hematomas or clip aneurysms. Complications include cerebral vasospasm, rebleeding, and hydrocephalus. Secondary stroke prevention focuses on controlling risk factors and treating
Hypertensive emergencies require immediate blood pressure reduction to prevent end organ damage. They are characterized by severely elevated blood pressure and signs of acute target organ injury. The goal is to lower mean arterial pressure by 20-25% within minutes to hours using intravenous antihypertensive drugs like sodium nitroprusside. Hypertensive urgencies also involve severely high blood pressure but without acute organ injury, allowing for oral drugs to safely lower blood pressure within 24 hours. Rapid blood pressure reduction is avoided to prevent hypotension in both conditions.
Hepatic Encephalopathy -Pathophysiology,Evaluation And ManagementSantosh Narayankar
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunting. It presents as a wide range of neurological or psychiatric abnormalities from mild alterations to coma. The prevalence is 30-40% in those with cirrhosis and risk of first episode is 5-25% within 5 years of cirrhosis diagnosis. Recurrence risk after an initial episode is 40% within 1 year. Ammonia, systemic inflammation, manganese, genetics, and oxidative stress may all contribute to pathogenesis. Diagnosis involves clinical exam and testing like serum ammonia levels or neuropsychological tests on phone apps. Management involves treating precipitating factors, lactulose, antibiotics like rifaximin, and
This document provides a clinical review of diabetic ketoacidosis (DKA) in adults. It begins with an introduction to DKA, defining it as a state of insulin deficiency causing extreme metabolic changes. It then covers diagnosis, epidemiology, pathophysiology, etiology, clinical presentation, laboratory evaluation, management, complications, topics for discussion, and references. The management section outlines the key treatment approach of correcting fluid loss, hyperglycemia, electrolyte disturbances, and acid-base balance primarily through intravenous fluids and insulin therapy. Controversies discussed include whether to use arterial or venous blood gases, the use of bicarbonate therapy, and choice of intravenous fluids.
1. The document discusses hypertensive emergencies and urgencies, their causes, manifestations, evaluation, and management.
2. Initial evaluation involves assessing for target organ damage by examining cardiovascular, neurological, and renal systems. Laboratory tests and imaging help identify secondary causes and end-organ effects.
3. Intravenous antihypertensives like sodium nitroprusside, nicardipine, and labetalol are used to lower blood pressure in hypertensive emergencies to prevent further organ damage, while oral medications are preferred for urgencies.
Hepatic encephalopathy occurs when the liver fails to detoxify toxic substances, such as ammonia, which are then able to pass into the brain. This causes neurological symptoms ranging from mild confusion to coma. Precipitating factors include gastrointestinal bleeding, infections, and certain drugs. Treatment focuses on reducing ammonia production in the gut through lactulose, antibiotics, and low-protein diets. Correcting electrolyte imbalances and removing precipitating medications or infections are also important for management of hepatic encephalopathy.
This document discusses hypertensive crises, including definitions, epidemiology, pathophysiology, assessment, diagnosis, and management. It defines hypertensive emergencies as elevated blood pressure with acute end-organ damage, while hypertensive urgencies involve impending end-organ damage. The typical patient presenting with crisis is middle-aged, noncompliant with medications, and may use substances. Treatment of emergencies requires immediate blood pressure reduction in the ICU to prevent further damage, while urgencies can be treated gradually as uncontrolled hypertension. Nitroprusside is very effective but has limitations like toxicity risks with prolonged use.
This document provides an overview of the management of hypertensive crisis. It begins with definitions of hypertensive urgency and emergency. It then covers etiology, pathophysiology, clinical evaluation, workup, and management. The goals of management are to lower blood pressure gradually in hypertensive urgencies, and more rapidly in emergencies to prevent end organ damage, while avoiding too rapid a drop in pressure. Drugs discussed for acute treatment include sodium nitroprusside, nicardipine, clevidipine, labetalol, and esmolol. Special scenarios like myocardial ischemia and aortic dissection are also addressed.
This document discusses hemorrhagic stroke, including intracerebral and subarachnoid hemorrhage. Intracerebral hemorrhage is caused by bleeding into the brain tissue and accounts for 10-15% of strokes. It has high mortality, especially if the patient is in a coma. Subarachnoid hemorrhage is caused by bleeding into the subarachnoid space, often due to ruptured aneurysms. Both require imaging like CT or MRI to diagnose and determine treatment, which may include surgery to remove hematomas or clip aneurysms. Complications include cerebral vasospasm, rebleeding, and hydrocephalus. Secondary stroke prevention focuses on controlling risk factors and treating
Hypertensive emergencies require immediate blood pressure reduction to prevent end organ damage. They are characterized by severely elevated blood pressure and signs of acute target organ injury. The goal is to lower mean arterial pressure by 20-25% within minutes to hours using intravenous antihypertensive drugs like sodium nitroprusside. Hypertensive urgencies also involve severely high blood pressure but without acute organ injury, allowing for oral drugs to safely lower blood pressure within 24 hours. Rapid blood pressure reduction is avoided to prevent hypotension in both conditions.
Hepatic Encephalopathy -Pathophysiology,Evaluation And ManagementSantosh Narayankar
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunting. It presents as a wide range of neurological or psychiatric abnormalities from mild alterations to coma. The prevalence is 30-40% in those with cirrhosis and risk of first episode is 5-25% within 5 years of cirrhosis diagnosis. Recurrence risk after an initial episode is 40% within 1 year. Ammonia, systemic inflammation, manganese, genetics, and oxidative stress may all contribute to pathogenesis. Diagnosis involves clinical exam and testing like serum ammonia levels or neuropsychological tests on phone apps. Management involves treating precipitating factors, lactulose, antibiotics like rifaximin, and
This document provides a clinical review of diabetic ketoacidosis (DKA) in adults. It begins with an introduction to DKA, defining it as a state of insulin deficiency causing extreme metabolic changes. It then covers diagnosis, epidemiology, pathophysiology, etiology, clinical presentation, laboratory evaluation, management, complications, topics for discussion, and references. The management section outlines the key treatment approach of correcting fluid loss, hyperglycemia, electrolyte disturbances, and acid-base balance primarily through intravenous fluids and insulin therapy. Controversies discussed include whether to use arterial or venous blood gases, the use of bicarbonate therapy, and choice of intravenous fluids.
1. The document discusses hypertensive emergencies and urgencies, their causes, manifestations, evaluation, and management.
2. Initial evaluation involves assessing for target organ damage by examining cardiovascular, neurological, and renal systems. Laboratory tests and imaging help identify secondary causes and end-organ effects.
3. Intravenous antihypertensives like sodium nitroprusside, nicardipine, and labetalol are used to lower blood pressure in hypertensive emergencies to prevent further organ damage, while oral medications are preferred for urgencies.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
This document provides information on hypertensive emergencies and urgencies, including their classification, evaluation, and management. It defines hypertensive emergencies as severe hypertension with evidence of acute target organ damage, while urgencies involve severe hypertension without organ damage. For emergencies, rapid parenteral treatment is needed to stop organ damage progression while avoiding hypoperfusion. Several parenteral agents are discussed for specific conditions along with their dosing and side effects. The goal is to lower blood pressure gradually to avoid complications. Hypertensive urgencies can often be treated orally as outpatients after initial control.
