Pathophys Immune Flashcards
Autoimmunity
Describes etiologic process
Cause of abnormal excess toward self
Hypersensitivity
Mechanisms of injury
May or may not be autoimmune
Type I Hypersensitivity Rxn
Involves IgE- immediate eaction
Normally will required multi exposures to produce enough IgE to cause a rxn
Atopic and anaphylactic
Primary Effectors of Type I hypersensitivity rxn
Mast Cells
Basophils
Symptoms of hypersensitivity rxn I
Hives, allergic rhinitis, eczema, asthma symptoms, tightening of throat, local edema, wheezing, tachycardia
Type II Hypersensitivity rxn
Tissue specific, cytotoxic, cytolytic
Antibodies attack antigens on surfaces of specific cells or tissue
Often immediate (but can occur over time)
Can be isoimmunity
Type II Hypersensitivity rxn is mediated by
Complement
Macophages, NK cells, neutrophils, eosinophils
IgM, IgG
Antigen binding –> complement fixation
Transfusion rxn
Type II hypersensitivity rxn
Agglutination due to mismatch ABO blood types
Destruction of RBCs
Fever, chills, flushing, tachycardia, hypotension
May progress to anaphylaxis
Hemolytic disease of newborn
Type II hypersensitivity rxn
Rh- mother with Rh+ fetus
Myasthemia Gravis
Type II hypersensitivity rxn
antibodies form to ach receptor on motor end plates of muscle
No effector cell
Loss of motor end plate function
antigen/ antibody and complement attack receptor
Graves Disease
Type II hypersensitivity rxn
Tissue to large to engulf and destroy
Build up on receptors and enhance normal function
Leads to hyperthyroidism
Hyperacute graft rejection
Type II hypersensitivity rxn
Donor tissue- antigen for which recipient has preformed antibodies
Lysis of donor tissue
inflammation, thromobsis & hemorrhage- 48 hours until donor tissue death
Type III Hypersensitivity Rxn
Failure of immune and phagocytic system to eliminate antigen/ antibody complex
Not tissue specific
Deposition of antigen/ antibody complex in tissues –> activation of complement and inflammatory reaction
What is this type III hypersensitivity rxn?
Cause by persistant low-grade infection
interaction of soluble exogenous antigen with soluble antibody
Damage to glomerular basement membrane due to immune complex deposited in glomerular basement membrane
Signs- protein uria, hypertension, oliguria
Immune complex glomerulonephritis
System lupus erythematosus
Type III hypersensitivity rxn
Autoimmune, connective tissue, collagen vascular or inflammatory disorder
Develop of antibodies against nuclear antigens
Autoantibodies will react with DNA from damaged cells anywhere in the body
Type IV Hypersensitivity Rxn
Delayed hypersensitivity
T cell mediated
Damage results from delayed cellular rxn to an antigen
Mast cell degranulation, lymphocyte and macrophage invasion
Cutaneous basophil hypersensitivity
Rapid type IV hypersensitivity
Soluble antigen triggers t cells –> release of cytokines –> basophil activation –> skin swelling
Contact hypersensitivity
Type IV hypersensitivity
Peaks in 48-72 hours
Hapten penetrates skin and become immunogenic
Activate of CD4+ cells –> inflammatory response and attraction of effector cells
From contact with various products/ chemicals
ex- posion ivy
Tuberculin- type Hypersensitivity
Type IV hypersensitivity rxn
Person with TB antibodies is exposed to tuberculin in a TB tests
Dermal phenom
Granulomatous hypersensitivity
Type IV hypersensitivity rxn
Antigen is not degraded in macrophages
Lymphocytes create inflammatory response
Primary defense against intracellular infections
Deficient Immune Responses
Function decrease in one or more immune system component
2 Types of Deficient Immune System Responses
Primary- congenital or acquired
Secondary- consequence of another process or treatment
SCID
Severe combined immunodeficiency disorder
embryonic defect
Autosomal recessive or X-linked recessive
Possible defective expression of MHC
Possible mutation of RAG1 & RAG2
only treatment is gene therapy/ bone marrow transplant
Reticular dysgensis
- type of SCID
- complete stem cell failure
- most severe
- No innate immune system
Wiskott-Aldrich Syndrome (WA)
X-linked B&T combined Mutation of WASP gene- cytoplasmic signaling Deficiency of platelets non-functional T cell Trouble mounting immune responses Only live 3 years
List the 3 primary B & T Cell Combined Disorders
SCID
reticular dysgensis (type of SCID)
Wiskott-Aldrich Syndrome (WA)
List the 2 primary T Cell Disorders
DiGeorge Syndrome
Chronic Muscuocutaneous Candidasis
DiGeorge Syndrome
Thymic hypoplasia
T cell develop affected due to mutation on chromosome 22
Normal B cells
Total loss of thymus
No immune memory- can’t coordinate a consistent immune response
Chronic Mucocutaneous Candidasis
Autosomal recessive T cell disorder
Selective deficiency of fights off Candidad albicans
Consistant yeast infections,
Other B and T cell functions are normal
List the 3 Primary B Cell Disorders
IgA deficiency
Bruton X-linked agammaglobulinemia
Transient hypogammaglobulinemia
IgA deficiency
Failure of IgA lymphocytes to become plasma cells
Autosomal dominant or recessive
Prone to respiratory, GI, and genitourinary infections
Bruton X-linked agammbloulinemia
B cells unable to complete maturation Mutation of btk gene Increase in T cells Prone to recurrent bacterial infections Fix by passoimmunotheraphy, serum from person with normal immune system
Transient hypogammaglobulinemia
Infant slow to acquire normal IgG levels
Normalcy achieved by age 4
Secondary B and T Cell Disorders Causes
Many types of linkages Direct and infirect linkages b/w brain and endocrine system T and B cells decrease after surgery Pharmaceuticals Nutritional Status Age
