Crystal Disease (Told) Flashcards
Crystal Disease
- the sadistic six
Monosodium urate (MSU)
Calcium Pyrophosphate Dihydrate (CPPD)
Basic Calcium PO4 (hydroxyapatite)
Calcium Oxalate
Cholesterol Crystals
Monoclonal Proteins
when do we think crystals?
If episodic or intermittent attacks, think crystals!
Rare birds
cholesterol crystals
monoclonal proteins
calcium phosphate hydroxyapatite
calcium oxylate
CALCIUM PO4 (HYDROXYAPATITE) DEPOSITION
CALCIFIC TENDONITIS
- MOST APATITE CRYSTALS
DO NOT REACT TO PORALIZED
LIGHT.
CALCIUM OXYLATE CRYSTALS
OXYLOSIS OF THE SPINE AND HAND +
NEPHROLYTHIASIS
Nephrolithiasis
terminal tuft calcification
OXYLOSIS OF THE RETINA
CHOLESTEROL CRYSTALS
LIQUID LIPID CRYSTALS IN THE JOINTS
LIPID CRYSTALS CAN BE SEEN IN LIPID LADEN JOINT EFFUSIONS OF RHEUMATOID ARTHRITIS AND CHRONIC INFECTION.
POLARIZED LIGHT- look like a picasso painting
MONOCLONAL PROTEINS
Multiple Myeloma can present with Plasma cell rich
joint effusions precluding the bone destruction.
gout vs pseudo gout
negative– YIPA
positive- pseudogout, little rectangles (not needles)
Hyperuricemia & Gout- Epidemiology
Increases with age & body mass
Risk increases with degree & duration of hyperuricemia
Middle-aged males
Incidence of gout in females approaches that in males after menopause
2 – 3% of adult male population
Hyperuricemia as a Marker for Atherogenesis
Hyperuricemia (gout) should alert the clinician to an overall increased risk of CVD and especially in those patients with other risk factors for CV events.
what we do with urate crystals
can be coated with IgG
or wraped in Apo-E like a weenie in a blanket
Both of these lead to responses by neutrophils, leukocytes, monocytes, fibroblasts, synoviocytes, renal cells
increased uric acid comes from
increased production or decreased excretion
or increased excretion can lead to stones
Pathogenesis of Hyperuricemia- decreased renal excretion
90% of Cases Impaired renal function Dehydration Acidosis Low dose salicylates Diuretics Pyrazinamide Cyclosporine Levodopa Ethambutol Nicotinic acid Hypothyroidism
Pathogenesis of Hyperuricemia: Increased Urate Production
10% of Cases Ethanol Myeloproliferative disorders Ineffective erythropoiesis Widespread psoriasis Cytotoxic drugs Glycogen storage disease G6PD deficiency HGPRTase deficiency Increased PRPP synthetase activity
Acute Gouty Arthritis
Abrupt onset & mono - articular
* Sudden changes in uric acid levels best predictor of an attack
Classically 1st attack “podagra”
Episodic Disease
Attacks polyarticular with time
Tophi indicative of chronic urate overload
Needle shaped negatively birefringent MSU crystals
Stages- clinical course of classical gout
*** Stage I: asymptomatic hyperuricemia. no arthritis. (? independent risk of atherogenesis)
*** Stage II: acute intermittent arthritis
acute attacks 1-2 weeks, intervals 210 years, joints 1-2
progresses to 1-3 weeks, every 6 mos-2 years
progresses to 1week - 2 months every 2-3 wks/ 3-4 months, involving 4-5 joints
*** STAGE III: chronic arthritis with acute exacerbations
Tophi- bone and cartilage
continuous arthritis
acute attacks superimposed
Indications for Urate Lowering
Tophacheous disease with erosions
Uric acid nephrolithiasis
Recurrent attacks despite prophylaxis
Prevent Acute cell lysis - e.g., chemo.
Allopurinol contraindicated in acute gout but do not stop during an attack
Asymptomatic hyperuricemia ???
Allopurinol hypersensitivity syndrome
calcification of the cartilage is
pseudogout
Management of Crystal Disease the Old Fashioned Way
Arthrocentesis
NSAIDs
Corticosteroids - p.o., i.v.
Colchicine - prophylaxis
Uric Acid Lowering Agents:
- Allopurinol, Febuxostat (Uloric ®), Uricosuric Agents
- Not during acute attacks!
MEDICAL STRATAGY 2015
ACUTE TX: NSAIDS Corticosteroids Colchicine Biologics (IL-1 inhibitors)
PROPHYLACTIC TX:
- Xantine Oxidase Inhibitors (Allopurinol, or Fabuxostat)
- Uricosurics (Probenicid, Fenofibrate, Losartan)
- Uricase (Procloticase)
Dr. Told’s Guide TREATING CRYSTAL DISEASES
Asymptomatic Hyperuricemia = no treatment but check diuretic use and ASA use and niacin use.
Acute Attack = NSAID’s Indomethacin still is the best. COX-2’s OK others are too slow.
CORTICOSTEROIDS= Good for poor renal function and Injectible use.
Uric Acid Lowering = Colchicine can be a “Crap Shoot” Allopurinal and Probenecid
and Fabuxostat are best bets.
important note about managing gout
NEVER ,NEVER STOP
ALLOPURINAL
PATIENTS MAY CHOOSE TO
BE MAINTAINED ON
INTERMITTANT INDOMETHACIN
So what about diet?…..
THE STRICTEST OF PURINE FREE DIETS WILL ONLY DECREASE
URIC ACID LEVELS 1 MG%. MEDICATION IS THE BEST Rx
highest things include meats, beans, raisins
