Stroke is an acute neurologic condition resulting from a disruption in cerebral perfusion, either due to ischemia or hemorrhage.
Hemorrhagic stroke is the cerebral infarction due to hemorrhage.
Subarachnoid hemorrhage is the extravasation of blood into the subarachnoid space. The most common cause is a ruptured saccular aneurysm, which accounts for 75% of cases. Clinical features include a sudden, severe "thunderclap" headache that reaches maximal intensity within minutes. Diagnosis is confirmed through brain CT scan or lumbar puncture. Treatment involves securing the ruptured aneurysm through surgical clipping or endovascular coiling to prevent rebleeding, managing vasospasm, and addressing complications like hydrocephalus.
This document discusses the surgical management of intracranial aneurysms. It begins by defining a cerebral aneurysm as a bulging, weakened area in the wall of an artery in the brain. It then discusses factors that can cause aneurysms like smoking, hypertension, and family history. The document covers types of aneurysms like ruptured vs unruptured, symptoms of subarachnoid hemorrhage, grading scales for severity, risks of rebleeding, hydrocephalus, and vasospasm. It concludes by noting that unruptured intracranial aneurysms can be incidental findings or detected as they grow and cause compression of brain structures.
Subarachnoid hemorrhage is caused most commonly by the rupture of a saccular aneurysm. The rupture causes blood to fill the subarachnoid space, which can lead to neurological deficits or death. Treatment involves securing the aneurysm through surgical clipping or endovascular coiling to prevent rebleeding, as well as managing complications like vasospasm, hydrocephalus, and seizures. Outcomes depend on the grade and location of the initial bleed and development of delayed cerebral ischemia.
Management Of Head Injury PK anesthesia.pptxAnaes6
1) Head injuries are a major cause of death and disability worldwide, especially in young men and children, due to falls, traffic accidents, and assaults.
2) CT scans and MRI are used to classify head injuries as mild, moderate, or severe based on Glasgow Coma Scale scores and to identify intracranial hemorrhages.
3) Immediate management focuses on maintaining oxygenation, circulation, and preventing rises in intracranial pressure through ventilation, fluids, osmotherapy and other measures to reduce secondary brain injury.
Head trauma, also called traumatic brain injury (TBI), occurs in two phases: primary and secondary brain injury. Primary injury involves direct damage to brain tissue from impact. Secondary injury involves downstream effects like edema and ischemia that start minutes after primary injury. Managing TBI focuses on preventing secondary injuries like hypotension, hypoxia, fever and intracranial hypertension that can exacerbate primary damage. Treatment involves intensive monitoring, ventilation, controlling blood pressure/ICP, anticonvulsants and early rehabilitation. The goal is to minimize further brain injury and maximize recovery.
This document discusses stroke, including its types, causes, pathophysiology, imaging findings, and clinical features. It provides the following key points:
1. Stroke is caused by ischemia or hemorrhage in the brain. The main types are cerebral infarction (80%), intracerebral hemorrhage (15%), and subarachnoid hemorrhage (5%).
2. Imaging plays an important role in assessing the parenchyma, vessels, perfusion, and penumbra to guide therapy and predict outcomes. Techniques include CT, MRI, CT/MR perfusion, and angiography.
3. CT findings evolve over time from hyperacute to chronic stages. Early signs include
Subarachnoid hemorrhage is the extravasation of blood into the subarachnoid space. The most common cause is a ruptured saccular aneurysm, which accounts for 75% of cases. Clinical features include a sudden, severe "thunderclap" headache that reaches maximal intensity within minutes. Diagnosis is confirmed through brain CT scan or lumbar puncture. Treatment involves securing the ruptured aneurysm through surgical clipping or endovascular coiling to prevent rebleeding, managing vasospasm, and addressing complications like hydrocephalus.
This document discusses the surgical management of intracranial aneurysms. It begins by defining a cerebral aneurysm as a bulging, weakened area in the wall of an artery in the brain. It then discusses factors that can cause aneurysms like smoking, hypertension, and family history. The document covers types of aneurysms like ruptured vs unruptured, symptoms of subarachnoid hemorrhage, grading scales for severity, risks of rebleeding, hydrocephalus, and vasospasm. It concludes by noting that unruptured intracranial aneurysms can be incidental findings or detected as they grow and cause compression of brain structures.
