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Rheumatology > 2 - Acute Arthritis and Urate Metabolism Crystal Arthritis > Flashcards

2 - Acute Arthritis and Urate Metabolism Crystal Arthritis Flashcards

1
Q

Acute Arthritis - “Acute”

A

Less than 6 weeks duration

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2
Q

Acute Arthritis - “Arthritis”

A

Inflammation localized to the articular surfaces
Swelling (Synovitis and/or effusion), warmth, discomfort, redness
Distinct from arthralgia, peri-arthritis, tendinitis, bursitis, etc

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3
Q

Acute Joint Complaints - Goals of the initial evaluation

A

Distinguish articular vs. non-articular pathology
Determine inflammatory vs. non-inflammatory features
Identify and triage musculoskeletal emergencies appropriately
Assess whether history, current symptoms and exam are consistent with a specific rheumatic disease
Obtain appropriate additional testing (imaging, labs, etc)
Establish short and long term treatment plans (when to refer)

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4
Q

Acute Joint Complaints - Timing

A

Rapid Onset:
Trauma
Septic
Crystalline

Slow Onset:
Systemic Rheumatic Disease
Non-Inflammatory Process (Osteoarthritis)

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5
Q

Acute Joint Complaints - Time of day the symptoms feel worst

A

AM:
Prolonged in systemic rheumatic disease

PM:
Sprain/strain/non-inflammatory

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6
Q

Acute Joint Complaints - Worse with Activity or Rest

A

Worse with activity:
Tendinitis
Bursitis
Non-Inflammatory Process

Worse with rest:
Systemic rheumatic diseases

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7
Q

Acute Joint Complaints - Time from no symptoms to maximal intensity

A

Rapid:
Trauma
Septic
Crystalline

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8
Q

Arthralgia

A

Pain in the joint that doesn’t appear to be inflammatory

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9
Q

Acute Joint Complaints - Confined to joints or inter-articular

A

Localized to joints:
Arthritis
Arthralgia

Inter-articular:
Diffuse pain syndromes

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10
Q

Acute Joint Complaints - Mono vs oligo vs polyarticular

A

Polyarticular:
Less likely to be septic arthritis (however, polyarticular septic arthritis is still possible)

Monoarticular:
Can still be an early presentation of a systemic rheumatic disease

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11
Q

Acute Joint Complaints - Pattern of joints affected

A

Small joint peripheral

vs.

Large joint

vs.

Axial involvement

These provide clues to the type of systemic rheumatic disease if presentation is polyarticular

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12
Q

Acute Joint Complaints - Recent Trauma

A

Possible fracture
Sprain
Strain
Tendon/ligamentous rupture

Also acute attacts of CCPD are often preceded by traumz

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13
Q

Acute Joint Complaints - Warmth & Swelling

A

Hot to touch:
Septic or crystalline

Cool:
Non-inflammatory

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14
Q

Acute Joint Complaints - Intensity and quality of symptoms

A

0 - 10 pain scale, “touch me not”:
Highest often in septic or crystalline

Sore vs ache vs stiff vs stabbing/lancinating vs burning vs numbness/tingling

Stiff>pain:
Systemic rheumatic diseases

Vague deep ache:
Hyperparathyroidism
Osteomalacia
Bone lesions (night pain)

Burning/numbness/tingling:
Neurogenic

Claudication:
Vascular vs. spinal stenosis

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15
Q

Acute Joint Complaints - Symmetry

A

Certain systemic rheumatic diseases

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16
Q

Acute Joint Complaints - Constitutional/prodromal symptoms

A

Infection or systemic rheumatic diseases, occasionally crystalline

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17
Q

Acute Joint Complaints - Prior similar episodes

A

Less likely to be infectious

Intercritical return to complete normality:
Crystalline arthritis

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18
Q

Specific indicators of systemic rheumatic diseases

A 
Cutaneous manifestations (Psoriasis, photosensitivity, purpura, skin thickening, erythema nodosum, nodules, etc)
Swollen glands
Raynaud's
Oral/nasal ulcers
Pleurisy/pericarditis
Eye inflammation
Nail changes
Dry eyes/mouth
Proximal muscle weakness
Sinusitis
Hearing loss
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19
Q

Acute Joint Complaints - Physical Exam - Articular

A

Inspection
Range of motion
Palpation (warmth, erythema, swelling, effusion, tenderness, deformity, crepitus, stability)

