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Lecture 121 Flashcards

1
Q

What general treatment principle should be considered with initiating ULT therapy?

A

Combine with an anti-inflammatory

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2
Q

What is the target serum uric acid level for the management of gout?

A

<6mg/dL

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3
Q

What is NSAIDs MOA for the acute treatment of gout?

A

Inhibits prostaglandin synthesis and inhibits urate crystal phagocytosis

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4
Q

What is the first-line treatment for acute gout?

if there are no contraindications

A

NSAIDs

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5
Q

What are the three primary NSAIDs used for the acute treatment of gout?

A

naproxen, indomethacin, sulindac

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6
Q

Full anti-inflammatory doses for acute gout are typically higher/lower than analgesic doses

A

Higher

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7
Q

What is the MOA of corticosteroids in the acute treatment of gout?

A

Supresses the immune/inflammatory response

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8
Q

First line therapy for acute gout if NSAIDs are contraindicated

A

Corticosteroids

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9
Q

Toxicities of corticosteroids include:

A

insomnia, mood changes, hyperglycemia, fluid retention

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10
Q

What is the MOA of colchicine in the acute treatment of gout?

A

Binds to tubulin, inhibiting microtubule polymerization and reducing inflammatory mediator release and leukocyte migration

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11
Q

Colchicine can be used for acute grout treatment if started within ____ of flare onset

A

36 hours

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12
Q

What drug used for treatment of acute gout is sometimes use as low-dose long-term prophylaxis?

A

Colchicine

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13
Q

Adverse effects of colchicine:

A

GI upset, potential for neuropathy or bone marrow suppression in chronic use

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14
Q

Which drug used for acute gout is metabolized by CYP3A4?

A

Colchicine

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15
Q

What is the MOA of pegloticase?

A

Converts uric acid to allantoin

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16
Q

What gout drug is used in severe/refractory cases?

A

Pegloticase

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17
Q

What is the MOA of canakinumab?

A

Blocks IL-1 to reduce inflammation

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18
Q

What three indications are considered for initiating urate-lowering therapy (ULT)?

A
  1. At least 1 tophus present
  2. Radiographic damage attributed to gout
  3. At least 2 gout attacks per year
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19
Q

What two drugs belong to the xanthine oxidase inhibitor (XOI) family?

A

Allopurinol and Febuxostat

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20
Q

Which ULT is usually first line for the treatment of gout?

A

Allopurinol

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21
Q

What is the MOA of allopurinol?

A

Competitive inhibition of xanthine oxidase leading to decreased uric acid production

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22
Q

What is allopurinol metabolized to?

A

Oxypurinol (alloxanthine), which also inhibits XO

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23
Q

What adverse effect requires immediate termination of allopurinol treatment?

A

Rash

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24
Q

Rare allopurinol hypersensitivity syndrome is associated with:

A

HLA-B5801 allele

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25
Fever, hepatitis, eosiniphilia, and renal failure are indications of hypersensitivity to which chronic gout medication?
Allopurinol | Rare allopurinol hypersensitivity syndrome
26
Allopurinol and Febuxostat can increase levels of which two drugs?
Azathioprine and mercaptopurine
27
What labs should be monitored during allopurinol therapy?
LFTs, creatinine, CBC
28
What is the MOA of febuxostat?
Non-purine xanthine osidase inhibitor
29
Febuxostat **does/does not** require renal dose adjustment
Does not
30
Toxicities associated with febuxostat include:
Elevated LFTs, nausea, rash, MSK pain
31
What Black Box Warning is associated with febuxostat?
Increased risk of cardiovascular death in patients with establish CVD
32
What labs should be monitored during febuxostat therapy?
LFTs, CBC
33
Probenecid belongs to what pharmacological group?
Uricosuric drugs
34
What is the MOA of probenecid?
Inhibits URAT1 transporter in the proximal tubule, reducing uric acid absorption
35
What is a lifestyle requirement for probenecid therapy?
Adequate hydration
36
What ULT is contraindicated in a patient with a prior history of urolithiasis?
Probenecid
37
Probenecid should be avoid in patients with an eGFR of less than ____
60mL/min
38
Toxicities of probenecid include:
Rash, precipitation of acute gout, nephrolithiasis
39
Reduced excretion of certain weak acids (e.g. penicillins) is associated with what ULT?
Probenecid
40
A low-dose anti-inflammatory should be used for ____ months after starting ULT to prevent flares
3-6 months
41
Acute therapy for gout should be started within ____
24 hours
42
Certain medications can trigger gout, including:
Thiazides
43
What is the classic single-joint location in gout?
First MTP joint
44
Pseudogout is also known as:
Calcium pyrophosphate deposition disease (CPPD)
45
Radiographs of patients with gout often show:
Chondrocalcinosis (calcification of cartilage)
46
Needle-shaped, negatively birefringement crystals typically indicates
Gout
47
Rhomboid, positively birefringent crystals indicates
Pseudogout
48
Dietary considerations for the prevention of gout flares includes limiting:
Red meat, seafood, beer
49
What medications are sometimes used to treat chronic CPPD flares?
Steroids, methotrexate, or colchicine
50
X-ray may show ____ in patients with gout
Joint erosions
51
Uric acid production is driven by:
Purine catabolism and urate synthesis
52
Uric acid excretion involves:
Filtration by the glomerulus with near-complete proximal tubule reabsorption
53
Partial HGPRT deficiency causes gout due to:
Increased uric acid production with normal excretion
54
Increased nucleic acid turnover results in secodnary gout due to:
Marked uric acid overproduction with increased excretion
55
Chronic renal disease results in secondary gout due to:
Normal uric acid production with decreased excretion
56
Congenital Lesch-Nyhan syndrome results in secondary gout due to:
Marked overproduction of uric acid with increased excretion
57
Renal complications caused by urate crystal or tophus deposition in the renal medulla or tubules is known as:
Urate nephropathy
58
Intense neutrophilic infiltrate with scattered lymphocytes, plasma cells, and macrophages in synovium indicates:
Acute gouty arthritis
59
Tophi are:
Large aggregates of urate crystal surrounded by intense inflammatory reaction
60
Foriegn-body giant cells are typically seen in what pathologic finding of gout?
Tophi
61
Urate encrusts articular surfaces, synovium becomes hyperplastic and fibrotic, and cartilage destruction and bone erosions can occur in this pathologic finding of gout
Chronic tophaceous arthritis
62
Which cytokine is primarily implicated in the pathogenesis of gout?
IL-1
63
Chronic gout is characterized by:
Joint destruction from persistent inflammation and crytsal deposition
64
Gain-of-function mutations in the ANKH gene results in:
Pseudogout
65
Secondary forms of pseudogout can be related to:
- Joint damage - Hyperparathyroidism - Hemochromatosis - Hypomagnesemia - Hypothyroidism - Diabetes
66
Deposition of ____ in articular cartilage, menisci, and intervertbral discs leads to pseudogout
Calciul pyrophosphate dihydrate (CPP) crystals

Block 3 (37 decks)

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