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MECHANISMS OF SELF-DEFENSE

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MECHANISMS OF SELF-DEFENSE Part 1 Charlotte A. Richmond, PhD, RN INNATE DEFENSES Body s 1st line of defense: anatomic barriers The skin & mucous membranes If ... – PowerPoint PPT presentation

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Title: MECHANISMS OF SELF-DEFENSE


1
MECHANISMS OF SELF-DEFENSE Part 1
  • Charlotte A. Richmond, PhD, RN

2
INNATE DEFENSES
  • Bodys 1st line of defense anatomic barriers
  • The skin mucous membranes
  • If these defenses are penetrated
  • Mechanical clearance
  • 2nd line of defense Inflammatory response

3
IMMUNE RESPONSE
  • 3rd Line of defense Immune Response
  • Slower specific compared to inflammatory
    response
  • Inflammatory immune responses complement each
    other interact in complex ways

4
THE IMMUNE SYSTEM
  • Extraordinary complex system
  • Elaborate dynamic communication network
  • Recognizes responds to antigens

5
Cells molecules of the immune system protect
the nose from attack by a virus
6
CHARACTERISTICS OF IMMUNE RESPONSE
  • Immunity
  • State of protection, primarily against infections
  • Characterized by memory specificity
  • Antigens
  • Chemical substances that react with preformed
    components of the immune response
  • Immunogens
  • Antigens that induce an immune response
  • Haptens
  • Antigens must be bound to carriers to induce an
    immune response

7
CHARACTERISTICS OF IMMUNE RESPONSE
  • Self-Antigens
  • Antigens on host cells
  • Not recognized as immunogenic by hosts immune
    system
  • A condition called tolerance

8
INDUCTION OF IMMUNE RESPONSE
  • Most immune system cells are WBCs
  • Immunocytes (lymphocytes) are 1 type of WBC
  • 2 major classes of immunocytes
  • T lymphocytes (T cells) B lymphocytes (B
    cells)
  • Immune response is characterized by the
    activation of B cells T cells

9
B CELLS
  • Develops from a stem cell that matures under
    hormonal control in bursal-equivalent tissues
    (bone marrow)
  • Develops into a mature plasma cell capable of
    producing antibody against a specific antigen
  • Antibody marks the antigen for destruction by
    other immune cells

10
ANTIBODIES
  • Plasma glycoproteins
  • Classified by chemical structure biologic
    activity
  • IgG, IgM, IgA, IgE, or IgD
  • Protect host from harmful antigens
  • Recognize and bind with antigens
  • Functions
  • Opsonize bacteria, neutralize toxins viruses
  • Activates inflammatory response

11
ANTIBODY CLASSIFICATION
  • IgG 80 plasma Ig, in all body fluids,
    secondary response, activates complement
  • IgM Primary response, large molecule, vascular
    system, activates complement
  • IgA 95 of body secretion Ig, respiratory and
    GI tract, coats bacteria some viruses
  • IgD Plasma, B cell surfaces, antigen receptor
  • IgE Hypersensitivity and allergic reactions
    (asthma)

12
T CELLS
  • Develop from stem cells that mature under
    hormonal control in thymus
  • Make up the cell-mediated immune response
  • Help to destroy infected cells
  • Coordinate the overall immune response

13
TYPES OF T CELLS
  • Cytotoxic T cells
  • Kill target cells directly
  • Delayed hypersensitivity T cell
  • Produces lymphokines that affect other cells
    (especially macrophages)
  • Helper T cell
  • Induces B cells to produce antibody
  • Recognize antigen fragments
  • Suppressor T cell
  • Suppresses antibody production immune function

14
T-CELL RECEPTOR
  • T cell has molecule on its surface called T-cell
    receptor
  • Interacts with molecules called MHC (major
    histocompatibility complex)

15
T cell (lymphocyte) with a T-cell receptor on its
surface
16
ANTIBODY PRODUCTION
  • Final stage of the process
  • Requires interaction of
  • B cells
  • Helper T cells
  • Antigen-presenting cells

17
Histocompatibility Antigens (Human Leukocyte
Antigens)
  • Proteins found on the surface of nearly every
    cell in the body
  • Recognizes substance is foreign

18
Major Histocompatibility Complex (MHC)
  • MHC (or HLA complex)
  • Major group of genes producing the HLA antigens
  • 4 closely linked foci located on short arm of
    chromosome 6 (A, B, C D complex)
  • Antigens produced by A, B C loci found on
    surface of most cells except erythrocytes
  • D complex consists of 3 independent loci (DR, DP,
    DQ)
  • Confined to B cells, macrophages, some epithelial
    cells some stimulated T lymphocytes

19
INNATE IMMUNITY
  • Nonspecific (species specific)
  • First line of defense
  • Present at birth
  • Found in multi-cellular organisms
  • Permanent immunity
  • Not product of immune response

