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Pharmacology > Gout > Flashcards

Gout Flashcards

1
Q

Gout?

A

Gout is the precipitation of urate crystals in joints or in and
around or into tissue causing recurrent acute or chronic
arthritis.

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2
Q

Types of Gout Treatment?

A

Acute Treatment is with :

  1. NSAIDs
  2. Colchicine
  3. Corticosteroids

Chronic Tx:

  1. Allopurinol,
  2. Probenecid
  3. Febuxostat
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3
Q

Signs and symptoms of gout?

A
  1. Pain(excruciating)
  2. Inflammation(swelling, redness ,warmth & tumor)
  3. Affects joints
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4
Q

How does Tophi develop?

A

Tophi occur in patients with chronic gout, but can occur in patients who have not ever had acute gouty arthritis.

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5
Q

Tophi?

A

Tophi are usually fine yellow or white papules or nodules

Deposits of monosodium urate
crystals in soS Nssues

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6
Q

Relationship between fever and leukocytosis?

A

Acute gout can even cause fever and leukocytosis

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7
Q

Chronic gout?

A

Characterized by chronic
arthri5s and tophi, resul5ng
in chronic inflammatory and
destruc5ve changes

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8
Q

Uric acid?

A

Uric acid is a metabolic by-product of purine catabolism

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9
Q

Purines to Uric Acid pathway?

A

Purines➡️hypoxanthine➡️xanthine➡️uric acid

Xanthine Oxidase

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10
Q

Nephrolithiasis?

A

Nephrolithiasis ( kidney stone disease), condiNon in which individuals form calculi
(stones) within the renal pelvis and tubular lumens
urate nephropathy - rapidly worsening (decreasing) kidney funcNon (renal
insufficiency) that is caused by high levels of uric acid in the urine (hyperuricosuria)

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11
Q

Gout risk factors?

A

MALE
M-Male or Mid 30s and up.
A-Alcohol drinker.
L-Loves high purine diet and lifestyle is sedendary.
E-Excessive weight.

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12
Q

Non-pharmacological interventions?

A
  1. DIET - Patients should be told to cut down on foods with a high level of purines in it like
    red meat.
  2. WEIGHT LOSS IS ESSENTIAL
    Patients should be
    encouraged to loose weight.
  3. Elimination of Alcohol intake.
    * Patients with hypertension
    should manage their
    hypertension with more care.
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13
Q

What treatment should be continued after initiating therapy?

A

Use prophylaxis for at least 3 months after
initiating gout therapy

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14
Q

Should we stop gout treatment?

A

Do not stop gout medication unless patient is
showing evidence of drug toxicity or adverse
reaction

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15
Q

Colchicine MOA(3)?

A
  • Inhibits the movement of granulocytes to the site of inflammation (inhibits chemiotaxis)
  • Inhibits phagocytosis
  • Arrests cell division in G1
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16
Q

Colchicine effect on metabolism and uric acid?

A

Has no effect on UA metabolism and
excretion

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17
Q

Colchine S/E?

A
  1. Diarrhoea/Nausea
  2. Abdominal pain
  3. Hair loss
  4. Bone marrow suppression
  5. Nausea & Vomitting
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18
Q

Colchicine and analgesic?

A

Not an analgesic
* Relieves pain and inflammation
* Indicated more specifically for gout
than NSAID’s

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19
Q

Colchicine and NSAIDS CI’s?

A
  • Can be used to treat gout in patients
    where NSAIDs are contraindicated.
  • used in conjunction with NSAIDS (for
    severe pain)
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20
Q

What do you prescribe in patients who have GIT ulcers because of NSAIDs treatment?

A

Proton Pump Inhibitor & Misoprostol

The most apt choice for treating the signs and symptoms of
inflammation
* However, they can lead to GIT ulcers Î decrease in prostaglandin
synthesis in the gastric mucosa from COX-1 inhibition.
* In these patients a proton pump inhibitor maybe prescribed as well.
* Misoprostol, a synthetic PGE1 analogue can be prescribed as well
and can prevent gastric ulcers in patients on long term NSAIDs

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21
Q

Do we prescribe Aspirin in patients with gout?

A

Avoid Aspirin at all costs

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22
Q

Why do we avoid Aspirin in patients with GOUT?

A

Aspirin can cause acute exacerbation of gout

23
Q

What is the effect of aspirin when prescribed at low and high doses?

A

At low daily doses it makes gout worse & At high doses Aspirin has a uricosuric effect. However, at low doses it has the opposite effect

24
Q

What is the dosage of aspirin for patients that it is absolutely necessary for?

A

Dose aspirin at 3-5g per day if you have no choice!!

25
Q

NSAIDS in Tx?

