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This Concept Map, created with IHMC CmapTools, has information related to: Summer Week 3 Mind Maps (RA, Kawasaki, OA), Case 2: Kawasaki Disease Anatomy autoimmune vasculitis characterized by inflammation of the mucous membranes, lymph nodes, lining of the blood vessels (vascular endothelium), and heart. Coronary artery involvement (major complication) Lymph nodes: enlargement and inflammation., Case 2: Kawasaki Disease Related Disorders Patients often develop coronary artery abnormalities resulting in aneurysms, thrombosis, and MI if left untreated. infantile periarteritis nodosa – pathologically identical. scarlet fever, staphylococcal toxic shock syndrome (TSS), Stevens-Johnson syndrome (erythema multiforme), leptospirosis, EBV, juvenile rheumatoid arthritis, measles, acrodynia, polyarteritis nodosa, Rocky Mountain spotted fever, drug reaction, and scalded skin syndrome., Case 3: Osteoarthritis Physiology Limited to joint affected Articular cartilage is connective tissue that lacks blood supply, innervation, or lymph drainage.It is made up of hyaline cartilage that is composed of cells (chondrocytes) and extracellular matrix (fibers and ground substance). Chondrocytes are responsible for the maintenance of the extracellular matrix and play a key role in the cartilage destruction found in osteoarthritis. Early stage, chondrocytes actively divide and produce extracellular matrix substances, but do not aggregate well to be stabilized. And it releases enzymes to degrade the extracellular matrix and inhibit matrix synthesis, ie, IL-1, TNF-α, TGF-β, and prostaglandins. Over time, remodeling and hypertrophy of the bone occur as a result of osteoclast and osteoblast activity. Osteoclast leading to appositional bone growth and sclerosis. At the margins of the joints there is further growth of bone and cartilage, resulting in osteophytes or bone spurs. Increased stress on the bone is one trigger for this process. Therefore, in osteoarthritis, increased repetitive stress on the articular surfaces of the bones of affected joints leads to the start of this remodeling process. The final result is thicker, denser bone that can better withstand the increased forces that occur once the cartilage has been lost. Osteoarthritis is due to mechanical stress on joints, so obesity is a risk factor due to increased mechanical stress. Prior trauma can also be a risk factor as can age., Case 3: Osteoarthritis Anatomy Osteoarthritis, a degenerative joint disease, is the most common form of arthritis. It is characterized by the slow progressive loss of articular cartilage, the formation of new bone at the appositional surfaces of the joint, as well as the formation of osteophytes at the joint margins. There are no systemic manifestations of this type of arthritis. Disease is often asymmetric and localized to just a few joints. The most commonly affected joints are weight-bearing joints, such as the hips, knees, and spine. However, small joints of the hands (first carpometacarpals, proximal and distal interphalangeals) and feet (metatarsophalangeals) can also be affected., Case 2: Kawasaki Disease Sign/symptoms Criteria: Fever for 5+ days +4: bilateral Conjunctival injection, Rash, Cervical lymphadenopathy, Oropharyngeal changes (strawberry tongue), Skin changes (Hand/foot swelling, peeling) 3 phases: Acute (cervical adenitis, conjunctivitis, changes in mucosa, rash, hand/foot swelling, and erythema); Subacute (Desquamation, coronary aneurysm +/- arthritis); Convalescent (Baeu lines of nails) Enlarged lymph nodes ; Labs: elevated ESR, neutrophil count, and platelet count, Case 3: Osteoarthritis Sign/symptoms Worsens with activity and better with rest. Heberden nodes OA mainly affects DIP, PIP, 1st CMC; hip; knee Joint pain in osteoarthritis typically worsens with activity and is relieved by rest. Stiffness is most pronounced after periods of immobility. The pain may initially be intermittent and mild but worsens as the disease progresses. With severe disease there is decreased range of motion in the affected joints as well as nocturnal pain., Case 1: Rheumatoid Arthritis Anatomy RA is a chronic, inflammatory disease that can affect multiple organ systems, including skin, blood vessels, heart, lungs, and muscles. destruction of articular cartilage = most common manifestation, Case 1: Rheumatoid Arthritis