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PHAR 255 - Therapeutics (3) > Misc. Autoimmune (RA / Gout) > Flashcards

Misc. Autoimmune (RA / Gout) Flashcards

1
Q

What is the underlying cause of Rheumatoid Arthritis?

A

AB development (triggered by some preceding event) within the Synovial Space, leading to joint & connective tissue inflammation / destruction.

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2
Q

What is “pannus”?

A

Non-functional scar tissue that develops within the joint space (due to chronic inflammation from RA disease state).

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3
Q

Is bone damage in RA reversible? Cartilage damage?

A

Bone: Slightly.

Cartilage: Nope (permanent).

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4
Q

What is the most well-defined trigger event for Rheumatoid Arthritis?

A

Smoking

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5
Q

What happens to ligaments in RA? Tendons?

A

Ligament: Laxity (overstretching leading to loss of supportive function & increased fall risk).

Tendon: Shorten & become non-pliable / tighter (causes joint to twist into locked positions).

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6
Q

Ligament Laxity most commonly affects what areas of the body? Tendon Contractures?

A

Ligament Laxity: Knees & Ankles.

Tendon Contractures: Hands & Wrists.

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7
Q

What gender is most commonly affected by RA? Most common age of onset?

A

Females (3:1); 30s - 50s.

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8
Q

When is Rheumatoid Arthritis worst throughout the day? Osteoarthritis?

A

RA: 1st thing AM worst, gets better as movement occurs.

Osteo: Best 1st thing AM, gets worse throughout the day.

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9
Q

Over what length of time (in wks) must symmetrical joint pain & stiffness be present for a Rheumatoid Arthritis diagnosis to be warranted?

A

6wks

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10
Q

What systemic symptoms accompany an RA flare-up?

A

-Muscle Pain
-Fatigue
-Weakness
-Low Grade Fever
-Reduced Appetite

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11
Q

What are the most important differences in clinical presentation between RA & Osteoarthritis?

A

RA: Symmetrical Distribution, Morning Stiffness, Presence of Systemic Symptoms (especially during flares).

Osteo: Typically Unilateral Distribution, Progressive Stiffness throughout the day, No Systemic Symptoms.

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12
Q

Is swelling of the joint more common in RA or Osteoarthritis?

A

RA; Little swelling with Osteoarthritis.

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13
Q

Does the intraarticular space & cartilage shrink in Early Stage RA? Late Stage RA?

A

Early Stage: No.

Late Stage: Yes (more closely resembles Osteoarthritis in this respect).

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14
Q

What percentage of RA patients demonstrate bone erosion at the time of their diagnosis?

A

30%

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15
Q

Extraarticular consequences of RA in blood vessels, lungs, & eyes?

A

Blood Vessels: Rheumatoid Vasculitis (commonly affects vessels supplying skin, can affect Kidney & Heart supplying vessels).

Lungs: Pleuritis / Pleural Effusion, Fibrosis, Nodule Formation.

Eyes: Iritis / Uveitis (permanent vision loss), Scleritis (just redness).

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16
Q

Extraarticular consequences of RA in the heart, muscles, & bones?

A

Heart: Pericarditis, Myocarditis (increases risk of CAD, HF, A. Fib).

Muscles: Weakness & Myalgias.

Bones: Osteopenia (leads to bone loss around affected joints).

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17
Q

Extraarticular consequences of RA at the level of the skin & hematologically?

A

Skin: Nodules & Ulcers.

Hematologic: Anemia (due to Chronic Disease).

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18
Q

What lab tests (coupled with signs & symptoms of RA) would suggest RA presence?

A

-Elevated Erythrocyte Sedimentation Rate (ESR) & Cross-Reactive Protein (CRP).

-Presence of Rheumatoid Factor (60-70% of patients).

-Anti-CCP as well.

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19
Q

A “Patient Assessment of Global Disease Activity” (PtGA) score of </= ___ is suggestive of RA disease remission or low disease activity.

A

2

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20
Q

Early recognition & diagnosis of RA is key, as significant damage occurs within the first ____ years of disease onset.

A

two

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21
Q

The “start low & go slow” approach to using DMARDs in RA is only appropriate to what patient demographic?

A

Very mild & early RA presentation… Otherwise, treat aggressively!

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22
Q

DMARD use should take place within ____ months of RA diagnosis.

A

three

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23
Q

Non-Pharm measures for treating RA?

A

-Balance of rest & exercise, as forced movement in states of 4 to 10 / 10 level pain worsens condition, but no movement at all causes muscular atrophy.

