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Musculoskeletal-First Aid > Musculoskeletal Pathology (424-427) > Flashcards

Musculoskeletal Pathology (424-427) Flashcards

1
Q

what is the etiology of osteoarthritis

A

mechanical forces; joint wear and tear destroys articular cartilage

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2
Q

what are the joint findings for osteoarthritis

A

subchondral cysts, sclerosis (thickened radiopacity and joint space narrowing on X-ray), osteophytes (bone spurs), eburnation (polished, sanded appearance of bone), Heberden nodes (DIP), Bouchard nodes (PIP), no MCP involvement

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3
Q

what factors predispose to developing osteoarthritis

A

age (more time spent on joints), obesity (more weight on joints), joint deformity, trauma

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4
Q

what is the classic presentation of osteoarthritis

A

pain in weight-bearing joints after use (e.g. at the end of the day) that improves with rest, knee cartilage loss that begins medially (bowlegged), NOT inflammatory, NO systemic symptoms

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5
Q

how do you treat osteoarthritis

A

NSAIDs, intra-articular glucocorticoids

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6
Q

what is the etiology of rheumatoid arthritis

A

autoimmune: inflammatory destruction of synovial joints mediated by cytokines and type III and type IV hypersensitivity reactions

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7
Q

what are the joint findings for rheumatoid arthritis

A

pannus formation in MCP and PIP (abnormal layer of fibrovascular tissue), subcutaneous rheumatoid nodules (fibrinoid necrosis), ulnar deviation of fingers, subluaxation, Baker cyst (in popliteal fossa), no DIP involvement

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8
Q

if you could only look at the patient’s hands how would you differentiate osteoarthritis from rheumatoid arthritis

A

in osteoarthritis there is no MCP involvement,

in rheumatoid arthritis there is no DIP involvement

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9
Q

what factors predispose to developing rheumatoid arthritis

A

female > male, 80% of patients have positive rheumatoid factor (anti-IgG antibody), anti-cyclic citrullinated peptide antibody is more specific,
associated with HLA-DR4

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10
Q

what is the classic presentation of rheumatoid arthritis

A

morning stiffness (lasting >30min and improving with use), symmetric joint involvement, systemic symptoms (fever, fatigue, pleuritis, pericarditis)

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11
Q

how do you treat rheumatoid arthritis

A

NSAIDs, glucocorticoids, disease-modifying agents (methotrexate, sulfalazine, TNF-alpha inhibitors)

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12
Q

what is Sjogren syndrome

A

autoimmune disorder characterized by destruction of exocrine glands (especially lacrimal and salivary)

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13
Q

what demographic is most commonly affected by Sjogren syndrome

A

females, ages 40-60

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14
Q

what are the clinical findings of Sjogren syndrome

A
  • xerophthalmia (decreased tear production and subsequent corneal damage)
  • xerostomia (dry mouth from decreased saliva)
  • bilateral parotid enlargement
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15
Q

what would you see on serology for Sjogren syndrome

A

antinuclear antibodies: SS-A (anti-Ro) and/or SS-B (anti-La)

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16
Q

is Sjogren syndrome a primary disorder or a secondary disorder

A

both; can be a primary disorder or a secondary syndrome associated with other autoimmune disorders such as rheumatoid arthritis

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17
Q

what are the complications arising from Sjogren syndrome

A

dental carries, MALT lyphoma (which may present as unilateral parotid enlargement)

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18
Q

what is gout

A

acute inflammatory monoarthritic condition caused by hyperuricemia, which leads to precipitation of monosodium urate crystals in joints

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19
Q

what are two general ways one can become hyperuricemic

A

underexcretion (seen in 90% of patients): largely idiopathic, can be exacerbated by thiazide diuretics
overproduction (seen in 10%): Lesch-Nyhan syndrome, PRPP excess, increased cell turnover (e.g. tumor lysis syndrome), von Gierke disease

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20
Q

what do gout crystals look like

A

needle shaped, negative birefringence (yellow under parallel light, blue under perpendicular)

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21
Q

does gout have a sex predilection

A

yes; more common in males

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22
Q

describe the location and character of the gout joints

A
  • asymmetric joint distribution,
  • joint is swollen red and painful,
  • classic joint= MTP of big toe (“podagra”=gout of the big toe)
  • tophus formation (monosodium urate crystal deposits, often in olecranon bursa, external ear or Achilles tendon)
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23
Q

when do gout attacks tend to happen and why

A

after meals or alcohol consumption because alcohol tends to compete for the same excretion sites as uric acid in the kidney leading to buildup in blood)

24
Q

how is gout treated

A

acute Tx: NSAIDs (e.g. indomethacin), glucocorticoids, colchicine (microtubule inhibitor)

chronic Tx: xanthine oxidase inhibitors (e.g. allopurinol and febuxostat) to prevent gout attacks

25
Q

what is podagra

A

gout of the big toe (MCP)

