1. Gouty Arthritis Quiz 류마티스내과 홍승재

2. Q1: Gout is caused by excess uric acid in the body. Uric acid results from the breakdown of purines. 1) True 2) False

3. Q2: Gout most commonly strikes a single joint with sudden, intense inflammation and pain. 1) True 2) False

4. Q3: Centuries ago, gout was known as "the disease of kings" and "the king of diseases" and was associated with high living and superior social status. 1) True 2) False

5. Q4: Men more commonly develop gout than women. Women typically don't develop gout until after they are postmenopausal. 1) True 2) False

6. Q5: Up to 18% of people with gout have a family history of gout, implying genetics may be a risk factor. 1) True 2) False

7. Q6: Foods which are high in purines such as certain meats, seafood, dried peas, and beans can increase uric acid levels and precipitate a gout attack. 1) True 2) False

8. Q7: Beer and other alcoholic beverages can raise the level of uric acid and provoke a gout attack. 1) True 2) False

9. Q8: Coffee and tea can raise the level of uric acid and provoke a gout attack. 1) True 2) False

10. Q9: Vegetables including kale, cabbage, parsley, green-leafy vegetables - good to eat if you have gout ! 1) True 2) False

11. Q10 Foods which are high in vitamin C -bad to eat if you have gout ! 1) True 2) False

12. Q11: Obesity and hypertension are NOT linked to gout. 1) True 2) False

13. Q12: Serum uric acid levels can be normal or low at the time of the acute gout attack 1) True 2) False

14. Q13: Which of the following drugs is NOT a known risk factor for gout? 1) aspirin/salicylates 2) diuretic 3) cyclosporine 4) methotrexate 5) Levodopa 6) Niacin

15. Q14: Which of the following diseases is NOT a known risk factor for gout? 1) leukemia 2) lymphoma 3) hemoglobin disorders 4) hypothyroidism 5) osteoarthritis

16. Q15: Urinalysis, blood urea nitrogen, serum creatinine, white blood cell (WBC) count, and serum lipids should be obtained in gout patients. 1) True 2) False

17. Q16: Elevated levels of uric acid in the blood can result in sharp needle-like crystals of monosodium urate deposited around the joints. 1) True 2) False

18. Q17: Tophi are masses of uric acid crystals which become deposited in various soft tissue areas of the body. 1) True 2) False

19. Q18: The following drugs are among those used to treat gout: NSAIDs, corticosteroids, colchicine, ACTH, allopurinol, probenecid, sulfinpyrazone, and analgesics. 1) True 2) False

20. Q19: aspirin and aspirin-containing products are generally avoided by persons with a known gout condition 1) True 2) False

21. Q20: Urate-lowering drugs should not be initiated during acute attacks. 1) True 2) False

22. Q21: Attempts to normalize serum uric acid to <300 mol/L (5.0 mg/dL) should be continued with a long-term hypouricemic regimens 1) True 2) False

23. Q22: In pseudogout, inflammation in the joints is caused by deposits of calcium pyrophosphate crystals. 1) True 2) False

24. Q23: Since gout and pseudogout are caused by the deposition of two different crystals, it is NOT possible to have gout and pseudogout at the same time. 1) True 2) False

25. Q24: Acute attacks of CPPD arthritis may be precipitated by trauma, arthroscopy, hyaluronate injections, or rapid diminution of serum calcium concentration. 1) True 2) False

26. Q25: Synovial fluid in acute CPPD gout, WBC count can range to 100,000 cells/L, the mean being about 24,000 cells/L, and the predominant cell being the neutrophil. 1) True 2) False

27. Q26: The Knee joint is a common site of (though it can affect other joints) pseudogout. 1) True 2) False

28. Q27: There is no effective way to remove CPPD deposits from cartilage and synovium 1) True 2) False

29. Classification of crystal-related arthropathies Monosodium urate (MSU) Calcium pyrophosphate dihydrate (CPPD) ; Pseudogout, ; pyrophosphate arthropathy ; Chondrocalcinosis Basic calcium phosphates (BCP) ; hydroxyapatite (HA) ; calcific periarthritis/tendinitis Oxalate crystals Cholesterol crystals Corticosteroid crystals