The document discusses pulmonary embolism (PE), which is a blockage in the pulmonary artery caused by blood clots that travel from deep veins. It covers the definition, sources, risk factors including Virchow's triad, pathogenesis, clinical presentation, differential diagnosis, investigations such as D-dimer and imaging tests, and management including anticoagulation, thrombolytic therapy, and prevention through prophylaxis. The management section also describes emergency resuscitation, thrombolysis to relieve obstruction, heparin therapy, warfarin therapy over 3-6 months, vena cava filters for recurrent cases, and embolectomy for massive PE.
The document discusses acute kidney injury (AKI), including its causes, diagnosis, and management. It provides details on prerenal, intrinsic, and postrenal forms of AKI. For prerenal AKI, management focuses on correcting the underlying cause, such as volume depletion, and restoring intravascular volume through fluid resuscitation. For intrinsic AKI, identifying and removing nephrotoxic agents is important. Dialysis may be needed for severe AKI with fluid/electrolyte imbalance or uremia.
1. Pericarditis is inflammation of the pericardium and is usually caused by viral or bacterial infections. It can occur acutely or become chronic.
2. The main symptoms are sudden onset of sharp chest pain that worsens with breathing or coughing. A pericardial friction rub may also be heard on examination.
3. Treatment focuses on relieving pain and inflammation, usually with NSAIDs. Corticosteroids may be used for refractory cases or certain causes like connective tissue diseases.
This document discusses acute heart failure, including its definition, causes, clinical presentations, and pathophysiology. Acute heart failure is rapid onset heart failure that can occur with or without previous cardiac disease. It is often life-threatening and requires urgent treatment. The patient may present with acute decompensated heart failure, hypertensive acute heart failure, pulmonary edema, cardiogenic shock, or high output failure. The pathophysiology involves a vicious cycle where the heart cannot maintain sufficient cardiac output to meet demands, leading to further worsening if not treated.
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by conditions present at birth like hypoplastic left heart syndrome. Symptoms include poor weight gain, fast breathing, and edema. Diagnosis involves chest x-ray, electrocardiogram, echocardiogram, and sometimes cardiac catheterization. Treatment focuses on underlying causes, medications to control symptoms like diuretics and digoxin, and surgery when possible to correct structural heart defects.
Infective endocarditis is a microbial infection of the heart valves or endocardium. It typically involves the valves and can be caused by many pathogens. The most common causes are streptococci, staphylococci, and enterococci. Untreated infective endocarditis has a high fatality rate. The pathogenesis involves endothelial damage, platelet-fibrin deposition forming nonbacterial thrombotic endocarditis (NBTE), and microbial colonization of the NBTE resulting in bacterial vegetations. Local effects include valvular damage, abscesses, fistulae, and conduction abnormalities. Distant effects occur via septic emboli that can lodge in organs like the brain, lungs,
The document discusses hypertensive emergencies, which are acute, severe elevations in blood pressure that can cause target organ damage. It notes key risk factors and various potential causes. It outlines goals for lowering blood pressure during hypertensive emergencies, which depend on the specific target organ(s) affected and time since presentation. Common medications used for treatment are discussed along with their indications and special considerations. Treatment goals differ for conditions like pregnancy, stroke, and aortic dissection. The importance of determining whether target organ damage is present and tailoring treatment accordingly is emphasized.
- Status epilepticus has a worldwide incidence of 3.8 to 38 per 100,000 people per year, with peaks in children and the elderly. Around 31-44% of cases are refractory to initial treatment.
- Initial treatment involves benzodiazepines like lorazepam or diazepam. If seizures continue, second-line drugs like phenytoin, fosphenytoin, or valproate are used.
- Refractory status epilepticus is defined as failure to control seizures with benzodiazepines and other antiepileptics. It requires general anesthesia with drugs like propofol, thiopental, or midazolam along with
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
This document discusses hemorrhagic stroke, specifically intracerebral hemorrhage. It defines intracerebral hemorrhage as bleeding within the brain tissue itself, accounting for 15% of strokes. Risk factors include hypertension and amyloid angiopathy. Clinical presentation includes sudden onset of focal neurological deficits like weakness or seizures. Diagnostics include CT scans. Prognosis is poor with 50% mortality at 1 year. Management focuses on controlling blood pressure, treating increased intracranial pressure, preventing seizures and infections. Surgical options include removing the hemorrhage via aspiration or craniotomy. Subarachnoid hemorrhage is also discussed as bleeding into the subarachnoid space, often from
This document summarizes chronic liver disease and cirrhosis. It describes cirrhosis as scarring of the liver caused by chronic liver disease leading to loss of liver function. Common causes include alcohol, hepatitis B/C, NASH, and genetic disorders. Complications include ascites, variceal bleeding, hepatic encephalopathy, hepatorenal syndrome, and hepatocellular carcinoma. Management involves treating the underlying cause, vaccinations, diuretics, banding/TIPS for varices, lactulose for encephalopathy, and liver transplantation for late stage disease.
Myocarditis is an inflammatory disease of the heart muscle that can be caused by infectious or non-infectious triggers. It has a variable clinical presentation ranging from mild symptoms to life-threatening conditions. The diagnosis is challenging due to the heterogeneity of symptoms but can involve electrocardiogram, cardiac biomarkers, echocardiogram, cardiac MRI and endomyocardial biopsy. About half of acute cases resolve in 2-4 weeks but some develop heart failure or arrhythmias. Treatment focuses on supporting heart function and managing symptoms while the disease runs its course.
Pulmonary hypertension is an abnormal elevation in pulmonary artery pressure. It is classified into 5 groups based on underlying causes. Group 1 includes pulmonary arterial hypertension which is characterized by pre-capillary pulmonary hypertension in the absence of other causes. Molecular abnormalities in pulmonary arterial hypertension include decreased prostacyclin and nitric oxide, and increased endothelin-1. Genetic mutations like in the BMPR2 gene are also associated. Idiopathic pulmonary arterial hypertension has no known cause. Symptoms include fatigue, chest pain and syncope with exertion. Signs include increased pulmonary component of heart sound and murmurs.
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
Rheumatic fever is an autoimmune disease that can develop as a result of a streptococcal throat infection. It causes inflammation of the heart, joints, brain, and skin. The disease is most common in children ages 5-15 in developing countries. It is diagnosed using the Modified Jones Criteria which looks for major criteria like heart inflammation, arthritis, subcutaneous nodules, and minor criteria like fever and joint pain along with evidence of a prior streptococcal infection. Treatment involves antibiotics to treat the infection as well as medications for symptoms while long term prevention relies on regular antibiotics.
Malignant hypertension is a rare but serious form of high blood pressure characterized by a sudden onset of very high blood pressure along with damage to the eyes and kidneys. It occurs when blood pressure in the arteries rises quickly to severely high levels, with diastolic pressure often over 130 mmHg. Common causes include essential hypertension, kidney disease, and pregnancy-related issues. Symptoms may include blurred vision, chest pain, seizures, reduced urine output, and headaches. Diagnosis involves examining physical signs of organ damage and testing for complications affecting the eyes, kidneys, heart, and brain. Treatment aims to lower blood pressure gradually over hours to days to avoid dangerous drops, using short-acting intravenous drugs like nitroprusside
Hypertension Emergencies and their managementpptxUzomaBende
This Presentation talks about Hyprtension, the mode of presentation of hypertensive crisis and the effective management of hypertensive crisis to prevent case fatalities.