Subarachnoid hemorrhage is caused most commonly by the rupture of a saccular aneurysm. The rupture causes blood to fill the subarachnoid space, which can lead to neurological deficits or death. Treatment involves securing the aneurysm through surgical clipping or endovascular coiling to prevent rebleeding, as well as managing complications like vasospasm, hydrocephalus, and seizures. Outcomes depend on the grade and location of the initial bleed and development of delayed cerebral ischemia.
Management Of Head Injury PK anesthesia.pptxAnaes6
1) Head injuries are a major cause of death and disability worldwide, especially in young men and children, due to falls, traffic accidents, and assaults.
2) CT scans and MRI are used to classify head injuries as mild, moderate, or severe based on Glasgow Coma Scale scores and to identify intracranial hemorrhages.
3) Immediate management focuses on maintaining oxygenation, circulation, and preventing rises in intracranial pressure through ventilation, fluids, osmotherapy and other measures to reduce secondary brain injury.
Head trauma, also called traumatic brain injury (TBI), occurs in two phases: primary and secondary brain injury. Primary injury involves direct damage to brain tissue from impact. Secondary injury involves downstream effects like edema and ischemia that start minutes after primary injury. Managing TBI focuses on preventing secondary injuries like hypotension, hypoxia, fever and intracranial hypertension that can exacerbate primary damage. Treatment involves intensive monitoring, ventilation, controlling blood pressure/ICP, anticonvulsants and early rehabilitation. The goal is to minimize further brain injury and maximize recovery.
This document discusses stroke, including its types, causes, pathophysiology, imaging findings, and clinical features. It provides the following key points:
1. Stroke is caused by ischemia or hemorrhage in the brain. The main types are cerebral infarction (80%), intracerebral hemorrhage (15%), and subarachnoid hemorrhage (5%).
2. Imaging plays an important role in assessing the parenchyma, vessels, perfusion, and penumbra to guide therapy and predict outcomes. Techniques include CT, MRI, CT/MR perfusion, and angiography.
3. CT findings evolve over time from hyperacute to chronic stages. Early signs include
This document discusses normal and increased intracranial pressure. It begins by stating normal ICP ranges in adults and babies. ICP is influenced by several factors and shows pressure fluctuations with cardiac systole and respiration. Increased ICP can be caused by obstruction of venous outflow, increasing blood and CSF volume in the cranium. Clinical signs of increased ICP include Cushing's response of hypertension and bradycardia. The document then discusses methods of monitoring ICP, both invasive and non-invasive.
This document discusses normal and increased intracranial pressure (ICP). It begins by defining normal ICP ranges in adults and babies. ICP is influenced by several factors and shows pressure fluctuations with cardiac systole and respiration. Increased ICP can be caused by factors that increase brain volume such as tumors or hematomas. Treatment aims to reduce ICP through general measures, induced cerebral vasoconstriction using techniques like hyperventilation, and osmotherapy using agents like mannitol. Careful monitoring of ICP is important for guiding therapy to prevent secondary brain injury.
Enoxaparin is used to treat strokes. Strokes are caused by interrupted blood flow to the brain and can be ischemic (caused by clots) or hemorrhagic (caused by bleeding). Timely treatment is important to reduce brain damage. Patients may experience symptoms like weakness or speech problems. Diagnosis involves imaging tests and ruling out other causes. Treatment focuses on rapidly restoring blood flow through thrombolysis or thrombectomy and preventing further issues.
Subarachnoid hemorrhage occurs when blood leaks into the subarachnoid space surrounding the brain. The most common cause is a ruptured intracranial aneurysm. Patients present with a sudden, severe headache and may experience nausea, vomiting, neck stiffness, loss of consciousness or neurological deficits. CT scans can detect bleeding in the first 12 hours, while lumbar puncture detects blood in the cerebrospinal fluid if CT is negative. Treatment involves stabilizing the patient, detecting and treating the aneurysm with clipping or coiling, and managing complications like vasospasm, delayed cerebral ischemia, hyponatremia, fever and rebleeding.
The document discusses the anesthetic management of patients undergoing treatment for cerebral aneurysms, including definitions, epidemiology, presentation, diagnosis, management of vasospasm, intracranial pressure, pre-operative assessment and testing, and radiological procedures such as coiling of aneurysms. Precise management of hemodynamics, fluid balance, and respiratory status is important due to the risks of re-bleeding, cerebral ischemia, and impaired autoregulation in these patients.
