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Year 2 > Pathophysiology Of Joint Disease > Flashcards

Pathophysiology Of Joint Disease Flashcards

1
Q

What is rheumatoid arthritis?

A

Symmetrical arthritis with inflammation of the synovial membrane with pain and swelling that leads to bone and articular cartilage erosion, affecting the MCP and PIP joints. It is worse after activity in the morning. It is a polyarticular arthritis affecting multiple joints.

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2
Q

What are the risk factors for rheumatoid arthritis?

A

->Age
-> Epigenetics
->Women post-menopause
->Smoking
->Porphyromonas gingivalis bacteria
->Injury or infection in synovial membrane causing synovial hyperplasia

These factors increase the recognition of autoantibodies against citrillunated components.

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3
Q

What are the epigenetics that increase risk of rheumatoid arthritis?

A

HLA-DR1
HLA-DR4

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4
Q

What is vimentin?

A

Fibroblast intermediate filament which is an auto-antigen in rheumatoid arthritis when citrullination occurs.

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5
Q

What is the pathophysiology of rheumatoid arthritis?

A

Auto-antigens are vimentin and citrillunated proteins. Macrophages release IL-1, IL-6 and TNF-alpha which induces inflammation. This activates fibroblast-like synoviocytes for T cells to express RANKL and bind to osteoclasts for activation and resorption and release of protease for articular cartilage degradation.

Auto-antigens of the synovial membrane are taken up by antibodies to lymph nodes and prime B and T cells for co-stimulation. Antibodies Rheumatoid factor and anti-citrillunated protein targets fibrin and fibrinogen on cartilage travel between the joints and result in symmetrical arthritis.

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6
Q

What is citrillunation?

A

Post-translational modification of arginine protein to citrilline which occurs in type 2 collagen and vimentin, which relies on Ca2+. When acumulated, these increase the risk of becoming immunogenicity and inducing action against synovial membrane.

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7
Q

How does the immune system work in rheumatoid arthritis?

A

Majority of rheumatoid arthritis is caused by Rheumatoid factor, a modified IgM antibody which acts on the Fc region of IgG to activate by forming an immune complex to be deposited into the articular cartilage and induce further destruction. High levels are associated with severe progressive disease

T cells produce IFN-alpha and IL-17 which further increase inflammation

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8
Q

What is the most common cause of death of rheumatoid arthritis?

A

Cardiovascular disease.

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9
Q

What is Hepicidin?

A

Liver enzyme which traps iron in macrophages and liver cells which results in anaemia

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10
Q

What is the composition of the nodules in rheumatoid arthritis?

A

Centre of necrosis tissue surrounded with macrophages and lymphocytes.

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11
Q

What are the autoantigens in rheumatoid arthritis?

A

Proteglycan mesh in Articular cartilage
Components of synovial membrane such as Vimentin and type 2 collagen, that have undergone citrillunation.

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12
Q

What are the deformities in rheumatoid arthritis?

A

Ulnar deviation at MCP joint
Boutonnierre’s deformity.
Swan’s neck’s deformity.

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13
Q

What is Boutonnière’s deformity?

A

Flexion of PIP, extension of DIP due to damage to extensor tendon.
-> DIP is unaffected in rheumatoid arthritis.

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14
Q

What is Swan’s neck deformity?

A

Hyperextension of PIP, extension of DIP joint.

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15
Q

What is the epidemiology of rheumatoid arthritis?

A

Symmetrical arthritis which affects more women and is generally progressive. The most common cause of death is coronary artery disease

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16
Q

What is the clinical presentation of rheumatoid arthritis?

A

Worse in the morning and improves during the day with increased activity but acute flares can occur . Affects the metacarpopharyngeal joints, metatarsopharyngeal joints with joint swelling and inflammatory signs. Dramatic alleviation of symptoms with NSAIDs.

X-rays should be performed.

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17
Q

Which cytokines inhibit inflammation effect?

A

IL-4
Il-10
TGF-beta

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18
Q

What is the role of TNF-alpha in inflammation in rheumatoid arthritis?

A

Increases inflammation, immune cell infiltration, angiogenesis
Acts on keratinocytes for hyperproliferation of keratinocytes, causing skin plaque formation.
Increases levels of the protease metalloproteinase for cartilage degradation of the proteogylcan mesh.

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19
Q

Why does CRP increase?

A

Liver enzyme elevated in inflammation due to being an acute phase reactant.

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20
Q

What is an acute phase reactant?

A

Proteins which respond to rise in inflammatory cytokines by INCREASING or DECREASING which makes it useful as an inflammation marker.

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21
Q

What are the effect of rheumatoid arthritis on joints?

A

It affects the MCP and PIP joints of the hands. Articular cartilage degrades so the joint space narrows and inflammation of the synovial membrane.

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22
Q

What are the systemic effects of rheumatoid arthritis?

A

Chronic inflammation, driving insulin resistance and osteoporosis due to high cortisol levels.
Skin nodules, typically in elbows which can also form in the lungs.

Liver: Elevated CRP and Hepicidin

Heart: Increased arthogenesis in coronary arteries, increasing risk of cardiovascular disease

Popliteal cyst in the knee joint

Felty Syndrome

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23
Q

How does rheumatoid arthritis affect the lungs?

A

It can cause intrapulmonary nodule formation
Fibrosis and interstitial lung disease
Pleural effusion
Bronchieactasis

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24
Q

How does rheumatoid arthritis affect the heart?

A

It can cause pericarditis and myocarditis and lead to increased atherosclerotic plaques for greater risk of cardiovascular disease due to greater cortisol.

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25
Q

What is Felty Syndrome?

A

Triad of factors with:
Rheumatoid arthritis, splenomegaly and neutropenia.

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26
Q

What is the markers for prognosis for mortality in rheumatoid arthritis?

A

Both Rheumatoid factor and Anti-CCRP antibodies involved in the condition.

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27
Q

What is the markers for prognosis for disability in rheumatoid arthritis?

A

Presence of nodules, affects many joints and patient is female.

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28
Q

What are the markers of prognosis for bone erosion in RA?

A

Both Rheumatoid Factor and anti-CCRP are involved in the immune response.

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29
Q

How is rheumatoid arthritis treated?

A

Early intervention to stop inflammation, prevent damage and preserve function to eventually achieve disease remission.

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30
Q

What is osteoarthritis?

A

Breakdown of articular cartilage combined with underlying bone growth, typically occurring in the weight-bearing joints such as the knees and hips. It also affects the small joints the DIP joints, cervical and lumbar vertebrae and metatarsopharyngeal joint. Most common disability in elderly and presents with osteophytes.

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31
Q

What is the clinical presentation of osteoarthritis?

A

First early sign is reduction in internal rotation.

Stiffness in the morning which worsens during the day with more activity with SHARP and aching pain. There are no swelling signs. Tenderness on joint palpation and osteophytes.
X-rays don’t show much for diagnosis, unless it is severe.

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32
Q

Which joins are affected in osteoarthritis?

A

DIP and PIP joints of the hands.
Weight bearing joints such as the sacro-iliac joint, hip joint and knee joint.

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33
Q

What are the risk factors for osteoarthritis?

A

Elderly due to thinning of articular cartilage with less hydration
Previous joint injury
Obesity
Post-menopausal women
Leg bone misalignment with bow legs/knock knees
Increased type 1 collagen which is less elastic.
Occupation

34
Q

What is the role of articular cartilage?

A

Provides friction-less movement with:
-> no tension due to type 2 collagen
-> no compression due to proteoglycans
Articular cartilage is not ossified.

35
Q

What is the composition of synovial membrane?

A

Type A cells are responsible for clearing cellular debris.
Type B cells are responsible for producing synovial fluid.

36
Q

What is the composition of articular cartilage?

A

Proteases break down by cartilage action due to TGF-alpha.

37
Q

What is menisci?

A

Weighted discs in the joint space of the knee for shock absorption.

38
Q

What is the pathophhysiology of osteoarthritis?

