Pathophys Immune

Question 1

Autoimmunity

Answer 1

Describes etiologic process

Cause of abnormal excess toward self

Question 2

Hypersensitivity

Answer 2

Mechanisms of injury

May or may not be autoimmune

Question 3

Type I Hypersensitivity Rxn

Answer 3

Involves IgE- immediate eaction
Normally will required multi exposures to produce enough IgE to cause a rxn
Atopic and anaphylactic

Question 4

Primary Effectors of Type I hypersensitivity rxn

Answer 4

Mast Cells

Basophils

Question 5

Symptoms of hypersensitivity rxn I

Answer 5

Hives, allergic rhinitis, eczema, asthma symptoms, tightening of throat, local edema, wheezing, tachycardia

Question 6

Type II Hypersensitivity rxn

Answer 6

Tissue specific, cytotoxic, cytolytic
Antibodies attack antigens on surfaces of specific cells or tissue
Often immediate (but can occur over time)
Can be isoimmunity

Question 7

Type II Hypersensitivity rxn is mediated by

Answer 7

Complement
Macophages, NK cells, neutrophils, eosinophils
IgM, IgG
Antigen binding –> complement fixation

Question 8

Transfusion rxn

Answer 8

Type II hypersensitivity rxn
Agglutination due to mismatch ABO blood types
Destruction of RBCs
Fever, chills, flushing, tachycardia, hypotension
May progress to anaphylaxis

Question 9

Hemolytic disease of newborn

Answer 9

Type II hypersensitivity rxn

Rh- mother with Rh+ fetus

Question 10

Myasthemia Gravis

Answer 10

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

Question 11

Graves Disease

Answer 11

Type II hypersensitivity rxn
Tissue to large to engulf and destroy
Build up on receptors and enhance normal function
Leads to hyperthyroidism

Question 12

Hyperacute graft rejection

Answer 12

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

Question 13

Type III Hypersensitivity Rxn

Answer 13

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

Question 14

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

Answer 14

Immune complex glomerulonephritis

Question 15

System lupus erythematosus

Answer 15

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

Question 16

Type IV Hypersensitivity Rxn

Answer 16

Delayed hypersensitivity
T cell mediated
Damage results from delayed cellular rxn to an antigen
Mast cell degranulation, lymphocyte and macrophage invasion

Question 17

Cutaneous basophil hypersensitivity

Answer 17

Rapid type IV hypersensitivity

Soluble antigen triggers t cells –> release of cytokines –> basophil activation –> skin swelling

Question 18

Contact hypersensitivity

Answer 18

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

Question 19

Tuberculin- type Hypersensitivity

Answer 19

Type IV hypersensitivity rxn
Person with TB antibodies is exposed to tuberculin in a TB tests
Dermal phenom

Question 20

Granulomatous hypersensitivity

Answer 20

Type IV hypersensitivity rxn
Antigen is not degraded in macrophages
Lymphocytes create inflammatory response
Primary defense against intracellular infections

Question 21

Deficient Immune Responses

Answer 21

Function decrease in one or more immune system component

Question 22

2 Types of Deficient Immune System Responses

Answer 22

Primary- congenital or acquired

Secondary- consequence of another process or treatment

Question 23

SCID

Answer 23

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

Question 24

Reticular dysgensis

Answer 24

• type of SCID
• complete stem cell failure
• most severe
• No innate immune system

Question 25

Wiskott-Aldrich Syndrome (WA)

Answer 25

``` 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 ```

Question 26

List the 3 primary B & T Cell Combined Disorders

Answer 26

SCID reticular dysgensis (type of SCID) Wiskott-Aldrich Syndrome (WA)

Question 27

List the 2 primary T Cell Disorders

Answer 27

DiGeorge Syndrome | Chronic Muscuocutaneous Candidasis

Question 28

DiGeorge Syndrome

Answer 28

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

Question 29

Chronic Mucocutaneous Candidasis

Answer 29

Autosomal recessive T cell disorder Selective deficiency of fights off Candidad albicans Consistant yeast infections, Other B and T cell functions are normal

Question 30

List the 3 Primary B Cell Disorders

Answer 30

IgA deficiency Bruton X-linked agammaglobulinemia Transient hypogammaglobulinemia

Question 31

IgA deficiency

Answer 31

Failure of IgA lymphocytes to become plasma cells Autosomal dominant or recessive Prone to respiratory, GI, and genitourinary infections

Question 32

Bruton X-linked agammbloulinemia

Answer 32

``` 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 ```

Question 33

Transient hypogammaglobulinemia

Answer 33

Infant slow to acquire normal IgG levels | Normalcy achieved by age 4

Question 34

Secondary B and T Cell Disorders Causes

Answer 34

``` 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 ```