-Diet Mods / Weight Loss, as less weight bearing down on affected joints is a good thing.

-Occupational / Physical Therapy (to maintain QOL & Functionality).

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24
Q

What classes of therapeutic options do we have for RA maintenance treatments? For RA flares?

A

Maintenance: tDMARDs, Biologic DMARDs, Synthetic DMARDs.

Flares: Corticosteroids, NSAIDs, Combo of Both.

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25
Q

What drugs are considered to be “Traditional DMARDs”?

A

Methotrexate, Leflunomide, Hydroxychloroquine, Sulfasalazine

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26
Q

tDMARDs have a _____ (fast / slow) onset of action.

A

slow

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27
Q

Which tDMARDs are considered to be the safest? Most potent?

A

Safest: HCQ, SSZ
Potent: MTX, Leflunomide

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28
Q

Why are Methotrexate & Leflunomide considered to be much more potent than HCQ & SSZ?

A

Directly target the immune system itself rather than inflammatory mediators.

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29
Q

MOA of HCQ? SSZ?

A

HCQ: Neutrophil / Chemotaxis Inhibition.

SSZ: Prodrug conversion to 5-ASA & Sulfapyridine; Modulates inflammatory mediators.

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30
Q

MOA of MTX? Leflunomide?

A

MTX: Anti-Folate (thus impairs DNA synthesis / repair / replication / immune response).

Leflunomide: XXX Pyrimidine Synthesis, leading to AI effects!

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31
Q

Dosing regimen for MTX in RA treatment?

A

7.5mg OW (to start), increase by 2.5 - 5mg / wk until 25mg OW target is met!

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32
Q

What’s an acceptable MTX dose for someone with tolerability concerns? Is going over 25mg dose more efficacious?

A

15mg acceptable; No additional efficacy & additional adverse effects when exceeding 25mg OW dose.

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33
Q

Can MTX be used with somebody who is renally impaired?

A

Yep! Can even use in dialysis patients (just have to cut target doses & titrations in 1/2).

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34
Q

Of the tDMARDs (HCQ, SSZ, Leflunomide, MTX) which one is best tolerated?

A

HCQ

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35
Q

Side effects of HCQ?

A

-NVD / Stomach Cramps
-Headache / Dizzy
-Skin Rxns (10%)

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36
Q

Side effects of SSZ?

A

-NVD
-Headache
-Photosensitivity

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37
Q

Side effects of Leflunomide?

A

-Rank Nausea & Diarrhea (60% d/c rate due to this)
-Weight Loss (indirectly from Nausea & Diarrhea)
-Rash / HTN
-Alopecia (is reversible)

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38
Q

Side effects of MTX?

A

-NV
-Tired
-Stomatitis
-Photosensitivity
-Alopecia
-Itchy / Burning Skin

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39
Q

How can we manage side effects of MTX?

A

1) Folic Acid 1-5mg OD (or 5-10mg OW)… Helps with NV / Fatigue / Stomatitis.

2) Split Dosing… Reduces fatigue & GI effects.

3) Sc MTX dosage form… Reduces GI effects.

4) PPI for 3d around MTX dose… Reduces GI effects.

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40
Q

Serious adverse effects of LT HCQ usage?

A

Ocular Toxicity… If on it beyond 5yrs duration, yearly eye exams important!

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41
Q

Serious adverse effects of MTX?

A

-Hepatotoxicity (get LFTs q6mth).

-Hematologic Abnormalities (get baseline counts).

-Pulmonary Toxicity (get baseline chest x-rays).

-Infection rate increases (typically URTIs most common, sometimes Pneumonia).

-Reversible Sterility (6mth - 1yr to return upon d/c).

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42
Q

Serious adverse effects of Leflunomide?

A

-Hepatotoxicity
-Wt. Loss
-Infection Increases

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43
Q

Outright CIs of the “safest” tDMARDs?

A

HCQ:
1) Pre-Existing Retinopathy

SSZ:
1) Salicylate / Sulfa Allergy

2) PPT. Asthma Attacks from ASA or NSAIDs

3) Sev. Renal / Hepatic Impairment

4) Existing GI Ulcers

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44
Q

Outright CIs of MTX?

A

1) Severe Hepatic Impairment

2) Existing Hematologic Abnormalities

3) Pregnant / Breastfeeding (BIG ONE!!!)

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45
Q

Outright CIs of Leflunomide use?

