A stroke is caused by the interruption of the blood supply to the brain, usually because a blood vessel bursts or is blocked by a clot. This cuts off the supply of oxygen and nutrients, causing damage to the brain tissue
A stroke is caused by the interruption of the blood supply to the brain, usually because a blood vessel bursts or is blocked by a clot. This cuts off the supply of oxygen and nutrients, causing damage to the brain tissue
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
3. Stroke
• Stroke is sudden loss of neurological function resulted due to
interruption of blood flow to the brain.
• Ischemic is the most common variant, affects 80% population of
the stroke which jeopardies the nutrients and O2.
• Hemorrhagic stroke occurs when blood vessels get ruptured and
blood sneaks out in and around brain.
• CVA is a term used interchangeably with stroke to refer vascular
conditions of brain.
4. Etiology
• Atherosclerosis is a major contributory factor in
cerebrovascular disease.
• It is characterized by plaque formation with an accumulation of
lipids, fibrin, complex carbohydrates, and calcium deposits on
arterial walls that leads to progressive narrowing of blood
vessels.
• Interruption of blood flow by atherosclerotic plaques occurs at
certain sites
5. • These generally include at the bifurcations,
angulations of arteries.
• The most common sites for lesions to occur are at the
origin of the common carotid artery.
• At its transition into the middle cerebral artery.
• At the main bifurcation of the middle cerebral artery.
• At the junction of the vertebral arteries with the
basilar artery
6. • Ischemic strokes are the product of a thrombus, embolism, or conditions
that produce low systemic perfusion pressures.
• The lack of Cerebral Blood Flow (CBF) compromises the brain’s needed
oxygen and glucose disrupts cellular metabolism leads to injury and death
of cerebral tissues.
• Haemorrhagic strokes, with abnormal bleeding into the extravascular areas
of the brain, are the result of rupture of a cerebral vessel or trauma.
• Haemorrhage results in increased intracranial pressures with injury to brain
tissues and restriction of distal blood flow.
7.
8. Risk Factors & Preventions
• Cardiovascular diseases affecting the brain and heart share number of
common risk factors important to the development of atherosclerosis.
• Major risk factors for stroke are hypertension, heart disease, disorders of
heart rhythm, and diabetes mellitus.
• Individuals with hypertension (blood pressure [BP] (140/90 mm Hg or
higher) have twice the lifetime risk of stroke.
• Hypertension (140/90 mm Hg or higher) have twice the lifetime risk of
stroke. Risk is increased with elevated total blood cholesterol
(hypercholesterolemia), 240 mg/dL or greater
9. • Risk is elevated with raised levels of low-density lipoprotein (LDL bad)
cholesterol. LDL levels are defined as borderline high levels of 130 to 159
mg/dL, high levels of 160 to 189 mg/dL, and very high levels of 190 mg/dL
or greater.
• Low levels of high-density lipoprotein (HDL-good) cholesterol, defined as
below 40 mg/dL in adult males and below 50 mg/dL in adult females, also
increases risk of stroke.
• Modifiable risk factors include cigarette smoking, physical inactivity,
obesity, and diet.
• Current smokers have 2 to 4 times increased stroke risk compared to non-
smokers or those who have quit for more than 10 years.
10. • Physical activity (moderate to vigorous exercise) is associated with an
overall 35% reduction in stroke risk whereas light exercise (walking) does
not appear to have the same benefit.
• Nonmodifiable risk factors include family history, age, gender, and race.
• Lifestyle changes can significantly reduce the risk of stroke, most
importantly it includes controlling BP, diet (cholesterol and lipids free),
weight loss, quitting smoking, and increasing physical activity, as well as
effective existing systemic disease management.
11. PATHOPHYSIOLOGY
• Sudden cessation of cerebral blood flow and oxygen- glucose deprivation
sets in motion a series of pathological events.
• Within couple of minutes neurons die within the ischemic core tissue, the
greater part of neurons located in the surrounding penumbra survive for a
slightly longer time.
• This Cell survival mechanism purely depends on the severity and the
duration of the ischemic episode.
• Without timely reperfusion, cells in the penumbra will die, neuronal
activity ceases, and the infarct expands.
12. • Ischemia triggers a number of damaging cellular events, called it as
ischemic cascade.
