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Pharmacology > MCPHS PA Pharmacology Gout DMARD Drug Info Exam 3 > Flashcards

MCPHS PA Pharmacology Gout DMARD Drug Info Exam 3 Flashcards

1
Q

WHat must be present for a Diagnosis of Gout?

A

Hyperuricemia

Plus

Deposition of monosodium urate crystals

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2
Q

What are normal uric Acid Levels?

A

Men

2.5-8.0 mg/dL

Women

1.5-6.0 mg/dL

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3
Q

What are the two types of Gout?

A

Acute Gout (Gouty Arthritis)

Severe Pain with erythema

-Usually Big Toe (Podagra)

Chronic Gout

Recurrant attacks

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4
Q

What are the complications of Gout?

A

Nephrolithiasis

AKI

CKD

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5
Q

What are the two primary causes of Gout?

A

Underexcretion of Urate

(90% of Cases)

Overproduction of Urate

(10% of Cases)

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6
Q

What are the principles of Gout Treatment?

A

Reduce swelling / Treat Pain

Accelerate Renal excretion of Uric Acid

Uricosuric Agents

Probenecid & Lesinurad

Reduce conversion of purines to Uric Acid by Xanthine Oxidase

Uricostatic Agents

Allopurinol & Febuxostat

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7
Q

What can be used in an acute Gout Attack?

A

Colchicine

NSAIDs

Corticosteroids

IL-1 Inhinitors (in some cases)

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8
Q

What is the MOA of Colchicine in an Acute Gout attack?

A

Selective inhibitor of Microtubule assembly

Reduces Leukocyte migration and phagocytosis decreasing inflammation

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9
Q

What is the administration window and onset of Colchicine?

A

Give within 48 hrs of an acute attack

Onset within 12-24 hrs pain relief comes not from the drug, but the anti-inflammitory affect.

Give with NSAID for pain

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10
Q

What are the ADEs of Colchicine?

A

Diarrhea (indicates toxicity - stop med)

GI discomfort - N/V and Abdominal pain

Bone Marrow Suppression

Neutropenia

Renal Failure - Monitor renal function / Avoid in Advanced Kidney disease

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11
Q

What DDIs does Colchicine have?

A

Strong 3A4 inhibitors (increase the toxicity of Colchicine (Grapefruit Juice!))

Protease Inhibitors (Lower Efficacy)

Azole Antifungals

Macrolides

Verapamil

Diltiazem

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12
Q

What are some facts we need to know about Colchicine?

A

Start treatment as soon as possible

NSAID pain therapy is faster

NSAID therapy preferred if no C/I

Avoid ASA (competes with Uric Acid for excretion)

If PTs have C/Is or Renal Insufficiency Corticosteroids can be used, but have more ADRs

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13
Q

What is the MOA of Anthine Oxidase Inhibitors like Allopurinol and Febuxostat?

A

Inhibit the Action of Xanthine Oxidase to inhibit production of Uric Acid

Used for both Underexcreters and Overproducers

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14
Q

What are Allopurinol’s ADEs?

A

GI Upset

Exfoliative Rash (serious, can happen acutely or years after exposure)

Bone Marrow Suppression

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15
Q

What are Febuxostat’s ADEs?

A

Rash (not as serious as Allopurinol)

LFT elevations (<2%)

Diarrhea

Reports of CV disease (Do not use in Cardiac PTs)

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16
Q

What DDIs do Xanthine Oxidase Inhibitors have?

A

Mercaptopurine

Azathioprine

(Increase in toxicity because these both need Xanthine Oxidase)

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17
Q

Does Allipurinol or Febuxostat have better Selectivity?

A

Febuxostat has better selectivity and may have better efficacy.

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18
Q

Is Allipurinol or Febuxostat better for Renal PTs?

A

Febuxostat

More expensive though

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19
Q

What is the metabolite of Allopurinol?

A

Oxypurinol

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20
Q

What is the MOA of Probenecid?

A

Antagonize URAT1 to block Uric Acid Reabsorption (increases Excretion)

(May also interfere with tubular secretion of multiple substrates via OAT1 and OAT3)

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21
Q

When is the use of Probenecid indicated?

