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    \vspace{-2pt}\large{\bf{\textcolor{DarkBackground}{\textrm{Gout and Hyperuricemia Cheat Sheet}}}} \\
    \normalsize{by \textcolor{DarkBackground}{HeirofFire} via \textcolor{DarkBackground}{\uline{cheatography.com/192916/cs/40316/}}}
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  \mymulticolumn{1}{p{5.377cm}}{\bf\textcolor{white}{Cheat Sheet}}  \\
   \vspace{-2pt}Not Yet Published.\\
   Updated 18th September, 2023.\\
   Page {\thepage} of \pageref{LastPage}.
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\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Pathophysiology}}  \tn
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Gout & Inflammatory condition. \tn 
% Row Count 2 (+ 2)
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{\emph{What makes Gout painful?}} & Build up of uric acid crystals in the joints, bones, or soft tissues. Usually affects one joint at a time and is most often the metatarsal phalangeal joint (MPJ) \tn 
% Row Count 11 (+ 9)
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What in the blood can lead to Gout? & Elevated uric acid levels \tn 
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Hyperuricemia for males is what level? & \textgreater{}7 mg/dL \tn 
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Hyperuricemia for & \textgreater{}6 mg/dL \tn 
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Hyperuricemia does {\emph{not}} always lead to... & does not always lead to gout. \tn 
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At 37 degrees C, serum urate concentrations \textgreater{}7 mg/dL begin to limit... & solubility for monosodium urate. \tn 
% Row Count 23 (+ 4)
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Higher concentrations of serum urate will lead to more what? & monosodium urate crystals (MSU) \tn 
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Gout is more prevalent societies with\_\_. & Lifestyles of overindulgence \tn 
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Uric acid is the {\emph{final}} step in the degradation of\_\_\_\_\_ & {\bf{Purines}} \tn 
% Row Count 31 (+ 3)
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Pathophysiology (cont)}}  \tn
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The two common abnormalitites in enzymes that lead to {\emph{increased uric acid}} & - Increased levels of PRPP (Phsphoribosyl pyrophosphate synthetase) -Deficiency of HGPRT \seqsplit{(HYPOxanthine-guanine} \seqsplit{phosphoribosyltransferase)} \tn 
% Row Count 7 (+ 7)
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{\bf{Tophi is created by}} & Uric acid binding to sodium and creating monosodium urate (msu) crystals that get deposited in tissues/joints \tn 
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{\bf{Tophi is}} & the build up of uric acid crystals in the {\bf{synovial fluid}} \tn 
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Non-Modifiable Risk factors of Gout & Age, Sex, Race, Genetic Variants \tn 
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Modifiable Risk Factors of Gout & Obesity, HTN, CKD, Diabetes, Medications altering urate balance \tn 
% Row Count 22 (+ 4)
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Medications that alter urate balance: & Diuretics, Ethanol, Salicylates (\textless{}2g/day), Nicotinic Acid, Pyrazinamide, Cyclosporin \tn 
% Row Count 27 (+ 5)
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Gout Prophylaxis}}  \tn
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First line for Gout Prophylaxis & NSAIDs, Colchicine \tn 
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Colchicine & 0.6 mg PO daily or BID (QD\textgreater{}BID) \tn 
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NSAID & Naproxen is an example (250 mg PO BID). May use a PPI if NSAID prolonged or increased GI bleeding risk. \tn 
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Alternative/First line contraindicated Prophylaxis dosing & Low dose corticosteroids (like prednisone 10 mg/day) \tn 
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Duration of Propphylaxis {\bf{without}} tophi & 3-6 months \tn 
% Row Count 16 (+ 3)
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Duration of Prophylaxis {\bf{with}} \textgreater{}1 tophi or radiographic evidence & 6-12 months \tn 
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\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Uricosuric}}  \tn
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2nd line Therapy for Gout Management & Probenecid \tn 
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Rarely used monotherapy... & but can be XOI is contraindicated or ineffective \tn 
% Row Count 5 (+ 3)
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Probenecid initial dosing & 250 mg PO BID x1 week \tn 
