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;
80 Cards in this Set
- Front
- Back
What is autoimmune adrenalitis?
|
The most common cause of adrenal failure in countries where TB is controlled
|
|
What is Anergy?
|
An irreversible inactivation of Tcells when tcells recognize self antigen, without costimulatory molecules
|
|
Autoimmune, males or females more?
|
10:1 female to male
|
|
Molecular mimicry happens by what vectors?
|
Bacteria and viruses
|
|
Name four examples of molecular mimicry as autoimmune dz
|
1. C. jejuni and anti-ganglioside ab = Guillan Barre
2. EBV and anti-myelin = MS 3. Coxsackie virus and anti-glutamic acid = diabetes mellitus 4. Yersinia and TSH ab = Graves |
|
How would molecular mimcry explain arthritic disorders?
|
1.Leukocyte CD11/CD18 looks a lot like B. burdoferi.
2. HLA B27 is the explanation of Reiter's and Rxt arthritis |
|
What are the 3 signs of Reiter's syndrome?
|
A Rxt arthritis, conjunctivitis and urethritis in response to a virus
|
|
What acne cream can induce autimmune dz?
|
minocycline
|
|
What is HLA?
|
Human leukocyte antigen, the HLA B27 is associated with spondyloarthropathies
|
|
What is autoimmune lymphoproliferative syndrome(ALPS)?
|
1.A mutation in the FAS and FASLigand that are upstream apoptotic effectors.
2. Lymphadenopathy, splenomegaly 3. Increase hodgkins risk |
|
How to link estrogen to autoimmune?
|
Estrogen withdrawal leads to upregulation of GM-CSF, IL-1, IL-6 and TNF. So all the immune cells with be increased.
|
|
Why administer IgG in an autoimmune?
|
Block the Fc receptors of macrophages, and attenuate complement induced injury. Decreases immune complex formation
|
|
What is RhoGAM and why give it for chronic ITP?
|
A serum antibody. It will induce hemolytic anemia and tie up the macrophages and prevent platelet destruction.
|
|
What is Immune Thrombocytopenic Purpura?
|
ITP is ab mediated platelet destruction. Happens to IIa/IIa or Ib/IX. Destroys the platelets in the spleen
|
|
What autoimmune is most associated with non-hodgkins lymphoma?
|
Sjorgrens then SLE
|
|
What is Rituximab and CD20?
|
All mature b-cells have CD20. Rituximab will tell those b-cells to stop producing CD20 and stop making antibodies
|
|
Primary Biliary Cirrhosis autoantibody?
|
Anti-mitochondrial
|
|
Diabetes mellitus Ab?
|
Anti insulin
|
|
Goodpasture's syndrome ab??
|
Anti basement membrane
|
|
Grave's Dz ab?
|
anti TSH-R
|
|
Hashimoto's ab?
|
antithyroglobulin
|
|
myasthenia gravis ab?
|
anti ACH-R
|
|
Pernicious anemia ab?
|
Anti parietal cell and anti intrinsic factor
|
|
Rheumatoid arthritis ab?
|
anti-EBV related antigen(mimicry)
|
|
Sjogren's syndrome ab?
|
Anti salivary duct epithelium, anti-SSA and antiSSB
|
|
Organ specific dz of the collagen system?(4)
|
1. Hashimoto's/graves
2. DM 1 3. Celiac 4. MS |
|
Multisystem dz of the collagen system?(4)
|
1.SLE
2. RA 3. Sjogren 4. ANCA related(wegener's, churg straus, RPGN) |
|
SLE epi?
|
1. 12 to 1 female to male in adults and 2 to 1 in children
2. 15-45 age of onset 3. Whites the least |
|
Give five criteria for Dx SLE?
|
1. Malar and discoid rash
2. Oral ulcer 3. Antinuclear antibodies(ANA, anti-dsDNA and anti-Smith) 4. Arthritis 5. Renal, neurologic, and hematologic disorder |
|
What is a discoid lesion?
|
A rash that looks like a 1/2 dollar
|
|
What is SLE prognosis based on?
|
Usually based on the kidney dz cause thats what most die from
|
|
What are some characteristics of male SLE?
|
1. More severe
2. Mitral valve prolapse |
|
What causes the malar rash?
|
Immune complex deposition at the dermal/epidermal junction
|
|
What happens to lymph nodes in SLE?
|
Hyperplasia
|
|
5 Main organ systems involved in SLE?
|
1. Kidney
2. Heart 3. Skin 4. Joints 5. Lymph nodes |
|
What is complete ankylosis?
|
Complete fusion of the synovial membrane and loss of movement in SLE
|
|
Why does 'onion skin' thickening of the splenic arteries occur in SLE?
|
Because of the increase in smooth muscle and fibroblasts
|
|
Describe focal segmental glomerulonephritis?
|
1. Focal = few
2. Segmental = parts 3. A few glomeruli in parts of the kidney are dying because of sub epithelial IC depositions from SLE |
|
Why does the lumpy bumpy occur in type 3 and smooth pattern occur in type 2?
|
Type 3 is caused by random immune complex deposition and Type two is caused by uniform destruction
|
|
Describe libman sach's endocarditis?(3)
|
1. non bacterial seen in SLE
2. Most common cardiac symptom is SLE 3. APLS causes a precipiation of platelets and fibrin |
|
What two things happen to the heart in SLE?
|
Endocarditis and premature atherosclerosis
|
|
What IL is increased in the spine during SLE?
