intro to autoimmune diseases and rhuematoid arthritis Flashcards
Development of autoimmune diseases
spectrum between organ specific and non-organ specific. E.g., hashimotos is thyroid specific, systemic lupus erythematous is non-organ specific
caused by antibodies targeting cell - leads to tissue damage. genetic factors that can be precipitated by pregnancy, infection, diet and environment.
Autoantigens are present in everyone, however some develop autoantibodies too. not everyone that has autoantibodies have autoimmune diseases. self-tolerance prevents auto antigens to activate the immune system. this tolerance is lost in autoimmune diseases.
Examples of autoimmune diseases
Hashimoto’s disease. hypothyroidism from antibodies for thyroid gland. causes fatigue, weight gain, cold. women 7x more likely to get it. age and heredity are factors in it. treated by levothyroxine.
Graves diseases is autoantibodies that stimulate the thyroid to produce thyroxine. treat by inhibiting thyroid hormone production
T1DM caused by a mix of autoantibodies: glutamic acid decarboxylase (in 80%), for B-cell proteins (70%) and for insulin (50-60%). treated by exogenous insulin.
systemic lupus erthematosus sees anti-dsDNA antibodies in 80%. sees joint pain, tiredness, skin rashes. severe cases cause lung, heart and renal inflammation. treated by immunosuppressants
Crohns and ulcerative colitis could be autoimmune. possible trigger of gut microbiome changes. autoantibodies found in 80-90% of UC patients and antibodies found against microbes in crohns. suggests UC had autoimmune component and crohns relates to bacteria
Osteoarthritis cause pathophysiology and treatments
Characterised by cartilage loss especially in knees hips and hands. linked to obesity. worsened by movement and worse at the end of the day. treated with steroids, NSAIDs/COX-2 inhibitors or surgery
COX-1 produces PGs in the GIT that increase bicarbonate secretion. COX-2 treat the pain with less GI disturbances
Steroids are injected intra-articular when the pain is moderate to severe and can cause cartilage loss or injury
Rheumatoid arthritis and rheumatoid disease cause and symptoms
a chronic inflammatory disorder caused by antibodies against citrullinarted proteins (such as fibrin, vimentin, fibronectin and collagenase) - structural proteins. causes joint damage, muscle wastage and deformity.
marked by increased WBC, increased erythrocyte sedimentation rate, anaemia, and rheumatoid factor (antibodies to IgG)
Older age, postpartum and smoking increase risk. women have heightened risk premenopausal, but equal risk after.
Pain improves with movement and is worse in the morning. affects small joints more
Rheumatoid disease is a systemic disease that mainly effects joints. 50% see eye inflammation. nodules can form on skin. Can see inflammation in lungs, vasculature (vasculitis), salivary glands, and pericardium (pericarditis)
RA symptomatic and steroid treatments mechanisms
treatment times to relieve pain or to modify the disease progression
NSAIDs (+ PPI) used to ease pain. DMARDs, steroids and biologics to slow progression
Steroids are given IM, IA, or IV. used to bridge therapy between or at beginning DMARDs. Prednisolone used orally for anti-inflammatory and immunosuppressive actions. Predfoam is a formulation used in enemas for rectal inflammation
Activity at glucocorticoid receptors stimulates transcription of Annexin A1, B2-AR, IKB (NF-KB inhibitor), MKP1 (phosphorylates MAPK - inhibitor), and promotes antiinflammatory cytokines. it represses transcription of inflammatory cytokines, chemokines, inflammatory enzymes (e.g.m iNOS, COX-2), and inflammatory peptides (e.g., endothelin-1)
Annexin A1 inhibits the synthesis of PGs and LTs. does this by inhibiting the activity of phospholipase A2 (PLA2), which forms arachidonic acid out of membrane phospholipids.