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20
Q

Acute Joint Complaints - Physical Exam - Extra-articular

A

Requires multi-system examination

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21
Q

Distinguishing Exam Features - Symmetry

A

Probably - Systemic Rheumatic Disease
Maybe - Non-inflammatory
Probably not - Tendinitis/bursitis

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22
Q

Distinguishing Exam Features - Inflammation

A

Tendinitis/bursitis - Over tendon/bursa
Systemic Rheumatic Disease - Common
Unusual in non-inflammatory

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23
Q

Distinguishing Exam Features - Tenderness

A

Tendinitis/bursitis - Focal

Systemic rheumatic disease - Over entire joint space

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24
Q

Distinguishing Exam Features - Locking

A

Tendinitis/bursitis - Unusual expect with tears
Noninflammatory - Possible, implies loose body or internal derangement
Uncommon in Systemic rheumatic disease

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25
Q

Acute Monoarthritis - Common Etiologies

A 
Infection
Crystal-induced
Trauma
Hemarthrosis
Osteonecrosis
Early monoarticular presentations of polyarticular diseases
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26
Q

Acute Monoarthritis - Infection

A

Bacteria (Gonococcal vs. non-gonococcal)
Viruses (often polyarticular)
Fungi/spirochetes/mycobacteria (Coccidiodomycosis, spirotrichosis, blastomycosis, lyme, M. marinum)

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27
Q

Acute Monoarthritis - Crystal induced

A 
Gout
Pseudogout (Calcium pyrophosphate deposition disease, CPPD)
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28
Q

Acute monoarthritis - Joint aspiration

A

IMPERATIVE to perform if septic joint ins suspected
Gout is a risk factor for septic arthritis
“If you think of it, do it”
Gram stain and culture should be performed prior to antibiotics
Warfarin is NOT a contraindication

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29
Q

Monoarthritis - Synovial fluid tests

A

Cell count & Differential:
Inflammatory WBC>2,000 or >75% PMN
Septic and crystal arthritis often much higher

Gram stain & culture:
Negative studies to not absolutely rule out septic joint
Aerobe, anaerobe, fungal, AFB and mycobacterial if clinically indicated
Crystal assessment using polarized light microscopy
Glucose, LDH, protein not very helpful

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30
Q

Inflammatory Joint Fluid (>2,000 WBC/μL)

A 
Rheumatoid arthritis
Psoriatic arthritis
Spondyloarthropathies
Juvenile chronic arthritis
Gout
Pseudogout
Systemic lupus erythematosus
Septic arthritis
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31
Q

Non-Inflammatory Joint Fluid (

A 
Osteoarthritis
Trauma
Charcot's joint
Pancreatitis
Hemochromatosis
Acromegaly
Glucocorticoid withdrawal
Hypertrophic osteoarthropathy
Avascular necrosis
Pigmented villonodular synovitis
Systemic lupus erythematosus
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32
Q

Monoarthritis - Additional testing

A

CBC
Blood cultures
Coagulation studies
Plain radiographs

Elevated uric acid level does not exclude septic arthritis

CT or MRI in specific situations (suspect osteomyelitis as focus, or soft tissue abscess

Specialized testing for specific pathogens (typically not sent initially)

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33
Q

Bacterial Septic Arthritis

A

Musculoskeletal EMERGENCY

Associated with:
Sepsis
Extensive joint damage
Mortality (10% overall, 19 - 33% in elderly or with comorbidities)
Permanent loss of joint function (40%)
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34
Q

Bacterial Septic Arthritis - Gonococcal

A

Incidence decreasing over past 2 decades
Typically sexually active young adults
Female > Male

Other clinical features (maybe, but not necessary):
Polyarthralgia can precede - monoarthritis in 50%, though
Constitutional symptoms
Tenosynovitis, especially wrist (68%)
Skin lesions (75%) - erythematous papules progress to vesicles or pustules on extremities and trunk

Anogenital infection often asymptomatic

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35
Q

Bacterial Septic Arthritis - Non-Gonococcal

A 
Gram positives (80%):
Staph aureus predominates (60%)
Gram negatives (10 - 20%):
E. Coli
Proteus
Klebsiella
Enterobacter
Very young, elderly, injection drug use, immunocompromised

Diabetes is a risk factor
Prodrome of malaise and fever (fever is often mild and only presents in 30 - 40% with temperatures >39C)
Large joint predilection (knees/hips>shoulders>wrist/ankles)

Requires aggressive management

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36
Q

Bacterial Septic Arthritis - Management

A

Serial aspiration to dryness vs. open surgical drainage with lavage
Parenteral antibiotics
Splinting and physical therapy to prevent contractures and muscle atrophy

