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Musculoskeletal 1 > Rheumatological 1 > Flashcards

Rheumatological 1 Flashcards

1
Q

Inflammatory response

  • morning stiffness lasts how long
  • synovial fluid analysis
  • other lab results
A
  • > 60 min
  • leukocyte ct >2,000/uL
  • elevated ESR and CRP
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2
Q

Non-Inflammatory response

  • morning stiffness lasts how long
  • synovial fluid analysis
  • other lab results
A
  • <30 min
  • leukocyte ct btwn 200 and 2,000/uL
  • nl ESR and CRP
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3
Q

Rheumatoid Arthritis

- etiology

A
  • risk increased in relatives: genetic
  • Heritability about 60%
  • 20 alleles IDed
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4
Q

Allele associated with RA

A

HLA-DRB1

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5
Q

List the 4 systems with extra-articular manifestations in RA

A
  • skin
  • eyes
  • pulmonary
  • cardiac
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6
Q

RA affects on skin

A
  • RA nodules, MC on pressure points like elbows
  • pyoderma gangrenosum
  • RA vasculitis (common)
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7
Q

RA affects on eyes

A
  • keratoconjunctivitis sick (dry eyes)

- episcleritis (sclera red and inflamed)

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8
Q

RA affects on pulmonary system

A
  • exudative pleural effusion

- interstitial lung disease

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9
Q

RA affects on cardiac system

A
  • CAD
  • CHF (dt CAD)
  • pericarditis (friction rub)
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10
Q

RA - felty syndrome

A
  • neutropenia
  • splenomegaly (MC)
  • RA (MC)
  • sometimes fever, anemia, thrombocytopenia
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11
Q

What is most appropriate autoantibody for RA

A

CCP

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12
Q

Is RA arthritis symmetrical or unilateral?

A

symmetrical

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13
Q

How does RA affect joints

A
  • small and large joints
  • small joints will be bilateral
  • might have single large joint
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14
Q

Osteoarthritis (OA)

  • how common
  • how relates to age
  • men vs. women
A
  • most common type of arthritis
  • incidence increases with age
  • men slightly more than women
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15
Q

Two classification for OA

A
  • primary: no specific predisposing event (injury for ex)

- secondary: degeneration of previously injured joint

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16
Q

OA

  • pain presentation
  • symmetry?
A
  • pain may be intermittent, occur with joint us
  • joints may be tender
  • asymmetric (diff from RA)
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17
Q

How does OA affect joints

A

oligoarthritic - 1 or 2 large joints or 1 or 2 small joints common

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18
Q

Two types of nodes found in OA

A
  • Bouchard: PIP joints

- Heberden: DIP joint

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19
Q

Baker cyst

A

chronic effusion of popliteal fossa

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20
Q

Lab and imaging for OA

A
  • no labs, may see elevated ESR during flair

- Imaging: plain film will show narrowing of joint space, subchondral sclerosis, osteophytes (bony outgrowths)

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21
Q

Overview of OA tx

A
  • NSAIDs
  • PT
  • Joint injection
  • steroids, esp with effusion
  • joint replacement
  • Glucosamine and chondroitin sulfate have little effect
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22
Q

Fibromyalgia

  • incidence
  • what is interesting about incidence
A
  • 0.06% to 10% WIDE range
  • misunderstanding about dx of fibromyalgia
  • many don’t believe it exists
  • many want to ignore
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23
Q

Fibromyalgia pathophysiology

A
  • aberrant chronic pain reflex arcs
  • centered on dorsal ganglia of spine
  • reflex arcs fn independently
  • may be exacerbated by acute or chronic pain inputs (arthritis or psych distress)
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24
Q

What do MRI studies show about fibromyalgia

A
  • pain is same as other pain perception but more easily triggered
  • elevation in pain-facilitating neurotransmitters (glutamate and substance P)
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25
Q

Fibromyalgia tx

A
  • validation is important
  • aerobic exercise
  • PT
  • SNRIs (duloxetine and milnacipram)
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26
Q

Spondyloarthritis

- three types

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Inflammatory bowel disease-associated arthritis (reactive arthritis)
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27
Q

Spondyloarthritis

- gene

A
  • HLA-B27 (MC with ankylosing spondylitis)

- insufficient to make dx

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28
Q

Ankylosing spondylitis

- m vs. f

A

3:1 M:F

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29
Q

Ankylosing spondylitis

- presentation

A
  • insidious low back pain MC
  • stiff worse after rest, better with use
  • bilateral buttock pain, sacroiliitis (XR of SI joint helpful)
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30
Q

Psoriatic arthritis

  • describe
  • seen with what co-morbidity
A
  • Severe inflammatory arthritis
  • like RA permanent destruction of joint
  • Oncholysis (painless separation of nail from nailbed)
  • oligo or symmetric
  • dactylitis (diffuse swelling of joint, tendon, ligament of digit) in 50%
  • 15-20% of people with psoriasis
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31
Q

Psoriatic arthritis

- dx

A
  • don’t use antibodies for dx
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32
Q

Inflammatory bowel disease related arthritis

  • incidence and progression
  • location of arthritis
A
  • 20-30% of people with Crohn’s or UC
  • up to 50% resolve in 6 months
  • axial or peripheral
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33
Q

Inflammatory bowel disease related arthritis is dt what

A
  • autoimmune, non-infectious
    BUT, associated with a few orgs:
    MC: Yersinia
    also: salmonella, shigella, campylobacter, rarely E. Coli
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34
Q

For each type of spondyloarthritis, what is the main thing to look for?