A

1) Mod - Sev Renal (anything < 60mL / min GFR) or Hepatic Impairment

2) Existing Hematologic Abnormalities

3) Pregnant / Breastfeeding (BIG ONE!!!)

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46
Q

DDIs of HCQ & SSZ?

A

HCQ: Other QT-Prolonging agents (ie. Anti-Arrythmics, Anti-Microbials, Certain ADs, Quetiapine).

SSZ: Warfarin (affects INR), MTX (increased nausea).

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47
Q

DDIs for Leflunomide?

A

Bile Acid Sequestrants (can be given deliberately to enhance drug elimination in cases of adverse reactions to the drug).

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48
Q

IS MTX CONCURRENT DOSING WITH NSAIDS INAPPROPRIATE???

A

NOOOOOO DUMBASS (CRA Position Statement got mad at us for this).

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49
Q

Why is it okay to dose NSAIDs concurrently with MTX in RA treatment?

A

Interactions were significant at anti-cancer doses of MTX (ie. 500 - 2000mg Weekly Doses)… WAAAAAY lower in RA management!

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50
Q

Christina comes in with the following prescription to treat an upper respiratory infection:

Septra DS (Sulfamethoxazole / Trimethoprim) 800 / 160mg

SIG: 1T OD x 10d

Her PIP Profile says she’s on the following meds:

Metformin 500mg (TIID)
Atorvastatin 20mg (Dyslipidemia)
Methotrexate 7.5mg (RA Management)
Naproxen 500mg (RA Flares)

Good to fill?

A

NOOOO!!!!! MTX interacts with Trimethoprim (greatly increases risk of Pancytopenia irrespective of dose). Don’t fill it!!!

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51
Q

Is Leflunomide or Methotrexate typically better tolerated?

A

MTX

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52
Q

Rank the tDMARDs by relative potencies.

A

MTX = Leflunomide > SSZ > HCQ

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53
Q

Biologic DMARD usage is reversed for what occasion?

A

tDMARD (ie. MTX) failure!

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54
Q

What are the four classes of Biologic DMARDs?

A

1) TNF-Alpha Inhibitors
2) IL-1 / IL-6 Inhibitors
3) T-Cell Co-Stim Inhibitors
4) B-Cell Depletors

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55
Q

Concerns for all Biologic DMARDs?

A

-ND / Headache / Malaise
-Injection Site Rxns
-Increased Infection Rates
-Neutropenia
-Malignant Disease Development (Skin Cancer & Lymphomas)
-AB Development

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56
Q

What can be done to mitigate injection-site reactions of administered Biologic DMARDs?

A

90min pre-treatment with Ace + Anti-Histamine + Corticosteroid

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57
Q

What opportunistic infections must be pre-screened for in those initiating Biologic DMARD therapies?

A

-Tuberculosis
-Mycobacterium
-Pneumocystis Pneumonia
-Cytomegalovirus
-Zoster Virus
-Hepatitis B & C
-HIV

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58
Q

Counseling Point for patients initiating Biologic DMARD therapies?

A

“Get up to date on your vaccines!!!”

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59
Q

Safest Biologic DMARD in high-risk infection patients?

A

Abatacept (is the least immunosuppressive option available).

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60
Q

Which of the Biologic DMARD classes is the only one without concern of AB development?

A

IL-6 Inhibitors

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61
Q

AB development against Biologic DMARDs typically occurs within the first ___ - ___ months of starting therapy.

A

two to six

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62
Q

Which Biologic DMARD(s) demonstrates the highest risk of AB development? Lowest risk?

A

Highest: Infliximab (50%)

Lowest: Adalimumab, Etanercept (12%)

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63
Q

What drugs would be considered TNF-Alpha Inhibitors?

A

Adalimumab, Certolizumab, Etanercept, Golimumab, Infliximab

64
Q

What strategy both increases the efficacy of and reduces AB development against TNF-Alpha Inhibitors?

A

Combination with MTX… Up from 40% to 60% ACR50 score.

65
Q

Of the TNF-Alpha Inhibitor drugs, which one(s) are indicated for MTX combination?

A

Golimumab & Infliximab

66
Q

T or F: TNF-Alpha Inhibitor drugs should always be avoided in pregnancy / lactation.

A

FALSE!!! All are very safe in pregnancy / lactation!

67
Q

Which of the TNF-Alpha drugs are available in IV dosage form?

A

Golimumab & Infliximab

68
Q

Outright CIs to TNF-Alpha Inhibitors?

