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Sem 2 Pharmacology > Week 2 - Gout > Flashcards

Week 2 - Gout Flashcards

(53 cards)

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1
Q

What is gout?

A

An inflammatory, intermittent arthritis.
Chronic hyperuricemia, leading to supersaturation of body tissues with urate
Causes formation of monosodium urate crystals in and around joint, particularly the Metatarsophalangeal joint (big toe)

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2
Q

What causes an acute attack of gout?

A

Shedding of urate crystals into the joint

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3
Q

How do you diagnose gout?

A

Very identifiable but also by urate crystals in synovial fluid

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4
Q

Why is incidence of gout increasing?

A

Ageing populations, obesity and sweet drink consumption

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5
Q

Which 6 foods are ‘bad’ for gout?

A 
Meat
Seafood
Sugary drinks
Fructose
Beer
Spirits
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6
Q

Which foods are ‘good’ for gout?

A

Coffee - over 6 cups
Dairy
Vit C
Maybe cherries

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7
Q

What are some risk factors of gout?

A

1 is genetic

Eating the ‘bad foods’
Gender - males x3 incidence
Hypertension/metabolic syndrome
Chronic renal failure as reduces filtration
Kidney/heart transplantation
Drugs like thiazide diuretics, low dose aspirin or cyclosporin

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8
Q

Describe the inflammatory process that urate crystals in synovial fluid produce

A
  1. Kinin, complement and plasmin system are activated
  2. Neutrophils infiltrate and engulf crystals
  3. Toxic oxygen metabolites are released
  4. Tissue lysis and release of proteolytic enzymes
  5. Goes back to the start to continue to the cycle
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9
Q

What are the clinical phases of gout?

A
  1. Preclinical - crystal deposits in joint tissues are accumulating. No attacks
  2. Intermittent attacks of acute gout with no symptoms in between
  3. Chronic tophaceous gout
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10
Q

What are common joints affected by gout?

A

70% with gout experience it in the MTP

Others include knee, ankle, mid-tarsal, wrist/elbow and fingers

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11
Q

When is gout poly-articular?

A

Usually in the elderly, particularly females

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12
Q

Is gout self-limiting?

A

Yes, usually over in 3-7 days

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13
Q

Describe how chronic tophaceous gout occurs

A

Recurrent acute attacks on gout inadequately treated by urate lowering medication

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14
Q

What’s the classic appearance of chronic tophaceous gout? What does this lead to?

A

Tophi - large crystal deposits on extensor surfaces of fingers/hands, elbows, tendons and the ear
Leads to erosion of neighbouring joints causing restricted movement and deformity, chronic renal failure, and contributes to CVD, stroke and CKD (chronic kidney disease)

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15
Q

What’s the current approach in treating chronic gout?

A

Treat early with use of urate lowering therapies, as increased uric acid is a risk factor for CVD, stroke and CKD

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16
Q

What is the main aim of acute gout? How is this achieved?

A

Pain relief
Using NSAIDs, otherwise colchicine
Glucocorticoids can be used, especially if intra-articular and not septic

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17
Q

When do you start urate lowering treatments?

A

2-4 weeks after an acute attack has resolved, otherwise you can make it worse

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18
Q

What is another arthritis you need to differentiate gout with?

A

Septic arthritis

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19
Q

What are the upper ranges of uric acid in males and females?

A

Males - 400 umol/L

Females - 360 umol/L

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20
Q

What is the level of uric acid in hyperuricemia in males?

A

420 umol/L

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21
Q

Why does hyperuricemia not always gout?

A

Hyperuricemia is seen in about 10% of men, and less than 25% of that population develop gout

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22
Q

Describe uric acid elimination and retention

Study These Flashcards
A

100% uric acid is filtered through glomerulus
99% is reabsorbed in proximal tubule by URAT1/GLUT9
6-10% is secreted in distal proximal tubule
Leads to only 10% loss of uric acid per cycle

23
Q

What is the usual cause of hyperuricemia?

