Pharma in rheumatic disease Flashcards

1
Q

2 mechs in NSAIDs

A
COX-1 
- prostaglandins for mucosal protection
- thromboxane for hemostatis
COX-2 
- prostaglndins for pain and inflammation
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2
Q

4 As of NSAID effects

A

Anti-inflamm
Analgesic
Antipyretic
Antiplatelet

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3
Q

5 things that differentaite NSAIDs

A
  1. cost - COX2 is expensive
  2. antiplatelet effect - ASA more than others
  3. Duration of action
  4. Route - most oral
  5. GI tolerance - unpredicatable
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4
Q

6 adverse effects of all NSAIDs

A
  1. bleeds - ASA most
  2. interference with renal funct
  3. Na retention
  4. dyspep and ulceration
  5. inhib. uterine motility
  6. allergic hypersens. reactions
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5
Q

def. NSAID gastropathy

A

endoscopic erosions in 20-40% of ppl

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6
Q

presentation of gastropathy

A
  • none for most
  • dyspepsia
  • bleeds
  • ulcer complications
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7
Q

5 risk factors for dev. of gastropath

A
  1. > 60
  2. Hx of ulcer
  3. use of glucocorticoids
  4. high dose/ multi NSAIDs
  5. anticoag use
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8
Q

3 ways to help prevent

A
  1. rational drug choice
    - try others or COX2
  2. acid supression
  3. prostagandin E1 analog
    - misoprostol
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9
Q

5 rheum uses of NSAIDs

A
  1. acute crystalline
  2. acute.subacute polyarth
  3. alternative analgesic for non-inflammatory
  4. adjunct to DMARD in RA, SpA
  5. first line mgmt in axial SpA
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10
Q

adv. of glucocoorticoids

A

cheap and powerful

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11
Q

3 general mechs. of glucocort

A
  1. non-genomic activation
  2. DNA-dep regulation
  3. protein interference mechs.
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12
Q

3 effects of glucocort.

A
  1. inhib. leukocyte access to inflammed tissue
  2. interfere with cell processes involved in inflammation
  3. supress the production of humoral factors involved in inflamm. (cytokines etc.)
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13
Q

4 acute SE of glucos

A
  1. infection
  2. avasc. necrosis
  3. steroid psychosis
  4. steroid myopathy
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14
Q

what is effect on osteoporosis

A
  • increase rate of bone loss

- effects are dose dependent

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15
Q

2 preps of glucos

A

oral - prednisone
IV
- doses based on prednisone and need to be adjusted

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16
Q

4 steroid sparing drugs

A

(all immunosuppressive)

  1. azathioprine
  2. methotrexate
  3. mycophenolate
  4. cyclophosphamide
17
Q

2 general goals of gout treatment

A
  1. treat acute flares

2. prevent recurrent disease

18
Q

how to reduce gout inflamm

A
  1. NSAIDS
  2. local injections
  3. RICE
19
Q

specific drug for gout flares

A

colchicine - dirputs chemotaxis + phag of urate by neutrophils

20
Q

cautions for colchicine

A
  1. toxicities

2. not well eliminated in people with renal disease

21
Q

when to use

A

within 24 hours of attack

22
Q

3 ways to prevent gout

A
  1. diet - esp alc
  2. avoid drugs that increase (ASA, diuetics)
  3. urate lowering therapy
23
Q

2 types of urate lowering therapy

A
  1. increase excretion of uric acid

2. block xanthine oxidase (allopurinol)

24
Q

SE of allopurinol

A
  1. flare of gout
  2. rash
  3. interstitial nephritis
25
mgmt of pseudo gout
1. same as gout | - no use of allpurinol or colchicine
26
key to mgmt of RA
DMARDs used early in disease
27
3 key DMARDs
1. methotrexate 2. sulfasalazine 3. leflunomide - all require regular monitoring
28
what are biologics
monoclonal ABs that target cytokines and immune cell surface receptors
29
3 keys mechanisms targeted by biologics
1. TNF 2. RF and other ABs from B-cells 3. block co-stim from T-cells
30
MOA of small molecule therapy
blocks pathway within T-cells that create pro-inflamm. molecules
31
3 major AE of biologics
1. immunosupresive 2. reactivation of latent TB 3. reactivation of hep B
32
mgmt of peripheral SpA (3)
1. DMARDs 2. biologics 3. NSAIDs
33
mgmt of axial SpA
1, NSAIDs | 2. anti-TNF
34
see treatment algorithms
yes