Inflammatory Response in Arthritis
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Questions and Answers

What is the primary cause of primary gout in 90% of cases?

  • Increased uric acid production
  • Dietary factors
  • Genetic predisposition
  • Decreased uric acid excretion (correct)

    • Which enzyme is responsible for purine metabolism leading to uric acid production?

  • Adenine deaminase
  • Hypoxanthine guanine phosphoribosyltransferase
  • Uricase
  • Xanthine oxidase (correct)

    • What renal process is enhanced to promote uric acid excretion?

  • Increased blood flow to kidneys
  • Decreased tubular reabsorption
  • Alkalization of urine (correct)
  • Renal filtration rate

    • Which of the following drugs is known to decrease uric acid excretion?

    <p>Loop diuretics</p> Signup and view all the answers

    What is the major dietary factor associated with increased uric acid production?

    <p>High protein diet</p> Signup and view all the answers

    What term describes the syndrome related to tissue breakdown during treatment of hematologic malignancies?

    <p>Tumor lysis syndrome</p> Signup and view all the answers

    What triggers the precipitation of monosodium urate crystals in joint tissue?

    <p>Increased serum uric acid levels</p> Signup and view all the answers

    Which of the following conditions is an example of a mixed cause of hyperuricemia?

    <p>Alcohol consumption</p> Signup and view all the answers

    What is the primary reason colchicine is not a first-choice treatment for acute gouty arthritis?

    <p>It has a high toxicity and slow onset</p> Signup and view all the answers

    Which of the following are characteristics of Familial Mediterranean Fever (FMF)?

    <p>Recurrent episodes last 1-3 days</p> Signup and view all the answers

    What is a recognized adverse effect of high oral doses of colchicine?

    <p>Diarrhea</p> Signup and view all the answers

    Which NSAIDs are FDA approved specifically for the treatment of acute gouty arthritis?

    <p>Indomethacin and naproxen</p> Signup and view all the answers

    What should be done to the dosage of NSAIDs when taken concurrently with probenecid?

    <p>Reduce the dosage</p> Signup and view all the answers

    Which of the following best describes the onset of action of colchicine compared to NSAIDs?

    <p>Colchicine has a slower onset than NSAIDs</p> Signup and view all the answers

    Among the adverse effects of colchicine, which is classified as the most severe?

    <p>Aplastic anemia</p> Signup and view all the answers

    What is the recommended initial oral dose of colchicine for an acute gout attack?

    <p>1.2 mg</p> Signup and view all the answers

    What is the primary mechanism of action of probenecid when used in small doses?

    <p>Inhibits tubular secretion of organic acids</p> Signup and view all the answers

    What occurs when probenecid is administered in large doses?

    <p>Inhibition of urate transporter URAT1</p> Signup and view all the answers

    What is the recommended timing for the use of uricosuric drugs like probenecid in relation to an acute gout attack?

    <p>2-3 weeks after the acute attack subsides</p> Signup and view all the answers

    Which of the following is a potential adverse effect of probenecid?

    <p>Interstitial nephritis</p> Signup and view all the answers

    How does the use of probenecid during an acute gout attack affect inflammation?

    <p>It aggravates inflammation due to rapid mobilization of uric acid crystals</p> Signup and view all the answers

    What is the primary therapeutic use of probenecid?

    <p>As a uricosuric agent in chronic gout</p> Signup and view all the answers

    What role do leukocytes play in the inflammation process of gout?

    <p>They release proteolytic enzymes and inflammatory mediators</p> Signup and view all the answers

    Why might probenecid not be suitable for treating acute gout attacks?

    <p>It can cause a mobilization of crystals leading to increased inflammation</p> Signup and view all the answers

    What is the mechanism of action of allopurinol in treating gout?

    <p>It inhibits xanthine oxidase enzyme.</p> Signup and view all the answers

    What is the target uric acid level for effective gout treatment with allopurinol?

    <p>5 mg/dl</p> Signup and view all the answers

    What is a common adverse effect of allopurinol therapy?

    <p>Gastric irritation</p> Signup and view all the answers

    Which medication should not be administered during an acute gout attack?

    <p>Allopurinol</p> Signup and view all the answers

    What condition is peglioticase especially indicated for?

    <p>Severe gout not responding to other agents</p> Signup and view all the answers

    What effect does colchicine have on leukocytes?

    <p>It inhibits their motility and phagocytosis.</p> Signup and view all the answers

    Which enzyme does pergloticase replace to enhance uric acid metabolism?

    <p>Uricase</p> Signup and view all the answers

    Co-administration of allopurinol with which of the following drugs may lead to increased toxicity?

    <p>Mercaptopurine</p> Signup and view all the answers

    Chronic hyperuricemia is defined as having uric acid levels greater than $7 mg/dl$.

    <p>True</p> Signup and view all the answers

    The renal excretion of uric acid is decreased by the alkalization of urine.

    <p>False</p> Signup and view all the answers

    Monosodium urate crystals precipitate when serum uric acid levels decrease.

    <p>False</p> Signup and view all the answers

    Diuretics are among the drugs that can increase uric acid retention in the body.

    <p>True</p> Signup and view all the answers

    Decreased uric acid excretion accounts for approximately 90% of primary gout cases.

    <p>True</p> Signup and view all the answers

    A high protein diet decreases production of uric acid in the body.

    <p>False</p> Signup and view all the answers

    Tumor lysis syndrome is associated with decreased uric acid production during treatment of hematologic malignancies.

    <p>False</p> Signup and view all the answers

    Gout is classified as an autoimmune disorder.

    <p>False</p> Signup and view all the answers

    Uric acid crystals cause swelling and inflammation of the joint tissue.

    <p>True</p> Signup and view all the answers

    Probenecid has a monophasic mechanism of action regardless of dosage.