A

-Active Severe Infection
-Mod - Severe HF

69
Q

TNF-Alpha Inhibitor drugs can cause transient liver enzyme elevations… An ALT above __x the upper limit of normal becomes concerning.

A

5x

70
Q

What other adverse effects can come about from TNF-Alpha Inhibitors?

A

-Cause / Worsen HF
-Cutaneous Rxns (Cellulitis, AI Skin Dx’s, Malignancies)
-Other AI Conditions (Lupus)
-Seizure Risk

71
Q

Which TNF-Alpha Inhibitor drugs have biosimilars?

A

Infliximab, Etanercept, Adalimumab

72
Q

Name of weak (Carter Berg Bench Press SAAAAD) IL-1 Inhibitor Drug?

A

Anakinra

73
Q

Two available IL-6 Inhibitor drugs?

A

Tocilizumab, Sarilumab

74
Q

Peak effects of IL-1 / IL-6 Inhibitors is ___ - ___ mths.

A

five to six

75
Q

What are the outright CIs of using Anakinra (IL-1i) & Sarilumab (IL-6i)?

A

NONE! However, would aim to withhold during active infections.

76
Q

Outright CI to using Tocilizumab?

A

Active Infection… Like other two related drugs but this is an explicitly labeled CI.

77
Q

Below a CrCl of ___ml / min would warrant a dose adjustment for IL-1 / IL-6i drugs.

A

< 30mL / min

78
Q

Unique adverse effects of the two IL-6 Inhibitor drugs?

A

-GI Perforation
-Dyslipidemia
-HTN

79
Q

Is AB development against IL-6i drugs linked to reduced effects (as seen with TNF-Alpha drugs)?

A

NOOO (unique to this class)!

80
Q

Tocilizumab has one unique DDI… It increases the systemic concentrations of this drug (what is it???) by 4-10x.

A

Simvastatin

81
Q

In addition to other usual lab tests that are ordered for DMARD patients (ie. Baseline CBCs, LFTs, CrCl, Disease Screens), what other lab test should be ordered for somebody initiating IL-6i drugs?

A

Lipid Panels (remember heightened dyslipidemia risk)!

82
Q

Abatacept is an example of a ___________ (what drug class is it part of).

A

T-Cell Co-Stimulation Inhibitor

83
Q

What would be an outright CI for T Cell Co-Stimulation Inhibitors?

A

COPD (exacerbates condition)

84
Q

Do T Cell Co-Stim Inhibitor drugs have impacts on Liver function?

A

Nope (main potential use case)

85
Q

What else can be considered adverse effects of T Cell Co-Stim Inhibitor drugs?

A

-HTN
-Blood Glucose Elevations

86
Q

“MAB” drug that is a B Cell Depletor?

A

Rituximab

87
Q

Onset of action for Rituximab?

A

6mths

88
Q

Rituximab requires pre-treatment with _________, __________, & __________.

A

methylprednisolone, acetaminophen, diphenhydramine

89
Q

HTN, GI Perforation & Blood Glucose increases are adverse effects of Rituximab. What other unique adverse effect can occur from its administration?

A

Mucocutaneous Rxn’s (SJS, TEN)

90
Q

Examples of JAKi drugs?

A

Tofacitinib, Baricitinib, Upadacitinib

91
Q

Adverse effects of JAKi drugs?

A

-Infection
-HTN
-Hepatotoxic
-Bradycardia
-GI Perforation

92
Q

Do ABs develop against JAKi drugs?

A

Nope

93
Q

Of the three JAKi for RA (Tofacitinib, Upadacitinib, Baricitinib), which ones are major CYP3A4 substrates?

A

First two!

94
Q

The main benefit of Corticosteroid usage in an RA flare is what?

A

Subjective Symptomatic Improvement

95
Q

A Prednisone equivalent dose of ___ - ___mg / day is appropriate for short-term use.

A

10 - 15mg

96
Q

What is the average Corticosteroid treatment duration for RA flare management?

A

2mths (includes time needed for tapering)

97
Q

A Prednisone equivalent dose of ___ - ___ mg / day is considered an appropriate dose for chronic usage.

A

5 - 10mg

98
Q

What would be some examples of good adjunctive therapies for chronic steroid users who have RA?

A

-Bisphosphonates
-Ca2+
-Vit. D

99
Q

If multiple yearly courses of Corticosteroids are required for RA management, what should we monitor for?

