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Julie Pharm > Gout And RA > Flashcards

Gout And RA Flashcards

0
Q

If NSAIDS or corticosteroids fail in acute gouty attack what is used

A

Colchicine

Orally every hour until symptoms improve or side effects become intolerable ( nausea, vomiting, diarrhea)

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1
Q

Treatment of an acute attack of gout

A

NSAIDS- indomethacin, naproxen
Corticosteroids - prednisone
ACTH

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2
Q

Colchicine - what is its moa

A

Binds to tubulin preventing Tubulin polymerization to form micro tubules
-> the hauls leukocyte migration and phagocytosis.
Also inhibits leukotriene b4 formation

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3
Q

Colchicine what does it do ? Why give it?

A

It decreases inflammation and pain associated with acute gouty arthritis and is more specific than NSAIDS
- at low doses can be used as a prophylaxis of gouty arthritis

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4
Q

What are side effects of colchicine and contraindications

A

Gi distress: diarrhea, vomiting,
Enterohepatic circulation : prolongs 1/2 life and increase exposure to GI tract
Acute high dose -> renal failure or bloody diarrhea
Chronic use ->bone marrow suppression, aplastic anemia, thrombocytopenia , alopecia

CONTRAINDICATIONS : renal disease, liver disease or GI disease

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5
Q

What is the goal of treatment for hyperuricemia

A

Decrease irate contraction to below 6.0 mg/dL

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6
Q

What is probenecid used for?

A

Increases uric acid elimination and thus decreases the body urate pool in pts with gout but not to be used in patients screwing large amounts of uric acid since it will precipitate Uric acid caliculi in the kidney . PREVENT GOUT ATTACK

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7
Q

What is the MOA of probenecid

A

Its secreted and reabsorbed from the proximal tubule of the kidney. COMPETES with Uric acid renal tubule anionic transport sites. There is a net decrease in Uric acid reabsorption

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8
Q

What are the side effects of probenecid

A

Decreases or halts secretion of weak acids ( penicillins)

GI irritation, rash, could aggravate gout at first ( give with colchicine) urate stones in kidney

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9
Q

Contraindications or limitations of giving probenecid

A
  • Pts with decreased function can’t be on it.
  • Uricosuric agents may case crystallization of urate if hydration isn’t maintained
  • potential for many drug interactions bc stops secretion of weak acids- alter the clearance of many drugs
    - methotrexate
    - oral hypoglycemics
    - zidovudine
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10
Q

Should aspirin be used in pts with gout?

A

NO ! Well just not in low doses. In low doses it will cause net UA retention by blocking the secretory transports

I large doses it will act as an uricosuric and compete with UA at receptors and therefore decrease the net UA reabsorption

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11
Q

What is allopurinol and what’s it’s MOA

A

It’s an isomer of hypoxanthine. A newer drug oxypurinol (alloxanthin)is more effective. Irreversibly blocks xanthine oxidase

It’s reduces the urate levels and increases hypoxanthine and xanthine which are more soluble

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12
Q

What is the MOA of methotrexate

A

NON BIOLOGICS - disease modifying antirheumatic drug

Inhibits dihydrofolate reductase decreases dTMP-> decreases DNA and protein synthesis / anti- inflammatory effect may be due to the enhanced adenosine release

[ dihydrofolate reductase : reduces dihydrofolate to tetrahydrofolate - which is essential for purine synthesis and unveil acid precursors]

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13
Q

What are the uses of methotrexate

A

RA, psoriasis, lupus , chemo, immunosuppression
Contraindicated with pregnancy
Non- biologic

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14
Q

What are adverse effects and drug interactions with methotrexate

A

Mucosal clerks, nausea, diarrhea, abnormal liver enzymes, bone marrow suppression

Competition for weak acid secreting pathway in proximal tubule so high dose of aspirin or probenecid can compete for excretion and cause toxicity.

converted to active metabolite in liver so must monitor liver enzymes.

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15
Q

How does febuxosat work and when should it be used

A

It is a non purine selective inhibitor of XO. I should be used with pts with renal insufficiency bc the liver metabolizes it. It’s chemically different that allopurinol so pts allergic to allopurinol can use this instead. It’s more effective than allopurinol but clinical effect doesn’t appear to be superior

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16
Q

Uricase enzymes what’s wrong with them

A

Metabolize UA to allantoin. Other species contain this enzyme naturally we don’t. A pegylated form of uricase is used to treat gout but some ppl are allergic and pts will develop antibodies toward it.

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17
Q

What is the MOA of hydroxychloroquine

A

NON BIOLOGIC DMARDS

The drug is a base and accumulates in the lysosomal compartment of connective tissue and white blood cells. It suppressed the intracelluar antigen processing and loading of peptides onto Mhc class II molecules in endosomes-> preventing T cell activation

18
Q

What are the adverse effects of hydroxychloroquine

A

Transient and not serious

Rashes , GI upset, leukopenia, peripheral neuropathy, and ocular effects.

