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Phys: Bone & Gen Med: Ortho > Arthritis > Flashcards

Arthritis Flashcards

1
Q

Define arthritis

A

Inflammation of >1 joints

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2
Q

What are the types of arthritis?

A
  1. Osteoarthritis (OA)- most common degenerative jt dz
  2. Rheumatoid arthritis (RA)- autoimmune disease
  3. Psoriatic arthritis- autoimmune disease
  4. Septic arthritis- infectious process
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3
Q

What is the pathophys of osteoarthritis?

A
  1. Joint cartilage deteriorates w/ aging
    A. Progressive loss of cartilage and bony overgrowth (osteophytes)
    B. Subchondral bone cysts may form
    C. Inflammation around articular surface of joint
    D. Irregular joint space, fragmneted cartilage, loss of cartilage, sclerotic bone, cystic change
    E. Advanced: osteophytes, periarticular fibrosis, calcified cartilage
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4
Q

What are the risk factors for OA?

A
  1. Age - #1 risk factor
  2. F>M
  3. Inc BMI
  4. Joint injury/trauma
  5. Contact sports
  6. Certain occupations
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5
Q

What are the sxs for OA?

A
  1. Joint Pain
    A. Worsens with activity or weight bearing (WB)
    B. Relieved with rest
  2. Joint Stiffness
    A. Morning joint stiffness < 30 minutes
    B. usually stiff minutes after waking and problems are worse through day and on activity
  3. Joint crepitus
  4. ↓ ROM
  5. Usually onset is insidious
  6. Commonly affects wrist, hand, hip, knee, back
  7. Impact of disease/pain on daily life?
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6
Q

Define heberden’s nodes

A

DIPJ swelling seen in OA

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7
Q

define Bouchard’s nodes

A

PIPJ swelling seen in OA

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8
Q

What must be inspected on the PE for OA?

A
  1. Effusion present +/-

2. Genu varus/valgus

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9
Q

What are the results of palpation on the PE for OA?

A
  1. Hard, bony joint
  2. dec ROM
    A. +/- Flexion contracture
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10
Q

What gait changes may be present in OA?

A
  1. Antalgic
  2. Trendelenburg
  3. Normal
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11
Q

What are the Xray results in OA?

A
  1. X-Rays (AP/Lat/Merchants Weight Bearing)
    A. Asymmetrical joint space narrowing
    B. Subchondral sclerosis
    -inc bone formation (density) of articular bone
    C. Bone cysts
    D. Bone spurs (osteophytes)
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12
Q

What are the synovial fluid assessment results in OA?

A 
1. Synovial fluid is NON-inflammatory
A. Color: clear to straw-colored
B. Clarity: transparent
C. <25%
E. Culture of fluid- negative
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13
Q

What is the treatment for OA?

A
  1. Weight loss
  2. Low impact physical activity
  3. Pain control
    A. Acetaminophen, NSAIDs, intra-articular cortisone (steroid) injection
  4. PT
    A. Quad strengthening / hamstring stretching
    B. Hip strengthening exercises
    C. Joint ROM
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14
Q

What joints does RA affect?

A

RA usually affects joints symmetrically, may initially begin in a few isolated joints, and most frequently attacks the wrists, hands, elbows, shoulders, knees, and ankles.

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15
Q

Define RA

A
  1. Chronic symmetric, inflammatory, peripheral polyarthritis of unknown etiology (autoimmune dz that 1st targets synovium)
    A. Major manifestation- synovitis of multiple joints
    B. Systemic extra-articular involvement- skin, eyes, vascular systems
    -Late in disease
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16
Q

What are the demographics of RA?

A
  1. F>M
  2. Mean age @ onset 35-55 yo
  3. Juvenile form (JRA) <16 yrs age
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17
Q

What is RA pathophys?

A
  1. TNF-alpha & IL-1 -> synovial cell growth/synovitis -> fibrosis -> pannus formation -> invades jt and causes cartilage destruction & bone erosion
  2. Joint damage: most rapid early in dz & cannot be reversed
    A. Need more aggressive treatment early in course of disease
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18
Q

What are the jt sxs of RA?

A
  1. Joint sxs
    A. Insidious onset vague joint pain (70%), 30% acute onset
    B. Morning stiffness >30 minutes
    -Very stiff and lasts > 1 hr after waking
    -Pain and stiffness gets better w/ mobility and as day progresses
  2. Symmetrical polyarthritis, most commonly affecting small joints hands & feet
    A. Wrists and MCP jts commonly involved
    B. DIP jts spared
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19
Q

What are the extra-articular sxs of RA?