A

Useful in underexcretors (most gout cases) when Allopurinol and Febuxostat are C/I or when Tophi present.

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22
Q

What are the ADEs of Probenecid?

A

Uric Acid Kidney Stones (Less reabsorption means more in kedney)

GI intolerance (Dyspepsia / Acid Reflux)

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23
Q

What extra considerations are there when evaluating use of Probenecid?

A

Requires Good Kidney function

Adequate Hydration

Urine pH monitoring

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24
Q

What DDIs does Probenecid have?

A

Penicillins

Cephalosporins

Methotrexate

ASA (Low doses <2g/day)

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25
What is the MOA of Lesinurad?
Antagonist of URAT1 and OAT4 transporters to block Uric Acid reabsorption (increases excretion)
26
What Black box warning does Lesinurad have?
It cannot be used as monotherapy, it is only cleared fro use with Allopurinol to reduce renal related events.
27
What are the ADEs of Lesinurad?
Headache Elevations in SCr Influenza
28
What DDIs does Lesinurad have?
Hormonal contreceptives (Reduced Efficacy) (Estrogen +/- Progestin) ASA
29
What is the MOA of Pegloticase?
It Catalyzes Oxidation of Uric Acid to readily eliminated metabolite (allantoin)
30
When is Pegloticase Use appropriate?
For Refractory Gout PTs unresponsive to conventional therapy
31
How is Pegloticase administered?
IV every other week (Extremely expensive)
32
What ADEs does Pegloticase have?
GI intolerence Anaphylaxis Development of antipegloticase antibodies Arthralgia Nephrolithiasis
33
How are IL-1 inhibitors used with gout?
Off label - Inhibits the inflammatory cytokines that are at work in a Gout attack. For PT's refractory to coventional therapies or that have C/I.
34
How do DMARDs treat RA?
Slow disease progression and preserve structure / function of joint by either Inhibiting Cytokines Suppressing activity of lymphocytes (T&B cells)
35
What is the Critical concern when using DMARDs?
Safety considerations are critical as these drugs are immunosuppressive.
36
What Cytokines are active in RA?
**_TNF-Alpha_** (Important mediator of acute inflammation; recruits neutrophils& macrophages to site of injury/infection) **_Interleukin-1 (IL-1)_** (Similar to TNF Alpha, also helps activate T-Cells) **_IL-6_** (Activates T-Cells; STimulates Fibroblasts)
37
What Effects do Cytokines have in RA?
**Increased Endothelial permiability to Leukocytes** **Stimulate Osteoclasts / Stimulates release of Collagenase** (Breakdown collagen and bone) **Progressive irreversible deformities in joints and functional impairment** (RA has to many pro-inflammitory and not enough anti-inflammitory effects)
38
What is JAK-STAT signaling?
Janus Kinase Signal Transducer and Activation of Transcription Ligand activation of JAK forms STAT dimer which travels to nucleus and changes Gene expression
39
How are they administered and what is the Onset of the Non-Biologic DMARDs?
Orally Methotrexate - 4-8 weeks Leflunomide - 4-12 weeks Sulfasalazine - 8-12 weeks
40
What is the MOA of Methotrexate?
**_Multifactorial_** **Reduce purine biosynthesis -\> reduces DNA synthesis** **At low doses (RA), selectively inhibits the replication of Tand B cells** (high doses treat cancer)
41
What is the preferred DMARD treatment for RA unless contraindicated?
Methotrexate
42
What are the C/Is for Methotrexate?
Pregnancy / breastfeeding (discontinue 3 months before conception)
43
What are Methotrexate's ADEs?
Decreased Immune response (Myelosupression) GI Toxicity (Nausea and Mucosal ulcers (mucositis)) Pulmonary Toxicity (Pneumonitis) Hepatic Fibrosis (Monitor LFT's every 3 mos (avoid if LFTs \>2x ULN)) THrombocytopenia Mild Apnea
44
Can anything decrease ADEs when on Methotrexate?
Folic Acid (1-5 mg daily) | (Reduces liver toxicity 5mg best)
45
What is Leflunomide's MOA?
