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Pharmacology III > Arthritis > Flashcards

Arthritis Flashcards

1
Q

Is osteoarthritis a inflammatory disorder?

A

No, it’s a non-inflammatory disorder

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2
Q

What does osteoarthritis involve?

A

primarily affecting weight-bearing joints of the peripheral and axial skeleton

deterioration and changes to the articular cartilage result in formation of new bone at the joint surfaces

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3
Q

What are the risk factors associated with osteoarthritis?

A 
Age
Gender
Obesity
Activities
Genetics 
Race
Osteoporosis
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4
Q

What are the risk factors for osteoarthritis associated with age?

A

Not a cause, but incidence increase with increased age.
Affects almost 50% of those >65 years of age
Almost all over 75 years of age

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5
Q

What are the risk factors for osteoarthritis associated with gender?

A

2:1 older women to older men with OA of the knee and hand.

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6
Q

What are the risk factors for osteoarthritis associated with obesity?

A

Increased body weight strongly associated with hip, knee, and hand OA
Increased body mass = increased risk of OA because of increased weight on weight-bearing joints.
Losing as little as 5 Kg can decrease the risk by up to 50 % of developing symptomatic OA.

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7
Q

What are the risk factors for osteoarthritis associated with activities?

A

Activities involving repetitive motion or injury are at increased risk. Work, sports and trauma have been implicated in OA.
If daily repetitive use: then duration and intensity play a major part in OA.
Trauma to the joint resulting in loss of ligament integrity and damage to the meniscus can lead to OA.

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8
Q

What are the risk factors for osteoarthritis associated with genetics?

A

Involved in certain types of OA. Genetic links that alter the cartilage matrix can lead to premature OA.

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9
Q

What are the risk factors for osteoarthritis associated with race?

A

Knee OA twice as likely in black women compared to white women

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10
Q

What are the risk factors for osteoarthritis associated with osteoporosis?

A

There may be an inverse relationship associated with OA of the knee and hip. Less dense bone may better distribute the load across the joint, slowing the development of OA. This is a controversial theory.

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11
Q

What does cartilage provide?

A

Low-friction surface covering the concave and convex ends of the bone to provide a load support and shock absorbing and smooth gliding surface during movement.

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12
Q

What is the major function of cartilage?

A

Enable movement within required ROM
Distribute loading across joint tissues, to prevent damage
Stabilize joint during use

Cartilage is avascular, aneural, and alymphatic

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13
Q

What is involved in the pathophysiology of osteoarthritis?

A
  • Damage to collagen fiber network
  • There is a resultant decrease in proteoglycan-collagen interaction in the cartilage causing failure of the cartilage to repair itself. This causes a loss of cartilage, leading to bony growth and severe pain.
  • Joint failure results from a progressive breakdown of cartilage surrounding weight-bearing joints.
  • Biochemical, biomechanical, inflammatory and immunologic factors contribute to the collapse of the cartilage.
  • NOT INFLAMMATORY ARTHRITIS
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14
Q

What is primary (idiopathic) osteoarthritis?

A

Failure of the cartilage in the absence of any known underlying predisposing factor

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15
Q

What are the most common types of primary osteoarthritis?

A 
Localized OA (one or two sites)
Generalized OA (3 or more sites)
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16
Q

What is erosive OA?

A

Presence of erosion and marked proliferattion in proximal and distal interphalangeal joints of hands

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17
Q

What is secondary osteoarthritis?

A

OA that occurs due to other disease states or trauma, i.e. metabolic or endocrine disorders or congenital factors

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18
Q

What is the ACR criteria for OA?

A

Presence of pain
Bony changes on exam
Normal erythrocyte sedimentation rate
Characteristic radiographs

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19
Q

What is the ACR criteria for Hip OA?

A

Hip pain plus 2 of the following
ESR <20 mm/hour
Radiographic femoral or acetabular osteophytes
Radiographic joint space narrowing

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20
Q

What is the ACR criteria for knee OA?

A

Knee pain and radiographic osteophytes plus one of the following
Age greater than 50
Morning stiffness of 30 minutes or less
Crepitus on motion

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21
Q

What are the clinical symptoms of OA?

