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NMSK Exam 3 > Gout/Pseudogout/ RA > Flashcards

Gout/Pseudogout/ RA Flashcards

1
Q

Hyperuricemia is when uric acid (end product of purine degradation) levels are _____

A

> 6.8 mg/dl

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2
Q

Hyperuricemia can cause what?

A

Gouty arthritis = supersaturation of monosodium urate crystals in fluids of joint or tophi (nodular monosodium urate crystal deposts in skin) due to overproduction or under-excretion of uric acid.

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3
Q

What do monosodium urate crystals look like under polarized light?

A

Needle-shaped, negative birifringence

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4
Q

Who is gout MC?

What can promote gout?

A
  1. 90% of gout in M (30-50s)
  2. Post-menopausal W
  3. Alcohol or anything high in purines
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5
Q

What is the MC presentation of acute gouty arthritis?

A
  • Acute onset, monoarticular, most often affecting the 1st MTP of the big toe.
  • Pain is so bad will wake you up at night.
  • Joints are hot, swollen, tender, dusky/red
  • Pt will have fever
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6
Q

Chronic gouty arthritis can lead to what?

A
  • Tophi = deposits in ears, forearms and achilles tendon
  • Renal insufficiency (urate stones that are radiolucent)
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7
Q

DDX for gouty arthritis

A
  1. Infectious arthritis (septic arthritis)
  2. Reative arthritis
  3. Pseudogout - CPPD disease (Ca+ pyrophosphate dihydrate)
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8
Q

Treatment for Gout

  1. Best medication for acute gouty flare?
  2. Treamtent for asymptomatic hyperuricemia?
A
  1. No single best agent
  2. Do not treat asymptomatic hyperuricemia, EXCEPT in patients about to receive cytotoxic therapy for neoplasm
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9
Q

How do we treat acute gouty flare?

A
  • ASAP within 12- 36 hours with NSAIDS (500mg of Naproxen BID / 50mg of Indomethicin TID).
  • Watch bc INC risk of GI bleeding.
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10
Q

What is a reasonable 1st line of treatment for Gout?

A

Steroids (Prednisone 40 mg PO/day x5-7days -taper)

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11
Q

What drug is effective for gout in the 1st 24 hours of an attack?

A

Colchicine

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12
Q

When would you use a uric acid lowering agent for gout?

What should you be cautious of?

A
  1. Recurrent gouty attacks, tophi, kidney stones or cytotoxic therapy
  2. Do not start during an acute attack because it cause flares.
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13
Q

How is pseudogout different from gout?

A
  1. Deposits of Calcium Pyrophosphate Dehydrate
  2. Affects larger joints and the knee
  3. Older patients
  4. Polyarticular
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14
Q

If chronic pseudogout, what do we see?

A
  • Resembles OA
  • Can cause chondrocalcinosis (Ca2+ deposits in articular cartilage)
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15
Q

What do the CPPD crystals in pseudogout look like on polarizing microscopy?

A
  • Short, blunt rods, rhomboids/cuboids
  • Weak POSITIVE birefringence
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16
Q

DDx for Pseudogout

A
  1. OA
  2. RA
  3. Gout
  4. Septic arthritis
  5. Aging
  6. If younger patients => primary hyperparathyroididm and hemochromatosis
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17
Q

Treatment for pseudogout

A
  1. NSAID
  2. Steroids (intra-articular injections)
  3. Colchicine (variable)
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18
Q

What is Rheumatoid Arthritis?

A
  • Chronic, inflammatory, systemic AI disease that affects synovial tissues and diarthrodial joints and other organs (lungs and skin)
    • _​_Symmetrical
    • Affects SMALL joints
    • Polyarthritis
    • Extraarticular features
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19
Q

Etiology of RA

A

Idiopathic, but thought to be have genetic susceptability (HLA-DRB4/DRB1 0401 or 0404) influences that is triggered by an environmental factor.

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20
Q

Rheumatoid Arthritis

  • MC in and when?
  • How is if affected by pregnancy?
  • What is it thought to be associated with?
A
  1. W 20-60 YO
    1. MC in Yakima & Inuit Native American Tribes
  2. Improves during pregnancy, but flare ups begin 4-6 weeks after delivery
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21
Q

What do we see in labs for RA?

A
  1. Acute phase reactants: ↑↑↑ ESR & ↑↑↑ CRP
  2. Serology: (+) RF + anti-CCP = 95% pt has RA
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22
Q

What is the purpose of Rheumatoid Factor (RF)?

A

RF is a IgM Ab made by B-cells in the RA synovium => binds to altered IgG Ab => forms immune complexes that go in synovial fluid => + comlpiment system.

