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Locomotor year 2 > DMARDs and Rheumatoid Arthritis > Flashcards

DMARDs and Rheumatoid Arthritis Flashcards

1.overview of RA 2.criteria for dignaosis of RA 3.basic management 4. NICE guidelines 5.Convential DMARDS 6.Biologicals

1
Q

prevelance

A

total NUMBER of cases of a disease in a population at a certain moment in time.

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2
Q

incidence

A

number of new cases occurring in a population over a defined time interval

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3
Q

UK prevelance of RA

A

400,000

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4
Q

UK incidence of RA

A

12,000

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5
Q

what areas of body are affected in RA? (reason it is more serious than OA)

A
  1. small joints of hands + feet = carpals + MCP + MTP
  2. tendon sheaths
  3. systemic inflammation - heart, lungs, kidneys, skin
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6
Q

which joint in the hand is usually spared in RA?

A

DIP (distal interphalangial) joint

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7
Q

Does RA present symmetrically or asymmetrically + why ?

A

RA- symmetrical - autoimuune disease - inflammation - occurs on BOTH sides of the body

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8
Q

why is treatment for RA agressive?

A

severity of symptoms if left untreated:

  1. hands + feet severly deformed
  2. systemic effect - IHD, CKD
  3. larger joints affected - shoulder, hips, knees
  4. premature mortality
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9
Q

4 diagnositic features for RA?

A
  1. affects small joints
  2. pain >6wks
  3. symmetrical
  4. seropostive for RF
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10
Q

What score for 2010 ACR/EULAR criteria qualifies RA diagnosis?

A

score ≥ 6/10

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11
Q

What is the aim of RA treatment?

A
  1. prevent sever joint deformity (slow progression of disease)
  2. prevent flare ups
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12
Q

What are the 2 types of drugs invovled in management of RA?

A
  1. DMARDs - disease modifying anti rheumatics
  2. Pain relief
    • analgesics= NSAIDs, corticosteroids
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13
Q

Management of newly diagnosised RA

A

NICE guidelines - high dosage DMARD combination therapy (symptoms >3mths)

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14
Q

What is the significance of having aggreesvie high dosage DMARD intially?

A
  • controls RA + prevent progression
  • 5yr- no DMARD = 60% patients = severe joint deformity
    - DMARD =<10% patients = severe joint deformity

(observable on X-ray - bone erosion + joint instability)

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15
Q

What is the management of RA if DMARDs combmination theraphy is not tolerated?

A

DMARD monotheraphy

cases - comorbidities + pregnancy (avoid MTX)

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16
Q

What are the 2 groups of DMARDs

A
  1. conventential

2. biologicals

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17
Q

List the 6 convential DMARDs

A
  1. methotrexate (MTX)
  2. leflunomide
  3. hydrochoroquine
  4. sulfasalazine
  5. azathioprine
  6. gold salts
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18
Q

Gold standard for RA from conventential DMARDs

A

methotroxate

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19
Q

METHOTREXATE (MTX)

  1. MOA
  2. dosage
  3. administration
  4. Side effects
  5. Time before benefits seen
A
  1. folic acid antagonist in ALL ACTIVELY DIVIDING cells
  2. 2.5mg tablets (intially 5-10mg) 1.pw
  3. oral /SC or IM injection
  4. affects haemtopoesis + liver function - affects all actively dividng cells - bone marrow + liver
  5. 3-12 wks
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20
Q

Describe MOA of methotrexate

hint-slide 8

A
  1. enters cell via A.T through folic acid transporter
  2. glutamination of MTX
  3. directly inhibits DIHYDROFOLATE REDUCTASE- prevents formation: dihydrofolic acid - tetrahydrofolic acid - block purine biodynthesis - blocks RNA synthesis
  4. indirectly inhibits THYMIDYLATE SYNTHESASE -blocks DNA synthesis
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21
Q

What treatment is methotrexate also involved in?

