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Revision Cards > Week 137 - Monoarthritis/Gout > Flashcards

Week 137 - Monoarthritis/Gout Flashcards

1
Q

What is the histology of OA?

A
  • Cartilage degradation /proteoglycan loss
  • Surface fibrillation
  • Chondrocyte clustering and apoptosis
  • Hyperplasia of synovium
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2
Q

Why does articular cartilage have limited capacity for self-repair?

A
  • Avascular
  • Slow diffusion of nutrients from synovial fluid.
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3
Q

What is a focal cartilage lesion?

A

Damage to cartilage from trauma or repetitive strain.

They can either be Chondral or Osteochondral.

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4
Q

What is a focal chondral lesion?

A

A lesion that lies entirely within the cartilage, do not repair spontaneously.

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5
Q

What is a focal osteochondral lesion?

A

These are lesions that penetrate through some subchondral bone - some spontaneous healing as it is vascular, osteoprogenitor cells invade the lesion.

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6
Q

What are the different classifications of cartilage defects?

A
  • Grade I - Some fissures extending into superficial cartilage.
  • Grade II - Multiple fissures extending half-depth into the cartilage.
  • Grade III - Fissures extending down to subchondral bone.
  • Grade IV - Complete loss of cartilage and exposure of subchondral bone.
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7
Q

What are the current repair strategies for intermediate/small localised cartilage defects?

A
  • Debridement
  • Microfracture
  • Osteochondral grafting
  • Cell-based therapies

• Osteotomy

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8
Q

Cartilage repair techniques: Debridement.

A
  • This is a palliative procedure which envolves shaving off the frayed edges of cartilage.
  • Aims to reduce friction and inflammation to improve pain and swelling.
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9
Q

Cartilage repair techniques: Microfracture.

A

A repairative technique, which drills small holes in the subchondrol bone with a arthroscope, this causes bleeding and initiates healing.

• Does not last long, and additional surgery will be required.

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10
Q

Cartilage repair techniques: Osteotomy.

A
  • This involves removing a wedge shaped bone in order to restore load-distribution and gait.
  • Edges of cut-bone are held together with nails.
  • Long recovery process, does not repair.
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11
Q

Cartilage repair techniques: Osteochondral grafting.

A
  • Regenerative procedure.
  • Healthy cartilage is removed from a location either self or donor and is then drilled into the site, which then multiplies to repair.
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12
Q

Cartilage repair techniques: Autologous chondrocyte implantation. (ACI)

A
  • This is a regenerative technique where healthy tissue is removed and sent to a lab where it undergoes processing for clonal expansion.
  • These are then injecting into the site and covered with a peiosteal patch which is sealed with fibrinogen and thombin.
  • This treatment is for injury from trauma or repetive action, it is **not **useful in OA.
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13
Q

Cartilage repair techniques: Matrix-induced autologous chondrocyte implantation (MACI).

A
  • This is an adaptation of ACI, where the chondrocytes are attached to a membrane which is directly implanted into the defect. A periosteal patch is not needed.
  • Surgery time is reduced.
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14
Q

What is septic arthritis?

A

This is acute inflammation of the joint due to direct infection.

Most frequently bacterial.

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15
Q

How does septic arthritis tend to present?

A

Acute

Pain

Swelling

Erythema

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16
Q

What are some of the predisposing factors for septic arthritis?

A
  • Prosthetic joint
  • Immunosupression / elderly / diabetes
  • Rheumatoid arthritis
  • Exisiting joint damage
  • IV drug abuse
17
Q

What is the outcome of septic arthritis if left untreated?

A
  • Rapid destruction of joint
  • Sinus/abcess formation
  • Septicaemia
  • Multiple organ failure
18
Q

What is the morbidity of septic arthritis when treated?

A

50%

19
Q

What investigations should be performed for a suspected septic arthritis?

A
  • Blood- FBC, U&Es, LFT, Culture, Urate etc..
  • X-ray

• Aspirate joint fluid (NOT prosthetic joint)
- culture

20
Q

How should antibiotics be given for septic arthritis?

A

2 weeks IV, 4 weeks oral.

21
Q

What is gout?

A

A clinical syndrome caused by an inflammatory response to monosodium urate monohydrate crystals which may form in people with hyperuricaemia.

22
Q

What is the type of crystal largely responsible for gout?

A

Monosodium urate monohydrate crystals.

23
Q

What essentially causes gout?

A

Overproduction/ underexcretion of urate.

Overproduction: Due to a purine-rich diet or increased synthesis of purines.

Under-excretion: **90% **of gout due to under-secretion, mainly sue to renal impairment.

24
Q

What are the non-modifiable risk factors for gout?

A
  • Age - 40-50 males, >60 females
  • Gender: Male
  • Genetic factors
  • Impaired renal function
25
Q

What are the modifiable risk factors for gout?

A
  • Hyperuricaemia
  • High-purine diet
  • Alcohol consumption
  • Obesity
26
Q

What is the clinical presentation of gout?

A
  • Acute, relapsing, self-limiting, severe inflammatory arthritis.
  • Exquisite pain, swelling and erythema.
  • >50% of 1st attacks occur in the 1st MTP.
27
Q

What % of acute attacks of gout occur mono-articularly?

A

90%

28
Q

What are tophi?

A

These are hard swellings of monosodium urate monohydrate crystals, responsible for the most disability during chronic gout.

29
Q

What investigations should be performed for Gout?

A
  • Joint fluid examination - presence of urate crystals.
  • Bloods, urinanlysis.
30
Q

What are the treatment aims for gout?

A
  • To treat acute attacks early and effectively.
  • Manage hyperuricaemia, to prevent build up of urate crystals.
31
Q

What is the medical treatment for an acute attack of gout?

A
  • NSAIDS
  • Cochicine
  • Oral and intra-articular steroids.
32
Q

What are some of the Urate-lowering drugs that can be used to treat chronic gout?

A
  • *• Xathine oxidase inhibitors**
  • Reduces production of uric acid.
  • Allopurinol
  • *• Uricosuric agents**
  • Increases secretion of uric acid.
  • Sulphinpyrazone - Used in normal renal function.
  • Benbromarone - Can be used in renal impairment.
33
Q

Explain the initiation of Urate-lowering therapy.

A
  • Should not be started during an acute attack.
  • It should be started at a low dose and titrated up.
  • It may cause an acute attack as urate crystals are mobilised.
  • Patients should recieve anti-inflammatory prophylaxis during the first few months of treatment.
34
Q

What is psuedogout?

A

This is similar to gout but is due to Calcium pyrophosphate crystals instead.

Attacks can last much longer and there is no specific treatment.

35
Q

What conditions are associated with pseudogout?

A

Hyperparathyroidism, osteoarthritis, haemochromatosis, diabetes, acromegaly.

36
Q
A

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