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Human Diseases > Rheumatic Disease > Flashcards

Rheumatic Disease Flashcards

1
Q

What is ankylosing spondylitis?

A

A form of spinal arthritis that eventually causes ankylosis of vertebral and sacroiliac joints

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2
Q

What are rheumatic diseases?

A

Autoimmune and inflammatory diseases that cause your immune system to attack your joints, muscles, bones and organs

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3
Q

What rheumatic disease can present with dental problems/symptoms?

A

Rheumatoid arthritis, polymyalgia pheumatica/giant cell arteritis, sepsis, multi system disease, and auto immune connective tissue diseases

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4
Q

What is a multi system disease?

A

Behcets

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5
Q

What are autoimmune connective tissue disease?

A

Systemic Lupus erythematosus, systematic sclerosis, and sjogren’s syndrome

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6
Q

What is rheumatoid arthritis?

A

A common severe inflammatory disorder affecting individuals of all ages

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7
Q

What is the origin of rheumatoid arthritis?

A

Multifactorial including a genetic predisposition, characterised by immune driven chronic inflammation

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8
Q

What are the main target organs in rheumatoid arthritis?

A

Synovial lining of joints, tendon sheaths, and bursae

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9
Q

What does synovitis result in?

A

Erosion of articular cartilage and bone with subsequent joint destruction

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10
Q

What is synovitis?

A

Inflammation of a synovial membrane

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11
Q

What is the course of rheumatoid arthritis?

A

Variable course, involving exacerbations and remissions of diseases activity

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12
Q

What are most cases of rheumatoid arthritis?

A

Chronic and progressive

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13
Q

What is the development of rheumatoid arthritis?

A

Genetic susceptibility, immune response, and insult/trigger

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14
Q

What is the anatomy of a normal joint?

A

Bone, cartilage, capsule, synovial membrane, and synoviocytes

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15
Q

What is the disease progression of early rheumatoid arthritis?

A

Neutrophils, hyperplastic synovial membrane, capillary formation, T cells, B cells, and hypertrophic synoviocyte

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16
Q

What is the disease progression of established rheumatoid arthritis?

A

Neutrophils, plasma cell, synovial villi, extensive angiogenesis, and eroded bone

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17
Q

What is antlanto axial subluxation?

A

A disorder of C1-C2 causing impairment in rotation of the neck

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18
Q

What is the common scenario of atlanto axial subluxation?

A

Longstanding deforming RA, increasing clumsiness, and increasing neurological symptoms both upper and lower limbs

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19
Q

What are the predisposing factors of atlanto axial subluxation?

A

Whiplash injury, forced extension of cervical spine (intubation), and aggressive treatment of disease (pulsed) causing instability as pannus ‘dissolved’

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20
Q

What is pannus?

A

A condition in which a layer of vascular fibrous tissue extends over the surface of an organ

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21
Q

What can periodontal disease severity correlate with?

A

RA disease severity

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22
Q

What does alveolar bone loss in RA patients with periodontal diseases paralell?

A

RA erosions at other sites

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23
Q

What may periodontal disease and RA share?

A

A number of pathobiological processes

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24
Q

What is polymagia rheumatic (PMR)

A

A clinical syndrome of middle aged and elderly patients

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25
Q

What is PMR characterised by?

A

Pain and stiffness in neck, shoulder, and pelvic girdle, systemic features, raised ESR (>60), and dramatic response to small disease of corticosteroids

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26
Q

What is ESR?

A

Erythrocyte Sedimentation Rate

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27
Q

What is giant cell arteritis (GCA)?

A

A vasculitis commonly accompanying PMR

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28
Q

What are the common features of GCA?

A

Headaches, jaw claudication, fatigue, and visual disturbance

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29
Q

What is jaw claudication?

A

Pain or discomfort in the jaw that typically occurs while chewing

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30
Q

What is the pathology of PMR?

A

Underlying pathological abnormality unknown

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31
Q

What is the pathology of GCA?