Cerebral vasospasm is a narrowing of cerebral arteries that occurs after subarachnoid hemorrhage, usually from a ruptured aneurysm. It develops in 50-90% of aneurysmal SAH cases on angiography but only 20-30% develop neurological deficits. Vasospasm typically begins 3-14 days after hemorrhage and can last up to 4 weeks. Risk is predicted by modified Fisher scale and thick subarachnoid blood. Transcranial Doppler is commonly used to screen for vasospasm. Prevention focuses on hydration, blood pressure control, nimodipine, and clot removal while treatments include "triple H" therapy and endovascular interventions like angiop
The Pathophysiology And Management Of Hemorrhagic StrokeLiew Boon Seng
1. The document discusses the pathophysiology and management of hemorrhagic stroke, specifically intracerebral hemorrhage (ICH). ICH is more common and more lethal than subarachnoid hemorrhage.
2. Risk factors for ICH include increasing age, hypertension, male gender, and alcohol use. CT scan is used to diagnose ICH. Management involves airway protection, blood pressure control, intracranial pressure monitoring, and seizure prophylaxis.
3. Treatment goals are to maintain blood pressure below 130 mmHg, intracranial pressure below 20 mmHg, and cerebral perfusion pressure above 70 mmHg. Surgical evacuation may be considered depending on hemor
This document discusses the pharmacotherapy of stroke. It begins by defining stroke and classifying it as either ischemic or hemorrhagic. Risk factors and pathophysiology are described. Clinical presentations include weakness, speech problems, or vision loss. Diagnosis involves imaging like CT or MRI to distinguish ischemic from hemorrhagic stroke. Treatment goals are to reduce injury, prevent complications and recurrence. For ischemic stroke, IV tissue plasminogen activator within 3 hours or aspirin within 48 hours are recommended. Secondary prevention includes managing conditions like atrial fibrillation, hypertension, and diabetes to prevent future strokes.
The document discusses the pharmacotherapy of stroke. It begins by defining stroke and classifying it as either ischemic or hemorrhagic. It then discusses risk factors, pathophysiology, clinical presentations, diagnosis, desired treatment outcomes, and general treatment approaches. It provides details on treatment for ischemic stroke, including IV tissue plasminogen activator and antiplatelet/anticoagulant therapy. Treatment for hemorrhagic stroke and rehabilitation are also summarized.
1. The document discusses intracranial pressure (ICP), cerebrospinal fluid (CSF) circulation and compensation mechanisms when ICP increases. It defines normal ICP and the factors that affect it, including the Monro-Kellie doctrine.
2. Symptoms of increased ICP are described, from early signs like headache to late signs like herniation and changes in vital signs. Different types of herniation are explained.
3. Methods for monitoring ICP are summarized, including invasive techniques like intraventricular and subdural monitors and non-invasive options. Indications for ICP monitoring include severe head injuries with abnormal CT scans or certain risk factors.
This document summarizes imaging findings related to subarachnoid hemorrhage (SAH). It describes that SAH appears as hyperdense linear structures on CT and hyperintense on FLAIR MRI. The location of blood can localize the source of bleeding such as anterior communicating artery aneurysms presenting with blood in the interhemispheric fissure. Complications include vasospasm, hydrocephalus, and superficial siderosis. Reversible cerebral vasoconstriction syndrome is also discussed, appearing as multifocal "string of beads" narrowing on angiography that resolves within 12 weeks.
Please find the power point on Management of Sub arachnoid hemorrhage. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
This document provides an overview of neurocritical care topics including: common neurologic emergencies like subarachnoid hemorrhage, aneurysms, seizures and tumors; classifications like Hunt and Hess for SAH; monitoring tools like ventriculostomy for ICP; treatments for increased ICP like hyperosmolar therapy; endovascular procedures like coiling; and surgical treatments including craniotomy, clipping and ventricular shunts.
This document discusses subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms. It covers the epidemiology, risk factors, presentation, diagnosis, grading scales, management of complications like vasospasm, and prognosis. SAH most commonly results from ruptured berry aneurysms, with a high rate of mortality and morbidity. Treatment involves securing the aneurysm with clipping or coiling, along with intensive care management including prevention of rebleeding, vasospasm, seizures and other complications.
Supportive management in neurological icuNeurologyKota
This document discusses neurointensive care, which aims to treat and prevent brain injury. It describes the role of the neurointensivist in comprehensively managing neurologic status while integrating knowledge of other organ systems. Various conditions treated in neurointensive care units are listed, along with assessments of neurologic function and scales used to evaluate levels of consciousness, motor response, and brainstem reflexes. Monitoring techniques and their indications are also outlined.