A

Reversible COX-inhibitors only i.e(Aspirin)

Examples:

  1. Indomethacin
  2. Diclofenac
  3. Ibuprofen ect..
26
Q

NSAIDS and ulcers and tx?

A

Can cause GIT ulcer

Admin with Misoprostol (PPI)-PGE-1 analogue

27
Q

What kind of people aren’t treated by COX-2 selective inhibitors?

A

GI diseases & Cardiotoxic

Tends not to be effective on those people with a history of GI diseases.Remember COX-II selective inhibitors are cardiotoxic and are best
avoided in patients with pre-existing heart conditions e.g. coronary
artery disease

COX-II inhibitors have been associated with gastroduodenal toxicity.

28
Q

Example COX-2 inhibitors ?

A

Etoricoxib

&

Celecoxib

29
Q

NSAIDS CI?

A

COX-2 Inhibitors
-Preexisting Conditions

30
Q

Cholchine CI?

A
  1. Renal & Hepatic Failure
  2. Blood dyscrasis
    3 Cardiac disorders
  3. Serious GIT problems
  4. Hypersensitivity
31
Q

Which medication should we not use on the acute gout attack?

A

Alopurinol & Uricosuric

DO NOT INITIATE TREATMENT with Allopurinol and uricosuric agents within 4 weeks of an acute gout attack

32
Q

Xanthine oxidase?

A

Xanthine Oxidase converts hypothaine to xanthine and urate acid formation

33
Q

Allopurinol MOA?

A

Xanthine oxidase inhibitor and thus blocks uric acid formation

34
Q

Oxypurinol & allopurinol elimination?

A

Oxypurinol, allopurinol metabolite, cleared by kidney and accumulates in patients with renal failure

35
Q

Oxypurinol & allopurinol hypersensitivity syndrome?

A

Increased oxypurinol related to risk of allopurinol hypersensitivity syndrome

36
Q

How do we increase excretion of allopurinol?

A

Make increase fluid intake to
increase excretion of the drug

37
Q

Allopurinol A/E(4)?

A
  • S/e:
  • Skin rashes
  • GIT disturbances
  • Can cause bone marrow suppression but this is rare
  • Acute gout attacks can be precipitated
38
Q

Allopurinol DI?

A

D/I:
*IMPT
* Allopurinol reduces clearance of 6-MP
*Mercaptopurine/Azathioprine

39
Q

Allupurinol DI explained?

A

Mercaptopurine/Azathioprine/Theophylline are metabolised by xanthine oxidase.

Allupurinol inhibits above drugs and thus their serum concentrations increaeses in presense of xanthine oxidase inhibitors such as Feboxosatte

40
Q

Allopurinol Hypersensitivity Syndrome Symptoms/

A

DRESS syndrome

Drug Reaction, Eosinophilia, Systemic Symptoms

41
Q

Allopurinol renal guidelines?

A

Allopurinol should
not be used in renal
insufficiency

42
Q

Febuxostat MOA?

A

Non-Purine Selec@ve Xanthine Oxidase inhibitor è Inhibits
uric acid produc5on

43
Q

Febuxost I?

A

Use for chronic management of hyperuricemia in pa5ents
with gout

44
Q

Febuxost and food/antacids during absorption?

A

Food & Antacids do not affect absorp5on

45
Q

Febuxost M & E?

A

Metabolized by liver, excreted by kidneys

46
Q

Febuxost Combination?

A

Can be combined with NSAIDs and Colchicine during an acute ➡️attach of gouty arthritis don’t need to disrupt therapy

47
Q

Febuxost DI?

A

Mercaptopurine, azathioprine, theophylline ➡️
metabolized by xanthine oxidase➡️therefore serum levels of these drugs with increase (POTENTIAL FOR TOXICITY!!)

48
Q

Allopurinol vs Febuxostat metabolism?

A

Allopurinol Renal Metabolism
Febuxostat Liver Metabolism

49
Q

Uricosurics MOA?

A

Probenecid

Probalan, is a medication that increases uric acid excretion in the urine. Prevents the re-absorp5on of UA from the kidney at the PCT . The medicine works by removing the extra uric acid from the body. Probenecid does not cure gout, but after you have been taking it for a few months it will help prevent gout attacks.

50
Q

Uricosurics DI?

A

Decreases the secretion of other weak acids e.g.Penicillin. This maybe a useful interaction as it can increase plasma levels of penicillin

51
Q

Uricosurics AE?

A
  • Gastro-intes5nal irrita5on
  • Can cause a rash
  • Nephro5c syndrome
52
Q

Uricosurics and urine?

A

Alkalinisation of the urine is advised

53
Q

What do you do if alkalinasation is too high for uricosurics?

A

Alkalinisation can be used if UA levels are too high ➡️it makes the UA more soluble and therefore easier to excrete

Pharmacology (44 decks)

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