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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
What condition does the release of the pro-inflammatory cytokines IL1,6,23 cause?
ankylosing spondylitis- chronic inflammatory disease of axial skeleton
26
What conditions does the release of pro-inflammatory cytokines IL17,22 cause?
IBD (ulcerative colitis)
27
What are the 2 systemic effects in RA caused by the activation of Th17 activation in the lamina propria of the gut?
1. IBD | 2. ankylosing spondylitis
28
Other than to treat RA what can sulfasalazine be used for?
antibioitic
29
what is sulfasalzine comprised of?
sulfapyridine + salicylate with azo bond
30
HYDROCHLOROQUINE 1. MOA 2. dosage 3. administration 4. Side effects 5. Time before benefits seen
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
What is the function of Toll 9 an which drug is thought to block its action?
Hydrochloroquine -toll like receptor 9 - recg DNA containing immune complexes- decreases act. of dendritic cells - present antigens to B cells - make autoantibody
32
What can hydrochloroquine be used to treat other than RA?
anti-malarial
33
LEFLUNOMIDE 1. MOA 2. dosage 3. administration 4. Side effects 5. Time before benefits seenWhat can hydrochloroquine be used to treat other than RA?
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
Under what circumstances would Leflunomide be used?
if methotrexate can not be tolerated -pregnancy + comorbitidies
35
AZATHIOPRINE 1. use 2. MOA 3. in combination with
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
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?
1. prevents inflammation at MCP 2. 50mg 3. injection 1 weekly (NOT ORAL) 4. painful + granulation/cysts surrounding injection 5. 4-6mnths
37
What are the 2 main disadvantages with using traditional DMARDs?
1. slow acting - 1 weekly | 2. target immune cells - immunosuppresion- monitor for infection (TB) + malignancy (skin cancer)
38
What is the effect of using traditional DMARDs on the production of pro-infl cytokines?
- 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
Which DMARDs target both T+ B cells?
MTX + LEF
40
Which DMARDs target both APC + T cells?
SSZ + Gold
41
Which DMARDs only targets APC?
Anti-malarials
42
What are the 5 possible targets for biological DMARDs?
1. TNFα 2. IL6 3. IL1 4. T cell 5. B cell
43
What are the most popular biological DMARDs?
TNFα blockers | ETANERECEPT + INFLIXAMAB + ADALIMUMAB
44
ETANERCEPT - define - components - dosage - administration - time for effect
- FUSION PROTEIN - TNF receptor 2 + Fc human IgI - 50mg weekly - SC - 1-4wks *OLDEST*
45
INFLIXIMAB - define - components - dosage - time for effect
- 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
MOA for Infliximab
- decoy for TNFα receptor | - binds to TNFα - unable to bind to receptor on synoviocyte - unable to act on joint- no inflammation
47
What can Infliximab treat other than RA?
pustular psoriasis
48
ADALIMUMAB - define - components - dosage - administration - time for effect
- monoclonal antibody - both Fc + Fv porion = HUMAN - 40mg - SC - 1-4wks *unlike inflixmab - no tolerance develops- all HUMAN*
49
Name the 3 anti-TNFα biological DMARDs
1. etanercept 2. infliximab 3. adalimumab
50
Which group of drugs are rarely used to treat RA and why?
- IL-1 blockers = ANAKINRA + RILONACEPT - daily injection - patient compliance - used to treat GOUT
51
RITUXIMAB - cell target? - what is it - dosage - administration - time for effect
- B cell - monoclonal antibody against CD20 receptor on B cell - X2 1000mg 2 wks apart - infusion - 3 months post infusion
52
What is the problem with use of Rituximab?
- depletes B cell population for 1 year (both normal + malignant)
53
ABATACEPT - cell target - what is it - dosage - administration - time for effect
- T cell | - FUSION PROTEIN -
54
MOA for Abatacept
CTLA-4 on Abatacept binds to CD28 on Tcell- prevents binding to APC - prevents activation of T cell - prevents release of inflam cytokines
55
TOCILIZUMAB - target - define - dosage - administration - use with
- IL6 receptor - HUMANISED monocloncal antibody - 8mg/kg MONTHLY - IV - MTX
56
Which 3 biological DMARDs are fusion proteins?
1. etanercept 2. rilonacept 3. abatacept *ending in CEPT = fusion protein*
57
Which 4 biological DMARDs are monoclonal antibodies?
1. rituximab 2. tocilizumab 3. adalimumab 4. inflixmab
58
MOA for Tocilizumab
binds to IL6 receptor - blocks IL6 binding to its receptor - block signalling from IL-6
59
What are the 2 advantages of using biological DMARDs over conventional DMARDs?
- faster effect | - do not damage body's immune cells - no immunosuppression
60
Gold standard for RA from biological DMARDs
TNFα blockers -less depression like symptoms

Locomotor year 2 (11 decks)

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