A

Limited to vessels with an internal elastic component and humoral and cellular mechanisms implicated in pathogenesis

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32
Q

What is the treatment of PMR?

A

10-20mg prednisolone and consider osteoporosis prophylaxis

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33
Q

What is the treatment of GCA?

A

40mg (60-80mg if ocular symptoms)

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34
Q

What does retinal artery occlusion cause?

A

Sudden, painless loss of vision in one eye

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35
Q

What are the autoimmune connective tissue disease?

A

Systemic Lupus Erythematosus (SLE), Anti-phospholipid Syndrome (APL), Systemic Sclerosis, Sjogren’s Syndrome and (inflammatory muscle disease)

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36
Q

What are the common symptoms of autoimmune connective tissue diseases?

A

Sicca symptoms (dry eyes, dry mouth), mouth ulcers, and annoying symptoms

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37
Q

What is SLE?

A

An inflammatory autoimmune disease, with multi-organ involvement, a wide variety of manifestations, and an unpredictable course

38
Q

What makes diagnosis of SLE particularly challenging?

A

Dynamic nature of disease, with changeable and intermittent signs and symptoms

39
Q

Why is SLE considered a great mimic?

A

Mimics a myriad of conditions often resulting in a delayed diagnosis

40
Q

What is SLE often recognised by?

A

Characteristic patterns of organ involvement and presence of particular autoantibodies usually to intranucleic acids

41
Q

What is prevalence of SLE in USA?

A

15-124/100,000

42
Q

What is prevalence of SLE in UK?

A

12-24.7/100,000

43
Q

What gender is SLE more prevalent in?

A

Women particularly in reproductive years

44
Q

What are the genetic factors of SLE?

A

High prevalence among monozygotic twins and family studies, hereditary predisposing 5-12% relatives of patients develop disease

45
Q

What are the human leukocyte antigen (HLA) associations for SLE?

A

HLA DR2 and DR3, C4a null allele, and immunoglobulin and T cell receptor genes

46
Q

What are the clinical features of SLE?

A

Constitutional, arthritis, skin, mucous membranes, pleurisy, pericarditis, Raynaud’s, thrombophlebitis, vasculitis, renal, Nephrotic Syndrome, CNS, gastrointestinal, pancreatitis, lymphadenopathy, and myositis

47
Q

What is pleurisy?

A

Inflammation of the pleurae, which impairs their lubricating function and causes pain when breathing

48
Q

What is myositis?

A

Inflammation and degeneration of muscle tissue

49
Q

What are the clinical features of systemic sclerosis?

A

Tightening and thickening of skin and involvement of internal organs including gastro-intestinal tract, lungs, heart, and kidneys which account for increased morbidity and mortality

50
Q

What is systemic sclerosis?

A

Disfiguring, multisystem disease that may alter every aspect of an individual’s life

51
Q

What is the risk of internal organ involvement in systemic sclerosis strongly linked to?

A

Extent and progression of skin thickening

52
Q

What is Raynaud’s phenomenon?

A

A disorder that causes decreased blood flow to the fingers

53
Q

What is Sjogren’s syndrome?

A

Disorder of exocrine function

54
Q

What are the types of Sjogren’s syndrome?

A

Primary and secondary associated with SLA and RA

55
Q

What are the symptoms of Sjogren’s syndrome?

A

Sicca symptoms

56
Q

What is Behcet’s disease?

A

Inflammatory condition rare and poorly understood

57
Q

What are the features of Behcet’s disease?

A

Mouth ulcers, genital ulcers, pathergy, inflammation in blood vessels, pulmonary, skin , and gastrointestinal

58
Q

What is pathergy?

A

An exaggerated skin injury occurring after minor trauma

59
Q

What are the first line therapies for rheumatic diseases?

A

NSAIDs, COX I, and COX II

60
Q

What are the second line agents for rheumatic diseases?

