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IDT exam #2 > Gout > Flashcards

Gout Flashcards

1
Q

Gout

A

an inflammatory disease resulting from the formation of urate crystals in joints and soft tissues.
Crystal formation is the consequence of improper handling of uric acid causing super saturated solution of urate precipitating crystals

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2
Q

Gout is associated with or aggravated by:

A 
Genetics
Obesity
Age
Adult males 
Postmenopausal women
Hypertension
 Diet (high purine, high fructose)
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3
Q

Disease states associated with Gout

A

Lesch-Nyhan syndrome
End stage renal disease
Cancers with cell lysis
major organ transplant

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4
Q

Drugs that can induce Gout

A 
Thiazides
low dose ASA
Niacin
immune suppressants
Cytotoxic agents that cause cell lysis
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5
Q

Lesch-Nyhan syndrome

A

AKA: juvenile gout

  • rare inherited disorder caused by a deficiency of the enzyme hypoxanthine-guanine phosphribosyltransferase (HGBRT)
  • X-linked trait
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6
Q

Phases of Gout

A

Acute
Intermittent
Chronic (advanced)

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7
Q

Acute Gout

A
  • Initial phase where crystals are starting to form, normally starts in a joint, like a toe or elbow.
  • Normally see a low grade fever
  • it is possible to only have one gout attack ever
  • attack may only last 3-14 days, acute attack doesn’t mean you need chronic therapy
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8
Q

Intermittent Gout

A

Start having acute attack 2 times or more per year

And most often start seeing the attack in more than one joint

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9
Q

Chronic (Advanced) Gout

A

You can see changes in renal function.

Significant inflammation.

Hand and feet start to look like RA

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10
Q

pathway to making urate

A

IMP –> Inosine –> Hypoxanthine (xanthine oxidase) –> Xanthine (xanthine oxidase) –> Urate (Uricase)–> Allantoin (more soluble form)

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11
Q

Renal elimination of uric acid

A

Uric acid enters glomerulus , undergoes glomerular filtration.
Proximal convoluted tubule reabsorbs about 90% of uric acid, and excretes only about 8-10%

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12
Q

inflamasomes

A

are created due to high levels of uric acid in the blood

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13
Q

the inflammatory response from gout

A

stimulated by metabolic, exogenous, and endogenous stimuli that active caspase-1. once caspase-1 is activated it actives IL-1b, IL-18, and IL-1a.
These IL’s then further active an even bigger inflammatory response (TNF-a, IL-6, KC).

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14
Q

Chronic Sequelae of Gout

A

Renal: Nephrolithiasis (kidney stones), and interstitial nephritis

Arthritic: deposition of tophi; erosion of cartilage and bone; joint deformities and loss of function

Metabolic(?): increasingly it is thought to be associated with metabolic syndrome, stroke and other types of cardiovascular disease

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15
Q

Diagnosis of gout

A

aspiration of synovial fluid and visualization of crystals, differential diagnosis can sometimes be difficult

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16
Q

Treatment goals of Gout

A

Acute: resolve inflammatory process rapidly

Intermittent/chronic: limit crystal formation, tophi (deposit of crystals and other substances on the surface of joints) and tissue damage by lowering serum uric acid, especially if there are comorbid conditions.

17
Q

Gout treatment guidelines

A

Treat to relieve symptoms not the level of uric acid in the blood.

18
Q

Medications that can treat acute gout symptoms

A

-colchicine
-NSAIDs (non-ASA)
-Steroids
Il-1 antagonists
ACTH (?)
Opioids (?)- just for pain

19
Q

A decision to initiate chronic therapy is made when:

A

Uric acid levels exceed 7 mg/dl AND

  • greater than 2 acute flares occur within one year OR
  • tophi are present OR
  • significant kidney disease OR
  • incidence of kidney stones
20
Q

Xanthine oxidase inhibitors

A

Allopurinol ( a purine, uric acid analog inhbitor)

Febuxstat ( a non-purine inhibitor)

Neither are preferred over the other, except in certain disease states.

21
Q

Allopurinol

A

Dosing: 100mg/d, can be slowly increase by 100mg/week. Maintenance dose: 300mg/day, can be pushed to 800mg/d (top of dosing curve.
Acute SE: Rash, fever, GI, malaise, itching
Excretion: 80% by the kidney (dose to be adjusted with decreased renal function)

-Allopurinol Hypersensitivity reaction
DI: Azathioprine, 6-mercaptopurine (both of these are degraded by xanthine oxidase)
-Has a lot of long term data for efficacy

22
Q

Allopurinol Hypersensitivity Reaction

A
  • SIGNIFICANT
  • Similar to SJS
  • Rash
  • Can lead to kidney failure
  • Would D/C therapy
  • Can screen for patients with HLA-B 58:01 Allele. It is associated with developing this hypersensitivity reaction
  • -> Asian populations generally have a high incidence of this allele
23
Q

Febuxostat

A
  • non-competitive inhibitor of xanthine oxidase
  • Acute SE: rash, GI, fever, malaise, itching
  • Hepatic metabolism- would want to monitor hepatic function
  • Dosing: 40 mg/day up to 80mg/day
  • no long term data for efficacy
24
Q

Colchicine

A

MOA: decreases microtubule formation, which limits(inhibits) chemotaxis (inhibits the inflammatory response)

  • Want to treat within 36 hours of flare up.
  • Dosing: 1.2 mg, then 0.6mg 1 hour later. if treating a flare up over a few days: 1.2 mg/d x 14 days
25
Q

NSAIDs

A

most common is Indomethacin, but naproxen is pretty common too.

26
Q

Steroids

A
  • Prednisolone 0.5 mg/kg (usually about 35 mg/day) and treat for about 5 days
  • Oral steroids are very effective, and intrajoint injections are also effective
27
Q

IL-1 antagonists

A

-Anakinda & Cankinumab

definitely not first line, mainly because to expensive

28
Q

Probenecid

A
  • Dosing: 250 mg BID up to 2000 mg daily
  • SE: GI upset, rash
  • CIearance: less than 50ml/min CrCl
  • Counseling point: make sure patient knows to stay adequately hydraded
  • DI: increase in concentrations of beta-lactam antibiotics, and methotrexate (this is bad)
  • decrease in Glucose-6-phosphate dehydrogenase, which increases incidence of hemolytic anemia
29
Q

Lisinurad

A

Just approved in December of 2015, by a SINGLE vote
-URAT-1 inhibitor
-Dosing: 200mg/d, can move up to 400mg/d but there is an increased risk of SE
SE: HA, malaise, GERD
-never used alone, always in conjunction with a xanthine oxidase inhibitor
–>when used alone it showed an increased risk of renal failure

IDT exam #2 (1 decks)

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