GLP-1 is an incretin (hormone that increases insulin secretion in response to a meal), which is a 30-amino acid peptide secreted in response to the oral ingestion of nutrients by intestinal L cells.
GLP-1 receptors (GLP-1R) are located in islet cells, central nervous system, and other organs. GLP-1 is metabolized by the enzyme dipeptidyl peptidase-4 (DPP-4).
Incretin effect is a phenomenon whereby a glucose load delivered orally produces a much greater insulin secretion than the same glucose load administered intravenously.
This presentation is an overview of the entire GLP-1 system, followed by an introduction to leveraging its therapeutic potential using GLP-1 analogues (Exenatide, Liraglutide, Lixisenatide, Albiglutide, Dulaglutide) and DPP-4 inhibitors (Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin, Anagliptin, Teneligliptin, Alogliptin, Trelagliptin, Omarigliptin).
Shashikiran Umakanth delivered this talk at Manipal on 30th November, 2015
Presentations by Tawfiq Choudhury and Rocco Hadland from the second webinar of the Mastering Cholesterol webinar series on Thursday 11 May 2023, focusing on Statins.
Osteoporosis is a poorly recognized entity in India, especially among the non-endocrine physicians. Talk given to chest physicians focusing on glucocorticoid induced osteoporosis
GLP-1 is an incretin (hormone that increases insulin secretion in response to a meal), which is a 30-amino acid peptide secreted in response to the oral ingestion of nutrients by intestinal L cells.
GLP-1 receptors (GLP-1R) are located in islet cells, central nervous system, and other organs. GLP-1 is metabolized by the enzyme dipeptidyl peptidase-4 (DPP-4).
Incretin effect is a phenomenon whereby a glucose load delivered orally produces a much greater insulin secretion than the same glucose load administered intravenously.
This presentation is an overview of the entire GLP-1 system, followed by an introduction to leveraging its therapeutic potential using GLP-1 analogues (Exenatide, Liraglutide, Lixisenatide, Albiglutide, Dulaglutide) and DPP-4 inhibitors (Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin, Anagliptin, Teneligliptin, Alogliptin, Trelagliptin, Omarigliptin).
Shashikiran Umakanth delivered this talk at Manipal on 30th November, 2015
Presentations by Tawfiq Choudhury and Rocco Hadland from the second webinar of the Mastering Cholesterol webinar series on Thursday 11 May 2023, focusing on Statins.
Osteoporosis is a poorly recognized entity in India, especially among the non-endocrine physicians. Talk given to chest physicians focusing on glucocorticoid induced osteoporosis
Primary Prevention of Cardiovascular Disease: The Role of Aspirin and StatinsCTSI at UCSF
Presented by Michael Pignone, MD, MPH, at UCSF's symposium "The Role of Risk Stratification and Biomarkers in Prevention of Cardiovascular Disease" in Jan 2012.
Treatment of Osteoporosis beyond Bisphosphonates therapy (2).pptxmehmoodriaz9
will gain valuable insights into emerging therapies, innovative strategies, and alternative approaches that hold promise in improving bone health and reducing fracture risk. The presentation will cover recent research findings, clinical trials, and real-world evidence, providing a comprehensive overview of the evolving
Update on the 18th International Conference on Co-morbidities and Adverse Drug Reactions in HIV
Daniel Lee, M.D.
January 20th, 2017
UCSD HIV & Global Health Rounds
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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.
