Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
82 Cards in this Set
- Front
- Back
What are the most common fracture sites in osteoporosis?
|
Vertebrae (most common), femoral neck, pubic rami, radius (wrist), rib
|
|
What are the non-modifiable risk factors for osteoporosis?**
|
Age, sex, race, body size, genetics, previous fx/ relatives w/ hx, chronic illness/ poor health, dementia, endocrine
|
|
What are the modifiable risk factors for osteoporosis?**
|
Low Ca+, low vit D, exercise (too little OR too much), low body weight.**
Also: etoh, caffeine, smoking, low sex hormones |
|
What are meds used for osteoporosis?**
|
Steroids, anti-seizures, thyroid replacement (synthroid), antisex hormones
|
|
What is the main treatment for osteoporosis?
|
Calcium, vit D, bisphosphonates
|
|
Dx of osteoporosis?
|
Labs, xray, DEXA to confirm
|
|
What are polymyalgia rheumatic and temporal arteritis (giant cell arteritis)?
|
Polymyalgia rheumatica is a rare, inflammatory condition that causes pain or aching in the large muscle groups, especially around the shoulders and hips.
TA: inflammation that damages large and med size arteries. Many ppl have both PMR and TA. |
|
What patient pops are usually at risk for PMR and TA?
|
Women more than men, >60 yo
|
|
What are the symptoms of PMR?**
|
Morning stiffness (shoulder, hip), sudden onset, knee effusions, carpel tunnel.
|
|
What lab changes would you see in PMR?
|
Increased ESR, CRP and anemia
|
|
What is tx for PMR?**
|
Low dose steroids (10-20 mgs prednisone). Most pts have a rapid response.
|
|
What are the classic sx of temporal arteritis?**
|
HA, Visual loss*, temporal artery tenderness, jaw claudication, fever, weight loss, PMR
|
|
What is treatment for TA/GCA?**
|
High dose steroids*, 60 mg prednisone IMMEDIATELY, then daily thereafter.
Call ophthalmologis for bx** |
|
For which (of PMR and TA) would you give low dose vs high dose steroids?
|
PMR: low dose.
TA: high dose. |
|
What would you use to treat RA as a combo therapy?
|
2/3 DMARD (disease modifying antirheumatic drug) + biological
Don't use two biologicals together --> side effects |
|
What should you know about RF in testing for RA?**
|
Never base diagnosis solely on RF! Not diagnostic. Many false positives and false negatives. RF positivity increases w/ disease duration, high titer more meaningful and worse prognosis.
|
|
What is anti-CCP (cyclic citrullinated peptide)?**
|
Newer test for RA. More specific and more sensitive, but not essential for dx. High titer = worse prognosis.
|
|
What would you see on PE in RA?**
|
Symmetry, soft tissue swelling, PIPs, MCPs and wrists
|
|
What xray findings would you expect in RA?**
|
Symmetrical and bilat joint space loss. PIPs, MCPs. Atlanto-axial subluxation (transverse ligament gets eroded), corner erosions of small joints ("mouse bite erosions")
|
|
What is an important extra-articular manifestation of RA?**
|
Pulmonary interstitial fibrosis (MAY INTERACT W/ METHOTREXATE). Very similar to methotrexate pulmonary toxicity.
|
|
What are some advances in RA treatment that have been made?**
|
Early, aggressive intervention improves outcome, Methotrexate! (main tx, low side effects, cheap, widely used). Biologic agents! (humira, remicade, etc).
Combo therapy!!: DMARD + another DMARD or biologic. |
|
What are 5 indications of a poor prognosis of RA?**
|
High anti-CCP, High RF, erosions, high esr or crp, extra-articular manifestations
|
|
What lab tests would you work up for RA?
|
ESR, CRP, RF, Anti-CCP, ANA, CBC
|
|
What are the pros of treating RA with oral steroids?**
|
Good for treating flares, minimizes or controls disease activity
|
|
What are the cons of treating RA with oral steroids?**
|
Higher doses or duration means more side effects. Difficult to discontinue
|
|
What are precautions to take into consideration with using oral steroids to treat RA?**
|
Glucose, bone density, bp, weight gain , cataracts
|
|
What is the Gold Standard treatment for RA?**
|
Methotrexate. - Basic first line treatment.
|
|
How is Methotrexate administered?**
Dose?** |
PO, IM, Subcu, IV or intra-articular. Parenteral absorbed better than PO>
2.5-25 mg once a week. |
|
What are possible side effects of Methotrexate?**
|
Megaloblastic anemia (folic acid deficiency), leukopenia, thrombocytopenia, rash, oral ulcers, increased liver enzymes, GI upset.
|
|
When would you want to treat RA with DMARDS (hydroxycholoroquine, sulfaslalzine) instead of Methotrexate?
|
Mild disease or if methotrexate isn't working well enough. (can also be given in combo w/ methotrexate).
|
|
What is a side effect of Hydroxychlloroquine (Plaquino) (DMARD)?
|
Can rarely cause macular inflammation. Need to have an eye exam once per year.
|
|
What is carpel tunnel syndrome?
|
Median Nerve dysfunction due to trauma, disease or compression
|
|
What are the symptoms of Carpel Tunnel syndrome?**
|
Numbness, pain, weakness of first 3.5 fingers
|
|
What are the signs of carpel tunnel syndrome?**
|
Swelling, Tinel's sign, Atrophy of thenar or interosseous muscles first 3.5 fingers.
|
|
What is Tinel's sign?
|
Way to detect irritated nerves. Involves light tapping over the area of the nerve looking for tingling or pain.
|
|
What risk factors are associated with carpel tunnel syndrome?**
|
Idiopathic, endocrinopathies (DM, hypothyroid), RA, PMR, isolated or repetative trauma (most common!)*, pregnancy, obesity
|
|
What should you do first if suspecting a Baker Cyst (PTP - pseudo- thrombophlebitis)?**
|
Rule out DVT!! with doppler US.
Then: PE, xray, labs if approp, synovial fluid analysis |
|
What are the extra-articular manifestations of a RA?
|
Anemia, fever, weight loss, vasculitis, pulm fibrosis, pericarditis, pleuritis, nodules, Felty's syndrome (RA, low WBC, enlarged spleen)
|
|
What is SLE?
|
Multi-system autoimmune disease/ connective tissue disease
|
|
What are the criteria for classification of SLE?
|
Malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis, nero disorder, hematologic disorder, immuno disorder, ANAs, renal disorder
|
|
What is a reasonable INITIAL lab screen for SLE?**
|
CBC, esr, UA, RF, ANA, CK, RPR or VRDL for syphilis, chem panel, thyroid functions
|
|
What is ANA?
|
Antinuclear antibody - INDIRECT immunofluorescent test, primary test for SLE
|
|
What is a reasonable SECONDARY lab screen for SLE when ANA is pos?**
|
Complement (decreased), DNA binding (increased), ACLs (anti cardiolipin), LAC (lupus anti-coag)
|
|
What systems are most invovled in SLE?
|
Joints (most), skin, serositis, kidney, Raynaud's, mucosa, CNS
|
|
What is Swan Neck deformities in SLE?
|
Extension deformity at PIP and flexion deformity at DIP. Due to lysis of flexor tendons at PIP
|
|
What are 6 joint issues in SLE?
|
Early inflammatory arthritis, non-deforming arthritis, Swan neck deformities, Ulnar drift, RA erosive arthritis, aseptic necrosis (bony mineralization increased)
|
|
What is indicated if a patient has renal involvement in SLE?
|
Much worse prognosis
|
|
What is treatment for SLE?
|
Usually benign, annoying and easily controlled. Treat clinically probs, not lab tests.
NSAIDS, Plaquenil, mtx, steroids, benlysta, immunizations |
|
What are two exceptions to minimal treatment for SLE?
|
High or increasing anti-DNA antibodies, Low or decreasing C3 or C4.
|
|
What is the correlation between thromboembolitic disease and SLE?
|
Increased risk. Anti-phospholipids, Lupus anti-coag. Plaquenil may help by inhibiting platelet aggregation and adhesion.
|
|
What is APLS (anti phospholipid antibody syndrom)?
|
Assoc w/ SLE or other connective tissue diseases, but can also be isolated. Hypercoagulable state.
|
|
What are the clinical criteria of APLS?**
|
Venous thrombosis, arterial thrombosis, miscarriage, thrombocytopenia, hemorrhage (due to treatment).
