Review of CT Conditions Flashcards

1
Q

Where is the CT in muscles?

A
  • dense regular CT sheaths around muscle fibres, groups of muscle fibres and muscle groups
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2
Q

What is tendinitis?

A
  • small tears to tendon causing a localised inflammation in tendon as repair mechanism
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3
Q

What are the causes of tendinitis?

A
  • overuse
  • collagen disorders (marfan’s)
  • renal dialysis (as affects clearance and new production of collagen)
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4
Q

What are the common sites of tendinitis?

A
  • lateral epicondylitis (Tennis elbow, extensor muscles attach)
  • achilles tendonitis
  • supraspinatus tendinitis
  • anywhere there is a tendon
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5
Q

What is the treatment for tendinitis?

A
  • rest, ice, compression, elevation (RICE)
  • analgesia and NSAIDs
  • stretching (otherwise forms unorganised collagen bundles as it forms)
  • surgery
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6
Q

What is tendinosis?

A
  • chronic injury and failed healing
  • disorganised collagen can make tendon weaker
  • can lead to full thickness tears
  • swelling 2-6cm above insertion point in belly
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7
Q

What is heterotopic ossification?

A
  • caused by achilles tendinitis
  • partial tears in achilles tendon may heal forming heterotopic calcified regions
  • due to inflammatory process so give COX2 inhibitors
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8
Q

What is the mechanism of heterotopic ossification?

A
  • inflammatory mediators induce differentiation of mesenchymal stem cells to chondrocytes via COX2
  • chondrocytes undergo hyperplasia and secrete osteoblastic factors like RANKL = osteogenesis, osteoclast recruitment, angiogenesis
  • previously damaged tendon which is calcified becomes more brittle and may rupture
  • COX2 inhibitors prevents these complications and reduces symptoms
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9
Q

Why does slow healing of tendons occur after injury?

A
  • tendons relatively avascular
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10
Q

What are the extrinsic factors of tendon healing?

A
  • peripheral fibroblasts

- for achilles, rotator cuffs as open/extrinsic

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11
Q

What are the intrinsic factors of tendon healing?

A
  • fibroblasts from tendon itself
  • hand flexors, any tendon covered by tendon sheath
  • takes longer than extrinsic as no way for peripheral mediators to enter
  • intrinsic as wrapped in tendon sheath
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12
Q

What is enthesis?

A
  • sites where ligaments/tendons insert into bone

- fibrous or fibrocartilaginous

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13
Q

What is fibrous enthesis?

A
  • fibrous tissue joins/extends directly to bone going through periosteum
  • collagen fibres coated with calcium hydroxyapatite (sharpey’s fibres)
  • when joint does not undergo a lot of movement
  • insert a long distance from joint
  • tendon ligament not moved by joint movement
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14
Q

What is fibrocartilaginous enthesis?

A
  • transitional material transitions through fibrocartilage regions
  • gradual change from tendon to bone
  • helps stiffen tendon/ligament (ensures any bending of tendon/ligament fibres during joint movements is spread gently away from bone)
  • inserts closely to joint allowing movement
  • majority of tendon
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15
Q

What is enthesitis?

A
  • inflammation of enthesis

- can occur at any point of attachment for tendon/ligament inserting into bone

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16
Q

What causes enthesitis?

A
  • recurring stress
  • autoimmune disease (spondyloarthritides, HLAB27 arthropathies)
  • interaction with different types of stress produces pro-inflammatory cytokines and danger PAMPS
  • activate inflammatory cells to produce cytokines at specific tissues sites (enthesis)
17
Q

What is the pathogenesis of enthesitis?

A
  • normal enthesis inserts into porous bone at location with small transcortical vessels
  • in mechanical trauma these vessels become inflamed =
    vasodilation, efflux of immune cells (neutrophils), osteoblasts form bone at enthesis
18
Q

What are some comorbidities of enthesitis?

A
  • IBS
  • psoriatic arthritis
  • ankylosing spondylitis

cytokines from gut or other arthritis conditions can travel to enthesis and cause damage

19
Q

What is the key difference between enthesitis and tendinitis?

A
  • tendinitis occurs halfway from muscle to insertion point at belly
  • enthesis occurs at insertion point itself, further down achilles
20
Q

What are the difference between enthesophytes and osteophytes?

A
  • enthesophytes originate from insertion point of tendon into bone (articular border not involved)
  • osteophytes originate from border of articular cartilage, at joint margins
21
Q

What is the mechanical treatment of enthesitis?

A
  • RICE

- NSAIDs

22
Q

What is the inflammatory treatment of enthesitis?

A
  • DMARDs
  • anti-TNF therapy
  • local radiotherapy
  • corticosteroid injection
  • injection of hyperosmolar dextrose
23
Q

What DMARDs are used for enthesitis?

A
  • sulfasalazine = prevents systemic release of pro-inflammatory enzymes from gut
  • methotrexate
24
Q

When can anti-TNF therapy be used for enthesitis?

A
  • cannot be used for isolated
  • can be used when multiple joints affected
  • ankylosing spondylitis and psoriatic arthritis
  • for severe autoimmune enthesitis
25
Q

Why are injections of hyperosmolar dextrose used for enthesitis?

A
  • irritant to cause proliferation of intrinsic fibroblasts

- higher rate of healing before it gets ossified

26
Q

What is the function of the tendon sheath?

A
  • protects and nourishes tendons
  • cushions tendons
  • guides tendons
  • allows only tendon nutrition
27
Q

What supplies nutrients to the tendon?

A
  • synovial fluid from tendosynovial sheath

- vincula blood supply via mesotendon

28
Q

What is tenosynovitis?

A
  • trigger finger (enlargement of tendon within sheath so tendon stuck, when make a fist then open finger stays as extensor tendon stuck then all of a sudden snaps back into place as muscle works)
  • de quervain’s tenosynovitis
  • isolated inflammation
  • fibrosis and narrowing of tendon sheath
  • tendon and sheath rubbing over radial styloid process
29
Q

What is the treatment for tenosynovitis?

A
  • RICE
  • splinting
  • anti-inflammatories
  • corticosteroid injections
  • surgery = cut annular ligament for chronic trigger finger, shave down radial styloid process
30
Q

What are the signs and symptoms of systemic lupus erythematosus?

A
  • non-specific fatigue
  • fever
  • arthralgia weight changes
  • dermatological changes
31
Q

What is undifferentiated CT disease?

A
  • rheumatoid arthritis (affecting synovial membrane)
  • Systemic Lupus erythematosus
  • Scleroderma
  • Sjogrens
32
Q

What specific symptoms are there of systemic lupus erythematosus?

A
  • affects soft tissue around small joints of hands, wrist, knees
  • migratory asymmetrical pain not related to swelling
  • malar facial rash in butterfly pattern extending over cheeks and bridge of nose, worse when exposed to UV light
  • photosensitivity
  • discoid lesions
  • alopecia
  • Jaccoud arthropathy (hand deformities due to tendinitis/tenosynovitis), swan neck and Z shape thumb like RA but can straighten them out
33
Q

What symptoms of lupus erythematosus are non-specific?

A
  • renal nephritic disease
  • neuropsychiatric
  • pulmonary
  • GI
  • cardiac
  • hematologic (immune complexes cause damage to blood vessels and CT, risk to any tissue with rich capillary network)
34
Q

How is lupus erythematosus diagnosed?

A
  • positive for ANA (anti-nuclear antigens)
  • stain
  • homogenous antigen double stranded DNA
  • speckled SS-A/RO
35
Q

How is lupus erythematous treated?

A
  • NSAIDs = mild to moderate
  • DMARDs = moderate to severe and flares
  • Biologicals (belimumab, rituximab)
  • Corticosteroids (flares)
  • IV immunoglobin
36
Q

What DMARDs are used for lupus erythematous?

A
  • cyclophosphamide

- mycophenolate mofetil

37
Q

What is the myotendinous junction?

A
  • go from striated skeletal muscle to tendon
  • CT connects to form tendon continuing
  • more damage to muscle here so more repair going on = more centrally located nuclei
  • tenocytes are fibroblasts in tendons making collagen I
38
Q

What is the significance of SLE and antibodies?

A
  • CT disease
  • more common in black people
  • linked to anti-nucelear antigen antibodies
  • against intranuclear proteins = deoxyribonucleic acid and ribonucleoproteins