Crystalline Arthritis - Postlethwaite Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Gout is defined as deposition of ____ due to prolonged _____?

A

monosodium urate (MSU), hyperuricemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hyperuricemia can result via what 2 ways? Think broadly

A

Overproduction, decreased efficiency of excretion

His fact: Excretion of uric acid (as in the # of mg you collect over 24 hours is normal). so its clearance that is decreased

requires a higher plasma level of uric acid such that production and clearance can be equal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the difference between monosodium urate and uric acid?

A

Uric acid is what is excreted in urine, monosodium urate (MSU) is what accumulates. So gout is an accumulation of MSU, not uric acid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hyperuricemia defines as plasma urate level greater than?

A

7.0 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of patient almost never gets gout? Why?

A

Premenopausal females, estrogen is thought to increase the excretion of uric acid. #feminism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Early manifestations/location of gout? Name given to this? Time length of involvement?

A

begins as a acute monoarticular arthritis of lower extremity joint. If it involves 1st MTP = podagra. Symptoms will usually resolves in 5-7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What factors (list 3) lead to early manifestations of gout? i.e. why the big toe

A

Lower extremity has:

  • decreased blood supply
  • decreased pH at night (increased acidosis)
  • decreased temperature at night.

These factors all lead to precipation of urate, forming crystals. Often patient wakes up in the morning in pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Chronic gout can cause urate crystals to accumulate in large deposits within joints. What are these deposits called?

A

Tophi. Path slides later in flashcards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In later stages, gout can resemble what other joint disorder? List common features? List differentiating feature?

A

Can resemble RA

Common features: polyarticular involvement

Joint involvement in gout is asymmetrical, RA is symmetrical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Is primary or secondary gout more common?

A

primary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In primary hyperuricemia, which has a greater impact on gout, decreased efficiency of excretion or increased production of uric acid?

A

Decreased effiency of uric acid excretion - 90%

Increased production of uric acid - 10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Secondary hyperuricemia and gout are usually related to what?

A

decreased renal urate clearance as a direct or indirect consequence of the primary disease process (meaning a disease is causing the gout)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What accounts for less than 1% of secondary hyperuricemia and gout?

A

Four known specific inborn errors of purine metabolism with overproduction of urate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Under excretion of uric acid is a misnomer. Why? Describe what they mean by this.

A

“under-excretors” actually still excrete the same amount of uric acid. They just require a higher serum concentration of uric acid to excrete this amount. This increased serum concentration is what causes gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Males or females have higher urate concentrations normally?

A

Males, 2x the amount of females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Intestinal metabolism of uric acid accounts for what % of total urate metabolism?

A

33%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Xanthine oxidase is involved in what step(s) of uric acid formation?

A

Hypoxanthine→ Xanthine → Uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Urate in kidney

What % of originally filtered urate wounds up being excreted?

A

8-12% of filtered is actually excreted

Urate freely filtered (100%) then 98-100% reabsorbed in PT. Again 50% secreted back into PT and largely reabsorbed. Back and forth game, lots of transporters we probably dont need to know.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In men, primary hyperuricemia begins when?

A

at puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What reduces the risk of developing gout in pre menopausal women?

A

Estrogen, increases urate clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Men or women experience highest incidence of gout b/t 30-45 years of age? At what age does the other sex usually get it?

A

Men 30-45

Women 55-70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What cells play a huge role in gout? How?

A

Neutrophils,

  • urate crystals deposit in joint, trigger acute inflammatory reaction (neutrophil influx and chemotaxis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Besides joints, what other parts of body can be affected by gout?

A

helix of ear, achilles tendon

24
Q

Does gout cause destruction of the joint?

A

Yes

25
Q

What radiographic finding of a joint is pathognomonic for gout?

A

Overhanging edges

26
Q

Kid bites his own lips and self mutilates himself? What disease? What genetic mutation?

