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1. Rheum RC > OA > Flashcards

OA Flashcards

1
Q

** OA physical exam findings **

A

-Crepitus
-Bony enlargement
-Mild swelling
-Joint instability
-Periarticular muscle atrophy
- Radiculopathy if facet hypertrophy causing neural foraminal compression
-Reduced ROM
-Facet OA worsens spinal stenosis w/ extension

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2
Q

** OA pathophysiology**

A

Repetitive trauma to articular cartilage → damage → DAMP release → activates innate immune system and adaptive (Th1>Th2; synovial fibroblasts secrete IL1/6/17, TNF cytokines causing less matrix synthesis and more apoptosis) *TNFb counters this and produces matrix and enhances chondrogenesis

-Chondrocytes increase proteoglycan synthesis but release more degradative enzymes → proteoglycan breakdown faster than it can be produced → articular cartilage thinning/softening → cracking/fissuring of cartilage → exposed underlying bone and synovial fluid forced into bone → subchondral cysts → remodelling/hypertrophy of subchondral bone → osteophyte and subchondral sclerosis

-Can occur under normal loads if underlying cartilage, bone, synovium, ligaments, muscles are abnormal from 2ndary cause

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3
Q

** How aging contributes to OA**

A
  • – DECREASED chondrocytes
  • – DECREASED proteoglycan synthesis – THINNER Collagen
  • – SHORTENED GAGs → less H2O retention and elasticity
  • – Increased “advanced glycation end products” accumulation (more rigid)
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4
Q

** Early Pathologic features of OA**

A

– Swelling of articular cartilage (Increased cartilage water content)
– Chondrocytes increase proteoglycan synthesis but release more degradative enzymes
– Loosening of collagen framework

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5
Q

** Late Pathologic features of OA**

A

– Degradative enzymes break proteoglycan faster than it can be produced by chondrocytes (less proteoglycan in cartilage)
– Articular cartilage thins and softens (joint space narrowing on XR)
– Fissuring/cracking of cartilage → underlying bone exposed → synovial fluid forced into bone by pressure of weight = subchondral cysts/geodes
– Remodeling/hypertrophy of subchondral bone → subchondral sclerosis and ostephyte (spur) formation

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6
Q

** Joint involved in primary idiopathic OA**

A

-CMC, PIP, DIP
-AC shoulder joint
-Hips, Knees, 1st MTPs
-Facet (apophyseal) joints of C/L spine

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7
Q

** Joints NOT involved in primary OA

AKA Joints in secondary OA**

A

Wrists, MCPs,
-Elbows, glenohumeral shoulder joint
-Ankles, 2nd-5th MTPs
-
-**If see these, search for 2ndary causes of OA

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8
Q

OA synovial fluid

A

Normal viscosity w/ good string sign
-Clear and yellow colored
-WBC <1000-2000
-No crystals
-Negative Cx

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9
Q

** OA XR findings**

A
  • Subchondral sclerosis/cysts
  • Osteophytes
  • NONuniform jointspace narrowing
  • Deformities: Heberden, Bouchard, distal phalanx deviation (lateral/palmar)
  • NONerosive (maybe gullwing in erosive OA)
  • Vacuum sign in DDD (nitrogen in a degenerated disk space)

No ankylosis, calcification, nail or soft tissue changes
-Alignment can be abN
-Bone mineralization N

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10
Q

OA classification

A

Primary idiopathic
– Localized: DIP, PIP, 1st CMC, 1st MTP, hip, knee, spine
– Generalized (aka Kellgren’s syndrome)

-Secondary

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11
Q

Joint involved in Nodal OA

A

DIP, PIP, first CMC

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12
Q

Joints involved in erosive inflamm OA

A

DIP, PIP, first CMC

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13
Q

** Generalized and Localized OA Risk factors**

A

Generalized OA
-Age
-Heredity
-Sex (women >50)
-Smoking (contrib to DDD)

Localized OA
-Previous joint trauma
-AbN joint mechanics (varus, valgus, hip dysplasia)
-Obesity
- Hemarthrosis
- Metabolic/Inflammatory/Septic Arthritis
- Repetitive loading (job, sports eg boxers MCPs, ballet ankles, basketball knees/ankles, drill operator shoulder/elbows)

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14
Q

** How does obesity predispose OA predisposition?**

A

-Increased loads causes chondrocyte mechanoR to produce growth factor, cytokine, MMP

-Adipose = source of proinflamm cytokines (leptin, adiponectin, resistin, IL1/6, TNFa) even in non weight bearing joints

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15
Q

Erosive OA XR findings

A

Osteophytes
-Central erosions with GULL WING or inverted T appearance
-Joint ankylosis

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16
Q

Differentiating erosive OA from inflammatory arthritis

A

NO systemic symptoms
-NO involvement of MCPs, wrists, 2nd-5th MTPs
-NORMAL inflammatory markers
-Negative RF and ANA

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17
Q

Erosive OA pathophys

A

-Synovial hypertrophy w/ IL1 release causing MMP and central cartilage destruction/clearing
-Lymphocytic/neutrophilic infiltration