|
|
What is Sjogren's syndrome?
|
Exocrine glands that produce tears and saliva dysfunction due to autoantibodies against them.
|
|
What should you expect to see in Sjogrens syndrome?**
|
Dry eyes, dry mouth, painful sex due to lack of lubrication.
|
|
What autoimmune disorders are associated with Sjogrens?
|
SLE, RA, PSS, PM/DM, Cryoglobulinemia, autoimmune hepatitis
|
|
What is the Schirmer test?
|
Paper put in eye to determine if eyes are being lubricated. If paper stays dry, decreased tears.
|
|
What is polymyositis and dermatomyositis (PM/DM)?
|
Weakness and pain in all muscles.
|
|
What is it important to test enzymes in PM/DM?**
|
Need to know them in order to identify medication side effects.
|
|
What enzymes effect the muscle only?**
|
CPK, Aldolase
|
|
What enzymes effect the liver only?**
|
ALT. If ALT is normal, then Myositis is not drug-induced
|
|
What does a normal ALT tell you in PM and DM when CPL and aldolase are elevated?**
|
Muscle is the source of PM
|
|
What does an elevated ALT but normal CK and aldolase tell you in PM?**
|
Liver is the source.
|
|
What is PSS (progressive systemic sclerosis, scleroderma)?
|
Extremely rare, progressive fibrosis/ sclerosis of skin and other organs. Pulmonary or renal involvement can be fatal.
|
|
What is Fibromyalgia?**
|
Chronic pain syndrome with painful points in characteristic locations. Muscular - NOT articular.
Assoc w/ a sleep abnormality. |
|
What is the criteria for dx fibromyalgia?**
|
Widespread pain, axial pain must be present, at least 11 of 18 tender points, pain present at least 3 months, can be assoc w/ illnesses
|
|
What is management of fibromyalgia?**
|
Education, meds, pt, exercise, trigger point injections of steroid + lidocaine or botox. Does not cure disease.
|
|
What are 9 tender point locations in fibromyalgia?
|
Occiput, low cervical, trap, supraspinatus, second rib, lateral epicondyle, gluteal, greater trochanter, knee
|
|
What are common drugs used for fibromyalgia?**
|
Approved: Savella, Lyrica, Cymbalta**
Unapproved: NSAIDS, Anti-depressants, analgesics, anti-seizure* TCAs* (amitriptyline, imipramine, nortriptyline) |
|
What is the SINGLE LARGEST CATEGORY of known "causes" of fibromyalgia?
Cause: precipitating event, not patho-phys |
Trauma - physical injury
|
|
What should be a concern when prescribing pain meds for fibromyalgia?
|
Addiction potential of opioids.
No perfect tx for chronic/ acute pain, numerous treatments. |
|
What are the 4 basic types of pain?
|
Nociceptive (pain caused by stimulus), neuropathic, acute, chronic
|
|
What occurs in chronic pain neurologically?
|
Pain signals are generated for no reason and may be intensified. Pain continues even after healing due to structural CNS changes that alter neural transmission.
|
|
What are several treatments for chronic pain?
|
Treat underlying disease, PT, Topical agents, tylenol, aspirin/nsaids, local injections, nerve blocks, opioids, implantable pumps, surgery
|
|
What are 4 types of topical pain treatments for chronic pain?
|
Steroids, capsaicin, lidocaine, nsaids
|
|
What are co-analgesics?
|
Enhance analgesia when combined w/ an opioid.
|
|
What are 3 examples of co-analgesics?**
|
Anti-depressants (tcas, snris), analeptics (anti-seizure), nsaids.
|
|
What is the most effective modality of pain control? No target organs..**
|
Opioids.
|
|
What are the disadvantages of opioids?**
|
Social stigma, regulatory pressures. **
Physical dependence doesn't necessarily signify addiction. |
|
Is physical dependence an addiction?**
|
NO**
|
|
What is addiction?**
|
Compulsive drug-seeking despite harm.
|
|
What is the most commonly prescribed opioid, most commonly prescribed analgesic, and most commonly prescribed medication in the US?
|
Hydrocodone
|
|
What are some side effects of opioids?
|
Constipation, itching, n/v, urinary retention, dependence, addiction potential, decreased sex hormones, sedation
|