FAST is an acronym used to help recognize the common signs of stroke. It stands for:
F - Face: Ask the person to smile. Does one side of the face droop?
A - Arms: Ask the person to raise both arms. Does one arm drift downward?
S - Speech: Ask the person to repeat a simple phrase. Is their speech slurred or strange?
T - Time: If you observe any of these signs, call emergency services immediately.
1. Stroke in children differs from adults, with congenital and developmental risk factors being more common than chronic risk factors. Presentation can also be more subtle.
2. Guidelines recommend brain imaging, preferably MRI, for any child presenting with clinical stroke symptoms. Further vascular imaging and cardiac echocardiography within 48 hours is also advised.
3. A thorough evaluation should include blood tests to check for coagulation disorders, inflammation, infection and other metabolic causes. Prothrombotic factor screening is important to identify inherited risks and guide family screening.
1) Pediatric strokes account for less than 5% of all strokes and affect 2-3 in 100,000 newborns and 12 in 100,000 children under 18 years of age. The annual incidence of pediatric strokes is reported to be between 2.5-2.7 per 100,000 children.
2) Risk factors for pediatric strokes include congenital heart defects, sickle cell anemia, coagulation disorders, and other conditions.
3) Prognosis after a pediatric stroke varies depending on the underlying cause, with 80% of children surviving 10 years after an ischemic stroke though most have residual hemiparesis. Hemorrhagic strokes carry a higher mortality risk than ischemic strokes.
1. Childhood stroke is more common than brain tumors and is among the top 10 causes of death in childhood. The incidence is about 8 per 100,000 children and risk factors include congenital heart disease and prematurity.
2. The most common causes of acute ischemic stroke are arteriopathy, cardioembolism from structural heart disease, and hematological conditions like sickle cell anemia. Diagnosis involves CT, MRI, and angiography. Treatment focuses on antithrombotics and rehab.
3. Hemorrhagic stroke risk factors include vascular malformations, blood disorders, and trauma. Subarachnoid hemorrhage is the most common type. Cerebral sinovenous
Stroke is an emergency condition caused by a blocked artery or burst blood vessel in the brain. It can lead to serious disability or death if brain cells are not quickly treated. The main types of stroke are ischemic, caused by a blockage, and hemorrhagic, caused by a burst blood vessel. Timely treatment is critical to minimize brain cell death and damage. Management involves stabilizing vital functions, rapidly diagnosing the type of stroke, and administering appropriate treatments such as clot-busting drugs to reduce disability. A multidisciplinary approach is needed for long-term care and rehabilitation.
This document discusses several inherited diseases including sickle cell disease, hemophilia, muscular dystrophy, cystic fibrosis, and Huntington's disease. Sickle cell disease is caused by a mutation that causes red blood cells to take on an abnormal sickle shape, leading to anemia and organ damage. Hemophilia is a bleeding disorder caused by deficiencies in clotting factors VIII or IX that is inherited in an X-linked recessive pattern. Muscular dystrophy encompasses genetic diseases that cause progressive muscle weakness and loss of muscle mass through defective muscle proteins. Cystic fibrosis is caused by a gene mutation that causes thick, sticky mucus to build up in the lungs and digestive system. Huntington's disease is an inherited
This document discusses the approach to diagnosing and treating histiocytosis syndromes in childhood. It is a diverse group of disorders involving an abnormal proliferation of histiocytes (monocyte-macrophage cells). The main types discussed are Langerhans cell histiocytosis (LCH), hemophagocytic lymphohistiocytosis (HLH), and reactive histiocytosis. LCH is characterized by Langerhans cells with Birbeck granules, while HLH involves an uncontrolled activation of macrophages and T-cells. Diagnosis involves biopsy and immunochemistry. Treatment depends on risk stratification and number of organ systems involved, ranging from monitoring to chemotherapy. Long-term follow-up is important due to the disease
Hematology oncology-nurs 3340 fall 2017Shepard Joy
This document outlines learning outcomes and content related to alterations in hematologic function and childhood malignancies. It begins by describing the functions of red blood cells, white blood cells, and platelets. It then discusses differences in pediatric hematopoiesis compared to adults. Specific topics covered include anemia, sickle cell disease, hemophilia, and childhood cancers. Nursing care is discussed for conditions such as vaso-occlusive crises, bleeding episodes, and cancer diagnosis and treatment.
This document summarizes information about cardiomyopathy in newborns and fetuses. It discusses definitions, classifications, etiologies, clinical features, diagnostic evaluations, and management strategies for various types of neonatal cardiomyopathy. It also reviews a journal article studying fetal cardiomyopathy detected on prenatal echocardiograms, finding reduced systolic function, valve issues, and chamber enlargement in some cases. Outcomes were generally poor, though early diagnosis may allow for improved postnatal management.
1. Stroke in children differs from adults, with congenital and developmental risk factors being more common than chronic risk factors. Presentation can also be more subtle.
2. Guidelines recommend brain imaging, preferably MRI, for any child presenting with clinical stroke symptoms. Further vascular imaging and cardiac echocardiography within 48 hours is also advised.
3. A thorough evaluation should include blood tests to check for coagulation disorders, inflammation, infection and other metabolic causes. Prothrombotic factor screening is important to identify inherited risks and guide family screening.
1) Pediatric strokes account for less than 5% of all strokes and affect 2-3 in 100,000 newborns and 12 in 100,000 children under 18 years of age. The annual incidence of pediatric strokes is reported to be between 2.5-2.7 per 100,000 children.
2) Risk factors for pediatric strokes include congenital heart defects, sickle cell anemia, coagulation disorders, and other conditions.
3) Prognosis after a pediatric stroke varies depending on the underlying cause, with 80% of children surviving 10 years after an ischemic stroke though most have residual hemiparesis. Hemorrhagic strokes carry a higher mortality risk than ischemic strokes.
1. Childhood stroke is more common than brain tumors and is among the top 10 causes of death in childhood. The incidence is about 8 per 100,000 children and risk factors include congenital heart disease and prematurity.
2. The most common causes of acute ischemic stroke are arteriopathy, cardioembolism from structural heart disease, and hematological conditions like sickle cell anemia. Diagnosis involves CT, MRI, and angiography. Treatment focuses on antithrombotics and rehab.
3. Hemorrhagic stroke risk factors include vascular malformations, blood disorders, and trauma. Subarachnoid hemorrhage is the most common type. Cerebral sinovenous
Stroke is an emergency condition caused by a blocked artery or burst blood vessel in the brain. It can lead to serious disability or death if brain cells are not quickly treated. The main types of stroke are ischemic, caused by a blockage, and hemorrhagic, caused by a burst blood vessel. Timely treatment is critical to minimize brain cell death and damage. Management involves stabilizing vital functions, rapidly diagnosing the type of stroke, and administering appropriate treatments such as clot-busting drugs to reduce disability. A multidisciplinary approach is needed for long-term care and rehabilitation.
