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Flashcards in Arthritis Deck (129):
1

Non-drug therapy for OA

- Rest
- PT
- ROM
- Muscle strengthening
- Assistive devices
- weight loss

2

What is the goal of OA drug therapy

- relieve pain and inflammation
- only treats sxs

3

What does drug therapy for OA NOT do

- It does not prevent the progression of OA

4

List of 8 analgesics to treat OA

- Oral acetaminophen (APAP)
- Oral NSAIDs
- topical capsaicin
- topical NSAIDs
- glucosamine/chondroitin
- intra articular injections (corticosteroids, viscosupplementation)
- opioids
- tramadol

5

How does acetaminophen treat OA

- used routinely to reduce pain
- does not decrease inflammation (NSAIDs may be better for treating NSAIDs)

6

What is the max dose of acetaminophen (APAP)

3g/day

7

what do you need to monitor with acetaminophen (APAP)

Liver and renal toxicity

8

How do NSAIDs treat OA

- Non selective NSAIDs equally effective as COX-2 specific inhibitors
- Analgesic effect at lower doses
- Anti inflammatory effect at higher doses
- Affects platelet fxn - reversible
- may take up to 2 weeks to feel effects

9

What to monitor for NSAIDS

- GI effects
-- Bleeding (CBC, stool guaiac)
- Renal toxicity
--Cr and BUN

10

How does Topical Capsaicin treat OA

- inhibits release of substance P in peripheral nerves (not present in cartilage)
- initially by sting/burn (subsides with use)

11

How long does it take for capsaicin to be effective

2-4 weeks

12

Where is the use of capsaicin most effective

-Studies show knees and hands (0.025%-0.075% cream q6)
- reduction in pain and tenderness

13

How does Glucosamine and Chontroitin treat OA

- provides materials to help rebuild cartilage

14

How long does it take for glucosamine to be effective

4-8 weeks

15

How long does it take for glucosamine to be effective

>2 weeks

16

How do Corticosteroid treat OA

- intra articular injections- short term of sxs in knee

17

How often and how long can corticosteroids treat OA

- injections q3 months x 3 years
- limit injections to no more than 3-4 times/year

18

Can Oral corticosteroids be used to treat OA

- No
-systemic effects
- not indicated or recommended to treat OA

19

How does viscosupplementation treat OA

- AKA hyaluronic acid (HA)
- intra articular injection
- Acts as viscous lubricant
- may reduce need for NSAID

20

Opioid Analgesics and OA

- should be reserved, potential for addiction
- may be combined with acetaminophen
- use caution whn using with other APAP (max APAP 3g/day)

21

Types of Opioid Analgesics used to treat OA

- Codeine/oxycodone/hydrocodone
- Tramadol

22

How to treat Hand OA

- One or more of:
--Topical capsaicin
--Topical NSAIDs (for > 75 years, topical is preferred)
--Oral NSAIDs
--COX-2 inhibitor

23

What do you NOT use to treat hand OA

- intra articular therapies
- opioid analgesics

24

How to treat Knee OA

- APAP
- oral NSAIDs
- topical NSAIDs
- tramadol
- intra-articular corticosteroid injections

25

What do you NOT use to treat Knee OA

- intra articular hyaluronates (HA)
- Opiate analgesics

26

How to treat Hip OA

- APAP
- oral NSAIds
- Tramadol
- intra articular corticosteroid injections

27

Why can mild opiates be used to treat Hip and Knee OA

- Knee and Hip OA can be painful
- May affect functionality
- May need to step up meds to increase function

28

What should you NOT use to treat Hip OA (Recommended)

- Glucosamine and Chondroitin

29

In treating Hip OA, what meds have no recommendation one way or the other

- Topical NSAIDs
- Intra articular HA

30

Basics of RA

- chronic/systemic inflammatory disease of the joints and related structures
- high disability rate and shortened life expectancy (by 5-7 years)

31

What is the pathophys of RA

- Immune mediated inflammation
- synovium, tissues, organs affected (eyes, heart, kidneys, blood vessels, RBCs)
- Synovial tissue exceeds bounds of joint structure eroding into bone and cartilage within joint capsule ("pannus")