    <p>False</p> Signup and view all the answers

    Leukocytes contribute to inflammation during an acute gout attack by releasing proteolytic enzymes.

    <p>True</p> Signup and view all the answers

    Probenecid should be given immediately during an acute gout attack to prevent inflammation.

    <p>False</p> Signup and view all the answers

    High doses of probenecid can lead to a decrease in uric acid excretion.

    <p>False</p> Signup and view all the answers

    Probenecid is effective as a treatment for acute gout attacks.

    <p>False</p> Signup and view all the answers

    Adverse effects of probenecid include interstitial nephritis and aplastic anemia.

    <p>True</p> Signup and view all the answers

    The therapeutic use of probenecid includes prolonging the half-life of some acidic drugs.

    <p>True</p> Signup and view all the answers

    Colchicine provides relief from pain within 1-3 hours after oral administration.

    <p>False</p> Signup and view all the answers

    Familial Mediterranean Fever (FMF) typically presents by the second decade of life.

    <p>True</p> Signup and view all the answers

    Diarrhea is considered one of the rare side effects of high oral doses of colchicine.

    <p>False</p> Signup and view all the answers

    Indomethacin and naproxen are not FDA approved for acute gouty arthritis.

    <p>False</p> Signup and view all the answers

    Corticosteroids are used only when colchicine and NSAIDs are sufficient to control acute attacks.

    <p>False</p> Signup and view all the answers

    Allopurinol is a potent inhibitor of xanthine oxidase and has a long duration of action.

    <p>True</p> Signup and view all the answers

    Probenecid enhances the renal excretion of NSAIDs.

    <p>False</p> Signup and view all the answers

    The most serious adverse effects of colchicine include aplastic anemia and agranulocytosis.

    <p>True</p> Signup and view all the answers

    The recommended starting dose of allopurinol for gout treatment is 300 mg once daily.

    <p>False</p> Signup and view all the answers

    Colchicine can inhibit neutrophil motility, making it useful for treating gout attacks.

    <p>True</p> Signup and view all the answers

    Attacks of Familial Mediterranean Fever (FMF) typically last between 3-5 days.

    <p>False</p> Signup and view all the answers

    Pegloticase is indicated for mild gout cases that respond to standard treatments.

    <p>False</p> Signup and view all the answers

    Allopurinol can lead to the precipitation of acute gout at the start of therapy due to mobilization of uric acid crystals.

    <p>True</p> Signup and view all the answers

    Aspirin is known to enhance uric acid excretion and support probenecid effects.

    <p>False</p> Signup and view all the answers

    Mercaptopurine and theophylline levels can increase dramatically when taken with allopurinol.

    <p>True</p> Signup and view all the answers

    Colchicine is a synthetic drug used primarily to treat rheumatoid arthritis.

    <p>False</p> Signup and view all the answers

    What pathological event initiates gouty arthritis when serum uric acid increases?

    <p>Monosodium urate crystals precipitate in joint tissue, causing irritation and inflammation.</p> Signup and view all the answers

    Explain how alkalization of urine affects uric acid excretion.

    <p>Alkalization of urine enhances the renal excretion of uric acid.</p> Signup and view all the answers

    Identify two factors that lead to decreased uric acid excretion.

    <p>Kidney diseases and the use of diuretics can decrease uric acid excretion.</p> Signup and view all the answers

    What are the major dietary factors influencing increased uric acid production?

    <p>A high protein diet and alcohol consumption are major dietary factors.</p> Signup and view all the answers

    Describe how diuretics contribute to the retention of uric acid.

    <p>Diuretics interfere with the renal excretion of uric acid, leading to its retention.</p> Signup and view all the answers

    How is the majority of body uric acid eliminated?

    <p>The majority of uric acid is excreted by the renal proximal convoluted tubule (PCT).</p> Signup and view all the answers

    What is the relationship between tissue breakdown and uric acid production during leukemia treatment?

    <p>During leukemia treatment, tissue breakdown increases uric acid production due to tumor lysis syndrome.</p> Signup and view all the answers

    What kind of syndrome is associated with sex-linked uric aciduria?

    <p>Lesch-Nyhan syndrome is associated with sex-linked uric aciduria.</p> Signup and view all the answers

    What biphasic action does probenecid exhibit at small doses?

    <p>At small doses, probenecid inhibits tubular secretion of organic acids, including uric acid.</p> Signup and view all the answers

    Explain the risk associated with administering probenecid during an acute gout attack.

    <p>Administering probenecid during an acute attack can aggravate inflammation due to rapid mobilization of uric acid crystals.</p> Signup and view all the answers

    How do leukocytes contribute to the inflammation seen in gout?

    <p>Leukocytes die and release proteolytic enzymes and inflammatory mediators, causing severe inflammation.</p> Signup and view all the answers

    What is a key therapeutic use of probenecid regarding other acidic drugs?

    <p>Probenecid is used to prolong the half-life of acidic drugs like penicillin by inhibiting their renal excretion.</p> Signup and view all the answers

    Describe the consequences of probenecid when given in large doses.

    <p>In large doses, probenecid inhibits the tubular reabsorption of uric acid, leading to increased excretion.</p> Signup and view all the answers

    What are the observed adverse effects when taking probenecid?

    <p>Adverse effects include gastric irritation, skin rash, and rarely interstitial nephritis and aplastic anemia.</p> Signup and view all the answers

    Why is it recommended to wait 2-3 weeks after an acute attack to use probenecid?

    <p>This waiting period allows for the acute inflammation to subside and reduces the risk of exacerbating symptoms.</p> Signup and view all the answers

    What inflammatory mediators are released by leukocytes during the gout inflammation process?

    <p>Leukocytes release mediators such as LT, TB4, and IL1 during the inflammation process.</p> Signup and view all the answers

    What condition is indicated for the lifelong use of allopurinol?

