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ICM - Infectious Disease > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

Definition of Rheumatoid Arthritis

A

Chronic Inflammatory Disorder primarily involving the joints.
Symmetric, Remitting
Can deform the joint

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2
Q

Pathogenesis of Rheumatoid Arthritis?

A

Etiology unknown, Some HLA assoications

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3
Q

What are the HLA associations with Rheumatoid Arthritis?

A

STAT4 Haplotypes Chromosome 2 (RA and SLE)

TRAF1-C5 on Chromosome 9

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4
Q

Pathophysiology of RA?

A

CD4 T cells activated, stimulate Macrophage with !L-2, IFN-g to make more cytokines.
Macrophage releases TNFa, IL1, IL6
Stimulated CD4s also make B cells release Igs (RF)

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5
Q

What do TNFa, IL1, and IL6 do together?

A

Stimulate chondrocytes, fibroblasts, and osteoclasts to make Metalloproteinases, Catalepsins, and other molecules that erode bone and cart.

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6
Q

IL1 and TNFa do what…

A

Stimulate adhesion molecules

Increase recruitment of PMN cells into a joint

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7
Q

What do PMNS do in a Rheumatoid Arthritis reaction

A

release elastase and proteases that degrade cartilage

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8
Q

What happens to the synovial membrane in Rheumatoid Arthritis?

A

Hyperplasia + Hypertrophy of Synovial lining cells

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9
Q

The growing Synovial membrane triggers what three things to happen?

A

Angiogenesis
CD4 predominant T and B cells infiltrate the membrane
Synovial membrane begins to invade cartilage

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10
Q

What happens to the synovial membrane by late RA?

A

Transformed into inflammatory tissue (Pannus)

The tissue invades and destroys cartilage and bone

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11
Q

Three cell types in a Pannus

A

Type A Synoviocytes (Macrophage Like)
Type B Synoviocytes (Fibroblast like)
Plamsa Cells

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12
Q

Typical Rheumatoid Arthritis patient history

A 
Gradual Onset (weeks-months), Can be pallindromic
Symmetrial, Usually Small Joints
Morning Stiffness for hours, Maybe Malaise+Fatigue
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13
Q

Men or Women – Who gets more Rheumatoid Arthritis?

A

Women

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14
Q

Average Rheumatoid Arthritis age of onset?

A

30-55

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15
Q

Physical findings common in a Rheumatoid Arthritis patient?

A 
Joints are warm, boggy, soft, squishy
Not in DIPS
NEVER, EVER in Lower Back
Characteristic Deformities
Extraarticular Involvement
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16
Q

List Characteristic Deformities of Rheumatoid Arthritis

A

Ulnar Deviation
Swan neck deformities, Boutenaire Deformities
Bayonet Deformities
Heel Valgus
Cervical Damage, atlantoaxial instability
MTP Subluxation

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17
Q

Non-MS systems that may be influenced by Rheumatoid Arthritis?

A

Lung
Cardiac
Hematologic
Ocular

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18
Q

Lung manifestations of Rheumatoid Arthritis?

A 
Pleuresy and Pleuritis
Parenchymal lung disease
Intersitital Fibrosis
Bronchiolitis obliterans w/ organizine pneumonia
Methotrexate pneumonitis
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19
Q

Cardiac manifestations of Rheumatoid Arthritis?

A

Pericarditis and Myocarditis

CV Disease

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20
Q

Hematologic manifestations of Rheumatoid Arthritis?

A

Anemia
Felty’s Syndrome
Large Granular Lymphocyte Syndrome
Lymphoma

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21
Q

What is Felty’s Sndrome?

A

Seropositive Rheumatoid Arthritis, neutropenia, splenomegaly, occasionally leg ulcers

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22
Q

Ocular manifestations of Rheumatoid Arthritis?

A

Sjogren’s Syndrome
Corneal Inflammation/Melt
Episcleritis/Scleritis
Uveitis

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23
Q

Occular problems associated with corticosteroid treatment?

A

Glaucoma and Cataracts

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24
Q

Treatment complications assocaited with hydroxychloroquin treatment?

A

Retinal pigment epithelial toxicity

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25
Q

Special studies to order for an Rheumatoid Arthritis patient?

A

Acute Phase Reactants
RF and CCP antibodies
Radiography

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26
Q

Rheumatoid Factors are only predictive for…

A

Patients with inflammatory polyarthritis

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27
Q

A patient with a postivie RF and CCP is at a high risk for

A

Erosions

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28
Q

An Anti-CCP test is looking at…

A

antibodies against the unusual amino acid sequence Citrulline

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29
Q

The CCP is very _____ for RA

A

Specific

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30
Q

The presence of both RF and CCP is _____ specific

A

Very (98%)

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31
Q

DDx diseases that should be considered in an RA patient?

A 
Inflam. Polyarthritises -- 
    SLE, Scleroderma, Vasculitis
    Seronegative Spondyloarthropathies
    Crystal Induced 
    Infectious
    Polymyalgia Rheumatica
    Sarcoidosis
    Cancer
32
Q

What is Polymyalgia Rheumatica?

A

An acute onset of pain in the shoulders and hips
Patients are over 50
Very high Sed rate
Very responsive to corticosteroids

33
Q

Causes of Infectious Arthritis?

A

Viral (Parvo B19, Rubella, Hep B)

Gonoccal

34
Q

Two major crystal induced arthritises?

