MSK disorders

Answer 1

Bursitis

1. Definition
2. Compare arthritis to bursitis
3. Risk factors?
4. Prepatellar first line?
5. Other site first lines
6. When to do cortisone shot? risks and SE?
7. Bursa and common presentations.

Lateral epicondyltis is tennis elbow

medial epicondylitis is golfers elblow

1. treatment
2. Grip strength for both is reduced.

Answer 2

Gout

1. Path/Epi:
2. Risk factors including medications.
3. Causes of secondary gout
4. OLDCarts - presentation
5. tophi description and locations
6. dx:
7. treatment
8. Medications for treatment indications and contraindications
9. Chronic gout medication
10. Prevention medications?

allopurinol, febuxostat, probenecid,

MOA and SE

11. dietary modifications?

12 purpose of 24 hour urine collection

13. Psudeogout path/symptoms
14. Risk factors and associations
15. Diagnosis
16. treatment

Question 3

Path:

Progressive loss of articular cartilage with reactive changes at joint margins and in subchondral bone

Primary osteoarthritis (OA)

Idiopathic: categorized by clinical features (localized, generalized, erosive)

Secondary OA

Posttraumatic

Childhood anatomic abnormalities (e.g., congenital hip dysplasia, slipped capital femoral epiphysis [SCFE], Legg-Calvé-Perthes disease)

Inheritable metabolic disorders (e.g., Wilson disease, alkaptonuria, hemochromatosis)

Neuropathic arthropathy (Charcot joints)

Hemophilic arthropathy

Endocrinopathies: acromegalic arthropathy, hyperparathyroidism, hypothyroidism

Paget disease

Noninfectious inflammatory arthritis (e.g., rheumatoid arthritis [RA], spondyloarthropathies)

Gout, calcium pyrophosphate deposition disease (pseudogout)

Septic or tuberculous arthritis

Femoral acetabular impingement (FAI)

System(s) affected: musculoskeletal

Synonym(s): osteoarthrosis; degenerative joint disease (DJD)

Epidemiology

Symptomatic OA most common in patients >40 years

Leading cause of disability in patients >65 years

Predominant sex: male = female

90% of hip OA is primary.

Hip OA is more common in whites.

Prevalence

Most common Joint disease

Etiology and Pathophysiology

Failure of chondrocytes to maintain the balance between degradation and synthesis of extracellular collagen matrix. Collagen loss results in alteration of proteoglycan matrix and increased susceptibility to degenerative change.

Biomechanical, biochemical, inflammatory, and immunologic factors contribute to cartilage loss. Attempts at repair most commonly manifest as osteophyte formation.

Risk Factors

• Increasing age: >50 years
• Age as a risk factor is greatest for hip and knee OA.
• Hand OA is most common in postmenopausal women.
• Obesity (weight-bearing joints); BMI >35
• Small critical shoulder angle (<30 degrees) can predispose to shoulder OA.
• Trauma, infection, or inflammatory arthritis
• Female gender (knee and hand)

Diagnosis s/sx

• Distinguish OA from other types of arthritis by:
• Absence of systemic findings
• Minimal articular inflammation
• Distribution of involved joints (e.g., distal and proximal interphalangeal joints)
• OA characterized by slowly developing joint pain. Pain often described as aching or burning in nature. Anecdotally, many patients describe pain changes with alterations in weather conditions.
• Transient stiffness (especially after awakening in morning and after sitting) that tends to lessen 10 to 15 minutes after joint movement

Most common locations?

OA more commonly affects hands, spine, and large weight-bearing joints (hip, knee).

Physical Exam

• Joint bony enlargement (Heberden nodes of distal interphalangeal joints; Bouchard nodes of proximal interphalangeal joints)
• Decreased range of motion of affected joints (2/2 effusion)
• Mechanical symptoms (clicking, locking) may be present, especially in knees with degenerative meniscal injury.
• Crepitation is a late sign.
• Local pain and stiffness with OA of spine; radicular pain (if compression of nerve roots)
• Changes in joint alignment (genu varum [bowlegs] and genu valgum [knock-knees])

Differential Diagnosis

• Crystalline arthropathies (gout; pseudogout): inflammatory arthritides (RA), spondyloarthropathies (reactive arthritis; psoriatic arthritis), septic arthritis
• Fibromyalgia; avascular necrosis; Lyme disease

Diagnostic Tests & Interpretation

Initial Tests (lab, imaging)

Routine chemistries are not helpful in diagnosis.