    <p>Lesch-Nyhan syndrome.</p> Signup and view all the answers

    How does allopurinol's mechanism of action affect uric acid levels?

    <p>Allopurinol inhibits xanthine oxidase, leading to decreased uric acid synthesis.</p> Signup and view all the answers

    What is the main reason to administer NSAIDs or colchicine when starting allopurinol therapy?

    <p>To prevent exacerbation of gout due to mobilization of uric acid crystals.</p> Signup and view all the answers

    What adverse effect is commonly associated with allopurinol treatment?

    <p>Gastric irritation and skin rash.</p> Signup and view all the answers

    What is the dosing adjustment protocol for allopurinol when treating gout?

    <p>Start at 100 mg daily, gradually increasing to a target of 300 mg daily.</p> Signup and view all the answers

    Which agent is used in severe gout cases unresponsive to other treatments?

    <p>Pegloticase.</p> Signup and view all the answers

    What is the mechanism of action of colchicine in managing gout?

    <p>Colchicine inhibits leukocyte motility and phagocytosis by binding to microtubules.</p> Signup and view all the answers

    Which drugs should be closely monitored when coadministered with allopurinol?

    <p>Mercaptopurine, azathioprine, and theophylline.</p> Signup and view all the answers

    What are the typical duration and features of attacks in Familial Mediterranean Fever (FMF)?

    <p>Attacks typically last 1-3 days and feature recurrent episodes of abdominal pain, pleurisy, and arthritis.</p> Signup and view all the answers

    What is the main reason colchicine is considered a second-line treatment for acute gouty arthritis?

    <p>Colchicine has a slower onset and higher toxicity, making it less preferable compared to NSAIDs or corticosteroids for acute presentations.</p> Signup and view all the answers

    Describe the primary mechanism by which high oral doses of colchicine can lead to diarrhea.

    <p>High doses inhibit the continuous renewal of the gastrointestinal epithelium, causing the accumulation of toxins and bacteria that result in diarrhea.</p> Signup and view all the answers

    What dosage adjustment should be made for NSAIDs when they are taken with probenecid?

    <p>The dosage of NSAIDs must be reduced when taken with probenecid because probenecid inhibits their renal excretion.</p> Signup and view all the answers

    What characterizes the adverse effects of colchicine, specifically in terms of severity?

    <p>The most severe adverse effects of colchicine include aplastic anemia and agranulocytosis, both indicating bone marrow depression.</p> Signup and view all the answers

    What is the recommended initial oral dose of colchicine for managing an acute gout attack?

    <p>The recommended initial dose is 1.2 mg orally, followed by one tablet (0.6 mg) every 12 hours until the attack resolves.</p> Signup and view all the answers

    How do indomethacin and naproxen compare to colchicine in terms of onset for relieving acute gout attacks?

    <p>Indomethacin and naproxen provide symptomatic relief faster than colchicine during acute gout attacks.</p> Signup and view all the answers

    What condition does the atypical presentation of recurrent polyserositis suggest?

    <p>It suggests Familial Mediterranean Fever (FMF), an autosomal recessive disorder with recurrent inflammatory episodes.</p> Signup and view all the answers

    Gout is a form of inflammatory arthritis due to deposition of monosodium urate crystals in the ______ tissue.

    <p>joint</p> Signup and view all the answers

    Chronic hyperuricemia is defined as having uric acid levels greater than ______ mg/dl.

    <p>7</p> Signup and view all the answers

    The renal excretion of uric acid is enhanced by ______ of urine.

    <p>alkalization</p> Signup and view all the answers

    Decreased uric acid excretion accounts for approximately ______% of primary gout cases.

    <p>90</p> Signup and view all the answers

    High protein diets can lead to ______ uric acid production.

    <p>increased</p> Signup and view all the answers

    Monosodium urate crystals are selectively precipitated around the joint tissue when serum uric acid levels ______.

    <p>increase</p> Signup and view all the answers

    Some drugs, such as ______, may interfere with the excretion of uric acid, leading to its retention.

    <p>diuretics</p> Signup and view all the answers

    Alcohol consumption is considered a ______ cause of hyperuricemia.

    <p>mixed</p> Signup and view all the answers

    Uric acid crystals cause swelling and inflammation of the ______ tissue.

    <p>joint</p> Signup and view all the answers

    Leukocytes eventually die with the release of ______ enzymes and inflammatory mediators.

    <p>proteolytic</p> Signup and view all the answers

    Probenecid inhibits tubular reabsorption of uric acid by acting on the ______ transporter.

    <p>urate</p> Signup and view all the answers

    During an acute attack, rapid lowering of serum uric acid can aggravate the acute ______.

    <p>inflammation</p> Signup and view all the answers

    Probenecid is used as a ______ agent in chronic gout.

    <p>uricosuric</p> Signup and view all the answers

    High doses of probenecid can lead to increased ______ of uric acid.

    <p>excretion</p> Signup and view all the answers

    Uricosuric drugs should not be used during the acute attack but rather ______ weeks after.

    <p>2-3</p> Signup and view all the answers

    Adverse effects of probenecid include gastric irritation and ______ rash.

    <p>skin</p> Signup and view all the answers

    Colchicine provides relief from pain and reduction of inflammation after ______ hours of oral administration.

    <p>12–24</p> Signup and view all the answers

    Familial Mediterranean Fever (FMF) is characterized by recurrent episodes of abdominal pain, pleurisy, and ______.

    <p>arthritis</p> Signup and view all the answers

    Common adverse effects of high oral doses of colchicine include diarrhea, alopecia, and ______.

    <p>myopathy</p> Signup and view all the answers

    NSAIDs such as ______ and naproxen are FDA approved for the treatment of acute gouty arthritis.

