Chapter 2 Body Defenses PDF

Chapter 2 Body Defenses LEARNINGOBJECTIVES  Describe the effect of stress on the body.  Explain the role of the body’s normal defenses in preventing disease.  Differentiate between innate and adaptive immunity.  Discuss some examples of altered immune responses.  Identif...

Chapter 2 Body Defenses LEARNINGOBJECTIVES  Describe the effect of stress on the body.  Explain the role of the body’s normal defenses in preventing disease.  Differentiate between innate and adaptive immunity.  Discuss some examples of altered immune responses.  Identify factors that enhance and impair the body’s defenses.  Stress  Stress is a state in which the external and/or internal demands that are appraised as taxing or exceeding the resources of the person  Stressors have been defined as environmental circumstances or chronic conditions that are appraised in a primary appraisal process, and then are seen as either benign or a threat to physical and/or psychological health or well- being (Grant et al., 2003).  Coping  It is an attempt to manage, master, or alter the stressful situation by reducing or tolerating it.  Two major types of coping have been suggested: Emotion focused and Problem focused  Stress can contribute directly to the development or exacerbation of disease, or negative behaviors such as smoking and drug abuse as individuals attempt to cope with this state.  Stress Response  General adaptation Syndrome is a cluster of systematic manifestations that represent an attempt to cope with the stressors.  The general adaptation syndrome includes three stages: alarm, resistance, and exhaustion Adrenocorticotropic hormone( ) Local Adaptation syndrome (is the localized version of the general adaptation) Response to stress vary and may depends on factors, such as :  Genetics  Age  gender  Life experience  Dietary status  Social support  Coping strategies  Positive adaptive strategies: minimize and eliminate negative stress effects including lifestyle modifications such as physical activity, adequate sleep, & optimal dietary status. Others include relaxation, distraction, & biofeedback.  Maladaptive coping strategies: include activities such as smoking, substance abuse, & overeating. Immune System  Self-regulated  Self-limiting  Defending & Attacking  Must be able to distinguish self from non-self  Antigen (foreign agent) Figure: Effects of Stress  First Line of Defense  Nonspecific  Distinguishes self from non-self  Does NOT distinguish between pathogens  Physical & Chemical barriers  First Line of Defense Physical barriers include:  Skin and mucous membranes  Chemicals Chemical barriers include:  A slightly acidic substance produced by the skin that inhibits bacterial growth.  Hydrochloric acid in the stomach destroys many ingested bacteria.  Tears and saliva contain lysozyme, an enzyme that dissolves bacterial cell walls.  Second Line of Defense  Responds to antigens that penetrate the first line Includes:  Inflammatory response  Pyrogens  Interferons  Complement proteins  Inflammatory Response  Vascular reaction  Triggered by mast cells; including histamine (vasodilation) & prostaglandin (pain receptors)  Manifestations include erythema (redness), edema (swelling), pain and warmth.  Figure: Inflammatory response. Chiras, D. (2011). Human biology (7th ed.). Sudbury, MA: Jones & Bartlett Learning.  Pyrogens  Fever producing molecules  Produced by macrophages  Create an unpleasant environment for bacterial growth  Interferons  Proteins released from cells infected by viruses  Bind to nearby uninfected cells which release an enzyme that inhibit viral replication  Interferons do not protect cells already infected by a virus but rather stop the spread of the virus to new cells.  In essence, interferon production is the dying cells’ attempt to protect other cells Figure : How interferon works. Chiras, D. (2011). Human biology (7th ed.). Sudbury, MA: Jones & Bartlett Learning.  Complement Proteins  Plasma proteins (approx. 20) that enhance antibodies‘ action.  Activated by antigens  Play a role in the immune and inflammatory response  Third Line of Defense  Specific  Develops over time  Uses memory system  Distinguishes self from non-self AND between pathogens Includes:  T cells-cell mediated immunity  Helper, suppressor, killer  Role in viral infection, cancer prevention, and hypersensitivity  B cells-humoral immunity  Antibody producing or memory  Acquired Immunity Active Immunity –Sources include having the disease and vaccinations –Long lasting but takes a few days to become effective Passive Immunity –Sources include maternal-fetal transfer of immunoglobumins and breastfeeding –Short lasting  Alterations in Immunity  Hypersensitivity Is an inflated immune response to a foreign substance (exaggeration)  Autoimmune The body’s normal defenses become self- destructive that is, they perceive the self as foreign.  Immunodeficiency (Diminution) A diminished or absent immune response increases susceptibility to infections  Figure 02.F07: Classification of hypersensitivity reactions Pommerville, J. C. (2011). Alcamo's Fundamentals of Microbiology (9th ed.). Burlington, MA: Jones & Bartlett Learning.  