26
Q

what is pseudogout

A

a condition characterized by pain and effusion in a joint caused by deposition of calcium pyrophosphate crystals within the joint space

27
Q

what do the crystals of pseudogout look like

A

basophilic, rhomboid crystals, weakly positively birefringent (blue on parallel, yellow on perpendicular)

28
Q

what joints are classically affected

A

large joints (e.g. knee)

29
Q

what demographic (age, sex)

A

> 50 years old, both sexes affected equally

30
Q

what conditions are associated with pseudogout

A

hemochromatosis, hyperparathyroidism, hypoparathyroidism

31
Q

how is pseudogout treated

A

NSAIDs (for acute attacks), steroids, colchicine

32
Q

what are the most common pathogens to cause infectious arthritis

A

S. aureus, Streptococcus, Gonococcus

33
Q

what does the joint look like in infectious arthritis

A

swollen, red, painful,

“STD”: synovitis (e.g. knee), tenosynovitis (e.g. hand), dermatitis (e.g. pustules)

34
Q

what is unique about the pattern of gonococcal infectious arthritis vs. other infectious arthritis

A

gonococcal arthritis presents as a migratory arthritis with an asymmetric pattern

35
Q

name four seronegative spondyloarthropathies

A

psoriatic arthritis, ankylosing spondylitis, inflammatory bowel disease, reactive arthritis (Reiter syndrome)

36
Q

what HLA allele are the seronegative spondyloarthropathies associated with

A

HLA-B27

37
Q

define seronegative spondyloarthropathies (why are they classified together in a group)

A

these are forms of arthritis with no rheumatoid factor (no anti-IgG)

38
Q

do seronegative spondyloarthropathies occur more often in women or men

A

men

39
Q

what characterizes psoriatic arthritis

A

joint pain and stiffness associated with psoriasis

40
Q

is psoriatic arthritis symmetric or asymmetric

A

asymmetric and patchy involvement

41
Q

what percentage of patients with psoriasis get psoriatic arthritis

A

less than 1/3

42
Q

what is seen on physical exam and on x-ray for in a patient with psoriatic arthritis

A

dactylitis (sausage fingers) on physical exam

“pencil-in-a-cup” deformity seen on x-ray

43
Q

what is ankylosing spondylitis

A

chronic inflammation of the spine and sacroiliac joints which leads to ankylosis (stiff spine due to fusion of joints)

44
Q

besides ankylosis what other abnormalities are seen in ankylosing spondylitis

A

uveitis and aortic regurgitation

45
Q

what is the association of inflammatory bowel disease to arthritis

A

Chron disease and ulcerative colitis are often accompanied by ankylosing spondylitis or peripheral arthritis

46
Q

what is the classic triad of reactive arthritis

A
  1. conjunctivitis, 2. urethritis, 3. arthritis

“can’t see, can’t pee, can’t bend my knee”

47
Q

after what infections is reactive arthritis commonly seen

A

post-GI (Shigella, Salmonella, Yersinia, Campylobacter) or Chlamydia

48
Q

what is the classic presentation of systemic lupus erythematosus

A

rash, joint pain, fever

49
Q

in what demographic is SLE most commonly seen

A

young, reproductive age women, African descent

50
Q

what cardiac complication can be seen with SLE

A

Libman-Sacks endocarditis: wart-like vegetations on BOTH sides of valve

51
Q

what kind of hypersensitivity reaction is Lupus nephritis

what two kinds of nephropathies are seen

A

type III:

  • nephritic kind= diffuse proliferative glomerulonephritis
  • nephrotic kind=membranous glomerulonephritis
52
Q

what are the most common causes of death in SLE

A

cardiovascular disease, infections, renal disease

53
Q

use the mnemonic to list all of the characteristic sof SLE

A

RASH OR PAIN:
Rash (malar or discoid), Arthritis, Soft tissue inflammation/ Serositis, Hematologic disorders (cytopenias), Oral/nasopharyngeal ulcers, Renal disease and Raynaud’s phenomenon, Photosensitivity and Positive VDRL/RPR, Antinuclear antibodies, Immunosuppresants (for Tx), Neurologic disorders (e.g. seizures, psychosis)

54
Q

what are the lab findings for SLE

A
  • ->positive anti-nuclear antibodies (ANA=sensitive, not specific)
  • ->anti-dsDNA antibodies (specific, poor prognosis, renal disease)
  • ->anti-Smith antibodies (specific; directed against snRNPs, which are proteins that make up spliceosome)
  • ->antihistone antibodies (sensitive for drug-induced lupus)
  • ->anticardiolipin antibodies (false pos. on syphilis test, prolongged PTT, paradoxically increased risk of AV thromboembolism)
  • ->low C3, C4 and CH50 due to immune complex formation
55
Q

how is lupus treated

A

NSAIDs, steroids, immunosuppresants, hydroxychloroquine

Musculoskeletal-First Aid (2 decks)

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