Cerebrovascular Accident or stroke is defined as an abrupt onset of neurological deficit caused by a focal vascular issue. Stroke is the second leading cause of death worldwide. The clinical manifestations of stroke can vary widely due to the complex anatomy of the brain and vasculature. Imaging such as CT and MRI are used to determine if the cause is ischemia or hemorrhage. Treatment focuses on rapid evaluation, managing risk factors, IV thrombolysis if appropriate, and rehabilitation to prevent complications and encourage recovery.
Management of Cerebral edema 1 [Autosaved].pptxChirayuRegmi2
This document discusses the management of cerebral edema, brain compression, and intracranial pressure. It begins by defining cerebral edema and describing the different types: vasogenic, cytotoxic, hydrostatic, and osmotic. It then discusses intracranial pressure, cerebral perfusion pressure, and ways of measuring them both invasively and noninvasively. The document concludes by outlining a tiered approach to treating elevated ICP and cerebral edema, including selective corticosteroids, osmotic therapy, CSF diversion and decompressive surgery.
This document discusses strokes, including definitions, types, risk factors, pathophysiology, clinical manifestations, diagnosis, and treatment. A stroke is defined as a neurological deficit lasting over 24 hours caused by a focal vascular issue. There are two main types: ischemic (caused by clot or embolism) and hemorrhagic (caused by bleeding). Risk factors include hypertension, atrial fibrillation, diabetes, and smoking. Treatment focuses on supporting vital functions, reversing damage with thrombolysis if given early, and rehabilitation.
1. Stroke can be caused by blockage of blood flow (ischemic) or bleeding in the brain (hemorrhagic). Treatment depends on the type and location of stroke.
2. Risk factors for stroke can be modifiable like hypertension, diabetes, smoking or non-modifiable like age, sex, family history. Managing modifiable risk factors is important for prevention.
3. Acute treatment of ischemic stroke may involve clot-busting drugs intravenously or surgery to remove clots, while hemorrhagic stroke management focuses on controlling blood pressure, reducing swelling in the brain.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
This document discusses normal and increased intracranial pressure. It begins by stating normal ICP ranges in adults and babies. ICP is influenced by several factors and shows pressure fluctuations with cardiac systole and respiration. Increased ICP can be caused by obstruction of venous outflow, increasing blood and CSF volume in the cranium. Clinical signs of increased ICP include Cushing's response of hypertension and bradycardia. The document then discusses methods of monitoring ICP, both invasive and non-invasive.
This document discusses normal and increased intracranial pressure (ICP). It begins by defining normal ICP ranges in adults and babies. ICP is influenced by several factors and shows pressure fluctuations with cardiac systole and respiration. Increased ICP can be caused by factors that increase brain volume such as tumors or hematomas. Treatment aims to reduce ICP through general measures, induced cerebral vasoconstriction using techniques like hyperventilation, and osmotherapy using agents like mannitol. Careful monitoring of ICP is important for guiding therapy to prevent secondary brain injury.
Enoxaparin is used to treat strokes. Strokes are caused by interrupted blood flow to the brain and can be ischemic (caused by clots) or hemorrhagic (caused by bleeding). Timely treatment is important to reduce brain damage. Patients may experience symptoms like weakness or speech problems. Diagnosis involves imaging tests and ruling out other causes. Treatment focuses on rapidly restoring blood flow through thrombolysis or thrombectomy and preventing further issues.
Subarachnoid hemorrhage occurs when blood leaks into the subarachnoid space surrounding the brain. The most common cause is a ruptured intracranial aneurysm. Patients present with a sudden, severe headache and may experience nausea, vomiting, neck stiffness, loss of consciousness or neurological deficits. CT scans can detect bleeding in the first 12 hours, while lumbar puncture detects blood in the cerebrospinal fluid if CT is negative. Treatment involves stabilizing the patient, detecting and treating the aneurysm with clipping or coiling, and managing complications like vasospasm, delayed cerebral ischemia, hyponatremia, fever and rebleeding.
The document discusses the anesthetic management of patients undergoing treatment for cerebral aneurysms, including definitions, epidemiology, presentation, diagnosis, management of vasospasm, intracranial pressure, pre-operative assessment and testing, and radiological procedures such as coiling of aneurysms. Precise management of hemodynamics, fluid balance, and respiratory status is important due to the risks of re-bleeding, cerebral ischemia, and impaired autoregulation in these patients.