32

Primary goal of treatment for RA

- improve/maintain fxnl status
- improve QOL

33

Goals of therapy for RA

- relieve pain
- preserve joint fxn
- prevent or control joint destruction and systemic complications

34

Non pharmacologic treatment of RA

- rest
- OT
- PT
- assistive devices
- weight reduction/mgmt
- splinting/joint protection

*****treat RA sxs early (pharma and non-pharma)***

35

What is a DMARD

Disease Modifying Anti-Rheumatic Drugs
- Misc group of drugs that have potential to reduce or prevent joint damage
- Includes biologics (Non-TNF, anti-TNF) and non-biologics

36

When should DMARDs be started to treat RA

- within 3 months
- joint space narrowing occurs in >80% of patients within 1st 2 years
- May need to start 1 or more DMARD and see how pt is responding

37

How do you select the appropriate DMARD

- Based on patient specific issues
- not every SAARD is appropriate or safe for every pt
- Things to consider
--severity of disease
--comorbidities
--likelihood of adherence
--Convenience and acceptability
--Monitoring requirements
--ADEs
--Costs

38

What is a SAARD - used to treat RA

Slow Acting Anti-Rheumatic Drug

39

What is TNF - used to treat RA

Tumor Necrosis Factor
- type of biologic

40

List the 5 DMARD non-biologics

- Hydroxychloroquine (HCQ)
- Methotrexate (MTX)
- Sulfasalazine (SSZ)
- Leflunomide (LEF)
- Minocycline

41

What are the 2 DMARD general biologics

- Anti TNF
- non TNF

42

List the 3 Non-TNF DMARD biologics

- Abatacept
- Rituximab
- tociluzimab

43

List the 5 Anti-TNF DMARD biologics

- Etanercept
- Adalimumab
- Infliximab
- Golimumab
- Certolizumab pegol

44

What should be done if pt's RA goes into remission?

- may consider tapering DMARD
- don't discontinue all

45

What DMARD monotherapy is most common (RA)

- MTX (methotrexate)

46

Other DMARD monotherapy drugs (RA)

- SSZ (sulfasalazine)
- HCQ (hydroxychloroquine)
- LEF (leflunomide)

47

What are examples of double DMARD therapy (RA)

- MTX+SSZ - most common
- MTX+HCQ
- SSQ+HCQ
--May combo with LEF

48

What are examples of triple DMARD therapy (RA)

- MTX+SSZ+HCQ

49

High dose vs Low dose

- low dose glucocorticoid: <10mg/day of prednisone (or equiv)
- high dose glucocorticoid: >10mg/day of prednisone (or equiv)
- short term glucocorticoid < 3 month treatment

50

What kind of drug is Hydroxychloroquine (RA)

- Antimalarial
- Used for mild disease or combo
- Reserved for pts unresponsive to NSAIDS
- Weaker DMARD properties than other 1st line

51

Time of onset for Hydroxychloroquine (RA)

- Relatively fast; 2-6 months
- DC if no response in 6 months

52

How can Hydroxychloroquine treat RA

- slows progression of erosive bone lesion
- may induce remission

53

Monitoring of Hydroxychloroquine (RA)

- Minimal monitoring
- Ophthalmologic exam 2x/year for retinal toxicity
--damage is initially reversible
- DOES NOT cause liver, kidney, or bone toxicities

54

What are the ADR's of Hydroxychloroquine (RA)

- GI: N/V/D (take w/food)
- Ocular toxicity
- Derm: pruritis, rash, alopecia, increased skin pigmentation
- Neuro: HA, insomnia, vertigo

55

What are the contraindications for Hydroxychloroquine (RA)

Pt's with significant:
- visual impairment
- hepatic impairment
- renal impairment

56

What is the theory on how Methotrexate (MTX) treats RA

- act as immunosupressive and anti-inflammatory agent
- it is a folic acid antagonist

57

How is Methotrexate (MTX) used to treat RA

- monotherapy or combo therapy
- Mainstay for pts not responding to NSAIDs
- slows appearance of new erosions
- may have significant reduction in CV mortality

58

Time of onset for Methotrexate (MTX) (RA)

- 2 weeks to 2 months
- max effect within 4-8 weeks

59

What is the long-term outcome for Methotrexate (MTX) (RA)