A

-Cataracts
-Dyslipidemia
-Hyperglycemia
-Osteoporosis
-Weight Gain

100
Q

If a patient goes in for an IA Corticosteroid injection, what is the limit for number of injections on said joint within 3mths?

A

1 injection / 3mths on a singular joint

101
Q

How long does symptomatic RA relief last when one undergoes an IA Corticosteroid injection?

A

4wks

102
Q

Issues with IA Corticosteroid injections?

A

-Tendon Rupture
-Acute Synovitis
-Local Skin Hypopigmentation
-Septic Arthritis

103
Q

Which NSAID is favored for LTU in RA pain management?

A

Celecoxib (is gastroprotective)

104
Q

Why do we advise against NSAID / Corticosteroid combinations when managing pain flares in RA patients?

A

Amplified potential for GI toxicity, ulcer risk, GI bleeds!

105
Q

Do Opioids have utility in RA pain management?

A

Nope… Avoid.

106
Q

After a timeframe of ___ mths with low disease activity or total remission, DMARD tapers can be initiated.

A

6mths

107
Q

According to CRA Guidelines, is it appropriate to totally discontinue DMARDs?

A

NOPE… Reduce dose as much as possible while keeping disease activity low (but not recommended to d/c drugs).

108
Q

When would be a suitable time to step-up DMARD therapies?

A

Failure to achieve remission or acceptable disease activity after 3 - 6mths at OPTIMAL DOSES!!!

109
Q

How many recurrent RA flares per year would warrant consideration for DMARD step-ups?

A

1 warrants consideration; 2 flares / yr definitely do it!

110
Q

For how many months prior to impregnation should MTX users have discontinued the drug?

A

3mths prior to conception (same for Leflunomide once levels < 0.02mg / mL)

111
Q

What is the only Biologic DMARD that does not have a favorable safety profile in pregnancy?

A

Rituximab

112
Q

Which Biologic DMARD has the most robust data for use in pregnancy?

A

Certolizumab

113
Q

For those who are breastfeeding, which NSAID is preferred for RA pain management?

A

Ibuprofen

114
Q

Prednisone doses below ___ mg / day are okay for RA pain management in lactation.

A

20mg / day

115
Q

In cases of Gout, what is the most common reason for hyperuricemia?

A

Purine overconsumption in the diet.

116
Q

Hyperuricemia is defined as having serum uric acid levels above ____ umol / L.

A

420 umol/L

117
Q

Why do Gout flares typically happen within peripheral extremities?

A

Cold Temps… Extremities have tendency to be colder & solubility of Uric Acid decreases with lowered temps.

118
Q

Aside from Purine Overconsumption, what disease states can cause Uric Acid Overproduction?

A

Obese
Hypertriglyceridemia

119
Q

How do diuretics cause hyperuricemia?

A

Fluid leaves joint space, hyperconcentration of Uric Acid within joints.

120
Q

What gender does Gout more commonly affect?

A

Men

121
Q

Which patients with Asymptomatic Hyperuricemia (ie. > 420 umol / L) should get drug treatments?

A

Poor Renal Health
> 800 umol / L & no sx

122
Q

Which joints are most commonly affected by gout attacks?

A

Toes, Instep, Ankle

-Knees, Wrists, Fingers less probable.

123
Q

What are the consequences of Chronic Tophaceous Gout?

A

-Joint Deformity
-Tissue Damage
-Joint Destruction
-Nerve Compression
-Kidney Stones & Urate Nephropathy

124
Q

Gout Flares typically self-resolve within how many days?

A

7d

125
Q

Instead of limiting Purine rich foods, what is a more feasible dietary adaptation to prevent Gout Flares?

A

Caloric Intake Restrictions

126
Q

First NSAID with an official Gout Flare indication?

A

Indomethacin

127
Q

Why caution Indomethacin use in elderly with Gout Flares?

A

Crosses BBB (more potential for Drowsiness / Confusion / CNS Effects than other NSAIDs).

128
Q

Naproxen & Ibuprofen dosing regimens for acute gout flares?

A

Nap: 500mg TID x 2-3d, then cut back to 250-500mg BID.

Ibu: 600-800mg TID x 2-3d, then cut back to 400-600mg TID.

129
Q

Why do we treat with NSAIDs a few days beyond a week even though gout flares self-resolve in one week?

A

NSAID discontinuation right at 1wk can re-exacerbate gout flares.

130
Q

Prednisone dosing for acute gout flare?