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23
Q

Pathophysiology of Rheumatoid Arthritis

A
  1. Genetic + environmental trigger =>
  2. Modification of our own antigens, like IgG ab, Type 2 Collagen and Vinmentin
  3. Type 2 collagen and vinmentin under citrullination: Argining => citrilline
  4. Our bodies immune cells no longer recognize them as self-antigens =>
  5. Antigens get picked up by APC => presented in LN
  6. CD4+ T-helper cells are (+) => stimulate B-cells
  7. B-cells => plasma cells => make autoAB against self-antigens
  8. T-helper cells & Ab NTR circulation => joints
    1. T-cells secrete IFN-y and IL-17 => recruit more inflammatory cells, like MO.
    2. B-cells secrete TNF-a, IL1 and IL6. =>
  9. => Synovial cells proliferate, creating a pannus (a thick, swollen, synovial membrame with granulation tissue (fibroblasts, myofibroblasts + inflammatory cells)
  10. Overtime:
    1. Pannus invades cartilage and bone and synovial cells release proteases, which break down articular cartilage, allowing bones to directly rub against one another.
    2. Inflammatory cytokines cause T-cells to express RANKL, which binds to RANK on osteoclasts => break down bone
    3. Rheumatoid factor, an IgM Ab, enters the joint space and binds to fc domain of altered IgG Ab
    4. Anti-CCP Ab targets citrillinated proteins
    5. When Ab bind to target, form immune complexes that accumulate in the synovial fluids
    6. => + compliment system => joint inflammation and injury
  11. Chronic inflammation =>
    1. Angiogenesis (new BV), which promotes more inflammatory cells
  12. As the disease progresses, affects MULTIPLE joints on BOTH sides of body.
  13. Inflammatory cytokines => mutliple organ systems and cause extraarticular problems.
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24
Q

Rheumatoid synovitis causes:

A
  • 1. Bursitis
  • 2. Tendinitis
  • 3. Synovitis
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25
Q

What imaging would you do in a patient with RA?

A
  1. XR of hand and feet = detect symmetrical involvament of MCP/MTP joints and erosion
  2. CT = more sensitive for erosions
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26
Q

Treatment of RA

A
  1. First, start off with RICE
  2. Begin with a full dose of NSAIDs ONLY for pain
  3. Goal= treat EARLY with DMARD immunosupression (bc take 2-6 months to work) to prevent damage to bone/cartilage to slow disease progression and radiographic progression => remission or low disease activity.
    1. Methotrexate = first line
  4. May need low dose of steroid for a few weeks, for flairs or until DMARDs work (bridge therapy)
  5. Monitor progress and toxicity
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27
Q

Why is Rheumatoid Arthritis so concerning?

A

Peaks in young adults, disables patients, it is associated with an ↑↑ of mortality due to endothelial damage from the chronic inflammation.

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28
Q

RA increases risk of mortality due to complications from what?

A
  1. Infection
  2. Renal disease
  3. GI disease
  4. Heart disease
  5. Cancer
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29
Q

2010 RA classification criteria includes what 4 categories?

A

Test patients who have at least 1 joint with definite clinical synovitis or with synovitis not better explained by another disease.

  1. Joint involvement: # of joints and size (smaller and more joints = more points)
  2. Serology: RF and anti-CCP
  3. Acute phase reactants: CRP and ESR
  4. Duration of sx’s: less than 6 weeks or more 6 weeks
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30
Q

Which score using the 2010 RA classification criteria indicates definite RA?

A

> 6/10

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31
Q

What is the articular manifestation of Rheumatoid Arthritis?

  • Affects what joints?
  • Typically starts where? Later affects?
  • What part of the spine does it affect?
  • INC risk of what?
A
  1. Affects any diarthrodial synovial joint
  2. Typically starts in hands and feet; MCP, PIP, MTP, spares DIP
    1. Later affects, larger joints: wrists, knees, elbows, ankles, hips, shoulders
  3. C1 – C2 / Not the rest of the axial spine
  4. Inc. risk osteoporosis
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32
Q

How does RA affect the hands?

A
  1. Affects MCP, PIP, MTP
  2. Spares DIP
  3. Swan neck deformity: hyperextension of PIP joints
  4. Bouttonniere deformity (button hole deformity): hyperflexion of PIP joints.
  5. Fingers = ulnar deviation; wrist = radial deviation
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33
Q

If a patient presents with Rhematoid nodules, for example on the elbow, what can we conclude?

A

100%, the patient will be RF (+)

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34
Q

In RA, how do the fingers deviate compared to wrist?

