Rheumatology 3 Flashcards

(42 cards)

1
Q

Fibromyalgia: Give the general overview

A

Characterized by WIDESPREAD chronic musculoskeletal pain with multiple tender points, cause is unknown
Pain and stiffness is diffuse, but predominates in the neck, shoulders, low back, and hips
Affects 3-10% of the general population, most common in women 20-50 years old

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2
Q

Fibromyalgia: Describe the clinical manifestations

A

1) Characterized by a NORMAL physical exam, except for “trigger points” in various areas of the trapezius, medial fat pad of the knee and lateral epicondyle of the elbow
2) This may be accompanied by other somatic symptoms, particularly fatigue and sleep disturbances, as well as cognitive and psychiatric disturbances
3) These symptoms occur in the absence of abnormal lab findings and negative imaging studies

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3
Q

How do you Dx fibromyalgia?

A

CRP/ESR will be normal, no specific autoantibodies noted
Radiographs will not show joint destruction, narrowing, or effusions
This is a DIAGNOSIS OF EXCLUSION
You must rule out other causes of symptoms first

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4
Q

Fibromyalgia:
1) What are the diagnostic criteria?
2) What must you rule out?

A

1) Multiple tender points (trigger points) that have been present for 3 months, and all lab tests and imaging studies are normal
2) You rule out other causes and other endocrine or rheumatological conditions (hypothyroidism, PMR, other seronegative rheumatoid diseases)

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5
Q

What meds show modest efficacy for fibromyalgia?

A

Amitriptyline (PANCE considers this treatment of choice)
Fluoxetine
Duloxetine
Gabapentin
Pregabalin
Cyclobenzaprine
Naltrexone

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6
Q

What is often helpful for fibromyalgia?

A

Mindfulness, meditation, CBT, exercise are often helpful

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7
Q

What is the prognosis for fibromyalgia?

A

All patients have chronic symptoms, but this is not a progressive disease, and objective findings do not develop
Patients may find comfort in earning a diagnosis since the road to it can be frustrating and long

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8
Q

Gout:
1) What is it characterized by?
2) What is the main lab finding?
3) Who is it seen in?
4) What causes most cases?

A

1) Characterized by recurring acute monoarticular arthritis that can develop into chronic deforming arthritis
2) Manifested by hyperuricemia (>6.8 mg/dL) or rapid fluctuations in serum urate levels
3) 90% of cases of primary gout are in males over 30 years old. In women onset is typically postmenopausal
4) Most cases caused by eating too much processed meats, fructose, alcohol, medications

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9
Q

What are the clinical manifestations of gout? Explain

A

1) Sudden onset of red, hot, swollen joint
-Podagra: large, erythematous, warm MTP joint of big toe, which is the most susceptible joint
2) Feet, ankles, knees can also be affected
3) Rapid onset, frequently nocturnal, exquisitely painful, fever common
4) Local desquamation and pruritus during recovery phase
5) Can have tophi formation: nodular deposits of urate crystals in soft tissue or joints that develop from elevated uric acid levels for prolonged periods of time
-Can lead to pain and ulcerations

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10
Q

What are the lab findings in gout?

A

Serum uric acid level may be elevated. It is better to do serial measurements since a single level can be normal in 12-43% of gout cases
A normal serum acid level does not EXCLUDE gout
May have neutrophilic leukocytosis, elevated ESR or CRP during flares

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11
Q

How is gout diagnosed? Explain

A

Establishes the diagnosis of gout
Aspirate shows negatively birefringent crystals that are “needle shaped” (this distinguishes from pseudogout which we will talk about next)
Culture-negative
Joint aspiration will rule out septic arthritis. If aspirate has WBC >50k, negative for crystals and starts growing something funky …it’s not gout

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12
Q

Describe gout on XR

A

X-rays are usually normal early in the disease
Later, they may show “punched out” erosions surrounding the joint, sometimes called “rat-bite” lesions

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13
Q

What are the 3 main ways to reduce inflammation during gout flareups? Explain each

A

1) NSAIDs (indomethacin or naproxen)
-Beware of NSAIDs contraindications: PUD, CKD, allergy
2) Colchicine (if symptoms have been present for less than 36 hours)
-Loading dose of 1.2mg, then 0.6mg one hour later
-Then 0.6mg BID until resolution of symptoms
-Do not use if there is kidney or liver impairment
3) Steroids (to be used as a last resort)
-May be given systemically, especially if other medicines are not an option
-Can be given as an intra-articular injection, but must r/o septic arthritis

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14
Q

How do you manage gout between attacks?