    <p>Indomethacin</p> Signup and view all the answers

    The recommended dose of colchicine for an acute gout attack starts with ______ mg.

    <p>1.2</p> Signup and view all the answers

    If taken with probenecid, the dose of NSAIDs must be ______ due to renal excretion inhibition.

    <p>reduced</p> Signup and view all the answers

    A serious adverse effect of colchicine includes ______ anemia, which affects bone marrow function.

    <p>aplastic</p> Signup and view all the answers

    Familial Mediterranean Fever (FMF) is inherited in an ______ fashion.

    <p>autosomal recessive</p> Signup and view all the answers

    Allopurinol inhibits the enzyme ______ oxidase to reduce uric acid synthesis.

    <p>xanthine</p> Signup and view all the answers

    Pegloticase converts uric acid into the water-soluble ______.

    <p>allantoin</p> Signup and view all the answers

    Colchicine is known for its action as a ______ blocker.

    <p>mitotic</p> Signup and view all the answers

    Patients with Lesch-Nyhan syndrome require allopurinol for ______.

    <p>life</p> Signup and view all the answers

    During acute gout attacks, colchicine inhibits the release of ______ by leukocytes.

    <p>LTB4</p> Signup and view all the answers

    Starting dose of allopurinol for gout treatment is typically ______ mg once daily.

    <p>100</p> Signup and view all the answers

    The adverse effect of allopurinol includes gastric irritation and ______ reactions.

    <p>hypersensitivity</p> Signup and view all the answers

    Allopurinol should not be given during an acute ______ attack.

    <p>gout</p> Signup and view all the answers

    Match the following drugs with their effect on uric acid levels:

    <p>Diuretics = Increase uric acid retention Aspirin = Decrease uric acid excretion Allopurinol = Decrease uric acid production Probenecid = Enhance uric acid excretion</p> Signup and view all the answers

    Match the following conditions with their relationship to hyperuricemia:

    <p>Kidney diseases = Decreased uric acid excretion High protein diet = Increased uric acid production Tumor lysis syndrome = Increased uric acid production Lessch-Nyhan syndrome = Sex-linked uric aciduria</p> Signup and view all the answers

    Match the following terms with their definitions related to gout:

    <p>Acute gouty arthritis = Swelling and inflammation caused by urate crystals Chronic hyperuricemia = Sustained high levels of uric acid in blood Monosodium urate = Primary crystal deposited in gout Alkalization of urine = Enhances renal excretion of uric acid</p> Signup and view all the answers

    Match the following dietary factors with their effect on uric acid:

    <p>High protein foods = Increase uric acid production Alcohol consumption = Mixed cause of hyperuricemia Diuretics = Decrease renal excretion of uric acid Low-purine diet = Decrease uric acid levels</p> Signup and view all the answers

    Match the following symptoms with their related processes in gout:

    <p>Joint inflammation = Urate crystal irritation Serum uric acid increase = Precipitation of urate crystals Chronic gout = Recurrent inflammatory episodes Acute gout attack = Sudden swelling and pain</p> Signup and view all the answers

    Match the following mechanisms with their descriptions:

    <p>Xanthine oxidase = Enzyme producing uric acid Renal PCT = Location of uric acid excretion Crystal deposition = Causes joint inflammation in gout Uric acid = End product of purine metabolism</p> Signup and view all the answers

    Match the following treatment strategies with their intended outcomes:

    <p>Colchicine = Relief of pain during acute attack Probenecid = Enhancement of uric acid excretion Allopurinol = Reduction of uric acid production NSAIDs = Anti-inflammatory for gout flares</p> Signup and view all the answers

    Match the following medications with their respective primary therapeutic uses:

    <p>Allopurinol = Recurrent attacks of gout Colchicine = Acute attacks of gout Pegloticase = Severe gout not responding to other agents Probenecid = Uricosuric therapy for chronic gout</p> Signup and view all the answers

    Match the following etiologies with their respective gout types:

    <p>Primary gout = Decreased uric acid excretion due to factors like diuretics Secondary gout = Increased uric acid production from conditions like malignancies Acute gout = Sudden inflammation due to crystal deposition Chronic gout = Long-term uric acid elevation resulting in joint damage</p> Signup and view all the answers

    Match the following drugs with their mechanisms of action:

    <p>Allopurinol = Inhibits xanthine oxidase Colchicine = Inhibits leukocyte motility Pegloticase = Converts uric acid to allantoin Probenecid = Inhibits uric acid reabsorption in kidneys</p> Signup and view all the answers

    Match the following adverse effects with their corresponding medications:

    <p>Allopurinol = Gastric irritation Colchicine = Diarrhea Pegloticase = Hypersensitivity reactions Probenecid = Aplastic anemia</p> Signup and view all the answers

    Match the following scenarios with the appropriate medication recommendations:

    <p>Allopurinol = Not during acute gout attack Colchicine = For immediate pain relief Pegloticase = Administer every 2 weeks Probenecid = Avoid in acute attacks</p> Signup and view all the answers

    Match the following conditions with the medications indicated for treatment:

    <p>Recurrent gout = Allopurinol Severe refractory gout = Pegloticase Acute gout attack = Colchicine Chronic gout management = Probenecid</p> Signup and view all the answers

    Match the following drug interactions with the relevant medication:

    <p>Allopurinol = Mercaptopurine Colchicine = NSAIDs Pegloticase = Not compatible with certain chemotherapeutics Probenecid = Penicillin</p> Signup and view all the answers

    Match the following drug classes with their effects on uric acid levels:

    <p>Xanthine oxidase inhibitors = Reduce uric acid production Uricosuric agents = Increase uric acid excretion Anti-inflammatory agents = Reduce inflammation during gout attacks Enzyme replacement therapy = Increase uric acid degradation</p> Signup and view all the answers

    Match the following patient scenarios with the appropriate medication guidance:

