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Therapeutics 1 Kappa Epsilon Version > Gout > Flashcards

Gout Flashcards

1
Q

Hyperuricemia levels

A

> 6.8 mg/dL

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2
Q

Gout results from increased levels of __________ in blood

A

uric acid

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3
Q

Gout is known as the deposition of ______________ in synovial fluid or tissue

A

monosodium urate crystals

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4
Q

Serum Urate Concentrations will increase with what factors?

A
  • age
  • body weight
  • gender (male)
  • alcohol
  • blood pressure
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5
Q

Humans (and apes) are at higher risk of gout because they do not make the ___________

A

uricase protein (pseudogene)

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6
Q

Uricase prevents ________ being made from ________

A

fat; sugar

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7
Q

Hypoxanthine gets made to xanthine by what enzyme?

A

xanthine oxidase

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8
Q

Xanthine gets made into Uric acid by what enzyme?

A

xanthine oxidase

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9
Q

Uric acid is (more or less) soluble than hypoxanthine and xanthine

A

less soluble!

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10
Q

Monosodium urate crystals can form when (low or high) plasma urate concentrations are present

A

high

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11
Q

Uric acid is made into Allantoin by the __________ enzyme

A

uricase

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12
Q

Uricase makes uric acid into ________

A

allantoin

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13
Q

Uric acid is excreted _________

A

renally

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14
Q

What 3 things will inhibit De Novo Synthesis of Purines

A

AMP, IMP, GMP

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15
Q

(Increase or Decrease) PRPP synthetase activity (Increase or Decrease) De Novo Synthesis of Purines

A

Increase; increases

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16
Q

Adenine and Guanine are broken down to ____________

A

hypoxanthine

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17
Q

What is the recycle pathway in purine metabolism?

A

Hypoxantine is made into GTP

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18
Q

When HGPRTase activity is DECREASED - what 2 effects are seen

A

1) increases hypoxanthine oxidation to uric acid

2) stimulates De Novo Synthesis through accumulated PRPP

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19
Q

De Novo Synthesis of Purines:

PRPP —–10 steps—-> ___________

A

IMP (inosine monophosphate)

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20
Q

Urate crystals are taken up by ________cytes and ________cytes

A

monocytes; synoviocytes

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21
Q

Once synoviocytes have taken in urate crystals, they release what?

A

prostaglandins, lysosomal enzymes, and interleukin (aka cause inflammation)

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22
Q

Synoviocytes take in urate crystals, release contents, and then attract _________ to increase inflammation

A

neutrophils

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23
Q

Uricase converts uric acid to _________ which is (more or less) solbule

A

allantoin; more

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24
Q

Urate crystals aka monosodium urate will deposit in the _________, _________, and may cause ________ in the kidneys

A

joints, cartilage, caliculi

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25
Q

Features of Acute Gout

A
  • acute arthritis
  • 1st metarsophalangeal joint
  • excruciating pain
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26
Q

Medication options for Acute Gout (Hazbun Lecture)

A

1 - NSAIDs
2 - Colchicine
3 - Glucocorticoids

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27
Q

Medication options for Chronic Gout (Hazbun Lecture)

A

allopurinol/Febuxostat;

Probenecid; Pegloticase

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28
Q

What are features of chronic gout?

A

Hyperuricemia; development of tophi; recurrent attacks of acute gout

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29
Q

Primary Gout vs Secondary Gout

A

Primary - happens because of overproduction or decreased secretion of uric acid

Secondary - uric acid increases due to cell death/lysis because nucleic acid is released

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30
Q

Reasons Primary Gout can occur

A

Ethanol, foods high in purines, Obesity

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31
Q

Why Does Ethanol increase uric acid levels

A
  • increases purine catabolism in liver
  • increases lactic acid which inhibits urate secretion

(ethanol competes with uric acid —> uric acid get secreted)

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32
Q

what are some foods high in purines

A

red meat, seafood

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33
Q

Reasons Secondary Gout can occur

A
  • chemotherapy
  • Myelo- and lymphoproliferative disorders
  • Polycythemia vera and anemia
  • Psoriasis
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34
Q

2/3 of Uric acid is excreted in the _______

A

kidneys

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35
Q

90% of uric acid is __________ in the ________ tubule

A

reabsorbed; proximal

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36
Q

How to tell if a patient with Hyperuricemia is a overproducer or underexcretor?

