University Of Fujairah BSN Pathophysiology Week 2 PDF

College of Health Sciences Department of Nursing Bachelor of Science in Nursing (BSN) Program PHL-2172 Pathophysiology Presented by: Dr. Huda Anshasi (Course Coordinator) & Dr. Ahmed...

College of Health Sciences Department of Nursing Bachelor of Science in Nursing (BSN) Program PHL-2172 Pathophysiology Presented by: Dr. Huda Anshasi (Course Coordinator) & Dr. Ahmed Loutfy  Week 2: Body Defenses By the end of this session students will be able to: 1. Use appropriately various Stress concepts. 2. Discuss the stages of the General Adaptation Syndrome. 3. Compare and contrast General Adaptation Syndrome with Local Adaptation Syndrome.  Week 2: Body Defenses By the end of this session students will be able to: 4. Discuss adaptive coping strategies used to treat stress. 5. Explain the role of the body’s normal defenses in preventing disease. 6. Compare between innate and adaptive immunity. 7. Discuss some examples of altered immune responses.  Lecture Outline ✓ Stress ✓ General Adaptation Syndrome ✓ Local Adaptation Syndrome ✓ Innate Immunity. ✓ Adaptive Immunity. ✓ Altered Immune Response. Hypersensitivity Transplant Reactions  Stress Stress is a perceived or anticipated threat that: ✓ Disrupts homeostasis ✓ Exceeds the individual’s capacity to meet the demands. Stress contributes to negative behaviors (e.g., smoking) to cope with this state.  Stress response Hans Selye noted that: the body responds to any stimuli, or stressor, with a series of nonspecific events. He described this stress response as the General Adaptation Syndrome  General Adaptation Syndrome ✓ Is a cluster of systemic manifestations ✓ Represent an attempt to cope with a stressor ✓ It includes 3 stages: 1. Alarm 2. Resistance 3. Exhaustion  Alarm Stage ✓ Emergency reaction ✓ Fight-or-flight response ✓ Includes a stimulation of the sympathetic nervous system resulting in the release of catecholamines and cortisol.  General Adaptation Syndrome 2. Resistance or adaptation stage ✓ Requires continued mobilization of the body’s resources to cope & overcome a sustained challenge. 3. Exhaustion ✓ Adaptation is NOT successful ✓ NO longer effectively cope with the stressor ✓ Marks the onset of diseases  Local adaptation syndrome ✓ is the localized version of the general adaptation syndrome. ✓ The body attempts to limit the damage associated with the stressor by: ✓ confining the stressor to one location. Example: Local inflammatory reaction that results from tissue trauma  Stress Adaptation Natural Age & Nutrition reserves Gender Factors can sleep–wake cycles affect Stress Genetics Adaptation Time Psychosocial factors  Coping Strategies = the ability to deal with the stressor. Adaptive coping strategies Maladaptive coping strategies ✓ physical activity, ✓Smoking ✓ adequate sleep ✓substance abuse ✓ optimal dietary, ✓overeating ✓ Relaxation, distraction  Immune System ❖ Responsible for: ✓ Protecting the body against an array of microorganisms. ✓ Removing damaged cells. ✓ Destroying cancer cells. ❖ Provides this protection through 2 major actions: 1. Defending. 2. Attacking.  Major Components of the Immune System Antigen A foreign agent that: triggers the production of antibodies by the immune system. Antibody a protein used by the immune system to identify foreign agents  Major Components of the Immune System Neutrophils Infection-fighting agents, usually the first to arrive on the scene of an infection, migrate to the site of infection, phagocytize microorganisms. Basophils White blood cells that bind immunoglobulin E (IgE) and release histamine in anaphylaxis.  Major Components of the Immune System Eosinophils White blood cells involved in allergic reactions. Monocytes White blood cells that replenish macrophages. Macrophages White blood cells within tissues, phagocytize and stimulate lymphocytes.  Major Components of the Immune System Mast cells ✓ Connective tissue cells. ✓ Contain histamine, heparin, and serotonin B cells ✓ Cells that mature in the bone marrow, (B lymphocytes) ✓ They differentiate into memory cells o eliminate bacteria, neutralize bacterial toxins, o prevent viral reinfection, o produce immediate inflammatory response.  Major Components of the Immune System T cells ✓ Produced in the bone marrow (T lymphocytes) ✓ mature in the thymus. Killer T cells ✓ destroy cells infected with viruses by releasing lymphokines that degrade cell walls Memory B cells recall the antigen as foreign, leading to rapid antibody production. Helper T- cells stimulate B-cells to make antibodies.  Innate & Adaptive Immunity Innate Immunity Adaptive Immunity ✓ Always present at birth ✓ Develops after exposure to specific ✓ Attacks non-self microbes antigen ✓ Does not distinguish between ✓ Attacks specific microbes (antigens) different microbes  Innate & Adaptive Immunity Innate Immunity Adaptive Immunity Mechanisms include: Mechanisms include: ✓ Barriers ✓ Humoral immunity ✓ Inflammatory response ✓ Cell –mediated immunity ✓ Pyrogens ✓ Interferons ✓ Complement proteins  Innate Immunity Barriers Physical barriers ✓ skin ✓ mucous membranes. Chemical barriers: ✓ Hydrochloric acid in the stomach destroys many ingested bacteria. ✓ Tears and saliva contain lysozyme, an enzyme that dissolves bacterial cell walls.  Innate Immunity Inflammatory Response ❖ This response is triggered by a set of mediators, or mast cells, including: ✓ Histamine (stimulates vasodilation) ✓ prostaglandins (stimulates pain receptors in the area).  Inflammatory Response Immediately after the injury, arterioles in the area constrict to limit bleeding Vasodilation increases blood flow to the injured area to dilute toxins & provide the area with essential immune cells, nutrients, & O2 Leukocytes will migrate to that area and begin phagocytosis  Inflammatory Response Fibrinogen is transformed into fibrin & used to wall off the injured area Blood clotting begins if blood vessels have been damaged.  Innate Immunity Pyrogens ❖ are molecules released by macrophages ❖ Pyrogens travel to the hypothalamus, producing ✓ fever & ✓ creating an unpleasant environment for bacterial growth ❖ Fever also increases metabolism, which facilitates healing and accelerates phagocytosis. ❖ Severe fever (more than 40.5 C) can be life threatening because it begins to denature vital proteins.  Innate Immunity Interferons  Innate Immunity Complement proteins ❖ circulate in the blood in an inactive state. ❖ When foreign substances invade the body these proteins become activated.  Innate Immunity Complement proteins ❖ Five complement system proteins join together to form membrane attack complex. ❖ It becomes embedded in the plasma membrane of bacteria, creating an opening into which water flows. ❖ The influx of water causes the bacterial cells to swell, burst, and die.  Adaptive Immunity Cell- mediated immunity ✓ Mediated by T cells, ✓ bind to the antigen, & ✓ trigger a response by other immune cells.  Adaptive Immunity/ Humoral Immunity B cells can begin this antigen production within 72 hours after initial antigen exposure Subsequent exposures to the antigen then trigger a quick response because memory cells recall the antigen as foreign This reaction is referred to as acquired immunity It is classified into: Active or Passive.  Adaptive Immunity Active immunity ✓ Acquired by having the disease (i.e., prior antigen exposure) or by vaccinations. ✓ Long lasting but takes a few days to become effective. ✓ Example: Chickenpox Passive immunity ✓ Receiving antibodies from external sources. ✓ Short lasting ✓ Example: Maternal–fetal transfer of immunoglobulins and breastfeeding  Alterations in Immunity Hypersensitivity ✓ Inflated response to antigen ✓ Can be immediate or delayed Autoimmune ✓ Mistakes self as non-self or foreign. Immunodeficiency ✓ A diminished or absent immune response ✓ increases susceptibility to infections.  Alterations in Immunity Hypersensitivity ✓ Four types: Type I: IgE mediated Type II: cytotoxic hypersensitivity reaction (tissue mediated) Type III: immune complex–mediated Type IV: delayed hypersensitivity reaction (cell mediated).  Type I (IgE mediated) ✓ Produces an immediate response. ✓ Local or systemic. Allergen activates T-helper cells lgE coats mast cells and basophils, sensitizing them stimulate B cells to produce IgE to the allergen. Examples: At next exposure, the antigen binds with the Hay fever, surface IgE, releasing mediators & triggering food allergies the complement system. anaphylaxis  Types of Hypersensitivity Type II (Cytotoxic hypersensitivity reaction) ✓ Usually immediate responses. ✓ IgG or IgM bind to antigen on ✓ Antigen may be intrinsic or extrinsic. individual’s own cells. ✓ Recognition of these cells by macrophages triggers antibody production. ✓ Lysis of cells occurs because of: the activation of the complement and by phagocytosis. Example: blood transfusion reactions & erythroblastosis fetalis  Types of Hypersensitivity Type III (immune complex–mediated hypersensitivity reaction) ✓ Circulating antigen–antibody complexes accumulate & are deposited in the tissue. ✓ Triggers the complement system, causing inflammation. ✓ Example: Autoimmune conditions (e.g., systemic lupus erythematosus)  Types of Hypersensitivity Type IV (delayed hypersensitivity reaction) ✓ Cell-mediated rather than antibody-mediated involving the T cells. ✓ Antigen presentation results in cytokine release, leading to inflammation. ✓ Causes severe tissue injury and fibrosis ✓ Examples: Tuberculin skin testing, transplant reactions, & contact dermatitis  Transplants Reactions ✓ Making the best match of tissue antigens is key for success. ✓ Donor sources may be living or a cadaver. Four types of tissue transplants are possible: Allogenic: donor and recipient are related or unrelated, but share similar tissue types Syngeneic: donor and recipient are identical twins Autologous: donor and recipient are the same person; most successful Xenogeneic: use tissue from another species  Classifications of Transplant Rejection Reactions based on timing Hyperacute tissue rejection ✓ Immediate or 3 days after transplant ✓ Due to the complement system ✓ Recipient has antibodies against the donor tissue ✓ Tissue becomes permanently necrotic Acute tissue rejection ✓ cell mediated & result in transplant cell destruction (lyses) ✓ Occurs between 4days and 3 months after transplant. ✓ Manifestations: fever, erythema, edema, site tenderness, & impaired function of transplanted organ.  Classifications of Transplant Rejection Reactions based on timing Chronic tissue rejection ✓ Occurs 4 months to years after transplant. ✓ Likely antibody-mediated response. ✓ Antibodies deposit in vessel walls of transplanted tissue, resulting in ischemia. Thank You!