lOMoARcPSD|70468202
Week 4: Midterm Study Guide
Thursday, May 22, 2025 9:24 AM
Week 4:
Chapter 59:
• General Information
○ COX Inhibitors have three useful effects:
§ Suppress inflammation
§ Relieve pain
§ Reduce fever
○ These effects are produced through the inhibition of COX, which is the enzyme responsible for the synthesis
of prostaglandins and related compounds.
• NSAIDs
○ AKA CycloOxygenase (COX) Inhibitors
○ Drugs that have anti-inflammatory properties
○ NSAIDs can be subdivided into two groups:
§ First generation NSAIDS
□ Conventional/traditional
□ Inhibit COX-1 and COX-2
□ These agents are unable to suppress pain and inflammation without posing a risk for serious
side effects
□ Used primarily for the treatment of inflammatory disorders, mild/moderate pain, fever
reducing, and dysmenorrhea
□ PROTOTYPE: Aspirin (ASA)
□ Black Box Warning: Increased risk for GI bleeding and cardiovascular events that can lead to
hospitalization or death.
§ Second Generation NSAIDS
□ Selective COX-2 inhibitors/coxibs
□ Only inhibit COX-2
□ In theory, these agents suppress pain and inflammation while causing fewer adverse effects.
□ However, these drugs appear even less safe than first-gen agents due to an increased risk for MI
and stroke.
• NSAIDs Adverse Effects
○ Serious adverse effects:
§ Gastric ulceration
§ Bleeding
§ Renal impairment
§ MI/Stroke (except ASA)
• NSAIDs Benefits of 2nd Gen
○ In theory can suppress pain and inflammation while causing fewer adverse effects, but in practice this is not
true as they increase the risk of MI and stroke the most of all NSAIDS
• NSAIDs: 1st Gen vs. 2nd Gen
• Nonacetylated Salicylates
○ Magnesium salicylate, sodium salicylate, and salsalate
○ Similarities to ASA:
§ Inhibit COX-1 and COX-2
§ Indicated for same uses
§ Most common adverse effects are GI disturbances
§ Should not be given to children with chickenpox or influenza d/t increase risk of Reye Syndrome
○ Contrasts to ASA:
§ Cause little to no suppression of platelet aggregation
§ Cannot protect against MI/Stroke and may increase the risk
§ Sodium Salicylate should be avoided in patients with sodium restrictions (HTN/HF)
, ○ Similarities to ASA: lOMoARcPSD|70468202
§ Inhibit COX-1 and COX-2
§ Indicated for same uses
§ Most common adverse effects are GI disturbances
§ Should not be given to children with chickenpox or influenza d/t increase risk of Reye Syndrome
○ Contrasts to ASA:
§ Cause little to no suppression of platelet aggregation
§ Cannot protect against MI/Stroke and may increase the risk
§ Sodium Salicylate should be avoided in patients with sodium restrictions (HTN/HF)
§ Magnesium Salicylate may be accumulate to toxic levels in patients with chronic renal insufficiency
§ Salsalate is a prodrug that breaks down to release two molecules of salicylate in the alkaline
environment of the small intestine and helps produce less gastric irritation that that of ASA
• Non-aspirin NSAIDs
○ Unlike ASA, these drugs cause reversible inhibition of COX
○ Primary indication for these drugs is RA and osteoarthritis along with mild/moderate pain, fever, bursitis,
tendinitis, and dysmenorrhea
○ Most NSAIDS are not proven to be save during pregnancy and should be discouraged for pregnant woman
○ These drugs do NOT protect against MI and stroke, in fact they increase the risk for a thrombotic event.
○ To minimize risk, these drugs should be used at lowest effect dosage for a short time
○ All NSAIDS can lead to the same adverse effects.
• NSAID: Ibuprofen
○ AKA: Advil, motrin, Caldolor
○ Prototype for propionic acid derivatives: ibuprofen
○ Inhibits COX and has all of the therapeutic effects of other NSAIDS
○ Ibuprofen is far superior to other NSAIDS for relief of primary dysmenorrhea, likely due to its inhibition of
COX in uterine smooth muscle
○ In clinical trials, ibuprofen was highly effective at promoting closure of the ductus arteriosus in preterm
infants
○ The drug produces less gastric bleeding and less inhibition of platelet aggregation than ASA
○ Ibuprofen is one of the safest NSAIDs to use with anticoagulants
• Acetaminophen Overdose
○ Can lead to severe liver injury and death
○ Intentional/unintentional Acetaminphen OD is the leading cause of acute liver failure (50% of all cases).
○ Risk for liver injury is increased by fasting, chronic alcohol use, and exceeding the 3500mg dose of
acetaminophen per day
○ s/s:
§ Principle feature of OD: hepatic necrosis
§ Early symptoms: N/V/D, sweating, abdominal pain
§ Severe poisoning can progress to: Hepatic failure, coma, death
§ Overt indications of Hepatic injury are not apparent until 48-72 hours after drug ingestion
○ Treatment:
§ Antidote: Acetylcysteine (Mucomyst)
□ Reduces injury by substituting depleted glutathione in the reaction that converts the toxic
metabolite of acetaminophen to its nontoxic form.
□ When given within 8 to 10 hours of acetaminophen ID, the drug is 100% effective at preventing
severe liver injury
□ Even when given as much as 24 hours after poisoning, it can still provide significant protection
□ Can be given PO or IV
• Drug Interactions with Acetaminophen
○ Alcohol
§ Regular alcohol consumption increases risk for liver injury if acetaminophen dosage is excessive.
□ First, alcohol induces synthesis of the p450 enzyme and increases production of
acetaminophen's toxic metabolite
□ Second, stores of glutathione are depleted in alcoholics and as a result the liver is unable to
convert the toxic metabolite to a nontoxic form.
□ Third, alcoholics often have pre-existing liver damage
§ Liver warning: product contains acetaminophen. Severe liver damage may occur if you take 3 or more
alcoholic drinks every day while using this product.
○ Warfarin
§ Increases the risk for bleeding when taken with warfarin d/t inhibition of warfarin metabolism, which
○ Vaccines
§ Blunts the immune response to childhood vaccines
Week 4: Midterm Study Guide
Thursday, May 22, 2025 9:24 AM
Week 4:
Chapter 59:
• General Information
○ COX Inhibitors have three useful effects:
§ Suppress inflammation
§ Relieve pain
§ Reduce fever
○ These effects are produced through the inhibition of COX, which is the enzyme responsible for the synthesis
of prostaglandins and related compounds.
• NSAIDs
○ AKA CycloOxygenase (COX) Inhibitors
○ Drugs that have anti-inflammatory properties
○ NSAIDs can be subdivided into two groups:
§ First generation NSAIDS
□ Conventional/traditional
□ Inhibit COX-1 and COX-2
□ These agents are unable to suppress pain and inflammation without posing a risk for serious
side effects
□ Used primarily for the treatment of inflammatory disorders, mild/moderate pain, fever
reducing, and dysmenorrhea
□ PROTOTYPE: Aspirin (ASA)
□ Black Box Warning: Increased risk for GI bleeding and cardiovascular events that can lead to
hospitalization or death.
§ Second Generation NSAIDS
□ Selective COX-2 inhibitors/coxibs
□ Only inhibit COX-2
□ In theory, these agents suppress pain and inflammation while causing fewer adverse effects.
□ However, these drugs appear even less safe than first-gen agents due to an increased risk for MI
and stroke.
