Pharmacology Part 2: NSAIDs Classification
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Pharmacology Part 2: NSAIDs Classification

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Questions and Answers

What are the potential effects of high doses of certain medications on oxidative phosphorylation?

  • Induction of hypopyrexia
  • Stimulation of uterine contractions
  • Tachycardia and hyperpyrexia (correct)
  • Inhibition of tachycardia

    • Which of the following is a consequence of using NSAIDs after 20 weeks of pregnancy?

  • Prolongation of pregnancy and delay of labor (correct)
  • Enhanced analgesic effects on severe pain
  • Prevention of tachycardia in mothers
  • Increased uterine contractions during labor

    • Why should salicylates not be used routinely as antipyretics?

  • They have no impact on inflammatory responses
  • Fever may serve as a protective mechanism (correct)
  • They are ineffective against mild pain
  • They can significantly reduce fever levels

    • In which condition are salicylates recommended as an anti-inflammatory and anti-rheumatic treatment?

    <p>Rheumatic fever and rheumatoid arthritis</p> Signup and view all the answers

    What type of pain is salicylates indicated for as an analgesic?

    <p>Mild-to-moderate pain such as headache</p> Signup and view all the answers

    What effect does high doses of aspirin (greater than 6 gm/day) have on prothrombin synthesis?

    <p>Decreases prothrombin synthesis</p> Signup and view all the answers

    What is a consequence of decreasing renal prostaglandins like PGE2 and PGI2 due to chronic aspirin use?

    <p>Chronic renal ischemia</p> Signup and view all the answers

    How does aspirin affect platelet aggregation?

    <p>Decreases platelet accumulation</p> Signup and view all the answers

    What potential renal effect can result from the chronic abuse of analgesics, including aspirin?

    <p>Analgesic nephropathy</p> Signup and view all the answers

    What is the impact of aspirin on uric acid excretion at small-to-moderate doses?

    <p>Lowers uric acid excretion</p> Signup and view all the answers

    What cardiovascular complications can arise due to the antagonistic effect of aspirin on diuretics?

    <p>Increased blood pressure along with antihypertensive medications</p> Signup and view all the answers

    What is a recommended use of aspirin regarding cardiovascular prophylaxis?

    <p>Should be continued if required for prophylaxis</p> Signup and view all the answers

    What can result from the decrease in renal blood flow due to aspirin use?

    <p>Increased aldosterone secretion</p> Signup and view all the answers

    Which of the following statements accurately describe the classification of non-steroidal anti-inflammatory drugs (NSAIDs)?

    <p>Propionic acid derivatives consist of ibuprofen and naproxen.</p> Signup and view all the answers

    What distinguishes aspirin from other non-steroidal anti-inflammatory drugs (NSAIDs) in terms of its mechanism of action?

    <p>Aspirin irreversibly inhibits COX enzymes.</p> Signup and view all the answers

    How does the acidity or alkalinity of urine impact the excretion of aspirin in the body?

    <p>Alkaline urine increases ionization, making aspirin less re-absorbable.</p> Signup and view all the answers

    What is the primary pharmacological effect of aspirin in relation to body temperature?

    <p>Aspirin can lower elevated body temperature without affecting normal body temperature.</p> Signup and view all the answers

    Which of the following is NOT a characteristic of aspirin’s analgesic action?

    <p>Effective for severe pain.</p> Signup and view all the answers

    Which of the following correctly outlines the anti-inflammatory mechanism of aspirin?

    <p>Decreases synthesis of inflammatory mediators such as PGs and TXs.</p> Signup and view all the answers

    Which physiological site is primarily targeted by aspirin's central analgesic effect?

    <p>Thalamus and hypothalamus</p> Signup and view all the answers

    Which of the following NSAID classifications includes drugs such as indomethacin and diclofenac?

    <p>Acetic acid derivatives</p> Signup and view all the answers

    What is the primary mechanism through which salicylates produce acute gastric ulcers?

    <p>Trapping of salicylate ions in gastric mucosal cells</p> Signup and view all the answers

    Which effect of salicylates is associated with low toxic doses?

    <p>Prolonged respiratory alkalosis</p> Signup and view all the answers

    What distinguishes severe hepatic injury from mild hepatic injury due to salicylates?

    <p>Reversibility and symptomatology</p> Signup and view all the answers

    What is a critical cardiovascular effect observed at toxic doses of salicylates?

    <p>Inhibition of vascular muscle contraction</p> Signup and view all the answers

    What is the significant hematologic action of aspirin related to platelet function?

    <p>Irreversible inhibition of the COX enzyme leading to decreased TXA2</p> Signup and view all the answers

    In which scenario is Reye's syndrome most likely to occur?

    <p>In children under 12 using aspirin for viral infections</p> Signup and view all the answers

    How does chronic ingestion of salicylates lead to chronic gastric ulcers?

    <p>Inhibition of protective prostaglandin synthesis</p> Signup and view all the answers

    What effect do high toxic doses of salicylates have on respiratory function?

    <p>Metabolic acidosis with inhibited respiratory center</p> Signup and view all the answers

    High doses of salicyclates can cause hypoperemia and tachycardia.

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

    The use of NSAIDs is recommended during labor to expedite uterine contractions.

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

    Salicyclates are indicated for the treatment of rheumatic fever and rheumatoid arthritis.

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

    Salicyclates should be used routinely as an antipyretic for fever management.

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

    Prolongation of pregnancy can result from the inhibition of uterine prostaglandins by salicyclates.

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

    Aspirin is a selective and reversible COX inhibitor that decreases both PGs and TXs.

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

    High doses of aspirin lead to elimination through a first-order process.

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

    The antipyretic effect of aspirin is achieved by lowering the body's normal temperature.