A

Destruction of articular cartilage creates fibrillation and increases the production of bradykinin for pain perception. This cartilage breaks off into the joint space and are taken up by type A cells of synovium.

The underlying subchondral bone is exposed and becomes the new articular surface, converted into ‘ivory’ bone in eburnation. This drives ossification of cartilage to form bony outgrowths called osteophytes.

39
Q

What is eburnation?

A

Degradation of articular cartilage causes friction in the joint with the conversion of subchondral bone to ivory-like bone at site of erosion.

40
Q

What is primary osteoarthritis?

A

Idiopathic cause of osteoarthritis.

41
Q

What is mild osteoarthritis?

A

Occurs naturally with aging where cartilage degeneration occurs and joint space narrows.

42
Q

What is secondary osteoarthritis?

A

Occurs due to pre-existing condition from infection, congenital abnormality, collagen defect, steroid use, previous inflammation and Ehler’s Danlos.

43
Q

What are the consequences of osteoarthritis?

A

Knee deformities such as:
Genu valga (knock knees)
Genu Vara (bow legs)
LOSS
L: loss of joint space
O: Osteophytes
S: subchondral sclerosis
S: subchondral cysts

44
Q

What is E-selectin?

A

Vascular adhesion molecule expressed in blood vessels for immune cell recruitment.

45
Q

How can osteoarthritis be viewed?

A

Viewed using X-rays initially and MRI to view progression.

46
Q

What is subarticular sclerosis?

A

Subarticular sclerosis, which is when there is increased density and hardening of bone in the articulation surface between the joints

47
Q

What is the presentation of osteoarthritis?

A

Pain which occurs due to prostaglandins and the presence of pain receptors in the periosteum. Muscle spasms and contractions can occur in the tendons. Synovitis can occur with inflammation of the synovial membrane due to immune response and presence of osteophytes.

48
Q

What is gout?

A

Inflammatory arthritis which causes sudden and severe joint pain in the metatarsopharyngeal joint, caused by defective uric acid metabolism that results in deposition of monosodium urate crystals in the joints. It is the most common inflammatory arthritis affecting men.

Causes fever and malaise

49
Q

What conditions increase the formation of mono sodium rate crystals?

A

Acidity/low pH
Low temperature
Stress

50
Q

What are the risk factors for gout?

A

**Typically affects middle aged men. ** High intake of shellfish, liver meat, organ meat and red meat. Intake of high fructose corn syrup drinks.

Dehydration
Obesity, kidney disease and hypertension
Kidney disease which impairs urate clearance
Chemotherapeutic agents like cyclosporine
Joint trauma
Thiazide diuretic

51
Q

What increases hyperuricaemia?

A

Dehydration from low water intake or high alcohol intake of (BEER > spirits > wine) causes reduced action by the kidneys for clearing uric acid.
Intake of shellfish, anchovies red meat and organ meat.

Diseases with a high cell turnover such as rhadomyolysis, haemolytic jaundice, psoriasis.

52
Q

Which hormonal imbalance can increase the risk of gout?

A

Hyperparathyoridism due to increased turnover of bone, increasing urate levels and the high free calcium can increase the risk of kidney stones and obstruct urate excretion in the urine.

53
Q

How do monosodium urate crystals form?

A

Purines such as adenine and guanine are broken down by xanthine oxidase into insoluble uric acid.

54
Q

What is hyperuricaemia?

A

Uric acid levels exceed a solubility at 6.8mg. This occurs when a pH of 7.4 causes uric acid to lose h+ ions and form urate ions.
Urate ion + sodium -> monosodiumurate crystals

55
Q

How does adenosine metabolism occur?

A

Adenosine is converted -> Inosine by adenosine deaminase.
Inosine -> hypoaxanthine by nucleoside phosphorylases.
** Hypoaxanthine** -> Xanthine -> Urate by urate oxidase.

56
Q

How does guanine metabolism occur?

A

Guanine -> Xanthine by guanine deaminase.
Xanthine -> Urate by Xanthine oxidase.

57
Q

Which conditions increase purine synthesis?

A

Lymphoma, leukaemia, anaemia, psoriasis, hyperparathyroidism due to high cell turnover.

