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LOCO 2 > Degenerative vs Inflammatory Joint Conditions > Flashcards

Degenerative vs Inflammatory Joint Conditions Flashcards

1
Q

Briefly explain the process of OA.

A

Chondrocytes have phenotypical alteration. Get old/stressed, and don’t produce good quality proteoglycans and collagen. They end up with ECM degradation which causes local low grade inflammation, which sets up the vicious cycle. Pro-inflammatory cytokines cause more stress to the chondrocytes. Eventually the cartilage is lost and this affects the subchondral bone, leading to osteophyte formation which will irritate the synovium, which leads to even more inflammation.

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2
Q

Briefly explain the process of RA.

A

RA is an autoimmune disease that creates large inflammatory response within the joints. It also affects the heart, kidney, gut, eyes (basically all body systems). Pro-inflammatory cytokines are not specific to the joint. Inflammation affects synovial membrane, which proliferates and grows to form pannus which degrades ECM of cartilage and bone. Cartilage is damaged and bone is exposed.

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3
Q

What is the prevalence of osteoarthritis in the US?

A

26.9 million

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4
Q

What is the prevalence of gout in the US?

A

6.1 million

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5
Q

RA is the most common autoimmune condition. What is the prevalence in the US?

A

1.3 million (860 per 100,000)

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6
Q

What is the prevalence of psoriasis in the US?

A

380 per 100,000

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7
Q

What is the prevalence of diabetes in the US?

A

192 per 100,000

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8
Q

What is the most common form of arthritis, with everybody developing age-related degenerative changes?

A

Osteoarthritis

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9
Q

What causes osteoarthritis?

A

Mechanical wear and tear on the joint

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10
Q

How many % of the population are affected by rheumatoid arthritis?

A

1%

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11
Q

Which joints are affected in OA?

A 
Distal and proximal IP joints
Big toe (as it carries more of the weight)
Big weight-bearing joints e.g. knee and hip
Spine
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12
Q

What is the main difference in the distribution of OA and RA in the body?

A

OA - bilateral or unilateral

RA - symmetrical

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13
Q

Which joints are affected in RA?

A

Any synovial joints can be affected
Cervical spine, shoulder, elbow, wrist, hip, knee, ankle, carpals, MCP…
Doesn’t affect distal joints in the hands/feet.

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14
Q

How does the age at which the condition starts differ between RA and OA?

A

RA – may begin at any time, usually mid 20s to 40s

OA – usually begins later in life

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15
Q

How does the speed of onset differ between RA and OA?

A

RA - Relatively rapid, over weeks to months

OA - Slow, over years

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16
Q

How do the joint symptoms differ between RA and OA?

A

RA - joints are painful, swollen (increased synovial fluid production), and stiff
OA – joints ache and may be tender but have little to no swelling

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17
Q

How does the pattern of joints that are affected differ between RA and OA?

A

RA - often affects small and large joints on both sides of the body (symmetrical), such as both hands, both wrists or elbows, or the balls of bothfeet.
OA - symptoms often begin on one side of the body and may spread to the other side. Symptoms are often limited to one set of joints, such as the DIPs and PIPs or the thumbs, largeweight-bearing joints (hips,knees), orthe spine.

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18
Q

How does the duration of morning stiffness differ between RA and OA?

A

RA - morning stiffness (synovial fluid gels at rest) lasts longer than 1 hour.
OA - morning stiffness lasts less than 1 hour. Stiffness returns at the end of the day or after periods of activity.

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19
Q

How does the presence of symptoms affecting the whole body (systemic) differ between RA and OA?

A

RA - frequentfatigueand a general feeling of being ill are present
OA - systemic symptoms are not present

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20
Q

Osteoarthritis is strongly __ related and is rare __ ___.

A

Age

<45 years

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21
Q

How many % of 65 year olds have OA on X-rays?

A

80%

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22
Q

When can degenerative changes begin to be seen on x-ray?

A

As early as 20 years old

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23
Q

Osteoarthritis mainly affects … joints.

A

Weight bearing

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24
Q

There is pronounced female preponderance for more severe symptoms and changes on radiographic examination, especially of what joints? Why?

A

Hand and knee

The knee is because women have wider pelvis, so have more severe OA of the knee (due to way the weight is carried).

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25
Q

OA of hips uncommon in…?

A

Africans and Asians

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26
Q

Polyarticular OA of the hand rare in…?

A

Africans and Malaysians

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27
Q

How many % of UK population over 55 years old have problematic knee pain? How many of these are severely disabled?

A

10%

25%

28
Q

OA is the leading cause of…?

A

Physical disability in people over 65 years

29
Q

What are the individual risk factors for OA? (11)

A
  • Obesity (esp OA knee)
  • Abnormal mechanical loading (e.g. meniscectomy, instability and dysplasia)
  • Inherited type II collagen defects in premature polyarticular OA
  • Inheritance in nodal and erosive OA
  • Occupation e.g. farmers & OA hip
  • Other arthritic conditions (e.g. RA or gout)
  • Previous knee injury
  • High-impact physical activity
  • Aged over 50 years
  • Genetic disorders such as deformed legs or knees
  • Habitual floor activities, such as kneeling, side-knee bending and squatting
30
Q

What are the three subsets of primary OA?