A
  • put on purine free diet
  • measure amount of uric acid in urine for 24 hours
  • if excreting < 600 mg = underexcretor
  • if excreting > 1000 mg = overproducer
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37
Q

Drugs that can induce Hyperuricemia

A
  • Diuretics (thiazides and loops)
  • Nicotinic acid
  • Salicylates
  • Ethanol
  • Cyclosporine
  • Pyrazinamide
  • Levodopa
  • Ethambutol
  • Cytotoxic Drugs
  • Urate lowering therapies
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38
Q

Patients will be (asymptomatic or symptomatic) between flare ups

A

asymptomatic

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39
Q

Clinical Presentation of Gout:

A

Fever, intense pain, erythema, warmth, swelling, and inflammation

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40
Q

Definition of Podagra

A

gout involving first metatarsophlalangeal joint “the great toe”

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41
Q

Definition of Tophi

A

deposits of monosodium urate in cartilage, tendons, synovial membranes

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42
Q

Gout is more common in (lower or higher) joints

A

lower

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43
Q

why is gout more common in lower joints?

A
  • lower temp

- are more of the “weight bearing joints” during the day

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44
Q

most flare ups happen during what time of the day?

A

nighttime/when you are sleeping!

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45
Q

Uric acid nephrolithiasis:

if urine is (acidic or basic) the uric acid is (less or more) soluble which leads to a risk of increased stone formation

A

acidic; less

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46
Q

Uric acid nephrolithiasis is more common when urine pH is < _____

A

6

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47
Q

What are the 3 long term conditions of Gout

A
  • uric acid nephrolithiasis
  • tophaceous gout
  • gouty nephropathy
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48
Q

what is tophaceous gout?

A

late complication of gout; seen at base of great toe, helix of ear, bursae, achillies, knees, wrists, ankles

Joint destruction, pain and nerve compression syndrome

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49
Q

Gouty Neprhopathy can be acute or chronic:

Facts about Acute Gout Nephropathy?

A
  • urine flow is blocked bc of uric acid precipitation collecting ducts/ureters
  • acute renal failure can occur
  • seen in ALL/CLL/CML pts
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50
Q

Gouty Neprhopathy can be acute or chronic:

Facts about Chronic Gout Nephropathy?

A
  • LONG TERM deposition of urate crystals in renal system
  • proteinuria can occur
  • assoc. w/ HTN, DM, atherosclerosis
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51
Q

What are some Non-Pharmacotherapy options to help with asymptomatic or symptomatic hyperuricemia

A
  • reduce purines rich foods
  • reduce fructose containing products
  • increase fluid intake (to decrease risk of nephrolithiasis)
  • increase consumption of low-fat or nonfat dairy products
  • encourage weight loss
  • rest joint 1 - 2 days/ice it/AVOID HEAT
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52
Q

Two main agents used to treat ACUTE GOUT

A
  • colchicine

- NSAIDs

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53
Q

Colchicine - (does or does not) alter the metabolism of excretion of urates

A

DOES NOT (it just relieves pain and inflammation)

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54
Q

Colchicine inhibits inflammation by slowing down what?

A

slowing (their movement) down macrophages

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55
Q

MOA of Colchicine = ?

