Gout Flashcards

1
Q

Gout is an excessive amounts of

A

uric acid (end product of purine metabolism)

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2
Q

What are the signs of Gout Arthritis?

A

Recurrent episodes of acute arthritis, large crystalline aggregates called tophi, and chronic joint deformity

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3
Q

Gout has precipitation of

A

Precipitation of monosodium urate crystals

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4
Q

Factors that contribute to Gout

A

Age of the individual and duration of the hyperuricemia: usually after 20to 30 years of hyperuricemia

Genetic predisposition: X-linked abnormalities of HGPRT, primary gout multifactorial inheritance

Heavy alcohol consumption

Obesity

Certain drugs (e.g., thiazides) reduce excretion of urate and predispose to the development of gout

Lead toxicity

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5
Q

Primary gout is

A

Overproduction of uric acid Normal excretion (majority) Increased excretion (minority)

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6
Q

Secondary Gout

A

Increased nucleic acid turnover ( leukemias )

Renal causes (Reduced excretion of uric acid with normal production (80 to 90% cases)

Inborn errors of metabolism (Lesch-Nyhan syndrome: (Overproduction of uric acid, increased urinary excretion - complete HGPRT deficiency

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7
Q

What is the morphology of Gout arthritis

A

Neutrophil infiltrate in synovium/synovial fluid

Needle-shaped monosodium urate crystals in cytoplasm of neutrophils and in synovium

Synovium is edematous and congested

Synovium: forms pannus

Location: articular cartilage of joints and peri-articular ligaments, tendons, soft tissue of ear lobes, nasal cartilages, skin of fingertips

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8
Q

What is Tophi?

A

pathognomonic, urate crystals surrounded by lymphocytes, macrophages, and foreign-body giant cells, attempting to engulf the masses of crystals

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9
Q

In Gouty Arthritis, how does the synovial fluid look with special polarization?

A

Negative birefringence (yellow)

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10
Q

Pathogenesis of Gout arthritis

A
  1. Hyperuricemia
  2. precipitation of rate crystals in joints
  3. activate complement pathway
  4. Neutrophil chemotaxis
  5. Phagocytosis of crystals by neutrophils
  6. lysis of neutrophils and release of lysosomal enzymes

Also

  1. phagocytosis of monocytes
  2. release iL-1, TNF, IL-6
  3. release proteases
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11
Q

Clinical features of Gout arthritis

A

95% cases in men > 30 years of age

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12
Q

Acute gouty arthritis

A

Mostly first attack is mono-articular; 50% in 1st metatarsophalangeal joint (great toe)

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13
Q

Four stages of gout

A

(1) asymptomatic hyperuricemia
(2) acute gouty arthritis
(3) “intercritical” gout
(4) chronic tophaceous gout

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14
Q

Asymptomatic hyperuricemia

A

around puberty in males and after menopause in women

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15
Q

Intercritical period:

A

Untreated acute arthritis may last for hours to weeks, but it gradually resolves and patient becomes asymptomatic

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16
Q

Chronic tophaceous gout:

A

After a decade of recurrent attacks, radiographs show characteristic juxta-articular bone erosion caused by the crystal deposits and loss of the joint space leading to severe crippling disease

17
Q

Treatment of Gouty arthritis

A

Non-pharmacologic - modify diet to eliminate diets high in purine, moderation in alcohol intake

Pharmacologic Rx
Acute gout: NSAIDs or colchicine (if intolerant then corticosteroids)

Chronic treatment to normalize serum uric acid:
Uricosuric agents for underexcretors (e.g., probenecid)

Allopurinol (xanthine oxidase inhibitor) for overproducers

18
Q

Pseudogout is caused by

A

Calcium pyrophosphate crystal deposition disease

19
Q

Most common joint involved in Pseudogout is

A

the knee

20
Q

Pseudogout happens in which population?

A

elderly population ( 50% of patients who are 85 years old )

21
Q

What is the pathogenesis of Pseudogout?

A

CPPD disease: ↑ with
Hemochromatosis, hemosiderosis – Iron is presumed to inhibit pyrophosphatase accounting for decreased degradation of pyrophosphate
(2) Primary hyperparathyroidism (HPTH) - Increase in calcium

Chondrocalcinosis: linear deposits of calcium pyrophosphate in articular cartilage

22
Q

Pseudogout is what type of birefringence?

A

Calcium pyrophosphate: positive birefringence

blue

23
Q

Suppurative Arthritis is caused by?

A

Haemophilus influenzae in children <2 years
S. aureus in older children and adults

Gonococcus in late adolescence/young adulthood (more in women)

Individuals with sickle cell disease – Salmonella

Septic arthritis/tendinitis due to cat/dog bite - Pasteurella multocida

24
Q

Suppurative Arthritis is characterized by?

A

Sudden onset of pain, redness, and swelling of the joint with restricted range of motion

Fever, leukocytosis, and elevated ESR (but in gonococcal infections – subacute)

In 90% of nongonococcal suppurative arthritis, single joint - usually the knee, followed by hip, shoulder, elbow, wrist, and sternoclavicular joints

Joint aspiration is typically purulent,allows identification of the causal agent

Deficiency of C6-9 predisposes to disseminated gonococcal infections (septic arthritis involving knee, tenosynovitis and dermatitis of the wrists & ankles)

Staphylococcus aureus - most common non-gonococcal cause, Treatment: Nafcillin + cephalosporin (third generation)

25
Q

Lyme Arthritis is caused by

A

spirochete Borrelia burgdorferi, transmitted by deer ticks of the Ixodes ricinus complex

26
Q

What are the stages of Lyme Arthritis?

A

Stage 1 : days, early localized, erythema chronicum migrans

Stage 2 : weeks, early disseminated
Flu like illnes, Cardiac, Neurologic symptoms

Stage 3 : months to years, Late
Lyme arthritis, Encephalopathy/ neuropathy (bilateral Bell’s palsy)

27
Q

Lyme Arthritis biopsy isn’t useful to diagnose, so what should you use?

A

Catch it in the 1st stage!

28
Q

What is Neuropathic arthropathy (Charcot’s joint)?

A

Because of Diabetes Mellitus, they lose sensation in the feet, they keep falling over or tripping, damaging the joint.

29
Q

Is Charcot’s joint inflammatory?

A

no