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ELM2 - integrated cases > case 4 - painful joints > Flashcards

case 4 - painful joints Flashcards

1
Q

What is inflammatory joint disease?

A

A condition involving autoimmunity to joint tissue, resulting in destruction of joint, loss of mobility, pain, etc.

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2
Q

What is degenerative arthritis?

A

Joint destruction caused by wear and tear to the joint

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3
Q

What is the difference between inflammatory joint disease and degenerative joint disease?

A

Inflammatory is caused by autoimmunity and affects many joints and causes systemic symptoms, while degenerative is caused by wear and tear to specific joints and has fewer systemic symptoms

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4
Q

What joints are typically affected in RA?

A

hands, wrists, feet, knees

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5
Q

What joints are typically affect in OA?

A

hands, back, knees, shoulders

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6
Q

What are the key systemic symptoms of RA?

A

Fatigue, anaemia of chronic disease, weight loss, fever

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7
Q

Why does RA cause fatigue?

A

Continuous inflammatory response results in cytokines that can trigger fatigue. Anaemia of chronic disease can reduce Hb, resulting in fatigue

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8
Q

What type of anaemia is common in patients with RA?

A

Anaemia of chronic disease - normocytic anaemia

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9
Q

Why does RA cause weightloss?

A

Proinflammatory cytokines, such as TNF, can cause weight loss

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10
Q

What are the key components of chronic disease management?

A

residential care, analgesic/anti-inflammatory use, mental health support, primary care, specialist team,

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11
Q

What are the members involved in a team approach to RA treatment?

A

GP, rheumatologist, physical therapist, occupational therapist, social worker, mental health professional, orthopaedic surgeon

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12
Q

What are the steps in RA development involving lymphocytes & macrophages?

A

1.) Inflammatory synovitis initiated when self-antigens presented to T-lymphocytes
2.) T cells recruit and activate macrophages and plasma cells in the synovium
3.) lymphocytes and macrophages produce cytokines (mostly TNF) that stimulates inflammation and cell proliferation, leading to cartilage destruction
4.) T cells activate osteoclasts leading to bone resportion

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13
Q

What immune interaction occurs to trigger RA?

A

Self-antigens are presented to T-cells

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14
Q

What cytokine is most heavily invovled with stimualting inflammation and cell proliferation in RA?

A

TNF (tumour necrosis factor)

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15
Q

How do T cells lead to the alteration of bone structure in RA?

A

T cells activate osteoclasts which leads to bone resorption

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16
Q

What is a pannus?

A

A chronically inflamed, thickened synovium found at the joint of patients with RA

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17
Q

What changes occur to the synovial membrane in patients with RA?

A

membrane becomes thick and opaque as synovial fibroblasts proliferate (pannus formation), pannus contains granulation tissue (is highly vascularised) then fibrosis occurs.

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18
Q

What is the consequence of the pannus being high vascularised in RA?

A

Leukocytes and inflammatory cytokines readily infiltrate the joint causing damage to cartilage

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19
Q

How does the pannus cause damage to articular cartilage in RA?

A

Invades the joint space and releases fluid containing proteolytic enzymes that erode cartilage matrix. The vascularisation also allows cytokines and chemokines to infiltrate and damage cartilage.

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20
Q

What are the changes to bone observed in RA?

A

Decreased bone mass at bone ends, eroded cartilage causes damage, bony ends may fuse together (bony ankylosis)

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21
Q

What 3 joint components show changes in RA and OA?

A

synovial membrane, articular cartilage, bone

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22
Q

What changes to the synovial membrane occur in OA?

A

inflammation and thickening in response to cartilage damage within the joint

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23
Q

Is there pannus formation in OA?

A

No, only slight thickening/inflammation of the synovial membrane

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24
Q

What changes occur to the articular cartilage in OA?

A

wear and tear thins cartilage narrowing the joint space, chondrocyte haemostasis altered leading to cartilage fibrillation.

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25
Q

What is cartilage fibrillation?

A

Sign of OA, splitting & fraying of articular cartilage, accompanied by local erosion and disintegration

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26
Q

What changes to bone occur in OA?

A

bone polishing (eburnation), increased density (sclerosis), fractures leading to subchondral cyst formation, osteophyte formation

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27
Q

What is eburnation?

A

In OA, the smooth polishing of bone ends to to loss of articular cartilage

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28
Q

What is bone sclerosis in OA?

A

Increased density of bone underneath damaged/lost cartilage

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29
Q

How are subchondral cysts formed in OA?

A

Small fractures in articulating bone surfaces can allow fluid to enter bone leading to subchondral cyst formation.

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30
Q

What is the name for the bony outgrowths that develop in OA?

A

Osteophytes

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31
Q

What are the key inflammatory mediators in RA?

A

cytokines (TNF alpha, IL-1, IL-6), chemokines

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32
Q

What releases the inflammatory mediators in RA?

A

Mostly macrophages

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33
Q

What is the role of TNF alpha in RA?

A

Cytokine, induces proliferation of synovial fibroblasts to form the pannus, activates osteoclasts for resorption

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34
Q

What is the role of IL-1 in RA?

