Musculoskeletal - Joint - Metabolic Disease Flashcards

1
Q

Monosodium Urate Gout

A
  • Term gout represents all of the various forms of crystal-induced deposition diseases of the joints. These diseases can be subdivided into three common types based on the type of crystals found in the synovial fluid:
    (1) monosodium urate (MSU)
    (2) calcium pyrophosphate dihydrate (CPPD)
    (3) calcium hydroxyapatite (HA)
    (4) calcium oxalate (CaOx) - very rare, primary oxalosis.

Note: some texts use term “pseudogout for CPPD form. These forms are of endogenous origin, however, numerous exogenous substances can also crystalize in a joint to span an arthritic situation.

AKA - MSU gout, Gout, Podagra (when confined to great toe); gouty arthropathy

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2
Q

Monosodium Urate Gout - History

A
  • In western cultures, 10% of total population has hyperuricemia.
  • Gout affects less than 0.5% of the total population; however, the incidence can be higher in some families.
  • In families affected by the disorder, the incidence is 6-80%
  • males beging experiencing gout at 18; women after menopause
  • Gout is an end point of a group of disorders resulting in hyperuricemia
  • Plasma urate levels above 7 mg/dl is considered hyperuricemia
  • Lack of the enzyme hypoxantine guanine phosphoribosyl transferase can elevate uric acid production
  • Precipitation of monosodium urate crystals into the joint cavity
  • distal joint most effected due to lower temperatures
  • Crystals are chemotaxic to leukocytes
  • cytokines released and joint inflammation follows
  • Phagocytosis of crystals, cell rupture and release of lysosomal enzymes
  • Repeated attacks lead to chronic gouty arthritis
  • Tophi (aggregates of crystalline monosodium urate) accumulate in teh synovium)
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3
Q

Monosodium Urate Gout - Risk Factors

A
  • Age
  • Genetics
  • Alcohol consumption
  • Obseity
  • Drugs (thiazides)
  • Lead toxicity
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4
Q

Monosodium Urate Gout- Presentation

A
  • Acute onset over a few hours of moderate to severe monoarthritic joint pain
  • Attack is usually at night and typically involves the first metatarslphalangeal joint
  • Heat, (intense) redness and swelling surround the joint
  • Hyperalgesia to touch
  • Synovial effusion and periarticular cellulitis
  • Intercritical periods tend to become shorter with time.
  • Repeated attacks (>10 year period) can lead to tophi formation termed chronic tophacceous gout
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5
Q

Monosodium Urate Gout - Diagnostic Testing

A
  • DIagnosed in part by clinical presentation
  • CBC, ESR, and C-reactive protein
  • Serum uric acid levels
  • Aspiration:
    -monosodium urate crystals seen under polarizing light microscopy
  • Gram-stain and culture
    *Radiographic studies - PA and lateral views of the joint; findings include:
  • soft tissue calcifications
    Bony overhangs from the edges of joints, can be very deforming
  • Erosion cysts in the periarticular bone
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6
Q

Monosodium Urate Gout

A
  • American College of Rheumatology criteria:
  • More than one attack of acute arthritis
  • maximum inflammation developed within 1 day
  • Monoarthritis attack
  • Redness observed over joints
  • First metatarsophalangeal joint painful or swollen
  • unilateral first metatarsalphalangeal joint attack
  • unilateral tarsal joint attack
  • tophus (proven or suspected)
  • hyperuricemia
  • asymmetric swelling within a joint on x-ray
  • subcortical cysts without erosions on x-ray
  • monosodium urate monohydrate microcrystals in joint fluid during attack
  • joint fluid culture negative for organisms during attack
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7
Q

Monosodium Urate Gout - treatment

A
  • Prove joint is not septic
  • Relieve pain and swelling; NSAIDS when appropriate
  • Oral and intra-articular corticosteroids
  • colchicine
  • Triamcinolone if not oral medication is possible
  • joint aspiration

Management with complications: Prophylaxis with colchicines or allopurinol when appropriate

Preventions: lifestyle changes

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8
Q

Calcium Pyrophosphate dihydrate-induced arthritis

A
  • pseudogout
  • CPPD is a calcium salt that is deposited into articular cartilage and released as crystals into the joint space.