This document discusses accelerated hypertension and provides information on defining and classifying hypertension. It begins by defining hypertension as a blood pressure of 140/90 mmHg or higher. It then discusses classifying hypertension based on severity from prehypertension to stage 1 and 2 hypertension. The document notes accelerated hypertension is associated with a rapid rise in blood pressure that causes retinal damage. It emphasizes controlling blood pressure to reduce risks of stroke, heart attack, and heart failure. The document provides guidelines for properly measuring blood pressure and evaluating patients with hypertension.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
This document provides information on hypertensive emergencies and urgencies, including their classification, evaluation, and management. It defines hypertensive emergencies as severe hypertension with evidence of acute target organ damage, while urgencies involve severe hypertension without organ damage. For emergencies, rapid parenteral treatment is needed to stop organ damage progression while avoiding hypoperfusion. Several parenteral agents are discussed for specific conditions along with their dosing and side effects. The goal is to lower blood pressure gradually to avoid complications. Hypertensive urgencies can often be treated orally as outpatients after initial control.
The document discusses pulmonary embolism (PE), which is a blockage in the pulmonary artery caused by blood clots that travel from deep veins. It covers the definition, sources, risk factors including Virchow's triad, pathogenesis, clinical presentation, differential diagnosis, investigations such as D-dimer and imaging tests, and management including anticoagulation, thrombolytic therapy, and prevention through prophylaxis. The management section also describes emergency resuscitation, thrombolysis to relieve obstruction, heparin therapy, warfarin therapy over 3-6 months, vena cava filters for recurrent cases, and embolectomy for massive PE.
The document discusses acute kidney injury (AKI), including its causes, diagnosis, and management. It provides details on prerenal, intrinsic, and postrenal forms of AKI. For prerenal AKI, management focuses on correcting the underlying cause, such as volume depletion, and restoring intravascular volume through fluid resuscitation. For intrinsic AKI, identifying and removing nephrotoxic agents is important. Dialysis may be needed for severe AKI with fluid/electrolyte imbalance or uremia.
1. Pericarditis is inflammation of the pericardium and is usually caused by viral or bacterial infections. It can occur acutely or become chronic.
2. The main symptoms are sudden onset of sharp chest pain that worsens with breathing or coughing. A pericardial friction rub may also be heard on examination.
3. Treatment focuses on relieving pain and inflammation, usually with NSAIDs. Corticosteroids may be used for refractory cases or certain causes like connective tissue diseases.
This document discusses acute heart failure, including its definition, causes, clinical presentations, and pathophysiology. Acute heart failure is rapid onset heart failure that can occur with or without previous cardiac disease. It is often life-threatening and requires urgent treatment. The patient may present with acute decompensated heart failure, hypertensive acute heart failure, pulmonary edema, cardiogenic shock, or high output failure. The pathophysiology involves a vicious cycle where the heart cannot maintain sufficient cardiac output to meet demands, leading to further worsening if not treated.
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by conditions present at birth like hypoplastic left heart syndrome. Symptoms include poor weight gain, fast breathing, and edema. Diagnosis involves chest x-ray, electrocardiogram, echocardiogram, and sometimes cardiac catheterization. Treatment focuses on underlying causes, medications to control symptoms like diuretics and digoxin, and surgery when possible to correct structural heart defects.
Infective endocarditis is a microbial infection of the heart valves or endocardium. It typically involves the valves and can be caused by many pathogens. The most common causes are streptococci, staphylococci, and enterococci. Untreated infective endocarditis has a high fatality rate. The pathogenesis involves endothelial damage, platelet-fibrin deposition forming nonbacterial thrombotic endocarditis (NBTE), and microbial colonization of the NBTE resulting in bacterial vegetations. Local effects include valvular damage, abscesses, fistulae, and conduction abnormalities. Distant effects occur via septic emboli that can lodge in organs like the brain, lungs,
The document discusses hypertensive emergencies, which are acute, severe elevations in blood pressure that can cause target organ damage. It notes key risk factors and various potential causes. It outlines goals for lowering blood pressure during hypertensive emergencies, which depend on the specific target organ(s) affected and time since presentation. Common medications used for treatment are discussed along with their indications and special considerations. Treatment goals differ for conditions like pregnancy, stroke, and aortic dissection. The importance of determining whether target organ damage is present and tailoring treatment accordingly is emphasized.
- Status epilepticus has a worldwide incidence of 3.8 to 38 per 100,000 people per year, with peaks in children and the elderly. Around 31-44% of cases are refractory to initial treatment.
- Initial treatment involves benzodiazepines like lorazepam or diazepam. If seizures continue, second-line drugs like phenytoin, fosphenytoin, or valproate are used.
- Refractory status epilepticus is defined as failure to control seizures with benzodiazepines and other antiepileptics. It requires general anesthesia with drugs like propofol, thiopental, or midazolam along with
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
This document discusses hemorrhagic stroke, specifically intracerebral hemorrhage. It defines intracerebral hemorrhage as bleeding within the brain tissue itself, accounting for 15% of strokes. Risk factors include hypertension and amyloid angiopathy. Clinical presentation includes sudden onset of focal neurological deficits like weakness or seizures. Diagnostics include CT scans. Prognosis is poor with 50% mortality at 1 year. Management focuses on controlling blood pressure, treating increased intracranial pressure, preventing seizures and infections. Surgical options include removing the hemorrhage via aspiration or craniotomy. Subarachnoid hemorrhage is also discussed as bleeding into the subarachnoid space, often from
This document summarizes chronic liver disease and cirrhosis. It describes cirrhosis as scarring of the liver caused by chronic liver disease leading to loss of liver function. Common causes include alcohol, hepatitis B/C, NASH, and genetic disorders. Complications include ascites, variceal bleeding, hepatic encephalopathy, hepatorenal syndrome, and hepatocellular carcinoma. Management involves treating the underlying cause, vaccinations, diuretics, banding/TIPS for varices, lactulose for encephalopathy, and liver transplantation for late stage disease.
Myocarditis is an inflammatory disease of the heart muscle that can be caused by infectious or non-infectious triggers. It has a variable clinical presentation ranging from mild symptoms to life-threatening conditions. The diagnosis is challenging due to the heterogeneity of symptoms but can involve electrocardiogram, cardiac biomarkers, echocardiogram, cardiac MRI and endomyocardial biopsy. About half of acute cases resolve in 2-4 weeks but some develop heart failure or arrhythmias. Treatment focuses on supporting heart function and managing symptoms while the disease runs its course.
Pulmonary hypertension is an abnormal elevation in pulmonary artery pressure. It is classified into 5 groups based on underlying causes. Group 1 includes pulmonary arterial hypertension which is characterized by pre-capillary pulmonary hypertension in the absence of other causes. Molecular abnormalities in pulmonary arterial hypertension include decreased prostacyclin and nitric oxide, and increased endothelin-1. Genetic mutations like in the BMPR2 gene are also associated. Idiopathic pulmonary arterial hypertension has no known cause. Symptoms include fatigue, chest pain and syncope with exertion. Signs include increased pulmonary component of heart sound and murmurs.
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
Rheumatic fever is an autoimmune disease that can develop as a result of a streptococcal throat infection. It causes inflammation of the heart, joints, brain, and skin. The disease is most common in children ages 5-15 in developing countries. It is diagnosed using the Modified Jones Criteria which looks for major criteria like heart inflammation, arthritis, subcutaneous nodules, and minor criteria like fever and joint pain along with evidence of a prior streptococcal infection. Treatment involves antibiotics to treat the infection as well as medications for symptoms while long term prevention relies on regular antibiotics.