58
Q

What are the features of acute gout?

A

Podagra occurs where monosodium urate crystals deposited in the 1st metatarsal joint where weight bearing causes solidification of crystals. Lymphocytes attempting to clear uric acid result in inflammation. Attacks start at night or in the morning and this condition resolves in 7-10 days without treatment. It is typically monoarticular.

59
Q

What are the sits of acute gout attacks?

A

Metatarsopharyngeal joints
Knee, ankle, wrist, finger joints, olecranon bursa

60
Q

What is the majority of gout caused by?

A

Low urate clearance due to renal impairment.

61
Q

What triggers gout?

A

Direct trauma
Dehydration
Rapid weight loss
Medications such as diuretics

62
Q

How is gout diagnosed?

A

Aspiration of tophi
Crystals examined under polarising light are
Blue perpendicular to light
Yellow parallel to light

63
Q

What is a tophi?

A

Mono sodium rate crystals surrounded by granulomas in chronic gout.

64
Q

What is chronic gout?

A

Formation of permanent large crystal depositions called tophi in the metatarsopharyngeal joints (MTP) and proximal interpharyngeal joints (PIP). Increased risk of kidney stones formed of uric acid and can attach to interstitial and cause interstitial nephropathy. It is an asymmetrical arthritis driven by neutrophils.

65
Q

What is septic arthritis?

A

Occurs 2-3 weeks post infection by
->Staphylococcus aureus, Group a STREP, neisseria gonnorhoea,
->Gram negative bacteria such as salmonella and E.coli involved in gastroenteritis which produce endotoxins
There is rapid destruction of muscle and bone with possible joint loss if left untreated

66
Q

What is the presentation of septic arthritis?

A

Fever, inflammatory mono arthritis in a single large joint like knee, ankle, feet or hips
Urethritis, conjuctivitis

67
Q

What is a risk factor for septic arthritis?

A

Pre-existing joint disease, IV drug abuse
Use of immunosuppressants and steroids.

68
Q

Common cause of septic arthritis in sickle cell patients?

A

Salmonella

69
Q

Common cause of septic arthritis in IV drug users?

A

Staphylococcus aureus (present in skin)
Pseudomonas

70
Q

Common cause of septic arthritis in infants?

A

Streptococcus
For unvaccinated infants, haemophilius

71
Q

How is septic arthritis investigated?

A

Joint aspiration and antibiotic treatment.

72
Q

What is pseudo gout?

A

Deposition of calcium pyrophosphate crystals which induces neutrophil mediated phagocytosis that causes a release of inflammatory cytokines. It is a polyarticular response which has a much slower onset than gout, lasts 3 weeks and is self-limiting.

Presents similarly to pseudo osteoarthritis, rheumatoid arthritis or arthritis of multiple joints.

73
Q

What are the risk factors for pseudogout?

A

Increasing age
Hyperparathyroidism
Hypothyroidism
Acromegaly

74
Q

What can trigger pseudogout?

A

Trauma
Dehydration
Illness
Surgery

75
Q

How is pseudogout diagnosed?

A

Arthrocentesis that shows rhomboid shaped crystals
X ray

76
Q

How is pseudogout treated?

A

NSAIDs and steroids to reduce inflammation
Rest
Aspiration of the joint with arthrocentesis

77
Q

Which areas of the body are affected in pseudogout?

A

Ankles, knees, wrists, MCP

78
Q

How is arthritis typically managed?

A

Intra-articular steroid injections
Analgesics (note: if using NSAIDs regularly, must be given with proton pump inhibitor)
Joint replacement.

79
Q

What type of hypersensitivity is rheumatoid arthritis?

A

Type III hypersensitivity typically, but may be type 3 hypersensitivity.

80
Q

What is psoriasis?

A
81
Q

What are rheumatoid nodules?

A

Subcutaneous lumps that are mobile and flesh coloured, found in areas of pressure like in fingers and elbows due to active rheumatoid arthritis. It has a centre of necrosis surrounded by macrophages and lymphocytes.

Year 2 (247 decks)

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