X-rays are usually normal early in disease process.

As OA progresses, plain films show?

• Narrowed, asymmetric joint space
• Osteophyte formation
• Subchondral bony sclerosis (increased density)
• Subchondral cyst formation
• Erosions may occur on surface of distal and proximal interphalangeal joints (erosive OA).

MRI may particularly demonstrate chondral degeneration and associated meniscal tears. 5–10% weight loss is associated with slowing of arthritic changes and decreased chondral loss on follow-up studies (1).

Follow-Up Tests & Special Considerations

May be useful in monitoring treatment with NSAIDs (renal insufficiency and GI bleeding)

In secondary OA, abnormal lab results associated with underlying disorder (e.g., hemochromatosis [abnormal iron studies])

Diagnostic Procedures/Other

Joint aspiration (not usually necessary for diagnosis)

Can help distinguish OA from other arthritides

OA: cell count usually <500 cells/mm3, predominantly mononuclear

Inflammatory: cell count usually >2,000 cells/mm3, predominantly neutrophils

Birefringent crystals in gout (−) and pseudogout (+)

Test Interpretation

Macroscopic patchy cartilage damage and bony hypertrophy

Histologic phases:

Extracellular matrix edema and cartilage microfissures

Subchondral fissuring and pitting

Erosion and formation of osteocartilaginous loose bodies

Subchondral bone trabecular microfractures and sclerosis with osteophyte formation

Degradation secondary to release of proteolytic and collagenolytic enzymes, prostaglandins, and associated immune response

Treatment

General Measures

Weight management combined with exercise/physical therapy demonstrates most improvement in patients with OA.

Physical therapy to maintain or regain joint motion and muscle strength

Quadriceps-strengthening exercises relieve knee pain and disability.

Transition to non–weight-bearing exercises (i.e., elliptical, stationary bike, swimming)

Exercise must be maintained; benefits are lost 6 months after exercise cessation.

Protect joints from overuse; ambulatory aides are beneficial as is proper-fitting footwear.

Bracing, joint supports, or insoles in patients with biomechanical instability:

Bracing is more beneficial in patients with unicompartmental disease of the knee.

For knee OA in particular, several nonpharmacologic modalities are strongly recommended: aerobic, aquatic, and/or resistance exercise and weight loss.

Nonpharmacologic modalities that are conditionally recommended for knee OA include medial wedge insoles for valgus knee OA, subtalar strapped lateral insoles for varus knee OA, medially directed patellar taping, manual therapy, walking aids, thermal agents, tai chi, self-management programs, and psychosocial intervention.

Medication

First Line
Manage pain and inflammation:

Acetaminophen up to 1,000 mg TID–QID: effective for pain relief in OA of knee and hip

Topical NSAID gels, creams have short-term (<4 weeks) benefits. Topical NSAIDs are a core treatment for hand and joints with minimal soft tissue–coverage (i.e., hand) OA. Diclofenac gel 1% can be applied as needed up to QID.

If acetaminophen or topical NSAIDs are insufficient, consider an oral NSAID/COX-2 inhibitor. Use the lowest effective dose for the shortest time possible.

May use nonacetylated salicylates (e.g., salsalate, choline-magnesium salicylate) or low-dose ibuprofen ≤1,600 mg/day

Topical NSAIDs and capsaicin as alternatives to oral analgesic/anti-inflammatory medications in knee OA

NSAID contraindications:

All PO NSAIDs/COX-2 inhibitors have analgesic effects of a similar magnitude but vary in their potential GI and cardiorenal toxicity.

NSAIDs should be avoided in patients with renal disease, CHF, HTN, active peptic ulcer disease, and previous hypersensitivity to an NSAID or aspirin (asthma, nasal polyps, hypotension, urticaria/angioedema).

Combination of NSAIDs and full-strength aspirin (325 mg) is contraindicated.

In patients at high cardiovascular risk: Combination of a nonselective NSAID and low-dose aspirin (81 mg) is recommended.

Oral or parenteral corticosteroids are contraindicated.

ALERT
http://www.health.harvard.edu/blog/fda-strengthens-warning-that-nsaids-inc…

Precautions:

If PO NSAID/COX-2 inhibitor use is necessary for a patient aged >65 years or a patient <65 years with increased GI-bleeding risk factors, proton pump inhibitors are recommended.

Significant possible interactions:

NSAIDs reduce effectiveness of ACE inhibitors and diuretics.

Aspirin and NSAIDs (except COX-2 inhibitors) may increase effects of anticoagulants.