A
  • Localized deep aching pain associated with the affected joint.
  • Relieved with rest or removal of weight from affected joint.
  • Later pain is associated with rest  it is not relieved by rest.
  • Weather changes or changes in barometric pressure aggravates the pain.
  • Limitation in motion, crepitus, stiffness and deformities may occur. Stiffness less than 30 minutes
  • With loss of articular surfaces, muscle spasms, capsular contracture, and mechanical blockage, with limited motion.
  • Joints most affected in idiopathic OA are DIP and PIP of the hand, the first carpometacarpal joint, knees, hips, cervical and lumbar spine, and the first (metatarsophalangeal) MTP joint of the toe.
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22
Q

What is found on PE for OA?

A

Pain, tenderness, decreased range of motion, +/-inflammation. Asymmetrical involvement

Feet: Pain, tenderness, stiffness of MTP joint.

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23
Q

What is found on PE for hands for OA?

A

Heberden’s nodes -bony enlargements (osteophytes) of the DIP joints. Heberden’s nodes usually develop slowly, nonpainful, lateral and medial aspects of joint.
Bouchard’s nodes-bony enlargements of the PIP joints.

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24
Q

What is found on PE for the feet for OA?

A

Pain, tenderness, stiffness of MTP joint.

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25
Q

What is found on PE for the knees for OA?

A

Pain, tenderness, crepitus, limitation of motion, joint instability. Area of involvement causes deviation toward opposite direction.

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26
Q

What is found on PE for the hips for OA?

A

Groin or buttock pain when bearing weight.

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27
Q

What is found on PE for the spine for OA?

A

Pain, tenderness, paresthesias, muscle weakness, & loss of reflexes.
Usually L3-L4 is the area of involvement.

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28
Q

Is radiological evaluation necessary for diagnosing OA? And what are the radiological findings?

A

Radiologic evaluation is essential in the diagnosis of OA.

Joint space narrowing, subchondral bony sclerosis, and marginal osteophyte and cyst formation.

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29
Q

What are the non-drug therapies used to treat OA?

A 
Rest
Physical therapy
ROM
Muscle strengthening
Assistive devices- canes, walkers
Diet-weight loss- more weight on the joints is harder on the joints so losing weight is beneficial.
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30
Q

What physical therapy can help with OA?

A
  • Heat and cold can maintain and regain joint range of motion, relieve pain, and decreased muscle spasm.
  • Transcutaneous electrical nerve stimulation (TENS)-transmission of an electrical current from the skin to the peripheral nerve may provide pain relief for acute pain.
  • Exercise programs using isometric techniques are designed to strengthen the muscle and improve joint function and motion.
  • Surgery-indicated for patients whose pain hinders their lifestyle, and can not be controlled with conservative therapy.
  • Laser-Red or Infrared light have been effective, as well as Helium-neon laser.
  • Acupuncture- been shown to be beneficial
  • Pulsed Electromagnetic Fields
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31
Q

What is the goal of drug therapy for OA?

A

Goal: To relieve pain and inflammation.

Drug therapy does not prevent progression of OA. Only treat symptoms.

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32
Q

What analgesics can be used to treat OA?

A

-Oral acetaminophen/NSAIDS
-Topical capsaicin
-Glucosamine/chondroitin
-Intra-articular injections- Corticosteroids, Viscosupplementation: Hyaluronic acid
Opioids

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33
Q

Acetaminophen

A

Used to reduce pain but not inflammation
Some evidence suggests that NSAIDS are moer efficacious than APAP
Max dose 3.2g/d, monitor for liver and renal toxicity

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34
Q

NSAIDS

A

Non-selective NSAIDs equally effective compared with COX-2 inhibitors
Analgesic effect at lower doses
Anti-inflammatory effect at higher doses.
Affects platelet function, but is reversible unlike ASA.

Renal toxicity:
monitor Cr, BUN

GI Side effects- concern
monitor for bleeding: CBC, stool guaiac

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35
Q

Topical capsaicin

A

Inhibits release of substance P in peripheral nerves
Substance P is not present in cartilage, but is present in nerves supplying other periarticular tissues

Initial applications result in stinging and burning that subsides with continued use
Initial release of substance P

Maximal efficacy after 2-4 weeks

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36
Q

Glucosamine

A

Prepared from shells of crabs and other crustaceans
Substrate for production of articular cartilage
Produces glycosaminoglycans

Symptom improvement usually reported at 4-8 weeks compared with 2 weeks with NSAIDs

1500 mg/day compared with ibuprofen and piroxicam 20 mg/day As effective in improving symptoms

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37
Q

Chondroitin

A

Prepared from bovine or porcine cartilage sources

Mucopolysaccharide used in synthesis of cartilage

1200 mg/day compared with diclofenac 150 mg/day as effective in decreasing pain at 3 months

Response appears later than NSAIDs

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38
Q

What corticosteroids are used in OA?