A
  1. Midday fatigue, +/- low grade fever*
  2. Subcutaneous Rheumatoid Nodules (20%)
    A. Most commonly over bony prominences
  3. Ocular Sxs
    A. Dry eyes
    B. Scleritis
  4. Other Sxs
    A. Vasculitis
    B. Palmar erythema
    C. Pulmonary fibrosis
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20
Q

What deformities may be present in RA pts?

A
  1. Deformities common with progressive disease
    A. Boutonniere deformity: PIP hyperflexion contracture
    B. Swan neck deformity: hyperextended PIP, hyperflexed DIP
    C. Ulnar deviated fingers
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21
Q

What are the PE components of an RA pt?

A
  1. Inspect
  2. Palpate
    A. “Spongy” feel to the joint
    B. Warm, tender
  3. ROM
  4. Strength
  5. Gait
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22
Q

What labs are ordered to dx RA?

A
  1. CBC w/diff
  2. Erythrocyte sedimentation rate (ESR)
  3. C-reactive protein (CRP)
  4. Antinuclear antibody (ANA)
    A. can be + in up to 1/3 of RA pts
  5. Rheumatoid factor (RF )& anti-cyclic citrullinated peptide antibodies (anti-CCP)
    A. Positive in 70-80% pts w/ RA
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23
Q

What are the x ray results in an RA pt?

A
  1. Soft tissue swelling & demineralization early signs
  2. Joint space narrowing and erosions usually late in dz
  3. MCP, MTP, and/or PIPJ involvement
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24
Q

What are the synovial fluid results in an RA pt?

A
  1. Synovial fluid is Inflammatory
  2. Color: straw to milky
  3. Clarity: translucent to opaque
  4. > 2000-7500 WBC/mcl
  5. PMNs 50% or more
  6. Culture- negative
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25
Q

How are RA and OA differentiated?

A 
1. joints affected: 
A. RA: MCP, proximal interphalangeal
B. OA: distal interphalangeal, CMC
2. Hebernden's Nodes:
A. RA: Absent
B. Present
3. Joint characteristics:
A. RA: soft, warm, tender
B. OA: hard and bony
4. Stiffness
A. RA: Worse after resting
B. OA; worse after effort
5. Lab findings:
A. RA; + RA factor, + anti-CCP antibody, inc ESR, inc C reactive protein
B. OA: - RA factor, - anti-CCP antibody, normal ESR, normal C reactive protein
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26
Q

What are the goals of RA treatment?

A
  1. dec inflammation & pain and prevent disease progression
  2. Preserve function/ROM joint(s)
  3. Prevent deformities
  4. flare-ups, remission, relapses
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27
Q

What are the first line drugs for RA treatment?

A
  1. Synthetic DMARDs
  2. Retard or halt disease progression
    -decrease pain and inflammation, reduce or prevent joint damage, and preserve the structure and function of the joints
    A. Methotrexate (Rheumatrex)- 1st synthetic DMARD
    -First Line for RA
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28
Q

What is the moa, and SE of methotrexate?

A
  1. Folate analog
    A. Inhibits dihydrofolate reductase, therefore inhibits DNA synthesis
    B. In RA, principle moa is inhibiting neutrophils
    C. Can be hepatotoxic- check LFTs and CBC
    D. Teratogenic
    E. 7.5 mg po weekly
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29
Q

What is the second line drug for RA treatment?

A

Sulfasalazine (Azulfidine)- second line for RA

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30
Q

What is the moa, and SE of sulfsalazine (Azulfidine)?

A
  1. Suppress T-cell or B-cell activation (etiology unknown)
  2. Side effects (n/v/ha/ skin rashes/leukopenia)
    A. causes about 30% pts to d/c drug
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31
Q

What other DMARDs are available to treat RA?

A

azathioprine, cyclosporine, hydroxychloroquine (Plaquenil)

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32
Q

What are biologic DMARDs? When are they used?

A
  1. Blocks signal transduction by either TNF or IL1
    A. TNF activates macrophages and monocytes
    B. IL1 activates other cytokines
  2. Often prescribed with methotrexate
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33
Q

What are the biologic options for RA treatment?

A
  1. Etanercept (Enbrel)- SQ
    A. Recombinant TNF receptor (TNF inhibitor)
  2. Adalimumab (Humira)- SQ
    A. Human monoclonal antibody->TNF inhibitor
  3. Infliximab (Remicade)- IV
    A. Monoclonal antibody->TNF inhibitor
    -Potential SE -> development of TB
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34
Q

What NSAIDs are used to treat RA? When are they used?