This document discusses several inherited diseases including sickle cell disease, hemophilia, muscular dystrophy, cystic fibrosis, and Huntington's disease. Sickle cell disease is caused by a mutation that causes red blood cells to take on an abnormal sickle shape, leading to anemia and organ damage. Hemophilia is a bleeding disorder caused by deficiencies in clotting factors VIII or IX that is inherited in an X-linked recessive pattern. Muscular dystrophy encompasses genetic diseases that cause progressive muscle weakness and loss of muscle mass through defective muscle proteins. Cystic fibrosis is caused by a gene mutation that causes thick, sticky mucus to build up in the lungs and digestive system. Huntington's disease is an inherited
This document discusses the approach to diagnosing and treating histiocytosis syndromes in childhood. It is a diverse group of disorders involving an abnormal proliferation of histiocytes (monocyte-macrophage cells). The main types discussed are Langerhans cell histiocytosis (LCH), hemophagocytic lymphohistiocytosis (HLH), and reactive histiocytosis. LCH is characterized by Langerhans cells with Birbeck granules, while HLH involves an uncontrolled activation of macrophages and T-cells. Diagnosis involves biopsy and immunochemistry. Treatment depends on risk stratification and number of organ systems involved, ranging from monitoring to chemotherapy. Long-term follow-up is important due to the disease
Hematology oncology-nurs 3340 fall 2017Shepard Joy
This document outlines learning outcomes and content related to alterations in hematologic function and childhood malignancies. It begins by describing the functions of red blood cells, white blood cells, and platelets. It then discusses differences in pediatric hematopoiesis compared to adults. Specific topics covered include anemia, sickle cell disease, hemophilia, and childhood cancers. Nursing care is discussed for conditions such as vaso-occlusive crises, bleeding episodes, and cancer diagnosis and treatment.
This document summarizes information about cardiomyopathy in newborns and fetuses. It discusses definitions, classifications, etiologies, clinical features, diagnostic evaluations, and management strategies for various types of neonatal cardiomyopathy. It also reviews a journal article studying fetal cardiomyopathy detected on prenatal echocardiograms, finding reduced systolic function, valve issues, and chamber enlargement in some cases. Outcomes were generally poor, though early diagnosis may allow for improved postnatal management.
This document summarizes information about cardiomyopathy in newborns and fetuses. It discusses definitions, classifications, etiologies, clinical features, diagnostic evaluations, and management strategies for various types of neonatal cardiomyopathy. It also reviews a journal article studying fetal cardiomyopathy detected on prenatal echocardiograms, finding reduced systolic function, valve issues, and chamber enlargement in some cases. Outcomes were generally poor, though early diagnosis may allow for interventions to improve prognosis.
Sickle cell anemia is a genetic blood disorder caused by a mutation in the beta-globin gene that results in abnormal hemoglobin S. When deoxygenated, hemoglobin S polymerizes and causes red blood cells to take on a sickle shape, which can block small blood vessels and damage tissues. Common complications include painful vasoclusive crises, acute chest syndrome, strokes, and infections. Treatment focuses on prevention of sickling through hydration and pain management of crises with opioids when they occur.
Sickle cell disease is a genetic disorder caused by a mutation in the beta-globin chain of hemoglobin. This causes red blood cells to become rigid and sickle-shaped, leading to anemia, pain crises, and damage to organs over time. The most common acute complications are vaso-occlusive pain crises, acute chest syndrome, and stroke. Treatment focuses on prevention, management of pain and infections, and addressing chronic organ damage through screening and medications.
Cardiomyopathy, or heart muscle disease, is a type of progressive heart disease in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart muscle's ability to pump blood is less efficient, often causing heart failure and the backup of blood into the lungs or rest of the body. The disease can also cause abnormal heart rhythms.
1) Birth asphyxia and hypoxic ischemic encephalopathy occur when there is impaired gas exchange or insufficient blood flow to the baby's brain during birth, leading to brain injury.
2) The document discusses the definitions, causes, effects on multiple organ systems, investigations, management including supportive care and therapeutic hypothermia, and long-term outcomes like cerebral palsy and developmental delays.
3) The goal of treatment is to maintain the baby's vital functions, optimize cardiac output and cerebral perfusion, control seizures, and use interventions to protect the brain such as therapeutic hypothermia.
This document discusses alterations in hematologic function and childhood malignancies. It covers the following key points:
1. It describes the functions of red blood cells, white blood cells, and platelets and how they differ in children compared to adults.
2. It discusses common pediatric hematologic disorders like sickle cell disease and hemophilia, outlining their pathophysiology, clinical manifestations, diagnosis, and treatment.
3. It provides an overview of childhood cancers, including incidence, causes, signs, diagnostic tests, treatment goals like chemotherapy and bone marrow transplant, and the most common types.
A 38-year-old man presented with seizures and was diagnosed with cortical venous thrombosis. He had multiple risk factors including diabetes, hyperhomocysteinemia, and dyslipidemia. He was treated with anticoagulation but continued having seizures. Imaging later revealed a venous infarct. His symptoms gradually improved with treatment but he was discharged with some residual neurological deficits. Cortical venous thrombosis can be challenging to diagnose but outcomes have improved with prompt diagnosis and treatment. Hyperhomocysteinemia is an increasingly recognized risk factor.
Tyler Lonergan, MD, of the UC San Diego Owen Clinic, presents "Stemming the Tide of Cardiovascular Disease: Transitioning from OI to CVD Prophylaxis" for AIDS Clinical Rounds at UC San Diego
Clinical Professor
UC San Diego Owen Clinic
This document discusses risk factors for ischemic stroke. It identifies non-modifiable risk factors such as age, sex, race and heredity. The major modifiable risk factors are hypertension, atrial fibrillation, diabetes, hyperlipidemia, cigarette smoking, and physical inactivity. Approximately 90% of strokes can be explained by 10 risk factors, including these medical conditions and behavioral risks. The document provides details on how each of these factors increases the risk of ischemic stroke. It also discusses additional potential risk factors that are still under investigation.
This document discusses 3 forms of cardiomyopathy:
1) Takotsubo cardiomyopathy, which causes transient left ventricular dysfunction and can mimic ACS but has lower cardiac enzyme levels, disproportionately affecting postmenopausal women.
2) Atrial fibrillation, which can occur in hypertensive patients with left ventricular hypertrophy.
3) Hypertrophic cardiomyopathy, an inherited genetic disorder causing excessive thickening of the heart muscle and increased risk of sudden cardiac death in children, requiring treatments like implantable cardioverter defibrillators.
Cardiomyopathy in HIV patients has been shown to progress faster than idiopathic Dilated Cardiomyopathy in the HIV negative population. It is therefore important to recognize this condition early in this population and manage it appropriately. Studies need to be done to validate the current therapy for cardiomyopathy in this population since it is still unclear that LV dysfunction in this population responds in a similar fashion as in HIV negative patients with Dilated Cardiomyopathy
Antiphospholipid syndrome was first described in the 1980s and is characterized by arterial or venous thrombosis, thrombocytopenia, or recurrent fetal loss associated with antiphospholipid antibodies. It is caused by autoimmune production of antibodies against cell membrane phospholipids such as cardiolipin and β2-glycoprotein I, which disrupt the body's normal regulation of blood coagulation and increase the risk of abnormal blood clotting. The syndrome can occur on its own or in association with other autoimmune diseases such as systemic lupus erythematosus.
This document discusses paediatric stroke, including its causes, presentation, diagnosis, and management. The main types of paediatric stroke are arterial ischemic stroke, cerebral sinovenous thrombosis, and hemorrhagic stroke. Common causes include arteriopathy, cardiac issues, hematologic disorders, and perinatal factors. Clinical presentation depends on the age of onset. Diagnosis involves neuroimaging such as MRI. Management is often supportive but may include anticoagulation, revascularization procedures, or transfusions depending on the underlying condition. Prognosis depends on factors like age of onset and severity of neurological deficits.
This document discusses non-traumatic coma in children. It begins by providing incidence rates for non-traumatic coma (30 per 100,000 children per year) and traumatic brain injury (670 per 100,000). The rest of the document discusses the definition, causes, evaluation, management, and outcomes of non-traumatic coma in children. Infection is the most common cause. Mortality depends on the underlying etiology and can range from 3-84%. Overall mortality in studies is around 46%.