Malignant hypertension is a rare but serious form of high blood pressure characterized by a sudden onset of very high blood pressure along with damage to the eyes and kidneys. It occurs when blood pressure in the arteries rises quickly to severely high levels, with diastolic pressure often over 130 mmHg. Common causes include essential hypertension, kidney disease, and pregnancy-related issues. Symptoms may include blurred vision, chest pain, seizures, reduced urine output, and headaches. Diagnosis involves examining physical signs of organ damage and testing for complications affecting the eyes, kidneys, heart, and brain. Treatment aims to lower blood pressure gradually over hours to days to avoid dangerous drops, using short-acting intravenous drugs like nitroprusside
Hypertension Emergencies and their managementpptxUzomaBende
This Presentation talks about Hyprtension, the mode of presentation of hypertensive crisis and the effective management of hypertensive crisis to prevent case fatalities.
This document discusses accelerated hypertension and provides information on defining and classifying hypertension. It begins by defining hypertension as a blood pressure of 140/90 mmHg or higher. It then discusses classifying hypertension based on severity from prehypertension to stage 1 and 2 hypertension. The document notes accelerated hypertension is associated with a rapid rise in blood pressure that causes retinal damage. It emphasizes controlling blood pressure to reduce risks of stroke, heart attack, and heart failure. The document provides guidelines for properly measuring blood pressure and evaluating patients with hypertension.
This document discusses hypertensive crisis, which can manifest as either an emergency or urgency depending on the presence of acute or progressive end-organ damage. Hypertensive emergencies require immediate treatment to reduce blood pressure to prevent irreversible organ damage and death. Examples include accelerated or malignant hypertension and hypertensive encephalopathy. Hypertensive urgencies involve elevated blood pressure without symptoms or organ damage, allowing more gradual blood pressure reduction. Proper classification and treatment can improve outcomes for patients experiencing hypertensive crisis.
Clevidipine is an intravenous calcium channel blocker approved by the FDA in 2008 for the management of acute, severe hypertension. It has a short half-life of 1-2 minutes and quick onset and offset of action. Studies have shown clevidipine to be effective in treating both preoperative and postoperative hypertension in cardiac surgery patients, with blood pressure control similar to other intravenous antihypertensives like nitroprusside, nitroglycerin, and nicardipine. Clevidipine lowers systemic vascular resistance and has greater effects on arterial vasodilation compared to other agents.
A 76-year-old male is admitted to the ICU for recovery after lung surgery. His BP is 168/96 mmHg without end-organ damage, so this represents a hypertensive urgency rather than emergency. Fundoscopic exam is not needed for this transient postoperative hypertension. Starting IV antihypertensives or consulting a hypertension specialist are not necessary actions at this time. The patient should be reassessed later since there is no end-organ damage currently.
A 76-year-old male is admitted to the ICU for recovery after lung surgery. His BP is 168/96 mmHg without end-organ damage, so this represents a hypertensive urgency rather than emergency. Fundoscopic exam is not needed for this transient postoperative hypertension. Starting IV antihypertensives or consulting a hypertension specialist are not necessary actions at this time. The patient should be reassessed later since there is no end-organ damage currently.
Hypertensive crisis refers to severely elevated blood pressure that can lead to organ damage and is categorized as hypertensive urgency or emergency depending on the presence of end-organ damage; treatment of urgency involves gradual oral medication while emergency requires immediate intravenous drugs to reduce blood pressure to prevent further damage; careful diagnosis and monitoring of blood pressure and organs is needed along with selecting appropriate drugs based on the situation.
This document provides an outline about hypertension in children. It defines hypertension and classifies it into different stages. It discusses hypertensive crisis, risk factors, pathophysiology, clinical presentations, diagnostic approach, and treatment. It notes that approximately 30% of children with a BMI over the 95th percentile have hypertension. It also outlines diagnostic testing, treatment considerations including medication options and goals, and provides algorithms for treating hypertensive urgency and emergencies. The treatment involves gradually lowering blood pressure over 24-48 hours while monitoring for side effects and end organ damage.
This document discusses hypertensive emergencies, which are severe cases of high blood pressure that result in acute organ damage. It defines categories of hypertensive states and provides details on etiology, pathophysiology, presentation, workup, and treatment of hypertensive emergencies. Treatment involves identifying the affected organ system and gradually lowering blood pressure over hours to days to prevent further organ injury, using intravenous medications like nitroprusside, labetalol, or nicardipine depending on the situation. Specific guidance is provided for rapidly lowering blood pressure in conditions like hypertensive encephalopathy, intracerebral hemorrhage, and ischemic stroke.
This document provides an overview of hypertensive crises, including hypertensive urgency and emergencies. It defines these conditions, discusses their epidemiology, risk factors, pathophysiology, clinical presentation, diagnosis, and management. Hypertensive urgency involves severe blood pressure elevations without end-organ damage, while emergencies involve elevations with end-organ damage. Management of urgency involves gradually lowering blood pressure over hours to days, while emergencies require faster reduction, usually with parenteral drugs initially then oral medications. Follow up care aims to identify and treat underlying causes while achieving long-term blood pressure control.
This document provides an overview of hypertensive crises, including hypertensive urgency and emergencies. It defines these conditions, discusses their epidemiology, risk factors, pathophysiology, clinical presentation, diagnosis, and management. Hypertensive urgency involves severe blood pressure elevations without end-organ damage, while emergencies involve elevations with end-organ damage. Management of urgency involves gradually lowering blood pressure over hours to days, while emergencies require faster reduction, usually with parenteral drugs initially then oral medications. Follow up aims to identify and treat underlying causes, and ensure blood pressure is well-controlled to prevent recurrence.
This document provides an overview of hypertensive crises, including hypertensive urgency and emergencies. It defines these conditions, discusses their epidemiology, risk factors, pathophysiology, clinical presentation, diagnosis, and management. Hypertensive urgency involves severe blood pressure elevations without end-organ damage, while emergencies involve elevations with end-organ damage. Management of urgency involves gradually lowering blood pressure over hours to days, while emergencies require faster reduction, usually with parenteral drugs initially then oral medications. Follow up aims to identify and treat underlying causes while achieving blood pressure control to prevent recurrence.
Hypertension is defined as persistent blood pressure readings of 140/90 mmHg or higher. It is a major risk factor for cardiovascular disease and premature death. While usually asymptomatic, regular screening is important for detection. Treatment involves lifestyle modifications and medication to lower blood pressure to under 140/90 mmHg to reduce health risks. Malignant hypertension is a medical emergency characterized by severely high blood pressure that requires urgent treatment and hospitalization.
A hypertensive crisis is a sudden spike in blood pressure to 180/120 mmHg or higher, which is a medical emergency that could lead to organ damage or be life-threatening. Symptoms include headaches, confusion, chest pain, nausea, and weakness. Causes include non-compliance with medications, high salt/fat diets, certain drugs, kidney disease, and hormone imbalances. Treatment involves reducing blood pressure in the ICU over hours to days depending on any organ damage present. Nursing care focuses on monitoring, medication administration, lifestyle changes, and education to prevent future crises.