A

Goal is to minimize urate deposition in tissues and to reduce frequency and severity of attacks
1) Lifestyle changes: Change diet, decrease high purine intake (meats, high fructose, shellfish), reduce alcohol
2) Medication changes: Stop thiazide diuretics, loop diuretics, and niacin (these can precipitate a gout attack due to increasing uric acid levels)

If attacks keep occurring with lifestyle and medication changes, check uric acid when not having a flare, if elevated, then this indicates the cause

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15
Q

How do you manage a pt between attacks if they have >2 attacks/ yr or uric acid levels high even when not in a flair?

A

1) Target uric acid with allopurinol to prevent flares
Sometimes initiation of urate-lowering therapy can precipitate flares, likely due to an acute fall in levels. May need colchicine treatment for 3-6 months
Goal of allopurinol is to maintain serum uric acid levels less than 6 mg/dL.
Do not start during an acute flare. Treat flare first.
If flare starts after initiation, treat flare and continue allopurinol
2) Other medications:
Probenecid-uricosuric drug. Treatment of choice if patient has a good diet and 24-hour uric acid level is normal. This means their issue is underexcretion
Pegloticase- porcine-like uricase that is used in patients with severe, refractory gout. Given IV every 2 weeks

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16
Q

Pseudogout:
1) Who is it seen in?
2) What joints is it found in?
3) What can it mimic Sx of?

A

1) Prevalence increases with age, often seen in people over 60
2) Typically involves the larger joints, knee and wrist are most common. Can also affect shoulders, ankles, feet, elbows, etc.
3) PMR

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17
Q

What is the main test for pseudogout? Explain

A

Joint Aspiration + Fluid Analysis
-Since patient will present with sudden onset of a red, hot, swollen joint, it’s ideal to aspirate to get a good idea of what you are working with
-Aspirate will show positively birefringent crystals with rhomboid shape
-And remember, you will need to r/o septic arthritis

18
Q

How do you Tx pseudogout?

A

1) NSAIDs are the most helpful in acute attacks.
2) Colchicine 1-2 times daily works better for prophylaxis than for treatment of acute flares
3) Intra-articular steroid injections work well for symptomatic relief, depending on the joint
4) Systemic steroids are the last resort

19
Q

How common is osteoporosis?

A

Causes 1.5 million fractures annually in the U.S.

20
Q

List some other Fxs that may be seen in osteoporosis

A

Hip fractures (15% of women and 5% of men by 80 years old)
Distal radius (Colles’ fracture)
Pelvic fractures

21
Q

Besides being found incidentally, when else may you see this present?

A

Sometimes a patient will come in with or without back pain and complaining that they are getting shorter as they get older

22
Q

What are some common causes of osteoporosis?

A

Aging
Ethnicity
Sex
Hormone deficiency
Alcohol use
Cigarette smoking
Long term PPI therapy
High dose and/or chronic steroid use

23
Q

Laboratory testing is required to screen for secondary causes of osteoporosis; list and describe these tests

A

1) If low T-score, it’s recommended to obtain: BUN, creatinine, albumin, serum calcium, phosphate, alkaline phosphatase, and 25-hydroxyvitamin D
-2) If serum calcium is abnormal, need to obtain serum PTH
-3) CBC is usually normal. If anemia present, screen for plasma cell myeloma and intestinal malabsorption
-4) Test for thyrotoxicosis, hypogonadism, celiac disease if clinically indicated

24
Q

How can you prevent osteoporosis?

A

1) Diet should be adequate in protein, total calories, calcium, and vitamin D
2) Steroids should be d/c or reduced if possible
3) Smoking cessation is key
4) Avoid excessive alcohol intake
5) Exercise is recommended to increase both bone density and overall strength
-Reduces the risk of fractures due to frailty falls
-Both aerobic and resistance training
-Weight bearing exercises are best

