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Pharmacology > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

Rheumatoid Arthritis (RA) afflicts – adults in the US

A

2.0 million

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2
Q

RA afflicts ~X:X women than men characterized by daily joint pain

A

3:1

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3
Q

most patients with RA also experience some degree of

A

depression
anxiety
feelings of helplessness

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4
Q

RA can interfere with routine

A

daily activities

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5
Q

what is RA

A

an inflammatory disease causing pain, swelling, stiffness, and loss of function in joints

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6
Q

how long does RA last for

A

few months and disappear w/o causing any noticeable damage

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7
Q

are there various degrees of RA

A

yes, some patients have mild or moderate forms of the disease with period of worsening symptoms (flares) and period they feel better (remission)

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8
Q

describe the severe form of RA

A

-diseaseis active most of the time, lasts for many years or a lifetime, leading to serious joint damage, disability

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9
Q

in RA, what happens to the synovium of a joint

A
  • it becomes inflamed causing warmth, redness, swelling and pain
  • as the disease progresses, the inflamed synovium invades and damages the cartilage and bone of the joint
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10
Q

in RA what happens to the surrounding muscle

A

muscles, ligaments and tendons become weakened

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11
Q

what effects does RA have on bones

A

can cause more generalized bone loss that may lead to osteoporosis

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12
Q

what type of disease is RA

A

autoimmune disease

  • a person’s immune system attacks joint tissues for unknown reasons
  • WBC travel to the synovium causing inflammation, characterized by typical symptoms of RA
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13
Q

RA effects in other parts of the body

A
  • anemia
  • neck pain
  • dry eyes and mouth
  • rarely ppl have inflammation of the blood vessels, the lining of the lungs, or the sac enclosing the heart
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14
Q

causes of RA

A
  1. genetic factors
  2. environmental factors
  3. hormonal factors
  4. state of the immune system
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15
Q

genetic factors causing RA

A

-some genes, involved in the immune system, are associated with a tendency to develop RA

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16
Q

environmental factors causing RA

A

appears that some viral or bacterial infections may trigger the disease process in people genetically susceptible to RA

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17
Q

hormonal factors causing RA

A

women are more likely to develop RA than men, pregnancy may improve the disease and RA may flare after a pregnancy

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18
Q

how can the state of the immune system cause RA

A

interleukin 12 and tumor necrosis factor-alpha may contribute to RA development

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19
Q

how can RA be diagnosed

A
  • difficult to diagnose in its early stages

- no single test for the disease, symptoms and their severity differ form person to person

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20
Q

how can laboratory test diagnose RA

A
  • Rheumatoid factor, antibody present in the blood of most people with RA: not all people with RA test positive for rheumatoid factor, especially early in the disease
  • some people test positive for R factor, yet never develop the disease
  • WBC count, C-reactive protein
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21
Q

clinical features of RA

A
  • tender, warm, swollen joints
  • symmetrical pattern of the affected joints
  • joint inflammation often affecting the wrist and finger joints closest to the hand
  • joint inflammation sometimes affecting other joints (eg. neck, shoulder, elbow, hips, knees, ankles, feet)
  • fatigue, occasional fevers, a general sense of not feeling well
  • pain and stiffness lasting for more than 30 mins in the morning or after a long rest
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22
Q

how long do RA symptoms last for

A

many years

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23
Q

what are the 2 primary objectives of treating inflammatory diseases

A
  1. relief of pain

2. relief of inflammation

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24
Q

what drugs are used to treat RA

A
  1. NSAIDs

2. Glucocortiocids

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25
Q

properties of NSAIDs

A

-have antinociceptive and anti-inflammatory properties

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26
Q

NSAIDs are useful in treating

A

acute and chronic pain

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27
Q

properties of glucocorticoids

A
  • have significant anti-inflammatory properties

- useful for the treatment of acute RA episodes

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28
Q

glucocorticoids have limited use as

A

chronic administration associated with serious toxicity

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29
Q

function of disease-modifying antirheumatic drugs (DMARDs)

A

slowing and stopping the tissue damage process

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30
Q

function of DMARDs in treating RA

A
  • slow rate of RA associated bone damage

* acts upon basic aspects of the immune response

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31
Q

what is the downfall of DMARDs

A

have significant side effects

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32
Q

most RA patients are treated with

A

-salicylates and other related agents having anti-inflammatory, analgesic and antipyretic effects

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33
Q

pain intensity of RA is related to what

A

the severity of the inflammation

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34
Q

what may be more effective in reducing or preventing joint damage

A

-treating RA with more powerful drugs and the use of drug combinations instead of one medication alone