• The release of excess neuro- transmitters (e.g., glutamate and aspartate)
produces a progressive disturbance of energy metabolism and anoxic
depolarization, this results in an inability of brain cells to produce
energy(ATP).
• This is followed by excess influx of calcium ions and pump failure of the
neuronal membrane, so this excess calcium reacts with intracellular
phospholipids to form free radicals.
• Calcium accumulation, stimulates the release of nitric oxide and cytokines
this furthermore damage the brain cells.
14. • Ischemic strokes produce cerebral edema, an accumulation of fluids
within the brain that begins within minutes of the insult and reaches a
maximum by 3 to 4 days.
• It is the result of tissue necrosis and widespread rupture of cell membranes
with movement of fluid from the blood into brain tissues.
• The swelling gradually subsides and generally disappears by 2 to 3 weeks.
Significant edema can elevate intracranial pressures and neurological
deterioration associated with contralateral and caudal shifts of brain
structures (brainstem herniation)
16. • Clinical signs of elevating intracranial pressure (ICP) include decreasing
level of consciousness (stupor and coma), widened pulse pressure,
increased heart rate, irregular respirations (Cheyne-Stokes respirations),
vomiting, unreacting(Dilated/No response to Light) pupils (cranial nerve
CN-III signs), and papilledema.
• Cerebral edema is the most frequent cause of death in acute stroke and is
characteristic of large infarcts involving the middle cerebral artery and the
internal carotid artery.
• Cheyne-Stokes Respiration - YouTubewww.youtube.com › watch
18. Anterior Cerebral Artery Syndrome
(HSLE>UE/“HASLE”)
• The anterior cerebral artery (ACA) is the first and smaller of two terminal
branches of the internal carotid artery.
• It supplies the medial aspect of the cerebral hemisphere (frontal and
parietal lobes) and subcortical structures, including the basal ganglia
(anterior internal capsule, inferior caudate nucleus), anterior fornix, and
anterior four-fifths of the corpus callosum.
• More distal lesions leads to more significant impairments.
• The clinical manifestations of anterior cerebral artery (ACA) syndrome
include contralateral hemiparesis and sensory loss with greater involvement
of the lower extremity (LE) than the upper extremity (UE) because the
somatotopic organization of the medial aspect of the cortex includes the
functional area for the LE.
19. Signs and Symptoms Structures Involved
• Contralateral hemiparesis involving mainly
the LE (UE is more spared)
• Primary motor area, medial aspect of
cortex, internal capsule
• Contralateral hemisensory loss involving
mainly the LE (UE is more spared)
• Primary sensory area, medial aspect of
cortex
• Urinary incontinence
• Posteromedial aspect of superior frontal
gyrus
• Problems with imitation and bimanual
tasks, apraxia
• Corpus callosum
20. Middle Cerebral Artery Syndrome (FUEL)
• The MCA is the second main branches of the internal carotid artery and supplies
the entire lateral aspect of the cerebral hemisphere. Mainly it covers frontal,
temporal, and parietal lobes and subcortical structures, including the internal
capsule posterior portion, corona radiata, globus pallidus (outer part), most of the
caudate nucleus, and putamen.
• Occlusion of the proximal MCA produces extensive neurological damage along
with marked cerebral edema, increased intracranial pressures typically lead to
loss of consciousness, brain herniation, and possibly death.
• The most common characteristics of the syndrome are contralateral spastic
hemiparesis and sensory loss of the face, UE, and LE, with the face and UE
more involved than the LE.
• Lesions of the parieto-occipital cortex of the dominant hemisphere (usually the
left hemi- sphere) typically produce aphasia. Lesions of the right parietal lobe of
the nondominant hemisphere (usually the right hemisphere) typically produce
perceptual deficits (e.g. unilateral neglect, anosognosia, apraxia, and spatial
disorganization).