A

Calcium Pyrophosphate Deposition Disease

Gout

35
Q

List the seronegative spondyloarthropathies

A

Psoriatic Arthritis
Reiter’s Syndrome
Enteropathic Arthritis (Crohn’s, UC, Sprue)
Reactive Arth.

36
Q

Function of COX1?

A

Important to constitutive functions (mucosal lining, platelet fxn)

37
Q

Function of COX2?

A

Mediation of pain, inflammation

38
Q

Role of NSAIDs in RA management?

A

Pain and Inflammation management

No modification of disease outcome

39
Q

Four functions of corticosteroids

A

Cytokine Inhibition
Diminished accumulation of inflammatory cells at site
Inhibition of Cox 2 synthesis
Decrease circulating T cells

40
Q

How do corticosteroids tend to influence skin?

A

Thinning, purpura, striae (stretch marks)

41
Q

How do corticosteroids tend to negatively influence eyes?

A

Cataracts, Glaucoma

42
Q

How do corticosteroids tend to negatively influence blood vessels?

A

Atherosclerosis

Raised BP

43
Q

How do corticosteroids tend to negatively influence GI?

A

Risk of peptic ulcers increased if taken with NSAIDS

44
Q

How do corticosteroids tend to negatively influence bones?

A

Osteoporosis

Can cause avascular necrosis in high dose

45
Q

How do corticosteroids tend to negatively influence pediatric patients?

A

Growth retardation

Steroid Psychosis

46
Q

How do corticosteroids tend to negatively influence CNS

A

Euphoria, Steroid Psychosis

47
Q

How do corticosteroids tend to negatively influence the endocrine system?

A

Glucose Intolerance, Diabetes

48
Q

Other potential concerns about corticosteroids?

A

Weight gain, obesity
Myopathy
Increased risk of infections

49
Q

Examples of Disease Modifying Antirheumatic Drugs?

DMARDS

A 
Antimalarials
Sulfasalazine
Gold
Nucleotide Pathways
TNF agonists, IL1 agonists
Costim. modulator
IL6 Ab
JAK inhibitor
50
Q

Classically prescribed antimalarial drug for RA?

A

Hydroxychloroquin

51
Q

Effects of antimalarial use?

A

Interference of cellular function in compartments in which there is an acid microenvironment (i.e. lysosomes, endosomes, golgi. This alters immune function, enzyme activity, and immune cell fxn.

52
Q

Side effects of antimalarial use?

A

Generally well tolerated, but watch for renal toxicity

53
Q

Molecular effects of Sulfasalazine?

A

Inhibits production of various prostanoids such as leukotriene B4, 5-hydroxyeicosatetraenoic acid, thromboxane A2.

54
Q

Result of taking Sulfasalazine?

A

Results in reduction of circulating lymphocytes, inhibition of B cell activation

55
Q

Side effects of Sulfasalazine?

A

Monitor for meylosuppressions, photosensitivity, rash

56
Q

Effects of Gold Therapy?

A

Inhibits acid P-ase, collagenase, PKC, P-lipase C
Reduced Ig synthesis
Inactivation of Classic and Alternative Complement pathways
Inhibition of lymphocyte proliferative response

57
Q

Side effects of Gold therapy?

A

Monitor for myelosuppression, oral ulcers, rash, proteinuria

58
Q

What drugs can be used to inhibit Purine nucleotide synthesis?

A

Methotrexate and Axathioprine

59
Q

What drugs can be used to inhibit pyramidine nucleotide synthesis?

A

Leflunomide (Arava)

60
Q

Why do nucleotide pathway drugs work?

A

Activiated lymphocytes require de novo synthesis

The combination of MTX and leflunomide can help with this

61
Q

Side effects of Methotrexate?

A

Monitor for oral ulcers, pneumonitis, hepatic toxicity, myelosuppression

62
Q

Side effects of Azathiprine?

A

Myelosuppression

63
Q

Side effects of Leflunomide?

A

Myelosuppression, hepatic toxicity, hair loss, diarrhea, weight loss

64
Q

Name Three common TNF agonists?

A

Etanercept (Enbrel)
Infliximumab (Remicade)
Adalimumab (Humira)

65
Q

What is Etanercept (Enbrel)?

A

A fusion protein of the TNF receptor and the Fc of IgG

66
Q

What is Infliximumab (Remicade)?

A

Binding region of a mouse antibody to TNF fused to th Tc of human Ig

67
Q

What is Adalimumab (Humira)?

A

Recombinant fully human IgG antibody to TNF

68
Q

Efficacy of TNF agonists for RA?

A

Very good

69
Q

Name an IL1 receptor agonist?

A

Anakinra (Kineret)

70
Q

Downsides of IL1 receptor agonist?

A

Painful, Daily injection

No shown benefit with etanercept

71
Q

What might you give to biologically support an RA patient who isn’t responsive to TNF blockers?

A

Abatacept, a costimulation modulator

It is a recombinant protein made of the Extracellular domain of CTLA4 and the constant portion of an IgG

72
Q

How might you promote RA heath by drugging B cells?

A

Give Rituximab (an anti CD20 antibody) with MTX

73
Q

Name the IL6 antibody?

A

Tocilizumba (Actemra)

74
Q

Example of a Janus Kinase inhibitor

A

Tofacitinib (Xeljanz)

75
Q

As of 1996, a triple drug combination has been dubbed the most effected treatment for RA. Name those 3 drugs

A

Methotrexate
Sulfasalazine
Hydroxychloroquin

76
Q

True or False, Timing of RA therapy is important?

A

True
Rates of remission were higher
Fewer erosions

ICM - Infectious Disease (11 decks)

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