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35
Q

NSAIDs are effective in treating

A
  • RA
  • seronegative sponduloarthropathies (eg. psoriasis arthritis)
  • osteoarthritis
  • localized musculoskeletal syndromes
  • gout
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36
Q

look at the COX-1 and COX-2 inhibitors slide 12

A

look at the COX-1 and COX-2 inhibitors slide 12

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37
Q

aspirin and select NSAIDs all have

A

-antipyretic, analgesic & anti-inflammatory properties

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38
Q

anti-inflammatory activity mediated mainly through the inhibition of

A

prostaglandin synthesis

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39
Q

when are NSAIDs found in the synovial fluid

A

after repeated dosing

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40
Q

what are the anti-inflammatory effects of aspirin

A
  • nonselective

- irreversible COX-1 and COX-2 inhibitor

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41
Q

what are the analgesic effects of aspirin

A

decreases mild to moderate intensity pain due to its anti-inflammatory effects and its probably inhibition of pain stimuli at a subcortical site

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42
Q

antipyretic effects of aspirin reduces fever though

A

COX inhibition in the CNS as well as blocking release of interleukin-1 from macrophages

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43
Q

aspirin also inhibits aggregation of

A

platelets

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44
Q

see brand names of aspirin slide 15

A

see brand names of aspirin slide 15

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45
Q

see combinations of aspiring slide 16 + 17

A

see combinations of aspiring slide 16 + 17

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46
Q

other possible NSAIDS mechanism of actin include

A
  • inhibition of chemotaxis
  • down regulation of interleukin-1 production
  • decreased production of free radicals and superoxide
  • interference with calcium mediated-mediated intracellular events
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47
Q

cylooxigenase-2 selective inhibitors (COXIBS) were developed to

A

inhibit prostalgandin synthesis by COX-2 isoenzyme induced at sites of inflammation, without affecting the constitutively active housekeeping COX-1 isoenzyme found in the GI tract, kidneys and platelets

48
Q

COXIBS bind to and block the active site of

A

COX-2 enzyme much more effectively than that of COX-1

49
Q

COX-2 inhibitors do not have a significant effect on

A
  • platelet aggregation, which is mediated by the COX-1 enzyme
  • do not offer aspirin cardioprotective effects
50
Q

where is COX-2 is constitutively active

A

kidneys

51
Q

COX-2 inhibitors produce – toxicities

A

renal toxicities similar to traditional NSAIDs

52
Q

why do COX-2 inhibitors have a limited use

A

-bc have a higher incidence of cardiovascular thrombotic effects resulting from the use of COX-2 inhibitors

53
Q

glucocorticoids are used in –% of RA patients

A

60-70%

54
Q

function of glucocorticoids in RA patients

A

rapid and dramatic effects, capable of slowing the appearance of new bone erosions

55
Q

prolonged use of glucocorticoids results in

A

serious toxic effects

56
Q

what is the primary function of NSAIDs

A
  • offer mainly symptomatic relief

- have little effect on the progression of bone and cartilage destruction

57
Q

DMARDs are used to

A

arrest or slow RA progression by modifying the disease itself

58
Q

DMARDs are – acting

A

slow acting and their beneficial effects may take 6 weeks to 6 months to become evident

59
Q

name 4 DMARDs

A
  1. methotrexate
  2. cyclosporine
  3. Azathioprine
  4. Sulfasalazine
60
Q

what DMARDs is the choice in RA treatment

A

methotrexate

61
Q

mechanism of action of methotrexate

A
  • inhibits aminoimidazolecarboxamide (AICAR) ribnucleotide transformylase and thymidalate synthetase thus decreasing polymorphonuclear chemotaxis
  • decreasing lymphocyte and macrophage function
62
Q

how is methotrexate absorbed

A

-from GI, hydroxulated, and both parent drug and metabolite intracellularly polyglutamated where they remain for prolong periods

63
Q

what is the plasma half life of methotrexate

A

6-9 hr which may go up to 24 hrs in some patients

64
Q

methotrexate decreases the rate of appearance of

A

new erosions, and is effective to treat juvenile chronic arthritis

65
Q

methotrexate also used to treat

A
  • psoriatic arthritis
  • psoriasis
  • systemic lupus erythematosus
66
Q

what are the side effects of methotrexate

A

nausea and mucosal ulcers are the common toxicities

-may cause cirrhosis

67
Q

-reports of “hypersensitivity” lung reaction or RA is characterized by

A

-shortness of breath, as well as pseudolymphomatus rxn

68
Q

what supplement is recommended to reduce GI and liver side effects of methotrexate

A

folic acid

69
Q

what are contraindications for using methotrexate

A

pregnancy

70
Q

mechanism of action of cyclosporine

A

inhibits synthesis of interleukin 1 and 2 receptors through gene transcription regulation

71
Q

cyclosporine results in decreased

A
  • macrophage T-cell interaction and T cell responsiveness

- affects T-cell dependent B cell function

72
Q

why is cyclosporine involved in a # of drug interactions

A
  • incomplete GI absorption

- metabolized by the liver P450 CYP3A

73
Q

what drugs can cyclosporine interact with

A

potassium-sparing diuretics

74
Q

FDA approved cyclosporine for the treatment of

A

RA; shown to delay new bony erosions

75
Q

cyclosporine use is limited by

A

serious toxicity including nephro- and liver effects, hypertension, hirsutism, etc.

76
Q

what is Azathioprine

A

a prodrug that is converted to its active metabolite 6-thioguanine

77
Q

mechanism of action of Azathioprine

A

inhibits inosinic acid synthesis, as well as B and T cell function

78
Q

FDA approved Azathioprine for use in the treatment of

A

RA

79
Q

what are serious adverse effects of Azathioprine

A
  • bone marrow suppression

- GI alterations

80
Q

metabolism to 6-thioguanine is

A

bimodal

-slower metabolizers accumulate azthioprine, are at high risk of developing symptoms of myelosuppression

81
Q

sulfasalazine is effective in treating

A

RA and juvenile chronic arthritis

82
Q

sulfasalazine is metabolized by

A

bacteria in the bowel to sulfapyridine and 5-aminosalicylic acid which appears to be active agent in the treatment of RA

83
Q

mechanism of action of sulfasalazine

A

-modify various immune response in RA patients (decreases production of IgA and IgM rheumatoid factors

84
Q

what are the serious side effects of sulfasalazine

A

GI alterations

neutropenia

85
Q

what are the tissue necrosis factor-alpha (TNF-A) Blocking Agents

A

Adalimumab
Infliximab
Etanercept
Leflunomide

86
Q

what is Adalimumab

A

-recombinant human anti-TNF monoclonal antibody

87
Q

what is infliximab

A

similar to adalimunab

88
Q

etanercept interacts with

A

TNF-a mediated process

89
Q

leflunomide interacts with

A

TNF-a mediated processes

90
Q

cytokines play a critcal role in the immune response and in

A

RA

91
Q

what factor appears to play a crucial role in the etiology of the inflammatory process

A

TNF-a

92
Q

what does TNF-a modulate

A

cellular functions by activating specific TNFR1 and 2 membrane bound receptors

93
Q

administration of soluble TNF receptors may combine with

A

soluble TNF, this inhibiting its effect

94
Q

monoclonal aniTNF antibody inhibits

A

T cell and macrophage function

95
Q

see diagrams 33-34

A

see diagrams 33-34

96
Q

in RA where are cytokines expressed

A

in the joints of patients

97
Q

what are cytokines

A

are a category of signalling proteins and glycoproteins that, like hormones and neurotransmitters are used extensively in cellular communication

98
Q

what is Adalimumab

A

fully human IgG1 anti-TNF monoclonal Ab

99
Q

Adalimumab is FDA approved to treat

A

RA, psoriatic arthritis and ankylosing spondylitis

100
Q

Adalimumab given subcutaneous forms a complex with

A

soluble TNF preventing its interaction with p55 and p75 cell surface receptors, thus down-regulating macrophage and T cell function

101
Q

methotrexate decreases the clearance of Adalimumab by

A

?40%

102
Q

function of Adalimumab

A

decreases ne bone erosion formation rate when used either as monotherapy or in combination with other DMARDS

103
Q

what are the adverse effects of Adalimumab

A
  • increases the risk of macrophage-dependent infection (including TB and other opportunistic infections)
  • vasculitis
  • leukopenias
  • evaluate for TB
104
Q

what is infliximab

A

chimeric IgG1 monoclonal Ab, binds to soluble and possibly membrane bound TNF-a

105
Q

mechanism of action of infliximab

A

similar to Adalimumab

106
Q

infliximab used to treat

A

RA

inflammatory diseases

107
Q

what combination simprove drug effectiveness of Infliximab

A
  • methotrexate, DMARDS
108
Q

use of Infliximab is limited by

A

toxic side effects

109
Q

contraindications of using Infliximab

A

latent or active tuberculosis

-this drug is a potent macrophage inhibitor, may activate latent TB

110
Q

Etanercept is used for

A
  1. surgery
  2. joint replacement
  3. tendon reconstruction
  4. synovectomy
111
Q

purpose of surgery

A
  • reduce pain

- improve the affected joint’s function and patients ability to perform daily activities

112
Q

purpose joint replacement

A
  • most frequently performed surgery for RA
  • artificial joints not always permanent and may have to be replaced
  • important for young ppl
113
Q

purpose of tendon reconstruction

A

used most frequently on the hands, reconstructs the damaged tendon by attaching an intact tendon to it
-can help to restore hand function

114
Q

function of synovectomy

A

-the inflamed synovial tissue is actually removed

115
Q

routine monitoring and ongoing care monitors

A
  • the course of the disease

- determines the effectiveness and any negative effects of medications, and changes therapies as needed

116
Q

what are alternative and complementary therapies for treating RA

A
  • special diets

- vitamin supplements

117
Q

see health behaviour change slide 42

A

see health behaviour change slide 42

Pharmacology (23 decks)

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