INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
Inflammation- General Pathology seminar PG 1st yearDr. Ritu Gupta
this seminar includes general inflammation, its etiology, acute inflammation, features, events, fate, chronic inflammation, causes, features, types, granulomatous inflammation, acute v/s chronic inflammation, inflammatory disorders of pulp and periradicular tissues
Inflammation is a fundamental process for human survival, this lecture covers the basics of the process, its components and affects. Developing an understanding of this process will enable the student to comprehend this omnipresent process and how it is directly linked to our survival.
Inflammation- General Pathology seminar PG 1st yearDr. Ritu Gupta
this seminar includes general inflammation, its etiology, acute inflammation, features, events, fate, chronic inflammation, causes, features, types, granulomatous inflammation, acute v/s chronic inflammation, inflammatory disorders of pulp and periradicular tissues
Inflammation is a fundamental process for human survival, this lecture covers the basics of the process, its components and affects. Developing an understanding of this process will enable the student to comprehend this omnipresent process and how it is directly linked to our survival.
Introduction, History , Types of inflammation, Cellular events, Vascular events, Morphology of inflammation, Systemic effects of inflammation, Fate of inflammation
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.
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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
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
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
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.
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.
4. Inflammation Triggers: Infectious organisms Trauma Objectives: Remove the trigger Remove any dead tissue End Result: Resolves when harmful stimulus is eliminated As Inflammation ends, Repair starts
5. Inflammation Protective in nature Removes harmful agents Enables tissue to heal May itself be harmful Too much Misdirected
6. The Cardinal Signs of Inflammation Rubor (redness) Tumor (swelling) Calor (heat) Dolor (pain) Functio Laesa (loss of function)
8. Inflammation Acute Rapid onset Short duration Neutrophils Exudation of fluid and plasma proteins Inflammation followed by Repair Chronic Slow onset; may follow acute Longer duration Lymphocytes and Macrophages Proliferation of blood vessels Simultaneous Inflammation and Repair
9. Acute Inflammation - Triggers Infections - Organisms and their toxins Tissue Necrosis - Ischemia, Chemical injury Foreign Bodies - Traumatic tissue injury Immune Reactions - Hypersensitivity
10. Acute Inflammation Changes in Vascular Caliber and Flow Increased Vascular Permeability Emigration of Leukocytes
12. Vasodilation Initial transient vasoconstriction of arterioles Histamine and NO act on vascular smooth muscle Vasodilation follows after a few seconds Increased blood flow in the area Opening of new capillary beds
13. Increased Vascular Permeability Retraction of endothelial cells Histamine, Bradykinin, NO, Substance P Endothelial injury Direct damage from burns Infectious organisms Neutrophils
17. Leukocyte Recruitment Rolling: Mediated by Selectins and their Ligands Histamine and Thrombin: Induce P-Selectin expression TNF and IL-1: Induce E-selectin and L-Selectin ligand Leukocytes: Express L-selectin and Ligand for E and P Selectins
18. Leukocyte Recruitment Activation: Chemokines (IL-8, PAF) activate leukocytes Integrins (VLA-4, LFA-1) converted to high affinity states
19. Leukocyte Recruitment Adhesion: Mediated by Integrins and their Ligands TNF, IL-1: Induce endothelial expression of ligands for Integrins VLA-4: VCAM-1 LFA-1: ICAM-1
20. Leukocyte Recruitment Diapedesis: Chemokines stimulate adherant leukocytes to migrate through inter-endothelial spaces PECAM-1 (CD31)
22. Chemotaxis Movement along a chemical gradient Leukocytes adhere to surrounding tissue cells Extend flopodia in the direction of movement Chemotactic agents: Exogenous: Bacterial products Endogenous: IL-8 C5a LTB4
24. Recognition Toll-like Receptors for Microbial Products Bind bacterial lipopolysaccharides, proteoglycans and lipids, and double stranded RNA (viral product) Stimulate production of mediators and microbicidal substances G Protein-coupled Receptors Bind bacterial peptides containing N-formylmethionyl residues Bind chemokines, complement proteins (C5a) and PAF Convert Integrin to high affinity state Stimulate chemotaxis