- best long-term outcome
- less toxic and less likely to be DC'd than other DMARDs
- most effective and least expensive

60

ADEs of Methotrexate (MTX) (RA)

Many side effects even though it is the most recommended
- GI: N/V/D, stomatitis (dose related)
- Hematologic: thrombocytopenia, leukopenia (dose related)
- Pulmonary: fibrosis, pneumonitis
- Hepatic: elevated liver enzymes, cirrhosis (DC if sustained increase in LFTs)

61

Drug interactions of Methotrexate (MTX) (RA)

- NSAIDs may decrease Methotrexate clearance and increase ADEs
- If you Rx MTX, DC NSAIDs and add folic acid

62

How can you alleviate some of the ADEs of Methotrexate (MTX)

- 1mg Folic Acid/day may alleviate some of the adverse effects

63

What is the antidote for Methotrexate (MTX) toxicity

- Leucovorin (folic acid derivative)

64

What do you need to monitor for Methotrexate (RA)

Baseline monitoring
--LFTs
--CBC
--Total bilirubin
--Hep B and C
--Serum creatinine
--Serum albumin
Q 1-2 months:
--CBC
--AST
--albumin

65

MOA for Sulfasalazine (SSZ) (RA)

- Prodrug cleaved by bacteria in the colon into sulfapyradine and 5-aminosalicylic acid
- Sulfapyridine is the agent responsible for anti-rheumatic properties

66

How is sulfasalazine (SSZ) used to treat RA

- treats mild RA or in combo

67

What do you need to monitor when using sulfasalazine (SSZ) to treat RA

Baseline CBC, then q week x1 month, then q 1-2 months

68

What are the ADRs of sulfasalazine (SSZ) (RA)

GI: N/V/D (minimized by slowly titrating dose), and anorexia
CNS: HA

***Life threatening reactions have occurred, stop med and try different DMARD***IDIOPATHIC

69

MOA for Leflunomide (LEF) in treating RA

- Reversible inhibitor of DHODH
- Interferes with RNA/DNA synthesis in lymphocytes

70

How does Leflunomide (LEF) treat RA

- reduces pain/inflammation associated w/RA
- slows progression of structural damage
- Overall efficacy similar to MTX and sulfasalazine

71

What are the ADRs of leflunomide (LEF) (RA)

- HA, nausea, diarrhea, rash, alopecia
- caution w/liver disease
- biliary and renal excretion

72

What do you need to monitor when using Leflunomide (LEF) to treat RA

MONTHLY
- CBC and ALT monthly initially, then q6-8 hours

73

Leflunomide (LEF) and pregnancy

- Pregnancy category X
- not recommended with pregnancy
- cholestyramine washout prior to conception

74

MOA and uses for Enteracept in treating RA - (Anti TNF)

- Soluble TNF receptor that competitively binds 2 TNF molecules (inactivating)
- Additive effects when in combo w/Methotrexate (MTX)

75

MOA and uses for Infliximab and adalimumab in treating RA - (Anti-TNF)

- Anti TNF- alpha monoclonal antibody IgG
- Inhibits progression of structural damage
- Additive effects when in combo w/Methotrexate (MTX)
- Never prescribed by themselves

76

What do you need to monitor when using infliximab and adalimumab to treat RA

- initial tuberculin skin test
- can't use this med if pt had TB

77

ADR of infliximab (RA)

infusion related
- HA/nausea in 20%
- antihistamine may help

78

ADR of etanercept and adalimumab

Injection site reactions

79

General ADRs of anti-TNF

-Risk of worsening infectious complications
-- DC in pts w/signs of active infections
- may worsen heart failure
- Rare reports of lupus-like syndromes (hepatotoxicity, pancytopenia)
- May exacerbate previous quiescent MS

80

MOA and for Anakinra (Interleukin-1 Receptor Antagonist) for RA

- Treats moderate to severe RA
- IL-1 induced by inflammatory stimuli
- antagonist slows degredation of cartilage and bone resorption

81

How is anakinra uses to treat RA (IL-I antagonist)

- monotherapy and combo with MTX

82

ADEs of anakinra (IL-1 antagonist) (RA)