20
INNATE IMMUNITY
  • Effectors
  • Neutrophils
  • Macrophages
  • Eosinophils
  • NK cells

21
INNATE IMMUNITY
  • Main Mediators
  • Lysosomal enzymes
  • Cytokines
  • Complement proteins
  • Acute phase proteins

22
ACQUIRED IMMUNITY
  • Highly specific, inducible discriminatory,
    unforgetting
  • T lymphocyte- dependent
  • Gained after birth

23
ACQUIRED IMMUNITY
  • Active
  • Natural exposure
  • Immunization

24
ACQUIRED IMMUNITY
  • Passive
  • Doesnt involve hosts immune response
  • Antibodies T cells transferred to recipient
  • Temporary immunity

25
IMMUNE RESPONSE
  • Primary
  • 5 7 days after exposure
  • Dominated by IgM
  • Lesser amounts of
  • IgG
  • Secondary
  • 2nd challenge by same antigen
  • Rapid production of
  • antibody
  • IgM same production
  • as primary
  • IgG predominant

26
HUMORAL IMMUNITY
  • Antigens stimulate B cells ? plasma cells
  • Mediated by antibodies secreted by B cells

27
CELL-MEDIATED IMMUNITY
  • Activation of sensitized T cells
  • T cells secrete cytokines
  • T cells become cytotoxic cells
  • T cells kill virus-infected or abnormal host cells

28
ACUTE INFLAMMATORY RESPONSE
  • Rapid nonspecific
  • Protective response to cellular injury
  • Occurs only in vascularized tissue

29
MACROSCOPIC HALLMARKS OF INFLAMMTION
  • Redness
  • Heat
  • Pain
  • Loss of function of the inflamed tissues

30
MICROSCOPIC HALLMARKS OF INFLAMMATION
  • Accumulation of fluid and cells at the
    inflammatory site

31
MAST CELLS
  • Most important activator of inflammatory response
  • Releases biochemical mediators
  • Histamine
  • Chemotactic factors
  • Synthesizes other mediators
  • Prostaglandins
  • Leukotrienes
  • Platelet-Activating Factor (PAF)

32
MAJOR VASOACTIVE AMINES OF INFLAMMATION
  • Histamine serotonin
  • Effects
  • Constricts vascular smooth muscles
  • Dilation of capillaries
  • Retraction of endothelial cells lining
    capillaries
  • Increases vascular permeability

33
ACUTE PHASE RESPONSE
  • Systemic changes present if inflammation is
    severe enough
  • May be transient, dissipating with recovery or
    persistent in chronic disease
  • Mediated by inflammation-associated cytokines
  • Changes in concentrations of large number of
    plasma proteins

34
ACUTE PHASE RESPONSE
  • Fever
  • Somnolence
  • Anorexia
  • Changes in plasma protein synthesis
  • Altered synthesis of endocrine hormones
  • Hormones effected
  • CRH
  • Glucagon
  • Insulin
  • ACTH
  • Cortisol
  • Catecholamines
  • Growth Hormones
  • TSH, Thyrpxine
  • Aldosterone
  • AVP

35
ACUTE PHASE PROTEINS
  • Major acute phase proteins (APP)
  • C-Reactive protein (CRP)
  • Serum amyloid A (SAA)
  • Negative APP
  • Albumin
  • Transthyretin
  • Transferrin
  • Other positive APP
  • Complement proteins
  • Ferritin
  • ?-1- antitrypsin (antiprotease)
  • Fibrinogen
  • Fibronectin
  • Hempexin
  • Haptoglobin
  • Ceruloplasmin

36
C-REACTIVE PROTEIN
  • Influences inflammatory tissue repair processes
  • Recognizes some foreign pathogens
  • Activates complement system
  • Bonds to phagocytic cells
  • Induces production of inflammatory cytokines
  • Main initiator of blood coagulation
  • Net effect may be antiinflammatory

37
PLASMA PROTEIN SYSTEM
  • Inflammation is mediated by 3 key plasma proteins
    systems
  • Complement system
  • Clotting system
  • Kinin system

38
COMPLEMENT SYSTEM
  • The complement cascade (Fig 7-7)
  • Activated by antigen-antibody reactions (classic
    pathway)
  • Activated by other products especially bacterial
    polysaccharides alternate (nonantibody) pathway
  • Produces biologically active (anaphylactic or
    chemotactic) fragments
  • Produces target cell lysis
  • Phagocytosis
  • Increases vascular permeability

39
CLOTTING SYSTEM
  • Extrinsic Intrinsic pathways (Fig 7-9)
  • Stops bleeding
  • Localizes microorganisms
  • Provides a meshwork for repair healing

40
KININ SYSTEM
  • Bradykinin most important kinin protein
  • Dilates vessels (low dosage)
  • Induces pain (along with prostaglandins)
  • Contracts extravascular smooth muscle
  • Increases vascular permeability
  • May increase leukocyte chemotaxis (Fig 7-6)

