Approach to Monoarthritis

Question 1

compare and contrast articular and extra-articular pain

Answer 1

Question 2

characteristics of degenerative vs inflammatory articular pain

Answer 2

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.

Question 3

5 factors of inflammation

Answer 3

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

Question 4

if the joint is red:

Answer 4

the tubes get fed.

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

Question 5

joint aspiration contra-indications

Answer 5

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.

Question 6

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

Answer 6

Question 7

tests to run when someone presents with monoarthritis

Answer 7

• 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.

Question 8

T/F biopsy is first line

Answer 8

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

Question 9

PMN deficiencies can predispose somseone to _____ infections

people with complement deficiencies can predispose someone to ____ infecitons

Answer 9

catalase positive infections like (staph auereus)

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

Question 10

note: people who are susceptible to a joint infection:

Question 11

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

Answer 11

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

Question 12

septic bursitis

Answer 12

• 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)

Question 13

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

Answer 13

Question 14

routes by which bacteria can reach the joint

Answer 14

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,

Question 15

first line Abx therapies for gram positive MSSA and MRSA bacterias

Answer 15

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

Question 16

first line Abx therapies for gram negative bacteria

Answer 16

REVIEW ABX SPREAD SHEET

Question 17

every septic arthritis should have an ____ consult

Answer 17

orthopedic consult

Question 18

number one cause of monoarthritsi

Answer 18

SEPTIC SPETIC SEPTIC (and gout)

Question 19

classic presentation of septic arthritis

Answer 19

IF THE JOINT IS RED THE TUBES GET FED

Question 20

which demographic really doesn’t get gout

Answer 20

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

Question 21

synovial fluid characteristics of gout

Answer 21

• 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)

Question 22

treatment for gout

Answer 22

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

Question 23

T/F allopurinol with CPPD

Answer 23

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

Question 24

CPPD can cause ___ in late stages

Answer 24

OA in late stages. may be asymptomatic chondrocalcinosis

Question 25

CPPD association

Answer 25

hyperparathyroid hemochromatosis hypomagnesemia -hypophosphateasia gout ra

Question 26

Answer 26

CPPD seen!›

Question 27

describe OA

Answer 27

• Usually chronic onset • Favors hips, knees, Carpometacarpal joint (CMC), distal interphalangeal joints (DIPs) * Limited morning stiffness * Worse with activity

Question 28

describe osteochondritis dessicans

Answer 28

* Children and teens * Favors the knee * Ischemic bone and its associated cartilage * Bone island may separate * May cause joint locking

Question 29

describe spontaenosu osteonecrosis of the knee

Answer 29

* Mostly older women * Typically weight bearing surface of the medial femoral condyle * Sudden and s**evere onset of pain** * May be effused * MRI helpful for diagnosis

Question 30

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

Answer 30

Question 31

outline diseases that fall into these inflammatory joint aspirate categories

Answer 31

Question 32

causes of reactive arthritis

Answer 32

- 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

Question 33

when might a reactive arthritis become chronic?

Answer 33

* Some reactive arthritis will become a chronic peripheral spondyloarthropathy * Especially if recurrent episodes and HLA-B27 Positive

Question 34

traumatic reactive arthritis is usually ____ and very wuick in onset

Answer 34

usually hemorrhaic.

Question 35

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

Answer 35

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

Question 36

most common tumor that might cause monoarthritis

Answer 36

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

Question 37

NOTE: General differentials for monoarthritis

Question 38

reference note: