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Winter P2 > Exam 2 - Medchem 753, Delander Gout > Flashcards

Exam 2 - Medchem 753, Delander Gout Flashcards

1
Q

What is gout?

A

Inflammatory disease that results in urate crystals in joints and soft tissues

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2
Q

What causes the formation of crystals in gout?

A

Crystals form due to improper handling of uric acid which causes a supersaturated solution of urate precipitating crystals

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3
Q

How many people in the US are affected with Gout?

A

8 million (4% of population)

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4
Q

What factors are associated w/or are aggravated by Gout?

A 
Genetics (big)
Obesity (Surface area?)
Age (older worse)
Adult Males
Potmenopausal women
HTN
Diet (high purine or high fructose)
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5
Q

What disease states might Gout be more prevalent in?

A

Lesch-Nyhan Syndrome
End Stage renal disease
Cancers w/ cell lysis
Major Organ Transplant

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6
Q

What Drugs may induce or exacerbate the presence of Gout?

A 
Thiazides (Diuretics) - compete for transporters
Low dose Aspirin
Niacin
Immune Suppressants
Cytotoxic agents causing cell lysis
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7
Q

What is Lesch-Nyhan Syndrome?

A

A disease characterized by a lack of HGPRT which results in problems in the breakdown and removal of Urate. It is a Problem w/ Metabolic Process that some people have that does not have salvage pathway which results in higher amounts of Uric Acid and gout like symptoms.

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8
Q

What are the disease stages of Gout?

A

Acute
Intermittent
Chronic

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9
Q

When do Acute phases of Gout generally occur?

A

At night while asleep, while not moving, increased likelihood of crystalizing out due to things cooling down.

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10
Q

What are the common characteristics of acute gout?

A
  • Crystals form in joint(Very common in big toe)
  • low grade fever
  • typically resolves in 3-14 days
  • May not have another attack for quite a while or ever
  • Intense pain
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11
Q

What are the common characteristics of intermittent gout?

A
  • Acute attacks x2 or more per year

- Usually in more than one joint (not always toe)

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12
Q

What are the common characteristics of chronic Gout?

A

Means that something is happening w/ disease state to cause other problems

  • Start therapy
  • Changes in renal
  • permanent crystals setting in joints
  • generally polyarticular (many joints)
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13
Q

What affect does change in diet have on disease state?

A

Generally very minimal effect

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14
Q

Where do Purines come from?

A
  1. Our cells, constantly breaking down and forming it

2. Food

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15
Q

What is the enzyme animals have to break down Uric Acid?

A

Uricase (urate oxidase) which breaks down urate into Allantoin

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16
Q

What animal species do not contain Uricase?

A

Humans, Apes and Dalmations (dog)

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17
Q

What percentage of Uric Acid enters the Proximal tubule from glomerulus?

A

100%

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18
Q

What percentage of Uric Acid is reabsorbed by glomerular filtration?

A

98-100%

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19
Q

Due to secretion and reabsorption of Uric Acid, what percentage of Uric Acid is actually excreted in Urine?

A

8-12%

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20
Q

Due to secretion and reabsorption of Uric Acid, what percentage of Uric Acid is actually excreted in Urine?

A

8-12%

increasing is current area of drug research

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21
Q

What are Inflammasomes?

A

When there are high levels of Uric Acid in plasma, the uric acid cystallize and are phagocytized and form these, which release IL-1b, which activates a huge inflammatory response.

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22
Q

How much Uric Acid is the “magic number”? At what level is treatment usually started?

A

~7mg/dL

23
Q

What are the chronic problems of gout that we are worried about with managing Gout?

A
  • Renal - Nephrolithiasis (stones) and Interstitial Nephritis
  • Arthritic - Deposition of Tophi, erosion of Cartilage and bone, loss of function
  • Metabolic - associated w/ metabolic syndrome, stroke and other CVD
24
Q

What is the gold standard in diagnosing Gout? What else is used?

A

Visualization of Uric Acid Crystals in aspirated synovial fluid

Differential Diagnosis by using colchicine to treat

25
Q

What are the treatment goals of Acute Gout?

A

Resolve inflammatory process rapidly

26
Q

What are the treatment goals of intermittent/chronic Gout?

A

Decrease Uric Acid so we don’t have long term problems of effects

New Guidelines state we don’t try to control serum level, we treat to control symptoms.

27
Q

What medication has traditionally been the go to therapy for Acute flares of Gout? Why is it no longer? What is the first line according to guidelines now?

A

Colchicine, Price

Steroid then NSAID

28
Q

Colchicine

  1. MOA
  2. Dosing
  3. SE
  4. Considerations
A
  1. Decrease Microtubule formation, which limits chemotaxis
  2. (1.2mg, prn 0.6mg an hour later) effective for 36hrs (1.2mg/day generally for 14 days)
  3. GI upset (25%), Muscle Weakness (inc w/ statins), Bone Marrow Suppression (penias)
  4. Price, Dose adjustments w/ Hepatic failure, inhibits 3A4 & PGP
29
Q

What other drug classes are often prescribed for acute Gout flares?

A 
NSAIDS
Steroids
IL-1 Antagonists (off label)
Adrenocorticotropic hormone (ACTH)
Opioids (?)
30
Q

When using NSAIDS to control Gout:

what Med do you not want to use, what is traditionally used, what is common now?

A
  • Don’t use Salicylates (Acetaminophen no effect, not an NSAID)
  • Historically use Indomethacin
  • Now Naprosyn or Naproxen common
  • Any can be used
31
Q

When using Steroids to control gout,

What is most common? dosing?

A

Prednisilone, 0.5mg/kg (~35mg/day) orally for 5 days, although can be given injection

32
Q

Interleukin 1 antagonists

Anakinra and Canakinumab

A
  • Not a lot known SE wise because they are rarely used,
  • Thought to stop Interleukin-1b from causing inflammasome response
  • Expensive as fuck
33
Q

Adrenocorticotropic Hormone in treatment of Gout

A

Increases availability of cortisol (endogenous steroid)

34
Q

Opioids in treatment of Gout?

A

Only treats the symptoms, covers up the pain.

35
Q

What behavioral changes can be adopted?

A
  • Weight loss
  • Diet (avoid foods high in purines, adequately hydrated)
  • Watch for Drugs that may aggravate

Historically doesn’t change a ton and is rarely adequate by itself

36
Q

When is chronic treatment generally pursued?

A

Increase in Uric Acid levels above 7mg/dL AND:

  • When patient is fed up with acute flares
  • > 2 flares per year
  • Tophi present
  • Kidney disease/presence of stones
37
Q

When you pursue Chronic therapy, what is a common side effect?

A

Increased incidence of acute flares within 6months of therapy

38
Q

Does pH have anything to do with acute flare ups?

A

Delander, doubtful, but it may increase amount of stones

39
Q

When you pursue Chronic therapy, what is a common side effect?

A

Increased incidence of acute flares within 6months of therapy (prophylaxis of acute attacks required)

40
Q

Does pH have anything to do with acute flare ups?

A

Delander, doubtful, but it may increase amount of stones.

Otherwise don’t know

41
Q

What are common Xanthine Oxidase inhibitors?

A

Allopurinol

Febuxostat

42
Q

Allopurinol

  1. MOA
  2. Dosing
  3. SE
  4. Considerations
A
  1. Is a purine and uric acid analog inhibitor, inhibits the Xanthine Oxidase, decreasing the amount of uric acid produced.
  2. initially 100mg/day, increase by 100mg weekly, usually 300mg, max 800mg]
  3. Rash, Fever, GI, malaise, itching
  4. Hypersensitivity (Steven Johnson), DDI (Azathioprine & Mercaptopurine) 80% renal clearance (adjust renal impairment)
43
Q

How to minimize the side effects of allopurinol?

A
  • slow titration of medication
    Hypersensitivity:
  • Limit use in HLA-B 5801 allele pts
44
Q

What populations more commonly express HLA-B 5801 allele?

A

Asians

  • Thai
  • Han Chinese (Taiwan)
  • Koreans
45
Q

What drugs should not be used alongside Allopurinol or Febuxostat?

A

Azathioprine

Mercaptopurine

46
Q

Febuxostat in the control of Gout

  1. MOA
  2. Dosing
  3. SE
  4. Considerations
A
  1. Non-purine inhibitor, non-competitively inhibits Xanthine Oxidase to reduce amount of Uric Acid produced
  2. 40mg/day up to 80mg/day, max 120mg
  3. Rash, Fever, GI, malaise, itching
  4. No hypersentivity rxn, Primarily Hepatic metabolism
47
Q

What uricosuric agents are used to control gout?

A

Probenecid

Lisinurad

48
Q

Probenecid

  1. MOA
  2. Dosing
  3. SE
  4. Considerations
A
  1. Relatively non specific transport inhibitor (facilitate excretion)
  2. usually 250mg bid, up to 2000mg
  3. Rash; GI
  4. DDI (Beta lactams, Methotrexate); Contraindicated in low CrCl (<50mL/min), those with G6P dehydrogenase deficiency
49
Q

What populations are generally deficient for G6P dehydrogenase?

A

Mediterraneans

Blacks (10%)

50
Q

Lisinuard

  1. MOA
  2. Dosing
  3. SE
  4. Considerations
A
  1. Inhibits Uric Acid Transporter 1 (URAT-1), reduces reabsorption from proximal tubule (facilitate excretion)
  2. 200mg/day
  3. Headache, Malaise, GERD
  4. Renal Failure in monotherapy
51
Q

What Drug class must accompany the use of Lisinurad?

A

Xanthine Oxidase Inhibitors

52
Q

When using Uricosurics, what counseling point is of the utmost importance?

A

Adequate Hydration

53
Q

If Disease state does not respond to Xanthine Oxidase inhibitors or Uricosurics what is another option? Why is it not common?

A

Recombinate Uricase
Expensive as fuck
Exceedingly immunogenic

54
Q

Rasburicase and Pegloticase

A

Rasburicase (only available w/ infusion)

Pegloticase (Pegylated uricase in order to not have a huge immune response)

Winter P2 (6 decks)

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