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BIO 325 - Pathophysiology > Autoimmune > Flashcards

Autoimmune Flashcards

(61 cards)

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1
Q

IgG

A

Most abundant of ABs
Activates complement proteins

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2
Q

IgA

A

Attached to epithelial cells
Prevents microbes from crossing mucus membrane

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3
Q

IgM

A

Activates complement proteins
Makes bacteria cells clump together

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4
Q

IgD

A

Never exposed to antigens
When they are exposed, they will create a mold of the antigen that can be used to make antibodies

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5
Q

IgE

A

Immediate allergic rxns & parasites

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6
Q

T-cells

A

Responsible for cell-mediated immunity where they kill targets directly or stimulate activity of other leukocytes

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7
Q

Adaptive immunity can be

A

Active or passive

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8
Q

Lymphoid organs contain

A

Large quantities of immune cells

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9
Q

Lymphoid organs

A

Lymph nodes, spleen, tonsils, appendix, bone marrow, thymus

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10
Q

Primary immune response

A

Latent period of 7-14 days following exposure before antibodies can be produced.
Dominated by IgM with some IgG

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11
Q

Secondary immune response

A

Occurs upon subsequent exposure to an antigen. Antibodies appear faster because memory cells recognize antigen and can make a faster immune response.

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12
Q

Autoimmunity

A

Immune reaction to self-antigens

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13
Q

Alloimmunity

A

Immune reaction to tissues of another individual

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14
Q

In hypersensitivity, what is the body injured by?

A

The immune response NOT the antigen/allergen

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15
Q

Immediate hypersensitivity rxn

A

Minutes to hours after exposure

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16
Q

Delayed hypersensitivity rxn

A

Hours to appear, at severity days after re-exposure to antigen

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17
Q

Anaphylaxis

A

Most rapid and severe rxn

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18
Q

Type 1 rxn

A

IgE mediated
Hay fever, allergies
Immediate rxn

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19
Q

Type 2 rxn

A

AB mediated
Tissue-specific
Immediate

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20
Q

Type 3 rxn

A

Complement-mediated immune disorders
Ag-AB complex deposited in tissues
Immediate

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21
Q

Type 4 rxn

A

T-cell mediated rxn
Delayed rxn

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22
Q

Type 1 rxn allergen

A

Contained within particle too large to be phagocytosed or protected by a nonallergenic coat.

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23
Q

Type 1 Pathogenesis

A

T-helper cells differentiate B cells into specific IgE-producing cells
IgE antibodies attach to receptors on mast cells or basophils
Allergen binds to cell-associated IgE
Binding triggers degranulation of mast cells/basophils to release histamine

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24
Q

Type 1 primary response

A

-Occurs 5-30 minutes after exposure, subsides within 60
-Mediated by mast cell degranulation

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25
Type 1 Late-phase response
-2-8 days after first phase - Result of lipid mediators and cytokines in inflammatory response - Influx of eosinophils and leukocytes to site of allergen causing tissue destruction
26
Possible mechanisms for tissue-specific rxns (type 2)
1. Complement-mediated lysis 2. Opsonization and phagocytosis 3. Antibody-dependent cell-mediated cytotoxicity 4. Modulation of cellular function
27
Graves Disease
Type 2 rxn AB binds to pit and stims TSH release = thyroxine release
27
Examples of type 2 rxn
Autoimmune hemolytic anemia, blood transfusion or Rh, medications are antigens and bind to cells, NK cells target killer cell, Graves Disease
28
Type 3 rxn
Produce damage - elicit inflammatory response - recruitment of neutrophils and other inflammatory cells responsible for injury
29
Glomerulonephritis
Thickening of glomerular capillary wall from immune complex deposition and destruction of ET cells by neutrophils
30
Symptoms of glomerulonephritis
Hematuria, proteinuria, hypertension, edema
31
Type 4 rxn responds to
Fungi, protozoa, parasites, poison ivy
32
Type 4 rxn mediated by
Sensitized T lymphocytes
33
Type 4 rxn t-cells
Macrophages/other cells release lysosomal enzymes that kill tissue cells with antigen on cell membrane ex. poison ivy causing contact dermatitis
34
Types of Type 4 rxns
Direct cell-mediated cytotoxicity Delayed-type hypersensitivity
35
Type 4 Direct cell-mediated cytotoxicity
Cytotoxic T lymphocytes kill target cells that show peptides from antigens prevented in association with class 1 major histocompatibility complex molecules
36
Type 4 rxn Delayed-type hypersensitivity
Activation of antigen-presenting cells, result in release of cytokines and recruitment/activation of inflammatory cells`
37
Type 4 rxn Delayed-type hypersensitivity
-24-72 hours to develop - Cause of several diseases like contact dermatitis - Patch testing can be used - Treatment usually limited to removal of irritant and topical preparations
38
Autoimmune diseases are
Familial
39
Autoimmunity
Self-tolerance breaks down and cytotoxic T cells/antibodies mistakenly attack the body's own cells
40
Two primary factors believed to cause autoimmune disease
Heredity and environment
41
T cell anergy
Self tolerance mechanism in which the T cell is inactivated after antigen encounter, but remains alive for an extended period of time in a hyporesponsive state.
42
Proposed environmental factor mechanisms include
1. Breakdown of T cell anergy 2. Release of sequestered antigens 3. Molecular imagery 4. Superantigens
43
Testing/diagnosis of autoimmune testing
1. Demonstration of antibodies that are directed against tissue antigens or cellular components 2. Assays involve diluting individual's serum and allow to react with antigen-coated surface 3. Serum serially diluted until it no longer produces a rxn
44
Treatment of autoimmune disease
Immunosuppressive drugs and corticosteroids, plasmapheresis, potential development of vaccines
45
Lupus
Chronic multisystem inflammatory disease Manifestations: fatigue, rashes, myalgia/arthritis, weight change and fever
46
Lupus characterization
Production of large variety of autoantibodies against: nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, etc.
47
Lupus Autoantibodies
Combine with antigens and form circulating immune complexes that can get stuck in various organs like kidneys, brain, heart, spleen, skin Some symptoms result from T3 rxn, others T2
48
Lupus - Clinical manifestations
Vasculitis, renal disease, hematologic changes, cardiovascular disease
49
Lupus - Common Findings
Need 4 Butterfly rash, discoid rash, photosensitivity, oral or nasopharyngeal ulcers, nonerosive arthritis, serositis (fatigue), renal disorder, neurologic disorder, hematologic disorder, immunologic disorder, presence of antinuclear antibodies
50
Lupus - Treatment (nonpharmaceutical)
Protection from sunlight, maintaining adequate nutrition, exercise, smoking cessation, receiving appropriate immunizations
51
Lupus - treatment (pharmacologic)
Hydroxychloroquine Other meds depending on severity and combination of clinical manifestation
52
Rheumatoid arthritis
Inflammatory joint disease characterized by inflammatory destruction of synovial membrane, articular cartilage, joint capsule, and surrounding ligaments and tendons. First joint affected is synovial membrane
53
What does rheumatoid arthritis affect
Heart, lungs, kidneys, skin, joints
54
Rheumatoid arthritis - antibodies
Antibodies against IgG fragments w/presence of rheumatoid factors (IgG and IgM) against self-antigens in blood and synovial membranes
55
Rheumatoid nodules could invade
Skin, lung, spleen, small and large arteries
56
Synovial fibroblasts
SFs undergo changes and develop exaggerated immune response. Produce proinflammatory cytokines, enzymes, and prostaglandins that thicken synovial tissue
57
Rheumatoid arthritis pathogenesis
Neutrophils in synovial fluid activated Inflammatory cytokines secreted by SFs T-cells interact with synovial fibroblasts Inflammation spreads to fibrous joint capsule and surrounding ligaments/tendons
58
Rheumatoid arthritis - manifestations
Insidious onset Inflammation - fever, fatigue, weakness, anorexia, weight loss, aching/stiffness Joints become painful, tender, swollen, warm, boggy Joint deformities
59
Rheumatoid arthritis evaluation
4 or more Morning joint stiffness Arthritis of 3+ joint areas Arthritis of hand joints Symmetric arthritis Rheumatoid nodules Abnormal amounts of serum rheumatoid factor Radiographic changes
60
Rheumatoid arthritis - treatment
Methotrexate, NSAIDS or corticosteroids, Leflunomide, Infliximab Biologics like Enbrel

BIO 325 - Pathophysiology (8 decks)

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