Osteoarthritis Flashcards
(50 cards)
1
Q
What is OA?
Symptoms?
A
- wearing out of hyaline articular cartilage of diarthrodial joints
- considered non-inflammatory, most common cause of chronic arthritis
- joint pain, inactivity stiffness, decreased ROM
2
Q
Causes leading to OA
A
- age
- injury
- obesity
- chronic inflammation of joint
- Paget’s (abnormal stiff subchondral bone)
- Avascular necrosis (abnormal weak subchondral bone)
- in hip specifically - shallow acetabulum, femoral head tilt, femoral acetabular impingement
3
Q
Where is OA common?
A
- large weight-bearing joints like hips/knees
- knee OA is most common
- can also be in the hands (DIPs, PIPs)
4
Q
Effect of OA on knees
A
- Varus deformity of the knees
5
Q
Diarthrodial Joints
A
- mobile, peripheral
- hyaline articular cartilage made of type 2 collagen and aggregated proteoglycans
- surrounded by fibrous capsule lined by synovium
6
Q
Describe articular cartilage - main cell present?
A
- chondrocytes are the only cells present - no blood or nerve supply, nutrients come from the synovial fluid
- chondrocytes produce both type II collagen and PGs
- # of chondrocytes is fixed once you reach adulthood
- does not regenerate once it wears out
- radiolucent (black/grey) on x-ray - not calcified
7
Q
What happens at a cellular level in OA?
A
- chondrocytes multiply in lacunae to try and synthesize more matrix
- however, this cannot keep up with the up-regulation of matrix metalloproteases
- less PG aggregates due to cleaving at hook region by aggrecanase
8
Q
Describe the matrix of articular cartilage
A
- 90% water - hydrophilia of PGs allows for compliance, deformability, shock absorption
- type II collagen - arranged in branch arches, helps prevent breakdown of PGs, tensile strength, impact loading
- proteoglycans - (-) charged combinations of protein and sugar
9
Q
Describe the structure of a proteoglycan
A
- bottle brush configuration
- central core protein with GAGs attached (- charged and thus attract water)
- hook region near amino terminal (aka hyaluronic acid binding region) which allows multiple PGs (aggrecans) to attach to HA
10
Q
What are the two different GAG types?
A
- chondroitin sulfate - larger, located superiorly (carboxyl end), mostly galactosamine disaccharides
- some revision from C-6s (adult) to C-4s (fetal) in OA
- keratin sulfate - shorter, located proximally (amino end), enriched in glucosamine
*core protein has a unique a.a. sequence that determines where these GAGs attach
11
Q
What is happening in the knee joint during compression/ relaxation?
A
- compression - water released by PGs into synovial space
- relaxation - water reimbibed into cartilage
12
Q
What are the different neutral matrix metalloproteases? What makes them?
A
- collagenase 1 (MMP 1) - targets type II collagen
- stromelysin (MMP 3) - targets PGs
- collagenase 13 (MMP 13) - targets type II collagen
*all made by chondrocytes
13
Q
What up regulates MMPs?
What inhibits them?
A
- IL-1 (made by chondrocytes, which have an IL-1 receptor), plasmin
- normally TIMPs block MMPs, but in OA MMPs overwhelm
14
Q
What happens in OA with regard to:
- water content
- PG aggregates
- collagen
- metachromatic stain
- surface
- chondrocyte number
- MMP enzymes
- subchondral bone
- osteophytes
A
- Initially there is swelling due to water influx, then water loss and the joint becomes dry
- PGs and collagen decrease
- There is decreased uptake in metachromatic staining
- Bone surface becomes irregular and fibrillated
- Chondrocyte # increases due to mitoses in brood capsules
- MMP enzymes increase
- Subchondral bone comes sclerotic and there is presence of osteophytes
15
Q
inflammatory mechanisms in OA
A
synovitis, IL-1, crystals
16
Q
Primary vs Secondary OA
A
primary - localized, generalized such as in hands
secondary - chronic inflammatory arthritis (RA), identifiable mechanical/ congenital/ metabolic factors (i.e. hemochromatosis)
17
Q
Names of enlargements at DIPs and PIPs
A
DIPs - Heberden’s nodes
PIPs - Bouchard’s nodes
18
Q
Examples of inflammatory back pain
- common sx
A
- ankylosing spondylitis, sero (-) spondyloarthropathy
- under 40, prolonged morning stiffness, better with activity and worse with rest, nocturnal awakening, alternating buttock pain
19
Q
Examples of infiltrative back pain
A
- malignancy (primary or metastatic from breast/lung/ prostate)
- infections (discitis, osteomyelitis, epidural abscess, TB)
20
Q
What are back pain red flags?
