Intro and module 1 Pathophysiology September 2024 (PDF)

Welcome Introduction to Patho and Module 1 will begin shortly Why you are waiting- please add to the chat box: Your name, University, Clinical area of employment (if applicable)  Introduction to Pathophysiology Module 1 September 11/12, 2024 Ins...

Welcome Introduction to Patho and Module 1 will begin shortly Why you are waiting- please add to the chat box: Your name, University, Clinical area of employment (if applicable)  Introduction to Pathophysiology Module 1 September 11/12, 2024 Instructor: Karen Harkness RN PhD CCN(C) CHFN-K Email: [email protected] [email protected] While you are waiting for the class to start, please type in the chat box: Your name and university Your clinical area of practice (if applicable)  Overview Time Topic Duration 6:00-6:15 Check in and introductions 15 min 6:15-6:40 Couse overview, general housekeeping 20 minutes 6:40-6:45 Epidemiology, social determinants of health 5 minutes 6:45-7:05 Inflammation- acute and chronic 20 minutes 7:05-7:30 Innate and Adaptive Immunity (video) 20 minutes 7:30-7:45 Break 7:45-7:50 Infection concepts (5 minutes) 5 minutes 7:50-8:10 Hypersensitivities (video) 20 min 8:10-8:25 Immunosuppression (concept map example) 15 min 8:25-8:45 Practice quiz 20 min 8:45-9:00 Wrap up 15 min 3 Introduction This course will: Provide you with a comprehensive understanding of the mechanisms of disease development, strengthen your clinical perspective of pathophysiological concepts, Challenge your critical thinking and Stimulate your curiosity. Above all, the solid working knowledge of pathophysiology offered in this course will help you make sound clinical decisions as a Nurse Practitioner. 4  The following learning outcomes have been developed for this course: 1. Synthesize knowledge of the pathophysiology of disorders affecting the musculoskeletal, cardiovascular, respiratory, endocrine, reproductive, renal, integumentary, gastrointestinal and nervous systems. Learning 2. Analyze and interpret diagnostic and imaging tests based on pathophysiological concepts. Outcomes 3. Use pathophysiological concepts to explain epidemiological and geographic disease patterns. 4. Explain environmental and occupational factors that influence disease progression. 5. Discuss the role of genetics in preventing and assessing risk factors for diseases. 5 6 12 Modules Sections within each module- examples You will not be specifically tested on the information presented within the supplementary videos. However, you are encouraged to watch these videos as they will enhance your understanding of the module objectives. 7 8  Focus on Module Objectives Information on each learning objective can be obtained through: Assigned textbook readings Research articles Evolve resources Module lecture videos Virtual classroom seminars 9 Methods of Evaluation 10  Module tests Each module has an associated module test There are a total of 12 module tests worth 10% of your final grade Each test consists of 15 multiple choice Module 1 Quiz questions and you have 15 minutes to starts complete the test Access to the module test starts following the Thursday sessions. You must complete each module test prior to the online session for the Module 1 quiz following module closes 5 pm You will know your mark when you submit your quiz responses Patho lecture dates You will not know what specific questions you did not answer correctly Concepts from items that appeared difficult for the group/class will be reviewed at the following class. 11 Clinical Consult The clinical consult presentation will be evaluated Presentation according to the following criteria: Content (50%) Presentation Skills (20%) Quality of Slides (10%) Facilitation of Discussion (20%) Please refer to the rubric provided for additional information about evaluation criteria within each section. 12 Clinical Consult What to include Tips: Visuals are encouraged Include more than 1 colour on your concept map Tips: Limit slide count to 15 to keep within the time frame See the rubric provided for additional information regarding expectations 13 CLINICAL CONSULT- housekeeping Please submit your presentation to me in a power point format at least 48 hours prior to the class. Please see the excel file for your Clinical Consult presentation date and topic. If you do not see your name assigned to a topic- please email me ASAP If you want to trade your date with another group member, please notify me by email by 2 weeks (minimum) prior to the presentation date. Both students must be included on the email. 