% Row Count 7 (+ 2)
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Probenecid maintenance dosing & 500 mg PO BID \tn 
% Row Count 9 (+ 2)
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Mainly for patients that... & underexcrete uric acid \tn 
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{\bf{MOA}} & {\bf{Competitively}} inhibits the reabsorption of uric acid at the proximal convoluted tubule, thereby promoting its excretion and reducing serum uric acid levels \tn 
% Row Count 19 (+ 8)
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Works where? & RENALLY \tn 
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Contraindicated & Nephrolithiasis, moderate-severe renal impairment (CKD 3) \tn 
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Effect of Salicylates on Probenecid & may impact the concentrations \tn 
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Recombinant Uricase}}  \tn
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{\bf{Pegloticase}} & 8 mg IV infusion ({\emph{over 120min}}) q2weeks \tn 
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{\bf{MOA}} & Pegylated recombinant form of urate-oxidase enzyme, also known as uricase; which converts uric acid to allantoin (an inactive and water soluble metabolite of uric acid) \tn 
% Row Count 11 (+ 9)
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ethicacy: & 4-6 months \tn 
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{\bf{MONOTHERAPY}} & Can only be used as monotherapy \tn 
% Row Count 14 (+ 2)
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Used for & Refractory gout {\bf{when failed conventional therapies.}} \tn 
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Produced from modified strain of & E. coli (Escherichia coli) \tn 
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Start prophylactic therapy & 1 week PRIOR to initiation (high risk of flares) \tn 
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Duration of prophylaxis while on Pegloticas & 6 months \tn 
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Requires... & Pre-treatment with antihistamines and corticosteroids to mitigate infusion reaction \tn 
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Recombinant Uricase (cont)}}  \tn
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Immunogenicity & develops antibodies against itself \tn 
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Discontinue therapy: & serum urate \textgreater{}6 mg/dL on more than one clinic visi \tn 
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Contraindicated: & G6PD-deficiency \tn 
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G6PD-deficiency & Increase risk of Hemolysis and methemoglobinemia \tn 
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Diagnosis, Signs, Symptoms, Classification}}  \tn
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{\bf{Diagnosis of Gout}} & Symptoms are used for diagnosis \tn 
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Signs and Symptoms of Gout & Intense pain, {\emph{Erythema}}, warmth, Fever, Tophi, Inflammation of Joint \tn 
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Where can inflammation of the joint be in Gout? & Toes, Knees, Fingers, Elbows, Ankles \tn 
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Uric Acid Levels & High uric acid levels do NOT always mean Gout! \tn 
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Leukocytosis in Gout & MSU crystals induce {\emph{inflammation}} and can {\emph{INCREASE}} white blood cell count \tn 
% Row Count 16 (+ 4)
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{\bf{Diagnostic Testing for Gout}} & {\emph{Arthrocentesis}} and {\emph{Radiography}} \tn 
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{\bf{Arthrocentsis}} & Removal of synovial fluid from the affected joint, microscopic examination, can give a definitive diagnosis of gout. \tn 
% Row Count 24 (+ 6)
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{\bf{Radiography}} & X-ray that can be used for more advanced gout, will be *unremarkable for first acute gout attacks, can help rule out other causes of arthritis. \tn 
% Row Count 32 (+ 8)
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\begin{tabularx}{5.377cm}{x{2.4885 cm} x{2.4885 cm} }
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Diagnosis, Signs, Symptoms, Classification (cont)}}  \tn
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Conditions that precipitate Gout Attack & Most can't identify a {\emph{trigger}}. Dehydration, Stress, excessive alcohol intake, excessive intake of purine-rich foods, increased physical activity, uric acid lowering agents, medications that increase uric acid levels \tn 
