Comparison of Degenerative versus Inflammation Flashcards

1
Q

what is more prevalent OA or RA

A

OA

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2
Q

What is more disabling OA or RA

A

RA - can cause more joint destruction

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3
Q

what is the most common form of arthritis

A

OA

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4
Q

describe OA

A

Everybody will develop age related degenerative changes

Mechanical wear and tear on the join

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5
Q

describe rheumatoid arthritis

A

Affects around 1% of the population

autoimmune

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6
Q

What type of joints does osteoarthritis affect

A

weight bearing joints

  • knee, hip, vertebral column
  • non symmetrical but can become symmetrical for example if you weight bear on the other joint this can cause more damage on it
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7
Q

describe the joints that RA affect

A
  • smaller joints to start with such as the metacarpal joints in the hands and feet
  • tends to start in the smaller joint and spread to the knee shoulder and elbow
  • alanto axis C1/C2 joint is affected
  • symmetrical joints are affected
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8
Q

describe the differences between RA and OA

  • age at which condition starts
  • speed of onset
  • joint symptoms
  • pattern of joints that are affected
  • duration of joint morning stiffness
  • presence of symptoms affecting the whole body (systemic)
A

Rheumatoid arthritis

  • age at which condition starts = begins at any time but usually between 30-60 years old
  • speed of onset = rapid, over weeks to months
  • joint symptoms = painful, swollen and stiff
  • pattern of joints that are affected = small and large joints on both sides of the body (symmetrical) such as both hands, both wrists or elbows
  • duration of joint morning stiffness = lasts longer than an hour
  • presence of symptoms affecting the whole body (systemic) = frequent fatigue and a general feeling of being ill is present

Osteoarthritis

  • age at which condition starts = later in life
  • speed of onset = slow over years
  • joint symptoms = joint ache and may be tender but have little or no swelling
  • pattern of joints that are affected = may begin on one side of the body and may spread, often limited to one set of joints such as the DIP, or PIPs, large weight bearing joints or the spine
  • duration of joint morning stiffness = less than an hour, returns at the end of the day or after periods fo activity
  • presence of symptoms affecting the whole body (systemic) = whole body symptoms are not present
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9
Q

describe the changes with age and OA

A

Rare <45 yrs
80% of 65 yr old have OA on X-rays
But 20 year olds have early degenerative changes

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10
Q

who is OA of the hips uncommon in

A

OA of hips uncommon in Africans and Asians

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11
Q

who is OA of the hand rare in

A

Polyarticular OA of the hand rare in Africans and Malaysians

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12
Q

who is at greater risk of OA

A
  • females
  • females also tend to have more severe symptoms and changes on radiographic examination
  • especially of the OA of the hand and knee
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13
Q

why in females is the knee more affected by OA

A
  • because the Q angle of the knee is larger therefore this puts more stress onto the medial side of the knee
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14
Q

what is the leading cause of physical disability in the country for those over 65 years old

A

OA

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15
Q

how many people over the age of 55 have knee pain

A

10% of UK population over 55 years old have problematic knee pain

Of these 25% are severely disabled

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16
Q

what are the risk factors for OA

A
  • obesity = especially in the knee
  • abdominal mechanical loading such as meniscectomy, instability and dysplasia
  • inherited type II collagen defects in premature polyarticular OA
  • inheritance in nodal and erosive OA
  • occupation e.g. farmers and OA hips
  • other arthritic conditions
  • age
    high impact physical activity
  • knee injury
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17
Q

what are the two different types of OA

A

primary and Secondary

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18
Q

What is Primary OA

A
  • this is when you cannot find a reason for the OA - therefore it is just age related and idiopathic
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19
Q

Describe primary osteoarthritis

A
  • idiopathic
  • generalise
  • erosive
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20
Q

Describe what secondary osteoarthritis is due to

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 such as rheumatoid arthritis
  • due to endocrine disorder such as diabetes, acromegaly
  • due to metabolic disorder such as calcium pyrrophophate dehydrate crystals, hemochrombtosis
  • miscellaneous (avascular necrosis)
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21
Q

what is OA primarily characterised by

A
  • it is primarily characterised by the degeneration of the articular cartilage with subsequent changes in other tissues
22
Q

What is the difference between bone versus cartilage regeneration

A

Bone
- bone has a good blood supply that brings in osteoblasts progenitor cells from the periosteum and endosteum which can replace the old bone with new bone

cartilage

  • relatively avascular
  • relient on the diffusion of nutrients from the synovial fluid into the top layers of the cartilage
  • therefore cartilage takes longer to heal and can take up to 3 months to heal
  • even then the cartilage is only replaced with fibrocartilage and not hyaline cartilage
  • deep cartilage is okay as it is close to the bone
23
Q