Salicylates reduce effectiveness of spironolactone (Aldactone) and uricosurics.

Corticosteroids and some antacids increase salicylate excretion, whereas ascorbic acid and ammonium chloride reduce salicylate excretion and may cause toxicity.

Pregnancy Considerations

ASA and NSAIDs have reported fetal risk during 1st and 3rd trimesters of pregnancy.

Compatible with breastfeeding

Second Line

Topical capsaicin is an adjunct therapy for knee and hand OA.

Topical NSAIDs (e.g., diclofenac gel) can lower gastric and renal risks associated with oral NSAIDs.

Rubefacients (e.g., oil of wintergreen) are not recommended.

Physical therapy: Core strengthening for hip OA and knee muscle strengthening for knee OA decrease joint reactive forces and can relieve pain.

Physical therapy demonstrates minimal benefit compared to sham treatment in randomized trial in patients with severe hip OA (2)[A].

Bracing; medial and lateral unloader braces are effective; long leg alignment x-rays can help determine the appropriate brace.

TENS modalities for pain may be more beneficial than hyaluronic acid (HA) injection (3)[A].

Third Line

Intra-articular corticosteroid injections can be used for acute flares and for patients failing first- and second-line treatments. Minimize injections (<2 per joint per year).

Long-lasting corticosteroid injections are increasingly available; outcomes have not yet been definitively compared to traditional corticosteroid injections.

The use of viscosupplementation injections for OA remains controversial. There is no clear evidence for benefit from HA injections.

Platelet-rich plasma (PRP) is more effective than HA injections for early-stage knee OA (4)[B].

Bone marrow aspirate concentrate (BMAC) demonstrates good outcomes for patients with mild to moderate knee OA; not recommended for patients with severe knee OA (5,6)[C]

HA combined with PRP demonstrated better outcomes in patients with knee OA than either in isolation (7)[A].

TENS is effective for pain relief in large-joint OA.

Ultrasound improves injection accuracy.

Additional Therapies

Address psychosocial factors (i.e., self-efficacy, coping skills). Screen for and appropriately treat anxiety and depression. Improve social support.

Surgery/Other Procedures

Total knee arthroplasty (TKA) may be necessary if conservative management fails.

Knee arthroscopy is not routinely recommended for the treatment of OA in the absence of clear mechanical symptoms (i.e., locking, clicking, etc.).

Complementary and Alternative Medicine

Nutritional supplements (glucosamine and chondroitin sulfate) may benefit some patients and have low toxicity. There is lack of standardized outcome assessments. Trial results using glucosamine and chondroitin have been mixed. If no response is apparent within 6 months, discontinue use.

TENS, yoga, and acupuncture have shown benefit.

Ongoing Care

Follow-up Recommendations

Patient Monitoring

Regularly assess range of motion and functional status.

Monitor for GI blood loss and cardiac, renal, and mental status in older patients on NSAIDs or aspirin.

Periodic CBC, renal function tests, stool for occult blood in patients on chronic NSAID therapy

Patient Education

American College of Rheumatology: http://www.rheumatology.org/public/factsheets/index.asp…

Arthritis Foundation: http://www.arthritis.org

Prognosis

Progressive disease: early in course, pain relieved by rest; later, pain may persist at rest and at night.

Joint effusions and enlargement may occur (especially in knees) as disease progresses.

Osteophyte (spur) formation, especially at joint margins

Advanced stage with full-thickness loss of cartilage at which point joint replacement is a consideration

Complications

Leading cause of musculoskeletal pain and disability

Decompensated CHF, GI bleeding, decreased renal function on chronic NSAID or aspirin therapy

Answer 3

OA

Most common joint disease in NA

1. S/sx?
2. Most common site and most problematic joints?
3. Risk factors
4. Path:
5. PE
6. Radiologic findings
7. expected lab findings
8. Therapeutic goals and lifestyle changes.
9. Exercise recommenations for hip and knee
10. Medication recommendations
11. Recommendations and AE of glucosamine and Chondroitin
12. Recommendations on intra-articular corticosteroid injection or hyaluronic.
13. when is joint replacement considered?

