Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
ARDS - Diagnosis and Management
Visit www.medicalgeek.com for more
http://www.medicalgeek.com/lecture-notes/36156-ards-diagnosis-management-presentation-ppt-pdf.html#post89045
https://www.facebook.com/MedicalGeek
https://only4medical.wordpress.com/
http://www.facebook.com/group.php?gid=129413628862&ref=nf
http://groups.yahoo.com/group/only4medical/
Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
ARDS - Diagnosis and Management
Visit www.medicalgeek.com for more
http://www.medicalgeek.com/lecture-notes/36156-ards-diagnosis-management-presentation-ppt-pdf.html#post89045
https://www.facebook.com/MedicalGeek
https://only4medical.wordpress.com/
http://www.facebook.com/group.php?gid=129413628862&ref=nf
http://groups.yahoo.com/group/only4medical/
Cardio pulmonary interactions during Mechanical Ventilation Dr.Mahmoud Abbas
Cardio pulmonary interactions during Mechanical Ventilation lecture presented by Dr Lluis blanch at the Egyptian Critical care Summit, the leading medical event in Egypt
Cardio pulmonary interactions during Mechanical Ventilation Dr.Mahmoud Abbas
Cardio pulmonary interactions during Mechanical Ventilation lecture presented by Dr Lluis blanch at the Egyptian Critical care Summit, the leading medical event in Egypt
Back to the Bedside: Internal Medicine Bedside Ultrasound ProgramAllina Health
David Tierney, MD. How bedside ultrasound is changing the practice of medicine and how Abbott Northwestern Hospital has become a national leader in integrating bedside ultrasound in its Internal Medicine Residency Program. "As internal medicine physicians, we are finding that everything we do with our hands, eyes and stethoscopes can be done a little better with ultrasound. That means our physical exam, which we consider our bread and butter, has more sensitivity and specificity. This gives us better diagnostic ability and results in earlier and more appropriate treatment."
The four phases of intravenous fluid therapy: Manu MalbrainSMACC Conference
Manu Malbrain presents the four phases of intravenous fluid therapy. He takes you through the big questions of fluids - What, when, why and how?
To Manu, there are four Ds of fluid therapy: Drug, dose, duration, and de-escalation
Drug
Fluids are drugs. This means, like any drugs, consideration must be taken about the type, indication, contraindication, and adverse effects of fluids whenever prescribing them. The evidence suggests that we should stop using starches in sepsis, albumin in TBI and stop using more than 2L of saline in resuscitation. For maintenance – eliminate the use of unbalanced isotonic fluids, and do not forget to cover daily needs. The bottom line is starting to consider fluids as drugs.
Dose
As Paracelsus famously said “The dose makes the poison”
This holds true when administering fluids. There are different doses for different patients dependent on the indication – whether using fluids for maintenance, resuscitation, or replacement.
Duration
When do you start and stop? You must weigh up the benefit and risk of fluid administration.
Duration should be appropriate – more often than not this means tending towards a shorter duration. Similarly, do not use fluids to treat numbers (such as low CVP or MAP) but rather to treat shock. Finally, fluids can be stopped when shock has resolved.
De-escalation
Water is a problem. Just as hypovolaemia is bad, so too is hypervolaemia.
Weigh up the benefit and risk of fluid removal. Manu describes the ROSE acronym – Resuscitation, Organ support, Stabilisation, Evacuation removal. Essentially, after early management with adequate and goal directed fluids, stop ongoing resuscitation, and move to conservative fluid management (de-resuscitation!)
We need to make good fluids better
So let Manu guide you through the complex world of fluids. Answer the four questions, address the four D’s and remember the four phases of ROSE.
For more like this, head to our podcast page. #CodaPodcast
presentation on SIRS septic shock and multiorgan failure,and their corelation together in increasing morbidity and mortalitiy in shocked patient explaning pathophysiology clinical picture and how to manage
CORTICAL SPREADING DEPOLARISATION IN NEUROLOGICAL DISEASE – AN INTRODUCTION
By Toby Jeffcote
Cortical spreading depolarization (CSD) is a spreading loss of ion homeostasis, altered vascular response, change in synaptic architecture, and subsequent depression in electrical activity following an inciting neurological injury.
