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Pharmacotherapy I > Exam 4 Gout > Flashcards

Exam 4 Gout Flashcards

1
Q

What factors can increase serum urate concentrations?

A

Age, Scr/BUN, male gender, blood pressure, body weight (obese pts twice as likely), and alcohol intake

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2
Q

What percent of patients with hyperuricemia develop gout?

A

20%

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3
Q

What 3 ways can we help with gout according to the purine metabolism mechanism?

A

Inhibit uric acid production, degrade uric acid, or help the body eliminate it

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4
Q

What enzyme overactivity can increase de novo purine synthesis and lead to gout?

A

PRPP synthetase

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5
Q

What lab value classifies as hyperuricemia?

A

> 6.0 mg/dL in women, >7.0 mg/dL in men

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6
Q

What cells and mediators are involved in acute inflammatory gouty response?

A

Monocytes, neutrophils, IL-1, IL-1B, and IL-8

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7
Q

What are some causes of secondary gout?

A

Cell death and lysis – chemotherapeutic agents, myelo- and lymphoproiferative disorders, polycythemia vera, anemia, psoriasis

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8
Q

What are some causes of primary gout?

A

Ethanol (increased purine catabolism, increased lactic acid), foods high in purines (meat, shellfish, veggies), obesity (urate production increases with surface area)

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9
Q

What conditions can be associated with hyperuricemia?

A

DKA/insulin resistance, myelo- and lymphoproliferative disorders, starvation/dehydration, hemolytic anemia, toxemia or pregnancy, psoriasis, polycythemia vera, renal transplantation, obesity, sarcoidosis, heart failure, renal dysfunction, metabolic syndrome, infection, hypo or hyperparathyroidism, alcoholism, aromegaly, hypothyroidism, stress/trauma

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10
Q

What drugs can induce hyperuricemia?

A

diuretics, nicotinic acid, salicylates, ethanol, cyclosporine, pyrazinamide, levodopa, ethambutol, cytotoxic drugs, urate lowering therapies

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11
Q

Name signs and symptoms of a gout exacerbation.

A

Fever, intense pain, erythema, warmth, swelling, and inflammation all leading to severe disability, peak severity within 12-24 hours but can last 3-14 days

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12
Q

How does gouty arthritis occur?

A

Aggregation of MSU crystals (tophi) over years of recurrent attacks can occur in cartilage, tendons, and synovial membranes, and can eventually lead to bone destruction.

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13
Q

What is podagra?

A

Gout involving first metatarsophalangeal joint (the big toe)

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14
Q

Why does gout occur more commonly in lower joints?

A

Lower temperature within those joints combined with high intraarticular urate concentration. Synovial effusions in these weight bearing joints during the day and at night water is reabsorbed, leaving supersaturated MSU

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15
Q

What is the gold standard for gout diagnosis?

A

Visualization of urate crystals from the joint or tophi through aspiration. However, clinical diagnosis is common.

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16
Q

What do you consider to clinically diagnose gout?

A

Pain, swelling, erythema, big toe involvement, monoarticular, > one attack, suspected or proven tophi, joint damage on Xray, pain free between episodes, hyperuricemia, peak inflammation within one day
Hyperuricemia can support diagnosis but not diagnostic

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17
Q

What is one long-term kidney complication of gout?

A

Uric acid nephrolithiasis. Uric acid is less soluble in acidic urine (

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18
Q

What is tophaceous gout?

A

A late complication characterized by joint destruction, pain, and nerve compression at the base of big toe, helix of ear, bursae, achilles, knees, wrists, and hands

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19
Q

Differentiate between acute and chronic gouty nephropathy.

A

Acute – urine blow blocked by MSU crystals, leading to acute renal failure
Chronic – long-term deposition of urate crystals can lead to proteinuria, often associated with HTN, DM, and atherosclerosis

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20
Q

What non-pharmacologic things can we do to help gout?

A

Reduce dietary purines (meat, seafood, alcohol, cheese), fructose-containing products (energy drinks, soft drinks), increase fluid intake (decreased nephrolithiasis risk), increase low-fat or nonfat dairy products, rest joint for 1-2 days, avoid heat, apply ice, weight loss

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21
Q

How does colchicine help in gout?

A

By binding to tubulin, it inhibits leukocyte migration, motility, and phagocytosis and inhibits LTB4 synthesis, relieving pain and inflammation but not altering urate metabolism/excretion.

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22
Q

What notable drugs interact with colchicine?

A

Cyclosporine, tacrolimus, and verapamil all increase levels of colchicine by inhibiting excretion in bile in urine

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23
Q

What NSAIDs inhibit urate crystal phagocytosis?