Hypertension, or high blood pressure, is defined as a systolic pressure above 140 mm Hg or a diastolic pressure above 90 mm Hg. It is a major public health problem affecting over 60 million Americans. Risk factors include family history, age, gender, ethnicity, stress, obesity, high sodium diet, and low calcium intake. Uncontrolled hypertension can lead to stroke, heart attack, and other cardiovascular diseases. Treatment involves lifestyle modifications and medication to prevent complications from this chronic condition.
Mr. A is a 61-year-old retired police officer who presented with headache and giddiness. His blood pressure was 150/90 mmHg. Tests showed grade 1 hypertension, obesity, impaired glucose tolerance, and dyslipidemia. He has a high cardiovascular risk level. An ACE inhibitor would be an appropriate initial treatment to aim for a target blood pressure of below 140/90 mmHg. Appropriate response would be a reduction in blood pressure of at least 25% over 24 hours without going below 160/90 mmHg. Hypertensive emergencies require rapid blood pressure reduction of 25% over 3-12 hours while monitoring for specific organ involvement.
This document summarizes the approach to hypertension in children. It defines hypertension and prehypertension based on blood pressure percentiles for age, gender and height. Secondary causes of hypertension in children include renal, cardiovascular, endocrine and neurological conditions. Evaluation involves assessing for target organ damage and investigating for underlying causes based on clinical features. Treatment involves lifestyle modifications and medications like ACE inhibitors, calcium channel blockers and diuretics based on the patient's age, gender and other health conditions. Hypertensive crisis requires prompt parenteral treatment to lower blood pressure over minutes to hours to prevent complications.
This document discusses managing hypertensive emergencies in the emergency department. It defines hypertension and hypertensive urgency versus emergency. For hypertensive urgency, when BP is markedly elevated but there are no symptoms, treatment is usually not required in the ED and patients can be referred for outpatient follow up. For hypertensive emergency, when there are progressive symptoms of end organ damage, treatment in the ED is warranted to lower BP by about 25% aiming to avoid hypotension. Goals of treatment and commonly used oral and IV antihypertensive agents are reviewed.
This document discusses hypertensive crisis and provides details on its etiology, pathophysiology, clinical evaluation, and management. It defines hypertensive crisis as an acute severe elevation in blood pressure of usually over 180/120 mmHg that may be associated with end organ dysfunction. It further categorizes hypertensive crisis into hypertensive urgency and hypertensive emergency based on the presence or absence of end organ damage. The document outlines the various causes, mechanisms, clinical assessment approach, and goals of treatment for hypertensive crisis, with an emphasis on preventing further organ damage while maintaining tissue perfusion.
Heart failure is a clinical syndrome where the heart is unable to pump enough blood to meet the body's needs. It can be caused by conditions that reduce the heart's ability to contract or fill properly and common symptoms include dyspnea, fatigue, and edema. Upon presentation, patients exhibiting signs of congestion such as elevated jugular pressure, rales, and edema are treated with diuretics, while those with low blood pressure or organ dysfunction may require inotropic support or mechanical circulatory support.
A 3-year-old girl has had loose stools for 2 months that often contain undigested food. She is otherwise well and thriving. The most probable diagnosis is chronic non-specific diarrhea (toddler's diarrhea). Management includes decreasing fluid intake, especially of fruit juice, providing high-fat foods to slow gastric emptying, and increasing fiber intake through bulking agents. Pharmacologic intervention is rarely required as symptoms usually resolve spontaneously by age 3-4 years.
The document discusses infant feeding and nutrition. It covers various topics including the types and definitions of breastfeeding, the physiology of lactation, problems associated with breastfeeding, infant growth phases and their energy requirements, and the importance of proper nutrition. The key components of human milk are discussed, including fat, proteins, carbohydrates, oligosaccharides, prebiotics and probiotics. Guidelines around establishing and maintaining breastfeeding are provided. Common breastfeeding and infant feeding problems are also outlined.
Postpartum hemorrhage (PPH) is excessive bleeding after childbirth, defined as blood loss over 500 ml for vaginal births or 1000 ml for C-sections. The main causes of PPH are uterine atony (failure of the uterus to contract), retained placenta, and trauma to the genital tract. Management involves bimanual uterine massage, uterotonic drugs, vaginal packing, balloon tamponade, and in severe cases surgical interventions like B-Lynch sutures or hysterectomy.
This document discusses the use of various imaging modalities for evaluating neck masses. Ultrasound is useful for differentiating cystic from solid lesions and assessing lymph node size and vascularity. CT provides details of soft tissues and their relationships. MRI is good for lesion detection and involvement of nearby structures but has limitations for nodal assessment. PET/CT is excellent for staging lymphoma and detecting unknown primary cancers. Biopsy is used when malignancy is suspected. The approach depends on whether the mass is in a child or adult, with ultrasound often the initial study. Location provides clues for cystic lesions. Features help characterize solid lesions and lymph nodes. Further tests are guided by ultrasound findings.
This document provides information about fetal cardiotocography (CTG), including:
1. CTG can be performed from 28 weeks of gestation as that is when the fetal autonomic nervous system is mature.
2. Normal CTG findings include a baseline heart rate between 110-160 bpm, variability between 5-25 bpm, and an absence of or early decelerations with at least 2 accelerations in 20 minutes.
3. Abnormal findings include bradycardia (<110 bpm), tachycardia (>160 bpm), decreased variability (<5 bpm), and late or variable decelerations which can indicate fetal hypoxia or distress.
This document discusses the partogram, a tool for recording the progress of labor. It explains that the partogram graphs cervical dilation, fetal descent, and uterine contractions on a chart to allow healthcare providers to monitor labor and identify complications early. The document outlines the components recorded on a partogram, including fetal heart rate, amniotic fluid, maternal vital signs, and medications. It describes how to interpret the alert and action lines plotted on the partogram to determine if labor is progressing normally or requires intervention. The partogram is an important tool that facilitates continuity of care during labor and allows early detection of problems like prolonged or obstructed labor.
Gestational trophoblastic disease (GTD) is a spectrum of tumors caused by abnormal proliferation of placental tissue. It includes hydatidiform moles (complete and partial), which are usually benign, as well as gestational trophoblastic neoplasms like invasive moles, choriocarcinoma, and placental site trophoblastic tumors, which are malignant. GTD is diagnosed using clinical features, ultrasound findings, and elevated human chorionic gonadotropin levels. Treatment may involve D&C for molar pregnancies as well as chemotherapy for malignant or persistent cases. Long term follow up is important to monitor for recurrence or progression to gestational trophoblastic neoplasia due to the
Gametogenesis conversion of germ cells into male and female gametes.pptJwan AlSofi
Gametogenesis refers to the formation of male and female gametes. It begins with primordial germ cells that migrate to the developing gonads. Oogenesis involves the formation of ova through meiotic divisions in females, arresting in prophase I until puberty. Spermatogenesis is the formation of sperm in males through mitotic and meiotic divisions of spermatogonia into spermatids. Spermiogenesis then transforms spermatids into mature spermatozoa through nuclear condensation and tail formation. Abnormal gametes can form with extra nuclei or morphological defects preventing fertilization.
Development of the male& female genital system.pptxJwan AlSofi
The document summarizes the development of the male and female genital systems from an indifferent stage. It describes how in males, the presence of SRY leads testes to develop from indifferent gonads, while in females without SRY ovaries develop. It outlines the development of testes, ovaries, male ducts including epididymis and vas deferens, and female ducts including uterus and vagina from indifferent ducts. External genitalia also develop differently in males under testosterone versus females.