A

Intra-articular injections
Triamcinolone acetonide
Methylprednisolone

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39
Q

Corticosteroids (Triamcinolone acetonide

Methylprednisolone)

A

Short-term improvement of symptoms in knee (1‐6 weeks)
Some studies indicate injections q3months over 2 years to be safe and may provide superior effects over placebo
Limit injections to 3-4 x/year
Animal studies show more frequent injections precipitate progressive cartilage damage

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40
Q

Are oral steroids recommended in OA?

A

NO

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41
Q

What is viscosupplementation?

A 
Intraarticular injection
Hyaluronic acid (HA)
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42
Q

Viscosupplementation (Hyaluronic acid)

A 
Naturally occuring glycosaminoglycan
Available products
Sodium hyaluronate and hylan G-F 20
Acts as a viscous lubricant
Mixed clinical trial results
May reduce need for NSAIDs
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43
Q

What narcotic or narcotic/analgesics can be used for OA?

A

propoxyphene
Codeine/oxycodone/hydrocodone
many of these agents are combined with acetaminophen, caution when using these agents with other acetaminophen agents (Max APAP = 4gm/day)

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44
Q

What is the biggest ADR for narcotic use?

A

Respiratory depression

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45
Q

What is rheumatoid arthritis?

A

A chronic systemic inflammatory disease of the joints and related structures

Genetic predisposition and exposure to unknown environmental factors

High disability rate and shortened life expectancy by 5-7 years

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46
Q

What is the pathophysiology involved in RA?

A

Immune-mediated inflammatory process

Attacks the synovium and other vital organs and tissues
Eyes, heart, kidneys, blood vessels, and RBCs

Erosive, symmetric joint involvement frequently involving hands and feet (not seen in the huge weight bearing joints)

Chronic inflammation of synovial lining
Layer becomes hyperplastic and hypertrophic
Tissue exceeds bounds of joint structure eroding into bone and cartilage within joint capsule “Pannus”

Leads to destruction of joint and results in deformities

47
Q

What is the onset of RA?

A

Sudden, acute in 10-25% of polyarticular

Insidious onset of weeks-months in >50% of polyarticular

48
Q

What is the joint involvement associated with RA?

A

Joint involvement can present unilaterally but progresses symmetrically.

49
Q

What are the prodromal symptoms of RA?

A 
Prodromal Symptoms (precede by weeks or months)
Fever, fatigue, weakness, malaise, anorexia, joint pain, weight loss, myalgia, and synovitis
50
Q

What is involved with morning stiffness and gelling after inactivity in RA?

A

Arthritis stiffness is usually worse in the morning, and last anywhere from 30 minutes to all day.

51
Q

What are the joints like in RA?

A

Stiff, painful, tender, and/or swollen joints
“Boggy” or “spongy” feel to joint
Affected joints are warmer, but not as warm as gout
Joints most involved are: the small bones of the hands, wrists, and feet.
Other joints that maybe involved are: Elbows, shoulders, hips, knees, and ankles. (not as common for the bigger joints to be affected)
Swelling of the joints may be visible or apparent only by palpation

52
Q

Is structural damage reversible in RA?

A

Structural damage is cumulative and irreversible

53
Q

Does RA fluctuate?

A

Disease activity fluctuates

54
Q

What is the clinical presentation in the hands and wrists of a patient with RA?

A

Grip weakness, instability, subluxation (partial joint dislocation)
Muscle atrophy, carpal tunnel syndrome

Deformities
Ulnar deviation of fingers
Swan neck deformity-Hyperextension of PIP and flexion of DIP
Boutonniere deformity- Flexion of PIP and hyperextension of DIP

55
Q

What is the clinical presentation in the feet of a patient with RA?

A

Subluxation of MP joint
“cock-up” or “hammer” toe deformities
Lateral deviations of toes: “hallux valgus”

56
Q

What is the extra-articular involvement associated with RA?

A

Rheumatoid nodules in 20-30%
Occur anywhere, usually benign
Primarily SQ tissues of extensor surfaces (elbows, forearms)

Anemia of chronic disease and hemolytic anemia
Vasculitis–Infarcts near end of digits

Pulmonary complications– Pleural effusions, insterstitial pneumonitis

Cardiac– Atherosclerotic CAD
Prescribe daily low-dose aspirin

Ocular complications– Sjogren’s syndrome (decreased tear formation)

Felty’s syndrome– Splenomegaly, neutropenia, and thrombocytopenia

57
Q

What is the primary objective for treatment of RA?

