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Alterations in the Immune Response - 681. Shirlee Ann Stokes, RN, EdD, FAAN. Immunodeficiency Disease. Alteration in the immune response Primary versus Secondary Primary Congenital Inherited – most are recessive traits Manifestations seen at birth and throughout childhood.

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alterations in the immune response 681

Alterations in the Immune Response - 681

Shirlee Ann Stokes, RN, EdD, FAAN

immunodeficiency disease
Immunodeficiency Disease
  • Alteration in the immune response
  • Primary versus Secondary
  • Primary
    • Congenital
    • Inherited – most are recessive traits
    • Manifestations seen at birth and throughout childhood
immunodeficiency disease1
Immunodeficiency Disease
  • Secondary
    • Acquired
    • Secondary to another disease
    • Malnutrition
    • Infection (e.g., acquired immunodeficiency syndrome [AIDS])
    • Neoplastic disease (e.g., lymphoma)
    • Immunosuppressive therapy (e.g., corticosteroids or transplant rejection medications)
    • Nephrotic syndrome
  • Absolute or partial loss if immune response
  • Categories
    • Humoral (B lymphocytes)
    • Cell-mediated (T lymphocytes)
    • Complement system
    • Phagocytic system (neutrophils and macrophages)
humoral immunodeficiency
Humoral Immunodeficiency
  • Alteration in
    • B-cell function
    • Antibody production (IgG, IgA, IgE, IgM, IgD)
humoral immunodeficiency1
Humoral Immunodeficiency
  • Diseases
    • Hypogammaglobulinemia
    • X-Linked Agammaglobulinemia
    • Common Variable Immunodeficiency
    • Selective IgA deficiency
    • Immunoglobulin G Subclass Deficiency
  • Review Figure 21-1
    • Shows how each are developed
humoral immunodeficiency2
Humoral Immunodeficiency
  • Common Manifestations
    • Recurrent infections – Particularly in children
      • Bacterial infections
        • Not intracellular bacteria (mycobacteria, fungi, or protozoa as these are handled by T cells
        • Not viral (except enterovirus causing GI infections) as these are handled by T cells
      • Bacterial with virulence factors
        • Toxins
        • Evasive factors – Capsulated polysaccharide
          • S. pneumoniae, H. influenzae, S. aureus, Neisseria meningitis
humoral immunodeficiency3
Humoral Immunodeficiency
  • Particularly prone to pyogenic organisms
    • Streptococcus pneumonia, Haemophilus influenzae, G- organisms
  • Infections that do not respond to therapy
  • Infections that respond slowly to therapy
  • Common sites of infection
    • Ear, Respiratory, Throat
cell mediated immunodeficiency
Cell Mediated Immunodeficiency
  • Alteration in T cell
    • Production
    • Function
cell mediated immunodeficiency1
Cell Mediated Immunodeficiency
  • Primary Cell-mediated Diseases
    • DiGeorge syndrome
    • X-Linked immunodeficiency with Hyper-IgM
  • Secondary cell-mediated Diseases
    • Secondary to infections
      • Viral – measles, cytomegalovirus
      • Hodgkin’s disease
      • HIV
cell mediated immunodeficiency2
Cell Mediated Immunodeficiency
  • Manifestations
    • Recurrent Infections
      • Often in children
      • Susceptible to wide range of pathogens
    • Severe infections
    • Infections resistant to therapy
    • Infections leading to death
      • Children rarely survive
combined t cell and b cell immunodeficiency
Combined T-cell and B-cell Immunodeficiency
  • Combined Immunodeficiency Syndrome (CIDS)
    • Genetic
    • Disruption in communication between T and B lymphocytes
combined t cell and b cell immunodeficiency1
Combined T-cell and B-cell Immunodeficiency
  • Combined Immunodeficiency Syndrome (CIDS)
    • Severe Combined Immunodeficiency Syndrome(SCIDSS)
      • X-linked Combined Immunodeficiency Syndrome
      • Autosomal Recessive Combined Immunodeficiency Syndrome
    • Combined Immunodeficiency
    • Ataxia-Telangiectasia
    • Wiskott-Aldrich Syndrome
combined t cell and b cell immunodeficiency2
Combined T-cell and B-cell Immunodeficiency
  • Manifestations
    • Present in children
    • Recurrent Infections
    • Failure to thrive
    • Infections leading to death
complement system disorders
Complement System Disorders
  • Alteration in
      • One or more complement components
      • Primary Disorders
        • Transmitted recessive trait
      • Deficiency in C1, C2, C, C4,
        • Increased susceptibility to infection
        • Increased incidence of Systemic Lupus Erythematosus (SLE)
          • Vasculitis, glomerulonephritis, rash
      • Deficiency in C5, C6, C7, C8, C9
        • Increased susceptibility to infection
      • Hereditary Angioneurotic Edema
complement system disorders1
Complement System Disorders
  • Secondary Disorders
    • Person with functionally normal complement system
    • Disease causing rapid activation and turnover
    • Diseases causing reduced synthesis of complement components
    • Diseases
      • Immune Complex disorders (Type III Hypersensitivity)
      • Cirrhosis
      • Malnutrition
phagocytic system disorders
Phagocytic System Disorders
  • Alteration in
    • Polymorphonuclear leukocytes
      • Neutrophils
      • Eosinophils
    • Mononuclear leukocytes
      • Monocytes/macrophages
phagocytic system disorders1
Phagocytic System Disorders
  • Reduction in number of phagocytes
  • Reduction in function of phagocytic cells
    • Chemotaxis
    • Adherence
    • Phagocytosis
    • Ability to kill
phagocytic system disorders2
Phagocytic System Disorders
  • Manifestations
    • Recurrent Infections – recur throughout life
    • Chronic Infections
    • Infections resistant to antibiotics
phagocytic system disorders3
Phagocytic System Disorders
  • Diseases
    • Primary
      • Chronic Granulomatous Disease (CGD)
    • Secondary
      • Side effect of drugs
        • Corticosteroids
        • Cyclosporine
      • Diabetes mellitus
      • HIV/AIDS
hypersensitivity reactions
Hypersensitivity Reactions
  • Excessive or inappropriate activation of immune system
  • Types
    • Type I (IgE- mediated)
    • Type II (IgM and IgG - Tissue-Specific)
    • Type III (Immune-Complex)
    • Type IV (Cell-Mediated)
type i hypersensitivity
Type I Hypersensitivity
  • IgE mediated
  • Most antigens (allergen) are environmental
  • Antigen response
    • Most potent when injected
    • Less potent when ingested
type i hypersensitivity1
Type I Hypersensitivity
  • First exposure or sensitization
  • Antigen changes B lymphocyte to plasma cell
    • Facilitated by Helper T (CD4 or TH2)
  • Plasma cell produces IgE
  • IgE coats surface of mast cells or Basophils
    • e.g. plugs into Fc receptor sites
type i hypersensitivity2
Type I Hypersensitivity
  • Second exposure allergen (Ag) binds to IgE which is bound to Fc receptor sites on mast cells or basophils
  • Causes mast cells and basophil degranulation
  • Each exposure become more rapid and severe
degranulation of mast cell
Degranulation of Mast Cell
  • Release of histamine
  • H1 receptor response
  • Vasodilatation
    • Local increase in blood flow
  • Increased vascular permeability
    • Extravasation of fluid into interstitial spaces
    • Edema of bronchi
    • Edema peripheral tissue (local)
    • Systemic drop in blood pressure (systemic)
  • Contract bronchial smooth muscles
    • Bronchial constriction
degranulation of mast cell1
Degranulation of Mast Cell
  • Release of histamine
  • H2 receptor Response
    • Increased gastric secretion
    • Decrease of histamine release from mast cell
degranulation of mast cell2
Degranulation of Mast Cell
  • Synthesis of Arachidonic acids
    • Prostaglandins
    • Leukotrienes
  • Stimulation of cytokines
primary and secondary phases type i hypersensitivity
Primary and Secondary PhasesType I Hypersensitivity
  • Primary Phase
    • Initial phase
    • Occurs in minutes
    • Lasts 60 minutes
  • Secondary Phase
    • Occurs 2-8 hours later
    • Lasts for days
type i hypersensitivity reactions
Type I Hypersensitivity Reactions
  • Individual with allergies
  • Genetic predisposition
  • Alteration
    • Increased IgE
    • Increased Fc receptors
  • Atopic – Local reaction
  • Systemic Reactions
type i hypersensitivity reactions1
Type I Hypersensitivity Reactions
  • Atopic – Local reaction
    • Urticaria (hives)
    • Allergic rhinitis
      • Hay fever
      • Seasonal allergies related to pollen, ragweed, etc
      • Recurrent allergies related to animal dander, dust mites, etc.
    • Atopic dermatitis
    • Food allergies (Milk, eggs, peanuts, soy, fish, etc.)
    • Certain types of asthma
type i hypersensitivity reactions2
Type I Hypersensitivity Reactions
  • Systemic Reaction
  • Anaphylaxis
    • Life threatening
    • Rapid deterioration
    • Vascular dilation leading to vasogenic shock
    • Widespread edema
    • Laryngeal edema
    • Bronchospasm
type i hypersensitivity manifestations2
Type I Hypersensitivity – Manifestations
  • Eye
    • Conjunctivitis
    • Discharge
  • Nasal
    • Itching
    • Discharge
type i hypersensitivity manifestations3
Type I Hypersensitivity – Manifestations
  • Bronchials
    • Spasm or smooth muscles
    • Edema
    • Increased production of mucous
  • Laryngeal edema
type i hypersensitivity manifestations8
Type I Hypersensitivity – Manifestations
  • Cardiac
    • Hypotension
    • Dysrhythmia
  • Gastrointestinal Tract
    • Cramps and malabsorption
testing for type i hypersensitivity
Testing for Type I Hypersensitivity
  • Skin Testing
  • Positive Radioimmunosorbent Testing (RIST)
    • Tests for IgE
type ii hypersensitivity
Type II Hypersensitivity
  • Tissue Specific Reaction
  • Antibody (IgG or IgM) formed to act against specific antigen on cell membrane
  • Cell is then destroyed by the antibody
  • Diseases
    • Graves disease
    • Drug sensitivities – anemia or thrombocytopenia
    • Hemolytic diseases
    • ABO incompatibility
    • Rh incompatibility
type ii hypersensitivity1
Type II Hypersensitivity
  • Type O is universal donner because has not antigens
  • Type AB is universal recipient because body does not develop antibodies (IgG or IgM) to the blood
type iii hypersensitivity
Type III Hypersensitivity
  • Immune-Complex mediated reaction
  • Immune complex is formed (antigen antibody complex)
type iii hypersensitivity1
Type III Hypersensitivity
  • Immune Complex deposited in
    • Walls of blood vessels leading to vasculitis
    • Glomerulus of kidneys leading to glomerulonephritis
    • Lung
    • Joints leading to arthritis
type iii hypersensitivity2
Type III Hypersensitivity
  • Damage occurs because
    • Immune Complex (Antibody) is deposited in tissues
    • Inflammatory response occurs
    • Complement is activated
    • Neutrophilic chemotaxis occurs
      • Neutrophils are drawn to the site of the deposited immune complex
      • Neutrophils try to ingest the immune complex
    • Lysosomal enzymes are released by neutrophils and cause tissue damage
type iii hypersensitivity3
Type III Hypersensitivity
  • Diseases
    • Raynaud Disease or Raynaud Phenomenon
    • Systemic Lupus Erythematosus (SLE)
    • Serum sickness
    • Arthus reaction
type iv hypersensitivity
Type IV Hypersensitivity
  • Mediated by T cell
  • Sensitized Tc or Cytotoxic T cell
  • Tc destroys the antigen
  • Produces lymphokines that attract macrophages
  • Tc releases
    • Lysosomal enzymes that destroy tissues
    • Toxic oxygen products that destroy tissues
type iv hypersensitivity1
Type IV Hypersensitivity
  • Diseases
  • Graft Rejection Alloimmune reaction
    • Reaction against antigen in donated tissue primarily HLA
    • Acute and/or chronic rejection
  • Tuberculin reaction
  • Poison ivy 
  • Rheumatoid arthritis
  • Type 1 Diabetes mellitus
  • Contact dermatitis
latex allergy
Latex Allergy
  • Combined
    • Type I Hypersensitivity
    • Type IV Hypersensitivity
categories of transplanted tissue
Categories of Transplanted Tissue
  • Allogeneic
    • The donor and recipient are related or unrelated but share similar HLA types
  • Syngeneic
    • The donor and recipient are identical twins
  • Autologous
    • The donor and recipient are the same person
autoimmune disease
Autoimmune Disease
  • Self-Tolerance
  • Immune system differentiates self from non-self
autoimmune disease1
Autoimmune Disease
  • Normal
    • Self recognizes the Human Leukocyte Antigen (HLA) of Class I and Class II Major Histocompatability Complexes (MHC) on the genes
  • Abnormal
    • Loss of self-tolerance
    • Can affect any cell of the body
    • Immune system sees self cells a antigens
    • Probably Autoimmune Diseases – Chart 21-2
autoimmune disease2
Autoimmune Disease
  • Immunologic Tolerance
  • B-Cell Tolerance
    • Development of autoantibodies
    • Antibodies against self cells
  • T-Cell Tolerance
    • T cells destroy self cells
    • T cells not regulated by usual methods of apoptosis
autoimmune disease3
Autoimmune Disease
  • Mechanism of Autoimmune Diseases
    • Failure of self-tolerance
    • Failure of T-cell suppression
    • Breakdown in T-cell anergy
    • Disorders of MHC-Antigen complex/Receptor interactions