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37
Q

Staph Aureus Septic Arthritis

A

Pathogenesis dependent on pathogen virulence factors and host factors

Virulence factors:
Adhesins
Bio-film (evasion mechanism)
Enzymes and toxins)

Consequence is inflammatory cell infiltration, synovitis, damage to cartilage and bone, erosion, joint destruction
Experimental limitation of virulence factors results in less joint damage
Host factors cause more damage than pathogen factors

38
Q

Lyme Arthritis

A

Features dependent on phase of disease

Early disseminated lyme:
Polyarthralgia
ELISA may be negative very early

Late lyme:
Weeks to months after primary infection (ELISA positive, if lyme infected)
Mono, oligo, occasionally polyarthritis
Tends to be symmetric
Large/medium joint
Large effusion in a single knee in most
39
Q

Polyarthritis Differential - Infection

A 
Gonococcal
Meningococcal
Lyme disease
Rheumatic fever
Bacterial endocarditis
Viral - Rubella, parvovirus, HBV, HCV
Fungal - Histoplasmosis, Disseminated Coccidiodomycosis
Mycobacterial
40
Q

Polyarthritis Differential - Systemic Rheumatic

A 
Rheumatoid Arthritis
Systemic Lupus Erythematosus
Sjogren's Syndrome
Reactive Arthritis
Psoriatic Arthritis
Polyarticular Gout
Sarcoid Arthritis
Vasculitis
Polymyalgia Rheumatica
Inflammatory myopathies
41
Q

Viral Arthritis

A

Usually self-limited, requires no specific therapy
Direct invasion of synovium by virus
Immune complex mediated synovitis
Virus acting as an antigenic target for the immune system

42
Q

Most common virus causing chronic polyarthralgia/arthritis

A

HCV

43
Q

Common viruses causing self-limited polyarthralgia/arthritis

A

HBV
Parvovirus
Alphaviruses
Dengue

44
Q

Viruses less likely to cause polyarthralgia/arthritis

A 
EBV
CMV
Mumps
Coxsackie
HSV
Adenovirus
45
Q

Viral serologies if high suspicion

A

HCV
HBV
Parvovirus

Viral cultures form joints are difficult and rarely performed

46
Q

Chikungunya - Locations

A

Caribbean
Parts of Africa
Mediterranean
Southeast Asia

47
Q

Gout

A

Intense inflammatory arthritis
Destructive potential for the joint
Caused by immunoreactivity to precipitated uric acid crystals in individuals with hyperuricemia

48
Q

Phases of gout

A

Acute:
Intermittent presentation

Chronic:
Episodic vs. persistent
Tophaceous vs. non-tophaceous

49
Q

Tophi

A

Uric acid crystals under the skin
Accumulate in places that are cooler
Can develop sinus tracks that can drain

50
Q

Acute Gout - Cardinal signs and symptoms

A 
Intense articular inflammation:
Calor
Dolor
Rubor
Tumor

Touch-me-not tenderness
Maximal symptoms in early morning after sleeping for hours
Inter-critical resolution of symptoms

51
Q

Acute Gout - Joint Predilection

A 
1st Metatarsophalangeal (called podagra)
Midfoot
Ankle
Knee
Wrist
Elbow
Distal Interphalangeal
52
Q

Chronic Gout - Cardinal signs and symptoms

A

Features/presentation extremely variable

Attacks more frequent or continuous symptoms
Tophi
Articular damage, destruction, disability
Nephropathy/Nephrolithiasis
Cardiovascular risk

53
Q

Gout - Radiograph

A

Preservation of the cortex around the erosion
Overhanging edge

“rat bite erosion”

54
Q

Gout - Epidemiology

A

Most common inflammatory arthritis
Prevalence estimates vary

Tophaceous gout: ~75% of untreated chronic gout patients with disease > 20 years

M>F
Very uncommon in pre-menopausal women
Incidence in women goes up after menopause

55
Q

Why is incidence of gout increasing?