A

To improve or maintain functional status, and improve QOL

58
Q

What are the goals of therapy for the treatment of RA?

A

To relieve pain, preserve joint function and prevent or control joint destruction and systemic complications.

59
Q

What are the nonpharmacologic treatments of RA?

A

Rest, OT, PT, assistive devices
Weight reduction or management
Splinting, joint protection

*these are not as beneficial as they are in the treatment of OA.

60
Q

What are DMARDS?

A

Disease modifying anti-rheumatic drugs

Miscellaneous group of drugs that have potential to reduce or prevent joint damage

61
Q

When should DMARDS be started in a RA patient?

A

Within 3 months

Joint space narrowing occurs in >80% of patients within 1st two years

62
Q

How should DMARDS be selected?

A 
Based on specific patient issues
No one SAARD is efficacious and safe in every patient
Severity of disease
Comorbid diseases
Likelihood of adherence
Convenience and acceptability
Monitoring requirements
ADEs
Costs
63
Q

What are the nonbiologic DMARDS?

A 
Hydroxychloroquine
Methotrexate
Sulfasalazine
Leflunomide
Minocycline
64
Q

what are the biologic DMARDS?

A

Non-TF
Abatacept
Rituximab
Tociluzimab

Anti-TF
Etanercept
Adalimumab
Infliximab
Golimumab
Certolizimab Pegol
65
Q

Hydroxychloroquine (Plaquenil®)- Indications

A

Antimalarial
Use for mild disease or in combination (Reserved for RA unresponsive to NSAIDS)
Weaker DMARD properties than other 1st line
Relatively fast onset (2-6 months)
D/C if no response in 6mo
Slows progression of erosive bone lesion, may induce remission

66
Q

Hydroxychloroquine (Plaquenil®)- monitoring

A

OPHTHALMOLOGIC EXAM TWICE YEARLY FOR RETINAL TOXICITY
Damage initially reversible but can move to irreversible
Does not cause liver, kidney, or bone toxicities

67
Q

Hydroxychloroquine (Plaquenil®)- ADRs

A

GI: N/V/D take with food
OCULAR TOXICITY- make sure you monitor for this.
Dermatology: pruritis, rash, alopecia, increased skin pigmentation
Neurological: HA, insomnia, and vertigo

Contraindicated in patients with significant visual, hepatic, or renal impairment

68
Q

Methotrexate- MOA and indications

A

Thought to act as an immunosuppressive and anti-inflammatory agent (folic acid antagonist)

Used as monotherapy or combination therapy
Mainstay of therapy for patients not responding adequately to NSAIDS (moderate to severe RA)
Best long-term outcome, because less toxic and is less likely to be D/C’d than other DMARD’s. Most effective and least expensive
Slows appearance of new erosions

69
Q

Methotrexate- onset

A

Onset at 2 weeks-2 months; max effect within 4-8 weeks
Possible survival benefits
Significant reduction in CV mortality

70
Q

Methotrexate- ADRS

A

-GI-N/V/D, stomatitis (dose related) (have them eat something)
-Hematologic-thrombocytopenia, leukopenia (dose related)
-pulmonary-fibrosis, pneumonitis
-hepatic-elevated liver enzymes, cirrhosis
Elevated LFTs in up to 15% of patients
Discontinue if sustained LFTs 2x ULN
Low serum albumin may signal liver toxicity

71
Q

Methotrexate- Interactions

A

NSAIDs may decrease Methotrexate clearance and increase ADEs (infrequent)
Folic Acid 1 mg QDay may alleviate some of the adverse effects caused by MTX.
Leucovorin (folic acid derivative) = antidote for MTX toxicity

72
Q

Methotrexate- Monitoring

A

Baseline: LFTs, CBC, total bilirubin, Hepatitis B and C studies (patients with these will not be candi- MOAdates for most of these meds), Serum creatinine, albumin
Q1-2 months: CBC, AST, albumin