1. Sickle cell disease is an inherited blood disorder that affects hemoglobin and causes red blood cells to take on a sickle, or crescent, shape.
2. The prevalence of sickle cell disease varies by ethnicity, with the highest rates seen in African Americans at about 1 in 375 individuals.
3. Complications of sickle cell disease include anemia, infections, acute pain episodes, stroke, and damage to organs like the lungs, kidneys, spleen, and liver over time if not properly managed.
This case report describes an unusual case of a 31-year-old male who presented with symptoms of Wallenberg syndrome due to simultaneous bilateral infarction of the anterolateral medulla. Extensive evaluation did not reveal a clear cause of the stroke. MRI showed subacute infarcts in the anterolateral aspect of the medulla bilaterally. CT angiogram showed a hypoplastic left vertebral artery but no significant stenosis. Investigations ruled out conditions like vasculitis, vascular malformations, and cardiac abnormalities. The patient was diagnosed with cryptogenic stroke and made a near complete recovery with treatment. This case highlights the importance of thorough evaluation for young patients presenting with stroke to identify potentially treatable causes.
This document describes a case of cerebral venous thrombosis (CVT) in a 20-year-old female patient who presented with worsening headache, nausea, dizziness, and blurred vision. It provides details on her medical history, physical exam findings, lab and imaging results. CVT is an uncommon type of stroke more common in young individuals. Risk factors include genetic thrombophilias, acquired conditions like pregnancy/puerperium and cancer. Clinical symptoms vary depending on increased intracranial pressure or focal brain injury. Management involves anticoagulation to stop thrombotic process along with supportive care. Outcomes range from full recovery in 80% of patients to mortality in 6-20% depending on severity of presentation
This document discusses sudden cardiac death (SCD), providing information on:
- SCD is an unexpected death from cardiac causes within one hour of symptoms. It often occurs in people with known or unknown heart disease.
- Autopsies show most SCD victims had prior heart attacks or coronary artery disease. About 92% of SCD victims do not survive.
- Risk factors for SCD include age, male sex, family history of heart disease, smoking, diabetes, and high blood pressure. EKG abnormalities like prolonged QT also increase risk.
- Causes of SCD include coronary artery disease, cardiomyopathies, genetic conditions, and electrical issues in the heart. The most common mechanism is
Renal function tests are important for identifying, diagnosing, monitoring renal dysfunction and disease. Key tests include urinalysis to detect abnormalities in urine appearance, composition and sediments. Glomerular filtration rate (GFR) is a key measure of renal function and can be estimated using creatinine clearance from plasma and urine creatinine levels or formulas. Other tests evaluate tubular function like handling of electrolytes, acids, proteins and determine if renal issues are pre-renal or intrinsic to the kidneys. Together these tests provide vital information about renal health and disease.
This document discusses hypoglycemic agents or anti-diabetic drugs used to treat diabetes mellitus. It describes diabetes as a metabolic syndrome caused by insulin deficiency and excess glucagon that can lead to acute manifestations like hyperglycemia and chronic complications affecting small blood vessels and arteries. It outlines the different types of diabetes and treatments including insulin therapies using rapid, short, intermediate and long-acting insulins. It also discusses oral hypoglycemic drugs for type 2 diabetes including sulfonylureas, biguanides, glitazones and alpha-glucosidase inhibitors providing details on their mechanisms, uses, and potential toxicities in treatment.
This document summarizes information about cardiomyopathy in newborns and fetuses. It discusses definitions, classifications, etiologies, clinical features, diagnostic evaluations, and management strategies for various types of neonatal cardiomyopathy. It also reviews a journal article studying fetal cardiomyopathy detected on prenatal echocardiograms, finding reduced systolic function, valve issues, and chamber enlargement in some cases. Outcomes were generally poor, though early diagnosis may allow for interventions to improve prognosis.
Sickle cell anemia is a genetic blood disorder caused by a mutation in the beta-globin gene that results in abnormal hemoglobin S. When deoxygenated, hemoglobin S polymerizes and causes red blood cells to take on a sickle shape, which can block small blood vessels and damage tissues. Common complications include painful vasoclusive crises, acute chest syndrome, strokes, and infections. Treatment focuses on prevention of sickling through hydration and pain management of crises with opioids when they occur.
Sickle cell disease is a genetic disorder caused by a mutation in the beta-globin chain of hemoglobin. This causes red blood cells to become rigid and sickle-shaped, leading to anemia, pain crises, and damage to organs over time. The most common acute complications are vaso-occlusive pain crises, acute chest syndrome, and stroke. Treatment focuses on prevention, management of pain and infections, and addressing chronic organ damage through screening and medications.
Cardiomyopathy, or heart muscle disease, is a type of progressive heart disease in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart muscle's ability to pump blood is less efficient, often causing heart failure and the backup of blood into the lungs or rest of the body. The disease can also cause abnormal heart rhythms.
1) Birth asphyxia and hypoxic ischemic encephalopathy occur when there is impaired gas exchange or insufficient blood flow to the baby's brain during birth, leading to brain injury.
2) The document discusses the definitions, causes, effects on multiple organ systems, investigations, management including supportive care and therapeutic hypothermia, and long-term outcomes like cerebral palsy and developmental delays.
3) The goal of treatment is to maintain the baby's vital functions, optimize cardiac output and cerebral perfusion, control seizures, and use interventions to protect the brain such as therapeutic hypothermia.
This document discusses alterations in hematologic function and childhood malignancies. It covers the following key points:
1. It describes the functions of red blood cells, white blood cells, and platelets and how they differ in children compared to adults.
2. It discusses common pediatric hematologic disorders like sickle cell disease and hemophilia, outlining their pathophysiology, clinical manifestations, diagnosis, and treatment.
3. It provides an overview of childhood cancers, including incidence, causes, signs, diagnostic tests, treatment goals like chemotherapy and bone marrow transplant, and the most common types.
A 38-year-old man presented with seizures and was diagnosed with cortical venous thrombosis. He had multiple risk factors including diabetes, hyperhomocysteinemia, and dyslipidemia. He was treated with anticoagulation but continued having seizures. Imaging later revealed a venous infarct. His symptoms gradually improved with treatment but he was discharged with some residual neurological deficits. Cortical venous thrombosis can be challenging to diagnose but outcomes have improved with prompt diagnosis and treatment. Hyperhomocysteinemia is an increasingly recognized risk factor.
Tyler Lonergan, MD, of the UC San Diego Owen Clinic, presents "Stemming the Tide of Cardiovascular Disease: Transitioning from OI to CVD Prophylaxis" for AIDS Clinical Rounds at UC San Diego
Clinical Professor
UC San Diego Owen Clinic
This document discusses risk factors for ischemic stroke. It identifies non-modifiable risk factors such as age, sex, race and heredity. The major modifiable risk factors are hypertension, atrial fibrillation, diabetes, hyperlipidemia, cigarette smoking, and physical inactivity. Approximately 90% of strokes can be explained by 10 risk factors, including these medical conditions and behavioral risks. The document provides details on how each of these factors increases the risk of ischemic stroke. It also discusses additional potential risk factors that are still under investigation.
This document discusses 3 forms of cardiomyopathy:
1) Takotsubo cardiomyopathy, which causes transient left ventricular dysfunction and can mimic ACS but has lower cardiac enzyme levels, disproportionately affecting postmenopausal women.
2) Atrial fibrillation, which can occur in hypertensive patients with left ventricular hypertrophy.
3) Hypertrophic cardiomyopathy, an inherited genetic disorder causing excessive thickening of the heart muscle and increased risk of sudden cardiac death in children, requiring treatments like implantable cardioverter defibrillators.