    <p>Patient with a history of recurrent gout attacks = Start allopurinol therapy Patient experiencing acute gout flare = Administer colchicine immediately Patient with Lesch-Nyhan syndrome = Lifetime allopurinol therapy Patient experiencing side effects from probenecid = Monitor for nephritis and anemia</p> Signup and view all the answers

    Match the following medications with their primary characteristics:

    <p>Colchicine = Inhibits cell division leading to gastrointestinal side effects Indomethacin = FDA approved NSAID for acute gouty arthritis Probenecid = Inhibits renal excretion of NSAIDs Corticosteroids = Used when colchicine and NSAIDs are ineffective</p> Signup and view all the answers

    Match the following drug classes with their primary mechanisms of action:

    <p>Uricosuric drugs = Inhibit tubular reabsorption of uric acid Probenecid = Inhibits organic acid transporters in tubular cells Colchicine = Inhibits leukocyte migration Allopurinol = Inhibits xanthine oxidase activity</p> Signup and view all the answers

    Match the following adverse effects with the respective drugs:

    <p>Probenecid = Gastric irritation Colchicine = Severe diarrhea Allopurinol = Rash and hypersensitivity reactions Pegloticase = Infusion reactions</p> Signup and view all the answers

    Match the following symptoms with their associated conditions:

    <p>Recurrent abdominal pain = Familial Mediterranean Fever (FMF) Aplastic anemia = Severe adverse effect of colchicine Diarrhea = Common side effect of high doses of colchicine Pleurisy = Characteristic of Familial Mediterranean Fever (FMF)</p> Signup and view all the answers

    Match the following characteristics to their respective medications:

    <p>Colchicine = Not first-choice in acute gout unless NSAIDs are contraindicated NSAIDs = Provide faster relief in acute attacks than colchicine Corticosteroids = Anti-inflammatory agents for acute attacks Familial Mediterranean Fever = Autosomal recessive disorder</p> Signup and view all the answers

    Match the following therapeutic uses with the appropriate drug:

    <p>Probenecid = Prolonging the half-life of penicillin Colchicine = Acute gout attacks relief Allopurinol = Chronic gout management Pegloticase = Treatment for chronic refractory gout</p> Signup and view all the answers

    Match the following conditions with their respective mechanisms:

    <p>Acute gout attack = Mobilization of uric acid crystals Chronic gout = Persistent hyperuricemia Leukocyte involvement = Release of inflammatory mediators Interstitial nephritis = Renal hypersensitivity reaction</p> Signup and view all the answers

    Match the following features with their descriptions:

    <p>High oral doses of colchicine = Inhibits GIT epithelium turnover Indomethacin = Works as an anti-inflammatory agent Attacks duration = Typically last 1-3 days in FMF Innovative mechanism of colchicine = Unclear but leads to significant pain relief</p> Signup and view all the answers

    Match the following mechanisms with their corresponding drug actions:

    <p>Probenecid in small doses = Inhibits tubular secretion Probenecid in large doses = Inhibits tubular reabsorption Allopurinol = Decreases uric acid production Colchicine = Reduces leukocyte activity</p> Signup and view all the answers

    Match the following conditions with their treatments:

    <p>Acute gouty arthritis = Colchicine, Indomethacin, NSAIDs Familial Mediterranean Fever (FMF) = Corticosteroids and colchicine if NSAIDs are ineffective Toxicity from colchicine = Leads to diarrhea and other gastrointestinal issues Recurrent polyserositis = Characteristic of Familial Mediterranean Fever (FMF)</p> Signup and view all the answers

    Match the following doses with their indications:

    <p>1.2 mg orally = Initial dose of colchicine for acute gout 0.6 mg every 12 hours = Follow-up dose of colchicine until attack resolves Dose reduction with probenecid = NSAIDs must be adjusted to avoid toxicity Gastrointestinal symptoms = High doses of colchicine lead to severe adverse effects</p> Signup and view all the answers

    Match the following precautions with the appropriate drug:

    <p>Probenecid = Avoid during acute attacks Colchicine = Careful with gastrointestinal issues Allopurinol = Monitor for skin reactions Pegloticase = Watch for infusion-related symptoms</p> Signup and view all the answers

    Match the following types of excretion alteration with their drugs:

    <p>Probenecid = Uricosuric agent Colchicine = Reduces excessive immune response Allopurinol = Inhibits uric acid synthesis Pegloticase = Enhances uricase enzyme activity</p> Signup and view all the answers

    Match the following adverse effects to their corresponding medications:

    <p>Colchicine = Diarrhea, alopecia, myopathy Corticosteroids = Increased risk of infections NSAIDs = Renal impairment when used with probenecid Probenecid = Interstitial nephritis and aplastic anemia</p> Signup and view all the answers

    Match the following clinical features to their related medications:

    <p>Recurrent attacks = Familial Mediterranean Fever (FMF) Not suitable for acute gout attacks = Probenecid Fast symptomatic relief = Indomethacin and NSAIDs Delayed onset of relief = Colchicine provides pain relief after 12-24 hours</p> Signup and view all the answers

    Match the following inflammatory mediators with their effects in gout:

    <p>LTB4 = Enhances leukocyte migration IL-1 = Promotes inflammation PGGs = Induces pain and swelling Proteolytic enzymes = Leukocyte death and tissue damage</p> Signup and view all the answers

    Study Notes

    Basic Information on Gout

    • Gout is an inflammatory arthritis caused by the deposition of monosodium urate crystals in joint tissue.
    • Chronic hyperuricemia, defined as uric acid levels > 7 mg/dL (0.42 mmol/L), is the primary cause.
    • Uric acid is the end product of purine metabolism, mainly excreted by the renal proximal convoluted tubule (PCT).
    • Certain drugs, such as diuretics, can interfere with uric acid excretion, causing retention.