Cerebral vasospasm is a narrowing of cerebral arteries that occurs after subarachnoid hemorrhage, usually from a ruptured aneurysm. It develops in 50-90% of aneurysmal SAH cases on angiography but only 20-30% develop neurological deficits. Vasospasm typically begins 3-14 days after hemorrhage and can last up to 4 weeks. Risk is predicted by modified Fisher scale and thick subarachnoid blood. Transcranial Doppler is commonly used to screen for vasospasm. Prevention focuses on hydration, blood pressure control, nimodipine, and clot removal while treatments include "triple H" therapy and endovascular interventions like angiop
The Pathophysiology And Management Of Hemorrhagic StrokeLiew Boon Seng
1. The document discusses the pathophysiology and management of hemorrhagic stroke, specifically intracerebral hemorrhage (ICH). ICH is more common and more lethal than subarachnoid hemorrhage.
2. Risk factors for ICH include increasing age, hypertension, male gender, and alcohol use. CT scan is used to diagnose ICH. Management involves airway protection, blood pressure control, intracranial pressure monitoring, and seizure prophylaxis.
3. Treatment goals are to maintain blood pressure below 130 mmHg, intracranial pressure below 20 mmHg, and cerebral perfusion pressure above 70 mmHg. Surgical evacuation may be considered depending on hemor
This document discusses the pharmacotherapy of stroke. It begins by defining stroke and classifying it as either ischemic or hemorrhagic. Risk factors and pathophysiology are described. Clinical presentations include weakness, speech problems, or vision loss. Diagnosis involves imaging like CT or MRI to distinguish ischemic from hemorrhagic stroke. Treatment goals are to reduce injury, prevent complications and recurrence. For ischemic stroke, IV tissue plasminogen activator within 3 hours or aspirin within 48 hours are recommended. Secondary prevention includes managing conditions like atrial fibrillation, hypertension, and diabetes to prevent future strokes.
The document discusses the pharmacotherapy of stroke. It begins by defining stroke and classifying it as either ischemic or hemorrhagic. It then discusses risk factors, pathophysiology, clinical presentations, diagnosis, desired treatment outcomes, and general treatment approaches. It provides details on treatment for ischemic stroke, including IV tissue plasminogen activator and antiplatelet/anticoagulant therapy. Treatment for hemorrhagic stroke and rehabilitation are also summarized.
1. The document discusses intracranial pressure (ICP), cerebrospinal fluid (CSF) circulation and compensation mechanisms when ICP increases. It defines normal ICP and the factors that affect it, including the Monro-Kellie doctrine.
2. Symptoms of increased ICP are described, from early signs like headache to late signs like herniation and changes in vital signs. Different types of herniation are explained.
3. Methods for monitoring ICP are summarized, including invasive techniques like intraventricular and subdural monitors and non-invasive options. Indications for ICP monitoring include severe head injuries with abnormal CT scans or certain risk factors.
This document summarizes imaging findings related to subarachnoid hemorrhage (SAH). It describes that SAH appears as hyperdense linear structures on CT and hyperintense on FLAIR MRI. The location of blood can localize the source of bleeding such as anterior communicating artery aneurysms presenting with blood in the interhemispheric fissure. Complications include vasospasm, hydrocephalus, and superficial siderosis. Reversible cerebral vasoconstriction syndrome is also discussed, appearing as multifocal "string of beads" narrowing on angiography that resolves within 12 weeks.
Please find the power point on Management of Sub arachnoid hemorrhage. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
This document provides an overview of neurocritical care topics including: common neurologic emergencies like subarachnoid hemorrhage, aneurysms, seizures and tumors; classifications like Hunt and Hess for SAH; monitoring tools like ventriculostomy for ICP; treatments for increased ICP like hyperosmolar therapy; endovascular procedures like coiling; and surgical treatments including craniotomy, clipping and ventricular shunts.
This document discusses subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms. It covers the epidemiology, risk factors, presentation, diagnosis, grading scales, management of complications like vasospasm, and prognosis. SAH most commonly results from ruptured berry aneurysms, with a high rate of mortality and morbidity. Treatment involves securing the aneurysm with clipping or coiling, along with intensive care management including prevention of rebleeding, vasospasm, seizures and other complications.