|
IL-6
|
|
What are the neurologic symptoms in SLE?
|
Serizures, dementia, meningitis etc
|
|
What are 4 abnormal immune responses in SLE?
|
1. Hyper active B Cells
2. Hyperactive T cells 3. Abnormal phagocytic function not as effective 4. Abnormal immunoregulation because of C2, C4 deficiency |
|
What is a classic LE cell?
|
1. Neutrophil or macrophage that has phagocytized the nucleus of an injured cell
|
|
What are the best SLE tests?
|
1. Anti-dsDNA
2. Anti-smith |
|
How would you test for ANA and give it more credibility?
|
1. Get blood
2. Add IgG and flourescent 3. Gives rim, speckled or nucleolar if positive |
|
What is Rim, speckled, nucleolar, and homegenous ANA tests associated with?
|
1. Rim = anti-dsDNA
2. Speckled = Mixed CT Dz 3. Nucleolar = Scleorderma 4. Homogenous = anti-histone |
|
What tests for Sjorgrens?
|
1.SS-A or SS-B, anti-Ro or anti-La
|
|
Best SLE test?
|
Speckled anti-Smith, but only 25% of all SLE people
|
|
Main drug that induces SLE?
|
Dilantin
|
|
Use ANA testing in these dz?
|
1. mixed CT DZ
2. Autoimmune hepatitis 3. drug induced SLE 4. SLE, sclerosis and sjorgrens |
|
What are the three criteria for hughes?
|
1. Thrombotic event
2. Thrombocytopenia 3. Multiple miscarriages |
|
What causes Lipman sach's endocarditis?
|
1. SLE
2. Proteins in the heart valve |
|
Why is clotting time prolonged in APLS?
|
1. Phospholipids are needed to add to the clot
2. The phospholipids are being destroyed in this syndrome |
|
Why is Sjogrens a problem?
|
1. Because it has a high association with malignant lymphomas
|
|
What should you look for in Sjogrens?
|
1. Swollen parotids
2. Dry eyes/mouth 3. Hypergammaglobulinemia |
|
What happens when you test coagulation in sjogrens?
|
1. Normal individual will have a small drop 10-15 mm
2. Sjorgrens will have an 80mm drop like multiple myeloma 3. The hypergammaglobulinemia has added so many extra cells |
|
What is morphea?
|
A white patch of localized skin thickening
|
|
How should you Dx Raynauds?
|
1. Exclude all other Dx
2. Make sure you get all CT symptoms listed 3. Check the nailbed capillaries 4. Check for autoantibodies |
|
What is sceleroderma?
|
1. Excessive fibrosis
2. Autoantibodies 3. Vascular alterations |
|
What is sclerodactyly?
|
Triangular fingers
|
|
What other part of the body does scleroderma involve?
|
The lungs as pulmonary fibrosis
|
|
What is CREST syndrome?
|
1. Limited Cutaneous Scleroderma
Calcinosis Raynauds Esophageal dysfunction Sclerodactyly Telangiesta |
|
What is Telangiesta?
|
Small dialated BV near the surface of the skin
|
|
What does CREST do to the skin?
|
The scleroderma causes scar tissue formation. Eventually destroys the BV, causes decreased circulation and necrosis in the capillaries.
|
|
What happens in acral sclerosis?(3)
|
The scleroderma at the fingertips. Causes Raynauds and sclerodactyly, Eventually necrosis.
|
|
What is Raynauds face?
|
1. Taught skin
2. Malar skin |
|
What happens in the lungs of progressive systemic sclerosis?
|
1. Reticulo nodular crossing
2. Increased collagen makes the lungs shorter |
|
What ab for CREST and progressive scleroderma?
|
1. Anti-centromere
2. Anti-Scl70 |
|
What can GAD causes?
|
1. Joint immobility
2. Want to use macrolytic(less free GAD) forms or Dialysis |
|
What is polymyositis?(3)
|
1. Chronic inflammatory myopathy
2. Inflammation, atrophy and apoptosis of SKM 3. Has Anti-synthetase ab |
|
3 ANCA dz associated with vasculitis? Plus 1?
|
1. Microscopic Polyangitis
2.Wegner's 3. Churg strauss Also Chronic Ulcerative Colitis |
|
Describe Microscopic Polyangitis?(5)
|
1. ANCA dz
2. Destruction of PMNs intravascular 3. Necrosis of endothelium 4. Crescenteric Glomerulonephritis 5. Pulmonary capillaritis |
|
Describe wegener's?(6)
|
1. ANCA
2. Sinusitis for 3ms 3.Hematuria 4. Cough 5. Antibiotics don't work 6. Saddle nose |
|
What is phemigus?
|
1. Seperation of epidermis from dermis at the desmosome
2. Areas become open sores |
|
What is rheumatoid arthritis?
|
A systemic inflammation of the skin, joints, lungs and BV
|
|
What is the pathology of rheumatoid arthritis?(5)
|
1. CMI synovitis
2. Synovial cell hyperplasia = pannus 3. Angiogensis 4. RANKL osteoclastic activity 5. Fibrosing ankylosis |
|
What is the Pannus?
|
Inflammatory matrix of B and T lymphocytes, macrophages, PMNs, capillary channels, and fibroblasts
|
|
D/D for rheumatoid arthritis?
|
1. Ghonorrhea can also invade PMNs in the synovial fluids
|