    Causes of Hyperuricemia

    • Decreased uric acid excretion accounts for 90% of primary gout cases, often due to:
      • Medications (e.g., diuretics, aspirin).
      • Kidney diseases.
    • Increased uric acid production can result from:
      • High-protein diets.
      • Treatment of hematologic malignancies, causing tissue breakdown (tumor lysis syndrome).
    • Alcohol consumption also contributes as a mixed cause.

    Pathogenesis of Gouty Arthritis

    • Elevated serum uric acid levels lead to the precipitation of urate crystals in joints, resulting in irritation and inflammation.
    • Polymorphonuclear leukocytes (PMNs) and macrophages phagocytize uric acid crystals, causing swelling and inflammation.
    • Leukocyte death releases proteolytic enzymes and inflammatory mediators (e.g., LTB4, IL-1), intensifying inflammation.

    Uricosuric Drugs: Probenecid

    • Probenecid has a biphasic action:
      • In small doses, it inhibits tubular secretion of organic acids (including uric acid).
      • In larger doses (≥500 mg twice/day), it inhibits tubular reabsorption of uric acid, enhancing its excretion.
    • Therapeutic uses include treatment of chronic gout and prolonging the half-life of certain acidic drugs.
    • Adverse effects may include gastric irritation, skin rash, and, rarely, interstitial nephritis or aplastic anemia.
    • Should not be used during acute gout attacks as it may aggravate inflammation.

    Inhibitors of Uric Acid Synthesis: Allopurinol

    • Allopurinol is a synthetic purine analogue that inhibits xanthine oxidase, reducing uric acid synthesis.
    • It has a long duration of action due to potent inhibition by both the drug and its metabolite.
    • Recommended for patients with recurrent gout attacks, targeting uric acid levels of 5 mg/dL (0.3 mmol/L).
    • May also be used in hematologic malignancies to prevent hyperuricemia.
    • Common adverse effects include gastric irritation and hypersensitivity reactions; can precipitate acute gout at therapy onset.

    Increase Uric Acid Metabolism: Pegloticase

    • Pegloticase is a recombinant form of porcine uricase, converting uric acid to the soluble allantoin.
    • Administered intravenously (8 mg every 2 weeks), it quickly lowers serum uric acid.
    • Indicated for severe gout cases resistant to other treatments.

    Anti-Inflammatory Drugs: Colchicine

    • Colchicine is a plant alkaloid that inhibits leukocyte motility, phagocytosis, and mitosis.
    • Mainly used for acute gout attacks; slower onset compared to NSAIDs, with pain relief occurring within 12–24 hours.
    • High doses can lead to gastrointestinal toxicity, especially diarrhea.

    NSAIDs: Indomethacin and Naproxen

    • Indomethacin and naproxen are FDA-approved NSAIDs for acute gout, providing faster relief than colchicine.
    • Dosage adjustments may be needed when co-administered with probenecid, which inhibits renal excretion.

    Corticosteroids

    • Used as anti-inflammatory agents when colchicine and NSAIDs are insufficient or contraindicated for acute attacks.

    Basic Information on Gout

    • Gout is an inflammatory arthritis caused by the deposition of monosodium urate crystals in joint tissue.
    • Chronic hyperuricemia, defined as uric acid levels > 7 mg/dL (0.42 mmol/L), is the primary cause.
    • Uric acid is the end product of purine metabolism, mainly excreted by the renal proximal convoluted tubule (PCT).
    • Certain drugs, such as diuretics, can interfere with uric acid excretion, causing retention.

    Causes of Hyperuricemia

    • Decreased uric acid excretion accounts for 90% of primary gout cases, often due to:
      • Medications (e.g., diuretics, aspirin).
      • Kidney diseases.
    • Increased uric acid production can result from:
      • High-protein diets.
      • Treatment of hematologic malignancies, causing tissue breakdown (tumor lysis syndrome).
    • Alcohol consumption also contributes as a mixed cause.

    Pathogenesis of Gouty Arthritis

    • Elevated serum uric acid levels lead to the precipitation of urate crystals in joints, resulting in irritation and inflammation.
    • Polymorphonuclear leukocytes (PMNs) and macrophages phagocytize uric acid crystals, causing swelling and inflammation.
    • Leukocyte death releases proteolytic enzymes and inflammatory mediators (e.g., LTB4, IL-1), intensifying inflammation.

    Uricosuric Drugs: Probenecid

    • Probenecid has a biphasic action:
      • In small doses, it inhibits tubular secretion of organic acids (including uric acid).
      • In larger doses (≥500 mg twice/day), it inhibits tubular reabsorption of uric acid, enhancing its excretion.
    • Therapeutic uses include treatment of chronic gout and prolonging the half-life of certain acidic drugs.
    • Adverse effects may include gastric irritation, skin rash, and, rarely, interstitial nephritis or aplastic anemia.
    • Should not be used during acute gout attacks as it may aggravate inflammation.

    Inhibitors of Uric Acid Synthesis: Allopurinol

    • Allopurinol is a synthetic purine analogue that inhibits xanthine oxidase, reducing uric acid synthesis.
    • It has a long duration of action due to potent inhibition by both the drug and its metabolite.
    • Recommended for patients with recurrent gout attacks, targeting uric acid levels of 5 mg/dL (0.3 mmol/L).
    • May also be used in hematologic malignancies to prevent hyperuricemia.
    • Common adverse effects include gastric irritation and hypersensitivity reactions; can precipitate acute gout at therapy onset.

    Increase Uric Acid Metabolism: Pegloticase

    • Pegloticase is a recombinant form of porcine uricase, converting uric acid to the soluble allantoin.
    • Administered intravenously (8 mg every 2 weeks), it quickly lowers serum uric acid.
    • Indicated for severe gout cases resistant to other treatments.