A

Idiopathic
Generalised
Erosive

31
Q

What are the subsets of secondary OA? (5)

A
  • Due to mechanical incongruity of joint, congenital or acquired (e.g. acetabular dysplasia of hip or internal knee derangement)
  • Due to prior inflammatory disease (e.g. RA)
  • Due to endocrine disorders (e.g. diabetes, acromegaly)
  • Due to metabolic disorders (e.g. calcium pyrophosphate dehydrate crystals, haemochromatosis)
  • Miscellaneous (e.g. avascular necrosis)
32
Q

Describe the joint in OA. (8)

A 
Thickened capsule
Frayed, cracked meniscus
Bone sclerosis
Bone osteophytes
Fibrillated/destroyed cartilage
Reduced viscosity of synovial fluid
Episodically inflamed synovium
Weakened and frayed tendons, ligaments, and muscles
33
Q

All tissues of the joint involved in the pathogenesis of OA, but primarily it is characterised by…?

A

Degeneration of the articular cartilage with subsequent changes in the other tissues

34
Q

What is seen in early-stage OA? (4)

A

Cartilage degeneration
Subchondral microdamage
Subchondral plate thickness decreases and porosity increases
Subchondral trabeculae deterioration

35
Q

What is seen in late-stage OA? (7)

A 
Progressive cartilage destruction
Increased calcified cartilage thickness
Reduplicated tidemarks
Increased subchondral plate thickness
Subchondral bone cyst
Subchondral microdamage
Subcondral trabeculae sclerosis
36
Q

What are the physical signs in OA? (7)

A 
Crepitus
Bony enlargement (osteophytes)
Deformity
Instability (pseudolaxity)
Restricted movement
Mild effusion
Muscle weakness or wasting
37
Q

What is the best means of assessment for OA?

A

Plain radiograph

38
Q

What four signs are seen on x-ray in OA?

A

Cartilage loss (joint space narrowing)
Osteophytes
Subchondral sclerosis
Trabeculae fractures/subchondral cysts

39
Q

Nodal generalised OA generally affects what joints?

A

Small joints of the hands

40
Q

Which joints get Herberden’s nodes in nodal OA?

A

DIP

41
Q

Which joints get Bouchard’s nodes in nodal OA?

A

PIP

42
Q

When does nodal OA usually start?

What is the relevance of this for treatment?

A

Around time of menopause

- But HRT does not help symptoms or progression

43
Q

Erosive OA is an inflammatory form of OA. What joints does it often affect?

A

DIPs

44
Q

What is erosive OA primarily characterised by?

A

Erosions of cartilage in the hands

45
Q

Who is most commonly affected by erosive OA?

A

Middle-aged or post-menopausal women

46
Q

How is OA treated (general)?

A

Management, no cure

No disease modifying drugs

47
Q

How is OA treated (specific)? (7)

A 
Weight loss and/or exercise
Acetaminophen
COX 2 inhibitors
NSAIDs
Intra-articular hyaluronic acid
Intra-articular steroids
Joint replacement surgery
48
Q

What is the shortcoming of acetaminophen?

A

Weak analgesic effects

49
Q

What are the shortcomings of COX 2 inhibitors?

A

Inadequate pain relief

GI complications and concerns

50
Q

What is the shortcoming of NSAIDs?

A

GI bleeding

51
Q

What are the shortcomings of intra-articular hyaluronic acid?

A

Weak analgesic effect

No proven efficacy

52
Q

What new treatment options are there for OA? (5)

A

Inhibition of synovial inflammation (synovium)
Inhibition of catabolic proteases (cartilage
Inhibition of osteoclast activity (subchondral bone)
Modulation of adipokine signalling (adipose tissue)
Inhibition of myofibrillar degradation (skeletal muscle)

53
Q

RA is a…?

A

Destructive inflammatory polyarthritis

54
Q

RA can affect any synovial joints, but particularly… (3)

A

PIPs
MCP
Carpals

55
Q

What deformities are seen in the hand in RA? (6)

A
  1. Z-deformity of thumb (flexion of MCP, extension of IP)
  2. Swan neck deformity (extension of PIP, flexion of DIP)
  3. Volar subluxation of MCPs (metacarpal heads appear prominent because proximal phalanges have subluxed under them)
  4. Ulnar deviation of fingers at MCPs
  5. Radial deviation of hand at the wrist
  6. Dorsal subluxation of ulnar head (due to interruption of radioulnar ligament)
56
Q

What may be the triggers for RA? (3)

A

Genetic disposition
Environmental factors
Acute trigger e.g. infection, trauma

57
Q

What autoantibodies are seen in RA?

A

Rheumatoid factor

Anti-citrullinated peptide antibodies

58
Q

What is rheumatoid factor?

How many % of RA patients have it?

A

IgM to Fc portion of IgG

60-80%

59
Q

Anti-citrullinated peptide antibodies - what can they cause?

What is the specificity for RA?

A

Can induce osteoclasts and cause destruction of the bone.

96%

60
Q

Cytokines cause…

and induce…

A

Proliferation of the fibroblasts in subintima and type B synoviocytes
Synovial fibroblasts to express RANKL and induce osteoclast production

61
Q

Which T cells are important in RA?

A

CD4 T helper cells, especially Th17 - this is the most important in orchestrating the other responses from the B cells and macrophages (via production of IL-17)

62
Q

What causes inflammation in RA?

A

Activation of T cells, B cells and macrophages which release cytokines such as IL-1, IL-6 and TNFα, causing local joint damage.

63
Q

How does systemic inflammation occur in RA?

What does this cause? (5)

A

IL-1, IL-6 and TNFα leak out into blood stream

Anaemia, thrombocytosis, fatigue, osteoporosis and the acute-phase response

64
Q

Anaemia of chronic disease - what type of anaemia is this?

A

Hypochromic normocytic anaemia (severe cases microcytic)

65
Q

What is seen in anaemia of chronic disease? (5)

A
  • Dysregulation of iron homeostasis
  • Decreased iron availability for RBC production
  • Impaired proliferation of erythroid progenitor cells
  • Shortened lifespan of RBC
  • Blunted EPO response

LOCO 2 (28 decks)

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