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Rheumatic Disease Flashcards

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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
What is PMR characterised by?
Pain and stiffness in neck, shoulder, and pelvic girdle, systemic features, raised ESR (>60), and dramatic response to small disease of corticosteroids
26
What is ESR?
Erythrocyte Sedimentation Rate
27
What is giant cell arteritis (GCA)?
A vasculitis commonly accompanying PMR
28
What are the common features of GCA?
Headaches, jaw claudication, fatigue, and visual disturbance
29
What is jaw claudication?
Pain or discomfort in the jaw that typically occurs while chewing
30
What is the pathology of PMR?
Underlying pathological abnormality unknown
31
What is the pathology of GCA?
Limited to vessels with an internal elastic component and humoral and cellular mechanisms implicated in pathogenesis
32
What is the treatment of PMR?
10-20mg prednisolone and consider osteoporosis prophylaxis
33
What is the treatment of GCA?
40mg (60-80mg if ocular symptoms)
34
What does retinal artery occlusion cause?
Sudden, painless loss of vision in one eye
35
What are the autoimmune connective tissue disease?
Systemic Lupus Erythematosus (SLE), Anti-phospholipid Syndrome (APL), Systemic Sclerosis, Sjogren’s Syndrome and (inflammatory muscle disease)
36
What are the common symptoms of autoimmune connective tissue diseases?
Sicca symptoms (dry eyes, dry mouth), mouth ulcers, and annoying symptoms
37
What is SLE?
An inflammatory autoimmune disease, with multi-organ involvement, a wide variety of manifestations, and an unpredictable course
38
What makes diagnosis of SLE particularly challenging?
Dynamic nature of disease, with changeable and intermittent signs and symptoms
39
Why is SLE considered a great mimic?
Mimics a myriad of conditions often resulting in a delayed diagnosis
40
What is SLE often recognised by?
Characteristic patterns of organ involvement and presence of particular autoantibodies usually to intranucleic acids
41
What is prevalence of SLE in USA?
15-124/100,000
42
What is prevalence of SLE in UK?
12-24.7/100,000
43
What gender is SLE more prevalent in?
Women particularly in reproductive years
44
What are the genetic factors of SLE?
High prevalence among monozygotic twins and family studies, hereditary predisposing 5-12% relatives of patients develop disease
45
What are the human leukocyte antigen (HLA) associations for SLE?
HLA DR2 and DR3, C4a null allele, and immunoglobulin and T cell receptor genes
46
What are the clinical features of SLE?
Constitutional, arthritis, skin, mucous membranes, pleurisy, pericarditis, Raynaud’s, thrombophlebitis, vasculitis, renal, Nephrotic Syndrome, CNS, gastrointestinal, pancreatitis, lymphadenopathy, and myositis
47
What is pleurisy?
Inflammation of the pleurae, which impairs their lubricating function and causes pain when breathing
48
What is myositis?
Inflammation and degeneration of muscle tissue
49
What are the clinical features of systemic sclerosis?
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
What is systemic sclerosis?
Disfiguring, multisystem disease that may alter every aspect of an individual’s life
51
What is the risk of internal organ involvement in systemic sclerosis strongly linked to?
Extent and progression of skin thickening
52
What is Raynaud's phenomenon?
A disorder that causes decreased blood flow to the fingers
53
What is Sjogren's syndrome?
Disorder of exocrine function
54
What are the types of Sjogren's syndrome?
Primary and secondary associated with SLA and RA
55
What are the symptoms of Sjogren's syndrome?
Sicca symptoms
56
What is Behcet's disease?
Inflammatory condition rare and poorly understood
57
What are the features of Behcet's disease?
Mouth ulcers, genital ulcers, pathergy, inflammation in blood vessels, pulmonary, skin , and gastrointestinal
58
What is pathergy?
An exaggerated skin injury occurring after minor trauma
59
What are the first line therapies for rheumatic diseases?
NSAIDs, COX I, and COX II
60
What are the second line agents for rheumatic diseases?
Methotrexate, Sulphasalazine, Leflunomide, Plaquenil, Gold, Cyclosporin, Azathioprine, and Penicillamine
61
What is the other treatment for rheumatic diseases?
Corticosteroids
62
What is the drug therapy for rheumatic diseases?
Analgesia, Nonsteroidal Anti-Inflammatories, Disease Modifying Anti-Rheumatic Drugs, steroids, and biologic agents
63
What is pharmacotherapy is most commonly used for rheumatic diseases?
Methotrexate and sulphasalazine
64
What are the Disease Modifying Anti-Rheumatic Drugs (DMARDS)
Methotrexate, Sulphasalazine, Leflunomide, and Hydroxychloroquine
65
What are the effects of DMARDS?
Stomatitis, relative immunosuppression, and effect on wound healing?
66
What is COX I?
Constitutive form, maintaining renal perfusion and normal gastric mucosa, brufen, diclofenac, and naproxen
67
What is COX II?
Inducible form, at sites of inflammation, different s/e profile, meloxicam, etodolac, and celecoxib
68
Where do corticosteroids act?
At specific cytoplasmic receptors
69
What do corticosteroids control?
Gene transcription
70
What do corticosteroids induce?
Changes in lymphocyte function, Fc receptor suppression and down regulation of many proinflammatory enzymes
71
What does prednisolone 7.5mg a day need prophylaxis of?
Steroid induced osteroporosis
72
What occurs in initial 3 months of corticosteroid use?
Bone loss
73
What is the treatment for bone loss?
Bisphosphonates, calcium, and vitamin D
74
What are examples of bisphosphonates?
Aldendronate, Risedronate, and Etidronate
75
What is the normal cytokine-receptor interaction?
Inflammatory cytokine, cytokine receptor, and inflammatory signal
76
What is the neutralisation of cytokines?
Monoclonal antibody, soluble receptor, and no signal
77
What is the receptor blockade?
Monoclonal antibody, receptor antagonist, and no signal
78
What is the activation of anti-inflammatory pathways?
Anti-inflammatory cytokine and
79
What are cytokines?
Intercellular messenger molecules
80
What is the function of cytokines?
Mediate effect by binding to cell-associated receptors on target cells, leading to intracellular signalling and activating gene transcription
81
What are cytokines produced in?
Small amounts
82
Where do cytokines act?
Principally in local milieu
83
What is anti-TNF therapy?
Biological therapy targeted against tumour necrosis factor
84
What are the anti-TNF therapy drugs available?
Infliximab, Etanercept, Adalimumab, Certolizumab, Golimumab, and Biosimilars
85
What is the strict criteria for usage of anti-TNF therapy drugs?
Fail >2 DMARDs including methotrexate and high DAS score
86
What is DAS?
Disease Activity Score
87
What are the functions of anti-TNF therapy?
Neutralisation of TNF-alpha, reduction in other proinflammatory cytokines, reduction of leucocyte migration into joint, and reduction of angiogenesis
88
What is anti-TNF therapy a major advance in treatment of?
Rheumatoid Arthritis
89
What is rituximab?
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
What does rituximab result in?
Rapid depletion of CD20+ive B cells in peripheral blood
91
When are normal B cells replenished by stem cells in most patients?
3-12 months after therapy
92
What type of treatment is rituximab?
Intravenous

Human Diseases (2 decks)

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