A

Colchicine binds to Tubulin –> no polymerization of tubulin occurs –> migration of leukocytes is inhibited –> decreased tyrsonie phosphorylation inhibits synthesis of LTB4

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56
Q

Drug interactions for Colchicine

A
  • Cyclosporine/Tacrolimus (only) will cause colchicine to get excreted in the urine
  • Cyclosporine/Tacrolimus/Verapamil will cause colchicine to get excreted in the bile
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57
Q

NSAIDs or Colchicine? which is preferred and why?

A

NSAIDs because they are less toxic than colchicine

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58
Q

NSAIDs: __________ can also increase ureate excretion in the urine

A

oxaprozin

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59
Q

2 main classes of drugs used to PREVENT Gout

A

Uricosuric Agents; Xanthine oxidase inhibitors

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60
Q

Which drugs are uricosuric agents

A

probenecid

sulfinipyrazone is but not used in practice anymore

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61
Q

Which drugs are Xanthine oxidase inhibitors?

A

Allopurinol, Febuxostat

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62
Q

Why do Uricosuric Agents work to prevent gout? (aka what is its MOA)

A

Uricosuric drugs compete with uric acid @ site of reabsorption in renal tubule - therefore uric acid is not reabsorbed as much/uric acid IS renally excreted

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63
Q

Drug interactions for Uricosuric Agents:

________ decreases effectiveness of uricosuric agents by competing @ kidney

A

aspirin

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64
Q

Drug interactions for Uricosuric Agents:

Aspirin

A

it decreases effectiveness of uricosuric agents by competing @ kidney’s reabsorption

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65
Q

Probenecid blocks _________ of other drugs or metabolites (sulfamides, penicillins, cephalosporins)

A

urinary secretion

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66
Q

Drugs that interfere with the excretion of uric acid and therefore increase serum uric acid - are …?

A

diuretics, salicylates, nicotinic acid

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67
Q

Allopurinol is a ________ of hypoxanthine

A

isomer

68
Q

Allopurinol is a isomer of _________

A

hypoxanthine

69
Q

MOA of Allopurinol

A

Allopurinol is substrate of xanthine oxidase; allopurinol is made into oxypurinol; oxypurinol will tightly bind to xanthine oxidase and inhibits the enzyme

70
Q

Difference b/w Allopurinol and Febuxostat (Uloric)

A

Febuxostat is a NON-PURINE inhibitor of xanthine oxidase

71
Q

Uloric is metbolized by the ________ and excreted by the ________

A

liver; kidney

72
Q

Uloric is (not very or very) strong at binding

A

very strong!! it can inhibit both the reduced and oxidized enzyme

73
Q

Uloric may be advantageous in what kind of patients? (3 groups)

A
  • pts w/ allopurinol hypersensitivity
  • pts w/ reduced kidney function
  • pts not responding o high doses of allopurinol
74
Q

Krystexxa is brand for ?

A

Pegloticase

75
Q

How does Krystexxa work to treat gout?

A

it is URICASE bound to mPEG; Uricase will oxidize uric acid to allantoin (a soluble product that can be excreted easily)

76
Q

Krystexxa is CONTRAINDICATED for what pts?

A

pts that are G6P dehydrogenase deficient

77
Q

which drug causes decreased immunogenicity

A

Krystexxa

78
Q

Elitek is brand for?

A

Rasburicase

79
Q

Elitek works how?

A

it is recombinant urate oxidase enzyme from aspergillus flavus - will catalyze the oxidation of uric acid to allantoin!

80
Q

how are Kyrystexxa and Elitek administered?

A

by IV

81
Q

Zurampic is brand for ?

A

Lesinurad

82
Q

Zurampic works how?

A

it is a selective uric acid reabsorption INHIBITOR aka will block URAT1 transporter

83
Q

Therapy goal for target serum uric acid < ___ mg/dL

A

6

84
Q

3 main options for an acute gout attach

A
  • NSAIDs
  • colchicine
  • corticosteroid
85
Q

FDA approved NSAIDs for gout?