A

Methotrexate, Sulphasalazine, Leflunomide, Plaquenil, Gold, Cyclosporin, Azathioprine, and Penicillamine

61
Q

What is the other treatment for rheumatic diseases?

A

Corticosteroids

62
Q

What is the drug therapy for rheumatic diseases?

A

Analgesia, Nonsteroidal Anti-Inflammatories, Disease Modifying Anti-Rheumatic Drugs, steroids, and biologic agents

63
Q

What is pharmacotherapy is most commonly used for rheumatic diseases?

A

Methotrexate and sulphasalazine

64
Q

What are the Disease Modifying Anti-Rheumatic Drugs (DMARDS)

A

Methotrexate, Sulphasalazine, Leflunomide, and Hydroxychloroquine

65
Q

What are the effects of DMARDS?

A

Stomatitis, relative immunosuppression, and effect on wound healing?

66
Q

What is COX I?

A

Constitutive form, maintaining renal perfusion and normal gastric mucosa, brufen, diclofenac, and naproxen

67
Q

What is COX II?

A

Inducible form, at sites of inflammation, different s/e profile, meloxicam, etodolac, and celecoxib

68
Q

Where do corticosteroids act?

A

At specific cytoplasmic receptors

69
Q

What do corticosteroids control?

A

Gene transcription

70
Q

What do corticosteroids induce?

A

Changes in lymphocyte function, Fc receptor suppression and down regulation of many proinflammatory enzymes

71
Q

What does prednisolone 7.5mg a day need prophylaxis of?

A

Steroid induced osteroporosis

72
Q

What occurs in initial 3 months of corticosteroid use?

A

Bone loss

73
Q

What is the treatment for bone loss?

A

Bisphosphonates, calcium, and vitamin D

74
Q

What are examples of bisphosphonates?

A

Aldendronate, Risedronate, and Etidronate

75
Q

What is the normal cytokine-receptor interaction?

A

Inflammatory cytokine, cytokine receptor, and inflammatory signal

76
Q

What is the neutralisation of cytokines?

A

Monoclonal antibody, soluble receptor, and no signal

77
Q

What is the receptor blockade?

A

Monoclonal antibody, receptor antagonist, and no signal

78
Q

What is the activation of anti-inflammatory pathways?

A

Anti-inflammatory cytokine and

79
Q

What are cytokines?

A

Intercellular messenger molecules

80
Q

What is the function of cytokines?

A

Mediate effect by binding to cell-associated receptors on target cells, leading to intracellular signalling and activating gene transcription

81
Q

What are cytokines produced in?

A

Small amounts

82
Q

Where do cytokines act?

A

Principally in local milieu

83
Q

What is anti-TNF therapy?

A

Biological therapy targeted against tumour necrosis factor

84
Q

What are the anti-TNF therapy drugs available?

A

Infliximab, Etanercept, Adalimumab, Certolizumab, Golimumab, and Biosimilars

85
Q

What is the strict criteria for usage of anti-TNF therapy drugs?

A

Fail >2 DMARDs including methotrexate and high DAS score

86
Q

What is DAS?

A

Disease Activity Score

87
Q

What are the functions of anti-TNF therapy?

A

Neutralisation of TNF-alpha, reduction in other proinflammatory cytokines, reduction of leucocyte migration into joint, and reduction of angiogenesis

88
Q

What is anti-TNF therapy a major advance in treatment of?

A

Rheumatoid Arthritis

89
Q

What is rituximab?

A

Chimeric monoclonal antibody, which mediates its effect via complement mediated and antibody dependent cell mediated-cytotoxicity, induction of apoptosis and inhibition of cell growth

90
Q

What does rituximab result in?

A

Rapid depletion of CD20+ive B cells in peripheral blood

91
Q

When are normal B cells replenished by stem cells in most patients?

A

3-12 months after therapy

92
Q

What type of treatment is rituximab?

A

Intravenous

Human Diseases (2 decks)

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