A
  • Fingers = ulnar deviation
  • Wrist = radial deviation
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35
Q

How can RA affect the feet, wrist, knees, neck?

A
  1. Feet: MTPs are affected
  2. Wrist: radial deviation, synovial prolfieration can compress median nerve => carpal tunnel
  3. Knees: Bakers cyst in the popliteal area that are v painful and can rupture (may be confused for venous thrombosis)
  4. Neck: C1- C2 are mainly affected => DO NOT force patient into flexion
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36
Q

Clinical manifestion of RA

A
  1. Pain, swelling and warmth in multiple small joints (>3) of hand and feet.
  2. Morning stiffness after a year
37
Q

When and where are extra-articular manifestations of RA most common?

A
  1. When RF (+) or anti-CCP (+)
  2. Skin: subQ nodules on the extensor surfaces of forearms,
38
Q

What are cutaneous manifestations of RA?

A

1. Pyoderma Gangrenosum: tender, red/purple papule that leads to a necrotic, non-healing ulcer.

2. Rheumatoid vasculitis: purple, petachial, splinter hemorrhages and digital infarcts.

39
Q

RA is an independent risk factor for which CV manifestation?

A

CAD: chronic endothelial inflammation - damage

40
Q

A 58-year-old male presents with a cough and dyspnea on exertion (climbing 1 flight of stairs and while working in the coal mine).

Medical history is positive for RA for ten (10) years and smoking (1-2 ppd x 30 years).

Chest x-ray reveals a nodular opacity in both lungs and diffuse hyper-lucency of the lungs.

What is diagnosis? What test should you order?

A
  • Coal miners pneumoconiosis with nodular opacities due to exposure to silicosis
    • Rheumatoid nodules too
  • CT of the chest
41
Q

MC lung manifestation in RA?

A

Pleuritis: pain on respiration

42
Q

A 36-year-old female presents to your office with a history of dry mouth, decreased tearing and a sandy- gritty feeling under her eye lids.

Recently she complains of “bright light” sensitivity. You have been treating her RA for give (5) years with NSAIDs and methotrexate.

Diagnosis? What tests would you order? Treatment

A
  1. Sjrogens syndrome = seen in 35% of RA patients
  2. Serology for anti-SSA (Ro) / SSB (La)
    1. Schimers test
    2. Slit-lamp test
  3. Antiflammatory + immunosuppresants; Lubrication with artifical tears, oral hygeine and drink H20
43
Q

Sjrogens Syndrome causes what?

A
  1. Keratoconjuctivitis Sicca (dry eyes)
  2. Dry mouth
  3. Vaginal dryness
  4. Tracheobronchial dryness
44
Q

What is pathognomic of RA?

A

NO single finding or PE or lab test is pathognomic

45
Q

What other lab findings would you see in RA?

A
  1. + ANA (30% of RA patients)
  2. Anemia
  3. Thrombocytosis
  4. Hyperglobinemia
  5. Leukopenia/granulocytopenia
  6. Low glucose in body
  7. Synovial fluid will have 2/3 PMNS: WBC = 5,000 - 100,000/mm3
46
Q

What is the goal of treatment of RA?

A

Treat to target: treat EARLY to prevent irreversible damage to bone and cartilage

Goal is remission (occurs in 50% of pts if tx early)

47
Q

Name the 4 spondyloarthropathies

A
  1. Ankylosing spondylitis (AS)
  2. Psoriatic arthritis (PsA)
  3. Reactive arthritis (ReA) = Reiters syndrome
  4. Enteropathic arthritis (EA) = occurs in ppl w IBD, Crohns or UC
  5. Undifferentiated (USpA)
48
Q

How is serology different for RA vs Spondylarthropathies?

A
  1. No (+) serology for RF or anti-CCP
  2. (+) HLA-B27
  3. Can involve axial spine
49
Q

What spondylopathies are more common in men?

A
  1. Reactive arthritis
  2. Ankylosing spondylitis
50
Q

What spondylopathies are seen equally men and women?

A
  1. Enteropathic arthritis
  2. Psoriatic arthritis
51
Q

What are common features in all 4 spondylopathies?

