1. Immunity's First line of defense
    • Innate Resistance
    • (Natural or Native Immunity)

    • Examples-
    • Physical and mechanical barriers-sloughing off of cells, coughing/sneezing, flushing, vomiting, mucus/cilia
    • Skin
    • Linings of GI, GU, and respiratory tracts
    • Biochemical barriers-saliva, tears, earwax, sweat, mucus
  2. Immunity's Second line of defense

    Inflammatory response activated to protect body from further injury, prevent infection of injured tissue, and promote healing
  3. Inflammation is caused by:
    • Trauma
    • Infection
    • Surgery
    • Caustic chemicals
    • Heat and cold extremes
    • Ischemic damage
  4. Vascular response to inflammation
    • 1. Vasodilation- slower blood velocity increases blood flod flow to injured site
    • 2. Increased vascular permeability-fluid escapes outside of vessel causing edema,
    • Edema
    • Increased concentration of red blood cells (warmth and redness)
    • 3. White blood cell adherence to the inner walls-migrate thru enlarged juctions in vessel
  5. Goals of Inflammation
    • Limit and control tissue damage
    • Prevent and limit infection and further damage
    • Initiates adaptive immune response
    • Initiates healing thru removal of bacterial products, dead cells, and other products of inflammation
  6. Cellular bags of granules located in loose connective tissues close to blood vessels.
    Mast cell

    Pg. 125:Figure 5-3
  7. Where are mast cells located?
    • Skin
    • Digestive lining
    • Respiratory tract
  8. Activation of mast cell
    • physical injury
    • chemical agents
    • immunologic processes
    • toll-like receptors
  9. Chemicals released from mast cell in two ways.
    • 1. Degranulation-release granules
    • 2. Synthesis-new production and release of mediators in response to stimulus
  10. Mast cell degranulation occurs 2 ways:
    Histamine-vasoactive amine that causes temporary, rapid constriction of large blood vessels and dilation of postcapillary venules. Retraction of endothelial cells lining capillaries

    • Chemotactic Factors-attration "recruit"
    • Neutrophil chemotactic factor:Predominant cells need to kill bacteria in early stages of inflammation
    • Eosinophil chemotactic factor of anaphylaxis-help regulate inflammatory response
  11. Mast cell synthesis of mediators:
    • Leukotrienes
    • Prostaglandins=pain
    • Platelet-activating factor

    (Review pg 126 in text for functions)
  12. Plasma Protein Systems Include:
    • Complement
    • Coagulation
    • Kinin
  13. Complement system:
    • Can destroy pathogens directly
    • Activates or collaborates with every other componenet of inflammatory response
  14. Coagulation (clotting) system
    Forms fibrinous meshwork at injured or inflamed site
  15. Kinin system
    Functions to activate and assist inflammatory cells

    Primary kinin is bradykinin

    Causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, and leukocyte chemotaxis
  16. Review Cellular components and products of inflammation
    pgs. 129-134
  17. Cardinal signs for Local manifestations of inflammation
    • Rubor=redness
    • tumor=swelling (histamine releases)
    • calor=heat
    • Dolor=Pain (bradykinin, prostaglandins)

    Results from vascular changes and corresponding leakage of circulating components into tissue
  18. 4 types of exudative fluids:
    • Serous-watery exudate from plasma indicating early inflammation
    • Fibrinous-thick, clotted exudate indicating more advanced inflammation
    • Purulent-contains pus, WBC, protein, tissue debris indicating bacterial infection (yellow, green)
    • Hemorrhagic-leakage of RBC from capillaries indicating bleeding
  19. Systemic manifestations of Inflammation
    • Fever-caused by exogenous and endogenous pyrogens. Pyrogens act directly on hypothalamus, portion of brain that controls body's thermostat
    • Leukocytosis-increased number of circulating leukocytes or white blood cells. Shift to the left refers to ratio of immature to mature neutrophils. Bacteria causes shift to the left and called bands.
    • Increased plasm portein synthesis-increased during inflammation, increased fibrinogen increases Erythrocyte Sedimentation Rate (ESR)
  20. Granuloma
    Consist of central area of amorphous caseous (cheeselike) necrosis that is surrounded by zone of activated macrophages, in which multinucleate macrophages (langerhans giant cells) are present. A wall of fibrin is laid down around granuloma, and the contents eventually breakdown and liquefy.
  21. Inflammation lasting 2 weeks or longer
    Chronic inflammation

    Often related to an unsuccessful acute inflammatory response.