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What are the 4 Gout Classifications & Asymptomatic, Acute Gouty Arthritis, Intercritical Gout, Chronic recurrent Gout \tn 
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{\bf{Asymptomatic}} & Hyperuricemia \tn 
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{\bf{Intercritical Gout}} & Intervals between attacks \tn 
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Severity of Chronic Tophaceous Gouty Arthritis {\bf{(CTGA)}} & Mild, Moderate, Severe \tn 
% Row Count 21 (+ 3)
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{\bf{CTGA Mild}} & One joint, {\emph{stable}} disease \tn 
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{\bf{CTGA Moderate}} & 2-4 joints, {\emph{stable}} disease \tn 
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{\bf{CTGA Severe}} & 4+ {\bf{OR}} Unstable, complicated, severe articular tophi \tn 
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% Row 16
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Large Joints: & Knee, ankle, wrist, elbow, hip, shoulder \tn 
% Row Count 30 (+ 2)
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Diagnosis, Signs, Symptoms, Classification (cont)}}  \tn
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Medium Joints: & Ankle, Wrist, Elbow \tn 
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Small Joints: & Interphalangeal \tn 
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Xanthine Oxidase Inhibitors (XOI)}}  \tn
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What are the Two XOI for Gout? & Allopurinol, Febuxostat \tn 
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Allopurinol Initial dose & 100 mg PO daily \tn 
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Allopurinol Maintenance dosing & 100-800 mg daily (average is 300 mg/day) \tn 
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Allopurinol Renal adjustment & 50 mg/day for CKD stage 4+ \tn 
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Febuxostat initial dose & 40 mg PO daily \tn 
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Febuxostat Maintenance dosing & 40-80 mg daily \tn 
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First line agent for & {\emph{Chronic management of gout}} \tn 
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Contraindications & CVD history or recent CV event \tn 
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Genotype contraindication & HLC-B*5801 haplotype \tn 
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Genotype is conditionally recommended for what race? & Southeast Asian descent, African Americans \tn 
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XOI MOA & Inhibits xanthine oxidase, an enzyme responsible for the conversion of hypoxanthine to xanthine to development of uric acid. Acts on purine metabolism, thereby reducing uric acid production without disrupting biosynthesis of vital purines \tn 
% Row Count 33 (+ 12)
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Xanthine Oxidase Inhibitors (XOI) (cont)}}  \tn
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{\bf{Black Box Warning}} & {\bf{Febuxostat}} \tn 
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Gout Management}}  \tn
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{\bf{Non-Pharmacological}} & Dietary Modifications, Promote Weight Loss, Adjuvant {\bf{ice}} therapy, {\emph{Avoid heat}} \tn 
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{\bf{Pharmacotherapy of {\emph{Acute}} Gout}} & Terminate acute attacks, Prevent Recurrent Attacks of gouty arthritis, Prevent complications associated with deposition of urate crystals in tissues, Prevent/reverse comorbidities associated with gout (Obesity, HTN) \tn 
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Dietary Modifications for Gout & Limit: Purine (meats, seafood), alcohol (beer, fortified wines/liquours), high-fructose corn syrup, maintain adequate hydration \tn 
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{\bf{Acute Gout Treatment}} & NSAIDS, Corticosteroids, Colchicine \tn 
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NSAIDS can be initiated when for a Acute attack? & 24-48 hours \tn 
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Celecoxib should be avoided if significant history of what? & CAD \tn 
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Gout Management (cont)}}  \tn
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NSAIDs with Acute Gout Attack FDA indication: & Indomethacin, Naproxen, Sulindac \tn 
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NSAIDs are contraindicated for & {\emph{Decompensated}} heart failure. \tn 
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NSAIDs MOA & Inhibit {\emph{prostaglandins}} for anti-inflammatory, analgesic and antipyretic effects via inhibition of cycloxygenase 1 and 2 enzymes \tn 