14 Pathophysiology Succinctly update members of your Letter of interprofessional team on recent developments in the underlying Information (20%) pathophysiological mechanisms of a specific disease. You will work along to create a three- Due Monday page double spaced paper. Also include a February 10th title page and a reference list. by 9 am One optional page, containing a figure or table relevant to your topic, is allowed Note- Additional information in the syllabus- we will revisit more information about this assignment in the next few virtual classes. 15 Note- Additional information in the syllabus- we will revisit more information about this assignment in the next few virtual classes. 16 Midterm and Final Exams Note, unlike the weekly module tests, you will NOT receive your mark as the conclusion of the test. Marks cannot be released until all students have completed the exam and reviewed by the course coordinator. Questions? 18  Define the terms incidence and prevalence. Discuss common social determinants of health. Learning Explain the influence of occupational factors on Outcomes the development of disease. These learning outcomes are not covered in the course textbook and will require you to review Introduction additional literature in this area, including the review articles below. to Jager, K.J., Zoccali, C., Kramar, R. & Dekker, F.W. (2007). Measuring disease Epidemiology occurrence. Kidney International. 72(4):412-415. Retrieved on July 4, 2017 from: https://www.ncbi.nlm.nih.gov/pubmed/17579664Links to an external site. Mikkonen, J. & Raphael, D. (2020). Social Determinants of Health: The Canadian Facts. https://www.thecanadianfacts.org/The_Canadian_Facts-2nd_ed.pdfLinks to an external site. Material not covered in lecture video 19  Definition of Terms Jager, K.J., Zoccali, C., Kramar, R. & Dekker, F.W. (2007). Measuring disease occurrence. Kidney International. 72(4):412-415. Retrieved on July 4, 2017 from: https://www.ncbi.nlm.nih.gov/pubmed/17579664Links to an external site. 20 Incidence and Prevalence of Diabetes in Canada- Example 21 https://health-infobase.canada.ca/ccdss/data-tool/index?V=1&M=2&S=B&Y=2021 Social Determinants of Health: The Canadian Facts (2nd Edition) 22 https://thecanadianfacts.org/The_Canadian_Facts-2nd_ed.pdf A Model of the Determinants of Health https://thecanadianfacts.org/The_Canadian_Facts-2nd_ed.pdf 23  Learning Describe the process of acute Outcomes inflammation using your knowledge of the cellular receptors, immune cells and Innate cytokines that are involved. Immunity and These concepts will come up repeatedly in the course Acute and it is important that you understand them. Inflammation You may wish to return to this outcome throughout the course to revisit these concepts. Lecture video covers a lot of this information 24  Acute Inflammation Acute inflammation is: A protective physiological response to injury or infection Neutralization and elimination of micro-organisms Promotes tissue repair Initiated within seconds to minutes and resides within days of the original injury or microbial invasion The inflammatory response is primarily carried out by the cells of the innate immune system Coordinated using signalling molecules known as cytokines and chemokines Memory trick- Cytokines tell ‘You’ what to do (organize roles of WBC) Chemokines have the Map on where help is needed. 25  Memory tips https://www.slideshare.net/dussavamshikrishna/inflammation-228942409 26  Local Manifestations of Acute Injury Primarily due to release of histamine from Mast cells Vasodilation causes redness and warmth (heat) Increased permeability leads to swelling Edema triggers pain fibres Inflammatory mediators release sensitized pain fibres (avoid movement in the affected area) 27 28  Learning Describe the causes and consequences of Outcomes chronic inflammation. Compare and contrast chronic inflammation Chronic and acute inflammation. Explain the process of granuloma Inflammation development during chronic inflammation. Material covered in the lecture video 29 Acute vs Chronic Inflammation 13 minutes https://www.youtube.com/watch?v=yIMz9pkT9xQ 30  Explain how professional antigen presenting Learning cells and T helper cells initiate humoral and cell-mediated adaptive immune responses. Outcomes Compare and contrast humoral and cell- mediated adaptive immune responses Adaptive based on the participating immune cells, the nature of the antigens being targeted Immunity and the mechanisms of defense that are used. Some material covered in lecture video 31 ALGORITHM 10.1 Host Defenses Against Pathogens Example- concept map 32  Antigens and Epitopes An antigen is a foreign molecule that is capable of producing an immune response in the host. The amino acid sequence is