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37 Cards in this Set

  • Front
  • Back
name the 3 syndromes associate with crystal deposition
- Gout
- Pseudogout
- Basic calcium phosphate (BCP) deposition diseases
what is the rate limiting step in making purine synthesis?

what enzyme, which is not found in humans but is found in other animals, prevents gout by breaking down uric acid to allantoin?
PRPP synthetase

uricase
what joints are most commonly affected by gout?
big toe > knee/ankles > tarsus
what's the mineral thats associated with:

-gout
-pseudogout
-BCP
gout: monosodium urate crystals (negatively birefringent)

pseudogout: calcium pyrophosphate dihydate (CPPD) crystals (postively birefringent)

BCP: Hydroxyapatite (non- birefringent)
differentiate b/w gout vs pseudogout
Gout is a heterogeneous group of diseases resulting from the deposition of monosodium urate (MSU) crystals in tissues or fluids.

Pseudogout is a form of acute arthritis that can mimics gout
Results from calcium pyrophosphate dihydate (CPPD) crystals deposition in articular cartilage
overweight pt presents with history chronic overeating. pt notes that he tends to eat large steaks 3-4 times a week. during meals, he consumes alcohol (but doesn't remember how much). more and more frequently, he has been having joint pains (starting with his right big toe, and now his knees and ankles).

dx?

what lab tests are indicated and what would you expect on them?
gout (acute attacks tend to occur after alcohol consumption or a large meal)

lab tests:
- microscopy of joint fluid (would see monosodium urate crystals due to hyperuricemia that are negatively birefringent)
- urine uric acid excretion >800-1000 mg/24 hrs
- serum urate concentration >6.8 mg/dL
pt comes into the clinic complaining of occassional attacks of pain in her right shoulder.

xray shows calcification. but there are non birefringent crystals that show up under light or polarizing light microscopy.

dx?
basic calcium phosphate (BCP) deposition diseases
within the purine metabolism pathway, mutations in _____ will lead to hyperuricemia, and eventually gout. Explain why?
HGPRT (The enzyme primarily functions to salvage purines from degraded DNA to renewed purine synthesis; keeps hypoxanthine from going down pathway towards xanthine --> uric acid --> hyperuricemia)
what is the mechanism of allopurinol?
blocks xanthine oxidase, so that there will be less conversion of hypoxanthine --> xanthine. this decreases amt of xanthine available to form additional uric acid (preventing further develop of hyperuricemia and gout)
hyperuricemia is defined as a serum urate conc level in excess of ___mg/dL
6.8 mg/dL (the risk for crystal deposition disease imparted by urate supersaturation of extracellular fluids begins at approximately this concentration)
name the 3 syndromes associate with crystal deposition
- Gout
- Pseudogout
- Basic calcium phosphate (BCP) deposition diseases
what is the rate limiting step in making purine synthesis?

what enzyme, which is not found in humans but is found in other animals, prevents gout by breaking down uric acid to allantoin?
PRPP synthetase

uricase
what joints are most commonly affected by gout?
big toe > knee/ankles > tarsus
what's the mineral thats associated with:

-gout
-pseudogout
-BCP
gout: monosodium urate crystals (negatively birefringent)

pseudogout: calcium pyrophosphate dihydate (CPPD) crystals (postively birefringent)

BCP: Hydroxyapatite (non- birefringent)
differentiate b/w gout vs pseudogout
Gout is a heterogeneous group of diseases resulting from the deposition of monosodium urate (MSU) crystals in tissues or fluids.

Pseudogout is a form of acute arthritis that can mimics gout
Results from calcium pyrophosphate dihydate (CPPD) crystals deposition in articular cartilage
overweight pt presents with history chronic overeating. pt notes that he tends to eat large steaks 3-4 times a week. during meals, he consumes alcohol (but doesn't remember how much). more and more frequently, he has been having joint pains (starting with his right big toe, and now his knees and ankles).

dx?

what lab tests are indicated and what would you expect on them?
gout (acute attacks tend to occur after alcohol consumption or a large meal)

lab tests:
- microscopy of joint fluid (would see monosodium urate crystals due to hyperuricemia that are negatively birefringent)
- urine uric acid excretion >800-1000 mg/24 hrs
- serum urate concentration >6.8 mg/dL
pt comes into the clinic complaining of occassional attacks of pain in her right shoulder.

xray shows calcification. but there are crystals that show up under light or polarizing light microscopy.