A

Indomethacin, naproxen, sulindac

86
Q

Dose for Indomethacin for Gout

A

50 mg TID

87
Q

Dose for Naproxen for Gout

A

750 mg followed by 250 mg PO q8H

88
Q

Dose for Sulindac for gout

A

200 mg BID

89
Q

NSAIDs for acute gout - how to take them

A

at SCHEDULED doses - not when feeling pain….

90
Q

NSAIDs are contraindicated in what situations?

A
  • pt has hypersensitivity to aspirin/NSAIDs
  • decompensated HF
  • Active peptic ulcer disease or GI bleed
  • Severe or Acute Renal impairment
91
Q

NSAIDs should be used with caution in what situations?

A
  • if pt is using anticoagulants or antiplatelet drugs
  • Hx of HF
  • Hx of peptic ulcer disease or GI bleed
  • Renal Impairment (CrCl < 50 mL/min)
  • Uncontrolled HTN
92
Q

Adverse effects of NSAIDs

GI effects and what to do to help prevent them?

A

can have Gastritis, bleeding, perforation

Consider PPI

93
Q

NSAIDs will effect the Kidney and this can be seen by a (decreased or increased) _______

A

increased SCr

94
Q

Colchicine should be started within ________ of attack onset

A

36 hours

95
Q

when should colchicine be used?

A

when pts do not tolerate NSAIDs or pt has a contraindication to NSAIDs

96
Q

Colchicine Dosing

A

LOADING and CONTINUING DOSE

Loading: 1.2 mg once then 0.6 mg one hour later

Continue: 0.6 mg PO QD or BID 12 hours after loading dose (depending on pt tolerability)

97
Q

what 4 things would indicate dose adjustments to colchicine

A
  • CrCl < 30 mL/min
  • Dialysis
  • Use of CYP3A4 inhibitors
  • Use of P-glycoprotein inhibitors
98
Q

How to dose Colchicine if pt has CrCl < 30 mL/min

A
  • DO NOT repeat dose w/in 14 days

- Prophylaxis: 0.3 mg PO QD (instead of 0.6)

99
Q

How to dose Colchicine if pt is on dialysis

A

Tx: 0.6 mg PO x 1 (DO NOT repeat dose w/in 14 days)

- Prophylaxis: 0.3 mg 2x a week

100
Q

Adverse Effects of Colchicine

A

GI - Diarrhea; Nausea Vomiting
Bone Marrow Suppression - Aplastic Anemia; Thrombocytopenia
Neuromuscular - Myopathy, Rhabdomyolysis

101
Q

Examples of Corticosteroids used for Gout

A
  • Prednisone
  • Methylprednisolone
  • Triamcinolone
102
Q

Corticosteroids are used for gout when…..

A
  • NSAID/Colchicine intolerance
  • Polyarticular involvement
  • Resistant Cases
103
Q

Dosing of Prednisone for Gout:
____ mg/kg per day for___ - _____ days followed by discontinuation
OR
____ mg/kg for ____ - ____ days followed by tapering for ____ - _____ days before discontinuation

A
  1. 5;5;10

0. 5; 2;5;7;10

104
Q

Dosing of Triamcinolone Acetonide
____ IM once then oral prednisone as above
OR
____ - ____ intra-articular injection x1

A

60 mg; 2.5 mg; 40 mg

105
Q

Adverse Effects of Corticosteroids
COMMON ones
______ in blood glucose
______ in appetite or weight gain
Dose Dependent ______ : ___/___/___
Fluid retention can lead to ________ or ____ concerns
CNS: HA, insomnia, mood swings, nervousness

A

increase; increase; GI upset; N;V;D; increase BP; HF

106
Q

What are the less common adverse effects of corticosteroids

A
  • neutropenia
  • hepatotoxicity
  • myleosuppresion
107
Q

caution with glucocorticoids with situations?

