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LOCO 2 > Review of Connective Tissue Disorders > Flashcards

Review of Connective Tissue Disorders Flashcards

1
Q

What type of tissue is tendon?

What cell type makes this tissue?

A

Dense regular connective tissue

Fibroblasts (tendinocytes)

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2
Q

What do centrally located nuclei in muscle signify?

A

Regenerating fibres

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3
Q

What is tendonitis?

A

Small tears in a tendon causing localised inflammation in a tendon.

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4
Q

What can cause tendonitis? (3)

A

Overuse
Collagen disorders
Renal dialysis (affects collagen metabolism and how it is turned over)

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5
Q

What sites are commonly affected by tendonitis? (3)

A 
Lateral epicondylitis (tennis elbow, over-use of extensor muscles of wrist)
Achilles tendonitis (calf muscles puts strain on tendon)
Supraspinatus tendonitis (can get impinged on acromion with repetitive activity of arm over head e.g. cricket)
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6
Q

Why do tendons take a while to recover/repair? (3 months)

A

Isn’t well vascularised

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7
Q

How is tendonitis treated? (4)

A

RICE (rest, ice, compression, elevation)
Stretching (organises new tendon collagen fibres into same orientation)
Surgery (if completely ruptured or torn)
Analgesia / NSAID (topical or oral)

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8
Q

How does ‘RICE’ work?

A

Rest - stops the activity that causes the pain/caused the damage
Ice - increases local blood flow and reduces inflammation
Compression - helps push oedema away.
Elevation - drains inflammation/oedema.

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9
Q

How may partial tears in Achilles tendon heal?

A

By forming heterotopic calcified regions (~30% of tendon injuries cause this) - bone forms rather than tendon or ligamente

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10
Q

Where do Achilles tendon ruptures usually occur?

What happens to the proximal part of the tendon (in complete ruptures)?

A

2–6 cm above the insertion point (calcaneal bone)

Moves up the leg (as the muscle contracts)

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11
Q

Why are partial tears in the Achilles tendon common?

A

Plantar flexors are a big muscle group, tendon is under stretch and tension all the time.

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12
Q

What is the common precursor for bone, cartilage and tendon?

A

Mesenchymal stem cells

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13
Q

How can COX-2 lead to heterotopic bone formation?

A

COX-2 (induced during inflammation) – more likely to push stem cells to chondrocyte differentiation (rather than fibroblast). This chondrocyte hypertrophies and creates cartilage, which then can lead on to osteogenesis and the formation of heterotopic bone (as well as angiogenesis, osteoclast recruitment, fracture bridging) due to production of VEGF and RANKL.

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14
Q

Why are NSAIDs useful in preventing heterotopic bone formation?

A

Inhibits COX-2 to prevent chondrocyte differentiation, osteogenesis etc
Prevents prostaglandin E2 synthesis (this induces osteoblast formation)

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15
Q

Why is a calcified tendon problematic?

A

It becomes more brittle and may rupture – this requires complete removal and then tendon grafting

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16
Q

How does healing occur after injury in Achilles tendon or rotator cuff?

A

Extrinsic – peripheral fibroblasts

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17
Q

How does healing occur after injury in hand flexors or any tendon covered by a tendon sheath?

A

Intrinsic – fibroblasts from tendon itself

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18
Q

How long can tendon healing and full recovery take?

A

Remodelling continues after 3 months, so full recovery can take up to 12 months

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19
Q

What are the stages of tendon healing?

A

Inflammation
Repair
Remodelling

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20
Q

What is an enthesis?

A

Tendon insertion into bone

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21
Q

What are the two types of enthesis?

A

Fibrous - fibrous tissue extends all way up to bone (inserts into the periosteum, then into bone)
Fibrocartilaginous - small section of fibrocartilage at attachment site, helps stiffen the tendon/ligament and creates a gradual change in mechanical properties (from dense regular connective tissue to unmineralised fibrocartilage, to mineralised fibrocartilage, to bone)

22
Q

What are Sharpey’s fibres?

A

Collagen type 1 fibres from a tendon insert through the periosteum and you can see these collagen bundles in the bone (bone is type 2 collagen).

23
Q

When are fibrous enthesis’ beneficial?

A

When the insertion is quite a distance away from the muscle belly (so tendon ligament not kinked by movement of the joint)

24
Q

When are fibrocartilaginous enthesis’ beneficial?

A

When the muscle is close to a joint and when a tendon changes angle with the muscle pulling on it (movement creates kinking of tendon and angle change)

25
Q

What is enthesitis?

A

Inflammation of the enthesis (any point of attachment for tendon / ligament inserting into bone)

26
Q

What causes enthesitis? (2)

A 
Recurring mechanical stress
Autoimmune disease (key pathological lesion in spondyloarthritide, associated with HLA B27 anthropathies and IL-23R)
27
Q

What cytokines drive the inflammatory process of enthesitis? (4)

A

IL-17, IL-22, IL-23, TNF

28
Q

What are some comorbid conditions of enthesitis? (3)

A

Inflammatory bowel disease
Psoriatic arthritis
Ankylosing spondylitis

29
Q

Tendonitis occurs where in relation to the insertion point?

What about enthesitis?

A

2-6cm from insertion points

Enthesitis occurs at the insertion point

30
Q

What is the difference between enthesophytes and osteophytes?

A

Enthesophytes originate from the insertion of joint capsule, ligament or tendons. The articular border is not involved.
Osteophytes originate from the border of the articular cartilage/affect the joint margin.

31
Q

How is enthesitis treated mechanically? (2)

A

RICE

Non-steroidal anti-inflammatories

32
Q

How is enthesitis treated (inflammatory)? (6)

A 
Sulfasalazine
Methotrexate
Anti-TNF therapy (infliximab) 
Local radiotherapy
Corticosteroid injection
Hyperosmolar dextrose injection
33
Q

How does sulfasalazine have effects on enthesitis?

A

HLA B27 changes the gut biome and makes it more leaky so there is a co-morbidity of gut inflammation. Sulfasalazine is not well absorbed across the gut, but acts locally on the gut to reduce inflammatory cytokines getting into circulation.

34
Q

Infliximab has restricted use for isolated enthesitis but it is useful for…?

A

RA and ankylosing spondylitis

35
Q

How does hyperosmolar dextrose work?

A

Irritant, causing proliferation of intrinsic fibroblasts

36
Q

What is ankylosing spondylitis?

A

Enthesitis of IV disc and anterior longitudinal ligament

37
Q

What is the role of the tendon sheath?

A 
Protects and nourishes tendons
Cushions tendons
Guides tendons
Tendon nutrition (synovial fluid from tendosynovial sheath, vincula blood supply via mesotendon)
38
Q

What is De Quervain’s tenosynovitis?

How is it treated?

A

Fibrosis and narrowing of tendon sheath caused by tendons and sheath rubbing over radial styloid process.
Pain on resisted movement, crepitus and positive Finkelstein’s test.
Shave down radial styloid process

39
Q

What is trigger finger?

How is it treated?

A

Tenosynovitis - enlargement (inflammation) of tendon within the sheath, gets stuck
Cut the annular ligament

40
Q

How is tenosynovitis treated? (4)

A

RICE
Anti-inflammatories
Corticosteroid injections
Surgery

41
Q

Systemic lupus erythematosus - how many people does it affect in Britain?
What is the ratio of female to males?

A

10-50:100,000 = over 30,000

90% female

42
Q

Which race is SLE more common in?

A

Black people

43
Q

What are there antibodies against in SLE?

A

Antibodies against a wide range of ‘self’ antigens:

  • ANA antibodies against intranuclear proteins
  • DNA
  • Ribonucleoproteins
44
Q

What is SLE?

A

An autoimmune disease is which there are hyperactive B-cells, and impaired immune complex clearance from tissues.
The immune complexes cause damage to blood vessels and connective tissue, so any tissue with a rich capillary network at risk.

45
Q

What are the signs and symptoms of SLE?

A 
Non-specific fatigue
Low-grade fever
Arthralgia weight changes
Migratory asymmetrical pain not related to swelling
Discoid lesions
Alopecia
Loss of appetite
Malar facial butterfly rash
Inflammation - pleuritis, pericarditis
Poor circulation to fingers and toes
Arthritis (small joints of hands, wrist and knees
Muscle aches
Mouth ulcers
Photosenstitvity
Renal nephritic disease
46
Q

What is Jaccoud anthropathy?

A 
Jaccoud arthropathy (non-erosive) hand deformities due 
to tendonitis/tenosynovitis – this is repositionable, stretching of tendon sheaths around tendons. Seen in SLE.
47
Q

How many % of SLE patients develop arthralgia?

A

90%

48
Q

How many % of SLE patients are positive for ANA?

A

More than 95%

49
Q

What patterns of ANA staining are seen in SLE?

A

Homogenous - antigen double stranded DNA (ds-DNA), histones

Speckled - SS-A /Ro, SS-B/La (Sjögren syndrome), Sm (Smith antigen), RNP

50
Q

How is SLE treated? (4)

A

NSAIDs
DMARDs
Corticosteriods (for flares)
IV immunoglobins

51
Q

What DMARDs are there for SLE?

A

Cyclophosphamide (cross links DNA, leads to cell death)
Mycophenolate mofetil (limits guanosine nucleotide synthesis)
Methotrexate
Tacrolimus
Biological DMARDS such as rituximab (targets B cells) and bortezomib (targets plasma cells)

LOCO 2 (28 decks)

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