    Chronic inflammation is characterized by dense infiltration of lymphocytes and macrophages. If macrophages are unable to protect the host from tissue damage, the body attempts to wall off and isolate the infected area, thus forming a granuloma
  22. Examples of chronic inflammation
    • splinters
    • sutures
    • viral
    • bacterial
    • TB lesion
  23. Wound healing involves:
    • Filling in the wound
    • Sealing the wound
    • Shrinking the wound
  24. Wounds that heal under conditions of minimal tissue loss
    • Primary intention
    • Paper cut
    • Sutured surgical wound
  25. An open wound involves a great deal more tissue and is known as
    • Secondary intention
    • Abdominal infection
    • Pressure ulcers
  26. Reconstructive phase of wound healing involves
    Begins 3 to 4 days after injury and continues for as long as 2 weeks

    • Fibroblast proliferation-lay foundation
    • Collagen synthesis by fibroblasts
    • Epithelialization
    • Contraction of wound
    • Cellular differentiation
  27. Most important cells during healing because they secrete collagen and other connective tissue proteins, which are deposited in debrided areas about 5 days after entering lesion
  28. Most abundant protein in body
  29. Continued cellular differentiation in wound healing, can persist for years
    Maturation phase
  30. Scar tissue formation and scar remodeling occur during which phase of wound healing
    Maturation phase

    During remodeling, cappillaries disappear, leaving scar avascular
  31. Dysfunctional wound healing during inflammatory response include:
    • Hemorrhage
    • Fibrous adhesions
    • Infection
    • Steriods
    • Hypovolemia
    • Wound Sepsis
  32. Dysfunctional wound healing during reconstructive phase:
    Impaired collagen matrix assembly- keloid scar, hypertrophic scar, scurvy

    Impaired epithelialization-steroids, hypoxemia, nutritional deficiency

    Impaired contraction-burns, can occur in liver constricting vascular flow
  33. Wound disruption
    dehiscence-pulls apart

    • Strain
    • Obesity
    • Increased risk of sepsis
  34. Third line of defense
    Adaptive (acquired) Immunity

    Often called immune response. Develops more slowly than the inflammatory response and is specific and has memory.

    • Involves:
    • Antigen/Antibody

    Humoral and cell-mediated immunity

    Active and passive Immunity

    Cell Mediated T and B lymphocytes
  35. Two types of lymphocytes involved in antigen process
    B lymphocytes- B cells- produce antibodies that enter blood and react with antigen

    T lymphocytes- T cells- attack antigen directly

    Both are extremely speciif and recognize only one specific antigen
  36. Produced by individual after either natural exposure to antigen or after immunization
    Active immunity

    Long lived
  37. Does not involve host's immune response. Occurs when preformed antibodies or T cells are transferred from donor to recipient
    Passive Immunity

    Only temporary because donor's antibodies or T cells are eventually destroyed
  38. Antigens that induce allergic response
  39. Altered immunologic response to antigen that results in disease or damage to host
  40. Four types of hypersensitivity reactions
    Type I: IgE mediated

    Type II: Tissue-specific reactions

    Type III: Immmune complex mediated

    Type IV: Cell Mediated
  41. Seasonal allergic rhinitis and asthma are examples of:
    IgE mediated reaction

    Rate of development-Immediate

    Antibody involved-IgE

    Effector cells involved-Mast cells

    Participation of complement-NO
  42. Autoimmune thrombocytopenic purpura, Graves disease, autoimmune hemolytic anemia are examples of:
    Tissue specific reaction

    Rate of development-Immediate

    Antibody involved- IgG and IgM

    Effector cells involved-Macrophages in tissues

    Participation of complement-Frequently
  43. Systemic lupu erythematosus is an example of:
    Immune complex mediated reaction

    Rate of development-Immediate

    Antibody involved-IgG and IgM

    Effector cells involved- Neutrophils

    Participation of complement-Yes
  44. Contact sensitivity to poison ivy and metals (jewelry) are examples of:
    Cell-mediated reaction

    Rate of development-Delayed

    Antibody involved-None

    Effector cells involved-lymphocytes and macrophages

    Participation of complement-No
  45. Type I hypersensitivity reaction
    IgE mediated-result of excessive or inappropriate production of IgE antibodies after exposure to some type of environmental antigen.

    With initial exposure to antigen, IgE (immunoglobulin) binds to Fc receptor on surface of mast cell. Individual now sensitized to antigen. Antigens cause allergic responses called allergens. With subsequent exposure to antigen, tiny sacs in mast cells called granules break open and release histamine, which then triggers inflammatory response
  46. Most potent mediator of Type I reaction

    • Contracts Bronchial smooth muscles
    • Increases Vascular permeability
    • Increases blood flow to affected area
    • Increased gastric acid secreation (N/V)
  47. Examples of Type I
    • Hay fever
    • Food and drug allergies
    • Bee stings
    • Asthma
    • Anaphylaxis
  48. Clinical manifestations of Type I:
    • Sudden onset
    • GI symptoms
    • Urticaria-hives
    • ENT and respiratory symptoms
    • Anaphylaxis-rapid onset, urticaria, cramps, difficulty breathing. Caused by bronchospasm, angioedema, hypotension, shock. Can be Lethal
  49. Who are atopic individuals?
    • Predisposition to develop allergies
    • Genetic tendency
    • Higher quantities of IgE
    • More Fc receptors on mast cells which connect IgE
  50. Type II:Tissue-specific Reactions
    Blood transfusions-red blood cell reaction