A
  • Diabetes
  • HTN
  • Peptic ulcer disease/GI bleed
  • CHF
  • Immunosuppression
  • Psychiatric disorder
108
Q

Possible Combination Therapy Options for ACUTE Gout ATTACKS

A
  • Colchicine + NSAIDs
  • Oral Corticosteroids + Colchicine
  • Intra-Articular Steroids + all other modalities

(just not Oral steroid AND NSAIDs)

109
Q

What are some disease states that are risk factors for Chronic Gout

A
  • HTN
  • Type 2 Diabetes
  • Obesity
  • Metabolic Syndrome
  • CKD
110
Q 
When to start Urate Lowering Therapy:
- Pt has Diagnosis of Gout
AND
one of the four other traits...
what are the 4 other traits
A
  • 2+ acute attacks per year
  • Presence of Tophi
  • CKD stage 2 or more
  • Presence of Renal Stones
111
Q

Urate lowering therapy is typically delayed for about ________ after acute attack resolution

A

2 weeks

112
Q

Goals of Therapy in Urate Lowering Therapy

A
  • Achieve a serum urate level < 6 mg/dL

- Prevent acute attacks

113
Q

Monitoring in Urate lowering therapy

During initiation monitor urate every ________

Once urate levels are under 6 mg/dL - monitor every _______

A

2 - 5 weeks; 6 months

114
Q

Agents that are used to Lower Urate Levels
1st line -
2nd line -
3rd line -

A

1st: Xanthine Oxidase inhibitors
2nd: Uricosurics
3rd: Uricase Agents

115
Q

Why is Allopurinol first line Xanthine Oxidase Inhibitors

A

efficacy, availability, low cost

116
Q

Starting Dose for Allopurinol

A

100 mg QD

117
Q

Starting dose of Allopurinol for patients with CKD stage 4

A

50 mg QD

118
Q

Max dose for Allopurinol

A

800 mg/day

119
Q

Slow titration of Allopurinol is recommended every _______

A

2 - 4 weeks

120
Q

Common Adverse Effects of Allopurinol

A
  • Skin rash
  • Itching
  • Leukopenia
  • Thrombocytopenia
  • GI intolerance
121
Q

Less Common Adverse Effects of Allopurinol

A
  • Hypersensitivity
  • Stevens-Johnson Syndrom o Toxic Epidermal necrolysis
  • Eosinophilia
  • Vasculitis
122
Q

Allopurinol Drug Interactions:

A
  • Warfarin (increase INR)
  • Antacids
  • Mercaptopurine and Azathioprine (because these also use Xanthine Oxidase)
123
Q

Allopurinol Monitoring - _________ screening in at-risk populations

A

HLA-B*580 (if have this, most likely people of asian decent, can put at high risk for life threatening hypersensitivity)

124
Q

Starting Dose for Uloric

A

40 mg QD

125
Q

Max dose for Uloric

A

80 mg QD

126
Q

which drug should NOT be initiated or discontinued during an acute attack

A

Uloric

127
Q

Dose Adjustments for Uloric if renal or hepatic impairment

A

No dose adjustment - data is limited; use with Caution

128
Q

Adverse Effects of Uloric

A
  • rash
  • nausea
  • Abnormal LFTs
  • Precaution for CV thromboembolic events (CV deaths, non fatal MI, non-fatal stroke)
129
Q

Largest Limitation of Uloric is?

A

Cost

130
Q

Things to Monitor when Pt is on Uloric

A

Check LFTs at baseline, 2 mos, 4 mos

131
Q

Contraindications for Uloric

A

concomitant use with azathioprine, mercaptopurine, or theophylline

132
Q

MOA for Uricosuric Agents

A

increases clearance of uric acid by inhibiting secretory reabsorption in the proximal tubule

133
Q

When is Probenecid used?

A
  • pts cant tolerate allopurinol
  • pts cannot reach target urate levels with just a XOI
  • pts have documented underexcretion of urate
134
Q

What is brand for probenecid

A

Benemid

135
Q

Can Probenecid be added to Allopurinol?