What are the physical signs in OA

A

Crepitus

Bony enlargement
- osteophytes

Deformity

Instability (pseudolaxity)

Restricted movement

Effusion (mild)

Muscle weakness or wasting

24
Q

what happens if the medial compartment of the knee is damaged

A
  • you get a pseudo laxity - medial collateral ligament is supposed to be working at a cm distance and if you loose the cartilage and the bone is closer then there is more loosesnes of the medial collateral ligmant
25
Q

what are the 4 signs of osteoarthritis on a radiogrpahy

A
  • Cartilage loss (joint space narrowing)
  • bone response (osteophytes)
  • subchondral sclerosis
  • trabecular fractures/subchondral cysts
26
Q

what is the best means of assessment of osteoarthritis

A
  • plain radiograph
27
Q

what are the nodes called affecting OA

  • DIP
  • PIP
A

DIP – Herberden’s node

PIP – Bouchard’s node

28
Q

when does OA usually start

A
  • disease often starts around the time of menopause

- but HRT does not help the symptoms or progression

29
Q

what is erosive OA

A

Severe subset of nodal generalised OA= a more inflammatory form of OA

  • May therefore be confused with RA

Primarily characterized by erosions of cartilagein the DIP and PIP joints

  • Gull-wing or saw-tooth
  • Erosions in centre and edges
30
Q

what is erosive OA primarily characterised by

A

Primarily characterized by erosions of cartilagein the DIP and PIP joints

  • Gull-wing or saw-tooth
  • Erosions in centre and edges
31
Q

who does erosive OA mainly caused in

A

Middle-aged or post-menopausal women are most commonly affected

32
Q

what is the treatment of OA

A
  • no cure
  • aim is management
  • at present there is no disease modifying drugs
  • pain management and then joint replacement surgery
33
Q

describe rheumatoid arthritis

A

1% of population

Destructive inflammatory polyarthritis

Symmetrical

attacks the small joint sin the hands and feet

34
Q

what joints does RA affect

A

Prevalence for attacking the small joints in hands and feet

  • Particularly PIPs, MCP, carpals
  • But can affect any synovial joint
35
Q

what are the risk factors for Rheumatoid arthritis

A
  • gender and hormal factors
  • prior inflammatory disease
  • environmental factors/gut flora
  • smoking
  • post viral immunomodulation
  • HLA-DR4
  • genetic disposition = monozygotic twins 15% compared to dizygotic twins 4%
36
Q

What gene is related to rheumatoid arthritis

A

HLA DR4

37
Q

what is the gut microbiome associated with

A

Core gut microbiome is associated with genotype but can be modulated by diet and other environmental factors

38
Q

what can gut flora influence

A

Gut flora can influence immune system locally and systematically

39
Q

what does NETs stand for

A

neutrophil extracellular traps

40
Q

describe the pathophysiology of RA

A
  • might have an infection
  • normally neutrophils are the first that responds
  • they tackle the viral infection via NETs
  • within the neutrophil they also have the enzyme that creates citrullinated peptides
  • these citrullinated peptides act against the synovial membrane
  • this initiates RA
41
Q

what does it mean in RA when you have Rheumatoid factor IgM to Fc portion of IgG

A

60-80% of RA patients

More severe disease

42
Q

what autoantibodies are affected in RA

A

Rheumatoid factor

Anti- citrullinated peptide antibodies

43
Q

what can autoantibodies be used for in RA

A

Used diagnostically and prognostically – both of them mean you have a high and active disease progress that is worse

44
Q

how do APCA affect RA

A
  • induce macrophages directly and switch it to an osteoclast and makes it more reactive
45
Q

what T cell is the most involved in the pathophysiology of RA

A

Th17

- produced IL-17

46
Q

How do cytokines produce a pannus

A

Cytokines cause proliferation of the fibroblasts in subintima and type B synoviocytes

Cytokines induce synovial fibroblasts to express RANKL and induce osteoclast production

Infiltration by CD4T helper cells
- TH17

47
Q

what is the inflammation in RA caused by

A

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

48
Q

what leads to systemic inflammation via RA

A

IL-1, IL-6 and TNFα also leak out into blood stream resulting in systemic inflammation

49
Q

what shows in systemic inflammation in RA

A

Anaemia, thrombocytosis, fatigue, osteoporosis and the acute-phase response
coronary artery disease such as MI and stroke increases

50
Q

what does anaemia look like when it is chronic disease

A

Hypochromic normocytic anaemia (severe cases microcytic)

51
Q

What can cause anaemia of chronic disease

A
  • dysregulation of iron homeostasis
  • impaired proliferation of erythroid progenitor cells
  • shortened lifespan of RBC
  • decreased iron availability for RBC production
  • Blunted EPO response