First week of development: Ovulation to Implantation Jwan AlSofi
The document summarizes key aspects of ovulation, fertilization, and early embryonic development. It describes the ovarian and menstrual cycles controlled by hormones like FSH and LH. Ovulation occurs mid-cycle due to an LH surge, releasing an egg. Sperm travel through the reproductive tract while undergoing capacitation. Fertilization typically occurs in the fallopian tubes, involving penetration of the egg's layers and fusion of gametes. This activates the egg and forms pronuclei, leading to cell division and pregnancy if implantation occurs. Otherwise, the corpus luteum regresses and menstruation begins.
Approach to patient with spinal cord lesions & diseases
Localize spinal cord lesions
Determining the Level of the Lesion in Myelopathy
Diseases of spinal cord
Multiple sclerosis is a chronic disease characterized by inflammation, demyelination, and gliosis in the central nervous system. It affects around 5 million people worldwide. The cause is unknown but involves genetic and environmental factors. Symptoms vary widely and can include sensory disturbances, motor symptoms, visual problems, ataxia, and cognitive impairment. Diagnosis involves demonstrating dissemination of lesions in the CNS over time via MRI imaging or evoked potentials testing, and sometimes analysis of cerebrospinal fluid. There are several disease courses including relapsing-remitting MS, primary progressive MS, and secondary progressive MS. Management aims to reduce inflammation and disability progression.
1. Short stature can be caused by familial, constitutional, or pathological factors. Familial short stature runs in families while constitutional short stature involves delayed puberty.
2. Pathological short stature can be disproportionate involving abnormal limb ratios, or proportionate involving prenatal issues like IUGR or postnatal diseases/nutritional disorders.
3. Evaluating a short child involves assessing growth charts, growth velocity, bone age, family history, and screening tests to classify the cause of short stature.
Headache is a common symptom in children and adolescents, with up to 75% experiencing a significant headache by age 15. Headaches can be primary, such as migraines or tension-type headaches, or secondary to other conditions such as viral infections. A thorough history and physical exam are usually sufficient for diagnosis, though imaging may be required if symptoms suggest increased intracranial pressure. Treatment involves acute medication to stop attacks as well as preventive medication and lifestyle modifications if headaches are frequent or disabling.
Neonatal seizures are the most common neurological emergency in newborns. The majority occur within the first day of life, and hypoxic ischemic encephalopathy is the most common cause, especially in term infants. In preterm infants, cerebral vascular events are more often the cause. Neonatal seizures are usually focal and often have identifiable underlying causes, unlike seizures in older children which are often idiophenic. The prognosis depends on the underlying etiology, with hypoxic ischemic encephalopathy carrying the worst prognosis. Phenobarbital remains the first-line treatment, though multiple anticonvulsants may be needed to control seizures.
this is a complete discussion and an approach to a child with febrile seizure / convulsion.
It contains:-
Case scenario
Causes of Seizures in the setting of fever
Definition of Febrile Seizure
Age of Occurrence
Types of Febrile Convulsions
Risks of Recurrent Febrile Seizures
Risk For Developing Epilepsy After Febrile Seizures
Workup for Febrile Seizure
Red Flags in Febrile Seizures
Treatment
Prognosis
Approach to Syncope in Children (Pediatric Syncope).pptxJwan AlSofi
Approach to Syncope in Children (Pediatric Syncope), includes:-
Introduction
Differential diagnosis of syncope
Syncope vs vertigo vs Presyncope vs light-headedness.
Comparison of Clinical Features of Syncope and Seizures
Neurocardiogenic (Vasovagal) syncope
MECHANISMS and Causes of Syncope
Cardiac causes of syncope
Life-threatening causes of syncope
Red Flags in Evaluation of Patients With Syncope
Non-cardiac causes of loss of consciousness.
Noncardiac Causes of Syncope
Differentiating Features for Causes of Syncope
EVALUATION of syncope:- History, Examination,Treatment.
Summary
The infant in choice c presents with signs of moderate encephalopathy after a known perinatal hypoxic event and meets criteria for therapeutic hypothermia based on guidelines. The other infants presented do not meet criteria either due to prematurity, mild encephalopathy findings, or presenting outside the time window.
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...Donc Test
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Study Guide Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Course Hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Answers Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Course hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Study Guide Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Ebook Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Questions Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Stuvia
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
One health condition that is becoming more common day by day is diabetes.
According to research conducted by the National Family Health Survey of India, diabetic cases show a projection which might increase to 10.4% by 2030.
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central19various
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
2. Outline of this lecture:
What is Heart Hypertensive Crisis?
Epidemiology.
Classification of Hypertensive Crisis.
Causes of Hypertensive Crisis
Clinical presentation of Hypertensive
Crisis
Managment of Hypertensive Crisis
Jwan Ali AlSofi
3. What is Hypertensive Crisis?
•The term hypertensive crisis is defined as a
severe elevation in blood pressure (BP),
generally considered to be a diastolic
blood pressure greater than 120 mm Hg
Jwan Ali AlSofi
4. What is Hypertensive Crisis?
•This disorder can be further classified as
hypertensive urgency or hypertensive
emergency when there is evidence of
acutely progressive end-organ damage.
•If these disorders are not treated promptly,
a high rate of morbidity and mortality will
occur the 5-year mortality for patients with
a history of hypertensive crisis is 26%
Jwan Ali AlSofi
5. Epidemiology
• Approximately 1% of hypertensive pts. may develop
hypertensive crises during their lifetime.
• Annual incidence of hypertensive emergencies being
1-2 cases/1,00,000 pts.
• Higher rates have been reported in African Americans, low
socioeconomic people, in developing countries.
• Incidence in men 2 times higher than in women
Epidemiology
Jwan Ali AlSofi
7. Definitions of hypertensive crisis:-
• Hypertensive emergencies:- are defined as severe
elevations in BP (>180/120 mm Hg) associated with
evidence of new or worsening target organ damage.
• Hypertensive urgencies:- are situations associated with
severe BP elevation (>180/120 mm Hg) in otherwise stable
patients without acute or impending change in target
organ damage or dysfunction.
• Accelerated hypertension (aka malignant hypertension):- A
severe increase in blood pressure to 180/120 mmHg or
higher (and often over 220/120 mmHg) with signs of
retinal haemorrhage and/or papilloedema (grade 3-4). It is
usually associated with new or progressive target organ
damage.
Jwan Ali AlSofi
10. • Renovascular Disease
• Pheochromocytoma
1. Non-adherence to anti-HTN medications (most
common)
2. Hyperaldosteronism
3. Anti-hypertensive withdrawal syndromes
4. Head injuries and CNS trauma
5. Post-op hypertension
6. Drug-induced hypertension
Causes of hypertensive emergencies ?
Jwan Ali AlSofi
11. • As with hypertensive emergencies ,severe BP
elevations may result from inadequate control or poor
adherence to current antihypertensive drug regimens.
• Another cause for patients reaching hypertensive
urgency is previous inaccurate BP measurements that
underestimate or do not detect increased BP at all
(e.g. poor patient technique for self‐monitoring).
Causes of hypertensive Urgencies ?
Jwan Ali AlSofi
13. Causes Hypertensive Urgencies
• Lifestyle:
- High salt diet, excessive alcohol use.
