Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
35 Cards in this Set
- Front
- Back
- 3rd side (hint)
What organs and tissues does systemic lupus erythematosus affect?
|
Systemic
Joints Skin Kidneys |
|
|
What organs and tissues does rheumatoid arthritis affect?
|
Systemic
Joints |
|
|
What organs and tissues does insulin dependent diabetes affect?
|
Pancrease
|
|
|
What organs and tissues does thyroiditis affect?
|
Thyroid
|
|
|
What organs and tissues does Addisons disease affect?
|
Adrenals
|
|
|
What organs and tissues do polyglandular autoimmune diseases affect?
|
Various endocrine organs
|
|
|
What organs and tissues does Graves disease affect?
|
Thyroid
|
|
|
What organs and tissues does Goodpastures disease affect?
|
Kidneys
Lungs |
|
|
What organs and tissues does immune hemolytic anermia affect?
|
erythrocytes
|
|
|
What organs and tissues does myasthemia gravis affect?
|
muscles
|
|
|
What organs and tissues does vasculitis?
|
Blood vessels
|
|
|
What organs and tissues does multiple sclerosis affect?
|
CNS
|
|
|
How does the body prevent autoimmune diseases?
|
Tolerance
|
|
|
How does the body maintain tolerance to prevent autoimmunity?
|
-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 |
|
|
Not all self antigens are presented in the thymus, how does the body prevent autoimmunity against these antigens?
|
-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 |
|
|
What are some possible causes of autoimmunity?
|
-release of autoantigen
-inappropriate MHC expression -Failure of suppression -Bypass of T-helper regulation -Cross reactivity and molecular mimicry |
|
|
Presence of HLA allele DR2 would increase the relative risks of which autoimmune diseases?
|
-Multiple sclerosis
-SLE |
|
|
The presence of HLA allele DR3 would increase the relative risk of which autoimmune diseases?
|
-SLE
-Sjogren's syndrome -Type I diabetes |
|
|
The presence of HLA allele DR4 would increase the risk of which autoimmune disease?
|
-Type I disease
-Rheumatoid arthritis |
|
|
The presence of HLA allele B27 would increase the risk of which auotoimmune diseases?
|
-Reiters syndrome
-Ankylosing spondylitis |
|
|
Systemic Lupus Erythematosus (SLE)
|
-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. |
-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 |
|
Rheumatoid Arthritis (RA)
|
-Chronic, recurrent, systemic inflammatory disease that primarily involves the joints
-Age of onset is usually 40-70 Describe the Immunologic features of RA |
-Rheumatoid factor
-Immune complex formation -Inflammation within the joints -Joint deformity and destruction -Rheumatoid nodules |
|
What is the mechanism by which RA works?
|
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 |
|
|
Insulin-dependent Diabetes Mellitus (IDDM)
|
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
|
|
|
Hashimoto Thyroiditis
|
-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. |
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 |
|
Addison's Disease
|
-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 |
|
|
Polyglandular autoimmune syndromes
|
-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) |
|
|
Graves Disease (Thyrotoxicosis)
|
-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? |
Autoantibodies against the TSH receptor which then stimulates the release of thyroid hormones.
|
|
Goodpasture's Syndrome
|
-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. |
-Plasma exchange
-Corticosteroids |
|
Immune Hemolytic Anemias
|
-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 |
Warm antibody types
Cold antibody types Paroxysmal cold antibody type |
|
Describe the difference between the direct and indirect antiglobulin test. What is this test used for?
|
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. |
|
|
Myasthenia Gravis
|
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? |
Muscle weakness.
|
|
Inflammatory Vasculitides
|
-Group of inflam. disorders that target the vascular system
-Inflammation of the blood vessels |
|
|
Pemphigus Vulgaris
|
-Autoantibody against keratinocytes
-Causes blistering of the skin and mucus membranes -Potentially fatal due to infection |
|
|
Multiple Sclerosis
|
-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? |
-Demyelinating plaques around the lateral ventricles.
|