A
  • ankylosing spondylitis: pain in sacroiliac joint
  • psoriatic arthritis: psoriasis of skin, hand findings
  • Inflammatory bowel: Sx of Crohn’s or UC
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35
Q

Management of spondyloarthritis

A
  • NSAIDs
  • glucocorticoid injections
  • DMARDS?
  • TNF-alpha inhibitors
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36
Q

Systemic Lupus Erythematosis

  • describe
  • inheritance
  • M vs. F
A
  • multi-organ
  • caused by auto-antibodies including antibodies vs. intranuclear antigens
  • polygenic inheritance
  • 90% women
37
Q

Systemic Lupus Erythematosis

- list the 7 organ systems involved

A
  • MSK
  • renal
  • neuropsychiatric
  • cardiovascular
  • pulmonary
  • hematologic
  • GI
38
Q

SLE

- MSK sx in acute, sub-acute, chronic dz

A
  • Acute: malar skin rash (butterfly) on face
  • Sub-acute: polycyclic rash with hyperpig. circular plaques
  • Chronic: infiltrative papules, plaques, red plaques on sun-exposed surfaces
39
Q

SLE

- other MSK sx

A
  • painless oral ulcers
  • alopecia
  • Raynaud’s (hypersensitive vascular endothelium)
  • 85% report myalgia
40
Q

SLE

- MSK joint involvement

A
  • 90% have joint issues
  • 40% get osteonecrosis of hips
  • peripheral or lrg joints
  • usually symmetrical but can be single
41
Q

SLE

  • Renal incidence
  • what is MC issue
A
  • up to 70%
  • usually glomerular dz
  • renal bx usually indicated - have a nephrologist do this!
42
Q

SLE

- What two markers associated

A
  • Anti-double stranded DNA

- Anti-smith antibody

43
Q

SLE

- neuropsychiatric involvement

A
  • vasculitis of the brain: common and hard to dx
  • esp difficult w/o arthritis or skin sx
  • 19 possible manifestations, be careful to not write off as psych issue
  • Can present with peripheral nervous dz
44
Q

Examples of peripheral nervous dz in SLE

A
  • mononeuropathy multiplex or single
  • autonomic lesions
  • cranial lesions
  • polyneuropathy
45
Q

What is mononeuropathy multiplex

A
  • Peripheral neuropathy that presents with numbness
  • Generally comes and goes
  • Caused by small vessel inflammation of peripheral nerves. Vessels get clogged up from autoimmune response and then reopen, clog and reopen again.
  • Pts most likely won’t tell you “I have numbness that comes and goes”
  • more likely to catch on ROS if ask
46
Q

SLE cardiovascular involvement

A
  • 40% pericarditis: find via exam, echo, MRI/CT

- cardiac valve thickening called “Libman-Sacks endocarditis”: non-infectious vegetations on valves

47
Q

SLE pulmonary involvement

A
  • pleuritis +/- effusion
  • interstitial lung dz
  • shrinking lung syndrome
48
Q

Define shrinking lung syndrome

A
  • pleuritic pain
  • SOB
  • progressive decrease in lung volume
  • unknown cause
49
Q

SLE hematologic involvement

A
  • All three cell lines possible (anemia, leukopenia, thrombocytopenia)
  • hemolytic anemia
  • pure red cell aplasia
  • aplastic anemia
50
Q

Describe warm antibodies in hemolytic anemia

A
  • attach to the cell membrane of the red cell
  • when cells try to get through sinusoids of spleen, spleen takes chunks of the membrane off
  • cell folds up on itself, no longer biconcave discs, now spherocytes
  • spherocytes seen on peripheral smear
51
Q

What do you always test for that is related to SLE if someone has a clot/DVT from unknown cause?

A
  • antiphospholipid antibody syndrome / lupus anticoagulant syndrome (APLA/LAC)
  • antibodies to endothelium, monocytes, platelets, which produce a pro-coagulant state
52
Q

SLE

- GI involvement

A
  • esophageal imotility
  • sterile peritonitis
  • mesenteric vasculitis
  • mesenteric thrombosis
53
Q

What is mesenteric vasculitis often confused with?

A

acute appendicitis

54
Q

What is much more common in SLE

A

malignancy. ..