A
  1. Provide symptomatic relief, but does not alter disease progression
  2. Used in conjunction with DMARDS
  3. Indomethacin (indocin)
    A. Nonselective cyclooxygenase inhibitor (inhibits COX 1 & 2)
    B. Inhibits prostaglandin production
  4. Celecoxib (Celebrex)
    A. Selective COX- 2 inhibitor
    B. Lower incidence gastric and duodenal ulcers
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35
Q

What low dose corticosteroids are used to treat RA? When are they used?

A
  1. Inhibit phospholipase A2 -> inhibit release arachidonic acid -> inhibit prostaglandin synthesis
  2. Oral prednisone 5-10 mg daily
    A. Prolonged use can lead to:
    Hyperglycemia, osteoporosis, poor wound healing
  3. Can be used short-term while other DMARDs take effect
36
Q

What is the prognosis for RA?

A
  1. Referral to Rheumatologist
  2. After months or years, deformities may occur
  3. Mortality asst w/ RA usually d/t cardiovascular dz -> chronic inflammation of vascular system
37
Q

Define Psoriatic arthritis

A
  1. Inflammatory arthritis w/ skin involvement

2. Psoriasis precedes onset of arthritis 80% of cases (up to 2 yrs)

38
Q

What are the sxs of psoriatic arthritis?

A
  1. Symmetric polyarthritis (resembles RA)
  2. “Sausage”digits (dactylitis) of fingers & toes (DIPs)
  3. Sacroliitis and spinal involvement common
  4. Pitting of nails and onycholysis (nail separation) are common
39
Q

What needs to be assessed on the PE for a psoriatic arthritis pt?

A
  1. HEENT- check hair/scalp
  2. Skin- ck gluteal cleft and umbilicus
  3. Nails
  4. MSK
40
Q

What labs need to be ordered for psoriatic arthritis? What are the results?

A
  1. ESR and CRP
  2. usually seronegative arthritis (RF neg.)* (15% can be positive)
  3. HLA-B27
41
Q

What x rays results may be present for psoriatic arthritis?

A
  1. Irregular destruction of joint & bone

2. In phalanx, may appear as sharpened pencil

42
Q

When are NSAIDs used in psoriatic arthritis pts?

A

Mild cases

43
Q

When is Methotrexate used in psoriatic arthritis pts?

A
  1. Drug of choice in pts who do not respond to NSAIDs

2. Improves cutaneous and arthritic manifestations

44
Q

When are biologics used in psoriatic arthritis pts?

A

Added if MTX not effective

45
Q

Define septic arthritis

A
  1. Infection of joint space, usually single joint involved
    A. Hematogenous spread of bacteria, osteomyelitis, non-sterile joint injection or cellulitis
    B. Most commonly knee, followed by hip, shoulder, ankle, wrist
46
Q

What is the most common pathogen for septic arthritis?

A

Staph aureus- most common pathogen in non-gonococcal bacterial arthritis

47
Q

What are the risk factors for septic arthritis?

A
  1. Previous joint damage
  2. IV drug use
  3. Immunocompromised pts
48
Q

What pts develop Neisseria gonorrhea septic arthritis?

A
  1. Healthy adults, esp young sexually active adults

A. Most common in young women onset of menses

49
Q

What are the sxs of septic arthritis?

A
  1. Acute joint swelling (effusion) over hrs
  2. Fever
  3. Joint warmth
  4. Erythema
  5. Tenderness
    A. ↑↑↑ pain with ROM of involved joint
50
Q

What is the joint fluid analysis in OA?

A
  1. Color: yellow
  2. WBCs: <25%
  3. Glucose: equal to serum
51
Q

What is the joint fluid analysis in RA?

A
  1. Color: white to yellow
  2. WBCs: >2000 - 5000
  3. PMNs: >50%
  4. Glucose: 25< serum
52
Q

What is the joint fluid analysis in septic arthritis?

A
  1. Color: green to yellow
  2. WBCs: 50,000 - 100,000
  3. PMNs: >75%
  4. Glucose:<25
53
Q

What are the xray results in septic arthritis?

A

Soft tissue swelling (STS)

54
Q

Why is a joint aspiration performed in septic arthritis?

A
  1. Differentiates between inflammation & infection

2. Send for aerobic and anaerobic cultures and sensitivities (C&S)

55
Q

What is the treatment for septic arthritis?

A
  1. Drainage of affected joint, culture, then empiric antibiotics
    A. Start w/ Broad Spectrum Abx
    B. Cover Staph, Strep and Gram neg. organisms
  2. Hospitalization always necessary
  3. Orthopedics Consult Immediately
    A. Arthroscopic lavage/washout, debridement and drain placement
    B. Open surgical drainage
56
Q

What is the prognosis for septic arthritis?