    Anti-Inflammatory Drugs: Colchicine

    • Colchicine is a plant alkaloid that inhibits leukocyte motility, phagocytosis, and mitosis.
    • Mainly used for acute gout attacks; slower onset compared to NSAIDs, with pain relief occurring within 12–24 hours.
    • High doses can lead to gastrointestinal toxicity, especially diarrhea.

    NSAIDs: Indomethacin and Naproxen

    • Indomethacin and naproxen are FDA-approved NSAIDs for acute gout, providing faster relief than colchicine.
    • Dosage adjustments may be needed when co-administered with probenecid, which inhibits renal excretion.

    Corticosteroids

    • Used as anti-inflammatory agents when colchicine and NSAIDs are insufficient or contraindicated for acute attacks.

    Basic Information on Gout

    • Gout is an inflammatory arthritis caused by the deposition of monosodium urate crystals in joint tissue.
    • Chronic hyperuricemia, defined as uric acid levels > 7 mg/dL (0.42 mmol/L), is the primary cause.
    • Uric acid is the end product of purine metabolism, mainly excreted by the renal proximal convoluted tubule (PCT).
    • Certain drugs, such as diuretics, can interfere with uric acid excretion, causing retention.

    Causes of Hyperuricemia

    • Decreased uric acid excretion accounts for 90% of primary gout cases, often due to:
      • Medications (e.g., diuretics, aspirin).
      • Kidney diseases.
    • Increased uric acid production can result from:
      • High-protein diets.
      • Treatment of hematologic malignancies, causing tissue breakdown (tumor lysis syndrome).
    • Alcohol consumption also contributes as a mixed cause.

    Pathogenesis of Gouty Arthritis

    • Elevated serum uric acid levels lead to the precipitation of urate crystals in joints, resulting in irritation and inflammation.
    • Polymorphonuclear leukocytes (PMNs) and macrophages phagocytize uric acid crystals, causing swelling and inflammation.
    • Leukocyte death releases proteolytic enzymes and inflammatory mediators (e.g., LTB4, IL-1), intensifying inflammation.

    Uricosuric Drugs: Probenecid

    • Probenecid has a biphasic action:
      • In small doses, it inhibits tubular secretion of organic acids (including uric acid).
      • In larger doses (≥500 mg twice/day), it inhibits tubular reabsorption of uric acid, enhancing its excretion.
    • Therapeutic uses include treatment of chronic gout and prolonging the half-life of certain acidic drugs.
    • Adverse effects may include gastric irritation, skin rash, and, rarely, interstitial nephritis or aplastic anemia.
    • Should not be used during acute gout attacks as it may aggravate inflammation.

    Inhibitors of Uric Acid Synthesis: Allopurinol

    • Allopurinol is a synthetic purine analogue that inhibits xanthine oxidase, reducing uric acid synthesis.
    • It has a long duration of action due to potent inhibition by both the drug and its metabolite.
    • Recommended for patients with recurrent gout attacks, targeting uric acid levels of 5 mg/dL (0.3 mmol/L).
    • May also be used in hematologic malignancies to prevent hyperuricemia.
    • Common adverse effects include gastric irritation and hypersensitivity reactions; can precipitate acute gout at therapy onset.

    Increase Uric Acid Metabolism: Pegloticase

    • Pegloticase is a recombinant form of porcine uricase, converting uric acid to the soluble allantoin.
    • Administered intravenously (8 mg every 2 weeks), it quickly lowers serum uric acid.
    • Indicated for severe gout cases resistant to other treatments.

    Anti-Inflammatory Drugs: Colchicine

    • Colchicine is a plant alkaloid that inhibits leukocyte motility, phagocytosis, and mitosis.
    • Mainly used for acute gout attacks; slower onset compared to NSAIDs, with pain relief occurring within 12–24 hours.
    • High doses can lead to gastrointestinal toxicity, especially diarrhea.

    NSAIDs: Indomethacin and Naproxen

    • Indomethacin and naproxen are FDA-approved NSAIDs for acute gout, providing faster relief than colchicine.
    • Dosage adjustments may be needed when co-administered with probenecid, which inhibits renal excretion.

    Corticosteroids

    • Used as anti-inflammatory agents when colchicine and NSAIDs are insufficient or contraindicated for acute attacks.

    Basic Information on Gout

    • Gout is an inflammatory arthritis caused by the deposition of monosodium urate crystals in joint tissue.
    • Chronic hyperuricemia, defined as uric acid levels > 7 mg/dL (0.42 mmol/L), is the primary cause.
    • Uric acid is the end product of purine metabolism, mainly excreted by the renal proximal convoluted tubule (PCT).
    • Certain drugs, such as diuretics, can interfere with uric acid excretion, causing retention.

    Causes of Hyperuricemia

    • Decreased uric acid excretion accounts for 90% of primary gout cases, often due to:
      • Medications (e.g., diuretics, aspirin).
      • Kidney diseases.
    • Increased uric acid production can result from:
      • High-protein diets.
      • Treatment of hematologic malignancies, causing tissue breakdown (tumor lysis syndrome).
    • Alcohol consumption also contributes as a mixed cause.

    Pathogenesis of Gouty Arthritis

    • Elevated serum uric acid levels lead to the precipitation of urate crystals in joints, resulting in irritation and inflammation.
    • Polymorphonuclear leukocytes (PMNs) and macrophages phagocytize uric acid crystals, causing swelling and inflammation.
    • Leukocyte death releases proteolytic enzymes and inflammatory mediators (e.g., LTB4, IL-1), intensifying inflammation.

