Exam 3 - Rheumatology Flashcards
(70 cards)
1
Q
What is fibromyalgia?
A
Disorder included with rheumatologic conditions - characterized by symptoms of widespread MS pain, fatigue, nonrestorative sleep, depression, HA, GI complaints (e.g. IBS)
- More than 3 months of MSK pain
2
Q
Fibromyalgia diagnostic considerations
A
- Must meet report of pain survey in 19 areas as well as severity of symptoms → replaced tender point examination
- More common in females, ages 40-50 years
3
Q
American College of Rheumatology criteria for diagnosing fibromyalgia
A
- WPI >7 and SSS score >5 OR WPI of 4-6 and SSS score >9
- Generalized pain (in at least 4-5 regions)
- Symptoms present for longer than 3 months
4
Q
Fibromyalgia clinical presentation
A
- Persistent widespread pain
- Chronic fatigue
- Somatic complaints → non restorative sleep, cognitive difficulties, auditory/vestibular/ocular complaints, chronic rhinitis or “allergies”, migraines, palpitations, IBS, subjective sense of joint swelling, mood disorders
5
Q
Fibromyalgia physical examination findings
A
- Normal muscle strength
- No evidence of synovitis or soft tissue inflammation
6
Q
Are labs indicated for the diagnosis of fibromyalgia?
A
- CBC, chem profile, TSH, ESR, CRP to exclude other disorders
- ANA, rheumatoid factor, anti-citrullinated protein antibody (ACPA) only in setting of synovitis, lupus, or RA
- Sleep study for OSA
7
Q
Can fibromyalgia be diagnosed back on history and physical examination alone?
A
Yes, but want to exclude other causes first
- Patient report of widespread pain present in up to 19 + fatigue + disordered sleep for >3 months
8
Q
Non pharmacological management of fibromyalgia
A
- CBT
- Exercise (to combat muscle wasting)
- Acupuncture
- Massage
- Chiropractor
9
Q
Pharmacological management of fibromyalgia
A
- TCAs (amitriptyline, cyclobenzaprine)
- SNRIs (duloxetine and milnacipran)
- Gabapentin (Neurontin) and pregabalin (Lyrica) for pain
- Tylenol
- Opioids ONLY after all other meds and therapies failed
10
Q
What are the four stages of a gout attack?
A
- Asymptomatic hyperuricemia → elevated serum urate but no acute attacks, crystals may deposit in joints and cause asymptomatic damage
- Acute gout attacks → activation of inflammatory response leading to intense pain, swelling, redness, warmth
- Intercritical gout (intervals between acute attacks)
- Chronic tophaceous gout → due to uncontrolled hyperuricemia
- Firm swelling most commonly found on digits of hands and feet, and olecranon bursa
11
Q
Risk factors for gout
A
- Use of diuretics or low dose aspirin use
- Obesity
- CKD
- Metabolic syndrome
- Advanced age
- Local trauma
- Binges of alcohol
- Overeating/fasting
- Newly initiated urate-lowering therapy
12
Q
How does gout appear in men vs women?
A
- Recurrent episodes of painful monoarthritis in men
- Oligoarticular arthritis (4 or fewer joints) in postmenopausal women and men with subsequent flares
13
Q
Acute gout clinical presentation
A
- Rapid onset (pain peak within 2-4 hours) and increasing pain
- First attack at night and patient wakes up from sleep
- Tenderness, warmth, redness, swelling, decreased ROM in affected joint (usually in first MTP)
- Heberden’s nodes
14
Q
Gout diagnostic studies
A
Confirmed with needle aspiration → MSU crystals in synovial fluid or tophi aspiration
15
Q
What are the goals of gout management?