Sign/symptoms Initial symptoms: insidious with vague prodromal symptoms of malaise, weight loss, and joint stiffness. The stiffness is most pronounced in the morning and after periods of inactivity. Symmetric joint swelling, warmth, tenderness, and pain are noted. Subcutaneous rheumatoid nodules located over bony prominences Extra-articular manifestations: pericarditis, pleural disease, and vasculitis (less common) Progressive joint destruction: Boutonniere deformity of the fingers (hyperextension of the DIP joint with flexion of the PIP joint), and swan neck deformity of the fingers (flexion of the DIP joint with extension of the PIP joint)., Case 1: Rheumatoid Arthritis Biochemistry Destruction of cartilage caused by the release of TNF-a and interleukin-1 (IL-1) → release of collagenases → inhibit the synthesis of proteoglycans in cartilage Proteases and elastases are released by neutrophils that alter the normal structure of the joint., Case 1: Rheumatoid Arthritis Microbiology RA is suspected to be caused by exposure to a microbial antigen, Case 2: Kawasaki Disease Biochemistry ROS can cause oxidative stress and damage to cells and tissues, contributing to the inflammatory response and endothelial dysfunction. endothelial cell dysfunction, characterized by increased expression of adhesion molecules and decreased production of nitric oxide (NO) platelet activation: thromboxane A2, platelet-derived growth factor (PDGF), and serotonin ( → inflammation, vasoconstriction, and the formation of blood clots)., Case 3: Osteoarthritis Biochemistry The inhibition of COX-1, which is constitutively active, is causing the stomach issues. COX-1 secretes gastroprotective substances that are inhibited by NSAIDS., Case 2: Kawasaki Disease Pharmacology Tx: IVIG and high-dose aspirin (100mg) Intravenous immunoglobulin (IVIG): administered within the first 10 days of the illness. Helps modulate the immune response, reduce inflammation, and decrease the risk of coronary artery complications. Aspirin: reduces inflammation, alleviates fever, and prevent the formation of blood clots during the acute phase. Anticoagulant: For coronary artery involvement, Case 2: Kawasaki Disease Microbiology Causes of infectious vasculitides: Neisseria, syphilis, Rocky Mountain spotted fever, herpes Potential viral triggers: human coronavirus, adenovirus, parvovirus B19, Potential bacterial triggers: Streptococcus pyogenes (group A streptococcus) and Staphylococcus aureus., Case 1: Rheumatoid Arthritis Related Disorders Differential diagnosis: ankylosing Spondylitis, Reiter Syndrome, SLE, Osteoarthritis, gout, chronic Lyme disease, polymyalgia rheumatica., Case 2: Kawasaki Disease Physiology secreted cytokines target vascular endothelial cells, producing cell-surface neoantigens. IL-6: acute febrile illness and increased acute phase reactants IL-2, TNF-α, IL-1a: acute cutaneous responses. triggered by an abnormal immune response following an infection or exposure to certain environmental factors. Immune system dysregulation, Vascular endothelial dysfunction, Inflammatory cascade, Formation of immune complexes, Case 3: Osteoarthritis Pharmacology NSAIDs will non-selectively inhibit COX-1 and COX-2, which is what is causing the stomach issues. Celecoxib is a selective COX-2 inhibitor that has been shown to reduce GI side effects usually associated with NSAIDS. Celecoxib can have adverse CV side effects and may be contraindicated in this patient due to hypercholesterolemia and obesity. Acetaminophen is a non-NSAID that works in the CNS to modulate pain and fever. It is not anti-inflammatory. It would likely be a good choice for this patient because she does not have inflammation or contraindications., Case 1: Rheumatoid Arthritis Physiology CD4 memory T cells: play primary role in immune reaction. Inflammation: Increased expression of intracellular adhesion molecules-1 (ICAM-1) at synovial vessels → neutrophils, plasma cells, and macrophages are recruited Progressive joint destruction: inflammatory infiltrate (CD4 cells, plasma cells, and macrophages) fills the synovial stroma and causes inflammation and erosion., Case 3: Osteoarthritis Related Disorders rheumatoid arthritis, SLE, seronegative spondylopathies (ankylosing spondylitis, Reiter syndrome, psoriatic arthritis), gout, pseudogout, and septic arthritis, obesity., Case 3: Osteoarthritis Microbiology None