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Rheumatology > OA and crystal arthropathies > Flashcards

OA and crystal arthropathies Flashcards

1
Q

Clinical subtypes of osteoarthritis?

A
  1. Nodal - most common
  2. Erosive - the radiographic evidence is centrally located. Osteophytes are present.
  3. Crystals
  • CPPD
  • – acute (pseudogout) or chronic, which is costrocalcinosis
  • Apatite
  • – Milwaukee shoulder - confined to elderly subjects predominantly women over 75. One or a few joints and looks like atrophic changed on xray, and there is joint instability.
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2
Q

what are the most common sites for OA?

A

hands (partic female) > knee (partic female) > hip

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3
Q

How does knee OA occur?

A

usually associated with age, female, obesity and nodal OA
- the medial compartment is most common

If it is strictly unilateral, then consider prev trauma or surgery as cause

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4
Q

Where does the majority of hip OA occur?

A

The most common is the “superior” pole of the ball-and-socket joint.

This is associated with symptoms of pain and restriction when hip abducted and ext rotated

on Xray see joint narrowing.

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5
Q

what makes up cartilage?

A

collagen - mostly type II, also XI

proteoglycans - rapidly turned over, electronegative and they are released into synovial fluid in OA.
— major one = aggrecan

proteinases - enzymes that help turnover of matrix. In OA, these overwhelm the chrondrocyte attempts to maintain the matrix. Include the MMP and counterbalanced by TIMPs (tissue inhibitory metalloproteinases)

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6
Q

what is the proposed pathogenesis of OA?

A

oedema of the extra-cellular matrix due to focal proteolysis and proteoglycan breakdown. The chondrocytes try to balance this by upregulating their proteoglycans, leading to more water. This leads to softened cartilage which takes direct force and degradation.

eventually these chondrocytes are replaced by fibroblasts

later we get subchondral sclerosis, cysts and osterophytes - this is being driven by angiogenesis from the other new tissue being laid down

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7
Q

Is there any evidence for glucosamine/chondroiton?

A

there is a little bit of evidence for glucosamine. there was approximately a 30% response rate (not much better than placebo).

general recommendation is to trial it for 4 months, then stop if no improvement.

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8
Q

What do you see under polarising microscopy in gout?

A

The finding is negatively birefringent crystals in gout

pseudo gout is the opposite

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9
Q

what are some medications to decrease serum uric acid?

A

probenecid is a medication used for hyperuricaemia. it decreases reabsorption of uric acid from the tubules.

allopurinol is a xanthine oxidase inhibitor

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10
Q

What are the locations of pyrophosphate arthropathy?

A

large joints are impacted more tan small joints

knees > wrists > shoulders > elbows > hips

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11
Q

are there any metabolic diseases that predispose to CPP disease?

A

haemochromatosis

hyperPTHism

hypophosphataemia

hypoMg

Hypothyroid

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12
Q

what is pseudogout?

A

this is an acute MONOarthritis seen in the elderly

it is self-limiting.

often triggered by trauma, or seen after surgery

positively birefringent under polarising microscopy

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13
Q

what are the therapies of acute pseudogout?

A

local treatment is best, including aspiration and steroid injections

treatment of any underlying metabolic process usually does not change disease process

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14
Q

what is calcium hydroxyapatite disease?

A

another crystal arthropathy - but no crystals seen on polarising microscopy

usually an idiopathic process, but can be seen in renal failure, scleroderma or even dermatomyositis

it can cause a whole bunch of different entities

  1. calcific PERIarthritis
  2. intra-articular hydroxyapatite disease

when there are large amounts of these crystals, it can cause a large joint to be destroyed - in the shoulder this can cause shoulder disintergration! (Milwaukee shoulder)

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15
Q

What is the characteristic xray finding that the college wants us to know for haemochromatosis related OA?

A

very important!

if you see severe OA of the 2nd and 3rd MCP of the hands, think of this condition. It is a common re-presenter

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16
Q

what is the condition associated with severe OA of the 1st carpo-metacarpal joint?

A

primary osteoarthritis

this can be very painful and function limiting - refer early to hand surgeon!

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17
Q

how do you officially use a walking stick?

describe it to me as if i had a painful RIGHT hip

A

hold the cane in the left (the contralat) hand, advance with the painful leg

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18
Q

when the college is describing an arthropathy in a Polynesian person, what is it likely to be?

A

gout.

19
Q

what is chondrocalcinosis?