(really only need blood work or imaging if these are present)
A
- pain at rest or at night
- history of trauma
- history of malignancy
- B symptoms (fever, weight loss, night sweats)
- incontinence
- saddle anesthesia
- substance use disorder
- steroids or immunocompromised
- first episode after the age of 50
- decreased passive range of motion
- midline tenderness
- new or progressive neuro issue (spasticity)
- loss of balance, abnormal gait
21
Q
Cauda Equina Syndrome
- sx
- dx
- tx
A
- occurs when end of the spinal cord (L4-S4) is compressed (tumor, disc, infection, metastases)
- acute or chronic back pain, saddle anesthesia (S3-5), bladder and bowel dysfunction (S2-3), lower leg weakness/ sensory changes
- Dx: CT or MRI
- Tx: emergency! surgical decompression
22
Q
Discogenic Back Pain
A
- often a normal asymptomatic part of aging, do NOT treat imaging findings if no pain or symptoms
- however, can be DDD or a herniation
23
Q
Degenerative Disc Disease (DDD)
A
- micro fracture of collagen and loss of PGs leading to a desiccated disc
- see disc space narrowing on X-ray
- chronic onset
24
Q
Disc Herniation
- imaging
- sx
A
- often acute due to lifting/ specific injury
- best seen on CT/MRI
- weakness, dermatomic pain, reflex loss, can be lateralized or central
25
Facet Arthropathy
- sx
- imaging
- facet joints (aka zygaphyseal joints) are synovial with hyaline surface, thus prone to OA
- most commonly due to aging
- unilateral neck/ lower back pain in non-dermatomic pattern
- pain worse with leaning back/ lumbar extension/ lateral flexion
- CT/MRI most useful, bone scan can demonstrate increased uptake suggesting active bone turnover and pain
26
Spondylolithesis
- sx
- one vertebra is sitting forward on the one below it
- non-union, lysis, fracture
- often developmental variation of neural arches (spondylolysis)
- worse pain with forward flexion
27
Spinal Stenosis
- sx for both spinal and vascular
- dx
- narrowing of the spinal canal
- can be congenital, osteophytes from facet hypertrophy, central disc herniation, mass effect from tumor or abscess, ligaments flavour hypertrophy
- if spinal claudication - worse with walking, spinal claudication worse with walking, better with sitting, better with bending forward, walking uphill is easier
- if vascular claudication - worse with walking, better with stop and stand, risk factors for PVD/ artherosclerosis, abnormal ABI, weak pedal pulses
- Dx: CT or MRI
28
Neural Foraminal Stenosis
- facet joints narrow due to osteophytes
- leaning to the affected side increases pain
29
SI Ligament Sprain
- sx
- causes
- buttock pain, difficulty sitting or standing
- acute injury, overuse, muscle weakness, imbalance
30
Scoliosis
- sx
- sideways curvature of the spine
- mild or asymptomatic, if severe can cause pain and respiratory issues
- often genetic and will develop overtime in chidlhood
31
In summary, which back pain syndromes are worse with flexion and which are worse with extension?
worse with flexion - spondylolitheis, discogenic pain
worse with extension - facet arthropathy, spinal stenosis
32
Role of PTs and OTs in OA?
PT - self management, therapeutic exercise, PA guidelines, manual therapy
OT - joint protection (splints, orthoses, footwear), energy conservation, ADLs
33
What is general non-surgical/pharmacological treatment for OA/ back pain?
EVIDENCE BASED: education, self-management, exercise (esp. quad strengthening), weight loss (dose-response relationship)
- avoid bed rest
- canes (NOT poles) are recommended for knee and hip OA (use opposite from affected side, wrist crease level when standing in shoes)
- neuromuscular training, aerobic exercise, flexibility
- potentially orthotics i.e. knee unloader brace/ braces/ laser/ TENS/ acupuncture, etc.
34
What role do adipocytes have in OA?