A 
1. Patient outcome varies:
A. Health of patient
B. Pathogen
-Staph aureus asst w/ poor functional outcome in 40% cases
C. Promptness of treatment
57
Q

What are the sxs of gonococcal arthritis?

A 
1. Prodromal migratory polyarthralgias involving wrist, knee, ankle or elbow
A. Joint pain occurs over 1-4 days
B. Fever
C. Abdominal pain
D. Dysuria; < 25% have GU sxs
58
Q

What are the 2 forms of gonococcal arthritis?

A
  1. Tenosynovitis (commonly wrists, fingers, ankles, or toes), skin rashes, polyarthralgia syndrome, fever, chills, generalized malaise
  2. Purulent monoarthritis w/o skin lesions (frequently knee, wrist, ankle or elbow)
  3. Most pts have characteristic skin lesions on palms and/or soles (small necrotic pustules)
59
Q

What labs are ordered for gonococcal arthritis?

A
  1. Joint fluid aspirate
    A. Cultures + in < 50% cases
    B. Urethral, rectal, throat cultures & BC should be done on all pts suspected of GC arthritis
    C. Often positive in absence of local sxs
  2. Urinary NAAT for N. gonorrhea
  3. X-rays
    A. Soft tissue swelling
60
Q

What is the treatment for gonococcal arthritis?

A
  1. Admission to hospital to confirm dx
  2. Joint aspiration to drain infected fluid
  3. IV Abx x 48-72 hrs, then change to IM Abx x 7-14 day course
    A. Third generation cephalosporin (Ceftriaxone/Rocephin) IV  cefixime po
    B. Ceftriaxone 250 mg IM Q24hrs 7-14 day course (no longer p.o. recommended d/t resistant strains of gonococci
61
Q

What is reactive arthritis?

A
  1. Formerly Reiter’s Syndrome: postinfectious arthritis, urethritis and conjunctivitis (clinical triad)
  2. Triad of urethritis, conjunctivitis and oligoarthritis
    A. Mouth ulcers are another common sign
  3. Uncommon, typically occurs in young adults, males>females
62
Q

What can reactive arthritis be preceeded by?

A
  1. Arthritic syndrome precipitated by antecedent GI or GU infections
    A. GI pathogens: Shigella, Salmonella, Yersinia, Campylobacter, Clostridium difficile
    B. GU pathogens: Chlamydia trachomatis, Chlamydia pneumoniae, E. coli
63
Q

What are the sxs of reactive arthritis?

A 
1. Asymmetric sterile oligoarthritis (1-4)
A. Large WB joints
B. Knee & ankle
2. Dactylitis
3. Painful oral ulcers
4. Penile lesions
5. Ulcers on extremities, palms and soles
6. Plantar heel pain
7. Fever & weight loss common
64
Q

What are the dx studies & results for reactive arthritis?

A
  1. ESR and CRP ↑
  2. HLA-B27- 80% are positive
  3. X-rays
    A. Nl in early stage
    B. Nonspecific STS
    C. sacroiliitis
65
Q

What is the treatment for reactive arthritis?

A
  1. Usually self-limited process (3-12 mos) but symptomatic tx needed
  2. NSAIDs
    A. Mainstay of treatment
  3. If one joint, cortisone injection
  4. Sulfasalazine
    A. Second line agent if not responding to NSAIDs
66
Q

What are crystal-induced arthritis?

A
  1. Gout

2. Pseudogout

67
Q

Define gout

A

Metabolic disease marked by uric acid deposits causing painful arthritic joints

68
Q

What can cause gout?

A
  1. Assoc w/ ↑ serum uric acid
    A. Major end product of purine metabolism
  2. Hyperuricemia results from:
    A. Under-excretion problem: Most common
    B. Overproduction problem
    C. Or both
  3. Formation of uric acid calculi in kidneys may also occur
69
Q

What is the pathophys of gout?

A
  1. Uric acid becomes supersaturated in blood & other body fluids -> Ur Ac crystallizes -> formation of tophi
    A. Tophi: Nodular deposit of urate salts in connective tissue throughout body w/ asst foreign body reaction
  2. Presence of uric acid crystals triggers an acute inflammatory response
    A. Neutrophils release lysosomes -> tissue damage
70
Q

What are the risk factors for gout?

A
  1. M>F
  2. Family hx of gout
  3. Alcohol: Beer
  4. Medications
    A. Diuretics
    B. Chemotherapy
    C. Niacin
  5. Diet
  6. Chronic kidney disease
  7. Hypothyroidism
71
Q

What are the sxs of gout?