Cardiomyopathy in HIV patients has been shown to progress faster than idiopathic Dilated Cardiomyopathy in the HIV negative population. It is therefore important to recognize this condition early in this population and manage it appropriately. Studies need to be done to validate the current therapy for cardiomyopathy in this population since it is still unclear that LV dysfunction in this population responds in a similar fashion as in HIV negative patients with Dilated Cardiomyopathy
Antiphospholipid syndrome was first described in the 1980s and is characterized by arterial or venous thrombosis, thrombocytopenia, or recurrent fetal loss associated with antiphospholipid antibodies. It is caused by autoimmune production of antibodies against cell membrane phospholipids such as cardiolipin and β2-glycoprotein I, which disrupt the body's normal regulation of blood coagulation and increase the risk of abnormal blood clotting. The syndrome can occur on its own or in association with other autoimmune diseases such as systemic lupus erythematosus.
This document discusses paediatric stroke, including its causes, presentation, diagnosis, and management. The main types of paediatric stroke are arterial ischemic stroke, cerebral sinovenous thrombosis, and hemorrhagic stroke. Common causes include arteriopathy, cardiac issues, hematologic disorders, and perinatal factors. Clinical presentation depends on the age of onset. Diagnosis involves neuroimaging such as MRI. Management is often supportive but may include anticoagulation, revascularization procedures, or transfusions depending on the underlying condition. Prognosis depends on factors like age of onset and severity of neurological deficits.
This document discusses non-traumatic coma in children. It begins by providing incidence rates for non-traumatic coma (30 per 100,000 children per year) and traumatic brain injury (670 per 100,000). The rest of the document discusses the definition, causes, evaluation, management, and outcomes of non-traumatic coma in children. Infection is the most common cause. Mortality depends on the underlying etiology and can range from 3-84%. Overall mortality in studies is around 46%.
1. Sickle cell disease is an inherited blood disorder that affects hemoglobin and causes red blood cells to take on a sickle, or crescent, shape.
2. The prevalence of sickle cell disease varies by ethnicity, with the highest rates seen in African Americans at about 1 in 375 individuals.
3. Complications of sickle cell disease include anemia, infections, acute pain episodes, stroke, and damage to organs like the lungs, kidneys, spleen, and liver over time if not properly managed.
This case report describes an unusual case of a 31-year-old male who presented with symptoms of Wallenberg syndrome due to simultaneous bilateral infarction of the anterolateral medulla. Extensive evaluation did not reveal a clear cause of the stroke. MRI showed subacute infarcts in the anterolateral aspect of the medulla bilaterally. CT angiogram showed a hypoplastic left vertebral artery but no significant stenosis. Investigations ruled out conditions like vasculitis, vascular malformations, and cardiac abnormalities. The patient was diagnosed with cryptogenic stroke and made a near complete recovery with treatment. This case highlights the importance of thorough evaluation for young patients presenting with stroke to identify potentially treatable causes.
This document describes a case of cerebral venous thrombosis (CVT) in a 20-year-old female patient who presented with worsening headache, nausea, dizziness, and blurred vision. It provides details on her medical history, physical exam findings, lab and imaging results. CVT is an uncommon type of stroke more common in young individuals. Risk factors include genetic thrombophilias, acquired conditions like pregnancy/puerperium and cancer. Clinical symptoms vary depending on increased intracranial pressure or focal brain injury. Management involves anticoagulation to stop thrombotic process along with supportive care. Outcomes range from full recovery in 80% of patients to mortality in 6-20% depending on severity of presentation
This document discusses sudden cardiac death (SCD), providing information on:
- SCD is an unexpected death from cardiac causes within one hour of symptoms. It often occurs in people with known or unknown heart disease.
- Autopsies show most SCD victims had prior heart attacks or coronary artery disease. About 92% of SCD victims do not survive.
- Risk factors for SCD include age, male sex, family history of heart disease, smoking, diabetes, and high blood pressure. EKG abnormalities like prolonged QT also increase risk.
- Causes of SCD include coronary artery disease, cardiomyopathies, genetic conditions, and electrical issues in the heart. The most common mechanism is
Renal function tests are important for identifying, diagnosing, monitoring renal dysfunction and disease. Key tests include urinalysis to detect abnormalities in urine appearance, composition and sediments. Glomerular filtration rate (GFR) is a key measure of renal function and can be estimated using creatinine clearance from plasma and urine creatinine levels or formulas. Other tests evaluate tubular function like handling of electrolytes, acids, proteins and determine if renal issues are pre-renal or intrinsic to the kidneys. Together these tests provide vital information about renal health and disease.
This document discusses hypoglycemic agents or anti-diabetic drugs used to treat diabetes mellitus. It describes diabetes as a metabolic syndrome caused by insulin deficiency and excess glucagon that can lead to acute manifestations like hyperglycemia and chronic complications affecting small blood vessels and arteries. It outlines the different types of diabetes and treatments including insulin therapies using rapid, short, intermediate and long-acting insulins. It also discusses oral hypoglycemic drugs for type 2 diabetes including sulfonylureas, biguanides, glitazones and alpha-glucosidase inhibitors providing details on their mechanisms, uses, and potential toxicities in treatment.
Echocardiography uses ultrasound to generate images of cardiac anatomy and function. The echocardiogram machine includes a transducer probe that transmits and receives ultrasound waves, and a display monitor. Different echocardiography modes exist, including M-mode for measuring dimensions, 2D/3D for morphology, and various Doppler modes for assessing blood flow velocity and direction. Trans-esophageal echocardiography uses a probe attached to an endoscope to obtain high resolution internal images of the heart. Echocardiography is used to evaluate conditions like thrombi, aneurysms, valves, and septal defects.
DISEASES OF THE THYROID GLAND NOVEMBER 2018.pptxKemi Adaramola
This document discusses diseases of the thyroid gland. It begins by describing the anatomy and physiology of the thyroid, including its location in the neck, histological structure, embryological development, and hormone production process. It then discusses the main thyroid diseases - thyrotoxicosis (Graves' disease, toxic nodular goiter, etc.) and hypothyroidism. For each condition, it outlines the etiology, clinical features, investigations, and treatment approaches. It also describes thyroid storm, a medical emergency representing severe thyrotoxicosis, and myxedema coma, a severe form of hypothyroidism.
This document discusses the management of diabetes mellitus in children beyond typical norms. It begins with an introduction to diabetes and classifications of types of diabetes including type 1, type 2, and maturity onset diabetes of the young (MODY). It then discusses epidemiology and the local experience with childhood diabetes at Ekiti State University Teaching Hospital. The remainder of the document focuses on treatment and management of type 1 diabetes in children, including insulin regimens, therapeutic goals, and sick day rules. It also briefly discusses type 2 diabetes in children and the differences between type 1 and type 2 diabetes.
Defibrillation is a process that delivers an electric shock to the heart to stop an irregular heartbeat and restore normal rhythm. It is the only effective treatment for cardiac arrest caused by ventricular fibrillation or pulseless ventricular tachycardia. Early defibrillation is critical, as survival rates decrease by 10% each minute without treatment. Different types of defibrillators include automated external defibrillators and implantable cardioverter defibrillators. Key factors that influence defibrillation success include transthoracic impedance, electrode placement and position, and shock waveform and energy level delivered.
