Pharmacology Part 2: NSAIDs Classification

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.

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.