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Junior - Pharm II - 1 > 5 - Arthritis And Gout > Flashcards

5 - Arthritis And Gout Flashcards

1
Q

Herbenden Nodes, PIP’s and DIP’s affected, think:

A

Osteoarthritis

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2
Q

APAP - MOA (for OA):

A

No significant anti-inflammatory effect

Acts centrally as an analgesic and antipyretic

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3
Q

APAP - clinical use in OA:

A

1st line for pain management of OA

Efficacy - similar pain relief to NSAID, less ADR’s

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4
Q

NSAID’s - clinical use in OA:

A

Anti-inflammatory and analgesic

Lower doses for analgesia, higher doses for inflammation

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5
Q

Topical NSAID’s for OA - who uses it

A

Knee-only arthritis

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6
Q

What is Diclofenac Gel 1%?

A

Topical NSAID for knee or hand osteoarthritis

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7
Q

Topical Salicylates (Bengay, Adpercreme, etc) for OA - MOA?

A

Local inhibition of COX-2 enzymes

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8
Q

Capsaicin in OA - MOA?

A

Releases and immediately depletes substance P from afferent nociceptive nerve fibers

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9
Q

Caspaicin - clinical use:

A

Muscle/joint pain

Neuropathic pain associated with diabetes or postherpatic neuralgia

Must use regularly 4x a day for maximum effect

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10
Q

Intra-articular corticosteroids - MOA:

A

decreases inflammation by suppression of

migration of polymorphonuclear leukocytes and reversal of increased capillary permeability

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11
Q

Intra-articular corticosteroids - clinical use:

A

OA/RA

Not to exceed 3 to 4 injections per year (significant degradation of cartilage)

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12
Q

Hyaluronate Injections - proposed MOA:

A

Hyaluronic acid is a viscous substance in synovial fluid that lubricates the joint

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13
Q

Hyaluronic injection - clinical use:

A

Not generally recommended

May try in patients who fail other therapies

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14
Q

Opioids for OA - for pt’s who:

A

Get no relief from APAP, NSAID’s, or topical therapy

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15
Q

Tramadol (Ultram) C-IV - MOA:

A

Partial Mu receptor agonist

Serotonin and norepinephrine reuptake inhibitor

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16
Q

Tramadol - clinical use in OA:

A

Moderate to severe pain that is not controlled by NSAID’s or APAP

Pt’s who can’t take NSAIDS

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17
Q

Tramadol - AE’s

A

Increased risk of serotonin syndrome

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18
Q

What labs tests will be positive in RA?

A

Rheumatoid factor (RF)
Elevated C-reactive protein (CRP)
Elevated erythrocyte sedimentation rate (ESR)

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19
Q

NSAID’s - use in RA?

A

Immediate relief of pain and inflammation

Preferred as ADJUNCT to DMARDs while they start to kick in

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20
Q

Preferred NSAID’s for RA:

A

Ibuprofen
Meloxicam
Nabumetone
Naproxen

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21
Q

Corticosteroids for RA?

A

Methylprednisolone IV
Prednisolone PO
Prednisone PO

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22
Q

What are DMARDs?

A

Disease-Modifying Anti-Rheumatic Drugs

Takes weeks to months to see full benefit

Screen pt’s for Hep B/C and TB prior to starting therapy

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23
Q

What are the four traditional DMARDs?

A

Methotrexate
Leflunomide
Hydroxychloroquine
Sulfasalazine

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24
Q

What is the preferred DMARD to start with according to ACR?

A

Methotrexate

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25
Q

Methotrexate - MOA?

A

Dihydrofolate reductase inhibitor

Interferes with DNA synthesis

Inhibits fast-growing cells

Leads to anti-inflammatory and, unfortunately, IMMUNOSUPPRESSIVE effects

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26
Q

Methotrexate - clinical use:

A

Preferred DMARD for RA tx

Also tx’s joint symptoms of psoriatic arthritis

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27
Q

Methotrexate - AE’s?

A

GI

Leukopenia (keep an eye on CBC, platelets), hepatic cirrhosis (keep an eye on AST/ALT)

28
Q

Methotrexate - pregnancy cat?

29
Q

What is the methotrexate toxicity reversal agent?