25. Recognition Receptors for Opsonins IgG specific for the particle Complement proteins (C3) Facilitate phagocytosis of microbes Receptors for Cytokines IFN-ɣ Cause production of microbicidal substances
30. Termination Stop signals (Switch in AA metabolism) Anti-inflammatory cytokines (IL-10, TGF-ß) Anti-inflammatory mediators (Resolvins, Protectins) Neutrophils have limited lives in tissue; die by apoptosis within a few hours after leaving blood vessel
36. Mediators of Inflammation Origin Cells or Plasma Proteins Preformed or Synthesized Activation In response to various triggers Amplification One mediator can stimulate release of others Actions Different effects on different cells Deactivation Inactivated / Decay / Inhibited quickly
37. Mediators of Inflammation Cell Derived Vasoactive Amines AA Metabolites PAF ROS NO Cytokines Chemikines Lysosomal Enzymes Neuropeptides Plasma Proteins Complement System Coagulation Pathway Kinin System
38. Vasoactive Amines - Histamine Preformed in Mast cells and Basophils Triggers Physical injury Ab’s binding to Mast cells Complement Proteins (C3a, C5a) Effects: Dilation of arterioles Increased permeability of venules (interendothelial gaps)
39. Vasoactive Amines - Serotinin Preformed in platelets Trigger for release: Platelet aggregation after contact with collagen Effect: Increased vascular permeability
40. Arachidonic Acid Metabolites Arachidonic Acid: 20-C Polyunsaturated Fatty Acid Normally esterified in membrane phospholipids Physical/Chemical injury activates Phospholipase A2 Releases AA from the membrane Metabolism through two pathways Cyclooxygenase Pathway Lipoxygenase Pathway AA-derived mediators act through G-Protein coupled receptors
41.
42. Platelet Activating Factor Originally described as a factor that causes platelet aggregation Released by: Platelets, Endothelial cells, Basophils, Mast Cells Effects: Vasodilation Increased vascular permeability Increased leukocyte ashesion Chemotaxis Oxidative burst
43. Reactive Oxygen Species Oxygen derived free radicals may be released extra-cellularly Production depends on Phagocyte Oxidase Effects: Endothelial damage, leading to Increased vascular permeability Injury to interstitial cells Inactivation of Anti-Proteases Anti-oxidants: Superoxide dismutase Catalase Ceruloplasmin Transferrin
46. Chemokines Small (8-10kD) proteins Diverse actions depending on cell type Act as chemoattractants 40 different chemokines in 4 groups 20 different receptors CXCR-4 and CCR-5 receptors are site of entry of HIV
47. Neuropeptides - Substance P Transmission of pain signals Regulation of blood pressure Increased vascular permeability
53. Coagulation and Kinin Systems Exposed Collagen activates Factor XII Extrinsic pathway starts Thrombin binds PAR1 Receptors Mobilization of P selectin Increased recruitment of leukocytes Induction of COX-2
54. Coagulation and Kinin Systems Kallikerin Activates Factor XII Chemotactic Bradykinin Activates Factor XII Increased vascular permeability Vasodilation Plasmin Activates Factor XII Lysis of fibrin clots Cleaves C3 to produce C3 fragments
55.
56. Chronic Inflammation Inflammation for a prolonged period (weeks-months) Onset After Acute Inflammation When injurious agent is not removed promptly More and more inflammatory cells are recruited to site of injury Insideous Onset Low intensity injury for long period of time Inflammatory response is not overwhelming Injury and inflammation persist
65. Chronic Inflammation - Cells Plasma Cells Develop from activated B lymphocytes Produce Ab’s against the target Ag Eosinophils IgE mediated immune reactions (Allergy) Parasitic infections Recruited by eotaxin Granules contain Major Basic Protein (Toxic to parasites)
66.
67. Chronic Inflammation - Cells Mast Cells Bind Fc portion of IgE Ab Degranulation when cell bound IgE Ab binds Ag Release Histamine, Serotinin Allergic reactions to food, drugs Neutrophils Persistent microbes (Osteomyelitis) Repeated injury (Lung damage due to smoking)
73. Systemic Effects of Inflammation Fever Induced by pyrogens Leukocytes release IL-1, TNF upon activation IL-1, TNF induce Cyclooxygenase; PG produced PGE2 stimulates production of cAMP in hypothalamus Temperature set point is reset to a higher level
74. Systemic Effects of Inflammation Acute Phase Proteins upregulated C Reactive Protein and Serum Amyloid A Protein Bind microbial cell walls; act as opsonins Serum Amyloid A Protein Faciltates transport of HDL to macrophages Fibrinogen Binds red cells and causes rouleaux formation Leads to increased ESR
75. Systemic Effects of Inflammation Leukocytosis Leukemoid reaction with Left Shift Lymphocytosis Leukopenia Eosinophilia