Study These Flashcards
A

Undersecretion of UA

24
Q

Describe the action of Xanthine oxidase in uric acid synthesis

Study These Flashcards
A

XO operates on hypoxanthine and turns it into xanthine. XO then turns xanthine to uric acid

25
What is Colchicine? What is it's action?
Colchicine is a tricyclic alkaloid It binds tubulin, stopping MT assemly and affecting cell division, neutrophil motility and reduces chemokine production Leads to prevention of inflammatory cell recruitment
26
Describe the absorption, distribution and excretion of colchicine
Absorbed rapidly orally Concentrates in WBCs Excreted - hepatobiliary, 10-20% renal
27
In what time frame should colchicine give pain relief?
12-24 hours
28
What are the common side effects of colchicine and why do we see them?
Diarrhoea and vomiting very common, may precede rare adverse effects like muscle damage, myelosuppression and multiple organ failure Common bc of narrow therapeutic window
29
To whom should you not give colchicine?
Those with poor renal function
30
What are some dangerous drug interactions of colchicine?
CYP3A4 and P-pgp inhibitors Antibiotics like erythromycin and clarithromycin Ca2+ channel blockers Cyclosporin/grapefruit juice
31
Describe the new low dosing of colchicine
``` 2 x 0.5mg at first sign 1 x 0.5mg 1 hour later No more than 1.5mg No more for at least 3 DAYS NO GRAPEFRUIT Stop if any N, V or D Ensure patient understanding ```
32
What is the aim of chronic gout treatment? What is targetted?
Long term reduction in uric acid | Address lifestyle i.e. alcohol, diet and weight
33
At what level of urate will gout attacks stop?
34
WHat should you do on a personal level with gout patients?
Stay positive - negative views reduce adherence Emphasize it's not their fault Gout is cruable
35
What are the main three drug groups for treating gout?
Xanthine oxidase inhibitors, uricase agents and uricosuric agents
36
What is allopurinol?
A hypoxanthine analog that competitively inhibits xanthine oxidase to decrease uric acid synthesis
37
What is allopurinol's mechanism of action?
Xo converts allopurinol to alloxanthine, which then non-competitively inhibits XO, decreasing uric acid synthesis
38
Which molecule in the allopurinol pathway is the pharmacologically active one?
Alloxanthine
39
Describe the treatment schedule of allopurinol
Well absorbed orally, half life 2-3 hours - 100mg once a day - Increase 100mg a month - Max of 800mg, until SUAA goal is reached at
40
How is allopurinol excreted?
Renally - balance between glomerular filtration nad tubular reabsorption
41
What would you need to be careful of in treating someone with renal insufficiency with oxypurinol?
Renal insufficiency elevates oxypurinol's half life, so doses would need to be adjusted
42
What are the adverse effects of allopurinol?
Adverse effects in 20%, 5% stop taking it Gastrointestinal, drug reactions, rash with eosinophilia and systemic symptoms (DRESS) and can lead to Steven-Johnson's syndrome --> particularly in East Asian populations
43
What are dangerous drug interactions with allopurinol?
Mercaptopurine and Azathioprine, which are purine analalogues
44
What does allopurinol do to the drug Mercaptopurine?
M is an antimetabolite chemotherapy agent which blocks DNA synthesis -> A increases its effects, leading to myelosuppression and gastrointestinal effects. Life threatening in large doses
45
WHat does allopurinol do to the drug Azathioprine?
Aza is a prodrug and immunosuppressent. Allopurinol increases it's effects, affecting fast replicating tissues and leading to myelopsuppression that can be life threatening
46
What is Febuxostat?
Non-purine selective inhibitor of XO Useful in patients with renal impairment because is hepatically excreted More expensive than Allopurinol
47
What is an example of a uricase drug, and what does it target? What's the effect of this?
Rasburicase Catalyzes the conversion of uric acid to allantoin. Rapidly decreases serum uric acid levels, and breaks down urate to remove tophi. IV only, short half life (18 hours)
48
Wat do uricosuric agents do?
Block urate uptake in the proximal tubule, useful for under-excretors (90%) with normal renal function
49
What are two examples of uricosuric agents?
Probenecid (can't use with aspirin) | Benzbromarone
50
Describe elimination of uric acid from the human body
1/3 enteric, 2/3 renal
51
What about uric acid causes it to affect peripheral joints?
Poorly soluble at low temperatures
52
What is uric acid?
Final product of purine metabolism in humans, but is broken down further to allantoin in other animals
53
How much uric acid do we get from our diet?
1/3

Sem 2 Pharmacology (4 decks)

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