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Abnormal Immune System > Pathophys Immune > Flashcards

Pathophys Immune Flashcards

1
Q

Autoimmunity

A

Describes etiologic process

Cause of abnormal excess toward self

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2
Q

Hypersensitivity

A

Mechanisms of injury

May or may not be autoimmune

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3
Q

Type I Hypersensitivity Rxn

A

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

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4
Q

Primary Effectors of Type I hypersensitivity rxn

A

Mast Cells

Basophils

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5
Q

Symptoms of hypersensitivity rxn I

A

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

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6
Q

Type II Hypersensitivity rxn

A

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

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7
Q

Type II Hypersensitivity rxn is mediated by

A

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

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8
Q

Transfusion rxn

A

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

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9
Q

Hemolytic disease of newborn

A

Type II hypersensitivity rxn

Rh- mother with Rh+ fetus

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10
Q

Myasthemia Gravis

A

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

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11
Q

Graves Disease

A

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

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12
Q

Hyperacute graft rejection

A

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

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13
Q

Type III Hypersensitivity Rxn

A

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

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14
Q

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

A

Immune complex glomerulonephritis

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15
Q

System lupus erythematosus

A

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

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16
Q

Type IV Hypersensitivity Rxn

A

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

17
Q

Cutaneous basophil hypersensitivity

A

Rapid type IV hypersensitivity

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

18
Q

Contact hypersensitivity

A

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

19
Q

Tuberculin- type Hypersensitivity

A

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

20
Q

Granulomatous hypersensitivity

A

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

21
Q

Deficient Immune Responses

A

Function decrease in one or more immune system component

22
Q

2 Types of Deficient Immune System Responses

A

Primary- congenital or acquired

Secondary- consequence of another process or treatment

23
Q

SCID

A

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

24
Q

Reticular dysgensis

A
  • type of SCID
  • complete stem cell failure
  • most severe
  • No innate immune system
25
Q

Wiskott-Aldrich Syndrome (WA)

A 
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
26
Q

List the 3 primary B & T Cell Combined Disorders

A

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

27
Q

List the 2 primary T Cell Disorders

A

DiGeorge Syndrome

Chronic Muscuocutaneous Candidasis

28
Q

DiGeorge Syndrome

A

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

29
Q

Chronic Mucocutaneous Candidasis

A

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

30
Q

List the 3 Primary B Cell Disorders

A

IgA deficiency
Bruton X-linked agammaglobulinemia
Transient hypogammaglobulinemia

31
Q

IgA deficiency

A

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

32
Q

Bruton X-linked agammbloulinemia

A 
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
33
Q

Transient hypogammaglobulinemia

A

Infant slow to acquire normal IgG levels

Normalcy achieved by age 4

34
Q

Secondary B and T Cell Disorders Causes

A 
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

Abnormal Immune System (1 decks)

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