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

    Alkalinization of urine increases the re-absorption of aspirin, making it less ionized.

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

    Peripheral effects of aspirin involve increasing PG synthesis in inflamed tissues.

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

    Salicylic acid derivatives include drugs such as naproxen and iboprufen.

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

    Aspirin's central analgesic effect primarily targets the thalamus and hypothalamus through increased PGE2 synthesis.

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

    The use of piroxicam is classified under pyrazolone derivatives.

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

    Irreversible acetylation of platelet cell membrane decreases platelet adhesions.

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

    High doses of aspirin can decrease platelet ADP synthesis, thus increasing platelet accumulation.

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

    Chronic abuse of analgesics can lead to renal failure due to chronic renal ischemia.

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

    Aspirin at doses of 75-150 mg is known to have significant effects on plasma urate levels.

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

    Aspirin can antagonize the diuretic effect of certain drugs by decreasing renal prostaglandin synthesis.

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

    Small-to-moderate doses of aspirin can enhance uric acid excretion, making it suitable for gout patients.

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

    Increased aldosterone production due to aspirin can lead to salt and water retention.

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

    The prolongation of bleeding time due to aspirin is associated with inhibition of prothrombin synthesis.

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

    Low toxic doses of salicylates lead to metabolic alkalosis due to compensatory hypoventilation.

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

    Chronic ingestion of salicylates inhibits the synthesis of PGE1, PGE2, and PGI2, resulting in acute gastric ulcers.

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

    Severe hepatic injury related to salicylates is characterized by fatty infiltration of the liver and is reversible.

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

    Aspirin's antiplatelet action occurs through reversible inhibition of the COX enzyme.

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

    Toxic doses of salicylates can lead to circulatory failure due to inhibition of the VMC.

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

    Chronic ingestion of salicylates leads to acute gastric ulceration primarily through the trapping of salicylate ions in the gastric mucosa.

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

    Reye's syndrome occurs in children below 12 years when aspirin is used to treat viral infections.

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

    Therapeutic doses of salicylates have a significant effect on the cardiovascular system.

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

    What are the implications of prolonged pregnancy due to the inhibition of prostaglandins by salicylates?

    <p>Prolonged pregnancy can lead to complications during labor and increased risks for both the mother and fetus.</p> Signup and view all the answers

    Explain how high doses of salicylates can lead to tachycardia and hyperpyrexia.

    <p>High doses disrupt oxidative phosphorylation, causing increased metabolic rate and heart rate, resulting in tachycardia and elevated body temperature.</p> Signup and view all the answers

    Discuss why the routine use of salicylates as antipyretics is not recommended.

    <p>Routine use can mask fever, which is a natural protective response that signals underlying issues needing attention.</p> Signup and view all the answers

    What consequences can arise from the chronic use of analgesics, including aspirin, on renal function?

    <p>Chronic use may lead to renal failure due to ischemia and damage from decreased prostaglandins required for kidney function.</p> Signup and view all the answers

    Why is it not recommended to use NSAIDs after 20 weeks of pregnancy?

    <p>Using NSAIDs can interfere with labor and prolong pregnancy by inhibiting prostaglandins that induce uterine contractions.</p> Signup and view all the answers

    Describe the primary difference in elimination processes of salicylates at low versus high doses.

    <p>At low doses, salicylates are eliminated through a first-order process, while at high doses, they follow a zero-order process.</p> Signup and view all the answers

    What physiological mechanisms allow aspirin to exert its antipyretic effect?

    <p>Aspirin lowers elevated body temperature by decreasing PGE2 synthesis in the hypothalamus and reducing the hypothalamic response to interleukin-1.</p> Signup and view all the answers

    Explain how the alkalinization of urine affects the excretion of aspirin.

    <p>Alkalinization of urine increases aspirin's ionization, making it less re-absorbable and thus enhancing its excretion.</p> Signup and view all the answers

    What distinguishes aspirin’s mechanism of action compared to other NSAIDs?

    <p>Aspirin is an irreversible COX inhibitor, while most other NSAIDs reversibly inhibit the COX enzyme.</p> Signup and view all the answers

    Identify the primary region affected by the central analgesic action of aspirin.

    <p>Aspirin primarily affects the thalamus and hypothalamus.</p> Signup and view all the answers

    What is the main anti-inflammatory mechanism through which aspirin operates?

    <p>Aspirin decreases the synthesis of prostaglandins (PGs) and thromboxanes (TXs), leading to reduced inflammatory mediators.</p> Signup and view all the answers

    Discuss the impact of aspirin on inflammatory cell activation and chemotaxis.

    <p>By inhibiting COX enzymes, aspirin decreases the activation and chemotaxis of inflammatory cells.</p> Signup and view all the answers

    How do high doses of aspirin influence the synthesis of prothrombin?

    <p>High doses of aspirin can decrease prothrombin synthesis, resulting in prolonged bleeding times.</p> Signup and view all the answers

    What is the primary renal complication associated with chronic misuse of analgesics, particularly aspirin?

    <p>Chronic analgesic misuse can lead to analgesic nephropathy, resulting in chronic renal failure.</p> Signup and view all the answers

    How does aspirin usage impact the synthesis of prostaglandins and the consequent effects on renal function?

    <p>Aspirin decreases the synthesis of renal prostaglandins such as PGE2 and PGI2, leading to renal ischemia and impaired blood flow.</p> Signup and view all the answers

    What effect does aspirin have on uric acid levels when administered in small-to-moderate doses?

    <p>Small-to-moderate doses of aspirin can decrease uric acid excretion, potentially contraindicating its use in gout patients.</p> Signup and view all the answers

    Describe how aspirin affects platelet aggregation in the context of its pharmacological properties.