AKA - Calcium pyrophosphate dihydrate-induced arthritis (CPPD arthritis); Chondrocalcinosis; Pseudogout

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9
Q

Calcium Pyrophosphate dihydrate-induced arthritis (pseudogout) - History

A
  • CPPD is a common condition that occurs with aging in all races
  • Usually occurs in people over 50
  • About 4% of the adult population has articular CPPD deposits at the time of death
  • Nearly 50% of people older than 85 years have radiologic evidence of chondrocalcinosis
  • Three categories of CPPD:
  • idiopathic form
  • Hereditary form
  • Secondary form
  • Hereditary form is associated with a mutation in the ANKH Gene
  • transmembrane inorganic pyrophosphate transport channel
  • Secondary form is associated with:
  • previous joint damage
  • hyperparathyroidism
  • hypomagnesemia
  • hemochromatosis
  • hypothyroidism
  • Ochronosis
  • Diabetes Mellitus
  • crystal first form in the articular matrix, menisci and intervertebral joint
  • Seeding of the joint space induces chemokines initiating a neutrophil invasion
  • Free radicals and cytokines are released and macrophages move in to the joint with associated fibrosis.
  • Individual crystals are small (0.5 - 5 mm in size)
  • Knee > wrist (triangular fibrocartilage) > elbow > shoulders > ankles
  • Depositions of CPPD are usually bilateral in nature
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10
Q

Calcium Pyrophosphate dihydrate-induced arthritis (pseudogout) - Presentation

A
  • Can be asymptomatic
  • Can produce acute, subacute or chronic arthritis
  • Can be monoarthicular or polyarticular
  • Rapid onset of painful swelling in the joint
  • Warmth, swellng and joint effusion
  • Can mimic any of the following: Gout, RA, OA, Charcot joint
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11
Q

Calcium Pyrophosphate dihydrate-induced arthritis (pseudogout) - Diagnostic Testing

A
  • Arthrocentesis and aspiration

* Culture of the aspirate and examination by polarized by polarized light microscopy

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12
Q

Hydroxyapatitie arthritis (HA)

A
  • Calcium apatite arthritis

AKA - Basic calcium phosphate hydroxyapitie deposition disease; Chondrocalcinosis; Calcium hydroxyapatitie

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13
Q

Hydroxyapatitie arthritis (HA) - History

A
  • No known association with the ANKH mutation
  • A very destructive form afflicts the shoulder in the elderly (termed Milwaukee shoulder)
  • crystals are often deposited on vessels
  • Basic calcium phosphate crystals can be found in the synovial fluid of 30-60% of patients with osteoarthritis
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14
Q

Hydroxyapatitie arthritis (HA) - Presentation

A
  • Can be asymptomatic
  • Can be acute, subacute or chronic in onset
  • Acute synovitis, bursitis, or tendinitis
  • Chronic destructive arthropathy, typically shoulder or knee
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15
Q

Hydroxyapatitie arthritis (HA) - DIagnostic Testing

A
  • Radiographic studies non-specific

* Synovial analysis necessary to rule out infection

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16
Q

Hemochromatosis

A
  • a disorder of iron metabolism characterized by the accumulation of iron in body tissues, typically liver and pancreas. Osteoarthritis-like symptoms can accompany the build up of iron.
17
Q

Hemochromatosis - Epidemiology

A
  • One of the most common hereditary diseases of humans
  • The hemochromatosis gene HFE is located on the short arm of chromosome 6
  • HFE encodes a molecule regulating iron absorption across the intestinal epithelium
18
Q

Hemochromatosis - Etiology

A
  • Iron accumulation occurs at the rate of 0.5 - 2.0 grams per year, thus the disease presents late in life
  • Symptoms begin between 40-60 years of age
19
Q

Hemochromatosis - Pathology

A
  • Proliferation of the synovium with fibrosis and limited inflammatory cells
20
Q

Hemochromatosis - Presentation

A
  • Arthritis presents in 20-40% of cases
  • Osteoarthritis-like presentation starting in the small joints of the hands followed by the larger joints of the upper and lower extremities later
  • Stiffness and pain in the morning
  • Enlargement of the joint and tenderness
21
Q

Hemochromatosis - Diagnosis

A
  • Hook like osteophytes on imaging
22
Q

Hemochromatosis - Treatment

A
  • Phlebotomy

* Does not reverse the arthropathy significantly