DRUGS USED IN GOUT

1
DRUGS USED IN GOUT

• DR.BILAL AHEED

2
DRUGS USED IN GOUT

• Gout (metabolic arthritis) is a disease created
  by a buildup of uric acid. In this condition,
  crystals of monosodium urate or uric acid are
  deposited on the articular cartilage of joints,
  tendons and surrounding tissues. These crystals
  cause inflammation and pain, both severe. If
  unchecked, the crystals form tophi, which can
  cause significant tissue damage. Gout results
  from a combination of elevated concentrations of
  uric acid and and overall acidity in the
  bloodstream. In isolation, neither elevated uric
  acid (hyperuricemia) nor acidity is normally
  sufficient to cause gout.

3
GOUT (METABOLIC ARTHRITIS)
4
PREVENTION OF GOUT ATTACK

• . Prevention strategies include
• reducing the supply of purine,
  dissolving crystals of uric acid so the uric acid
  can return to the blood, and increasing the
  excretion of uric acid from the blood into the
  urine (without causing lithiasis there).
• careful diagnosis of the factors
  contributing to the gout, followed by appropriate
  use of medication, diet, and over the counter
  remedies.

5
THERAPEUTIC STRATEGIES

1. Interfering with uric synthesis.
2. Increasing uric acid excretion.
3. Inhibiting leukocyte entry into the affected
   joint .
4. Administered non steroidal anti-inflammatory
   agents.

6
DRUGS USED IN GOUT.

• ACUTE TREATMENT
• Non-steroidal anti-inflammatory drugs
• Colchicine
• Steroids
• intra-articular
• oral
• Joint aspiration
• Analgesics
• CHRONIC TREATMENT
• URICOSURIC AGENTS ( PROBENECID AND
  SULFINPYRAZONE).
• ALLOPURINOL (xanthine oxidase inhibitor).
• FEBUXOSTAT (non purine inhibitor of xanthine
  oxidase).

7
ACUTE GOUTY ARTHRITISTREATMENT
OPTIONS.COLCHICINE

• Colchicine inhibits microtubule polymerization by
  binding to tubulin, one of the main constituents
  of microtubules. Availability of tubulin is
  essential to mitosis, and therefore colchicine
  effectively functions as a "mitotic poison" or
  spindle poison.
• It impairs the motility of granulocytes and can
  prevent the inflammatory phenomena that initiate
  an attack. Colchicine should be taken within the
  first 12 hours of the attack and usually relieves
  the pain within 48 hour
• It reduces the inflammatory response by
  decreasing leukocyte migration and phagocytes.
• Administered orally
• Peak plasma levels within 2 hours and its
  eliminated with a serum half life of 9 hours.
• Excreted through intestinal tract and urine.
• Side effects include diarrhea, nausea and
  vomiting,
• Other includes agranulocytosis , alopecia,
  peripheral neuritis and myopathy.

8
Acute Gouty Arthritis
9
DRUGS USED IN ACUTE GOUT.

• The first line of treatment should be pain
  relief. Once the diagnosis has been confirmed,
  the drug options are of nonsteroidal
  anti-inflammatory drugs (NSAIDs)
• INDOMETHACIN is drug of choice for acute gouty
  arthritis, although other NSAIDS also effective.
• ACETAZOLAMIDE, one of the first diuretics
  discovered. This drug inhibits the action of
  carbonic anhydrase on the proximal convoluted
  tubules within the kidneys, which effectively
  inhibits reabsorption of bicarbonate, thus
  alkalinizing the urine. The alkalinization of
  urine persists, and this basic urine attracts
  weak acids such as uric acid and cystine into the
  urine, thus increasing their urinary excretion.

10
Chronic Tophaceous GoutTreatment Options

• Control and prevent acute gouty arthritis
• Non-steroidal anti-inflammatory drugs
• Colchicine
• Steroids
• Analgesics
• Reduce serum uric acid levels (lt 4.0 mg/dL)
• decrease uric acid production (inhibit xanthine
  oxidase)
• increase uric acid excretion (uricosuric drugs)

11
Chronic Tophaceous Gout
12
Chronic Tophaceous Gout
13
Chronic Tophaceous Gout
14
Chronic Tophaceous GoutTreatment
OptionsALLOPURINOL
15
Chronic Tophaceous GoutTreatment
OptionsALLOPURINOL

• Blocks conversion of hypoxanthine to xanthine,
  and xanthine to uric acid
• Accumulation of hypoxanthine inhibits de novo
  purine biosynthesis (negative feedback)
• It absorbed 80 by oral administration.
• Its half life 1-2 hours.
• DO NOT USE allopurinol with azathioprine or
  6-mercaptopurine
• It is safe to use in patients with renal
  impairment and urate stones
• The most serious adverse effect is a
  hypersensitivity syndrome consisting of fever,
  skin rash, eosinophilia.
• Other adverse effects gastrointestinal
  intolerance, including nausea, vomiting and
  diarrhea. Peripheral neuritis, its rarely cause
  bone marrow depression like aplastic anemia.

16
(No Transcript)
17
MECHANISM OF ACTION OF URICOSURIC AGENTS
18
Chronic Tophaceous GoutTreatment Options
URICOSURIC AGENTS

• URICOSURIC AGENTS ( PROBENECID AND
  SULFINPYRAZONE).
• Probenecid is a uricosuric drug, primarily used
  in treating gout and hyperuricemia, that
  increases uric acid removal in the urine.
• Probenecid also decreases the renal excretion of
  some drugs.
• The kidney's organic anion transporter (OAT)
  reclaims uric acid from the urine and returns it
  to the plasma. Probenecid interferes with these
  systems.If probenecid (an organic acid) is
  administered to a patient, the OAT binds to
  probenecid instead of to uric acid, preventing
  the reabsorption of uric acid. As a result, more
  uric acid leaves the body in the urine, lowering
  the uric acid concentration in the plasma.
• Probenecid, a uricosuric drug, often is
  prescribed for gout in conjunction with
  colchicine

19
(No Transcript)
20
(No Transcript)