It was first described by Leão in 1944, a disturbance in neuronal electrophysiology has since been demonstrated in a number of animal studies, and recently a few human studies that examine the occurrence of this depolarizing phenomenon in the setting of a variety of pathological states, including migraines, cerebrovascular accidents, epilepsy, intracranial hemorrhages, and traumatic brain injuries. The onset of CSD has been demonstrated experimentally following a disruption in the neuronal environment leading to glutamate-induced toxicity. This initial event leads to pathological changes in the activity of ion channels that maintain membrane potential. Recovery mechanisms such as sodium-potassium pumps that aim to restore homeostasis fail, leading to osmolar shifts of fluid, swelling of the neuron, and ultimately a measurable depression in cortical activity that spreads in the order of millimeters per minute. Equally important is the resulting change in vascular response. In healthy tissue, increased electrical activity is coupled with release of vasodilatory factors such as nitric oxide and arachidonic acid metabolites that increase local blood flow to meet increased energy expenditure. In damaged tissue, not only is the restorative vascular response lacking but a vasoconstrictive response is promoted and the ischemia that follows adds to the severity of the initial injury. Tissue threatened by this ischemic response is then at elevated risk for CSD propagation and falls into a vicious cycle of electrical and hemodynamic disturbance. Efforts have been made to halt this spreading cortical depression using N-methyl-D-aspartate receptor antagonists and other ion channel blockers to minimize the damaging effects of CSD that can persist long after the triggering insult.
Celia Bradford takes us through the latest on the management of subdural haemorrhage (SDH). She covers acute SDH, chronic SDH and middle meningeal artery embolisation, a novel treatment for chronic SDH management in certain circumstances.
Andy Neill - More neuroanatomy pearls for neurocritical careSMACC Conference
Andy Neill shares some more neuroanatomy wisdom that's highly practical for anyone working with neuro emergencies. This time he covers brain herniation syndromes, hydrocephalus, extradural vs subdural haematomas, cervical spinal imaging, vertebral artery dissection and "things you read on CT reports but don't know what they mean"!
Andrew Udy talks about Brain Tissue Oxygen Monitoring:
It’s Not What You’ve Got It’s What You Do With It
The BONANZA Trial
Andrew Udy talks about the ongoing BONANZA Trial which is assessing whether an algorithm that incorporates both ICP and brain tissue oxygen (PbTO2) can improve outcomes after traumatic brain injury (TBI). Like with all monitoring, how the PbTO2 is interpreted and managed is critical and the devil is in the detail!
More on BONANZA here
More on BOOST3 here
R. Loch Macdonald, M.D., Ph.D.
Community Neurosciences Institute
Fresno, California, USA
Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.
By Catherine Bell and Andrew Udy
Catherine Bell takes us through how to troubleshoot problems commonly encountered when looking after patients who have an external ventricular drain (EVD) in situ. Issues with using brain tissue oxygen monitors are also discussed. A highly practical session aimed at bedside clinicians.
There is no such thing as mild, moderate and severe TBI - by Andrew UdySMACC Conference
Part 2 of a debate over the classification of TBI. Andrew Udy then argues that this classification is fundamentally flawed. He discusses the issues with the Glasgow Coma Scale, and therefore the follow-on issues in TBI classification, including all the confounders to the GCS, the issues with timing of the score as well as GCS not taking baseline function or specifics subtypes of TBI into account. He makes teh argument that biomarkers may better categorise the diffuse entity we call TBI.
TBI Debate - Mild, moderate and severe categories workSMACC Conference
Andrew Chow, Intensivist with a neurosurgical background, argues that the current categorisation system for traumatic brain injury (TBI) works, and makes sense! He tackles us through the history of this system, and why it’s important to differentiate different types of TBI. The arguments in favour of this categorisation include the consistency and benefits of a universal language, the implications for triage and management, and the fact that this system has been endorsed by all major organisations
Dr Nick Little is an experienced Neurosurgeon who's looked after patients with traumatic brain injury for his whole career. Here he discusses the difficulties of prognostication following traumatic brain injury (TBI). He talks about the statistics of outcomes following mild, moderate and severe TBI and then goes on to tackle the harder topic of how we try to work out what an individual would want if they knew the spectrum of outcomes that they may face. The issues with the clinical examination findings we use to prognosticate are covered, as well as which imaging findings he finds most helpful. He also mentions the difficulties with current prognostic calculators.