25
Do you need to treat osteoporosis patients?
Treatment is indicted for most patients with osteoporosis, particularly if they have a recent or previous fragility fracture
26
Explain the role of Vit D in osteoporosis
Deficiency of vitamin D or calcium causes osteomalacia, rather than osteoporosis, but they often coexist and cannot be distinguished by DXA bone densitometry Hard to get recommended daily amount of vitamin D (600-800 IU/day) from diet alone, the sun, or in patients with intestinal malabsorption Oral vitamin D3 (cholecalciferol) is given as a supplement of 800-2000 IU/day Do not exceed 4000 IU/day since there is a risk of GI side effects or hypercalcemia
27
What hormones can help prevent osteoporosis?
Low dose transdermal systemic estrogen Testosterone replacement of low-dose transdermal estradiol therapy
28
Bisphosphonates: How do they work for osteoporosis? Who are they indicated for? Explain
Work by inhibiting osteoclast-induced bone resorption Alendronate, risedronate, ibandronate as examples Indicated for patients with osteoporosis in spine or hip or for patients with a pathological spine fracture or low-impact hip fracture To ensure intestinal absorption, must be taken in the morning with 8oz of water at least 40 mins before anything else. Typically given once weekly or monthly. Must remain upright to reduce risk of esophagitis Avoid in patients with CKD that have creatine clearance less than 35 IV options (infusions) are available (zoledronic acid)
29
Osteonecrosis of the jaw is a RARE complication of bisphosphonate therapy; explain
It is a painful, necrotic, nonhealing lesion of the mandible or maxilla, usually after a tooth extraction Risk increased with older age, in women, and in patients also receiving chemotherapy or corticosteroid therapy 95% of cases occurred with IV high-dose therapy. Only 5% have occurred with oral therapies or once-yearly infusions Important that patients on bisphosphonates receive regular dental care and try to avoid extractions when possible
30
Denosumab (Prolia) 1) What is it/ how does it work? 2) Is it well tolerated? 3) Does it work well?
1) Monoclonal antibody that inhibits proliferation and maturation of preosteoclasts into mature osteoclast bone-resorbing cells 2) Overall, very well tolerated, used if patient cannot tolerate bisphosphonate therapy due to side effects 3) Compared to oral bisphosphonates, denosumab appears to be slightly superior at improving BMD of the spine, total femur, and femoral neck and at reducing fracture risk after 2 years of therapy
31
PTH and PTHrP Analogs: 1) Give examples 2) Who is it indicated for? 3) How do they work?
1) Teriparatide (Forteo) and abaloparatide (Tymlos), feriparatide 2) Indicated only for patients with osteoporosis who are at a very HIGH fracture risk, especially if they have had multiple or severe vertebral fractures 3) Work by stimulating production of new collagenous bone matrix, particularly vertebral trabecular bone Must have sufficient intake of vitamin D and calcium
32
PTH and PTHrP Analogs: 1) How is it given? 2) What is a risk?
1) Given as a daily subcutaneous injection for up to 2 years 2) After 2 years, bisphosphonates should be given to retain improved bone density Potential risk of developing osteosarcoma with prolonged use
33
Selective Estrogen Receptor Modulators (SERMs) (Raloxifene): What is a positive side effect? What is it used in place of? What is a risk?
Also decreases risk of breast cancer by 76% Taken in place of estrogen therapy Increased risk of thromboembolic events
34
T/F: BMD densitometries (DXA scans) can detect whether progressive osteopenia or frank osteoporosis is developing
True
35
T/F: Dexa scans may need to be done earlier if patient at high risk or has had a previous fracture or an incidental finding on other imaging
True
36
Paget Disease of Bone (PDB): 1) What did it used to be called? 2) What does it do to the body? 3) What causes it?
1) Known historically as osteitis deformans 2) Characterized by abnormal and accelerated bone remodeling, resulting in overgrowth of bone at a single (monostotic PDB) or multiple (polyostotic PDB) sites -Leads to impaired integrity of the bone -Commonly affects the skull, spine, pelvis, and long bones of the lower extremity 3) Both environmental and genetic causes
37
Paget Disease of Bone (PDB): 1) How is it often found? 2) Where does it occur in the body?
1) Majority of patients are asymptomatic, so found incidentally on radiographs or because of high alkaline phosphatase found on routine labs -Serum calcium and phosphate levels are normal in most patients 2) Bone pain: most common symptom, classically in pelvis (most common site), axial skeleton, skull, long bones or femur pain due to stress fractures. May have secondary osteoarthritis
38
Paget Disease of Bone (PDB): Describe each body part it affects
1) Soft bones: bowed tibias, kyphosis, frequent fractures with slight trauma 2) Skull involvement: deafness (seen in 50% due to CN VIII compression), headache, vertigo 3) Bone tumors: Increased risk for primary bone neoplasms, particularly osteosarcoma
39
Paget Disease of Bone (PDB): What will labs show?
1) Markedly increased alkaline phosphatase, normal calcium and phosphate levels 2) Increase in urinary pyridinolines or increase in urinary/serum N-telopeptide (collagen breakdown markers increased during bone resorption)
40
Describe how radiographs will appear with PDB
Lytic phase: “blade of grass/flame shaped” lucency Mixed phase: lucency + sclerosis Sclerotic phase: coarsened trabeculae, denser/expanded bones Long bones may show multiple fissures Skull: “cotton-wool appearance”
41
Do most PDB pts need Tx?
Asymptomatic patients typically require no treatment
42
What are the 2 main PDB Txs? Explain each
1) Bisphosphonates -Treatment of choice (Alendronate, risedronate) -MOA = inhibits osteoclast activity (decreasing bone resorption & turnover) -Remember your counseling points for bisphosphonates 2) Calcitonin -Works by decreasing osteoclast activity -Typically given SQ or intranasally