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
- 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
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
1. Drug-induced osteoporosis Juliet Compston Professor of Bone Medicine University of Cambridge School of Clinical Medicine Cambridge UK
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6. Glucocorticoids increase fracture risk independently of BMD 0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5 OP fracture Hip fracture 50 55 60 65 70 75 80 Age (yrs) BMD-adjusted RR (from Kanis et al, JBMR 2004;19:893-7)
7. Use of oral glucocorticoids and risk of fracture 0 1 2 3 4 5 6 Hip Spine 0.8-1.2 1.2-2.0 1.6-2.0 2.2-3.1 1.9-2.7 4.3-6.3 (from van Staa et al 2000;15:993-1000) RR < 2.5 mg/d 2.5 - 7.5 mg/d > 7.5 mg/d N=244,235 Mean age 57 yr 59% female
8. Time course of vertebral fractures during glucocorticoid use 0 0.5 1 1 year before 0-3 3-6 6-9 9-12 Months % (from van Staa et al, OI 2002;13:777-87) >7.5 mg daily 2.5 - 7.5 mg daily <2.5 mg daily
9. Effect of interventions on glucocorticoid-induced bone loss and fracture nae: not adequately assessed nd: not demonstrated *: not a 1˚ end-point #: data inconsistent Intervention Spine BMD Proximal femur BMD Vertebral fracture Alendronate A A A * Alfacalcidol A A nae Calcitonin A A nae Calcitriol A A nae Calcium nd nd nae Calcium + vitamin D A A nae Clodronate A A nae Cyclic etidronate A A A * Fluoride A nd nae Ibandronate A A A* Pamidronate A A nae PTH A A nae Raloxifene no data no data no data Risedronate A A A * Teriparatide A A A*
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12. Similarities and differences between GIOP and PMO GIOP PMO Bone turnover/resorption Increase is early and transient Increased long-term Bone formation at BMU level Reduced ++ Reduced + Fracture risk Increase mainly in first few months Risk increases with time Distribution of bone loss Cancellous and cortical sites Cancellous and cortical sites
13. Comparison of efficacy of bisphosphonates in PMO and GIOP 0.0 0.5 1.0 1.5 2.0 PMO GIO PMO GIO RR N = 9,681 987 14,551 500 Vertebral fracture Non-vertebral fracture RR= 0.58 0.48 0.81 0.79 From Kanis et al, Health Tech Assess 2007;11:1-258
14. Effects of teriparatide and alendronate on lumbar spine BMD M o n t h s 0 3 6 1 2 1 8 E n d p o i n t Mean % change from baseline ± SE 0 2 4 6 8 1 0 T e r i p a r a t i d e A l e n d r o n a t e Alendronate N= 195 184 173 159 148 195 Teriparatide N= 198 183 178 170 156 198 ‡ P<0.001 Teriparatide vs. Alendronate ‡ ‡ ‡ ‡ Saag KG et al. N Eng J Med 2007; 357:2028-39
15.
16. Cost-effectiveness of bisphosphonates in GIOP 0 20 40 60 80 100 0 20 40 60 80 100 Cost (£000)/QALY gained 0 20 40 60 80 100 0 20 40 60 80 100 Cost (£000)/QALY gained 0 20 40 60 80 100 -10 0 10 20 30 40 50 Cost (£000)/QALY gained 0 20 40 60 80 100 -20 -10 0 10 20 30 40 50 Cost (£000)/QALY gained Age=80 years No prior fracture Prior fracture Age=70 years Age=50 years Age=60 years Cumulative frequency (%) T-score = -2.5 T-score = -2.5 T-score = -2.5 T-score = -2.5 From Kanis et al, Health Tech Assess 2007;11:1-258
17. ACR and RCP guidelines for GIOP From Compston, Curr Rheumatol Rep 2004;6:66-9 ACR RCP (UK) Calcium and vitamin D All patients Those with low ca intake and/or vit D insufficiency Bisphosphonates for 1˚ prevention All patients taking GCs ≥ 5mg/d for 3 months Age ≥ 65yrs PH fragility fracture Bisphosphonates for 2˚ prevention BMD T-score ≤-1 BMD T-score ≤ -1.5
23. Annualised rates of bone loss (lumbar spine) IBMS June 07 0 3 6 9 Annual LS-BMD loss (%) Normal men Late PM women Early PM women Aromatase inhibitor (AI) Androgen deprivation therapy Gonadorelin plus AI Treatment induced ovarian failure Guise, T. A. Oncologist 2006;11:1121-1131