30. Crystal or particle in SF

31. Particles in SF under high power

32. Polarizing microscopy

33. Plain light Crossed polarisers Compensated polarised light MSUM "Beachball"  U Pay Peb

34. CPPD Mixed SF Crystals MSUM & Cholesterol CPPD ‘Yun-bpp’

35. PMN cells plus crystal (CPPD) "ghosts" Cartilage fragments Starch granulesCorticosteriod crystals

36. MONOSODIUM URATE GOUT ( 단일나트륨요산염 통풍 )

37. metabolic disease approximately 840 out of every 100,000 people. Adult men, particularly ages of 40 and 50 increased uric acid, hyperuricemia episode of acute and chronic arthritis deposition of MSU crystals in connective tissue tophi and kidneys Epidemiology

38. Recent demographic and clinical trends in gout Bieber et al, Arthritis Rheum 2004;50:2400-14

39. principal factors to the increased prevalence of gout Bieber et al, Arthritis Rheum 2004;50:2400-14

40. Obesity, metabolic syndrome, and gout

43. Pathogenesis of GOUT

44. GOUT promotors and inhibitors

45. Asymptomatic hyperuricemia ; A person in this stage does not usually require treatment.  ?? Acute gouty arthritis ; sudden onset of intense pain, swelling, warm, tender  ‘attack’ ; occurs at night and triggered by stressful events, alcohol or drugs ; subside within 3 to 10 days, even without Tx ; The next acute attack? - 50% or more of gout sufferers will have a second attack - which may not occur for months or years. - Subsequent attacks, are more frequent, severe, destructive to joints Stages

46. Interval/intercritical gout ; the period between acute attacks ; not have any symptoms and has normal joint function Chronic tophaceous gout ; the most disabling stage of gout, over a long period, such as 10 yrs. ; permanent damage to the affected joints and kidneys. Stages

47. Distribution of joints in acute and chronic gouty arthritis

48. WHY ? Big toe is the most common site or an initial gout attack

52. Diagnosis of GOUT (ROME and NEW YORK criteria)

53. ACR criteria for acute arthritis of primary GOUT

54. MSU Cystals  U Pay Peb

55. Radiologic finding Martel's sign (G sign) ; punched-out lytic lesions with overhanging bony edges Cystic change Soft tissue calcified masses DDx. erosive osteoarthritis apatite arthropathies rheumatoid arthritis

57. General approaches to the management of GOUT What should patients be told about aspirin and Gout ? Will aspirin cause Gout ?

58. Site of action and Timetable to the management of GOUT

59. Indications for allopurinol Urate overproduction, primary and secondary Acute uric acid nephropathy Nephrolithiasis of any type Renal impairment (dose 100 mg/day per 30 ml/min GFR) Low urine volume 24hr urinary uric acid > 0.42 g (2.5 mmol) Intolerance or allergy to uricosuric agents

60. Recommended Foods To Eat Fresh cherries, strawberries, blueberries, and other red-blue berries Bananas, Celery, Tomatoes Vegetables including kale, cabbage, parsley, green-leafy vegetables Foods high in bromelain (pineapple) Foods high in vitamin C Drink fruit juices and purified water (8 glasses of water per day) Low-fat dairy products Complex carbohydrates Chocolate, cocoa Coffee, tea Carbonated beverages Essential fatty acids (tuna and salmon, flaxseed, nuts, seeds) Tofu, although a legume and made from soybeans, may be a better choice than meat

62. New therapeutic directions for gouty inflammation:lessons learned from pathogenesis of the acute gouty attack

63. Calcium pyrophosphate dihydrate (CPPD) deposition disease ( 이수소칼슘피로인산염 통풍 )

64. Epidemiology age range (yr)63-93 peak age (yr)65-75 sex distribution (F:M)2-7:1 prevalence rate (/100,000)8100 annual incidenceunknown geopraphyubiquitous genetic associationschr. 5p

