Cardiac Arrhythmias ppt
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Cardiac arrhythmias : VF,VT,AF,A FLUTTER, SVT, HEART BLOCKS, JUNCTIONAL RHYTHMS , ECG Interpretations, management,Latest research findings, Technological advancement in treatment
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5. dic dr. sinhasan- mdzah
DIC is an acquired syndrome characterized by systemic intravascular coagulation and thrombosis. It has multiple potential causes including infection, cancer, trauma, and obstetric complications. The morbidity and mortality of DIC depends on the extent of thrombosis and bleeding from depletion of platelets and coagulation factors. Diagnosis involves evaluating for a condition associated with DIC, signs of thrombosis or bleeding, and abnormal lab tests like low platelet count and elevated D-dimer. Treatment focuses on treating the underlying cause and providing supportive care like plasma or platelet transfusions.
14 diminished concentration of contrast material in the
Diminished concentration of contrast material in the pelvicalyceal system can be seen in three conditions:
1) Nephrotic syndrome causing renal failure where enlarged kidneys show decreased opacification of collecting systems.
2) Malignant nephrosclerosis where small, smooth kidneys demonstrate minimum opacification five minutes after contrast injection.
3) Renovascular hypertension where a film three minutes after contrast shows no left calyceal opacification in a patient with left renal artery stenosis.
Infarct
This document discusses infarcts, which are areas of ischemic necrosis caused by occlusion of the arterial supply or venous drainage. It defines infarcts and lists common causes like thrombotic occlusion. It describes different types of infarcts based on color, age, and presence of infection. Pathogenesis involves local hyperemia, edema, hemorrhage, and cellular changes leading to necrosis replaced by fibrous tissue. Gross morphology shows wedge-shaped areas pointing toward the occluded vessel. Microscopy shows coagulative necrosis and inflammatory reaction at the periphery replaced by fibrous tissue. Commonly affected organs and outcomes are also outlined.
Approach to Disseminated intravascular coagulation
This document from Williams Hematology discusses disseminated intravascular coagulation (DIC). It defines DIC as occurring when procoagulants overwhelm the body's natural anticoagulation mechanisms, leading to systemic thrombin generation and microthrombi formation. Common triggers of DIC include tissue factor exposure, infections, tumors, trauma, and pregnancy complications. The document outlines various underlying conditions that can predispose patients to DIC and discusses approaches to diagnosis and treatment.
Cavernous malformations
Cavernous malformations are vascular lesions composed of thin-walled, blood-filled sinusoids known as caverns. They are angiographically occult and low-pressure. These lesions are caused by mutations in CCM genes that result in abnormal angiogenesis and vascular integrity. This leads to immature and fragile vasculature that is prone to hemorrhage, further activating lesion growth. Histologically, they appear as lobulated reddish lesions containing blood-filled caverns surrounded by hemosiderin staining from previous hemorrhages.
Pathophysiology of Diabetic retinopathy
Diabetic retinopathy is caused by pathological changes to the retina due to hyperglycemia. The breakdown of the blood-retinal barrier leads to vascular permeability and leakage. This results in retinal edema, hemorrhages, and exudates. Over time, there is loss of pericytes and endothelial cells, capillary nonperfusion, and upregulation of growth factors like VEGF. Eventually, this causes the development of proliferative retinopathy characterized by neovascularization and fibrovascular proliferation. The pathological effects of hyperglycemia are mediated through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and increased oxidative stress - all of which disrupt the normal vascular physiology in
Ischemia,necrosis,hypoxia
This document provides information on ischemia, necrosis, and their causes and types. It defines ischemia as insufficient blood supply causing oxygen and nutrient shortage. Causes include embolism, thrombosis, and aneurysm. Signs include tissue damage within minutes in highly aerobic tissues. Types are discussed like cardiac and limb ischemia. Necrosis is defined as cell death from loss of membrane integrity. Causes include anoxia, ischemia, chemicals and infections. Changes include cytoplasmic and nuclear changes. Necrotic cells may persist or be digested. Types discussed are coagulative, liquefactive, and caseous necrosis.