A
  1. chemotherapy

2. abortions

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22
Q

SULFASALAZINE

  • special use*
    1. MOA
    2. dosage
    3. administration
    4. Side effects
    5. Time before benefits seen
A
  • special use* - treat systemic effects of RA
    1. remains in L.I - metabolism to 5ASA -treats ULCERATIVE COLITIS
    2. 500mg daily
    3. oral- tablet
    4. haemolytic anaemia
    5. 12 wks
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23
Q

Why does sulfasalazine remain in the large intestine?

A

metabolite 5ASA (5-aminosalicylic acid) =poorly absorbed into bloodstream

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24
Q

Activation of which Th cell causes the release of pro-inflammatory cytokines?

A

Th17 in lamina propria

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25
Q

What condition does the release of the pro-inflammatory cytokines IL1,6,23 cause?

A

ankylosing spondylitis- chronic inflammatory disease of axial skeleton

26
Q

What conditions does the release of pro-inflammatory cytokines IL17,22 cause?

A

IBD (ulcerative colitis)

27
Q

What are the 2 systemic effects in RA caused by the activation of Th17 activation in the lamina propria of the gut?

A
  1. IBD

2. ankylosing spondylitis

28
Q

Other than to treat RA what can sulfasalazine be used for?

A

antibioitic

29
Q

what is sulfasalzine comprised of?

A

sulfapyridine + salicylate with azo bond

30
Q

HYDROCHLOROQUINE

  1. MOA
  2. dosage
  3. administration
  4. Side effects
  5. Time before benefits seen
A

1.

  • acc in lysosomes - acidic- prevents protein modifications- decreases proteolyitc enzymes- in synovcytes type B
  • blocks Toll like receptor 9
    2. 400mg daily
    3. ORAL
    4. psoriatic rash + skin plaques
    5. 12wks for benefit
31
Q

What is the function of Toll 9 an which drug is thought to block its action?

A

Hydrochloroquine
-toll like receptor 9 - recg DNA containing immune complexes- decreases act. of dendritic cells - present antigens to B cells - make autoantibody

32
Q

What can hydrochloroquine be used to treat other than RA?

A

anti-malarial

33
Q

LEFLUNOMIDE

  1. MOA
  2. dosage
  3. administration
  4. Side effects
  5. Time before benefits seenWhat can hydrochloroquine be used to treat other than RA?
A
  1. inhibits DIHYDROOROTATE DEHYDROGENASE - inhibits PRYADMIDINE BIOSYNTHESIS - blocks DNA + RNA synthesis
  2. 10-20mg daily
  3. oral
  4. liver damage, lung disease, immunosuppression, diarrhoea, hair loss
  5. 12wks
34
Q

Under what circumstances would Leflunomide be used?

A

if methotrexate can not be tolerated -pregnancy + comorbitidies

35
Q

AZATHIOPRINE

  1. use
  2. MOA
  3. in combination with
A
  1. immunosuppression (see transplantation - to prevent rejection)
  2. interferes with purine synthesis - DNA synthesis
  3. prednisolone - can use smaller dose (if used with AZT)
36
Q

GOLD SALTS

  1. MOA
  2. dosage
  3. administration
  4. Side effects
  5. Time before benefits seenWhat can hydrochloroquine be used to treat other than RA?
A
  1. prevents inflammation at MCP
  2. 50mg
  3. injection 1 weekly (NOT ORAL)
  4. painful + granulation/cysts surrounding injection
  5. 4-6mnths
37
Q

What are the 2 main disadvantages with using traditional DMARDs?

A
  1. slow acting - 1 weekly

2. target immune cells - immunosuppresion- monitor for infection (TB) + malignancy (skin cancer)

38
Q

What is the effect of using traditional DMARDs on the production of pro-infl cytokines?

