Autoimmunity And Autoimmune Disease

Front 1

What organs and tissues does systemic lupus erythematosus affect?

Back 1

Systemic
Joints
Skin
Kidneys

Front 2

What organs and tissues does rheumatoid arthritis affect?

Back 2

Systemic
Joints

Front 3

What organs and tissues does insulin dependent diabetes affect?

Back 3

Pancrease

Front 4

What organs and tissues does thyroiditis affect?

Back 4

Thyroid

Front 5

What organs and tissues does Addisons disease affect?

Back 5

Adrenals

Front 6

What organs and tissues do polyglandular autoimmune diseases affect?

Back 6

Various endocrine organs

Front 7

What organs and tissues does Graves disease affect?

Back 7

Thyroid

Front 8

What organs and tissues does Goodpastures disease affect?

Back 8

Kidneys
Lungs

Front 9

What organs and tissues does immune hemolytic anermia affect?

Back 9

erythrocytes

Front 10

What organs and tissues does myasthemia gravis affect?

Back 10

muscles

Front 11

What organs and tissues does vasculitis?

Back 11

Blood vessels

Front 12

What organs and tissues does multiple sclerosis affect?

Back 12

CNS

Front 13

How does the body prevent autoimmune diseases?

Back 13

Tolerance

Front 14

How does the body maintain tolerance to prevent autoimmunity?

Back 14

-clonal deletion-deleting T cells in the thymus
-clonal anergy-silencing T cells that recognize self
-Suppression-mechanisms that suppress self reactions
-Regulatory T-cells (treg)- responsible for peripheral tolerance

Front 15

Not all self antigens are presented in the thymus, how does the body prevent autoimmunity against these antigens?

Back 15

-antigens may be sequestered- cannot reach certain cells, ex CNS
-antigen levels may be too low to stimulate a response
-insufficient levels of MHC I or II- prevents costimulation
-Accessory signals may be missing
-active suppression

Front 16

What are some possible causes of autoimmunity?

Back 16

-release of autoantigen
-inappropriate MHC expression
-Failure of suppression
-Bypass of T-helper regulation
-Cross reactivity and molecular mimicry

Front 17

Presence of HLA allele DR2 would increase the relative risks of which autoimmune diseases?

Back 17

-Multiple sclerosis
-SLE

Front 18

The presence of HLA allele DR3 would increase the relative risk of which autoimmune diseases?

Back 18

-SLE
-Sjogren's syndrome
-Type I diabetes

Front 19

The presence of HLA allele DR4 would increase the risk of which autoimmune disease?

Back 19

-Type I disease
-Rheumatoid arthritis

Front 20

The presence of HLA allele B27 would increase the risk of which auotoimmune diseases?

Back 20

-Reiters syndrome
-Ankylosing spondylitis

Front 21

Systemic Lupus Erythematosus (SLE)

Back 21

-autoimmune disease that involves chronic systemic inflammation
-Lupus butterfly rash
-multiple organs involved including hematologic > arthritis > skin > fever > renal > myalgia > pericarditis > gastrointestinal > CNS > Ocular

Describe the immunologic features of SLE.

Hint 21

-antinuclear antibody-self reactive bind to certain ribonuclear proteins found in the cell nucleus
-antibody against DS DNA-specific for SLE
-Increased serum complement levels
-Immune comlex deposition cuases renal disease
-Numerous other autoantibodies

Front 22

Rheumatoid Arthritis (RA)

Back 22

-Chronic, recurrent, systemic inflammatory disease that primarily involves the joints
-Age of onset is usually 40-70

Describe the Immunologic features of RA

Hint 22

-Rheumatoid factor
-Immune complex formation
-Inflammation within the joints
-Joint deformity and destruction
-Rheumatoid nodules

Front 23

What is the mechanism by which RA works?