Ischemia reperfusion
This document discusses ischemia-reperfusion injury, which occurs when blood flow returns to tissues that had previously lost their blood supply. It causes further damage beyond what occurred during ischemia alone. The two phases of injury - ischemic and reperfusion - each have unique cellular and systemic consequences. Clinically, it can cause issues like compartment syndrome, gastrointestinal/renal injury, and myocardial dysfunction. The pathophysiology involves hypoxia, inflammation, apoptosis, reactive oxygen species generation, and nitric oxide imbalance. Strategies to prevent or reduce injury include ischemic preconditioning, antioxidant therapy, anti-complement therapy, and antileukocyte therapy.
Recommended
5. dic dr. sinhasan- mdzah
DIC is an acquired syndrome characterized by systemic intravascular coagulation and thrombosis. It has multiple potential causes including infection, cancer, trauma, and obstetric complications. The morbidity and mortality of DIC depends on the extent of thrombosis and bleeding from depletion of platelets and coagulation factors. Diagnosis involves evaluating for a condition associated with DIC, signs of thrombosis or bleeding, and abnormal lab tests like low platelet count and elevated D-dimer. Treatment focuses on treating the underlying cause and providing supportive care like plasma or platelet transfusions.
14 diminished concentration of contrast material in the
Diminished concentration of contrast material in the pelvicalyceal system can be seen in three conditions:
1) Nephrotic syndrome causing renal failure where enlarged kidneys show decreased opacification of collecting systems.
2) Malignant nephrosclerosis where small, smooth kidneys demonstrate minimum opacification five minutes after contrast injection.
3) Renovascular hypertension where a film three minutes after contrast shows no left calyceal opacification in a patient with left renal artery stenosis.
Infarct
This document discusses infarcts, which are areas of ischemic necrosis caused by occlusion of the arterial supply or venous drainage. It defines infarcts and lists common causes like thrombotic occlusion. It describes different types of infarcts based on color, age, and presence of infection. Pathogenesis involves local hyperemia, edema, hemorrhage, and cellular changes leading to necrosis replaced by fibrous tissue. Gross morphology shows wedge-shaped areas pointing toward the occluded vessel. Microscopy shows coagulative necrosis and inflammatory reaction at the periphery replaced by fibrous tissue. Commonly affected organs and outcomes are also outlined.
Approach to Disseminated intravascular coagulation
This document from Williams Hematology discusses disseminated intravascular coagulation (DIC). It defines DIC as occurring when procoagulants overwhelm the body's natural anticoagulation mechanisms, leading to systemic thrombin generation and microthrombi formation. Common triggers of DIC include tissue factor exposure, infections, tumors, trauma, and pregnancy complications. The document outlines various underlying conditions that can predispose patients to DIC and discusses approaches to diagnosis and treatment.
Cavernous malformations
Cavernous malformations are vascular lesions composed of thin-walled, blood-filled sinusoids known as caverns. They are angiographically occult and low-pressure. These lesions are caused by mutations in CCM genes that result in abnormal angiogenesis and vascular integrity. This leads to immature and fragile vasculature that is prone to hemorrhage, further activating lesion growth. Histologically, they appear as lobulated reddish lesions containing blood-filled caverns surrounded by hemosiderin staining from previous hemorrhages.
Pathophysiology of Diabetic retinopathy
Diabetic retinopathy is caused by pathological changes to the retina due to hyperglycemia. The breakdown of the blood-retinal barrier leads to vascular permeability and leakage. This results in retinal edema, hemorrhages, and exudates. Over time, there is loss of pericytes and endothelial cells, capillary nonperfusion, and upregulation of growth factors like VEGF. Eventually, this causes the development of proliferative retinopathy characterized by neovascularization and fibrovascular proliferation. The pathological effects of hyperglycemia are mediated through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and increased oxidative stress - all of which disrupt the normal vascular physiology in
Ischemia,necrosis,hypoxia
This document provides information on ischemia, necrosis, and their causes and types. It defines ischemia as insufficient blood supply causing oxygen and nutrient shortage. Causes include embolism, thrombosis, and aneurysm. Signs include tissue damage within minutes in highly aerobic tissues. Types are discussed like cardiac and limb ischemia. Necrosis is defined as cell death from loss of membrane integrity. Causes include anoxia, ischemia, chemicals and infections. Changes include cytoplasmic and nuclear changes. Necrotic cells may persist or be digested. Types discussed are coagulative, liquefactive, and caseous necrosis.