A

this is calcium (pyrophosphate) deposition in the hyaline cartilage. almost a precursor to pseudogout.

20
Q

what is the likely diagnosis for a 75+ yr old woman with two weeks painful knee with no prior trauma.

decreased ROM

xray shows medial compartment joint space narrowing

maybe calcium in the hyaline cartilage of contralateral compartment

A

the calcium deposition is chondrocalcinosis

the diagnosis is pseudogout, the acute arthopathy presentation of this condition

21
Q

where does diabetic neuropathic arthropathy most commonly affect?

A

mid-foot is most common

22
Q

how do we provide diagnosis for:

75 yr old woman with bilat knee OA. presents with 4/52 severe right knee pain. tender medial joint line. no evidence of sepsis. small effusion. xray shows mod changes of OA

what is the next best scan to prove what’s going on?

A

MRI is the best choice. it will demonstrate a meniscal tear of the medial compartment.

this would be leading to bone oedema and pain etc

referring to surgeon would be bad, because they would chop out more cartilage

23
Q

what happens with you give allopurinol and azathioprine together?

A

you can get azathioprine related bone marrow depression (need to decrease the dose of aza if giving allopurinol)

24
Q

where do we feel pain if there is hip pathology?

A

it is felt in the groin usually

25
Q

where should you aspirate a small knee effusion?

A

medial to the upper/middle third of patella

realistically though, if there’s fluid in the suprapatellar pouch - go for that

26
Q

what is the goal with allopurinol treatment? do we have a number we are trying to achieve?

A

Yes - “Treat to Target”
Aim <0.30mmol/L (300micromol/L) in tophaceous gout.

[This is substantially below the urate concentration at which monosodium urate is saturating in extracellular fluids: approx 0.405mmol/L].

Titrate the allopurinol to achieve these targets, but aim to decrease by ≤0.6-1mmol/L per month, to reduce risk of acute episode.

27
Q

knee pain walking down stairs - where’s the pathology?

A

retropatellar compartment.

basically you are jamming the femur into the patella with every step down the stairs

suggests early chondromalacia or OA of patella

28
Q

what sort of pain does a hip abductor tendinopathy cause?

A

it can cause a trochanteric bursitis. it’s like tennis elbow for the hip.

passive ROM is okay, but extremely tender on direct palpation

the pain is lateral thigh and is worse when crossing leg and when walking

stops patient from lying on that side

29
Q

How is obesity related to OA?

A

Not just pressure effect of joint-loading:

  1. Cytokines produced by adipose tissue lead to inflammation and cartilage damage. Eg. leptin, adiponectin, resistin
  2. Mechanoreceptors on chondrocytes detect obesity load –> trigger cascade of cytokines, GFs and metalloproteinases, TNF, IL-1
30
Q

What is the correlation between osteoporosis and osteoarthritis?

A

There isn’t a correlation.

Although, may get OA at site of previous osteoporotic fracture.

31
Q

Modifiable risk factors / secondary prevention for OA:

A
  1. Obesity - losing weight reduces OA and OA-related pain
  2. Injury, occupational use
  3. Oestrogen deficiency (note- common to see rapidly progressive postmenopausal OA; inverse relationship between HRT and OA, but once starts, going back on HRT does not reverse it).
32
Q

What are Heberden’s nodes?

A

hard, bony swellings of DIP joints, seen in primary generalised (nodal) OA.

33
Q

What are Bouchard’s nodes?

A

bony swelling of PIP joints.

34
Q

Do XR findings predict pain in OA?

A

No, XR findings often do not correlate with pain in OA. Nor do arthroscopic findings.

Pain in OA is most related to:

  • Bone oedema
  • Erosions and ulcers in cartilage (not seen on XR)

Bone oedema can be seen on MRI.

35
Q

OA management:

A
  1. Education
  2. Pharmacological: Paracetamol; +/- NSAIDs (more effective than paracetamol but more ASEs; no evidence for a particular NSAID); Glucosamine still trialled.
    Doxycycline occasionally used in inflammatory OA (inhibits metalloproteinases and collagenases)
  3. Exercise - optimise function (eg. quads strength for knee OA)
  4. Reduce handicap - aids, braces
  5. Viscosupplementation eg. synvisc (hylan G-P 20) - expensive, effect lasts only 3-6 months
  6. Flexible splints, eg. unloading orthopaedic osteoarthritic knee brace - shifts load from medial compartment to brace.
  7. Surgery
    eg. Early referral to hand surgeon
  8. Podiatry
  9. Support groups (eg. Arthritis Association)

Future areas: ?stem cells

36
Q

What is podagra?