Types of Hypersensitivity Type 1 “IgE mediated" – Produces an immediate response – Local or systemic – Allergen activate IgE which bind to mast cells – At next exposure, the antigen binds with the surface IgE, releasing mediators (histamine, Cytokines, and prostaglandins) and triggering the complement system – Examples: hay fever, food allergies, and anaphylaxis – Treatment: epinephrine, antihistamines, corticosteroids, and desensitizing injections  Types of Hypersensitivity Type II (tissue specific), cytotoxic hypersensitivity reaction – IgG or IgM type antibodies that react to foreign tissue of cells – Lysis and phagocytosis of blood cells occurs because of the activation of the complement – Usually immediate responses – Examples: Blood transfusion reaction and erythroblastosis fetalis – Treatment: ensuring blood compatibility and administering medication to prevent maternal antibody development (corticosteroids, cyclosporine)  Types of Hypersensitivity Type III, immune complex-mediated hypersensitivity reaction – Circulating antigen-antibody complexes accumulate and are deposited in the tissue – Triggers the complement system and inflammation – Example: Autoimmune conditions (e.g. systemic lupus erythematosus) – Treatment is disease specific  Types of Hypersensitivity Type IV, delayed hypersensitivity reaction – Cell-mediated rather than antibody- mediated involving the T cells – The antigen will be processed by macrophages. – T- cells will release of lymphokines (cytokine) cause antigen destruction. – Examples: tuberculin skin testing, transplant reactions, & contact dermatitis – Treatment is disease specific  Transplants Making the best match of tissue antigens is the core for success Donor sources may be living or a cadaver 4 Categories: – Allogenic-donor and recipient are related or unrelated, but share similar tissue types – Syngenic-donor and recipient are identical twins – Autologous-donor & recipient are the same person; most successful – Xenogenic- Transplant from a different species. Patterns of Transplant Reactions Hyperacute rejection Acute rejection  immediate or 3 days after  most common transplant  treatable  due to the complement system  occurs between 4 days  before the new organ can and 3 months after establish vascularization. transplant  Can lead to lyses or Chronic rejection  occurs 4 months to years after necrosis of the new organ transplant or impaired function.  likely antibody-mediated  Manifestations: fever, response erythema, edema, site  Antibodies and complements tenderness, & impaired deposit in vessel walls of function of transplanted transplanted tissue, resulting in organ ischemia Transplant Reaction Classifications Host vs Graft Disease Graft vs Host Disease  Host fights the graft  Graft fights the host  Frequent and potentially fatal  The recipient’s immune system complication of bone marrow attempts to eliminate transplants the donor cells  Occurs when immunocompetent fatal cells recognize host tissue as foreign and mount a cell- mediated immune response  Host usually immunocompromised and unable to fight graft cells, and the host’s cells are destroyed  Autoimmune Disorders  Immune system losses the ability to recognize itself  Defenses are directed against host  Can affect any tissue  Mechanism that triggers this response is not clear  Known characteristics  Genetics play a role  More prevalent in females  Onset is frequently associated with an abnormal stressor, either physical or psychological  Are frequently progressive relapsing-remitting disorders characterized by periods of exacerbation and remission  Systemic Lupus Erythematosus SLE  Chronic inflammatory condition  Remission and exacerbations-stressors tend to trigger  May affect connective tissue of any body organ  Disease progression varies from mild to severe  More common in women  Cause is unclear, but thought that B cells are activated to produce autoantibodies and autoantigens that combine to form immune complexes, which attack the body’s own tissues Diagnostic criteria (four or more of the following) 1. Butterfly rash over the cheeks of the face 2. Skin rash of patchy redness with hyperpigmentation and hypopigmentation that can cause scarring 3. Photosensitivity 4. Mucous membrane ulcers 5. Arthritis 6. Pleuritis or pericarditis 7. Renal abnormalities 8. Brain irritation 9. Blood abnormalities 10. Immunologic disorder 11. Antinuclear antibody  SLE  Prognosis improves with early diagnosis and treatment  Diagnosis: 11 criteria, X-rays, elevated sedimentation rate, c- reactive protein, and blood testing for complications  Treatment:  no cure  Stress management and health promotion behaviors  Pharmacological: NSAIDs, antimalarials, corticosteroids, and immunosuppressants  Plasmapheresis  Table: Common Manifestations of Systemic Lupus Erythematosus Pommerville, J. C. (2011). Alcamo's Fundamentals of Microbiology (9th ed.). Burlington, MA: Jones & Bartlett Learning.  Immunodeficiency  Diminished or absent immune response  Renders the person susceptible to disease normally prevented  Opportunistic infections  May be acute or chronic  Classifications  Primary  Secondary Acquired Immunodeficiency Syndrome (AIDS)  HIV – parasitic retrovirus that infects CD4 & macrophages upon entry  Two primary types – Type I is the most common strain – Type 2 is more common in West Africa; progresses to disease more slowly  Transmission – Blood and bodily fluids  Pathogenesis – Retrovirus Genetic information is in the form of RNA Contains reverse transcriptase to convert RNA into double-stranded DNA Integrase This enzyme integrates the DNA produced by reverse transcriptase into the host's genome. Protease A protease is any enzyme that cuts proteins into segments. HIV's gag and pol genes do not produce their proteins in their final form, but as larger combination proteins; the specific protease used by HIV cleaves these into separate functional units. Protease inhibitor drugs block this step. Human Immunodeficiency Virus (HIV)  Human Immunodeficiency Virus (HIV) (cont’d)  Structure – gp120 protein binds to the CD4 molecule found primarily on surface of helper T cells Destroys CD4+ Th cells – Typically 800 to 1000 cell/mm3 – Reverses CD4/CD8 ratio © BioMedical/Shutterstock, Inc.  AIDS Progression  Asymptomatic phase – virus is reproducing, usually for several years  Infections begin as the viral number rise destroying the CD4  Progression takes three forms – Immunodeficiency – Autoimmunity – Neurological dysfunction  AIDS Progression Diagnostic test (used for diagnosis and determine progression) – HIV antibody Rapid test Home test Polymerase chain reaction – Measures amount HIV DNA or viral load – Good for infants and infected mothers  AIDS Classification System Two systems, one based on lab findings and the other based on clinical manifestations Laboratory findings – Category 1: >500 cells/microL – Category 2: 200-499 – Category 3: