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BMSc Orthopaedic medicine > Unit 1 - Joint conditions > Flashcards

Unit 1 - Joint conditions Flashcards

1
Q

What causes OA?

A

Excessive wear of articular cartilage resulting from a breakdown of the balance between wear & tear process in joint

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2
Q

What is primary OA

A

Of unknown cause

Most common

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3
Q

What is secondary OA?

A

Of known cause

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4
Q

Causes of secondary OA?

A
  • Congenital - congenital dislocation of the hip.
  • Childhood - Perthe’s disease, infection.
  • Trauma - fracture into a joint.
  • Metabolic - gout, crystal arthropathy.
  • Infection - TB (tuberculosis).
  • Chronic inflammatory - rheumatoid.
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5
Q

Presentation of OA?

A

Pain (during activity)

Loss of function

Stiffness

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6
Q

Conservative management of OA?

A

Weight loss

Walking stick

Physio

Analgesia

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7
Q

What surgical options are available for OA?

A

(Nothing)

Arthrodesis

Osteotomy

Arthroplasty

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8
Q

What does arthrodesis involve?

A

Surgical stiffening of a joint

Useful in young person with painful & limited RoM

Useful in smaller joints

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9
Q

What does an osteotomy involve?

A

Surgical realignment of a joint, aiming to redirect forces across a joint to more evenly distribute load

Good operation in young people who have retained a good range of motion and have a reasonable preservation of articular cartilage

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10
Q

What is arthroplasty?

A

Joint replacement

Literally means ‘to reshape joint’

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11
Q

Limitations of arthroplasty?

A

Only suitable for elderly inactive people

From the moment it is put in, it begins to wear out (no regenerative capacity)

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12
Q

Arthroplasty:

New joint must be capable of?

A

Functional & pain free range of motion

Able to withstand forces placed upon it without undue wear & tear

Same stability as natural joint

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13
Q

General complications of undergoing arthroplasty?

A

Chest infection/UTI

Pressure sores

DVT/PE

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14
Q

Specific (early) complications of arthroplasty?

A

Dislocation - immediately the prosthesis will not be fully supported by soft tissues. Muscles and their proprioceptors may be out of action, through surgical trauma and pain inhibition. A capsule of scar tissue will not yet have formed around prosthesis

DVT - give prophylaxis (heparin, support stockings)

Infection - S. aureus, S. albus. Prevent with ABx prophylaxis & ultra-clean operating environment

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15
Q

Specific (late) complications of arthroplasty?

A

Infection - S. aureus & albus (as with early) but also may be blood borne because of contaminations of blood stream commonly encountered in normal life

Loosening & wear

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16
Q

What causes RA?

A

Unknown

Links with abnormalities of the immune system and there is growing evidence that there may be a genetic abnormality which causes an abnormal reaction to certain types of bacteria

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17
Q

Presentation of RA?

A

Severe pain, swelling & joint deformity

Morning stiffness (improving through the day)

Primarily affects small joints of hands and feet (symmetrically)

Higher incidence in women

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18
Q

Role of surgery in RA?

A

Soft tissue surgery (synovectomy) - removing synovium useful in preventing damage to tendons & tendon sheaths (useful in early disease with retained movement)

Excision arthroplasty - may be combined with synovectomy to relieve pain, however limits future function

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19
Q

What is avascular necrosis (AVN)?

A

Bone tissue death through loss of blood supply

20
Q

Causes of AVN?

A

Post traumatic:
- areas at risk incl femoral head, prox scaphoid, prox talus

AVN of unknown cause:

  • lunate & femoral head
  • AVN of femoral head may be seen in chronic alcohol abuse, high dose steroids, Caisson’s disease (deep sea divers)
21
Q

AVN presentation?

A

Acute severe pain, made worse by movement (relieved by rest to some degree)

Becomes indistinguishable from OA with time

Patients are young

22
Q

Diagnosis of AVN?

A

Initially no x-ray changes

Later bone appears less dense due to absence of blood vessels

23
Q

Management of AVN?

A

Affected joint should be rested

May be reversed if blood supply is re-established naturally. However, in the re-vascularising phase bone is very soft and prone to distort, with secondary arthritic changes. Surgical restoration of bone blood supply is not possible at that moment

Surgery is of no value in treating underlying condition and often the surgeon is left to salvage situation with a joint replacement (problematic as patients are often young)

24
Q

What 2 crystal arthropathies do we look at & what crystals do they deposit in joints?

A

Gout:
- Urate crystals

Pseudogout:
- Pyrophosphate crystals

25
Q

Causes of gout?

A

Dehydration (post-surgery)

Chemo

Diuretics

(urate is a waste product of cell metabolism)

26
Q

Presentation of gout?

A

Hot tender swollen joint

Most commonly 1st metatarsophalangeal joint (knee less common)

27
Q

Diagnosis of gout?

A

Uric acid levels in blood (more accurate to test synovial fluid for urate crystals)

(uric acid normally a waste product passed in urine)

28
Q

Treatment of gout?

A

Anti-inflammatory drugs (help kidneys eliminate urate)

29
Q

Presentation, cause & treatment of pseudogout?

A

Mimic gout but less acute

Origin of pyrophosphate crystals unknown.

Chronically causes calcification of joint surfaces & menisci

Symptoms controlled with anti-inflammatory drugs (long-term degeneration likely)

30
Q

Causes of acute septic arthritis?

A

Rarely from direct penetration of joint

Usually spread there through blood

(Rare in adults unless joint it damaged or immunodeficiency)

Most likely gonococcus in young adults

31
Q

Presentation of acute septic arthritis?

A

Children - acute illness & fever with stiff, hot & tender joint

Adults - less acute & remains unwell for many days before presenting with bacteraemia

32
Q

Treatment of acute sepctic arthritis?

A

Surgical washout & IV ABx

prophylactic anti-staph agent in children as this is most likely

33
Q

Causes of chronic septic arthritis?

A

TB

AIDS patients particularly prone

Kidney & joint TB often found together

34
Q

Presentation of joint TB?

A

Chronic ill health

Weight loss

Muscle wasting around joint

X-ray shows thinning of bone

35
Q

Treatment of chronic septic arthritis?

A

2 RIPE 4 RI

36
Q

Presentation of meniscal lesions?

A

Pain, joint effusion, locking, giving way

More common in men (more vigorous contact sport)

37
Q

Causes of meniscal lesions?

A

Twisting injury (foot gets stuck on the ground and the femur twists over stationary tibia causing a wrench to the meniscus which may be torn or pulled off the bone)

Medial meniscus more frequently torn

38
Q

Types of meniscal tear?

A

Horizontal (cleavage lesion) - common in old age. may act like flap and allow build up of fluid, forming a cyst

A vertical split, which is anchored at both ends - bucket handle tear

Split off one end of the lateral meniscus - parrot beak tear

Tear due to degeneration - degenerate tear

39
Q

Management of meniscal lesion?

A

Examination by arthroscopy and most meniscal lesions can now be removed via arthroscopic meniscectomy, although some require a small opening to be made in the joint (arthrotomy) leading to a longer recovery

As much should be preserved during surgery to help in distributing the load between femur and tibia

Peripheral tears can be reattached with sutures.

Tears within the substance of the meniscus have no capacity to repair and so the torn peripheral part should be removed

40
Q

What are loose bodies in the knee?

A

Osteochondral fragments that shear off in injury

Knee swells (haemarthrosis)

Often not resorbed but lives floating free in synovial fluid

41
Q

Presentation of loose body?

A

1st incident may settle but later (months/years) patient presents with locking, pain, giving way & effusion

Rarely, in adolescents, osteochondral fragments occur spontaneously. Known as osteochondritis dissecans. Tends to settle spontaneously but loose bodies may require removal

42
Q

Treatment of loose bodies?

A

Removal via arthroscope

43
Q

Cause of cruciate ligament lesions?

A

Commonly injured by hyperextension or a twist, often in association with the foot being anchored

Cruciate ligaments not capable of spontaneous healing because if torn, the blood supply is lost.

In rare circumstances the cruciate ligament may be pulled off with a fragment of bone at one end. If the fragment and associated ligament are put back within a few hours then the whole ligament may survive with its blood supply relatively undamaged

44
Q

Presentation of cruciate ligament tear?

A

Acute injury - knee swells quickly (haemarthrosis).

May feel “pop” of ligament tearing

Loss of a cruciate leads to loss of antero-posterior (particularly in flexion), and rotatory stability (when twisting and turning).

Some have no symptoms and there is no explanation for this.

Many patients only experience symptoms when descending stairs or when twisting or turning.

Rotatory instability and pivot shift follow some cruciate ligament injuries

45
Q

Management of cruciate ligament tear?

A

Left untreated for a while and the knee muscles rehabilitated

Treatment offered only if symptoms interfere with daily life or if the patient wishes to return to sport.

Treatment consists of replacing torn ligament with a synthetic one

46
Q

Causes of patella dislocation?

A

Malformation of patella or lateral femoral condyle

Leads to patella moving abrasively on femur (painful due to muscle spasm)

Leads to spontaneous dislocation of patella & failure of quadriceps to act as extensor (person falls to ground)

47
Q

Management of patella dislocation?

A

Minor degrees of mal-tracking dealt with by surgical splitting of vastus lateralis muscle insertion into patella, allowing patella to fall back into a normal relationship to femur

If recurrent and severe then medial tightening (plication) of vastus medialis muscle may be required. In adulthood, the patellar tendon may be re-sited more medially.

BMSc Orthopaedic medicine (5 decks)

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