Historically, when it came to brain injury, ketamine had a bad rap. Much of that dogma was dispelled in the last decade, and ketamine is now frequently used as an induction agent in acute brain injury, especially traumatic brain injury, due to it’s favorable effects on haemodynamics.
However a new application of ketamine is now being explored - whether ketamine may be able to reduce secondary brain injury.
Managing Complications of Chronic SCI by Bonne LeeSMACC Conference
20 million people around the world are living with a spinal cord injury (SCI). The medical issues they develop over the years differ to any other patient cohort.
These complications include autonomic dysreflexia, management of pressure areas, specific infections, nuanced peri-operative care and highly specific issues such as baclofen pump management and syringomyelia
Do look at the NeuroResus section on this and listen to Spinal Rehab Specialist Bonne Lee talk about this side of SCI care.
Keywords
SCI, spinal, spinal cord injury, autonomic dysreflexia, pressure areas, infection, peri-operative care, baclofen pump, syringomyelia, chronic SCI, spinal trauma, spinal rehab, incomplete SCI
Tania is a neurologist and epileptologist with expertise in continuous EEG (cEEG) and status epilepticus (SE). This talk covers what a seizure is, what status is, including focal and generalised status epilepticus.
So why do we do cEEGs for patients with suspected SE?
To confirm the diagnosis
To see if patient just post ictal or still seizing
To establish that the clinical and electric seizures have stopped
To see if burst suppression is achieved
To exclude other differential diagnoses
She makes a good argument for why cEEG is such an important tool in managing SE.
In the questions after the talk, the issue of availability of cEEG in the Australian setting was discussed. Limited montage EEGs are discussed including their pros and cons.
Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. He discusses what "severe disability" really means.
Severe disability is more common than many realise - about 6% of the Australian population.
Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated.
He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being.
Stuart also covers how severely disabled people face various forms of discrimination.
Shree Basu is a Paediatirc Intensivist in Sydney. These slides from the Brain Symposium 2023 accompany the talk she gave. She discusses how Paediatric stroke presents, what neuroimaging is required and what interventions are available, including thrombolysis and the role of endovascular thrombectomy.
Hypertensing Spinal Cord Injury - gold standard or wacky?SMACC Conference
After spinal cord injury (SCI), there aren’t many interventions we have available that actually make a difference.
Augmenting blood pressure to increase spinal cord perfusion pressure is an attractive concept that may improve neurological outcomes following SCI. We know that hypotension can make SCI worse. Clinical studies looking at blood pressure augmentation are mostly old, retrospective and flawed in various ways.
Aiming for a MAP of > 85 for 5-7 days is recommended by guidelines but why this pressure and duration are good questions.
Hypertensive therapy is relatively safe and easy to implement but not without risk.
Tessa discusses the pros and cons, how this is managed practically and what the future may hold in this area.
Mark Weedon takes us through the increasingly utilised concept of an optimal cerebral perfusion pressure (CPPopt) for each unique patient. He discusses the background to CPPopt, including intrcranial pressure (ICP), the Monroe Kelly hypothesis, neurovascular coupling, and cerebral autoregulation in health and following brain injury. He shows how intracranial pressure is affected by intracranial compliance and how this affects ICP waveforms. Cerebral perfusion pressure in relation to the Brain Trauma Foundation guidelines is covered including management of elevated ICP (EICP). The currently recommended tiered approach to managing cerebral perfusion pressure and EICP is mentioned citing recent guidelines. He uses a clinical case of a TBI to illustrate how the CPPopt can be ascertained and used to guide therapy, including the easy to perform “MAP Challenge”. Mark also describes the Pressure Reactivity Index (PRx) and how it can be used as a target for therapy. Finally, he covers the exciting results of the preliminary COGiTATE pilot study.