-Risk of worsening infectious complications
-- DC in pts w/signs of active infections
- may worsen heart failure
- Rare reports of lupus-like syndromes (hepatotoxicity, pancytopenia)
- May exacerbate previous quiescent MS
- SIMILAR to TNF antagonists

83

What do you need to monitor when using anakinra to treat RA

- none
- Never give TNF antagonist with anakinra

84

How is abtacept used to treat RA

- Moderate to severe RA refractory to treatment
- Use as monotherapy or combo therapy

85

MOA and drug info for abtacept for RA

- soluble fusion protein
- inhibits human cytotoxic t-lymphocyte- associated antigen 4 (CTLA-4) linked to the modified Fc portion of IgG1
- Inhibit T lymphocyte activation
- Cost 12k-24k/year

86

MOA for rituximab for RA

- depletes B lymphocytes
- reduces antibody formation

87

Uses of rituximab for RA

- Combo w/MTX in moderate to severe active RA with inadequate response to TNF antagonist
- IV infusion separated by 2 weeks,

88

MOA of Tofacitinib for RA

- Tofacitinib enzymes inhibits Janus Kinase (JAK) enzymes
- These enzymes which are intracellular enzymes in stimulating hematopoiesis and immune cell function through signaling pathway

89

When is Tofacitinib indicated for RA

- monotherapy or combined therapy with MTX or nonbiologics
- Used to treat moderate or severe RA

90

Black box warning for Tofacitinib

Infections and malignancy

91

How is Tofacitinib metabolized

- 70% hepatic, P450
- potential for drug interactions for P450 metabolism

92

Symptom relief of RA - What we'll do as providers

- NSAIDs at anti-inflammatory doses
- oral prednisone <10mg/day can help with flare up or add to current therapy (mild-mod for 1-3 months; mod-severe for 3-6 months)
- intraarticular injections of glucocorticoids (no more frequent than q3 months)
- Opioids
- Surgical treatment (unacceptable pain, ROM, or fxn)

93

Corticosteroids for treating RA

- anti inflammatory and immunosuppressive
- can be used as a bridge to control debilitating sxs until DMARDS take effect
- Used as oral therapy - low dose and short term or high dose burst

***Long term use can lead to osteoporosis***

94

What is gout

- most common rheumatic disease of adulthood
- more common in pts with HTN, obesity, CKD, metabolic syndrome, DM2
- Dietary trends and use of thiazide and loop diuretics can also contribute
- characterized by high levels of uric acid in blood
- Sodium urate is end product of purine metabolism

95

Treatment strategies for gout

- pt education and diet and lifestyle
- mgmt of comorbidities
- Administer NSAIDs

96

How does allopurinol treat gout

- It's a xanthine oxidase inhibitor (XOI)
- recommended as first line urate lowering therapy
- interferes with uric acid synthesis
- adjust dose with kidney disease

97

How do probenecid or sulfinpyrazone treat gout

- increase uric acid excretion

98

How does colchicine treat gout

- inhibit leukocyte entry into affected joint

99

Patient education on gout

- diet, education, lifestyle, treatment objectives, mgmt of comorbidities
- consider eliminating serum elevating non-essential medications (thiazides, loop diuretics, niacin, calcineurin inhibitors, ASA)

100

What to avoid when pt has gout

- alcohol overuse
- complexe avoidance in acute attack

101

What to limit when pt has gout

- purine rich meat and seafood
- high fructose corn syrup soft drinks and energy drinks

102

What to encourge when pt has gout

- low fat or non fat dairy products
- vegetables

103

When are meds recommended with gout

- gout w/CKD stage 2-5 or end stage renal disease
- pts w/ prior gout attacks
- current hyperurecemia

104

ADRs of allopurinal when treating gout

- HA, somnolence
- N/V/D, dyspepsia, abdominal cramping
- jaundice liver problems
- hypersensitivity
- acute exacerbation of gout (can prevent with use of anti-inflammatories)

105

Drug interactions of allopurinol (gout)

- interferes with metabolism of 6-mercaptopurine
- interferes with azathioprine

106

Considerations before using allopurinol for gout

- rapid PCR screening for high risk groups
- genetic complications for allopurinol hypersensitivity rxn

