Crystal-Induced Arthritis Flashcards
Who tends to get gout, men or women, and why?
Tends to occur in men, because estrogen has a uricosuric effect
Women can start getting gout after menopause
Happens most commonly in blacks in their 30s-50s
What is the definition of hyperuricemia and what signifies you definitely have an active gout infection in a joint?
Hyperuricemia = >7.0 mg/dL in the blood in men, >5.7 mg/dL in women
Active infection is when monosodium urate (MSU) crystals can actually be seen in neutrophils, not just in the joint space. This is classical but NOT required for diagnosis.
Why do humans develop gout easily? If you have hyperuricemia, do you have gout?
Humans lack the enzyme uricase (present in animals) which breaks down uric acid to allantoin.
Hyperuricemia =/= gout. Need to have crystals actually precipitating for this to happen. This can first start occurring at the saturation point (6.8 mg/dL). Only 15% of those with asymptomatic hyperuricemia will go on to develop gout.
What causes lipid crystals in a joint and what do they look like?
Caused by intraarticular fracture
Looks like “maltese cross” crystals
Give the breakdown pathway of adenine to uric acid and the rate limiting step.
Purine breakdown pathway:
Adenine -> Hypoxanthine via adenosine deaminase.
HX -> Xanthine via xanthine oxidase (XO)
X -> uric acid via XO
Rate limiting step is xanthine oxidase.
What is the cause of hyperuricemia in most patients and give a few examples of what can cause this?
90% of patients have hyperuricemia due to underexcretion
Causes: renal insufficiency, keto or lactic acidosis, ethanol, thiazide diuretics, lead nephropathy, pyrazinamide (all complete for uric acid excretion in the kidney).
What are the causes of hyperuricemia due to overproduction?
10% of patients:
HGPRT deficiency (Lesch-Nyhan)
PRPP synthetase overactivity (overproduction of purines)
G6PD deficiency (too much hemolysis)
Myeloproliferative disorders, cytotoxic chemotherapy, sickle cell anemia (cell turnover and tumor lysis syndromes)
How does von Gierke disease cause gout?
von Gierke -> Glucose-6-phosphatase deficiency
Lack of phosphate leads to ATP -> AMP -> adenine -> broken down to uric acid more readily.
Furthermore, glucose is forced to be used in glycolysis -> high blood lactate levels. Lactic acidosis compete with uric acid transporter
What is acute vs chronic gout characterized by? What is the midpoint between these two.
Acute - usually single joint but sometimes oligoarticular joint involvement
Intercritical: midpoint between these two. Only a small% will never have an attack again.
Chronic (tophaceous) - development of tophi with frequent attacks of arthritis or persisting symptoms of gout between acute attacks.
How long do gout attacks last? When do they usually start? What is it called when they affect the first MTP joint?
They usually last 3-10 days. Will self-resolve without intervention
Usually starts during the night -> cold probably precipitates the crystals
Painful MTP of big toe = Podagra.
What are tophi? What does the material look like?
Aggregated deposites of monosodium urate commonly observed as subcutaneous lumps overlying joints or bony prominences. Often found in ear and olecranon process.
Looks like white, chalky material that may appear like pus
Where does gout usually appear other than podagra? What provides a nidus for its development?
Usually appears on lower extremities, i.e. ankle, heel, knee. Sometimes upper extrem.
Nidus - underlying degenerative changes (i.e. osteoarthritis). I.e. Arising in Heberden’s nodes of osteoarthritis.
What are some common precipitants of an acute gout attack?
Dehydrating, fasting, adding a thiazide diuretic.
Discontinuation or introduction of a urate-lowering medication (i.e. allopurinol)
Higher intakes of meat, seafood, or alcohol -> think of a cruise ship. This was once thought to be a disease of the rich
What are the most common bursae to be affected by gout?
Prepatellar and olecranon bursae
Particularly happens if nearby knee or elbow are affected, respectively
What should be done the joint-aspirated material from a joint with suspected gout? Are blood urate levels always elevated in acute gouty attack?
Check the WBC count, should be >2,000 and <50,000 with mostly PMNs.
Check for monosodium uric acid crystals under POLARIZED light. Intracellular crystals may be seen. Blood urate levels need not be elevated for attack.
