1. Stroke is defined as a clinical syndrome of rapid onset of focal deficits of brain function lasting more than 24 hours or leading to death. There are two main types - ischemic and hemorrhagic.
2. Ischemic strokes account for 80% of cases and result from arterial occlusion blocking blood flow. Hemorrhagic strokes can be either intracerebral hemorrhage from ruptured small arteries damaged by hypertension, or subarachnoid hemorrhage from ruptured aneurysms.
3. The pathophysiology of ischemic stroke involves development of an ischemic core with immediate cell death surrounded by an ischemic penumbra of reversibly dysfunctional tissue that can potentially be salvaged by reperfusion
Is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke.
It can occur
in the carotid
artery of the
neck as well as
other arteries.
When an artery is acutely occluded by thrombus or embolus, the area of the CNS supplied by it will undergo infarction if there is no adequate collateral blood supply.
Surrounding a central necrotic zone, an ‘ischemic penumbra’ remains viable for a time, i.e. it may recover function if blood flow is restored.
CNS ischemia may be accompanied by swelling for two reasons:
● cytotoxic oedema – accumulation of water in damaged glial cells and neurones,
● vasogenic oedema – extracellular fluid accumulation as a result of breakdown of the blood–brain barrier.
In the brain, this swelling may be sufficient to produce clinical deterioration in the days following a major stroke, as a result of a rise in intracranial pressure and compression of adjacent structures.
Is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke.
It can occur
in the carotid
artery of the
neck as well as
other arteries.
When an artery is acutely occluded by thrombus or embolus, the area of the CNS supplied by it will undergo infarction if there is no adequate collateral blood supply.
Surrounding a central necrotic zone, an ‘ischemic penumbra’ remains viable for a time, i.e. it may recover function if blood flow is restored.
CNS ischemia may be accompanied by swelling for two reasons:
● cytotoxic oedema – accumulation of water in damaged glial cells and neurones,
● vasogenic oedema – extracellular fluid accumulation as a result of breakdown of the blood–brain barrier.
In the brain, this swelling may be sufficient to produce clinical deterioration in the days following a major stroke, as a result of a rise in intracranial pressure and compression of adjacent structures.
Heart failure, sometimes known as congestive heart failure, occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently.
Heart failure, sometimes known as congestive heart failure, occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently.
In medicine, a loss of blood flow to part of the brain, which damages brain tissue. CVAs are caused by blood clots and broken blood vessels in the brain. Symptoms include dizziness, numbness, weakness on one side of the body, and problems with talking, writing, or understanding language.
Handout for Inhalational Anaesthesia CME held in 2013 by the Department of Anaesthesiology, JNMC, Belagavi. Authors have been credited in each chapter.
A brief overview of the physiology of the neuromuscular junction.It includes a video towards the end sourced from the internet with the copyright watermarks intact.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Approach to a patient with stroke - Pathophysiology of stroke
1. Approach to a patient with stroke AshwinHaridas Asem Ali Ashraf Adam EAH Adam
2. Definitions Stroke Clinical syndrome of rapid onset of focal deficits of brain function lasting more than 24 hours or leading to death Transient Ischemic attack (TIA) Clinical syndrome of rapid onset of focal deficits of brain function which resolves within 24 hours
3. Definitions Progressive Stroke A stroke in which the focal neurological deficits worsen with time Also called stroke in evolution Completed Stroke A stroke in which the focal neurological deficits persist and do not worsen with time
4. Epidemiology Third most common cause of death after cancer and ischeamic heart disease Most common cause of severe physical disability Prevalence of stroke in India is about 1.54 per 1000 Death rate is about 0.6 per 1000 Incidence and prevalence of stroke is on the rise due to increasing adoption of unhealthy lifestyle & an increasing life expectancy
13. Thrombotic Stroke Atherosclerosis is the most common pathology leading to thrombotic occlusion of blood vessels Hypercoagulable disorders – uncommon cause Antiphospholipid syndrome Sickle cell anemia Polycythemiavera Homocysteinemia Vasculitis: PAN, Wegener’s granulomatosis, giant cell arteritis
14. Thrombotic Stroke Lacunar stroke Accounts for 20% of all strokes Results from occlusion of small deep penetrating arteries of the brain Pathology: lipohyalinosis & microatheroma Thrombosis leads to small infarcts known as lacunes Clinically manifested as lacunar syndromes
15. Embolic Stroke Cardioembolic stroke Embolus from the heart gets lodged in intracranial vessels MCA most commonly affected Atrial fibrillation is the most common cause Others: MI, prosthetic valves, rheumatic heart disease Artery to artery embolism Thrombus formed on atherosclerotic plaques gets embolized to intracranial vessels Carotid bifurcation atherosclerosis is the most comon source Others: aortic arch, vertebral arteries etc.
17. Blood supply to the brain is autoregulated Blood flow If zero leads to death of brain tissue within 4-10min <16-18ml/100g tissue/min infarction within an hour Ischemia leads to development of an ischemic core and an ischemic penumbra Pathophysiology of Ischemic Stroke
18.
19. Ischemic Penumbra Tissue surrounding the core region of infarction which is ischemic but reversibly dysfunctional Maintained by collaterals Can be salvaged if reperfused in time Primary goal of revascuralization therapies
20. Thrombus/embolus Hypoperfusion ATP depletion Failure of Na+/K+ATPase membrane ionic pump Activation of pro-coagulant pathways Membrane depolarization & cytotoxic cellular edema Free fatty acid release Calcium entry Glutamate release Activation of lipid peroxidases, proteases & NO synthase Destruction of intracellular organelles, cell membrane & release of free radicals Liquefactive necrosis
21. Hemorrhagic Stroke Two types Intracerebral hemorrhage(ICH) Subarachnoid hemorrhage(SAH) Higher mortality rates when compared to ischemic stroke
26. Pathophysiology Of Hemorhagic Stroke Explosive entry of blood into the brain parenchyma structurally disrupts neurons White matter fibre tracts are split Immediate cessation of neuronal function Expanding hemorrhage can act as a mass lesion and cause further progression of neurological deficits Large hemorrhages can cause transtentorial coning and rapid death