Arthritis Flashcards
(129 cards)
1
Q
Non-drug therapy for OA
A
- Rest
- PT
- ROM
- Muscle strengthening
- Assistive devices
- weight loss
2
Q
What is the goal of OA drug therapy
A
- relieve pain and inflammation
- only treats sxs
3
Q
What does drug therapy for OA NOT do
A
- It does not prevent the progression of OA
4
Q
List of 8 analgesics to treat OA
A
- Oral acetaminophen (APAP)
- Oral NSAIDs
- topical capsaicin
- topical NSAIDs
- glucosamine/chondroitin
- intra articular injections (corticosteroids, viscosupplementation)
- opioids
- tramadol
5
Q
How does acetaminophen treat OA
A
- used routinely to reduce pain
- does not decrease inflammation (NSAIDs may be better for treating NSAIDs)
6
Q
What is the max dose of acetaminophen (APAP)
A
3g/day
7
Q
what do you need to monitor with acetaminophen (APAP)
A
Liver and renal toxicity
8
Q
How do NSAIDs treat OA
A
- 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
Q
What to monitor for NSAIDS
A
- GI effects
- Bleeding (CBC, stool guaiac)
- Renal toxicity
- -Cr and BUN
10
Q
How does Topical Capsaicin treat OA
A
- inhibits release of substance P in peripheral nerves (not present in cartilage)
- initially by sting/burn (subsides with use)
11
Q
How long does it take for capsaicin to be effective
A
2-4 weeks
12
Q
Where is the use of capsaicin most effective
A
- Studies show knees and hands (0.025%-0.075% cream q6)
- reduction in pain and tenderness
13
Q
How does Glucosamine and Chontroitin treat OA
A
- provides materials to help rebuild cartilage
14
Q
How long does it take for glucosamine to be effective
A
4-8 weeks
15
Q
How long does it take for glucosamine to be effective
A
> 2 weeks
16
Q
How do Corticosteroid treat OA
A
- intra articular injections- short term of sxs in knee
17
Q
How often and how long can corticosteroids treat OA
A
- injections q3 months x 3 years
- limit injections to no more than 3-4 times/year
18
Q
Can Oral corticosteroids be used to treat OA
A
- No
- systemic effects
- not indicated or recommended to treat OA
19
Q
How does viscosupplementation treat OA
A
- AKA hyaluronic acid (HA)
- intra articular injection
- Acts as viscous lubricant
- may reduce need for NSAID
20
Q
Opioid Analgesics and OA
A
- should be reserved, potential for addiction
- may be combined with acetaminophen
- use caution whn using with other APAP (max APAP 3g/day)
21
Q
Types of Opioid Analgesics used to treat OA
A
- Codeine/oxycodone/hydrocodone
- Tramadol
22
Q
How to treat Hand OA
A
- One or more of:
- -Topical capsaicin
- -Topical NSAIDs (for > 75 years, topical is preferred)
- -Oral NSAIDs
- -COX-2 inhibitor
23
Q
What do you NOT use to treat hand OA
A
- intra articular therapies
- opioid analgesics
24
Q
How to treat Knee OA
A
- 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