19
Q

What are the clinical uses of hydroxychloroquine

A

Used for pts not responding to NSAIDS. Reduces rheumatoid factor but does not effect erosive bony lesions

Malaria

20
Q

What’s the MOA of sulfasalazine

A

Unknown- but it decreases Rheumatoid factor. , suppresses T-cell activation and inhibit release of inflammatory cytokines

NONBIOLOGIC DMARDS

21
Q

What are the adverse effects of sulfasalazine

A

GI and Cns complications, neutropenia, skin rashes a hepatotoxicity

22
Q

What is the clinical use of sulfasalazine

A

Early treatment of arthritis and second line drug for ra

23
Q

3 TNF alpha inhibitor drugs

A

Etanercept ( enbrel)
Infliximab ( remicade)
Adalimumab ( humira)

Can cause serious infractions

Remember TNF alpha - is part of the acute phase response

24
Q

What is the clinical use of etanercept

A

RA, ankylosing spondylitis, juvenile idiopathic arthritis, psoriatic arthritis, plaque psoriasis

Can wine used with methotrexate or alone

25
Q

What is the MOA of entanercept

A

I consists of two soluble TNF p75 receptor moieties linked to the Fc portion of human IgG1. I binds two TNF alpha molecules, but it also binds beta. Blocks the action of TNF decreases the expression of adhesion molecules responsible for leukocyte migration and serums levels of cytokines and metalloproteinase

26
Q

What are the adverse effects of etanercept

A

Injection site rxns. Increase serious infections including respiratory tract infections, activate latent tb, not to be used in pts with ms

27
Q

What is they MOA of adalimumab ( humira)

A

Fully human anti- tnfalpha antibody. Blocks the ability of tnfalpha to interact with the p55 and p75 cell surface TNF receptors

28
Q

Adverse effects of adalimumab and clinical uses

A

Injection site rxn, headache, development of antibodies to adalimumab, antinuclear antibodies, activation of latent tb , sinusitis and upper respiratory tract infections.

Uses: alone or with methotrexate. RA , ankylosing spondylitis , juvenile idiopathic arthritis , psoriatic arthritis, plaque psoriasis, and moderate to severe Crohn’s disease / ulcerative colitis

29
Q

Interleukin -1 inhibitor

A

Anakinra( kineret)

30
Q

Anakinra MOA and uses

A

Recombinant form of human IL-1 receptor antagonist . It blocks the actions of IL-1 . IL-1 causes cartilage degradation by its induction of loss of proteoglycans as well as stimulation of bone resorption

Uses: pt over 18 who failed one or more DMARDS . Can be used in combo with non-BIOLOGICS but not antiTNF drugs

Adverse effects - serious infection and injection site rxn

31
Q

Interleukin-6

A

Tocilizumab

32
Q

Tocilizumab MOA , clinical use , adverse effects

A

Antibody against IL-6 receptor - IL-6 is produced by synovial cells in the joints in response to inflammatory processes

Juvenile idiopathic arthritis, RA if the pt has not responded to other BIOLOGICS

Injection site rxn, rash, GI symptoms, headache, respiratory tract infection, nasopharyngitis , activation of latent tb, elevated liver enzymes

33
Q

Lymphocyte antagonist

A

Leflunomide

34
Q

MOA of of of leflunomide

A

Activated lymphocytes require increased DNA/RNA synthesis. Activated lymphocytes depend on de novo synthesis of nucleotides. Leflunomide inhibits dihydroorotate dehydrogenase leading to a decrease in UMP. This causes cells to be arrested in the G1 phase. Mostly reduces B cells but also effects T lymphocytes

35
Q

What is the pharmokinetics , side effects and uses leflunomide

A

Leflunomide is converted to the active drug in the intestinal mucosa and liver.
It has an average plasma half-life of 15 days due to plasma protein binding and enterohepatic
circulation. Cholestyramine can interrupt the enterohepatic circulation and increase the rate of
elimination.

Adverse effects: Diarrhea, reversible alopecia, rash, headache, dizziness, respiratory tract infection, and elevation of liver enzymes and hepatoxicity. Contraindicated in pregnancy.

Clinical use: Efficacy of leflunomide is similar to methotrexate and can be used in combination with it. May be combined with biologic DMARDs.

36
Q

What is the MOA of Abatacept

A

Abatecepta recombinant fusion protein that binds to CD80 and CD86 on antigen presenting cells (APCs), preventing these molecules from binding CD28 on T lymphocytes. This inhibits T cell activation by preventing the co-stimulatory signal.

37
Q

What is the clinical use of Abatacept

A

Moderate to severe active rheumatoid arthritis who have had an inadequate response to or more DMARDS. May be used alone or with a non-biologic DMARD, but not with a biologic

38
Q

What are the side effects and pharmokinetics of Abatacept

A

Pharmacokinetics: Abatacept is administered by IV approximately every two weeks.

Adverse reactions: May cause an increase in infections nasopharyngitis, exacerbates COPD, headache, nausea.

39
Q

JANUS KINASE (JAK) PATHWAY INHIBITOR

A

Tofacitinib

40
Q

MOA of Tofacitinib

A

Janus kinases that are intracellular tyrosine kinases that will phosphorylate the cytokine receptor when it is activated. This recruits Signal Transducers and Activators of Transcription (STATs) that become phosphorylated and then dimerize. The dimmers then enter the nucleus and regulate gene expression. These signals are important in inflammation. This drug inhibits the JAK

41
Q

What are the uses of Tofacitinib

A

Rheumatoid arthritis in patients who have not responded to methotrexate. It may be used alone or in combination with methotrexate or other non-biologic DMARDs. It should not be used in combination with biologics such as a TNF or IL inhibitor. It is considered to be an oral molecule with biologic-like efficacy

42
Q

What are the adverse effects and pharmokinetics of Tofacitinib

A

Administered orally two times a day.

Potential for cytochrome p450 interactions, increased risk of infections, headache, diarrhea, nasopharyngitis

Julie Pharm (14 decks)

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