• NSAIDs Adverse Effects
○ Serious adverse effects:
§ Gastric ulceration
§ Bleeding
§ Renal impairment
§ MI/Stroke (except ASA)
• NSAIDs Benefits of 2nd Gen
○ In theory can suppress pain and inflammation while causing fewer adverse effects, but in practice this is not
true as they increase the risk of MI and stroke the most of all NSAIDS
• NSAIDs: 1st Gen vs. 2nd Gen
• Nonacetylated Salicylates
○ Magnesium salicylate, sodium salicylate, and salsalate
○ Similarities to ASA:
§ Inhibit COX-1 and COX-2
§ Indicated for same uses
§ Most common adverse effects are GI disturbances
§ Should not be given to children with chickenpox or influenza d/t increase risk of Reye Syndrome
○ Contrasts to ASA:
§ Cause little to no suppression of platelet aggregation
§ Cannot protect against MI/Stroke and may increase the risk
§ Sodium Salicylate should be avoided in patients with sodium restrictions (HTN/HF)
, ○ Similarities to ASA: lOMoARcPSD|70468202
§ Inhibit COX-1 and COX-2
§ Indicated for same uses
§ Most common adverse effects are GI disturbances
§ Should not be given to children with chickenpox or influenza d/t increase risk of Reye Syndrome
○ Contrasts to ASA:
§ Cause little to no suppression of platelet aggregation
§ Cannot protect against MI/Stroke and may increase the risk
§ Sodium Salicylate should be avoided in patients with sodium restrictions (HTN/HF)
§ Magnesium Salicylate may be accumulate to toxic levels in patients with chronic renal insufficiency
§ Salsalate is a prodrug that breaks down to release two molecules of salicylate in the alkaline
environment of the small intestine and helps produce less gastric irritation that that of ASA
• Non-aspirin NSAIDs
○ Unlike ASA, these drugs cause reversible inhibition of COX
○ Primary indication for these drugs is RA and osteoarthritis along with mild/moderate pain, fever, bursitis,
tendinitis, and dysmenorrhea
○ Most NSAIDS are not proven to be save during pregnancy and should be discouraged for pregnant woman
○ These drugs do NOT protect against MI and stroke, in fact they increase the risk for a thrombotic event.
○ To minimize risk, these drugs should be used at lowest effect dosage for a short time
○ All NSAIDS can lead to the same adverse effects.
• NSAID: Ibuprofen
○ AKA: Advil, motrin, Caldolor
○ Prototype for propionic acid derivatives: ibuprofen
○ Inhibits COX and has all of the therapeutic effects of other NSAIDS
○ Ibuprofen is far superior to other NSAIDS for relief of primary dysmenorrhea, likely due to its inhibition of
COX in uterine smooth muscle
○ In clinical trials, ibuprofen was highly effective at promoting closure of the ductus arteriosus in preterm
infants
○ The drug produces less gastric bleeding and less inhibition of platelet aggregation than ASA
○ Ibuprofen is one of the safest NSAIDs to use with anticoagulants
• Acetaminophen Overdose
○ Can lead to severe liver injury and death
○ Intentional/unintentional Acetaminphen OD is the leading cause of acute liver failure (50% of all cases).
○ Risk for liver injury is increased by fasting, chronic alcohol use, and exceeding the 3500mg dose of
acetaminophen per day
○ s/s:
§ Principle feature of OD: hepatic necrosis
§ Early symptoms: N/V/D, sweating, abdominal pain
§ Severe poisoning can progress to: Hepatic failure, coma, death
§ Overt indications of Hepatic injury are not apparent until 48-72 hours after drug ingestion
○ Treatment:
§ Antidote: Acetylcysteine (Mucomyst)
□ Reduces injury by substituting depleted glutathione in the reaction that converts the toxic
metabolite of acetaminophen to its nontoxic form.
□ When given within 8 to 10 hours of acetaminophen ID, the drug is 100% effective at preventing
severe liver injury
□ Even when given as much as 24 hours after poisoning, it can still provide significant protection
□ Can be given PO or IV
• Drug Interactions with Acetaminophen
○ Alcohol
§ Regular alcohol consumption increases risk for liver injury if acetaminophen dosage is excessive.
□ First, alcohol induces synthesis of the p450 enzyme and increases production of
acetaminophen's toxic metabolite
□ Second, stores of glutathione are depleted in alcoholics and as a result the liver is unable to
convert the toxic metabolite to a nontoxic form.
□ Third, alcoholics often have pre-existing liver damage
§ Liver warning: product contains acetaminophen. Severe liver damage may occur if you take 3 or more
alcoholic drinks every day while using this product.
○ Warfarin
§ Increases the risk for bleeding when taken with warfarin d/t inhibition of warfarin metabolism, which
○ Vaccines
§ Blunts the immune response to childhood vaccines
