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Session 4 CM Rheum-2
CM- Rheum -2- OA
| Question | Answer |
|---|---|
| What is the most common type of arthropathy | Osteoathritis |
| Is OA typically inflammatory or non-inflammatory | Non- Inflammatory |
| Does the pahtophysiology of OA vary depending on the joint type involved | no it is the same regardless of joint involved |
| What is OA | progressive deterioration and loss of articular cartilage leading to loss of normal joint strucutre and function |
| What is the primary etiology of OA | aging or idiopathic there cand be gentic such as Nodal OA |
| What is secondary OA | OA caused by disorders that damage joint surface |
| What are the pathological characterisitcs of OA | Altered chondrocyte function, loss of cartilage (thinning), subchondral bone thickening (sclerosis), Remodeling of bone, marginal spurs (osteophytes), cystic changes in subchondral bone and mild reactive synovitis |
| What are some systemic risk factors for OA | age, obesity, gentics, gender, menopause(?) |
| What are some local factors that can influence risk of OA | Muscle strenght, joint proprioception, repetitive use, configuration of joint, trauma |
| What are the common locations for OA | cervical spine, lumbar spine, 1st cmc (carpometacarpophalangeal), PIP, DIP, Hip, Knee, 1st MTP (metatarsophalangeal) |
| What are some uncommon locations for OA | SHoulder, Thoracic Spine, Elbow, Wrist, MCP (metacarpophalangeal), Ankle, Subtalar |
| What are the 7 subsets of OA | Generalized OA, Nodal OA, Spondylosis, Erosive OA, Inflammatory OA, Diffuse idiopathic skeletal hyperostosis (DISH), Chondromalacia patellae |
| Where are heberden's nodes found | DIP |
| Where are bouchards nodes found | PIP |
| Where is the most common location to find nodes in OA | Knees 3 compartments med/lat/pat-fem |
| What are the common symptoms of OA | insidious onset of joint pain w/ movement, limitation of motion, referred pain, minimal stiffness after rest, (systemic symptoms are rare)- acute flares of these symptoms suggest another dx |
| Why do you get pain in OA if the cartilage is avascualr and aneuritic | could cause synovitis, joint capsule/ligament stretchin, periosteal irritation from osteophytes, travecular microfractures, muscle spasm, intraosseous hypertension |
| What physical exam findings would you expect to find in an OA patient | Bondy changes in joint shape, crepitus, malalignement/instability, limited ROM, join line tenderness, cool effusions, spasm or atrophy of adjacent muscle |
| What lab tests are indicative of OA | non really but ESR and RF appropriate for age and synovial fluid shiould be class 1 (non-inflammatory) |
| What x-ray findings are indicative of OA | cartilage loss/joint space narrowing, subchondral sclerosis, osteophytes at joint margins, subchondral cysts |
| What is Genu Varus | bowleg |
| This type of OA is marked by exuberant osteophytosis of the spine spanning 3-4 vertebral segments with preservation of disc spaces. Ligament calcification is noted. | Diffuse Idiopathic Skeletal Hyperostosis (DISH) |
| Who is more affected with DISH diffuse idiopathic skeletal hyperostosis | M>F |
| What other pathology is diffuse idiopathic skeletal hyperostosis (DISH) associated with | Diabetes Mellitus |
| A person with dish may develop anterior cervical osteophytes what may that cause them to have | dysphagia |
| What are some of the ways to manage a pt with OA | education, weight reduction, nutriceuticals, topical agents, analgesics, NSAIDs, phyical therpay, occupational therapy, surgery, conditioning, Intra-articular steroids, Viscosupplementation, SMOADS (systemic modulating osteoarthritic drugs) |
| What are SMOADS (systemic modulating osteoarthritic drugs) in management of OA | MMPI, Residronate, Doxycycline, Glucosamine, Chondroitin |
| How is capsaicin work in tx of OA | it is a topical agent that can be rubbed on the joint it causes a rxn that with time will cause a person to exhaust their supply of substance P which without they don't have pain. |
| What is the primary analgesic in management of OA | acetaminophen (3g maximum per day) easily overdosed on |
| What is the definitive tx for OA | Surgery |
| What are the tx goals for OA | pain control, improve function, enhance health related quality of life, avoid Rx related side effects. Sadly there is not cure |
| What are the essential to dx of OA | degenerative disorder w/o systemic manifestations, pain relived by rest, morning stiffness, articular inflammation is minimal, x-ray finding of joint space narrowing, osteophytes, increased subchondral bone, bone cysts |
Created by:
smaxsmith
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