A

Gout of 1st MTPJ

37
Q

How do you distinguish inflammatory from non-inflammatory OA? Why is this relevant?

A

Noninflammatory versus inflammatory OA:

The distinction is particularly useful in treatment.

Both inflammatory and noninflammatory OA can be polyarticular, pauciarticular, or monoarticular.

● Noninflammatory OA: 
SYMPTOMS: 
pain and disability-related complaints usually the only symptoms.
SIGNS in affected joints: tenderness, 
bony prominence, 
crepitus.
● Inflammatory OA:  
SYMPTOMS: 
articular swelling, 
morning stiffness >30 minutes,
night pain. 
SIGNS of inflammation: 
joint effusion on examination or radiography, 
warmth on palpation of the joint,
synovitis on arthroscopy
38
Q

Safety of long-term paracetamol use:

A

Adverse effects of therapeutic doses are generally mild (safety profile similar to placebo in a 2006 meta-analysis of paracetamol for OA).

Hepatotoxicity can occur (At therapeutic doses is primarily seen only in patients who concurrently consume excessive amounts of alcohol).
Monitor LFTs periodically in those with liver impairment or excess alcohol use.

  • Need to warn about unintentional OD (using multiple paracetamol-containing products).

Increased risk of GIB / perforation if >2g/day suggested by one study.
The risk of GI complications was greater with the combination of acetaminophen and an NSAID than with either alone.

May increase the anticoagulant effect of warfarin.

There is suggestive but not definitive evidence that chronic, especially daily acetaminophen use has dose-dependent, long-term nephrotoxicity.

39
Q

NSAIDs in people with known IHD - principles of use?

A
  • avoid if possible
  • if needed, short term use only
  • use naproxen, rather than ibuprofen or diclofenac, as 2013 meta-analysis showed increased risk of major CV events with these.

Note: can also cause / exacerbate heart failure.

40
Q

Main ASEs of NSAIDs?

A

● Rash and hypersensitivity reactions
● Abdominal pain and gastrointestinal bleeding
● Impairment of renal, hepatic, and bone marrow function, and platelet aggregation
● Increased risk of cardiovascular disease, including myocardial infarction and stroke, increased blood pressure, worsening of heart failure, and arrhythmia
● Interference with cardiopreventive antiplatelet effects of low-dose aspirin
● Central nervous system dysfunction in older adults

41
Q

Tell me about lifestyle and dietary modifications in the prevention of gout:

A
  1. Lose weight - reduces likelihood of attacks
  2. Diet: high protein, low saturated fat, low refined carbs (replace with complex carbs).
    - Type of protein important: meat and fish high risk; dairy (low fat) lowers risk
  3. Reduce Alcohol intake (strongly associated with risk of gout)
  4. Decrease sugar-sweetened beverages or foods or beverages that contain fructose.
    (Note: drinking diet soft drinks is not associated with an increased risk of gout).
42
Q

Are there medications that should be avoided in gout, or can lead to a flare?

A

Primary HTN and diuretics are independently associated with gout. The risk is relatively low with low dose thiazide.

Losartan actually has a mild uricosuric effect, and so it may be a good alternative for hypertension.

Aspirin can increase the risk of a flare, but the risk is low if they are not hyperuricaemic prior to starting aspirin. Also, this risk can be countered with allopurinol.

43
Q

Treatment of Ankylosing Spondylitis:

A
  1. NSAIDs
    - if no contraindications
    - with acid-lowering agent for protection
    - need sustained, long term therapy to prevent flare
    * Are disease modifying (slow radiographic progression when used continuously - cf. intermittent dosing)*
  2. Physiotherapy
  3. Anti-TNF agents
    (adalimumab, infliximab, etanercept, golimumab)
    - saved for severe disease, due to cost
    - also, not shown to be disease-modifying, but helpful symptomatically
  4. Sulfasalazine for peripheral arthritis
    - no effect on axial disease
    - disease-modifying in peripheral joints
    - used less now anti-TNF agents available

MTX and leflunomide have been used, but limited evidence shows not particularly beneficial.

44
Q

Concern re: NSAIDs in patient with AS and inactive Crohn’s?

A

NSAID can reactivate inactive Crohn’s disease

Rheumatology (8 decks)

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