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BIO 325 - Pathophysiology > Autoimmune > Flashcards

Autoimmune Flashcards

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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
Q

Type 1 Late-phase response

A

-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
Q

Possible mechanisms for tissue-specific rxns (type 2)

A
  1. Complement-mediated lysis
  2. Opsonization and phagocytosis
  3. Antibody-dependent cell-mediated cytotoxicity
  4. Modulation of cellular function
27
Q

Graves Disease

A

Type 2 rxn
AB binds to pit and stims TSH release = thyroxine release

27
Q

Examples of type 2 rxn

A

Autoimmune hemolytic anemia, blood transfusion or Rh, medications are antigens and bind to cells, NK cells target killer cell, Graves Disease

28
Q

Type 3 rxn

A

Produce damage - elicit inflammatory response - recruitment of neutrophils and other inflammatory cells responsible for injury

29
Q

Glomerulonephritis

A

Thickening of glomerular capillary wall from immune complex deposition and destruction of ET cells by neutrophils

30
Q

Symptoms of glomerulonephritis

A

Hematuria, proteinuria, hypertension, edema

31
Q

Type 4 rxn responds to

A

Fungi, protozoa, parasites, poison ivy

32
Q

Type 4 rxn mediated by

A

Sensitized T lymphocytes

33
Q

Type 4 rxn t-cells

A

Macrophages/other cells release lysosomal enzymes that kill tissue cells with antigen on cell membrane

ex. poison ivy causing contact dermatitis

34
Q

Types of Type 4 rxns

A

Direct cell-mediated cytotoxicity
Delayed-type hypersensitivity

35
Q

Type 4 Direct cell-mediated cytotoxicity

A

Cytotoxic T lymphocytes kill target cells that show peptides from antigens prevented in association with class 1 major histocompatibility complex molecules

36
Q

Type 4 rxn Delayed-type hypersensitivity

A

Activation of antigen-presenting cells, result in release of cytokines and recruitment/activation of inflammatory cells`

37
Q

Type 4 rxn Delayed-type hypersensitivity

A

-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
Q

Autoimmune diseases are

A

Familial

39
Q

Autoimmunity

A

Self-tolerance breaks down and cytotoxic T cells/antibodies mistakenly attack the body’s own cells

40
Q

Two primary factors believed to cause autoimmune disease

A

Heredity and environment

41
Q

T cell anergy

A

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
Q

Proposed environmental factor mechanisms include

A
  1. Breakdown of T cell anergy
  2. Release of sequestered antigens
  3. Molecular imagery
  4. Superantigens
43
Q

Testing/diagnosis of autoimmune testing

A
  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
Q

Treatment of autoimmune disease

A

Immunosuppressive drugs and corticosteroids, plasmapheresis, potential development of vaccines

45
Q

Lupus

A

Chronic multisystem inflammatory disease
Manifestations: fatigue, rashes, myalgia/arthritis, weight change and fever

46
Q

Lupus characterization

A

Production of large variety of autoantibodies against: nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, etc.

47
Q

Lupus Autoantibodies

A

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
Q

Lupus - Clinical manifestations

A

Vasculitis, renal disease, hematologic changes, cardiovascular disease

49
Q

Lupus - Common Findings

A

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
Q

Lupus - Treatment (nonpharmaceutical)

A

Protection from sunlight, maintaining adequate nutrition, exercise, smoking cessation, receiving appropriate immunizations

51
Q

Lupus - treatment (pharmacologic)

A

Hydroxychloroquine
Other meds depending on severity and combination of clinical manifestation

52
Q

Rheumatoid arthritis

A

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
Q

What does rheumatoid arthritis affect

A

Heart, lungs, kidneys, skin, joints

54
Q

Rheumatoid arthritis - antibodies

A

Antibodies against IgG fragments w/presence of rheumatoid factors (IgG and IgM) against self-antigens in blood and synovial membranes

55
Q

Rheumatoid nodules could invade

A

Skin, lung, spleen, small and large arteries

56
Q

Synovial fibroblasts

A

SFs undergo changes and develop exaggerated immune response. Produce proinflammatory cytokines, enzymes, and prostaglandins that thicken synovial tissue

57
Q

Rheumatoid arthritis pathogenesis

A

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
Q

Rheumatoid arthritis - manifestations

A

Insidious onset
Inflammation - fever, fatigue, weakness, anorexia, weight loss, aching/stiffness
Joints become painful, tender, swollen, warm, boggy
Joint deformities

59
Q

Rheumatoid arthritis evaluation

A

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
Q

Rheumatoid arthritis - treatment

A

Methotrexate, NSAIDS or corticosteroids, Leflunomide, Infliximab
Biologics like Enbrel

BIO 325 - Pathophysiology (8 decks)

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