24. Effect of anastrozole treatment on fracture risk Median duration of 60 months’ treatment IBMS June 07 p-value <0.0001 0.5 0.03 0.4 <0.0001 Any fracture Hip Spine Wrist / Colles All other sites Number of patients (%) ATAC Trialists’ Group. Lancet 2005;365:60-62 Anastrozole (n=3092) 340 (11.0) 37 (1.2) 45 (1.5) 72 (2.3) 220 (7.1) Tamoxifen (n=3094) 237 (7.7) 31 (1.0) 27 (0.9) 63 (2.0) 142 (4.6)
25. Fracture rates with anastrozole during and after treatment IBMS June 07 Time since randomisation (years) Annual fracture episode rates (%) Tamoxifen (T) Anastrozole (A) 0 1 2 3 4 5 6 7 8 9 0 2 3 4 1 The ATAC Trialists’ Group. Lancet Oncol 2008; 9: 45-53
26. Fracture risk in men treated with ADT Vertebral fractures RR 1.45 (1.19,1.75) Hip/femur fractures RR 1.30 (1.10,1.53) From Smith et al, J Clin Oncol 2005 Retrospective study Using Medicare claims data
27. Androgen deprivation therapy and fracture risk IBMS June 07 GnRH therapy and orchiectomy associated with increased bone loss at spine and hip. Relative risk of fracture increased by up to 50-60% All skeletal sites affected Shahinian et al, NEJM 2005 50,613 men in the Surveillance, Epidemiology, and End Results (SEER) program with diagnosis of prostate cancer from 1992 through 1997
28. Management algorithm for patients with cancer treatment-induced bone loss Risk assessment with BMD at baseline T score≤ -2.5 Repeat BMD at 5 yrs Treat: ADT: alendronate zoledronic acid AIs: risedronate zoledronic acid T score≥ -1 T score≤ -1 to -2.5 Reassure Reassess risk at 1-2 yrs No other risk factors Other risk factors
29.
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32. Effect of proton pump inhibitors on fracture risk 0 0.2 0.4 0.6 0.8 1 1.2 1.4 1.6 1.8 All Hip Spine Odds ratio (from Vestergaard et al, CTI 2006;79:76-83) 1.12-1.43 1.28-1.65 1.25-2.04 124,655 cases 373,962 controls
33. Effect of proton pump inhibitors on hip fracture risk according to duration of use 0 0.2 0.4 0.6 0.8 1 1.2 1.4 1.6 1.8 1 yr 2 yrs 3 yrs 4 yr s (from Yang et al, JAMA 2006;296:2947-53) Adjusted odds ratio 1.15-1.30 1.28-1.56 1.37-1.73 1.39-1.80 13,556 hip # 135,386 controls
34. Association between osteoporotic fracture and PPI exposure From Targownik et al, CMAJ 2008;179:319-26 Retrospective matched cohort study using claims databases
35. PPIs and fracture risk: GPRD data 0 0.2 0.4 0.6 0.8 1 1.2 1.4 1.6 1.8 Any Fragility Hip Wrist Low dose Medium dose High dose Spine * * * * * * * * Adjusted OR Data courtesy of Cyrus Cooper
36.
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39. Anti-depressant medication use and fracture risk Study Result Fracture site SOF (Ensrud et al, 2003) Increased risk for TCAs and SSRIs Non-spine fractures MrOS (Lewis et al, 2007) Increased risk with TCAs Non-spine fractures CaMOS (Richards et al, 2007) Increased risk with SSRIs Clinical fractures Danish study (Vestergaard et al, 2006) Increased risk for TCAs and SSRIs Clinical fractures GPRD (UK) (Hubbard et al, 2003) Increased risk for TCAs and SSRIs Hip fractures WHI (Spangler et al, 2008) Increased risk for SSRIs All clinical fractures
40.
41. Effect of 5-HTT deficiency in mice (From Warden et al, Endocrinology 2005;146:685-93)
42. Fracture Free Survival by SSRI Use (Richards et al, Arch Intern Med 2007;167:188-94) HR 2.1(1.3-3.4)
43. Adjusted % difference in BMD associated with SSRI Use (95% CI) (Richards et al, Arch Intern Med 2007;167:188-94)
44. The association between SSRI use and falls at baseline interview (Richards et al, Arch Intern Med 2007;167:188-94)
45.
46. PPAR effects on differentiation of osteoblasts and adipocytes Pluripotent stem cell Osteoblasts Adipocytes - PPAR (from Cock et al, EMBO reports, 2004;5:1007-12)