Ischemia reperfusion
This document discusses ischemia-reperfusion injury, which occurs when blood flow returns to tissues that had previously lost their blood supply. It causes further damage beyond what occurred during ischemia alone. The two phases of injury - ischemic and reperfusion - each have unique cellular and systemic consequences. Clinically, it can cause issues like compartment syndrome, gastrointestinal/renal injury, and myocardial dysfunction. The pathophysiology involves hypoxia, inflammation, apoptosis, reactive oxygen species generation, and nitric oxide imbalance. Strategies to prevent or reduce injury include ischemic preconditioning, antioxidant therapy, anti-complement therapy, and antileukocyte therapy.
08 dic
patholophysiology of DIC Disseminated intravascular coagulation
Pathophysiology（病理生理学）
Pathology
uploaded by prabesh 杰诗
Neurology
The document provides information on several neuropathology topics including glioblastoma multiforme, recent infarct, meningioma, Alzheimer's disease, spinal bifida, astrocytoma, and cerebral atrophy. It describes the etiology, pathogenesis, epidemiology, gross and microscopic features, and clinical correlations for each condition over multiple paragraphs.
Infarction
This document provides information about myocardial infarction including:
- Myocardial infarction is caused by interruption of blood supply to the heart muscle, usually due to blockage of a coronary artery.
- Risk factors that can lead to coronary artery blockage include hypertension, hyperlipidemia, diabetes, and smoking.
- A thrombus or embolism in a coronary artery cuts off the blood supply, causing cell death in the affected heart muscle area.
- The location and size of the infarction depends on which coronary artery is blocked. Transmural infarcts that penetrate the full heart wall thickness are more likely to cause complications than smaller subendocardial infarcts.
DISSEMINATED INTRAVASCULAR COAGULATION
DIC is one condition that always trouble patients and doctor, though its a nightmare for any clinician , its also a potent question in both UG and PG exams. I hope this will help you in answering those questions well.
Berry aneurysm
This document discusses berry aneurysms, which are thin-walled bulges that can form on arteries in the brain. Specifically:
- Berry aneurysms are the most common type of intracranial aneurysm, forming at arterial branch points in the circle of Willis which supplies blood to the brain.
- Risk factors for berry aneurysms include smoking, high blood pressure, age over 40, and genetic factors. Ruptured aneurysms have a high risk of death or permanent neurological deficits.
- Symptoms of an unruptured aneurysm include vision changes and headaches, while a ruptured aneurysm causes a sudden and painful headache along with potential nausea, stiffness, and loss of consciousness.
Hypertensive retinopathy
Hypertensive retinopathy is retinal vascular damage caused by systemic hypertension. It can be detected by examining the ocular fundus, where changes to the arterioles and veins may indicate vascular damage from high blood pressure. These changes include arteriolar narrowing, hemorrhages, cotton wool spots, hard exudates, and optic disc swelling. The risk factors include age, family history of hypertension, obesity, smoking, stress, alcohol consumption and lack of exercise. Treatment focuses on lowering blood pressure through lifestyle changes like exercise and diet, as well as medication if needed, to prevent further organ damage.
1 dilated cerebral ventricles Radiology
1. The document discusses dilated cerebral ventricles as seen on clinical imaging. It provides 10 figures showing examples of ventricle dilation caused by various conditions, such as congenital hydrocephalus, choroid plexus papilloma, normal aging, Alzheimer's and Huntington's disease.
2. The figures demonstrate examples of generalized and localized ventricular enlargement, obstructive vs communicating hydrocephalus, loss of brain volume from cerebral hemiatrophy and occipital atrophy from intrauterine infection.
3. Imaging is useful for diagnosing the underlying causes of ventricle dilation and assessing treatment needs like ventricular shunting.