A
  1. HLA-B27
  2. Target axial spine (cranium + vertebra) and SI joints, NOT peripheral arthritis like RA
  3. Asymmetric peripheral arthritis
  4. New bones form at sites of inflammation
  5. Joint ankylosing occurs = fusion that causes rigidity
  6. Enthesitis = inflammation where tendons/ligaments insert into bone
  7. GI/GU inflammation; sometimes due to bacterial infection
  8. Ocular inflammation
52
Q

Terminology

  1. Dactylitis =
  2. Osteitis =
A
  1. Dactylitis = swelling of finger or toe due to reactive arthritis or psoriatic arthritis
  2. Osteitis = inflammation of bone
53
Q

Terminology

  1. Spondylitis =
  2. Spondylolisthesis =
  3. Spondylolysis =
A
  1. Spondylitis = Inflammation of vertebrae
  2. Spondylolisthesis = Anterior displacement of a vertebral body relative to the adjacent vertebral body below
  3. Spondylolysis = Defect of the portion of bone in between the inferior and superior articular process of vertebrae (pars interarticularis)
54
Q

Which spondylopathies affect SYMMETRICAL SI joints?

A
  1. Ankylosing spondylitis
  2. Enteropathic Arthritis
55
Q

Which spondylopathies affect ASSYMMETRICAL SI joints?

A
  1. Psoriatic arthritis
  2. Reactive arthirits
56
Q

What is the hallmark of spondyloarthropathy in children?

A

Enthesitis: inflammation at sites where tendons, ligaments and joint capsule insert into bone

57
Q

What type of spondylopathies has the HIGHEST association with HLA-B27?

A

Ankylosing spondylitis (90%) > ReA

Not all spondylopathies are HLAB27 (+)

58
Q

A 28-year-old male presents with a history of low back pain for the past four (4) months. He denies trauma, heavy lifting or unusual physical activity. He indicates the lower portion of the back over the lumbar – sacral-iliac region, right side worse than left side. He admits to morning stiffness, fatigue and 9lb. weight loss over three (3) months

What other question do you want to ask?

A

•Does physical activity/exercise improve the pain?

59
Q

PEARL: How is pain in spondyloarthropaties affected with physical activity/exercise?

A

Physical activity or XRCISE = improves pain in spondyloarthopaties

60
Q

Tests and imaging for Spondylarthropathies

A
  1. HLA B27
  2. CRP and ESR
  3. XR of pelvis (SI joint)
  4. XR of lumbar vertebra
  5. CT of lumbar and pelvis if XR is non-diagnostic
61
Q

What is the MC inflammatory disease of axial skeleton?

A

Ankylosing Spondylitis (AS)

62
Q

What is ankylosing spondylitis?

  • MC in who and when?
A

Ankylosing spondylitis (spondyloarthritis) is a chronic inflammatory disease of the axial skeleton that leads to partial or even complete fusion and rigidity of the spine

  • 20-30YO M
63
Q

Pathogenesis of AS?

A
  • Immune mediated: CD4/8 T-cells infiltrate SI joint => inflammation; high amount of TNF-a
64
Q

Clinical manifestations of Ankylosing Spondylitis

A
  1. Insideous onset of pain and stiffness in the neck and lower back > 3 months => loss of mobility/flexibility
  2. Symmetrical SI joint pain (sacroilitis)
  3. Pain typically improves with activity and is prominent at night.
  4. Morning stiffness that improves with activity
  5. Tendonitis, plantar fasciitis (pain at achilles heel area)
  6. Enthesitis
  7. + family history
65
Q

Extraarticular manifestations of Ankylosing Spondylitis

A
  1. Anterior uveitis (iritis) => photophobia, eye pain, blurry vision
  2. Restrictive pulmonary fibrosis
  3. IBD
66
Q

How to test for Ankylosing Spondylitis on PE?

A
  1. Schober Test = restricted forward flexion due to ↓ lumbar spine mobility (less than 4 cm)
  2. FABERE test = restricted chest expansion less than 5cm
67
Q

Which imaging modality is most sensitive for detecting erosions and which is able to detect inflammation earliest?

A
  • CT = more sensitive for erosions
  • MRI = detects inflammation before changes seen on X-ray and CT
68
Q

What unique XR finding can be seen in Ankylosing Spondylitis?

A
  1. Syndesmophytes = symmetrical, vertical bridging of vertebrae resulting in a ‘bamboo spine’ in AP XR in the later stages
  2. Osseous erosion and sclerosis
69
Q

DDx of Ankylosing Spondylitis

A
  1. DISH (diffuses idiopathic skeletal hyperosteosis) = Calcification along lateral aspect of four (4) contiguous vertebrae bodies. SI joints okay
70
Q

What are some of the late complications which may arise with Ankylosing Spondylitis?

A
  1. Cauda equina syndrome: bladder, bowel, pelvis and LBP
  2. Compression fractures
  3. Restrictive lung disease
71
Q

Which pharmacologic agents can decrease the inflammation of the axial spine and improve mobility in pt’s with Ankylosing Spondylitis?