Social Worker Victoria Whitfield and Bereavement councilor Louise Sayers discuss the power of words when health professionals are communicating topics around of death and serious injury with relatives and patients in critical care. They use role plays to bring theories to life.
Sepsis and Antimicrobial Stewardship - Two Sides of the Same CoinSMACC Conference
Appropriate use of antimicrobials is primarily a patient safety issue, and is the key aim of an effective antimicrobial stewardship program. We discuss the challenges in the management of a patient with sepsis, and how decision-making is usually done in the absence of effective diagnostics. Time dependent protocols and the knowledge that undertreatment of a patient with sepsis will lead to poor outcomes will lead to prescribing that may be driven by fear. Antimicrobial resistance is associated with over-use of antimicrobials but is usually not the immediate concern. Antimicrobial stewardship programs should work closely with sepsis teams to ensure that sepsis pathways are implemented across the whole hospital, and that key principles of judicious use are embedded within the clinical pathway.
Being able to prognosticate in the aftermath of a traumatic brain injury (TBI) is important as it assists with counselling patients and families. Moreover, it helps rationally allocate healthcare resources.
However, due to the heterogenous nature of TBI and variable pre brain injury patient factors and post brain injury course, this has proven to be a difficult task.
Large cohort studies have enabled improved accuracy in the prediction of 6 month mortality and unfavourable outcome.
Furthermore, many of the factors that contribute to long-term outcome have also emerged. However, it is not yet possible to use them in prediction algorithms or mathematical models.
There is emerging evidence that pre injury psychosocial and demographic factors may be of more relevance than injury severity. Moreover, that 'outcome' becomes increasingly subjective and complex as the post injury duration increases.
We end with three brief vignettes which highlight the fraught nature of long term outcome prediction.
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
- 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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
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.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
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
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...
ARDS: An Evidence-based Update. By Mac Sweeney.
1. ARDS
An Evidence Based Update
Rob Mac Sweeney
SMACCgold 2014
rob@criticalcarereviews.com / @critcarereviews
2. Disclosure
• Research funding from Northern Ireland Health and Social Care
Research and Development Board
• Research into ARDS biomarkers
References
• http://www.criticalcarereviews.com/index.php/smacc-2014
3. ARDS
An Evidence Based Update
Rob Mac Sweeney
SMACCgold 2014
rob@criticalcarereviews.com / @critcarereviews
4. A Condition That….
1. can’t diagnose
2. of limited use
3. no specific treatment for
4. people don’t die from
……….. doesn’t actually exist
12. Original Description
• Syndrome of
• Severe Dyspnoea
• Tachypnoea
• Cyanosis refractory to oxygen therapy
• Loss of lung compliance
• Benefit with PEEP
• Possible benefit with steroids
• Diffuse alveolar infiltration
53. ARDS – A Condition That….
1. can’t diagnose (we can’t agree to diagnose)
2. of limited use (doesn’t change management)
3. no specific treatment for (getting to it)
4. people don’t die from (mostly)
5. doesn’t actually exist (half the time)
54. ARDS – A Condition That….
1. can’t diagnose (we can’t agree to diagnose)
2. of limited use (doesn’t change management)
3. no specific treatment for (getting to it)
4. people don’t die from (mostly)
5. doesn’t actually exist (half the time)
55. ARDS – A Condition That….
1. can’t diagnose (we can’t agree to diagnose)
2. of limited use (doesn’t change management)
3. no specific treatment for (getting to it)
4. people don’t die from (mostly)
5. doesn’t actually exist (half the time)
56. ARDS – A Condition That….
1. can’t diagnose (we can’t agree to diagnose)
2. of limited use (doesn’t change management)
3. no specific treatment for (getting to it)
4. people don’t die from (mostly)
5. doesn’t actually exist (half the time)
57. ARDS – A Condition That….
1. can’t diagnose (we can’t agree to diagnose)
2. of limited use (doesn’t change management)
3. no specific treatment for (getting to it)
4. people don’t die from (mostly)
5. doesn’t actually exist (half the time)
58. ARDS – A Condition That….
1. can’t diagnose (we can’t agree to diagnose)
2. of limited use (doesn’t change management)
3. no specific treatment for (getting to it)
4. people don’t die from (mostly)
…….doesn’t actually exist (half the time)
59.
