Musculoskeletal Disorders Flashcards
What is osteoporosis?
Loss of matrix, porous matrix, atrophy of bone.
What is a complication of OP because of the fragile bone?
Fracture (minimal force).
What are 3 etiologic factors for OP? 2 major risk factors?
Ageing, genetic predisposition (PBM), endocrine changes. RF: low PBM, post-menopause (loss of E)
What role does E play in maintaining bone health?
Limits bone breakdown/osteoclast activity
What is the patho for OP? When does one reach PBM? When does longitudinal bone growth stop?
30 years. 20 years. Architectural changes inside bone + microscopic damage sets in. Basically more matrix is being removed than is being laid, therefore the matrix becomes porous and bone density is reduced.
Up until when are manifestations of OP usually silent? What areas of the body are affected by OP (3)?
Fracture (acute, severe pain). Damage to vertebrae (change in stature - hunched over), distorted spine (breathing issues), dentition issues.
How can OP be diagnosed?
XRAY in advanced cases (substantial porosity), bone density scan (looks at absorption and transmission of light through radius, neck of femur + lumbar spine - lower value = more porous).
What is a major thing we want to avoid in OP? What are 5 treatment methods?
Prevent fractures. Pain + disability, weight bearing activities, antiresoprtive agents (osteoclasts), anabolic agents (osteoblasts), adequate Vit D, protein, calcium.
What is OA? Which joints are affected first? What is lost in this disease? How fast is the progression?
Degenerative joint disease. Weight bearing joints. Cartilage between bones in joints + sunchondrial bones. Slow.
What are the 2 etiologic factors for primary OA? alte
Wear + tear with ageing, genetic predisposition (defective gene coding for protein that maintains cartilage - cartilage injures easily + does not repair properly)
What is the etiologic factor for secondary OA? What two factors does obesity play?
Injury, obesity, professional sports (repetitive joint movement). OBESITY: 1. carry more weight therefore more stress on joints (wear + tear) 2. low-grade systemic disease of inflammation - adipose tissue somehow has some metabolic impact on joint.
Normal, physiologic cartilage has what 3 features?
Smooth + is surrounded by fluid for a no friction environment, is weight bearing, and will dissipate force to bone by “deforming”
What is the patho for OA?
Composition + properties of cartilage, then cytokines are released by chondrocytes triggering the release ++ proteases which destroys cartilage. Chondrocyte damage leads to an impaired ability to heal cartilage.. Cartilage deteriorates - the bone makes contact with bone - sclerosis of bone (inc density to make stronger so it doesn’t erode) - then cysts and fissures appear as fluid enters cracks in bones - and bone forms osteophytes (projections) inside joints resulting in joint enlargement + deformity
What is an initial manifestation of OA? Later? Finally, 2 more manifestations?
Non-localized aching pain. Activity-related pain to weight bearing joints. Crepitus + stiff, inflamed joints.
How is OA diagnosed (4)?
Hx, Px, xray (not always useful), labs (to rule out other joint problems like septic arthritis)
What are 3 treatment methods for OA? 1st line? What are 3 treatments for severe OA?
Monotherapy pain meds PRN. Acetaminophen (1st line), COX 2 inhibitors. SEVERE: intra articular steroid injection (is cortisone), PT, Sx (joint replacement).
What 2 things does the enzyme cyclooxygenase 2 do? By giving COX 2 inhibitors what are we achieving?
Mediates/advances inflammation + leads to the production of prostaglandin (PG). Preventing both of those from happening.
What is RA? Which joints are affected first? Then later which joints? What type of HS reaction is this? Is this disease systemic or localized to an area of the body?
Chronic autoimmune CT disease resulting in inflamed + deformed synovial joints. Non weight-bearing + then weight bearing. Type 3. Systemic.
What is the etiology for RA?
Complex trait - viral trigger (EBV?), genetic mutation (MHC/HLA).
Touch on the 3 main patho points for RA.
- altered T cell response results in targeting of synovial membrane leading to inflm + damage to joint. 2. Altered B cells produce rheumatoid factors (RF) autoantibodies that target tissue. 3. RF forms IC that deposit in synovial membrane resulting in inflm. Repeated inflm - deformity of joint - pannus forms inside joint
In RA, what is a pannus? What 4 issues arise when this is formed?
A pannus is granulation tissue that forms within a joint. It: occupies space in the joint, releases enzymes that destruct the cartilage, has damaging inflammatory cells, and reduces the joints mobility.
What two types of deformities are there in the hands of someone with RA?
Swan neck deformity + ulnar drift/shift
Are the manifestations limited to the joints, or are there some unrelated to joints? Which manifestations appear subtly (2) in RA? What are 3 other articular manifestations? What body systems/structures are also affected in RA (5), and why?
Both. SUBTLE: low grade fever, malaise. Increased fatigue, AM joint pain (stiffness), and stiffness after activity. NON ARTICULAR: heart, BVs, skin, eyes, lungs. Because there is CT distributed throughout the body.
How is RA diagnosed? (5)
Hx, Px, exclude other diseases of the skeleton, X-ray (not revealing early on), labs (RF antibodies).
What is an issue with the validity of testing for RF antibodies in RA?
Not everyone tests positive for these Ab, only about 75% of people do, especially in early stages of RA.
What is important to remember about the treatment of RA? What pain management can we do? Other meds? What if the immunomodulatory doesn’t work, what’s next?
Limit progression. Meloxicam or naproxen (NSAID). Immunomodulatory (Plaquenil). Maintain pain meds + Sulfasalazine (anti-inflammatory + immunomodulatory) + methotrexate
What is an issue with using Plaquenil as a drug for RA? What class of drug is this? What 2 properties does this drug have?
Antimalarial. The drug deposits in the eye so need an eye exam every 6-12 months. It is an anti-inflm + immunomodulatory.
If someone is receiving methotrexate for RA, what are some important diagnostics to get?
CBC (antifolate), liver Es (hepatotoxic), creatinine monthly.
What is gout? What compound causes this?
Crystal-induced joint disease. Uric acid crystal deposit in joints from building up in circulation.
For primary gout, who does it most commonly affect? What is the main cause?
95% men. Metabolic issue.
For secondary gout, what are 4 etiologic factors?
Excessive cell turnover/destruction, renal problem, alcohol ingestion (beer), and chemo.
What is the patho for primary gout?
Altered purine (adenine + guanine) breakdown which leads to asymptomatic hyperuricemia. Later: crystals deposit in synovial joints, WBC influx + complement action occurs - WBC phagocytize the crystals resulting in WBC necrosis and enzyme release resulting in inflammatory joint damage - recurrent acute attacks happen and tophi form
What is a tophi/tophus?
Accumulation of uric acid crystal, the lesion present in gout.
What are the stages one progresses through in gout?
- Asymptomatic hyperuricemia. 2. acute inflm (over night - usually in one joint like big toe and usually following alcohol binge or heavy meal, drugs, or excessive exercise). 3. issue subsides in about a week. 4. asymptomatic hyperuricemia maintains and joints are affected more frequently + different joints now affected too.