    Uricosuric Drugs: Probenecid

    • Probenecid has a biphasic action:
      • In small doses, it inhibits tubular secretion of organic acids (including uric acid).
      • In larger doses (≥500 mg twice/day), it inhibits tubular reabsorption of uric acid, enhancing its excretion.
    • Therapeutic uses include treatment of chronic gout and prolonging the half-life of certain acidic drugs.
    • Adverse effects may include gastric irritation, skin rash, and, rarely, interstitial nephritis or aplastic anemia.
    • Should not be used during acute gout attacks as it may aggravate inflammation.

    Inhibitors of Uric Acid Synthesis: Allopurinol

    • Allopurinol is a synthetic purine analogue that inhibits xanthine oxidase, reducing uric acid synthesis.
    • It has a long duration of action due to potent inhibition by both the drug and its metabolite.
    • Recommended for patients with recurrent gout attacks, targeting uric acid levels of 5 mg/dL (0.3 mmol/L).
    • May also be used in hematologic malignancies to prevent hyperuricemia.
    • Common adverse effects include gastric irritation and hypersensitivity reactions; can precipitate acute gout at therapy onset.

    Increase Uric Acid Metabolism: Pegloticase

    • Pegloticase is a recombinant form of porcine uricase, converting uric acid to the soluble allantoin.
    • Administered intravenously (8 mg every 2 weeks), it quickly lowers serum uric acid.
    • Indicated for severe gout cases resistant to other treatments.

    Anti-Inflammatory Drugs: Colchicine

    • Colchicine is a plant alkaloid that inhibits leukocyte motility, phagocytosis, and mitosis.
    • Mainly used for acute gout attacks; slower onset compared to NSAIDs, with pain relief occurring within 12–24 hours.
    • High doses can lead to gastrointestinal toxicity, especially diarrhea.

    NSAIDs: Indomethacin and Naproxen

    • Indomethacin and naproxen are FDA-approved NSAIDs for acute gout, providing faster relief than colchicine.
    • Dosage adjustments may be needed when co-administered with probenecid, which inhibits renal excretion.

    Corticosteroids

    • Used as anti-inflammatory agents when colchicine and NSAIDs are insufficient or contraindicated for acute attacks.

    Basic Information on Gout

    • Gout is an inflammatory arthritis caused by the deposition of monosodium urate crystals in joint tissue.
    • Chronic hyperuricemia, defined as uric acid levels > 7 mg/dL (0.42 mmol/L), is the primary cause.
    • Uric acid is the end product of purine metabolism, mainly excreted by the renal proximal convoluted tubule (PCT).
    • Certain drugs, such as diuretics, can interfere with uric acid excretion, causing retention.

    Causes of Hyperuricemia

    • Decreased uric acid excretion accounts for 90% of primary gout cases, often due to:
      • Medications (e.g., diuretics, aspirin).
      • Kidney diseases.
    • Increased uric acid production can result from:
      • High-protein diets.
      • Treatment of hematologic malignancies, causing tissue breakdown (tumor lysis syndrome).
    • Alcohol consumption also contributes as a mixed cause.

    Pathogenesis of Gouty Arthritis

    • Elevated serum uric acid levels lead to the precipitation of urate crystals in joints, resulting in irritation and inflammation.
    • Polymorphonuclear leukocytes (PMNs) and macrophages phagocytize uric acid crystals, causing swelling and inflammation.
    • Leukocyte death releases proteolytic enzymes and inflammatory mediators (e.g., LTB4, IL-1), intensifying inflammation.

    Uricosuric Drugs: Probenecid

    • Probenecid has a biphasic action:
      • In small doses, it inhibits tubular secretion of organic acids (including uric acid).
      • In larger doses (≥500 mg twice/day), it inhibits tubular reabsorption of uric acid, enhancing its excretion.
    • Therapeutic uses include treatment of chronic gout and prolonging the half-life of certain acidic drugs.
    • Adverse effects may include gastric irritation, skin rash, and, rarely, interstitial nephritis or aplastic anemia.
    • Should not be used during acute gout attacks as it may aggravate inflammation.

    Inhibitors of Uric Acid Synthesis: Allopurinol

    • Allopurinol is a synthetic purine analogue that inhibits xanthine oxidase, reducing uric acid synthesis.
    • It has a long duration of action due to potent inhibition by both the drug and its metabolite.
    • Recommended for patients with recurrent gout attacks, targeting uric acid levels of 5 mg/dL (0.3 mmol/L).
    • May also be used in hematologic malignancies to prevent hyperuricemia.
    • Common adverse effects include gastric irritation and hypersensitivity reactions; can precipitate acute gout at therapy onset.

    Increase Uric Acid Metabolism: Pegloticase

    • Pegloticase is a recombinant form of porcine uricase, converting uric acid to the soluble allantoin.
    • Administered intravenously (8 mg every 2 weeks), it quickly lowers serum uric acid.
    • Indicated for severe gout cases resistant to other treatments.

    Anti-Inflammatory Drugs: Colchicine

    • Colchicine is a plant alkaloid that inhibits leukocyte motility, phagocytosis, and mitosis.
    • Mainly used for acute gout attacks; slower onset compared to NSAIDs, with pain relief occurring within 12–24 hours.
    • High doses can lead to gastrointestinal toxicity, especially diarrhea.

    NSAIDs: Indomethacin and Naproxen

    • Indomethacin and naproxen are FDA-approved NSAIDs for acute gout, providing faster relief than colchicine.
    • Dosage adjustments may be needed when co-administered with probenecid, which inhibits renal excretion.

    Corticosteroids

    • Used as anti-inflammatory agents when colchicine and NSAIDs are insufficient or contraindicated for acute attacks.

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    Description

    This quiz explores the role of PNLLs and macrophages in phagocytosing uric acid crystals, resulting in joint swelling and inflammation. It also delves into the impact of leukocytes and their enzymes and inflammatory mediators on the process of arthritis. Test your understanding of the cellular mechanisms behind this condition.

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