Answer 4

RA

1. Path
2. Epidemology
3. Risk factors:
4. Clinical picture
5. progression/sequalae of RA
6. Classification for RA in new patients

7 radiographic findings

8. general lab values
9. Hemogram
10. Treatment goal; lifestyle and exercise management.
11. Medications for symptom control and reduced disease progression.
12. recommended use of corticosteroids? Dmards? Biologics?

antimalarial drugs: hydroxycholroquine

Immune suppressors: methotrexate, axathiopine,

TNF-1 inhibitors: infliximab

NO tofacitinib: JAKs inhibitor - antiinflammatory path

13. vaccinations when starting a biologic
    14: COX-1
    15: COX-2
    16: Serious side effects of Benlysta? belimumab

increased SI; progressive multifocal leukoencephalopathy; life-threatening infections.

Answer 5

Sjogren syndrome

1. Path
2. S/Se
3. Labs and procecdures for diagnosis
4. Intevention

Answer 6

SLE

1. path:
2. s/sx?

Oral/nasal ulcers (usually painless)

Arthritis, arthralgia, myalgia, weakness

Pleuritic chest pain, cough, dyspnea, hemoptysis

Early stroke (age <50 years), unexplained seizure/psychosis (LR+) = 13,

cognitive deficits

Proteinuria, cellular casts

Hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia

Abdominal pain, anorexia, nausea, vomiting

Raynaud phenomenon

3. Pregnancy concerns?
4. dx:
5. Treatment including medications?

5a Exams needed for use of hydroxycholorquinone.

6. SE of treatment with specific s of belimumab.

Answer 7

Meniscal tears

1. Where most often seen?
2. S/sx?
3. Classification?
4. Describe McMurry test
5. Describe the epley

6 What imaging? When?

7. Initial treatment? when to aspirate?
8. Next steps if no response to initial treatment?

Answer 8

carpal tunnel

1. Path
2. risk
3. Primary prevention
4. Type of pain reported? classic presentation and name
5. PE findings? phalen, tinels, best test, later disease?

6 What are two diagnositc tests?

7. Compare/contrast EMG and nerve conduction studies

8, treatment: including

9. medications
10. Failure of treatment next step and purpose.

Answer 9

Sarcoidosis

1. Path: What are the primary locations?
2. Epidemiology?

3, What are s/sx?

4. PRoblems with diagnosis?
5. Common labs? imaging? Confirmation?

Answer 10

Low back pain

1. How soon does acute low back pain end without intervention? %?
2. Risk factors
3. Most common type of low back pain?
4. s.sx?
5. When should immediate xray imaging be done? MRI/CT scan?
6. When to choose MRI? When to choose CT?
7. Description and risk factors for disk herniation
8. Most common sites? Symptoms of radiculopathy
9. Neck pain causes common causes/ most common site?
10. Herniated disk early sign?
11. Management including lifestyle and pharm.
12. Referral? what are some red flags?

13 What nerve roots does straight leg test evaluate?

L5 and S1

14 What does a loss of posterior tibial relfex show leson?

L 5

15. Loss of achilles tendon reflex?

L5 to S1

16/ Test pf a[[;oed [resire to head with neck bending forward, pain or numbness in upper extremetires?

spurling

Answer 11

Reactive arthritis or Reieter syndrome\seronegative multisystem inflammatory disorder: involves joints, eye, lower GU, Axial joints ( spine sacroiliac joints) and dermatoligic involvement. (can’t see. can’t pee, can’t bend my knee)

TRiggers

sexually transmitted infection or infectious diarrhea

1. Dx. two or more symptoms with one muskleoskeltela.
2. Onset?
3. Lab values of significance?
4. Treatment? when should an ABX be considered?
5. What abx for urethritis?

Answer 12

Osteoporosis

1. Calcium requirements for men 50-70? women 51 and older + men > 70? Vitamin D for individual > 50?
2. Screening recommendations?
3. first line antiresoprtive medicaitons?
4. second line anti resorptive medications?
5. RANKL inhibitor
6. anabolic medications?

Answer 13

Sprain

1. What is a sprain?
2. pathology of Grade I, intervention and length of rest
3. pathology of Grade II, intervention and length of rest
4. pathology of Grade III, intervention and length of rest
5. When is referral recommended?

Answer 14

Tendonitis

1. Tendinitis vs tendonosis definition?
2. Tendinitis vs tendonosis healing time and use of medication
3. Common sites
4. Clinical presentation
5. Rotator cuff symptoms and associated activities
6. Bicep tendonitis associated activites and symptoms
7. Wrist tendonitis
8. Dx and any required studies?
9. Treatment of tendonitis

Answer 15

Fibromyalgia

1. 1.Path?
2. Epidemiology?
3. dx:
4. ACR criteria?
5. Life style interventions?
6. Medication?