Supportive management in neurological icuNeurologyKota
This document discusses neurointensive care, which aims to treat and prevent brain injury. It describes the role of the neurointensivist in comprehensively managing neurologic status while integrating knowledge of other organ systems. Various conditions treated in neurointensive care units are listed, along with assessments of neurologic function and scales used to evaluate levels of consciousness, motor response, and brainstem reflexes. Monitoring techniques and their indications are also outlined.
Cerebrovascular Accident or stroke is defined as an abrupt onset of neurological deficit caused by a focal vascular issue. Stroke is the second leading cause of death worldwide. The clinical manifestations of stroke can vary widely due to the complex anatomy of the brain and vasculature. Imaging such as CT and MRI are used to determine if the cause is ischemia or hemorrhage. Treatment focuses on rapid evaluation, managing risk factors, IV thrombolysis if appropriate, and rehabilitation to prevent complications and encourage recovery.
Management of Cerebral edema 1 [Autosaved].pptxChirayuRegmi2
This document discusses the management of cerebral edema, brain compression, and intracranial pressure. It begins by defining cerebral edema and describing the different types: vasogenic, cytotoxic, hydrostatic, and osmotic. It then discusses intracranial pressure, cerebral perfusion pressure, and ways of measuring them both invasively and noninvasively. The document concludes by outlining a tiered approach to treating elevated ICP and cerebral edema, including selective corticosteroids, osmotic therapy, CSF diversion and decompressive surgery.
This document discusses strokes, including definitions, types, risk factors, pathophysiology, clinical manifestations, diagnosis, and treatment. A stroke is defined as a neurological deficit lasting over 24 hours caused by a focal vascular issue. There are two main types: ischemic (caused by clot or embolism) and hemorrhagic (caused by bleeding). Risk factors include hypertension, atrial fibrillation, diabetes, and smoking. Treatment focuses on supporting vital functions, reversing damage with thrombolysis if given early, and rehabilitation.
1. Stroke can be caused by blockage of blood flow (ischemic) or bleeding in the brain (hemorrhagic). Treatment depends on the type and location of stroke.
2. Risk factors for stroke can be modifiable like hypertension, diabetes, smoking or non-modifiable like age, sex, family history. Managing modifiable risk factors is important for prevention.
3. Acute treatment of ischemic stroke may involve clot-busting drugs intravenously or surgery to remove clots, while hemorrhagic stroke management focuses on controlling blood pressure, reducing swelling in the brain.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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.
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.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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.
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).
3. What is stroke?
It is an acute neurologic condition resulting from a disruption in
cerebral perfusion, either due to ischemia or hemorrhage.
A blocked artery: Ischemic 87%
A ruptured artery: Bleeding 13%
4.
5. What is Hemorrhagic stroke?
It is the cerebral infarction due to hemorrhage.
1- Intracerebral hemorrhage 2- Subarachnoid hemorrhage
Bleeding within the brain parenchyma Bleeding into the subarachnoid space
6. 1- Intracerebral hemorrhage
High mortality rate (50% at 30 days).
Significant morbidity.
Hematoma formation and enlargement may lead to
local injury and increase in intracerebral pressure.
8. 1- Intracerebral hemorrhage
Causes?
B- Ischemic stroke A- HTN (Particularly a sudden increase in BP)
May convert to a
hemorrhagic stroke
HTN causes a rupture of small vessels deep within the brain parenchyma.
Chronic HTN causes degeneration of small arteries,
leading to microaneurysms, which can rupture easily.
It is typically seen in older patients; risk increases with age
C- Others Amyloid angiopathy (10%), Anticoagulant/Antithrombolytic use (10%),
brain tumors (5%), and AV malformations (5%)
HIT: Cocaine is one of the main causes of stroke in young patients. ICH, ischemic stroke, and SAH are all associated with cocaine use.
9. Clinical Features
1- Intracerebral hemorrhage
● Altered level of
consciousness, stupor,
or coma
● Headache, vomiting
● Signs of increased ICP
● Abrupt onset of a focal
neurologic deficit that
worsens steadily over
30 to 90 minutes
10. Diagnosis
a. CT scan of the head diagnoses 95% of ICH (may
miss very small bleeds)
b. Coagulation panel and platelets-check these to
evaluate for bleeding diathesis.
1- Intracerebral hemorrhage
12. Treatment
1- Intracerebral hemorrhage
1- Admission to the ICU
2- ABC's (airway, breathing,
and circulation)-airway
management is important
due to altered mental status
and decreased respiratory
drive. Patients often require
intubation.
