235. Crystalline Diseases

Question 1

Characteristics of Inflammatory Synovial Fluid

Three main crystal types

Answer 1

Inflammatory - Slightly turbid, 2k-50k total WBC, 20-70% PMNs

1. Basic Calcium Phosphate (BCP)
2. Calcium Pyrophosphate Dihydrate (CPPD)
3. Monosodium Urate (GOUT)

Question 2

Three types of presentations of BCP crystals (with age/sex)

Answer 2

1. soft tissues: Acute calcific periarthritis, Atypical gout (young women) on 1st MTP, intense local inflammation
2. joints: Bcp arthropathy: Milwaukee shoulder syndrome (loss of rotator cuff fx with swelling) women >70s
3. tendons: Calicific tendinitis: most commonly shoulder Cuff

Question 3

Microscopic appearance of BCP crystals

Answer 3

1. Aspirate of joint stained for Alizarin red
2. NOT Birefirengent on polarized LM
3. shiny Coins on ordinary LM

Question 4

Tx for BCP crystal diseases

Answer 4

NSAIDs
PT
intraarticular steroids
surgery if indicated

Question 5

CPPD Arthropathy: risk factor, joint types, age/sex, causes

Answer 5

“pseudogout”
F>M, Risk Factor: AGING (peak 65-75yrs)
Assoc with numerous metabolic disturbances
Secondary cause: HPTH, hypoMg, hypothyroidism

Question 6

clinical presentation of CPPD arthropathy

Answer 6

Acute monoarthritis (in KNEE)
Chronic polyarthritis in symmetric small joints
Progressive OA in large + small joints (may involve spine)
Asx Chondrocalcinosis - in meniscus of knee and fibrocartilage of wrists
RHOMBOID CRYSTALS, weakly positively birefringent on polarized LM

Question 7

Treatment for CPPD arthropathy

Answer 7

1. NSAIDS
2. Intraarticular/oral steroids
3. Colchicine - given to elderly, use caution
   just tx for acute attack

Question 8

Epidemiology of GOUT

Answer 8

Increased prevalence with aging and high serum uric acid

M>F until menopause then M=F

Question 9

Risk Factors for GOUT

Answer 9

1. High alcohol consumption (high ATP degradation = high urate synthesis; high lactic acid load = less urate excretion)
2. Obesity, Metabolic Syndrome, insulin resistance
3. High Purine Diet (Meat, Shellfish, Alcohol, Soft Drinks, HFCS)
   Drugs: thiazides, low dose ASA

Question 10

Two mechansims of GOUT Pathophysiology

Answer 10

1. Overproduction of uric acid - enzyme abnormalities, hemolytic disease, myeloproliferative disease, or alcohol use causes this
2. Underexcretion of uric acid (90% GOUT) - low renal fx, drugs, and alcohol use cause this

Question 11

Stages of Disease with clinical sx of GOUT

Answer 11

1. Asx hyperuricemia
2. Acute Gouty Arthritis (usually 1st MTP -podagra, pain very acute in early morning - bed sheets- usually self-limited first attack)
3. Intercritical Gout: quiescent intervals between gout attacks (become more frequent and severe)
4. Chronic Tophaceous Gout: deposits in distal phalanges, ear, olecranon of ulna (non-painful)

Question 12

Diagnosis of Gout (LM, Xray)

Answer 12

LM: needLe shaped, yeLLow when paraLLel to poLarizer (blue when perpendicular)
Tx with aLLopurinol

XR: Large erosions of random joints, punched out lesions, sclerotic overhanging edges, preserved joint spaces

Question 13

Acute Tx of Gout

Answer 13

NSAIDs, Colchicine, Corticosteroids

DO NOT ALTER URATE LOWERING TX during acute attacks!! these are chronic agents!

Question 14

Chronic Tx of Gout indications

Answer 14

Frequent gout attacks in 1-2 years, renal stones, tophaceous gout, erosions on xray

Question 15

Chronic Tx of Gout

Answer 15

Xanthine Oxidase Inhibitor (allopurinol) - decreases production of urate

Uricosuric Agents (Probenecid) increase urate excretion (more risk of kidney stones)

Risk precipitating acute attack with chronic tx!

Pegloticase - uricase enzyme given IV

Anakinra - anti-IL-1 biologic tx - not FDA approved