Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
what is the end product of purine metabolism in humans due to loss of uricase activities?
|
uric acid
|
|
what are the four evolutionary advantages of uric acid?
|
anti-oxidant, BP control in times of low salt ingestion, intelligence, neurodegenerative protective effects.
|
|
what is hyperuriciemia an independent risk factor for?
|
atherogenesis
|
|
why are inflammatory mediators produced in response to urate crystals?
|
because the urate crystal are coated by IgG which stimilates the neutrophils, leukocytes, monocytes, fibroblasts, synoviocyte, and renal cell to produce inflammatory mediators.
|
|
Out of all of the inflammatory mediators produced in response to urate crystals, which one is the most imporant in atherogenesis?
|
oxygen radicals
|
|
what lipoprotein inhibits urate crystals from initiating a production of inflammatory mediators?
|
APOE
|
|
what gender is most affected by hyperuricemia and gout before the age of 55? after?
|
men; by 65 yoa both men and women are equal because after menopause women quickly catch up to men.
|
|
what is the best predictor of acute gout?
|
change in serum uric acid
|
|
20 yoa female not currently on any medications with regular periods comes in complaining of joint pain and has a high serum uric acid level, what can you immediately rule OUT?
|
an attack of gout
you will NEVER EVER see an attack of gout in a menstrating woman unless they are on diuretics. |
|
anything that causes a shift of uric acid through the joint where polies may form will cause what?
|
a precipitation of gout.
|
|
what is the most common form of inflammatory arthritis in men >40 yoa?
|
gout
|
|
90% of hyperuriciemia cases are caused by? give examples
|
underexcretion
renal defect, dec GFR, diuretics, tubular toxins, lead, hypothyroidism |
|
what is the most common cause of hyperurecemia via overproduction?
|
alcohol, esp beer consumption
|
|
10% of hyperuriciemia cases are caused by? give examples.
|
overproduction
HGPRTase/ PRPP synthestase, increase purine intake, alcohol, myeloproliferative dz, psoriasis |
|
56 yo Male comes in complaining of recurring attacks of pain in 4 of his joints that has been going on every 2 weeks that last for a week. what stage is he in?
|
stage II- last subcategory of stage II before it becomes stage III
-acute intermittent arthritis acute attacks: 1 week- 2 months intervals: 2-3 wks, 3-4 mos joints: 4-5 |
|
59 yo male comes in complaining of pain in his knee that last for about a week, but happens once every couple of years. what stage is this guy in? what do you give him?
|
stage II- 1st subcategory of stage II
-acute intermittent arthritis acute attacks: 1-2 weeks intervals: 2-10 yrs joints: 1-2 give him NSAIDs unless CI (HTN, GI problems) forman would give corticosteroids. |
|
50 yo male comes into your office complaining of knee pain that lasted for 2 weeks and occurs every 6 months. what stage is he in?
|
stage II- 2nd subcategory
-acute intermittent arthritis acute attacks: 1-3 weeks intervals: 6 months-2 yrs joints: 1-2 |
|
how do you differentiate stage III gout from RA?
|
by ordering an RF test. If it's positive then it must be RA.
|
|
what is the 1st attack in acute gouty arthritis called? where is it usually located?
|
podagra- 1st MTP
|
|
what is a Tophi indicative of?
|
chronic urate overload
|
|
if a pt comes in with recurrent attacks of gout even though he is on a prophylaxis, what should you give him?
|
a uric acid excreter like probenecid
|
|
T/F
Cochicine changes uric acid level. |
FALSE
it does not change uric acid level. |
|
what are the indications for urate lowering?
|
tophacheaous disease w/ erosion
uric acid nephrolithiasis recurrent attacks despite prophylaxis to prevent acute cell lysis |
|
89 yo male presents with oligoarthritis and linear or stippled calcifications on x-ray. What should be your #1 ddx? what other clinical features would confirm this ddx?
|
- calcium pyrophosphate deposition disease (CPPD)
other clinical features: - multiplicity of presentations -superimposed one existing OA -knee, shoulder, wrist and MCPs |
|
what are the five CPPD presentations?
|
pseudogout, pseudo-RA, pseudo-OA, pseudo-neuropathic joints, and asymptomatic chondrocalcinosis
|
|
what is chondrocalcinosis?
|
calcification in the hyaline cartilage
|
|
what are the associated medical conditions for CPPD?
|
hyperparathyroidism, hypothyroidism, hemochromatosis, and hypomagnesemia
|
|
what is the most frequently involved joint in pseudogout?
|
knee
runner ups: hip wrist shoulder |
|
what do CPPD crystals look like?
|
rhomboid, weakly positively birefringent
|
|
how do you manage crystal disease?
|
NSAIDs and Corticosteroids. For chronic lowering of uric acid use allopurinol or febuxostat
can use colchicine as a prophylaxis (1 tab/ day) |