A

Lesch-Nyhan Syndrome; X-linked deficiency of HGPRT (hypoxanthine-guanine phosphoribosyltransferase…try saying that 3 times)

27
Q

What diuretics promote hyperuricemia?

A

Loop, Thiazide diuretics

28
Q

What drug did Dr. P do research on that causes hyperuricemia? List other drugs that can cause it

A

Ethambutol

Loop and thiazide diuretics, pyrazinamide, Salicylates (low dose), Nicotinic acid, Cyclosporine, Ethanol

29
Q

Uric acid stones account for what % of urinary tract stones?

A

5-10%

30
Q

3 major risk factors for uric acid nephrolithiasis?

A

increased uric acid excretion, reduced urine volume, low urine pH

31
Q

What do you want to do to urine to decrease risk for uric stones?

A

alkalinize the urine

32
Q

What clnical conditions are commonly associated with hyperuricemia and gout?

A

HTN, CAD, Dabeetus, obesity, alcoholism, renal insuffiency, lead poisoning, hypothyroidism

33
Q

What foods increase risk for gout?

A

alcohol consumption (beer), seafood (shrimp,lobster) red meat

red wine may actually be protective

34
Q

Moonshine can cause what that leads to gout? How?

A

lead poisoning (produces interstitial nephritis, which interferes with uric acide excretion)

35
Q

Gross description of tophi?

A

White chalky aggregates of uric acid crystals

36
Q

Microscopic description of tophi?

A

fibrosis and giant cell formation

37
Q

Gout under polarized light (3 features)

A

Negative birefringence, needle shaped, yellow under parallel

38
Q

What slide fixation ruins microscopy of gout? What is best method to view it?

A

Formalin fixation dissolves urate deposits

Alcohol fixation with silver stain is best (shown in picture, dark stained stuff is urate crystals)

39
Q

This is an image of what?

A

Urate deposits in kidney, almost look like stellate stars

40
Q

Other disease that involves crystal deposition?

A

Calcium pyrophosphate Dihydrate (CPPD) Crystal Deposition Disease

41
Q

List some metabolic abnormalities associated with CPPD?

A
  • hyperparathyroidism
  • hemochromatosis
  • gout
  • hypophosphatasia
  • hypomagnesmia
  • ochronosis
42
Q

Biggest factor for CPPD?

A

Age, average age is 70-75

43
Q

CPPD sex preference?

A

M = F

44
Q

Most common form of CPPD?

A

Asymptomatic form, not pseudogout

45
Q

Recurrent acute inflammatory monoarticular arthritis associated with CPPD is called what?

A

pseudogout

46
Q

Injection of what into joint space can actually worsen pseudogout?

A

Intra-articular hyaluronan (used to treat other joint disorders)

47
Q

RA and CPPD common radiographic findings? Differentiating findings?

A

Similar: Subchondral sclerosis, joint space narrowing

Different: No erosions (erosions present in RA)

48
Q

Familial CPPD disease is linked with what gene?

A

ANKH gene on chromosome 5p

49
Q

Main way to tell CPPD from OA?

A

Location of joint involvement. CPPD will involve MCP joints, wrist, elbows, glenohumeral joints)

50
Q

If patient has CPPD under the age of 55, what disorder should also be considered?

A

Hyperparathyroidism

51
Q

What disease is associated with accumulations of hydroxyapatite?

A

Calcium Hydroxyapatite (HA) Deposition Disease

52
Q

Hyperphosphatemia in HA deposition disease is usually associated with what other condition?

A

Chronic renal failure, hyperphosphatemia enhances HA deposition both in and around joints.

  • CPPD deposition disease can be seen in these patients too
53
Q

Unlike urate and CPPD crystal deposition, what is NOT seen in HA deposition disease?

A

Acute synovitis is unusual

54
Q

CPPD under polarized light (3 features)?

A

positively birefringent, rhomboid shaped, blue under parallel light

55
Q

What are these? What disease can they be seen in?

A

Cholesterol crystals, may be seen in RA