41
INHIBITORY INFLAMMATORY ENZYMES
  • Histaminase
  • Carboxypeptidase
  • C1 esytrase inhibitor
  • ?1-antitrypsin

42
CELLULAR COMPONENTS OF INFLAMMATION
  • Phagocytic leukocytes
  • Neutrophils
  • Macrophages
  • Eosinophils
  • Platelets
  • Lymphocytes

43
PHAGOCYTIC CELLS
  • Engulf destroy microorganism (Fig 7-16)
  • Enclose in phagocytic vacuoles (phagolysosomes)
  • Toxic products degradative lysosome enzymes
    kill digest

44
OPSONINS
  • Antibody complement component (C3b) coat
    microorganisms (Fig 7-15)
  • This makes them more susceptible to phagocytosis
  • Binds microorganism more tightly to the phagocyte

45
ENDOTHELIAL CELLS
  • Line the blood vessels capillaries
  • Retract during inflammation
  • Permit fluid, nutrients phagocytic cells into
    area of injury

46
POLYMORPHONUCLEAR NEUTROPHIL (PMN)
  • Predominant phagocytic cell in early inflammatory
    response
  • Enters inflammatory site within 6-12 hours
  • Attracted by chemotactic factors
  • Short lived
  • Gradually replaced by macrophages lymphocytes
  • Primary role removal of debris phagocytosis

47
MONOCYTES
  • Largest normal blood cell
  • Produced in bone marrow
  • Enters circulation migrates to inflammatory
    site
  • Develops into a macrophage

48
MACROPHAGES
  • Larger more active phagocyte
  • Characterizes chronic inflammation
  • May appear within 24 hours of injury
  • Usually arrive 3-7 days later
  • Attracted by chemotactic factor released by PMN
    monocytes
  • Survive longer at site

49
ROLE OF MACROPHAGES
  • Responsive to products secreted by T cells
  • Participate in activating the immune response
  • Stimulates the growth differentiation of
    granulocytes monocytes in bone marrow
  • Produce inflammatory cytokines
  • Secrete substances to promote wound healing
  • Phagocytic activity

50
EOSINOPHILS
  • Release products to control inflammatory response
  • Contain biochemical mediators to control effects
    of histamine serotonin
  • Contains a caustic protein that dissolves surface
    membranes of parasites
  • Induced by IgE-mediated mechanisms of
    hypersensitivity (Fig 7-18)

51
CELLULAR PRODUCTS
  • Interleukins
  • Lymphokines
  • Chemokines
  • Interferon
  • See Fig 7-19

52
INTERLEUKINS
  • Biochemical messengers
  • Cytokines produced by macrophages or lymphocytes
  • Stimulated by antigens or inflammation
  • Stimulate other leukocytes to proliferate (?
    immune function)
  • Chief effect ? the immune response

53
LYMPHOKINES
  • Cytokines produced by T cells
  • Also biochemical mediators
  • Most important effects on macrophages
  • Tumor necrosis factor (TNF)

54
CHEMOKINES
  • Generally proinflammatory cytokines
  • Effects on leukocytes
  • Chemotaxis
  • Growth
  • Activation
  • Release stored chemicals from intracellular
    storage granules (degranulation)

55
INTERFERON
  • Defense against viral infections
  • Cytokine produced released by host cells
    invaded by virus
  • Prevents virus from infecting healthy cell
  • Stimulates uninfected cells to produce antiviral
    proteins (Fig 7-20)
  • INF-? INF-? are antiinflammatory
  • INF-? is proinflammatory and enhances
    cell-mediated immunity

56
CHRONIC INFLAMMATION
  • Lasts 2 or more weeks
  • Can occur without much acute inflammation
  • Dense infiltration of lymphocytes macrophages
  • Granulomas form to isolate tissue damage

57
RESOLUTION REPAIR
  • Begin during inflammation (debridement)
  • Phagocytosis
  • Dissolution of fibrin clot
  • 2 phases reconstruction maturation
  • Resolution
  • Restoration of original structure function
  • Repair
  • Replacement of destroyed tissue with collagen
  • Fill in the wound
  • Cover or seal wound
  • Shrink the wound

58
WOUND HEALING
  • Primary Intention
  • Conditions of minimal tissue loss
  • Clean incision
  • Paper cut
  • Surgical incision
  • Secondary Intention
  • Healing requiring more tissue replacement
  • Wound healing takes longer
  • Open wound
  • Stage IV decubitus

59
NEONATAL CONSIDERATION
  • Immature depressed immune function
  • Transient depressed inflammatory function
  • Partially deficient in complement (components of
    alternative pathway)
  • Develop severe sepsis meningitis when infected
    with bacteria with no transferred maternal
    antibody

60
GERIATRIC CONSIDERATIONS
  • Impaired wound healing
  • Associated with chronic illness
  • Medications that interfere with healing
  • Diminished immune function
  • Decrease perfusion to the skin
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