A

Aging population
Increasing obesity
Treatment of cardiovascular risk factors (diuretics)
Improved longevity with CKD/Transplant

56
Q

Risk factors for Incident Gout

A

Hyperuricemia (main risk factor, necessary but not sufficient)
Obesity
Hypertension
Medications (Diuretics, cyclosporine, tacrolimus, low dose aspirin)
Dietary (Red meat, shellfish, other fish, beer, liquor)

57
Q

Urate Metabolism

A

Diet and cell breakdown
Purines
Hypoxanthine (broken down by Xanthine Oxidase)
Xanthine (broken down by Xanthine Oxidase)
Uric acid (broken down by Urate oxidase/Uricase)
Allantoin + CO2 + H2O

58
Q

Allantoin

A

Soluble and easy to excrete

59
Q

Primary contributors to the urate level

A

Endogenous purine synthesis

Dietary purine load (less so)

60
Q

Primary contributors to urate excretion

A 
Renal excretion
Gut excretion (less so)
61
Q

Urate: Overproduction vs. Underexcretion

A 
Underexcretion = 90% of gout patients
Overproduction = 10% of gout patients
62
Q

How much urate is excreted after passing through the proximal tubule?

A

7 - 12%

63
Q

Urate exchanger at the proximal tubule

A

URAT1

Urate reabsorbed in order to trade and excrete lactate, nicotinate, pyrazinamide

64
Q

Genetics of hyperuricemia

A

Mutations in hypoxanthine guanine phosphoribosyltransferase (HPRT) and phosphoribosyl pyrophosphatase synthetase (PRPSI):
Early onset gout
Lesch-Nyhan Syndrome

Idiopathic hyperuricemia:
Likely polygenic
Polymorphisms in URAT1 and other urate transport proteins are likely contributors

65
Q

Acute Gout - Hallmark Crystal Finding

A

Needle shaped
Intracellular
Negative birefringence with polarized light microscopy

66
Q

How do the crystals trigger inflammation?

A

Crystals bind TLRs on macrophages
TLRs signal the NALP3 Inflammasome (IL-1, TNF-α, IL-18)

Cytokine cascade:
Endothelial priming
Neutrophil influx
Leukotriene production
Bradykinin generation
67
Q

Neutrophil Extracellular Traps (NETs)

A 
Neutrophils die and extrude their DNA
This forms a net
This aggregates inflammatory cytokines and chemokines
This breaks the inflammatory cascade
Resolves acute gouty inflammation
68
Q

Gout - Diagnostic Pearls

A

Demonstration of uric acid crystals should be attempted in all patients.
Asymptomatic joints often demonstrate uric acid crystals
Serum uric acid levels can be low or normal during an acute attack
Acute gout and septic arthritis can coexist
Gout and rheumatoid arthritis are rarely seen together
Rapidity of onset, intensity of symptoms, intercritical resolution of symptoms distinguish gout from other inflammatory arthritidies

69
Q

Gout - Treatment

A

Acute attack:
Reduce inflammation, Pain

Chronic Gout:
Reduce hyperuricemia
Reduce the frequency/prevent flares

70
Q

Acute Gout - Treatment

A 
Colchicine
NSAIDs
Intra-articular steroids (preferred)
Systemic corticosteroids/ACTH
Analgesics
Ice
Investigational - Systemic anti-IL-1 therapy and other anti-cytokine biologics
71
Q

Acute Gout - Colchicine

A

Used for decades, but only one clinical trial
Mechanism unknown
Likely interferes with PMN chemotaxis
Best outcome when used early (first 12 - 24 hours of attack)

Toxicities:
Diarrhea
Myopathy (especially in those with renal/hepatic insufficency, those on HMG-CoA reductase inhibitors, cyclosporine)
Bone marrow suppression

Low dose colchicine plus lower doses 1 hour later is as effective as a higher dose regimen

72
Q

Acute Gout - NSAIDS

A

Well established
Little studied
All NSAIDs are likely effective

Indomethacin traditionally used (but risk of GI toxicity)

COX-2 inhibitors appear to be as effective as non-selective NSAIDs
Etoricoxib is as effective as indomethacin in a randomized, double blind clinical trial

73
Q

Acute Gout - Corticosteroids

A

Intra-articular corticosteroids = treatment of choice for acute mono/oligo articular gout

Refractory to NSAIDs/colchicine
Contraindications to NSAIDs/colchicine
May be associated with rebound flares when used without NSAIDs/colchicine
Side effect profile often an issue for those with gout and multiple comorbidities
Intramuscular corticotropin an option, but not seen often

74
Q

Acute Gout - Cytokine Inhibition

A

IL-1 antagonism
Pain after acute flare is lower for Canakinumab compared to intramuscular Triamcinolone
It is for patients are unable to take NSAIDs or colchicine
Can’t hold a candle to NSAIDs/colchicine

75
Q

Gout Flare Prophylaxis - Cytokine Inhibition

A

IL-1 antagonism
Acute flares lower in patients treated with Canakinumab compared to colchicine
Acute flares after starting allopurinol reduced patients treated with rilonacept compared to placebo