3- BP reduction
● Elevated BP increases ICP and can cause further
bleeding. However, hypotension can lower
cerebral blood flow, worsening the neurologic
deficits. Therefore, BP reduction must be gradual.
● Treatment is indicated if systolic BP is >180 or the
MAP is >130. Common IV agents used include
nicardipine, labetalol, nitroprusside, and others.
13. 1- Intracerebral hemorrhage
4- Initial management of elevated ICP
includes elevating the head of the bed to
30 degrees and appropriate sedation and
pain control. Mannitol (osmotic agent) is
often used to lower ICP; other options
include hyperventilation, barbiturates,
neuromuscular blockade, and CSF drainage.
5- If the patient is on anticoagulation
or an antiplatelet agent, reversal
agents (e.g., vitamin K for warfarin,
protamine sulfate for heparin,
prothrombin complex concentrate
for warfarin and the newer oral
anticoagulants, etc.)
6- Use of steroids is harmful
and is not recommended.
7- Rapid surgical evacuation of cerebellar
hematomas can be lifesaving. However,
surgery is not helpful in most cases of ICH.
Treatment
14. 2- Subarachnoid Hemorrhage
a. Mortality rate can be as
high as 40% to 50% at 30
days.
b. Berry aneurysms occur
at bifurcations of arteries
of the circle of Willis.
15. Causes
2- Subarachnoid Hemorrhage
B. Trauma is also a common cause.
C. AV malformation.
A. berry aneurysms are the most
common cause
Arteriovenous
angioma
(arteriovenous
malformation)
16. Clinical features
2- Subarachnoid Hemorrhage
D. Retinal hemorrhages in up
to 30% of patients.
A. Sudden, severe
(often excruciating)
headache in the
absence of focal
neurologic symptoms;
the classic description
is "the worst
headache of my life"
but may also be more
subtle.
B. Sudden, transient loss of consciousness in approximately
50% of patients.
C. Vomiting (common).
F. Meningeal irritation, nuchal rigidity, and photophobia
can take several hours to develop Death-25% to 50% of
patients die with the first rupture. Those who survive will
recover consciousness within minutes.
17. Diagnosis
2- Subarachnoid Hemorrhage
c. Once SAH is
diagnosed,
order a cerebral
angiogram. It is
the definitive
study for
detecting the
site of bleeding
(for surgical
clipping).
a. Noncontrast CT
scan identifies the
majority of
subarachnoid
hemorrhages
(SAHs).
However, CT scan
may be negative in
up to 10% of cases.
b. Perform lumbar puncture (LP) if
the CT scan is unrevealing or negative
and clinical suspicion is high.
Xanthochromia (yellow color of the CSF) is
the gold standard for diagnosis of SAH.
Xanthochromia results from RBC lysis.
Xanthochromia implies that blood has
been in CSF for several hours and that it is
not due to a traumatic tap.
18. Complications
2- Subarachnoid Hemorrhage
c. Hydrocephalus (communicating)-
secondary to blood within the
subarachnoid
space hindering normal CSF flow.
a. Rerupture-occurs in up to 30% of
patients.
b. Vasospasm-occurs in up to 50% of
patients (more often with aneurysmal
SAH);
can cause ischemia/infarction and
therefore stroke.
d. Seizures may occur (blood acts as
an irritant).
e. Siadh
19. Treatment
2- Subarachnoid Hemorrhage
c. Medical-therapy reduces the risks
of rebleeding and cerebral vasospasm.
• Bed rest in a quiet, dark room.
• Stool softeners to avoid straining
(increases ICP and risk of rerupture).
• Analgesia for headache
(acetaminophen).
• IV fluids for hydration.
a. Minimally invasive-consult
interventional neuroradiology.
Recent studies have shown
endovascular coiling to have better
outcomes than surgical clipping.
b. Surgical-consult neurosurgery
Surgically clip the aneurysm to
prevent rebleeding.
20. 2- Subarachnoid Hemorrhage
E. Calcium channel blocker
(nimodipine) for vasospasm-lowers
the incidence of cerebral infarction by
one-third.
D. Control of HTN-lower the BP
gradually because the elevation in
BP may be a compensation for the
decrease in cerebral perfusion
pressure (secondary to increased
ICP or cerebral arterial narrowing).
Treatment