    <p>Aspirin irreversibly acetylates platelets, leading to decreased platelet adhesion and aggregation.</p> Signup and view all the answers

    What is the consequence of high doses of aspirin on prothrombin synthesis and bleeding time?

    <p>High doses of aspirin inhibit hepatic prothrombin synthesis, resulting in prolonged bleeding time.</p> Signup and view all the answers

    In what way does aspirin antagonize the effects of diuretics?

    <p>Aspirin antagonizes diuretic effects by decreasing renal blood flow and prostaglandin synthesis.</p> Signup and view all the answers

    Explain the implications of decreased plasma urate levels in patients taking sustained aspirin therapy.

    <p>Sustained aspirin therapy can lead to increased plasma urate levels, which is detrimental for patients with gout.</p> Signup and view all the answers

    What role does aspirin play in the management of cardiovascular conditions regarding thrombus formation?

    <p>Aspirin is used to manage cardiovascular conditions by decreasing thrombus formation through its antiplatelet effects.</p> Signup and view all the answers

    What mechanism does aspirin utilize to inhibit platelet aggregation?

    <p>Aspirin irreversibly inhibits the COX enzyme, leading to a decrease in thromboxane A2 (TXA2) and thus reducing platelet aggregation.</p> Signup and view all the answers

    Explain how chronic ingestion of salicylates can lead to chronic gastric ulcers.

    <p>Chronic ingestion of salicylates inhibits the synthesis of protective prostaglandins like PGE1 and PGE2, resulting in chronic gastric ulceration.</p> Signup and view all the answers

    What are the respiratory effects associated with high toxic doses of salicylates?

    <p>High toxic doses of salicylates can cause metabolic acidosis combined with respiratory failure, leading to severe acidosis and potential death.</p> Signup and view all the answers

    Describe the pathogenesis of Reye's syndrome in relation to salicylate use in children.

    <p>Reye's syndrome occurs when aspirin is used in children to manage viral infections, causing severe fatty infiltration of the liver and other organs, leading to encephalopathy.</p> Signup and view all the answers

    How does inhibition of the vascular motor center (VMC) at toxic doses affect cardiovascular function?

    <p>Inhibition of the VMC at toxic doses of salicylates leads to circulatory failure due to compromised vascular tone.</p> Signup and view all the answers

    What is the relationship between low toxic doses of salicylates and respiratory alkalosis?

    <p>Low toxic doses of salicylates induce metabolic acidosis, prompting compensatory hyperventilation which can result in prolonged respiratory alkalosis.</p> Signup and view all the answers

    Identify the liver effects of salicylate toxicity and differentiate between mild and severe hepatic injury.

    <p>Mild hepatic injury from salicylates is dose-dependent and reversible, while severe hepatic injury, like Reye's syndrome, is fatal and involves significant fatty infiltration.</p> Signup and view all the answers

    What types of gastric ulcers are associated with salicylate use, and what is their primary mechanism?

    <p>Salicylates can cause acute gastric ulcers due to acute ingestion and chronic gastric ulcers from long-term use, both mechanisms involving damage to the gastric mucosa.</p> Signup and view all the answers

    High doses can cause tachycardia and hypoperpyrexia due to coupling of oxidative ______.

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

    The use of NSAIDs after 20 weeks of pregnancy is not ______.

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

    Salicylates should not be used routinely as an antipyretic because fever may be a normal ______ mechanism.

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

    Salicylic acid is indicated as anti-inflammatory and anti-rheumatic in conditions such as rheumatoid ______ and osteoarthritis.

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

    High doses of salicylic acid can lead to the inhibition of ______ necessary for uterine contraction during labor.

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

    Irreversible acetylation of platelet cell membrane leads to decreased platelet ______.

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

    Aspirin in high doses (> 6 gm/day) inhibits hepatic ______ synthesis, prolonging bleeding time.

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

    Chronic abuse of analgesics can lead to chronic renal ______ due to renal ischemia.

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

    Small-to-moderate doses of aspirin can decrease uric acid ______, making it contraindicated in gout patients.

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

    Aspirin is a non-selective and irreversible ______ inhibitor leading to inhibition of both PGs and TXs.

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

    Aspirin's antipyretic effect works by decreasing ______ synthesis in the hypothalamus.

    <p>PGE2</p> Signup and view all the answers

    Salt and water retention due to aspirin use is a result of decreased renal ______ flow.

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

    Aspirin can antagonize the diuretic effect of certain medications by decreasing renal synthesis of ______.

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

    The excretion of aspirin is increased by the alkalinization of ______.

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

    Chronic use of aspirin can lead to analgesic nephropathy, resulting from ______ renal ischemia.

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

    At low doses, elimination of salicylates occurs through a first-order ______.

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

    NSAIDs like aspirin can provide analgesic action for ______ to moderate intensity pain.

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

    Increased aldosterone production due to aspirin can result in salt and water ______.

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

    The inhibition of COX enzymes leads to a decrease in inflammatory cell activation and ______.

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

    High doses of aspirin can lead to a zero-order ______ process for elimination.

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

    Selective COX-2 inhibitors, such as ______, are designed to reduce inflammation without affecting COX-1.

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

    Toxic doses of salicylates can inhibit the ______ leading to circulatory failure.

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

    Low toxic doses of salicylates can produce metabolic acidosis followed by prolonged respiratory ______.

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

    Chronic ingestion of salicylates can lead to inhibitory effects on the synthesis of protective ______ which may result in chronic gastric ulceration.

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

    Reye's syndrome is a severe condition associated with ______ use to control fever in children.

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

    The acute gastric ulcer caused by salicylates is primarily due to the trapping of salicylate ions inside the gastric ______.

    <p>mucosal cells</p> Signup and view all the answers

    Mild hepatic injury caused by salicylates is dose-dependent, reversible, and often ______.