foreign and will be detected by immune cells. An epitope is the part on the antigen that is actually recognized by immune cells. Foreign molecules are detected by receptors expressed by immune cells. Most of these receptors are found embedded in the plasma membrane, but some can be found intracellularly. Innate immune cells are non-specific. They can detect the presence of foreign material but have a tough time distinguishing from the source of that material. E.g. they know that a gram-negative bacterium is present but can’t distinguish between different species such as E. coli and A. faecalis. Receptors of the adaptive immune system are highly specific. A receptor will only be activated by a single epitope from a single antigen. The cell expressing the receptor that is activated will then only be able to fight foreign material containing that specific epitope e.g. through antibodies or cytotoxic T cells. 33 4 protein chains- 2 heavy (green) and 2 light (pink) linked together by disulphate bonds (yellow-hinge regions) Antigen binding sites- the variable region of the N terminal of the protein chains on the antibody and determines specificity Heavy chain C-terminus- determines the type of antibody (antibody isotope) 34 Antibodies are categorized into five classes according to their location. Each one is labeled by a letter, which is attached to an abbreviation of the term “immunoglobulin” (Ig). 35 Antibody types and function- Supplemental information 36  G.A.M.E.D. https://www.yo utube.com/wat ch?v=Uxvx7sr W6CI See Appendix for memory tricks  9 minutes https://www.youtube.com/watch?v=4NeHU79qBkw 38 Break Time 39 Learning Describe the process of infection and the Outcomes clinical course it takes within the patient. Explain how antibiotics, vaccines and passive immunizations can be used to counter Infection infectious diseases. Discuss the primary causes and consequences Concepts of antibiotic resistance in pathogenic bacteria. 40 Stages of Infection- from text book The clinical process of infection occurs in the following four distinct stages: Incubation period: The period from initial exposure to the infectious agent and the onset of the first symptoms; during this time, the microorganisms have entered the individual, undergone initial colonization, and begun multiplying but are at insufficient numbers to cause symptoms. This period may last from several hours to years. The time between exposure and symptoms is often termed clinical latency. With some infections (e.g., HIV and varicella zoster infection), there is an acute symptomatic phase, followed by a latency period that can last months or even years. Prodromal stage: The occurrence of initial symptoms, which are often mild and include a feeling of discomfort and tiredness; pathogens continue to multiply during this stage. Invasion or acute illness period: The pathogen is multiplying rapidly, invading farther and affecting the tissues at the site of initial colonization as well as other areas; the immune and inflammatory responses have been triggered; symptoms may be specifically related to the pathogen or to the inflammatory response. Convalescence: In most instances, the individual's immune and inflammatory systems successfully remove the infectious agent and symptoms decline; alternatively, the disease may be fatal or enter a latency phase with resolution of symptoms until pathogen reactivation at a later time. 41 Simple explanation of stages of Infection https://www.youtube.com/watch?v=6wrrbulWxPY 3 minutes 42  Some antibacterial antibiotics are bactericidal (kill the microorganism), whereas others are bacteriostatic (inhibit growth until the microorganism is destroyed by the individual's own protective mechanisms). Mechanisms of most The mechanisms of action of most antibiotics are: antibiotics (1) Inhibition of the function or production of the Key concepts cell wall/membrane, (2) Prevention of protein synthesis, (3) Blockage of DNA replication, or (4) Interference with folic acid metabolism Because viruses use the enzymes of the host's cells, there has been less success in developing antivirals. 43  Overview of types of Vaccines video using examples of different COVID-19 vaccines Attenuated Active Virus Inactivated Virus Subunit (e.g., Antigen portion only, Empty call, toxin) Nucleic Acid: – DNA Viral Vector – mRNA https://www.youtube.com/watch?v=osRo-yz1VQ8 6 minutes 44 Mechanisms of Antibiotic Resistance (textbook) Key concepts Mechanisms of antibiotic resistance include the following: 1. Resistance genes that are spread within the bacterial community by horizontal gene transfer to other generations of microbes. 