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

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

Gout Flashcards by Lethibe Mokgwadi

Gout?

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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Types of Gout Treatment?

Acute Treatment is with :

NSAIDs
Colchicine
Corticosteroids

Chronic Tx:

Allopurinol,
Probenecid
Febuxostat

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Signs and symptoms of gout?

Pain(excruciating)
Inflammation(swelling, redness ,warmth & tumor)
Affects joints

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How does Tophi develop?

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

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Tophi?

Tophi are usually fine yellow or white papules or nodules

Deposits of monosodium urate
crystals in soS Nssues

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Relationship between fever and leukocytosis?

Acute gout can even cause fever and leukocytosis

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Chronic gout?

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

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Uric acid?

Uric acid is a metabolic by-product of purine catabolism

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Purines to Uric Acid pathway?

Purines➡️hypoxanthine➡️xanthine➡️uric acid

Xanthine Oxidase

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Nephrolithiasis?

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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Gout risk factors?

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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Non-pharmacological interventions?

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

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What treatment should be continued after initiating therapy?

Use prophylaxis for at least 3 months after
initiating gout therapy

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Should we stop gout treatment?

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

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Colchicine MOA(3)?

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

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Colchicine effect on metabolism and uric acid?

Has no effect on UA metabolism and
excretion

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Colchine S/E?

Diarrhoea/Nausea
Abdominal pain
Hair loss
Bone marrow suppression
Nausea & Vomitting

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Colchicine and analgesic?

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

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Colchicine and NSAIDS CI’s?

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

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

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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Do we prescribe Aspirin in patients with gout?

Avoid Aspirin at all costs

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Why do we avoid Aspirin in patients with GOUT?

Aspirin can cause acute exacerbation of gout

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

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

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

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

NSAIDS in Tx?

Reversible COX-inhibitors only i.e(Aspirin) Examples: 1. Indomethacin 2. Diclofenac 3. Ibuprofen ect..

NSAIDS and ulcers and tx?

Can cause GIT ulcer Admin with Misoprostol (PPI)-PGE-1 analogue

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

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.

Example COX-2 inhibitors ?

Etoricoxib & Celecoxib

NSAIDS CI?

COX-2 Inhibitors -Preexisting Conditions

Cholchine CI?

1. Renal & Hepatic Failure 2. Blood dyscrasis 3 Cardiac disorders 4. Serious GIT problems 5. Hypersensitivity

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

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

Xanthine oxidase?

Xanthine Oxidase converts hypothaine to xanthine and urate acid formation

Allopurinol MOA?

Xanthine oxidase inhibitor and thus blocks uric acid formation

Oxypurinol & allopurinol elimination?

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

Oxypurinol & allopurinol hypersensitivity syndrome?

Increased oxypurinol related to risk of allopurinol hypersensitivity syndrome

How do we increase excretion of allopurinol?

Make increase fluid intake to increase excretion of the drug

Allopurinol A/E(4)?

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

Allopurinol DI?

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

Allupurinol DI explained?

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

Allopurinol Hypersensitivity Syndrome Symptoms/

DRESS syndrome Drug Reaction, Eosinophilia, Systemic Symptoms

Allopurinol renal guidelines?

Allopurinol should not be used in renal insufficiency

Febuxostat MOA?

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

Febuxost I?

Use for chronic management of hyperuricemia in pa5ents with gout

Febuxost and food/antacids during absorption?

Food & Antacids do not affect absorp5on

Febuxost M & E?

Metabolized by liver, excreted by kidneys

Febuxost Combination?

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

Febuxost DI?

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

Allopurinol vs Febuxostat metabolism?

Allopurinol Renal Metabolism Febuxostat Liver Metabolism

Uricosurics MOA?

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.

Uricosurics DI?

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

Uricosurics AE?

* Gastro-intes5nal irrita5on * Can cause a rash * Nephro5c syndrome

Uricosurics and urine?

Alkalinisation of the urine is advised

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

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