This document discusses the anatomy, pathophysiology, and factors related to ischemic stroke. It begins by outlining the arterial supply of the brain and clinical findings associated with occlusion of the anterior, middle, and posterior cerebral arteries. It then explains key aspects of cerebral blood flow such as normal rates, autoregulation, and thresholds for ischemia and infarction. Finally, it lists several factors that can influence the occurrence of ischemic stroke such as the rate and duration of reduced blood flow, collateral circulation, systemic conditions, and temperature and glucose levels.
Craniotomy
A craniotomy involves making an incision in the scalp and creating a hole known as a bone flap in the skull. The hole and incision are made near the area of the brain being treated.
During open brain surgery, it is done to remove tumors, clip off an aneurysm, drain blood or fluid from an infection & remove abnormal brain tissue
Decompressive craniectomy
It is a neurosurgical procedure in which part of the skull is removed to allow a swelling brain room to expand without being squeezed. It is performed on victims of traumatic brain injury, stroke and other conditions associated with raised intracranial pressure.
Increased intracranial pressure is defined as cerebrospinal fluid pressure greater than 15 mm Hg.
Infections
Tumors
Stroke
Aneurysm
Epilepsy
Seizures
Hydrocephalus
Hypertensive brain injury
Hypoxemia
Meningitis
Due to etiological factors
Components of ICP is disturbed- brain tissue, CSF, blood volume
An increase in the volume of ANY ONE component must be accompanied by a reciprocal decrease in one of the other components.
When this volume-pressure relationship becomes unbalanced, ICP increases.
Craniotomy
A craniotomy involves making an incision in the scalp and creating a hole known as a bone flap in the skull. The hole and incision are made near the area of the brain being treated.
During open brain surgery, it is done to remove tumors, clip off an aneurysm, drain blood or fluid from an infection & remove abnormal brain tissue
Decompressive craniectomy
It is a neurosurgical procedure in which part of the skull is removed to allow a swelling brain room to expand without being squeezed. It is performed on victims of traumatic brain injury, stroke and other conditions associated with raised intracranial pressure.
Increased intracranial pressure is defined as cerebrospinal fluid pressure greater than 15 mm Hg.
Infections
Tumors
Stroke
Aneurysm
Epilepsy
Seizures
Hydrocephalus
Hypertensive brain injury
Hypoxemia
Meningitis
Due to etiological factors
Components of ICP is disturbed- brain tissue, CSF, blood volume
An increase in the volume of ANY ONE component must be accompanied by a reciprocal decrease in one of the other components.
When this volume-pressure relationship becomes unbalanced, ICP increases.
An overview of how to perform a paramedic neurological assessment. For more information about this lecture, please go to www.paramedicine.com/episode6.
An overview of how to perform a paramedic neurological assessment. For more information about this lecture, please go to www.paramedicine.com/episode6.
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.
STROKE is cerebrovascular event with rapidly developing clinical signs of focal or global disturbances of cerebral functions with signs lasting 24 hours or longer or leading to death ,with no apparent cause other than of vascular origin (by WHO)
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
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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
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
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdf
Basic Anatomy & Pathophysiology of ischemic stroke
1. Ischemic Stroke: Basic
Anatomy and Pathophysiology
Dr. Ajay Kumar Agarwalla
Phase- A Resident (Neurology)
Blue Unit, Neurology dept. ,
BSMMU
2. Road Map
• Artery supply of the brain
• Findings associated with occlusion
• Key features of cerebral blood flow
• Auto regulation of cerebral blood flow
• Pathophysiology of infarction in brain
• Factors influence ischemic stroke
4. Anterior Cerebral Artery Occlusion
Contralateral hemiparesis and hemisensory loss involving mainly the
leg and foot (paracentral lobule of cortex)
Inability to identify objects correctly, apathy, and personality changes
(frontal and parietal lobes)
5. Contralateral hemiparesis and
hemisensory loss involving
mainly the face and arm
(precentral and postcentral
gyri)
Aphasia if the left hemisphere
is affected (rarely if the right
hemisphere is affected)
Contralateral homonymous
hemianopia (damage to the
optic radiation)
Middle Cerebral Artery
Occlusion
6. Contralateral homonymous
hemianopia with some
degree of macular sparing
(damage to the calcarine
cortex)
Visual agnosia (ischemia of
the left occipital lobe)
Impairment of memory
(damage of medial aspect
of the temporal lobe)
Posterior Cerebral Artery
Occlusion
7. Key features of blood flow in
BRAIN
• In an adult, CBF is typically
750 ml/min or
45-50ml/100g/min or
15 % of the cardiac output (CO)
In normal individuals, CBF remains constant when
the mean arterial pressure varies between
“60 and 160 mmHg”
8. Ideal Cerebral Auto regulationIdeal Cerebral Auto regulation
Lassen NA. Physiol Rev. 1959;39:183-238
Strandgaard S, Paulson OB. Stroke.1984;15:413-416
9. Matter of Concern
Cerebral Blood Flow (CBF) :
• Less than 23ml/100g/min, physiological
electrical function of the cell begins to fail-
“ischemic penumbra”.
• Below 10 ml/100g/min, ionic membrane
transport failure, Irreversible cell death- which
leads to- “infarction”.
10.
11. Factors Influence Ischemic Stroke
• Rate and onset of duration
• Collateral circulation
• Systemic circulation
• Hypercoagulable states
• Increased temperature
• Hyper/hypo glycemia
12. Reference
Snells Clinical Neuroanatomy, 7th
edition
Davidson’s Principles and Practice of Medicine, 22nd
edition
Harrison’s Principles of Internal Medicine, 19th
edition
http://what-when-how.com/neuroscience/blood-supply-of-the-
http://en.wikipedia.org/wiki/Cerebral_blood_flow
Stroke Pathophysiology Sid Shah, MD
Editor's Notes
It is a characteristic of the brain to adjust its own blood supply. The brain accounts for only 2-3% of total body weight and does not do any mechanical work, yet it receives 20% of all cardiac output.
Ideally, when aterial blood pressure increase or decrease between 70-150 mmhg , the cerebral autoregulation can make the blood flow velocity constant , beyond the range, the blood flow velocity will increase or decrease dramaticaly with the blood pressure
A thrombus or an embolus can occlude a cerebral artery and cause ischemia in the
affected vascular territory. It is often not possible to distinguish between a lesion caused
by a thrombus and one caused by an embolus. Thrombosis of a vessel can result in
artery-to-artery embolism. Mechanisms of neuronal injuy at the cellular level are
governed by hypoxia or anoxia from any cause that is reviewed below.
At a gross tissue level, the vascular compromise leading to acute stroke is a dynamic
process that evolves over time. The progression and the extent of ischemic injury is
influenced by many factors.
2-5
Rate of onset and duration: the brain better tolerates an ischemic event of short duration
or one with slow onset.
Collateral circulation: the impact of ischemic injury is greatly influenced by the state of
collateral circulation in the affected area of the brain. A good collateral circulation is
associated with a better outcome.
Health of systemic circulation: Constant cerebral perfusion pressure depends on
adequate systemic blood pressure. Systemic hypotension from any reason can result in
global cerebral ischemia.
Hematological factors: a hypercoagulable state increases the progression and extent of
microscopic thrombi, exacerbating vascular occlusion.
Temperature: elevated body temperature is associated with greater cerebral ischemic
injury.
Glucose metabolism: hyper- hypoglycemia can adversely influence the size of an infarct.