A
1) treat acute attacks
2) lowering of total body uric acid pool to prevent tissue deposition of MSU crystals
3) anti-inflammatory prophylaxis to prevent further acute attacks
16
Q
Non pharmacologic management of gout
A
- Avoid diuretics
- Control weight
- Limit alcohol consumption
- Consume low fat dairy products, cherry juice concentrate
- DASH diet
- Topical ice
17
Q
Pharmacologic management of acute gout attacks
A
- NSAIDs and oral corticosteroids for initial treatment (corticosteroids preferred of CrCl <50, on anticoagulant therapy, or hepatic dysfunction)
- Colchicine should be used within 36 hours of onset of acute attack
- NOT used if GFR is <50
18
Q
Pharmacologic management of chronic gout attacks
A
- Urate lowering therapy (ULT) should be started 4-8 weeks after attack is resolved
- Xanthine oxidase inhibitors (allopurinol, febuxostat)
- Uricosuric agents (probenecid, lesinurad)
- Recombinant uricase (pegloticase)
19
Q
What is considered chronic gout?
A
Patients who have 2+ gout attacks a year
20
Q
True/false: There is an increase in acute attacks after ULT therapy initiation for gout
A
True - due to inflammation caused by changes in the chemical and/or physical state of preexisting MSU crystals
21
Q
What medication should be prescribed to patients prophylactically for patients starting ULT therapy for gout?
A
- Give prophylactic low dose anti inflammatory treatment when initiating patient on ULT → e.g. colchicine
- Alternative → NSAIDs
22
Q
What are the three types of treatment for gout?
A
- Medications to control attacks of joint pain (NSAIDs, colchicine, corticosteroids)
- Prophylaxis (colchicine, NSAIDs)
- Medications to lower uric acid levels (allopurinol, febuxostat)
23
Q
OA risk factors
A
- Female (middle age and older)
- Obesity
- Prior trauma
- Genetics
- Repetitive activities
- Metabolic disorders
- Neurologic disease
- Hematologic conditions
24
Q
OA vs RA
A
25
OA clinical presentation (history)
* Insidious, progressive pain/stiffness of one or more joints
* Symptoms common after waking up (duration \<1 hour)
* Pain with weight bearing activities
* Crepitus, swelling, joint deformity, gradual loss of motion
26
OA physical examination findings
* If cervical or lumbar spine spine is involved, neuropathy and radiculopathy → groin/butt pain causes patient to “favor” the hip → Trendelenburg gait
* Heberden nodes (distal) and Bouchard nodes (proximal)
27
OA diagnostic studies
X-ray (will see radiographic changes as disease progresses)
28
Pharmacological management of OA
* Pills
* Acetaminophen → **first line**
* Tramadol for moderate to severe pain
* NSAIDs (may be given with H2 blockers or PPIs to reduce GI intolerance)
29
Pharmacological management for OA
* Injectables
* Hyaluronan injections for mild to moderate OA (improves fluid viscosity)
* Intra articular corticosteroid injections → not recommended more often than every 3-4 months
30
Non pharmacological management of OA
* Exercise
* Locally applied heat, ice
* Warm baths
* Custom orthotics
* Weight reduction
31
What is poly myalgia rheumatica (PMR)?
Treatable, chronic systemic inflammatory condition of unknown cause most often in older adults
* Does not occur in adults younger than 50 years
32
PMR clinical manifestations
* Stiffness/aching of shoulder girdle, pelvic girdle, neck
* Pain worse at night and can radiate to elbows and knees (can have morning stiffness \>1 hour)
* Low grade fever, depression, fatigue, malaise, weight loss
33
How is PMR different from RA?