A
  • TNF-alpha blockers: Infliximab, Adalimumab
72
Q

Tx for Ankylosing Spondylitis

A
  1. Exercise, physical therapy, swimming, stretching, (preserve mobility/prevent kyphosis)
  2. NSAIDS
  3. TNF-a inhibits
  4. Non-biologic DMARDS are okay, but work best for peripheral arthritis, NOT axia
73
Q

A 26-year-old male presents with pain, swelling and warmth in the right knee. Onset two (2) weeks prior to office visit. Admits to pain in achilles tendon on right side and sore soles of the feet. He does admit to swelling and soreness of the 2nd and 3rd toes on the right foot. He denies eye pain, rash or urethral discharge.

What questions do you want to ask? Diagnosis?

A
  1. Any history of a recent GU or GI track infection?
  2. Any history of oral ulcers, penile rash, fever?
  3. Any history of venereal disease (GC, syphilis)?
  4. Any IV drug use?

•Reactive arthritis

74
Q

What is reactive arthritis?

A

AI condition that occurs after a bacterial infection of the GI/GU tract. Primarily affects young men and usually presents with MSK or extra‑articular symptoms. The characteristic triad consists of arthritis, conjunctivitis, and urethritis.

75
Q

Describe the arthritis experienced in Reactive Arthritis?

A
  • Acute onset (1-4 weeks after infection)
  • Asymmetric
  • Migratory
  • Monoarthritis or oligoarthritis of large joints (SI, knee) of LE
76
Q

Reactive Arthritis can typically occur after GI/GU infections?

A

ShY ChiCS:

  1. Shigella
  2. Yersinia
  3. Chlamydia
  4. Campylobacter
  5. Shigella
77
Q

Triad for Reactive Arthritis

A
  1. Arthritis
  2. Urethritis
  3. Conjunctivitis
78
Q

MSK manifestations of Reactive Arthritis

A
  1. Enthesitis = achilles tendon/plantar fascitis
  2. Dactylitis = sausage finger or toe
79
Q

Other manifestions of Reactive Arthritis

A
  1. Oral ulcers (mucocutaneous lesions)
  2. Circunate balanitis = vesicles and ulcers on glans penis
  3. Kertoderma blennorrhagicum = painless eruption on palms/soles
80
Q

Labs and imaging for Reactive Arthritis

A
  1. Same as AS
  2. Inflammatory synovial fluid (WBC = 2,000 - 50,000 PMNS)
  3. Asymmetrical SI joint affected
81
Q

Treatment of Reactive Arthritis

A
  • Usually self-limiting: 6 months
  • NSAIDS, steroids (intra-articular)
  • If chronic, use DMARDS (sulfasalazine, metrotrex, leflunomide)
  • If uretheritis: treat chylamidia with azithromycine or doxycycline.
82
Q

What is Psoriatic Arthritis?

A

Seronegative spondyloarthritis that occursin 5-20% of ppl w skin psoriasis that occurs equally in M=F around 30-50YO.

83
Q

Describe the arthritis in Psoriatic Arthritis

A
  1. Asymmetric or symmetric peripheral arthritis
  2. Often DIP, PIP, MCP, MTP, can also involve large joints.
  3. C1-C2 spine can be involved
  4. Joint pain and stiffness worse in the morning
84
Q

MSK manifestions of PsA

A
  1. Enthesitis
  2. Dactylitis
  3. Pitting nails due to DIP arthritis
  4. STS (soft tissue swelling)
  5. Erosions
  6. Periostitis
  7. Destruction of interphalangeal joints
85
Q

PsA flare ups may be due to what?

5-10% of ppl with PsA have what?

A
  1. Co-infection with HIV
  2. (+) RF or antiCCP Ab
86
Q

What is the progression of DIP arthritis seen in Psoriatic Arthritis?

A
  1. Narrowed joint space and condylar erosions
  2. Reactive subperiosteal new bone
  3. Pencil in cup appearance
87
Q

What is Enteropathic Arthritis?

A

Arthritis associated with Crohn’s Disease (CD) or ulcerative colitis (UC) that affects M=F equally.

88
Q

Describe arthritis seen in Enteropathic arthritis

A
  1. Axial involvement
  2. Symmetric SI involvement
  3. Peripheral arthritis: Parallels activity of IBD
    • Large joints of LE.
    • Small joints of UE
    1. All extra-articular manifestations occur more commonly in CD
89
Q

Extraarticular manfiestations of Enteropathic Arthritis.

A
  1. Pyoderma Gangrenosum
  2. Erythema Nodosum
  3. Uveitis
  4. Nephrolitiasism

NMSK Exam 3 (17 decks)

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