A

Stimulates matrix degradation and chondrocyte apoptosis

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35
Q

What is the role of IL-6 in RA?

A

Cytokine, involved in synovial inflammation, pannus formation, osteoclast activation

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36
Q

What are the 3 key cytokines in RA inflammatory mediation?

A

TNF alpha, IL-1, IL-6

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37
Q

What is the role of chemokines in RA?

A

Immune cell recruitment to joints

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38
Q

What are the 3 key autoantibodies found in RA?

A

Rheumatoid factor, Anti-CCP antibodies, Anti-nuclear antibodies

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39
Q

What is Rheumatoid Factor an antibody to?

A

IgG

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40
Q

What is Rheumatoid Factor produced by?

A

B cells in lymphoid follicles in the synovium

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41
Q

What autoantibody is found in the plasma of the majority of RA patients

A

Rheumatoid Factor

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42
Q

What are Anti-CCP antibodies autoantibodies to?

A

Cyclic Citrullinated Peptides (CCP), which are citrullinated proteins that are thus foreign to the immune system in patients with autoimmunity.

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43
Q

What are Anti-nuclear antibodies autoantibodies to in RA?

A

Protein contents of cell nuclei

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44
Q

What autoantibody is a general sign of autoimmunity and is not always found in RA patients?

A

Anti-nuclear antibodies

45
Q

What are the structural differences between the synovial membrane in OA & RA?

A

In OA the membrane becomes inflamed and thickened, while in RA the synvovium is degraded and then pannus is formed

46
Q

What are the structural differences between articular cartilage in OA & RA?

A

In OA, cartilage is worn away by wear and tear and fibrillation leading to exposure of bone ends, while in RA cartilage is partially destroyed by the pannus and inflammatory cells and chemicals in the autoimmune response.

47
Q

What are the structural differences between bone in OA & RA?

A

In OA, bones become polished and are prone to fractures, subchondral cyst formation and osteophyte formation. In RA, osteoclast activity causes bone breakdown and bone ends may fuse together (ankylosis) causing joint fixation.

48
Q

What are the key physical findings in RA?

A

symmetrical joint pain, morning stiffness, persistent synovitis (joint swelling), deformities of hand, wrist, fingers, rheumatoid nodules, systemic symptoms

49
Q

What joints are particularly susceptible to persistent synovitis in RA?

A

Metacarpophalangeal and interphalangeal jopints of the hands

50
Q

What are the hand deformities common in RA?

A

Radial deformation of wrist, ulnar deviation of fingers

51
Q

What are the common finger deformities in RA?

A

Swan neck, Boutonniere

52
Q

What are Rheumatoid nodules?

A

Firm lumps under the skin close to affected joints in RA

53
Q

What are the key physical findings in OA?

A

assymetrically affected joints, reduced range of motion, crepitus, bone enlargement, joint line tenderness, Heberden & Bouchard nodes

54
Q

What are Heberden Nodes?

A

Osteophyte formation at the distal interphalangeal joints of the hands

55
Q

What are Bouchard nodes?

A

Osteophyte formation at the proximal interphalangeal joints

56
Q

What is the ratio of females to males with RA?

A

3:1

57
Q

What age does RA typically onset?

A

Middle age

58
Q

What is the most common RA-linked allele in patients with RA?

A

The ‘shared epitope’ a region of MHC genes

59
Q

What is the mechanism by which the ‘shared epitope’ may lead to RA?

A

mutations may cause the presentation of citrullinated antigens, leading to autoimmunity

60
Q

What is the greatest lifestyle risk factor for developing RA?

A

Smoking

61
Q

How does smoking exacerbate RA symptoms?

A

Worsens chronic inflammation

62
Q

How does alcohol alter the risk of developing RA?

A

Moderate consumption can decrease risk of developing RA by decreasing some cytokine.

63
Q

Why should alcohol be avoided in patients with RA?

A

Can have dangerous interactions with medications

64
Q

What are the genetic factors in OA?

A

Often strong history, unknown genetic cause, likely polygenic

65
Q

What are the key environmental factors in OA?

A

Occupation/sport, obesity, physical inactivity, metabolic syndromes, poor diet, joint trauma

66
Q

Why does obesity increase the risk of OA?

A

Increases the joint load causing strain, and also increases chronic systemic inflammation

67
Q

Why is physical inactivity a risk factor for OA?

A

Leads to muscle wasting decreasing joint support, lack of joint loading decreases nutrient supply to articular cartilage

68
Q

Why is joint trauma a risk factor for OA?

A

Causes abnormal stress to the joint, and can force immobility and inactivity

69
Q

What are the 3 key drug types used in the treatment of inflammatory joint disease?

A

NSAIDs, DMARDs, corticosteroids

70
Q

What is the ‘Treat to Target’ method of RA management?

A

Goal of remission or low level disease, with target setting for treatment which are measured through regular disease monitoring.

71
Q

What does DMARD stand for?

A

Disease Modifying Anti Rheumatic Drug

72
Q

What are DMARDs used for in RA?