Inflammatory arthritis of knees and wrists
* Asymmetric, self limiting, responsive to systemic corticosteroids
34
PMR physical examination findings
* Painful active ROM of shoulder and hips
* No signs of synovitis
35
American College of Rheumatology diagnostic criteria for PMR
* Patient 50+ years with new onset bilateral shoulder pain
* Elevated ESR and/or CRP
* Negative RF and anti-CCP
* Morning stiffness \>45 minutes
* New hip pain in the absence of peripheral synovitis
36
PMR lab studies to rule out other inflammatory diseases
* CBC, ESR, CRP, CMP, LFTs, serum protein electrophoresis, RF and anti-CCP, UA, TSH
* Chest x-ray
37
PMR management/treatment
* Referral to rheumatologist
* Referral to ophthalmologist or plastic surgeon with any sign of temporal arteritis
* Systemic corticosteroids (low dose prednisone)
* Consider bone protective measures for patients with chronic PMR and require lifelong corticosteroids
38
What is the most significant complication of PMR?
Giant cell arteritis → report any new headache, change in vision, scalp tenderness, pain on chewing
39
Giant cell arteritis clinical manifestations
* Involvement of CNs → severe headache (temporal region), jaw claudication, visual impairment, scalp tenderness, prominent or tender temporal artery, tongue infarction, stokes, neuropsychiatric symptoms
40
Giant cell arteritis diagnostic studies
* Color doppler ultrasound of temporal arteries → halo sign
* **Gold standard** → unilateral temporal artery biopsy
41
Giant cell arteritis management/treatment
* Prednisone
* Pulse IV methylprednisolone for visual impairment
* Adjunctive therapy with steroid sparing agents (e.g. methotrexate)
* Low dose aspirin
42
What is rheumatoid arthritis?
Autoimmune disorder characterized by bilateral symmetrical inflammatory polyarthritis and varying degrees of extra-articular involvement
* Insidious onset
43
Systemic symptoms of RA
* Weakness
* Weight loss
* Malaise
* Fatigue
* Anorexia
* Aching
* Stiffness
44
Localized symptoms of RA
* Painful, tender, swollen joints
* Morning stiffness for \>1 hour
45
Extra articular symptoms of RA
* Sjogren syndrome (dry eyes and mouth)
* CV disease
46
RA diagnostic studies
* X-rays
* Labs → CBC, ESR, CRP, creatinine, hepatic panel, UA, RF, anti-CCP
* Normocytic, normochromic anemia common
* Synovial fluid analysis (aspiration)
47
Non pharmacologic management of RA
* PT, OT, psychological interventions, exercise
* Warm showers in the morning
* Frequent position changes during sleep to alleviate stiffness
* Assess CV risk yearly
48
Pharmacologic management of RA
DMARDs (methotrexate) + folic acid supplementation, biosimilar medications, NSAIDs, glucocorticoids
49
Clinical manifestations of ankylosing spondylitis
* Chronic back pain and stiffness (in pelvis and lower back) due to involvement of spine or sacroiliac joints
* Back pain improves with exercise and worsens with inactivity/rest and in the morning
* Buttock pain; hip pain
* Deep ache or nagging discomfort
* Sleep disturbance (wake up to “walk to pain off”)
* Asymmetric joint arthritis (commonly in lower limbs)
50
Extra articular manifestations of ankylosing spondylitis
* Low grade fever, fatigue, weight loss
* Acute anterior uveitis → unilateral or unilateral alternating
51
Physical exam findings of ankylosing spondylitis
* Loss of normal lumbar lordosis
* Decreased spine mobility
52
Ankylosing spondylitis diagnostic studies
* Presence of sacroiliitis on MRI associated with one clinical criterion
* X-ray may not show changes early on in disease process
* “Bamboo” spine appearance
53
Referrals for ankylosing spondylitis
* Referral to rheumatology
* Referral to orthopedic surgeon (for patients who develop hip arthritis), evaluation by cardiologist
* Periodic ophthalmic monitoring
54
Non pharmacologic management of ankylosing spondylitis
* Perform exercises tailored for AS (PT)
* Local heat and massage
* Avoid contact sports (can go swimming)