Aneurysm ppt
1. An aneurysm is an abnormal dilatation of an artery caused by atherosclerosis or trauma that weakens the arterial wall. There are true, false, fusiform, and saccular aneurysms.
2. Mycotic aneurysms are caused by bacterial infections like Staphylococcus aureus. Dissecting aneurysms involve a tear in the arterial intima allowing blood to dissect between the media layers.
3. Cirsoid aneurysms are rare arteriovenous fistulas or malformations usually involving the superficial temporal artery that appear as pulsating swellings. Diagnosis involves Doppler, CT, or angiogram and treatment requires ligation of the feeding artery.
Infarction
1. Infarction is localized tissue death caused by reduced blood supply, usually from arterial blockage.
2. The main causes of infarction are arterial obstruction, capillary occlusion, or venous obstruction which leads to ischemia, hypoxia, thrombus formation, and ultimately necrosis in the affected tissue.
3. Infarctions are classified based on their color (red hemorrhagic or white anemic) and presence of infection. Factors that influence infarction development include the anatomy of blood supply, rate of occlusion, tissue susceptibility to hypoxia, and degree of hypoxemia. Common sites of infarction include the heart, brain, intestines, kidneys, and liver.
Lecture 16 cardiovascular system
The document discusses diseases of the cardiovascular system, focusing on diseases of arteries and veins. It describes atherosclerosis as a hardening and thickening of arteries due to plaque buildup. Other artery diseases discussed include arteriosclerosis, medial sclerosis, endarteritis obliterans, and arteritis. Aneurysms, which are local artery dilations, are also covered. Finally, the document touches on varicose veins, phlebitis, and venous thrombosis as common diseases of veins.
Coagulation failure in pregnancy
This document discusses alterations in coagulation and fibrinolysis during pregnancy. It covers the normal coagulation cascade and triggers, as well as classifications of coagulation failure in pregnancy. Specific conditions covered include disseminated intravascular coagulation (DIC), thrombocytopenic coagulopathies, anticoagulant therapy, and von Willebrand disease. Diagnosis and management of DIC and thrombocytopenia are outlined. The importance of promptly diagnosing and treating coagulation disorders to prevent maternal morbidity and mortality is emphasized.
acute coronary syndrome
Acute coronary syndrome (ACS) occurs when a plaque in the coronary arteries ruptures or erodes, restricting blood flow. Plaque forms over time as LDL cholesterol builds up in artery walls due to risk factors like smoking, diabetes, and hypertension. The plaque contains an inflammatory necrotic core covered by a fibrous cap. Rupture occurs when the cap thins, exposing the core and triggering a clot. Medications treat ACS by lowering cholesterol and inflammation to stabilize plaques and prevent clots.
Carotid Cavernous Fistula
Carotid cavernous fistulas (CCFs) are abnormal connections between the carotid artery and cavernous sinus. They are classified as direct or indirect based on their anatomy and cause. Clinical presentation depends on flow rate, with high-flow CCFs causing rapid onset symptoms like proptosis and orbital bruit, while low-flow CCFs have slower onset. Diagnosis is by cerebral angiography, though other imaging can provide clues. Endovascular intervention is usually the treatment of choice, with conservative management or surgery also options depending on type. Prognosis is good if successfully treated, with symptom resolution and low recurrence rates.
Blood vessels and cvs
This document discusses the structure and pathology of blood vessels. It begins by stating that vascular pathology is a major cause of morbidity and mortality, affecting both arteries and veins. It then describes the layers of blood vessel walls and how they vary in thickness and composition between arteries, veins, and capillaries. The document discusses several vascular conditions, including atherosclerosis, aneurysms, hypertension, and vasculitis. It provides details on the pathogenesis, risk factors, morphology, and complications of these different diseases affecting the blood vessels.
Venous pathophysiology
1. Venous pathophysiology involves a complex interplay between genetic, environmental, and acquired factors that can disrupt the normal balance between procoagulant and anticoagulant mechanisms in the veins.
2. The venous endothelium plays a critical role in homeostasis by maintaining an anticoagulant state, but this can be damaged by various disease processes, promoting thrombosis.