60.
61. Therapeutic
Evidence-
Base
?
DAD
Severity Mortality
Temporary Function Clinical
Timing Oedema PaO2/FiO2 Infiltrates
63. Tidal Volume
• 861 ARDS patients (P/F < 300 cm H20)
• 6 ml/kg & Pplt ≤ 30 cm H20
versus
• 12 ml/kg & Pplt ≤ 50 cm H20
• 9% absolute risk reduction in 28 day
mortality
64. Tidal Volume
• 150 critically ill mechanically
ventilated patients
• 6 ml/kg vs 10 ml/kg
Development of ARDS
• 2.6% versus 13.5%; p = 0.01
65. Tidal Volume
• 400 patients undergoing major
abdominal surgery
• 10-12 ml/kg & ZEEP & no recruitment
versus
• 6-8 ml/kg & PEEP 6-8 cm H20 & RM
• Postoperative Respiratory Support
• 5% vs 17%
• RR 0.29 (95% CI 0.14 to 0.61)
66. Oscillate
• 548 ARDS patients
• PaO2/FiO2 < 200 cmH20
• Fi02 > 0.5
In-hospital mortality
• HFOV 47% vs Control 35%
(RR 1.33; 95% CI 1.09 to 1.64;
P = 0.005)
67. Oscar
• 548 ARDS patients
• PaO2/FiO2 < 200 cmH20
• PEEP > 5 cmH20
30 day mortality
• HFOV 41.7% vs Control 41.1%
• Difference 0.6%, 95% CI −6.1 to 7.5
70. ACURASYS Study
• 340 ARDS patients
• PaO2/FiO2 < 150 mmHg
Adjusted Mortality at Day 90
• NMB: 31.6% vs placebo: 40.7%
• HR 0.68 (95% CI 0.48 to 0.98; P = 0.04)
71. PROSEVA Study
• 466 ARDS patients
• PaO2/FiO2 < 150 cmH20
28 day mortality
• Prone: 16% vs Control 32.8%
Unadjusted 90-day mortality
• Prone: 23.6% vs supine 41.0%
72. Prone Ventilation
• 4 RCTS
• 1,573 patients
In the most hypoxaemic
• 486 patients
• PaO2/FiO2 < 100 mmHg
• absolute mortality reduction 10%
(6% to 21%)