Inhibits autoimmune T-Cell proliferation and production of autoantibodies by B cell
46
Does Leflunomide have comparable efficacy to Methotrexate?
Yes, and it has a longer half-life.
47
What are Leflunomide's C/Is?
C/I in pregnancy and Breast feeding (will need to stop sooner than methotrexate due to Half-life)
48
What are Leflunomide's ADEs?
Alopecia Hematologic Toxicity Diarrhea -\> significant (25%) Rash -\>Steven's Johnson Syndrome (Very bad) Severe Hepatotoxicity (avoid if LFTs \>2x ULN)
49
What is the MOA and Efficacy of Sulfasalazine?
The MOA is not known, and the efficacy is less than the other drugs we have covered.
50
Is Sulfasalazine safe to use in pregnancy?
Rated B, Probably safe to use while pregnant, but not for breastfeeding. (May cause neonatal Jaundice)
51
What are Sulfasalazine's ADEs?
GI effects (less with EC coated tabs) Lupus-like Syndrome HA / Fever / Rash Hepatotoxicity Avoid if documented Sulfa Allergy
52
What is monitored on non-biologic DMARDS?
**CBC / LFT / SCr** for **_Methotrexate / Leflunomide / Sulfasalazine_** Every _**2-4 weeks** for first **3 months**_ then every **_8-12 weeks after_**
53
What are the advantages of Biologic DMARDS?
These Monoclonal Anti-bodies are Rapid onset 1-4 weeks for most!
54
What are the disadvantages of Biologic DMARDs?
They are Expensive More immunosuppressive increasing infection risk.
55
Which type of DMARDs are the First Line biologics?
Tumor Necrosis Factor (TNF) inhibitors | (Anti-TNFs)
56
How are Anti-TNFs administered?
MABs are always injected. All are SQ except **Infliximab** which is **IV**
57
What is the MOA of Etanercept?
Soluble TNF receptor blockade
58
What is the MOA of Adalimumab and Golimumab?
Human Anti-TNF antibody
59
What is the MOA of Infliximab?
Chimeric anti-TNF antibody
60
What is the MOA of Certolizumab Pegol?
Pegylated humanized Fab fragment of TNF-alpha antibody
61
What are the ADEs of anti-TNF antibodies?
**Increased susceptibility to infection** - Bacterial and fungal infection - Potential for reactive TB -\> check PPD before use - No live vaccines while on drug **New or worsening cases of HF** -Changes in LV remodeling, negative inotropic effect **Increased risk of Lymphoma (low incidence to date)** **Injection site reactions, arthralgia, rash, cough**
62
Are there any C/Is for anti-TNF DMARDs?
DO not use with HF
63
What are the Routes of administration for the Non Anti-TNF Biologic DMARDs?
**_SQ_** Anakinra Sarilumab **_IV_** Toclizumab Abatacept Rituximab
64
What is the Specific Action of Anakinra?
IL-1 receptor inhibitor
65
What is the Specific Action of Rituximab?
B-Cell inhibitor
66
What is the Specific Action of Abatacept?
T-Cell co-stimulation inhibitor
67
What are the Specific Actions of Toclizumab and Sarilumab?
IL-6 receptor inhibition / antagonist
68
What are the ADEs of Abatacept?
Avoid combining with anti-TNF biologics -\> increased infection Malignancy -Respiratory events in COPD PTs
69
What are the ADEs of Rituximab?
Fatal infusion related reactions Severe mucocutaneous reactions Hep B reactivation Infections
70
What are the ADEs of Toclizumab?
Severe infections GI perforations Netropenia Thrombocytopenia LFT elevations Dyslipidemia (Most Lab complications / Most headache to monitor)
71
What are the ADEs of Anakinra?
Avoid with anti-TNF biologics
72
What are the Oral biologics?
Small non-protein molecules Tofacitinib Baricitinib -Citi**nibs** Nibs are small
73
What is the MOA of Oral Biologics?
Inhibits activity of JAK enzyme at the Cytokine receptor -\> Reduces Cytokine transmission signaling -\> Decrease inflammation
74
What are the ADEs of JAK inhibitors (oral biologics)?
Similar to other biologics Infection Reactivation of TB Risk of malignancy Avoid live Vaccines GI perforation Dyslipidemia Anemia / Neutropenia Hepatoxixity Thrombosis (screen for risk)

Pharmacology (14 decks)

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