65. Trigger factor acute Pseudogout Direct trauma Intercurrent medical illness (chest infection, AMI) Surgery (esp. parathyroidectomy) Blood transfusion, parenteral fluid administration Institution of thyroxine replacement therapy Joint lavage, arthroscopy, or hyaluronate injection MOST cases of pseudogout develop sponteneously

66. Aging Disease - associated Primary hyperparathyroidism Hemochromatosis Hypophosphatasia Hypomagnesemia Chronic tophaceous gout Post - meniscectomy Epiphyseal dysplasia Hereditary Conditions Associated with Pseudogout

67. Roles of crystals

68. Tissue sites of CPPD deposition

70. Diagnostic criteria for Pseudogout

71. Comparison of Gout and Calcium pyrophosphate crystal arthropathy (pseudogout) Gout Pseudogout Sex ratio (M:F) 2-7:1 1:4 Peak age 40-50 65-75 Most common jt 1 st MTP jt knee Serum urate high normal Radiology Calcification usually absent chondrocalcinosis Erosion characteristic often degenerative Crystals Type MSUM CPPD Shape needle small rod-like Birefringence strong, negative weak, positive

72. Calcium hydroxyapatite(HA) Deposition disease ( 칼슘수산화인회석 통풍 )

73. Pathogenesis

74. Aging Osteoarthritis Hemorrhagic shoulder effusions in the elderly (Milwaukee shoulder) Destructive arthropathy Tendinitis, bursitis Tumoral calcinosis (sporadic cases) Disease-associated Hyperparathyroidism Milk alkali syndrome Renal failure/long-term dialysis Connective tissue diseases (e.g., systemic sclerosis, CREST syndrome, idiopathic myositis, SLE) Heterotopic calcification following neurologic catastrophes (e.g., stroke, spinal cord injury) Hereditary Conditions Associated with HA Deposition Disease

75. Clinical features Common sites of HA deposition - bursae and tendons - around the knees, shoulders, hips, and fingers Clinical manifestations - elderly - indolent progression - from minimal to severe pain and disability - asymptomatic radiographic abnormalities, acute synovitis, bursitis, tendinitis chronic destructive arthropathy

76. - WBC count < 2000/µL - predominance of mononuclear cells - definitive diagnosis ; clumps of crystals by EM Synovial fluid

77. BCP Crystals Clumps of crystals by Alizarin red S stain Small, nonbirefringent crystal, seen by EM

78. Radiologic finding Not diagnostic Intra- and/or periarticular calcifications with/without erosive, destructive, or hypertrophic changes

79. Milwaukee shoulder

80. Treatment Nonspecific Acute attacks of bursitis or synovitis ; resolving in from days to several weeks Use of either NSAIDs or oral colchicine for 2 weeks Intra- or periarticular injection of glucocorticoid salts

81. Case Male / 65 years old Chief complaint: polyarthralgia for one week PI) 평소 Essential hypertension 과 Gouty arthritis 로 개 인 의원에서 투약 중인 환자로 1 주전 Cerebral infarction 으로 신경과 입원 Thrombolytic therapy 진 행 중 polyarthralgia esp, hand & wrist, both 의 swelling 심해지며 low grade fever 발생

82. Past Medical history Hypertension : 10 yrs ago Gouty arthritis : 7 yrs ago - 현재 allopurinol 복용 중 - 당시 손가락 마디, 손목, 무릎, 어깨, 다리 관절 통증 - 1 st MTP joint 의 종창 소견은 없었음 Cerebellum infarction (Both PCA territory) : 3 yrs ago Personal Hx trauma (-) Occupation: agriculture Smoking: 40 pack-year, 5 년 전 금연 Alcohol (-)

83. Lab. Findings WBC 19,400/uL, Hgb 15.6g/dL, Hct 46.1%, PLT 273K/uL (Segment 93%, Lymphocytes 5%) ESR 30 mm/hr, CRP 2.2 mg/dL BUN 14.3 mg/dL, Cr 2.0 mg/dL Uric acid 5.4 mg/dL Others ; within normal limit

89. Thank you for your attention !