73
Q

Sulfasalazine (Azulfidine®)- MOA

A

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

74
Q

Sulfasalazine (Azulfidine®)- indications and monitoring

A

Treatment mild RA or in combination

Monitor- Baseline CBC then q week for 1 month, then q 1-2 months

75
Q

Sulfasalazine (Azulfidine®)- adverse reactions

A

GI: N/V/D (minimize by slowly titrating dose)and anorexia
CNS: HA
Life-threatening reactions have occurred…stop med and try different DMARD

76
Q

Leflunomide (Arava®)- MOA

A

Reversible inhibitor of DHODH interferes with RNA and DNA synthesis in lynphocytes
Reduces pain and inflammation associated with RA; slows progression of structural damage
Overall efficacy similar to MTX and sulfasalazine

77
Q

Leflunomide (Arava®)- ADRs

A

HA, nausea, diarrhea, rash, alopecia
Caution with liver disease -> biliary and renal excretion

PREGNANCY CATEGORY X
Cholestyramine washout prior to conception

78
Q

Leflunomide (Arava®)- Monitor

A

Monitor: CBC and ALT monthly initially, then q6-8 weeks

79
Q

Etanercept (Enbrel®)

A

Soluble TNF receptor that competitively binds 2 TNF molecules rendering inactive

Additive effects when in combination with methotrexate (improvement when added on top of methotrexate)

80
Q

Infliximab (Remicade®) and adalimumab (Humira®)

A
  • Anti-TNF-alpha monoclonal Antibody (IgG)
  • Inhibits progression of structural damage
  • Additive effects when combined with MTX
  • Infliximab only in combination with MTX
  • Human antichimeric molecule antibodies development
81
Q

What sound be monitored for tumor necrosis factor antagonists (biologics)?

A

Initial tuberculin skin test

82
Q

TNF antagonists (Etanercept, infliximab, and adalimumab)- ADEs

A
  • Infliximab: infusion-related HA/Nausea in 20%-may use antihistamines
  • Etanercept/Adalimumab: Injection site reactions
  • Risk of worsening infectious complications
  • Discontinue is patients with signs of active infections
  • May worsen heart failure
  • Rare reports of lupus-like syndromes, hepatotoxicity, pancytopenia
  • May exacerbate previous quiescent multiple sclerosis
83
Q

What are the Biologics- Interleukin-1 Receptor Antagonists?

A

Anakinra (Kineret®)
Abtacept (Orencia)
Rituximab

84
Q

Anakinra (Kineret®)- MOA

A 
moderate to severe RA
IL-1 receptor antagonist
IL-1 induced by inflammatory stimuli
Antagonist slows degradation of cartilage and bone resorption
Monotherapy and combination with MTX
85
Q

Anakinra (Kineret®)- ADEs

A

Similar ADE to TNF antagonists
Injection site reactions and risk of infections
Don’t use in combination with TNF antagonists
Reserve for failure after TNF antagonists

No monitoring necessary

86
Q

Abtacept (Orencia)

A

-Moderate to severe RA refractory to other treatment
-Use as monotherapy or combination therapy
-Soluble fusion protein
Human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to the modified Fc (hinge, CH2, and CH3 domains) portion of human immunoglobulin G1 (IgG1)

-Inhibit T lymphocyte activation
Can cause a lot of problems for patients like opening up for infections
Very expensive ($12,000-24,000 yearly)

87
Q

Rituximab

A
  • Depletes B lymphocytes, reducing antibody formation
  • FDA indication: Combo with MTX I modsevere active RA with inadequate response to TNF antagonists
  • IV infusion separated by 2 weeks, premedicate with methylprednisolone
88
Q

What are the pharmacologic therapy-symptom relief for RA?

A

–NSAIDs at antiinflammatory doses
–Oral prednisone <10 mg/day- still has SE
Mild-mod for 1-3 months
Moderate-severe for 3-6 months
–Intraarticular injections of glucocorticoids (no more freq. than q3months)
–Opioids
–Surgical treatment– Unacceptable pain, ROM, or function

89
Q

Corticosteroids

A

Anti-inflammatory and immunosuppressive
Can be used as a bridge to control debilitating
symptoms until DMARDs take effect.
Used as oral therapy-low dose and short-term or high-dose burst
Long term use can lead to osteoporosis

90
Q

What is gout?

A

Metabolic disorder characterized by high levels of uric acid in blood

91
Q

What is the process that leads to gout?

A

Hyperuricemia leads to deposition of Na+ urate crystals in tissues (kidneys and joints)->inflammatory process ->release of mediators
Na+ urate is end product of purine metabolism:
Purine ->hypoxanthine->xanthine->uric acid

92
Q

What is hyperuricemia?