-**Erosion NOT from synovial pannus invasion

-Another hypothesis is role of hydroxyapatite and CPP crystals

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18
Q

Generalized OA

A

4+ sites symmetrically involved

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19
Q

DISH (diffuse idiopathic skeletal hyperostosis) clinical manifestations

A
  • Most frequently T spine → stiffness & decreased ROM
    -Pain is NOT significant
    -Dysphagia if C spine involved
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20
Q

DISH radiologic findings

A

-Flowing ossification of anterior longitudinal ligament connecting at least 4 contiguous vertebral bodies
-Ossification separated from anterior vertebral body by thin radiolucent line (flowing candle wax)
-NORMAL disk spaces, apophyseal joints, and SI joints

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21
Q

** Secondary OA features**

A

Early age of onset

Atypical joints:
- MCP, Wrists,
- Elbows, Shoulders (GH NOT AC)
-Ankles, MTP2-5

22
Q

** Causes of shoulder OA**

A

Chronic dislocation or hypermobility (EDS)
-Trauma
-Surgery
-AVN
-Inflammatory arthritis
-Rotator cuff tendinopahy/tear
-Crystal arthropathy (eg Milwaukee)
-Infection (septic joint)

23
Q

** Secondary causes of OA **

A

Congenital
- Hip: Perthes disease, SCFE, FAI, congenital shallow acetabulum
- Dysplasia: epiphyseal or spondyloepiphyseal dysplasia
-Mechanical: hypermobility, leg length discrepancy, varus/valgus, scoliosis

-Trauma: ACL tear, fracture, meniscectomy

-Metabolic: hemochromatosis, gaucher’s, crystal deposition, hemoglobinopathy,Paget

-Endocrine: hyPOthyroid, hyPERPTH, acromegaly, DM

-Infectious: syphilis,septic

-Other: AVN, inflamm arthropathy, osteochondropathy 2/2 mycotoxin or selenium def

24
Q

FAI clinical manifestations

A

-Groin pain w/ sitting/athletics
-Hip flexion limited to 90deg w/ painful internal rotation from impingement
-Click/snap w/ hip rotation 2/2 labral/chondral lesion

25
Q

How does FAI cause OA

A

Flexion → abN contact between femoral head or prox femur (at head-neck jcn) with anterior rim of acetabulum → labral tears and early OA
-Due to deep acetabular socket or cam deformity

26
Q

How does pes planus cause knee OA

A

-Rotation stress on medial knee from pronation
-Patella tracks laterally → patellofemoral OA

27
Q

Why no ankle OA vs knee/hips

A
  • Ankle = rolling joint w/ congruent surfaces at high load (vs knee=less congruent w/ sliding/rolling/rotation → more stress)
  • Ankle cartilage thickness and composition makes it more resistant to catabolic cytokines
28
Q

** OA nonpharm Tx**

A

ACR strong recommendation:
-Exercise
-Weight loss
-Tai Chi
-Cane, tibiofemoral knee brace, 1st CMC orthosis

-Conditional recommend:
-Heat/therapeutic cooling
-CBT
-Acupuncture
-Kinesiotaping
-Balance taping
-Patellofemoral knee brace, other hand orthoses
-Yoga
-Paraffin bath (hands)
-Radiofrequency ablation

29
Q

** OA Tx - pharm**

A

-Tylenol
-Intermittent NSAIDs + PPI

If GI issues:
- Topical NSAIDs,
- Tramadol,
- Duloxetine

-IA steroids
-NO role for PO steroids

30
Q

Erosive OA tx

A

Topical/PO NSAIDs
-IA steroids

-Varying success: HCQ, MTX, anti-TNF, IL1 ANT

31
Q

** How does Glucosamine and chondroitin supplements work, do you support it **

A

Glucosamine and chondroitin are GAGs
-Can be incorporated into and increase chondrocyte production of proteoglycans
-Mild anti-inflamm fx
-Can block certain proteases

** 2020 guidelines recommend AGAINST given discrepancy between studies. VAS pain benefit in some trials

32
Q

Glucosamine and chondroitin dosing

A

Glucosamine 1500mg daily
-Chondroitin 1200mg daily

33
Q

Glucosamine and chondroitin side fx

A

Cause allergy in ppl w/ shellfish allergy
-May increase warfarin effect

34
Q

How does hyaluronan work?

