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MDCN 360: Course 2 > Approach to Monoarthritis > Flashcards

Approach to Monoarthritis Flashcards

1
Q

compare and contrast articular and extra-articular pain

A
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2
Q

characteristics of degenerative vs inflammatory articular pain

A

degenerative: instability, locking, crepitis, pain with motion, <30 min morning stiffness
inflammatory: warmth and swelling, extra-articular featurs, morning stiffness>1 hr, pain better with movement.

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3
Q

5 factors of inflammation

A
  1. dolor (pain)
  2. swelling (tubor)
  3. redness (rubor)
  4. warmth (calor)
  5. functional loss (functio laisa)
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4
Q

if the joint is red:

A

the tubes get fed.

do a test of fluid! (unless contra-indicated)

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5
Q

joint aspiration contra-indications

A

relative: overlying infection on hte skin, coagulopathy, tattoos (not really applicable anymore)
- absolute: prosthetic joint (get ortho in), anatomically inaccessible, lack of proficiency or consent.

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6
Q

what does synovial fluid look like in a nomral, degenerative, inflammatory, septic or hemorrhagic joint? what would the culture, viscosity and PMN counts be?

A
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7
Q

tests to run when someone presents with monoarthritis

A
  • CBC (check WBC)
  • CRP, Uric Acid
  • INR, ASOT, Igs
  • blood and urine cultures if septic arthritis is usspected
  • RF, ANA, ANCA, CCP, HLAB27 only if you have reason based on history to suspect a diagnosis supported by one of these, never to rule an AI disease out
  • XRay of the affected joint and the contralateral side.
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8
Q

T/F biopsy is first line

A

FALSE. aspiration FLUID might but not bone. Can biopsy synovium with a needly, arthroscopy or openly.

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9
Q

PMN deficiencies can predispose somseone to _____ infections

people with complement deficiencies can predispose someone to ____ infecitons

A

catalase positive infections like (staph auereus)

complement deficiencies can predispose someone to ENCAPSULATED infections (yersinia, strep, klevsiella, bacillus, neisseria etc)

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10
Q

note: people who are susceptible to a joint infection:

A
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11
Q

first bacteria to suspect for septic arthritis/osteomyelitis, then secondary

A
  • most common is staph aureus– usually a monoarthritis in the extremems of age
  • in you, otherwise think gonococcol infection (neusseria)
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12
Q

septic bursitis

A
  • may mimic septic arthritis
  • many joints have a geographically related bursa, often more superficial
  • olecranon bursa is most common

(bursa is a space that can fill with fluid that allows tissues to slide around without friction)

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13
Q

gonococcal vs nongonococcal arthritis: compare population, pattern, tenosynocitis, dermatitis, joint cultures, blood cultures, outcome.

A
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14
Q

routes by which bacteria can reach the joint

A
  1. the hematogenous route
  2. dissemination from osteomyelitis
  3. spread from an adjacent soft tissue infection
  4. diagnostic or therapeutic measures
  5. penetrating damage by puncture or trauma,
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15
Q

first line Abx therapies for gram positive MSSA and MRSA bacterias

A

*usually IV vanco cause it won’t get absorbed if given orally, which is also why it’s good for Cdiff.

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16
Q

first line Abx therapies for gram negative bacteria

A

REVIEW ABX SPREAD SHEET

17
Q

every septic arthritis should have an ____ consult

A

orthopedic consult

18
Q

number one cause of monoarthritsi

A

SEPTIC SPETIC SEPTIC (and gout)

19
Q

classic presentation of septic arthritis

A

IF THE JOINT IS RED THE TUBES GET FED

20
Q

which demographic really doesn’t get gout

A

premenopausal women don’t usually get gout unless they have a a hardcore hormonal issue

  • gout: overweight, metabolix syndrome, women who are taking diuretics post menopausal
21
Q

synovial fluid characteristics of gout

A
  • thin yellow cloudy fluid
  • high WBC count 90% neutrophils (still gotta rule out infection– need to do culture or gram staining)
  • negatively birefringent needle shaped crystals seen, some wihtin neutrophils (actively phagocytosing)
22
Q

treatment for gout

A
  1. treat at the first attack (prednisone and colchicine)
  2. always treat with prophylaxis when using urate lowering therap (allopurinol except in HLA+ then use Febaxostat)
  3. continue prophylaxis until target urate reached for 4-6 monts
  4. for those with tophi target <300

if you can’t distinguish between gout and septic arthritis, start Abx before the cultures come back

23
Q

T/F allopurinol with CPPD

A

false .allopurinol lower urate which will help with gout but CPPD is pseudogout. prednisone and NSAIDs can treat flares but colchicine and allopurinol is of little utility.

there is no way to prevent recurrent flares of CPPD and is more common in elderly

-CPP crystals tend to deposit into hyaline and fibrocartilage and called chondrocalcinosis on Xray

24
Q

CPPD can cause ___ in late stages

A

OA in late stages. may be asymptomatic chondrocalcinosis

25
Q

CPPD association

A

hyperparathyroid

hemochromatosis

hypomagnesemia

-hypophosphateasia

gout

ra

26
Q
A

CPPD seen!›

27
Q

describe OA

A

• Usually chronic onset
• Favors hips, knees, Carpometacarpal joint (CMC), distal interphalangeal joints
(DIPs)

  • Limited morning stiffness
  • Worse with activity
28
Q

describe osteochondritis dessicans

A
  • Children and teens
  • Favors the knee
  • Ischemic bone and its associated cartilage
  • Bone island may separate
  • May cause joint locking
29
Q

describe spontaenosu osteonecrosis of the knee

A
  • Mostly older women
  • Typically weight bearing surface of the medial femoral condyle
  • Sudden and severe onset of pain
  • May be effused
  • MRI helpful for diagnosis
30
Q

two key genetic disorders that can leas to a degenerative mono or poly arthritis

A
31
Q

outline diseases that fall into these inflammatory joint aspirate categories

A
32
Q

causes of reactive arthritis

A
  • typically is a large joint, lower rextremity monoarthritis or asymmetric oligoarthritis
  • check HISTORY for Upper resp tract infection, UTI, or FI infection
  • may have had a flu a week ago, now they ahve a sore ankle– reactive arthritis
  • may also have uveitis, keratoderma blennorrhagicum (resembles psoriasis)
  • Some reactive arthritis will become a chronic peripheral spondyloarthropathy
  • Especially if recurrent episodes and HLA-B27 Positive
33
Q

when might a reactive arthritis become chronic?

A
  • Some reactive arthritis will become a chronic peripheral spondyloarthropathy
  • Especially if recurrent episodes and HLA-B27 Positive
34
Q

traumatic reactive arthritis is usually ____ and very wuick in onset

A

usually hemorrhaic.

35
Q

a patient presents with a hugely swollen painful knee and on biopsy, brown looking synovium was seen. On MRI, synovium shows arborescence.

A

Giant cell tumor of the synobium. the brown looking synovium is due to hemosiderin laden macrophages.

36
Q

most common tumor that might cause monoarthritis

A

Lipoma Arborescence
• Benign tumor usually of the knee
• Synovium replaced by adipose cells
• Villous pattern on MRI is characteristic

37
Q

NOTE: General differentials for monoarthritis

A
38
Q

reference note:

A

MDCN 360: Course 2 (70 decks)

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