A

yes

136
Q

Max dose of Probenecid

A

2 gm QD

137
Q

Encourage _______ when on Probenecid

A

adequate hydration - to prevent renal stone formation

138
Q

Dosing of Probenecid

A

TITRATE UP

250 BID x 7 then 500 BID x 14

139
Q

Why start at a low dose with Probenecid

A

to prevent uricosuria and renal stone formation

140
Q

Adverse Effects for Probenecid

A
  • flushing
  • HA
  • pruritis
  • GI upset
  • STONE FORMATION
  • Aplast Anemia/Leukopenia
141
Q

Contraindications for Probenecid

A
  • Hypersensitivity
  • Salicylates
  • Blood Dyscrasias
  • Uric Acid Kidney Stones
  • CrCl < 50 mL/min
  • Acute Attack
142
Q

Example of Uricase Agents

A

Pegloticase

143
Q

MOA of Uricase Agents

A

converts Uric acid to allantoin (which is more SOLUBLE IN WATER)

144
Q

Brand for Pegloticase

A

Krystexxa

145
Q

Pegloticase is a ________ line agent

A

LAST

146
Q

How is Pegloticase administered?

A

by IV

147
Q

Dose for Pegloticase

A

8 mg IV infusion q 2 weeks

Administered over 120 minutes

148
Q

for Pegloticase - Patients should be PRE-TREATED with what?

A

antihistamines and corticosteroids (bc of infusion related rxns)

149
Q

When is Pegloticase indicated

A

for REFRACTORY GOUT
- pt with significant disease burden
or
pt has intolerance to conventional urate lowering therapy

150
Q

Adverse Effects for Pegloticase

A
  • infusion related rxns
  • Anaphylaxis
  • Nephrolithiasis
  • Arthralgias
  • HF exacerbation
  • Nausea
151
Q

Contraindications/Cautions for Pegloticase

A
  • G6PD deficiency (bc puts them at risk for hemolysis and methemeoglobinemia - perform G6PD test)
  • Caution: HF pts
152
Q

Lesinurad is generic for ?

A

Zurampic

153
Q

MOA for Lesinurad

A

URAT1 inhibitor - aka will enhance uric acid excretion

154
Q

Lesinurad has been approved to be used in combination with what med?

A

XOI (xanthine oxidase inhibitor)

155
Q

Dose of Lesinurad

A

200 mg QD PO

156
Q

Adverse Effects for Lesinurad

A

BLACK BOX WARNING: for Acute Renal Failure

  • HA
  • GERD
157
Q

Fenofibrate can be used for gout - how/what is the MOA

A

increases the clearance of both hypoxanthine and xanthine (decreases levels ~ 20 - 30%)

158
Q

Losartan can be used for gout - how/what is the MOA

A

inhibits tubular reabsorption of uric acid

unique to losartan - no other ARB will do this

159
Q

Fenofibrate or Losartan can be used to help with gout - can they be used with another gout med?

A

yes - XOI and one of those can be used for refractory cases

160
Q

What are two off label drugs that can be used for gout

A

fenofibrate, Losartan

161
Q

Options for Prophylaxis

A
  • Colchicine (preferred)
  • Low Dose NSAIDs
  • Low dose Prednisone/Prednisolone (< 10 mg /day tho)
162
Q

Prophylaxis regimen should be initiated along with _________

A

ULT (urate lowering therapy)

163
Q

Colchicine dosing - Prophylaxis

A

0.6 mg PO QD or BID

colchicine is preferred over NSAIDs but both are first line options

164
Q

Low Dose NSAIDs dosing - Prophylaxis

A

Naproxen 250 mg PO BID

165
Q

Low dose Prednisone/Prednisolone dosing - Prophylaxis

A

ONLY if other options are contraindicated or not tolerated

Therapeutics 1 Kappa Epsilon Version (17 decks)

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