55
Pharmacologic management of ankylosing spondylitis
* **NSAIDs** first line therapy
* DMARDs (methotrexate), TNF agents (etanercept, -umab), IL-17 monoclonal antibodies (secukinumab)
* Systemic corticosteroids for short term relief (NOT long term)
* Acetaminophen and muscle relaxants to minimize chance of spine deformity
56
Psoriatic arthritis clinical manifestations
* Can occur before, with, or after onset of psoriasis
* Nail pitting before rash
* Enthesitis and dactylitis, arthritis mutilans
* Asymmetric sacroiliitis (in AS it is bilateral)
57
Psoriatic arthritis diagnostic studies
* X-ray of affected joints → subchondral erosions, periostitis, ankylosis
* Late disease will show whittling and “pencil in cup” appearance
58
Non pharmacologic management of psoriatic arthritis
* Regular exercise (swimming, cycling, walking)
* Referral to rheumatologist and dermatology
59
Pharmacologic management of psoriatic arthritis
* **NSAIDs** are first line
* DMARDs are second line (methotrexate)
* Anti-TNF agents → etanercept, infliximab, adalimumab, golimumab, certolizumab)
60
Clinical manifestations of SLE
* Early symptoms are nonspecific → fatigue, oral ulcers, joint pain, malaise
* Malar (butterfly) rash
* Discoid rash
* Photosensitivity
* Arthritis
* Serositis (pleuritis, pericarditis)
* Persistent proteinuria, cellular casts
* Seizures, psychosis; mood changes, depression, migraines, headaches
* Raynaud phenomenon
61
SLE diagnostic studies
* Elevated ESR, CRP, serum gamma globulins
* Hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia
* UA, BUN, creatinine, 24 hour urine protein excretion, CrCl
62
Non pharmacologic management of SLE
* Referral to rheumatology at diagnosis; dermatologist, ophthalmologist, nephrologist, cardiologist, orthopedic surgeon, hematologist, OT, PT, nutritionist
* Visits to gynecologist at shorter intervals (higher risk of HPV and cervical dysplasia)
* Avoid prolonged sun exposure (wear SPF \>30)
63
Pharmacologic management of SLE
* Statins for hyperlipidemia, calcium and vitamin D for osteoporosis
* Antibiotic prophylaxis before dental procedures
* NSAIDs
* PPIs in addition to corticosteroids or aspirin therapy
* Hydroxychloroquine for MSK, mucocutaneous, and serosal manifestations
64
What is juvenile idiopathic arthritis?
Persistent arthritis for more than six weeks in a child younger than 16 years old
65
Clinical manifestations (history) of juvenile idiopathic arthritis
* Arthritis → pain (aching), joint stiffness (worse in the morning and after rest), joint effusion and warmth, younger children may be irritable or have behavioral regression
* Nonspecific symptoms → decreased appetite, myalgia, nighttime joint pain, inactivity, FTT
66
MSK exam findings for juvenile idiopathic arthritis
* Swelling of joint with effusion or thickening of synovial membrane
* Heat over inflamed joint and tenderness along joint line
* Loss of joint ROM and function
* Observe gait abnormalities (may walk with a limp)
* Holds affected joint in flexion
67
Physical exam findings for juvenile idiopathic arthritis
* Vision screening
* Nail pits or onycholysis
* Ciliary injection
* Fleeting salmon-color rash that is more prominent on the trunk
68
Juvenile idiopathic arthritis diagnostic studies
* Diagnosis of exclusion
* Watchful waiting since joint pain must be present for \>6 weeks
69
Non pharmacologic management of juvenile idiopathic arthritis
* Referred to pediatric rheumatologist and ophthalmologist
* High risk for uveitis → slit lamp examination every 3-4 months for four years
* Physical therapy mainstay of treatment for chronic childhood arthritis
* Water therapy and using heat or cold to reduce pain and stiffness (e.g. swimming)
70
Pharmacologic management for juvenile idiopathic arthritis
* Aggressive early pharmacological therapy
* NSAIDs
* DMARDs (managed by pediatric rheumatologist)
* Oral glucocorticoids if there has not yet been a prompt response