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

    Aspirin irreversibly inhibits the ______ enzyme, which decreases thromboxane A2 and affects platelet aggregation.

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

    At high toxic doses, salicylates can produce metabolic acidosis and inhibit ______, leading to potential death.

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

    Match the following types of gastric ulcers caused by salicylates with their descriptions:

    <p>Acute gastric ulcer = Results from acute ingestion of large doses, leading to painful gastric bleeding Chronic gastric ulcer = Occurs due to chronic intake, causing chronic blood loss through inhibition of protective prostaglandins</p> Signup and view all the answers

    Match the following hepatic injuries associated with salicylates to their characteristics:

    <p>Mild hepatic injury = Dose-dependent, reversible, asymptomatic with slight increase in transaminases Severe hepatic injury = Rare, fatal condition characterized by fatty infiltration, notable in children with viral infections</p> Signup and view all the answers

    Match the effects of salicylates on the respiratory system with their doses:

    <p>Low toxic doses = Produce metabolic acidosis followed by compensatory hyperventilation leading to respiratory alkalosis High toxic doses = Lead to severe acidosis and potential death due to inhibition of respiratory control</p> Signup and view all the answers

    Match the effects of different doses of salicylates on cardiovascular function:

    <p>Therapeutic doses = No significant effect on the cardiovascular system Toxic doses = Inhibit vasomotor centers leading to circulatory failure</p> Signup and view all the answers

    Match the effects of aspirin on platelet aggregation with their mechanisms:

    <p>Irreversible inhibition of COX enzyme = Decreases synthesis of TXA2 leading to reduced platelet aggregation Inhibition of platelet aggregation = Involves reduction in thromboxane levels affecting clotting</p> Signup and view all the answers

    Match the following conditions with their related effects of salicylates:

    <p>Acute ingestion of salicylates = Causes acute gastric ulcers due to trapping salicylate ions Chronic ingestion of salicylates = Leads to chronic gastric ulcers due to PG synthesis inhibition</p> Signup and view all the answers

    Match the therapeutic uses of salicylates with their respective indications:

    <p>Analgesic = Mild-to-moderate pain relief Anti-inflammatory = Rheumatic fever and osteoarthritis Antipyretic = Fever management in routine cases Antithrombotic = Prevention of cardiovascular events</p> Signup and view all the answers

    Match the effects of high doses of salicylates with their consequences:

    <p>Tachycardia = Increase in heart rate due to oxidative phosphorylation coupling Hypoperia = Decreased blood flow due to hemodynamic changes Hypopyrexia = Reduction of fever contrary to its primary use Uterine contraction inhibition = Prolongation of pregnancy</p> Signup and view all the answers

    Match the following physiological responses with the respective concentrations of salicylates:

    <p>High doses = Associated with risk of Reye's syndrome in children Low to moderate doses = Safe for conditions like gout due to uric acid excretion enhancement</p> Signup and view all the answers

    Match these NSAIDs’ potential effects with their corresponding characteristics:

    <p>Peripheral effects = Increase in prostaglandin synthesis in inflamed tissues Urinary alkalinization = Increases re-absorption and reduces ionization of aspirin Chronic ingestion = Leads to chronic gastric ulcers Selective COX inhibition = Decreases both prostaglandins and thromboxanes</p> Signup and view all the answers

    Match the following non-steroidal anti-inflammatory drug (NSAID) classes with their examples:

    <p>Salicylic acid derivatives = Aspirin Acetic acid derivatives = Indomethacin Propionic acid derivatives = Ibuprofen Oxicams = Piroxicam</p> Signup and view all the answers

    Match the salicylates' action on the gastrointestinal system with its consequences:

    <p>Acute gastric bleeding = Resulting from acute gastric ulcer due to high salicylate levels Chronic ulceration = Secondary to PG synthesis inhibition, causing serious long-term damage</p> Signup and view all the answers

    Match the circumstances under which the use of NSAIDs is discouraged:

    <p>After 20 weeks of pregnancy = Prolongation of labor Routine antipyretic use = Masking of fever as protective mechanism High dosage in chronic cases = Risk of renal failure Competing with diuretics = Decreased renal prostaglandin synthesis</p> Signup and view all the answers

    Match the following mechanisms of aspirin with their effects:

    <p>Analgesic action = Decrease PG synthesis in inflamed tissues Antipyretic effect = Decrease hypothalamic response to interleukin-1 Anti-inflammatory effect = Decrease capillary permeability Central effect = Decrease PG synthesis in thalamus</p> Signup and view all the answers

    Match the following categories of NSAIDs with their characteristics:

    <p>Non-selective COX inhibitors = Inhibit both COX-1 and COX-2 Selective COX-2 inhibitors = Specifically inhibit COX-2 Salicylic acid derivatives = Include aspirin and diflunisal Pyrazolone derivatives = Include phenylbutazone and azapropazone</p> Signup and view all the answers

    Match the effects associated with chronic use of salicylates:

    <p>Gastric ulceration = A result of direct mucosal damage Hepatic injury = Variability between mild and severe outcomes Renal failure = Due to chronic renal ischemia Increased urate levels = Facilitated by low to moderate doses</p> Signup and view all the answers

    Match the following NSAID properties with their descriptions:

    <p>Aspirin = Non-selective and irreversible COX inhibitor Celecoxib = Selective COX-2 inhibitor Ibuprofen = Propionic acid derivative Indomethacin = Acetic acid derivative</p> Signup and view all the answers

    Match the following effects of aspirin with their mechanisms:

    <p>Analgesic = Peripheral and central decrease in PG synthesis Antipyretic = Inhibition of PGE2 synthesis in hypothalamus Anti-inflammatory = Decreased inflammatory cell activation Decrease in capillary permeability = By inhibition of COX enzyme</p> Signup and view all the answers