75. FACTT Study
• 1000 patients with ALI
• 0 ml vs 7000 ml fluid balance at day 7
60 Day Mortality
• Conservative: 25.5% vs liberal 28.4%
95% CI difference −2.6 to 8.4 %, P=0.3
76. FACTT Study
• 1000 patients with ALI
• 0 ml vs 7000 ml fluid balance at day 7
60 Day Mortality
• Conservative: 25.5% vs liberal 28.4%
95% CI difference −2.6 to 8.4 %, P=0.3
77. FACTT Study
• 1000 patients with ALI
• 0 ml vs 7000 ml fluid balance at day 7
60 Day Mortality
• Conservative: 25.5% vs liberal 28.4%
95% CI difference −2.6 to 8.4 %, P=0.3
81. Drugs
Clinically Tested
1. NMBs √
2. Steroids ?
3. Surfactant X
4. β2 agonists X
5. Diuretics ?
6. Ketoconazole X
7. Activated Protein C X
8. Nitric Oxide X
9. Silvelestat X
10. Lisofylline X
11. Pharmaconutrients X
82. Drugs
Clinically Tested
1. NMBs √
2. Steroids ?
3. Surfactant X
4. β2 agonists X
5. Diuretics ?
6. Ketoconazole X
7. Activated Protein C X
8. Nitric Oxide X
9. Silvelestat X
10. Lisofylline X
11. Pharmaconutrients X
Clinically Untested
1. Prostacyclin
2. Almitrine
3. Ibuprofen
4. N-Acetylcysteine
5. Mucolytics
6. Albumin
83. Drugs
Clinically Tested
1. NMBs √
2. Steroids ?
3. Surfactant X
4. β2 agonists X
5. Diuretics ?
6. Ketoconazole X
7. Activated Protein C X
8. Nitric Oxide X
9. Silvelestat X
10. Lisofylline X
11. Pharmaconutrients X
Clinically Untested
1. Prostacyclin
2. Almitrine
3. Ibuprofen
4. N-Acetylcysteine
5. Mucolytics
6. Albumin
Next Wave
1. Statins
2. Aspirin
3. ACEI / ARB
4. Macrolides
5. Insulin
6. Vitamin D
7. Antibodies
• Complement
• Interleukins
8. Stem cells
9. Growth factors
10. Gene therapy
84. Drugs
Clinically Tested
1. NMBs √
2. Steroids ?
3. Surfactant X
4. β2 agonists X
5. Diuretics ?
6. Ketoconazole X
7. Activated Protein C X
8. Nitric Oxide X
9. Silvelestat X
10. Lisofylline X
11. Pharmaconutrients X
Clinically Untested
1. Prostacyclin
2. Almitrine
3. Ibuprofen
4. N-Acetylcysteine
5. Mucolytics
6. Albumin
Next Wave
1. Statins
2. Aspirin
3. ACEI / ARB
4. Macrolides
5. Insulin
6. Vitamin D
7. Antibodies
• Complement
• Interleukins
8. Stem cells
9. Growth factors
10. Gene therapy
85. ALTA Study
• 282 patients with ALI
• Aerosolized albuterol vs saline
Ventilator-free days
• albuterol 14.4 vs control 16.6 d
• 95% CI difference –4.7 to 0.3 d; P =
0.087
Hospital death
• albuterol 23.0% vs control 17.7%
• 95% CI difference –4.0 to 14.7%, P=0.30
86. BALTI 2 Study
• 326 ARDS patients
• PaO2/FiO2 < 200 mmHg
• IV salbutamol vs placebo
28 day mortality
• salbutamol: 34% vs Control 23%
• RR 1∙47, 95% CI 1∙03 to 2∙08
87. Nitric Oxide
Severe ARDS
• n = 329, six trials
• RR 1.01; 95% CI 0.78 to 1.32; p = 0.93
Mild to Moderate ARDS
• n = 740, seven trials
• RR1.12, 95% CI 0.89 to 1.42; p = 0.33
90. ECMO
CESAR STUDY
• 170 patients with severe respiratory
failure
6 month mortality outcome
• ECMO centre 63% vs referral 47%
• RR 0·69; 95% CI 0·05 to 0·97, p=0·03
91. ECMO
ANZICS H1N1 ECMO Case Series
• 2009 influenza A(H1N1) - associated
ARDS
• 68 patients
• Median PaO2/FiO2 56 (48-63) mmHg
• 71% survival
98. To Summarise
1. The positive studies would likely be positive in
any critical care condition
2. The negative studies are probably negative
because they have been studied in any critical
care condition (i.e. ARDS) rather than the
specific condition that they are intended for
(i.e. DAD)
99. To Summarise
1. The positive studies would likely be positive in
any critical care condition
2. The negative studies may be negative because
they have been studied in any critical care
condition (i.e. ARDS) rather than the specific
condition that they are intended for (i.e. DAD)
100. To Summarise
1. The positive studies would likely be positive in
any critical care condition
2. The negative studies may be negative because
they have been studied in any critical care
condition (i.e. ARDS) rather than the specific
condition that they are intended for (i.e. DAD)
101. To Summarise
1. The positive studies would likely be positive in
any critical care condition
2. The negative studies may be negative because
they have been studied in any critical care
condition (i.e. ARDS) rather than the specific
condition that they are intended for (i.e. DAD)
102. ARDS – A Condition That….
1. can’t diagnose
2. of limited use
3. no specific treatment for
4. people don’t die from
…….doesn’t actually exist
103. Final Thoughts
1. ARDS studies need to be able to identify
alveolar injury
2. Did the AECCC prevent us from adequately
investigating some therapies?
3. Are critical care syndromes really of any use?