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36 Cards in this Set

  • Front
  • Back
Monoarticular vs. Oligoarticular vs. Polyarticular
Mono= single joint
Oligo= <4 joints
Poly= >4 joints
If you do a diagnostic arthrocenthesis and find turbid synovial fluid which is pyarthrotic and contains a WBC count of >50,000, what do you have to be suspicious for?
Septic arthritis- give Abx (consider a tap?)
Identifying crystals under polarized light:

Yellow and perpendicular to the axis= ___.
Blue and perpendicular to the axis= ___.
Yellow and parallel to the axis= ___.
Blue and parallel to the axis= ____.
Yellow and parallel= monosodium urate (gout)
Blue and perpendicular= monosodium urate (gout)

Blue and parallel= pyrophosphate (pseudo-gout)
Yellow and perpendicular= pyrophosphate (pseudo-gout)
A synovial tap was placed under a polarized microscope and you saw this (parallel to axis). What can you diagnose the patient with?
A synovial tap was placed under a polarized microscope and you saw this (parallel to axis). What can you diagnose the patient with?
Yellow crystal that is parallel to the axis= uric acid

GOUT
What is the main crystal that's involved in gout? What are the levels of individuals who have gout?

Why is there a gender predominance?
Uric Acid, typically > 6.8 mg/dl

M>F (because E2 is uricosuric- which is why women are more susceptible after menopause)
What is Podagra?
Inflammation of the big toe (common area of initial presentation of gout). Also in wrists, fingers, ankles, etc. 

*typically starts as monoarticular and then becomes polyarticular.
Inflammation of the big toe (common area of initial presentation of gout). Also in wrists, fingers, ankles, etc.

*typically starts as monoarticular and then becomes polyarticular.
What is the cause of hyperuricemia/gout?
1. Genetic makeup
2. Western Diet (meat, liquor, seafood)
3. Behavior (ex: lasix)
4. Environment
How is Uric acid excreted?
Kidneys (2/3), Gut (1/3)

*Many patients with gout have renal impairment and problems with excretion of uric acid
Uric Acid crystals begin to precipitate out of solution when the level of UA is ____.
>6.8 (cutoff after which gout occurs)
What is the gold standard for diagnosing any crystal syndrome (esp. gout)?
Synovial fluid analysis (look for crystals under polarized light)
What percentage of patients with hyperuricemia and gout have abnormal OVERPRODUCTION of uric acid?

What are some causes of this?
10%

Primary- genetic defects, HGPRT deficiency (inhibits the purine salvage pathway so more urate is produced). PRPP overactivity (increase uric acid)

Secondary- ↑ cell turnover, tumors, dietary indiscretion
Lesch Nyhan syndrome vs. Kelley Geegmiller Syndrome
Lesch Nyhan (complete x-linked, MR and self-mutilation)
Kelley Geegmiller (incomplete x-linked, no neurologic/behavioral feature)
What percentage of patients with hyperuricemia and gout have a deficient RENAL EXCRETION of gout?

Primary vs. Secondary
90% are under excreters

Primary: genetic/idiopathic
Secondary: ↓ GFR of any cause, diuretics, age
Risk factors for development of gout
Male, post-menopausal women
Advanged Age
Drugs (diuretics, aspirin at low dose)
High Alcohol
High BMI
Diet that is high in meat/seafood
What is the transporter that is principally responsible for uric acid secretion in the nephron?

Where in the nephron does it work?
URAT-1 (Probenecid acts here)

GLUT0 is a fructose transporter, ABCG2 as well
What is this an example of? What are other sites of gout?

Why does having Psoriasis predispose you to gout?
What is this an example of? What are other sites of gout?

Why does having Psoriasis predispose you to gout?
Acute flare of gout. Other sites: elbow, hands, ankle

Psoriasis= rapidly turning over dead skin cells --> ↑ uric acid production
What is the role of uric acid in the body?
Good: potent antioxidant (works like vitamin C)

Bad: excess induces inflammation and oxidative stress
Uric acid crystals activate the ______.

Describe how MSU initiates inflammation (what is the key inflammatory mediator?)
Inflammasome (activated by uric acid crystals) --> IL-1B production --> this amplifies neutrophil recruitment & activation --> ↑ amplification and neutrophil entry into cell

Pro IL-1B --> IL-1B
What is shown in this picture? 

Is it possible for a person to have gout without having elevated serum urate?
What is shown in this picture?

Is it possible for a person to have gout without having elevated serum urate?
Tophus of gout in prepatellar area (body is walling off the crystals)

Yes! Inflammatory mediators might initially cause increased excretion of urate. Vice versa- someone with elevated urate might not show gout (pre-clinical and asymptomatic)
What medications can be used to terminate an acute gout flare?