    Match the following pharmacokinetic characteristics with their details regarding aspirin:

    <p>Oral absorption = Complete from stomach and upper GIT Metabolism = Hepatic microsomal enzymes Elimination at low doses = First-order process Excretion influenced by urine pH = Increased at pH 8</p> Signup and view all the answers

    Match the following aspirin effects with their consequences:

    <p>Decrease of inflammatory mediators = Decreased chemotaxis Alkalinization of urine = Increases aspirin ionization Chronic use = May lead to gastric ulcers High doses = Zero-order elimination process</p> Signup and view all the answers

    Match the following terms related to aspirin with their definitions:

    <p>PGs = Prostaglandins TXs = Thromboxanes CNS distribution = Widely distributed to all tissues First-order process = Elimination rate depends on drug concentration</p> Signup and view all the answers

    Match the following effects of aspirin with their corresponding descriptions:

    <p>Decreased platelet adhesions = Irreversible acetylation of platelet cell membrane Chronic renal ischemia = Analgesic nephropathy from chronic analgesic abuse Decrease in plasma urate levels = Antagonizes diuretic effects due to decreased renal prostaglandin synthesis Salt and water retention = Increased aldosterone production due to decreased renal blood flow</p> Signup and view all the answers

    Match the following doses of aspirin with their effects on platelet function:

    <p>High doses (&gt; 6 gm/day) = Inhibits hepatic prothrombin synthesis 75-150 mg = Not thought to have a significant effect on plasma urate levels Moderate doses = Can enhance uric acid excretion in gout patients Chronic abuse = Leads to chronic renal failure due to sustained ischemia</p> Signup and view all the answers

    Match the following effects of aspirin with their clinical implications:

    <p>Prolonged bleeding time = Inhibition of prothrombin synthesis Decreased platelet ADP synthesis = Increased platelet accumulation Decreased synthesis of renal PGE2 = Antagonizes the effect of β-blockers Small-to-moderate doses = Can contraindicate use in gout patients due to uric acid retention</p> Signup and view all the answers

    Match the following aspirin mechanisms with their physiological outcomes:

    <p>Irreversible acetylation = Inhibition of platelet aggregation Decreased renal prostaglandins = Salt and water retention Increased aldosterone = Decreased renal blood flow Chronic analgesic abuse = Chronic renal ischemia leading to failure</p> Signup and view all the answers

    Match the following aspirin-related pathophysiological effects:

    <p>Decreased uric acid excretion = Antagonism of diuretic effects Salt retention = Due to decreased renal blood flow Chronic abuse of analgesics = An increased risk of renal failure Inhibition of hepatic synthesis = Prolonged bleeding times due to decreased prothrombin</p> Signup and view all the answers

    Match the following clinical scenarios with aspirin effects:

    <p>Patient on high dose aspirin = Prolonged bleeding time and increased risk of hemorrhage Patient with gout = Avoid aspirin due to uric acid retention Chronic analgesic user = Risk for renal failure due to chronic ischemia Patient receiving diuretics = Diminished efficacy due to aspirin's renal effects</p> Signup and view all the answers

    Match the following pharmacological aspects of aspirin with their outcomes:

    <p>Prolonged bleeding time = Associated with inhibition of platelet function Decreased renal PGE2 and PGI2 = Results in salt and water retention Aspirin at 75-150 mg = Minimal effect on plasma urate levels High doses of aspirin = Inhibits hepatic prothrombin synthesis</p> Signup and view all the answers

    Match the following descriptions of aspirin’s actions with their respective consequences:

    <p>Irreversible acetylation of platelet membrane = Decreases platelet adhesions Inhibition of ADP synthesis = May lead to increased platelet accumulation Chronic renal ischemia = Caused by prolonged analgesic use Uric acid retention = Can lead to gout exacerbation with chronic aspirin use</p> Signup and view all the answers

    Study Notes

    Non-steroidal Anti-inflammatory Drugs (NSAIDs) Classification

    • Non-selective COX inhibitors affect both COX-1 and COX-2 enzymes.
    • Categories include salicylic acid derivatives (e.g., aspirin), acetic acid derivatives (e.g., indomethacin, diclofenac), and propionic acid derivatives (e.g., ibuprofen, naproxen).
    • Selective COX-2 inhibitors comprise celecoxib, etoricoxib, and meloxicam.

    Acetylsalicylic Acid (Aspirin)

    Chemistry and Pharmacokinetics

    • Complete oral absorption predominantly occurs in the stomach and upper gastrointestinal tract.
    • Aspirin is widely distributed across tissues, including the central nervous system.
    • Metabolism by hepatic microsomal enzymes varies with dosage: first-order at low doses and zero-order at high doses.
    • Urinary excretion increases with alkaline urine (pH 8), enhancing ionization and reducing reabsorption.

    Mechanism and Pharmacological Effects

    • Acts as a non-selective and irreversible COX inhibitor, leading to decreased production of prostaglandins (PGs) and thromboxanes (TXs).
    • Analgesic for mild to moderate pain through:
      • Peripheral effects: reduction of PG synthesis in inflamed tissues.
      • Central effects: decreased PG synthesis in the thalamus and hypothalamus.

    Antipyretic Effect

    • Lowers elevated body temperature without inducing hypothermia.
    • Mechanisms involve decreasing PGE2 synthesis and the hypothalamic response to interleukin-1, promoting sweating and vasodilation.

    Anti-inflammatory, Immunological, and Rheumatic Effects

    • Inhibiting COX leads to decreased activation and chemotaxis of inflammatory cells, reduced capillary permeability, and stabilization of lysosomal membranes.

    Respiratory Effects

    • Low toxic doses result in metabolic acidosis followed by compensatory hyperventilation and possible prolonged respiratory alkalosis.
    • High toxic doses can cause severe acidosis, potentially leading to death.