Back 23

CD4+ T cells activate
-B cells-> autoantibodies-> Immune complex formation-> Joint injury
-Macrophages-> cytokines-> fibroblasts, chondrocytes, synovial cells; release destructive enzymes
-Recruit leukocytes
All of this leads to pannus formation, destruction of bone, cartilages, fibrosis, ankylosis

Front 24

Insulin-dependent Diabetes Mellitus (IDDM)

Back 24

Type I diabetes occurs when autoantibodies and autoreactive T cells are produced against the B cells of the pancreatic Islets of Langerhans, resulting in diminished insulin production and chronic hyperglycemia

Front 25

Hashimoto Thyroiditis

Back 25

-Inflammatory disorder of the thyroid with unknown etiology
-cellular infiltration of the htyroid
-Enlarged thyroid (goiter) and abnormal thyroid function
-Hypothyroidism-fatigue, weakness, weight gain, cold intolerance, muscle cramps, dry pale skin

Describe the mechanism by which Hashimoto Thyroiditis occurs.

Hint 25

T-cell mediated cytotoxicity- CD8+ cytotoxic T cell
Thyrocyte injury due to CD4+ activation of macrophages
Antibody-dependent cell mediated cytotoxity- plasma cells release anti-thyroid antibodies which the Fc receptor of NK then binds

Front 26

Addison's Disease

Back 26

-Disease of adrenal insufficiency
-autoantibody against the adrenal cells
-Target auto-antigens may be enzymes involved in steroid synthesis
-Patients show hypotension, anorexia, malaise, and hyperpigmentation
-often associated with other endocrine diseases including polyglandular autoimmune syndromes

Front 27

Polyglandular autoimmune syndromes

Back 27

-Circulating autoantibody against multiple endocrine glands
-Type I, II, and III
-As many as 25% of pts with evidence of hypofunciton of one gland will also have evidence of other endocrine dieases (thyroid, diabetes)

Front 28

Graves Disease (Thyrotoxicosis)

Back 28

-7:1 female to male
-Signs and symptoms- hand tremors, irritability, nervousness, weight loss, tachycardia, fatigue, heat sensitivity, eye proptosis, goiter

What causes the increases release of thyroid hormone?

Hint 28

Autoantibodies against the TSH receptor which then stimulates the release of thyroid hormones.

Front 29

Goodpasture's Syndrome

Back 29

-Autoimmune
-Affects primarily young males
-Characterized by the triad of pulmonary hemorrhage, glomerulonephritis, and circulating antibody to basement membranes.
-Ig and complement deposits common
-May be rapidly fatal

Describe the treatment.

Hint 29

-Plasma exchange
-Corticosteroids

Front 30

Immune Hemolytic Anemias

Back 30

-Group of disorders
-Immunologic reactions against rbc proteins
-usually mediated by antibody, complement, or phagocytes.
-many drugs can bind to rbc membranes, induce antibody responses, and cause the immune mediated destruction of the rbc

List the three classes

Hint 30

Warm antibody types
Cold antibody types
Paroxysmal cold antibody type

Front 31

Describe the difference between the direct and indirect antiglobulin test. What is this test used for?

Back 31

Tests for Immune Hemolytics Anemias

-Direct determines if there is in vivo antibody coated RBCs which with the addition if antiIg will agglutinate.
-Indirect- the RBC is not coated with antibody but the tests checks to see if it will react if antibody is added. THis is important for blood transfusions.

Front 32

Myasthenia Gravis

Back 32

Auto-reactive antibodies are directed against the acetylcholine receptors at the neuromuscular junctions. Complement is then activated and the post-synaptic membrane is destroyed.

What is the result of this?

Hint 32

Muscle weakness.

Front 33

Inflammatory Vasculitides

Back 33

-Group of inflam. disorders that target the vascular system
-Inflammation of the blood vessels

Front 34

Pemphigus Vulgaris

Back 34

-Autoantibody against keratinocytes
-Causes blistering of the skin and mucus membranes
-Potentially fatal due to infection

Front 35

Multiple Sclerosis

Back 35

-Inflammatory demyelination of the CNS via macrophages and T cells
-Results in progressive motor weakness, parethesias, visual impairment, and ataxia
-Oligoclonal immunoglobulin bands in the CSF
-HLA antigen associations
-Altered immunoregulatory T cell populations

What characteristics would an MRI show?

Hint 35

-Demyelinating plaques around the lateral ventricles.