A

Long term disease control, prevention of joint damage, therapeutic remission

73
Q

What is the protocol for onset of DMARD treatment in RA?

A

Treat with DMARDs as soon as diagnosis is confirmed

74
Q

What drugs are used in bridging therapy until the effects of DMARDs appear?

A

NSAIDS and glucocorticoids

75
Q

How should DMARD induced immunosuppression be monitored?

A

Regular blood tests, monitoring for signs of infection (fever, etc.)

76
Q

What is the ‘first choice’ DMARD for RA treatment?

A

Methotrexate

77
Q

What is the mechanism of action of methotrexate?

A

Antagonist of folate, blocking DHFR enzymes, which are required for nucleotide and therefore DNA production

78
Q

What is the target site of methotrexate?

A

Dividing cells in bone marrow, progenitor cells in immune system, tumour cells

79
Q

What are the side effects of methotrexate?

A

infection, nausea, vomiting, headache, ulcers, fatigue

80
Q

what are the 4 key common DMARDs?

A

Methotrexate, Etanercept, Tofacitinib, Infliximab

81
Q

What is the mechanism of action of Etanercept?

A

Acts as soluble TNF (tumour necrosis factor) receptor to bind and neutralise TNF alpha (cytokine) to inhibit its inflammatory processes

82
Q

What is the mechanism of action of Tofacitinib?

A

Janus kinase enzyme inhibitor

83
Q

What is the mechanism of action of Infliximab?

A

Antibody against the cytokine TNF alpha

84
Q

What is an NSAID?

A

Non-steroidal anti-inflammatory drug

85
Q

What is the mechanism of action of most NSAIDs?

A

Binding and inhibiting COX1 or COX2 enzymes to block prostaglandin production and thereby prevent inflammation

86
Q

Why are NSAIDs used alongside DMARDs?

A

They reduce pain and inflammation but do not alter disease progression, which is the role of DMARDs

87
Q

What is the most common/major side effect of NSAIDs?

A

gastric complications - ulcers, bleeding, heart burn.

88
Q

Why do NSAIDs cause gastric complications?

A

Are weak acids that concentrate on stomach wall and deprotonate. COX enzymes, which NSAIDs inhibit, have a role in maintaining the mucosal barrier

89
Q

What is a common NSAID that should not be used for RA treatment due to its gastric complications?

A

Aspirin

90
Q

Why should aspirin not be used in the long term treatment of pain in RA?

A

Causes cumulative GI toxicity because of its low pKa and irreversible binding to COX-2 enzymes

91
Q

How does aspirin inhibit platelet aggregation?

A

By inhibiting the COX-1 enzyme

92
Q

What is the mechanism of action of aspirin?

A

Blocks prostaglandin synthesis by binding non-selectively to COX 1 and 2 enzymes

93
Q

What is the mechanism of action of Naproxen?

A

Inhibits COX-1 and COX-2 reducing prostaglandin synthesis

94
Q

What is the action of Naproxen?

A

reducing pain and inflammation

95
Q

What is the mechanism of action of Diclofenac?

A

Inhibits COX-1 and COX-2 enzymes, reducing prostaglandin synthesis

96
Q

What enzyme is Diclofenac selective for?

A

COX-2

97
Q

What is the action of Diclofenac?

A

Reduce inflammation and pain (NSAID)

98
Q

What is the role of prostaglandin in pain and inflammation?

A

Synthesised in infected/damaged tissues to trigger fever, inflammation and pain

99
Q

What are corticosteroids?

A

Steroid hormones naturally synthesised by the adrenal cortex, but also used as drugs

100
Q

What are the actions of glucocorticoid drugs?

A

Anti-inflammatory, analgesic, immunosuppressive

101
Q

What is the general mechanism of action of glucocorticoids?

A

Act on nuclear cell glucocorticoid receptors to alter gene transcription and thereby suppress inflammatory and immune responses.

102
Q

How are glucocorticoids used in conjunction with DMARDs in RA treatment?

A

Used as bridging therapy until DMARDs are effective, but can be used as a DMARD itself at high doses

103
Q

What is the major side effect of prolonged glucocorticoid use, and why?

A

Cushingoid effects, due to increased coritsol levels

104
Q

What is the standard glucocorticoid used in RA treatment?

A

Prednisone

105
Q

What is the mechanism of action of prednisone?

A

Binds to glucocorticoid receptor leading to downstream decreases in vasodilation, and decrease leukocyte migration to sites of inflammation.

106
Q

What is the target site of prednisone?

A

Glucocorticoid receptor

107
Q

What is the action of prednisone?

A

Steroid that reduces inflammation, suppresses immune reactions and reduces pain

108
Q

What are the side effects of prednisone?

A

weight gain, mood changes, insomnia, headache

109
Q

What is the non-pharmacological management of RA?

A

Treatments used in conjunction with drugs to offer best outcomes. Include patient education, psycho-behavioural interventions, physical therapy, occupational therapy, nutritional/dietary changes

ELM2 - integrated cases (9 decks)

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