What is the limitation to these medications?
NSAIDs, low dose oral colchicine, corticosteroids

Limitation: can only relieve SYMPTOMS, uric acid levels stay the same (not curing the problem, just masking it). However treating with these meds is shown to ↓ Flares overall.
What are three broad categories of agents that treat gout?
1. decrease production (XOis)
2. increase excretion (Uricosurics)
3. Biologic
What is the MoA of Allopurinol?

What about Febuxostat?

*what class of patients are these drugs good for?
Xanthine Oxidase inhibitor --> blocks hypoxanthine to xanthine (prevents Uric Acid formation)

Febuxostat --> non-purine XOi

*note- both drugs are safe in patients with renal insufficiency!
How does the biologic therapy Pegloticase (krystexxa) work?
It pegylates Uricase extending it's half life so it can work longer. Uricase breaks down uric acid to allantoin which is soluble and excreted.

*mammals lost uricase enzyme through process of evolution
What is CPPD?

What kinds of crystals are found in this condition?
Calcium Crystal Deposition Disease

- Ca2+ pyrophosphate dihydrate
- Calcium Phosphate (includes hydroxyapatite)
- Calium oxalate
What type of crystal disease is shown here? How can you tell?
What type of crystal disease is shown here? How can you tell?
Crystals in CPPD like to form in the cartilage (especially articular cartilage of knee and hands). Thus you can see the deposits.

(also note the deposits in the medial meniscus)
Crystals in CPPD like to form in the cartilage (especially articular cartilage of knee and hands). Thus you can see the deposits.

(also note the deposits in the medial meniscus)
This is an x-ray of linear deposition of material. What crystal related condition has this pattern?
This is an x-ray of linear deposition of material. What crystal related condition has this pattern?
CPPD - where there is chondrocalcinosis (or linear deposits of calcium into cartilage). 

Knees and hands are commonly affected (as is wrist in post-menopausal women). Calcification also seen in pubic symphisis.
CPPD - where there is chondrocalcinosis (or linear deposits of calcium into cartilage).

Knees and hands are commonly affected (as is wrist in post-menopausal women). Calcification also seen in pubic symphisis.
How do you identify pyrophosphate crystas on polarized light microscopy?
How do you identify pyrophosphate crystas on polarized light microscopy?
They are rhomboid shaped. Blue when parallel, Yellow when perpendicular.
A person comes in to you with painful gouty symptoms in her hands and CPPD deposition in the 2nd and 3rd MCP. What is this disease?
A person comes in to you with painful gouty symptoms in her hands and CPPD deposition in the 2nd and 3rd MCP. What is this disease?
Hemochromatosis

-causes psuedo RA (patient can have gout at younger age). Very specific when swelling is in 2nd and 3rd MCP.
What is the syndrome shown here?
What is the syndrome shown here?
Crowned Dens Syndrome (cause of neckpain). Deposits of pyrophosphate crystals in the neck.
What familial condition causes enhanced CPPD deposition? (hint: disease is CCAL2)
CCAL2 autosomal dominant disease --> ANKH gene

It codes for a pyrophosphate transformer that moves minerals in and out of cells (prevents Hydroxyapetite crystal formation). GAIN OF FXN mutation causes increased prophosphate out of cell --> combines with Ca2+ -->forms calcium pyrophosphate
What condition (shown above) is associated with HADD disease?
What condition (shown above) is associated with HADD disease?
Calcific tendinopathy (some erosion can be seen).

Condition is associated with aging as well as with other disease (Hyperpara, Crest, SLE, etc.)
This is a destructive arthritis that causes hemorrhagic shoulder effusions. What might it be and what crystal arthropathy is it associated with?
This is a destructive arthritis that causes hemorrhagic shoulder effusions. What might it be and what crystal arthropathy is it associated with?
Milwaukee Shoulder (associated with HADD). Tends to occur in older women.
What do the following three agents have in common and how are they different:

1. Anakinra
2. Rilonacept
3. Canakinumab
1. Anakinra: IL-1 receptor antagonist (blocks IL-1a and IL-1B). Daily injection.

2. Rilonacept- IL-1 receptor antagonist (fused protein). Not used for gout.

3. Canakinumab- Monoclonal antibody against IL-1B
MSU, CPPD, and HA all act through the same mechanism which is activation of the ______ causing the release of ______ inflammatory mediator.
Inflammasome ---> cause release of IL-1B
This type of crystal is commonly seen in patients with renal failure on hemodialysis.
This type of crystal is commonly seen in patients with renal failure on hemodialysis.
Calcium Oxalate Crystals
This type of crystal is entirely NON-INFLAMMATORY. What could it be? 

(hint: found in chronic effusions)
This type of crystal is entirely NON-INFLAMMATORY. What could it be?

(hint: found in chronic effusions)
Cholesterol crystal!