A
  • target immune cells: APC, T cell, B cell
  • prevent active division
  • decrease production of pro-infl cytokines
  • decrease synovial inflammation, systemic inflammation, destructive changes
39
Q

Which DMARDs target both T+ B cells?

A

MTX + LEF

40
Q

Which DMARDs target both APC + T cells?

A

SSZ + Gold

41
Q

Which DMARDs only targets APC?

A

Anti-malarials

42
Q

What are the 5 possible targets for biological DMARDs?

A
  1. TNFα
  2. IL6
  3. IL1
  4. T cell
  5. B cell
43
Q

What are the most popular biological DMARDs?

A

TNFα blockers

ETANERECEPT + INFLIXAMAB + ADALIMUMAB

44
Q

ETANERCEPT

  • define
  • components
  • dosage
  • administration
  • time for effect
A
  • FUSION PROTEIN
  • TNF receptor 2 + Fc human IgI
  • 50mg weekly
  • SC
  • 1-4wks

OLDEST

45
Q

INFLIXIMAB

  • define
  • components
  • dosage
  • time for effect
A
  • monoclonal antibody against TNFα
  • IgI + mouse Fv
  • 3mg/kg 2-3hrs in 2-6hr duration
  • INFUSION
  • days

tolerance- create antibody’s to foreign mouse part of drug

46
Q

MOA for Infliximab

A
  • decoy for TNFα receptor

- binds to TNFα - unable to bind to receptor on synoviocyte - unable to act on joint- no inflammation

47
Q

What can Infliximab treat other than RA?

A

pustular psoriasis

48
Q

ADALIMUMAB

  • define
  • components
  • dosage
  • administration
  • time for effect
A
  • monoclonal antibody
  • both Fc + Fv porion = HUMAN
  • 40mg
  • SC
  • 1-4wks

unlike inflixmab - no tolerance develops- all HUMAN

49
Q

Name the 3 anti-TNFα biological DMARDs

A
  1. etanercept
  2. infliximab
  3. adalimumab
50
Q

Which group of drugs are rarely used to treat RA and why?

A
  • IL-1 blockers = ANAKINRA + RILONACEPT
  • daily injection - patient compliance
  • used to treat GOUT
51
Q

RITUXIMAB

  • cell target?
  • what is it
  • dosage
  • administration
  • time for effect
A
  • B cell
  • monoclonal antibody against CD20 receptor on B cell
  • X2 1000mg 2 wks apart
  • infusion
  • 3 months post infusion
52
Q

What is the problem with use of Rituximab?

A
  • depletes B cell population for 1 year (both normal + malignant)
53
Q

ABATACEPT

  • cell target
  • what is it
  • dosage
  • administration
  • time for effect
A
  • T cell

- FUSION PROTEIN -

54
Q

MOA for Abatacept

A

CTLA-4 on Abatacept binds to CD28 on Tcell- prevents binding to APC - prevents activation of T cell - prevents release of inflam cytokines

55
Q

TOCILIZUMAB

  • target
  • define
  • dosage
  • administration
  • use with
A
  • IL6 receptor
  • HUMANISED monocloncal antibody
  • 8mg/kg MONTHLY
  • IV
  • MTX
56
Q

Which 3 biological DMARDs are fusion proteins?

A
  1. etanercept
  2. rilonacept
  3. abatacept

ending in CEPT = fusion protein

57
Q

Which 4 biological DMARDs are monoclonal antibodies?

A
  1. rituximab
  2. tocilizumab
  3. adalimumab
  4. inflixmab
58
Q

MOA for Tocilizumab

A

binds to IL6 receptor - blocks IL6 binding to its receptor - block signalling from IL-6

59
Q

What are the 2 advantages of using biological DMARDs over conventional DMARDs?

A
  • faster effect

- do not damage body’s immune cells - no immunosuppression

60
Q

Gold standard for RA from biological DMARDs

A

TNFα blockers -less depression like symptoms

Locomotor year 2 (11 decks)

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