3. Abnormal venous biomechanics and valve incompetence, as seen in varicose veins and post-thrombotic syndrome, can lead to ambulatory venous hypertension from impaired flow and reflux of blood in the veins.
Cell injury< Necrosis
This document describes different patterns of tissue necrosis:
- Coagulative necrosis preserves tissue architecture for days as cells remain intact due to blocked proteolysis, eventually being removed by phagocytosis. It can result from ischemia.
- Liquefactive necrosis transforms tissue into a liquid mass as cells are digested. It is seen with infections.
- Specific types include caseous necrosis in tuberculosis, fat necrosis affecting fatty tissues, and fibrinoid necrosis in immune reactions of blood vessels.
Atherosclerosis morphology
description of gross and microscopic morphology of an atherosclerotic lesion, includes fatty streak, simple plaque and fatty plaque.
Liver cirrhosis (Causes, clinical manifestation, complications, diagnosis, tr...
Cirrhosis is a diffuse process characterized by liver necrosis and fibrosis that converts the normal liver architecture into abnormal nodules lacking lobular organization. It has many causes including alcohol, viral hepatitis, fatty liver disease, and genetic disorders. Clinically, it manifests as asymptomatic or symptoms like vomiting and weight loss. Complications arise from portal hypertension and include ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome. Diagnosis involves liver function tests, imaging, and biopsy. Treatment focuses on managing complications and the underlying cause. For end-stage disease, liver transplantation may be required.
Cerebral aneurysm
Cerebral aneurysms are localized dilations of arteries in the brain. They can be saccular, fusiform, or dissecting in shape. The most common location is on arteries in the Circle of Willis. Risk factors include hypertension and smoking. Symptoms may include sudden headache, nausea, vision changes, or seizures. Diagnosis is made using CT, MRI, or CT angiography. Treatment options are surgical clipping or endovascular coiling to prevent rupture and bleeding in the brain. Nursing management focuses on monitoring for complications and educating on risk factor modification.
Cerebral edema and its management
This document discusses different types of cerebral edema including cytotoxic, vasogenic, hydrostatic, osmotic, and hydrocephalic edema. It provides details on the causes, mechanisms, and management of each type. The key management strategies for cerebral edema discussed are head elevation, oxygenation, fluid management, seizure prophylaxis, fever control, nutrition, hyperventilation, osmotherapy using mannitol, and other adjunctive therapies.
Clinical teaching on electroencephelography
The document discusses a clinical teaching session on electroencephalography (EEG) for 4th year nursing students. The session objectives were to define EEG, describe its indications, mechanism, procedure, and waveforms. EEG measures electrical activity in the brain using electrodes attached to the scalp. It is used to detect problems associated with brain disorders like seizures, tumors, or injuries. During an EEG, technicians attach electrodes to the scalp to record brain wave patterns over 30-60 minutes.
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08 dic
patholophysiology of DIC Disseminated intravascular coagulation
Pathophysiology（病理生理学）
Pathology
uploaded by prabesh 杰诗
Neurology
The document provides information on several neuropathology topics including glioblastoma multiforme, recent infarct, meningioma, Alzheimer's disease, spinal bifida, astrocytoma, and cerebral atrophy. It describes the etiology, pathogenesis, epidemiology, gross and microscopic features, and clinical correlations for each condition over multiple paragraphs.
Infarction
This document provides information about myocardial infarction including:
- Myocardial infarction is caused by interruption of blood supply to the heart muscle, usually due to blockage of a coronary artery.
- Risk factors that can lead to coronary artery blockage include hypertension, hyperlipidemia, diabetes, and smoking.
- A thrombus or embolism in a coronary artery cuts off the blood supply, causing cell death in the affected heart muscle area.
- The location and size of the infarction depends on which coronary artery is blocked. Transmural infarcts that penetrate the full heart wall thickness are more likely to cause complications than smaller subendocardial infarcts.
DISSEMINATED INTRAVASCULAR COAGULATION
DIC is one condition that always trouble patients and doctor, though its a nightmare for any clinician , its also a potent question in both UG and PG exams. I hope this will help you in answering those questions well.