A

25-50mg OD x 3-5d

131
Q

What would be some circumstances where acute steroid usage in a gout flare warrants a taper?

A

-Long course of steroids required (ie. Couple Weeks).

-Multiple Flares / Short Intercritical Period (so bulk intake of steroid is greater in a shorter span of time).

132
Q

Colchicine is a historically old drug (1500BC)… What plant was it derived from?

A

Autumn Crocus

133
Q

Colchicine should only be initiated within how many hours of a gout flare?

A

24hrs

134
Q

Optimal Colchicine dosing?

A

Day 1: 1.2mg (2T) stat, then 0.6mg (1T) 1hr later for a total daily intake of 1.8mg.

Next 7-10d: 0.6mg (1T) OD or BID until resolution of flare.

135
Q

In Renal Impairment, appropriate to use Colchicine?

A

Probably pick something else… Evidence for how to dose reduce in renal failure not well studied.

136
Q

Outright Colchicine CI?

A

Concurrent Renal / Hepatic Impairment with co-admin of CYP3A4i drugs!

137
Q

Side effects of Colchicine?

A

GI Related & Myopathy / Rhabdo potential.

138
Q

Important DDIs with Colchicine?

A

-Statins (increased myopathy risk).

-Azole Antifungals (ie. Ketoconazole), Clarithromycin (strong CYP Inhibitor).

-Verapamil, Diltiazem, Grapefruit Juice (moderate CYP Inhibitor).

139
Q

Patient has CKD &/or CVD… What drugs do we avoid with acute gout flares?

A

Colchicine & NSAIDs… Use Corticosteroids with caution.

140
Q

Patient has history of GI problems / Ulcers… Avoid what drugs for acute gout flare treatment?

A

NSAIDs & CSs… Use Colchicine with caution at its optimized dose range (heightened GI upset potential at weird high dose regimen Dr. Enweani likes to use).

141
Q

Patient is diabetic… Which drugs do we avoid giving for acute gout flares?

A

CSs (increase blood glucose).

142
Q

Who are candidates for Gout Prophylaxis?

A

-Hx Complicated Kidney Stones.

  • > 800umol / L Serum Uric Acid levels.
  • > /= 2 Gout Attacks per year.
143
Q

Reasonable serum uric acid targets for gout prophylactic treatment?

A

< 300 - 360umol / L

144
Q

When bridging prophylactic treatments with NSAIDs or Colchicine, how long do we treat? Why bridge at all?

A

3-6mths; Prevent flares when lowering Serum Urate levels.

145
Q

Main concerns with Uricosuric Agents (ie. Probenecid, Sulfinpyrazone)?

A

-Ppt. gout flares & nephrolithiasis

-Bleed risk (Sulfinpyrazone)

146
Q

Outright CIs of Probenecid & Sulfinpyrazone?

A

CrCl < 60mL / min
ASA Concurrent Use
Hx Kidney Stones

147
Q

XOi drugs?

A

Allopurinol
Febuxostat

148
Q

Maximal effect of XOi drugs takes place in how many weeks?

A

2wks

149
Q

Average maintenance dose of Allopurinol is what?

A

300mg / d

150
Q

How often do we titrate Allopurinol doses?

A

q4wks

151
Q

Common side effects of Allopurinol?

A

-Rash & Pruritis (caution presents same as SJS hypersensitivity Rxn!!!)

-Diarrhea

-Ppt. Acute Gout Flare (hence treatment with NSAIDs / Colchicine)

152
Q

Which nationalities of people are more commonly affected by the HLA-B genotype expression (which can predict hypersensitivity syndrome brought upon by Allopurinol use)?

A

Korean, Thai, Chinese

153
Q

Febuxostat’s one outright CI?

A

Azathioprine / Mercaptopurine use (immunosuppressive nature of these drugs greatly increased with Febuxostat use).

154
Q

Important DDIs of Allopurinol (because both interactions increase Hypersensitivity Syndrome risk)?

A

ACEi’s, All Diuretics

155
Q

Uricase Enzyme drugs (ie. Pegloticase, Rasburicase) convert Uric Acid into what water-soluble metabolite?

A

Allantoin

156
Q

Main concern with Uricase Enzyme drugs?

A

AB Development (92%)… Not intended for LTU for this exact reason (require transfer onto Allopurinol or Febuxostat).

157
Q

Best choice for gout prophylaxis in pregnant women?

A

Allopurinol… Avoid Febuxostat (limited evidence).

PHAR 255 - Therapeutics (3) (7 decks)

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