107

What do you need to monitor when a pt is taking allopurinol

- regular monitoring of serum urate levels (every 2-5 weeks) during titration dose
- monitor serum urate levels once target levl is achieved every 6 months

108

MOA for Febuxostat (gout)

- selectively inhibits xanthine oxidase (XOI)
- used to treat hyperuricemia

109

What do you need to monitor for a pt taking Febuxostat for gout

- LFTs at baseline and then periodically
- serum uric acid levels every 2 weeks initially
- s/s of MI or stroke
- s/s of hypersensitivity or severe skin rxn

110

ADRs of Febuxostat (gout)

- liver fxn abnormalities
- hypersensitivity
- rare but possible MI or stroke
- rare but can see severe skin rxns

111

How can a gout flare be prevented

- take NSAID or colchicine to help prevent flares when taking febuxostat

112

What is the first line alternative with contraindication to XOI therapy (gout)

- Probenecid: first choice among uricosuric agents for ULT monotherapy

113

When is probenecid not the first line alternative

- in gout pts with a creatinine clearance of 50lm/min

114

MOA and drug info for Probenecid (gout)

- Inhibits resorption of urate at proximal convoluted tubule which increases excretion of uric acid
- do not start treatment until acute gouty attack
- take with plenty of water to prevent kidney stones
- alkization of urine and purine restriction is recommended

115

ADRs of Probenecid (uricosuric) (gout)

- HA, dizziness, anemia, flushing, sore gums
- GI: N/V, anorexia (taking food can decrease ADR)

116

Drug interactions of taking probenecid for gout

- probenecid increases plasma levels of weak acids (PCN, cephalosporins, beta-lactams) by competitively inhibiting renal tubular secretion
- salicylates may increase levels of probenecid

117

Anti-inflammatory treatment for gout

- recommended for all gout pts when pharma urate lowering is initiated
- should be continued if evidence of continuing gout disease
- low dose NSAID therapy is appropriate choice for first line gout attack prophylaxis

118

How is colchicine used to treat gout

- appropriate first line gout attack prophylaxis therapy
- approgriate dose adjustment in CKD and for drug interaction

119

When is pegloticase indicated for treatment of gout

- pts with burden of severe gout disease
- refractory gout
- discontinue use of oral anti-hyperuricemic agents prior to initiating
- Premedicate with antihistamines and corticosteroids

120

MOA of pegloticase (gout)

- peglylated recombinant form of urate-oxidase enzyme
- known as uricase which converts uric acid to allantoin

121

What do you have to monitor in pts taking pegloticase for gout

- serum uric acid levels (prior to infusions)
- consider DC if levels increase to >6mg/dL
- infusion rxns and anaphylaxis

122

ADRs of Pegloticase (gout)

-antibody formation
- gout flare (74% within 1st 3 months)
- infustion rxn
- nausea

123

Treating acute gout

- treat with pharma therapy within 24 yours of onset
- continue established pharam urate lowering therapy (ULT) without interruption
- NSAIDs, corticosteroids, oral colchicine appropriate 1st line option

124

Use of NSAIDs in Acute gout

- inhibit anti-inflammatory response
- indomethacin, naproxen, sulindac
- celecoxib (cox-2 inhibitor)

125

ADRs for NSAIDs in acute gout

- HA
- dizziness
- risk of GI bleed
- stomach upset
-indomethacin may aggravate depression or other CNS disturbances (epilepsy and parkinsonism)

126

What meds are contraindicated in treating acute gout

- ASA and other salicylates are contraindicated
- inhibit uric acid excretion in urine which exacerbates serum cxns

127

MOA of colchicine in treating gout

- prevent migration of leukocytes and phagocytosis by binding tubulin
- inhibits mitotic spindle formation
- not uricosuric nor alalgesic agent
- reduction of pain and inflammation within 12 hours of administration

128

ADRs of colchicine in treating gout

- N/V/D
- with chronic use: myopathy, bone marrow depression alopecia

129

Corticosteroid use for treating gout

Intraarticular injections
- consider if large joints involved

Systemic steroids
- Oral prednisone or methylprednisone
- IM triamcinolone