    Cardiovascular Effects

    • Therapeutic doses have no significant effect, while toxic doses can inhibit vasomotor center leading to circulatory failure.

    Gastrointestinal Effects

    • Acute gastric ulcers arise from large doses; acute ingestion traps salicylate ions in gastric mucosal cells, leading to bleeding.
    • Chronic ulcers develop from repeated use, as inhibition of protective PG synthesis contributes to sustained injury.

    Hepatic Effects

    • Mild, reversible hepatic injury characterized by asymptomatic increases in transaminases.
    • Severe injury, known as Reye’s syndrome, involves fatty infiltration of organs when aspirin is given for viral infections in children, leading to encephalopathy.

    Hematologic Effects

    • Antiplatelet action through irreversible COX inhibition decreases thromboxane A2 and platelet aggregation, leading to prolonged bleeding times in high doses.

    Renal Effects

    • Chronic analgesic nephropathy may develop from long-term aspirin abuse, causing renal ischemia due to reduced renal prostaglandin synthesis.
    • Aspirin can decrease the effectiveness of diuretics and antagonize their effects on blood pressure.

    Metabolic Effects

    • High doses can lead to accelerated oxidative phosphorylation, resulting in tachycardia and hyperpyrexia.

    Uterine Effects

    • Aspirin can delay labor and prolong pregnancy by inhibiting prostaglandins necessary for uterine contractions; use after 20 weeks of pregnancy is discouraged.

    Therapeutic Uses of Salicylates

    • Analgesic and antipyretic for mild-to-moderate pain but should not be routinely used to manage fever as it may interfere with protective responses.
    • Anti-inflammatory and anti-rheumatic properties beneficial for conditions like rheumatoid arthritis and osteoarthritis.
    • Used as an antithrombotic to reduce clot formation.

    Non-steroidal Anti-inflammatory Drugs (NSAIDs) Classification

    • Non-selective COX inhibitors affect both COX-1 and COX-2 enzymes.
    • Categories include salicylic acid derivatives (e.g., aspirin), acetic acid derivatives (e.g., indomethacin, diclofenac), and propionic acid derivatives (e.g., ibuprofen, naproxen).
    • Selective COX-2 inhibitors comprise celecoxib, etoricoxib, and meloxicam.

    Acetylsalicylic Acid (Aspirin)

    Chemistry and Pharmacokinetics

    • Complete oral absorption predominantly occurs in the stomach and upper gastrointestinal tract.
    • Aspirin is widely distributed across tissues, including the central nervous system.
    • Metabolism by hepatic microsomal enzymes varies with dosage: first-order at low doses and zero-order at high doses.
    • Urinary excretion increases with alkaline urine (pH 8), enhancing ionization and reducing reabsorption.

    Mechanism and Pharmacological Effects

    • Acts as a non-selective and irreversible COX inhibitor, leading to decreased production of prostaglandins (PGs) and thromboxanes (TXs).
    • Analgesic for mild to moderate pain through:
      • Peripheral effects: reduction of PG synthesis in inflamed tissues.
      • Central effects: decreased PG synthesis in the thalamus and hypothalamus.

    Antipyretic Effect

    • Lowers elevated body temperature without inducing hypothermia.
    • Mechanisms involve decreasing PGE2 synthesis and the hypothalamic response to interleukin-1, promoting sweating and vasodilation.

    Anti-inflammatory, Immunological, and Rheumatic Effects

    • Inhibiting COX leads to decreased activation and chemotaxis of inflammatory cells, reduced capillary permeability, and stabilization of lysosomal membranes.

    Respiratory Effects

    • Low toxic doses result in metabolic acidosis followed by compensatory hyperventilation and possible prolonged respiratory alkalosis.
    • High toxic doses can cause severe acidosis, potentially leading to death.

    Cardiovascular Effects

    • Therapeutic doses have no significant effect, while toxic doses can inhibit vasomotor center leading to circulatory failure.

    Gastrointestinal Effects

    • Acute gastric ulcers arise from large doses; acute ingestion traps salicylate ions in gastric mucosal cells, leading to bleeding.
    • Chronic ulcers develop from repeated use, as inhibition of protective PG synthesis contributes to sustained injury.

    Hepatic Effects

    • Mild, reversible hepatic injury characterized by asymptomatic increases in transaminases.
    • Severe injury, known as Reye’s syndrome, involves fatty infiltration of organs when aspirin is given for viral infections in children, leading to encephalopathy.

    Hematologic Effects

    • Antiplatelet action through irreversible COX inhibition decreases thromboxane A2 and platelet aggregation, leading to prolonged bleeding times in high doses.

    Renal Effects

    • Chronic analgesic nephropathy may develop from long-term aspirin abuse, causing renal ischemia due to reduced renal prostaglandin synthesis.
    • Aspirin can decrease the effectiveness of diuretics and antagonize their effects on blood pressure.

    Metabolic Effects

    • High doses can lead to accelerated oxidative phosphorylation, resulting in tachycardia and hyperpyrexia.

    Uterine Effects

    • Aspirin can delay labor and prolong pregnancy by inhibiting prostaglandins necessary for uterine contractions; use after 20 weeks of pregnancy is discouraged.

    Therapeutic Uses of Salicylates

    • Analgesic and antipyretic for mild-to-moderate pain but should not be routinely used to manage fever as it may interfere with protective responses.
    • Anti-inflammatory and anti-rheumatic properties beneficial for conditions like rheumatoid arthritis and osteoarthritis.
    • Used as an antithrombotic to reduce clot formation.