A

Leucovorin (supplies the necessary cofactor blocked by methotrexate)

30
Q

Leflunomide - MOA:

A

PRODRUG

Inhibits pyrimidine synthesis

Antiproliferative, anti-inflammatory

31
Q

Leflunomide - pharmacokinetics:

A

Detectable levels 2 years after stopping medication

If you need to rapidly clear the drug you can use CHOLESTYRAMINE

32
Q

Leflunomide - AE’s?

A

Severe liver injury

Peripheral neuropathy

33
Q

Leflunomide - pregnancy cat?

34
Q

Hydroxychloroquine - MOA:

A

Inhibits locomotion of neutrophils chemotaxis of eosinophils

35
Q

Hydroxychloroquine - clinical use:

A

Anti-malarial (only labelled use)

RA and SLE (off-label)

36
Q

Sulfasalazine - MOA:

A

PRODRUG

Cleaved by bacteria in the colon and 5-aminosalicylic acid

Decreased production of IgA and IgM

37
Q

Sulfasalazine - clinical use:

A

Used for mild RA

Not as effective as methotrexate

Also used for ulcerative colitis

38
Q

Sulfasalazine - drug interactions

A

ABX can cause decreased absorption

Sulfasalzine binds iron in the GI tract

Can displace warfarin

39
Q

All biologic DMARD’s can increase risk of:

40
Q

Black box warning for biologic DMARD’s:

A

All anti-TNF-alpha can cause increased lymphoproliferative cancers in peds and adults

41
Q

Etanercept typically for pt’s who:

A

Have failed methotrexate

42
Q

MOA for biologic DMARD’s:

A

Block the pro-inflammatory cytokines TNFa, interleukin, or bind on target receptors on T-cells to prevent the co-stimulation needed to fully activate T-cells

43
Q

Predisposing factors for gout:

A
  1. Diet - meat, fatty food, alcohol, high-fructose

2. Medical - DM, HTN, HLP

44
Q

What is the serum urate target in tx of gout:

45
Q

Non-pharm management of gout:

A 
Weight loss
Healthy diet
Exercise
Smoking cessation
Adequate hydration
46
Q

3 primary classes of meds for acute gout:

A

NSAID’s
Colchicine
Glucocorticoids

47
Q

What are the three primary med classes for urate-lowering (chronic suppression):

A
  1. Xanthine Oxidase Inhibitors
  2. Uricosuric agents
  3. Uricase
48
Q

Most appropriate first-line drugs for acute gout attack?

A

NSAID’s and Colchicine

49
Q

Colchicine only if initiated within ___ hours of attack onset

50
Q

NSAID’s plus corticosteroids are NOT recommended in acute gout due to:

A

GI ADE’s

51
Q

Which NSAID’S are FDA approved for gout?

A

Naproxen
Indomethacin
Sulindac

52
Q

Colchicine - MOA:

A

Binds to intracellular protein tubulin; prevents activation, degranulation, and migration of neutrophils associated with mediating some gout symptoms

53
Q

Colchicine - clinical use:

A

Treatment of gout flares

Prophylaxis of gout flares

54
Q

Colchicine - drug interactions?

A

Significant - CYP3A4

55
Q

Urate-Lowering Therapy (ULT) - clinical use:

A

Chronic management of hyperuricemia

Tophi present

Two or more attacks per year

CKD

Past urolithiasis

56
Q

What is the first-line ULT?

A

Xanthine Oxidase Inhibitor - Allopurinol or Febuxostat

57
Q

XOI - MOA:

A

Inhibits uric acid synthesis by inhibiting xanthine oxidase (therefore no conversion to uric acid)

58
Q

Which XOI has a higher risk of thromboembolic events?

A

Febuxostat

59
Q

Uricosuric Agents - MOA:

A

Weak organic acids that promote renal clearance of uric acid by inhibiting proximal tubule urate-anion exchangers that mediate urate reabsorption

In english -> stop reabsorption of urate

60
Q

What type of meds are Probenecid and Lesinurad?

A

Uricosuric Agents

61
Q

What type of meds of Pegloticase and Rasburicase?

62
Q

Uricase - MOA:

A

It’s an enzyme that humans don’t normally have

Lowers serum uric acid

63
Q

Clinical use of uricase:

A

Severe gout disease refractory to traditional ULT’s

64
Q

What can uricase exacerbate?

65
Q

What is uricase contraindicated in?

A

G6PD deficiency

Junior - Pharm II - 1 (6 decks)

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