A

-Stimulates proteoclycan synthesis
-Antiinflammatory fx
-Antinociceptive fx

35
Q

Hyaluronan side fx

A

Local injxn rxn
-Systemic allergic rxn (egg and feather component)
-Pseudoseptic rxn

36
Q

** Indications for joint replacement in OA **

A

Severe pain unresponsive to medical therapy
- Consistent Night pain
- Unable to stand for >20-30 min

Loss of joint fcn
- Cannot walk 1+ block,
- Can’t put on shoes,
-Moved to aptment bc of inability to climb stairs

37
Q

New therapies for OA

A

Autologous chondrocyte implantation or mesenchymal stem cell injxn

-Abrasion and microfracture surgery (micro drilling releases mesenchymal stem cells from marrow to repair cartilage)

-PRP (degranulated PLT releases TGFb, platelet derived GF, epidermal GF, insulin like GF that inhib inflamm, increases cartilage synthetic activity)

-Genicular nerve block (cooled radiofreq ablation of genicular nerve in knee)

38
Q

** Name the 2 most frequent components of cartilage by dry weight?**

A
  • Collagen (>90% type 2)
  • Proteoglycan (glycosylated prot monomers)
39
Q

** How does cartilage or chondrocytes get nourished? **

A
  • Adult cartilage is avascular,
  • Chondrocytes obtain nutrients through diffusion from synovial fluid (cartilage water squeezed out during weightbearing and sucked back when unloaded)
40
Q

** Name the 3 constituents of normal cartilage and their relative proportions? **

A

Articular cartilage (wet weight) is more than 70% water, 15% collagen, 10% proteoglycans.

Chondrocytes constitute only 1% to 2% of its total volume.

41
Q

** Describe the structure of the proteoglycans**

A

Proteoglycans are glycoproteins with 1+ glycosaminoglycan (GAG) chains made of either:

-Chondroitin sulfate/dermatan sulfate,
-Heparan sulfate/heparin,
-Keratan sulfate or
-Hyaluronic acid (usually the backbone)

42
Q

** List 3 structural differences in proteoglycans in OA vs normal aging?**

A

Concentration: OA = early increase (not in aging), then decreases later (occurs in aging but not as much)
Molecular weight: decreased in both
Keratin sulfate [ ] : decreased in OA (INCREASED in aging)
Chondroitin sulfate [ ]: INCREASED in OA (decreased in aging)
Aggregation of proteoclycan: decreased in both (less in aging)

43
Q

** Role of proteoglycan **

A
  • Structural support to ECM
  • Binds water to absorb high compressive loads
  • Regulate cell adhesion, proliferation, migration, differentiation, survival, and death
44
Q

** List the cell type most important in the cartilage degeneration in OA?**

A

Chondrocytes

  • Increase proteoglycan synthesis but also release degradative enzymes (MMPs, ADAMTS-4) = more breakdown than production
  • Damaged cartilage (chondrocytes) release DAMPs to activate innate immune system.
  • The adaptive system, responds due to the DAMPS. T cells (Th1 > Th2) and synovial fibroblasts secrete IL-1, IL-6, IL-17, and TNF.
45
Q

** List 1 family and 2 examples of substances that mediate degradation of cartilage in OA? List 2 molecules which inhibit the above 2 examples?**

A

MMP = cleave collagen & proteoglycans
- Collagenases,
- Gelatinases,
- Aggrecanases,
- Serine/cysteine proteases

Inhibitors of MMP
- Tissue inhibitor of MMP (TIMP) 1,2,3,4
- Synthetic zinc binding globulins (ZBG) or nonZBG

46
Q

** What 3 enzymes or factors are important in OA? **

A

Anabolic factors:
- TGFb, IGF1,
- Bone morphogenic proteins (BMPs),
PGE2

Catabolic:
- IL1, IL6, TNFa
- MMP (collegenase, gelatinase, aggrecanase)

47
Q

DISH Exam maneuvers

A

-Decreased spinal ROM of T spine, especially lateral flexion
- Nodules at enthesis (elbow, knee, Achilles)

48
Q

** List 2 indications for intra-articular corticosteroid injection in OA of the knee? How long does an intra-articular injection last to the knee for OA?**

A

Pain
Failed other treatment options

Cohcrane review: up to 6 weeks relief

49
Q

** List 3 potential complications of TKA or THA **

A
  • Reaction to anesthetic or transfusions
  • Vascular/nerve injury
  • VTE
  • Surgical site infection, PJI
  • Periprosthetic fracture, dislocation, osteolysis
  • Heterotopic ossification
  • Patellofemoral disorders
  • Wear and tear of prosthetic
  • Aseptic loosening
50
Q

** Indications for THA**

A

Same as for TKA, but includes:
- #
- AVN
- Periarticular pagets
- Hardware failure from previous replacement

51
Q

**OA nonpharm recommended against **

A

AGAINST:
-TENS (transcutaneous electrical nerve stimulator)

-Massage, modified shoes, wedged insoles, vibration therapy, iontophoresis, Cspine collar, traction, distraction

Topical lidocaine, capsaicin (deplete Hydrotherapy

Not effective: pulsed electromagnetic fields, magnets

52
Q

** Lumbar facet joint spinal stenosis:
List 2 activities which cause worsening of symptoms?
List 2 activities which cause improvement in symptoms?
List 4 findings on CT-Scan?**

A

Worsens
-Prolonged walking (esp downhill)
-Leaning backwards
-Spinal phalen’s (30s back extension)

Improves
- Leaning forward
- Sitting

CT findings (need <10mm AP diameter to consider it central stenosis)
- Oval spinal canal looks triangular
- Central disc bulge
- Facet hyperostosis
- Spondylosis (aka OA of the spine)
- Ligamentum flavum hypertrophy

1. Rheum RC (23 decks)

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