• Comorbid Conditions:
- Thyroid storm, trauma, renovascular disease, acute
ischemic stroke or adrenal dysfunction
Causes of hypertensive Urgencies ?
Jwan Ali AlSofi
14. Clinical Presentation of HC
Emergency
• Characterized by severe increase in
systolic and/or diastolic blood pressure
associated with signs or symptoms of
acute end-organ damage.
• Usually, SBP > 180 mm Hg - DBP >
120 mm Hg
• Requires an immediate BP reduction in
few minutes - hours.
• Requires an ICU care & IV drugs
Urgency
• Elevated BP ( usually systolic > 180
mmHg &/or diastolic > 120 mmHg ) but
without evidence of end-organ
damage.
• Usually asymptomatic; severe
headache, shortness of breath,
epistaxis, severe anxiety.
• Adequate treatment of these conditions,
a BP lowering within 24-48 hrs by
administration of oral drugs.
• ICU admission is usually not required
• Controlled by oral medications.
Jwan Ali AlSofi
15. Clinical Presentation of HC
Emergency
• Rarely develop in patients without a
previous history of hypertension
• occur in patients with
pheochromocytoma or renal vascular
disease
• CNS:-
• Cerebral infarctions,
• HTN Encephalopathy
• intracranial or subarachnoid hemorrhage.
• Heart:-
• acute heart failure (HF) and pulmonary
edema
• acute myocardial infarction,
• unstable angina.
• Acute dissection,
• Eclampsia .
Urgency
• Not all patient present with
same symptoms
• 90% of patients had a history
of hypertension
• Headache (42%) and dizziness
(30%).
• visual changes,
• chest discomfort,
• nausea,
• epistaxis,
• Fatigue
• psychomotor agitation.
Jwan Ali AlSofi
17. • Single organ damage in approximately 83%.
• Two organ damage found in 14%,multiorgan damage
in 3 % pts.
Most common clinical presentations :
- cerebral infarction (24%)
- pulmonary oedema (22%)
- HTN encephalopathy (16%)
- Cong. HF (12%)
•Less common presentations –
- IC hemorrhage,
- Aortic dissection
Acute End-organ Damage
(Complication of HC).
Jwan Ali AlSofi
22. Hypertensive Encephalopathy
• Is a presentation of hypertensive emergency
• Our brains are under tight control. With severe rises in BP,
autoregulation fails and leads to cerebral edema.
• Hypertensive encephalopathy is defined as the presence of
signs or symptoms of cerebral edema secondary to severe
and/or sudden rises in BP. It’s characterized by:
• Severe Hypertension with 1+ of:
1. Seizures
2. Lethargy
3. Cortical Blindness
4. Coma
• It is a diagnosis of exclusion
Jwan Ali AlSofi
23. Of note, there is little evidence to
suggest that headache alone is a sign
of a hypertensive emergency, however,
in combination with visual changes,
lethargy, seizures or altered mental
status it may be an indication of
hypertensive encephalopathy.
24. ACUTE END ORGAN DAMAGE- CVS
2. Cardiovascular
- Myocardial ischemia/infarction – 4TH (12%).
- Acute left ventricular dysfunction
- Acute pulmonary edema – 2ND MOST COMMON
(22.5% )
- Aortic dissection
Jwan Ali AlSofi
25. ACUTE END ORGAN DAMAGE- Renal
3. RENAL
ARTERIOSCLEROSIS, FIBRINOID NECROSIS overall
impairment of renal protective autoregulation mechanisms!
RESAULT:
- Worsening renal function - Acute renal failure/insufficiency (↑BP)
- Hematuria + red blood cell (RBC) cast formation
- Proteinuria.
4. Microangiopathic hemolytic anemia
Jwan Ali AlSofi
26. MALIGNANT HYPERTENSION
- Is a HYPERTENSIVE EMERGENCY!!!
- Leading to an acute end organ damage
- Less than 1% of ht patients develop the
malignant phase
- Avarage age of diagnosis is 40
- Men>women
Jwan Ali AlSofi
27. MALIGNANT HYPERTENSION-
PATHOPHYSIOLOGY
BP =PVR*CO(SV*HR)
Rate at which MAP rises more important than absolute rise
Acute rise in BP Failure of vasoconstriction Endothelial
by autoregulation damage
FIBRINOID Activates coag. and Deposition. of proteins/
NECROSIS inflammation fibrinogen in vessel
wall
- RAAS plays an important role in initiating and perpetuating BP rise by causing
vasoconstriction and fluid retention.
- THIS CYCLE MUST BE STOPPED IN ORDER TO PREVENT FURTHER VASCULAR
INJURY AND TISSUE ISCHEMIA!
Jwan Ali AlSofi
29. • The treatment of hypertensive crises must balance
preventing further end-organ damage while
maintaining tissue perfusion.
• The initial goal for blood pressure reduction is not to
obtain a normal blood pressure.
• Rapid and aggressive reductions in blood pressure can
actually induce cerebral, myocardial, or renal
ischemia or infarction if the blood pressure falls below
the range at which tissue perfusion can be maintained
by autoregulation.
MANAGEMENT
History Examination Assessment Treatment
Jwan Ali AlSofi
30. • Duration and degree of pre existing hypertension
• Details of antihypertensive therapy
• Compliance with medications
• Use of the over counter drugs
• History of recent operations.
History Examination Assessment Treatment
HISTORY
Jwan Ali AlSofi
34. Lab tests & investigations may be required:-
- CBC,
- ECG,
- urinalysis,
- renal function
- Echo.
- consider head imaging if neurological symptoms
are present
ASSESMEN with INVESTIGATION
Jwan Ali AlSofi
37. Clinical Presentation of HC
Emergency
• rarely develop in patients
without a previous history of
hypertension
• occur in patients with
pheochromocytoma or renal
vascular disease
• Cerebral infarctions,
encephalopathy and
intracranial or subarachnoid
hemorrhage.
• acute heart failure (HF) and
pulmonary edema and acute
myocardial infarction, unstable
angina. Acute dissection,
eclampsia.
Urgency
• headache (42%) and
dizziness (30%). Other
symptoms include visual
changes, chest discomfort,
nausea, epistaxis, fatigue,
and psychomotor agitation.
• Not all patient present with
same symptoms
• 90% of patients had a
history of hypertension
Jwan Ali AlSofi
39. MALIGNANT HYPERTENSION-
THERAPY - general
- HOSPITALIZATION
- RELAXATION (NON STRESSED ENV.)
SCREEN FOR END ORGAN DAMAGE
INITIAL AIMS:
1. CORRECTION OF MEDICAL COMPLICATION
2. REDUCTION OF MAP BY 20-25% IN THE 1ST HOUR
3. REDUCTION OF DIASTOLIC PRESSURE TO 13 OVER MINUTES
TO HOURS HOURS=110 mmHg (BUT NOT BELOW <95 mmHg –
IN ORDER NOT TO CAUSE CEREBRAL HYPOPERFUSION)
BP should be reduced
- immediately-
- gradually
(Specifically)
DRUGS should be used i.v
Jwan Ali AlSofi
42. Hypertensive Emergency
THERAPY – IV DRUGS cont.
