Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Seminar present the Upper Gastrointestinal Bleeding problems
Edited by : Dr. Inzar Yassen & Dr. Ammar L. Aldwaf
in Hawler Medical Uni. collage of medicine in 14/01/2014
Iraq - Kurdistan - Erbil
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Seminar present the Upper Gastrointestinal Bleeding problems
Edited by : Dr. Inzar Yassen & Dr. Ammar L. Aldwaf
in Hawler Medical Uni. collage of medicine in 14/01/2014
Iraq - Kurdistan - Erbil
Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
Dr. Roberto Machado from the University of Illinois at Chicago presented an update on PAH at a Patient Education Conference on March 15, 2014 hosted by the Scleroderma Foundation, Greater Chicago Chapter.
CAD – leading cause of death
Cardiac SPECT – steady growth in last two decades & played an important role in clinical mangement
Radionuclide ventriculography (MUGA)
First pass studies
PET/CT
Pierre Janin talks targets in neuro-icu, zoning in on blood pressure management in patients with ICH. This resource was recorded at Bedside Critical Care Conference 4.
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.
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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.
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.
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.
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?
Rockall score in non-variceal upper gastrointestinal bleeding
1. The use of Rockall Score in predicting mortality, recurrent bleeding and need for surgery in non-variceal upper gastrointestinal bleeding at a University Hospital in the East Coast of Peninsular Malaysia Yeong Yeh Lee MD MRCP(UK) MMed ORAL PRESENTATION APDW 2008
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5. Calculation of Rockall Score High risk score > 5 Low risk score ≤ 5 1 1. Church NI, Palmer KR (2001). Eur J Gastroenterol Hepatol 13:1149–52. SBP = systolic blood in mmHg PR = pulse rate IHD=Ischaemic heart Disease GI= gatrointestinal SRH= Stigmata recent Haemorrhage Variable Score 0 1 2 3 Age Shock Co Morbidity Diagnosis Major SRH <60 No shock SBP≥100 PR<100 No major Co-morbidity Mallory-Weiss tear, no lesion identified, no SRH or blood None or dark spot 60-79 Tachycardia SBP≥100 PR≥100 All other diagnosis >80 Hypotension SBP≤100 Cardiac Failure, IHD, any major co-morbidity Malignancy of upper GI tract Blood in upper GI tract, adherent clot, visible or spurting vessel Renal failure, liver failure disseminated malignancy
6. Rockall Score and outcome Rockall score Mortality n(%) p Recurrent bleeding n(%) p Need for surgery n(%) p Score > 5 Score≤5 7(2.8) 2(0.8) <0.001 10(4) 14(5.6) <0.01 6(2.4) 5(2.0) 0.43 Score >5 Sensitivity Specificity 0.78 0.86 0.42 0.87 0.45 0.85
7. Demographic Frequency Mean ±SD Total n(%) Mortality n (%) Recurrent Bleeding n (%) Need for Surgery n (%) Total Age(years) Gender Male Female Race Malay Non-malay Smoking Current Ex 62.1 ±16 250(100) 144(57.6) 106(42.4) 209(83.6) 41(16.4) 33(13.2) 38(15.2) 9(3.6) 5(55.6) 4(44.4) 7(77.8) 2(22.2) 1(11.1) 0 24(9.6) 17(70.8) 7(29.2) 22(91.7) 2(8.3) 5(20.8) 2(8.3) 11(4.4) 8(72.7) 3(27.3) 11(100) 0 2(18.2) 1(9.1)
8. IHD = Ischaemic Heart Disease PUD = Peptic Ulcer Disease CRF = Chronic Renal Failure CLD = Chronic Liver Disease Op = operation / surgical interventtion NS= Not significant Comorbidity and association with outcome Co-morbidity Frequency /association (p value) Total (n) Death (n) p Recurrent bleeding (n) p Need for op (n) p High risk group (n) p Total (n) 9 24 11 37 IHD Prior PUD CRF CLD Sepsis 53 41 41 11 12 2 1 2 2 4 NS NS NS 0.008 <0.001 1 6 7 3 4 NS NS NS 0.042 0.004 0 2 3 1 1 NS NS NS NS NS 14 11 12 4 6 0.007 0.018 0.004 0.039 <0.001
9. BP = Diastolic Blood Pressure in mmHg Op = operation/ surgical intervention Risk factors , symptoms, clinical parameters - association with outcome Risk factors Frequency / association (p value) n Mortality (n) p Recurrent bleeding (n) p Need for op(n) p High risk group (n) p Total 9 24 11 37 Aspirin Warfarin Herbs 57 14 4 2 2 0 NS 0.019 NS 1 0 0 0.022 NS NS 0 0 2 NS NS NS 9 4 2 NS NS 0.046 Symptoms Epigastric pain S ymptomatic anaemia 103 168 2 8 NS NS 11 23 NS 0.002 9 11 0.005 0.018 16 30 NS 0.05 Clinical parameter mean±SD mean±SD mean±SD mean±SD mean±SD DBP 71±15 67±26 NS 71±19 NS 64±10 0.031 67±14 NS
10. RT= Ryles tube Hb=Haemoglobin in grams/deciliter PR = Per rectal APTT=Activated partial thromboplastin time in seconds Examination, laboratory parameters and association with outcome Examinations Frequency/ association (p value) n Mortality (n) p Recurrent bleeding (n) p Need for op (n) p High risk(n) p Total 9 24 11 37 Unconscious RT coffee ground PR malaena Tender epigastrium 13 58 17 45 5 5 9 1 <0.001 0.019 0.038 NS 4 0 2 5 0.008 NS NS NS 1 5 7 5 NS NS NS 0.015 5 11 28 9 0.014 NS NS NS Laboratory parameters mean±SD mean±SD mean±SD mean±SD mean± SD Hb (g/dl) APTT(secs) Urea(mmol/L) Creatinine (mmol/L) 15.5±8.2 33.9±11 14.1±12 170±187 6.4±2.0 39.9±12 22.5±13 317±255 0.030 NS 0.040 NS 6.8±1.6 38.8±15 21.0±15 290±230 0.006 NS 0.028 0.029 6.4±1.3 35.6±66 20.7±13 213±153 0.001 NS NS NS 7.3±2.4 37.9±9.4 18.3±14 196±192 0.022 0.026 NS NS
11. SRH=Stigmata of Recent Haemorrhage Multiple Logistic Regression Analysis of factors with outcome variable P Value Odd Ratio 95% Confidence Interval Mortality Sepsis 0.021 9.910 1.413-69.513 Recurrent Bleeding Creatinine 0.012 1.002 1.000-1.004 High risk Group SRH Sepsis Warfarin <0.001 0.013 0.028 0.063 0.149 0.182 0.26-0.152 0.034-0.664 0.040-0.832