PULMONARYHYPERTENSION IN HEART FAILURE.pptxKemi Adaramola
This patient presented with bilateral leg swelling, abdominal swelling, facial swelling, and exertional dyspnea over the past 2 years. She has a history of recurrent productive cough as a child treated with antibiotics. On examination she had clubbing, leg swelling up to the knees, enlarged liver, ascites, and signs of right heart failure. Investigations showed features consistent with constrictive pericarditis and severe pulmonary hypertension likely due to tuberculous pericarditis in the past. She was treated unsuccessfully for heart failure and later developed venous thrombosis, remaining in the hospital for over 50 days before leaving against medical advice due to financial constraints.
This document outlines the causes, clinical features, diagnosis, and management of an Addisonian crisis, which is a life-threatening adrenal insufficiency emergency. It may be triggered by stress, infection, trauma, or withdrawal from steroids. Symptoms include nausea, vomiting, abdominal pain, hypotension, and electrolyte imbalances. Treatment involves intravenous hydrocortisone, fluids, glucose, and identifying and treating any precipitating causes. Long term management consists of glucocorticoid and mineralocorticoid replacement therapy and patient education.
This document outlines an introduction to pulmonary hypertension including its epidemiology, etiology, pathogenesis, clinical features, treatment, and future directions. It defines pulmonary hypertension and notes the most common causes are lung diseases like COPD. In Nigeria, common causes include COPD, tuberculosis, connective tissue diseases, and sickle cell disease. The pathogenesis involves remodeling of the pulmonary vasculature from factors like endothelial dysfunction and an imbalance of vasoconstrictors and vasodilators. Over time, this can lead to right heart failure if the right ventricle can no longer compensate for the increased resistance.
This document discusses cardiovascular disease risk factors. It begins by introducing the topic and outlines the sections. The introduction notes that CVD is a leading cause of death worldwide. The epidemiology section describes the prevalence of CVD globally and in certain regions. The pathophysiology section explains the development of atherosclerosis. The traditional risk factors section lists established risks like hypertension, diabetes, and smoking. The document focuses on emerging risk factors, describing biomarkers like lipoprotein(a), apolipoprotein B, and homocysteine that can help identify risk beyond traditional factors. It discusses the evidence supporting these novel factors and their clinical implications.
This document provides an overview of the management of ascites. It discusses the epidemiology, etiology, pathophysiology, evaluation, treatment, and complications of ascites. Ascites is most often caused by portal hypertension from liver cirrhosis. Other causes include malignancy, infection, heart failure, and nephrotic syndrome. Evaluation involves diagnostic paracentesis and ascitic fluid analysis. Treatment depends on the underlying cause but typically involves dietary sodium restriction and diuretic medication. Complications include spontaneous bacterial peritonitis.
Bronchiectasis, lung abscess, and empyema are chronic lung infections that can result from complications of pneumonia. They often occur in people with underlying lung disease or immune disorders. Key features include recurrent chest infections, coughing, sputum production, and life-threatening complications like respiratory failure. Treatment involves identifying and addressing the underlying cause, airway clearance techniques, long-term antibiotics, and surgery in some cases.
This document discusses impetigo, a common bacterial skin infection caused by Staphylococcus aureus or Streptococcus pyogenes. It presents in two forms: non-bullous and bullous. Symptoms include lesions on the face or limbs that may crust over. While usually mild, impetigo can develop into ecthyma if untreated. Treatment involves cleaning the skin, removing crusts, and using topical or oral antibiotics like mupirocin, retapamulin, cloxacillin, or erythromycin. Complications may include regional lymphadenopathy or ecthyma, a deeper skin ulceration.
This document discusses acute leukaemias in adults, including acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). It covers the incidence, risk factors, pathogenesis, clinical features, classification, prognostic factors, treatment for induction and post-remission, and supportive care for AML and ALL. The prognosis for ALL in adults remains poor despite high initial response rates to therapy. Improved supportive care and bone marrow transplantation are utilized while awaiting new, better therapies for these aggressive malignancies.
This document provides an overview of blood components therapy, including their indications and guidelines for use. It discusses the various components that can be derived from whole blood, such as packed red blood cells, platelets, fresh frozen plasma, cryoprecipitate, and granulocytes. Storage conditions, shelf lives, and therapeutic doses are provided. The main reasons for transfusion in Africa are described as childhood malaria, hemoglobinopathies, obstetric bleeding, trauma, and certain surgical procedures. Contraindications and risks of transfusion-transmitted infections are also covered. The document emphasizes considering alternatives to transfusion and whether benefits outweigh risks in each clinical situation.
This document provides an overview of haemoglobinopathies with an emphasis on sickle cell anaemia (SCA). It describes the complications and types of crises seen in SCA, how to identify them, and the modalities for treating various crises in the local environment. The introduction defines qualitative and quantitative haemoglobin abnormalities. It then outlines SCA pathogenesis, epidemiology, complications including vaso-occlusive crisis, management of crises through treatment of pain and infections, and prevention of sickle cell crises.
This document discusses Lassa fever, an endemic viral hemorrhagic fever found in parts of West Africa including Nigeria. It was first identified in 1969 after an outbreak infected and killed healthcare workers. The virus is transmitted from rodents to humans and can also spread between humans. Symptoms include fever, headache and bleeding. Diagnosis involves ELISA, virus isolation or PCR. Treatment is supportive, though the antiviral ribavirin may help if given early. Prevention focuses on rodent control, barrier nursing and safe medical practices. Nosocomial outbreaks remain a risk where infection control is poor. The document provides extensive details on the virus, epidemiology, transmission, clinical features, treatment and control of Lassa fever.
This document provides an overview of pituitary disorders, including:
- The pituitary gland regulates other endocrine glands and is regulated by the hypothalamus. It has anterior and posterior lobes.
- Anterior pituitary disorders include hyposecretion (hypopituitarism), hypersecretion (adenomas like prolactinomas and Cushing's disease), and sella enlargement.
- Causes of hypopituitarism include invasion, infarction, infiltration, injury, infections, immunologic issues, being iatrogenic, or being idiopathic. Symptom onset is gradual and follows a sequence of hormone deficiencies.
- Hyperfunctioning disorders include prolactinomas, acromegaly/
1. Stroke is defined as an acute brain attack caused by a disruption of blood flow, leading to neurological dysfunction lasting more than 24 hours.
2. Stroke is a leading cause of long-term disability worldwide and a major risk factor is hypertension. Diagnosis involves assessing symptoms, risk factors, and imaging of the brain.
3. There are two main types of stroke - ischemia caused by blockage of a blood vessel and hemorrhage caused by bleeding within the brain. Imaging is needed to distinguish between types and guide treatment.
Primary adrenal insufficiency, also known as Addison's disease, is caused by destruction or dysfunction of the adrenal cortex resulting in deficiencies of glucocorticoids and mineralocorticoids. Thomas Addison first described the clinical presentation in 1855. It most commonly presents with hyperpigmentation, dizziness, weakness, and weight loss. Diagnosis involves tests showing a lack of response to ACTH stimulation and electrolyte abnormalities. Treatment is lifelong glucocorticoid and mineralocorticoid hormone replacement to prevent adrenal crises.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th 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.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
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.
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.
Tests for analysis of different pharmaceutical.pptx
stroke2.ppt
1. A Lecture delivered on the 6th of August 2012 at the
REVISION / UPDATE COURSE
Organized by
The West African College of Physicians
on
MANAGEMENT OF STROKE
By
Prof. Yomi Ogun
BSc (Hons); MBChB; Cert. Neurol. (Lond); FWACP; FACP.
Professor of Internal Medicine / Neurology
Consultant Physician / Neurologist.
