Intro to joint disease mono and polyarthritis

Question 1

patterns of arthritis (2 categories; 4 kinds)

Answer 1

inflammatory vs noninflammatory; monoarthritis vs polyarthritis

Question 2

causes of inflammatory monoarthritis (3)

Answer 2

trauma
crystals: monosodium urate (gout) vs calcium pyrophosphate (pseudogout)
septic joint

Question 3

Clinical presentation of joint inflammation (5)

Answer 3

morning stiffness;
erythema and warmth (in crystals and septic joints) may not be prominent in others
synovitis: thickening of synovium around joints/TTP

Question 4

Joint inflammation

diagnostic tools-4 lab tests and 1 imaging technique

Answer 4

-lab tests for inflammation:
    ESR
    CRP
-peripheral blood leukocytosis (septic arthritis)
-joint fluid analysis
-xray

Question 5

WBC and PMN values for synovial fluid analysis for:
noninflammatory
Inflammatory
Septic

Answer 5

noninflammatory: WBC 2,000 PMN2,000; PMN 50-90%
septic: WBC > 50,000; PMN >90%

Question 6

Gout
Definition
cause (general)

Answer 6

metabolic disorder resulting in elevated uric acid levels (hyperuricemia) beyond saturation.

Could be due to underexcretion (90%) or overproduction (10%)

Question 7

Gout
Patient population
Estrogen’s effect on urate excretion?
one increasing risk factor in the US

Answer 7

elderly men more than women, but increased incidence in women post menopause (because estrogen promotes urate renal excretion)

Obesity is a risk factor

Question 8

Input sources of nucleoproteins and nucleotides? where do we get it from?

Answer 8

1/3 nucleoproteins and nucleotides come from diet and 2/3 comes from our own cells.

Question 9

What happens to the nucleoproteins and nucleotides we consume?

Answer 9

converted to adenine and guanine nucleotides

Question 10

metabolized adenine and guanine become what? about how much is that? in mg

Answer 10

uric acid (about 1,000 mg)

Question 11

How is uric acid excreted? in what proportions? in mgs?

Answer 11

1/3 gut excretion (bacterial degradation) about 200mg/day

2/3 renal excretion (10% of filtered load (AKA 80%) reabsorbed) 600mg/day

Question 12

Hyperuricemia
causes of overproduction (4)
causes of underexcretion (4)

Answer 12

Overproduction (10%):
enzymatic abnormalities, increased cell turnover, diet, ETOH

Underexcretion (90%):
metabolic syndrome, renal disease, drugs (diuretics, cyclosporine), ETOH

Question 13

Physical findings of Gout
(2 sx; 1 microscopic finding)
potential presentation in more serious gout disease (2)

Answer 13

• joint/extremity pain
• swelling, warmth (Podagra-joint swelling)
• MSU crystals upon microscopy; often phagocytosed by PMNs
• potentially polyarticular
• potentially tophaceous gout (nodules on ears; “punched out” lesions and over hanging edges upon x-ray)

Question 14

Precipitation of gout attack (3)

Answer 14

• elevation of uric acid
• reduction of uric acid–because stored crystals start mobilizing
• release of crystals from preformed deposits

Question 15

Kidney filtration of uric acid: What percent is filtered at each of the following parts?

proximal tubule
descending limb
ascending limb
collecting duct

Answer 15

Proximal tubule 99% reabsorbed
Descending limb loop of henle 50% is secreted
Ascending loop of henle 80% is reabsorbed
collecting duct 10% is excreted

Question 16

Onset of Gout is closely correlated to what?

At what value will 90% of men experience gout?

Answer 16

Gout is correlated to uric acid levels… at 9 or above 90% of men will have gout

Question 17

Gout vs. CPPD
Crystal name
clinical description upon lab examination
color

Answer 17

Gout:

• monosodium urate crystals;
• negative bifrengent when indicator is PARALLEL
• YeLLOW when parallel

Pseudogout:

• calcium pyrophosphate
• positive bifrengent when indicator is parallel
• blue when parallel

Question 18

What is polyarticular gout?

Answer 18

Gout involving multiple joints

Question 19

What is Tophaceous gout? 
Clinical presentation (4)

Answer 19

presence of crystal accumulation. presentation include nodules on ears, large abscesses of calcium pockets, overhaning joint edges, and punched out bone

Question 20

Inflammation cascade induced by MSU crystals. What does it end it? What are the steps? (5)

Answer 20

ends in recruitment of neutrophils.
Phagocytosis of crystals by monocyte–>activation of inflammation signals within inflammasome–> IL1B is produced–> IL1B triggers endothelial cells to produce inflammatory cytokines–>recruitment of neutrophils

Question 21

Calcium pyrophosphate dihydrate Depositing disease.
etiology of majority cases?
patient population?

Answer 21

• mostly due to overproduction of inorganic pyrophosphate

- patient population is 12% of elderly. 5% at 60 years rise to 30% in 90 year olds

Question 22

How do calcium pyrophosphate crystals form?

Answer 22

pyrophosphate crystals exit cell via the “ank” channel and bind to calcium to form calcium phyrophosphate

Question 23

Common causes of CPPD (4) and the labs to test for CPPD?

Answer 23

1. Hemochromatosis-Fe, Total Iron binding capacity (TIBC)
2. Hypophosphatasia- alkaline phosphatatase function
3. Hypomagnesemia-Mg level
4. Hyperparathyroidism-Ca and PTH level

Question 24

Psuedogout target joints

Answer 24

similar to gout but LARGER joints such as

Knee, wrist, shoulders

Question 25

How to diagnose CPPD?

What is an indication for CPPD?

Answer 25

indication is “chondrocalcinosis” upon x-ray; this is not always seen.
Dx: positive bifringent crystals upon joint fluid analysis

Question 26

Clinical Presentation of CPPD (pseudogout) (3) and the most common presentation of pseudogout

Answer 26

1. asymptomatic-most common
2. pseudogout
3. Osteoarthritis–often widespread including shoulder/wrist…then you should be suspicious of pseudogout
4. RA-like (MCP joint enlargement)

Question 27

What is chondrocalcinosis?

Answer 27

deposition of calcium pyrophosphate crystals in hyaline cartilage

Question 28

Therapeutic goals of treating Gout (4)

Answer 28

1. increase urate excretion
2. decrease urate synthesis
3. inhibit inflammation
4. symptomatic relief