Berry aneurysm
This document discusses berry aneurysms, which are thin-walled bulges that can form on arteries in the brain. Specifically:
- Berry aneurysms are the most common type of intracranial aneurysm, forming at arterial branch points in the circle of Willis which supplies blood to the brain.
- Risk factors for berry aneurysms include smoking, high blood pressure, age over 40, and genetic factors. Ruptured aneurysms have a high risk of death or permanent neurological deficits.
- Symptoms of an unruptured aneurysm include vision changes and headaches, while a ruptured aneurysm causes a sudden and painful headache along with potential nausea, stiffness, and loss of consciousness.
Hypertensive retinopathy
Hypertensive retinopathy is retinal vascular damage caused by systemic hypertension. It can be detected by examining the ocular fundus, where changes to the arterioles and veins may indicate vascular damage from high blood pressure. These changes include arteriolar narrowing, hemorrhages, cotton wool spots, hard exudates, and optic disc swelling. The risk factors include age, family history of hypertension, obesity, smoking, stress, alcohol consumption and lack of exercise. Treatment focuses on lowering blood pressure through lifestyle changes like exercise and diet, as well as medication if needed, to prevent further organ damage.
1 dilated cerebral ventricles Radiology
1. The document discusses dilated cerebral ventricles as seen on clinical imaging. It provides 10 figures showing examples of ventricle dilation caused by various conditions, such as congenital hydrocephalus, choroid plexus papilloma, normal aging, Alzheimer's and Huntington's disease.
2. The figures demonstrate examples of generalized and localized ventricular enlargement, obstructive vs communicating hydrocephalus, loss of brain volume from cerebral hemiatrophy and occipital atrophy from intrauterine infection.
3. Imaging is useful for diagnosing the underlying causes of ventricle dilation and assessing treatment needs like ventricular shunting.
Aneurysm ppt
1. An aneurysm is an abnormal dilatation of an artery caused by atherosclerosis or trauma that weakens the arterial wall. There are true, false, fusiform, and saccular aneurysms.
2. Mycotic aneurysms are caused by bacterial infections like Staphylococcus aureus. Dissecting aneurysms involve a tear in the arterial intima allowing blood to dissect between the media layers.
3. Cirsoid aneurysms are rare arteriovenous fistulas or malformations usually involving the superficial temporal artery that appear as pulsating swellings. Diagnosis involves Doppler, CT, or angiogram and treatment requires ligation of the feeding artery.
Infarction
1. Infarction is localized tissue death caused by reduced blood supply, usually from arterial blockage.
2. The main causes of infarction are arterial obstruction, capillary occlusion, or venous obstruction which leads to ischemia, hypoxia, thrombus formation, and ultimately necrosis in the affected tissue.
3. Infarctions are classified based on their color (red hemorrhagic or white anemic) and presence of infection. Factors that influence infarction development include the anatomy of blood supply, rate of occlusion, tissue susceptibility to hypoxia, and degree of hypoxemia. Common sites of infarction include the heart, brain, intestines, kidneys, and liver.
Lecture 16 cardiovascular system
The document discusses diseases of the cardiovascular system, focusing on diseases of arteries and veins. It describes atherosclerosis as a hardening and thickening of arteries due to plaque buildup. Other artery diseases discussed include arteriosclerosis, medial sclerosis, endarteritis obliterans, and arteritis. Aneurysms, which are local artery dilations, are also covered. Finally, the document touches on varicose veins, phlebitis, and venous thrombosis as common diseases of veins.
Coagulation failure in pregnancy
This document discusses alterations in coagulation and fibrinolysis during pregnancy. It covers the normal coagulation cascade and triggers, as well as classifications of coagulation failure in pregnancy. Specific conditions covered include disseminated intravascular coagulation (DIC), thrombocytopenic coagulopathies, anticoagulant therapy, and von Willebrand disease. Diagnosis and management of DIC and thrombocytopenia are outlined. The importance of promptly diagnosing and treating coagulation disorders to prevent maternal morbidity and mortality is emphasized.
acute coronary syndrome
Acute coronary syndrome (ACS) occurs when a plaque in the coronary arteries ruptures or erodes, restricting blood flow. Plaque forms over time as LDL cholesterol builds up in artery walls due to risk factors like smoking, diabetes, and hypertension. The plaque contains an inflammatory necrotic core covered by a fibrous cap. Rupture occurs when the cap thins, exposing the core and triggering a clot. Medications treat ACS by lowering cholesterol and inflammation to stabilize plaques and prevent clots.