A
  1. Sudden onset joint PAIN
    A. Frequently nocturnal
  2. 1st MTP jt (Podagra)
    A. Can affect knee, ankles & other toes also
  3. Localized erythema, swelling, warmth
    A. Dusky red, tense, warm skin over jt
  4. +/- fever
  5. Tophi may be found in chronic disease:
    A. Ears, hands, feet, olecranon, prepatellar bursa
    B. Develop years after initial gout attack
72
Q

What dx tests are used for gout and what are the results?

A
  1. Serum uric acid > 6 mg/dl
    A. Not always high
    -More important is a significant change in level of Ur Ac
    -Asymptomatic hyperuricemia should not be treated
  2. ESR inc
  3. WBC inc
  4. Joint aspiration
    A. Monosodium urate crystals
    B. Needle- like negatively birefringent crystals
73
Q

What xray results may be present in gout?

A
  1. “Rat bite” may be seen late in disease

2. Punched out erosions with an overhanging rim of cortical bone

74
Q

What is the acute treatment of gout?

A
  1. NSAIDs: Medication of choice
    A. Nonselective COX inhibitor
    -Indomethacin / indocin 25-50 mg po q 8 h x 5-10 days
    B. COX-2 inhibitor: Celebrex
    C. Contraindications:
    Active PUD, renal disease, allergy to NSAIDs
  2. Colchicine (0.6 mg)
    A. 2 tabs @ onset of pain and then 1 tab 2 hours later
    B. Useful if pt cannot take NSAID
    C. Inhibits leukocyte migration, phagocytosis, metabolic activity and release of proinflammatory autacoids
    D. Caution in renal pts
  3. Oral corticosteroids: used in pts who cannot take NSAIDs
  4. Intra-articular Corticosteroid injection
    A. Triamcinolone 10-40 mg
    B. Depo-Medrol 40-80 mg
75
Q

What are the goals of chronic gout treatment?

A
  1. Minimize urate deposition in tissues

2. Reduce frequency and severity of recurrences

76
Q

What are the diet changes in treating gout?

A
  1. Wt loss if inc BMI
  2. Avoid:
    High purine diet, alcohol, certain medications
77
Q

What are the chronic treatment options for gout?

A
  1. Colchicine prophylaxis
    0.6 mg po Qdaily to BID
  2. Xanthine oxidase inhibitors:
    Allopurinol (zyloprim)
  3. Uricosuric drugs : Probenacid
78
Q

When is Allopurinol used? What is the moa and SE?

A
  1. Allopurinol (zyloprim) (maintenance) 100 mg po Daily
    A. more then 3 episodes of acute gout
    B. Used in treating over-producers, Urine Ur ac > 800 mg/day
    C. Can reduce tophi size
    D. Side effects:
    Can potentially precipitate acute gout attack
79
Q

What is the mechanism of probenacid?

A
  1. Reduction of serum uric acid
  2. Blocks tubular re-absorption of filtered urate
  3. Prevents formation new tophi and reduces size of tophi
80
Q

What is the prognosis of gout?

A
  1. With treatment, acute gout attack can last days to several weeks
    A. Intervals btw acute gouty attacks varies
  2. Chronic gouty arthritis occurs after repeated attacks of gout
    A. 3 or more acute episodes allopurinol
    B. Refer to Rheumatologist
  3. Younger age of onset, inc tendency for progressive course
81
Q

What is pseudogout?

A
  1. Calcium pyrophosphate dihydrate (CPPD) deposition disease in fibro- and hyaline cartilage -> acute crystal-induced arthritis
    A. Chondrocalcinosis of affected joints
  2. Acute and recurrent arthritis involving large joints
    A. Most common: knees and wrists
82
Q

What are the risk factors for pseudogout?

A
  1. Age > 60 yrs
  2. Occurs at higher rate in pts w/ OA
  3. Most cases have no associated condition
    A. Hyperparathyroidism, hemochromatosis, hypothyroidism can inc risk of CPPD
83
Q

What are the sxs of pseudogout?

A

Painful inflammation of a joint

84
Q

What dx studies are used for pseduogout?

A
  1. Joint fluid: Calcium pyrophosphate crystals
    A. Rhomboid-shaped positively birefringent
  2. X ray: Fine linear calcifications in cartilage -> chondrocalcinosis
85
Q

What treatment is used for pseudogout?

A
  1. Treat underlying disease, (OA) if present
  2. NSAIDs – acute pain
    A. Indomethacin / Indocin
    B. Naproxen / Naprosyn
    C. Celebrex
  3. Intra-articular steroid injection when NSAIDs contraindicated

Phys: Bone & Gen Med: Ortho (14 decks)

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