A

overproduction of uric acid relative to ability to excrete it

93
Q

What are the treatment strategies for hyperuricemia?

A
  • Interfere with uric acid synthesis with allopurinol
  • Increase uric acid excretion with probenecid or sulfinpyrazone
  • Inhibit leukocyte entry into affected joint with colchicine
  • Administer NSAIDS
94
Q

What can be used to treat an acute gout attack?

A

Colchicine

NSAIDS

95
Q

Colchicine- MOA

A

MOA: prevents migration of leukocytes and phagocytosis by binding tubulin (a microtubular protein), also inhibits mitotic spindle formation thus affecting dividing cells.
Not uricosuric nor analgesic agent (works to decrease pain due to MOA, doesn’t affect the uric acid deposits at all)
Reduction of pain and inflammation w/in 12 hours of administration

96
Q

Colchicine- ADRs

A

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

97
Q

How long should you wait before initiating another course of therapy after giving colchicine?

A

3 days

98
Q

NSIADs- Indomethacin (Indocin)- MOA

A

Inhibit inflammatory response

Other NSAIDS used: naproxen, ibuprofen, sulindac.

99
Q

NSAIDs- Adverse reactions

A 
Headache
Dizziness
Risk of GI bleed
Stomach upset
Indomethacin may aggravate depression or other CNS disturbances, epilepsy and parkinsonism
100
Q

What medications are contraindicated for acute gout treatment?

A

Aspirin and other salicylates contraindicated because they inhibit uric acid excretion in the urine thus exacerbating serum concentrations.

101
Q

What can be done to prevent gout?

A

Avoid heavy alcohol use
Avoid foods rich in purines–fish, poultry, meat, concentrated sweets, rich pastries, fried foods
Weight loss

102
Q

What medications are sued to treat CHRONIC gout?

A

Allopurinol

Uricosuric agents- Probenecid and sulinpyrazone

103
Q

Allopurinol- MOA

A

MOA: Reduces uric acid synthesis-inhibits xanthine oxidase (enzyme that converts purines to uric acid).
Not to be used in acute gout attack
Indications:

104
Q

Allopurinol- Indications

A

Hyperuricemia of gout
Pts. w/allergy to uricosuric agents (probenecid, sulfinpyrazone)
Recurrent renal stones

105
Q

Allopurinol-ADRS

A

ADRs-Headache, somnolence
N/V/D, dyspepsia, abdominal cramping
Jaundice, liver problems
Acute exacerbation of gout (NSAIDS and colchicine concurrently)

106
Q

Allopurinol- drug interactions

A

Allopurinol interferes with metabolism of 6-mercaptopurine (anticancer agent) and
azathioprine

107
Q

Uricosuric agents- Probenecid and sulinpyrazone- MOA

A

Inhibits resorption of urate at proximal convoluted tubule->increasing excretion of uric acid.

108
Q

Probenecid (Benemid®)- indications

A

Do not start treatment until acute gouty attack has subsided. Take with plenty of water to prevent kidney stones. Alkalization of urine and purine restriction is recommended. Dose 0.25 g twice a day for 1 week then 0.5 g twice daily thereafter.

109
Q

Probenecid (Benemid®)- ADRS

A

Headache, dizziness, anemia, flushing, sore gums
GI effects-nausea, vomiting, anorexia
uric acid stones, exacerbation of gout

110
Q

Probenecid (Benemid®)- Drug interactions

A

Probenecid blocks secretion of PCN (only a problem if the patient is currently taking this med) also inhibits excretion of naproxen, ketoprofen, and indomethacin (these are meds used for symptomatic therapy)

111
Q

Sulfinpyrazone- Indications

A

Treatment of chronic and intermittent gouty arthritis
Initially 100 to 200 mg twice a day with meals or milk, increase to maintenance dose 200 to 400 mg twice a day. Once urate levels are controlled reduce to 200 mg a day.

112
Q

Sulfinpyrazone- ADRS

A

Upper GI disturbances, may reactivate ulcer

Rash, anemia

113
Q

What are the interactions of sulfinpyrazone?

A

Probenecid + sulfinpyrazone = additive effect

Salicylates inhibit uricosuric effects of probenecid & sulfinpyrazone (even though salicylates can be uricosuric). Use Ibuprofen or APAP, not ASA

Highly protein bound -> can affect plasma levels of other highly bound drugs

Pharmacology III (19 decks)

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