Intro to joint disease mono and polyarthritis Flashcards

1
Q

patterns of arthritis (2 categories; 4 kinds)

A

inflammatory vs noninflammatory; monoarthritis vs polyarthritis

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2
Q

causes of inflammatory monoarthritis (3)

A

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

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3
Q

Clinical presentation of joint inflammation (5)

A

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

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4
Q

Joint inflammation

diagnostic tools-4 lab tests and 1 imaging technique

A
-lab tests for inflammation:
    ESR
    CRP
-peripheral blood leukocytosis (septic arthritis)
-joint fluid analysis
-xray
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5
Q

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

A

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

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6
Q

Gout
Definition
cause (general)

A

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

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

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7
Q

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

A

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

Obesity is a risk factor

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8
Q

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

A

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

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9
Q

What happens to the nucleoproteins and nucleotides we consume?

A

converted to adenine and guanine nucleotides

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10
Q

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

A

uric acid (about 1,000 mg)

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11
Q

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

A

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

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

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12
Q

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

A

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

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

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13
Q

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

A
  • 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)
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14
Q

Precipitation of gout attack (3)

A
  • elevation of uric acid
  • reduction of uric acid–because stored crystals start mobilizing
  • release of crystals from preformed deposits
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15
Q

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

proximal tubule
descending limb
ascending limb
collecting duct

A

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

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16
Q

Onset of Gout is closely correlated to what?

At what value will 90% of men experience gout?

A

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

17
Q

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

A

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
18
Q

What is polyarticular gout?

A

Gout involving multiple joints

19
Q
What is Tophaceous gout? 
Clinical presentation (4)
A

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

20
Q

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

A

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

21
Q

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

A
  • mostly due to overproduction of inorganic pyrophosphate

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

22
Q

How do calcium pyrophosphate crystals form?

A

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

23
Q

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

A
  1. Hemochromatosis-Fe, Total Iron binding capacity (TIBC)
  2. Hypophosphatasia- alkaline phosphatatase function
  3. Hypomagnesemia-Mg level
  4. Hyperparathyroidism-Ca and PTH level
24
Q

Psuedogout target joints

A

similar to gout but LARGER joints such as

Knee, wrist, shoulders

25
How to diagnose CPPD? | What is an indication for CPPD?
indication is "chondrocalcinosis" upon x-ray; this is not always seen. Dx: positive bifringent crystals upon joint fluid analysis
26
Clinical Presentation of CPPD (pseudogout) (3) and the most common presentation of pseudogout
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)
27
What is chondrocalcinosis?
deposition of calcium pyrophosphate crystals in hyaline cartilage
28
Therapeutic goals of treating Gout (4)
1. increase urate excretion 2. decrease urate synthesis 3. inhibit inflammation 4. symptomatic relief