    Specific cell or tissue (tissue specific antigens) is target of immune response. Direct interaction b/t IgG and IgM class antibodies and tissue or cell surface antigens.
  51. Five mechanisms of Type II
    • 1. Cell is destroyed by antibodies and complement
    • 2. Antibody may cause cell destruction through phagocytosis
    • 3. Toxic products produced by neutrophils
    • 4. Antibody dependent cell mediated cytotoxicity (ADCC)
    • 5. Cell malfunctions
  52. Examples of Type II
    Erythroblastosis Fetalis-Rh or Abo incompatibility b/t blood of mother and fetus

    Hemolytic anemia-antibodies produced against red blood cells could be drug induced

    Transfusion reaction-Antibodies produced against donor cells
  53. Type III:Immune complex mediated
    Abnormal creation that forms. ex-autoimmune disorder

    caused by antigen antibody immune complexes formed in circulation and deposited later in vessel walls and other tissue.

    Size influences whether remain in plasma or lodge in tissues where they result in tissue damage.

    Complement activated and neutrophils degranulate enzymes damage tissue. can damage and destroy healthy tissue
  54. Examples of Type III
    • Serum sickness
    • Systemic lupus erythematosus
    • arthus reaction-local reaction
    • Acute glomerulonephritis that follows strept infection
  55. Type IV Hypersensitivity Reaction
    • Mediated by Sensitized T lymphocytes
    • Don't involve antibody
    • Reaction delayed-24-72 hours after exposure
  56. Examples of Type IV reaction
    • Graft rejection
    • Skin test for TB
    • Allergic contact dermatitis- poison ivy and metals
  57. Autoimmunity
    Breakdown of tolerance to own antigens

    • Examples-pg 171 other examples
    • SLE
    • Chronic multisystem inflammatory disease-abnormal antibodies attack RBC's

    Autoantibodies against nucleic acids, erythrocytes, Coagulation porteins, platelets

    Deposition of circulating immune complexes containing antibody against host DNA

    More common in females

    Clinical manifestation-Butterfly rash, Lupus
  58. Common Findings of SLE-serial or simultaneous presence of at least four

    Not just localized-can become systemic
    • facial rash
    • discoid rash
    • photosensitivity
    • Oral or nasophyaryngeal ulcers
    • arthritis
    • serositis
    • renal disorders
    • neurologic dis
    • hematologic disorder
    • immunologic disorder
    • Presence of antinuclear antibody-blood test of ANA-titer. some reaction going on in body if ANA is elevated
  59. alloimmunity
    Immunse sys reacts w/antigens on tissue of genetically dissimilar members of same species

    • ex.
    • graft rejection
    • transplant rejection classified to time:hyper, acute, chronic
    • Hyperacute;immediate rejection
  60. Graft-versus-host disease (GVHD)
    cellular immune system of transplant tissue can attach unrelated recipient tissue
  61. Immune Deficiencies
    Failure of immune mechanisms of self defense

    Primary (congenital) immunodeficiency (Pg 196:Table 7-13)

    Secondary (acquired) immunodeficiency-caused by another illness (cancer, infection) More common
  62. Syndrome caused by viral disease-Human Immunodeficiency virus (HIV).
    Acquired Immunodeficiency Syndrome (AIDS)

    Blood borne pathogen. Increasing faster in women than men.

    • Depletes CD4 Th cells
    • Incidence:Worldwide 5 mill/yr
    • US 31K/yr
  63. Pathogenesis of AIDS

    Genetic information stored in RNA rather than DNA

    Contains reverse transcriptase to convert RNA into double stranded DNA

    Integrase inserts new DNA into infected cells genetic material

    Structure:GP 120 proteins bind to CD$ molecule found on surface of CD4 Th cells
  64. Normal CD4 count
    800-1000 cells/mm3
  65. Clinical manifestations of AIDS
    • Antibody 4-7 wks after blood products
    • Antibody 6-14 mo after sexual transmission
    • Window period
    • Can still be infectious

    Early signs-flu symptoms, swollen lymph glands, diarrhea, fatigue
  66. Opportunistic infections (pg 201, Box 7-2)
    Organisms produce infection in persons w/impaired immune function
  67. Neurologic Complications of AIDS
    • Encephalopathy
    • Myelopathy
    • Neuropathy
    • Viral meningitis
    • Opportunistic infections
    • Neoplasms
    • Bleeding
Card Set
test 2 patho section 1