A

Indomethacin and other NSAIDs except aspirin

Oxaprozin also increases urate excretion in urine

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24
Q

What agents reduce serum urate levels?

A

Probenecid, allopurinol, and febuxostat.

These decrease the pool of urate (goal

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25
Q

How do uricosuric agents like probenecid and sulfinpyrazone function?

A

They compete with uric acid at the anionic transport site of reabsorption in the renal tubule so that more uric acid will be excreted.

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26
Q

What drugs interact with uricosuric agents?

A

Salicylates, nicotinic acid, diuretics decrease effectiveness by competing for same transporter. Probenecid blocks secretion of sulfonamides, penicillins, cephalosporins.

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27
Q

How does allopurinol help with gout?

A

It is an isomer of hypoxanthine that binds xanthine oxidase and is converted to oxypurinol which tightly binds and inhibits the enzyme. Inhibition is lost upon re-oxidation of the enzyme.

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28
Q

What non-purine inhibitor of xanthine oxidase functions slightly better than allopurinol?

A

Febuxostat – inhibits both reduced AND oxidized enzyme.
Metabolized in liver, excreted via kidney.
Good for patients who cant get allopurinol, reduced kidney function, or not responding to high allopuriniol doses.

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29
Q

What two biologic drugs are enzymes that break down uric acid to allantoin?

A

Pegloticase (Krystexxa)–mammalian uricase covalently attached to mPEG (lower immunogenicity). Long half life. NOT for G6PD deficiency pts.
Rasburicase (Elitek)–recombinant enzyme from aspergillus cultured in yeast. Given IV before chemotherapy to pediatric leukemia patients. Not FDA approved for gout. Short half life, high cost.

30
Q

True or false: Some NSAIDs are better than others at treating an acute gout attack.

A

False–all NSAIDs are equally effective.

Indomethacin, naproxen, and sulindac are FDA approved

31
Q

How are NSAIDs dosed in an acute gout attack?

A

Use MAX dose at onset of symptoms, continue for 24 hours after symptom resolution. Taper quickly over 2-3 days.

32
Q

What are the first-line treatments in an acute gout attack? In what order do you consider them?

A

NSAIDS, colchicine, and corticosteroids. NSAIDs are used unless the patient has a contraindication. If so, consider time since onset. If 36 hours since onset, use corticosteroid.
Idealy, initiate within 24 hours and continue ongoing urate-lowering therapy.

33
Q

What would contraindicate NSAID therapy for an acute attack? What conditions would make us cautious about NSAIDs?

A

Contraindications – hypersensitivity, decompensated HF, active PUD or GI bleed, and severe/acute renal impairment
Cautions – uncontrolled HTN, h/o HF or CAD, h/o PUD or GI bleed, renal impairment (CrCl

34
Q

What effect do NSAIDs have on kidney function?

A

Increased SCr, decreased CrCl, sodium/fluid retention that can worsen edema, HTN, and HF

35
Q

What CNS NSAID side effect is a concern in our elderly patients?

A

Impaired cognition especially, but also HA, dizziness

36
Q

How do we dose sulindac for acute gout?

A

200mg BID

37
Q

How do we dose indomethacin for acute gout?

A

Start at 50mg TID then taper to 50mg BID

38
Q

How do we dose naproxen for acute gout?

A

Start at 750mg for the initial dose, then 250mg q8h after OR 500mg BID

39
Q

What should we monitor in NSAID therapy?

A

Improvement of s/sx, renal function (BUN, SCr), GI side effects.

40
Q

When should colchicine be initiated?

A
41
Q

How is colchicine dosed?

A

1.2mg initially, then 0.6mg in 1 hour
Wait two weeks to redose in pts with hepatic or renal disease
Dialysis: 0.6mg x 1 dose only
Low dose good response and lower SEs vs high dose

42
Q

What adverse effecs are associated with colchicine?

A

Dose-dependent GI toxicity (N/V/D), myelosuppression including aplastic anemia and thrombocytopenia.

43
Q

What drugs interact with colchicine?

A

Through CYP3A4 and Pgp –> protease inhibitors, azole AF, clarithromycin, erythromycin, verapamil, statins, cyclosporine

44
Q

What gout patients receive corticosteroids?

A

Those intolerant to NSAIDs and colchicine, if >36h since onset, polyarticular involvement, and resistant cases.

45
Q

How are corticosteroids dosed for gout?

A

Prednisone 0.5 mg/kg/day x 5-10 days then stop or taper

Can also inject IA ONLY if 1-2 large joints

46
Q

When should you be cautious about giving corticosteroids to a patient?

A

If they have hyperglycemia, CHF, immunosuppression, GI bleed, PUD, psychiatric disorder

47
Q

When should you consider combination therapy for an acute gout attack? What is the only combination of the three that you cannot do?