Provost Obafemi Awolowo College of Health Sciences
Olabisi Onabanjo University Teaching Hosp. Sagamu
Venue: University College Hospital; Ibadan
11/7/2022 1
2. Management of stroke
Cerebral Infarction (CI),
Intracerebral Haemorrhage (ICH)
Sub – Arachnoid Haemorrhage (SAH)
11/7/2022 2
3. What is stroke?
Historical remarks:
Hippocrates (460 – 370BC) “first describtion of phenomenon of
sudden paralysis”
Greek word “Apoplexy” ( “struck by violence”),
spiritual attacks
Witch theory / Step-mum theory / Wicked Mother in law
offended the gods /godesses (unable to speak, move part of the
body; “Agbero”; “Ofa” “Ota”, “Ita”)
3
4. Definition – new concept
• The 24 hrs time based no longer acceptable: confusing;
misleading; outdated
• It does not suggest a medical emergency (Brain attack) and the
mantra “time’s neuron
• (cf Time’s muscle by cardiologist)
• Does not take into cognizance the use of thrombolytics within 270
mins (4 ½ hrs) in CI or Recombinant activated factor VII within 4
hours in ICH
• TIA no longer considered as benign
• Risk of developing stroke- 10% in one wk; 15% in one month,
20% in 90 days;
• (½ of these in 24 –48 hrs.)
• age ; D.M; > 10 mins; weakness; impaired speech
• TIA and stroke = One hour
• Most (90%) TIA lasts 10 mins; resolve in 30 mins. If symptoms last
> I hr; chances of resolution:15%
4
5. TIA / Stroke – new definition
Tissue – based / Time – based definition
• TIA: No objective evidence of acute infarction in
the affected region of brain or retina; < I hour
• Stroke : objective evidence of infarction
irrespective of duration of clinical symptoms.
• (Compared to Angina pectoris vs Myocardial
infarction )
• CT/MRI necessary to increase diagnostic accuracy
• CITS = RIND.
5
9. STROKE EMERGENCY BRAIN IMAGING:
NONCONTRAST CT SCAN
Acute (4 hours)
Infarction
Subtle blurring of gray-white
junction & sulcal effacement
Subacute (4 days)
Infarction
Obvious dark changes &
“mass effect” (e.g.,
ventricle compression)
R
R L L
10. Epidemiology
• Stroke is a common neurological problem
• 1 out of every 6 adults would develop stroke in a lifetime
• Every 12 seconds, one adult develops stroke in the world.
• (six adults in every one minute)
• 15 million cases yearly (2/3rd developing world)
• 6 million deaths yearly; Second leading cause of all deaths
worldwide
• Leading cause of disability in adults (5 million).
• One of the most costly disease in low and middle income
countries (T he inverse burden-knowledge relationship)
• 1 person dies of stroke every 6 seconds in the world,
• Account 4.5-17% of all admissions in hospital based studies- Nig
• 2.8 – 4.5% of deaths case fatality: = 35% (14.9 – 77%)
• community prevalence = 58 – 400/ 100,000
10
12. Possible Aetiology/ Risk factors - CI
• Migraine / Cigarette
• Hyperlipidaemia / Obesity
• Lack of exercise (physical inactivity)
• Hypotension / Dehydration
• Hypothyroidism / Hyperuricaemia
• Hypercoagulable states – anti-phospholipid syndrome ;
Protein C / S def.; Anti-thrombin 1 def.
• CCF / Severe Anaemia ; Low S – E status (unknown
hypertensive; undernutrition; infectn) Black race; male
sex; positive family hx ; HIV ;
12
13. Aetiology / Risk factors - CI
Modifiable
Well documented HTN, DM, Smoking, non-valvular
atrial fibrillation, asymptomatic carotid stenosis,
hyperlipidemia, sickle-cell dx.
Less well documented / potentially doc;
Alcohol abuse, obesity, physical inactivity,
hyperhomocystenemia, drug abuse, hypercoagulable
state, HRT, OCP and inflammatory processes.
non-modif. age, race, sex, family hx stroke/ TIA
severity of stroke at onset; comorbidities
13
14. Stroke in the Young
• Age grp: 15-45yrs; (40% Haemorrhagic)
• Migraine ;
• Heroine, cocaine, methamphetamine, oral
contraceptives ;
• prothrombotic state; Coagulopathies vasculitis
/ connective tissue dx
• Haemoglobinopathy
• HIV
11/7/2022 14
15. Stroke in the young
• Arteritis (Takayasu ,kawasaki)
• Moyamoya syndrome
• Cardiac: - congenital cardiac lesions atrial
ventricular and pulmonary vascular shunting,
Mitral valve prolapse ;
• Patent foramen ovale;
• Tetralogy of Fallot’s
• Cardiomyopathies
• Dissection and traumatic vascular injuries
• Cerebral venous thrombosis
• Infection of the endothelium
11/7/2022 15
16. Stroke and HIV
AIDS patients - higher risk for CI than ICH.
cerebral ischemia
non-bacterial thrombotic endocarditis
CI ( stroke-like syndrome: stroke mimics)
concomitant opportunistic CNS infection
Cryptoccocoma; Tuberculoma; Toxoplasma abscess;
Kaposis sarcoma;cerebral lymphoma
Intra cerebral haemorrhage
thrombocytopenia/Thromboasthenia
(Thrombocytopathy),
primary CNS lymphoma or metastatic kaposis sarcoma.
11/7/2022 16
17. Stroke and HIV
Pathobiology – ? clear
Vasculitis - HIV associated vasculopathy
> deposition of circulating Ig complexes
direct toxic effect of virus on the vascular
endothelium.
Anti-phospholipidsantibodies,including
anticardiolipin antibodies - high frequency
11/7/2022 17
18. ICH : Risk factors
• Age, male sex, hypocholesterolaemia / low
Triglyceride
• Alcohol abuse,(SAH: Linear; ICH: U; CI: J)
• illicit drugs, iatrogenic
• Diet high in salt and saturated fat intake
• Diet low in K+, polyunsaturated fatty acids and
fish oil.
• Physical inactivity , stressful life events; Low
socio-economic class
• The association is strong, dose related and
consistent
11/7/2022 18
19. Potential new Risk factors
Genetic polymorphisms
(e.g phosphodiesterase 4D, 5-lipoxygenase activating
protein, methylane tetrahydrofolate reductase
(MTHFR) C677T, angiotensin-converting enzyme,
Factor V Leiden Arg 506 Gln, prothrombin G 20210
A, and apolipoprotein E),
Inflammatory markers (C- reactive protein ,
interleukins [e.g IL-6, IL-18]), soluble CD 40 ligand,
leucocyte count, monocyte count, serum amyloid A),
11/7/2022 19
20. Potential new Risk factors
11/7/2022 20
Infectious agents (cytomegalovirus,
Chlamydia pneumonia, Helicobacter
pylori, herpes simplex virus, peridontal
disease)
Lipid-related factors (apolipoproteins B
and A1, LDL particle size, small dense low
density lipoprotein [LDL], lipoprotein (a),
oxidized LDL),
21. Potential new Risk factors
Haemostasis/thrombosis markers (fibrinogen, protein Z, von
Will-brand factor antigen, plasminogen activator inhibitor 1,
tissue-type plasminogen activator, factor V, VII and VIII; D-
dinner, fibrinopeptide A, prothrombin fragment 1 and 2
antiplatelet drug resistance).
Behavioural factors (alcohol, inactivity, poor nutrition,
obesity).
