Lecture 40 March 14th-msk

1DDX: LECTURE 40 – MARCH 14th, 2007 CONDITIONS OF THE MUSCULOSKELELTAL SYSTEM Page 1 This presentation will be on E-College, for the slides that we can’t read. Case What are her signs and symptoms? What jumps out at you in this case? Post-menopausal, she smokes and drinks. History of HRT, has back pain. The majority of these are not “signs and symptoms” but rather, they are risk factors. OSTEOPOROSIS Osteoporosis is a disease that presents as “risk factors”. Takes about 4 months for bone remodelling to occur (see diagram) It is normal to lose bone as we age (0.7% per year) After menopause: rapid bone loss (about 5%). Levels out at 1-2% per year. Osteoporosis: DEXA T score is used: measure of skeletal bone density. (we will talk about this test later in lecture) Assesses fracture risk. Page 2 10-20 million Canadians and Americans have been diagnosed with osteoporosis 20-30 million have osteopenia (precursor to osteoporosis). Role for us as NDs. If you are 50 or over, you have a 40% chance of having an osteoporotic fracture in your life. Consequences of fracture: loss of mobility, independence. Psychological effects. Major risk factors: age, gender, race. Age: 5X increased risk / decade Genetics: plays a big role: this is being investigated currently. Asymptomatic presention (often) until there is a fracture. Vertebrae: first area of complaints (pain, fracture) Palpate area of pain: identify deformity, pain, tenderness. Look at curvature of spine. PE will often be completely normal. Even if there is a fracture, it may not present with pain. Measure height over time! See other points on PE (notes) Page 3 Can have primary or secondary OP. Look at the systemic hormones that are involved in bone growth. Parathyroid hormone: decreases bone mass (leads to bone loss) Calcitriol: Increases bone mass Calcitnin: increases bone mass Estrogen/testosterone: increases bone mass Growth hormone: increases bone mass Thyroid hormone: decreases bone mass Cortisol: decreases bone mass Causes: anything that affects these hormones will have effect on bone density. M/C causes of osteoporosis: aging and glucocorticosteroid use. DDX to consider: • Sex hormone deficiency: hard to DDX: rapid onset of bone loss, no sxs until fracture, hot flashes, differentiate this through blood testing. (MC cause of osteoporosis) • Excess oral glucocoricoids (especially those on chronic doses: worse prognosis re: fractures). Can be exogenous intake or endogenous (Cushings). Bone loss (dose-dependent), First 3 months of intake of steroid: worst fracture risk. • Osteomalacia: abnormal metabolism of minerals (Ca, Mg, Vit D). Can happen at same time as osteoporosis (what came first?) • Hyperparathyroidism: Look at lab tests: see increased serum calcium, decreased phosphorus. X-rays look a little DDX LECTURE 40, MARCH 14th, 2007 – PAGE 1

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different: see subperiosteal bone resorption happening in hyperparathyroidism. Osteogenesis imperfecta: often presents in children (see path notes!), blue sclera, tendency to fracture (brittle bone disease) Mutiple myeloma: other symptoms: anemia, thrombocytopenia.

Lab tests: used to decide if this is a primary or secondary condition. (not covered in detail) Page 4 Clinical risk categories: Extremely high: has diagnosis of OP and has had fracture. Should have DEXA T scan in 6 months to a year (other categories are 2 years). Fracture is not obvious, compound fracture: may be miniscule compression fracture that the person doesn’t notice. MC preliminary fractures are in vertebrae. Very high: (whether post-menopausal or not!) High: this category would apply to patient in our case at beginning of class. Frailty fracture: an immediate diagnosis of osteoporosis. Moderate: can be any of these factors. Diagnosis: based on bone mineral density. Estimate fracture risk factor. Criteria determining whether someone should undergo BMD testing. Major diagnostic test: DEXA. 2 different x-ray frequencies sent through body, subtracts soft tissue effects, you are left with measure of bone mass (this is “bone scan”) SPXA: old system CT: not used much QUS: done on the foot: some controversy over this. Not diagnostic: can be used as a general screen, but have to follow up with a DEXA anyway, so not highly recommended. Biochemical markers: not clinically used. Not enough standardization in markers themselves. Just used to ID drug treatment and effects on bone remodelling. (blank slide in notes: picture of patient getting DEXA scan. Same radiation per site as what we are exposed to in a day) Trabecular bone is most affected by bone loss. Measure non-dominant hip. Below –2.5 is OP In hips, won’t see compression fractures, other factors that make the bones look denser than they are. Treatment is long-term (life long, as bone loss is life long) If you are post-menopausal and have a fracture, you will start treatment regardless of BMD. Page 5 First 2 items on Allopathic list are considered for all patients (osteopenic, osteoporotic). Should be considered even prior to menopause. Bisphosphoates: drugs given 1x per week, (used to be low dose, daily). Inhibit bone resorption. Problem: give too much, will inhibit bone mineralization. Decrease risk of hip fracture by 30-50%. (FYI: eg. Of this type of drug is alendronate, risedronate). HRT: women with high risk factors, or who have not been helped by other treatments. Raloxifene: affects estrogen receptors. Helps vertebral fractures, not helpful with hip fractures. Calcitriol (Vit. D) More effective with vertebral fractures, esp. for pt. With KI issue. Cacitoin: not very effective Teriparatide: Human parathyroid hormone. Only treatment to increase bone formation. (we just said that PTH leads to bone loss!) In intermittent treatment, stimulates bone formation. In constant dose, decreases bone formation. “success” of treatment is decreasing fracture risk factor. 20-30% of those with hip fracture need to be institutionalized and 30% die (men more so than women. Psychological impact harder on men?) DXA=DEXA (chief DX tool, progress monitoring) **Prevention is key** Once bone is lost: impossible to replace it with structurally normal bone. Can replace 5-10 over 5 years (this is optimistic) Naturopathic treatment options (didn’t cover this in detail)

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Page 6 Case #2 Enlarged joints vs. swollen joints. Is it bony enlargement, or is it tissue effusion/swelling? (Important DDX) In slide: Heberden nodes, Bouchard nodes without redness (in hands): leaning towards OA. OSTEOARTHRITIS “Degenerative Bone Disease” is a better description, there isn’t constant inflammation. There may be secondary inflammation, but it is not an inflammatory disease. Almost the entire population will have some joint degeneration over their lifetime. Unlike OP, OA is not a disease of “risk factors”: there are definite symptoms. Not the same differences in age, race, gender as with osteoporosis. Men get OA earlier than women. Page 7 Significant factors: mechanical factors (can include obesity) and age. Presentation: Stiffness on waking, but it is very brief. 15-20 minutes. Once it is limbered up, it improves. Signs: crepitus of knee, hip. Locking/catching of joint during manipulation. Limit in ROM. No lab tests: everything seems normal. Exclusionary diagnosis. Synovial fluid analysis: can be useful. (see next slide) “Clear glass test” of synovial fluid. If you can read print through it, not an inflammatory condition. Poly: = polymorphonucleocytes (general categories: includes WBC and others). Definitive diagnosis through radiograph. Key features: decrease in joint space (cartilage destroyed and narrows joint space). Decrease in cushioning, of bones, bone responds with increased sub-chondral bone density. Might see osteophytes, pseudocysts. Can be erosive, inflammatory, rapidly destructive. Pain is characteristic: better rest, worse movement and weight bearing. Know that the PE distinguishes between inflammatory and non-inflammatory condition We are not responsible for the “clinical classification charts” Page 8 X-ray of arthritic/normal hips: No joint space Increase of sub-cortical bone density See pseudocyst (darker area) Page 9 Morning stiffness? Yes: could be variety of things Short lived? OA = short lived Obesity risk factor in OA Allopathic treatment: reduce pain. Paracetamol=acetaminophen (Tylenol) First drug of choice. Know first and last drug for test (don’t need to know rest of flow chart on this page.) First: Acetaminophen. 2nd: topical agents/glucosamine 3rd: NSAIDS Opiates/Tramadol Last: injections of glucocorticoids.

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Page 10 Naturopathic modalities: every one will have an impact! This is a “tip of the iceberg” list. Not tested ND treatments. Exercise: should be the first focus of treatment. All mammals show signs of degenerative disease of vertebrae. Exceptions: the bat and the sloth. They hang upside down: joint decompression! Inversion table? Prognosis: All slides on this page covered quickly: not much detail. Page 11 Bone tumours OSTEOSARCOMA (OSTEOGENIC SARCOMA) Diagnosis by X-ray, but the effectiveness of this is variable. May get chemo with or before surgery. Most common malignant tumour. Page 12 CHONDROSARCOMA Outstanding feature: likes to seed to soft tissue. Also: this occurs in adulthood, not in rapid-growth years. Biopsy is definitive High recurrence and mortality rate. Have to ensure that all of tumour is removed. Page 13 EWING’S SARCOMA Very proliferative: can involved entire shaft of long bone. Biopsy is devinitive diagnosis. Radiograph: there is a slight elevation on tibia on medial aspect. Tumour in SC region: much worse prognosis. Page 14 Benign tumours of the bone OSTEOCHONDROMA Young age group again. Characteristic: cartilaginous cap. Benign bone tumour, but if it presents in multiple sites, it has a 10% chance of becoming malignant chondrosarcoma. CHONDROMAS Umbrella term for group of benign tumours. Will look at Enchondromas. Can happen at any age or sex. Tends to occur in hands. Page 15 GIANT CELL TUMOURS Rare, benign, but aggressive. Would see soft tissue swelling, depending on size of tumour. Occur spontaneously: no known risk factors, although may be linked to hyperparathyroidism? DDX for OA: worse activity, better rest. Doesn’t stop growing: leads to destruction of bone and joint. Page 16 Embolization: cut off blood supply to the tumour. Has a tendency to re-occur, but it doesn’t metastasize. Case: Radiograph: see growth in proximal femur. Circular opacity with luminescent centre (typical of osteoid osteoma) Very characteristic presentation is paid worse at night, better with low dose ASA.

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OSTEOID OSTEOMA It is believed that it will correct itself: respond spontaneously, but surgery usually performed d/t intensity of pain.

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