2. Antibiotics are degraded by enzymes released from the microbe. 3. Antibiotics are altered by enzymes within the microbe. 4. Antibiotics are ejected from inside the microbe by efflux pumps in the cell membrane. 5. The cell wall can be modified to prevent antibiotic binding or uptake. 6. Modification of the cellular target of the antibiotic. 45  Learning Define the term sensitization as it relates to hypersensitivity reactions. Outcomes Compare and contrast Type I-Type IV hypersensitivity reactions based on the: Hypersensitivity Participating immune cells, Reactions Pathophysiological mechanisms involved, and Consequences of each type of hypersensitivity reaction. Material covered in the lecture video 46  Types of Hypersensitivity Reactions General Overview 9 minutes https://www.youtube.com/watch?v=WgcCZdVyIJ8 47  Hypersensitivity pneumonic https://www.youtube.com/watch?v=IpHaGrYNTag 10.5 minutes 48 Comparison of Different Types of Hypersensitivity 49 50  Learning Discuss the consequences of primary and secondary immunodeficiency. Outcomes Describe the mechanisms used by HIV to target CD4+ T helper cells. Immunodeficiency Explain the clinical course of HIV infection. Material covered in the lecture video 51 52  Retrovirus- any of a family of RNA viruses that have an enzyme (reverse transcrip tase) capable of making a complementary DNA copy of the viral RNA, which then is integrated into a host cell’s DNA. The family includes a number of significant pathogens, typically causing tumors or affecting the function of the immune system, e.g. HIV. NK- Natural Killer cells 53 (CD4 T lymphocyte) 54 Stages of Viral Infection of a Host Cell (textbook) FIG. 10.7 Stages of Viral Infection of a Host Cell. Viral life cycle includes several steps. (1) Recognition and attachment of the virus to a host receptor or cell wall molecule. (2) Penetration into the host cell by fusion or endocytosis. (3) Uncoating of the viral genome within the cell cytoplasm. (4) Replication of the viral genome using host or viral transcriptases and polymerases. (5) Translation with viral structural protein synthesis in the host cell endoplasmic reticulum and Golgi apparatus. (6) Assembly of the virus. (7) Release of the virus by budding or exocytosis, or by lysis of the host cell. 55 Human Immunodeficiency Virus-1 (HIV-1)- Life Cycle and Sites of Drug Interaction Figure from text book and lecture video 56 57 58 Learning Outcomes Describe the role of cytokines in initiating a fever during acute infection. Sickness Explain the causes and consequences Behaviour of cachexia. Material covered in the lecture video Lecture video 59 60 Cachexia is a complicated Cachexia metabolic syndrome related to underlying illness and characterized by: muscle mass loss with or without fat mass loss that is often associated with anorexia, an inflammatory process, insulin resistance, and https://www.slideserve.com/opal/research-opportunities-in-the-department-of-otolaryngology-head- increased protein turnover. and-neck-surgery#google_vignette 61 Supplemental information 62 Practice Quiz 63 Wrap up- Wed pm These slides are intended to be an additional resource to support your learning- supplemental information that extends beyond your learning objectives and not part of test material. Module 1 test – opens Thursday, Sept 12th- afternoon and closes by 5 pm on Sept 25th. Clinical consults Sept 25th: Wrap up- Thurs am These slides are intended to be an additional resource to support your learning- supplemental information that extends beyond your learning objectives and not part of test material. Module 1 test – opens Thursday, Sept 12th- afternoon and closes by 5 pm on Sept 25th. Clinical consults Sept 26th: Appendix Spare Slides from lecture video 67 How has epigenetics changed our understanding of genetic susceptibility and our ability to screen for genetic diseases? 70 https://en.wikipedia.org/wiki/Chromatin_remodeling  Pediatrics Special populations Elderly 71 72 73 Hypersensitivity reactions 74 75 76 77 78 79 80 81 82 83 84 Supplemental Slides 85 Antibodies/Immunoglobulins Memory Tricks G.A.M.E.D. https://www.yo utube.com/wat ch?v=Uxvx7sr W6CI  IgG you have “GOB”s of it to Gobble up” Germs https://www.youtube.com/watch?v=Uxvx7srW6CI  IgM is the first antibody to be produced after exposure to an antigen “me goes first” (IgM followed by IgG in immune response) https://www.youtube.com/watch?v=Uxvx7srW6CI https://www.youtube.com/watch?v=oCOrUYLK2mU IgA Aaahhh- this one messy- mucosal surfaces exposed to the environment IgE is about allergy “allergeee”  IgD We don’t know what it will Be (not sure of the function, but it is secreted from B cells) https://www.youtube.com/watch?v=oCOrUYLK2mU