Pyschosocial factors (depression, social isolation, lack of social
support)
Other factors (homocysteine, microalbuminuria/renal disease,
metabolic syndrome, obstructive sleep apnoea)
11/7/2022 21
22. Genetics of stroke - Polygenic
• Majority of px- Genetic factors may interact with other risk
factors (aging, hypertension) to increase risk of ICH
• Confers only a low risk to1st degree relatives
• Huge genetic heterogeneity wth wide spectrum of low risk
alleles involved
• 2 genes identified in ICELAND: - No practical clinical
implication
• Search for a stroke gene continues: Loci on chromosomes 5
and 19 (Apolipoprotein E); KRITI gene mutation are assoc wth
vascular events / malformations.
• A) PDE4D (Phosphodiesterase 4D)
• B) 5 Lipooxygenase activating protein (ALOX5AP)
11/7/2022 22
23. Stroke genetics - CI
• A familial dx with unclear genetic risk
factor
• +ve family hx - increase the odds of
having stroke by about 30%
• Hereditary of stroke is heterogeneous
across ischemic stroke subtypes, with
cardioembolic stroke being least
heritable.
23
24. Stroke genetics: Monogenic
• Minority
• confers high risk to mutation carriers and relatives
• > 50 varieties reported in small and large artery
diseases, CTD, Prothrombotic disorders, carvernous
malformation
• CADASIL, CAA = Monogenic autosomal dominant
varieties
• SAH : marfans, polycstic kidney disease coarctation
of the Aorta Connective Tissue disease
• Locus 7q11
11/7/2022 24
25. Risk factors – ICH - genetic
Inherited amyloidopathies
• Vascular malformations
• Coagulopathies
• Polymorphism in apolipo protein E gene
(ApoE) - major risk factor for lobar ICH
• ApoEe4 allele increase risk of ICH in CAA
11/7/2022 25
26. Pathophysiology / genesis
progression and extent of ischemic injury
is influenced by;
• Health of systemic circulation
• Status of collateral circulation
• age
• co-existing metabolic abn (hyperglycaemia)
• Premorbid medicationn + confounding factor
• The rate of onset and duration,-
• Hematological factors,-
• Temperature
• glucose metabolism.
26
27. Virchow’s triad
• Flow: stasis
• Wall: endothelium (largest organ in d body) -
vascular injury
• Blood cellular components: viscosity/coagulablty
• white clots: platelets + fibrin (slow circltn)
• red clots: rbc+fibrin(damaged endothl + fast circl
• CI is an heterogenous entity: Interactn bt platelets,
plasma proteins (embolism; homostatic coagulation
abnormality)
• and vascular wall (penetrating small A. vasculopathy
+ vascular irregularity)
11/7/2022 27
28. EXTRACRANIAL / INTRACRANIAL
EXTRACRANIAL
• endothelial plaque / plaque
rupture
• Common in whites
• Common in males
• Associated with
hyperlipidaemia
• Smoking
• Assoc PVD and CAD
• > CRP (? Genetics)
INTRACRANIAL
• Insitu thrombus
• Smaller vessels
• Common in blacks and
Hispanics
• Commoner in females
• Associated with
hypertension
• Associated with D.M /
Metabolic Syndrome.
11/7/2022 28
32. Clinical features
• Depends on location/extent
• CLINICAL
• PATHOLOGICAL
• AETIOLOGICAL
• ANATOMICAL Diagnosis
11/7/2022 32
33. Pathological: WHO Criteria
C.I C.H
• L.O.C. -ve +ve
• Headache - ve +ve
• Vomiting - ve +ve
• T.I.A. +ve - ve
• Gradual onset +ve -ve
• Activity -ve + ve
• HBP mild /-ve mod/severe
• Bldy csf -ve + ve
• Meningeal signs -ve +/-ve
11/7/2022 33
34. Table 1 :PHASES OF CONTEMPORARY MANAGEMENT OF STROKE
Phases Period from onset Activities Prefered location
1Acute (emergency)
care:
Hyperacute: 4.5hrs
Acute : 48hrs
1st-7th day a)Assessment
b)Early supportive
care
Stroke Unit
Hospital
2 Early sub-
acute(supportive)
care
2nd-4th week a) prevention and
treatment of
complications
Hospital
3 Late sub-
acute(maintIanance)
care
2nd-6th month a)Rehabilitation
b)Psychological
support
c)Prevent recurrence
Hospital/Community
4.Long-term (chronic)
care
7th month onwards a) Rehabilitation
b)Psychological support
c)Social support
d)Prevent recurrence
Community
11/7/2022 34
37. Act FAST
• What is FAST? FAST requires an assessment of 3 spp.
symptoms of stroke:
• Facial weakness - can the person smile? Has their
mouth or eye drooped?
• Arm weakness - can the person raise both arms? Is one
arm or leg weak?
• Speech problems - can the person speak clearly and
understand what you say?.
• Time to call or go straight to the hospital.
• If failed any one of these 3 tests , act fast.
38. “Brain attack”
Time is brain is the key concept Time lost = Brain
lost 200 billion neurons in the brain 2 million
neurons lost per minute Age 3.6 years per hour of
hypoxia
Lost / hr : 830 billion synapses (14 billion
synapses /min)
Lost / hr: 714 km of myelinated fibres
(12 km fibres / min)
39. TIME IS BRAIN;
TIME IS NEURONE
• TIME IS BRAIN;
• TIME IS NEURONE
11/7/2022 39
40. Acute Neuro-Vascular Syndrome:
Stroke care
• Pre-hospital: Train emergency paramedics
Pre-arrival notification
• Emergency dept
• Stroke unit
• acute care:
• in a vascular unit (includes CI; MI; TIA, PE) or
Neuro ICU
11/7/2022 40
41. Treatment
Aims to
Rx underlying disease process if possible
Protect ischemic brain tissue from necrosis
attempt to reverse/limit the degree of brain
dysfunction
Prevent and treat complications
Rehabilitate the disabled patient physio /ccupational
/speech / swallow therapy
Prevent reoccurrence
11/7/2022 41
42. Treatment
• Thrombolytic therapy
• Early antithrombotic treatment
• Treatment of elevated intracranial pressure
• Prevention and management of complications
• No 2 strokes are alike / same for 2 individuals
• Need to individualize Rx
• Response not the same for 2 individuals
11/7/2022 42
43. Treatment
• Traditional: ‘wait and see’
• Now: ‘Watch and intervene as appropriate’
• Stroke unit:
– multidisciplinary committed professional staff: Physician:
neurosurgeon; physiotherapist; occupational / Speech (largo
paedics) swallow therapist; nursing staff and social worker
– < mortality; < morbidity in survivors (> 20%)
– < need for institutional care; < dependency
43
44. Stroke Unit
• All stroke pts: irrespective of gender, age, stroke
type, subtype and severity,
• dedicated / geographically defined part of a hospital
/ specialised staff with coordinated multidisciplinary
expert approach to Rx/ care
• Keep > = 24 hrs
• Assessment and diagnosis (exclude mimics)
• Early assessment of nursing and therapy needs
• Early mobilization, prevention of complications, Rx of
hypoxia, >glycaemia, pyrexia and dehydration.
• Ongoing rehabilitation; Coordinated multidisciplinary team
care; early assessments of needs > discharge
11/7/2022 44
45. Stroke Unit
• diagnostic tests to df types of stroke, assess underlying
cause of CI, prognosis, rule out other brain diseases or
stroke mimics, identify concurrent diseases or
complications
• Assessment of neurological and vital functions parallels Rx of acutely
life-threatening conditions.