- release leptons and adiponectins that can lead to joint damage directly
35
Oral treatments for OA
Acetaminophen - can push to 3-4g/day if normal kidney and liver function
NSAIDs - helps with inflammation and pain
Opiates - i.e. tramadol, tramacet... controversial, can try Tylenol T3s or start with tramadol
Duloxetine (SNRI) - moderate evidence for knee OA
Alternatives - ginger, apple cider vinegar, CBD oil
36
Cons of NSAIDs (non-selective and selective)
non-selective - gastropathy especially if over 55
- use PPI for protection
- COX-2 selective (celecoxib) - no effect on upper GI mucosa
Both - affect renal function, increase BP, CV risks, lower GI upset (do NOT give if IBD)
- if on them chronically, need to monitor liver and creatinine/ CBC
37
Topical anti-inflammatories or analgesics for OA
- diclofenac (voltaren) - some efficacy, 1st line
- capsaicin - less evidence, more for neuropathic pain
38
Injections
- injectable corticosteroids - i.e. kenalog, Depomedrol
- no more than 3 injections in one joint EVER, no more than 2-3 per year
- inhibit IL-1 and MMPs, decrease inflammation
- viscosupplementation/HA - not recommended, unclear efficacy, still widely done
- platelet rich plasma (PRP) - centrifuged platelets, GFs, and cytokines re-injected
- does NOT regenerate cartilage, no current evidence
39
Glycosamine Sulfate (GLS-500) and Chondroitin Sulfate
- provide GAG substrate
- inhibit IL-1 and MMPs
- however, no proven role yet
40
DMOADs
- disease modifying anti-OA drugs
- some efficacy seen in strontium and tetracycline - inhibit MMPs
41
Possible future treatments in OA
- cartilage/ chondrocyte transplants
- growth peptide
- TIMPs (tissue inhibitors of metalloproteases)
- mesenchymal stem cells, bone marrow aspirate concentrate
42
What are some tools used to assess outcomes in OA?
- WOMAC and AIMS2
43
OA history taking
- always ask about arthritis or psoriasis
44
What is an acute onset of joint pain likely to be?
- infection (septic arthritis) i.e MRSA, will see r-sided endocarditis
- trauma
- gout or pseudogout
- renters disease
45
Gout
- acute onset, older age, diuretics, beer, rich food, past history
- can get in the knee, but big toe most common
- will likely see high serum uric acid, check fasting lipids as often metabolic
- arthrocentesis (joint aspiration) - look for infection/ crystals (yellow parallel, negatively bi-refringent)
46
Pseudogout
- often caused by calcium pyrophosphate dehydrate crystals (CCPD)
- will see chonedrocalcinosis on xray
- blue parallel, yellow perpendicular crystals
47
Indications for surgery in OA
1. Nonoperative management has been maximized
2. Pain interfering with QoL
3. Reasonable expectations of joint replacement from the patient
4. Pathology resulting in adult arthritis
Knee - medial OA, over 60, correctable deformity, stable knee
48
Surgical treatment for Hip OA
- total hip arthroplasty - very successful, replacements last 30+ years
49
Surgical treatment for knee OA
- arthroscopic debridement
- arthroscopic microfracture
- autologous cartilage implantation
- allograft osteochondral transplant
- high tibial osteotomy
- knee arthroplasty
- arthroscopic debridement - not common but maybe if unstable meniscus
- arthroscopic microfracture - creating small fractures to stimulate bone marrow cells for cartilage regeneration
- best for small symptomatic lesions under 2cm
- requires careful rehab, mod improvement, but inconsistent results
- autologous cartilage implantation - great results
- take several cylindrical plugs from non-weight bearing zone to deficient area
- allograft osteochondral transplant - harvested from cadaver (needs immediate transplant)
- high tibial osteotomy - consider if medial compartment is arthritic and nothing else
- offloads the medial compartment by realigning the tibia
- good for young active patients with moderate arthritis in the medial compartment
- knee arthroplasty - partial or total, replaces entire tibiofemroal joint and patella
- not as good as total hip replacement
- meant to treat pain, NOT to restore athleticism
50
Contraindications for surgery in OA
- panarthroses
- young
- obese
- labourer
- varus over 10
- ACL deficiency
- crystalline/inflammatory arthropathy