    Non-steroidal Anti-inflammatory Drugs (NSAIDs) Classification

    • Non-selective COX inhibitors affect both COX-1 and COX-2 enzymes.
    • Categories include salicylic acid derivatives (e.g., aspirin), acetic acid derivatives (e.g., indomethacin, diclofenac), and propionic acid derivatives (e.g., ibuprofen, naproxen).
    • Selective COX-2 inhibitors comprise celecoxib, etoricoxib, and meloxicam.

    Acetylsalicylic Acid (Aspirin)

    Chemistry and Pharmacokinetics

    • Complete oral absorption predominantly occurs in the stomach and upper gastrointestinal tract.
    • Aspirin is widely distributed across tissues, including the central nervous system.
    • Metabolism by hepatic microsomal enzymes varies with dosage: first-order at low doses and zero-order at high doses.
    • Urinary excretion increases with alkaline urine (pH 8), enhancing ionization and reducing reabsorption.

    Mechanism and Pharmacological Effects

    • Acts as a non-selective and irreversible COX inhibitor, leading to decreased production of prostaglandins (PGs) and thromboxanes (TXs).
    • Analgesic for mild to moderate pain through:
      • Peripheral effects: reduction of PG synthesis in inflamed tissues.
      • Central effects: decreased PG synthesis in the thalamus and hypothalamus.

    Antipyretic Effect

    • Lowers elevated body temperature without inducing hypothermia.
    • Mechanisms involve decreasing PGE2 synthesis and the hypothalamic response to interleukin-1, promoting sweating and vasodilation.

    Anti-inflammatory, Immunological, and Rheumatic Effects

    • Inhibiting COX leads to decreased activation and chemotaxis of inflammatory cells, reduced capillary permeability, and stabilization of lysosomal membranes.

    Respiratory Effects

    • Low toxic doses result in metabolic acidosis followed by compensatory hyperventilation and possible prolonged respiratory alkalosis.
    • High toxic doses can cause severe acidosis, potentially leading to death.

    Cardiovascular Effects

    • Therapeutic doses have no significant effect, while toxic doses can inhibit vasomotor center leading to circulatory failure.

    Gastrointestinal Effects

    • Acute gastric ulcers arise from large doses; acute ingestion traps salicylate ions in gastric mucosal cells, leading to bleeding.
    • Chronic ulcers develop from repeated use, as inhibition of protective PG synthesis contributes to sustained injury.

    Hepatic Effects

    • Mild, reversible hepatic injury characterized by asymptomatic increases in transaminases.
    • Severe injury, known as Reye’s syndrome, involves fatty infiltration of organs when aspirin is given for viral infections in children, leading to encephalopathy.

    Hematologic Effects

    • Antiplatelet action through irreversible COX inhibition decreases thromboxane A2 and platelet aggregation, leading to prolonged bleeding times in high doses.

    Renal Effects

    • Chronic analgesic nephropathy may develop from long-term aspirin abuse, causing renal ischemia due to reduced renal prostaglandin synthesis.
    • Aspirin can decrease the effectiveness of diuretics and antagonize their effects on blood pressure.

    Metabolic Effects

    • High doses can lead to accelerated oxidative phosphorylation, resulting in tachycardia and hyperpyrexia.

    Uterine Effects

    • Aspirin can delay labor and prolong pregnancy by inhibiting prostaglandins necessary for uterine contractions; use after 20 weeks of pregnancy is discouraged.

    Therapeutic Uses of Salicylates

    • Analgesic and antipyretic for mild-to-moderate pain but should not be routinely used to manage fever as it may interfere with protective responses.
    • Anti-inflammatory and anti-rheumatic properties beneficial for conditions like rheumatoid arthritis and osteoarthritis.
    • Used as an antithrombotic to reduce clot formation.

    Non-steroidal Anti-inflammatory Drugs (NSAIDs) Classification

    • Non-selective COX inhibitors affect both COX-1 and COX-2 enzymes.
    • Categories include salicylic acid derivatives (e.g., aspirin), acetic acid derivatives (e.g., indomethacin, diclofenac), and propionic acid derivatives (e.g., ibuprofen, naproxen).
    • Selective COX-2 inhibitors comprise celecoxib, etoricoxib, and meloxicam.

    Acetylsalicylic Acid (Aspirin)

    Chemistry and Pharmacokinetics

    • Complete oral absorption predominantly occurs in the stomach and upper gastrointestinal tract.
    • Aspirin is widely distributed across tissues, including the central nervous system.
    • Metabolism by hepatic microsomal enzymes varies with dosage: first-order at low doses and zero-order at high doses.
    • Urinary excretion increases with alkaline urine (pH 8), enhancing ionization and reducing reabsorption.

    Mechanism and Pharmacological Effects

    • Acts as a non-selective and irreversible COX inhibitor, leading to decreased production of prostaglandins (PGs) and thromboxanes (TXs).
    • Analgesic for mild to moderate pain through:
      • Peripheral effects: reduction of PG synthesis in inflamed tissues.
      • Central effects: decreased PG synthesis in the thalamus and hypothalamus.

    Antipyretic Effect

    • Lowers elevated body temperature without inducing hypothermia.
    • Mechanisms involve decreasing PGE2 synthesis and the hypothalamic response to interleukin-1, promoting sweating and vasodilation.

    Anti-inflammatory, Immunological, and Rheumatic Effects

    • Inhibiting COX leads to decreased activation and chemotaxis of inflammatory cells, reduced capillary permeability, and stabilization of lysosomal membranes.

    Respiratory Effects

    • Low toxic doses result in metabolic acidosis followed by compensatory hyperventilation and possible prolonged respiratory alkalosis.
    • High toxic doses can cause severe acidosis, potentially leading to death.

    Cardiovascular Effects

    • Therapeutic doses have no significant effect, while toxic doses can inhibit vasomotor center leading to circulatory failure.