• Hx on risk factors for arteriosclerosis/cardiac dx
• Initial o/e: breathing and pulmonary function
• BP / HR; Targeted neurological examination
• Observation of early signs of dysphagia
• arterial oxygen saturation; clinical chemistry, coagulation ;
haematology
11/7/2022 45
46. Assessment
• All pts: Brain Imaging: CT or MRI
• Chest X-ray; ECG; Echocardiography;
• FBC; platelet count, PT or INR, PTT; CRP/ESR electrolytes,
glucose; LFT / Renal fn
• correlation between lacunar stroke and HB, None
between Hb and non-lacunar; leucocytosis is associated
with poor prognosis
• Urinalysis - Microalbuminuria predicts haemor
transformation in CI– endothelial dysfunctn
• In selected patients: Duplex / Doppler ultrasound MRA or
CTA
• Diffusion and perfusion MR or perfusion CT
• Pulse oximetry and arterial blood gas analysis
• Lumbar puncture; EEG ;Toxicology screen
11/7/2022 46
47. Stroke bio-markers
• Cf cardiac specific Troponin, CPK, LDH)
• Serum S 100 β - CI (Astroglial protein)
• Serum Glial fibrillary acidic protein (GFAP) -
ICH
• H –fatty acid binding protein (H-FABP)
• Apo lipoprotein CI (Apo CI) - CI
• Apo lipoprotein C III (Apo C III) - CI
• Serum Amyloid A (SAA)
• Antithrombin III (AT-III) fragment
47
61. rtPA
• iv rtPA : 0.9 mg/kg BW, maximum 90 mg), with 10%
of the dose given as bolus followed by a 60-minute
infusion)
• BP >= 185/110 must be lowered; < 80 yrs
• ia Rx: < 6hrs : MCA / Basilar occlusion.
• Contraindication wake –up stroke
– DM + previous stroke
– pts on oral anticoagulants
– BP > 185 / 105 (>> haem risk)
– age > 80 years; minor stroke ????
11/7/2022 61
62. rtPA
• > bleeding risk: > glucose, hx of DM / CCF
• baseline symptom severity, advanced age, increased
time to Rx, previous aspirin use.
• 3-15% qualify; One out of 3 recover
• > ½ not fully recover. rtPA not panacea
• Complete recanalisation: 20%
• Partial recanalisatn:30% No recanalisatn: 25%
• TCD / DSA: Recanalisation not equal to reperfusion
(different scales); reperfusion better
• MRI/CTscan perfusion mismatch at 24hrs
11/7/2022 62
63. Desmotelpase
• Fd in saliva of Vampire bats
• 80% recanalisation achieved
• Time 8hrs
• < Risk benefit ratio
• No phase 3 evidence yet
• No BBB damage
• Not neurotoxic (cf Alteplase)
• No age restrictions
11/7/2022 63
64. Other treatment options
• Newer Anti-thrombotics
• Neuroprotectants (Mg So4) – vasodilator)
• +IV cooling with iced saline via IVC
• USS clot lysis
• Endovascular Rx.
• Mechanical recanalisation
11/7/2022 64
65. Antithrombotics
• Aspirin/ Trifluzal 600 mg/dly : structurally related;
no > B.time; efficacy same. Prasogrel
• within 48hrs – reduce risk of mortality/ disability
• Binding site of platelets with fibrin: GP inhibitors
Abciximab-antibody: GPIIB / III A receptor inhibitor < 5hrs
• Phase 3 trial stopped b/c of > bleeding
• Thienopyridines : Ticlopidine; clopidogrel
• (prevents binding of PL to fibrinogen/inhibits PL aggregation/prevents ADP binding to PL receptor: & impair ADP
mediated action of GP Iib/IIIa complex): impair PL degranulation). not block GP receptor)
• Binding site of platelets to endothelium:
– PDI: Dipyridamole (PDE5) ; Cilostazole (PDE3)
(suppress cAMP degradation; > cAMP= inhibit PL aggregation; vasodilatation +)
11/7/2022 65
69. New antithrombotic agents in stroke Rx
and prevention
• Ximelagatran – direct thrombin (? Trypsin) inhibitor –
• prevent clot formation, propagation and embolisation.
• Not require frequent monitoring of coagulation or dose
adjustment Risk of bleeding is reduced compared with warfarin.
• Withdrawn b/c of hepatotoxity .
• DABIGATRAN is recommended.
• Not cross BBB; not hepatotoxic
• Cardioembolic stroke:
• (30 days case fatality: 25%;1 year case fatality: 50%)
11/7/2022 69
70. statins
• < platelet aggregation: < thrombus formation
• < BP (prevent haemorrhage)
• Neuroprotectives
• Plaque stabilisation
• improve endothelial function
• Anti-inflammatory
• Upregulate Nitric oxide synthase
• ( > HDL: Niacin; exercise; red wine; ? Life style
modification)
• Aim: High risk: < LDL100; v hg risk: <70
• > ?? Haemorhagic stroke
11/7/2022 70
71. Neuroprotective agents (Neuroprotectants)
• Neurorestorative / Neuroregenerative
• Neuroprotective / Neuroproliferative
Protect N from adverse milleu created by the biochemical changes triggered
by ischaemia:
attenuate neuronal injury
• free radical scavengers – Vit C ; E ; 21-aminosteroid ; antioxidants
tirilazad
• inhibitors of excitatory A.A. (NMDA receptor blockers – MK – 801)
Glutamate antagonists
• Caspace (apoptosis) inhibitors
• Lysosomal protease (necrosis) inhibitors
• Ca2+ antagonist – nimodipine
• Barbiturates; hypothermia; steroids (<met. Demand)
• Citicoline
11/7/2022 71
72. Neuroprotectants
• Naftidrofuryl
> efficiency of substrate use;
< lactate level; >supply of ATP
• lengthens the window period
NO (Nitric oxide) synthase inhibitors
(neuronal / inducible) cytotoxic
endothelial vasodilate protective
Repinotan - 5 HT1a Agonist - CI
Mg failed; Citicoline promising
11/7/2022 72
73. Neuroprotectants
• Cerebrolysin: a peptide with neurotrophic effect
• BDNF: (Brain Derived Neurotrophic Factor)
• one of the “Neurotrophin” family of growth factors th
regulates neuronal survival and protects from
glutamate induced damage.
• encourages proliferatn,differentiatn of new Neurons
• BDNF pathways are involved in cell survival, neuron –
protection, brain plasticity and neurogenesis.
• Neuronal cells require BDNF to regenerate
11/7/2022 73
74. Stem cell transplantation
• Rationale:Replace necrotic cell / take over fn
• Secrete trophic factors to maintain marginally surviving cells or
enhance local environment
• Sprouting new axons and synapse formation .
• Sources:
– Fetal stem cells
– Neuroprogenitor cells (fd in periventricular region of developing/adults B. –migrates to area of
injury and differentiate. autologous neural progenitor: paracrine / indirect effecteg: adipose
tissue derived is minimally invasive
– Bone marrow stromal cells: diffrentiate to multiple cell types including N
– Multipotential cells: from umbilical cord blood
– Immortalised cell line : Human embryonic carcinoma derived cell lines.
11/7/2022 74
75. Stem cell transplantation
• PD: dopaminergic cell replacement.
• Stroke: multiple cell types and neurotransmitters
lost.
• Several Potential pitfalls;
• Success in animals yet to translate to humans
• Cautious optimism and healthy skeptical reserve;
• Ethical concerns
• Depends:Subtypes of Stem cell/time after ictus
11/7/2022 75
76. Experimental sonothrombolysis:
• USS has thrombolytic potentials and can be
used for pure mechanical thrombolysis or
facilitate enzymatic mediated thrombolysis
• TCD use for 3hours (2 hrs whilst on rtPA and I
hr thereafter).
• Operator independence: hand held TCD
11/7/2022 76