Not compared against colchicine
Not FDA approved for this indication

76
Q

Chronic Gout - Management

A

Reduce/Eliminate Flares by lowering Urate
Reduce exogenous purines
Reduce endogenous purines
Facilitate urate handling

Prophylax against flares (important during lowering of urate)
Urate therapy recommended for 2+ significant attacks per year, tophi or radiographic damage

77
Q

Chronic Gout - Xanthine Oxidase Inhibitors

A

Allopurinol
Febuxostat
Oxypurinol

Can be used in over-producers, under-excretors, and those with urate nephrolithiasis

78
Q

Allopurinol

A

Requires renal function based on dosing adjustment

Toxicities (

79
Q

Febuxostat

A

Non-purine selective inhibitor of xanthine oxidase
Less toxicity in patients with chronic kidney disease
No cross-reactivity in patients with allopurinol hypersensitivity
Flares common with initiation - colchicine prophylaxis recommended

80
Q

Chronic Gout - Uricosurics

A

Less commonly used
May precipitate nephrolithiasis in uric acid over-excretors or patients with a history of renal calculi

Probenecid
Benzbromarone/Sulfinpyrazone (not available in the USA)
Combining with Allopurinol is an option (requiring CAREFUL monitoring)

81
Q

Probenecid

A

Molecular target: Renal URAT1 exchanger
Common clinical utility in patients refractory or intolerant to allopurinol (eg allopurinol hypersensitivity)
Ineffective in conjunction with low-dose aspirin
Ineffective in chronic kidney disease

82
Q

Chronic Gout - “Surprise” uricosurics

A

Losartan (other ARBs)?
Blocks URAT1 exchanger in proximal renal tubule

Fenofibrates
Statins (maybe?)
Vitamin C
Cherries/Cherry extract
Low fat dairy products
83
Q

Chronic Gout - Uricase Replacement

A 
Rasburicase
PEGylated uricase (Pegloticase)
84
Q

Rasburicase

A

Uricase replacement
Available for the prevention of tumor lysis syndrome
Immunogenicity prevents repeated infusions

85
Q

PEGylated Uricase (Pegloticase)

A

Less immunogenic than Rasburicase
Shows promise for rapid resorption of tophi
Long-term safety unknown
FDA approved for refractory gout (appropriate for

86
Q

Chronic Gout - Concomitant Management

A

Diet:
Less red meat, shellfish, fatty fish, alcohol, sugar, sweetened soda
More water, low fat dairy

Weight Loss

Treat other risk factors:
Hypertension, psoriasis, chronic dehydration

Consider alternates to diuretics

87
Q

Acute Gout Prophylaxis during Urate Lowering Therapy - Rules of thumb

A

Do not start urate lowering therapy during an acute attack
Do not discontinue urate lowering therapy if an attack occurs
Prophylax with colchicine (0.6mg BID) or NSAIDs (colchicine preferred) for the first months of urate therapy
Acute attacks more likely when rapid uric acid shifts occur

If the patient is prone to attacks, stat low and slowly titrate urate lowering therapy

88
Q

Acute Gout Prophylaxis during Urate Lowering Therapy - Typical timeframes

A

4 to 12 months to normalize serum uric acid levels

12 to 24 months for noticeable tophi reduction

89
Q

Calcium Pyrophosphate Deposition Disease (CPDD) - Multiple Presentations

A

Asymptomatic Chondrocalcinosis:
In isolation or in conjunction with osteoarthritis

Acute CPPD inflammatory arthritis

Chronic CPPD inflammatory arthritis:
Can be mono-, oligo- or polyarticular
Rarely can resemble rheumatoid arthritis

Knee usually involved, especially in acute pseudogout
Hip, wrist and shoulder often involved, especially in chronic pyrophosphate-related osteoarthritis

90
Q

CPPD Epidemiology

A

Prevalence unknown
There are hereditary forms

Associated with:
Prior joint damage/injury
Hemochromatosis
Hyperparathyroidism
Hypophosphatasia
Hypomagnesemia
Age
91
Q

CPPD - Pathophysiologic Mechanism

A

ANKH gene linked to chondrocalcinosis
Gain of function mutations associated with increased extracellular inorganic pyrophosphate (ePPi)
Higher ePPi associated with CPPD deposition in chondrocytes

92
Q

Hydroxyapatite Deposition Disease

A

Another crystal-induced arthritis

Intra-articular and periarticular hydroxyapatite deposition
Milwaukee shoulder
Predisposing factors - age, CPPD, dialysis, trauma

Rheumatology (16 decks)

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