Carotid Cavernous Fistula
Carotid cavernous fistulas (CCFs) are abnormal connections between the carotid artery and cavernous sinus. They are classified as direct or indirect based on their anatomy and cause. Clinical presentation depends on flow rate, with high-flow CCFs causing rapid onset symptoms like proptosis and orbital bruit, while low-flow CCFs have slower onset. Diagnosis is by cerebral angiography, though other imaging can provide clues. Endovascular intervention is usually the treatment of choice, with conservative management or surgery also options depending on type. Prognosis is good if successfully treated, with symptom resolution and low recurrence rates.
Blood vessels and cvs
This document discusses the structure and pathology of blood vessels. It begins by stating that vascular pathology is a major cause of morbidity and mortality, affecting both arteries and veins. It then describes the layers of blood vessel walls and how they vary in thickness and composition between arteries, veins, and capillaries. The document discusses several vascular conditions, including atherosclerosis, aneurysms, hypertension, and vasculitis. It provides details on the pathogenesis, risk factors, morphology, and complications of these different diseases affecting the blood vessels.
Venous pathophysiology
1. Venous pathophysiology involves a complex interplay between genetic, environmental, and acquired factors that can disrupt the normal balance between procoagulant and anticoagulant mechanisms in the veins.
2. The venous endothelium plays a critical role in homeostasis by maintaining an anticoagulant state, but this can be damaged by various disease processes, promoting thrombosis.
3. Abnormal venous biomechanics and valve incompetence, as seen in varicose veins and post-thrombotic syndrome, can lead to ambulatory venous hypertension from impaired flow and reflux of blood in the veins.
Cell injury< Necrosis
This document describes different patterns of tissue necrosis:
- Coagulative necrosis preserves tissue architecture for days as cells remain intact due to blocked proteolysis, eventually being removed by phagocytosis. It can result from ischemia.
- Liquefactive necrosis transforms tissue into a liquid mass as cells are digested. It is seen with infections.
- Specific types include caseous necrosis in tuberculosis, fat necrosis affecting fatty tissues, and fibrinoid necrosis in immune reactions of blood vessels.
Atherosclerosis morphology
description of gross and microscopic morphology of an atherosclerotic lesion, includes fatty streak, simple plaque and fatty plaque.
Liver cirrhosis (Causes, clinical manifestation, complications, diagnosis, tr...
Cirrhosis is a diffuse process characterized by liver necrosis and fibrosis that converts the normal liver architecture into abnormal nodules lacking lobular organization. It has many causes including alcohol, viral hepatitis, fatty liver disease, and genetic disorders. Clinically, it manifests as asymptomatic or symptoms like vomiting and weight loss. Complications arise from portal hypertension and include ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome. Diagnosis involves liver function tests, imaging, and biopsy. Treatment focuses on managing complications and the underlying cause. For end-stage disease, liver transplantation may be required.
Cerebral aneurysm
Cerebral aneurysms are localized dilations of arteries in the brain. They can be saccular, fusiform, or dissecting in shape. The most common location is on arteries in the Circle of Willis. Risk factors include hypertension and smoking. Symptoms may include sudden headache, nausea, vision changes, or seizures. Diagnosis is made using CT, MRI, or CT angiography. Treatment options are surgical clipping or endovascular coiling to prevent rupture and bleeding in the brain. Nursing management focuses on monitoring for complications and educating on risk factor modification.
Cerebral edema and its management
This document discusses different types of cerebral edema including cytotoxic, vasogenic, hydrostatic, osmotic, and hydrocephalic edema. It provides details on the causes, mechanisms, and management of each type. The key management strategies for cerebral edema discussed are head elevation, oxygenation, fluid management, seizure prophylaxis, fever control, nutrition, hyperventilation, osmotherapy using mannitol, and other adjunctive therapies.
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Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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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
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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