21. Signs and Symptoms Structures Involved
• Contralateral hemiparesis involving
mainly the UE and face (LE is more
spared)
• Primary motor cortex and internal
capsule
• Contralateral hemisensory loss involving
mainly the UE and face (LE is more
spared)
• Primary sensory cortex and internal
capsule
• Motor speech impairment: Broca’s or
nonfluent aphasia with limited
vocabulary and slow, hesitant speech
• Broca’s cortical area (third frontal
convolution) in the dominant hemisphere,
typically the left hemisphere
• Receptive speech impairment:
Wernicke’s or fluent aphasia with
impaired auditory comprehension and
fluent speech with normal rate and
melody
• Wernicke’s cortical area (posterior
portion of the temporal gyrus) in the
dominant hemisphere, typically the left
22. Signs and Symptoms Structures Involved
• Global aphasia: nonfluent speech with
poor comprehension
• Both third frontal convolution and
posterior portion of the superior temporal
gyrus
• Contralateral homonymous hemianopsia
• Loss of conjugate gaze to the opposite side
• Ataxia of contralateral limb(s) (sensory
ataxia) Pure motor hemiplegia (lacunar
stroke)
• (https://youtu.be/5ji0ZwcP4vs)
• Optic radiation in internal capsule.
• Frontal eye fields or their descending
tracts.
• Parietal lobe.
• Limb-kinetic apraxia
• Premotor or parietal cortex
• Perceptual deficits: unilateral neglect,
depth perception, spatial relations, agnosia
• Parietal sensory association cortex in the
nondominant hemisphere, typically the
right
23. Posterior Cerebral Artery Syndrome
• Arise as terminal branches of the basilar artery and each supplies the
corresponding occipital lobe and medial and inferior temporal lobe.
• It also supplies the upper brainstem, midbrain, and posterior diencephalon,
including most of the thalamus.
• Occlusion of thalamic branches may produce hemianesthesia
(contralateral sensory loss) or central post-stroke (thalamic) pain,
Occipital infarction produces homonymous hemianopsia, visual agnosia,
prosopagnosia, or if the lesion is bilateral, cortical blindness are common,
whereas Temporal lobe ischemia results in amnesia
24. Signs and Symptoms
(Peripheral Territory) Structures Involved
• Contralateral homonymous hemianopsia
• Bilateral homonymous hemianopsia with
some degree of macular sparing
• Visual agnosia
• Primary visual cortex or optic radiation
• Calcarine cortex (macular sparing is due to
occipital pole receiving collateral blood
supply from MCA)
• Left occipital lobe
• Prosopagnosia (difficulty naming people
on sight)
• Visual association cortex
• Dyslexia (difficulty reading) without
agraphia (difficulty writing), colour
naming (anomia), and colour
discrimination problems
• Dominant calcarine lesion and posterior
part of corpus callosum
• Memory defect
• Topographic disorientation
• Lesion of inferomedial portions of
temporal lobe bilaterally or on the
dominant side only
• Nondominant primary visual area, usually
bilaterally
25. Signs and Symptoms
(Central Territory)
Structures Involved
• Central post-stroke (thalamic) pain
Spontaneous pain and dysesthesias;
sensory impairments (all modalities)
• Ventral posterolateral nucleus of
thalamus
• Involuntary movements; choreoathetosis,
intention tremor, hemiballismus
• Subthalamic nucleus or its pallidal
connections
• Contralateral hemiplegia
• Weber’s syndrome
Oculomotor nerve palsy and contralateral
hemiplegia
• Cerebral peduncle of midbrain
• Third nerve and cerebral peduncle of
midbrain
• Paresis of vertical eye movements, slight
miosis and ptosis and sluggish pupillary
light response
• Supranuclear fibres to third cranial nerve
26. Lacunar Stroke
• Lacunar strokes are caused by small vessel disease deep in the cerebral
white matter.
• They are strongly associated with hypertensive haemorrhage and diabetic
microvascular disease & are consistent with specific anatomical sites.
• Pure motor lacunar stroke are associated with involvement of the posterior
limb of the internal capsule, pons, and pyramids. Pure sensory lacunar
stroke is associated with involvement of the ventrolateral thalamus or
thalamocortical projections.
• Other lacunar syndromes include dysarthria/clumsy hand syndrome
(involving the base of the pons, genu of anterior limb, or the internal
capsule)
27. • Ataxic hemiparesis (involving the pons, genu of internal capsule, corona
radiata, or cerebellum).
• Sensory/motor stroke which involving the junction of the internal capsule
and thalamus, or dystonia/involuntary movements such as choreoathetosis
with lacunar infarction of the putamen or globus pallidus; hemiballismus
with involvement of the subthalamic nucleus.