AntiGout Flashcards

(72 cards)

1
Q

a metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium
urate in joints and cartilage

A

Gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Gout is a metabolic disease characterized by recurrent episodes of _____________ due to deposits of monosodium
urate in joints and cartilage

A

acute athritis; monosodium
urate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

a systemic disease caused by the buildup of uric acid in the joints, causes inflammation, swelling and pain

A

Gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

urate level > 8mg/dL in men and 7 mg/dL in women

A

Hyperuricemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ost common first symptom of gout

A

Pain in one joint of the lower extremity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

end product of purine metabolism

A

Uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

rate limiting step in the formation of the uric
acids

A

Xanthine oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

serves no known biological functions, but the body has
content of 1.0-.2g

A

Uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Approximately ________ of Uric acid is excreted via the ________

A

70-80%; kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

result of an innate defect in purine metabolism of uric acid excretion

A

Primary gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of primary gout

A

Uric acid overproduction (overproducers)
Impaired renal clearance of uric acid (underexcreters)
Combination of both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

causes of Secondary gout

A
  • Hematologic disorders
  • Drug induced – salicylates,diuretics (thiazide), ethambutol, pyrazinamide, nicotinic acid, ethanol, niacin and cyclosporine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment Goals for gout

A
  • Relieve pain and inflammation
  • Reduce serum uric acid concentration (urate lithiasis)
  • Prevent recurrent gout attacks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Treatment for acute gouty athritis attack

A
  • Colchicine
  • NSAIDs
  • Corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Antimitotic drug that is highly effective in relieving acute gout attack

A

Colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Has low –benefit to toxicity ratio, thus it is used less often than NSAIDs

A

Colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Colchicine is most effective when initiated within ____________ of the attack

A

12-36 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

T/F: Colchicine’s likelihood of success increase substantially if treatment is delayed longer than 48 hours after symptom onset.

A

false: decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

type of colchicine that causes dose-dependent GI adverse effect (nausea, vomiting, bloating, emesis and diarrhea) that occur in up to 80% of patients

A

oral colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

first-line drugs for acute gout

A

NSAIDs, corticosteroids, or

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

was the primary treatment for many years due to its efficacy in treating and preventing acute gout flares

A

colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Colchicine can be taken with or without food and is sometimes given in combination with
NSAIDs

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Colchicine is an alkaloid isolated from the autumn crocus, ______________

A

Colchicum autumnale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

relieves the pain and inflammation of gouty arthritis in 12–24 hours without altering urate metabolism or excretion and without other analgesic effects