2 MAIN CLASSES OF DRUGS:
1.Vasodilators:
Nitroprusside
Nitroglycerine
Nicardipine
Hydralazine
Enalapril
Fenoldopam
2. Adrenergic inhibitors
Labetalol (a+b blocker)
Esmolol (b-1 selective blocker)
Phentolamine (a1 blocker)
Jwan Ali AlSofi
43. Hypertensive Emergency
THERAPY – SPECIFIC DRUGS
1. NITROPRUSSIDE :
- 1ST CHOICE FOR HT CRISIS!
- ONSET 30 SEC FOR FEW MIN
VEINS + ARTERIES
DECREASE PRELOAD = USED IN ACUTE MI!
SIDE EFFECT: THIOCYANIDE TOXICITY, METHEMOLOBINEMIA,
HYPOTHYRODISM
2. NITROGLYCERIN:
- Coronary vasodilator
- Direct venodilator (variable arterial effects)
SIDE EFFECT: headaches and tachycardia ,Methemoglobinemia
3. LABETALOL:
Combined alpha & beta blocker
Beta blockade blunts reflex tachycardia from alpha blockade
Myocardial depression
Caution in patients with reactive airway disease
Jwan Ali AlSofi
44. Hypertensive Emergency –
THERAPY – SPECIFIC DRUGS
4. FENOLDOPAM : (DOPAMIN AGONIST)
Short acting (30 MIN)
Rapid elimination upon discontinuation
No dosing adjustment for pre-existing renal or hepatic impairment
Increases renal blood flow and maintains GFR
5. HYDRALAZINE (oral):
- Strict arteriole vasodialator
-3rd 4th option in HT crisis.
Jwan Ali AlSofi
45. Hypertensive Emergency THERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
1. Hypertensive encephalopathy
Preferred medications :
Labetalol
Nicardipine
Esmolol
Medications to avoid :
Nitroprusside (was used in the past- caused ICP )
Hydralazine
Treatment guidelines: Reduce mean arterial pressure (MAP) 25% over 8
hours.
Jwan Ali AlSofi
46. Hypertensive EmergencyTHERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
2. Aortic dissection –
Immediate redn. In BP and mainly shear stress (change in BP with change in time)
is essential to limit the extension of damage as surgery is being considered.
Preferred medications
Labetalol
Nicardipine
Nitroprusside (with beta-blocker)
Esmolol
Morphine sulfate
Medications to avoid
Avoid beta-blockers if there is aortic valvular regurgitation or suspected
cardiac tamponade, HYDRALAZINE (increase shear stress)
Treatment guidelines: Maintain SBP <110 mm Hg, unless signs of end-organ
hypoperfusion are present.
+Narcotic analgesics
TIME TO ACHIEVE: 20 MINUTES!!!!!
Jwan Ali AlSofi
47. Hypertensive Emergency THERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
3. Preeclampsia/eclampsia
Preferred medications
Hydralazine
Labetalol
Nifedipine
Medications to avoid
Nitroprusside
Angiotensin-converting enzyme inhibitors
Esmolol
Treatment guidelines: In women with eclampsia or preeclampsia, SBP should
be <160 mm Hg and DBP <110 mm Hg in the prepartum and intrapartum
periods. If the platelet count is <100,000 cells mm3 BP should be
maintained below 150/100 mm Hg. Patients with eclampsia or
preeclampsia should also be treated with IV magnesium sulfate to
avoid seizures
Jwan Ali AlSofi
48. Hypertensive Emergency THERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
4. CARDIAC CRISIS
L.V FAILURE AND PUL. EDEMA
Preferred medications
Nitroglycerin
Enalaprilat
Nitroprusside
Treatment guidelines: Treatment with vasodilators (in addition to diuretics) for SBP
≥140 mm Hg. IV or sublingual nitroglycerin is the preferred agent
BP CONTROL IS SECONDARY to the primary problem - open the infarct
related artery and treat pain, diurese and oxygenate those in pulmonary
edema
Jwan Ali AlSofi
49. Hypertensive Emergency THERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
4. RENAL INSUFFICENCY:
Goal is to prevent further renal damage by
maintaining adequate blood flow.
Preferred medications:
Nitroprusside
Jwan Ali AlSofi
52. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
• reduce MAP by no more than 20-25%, DBP to 100-
110mm Hg within few minutes to 2 hours.
• More aggressive and rapid BP reduction (Acute
Pulmonary edema ,Aortic dissection)
• More slowly for acute cerebrovascular damages with
monitoring of neurological status.
• Constant infusion of intravenous agents required
MANAGEMENT
Jwan Ali AlSofi
53. Target of BP in HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi
54. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
• reduce MAP by no more than 20-25%, DBP to 100-
110mm Hg within few minutes to 2 hours.
• More aggressive and rapid BP reduction (Acute
Pulmonary edema ,Aortic dissection)
• More slowly for acute cerebrovascular damages with
monitoring of neurological status.
• Constant infusion of intravenous agents required
TREATMENT OF HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi
55. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
• reduce MAP by no more than 20-25%, DBP to 100-
110mm Hg within few minutes to 2 hours.
• More aggressive and rapid BP reduction (Acute
Pulmonary edema ,Aortic dissection)
• More slowly for acute cerebrovascular damages with
monitoring of neurological status.
• Constant infusion of intravenous agents required
TREATMENT OF HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi
59. GOAL
• Overall Goal of Management: reduce SBP by ~ 25% over
24‐48 hours.
• More conservative BP lowering reduces the risk of
potential adverse effects (i.e. perfusion complications
worsening incidence of MI, stroke, and death) associated
with more aggressive BP lowering if the blood pressure
falls below the range at which tissue perfusion can be
maintained by autoregulation .
• All treatment strategies should consider the patient’s
comorbidities and risk of adverse events.
• Treated by oral medications not IV.
TREATMENT OF HYPERTENSIVE
URGENCY
Jwan Ali AlSofi
60. TREATMENT OF HYPERTENSIVE URGENCY
GOAL
• Overall Goal of Management: reduce SBP by ~ 25% over
24‐48 hours.
• More conservative BP lowering reduces the risk of
potential adverse effects (i.e. perfusion complications
worsening incidence of MI, stroke, and death) associated
with more aggressive BP lowering if the blood pressure
falls below the range at which tissue perfusion can be
maintained by autoregulation .
• All treatment strategies should consider the patient’s
comorbidities and risk of adverse events.
MANAGEMENT
Jwan Ali AlSofi
61. Take-Home Points
Fundoscopy and urine dip are key in the
assessment of the severely hypertensive
patient who you are working up for a possible
hypertensive emergency
Keep a high index of suspicion for
hypertensive encephalopathy in the severely
hypertensive and altered or comatose patient
with or without seizures or cortical blindness
Treat the patient and not the number
Jwan Ali AlSofi
Diagnosis and management of a hypertensive crisis. Colors correspond to Class of Recommendation in Table 1. *Use drug(s) specified in Table 19. †If other comorbidities are present, select a drug specified in Table 20. BP indicates blood pressure; DBP, diastolic blood pressure; ICU, intensive care unit; and SBP, systolic blood pressure.
Management of hypertension in patients with acute ICH. Colors correspond to Class of Recommendation in Table 1. BP indicates blood pressure; ICH, intracerebral hemorrhage; IV, intravenous; and SBP, systolic blood pressure.
Management of hypertension in patients with acute ischemic stroke. Colors correspond to Class of Recommendation in Table 1. BP indicates blood pressure; DBP, diastolic blood pressure; IV, intravenous; and SBP, systolic blood pressure.