A

If it is severe (>7/10 on pain scale), polyarticular involvement, or monotherapy ineffective
Do NOT do NSAID + corticosteroid (GI toxicity)

48
Q

When should you start chronic gout therapy relative to an attack?

A

Wait 6-8 weeks after an attack before starting ULT because an acute drop in blood levels can precipitate urate and new attack.

49
Q

What urinary urate amount would classify a patient as an overproducer? As an underexcretor?

A

Overproducer: >1000mg
Underexcretor:

50
Q

What factors would make you start ULT after a patient’s first attack?

A

A severe attack (polyarticular, tophi), complicated nephrolithiasis, serum uric acid >10 mg/dL, urinary uric acid >1000/24 hours

51
Q

In severe cases, what might your serum uric acid goal be?

A
52
Q

How often should serum urate be monitored?

A

Every 2-5 weeks during ULT titration, then every 6 months to measure adherence

53
Q

What first-line chronic gout therapy drugs inhibit xanthine oxidase?

A

Allopurinol and febuxostat

54
Q

How do we dose allopurinol?

A

Start at 100mg/day and titrate up by 100mg/day every 2-5 weeks to achieve 300/day (GI upset)

55
Q

What side effects are associated with allopurinol?

A

GI upset, skin rash, leukopenia, thrombocytopenia, increased LFTs, HA
Rare but severe allopurinol hypersensitivity syndrome (20-25% mortality) Stevens Johnson syndrome and toxic epidermal necrolysis – test HLA-B5801 in all Chinese patients and Korean descent with stage 3 CKD

56
Q

What drugs interact with allopurinol?

A

Mercaptopurine and azathioprine (reduce doses of these by 25-75% empirically), warfarin (increase INR), cyclophosphamide increased bone marrow suppression/toxicity

57
Q

What else can allopurinol be used for?

A

Recurrent kidney stones and blood dyscrasias to prevent tumor lysis syndrome.

58
Q

What patients receive febuxostat (Uloric)?

A

Patients with allopurinol intolerance, due to cost.

59
Q

How do we dose febuxostat?

A

Start at 40 mg/day and titrate up to 80 mg/day, even 120mg if needed.

60
Q

What adverse effects are associated with febuxostat? How do we monitor them?

A

Rash, nausea, abnormal LFTs, arthralgias, precaution for CV thromboembolic events.
Monitor LFTs at baselin, 2 months, and 4 months

61
Q

What three drugs are contraindicated for use with febuxostat?

A

Azathioprine, mercaptopurine, and theophylline – metabolism inhibition too strong by febuxostat

62
Q

What patients should receive probenecid?

A

Patients with documented underexcretion of urate (

63
Q

How is probenecid (Benemide) dosed?

A

Start at 250mg BID x 7 days, then 500mg BID for 2 weeks, may titrate up by 500mg every 1-2 weeks
MAX 2g/day

64
Q

What side effects are associated with probenecid?

A

Rash, GI upset, stone formation (especially with dehydration–counsel pts re hydration!!)

65
Q

What patients should not receive probenecid?

A

patients with uric acid kidney stones, concomitant salicylates, especially >325mg/day, overproducers, CrCl

66
Q

What is our last line therapy for gout, reserved for patients unresponsive or intolerant to standard therapy? How do we dose it?

A

Pegloticase (Krystexxa) – dosed 8mg IV infusion given over 120min every 2 weeks
Pretreat with antihistamines and corticosteroids

67
Q

What adverse effects are associated with pegloticase?

A

Nephrolithiasis, arthralgia, exacerbations of HF, infusion-related adverse effects, anaphylaxis

68
Q

What patients should NOT receive pegloticase?

A

Patients with G6PD deficiency and caution in HF patients

69
Q

What agent, commonly used for HLD, also decreases urate levels by 20-30%?

A

Fenofibrate

Can use with XO inhibitor

70
Q

What ARB uniquely inhibits tubular reabsorption of uric acid?

A

Losartan

Can use with XO inhibitor

71
Q

What agents can we use prophylactically against gout flares that are a sign of successful therapy when starting ULT therapy?

A

Colchicine 0.6mg once or BID, (indomethacin 25mg BID, or naproxen 250mg BID as alternatives)
Administer for first 8 weeks of ULT, discontinue 3-6 months after achieving goal serum urate of

72
Q

How can we prevent nephrolithiasis?

A

Hydration (goal UOP 2-3L/day), alkalinization of urine (pH >6) with potassium bicarb or citrate or acetazolamide 250mg PO HS, decrease purine-rich foods and limit protein to

Pharmacotherapy I (15 decks)

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