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Corticosteroids can be initiated when for an acute gout attack? & 24-48 hours \tn 
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Corticosteroids for Acute Gout attack: & Prednisone, Methylprednisolone, Triamcinolone, ACTH \tn 
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ACR guidelines recommend this as an option for acute gout flare: & Corticosteroids \tn 
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Corticotropin's anti- inflammatory properties work through: & melanocortin type-3 receptor \tn 
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Corticosteroids are contraindicated when? & Active systemic infections (can worsen them), IA injections if septic arthritis, long term use decreases amoutn of physiological steroids so there can be rebound which is why we taper \tn 
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Gout Management (cont)}}  \tn
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Adverse event of corticosteroid use: & HPA axis suppression \tn 
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When can {\emph{Colchicine}} be initiated for Acute Gout attack? & 12-24 hours of symptom onset. if \textgreater{}36 hours, consider alternative therapies \tn 
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Colchicine for acute gout attack initial dosing: & Day 1: 1.2 mg PO {\emph{once}}, then 0.6 mg PO 1-6 hour later \tn 
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Colchicine for acute gout attack {\emph{mainenance}} dosing: (Day 2) & 12 hours after Day one, 0.6 mg PO daily or BID \tn 
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{\bf{Colchicine MOA}} & Decreases inflammation during gout flare by decreasing activation, degranulation and migration of neutrophils through inhibiting betatubulin polymerization into microtubules \tn 
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Colchicine is Contraindicated when: & Blood dyscrasias, severe renal disease (CrCl \textless{}10 ml/min) \tn 
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If gout is seen on an x-ray, it's immediately classified as & Severe \tn 
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Initiate Monotherapy & Mild/Moderate Pain intensity \tn 
% Row Count 30 (+ 2)
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\par\addvspace{1.3em}

\vfill
\columnbreak
\begin{tabularx}{5.377cm}{x{2.4885 cm} x{2.4885 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Gout Management (cont)}}  \tn
% Row 22
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Initiate Combination Therapy & Severe, X-ray \tn 
% Row Count 2 (+ 2)
% Row 23
\SetRowColor{white}
Combination therapy includes & Colchicine + NSAID, Colchicine + Oral Corticosteroid, NSAID + IA injection, Colchicine + IA, Oral Corticosteroid + IA \tn 
% Row Count 8 (+ 6)
% Row 24
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{\bf{Goal Serum Urate level to maintain}} & \textless{}6 mg/dL \tn 
% Row Count 10 (+ 2)
% Row 25
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When using a ULT, what should also be used? & Anti-inflammatory to overlap \tn 
% Row Count 13 (+ 3)
% Row 26
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High level of evidence/Strong recommendation for Initiation of ULT & 1 or more subcutaneous tophi, evidence of radiographic damage from gout, \textgreater{}2 gout flares per year \tn 
% Row Count 18 (+ 5)
% Row 27
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Moderate Evidence, Conditional recommendation & ULT is recommended for patients who have previously experienced \textgreater{}1 flare but have infrequent flares (\textless{}2 per year) \tn 
% Row Count 24 (+ 6)
% Row 28
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ULT options for Gout & Xanthine Oxidase Inhibitors (XOI), Recombinant Uricase, Probenecid \tn 
% Row Count 28 (+ 4)
% Row 29
\SetRowColor{white}
{\bf{Fenofibrate}} & Increase clearance of hypoxanthine and xanthine. Consider if concomitant \seqsplit{Hypertriglyceridemia} \tn 
% Row Count 33 (+ 5)
\end{tabularx}
\par\addvspace{1.3em}

\vfill
\columnbreak
\begin{tabularx}{5.377cm}{x{2.4885 cm} x{2.4885 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Gout Management (cont)}}  \tn
% Row 30
\SetRowColor{LightBackground}
{\bf{Losartan}} & Inhibits tubular reabsorption of uric acid and increases excretion. Alkalinizes urine to reduce risk of calculi \tn 
% Row Count 6 (+ 6)
% Row 31
\SetRowColor{white}
{\bf{Asymptomatic Hyperuricemia treatment}} & {\bf{No pharmacotherapy required}} , Target lifestyle modifications \tn 
% Row Count 10 (+ 4)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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% That's all folks
\end{multicols*}

\end{document}