A

Colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Colchicine relieves the pain and inflammation of gouty arthritis in ________ without altering ___________ and without other analgesic effects
12–24 hours; urate metabolism or excretion
26
Colchicine relieves the pain and inflammation of gouty arthritis in 12–24 hours _________ (with/without) altering urate metabolism or excretion and without other analgesic effects
without
27
mainstay of therapy because of their excellent efficacy and minimal toxicity with short-term use.
NSAIDs
28
NSAIDs Therapy should be initiated with ____________ (maximum/minimum) recommended dose for gout at the onset of symptoms and continued for ______- after resolution of an acute attack, then tapered quickly over _____
maximum; 24 hours; 2-3 days
29
NSAID most common adverse effects involve _____
GI system
30
most extensively studied NSAID in the treatment of an acute gouty arthritis attack
Indomethacin
31
In addition to inhibiting prostaglandin synthase, __________ inhibit urate crystal phagocytosis and reduce inflammation and pain in acute gout flare
NSAIDs
32
NSAIDs inhibit
-prostaglandin synthase -urate crystal phagocytosis
33
Why is Aspirin not used in Gout treatment?
because it causes renal retention of uric acid at lower doses (≤2.6 g/d); it is uricosuric at doses >3.6 g/d.
34
T/F: All NSAIDs except aspirin, salicylates, and tolmetin have been successfully used to treat acute gouty episodes
true
35
lowers serum uric acid, is theoretically a good choice and all NSAIDs appear to be as effective and safe as the older drugs like indomethacin
Oxaprozin
36
equivalent to NSAIDs for treatment of acute gout flares
Corticosteroids
37
Corticosteroids are effective when given _________
intra-articulary, IV or orally.
38
Oral Corticosteroid
Prednisone
39
long acting corticosteroid, IM, ntra-articular (can be given if the patient is unable to take oral medications)
Triamcinolone acetonide or methlyprednisolone
40
decrease activation, proliferation, and survival of various inflammatory cells
corticosteroids
41
decrease the migration of neutrophils, and they inhibit prostaglandins and proinflammatory cytokines such as IL-1β.
corticosteroids
42
a good alternative for patients in whom NSAIDs or colchicine are contraindicated and in those with renal impairment or chronic kidney disease.
Corticosteroids
43
sometimes used in the treatment of severe symptomatic gout, by oral, intra-articular, systemic, or subcutaneous routes.
Corticosteroids
44
The goal of _____________ is to achieve and maintain a serum uric acid concentration < 6mg/dL and preferably < 5mg/dL
urate lowering therapy
45
Reduction of the serum urate concentration un Uric Acid Lowering Therapy can be accomplished b
* decreasing uric acid synthesis (xanthine oxidase inhibitor) * Increasing the renal excretion of the uric acid (uricosurics)
46
Uric Acid Lowering therapy are not be used during as ______
acute gouty arthritis attack
47
Allopurinol, Febuxostat
Xanthine Oxidase Inhibitors
48
reduce uric acids by impairing the conversion of hypoxanthine to xanthine and xanthine to uric acid.
Xanthine Oxidase Inhibitors
49
effective in both overproducers and underexcretion of uric acids
Xanthine Oxidase Inhibitors
50
most widely prescribed agents for long-term prevention of recurrent gout attacks
Xanthine Oxidase Inhibitors
51
responsible for the conversion of xanthine and hypoxanthine to uric acid
Xanthine oxidase
52
a purine analogue that inhibits this enzyme, resulting in a fall in the plasma urate level and a decrease in the overall urate burden.
Allopurinol
53
Allopurinol is a _________ analogue that inhibits this enzyme, resulting in a fall in the _________ and a decrease in the _____
purine; plasma urate level; overall urate burden
54
The result of xanthine oxidase inhibition is
build-up of its substrates, the more soluble xanthine and hypoxanthine
55
The result of xanthine oxidase inhibition is a build-up of its substrates, the _______ (more/less) soluble xanthine and hypoxanthine.
more
56
is often the first-line agent for the treatment of chronic gout in the period between attacks, and it tends to prolong the intercritical period
Allopurinol
57
Allopurinol is often the first-line agent for the treatment of chronic gout in the period between attacks, and it tends to prolong the ________
intercritical period
58
T/F: Allopurinol Therapy is continued for years if not for life.
true
59
a potent and selective non-purine inhibitor of xanthine oxidase thereby reducing the formation of xanthine and uric acid without affecting other enzymes in the purine or pyrimidine metabolic pathway
Febuxostat
60
Febuxostat is a potent and ___________ non-purine inhibitor of xanthine oxidase thereby reducing the formation of _______ without affecting other enzymes in the ________
selective; xanthine and uric acid; purine or pyrimidine metabolic pathway
61
Febuxostat is a potent and selective __________ inhibitor of xanthine oxidase thereby reducing the formation of xanthine and uric acid ________ (with/without) affecting other enzymes in the purine or pyrimidine metabolic pathway
non-purine; without
62
uricosuric agent have been discontinued in the USA
Sulfinpyrazone and Lesinurad
63
Probenecid
Uricosuric Drug
64
They increase the renal clearance of uric acid by inhibiting the postsecretory renal proximal tubular reabsorption of uric acid.
Uricosuric Drugs
65
should be initiated in gouty patients with underexcretion of uric acid when allopurinol or febuxostat is contraindicated
Uricosuric therapy (Probenecid)
66
Uricosuric therapy (Probenecid) should be initiated in gouty patients with underexcretion of uric acid when ________ or _________ is contraindicated
allopurinol; febuxostat
67
T/F: Probenecid can be used as monotherapy or in combination with a xanthine oxidase inhibitor
True
68
Canakinumab, Anakinra, and Rilonacept
INTERLEUKIN 1 INHIBITORS IN GOUT
69
inhibit the IL-1 receptor pathway
INTERLEUKIN 1 INHIBITORS IN GOUT
70
main proinflammatory cytokine responsible for the crystal-induced inflammation of gout.
IL-1β
71
T/F: Canakinumab, Anakinra, and Rilonacept are not yet FDA-approved for the treatment of gout.
True
72
All three IL-1 inhibitors are administered
subcutaneously