    Gastrointestinal Effects

    • Acute gastric ulcers arise from large doses; acute ingestion traps salicylate ions in gastric mucosal cells, leading to bleeding.
    • Chronic ulcers develop from repeated use, as inhibition of protective PG synthesis contributes to sustained injury.

    Hepatic Effects

    • Mild, reversible hepatic injury characterized by asymptomatic increases in transaminases.
    • Severe injury, known as Reye’s syndrome, involves fatty infiltration of organs when aspirin is given for viral infections in children, leading to encephalopathy.

    Hematologic Effects

    • Antiplatelet action through irreversible COX inhibition decreases thromboxane A2 and platelet aggregation, leading to prolonged bleeding times in high doses.

    Renal Effects

    • Chronic analgesic nephropathy may develop from long-term aspirin abuse, causing renal ischemia due to reduced renal prostaglandin synthesis.
    • Aspirin can decrease the effectiveness of diuretics and antagonize their effects on blood pressure.

    Metabolic Effects

    • High doses can lead to accelerated oxidative phosphorylation, resulting in tachycardia and hyperpyrexia.

    Uterine Effects

    • Aspirin can delay labor and prolong pregnancy by inhibiting prostaglandins necessary for uterine contractions; use after 20 weeks of pregnancy is discouraged.

    Therapeutic Uses of Salicylates

    • Analgesic and antipyretic for mild-to-moderate pain but should not be routinely used to manage fever as it may interfere with protective responses.
    • Anti-inflammatory and anti-rheumatic properties beneficial for conditions like rheumatoid arthritis and osteoarthritis.
    • Used as an antithrombotic to reduce clot formation.

    Non-steroidal Anti-inflammatory Drugs (NSAIDs) Classification

    • Non-selective COX inhibitors affect both COX-1 and COX-2 enzymes.
    • Categories include salicylic acid derivatives (e.g., aspirin), acetic acid derivatives (e.g., indomethacin, diclofenac), and propionic acid derivatives (e.g., ibuprofen, naproxen).
    • Selective COX-2 inhibitors comprise celecoxib, etoricoxib, and meloxicam.

    Acetylsalicylic Acid (Aspirin)

    Chemistry and Pharmacokinetics

    • Complete oral absorption predominantly occurs in the stomach and upper gastrointestinal tract.
    • Aspirin is widely distributed across tissues, including the central nervous system.
    • Metabolism by hepatic microsomal enzymes varies with dosage: first-order at low doses and zero-order at high doses.
    • Urinary excretion increases with alkaline urine (pH 8), enhancing ionization and reducing reabsorption.

    Mechanism and Pharmacological Effects

    • Acts as a non-selective and irreversible COX inhibitor, leading to decreased production of prostaglandins (PGs) and thromboxanes (TXs).
    • Analgesic for mild to moderate pain through:
      • Peripheral effects: reduction of PG synthesis in inflamed tissues.
      • Central effects: decreased PG synthesis in the thalamus and hypothalamus.

    Antipyretic Effect

    • Lowers elevated body temperature without inducing hypothermia.
    • Mechanisms involve decreasing PGE2 synthesis and the hypothalamic response to interleukin-1, promoting sweating and vasodilation.

    Anti-inflammatory, Immunological, and Rheumatic Effects

    • Inhibiting COX leads to decreased activation and chemotaxis of inflammatory cells, reduced capillary permeability, and stabilization of lysosomal membranes.

    Respiratory Effects

    • Low toxic doses result in metabolic acidosis followed by compensatory hyperventilation and possible prolonged respiratory alkalosis.
    • High toxic doses can cause severe acidosis, potentially leading to death.

    Cardiovascular Effects

    • Therapeutic doses have no significant effect, while toxic doses can inhibit vasomotor center leading to circulatory failure.

    Gastrointestinal Effects

    • Acute gastric ulcers arise from large doses; acute ingestion traps salicylate ions in gastric mucosal cells, leading to bleeding.
    • Chronic ulcers develop from repeated use, as inhibition of protective PG synthesis contributes to sustained injury.

    Hepatic Effects

    • Mild, reversible hepatic injury characterized by asymptomatic increases in transaminases.
    • Severe injury, known as Reye’s syndrome, involves fatty infiltration of organs when aspirin is given for viral infections in children, leading to encephalopathy.

    Hematologic Effects

    • Antiplatelet action through irreversible COX inhibition decreases thromboxane A2 and platelet aggregation, leading to prolonged bleeding times in high doses.

    Renal Effects

    • Chronic analgesic nephropathy may develop from long-term aspirin abuse, causing renal ischemia due to reduced renal prostaglandin synthesis.
    • Aspirin can decrease the effectiveness of diuretics and antagonize their effects on blood pressure.

    Metabolic Effects

    • High doses can lead to accelerated oxidative phosphorylation, resulting in tachycardia and hyperpyrexia.

    Uterine Effects

    • Aspirin can delay labor and prolong pregnancy by inhibiting prostaglandins necessary for uterine contractions; use after 20 weeks of pregnancy is discouraged.

    Therapeutic Uses of Salicylates

    • Analgesic and antipyretic for mild-to-moderate pain but should not be routinely used to manage fever as it may interfere with protective responses.
    • Anti-inflammatory and anti-rheumatic properties beneficial for conditions like rheumatoid arthritis and osteoarthritis.
    • Used as an antithrombotic to reduce clot formation.

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    Non-steroidal anti-inflammatory drugs (NSAIDs) PDF

    Description

    Explore the classification of non-steroidal anti-inflammatory drugs (NSAIDs) in this quiz. Learn about various types including non-selective COX inhibitors, salicylic acid derivatives, acetic acid derivatives, and propionic acid derivatives. Test your knowledge on their characteristics and examples.

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