dx?
basic calcium phosphate (BCP) deposition diseases
within the purine metabolism pathway, mutations in _____ will lead to hyperuricemia, and eventually gout. Explain why?
HGPRT (The enzyme primarily functions to salvage purines from degraded DNA to renewed purine synthesis; keeps hypoxanthine from going down pathway towards xanthine --> uric acid --> hyperuricemia)
what is the mechanism of allopurinol?
blocks xanthine oxidase, so that there will be less conversion of hypoxanthine --> xanthine. this decreases amt of xanthine available to form additional uric acid (preventing further develop of hyperuricemia and gout)
hyperuricemia is defined as a serum urate conc level in excess of ___mg/dL
6.8 mg/dL (the risk for crystal deposition disease imparted by urate supersaturation of extracellular fluids begins at approximately this concentration)
what are the 2 physiological processes that can lead to gout?

which is more common?
- excessive urate synthesis
- decreased excretion (more common!!)
Over activity of ___ _____ and deficiency of _____ have been implicated as potential mechanisms within the purine metabolism for causing excessive urate synthesis.
PRPP synthetase; HGPRT
"Overproducers" (people who have excessive urate synthesis) can be expected to have what amount of uric acid excreted in their urine every 24 hrs?
>800 -1000 mg/24 hrs
Most of the uric acid in our bodies is removed through KIDNEYS/LIVER.
kidneys (so kidney failure pts are for sure going to get hyperuricemia and be at risk for gout development)
what particular drug is implicated in causing hyperuricemia predisposing to acute gout?

do they increase or decrease urate excretion?
diuretics (eg. thiazide)

decrease urate excretion by increasing net urate reabsorption.
what is the mechanism of gout development following hyperuricemia?
So now you have crystals of urate floating around, they get deposited in joints and other places --> the body perceives these particles are foreign and mount immune response against them (opsonization and phagocytosis) --> leading to activation of acute inflammation
what is the natural history of untreated gout?
the likelihood of someone developing gout is based on the level of hyperuricemia that one has.

with time, the pain between gout attacks increase. chronic gout will develop >10 yrs of acute intermittent gout (Once you have chronic gout, the deposition is not only in joints, but outside of joints)
what are the major patterns of renal involvement with gout?

which is most common?
- urate nephropathy (#1): deposition of MSU in renal parenchyma in pts with severe tophaceous gout

- acute uric acid nephropathy: uric acid (not MSU) precipitates in collecting tubules

- nephrolithiasis (kidney stones): related to magnitude of urate excretion
What is the definitive dx of gout based upon?
take synovial joint fluid and examine under a microscope.

You must see negatively birefringent crystals of MSU intracellularly on polarizing microscope!
if pt does not have negatively birefringent crystals in their joint fluid, can you still dx gout?
yes, you can dx gout based on presumptive criteria.

>6 of a long list of features:

hyperuricemia
acute arthritis
maximum inflammation developing in 24 hours
monoarticular attack
erythema over joints
unilateral first MTP arthritis

unilateral tarsal arthritis

suspected tophus

asymmetric swelling of joints on x-ray

sub-cortical cysts without erosions

joint fluid is culture negative
tx:

- asymptomatic hyperuricemia
- acute gout
- intercritical gout (between attacks)
- chronic tophaceous gout
asymptomatic gout:
- no tx, stop offending drug
- reduce intake of purine-rich/weight loss

acute gout:
- NSAIDs (indomethacin) for pain
- corticosteroids (if NSAID is contraindicated, like in peptic ulcers)

intercritical gout:
- colchicine and/or NSAIDS
- drugs that lower serum urate, like uricosuric drugs (probenecid or sulfinpyrazone) and xanthine oxidase inhibitors (allopurinol and febuxostat)

chronic gout:
- allopurinol
- colchicine/NSAIDs to prevent acute arthritis
what drug is useful to prevent gout attacks, but not for tx during gout attack?
colchicine
if pt with chronic gout has now developed renal insufficiency, what drug can you give him that will allow him to tx his hyperuricemia and acute gout attacks
Febuxostat (works like allopurinol, but removed by liver rather than kidneys and better for kidney failure pts)
80 y/o female presents with history of hemochromatosis complaining of intermittent joint pains. xrays of her knee show chondrocalcinosis.

dx?

what is the definitive diagnostic test to do for a pt like this?
pseudogout

should do a joint fluid microscopy; will see CPPD cystals that are weakly positively birefringent
tx of:

- asymptomatic chondrocalcinosis
- acute arthritis due to pseudogout
asymptomatic:
- no tx

acute arthritis:
- NSAIDs, corticosteroids, colchicine
30 y/o female pt comes in with sudden shoulder pain. Xray shows opacity in the shoulder. Under the microscope show non birefrignence. Dx?
basic calcium phosphate (BCP) deposition dz
tx:

- asymptomatic BCP deposits
- acute tendonitis/bursitis
- large deposits that impinge or cause erosive changes
asymptomatic:
- no tx

acute tendonitis:
- NSAIDs/corticosteroids

large deposits;
- surgery