- 7 times increase in non-hodgkin lymphoma

55
Q

How to diagnose SLE

A
  • consider in anyone with otherwise unexplained multi system dz
  • antibodies: many, Anti-double stranded DNA and Anti-Smith are two tow know
56
Q

SLE how to interpret ANA results

A
  • in light of pre and post test probability
57
Q

ESR vs. CRP in SLE

A
  • ESR preferred over CRP (CRP can be negative in acute flare)
58
Q

What else should be tested for if suspect SLE

A
  • C3 and C4 dt potetential for immune complex dz
59
Q

Sjogren syndrome

- describe

A
  • immune-mediated
  • unknown cause
  • infiltrative inflammation damages exocrine glands
  • major/minor salivary glands, lacrimal glands, possibly others like pancreas
  • 1.5% prevalence
60
Q

Sjogren’s pathophys

A
  • inflammatory infiltrates of CD-4 positive T lymphocytes

- some B cell action

61
Q

Sjogren’s clinical manifestations

A
  • Keratoconjunctivitis sick (dry eyes): dx via shimmer test (strip under lower eyelid)
  • Xerostomia (dry mouth)
62
Q

What are the best markers for Sjogrens

A
  • Anti-Ro / SSA

- Anti-La / SSB

63
Q

What is the definitive dx test for Sjogrens?

A

Lip bx

- would do if still suspect but negative antibodies

64
Q

Sjogren’s management

A
  • symptomatic

- local (eye drops, etc)

65
Q

Mixed Connective Tissue disease (MCTD)

  • describe
  • markers
A
  • overlap syndrome
  • includes features of SLE, systemic sclerosis, polymyositis
  • anti-U1-ribonucleoprotein (RNP) antibodies
  • ANA with speckled pattern
66
Q

Mixed Connective Tissue disease (MCTD)

- presentation

A
  • 50% hand swelling and synovitis

- also: esophageal reflux, interstitial lung dz, pulmonary HTN

67
Q

Mixed Connective Tissue disease (MCTD)

- recommended testing

A
  • high resolution CT of chest
  • PFTs
  • Cardiac echo
68
Q

Mixed Connective Tissue disease (MCTD)

- management

A
  • individualized
  • glucocorticoids, azathioprine, methotrexate
  • help from a rheumatologist!
69
Q

what are the two crystalopathies?

A
  • Gout

- Calcium pyrophosphate deposition (pseudo gout)

70
Q

Gout

- description

A
  • intermittent attacks of inflammatory arthritis

- results from crystallization of excessive levels of uric acid

71
Q

Gout

- incidence

A
  • increasingly common in older people

- 13% >80 yo

72
Q

Gout

- pathophys

A
  • Elevated serum uric acid
  • when in cooler joints, crystalizes
  • crystals recruit inflammatory response (IL-6 , IL-1B, TNF alpha, neutrophils)
  • uric acid is end product of purine metabolism
73
Q

What do free purines arise from (3)

A
  1. ATP turnover
  2. purine metabolism
  3. cell turnover
74
Q

What is the rate limiting step to purine metabolism?

A

Xanthine oxidase

**know this one

75
Q

What is the saturation concentration of serum rate? what does this mean

A
  • 6.8 mg/dL
  • crystals unlikely to form at concentration lower than 6.8
  • above 6.8 is considered hyperuricemia
76
Q

What 5 variables affect crystal formation in gout?

A
  • serum concentration
  • temp
  • other unknowns
  • some people overproduce
  • some people underexcrete
77
Q

Gout Pathophys

- what is the hallmark finding of established gout attack?

A
  • neutrophil infiltration
78
Q

Acute gout

  • when MC
  • presentation
A
  • MC in early am (lowest temp of toe)
  • extreme pain, even sheet hurts
  • red toe
79
Q

Gout

- dx

A
  • clinical presentation
  • crystal analysis (microscope), gram stain, culture
  • Elevated ESR and CRP
80
Q

What do gout crystals look like under microscop

A
  • negatively birefringent urate crystals
  • yellow when parallel and blue perpendicular
  • long like a spear
81
Q

Three gout presentations

A
  1. acute - dx via microscopic exam of fluid
  2. inter critical: time between acute attacks
  3. chronic: frequent attacks
82
Q

Gout

- acute management

A
  • colchicine
  • once acute phase over, start allopurinol and treat until serum uric acid <6.5 mg/dL
  • continue allopurinol for life

*allopurinol is a xanthine oxidase inhibitor

83
Q

Gout

- common reasons for tx failure

A
  • failure to treat to target (<6.5 mg/dL)

- not using high enough dose, can go up to 800 mg per day

84
Q

What is the best name for pseudo gout?

A

osteoarthritis with calcium pyrophosphate deposition (CPPD)

85
Q

CPPD pathophysiology

A
  • mech not understood

- deposition of calcium pyrophosphate crystals in CT

86
Q

What should consider if in young person who presents with CPPD?

A
  • hyperparathyroidism
  • hemochromatosis**
  • hypomagnesemia
  • hypothyroidism
87
Q

What physical finding is associated with CPPD?

A
  • calcium deposits in cartilage

- linear density parallel to surface of cartilage

88
Q

CPPD

- management

A
  • symptomatic
  • decrease inflammation
  • nothing to reduce likelihood of crystal depostion
89
Q

Why does acute mono-articular arthritis require needle aspiration for dx?

A

differentiate between

  • gout
  • CPPD
  • infection

Musculoskeletal 1 (14 decks)

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