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Questions and Answers
What is the elimination half-life of ibuprofen after absorption?
What is the elimination half-life of ibuprofen after absorption?
How long does it take for a single therapeutic dose of ibuprofen to be completely eliminated from the body?
How long does it take for a single therapeutic dose of ibuprofen to be completely eliminated from the body?
What happens to the elimination half-life of ibuprofen during an acute overdose?
What happens to the elimination half-life of ibuprofen during an acute overdose?
Which of the following statements about ibuprofen metabolism is incorrect?
Which of the following statements about ibuprofen metabolism is incorrect?
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Which duration most accurately reflects the elimination timeline of a therapeutic dose of ibuprofen?
Which duration most accurately reflects the elimination timeline of a therapeutic dose of ibuprofen?
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What effect do salicylates have on blood glucose levels?
What effect do salicylates have on blood glucose levels?
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What is the ultimate consequence of salicylate interference with glucose regulation?
What is the ultimate consequence of salicylate interference with glucose regulation?
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Which physiological process is directly affected by the presence of salicylates?
Which physiological process is directly affected by the presence of salicylates?
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What condition results from the depletion of glucose stores due to salicylates?
What condition results from the depletion of glucose stores due to salicylates?
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How do salicylates impact amino acids in the body?
How do salicylates impact amino acids in the body?
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What physiological response is expected as a result of salicylate poisoning?
What physiological response is expected as a result of salicylate poisoning?
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Which of the following best describes the acid-base status in salicylate poisoning?
Which of the following best describes the acid-base status in salicylate poisoning?
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What is the primary goal of managing salicylate poisoning?
What is the primary goal of managing salicylate poisoning?
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What symptom most likely indicates respiratory alkalosis in a patient with salicylate poisoning?
What symptom most likely indicates respiratory alkalosis in a patient with salicylate poisoning?
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In the management of salicylate poisoning, which of the following methods is NOT typically employed?
In the management of salicylate poisoning, which of the following methods is NOT typically employed?
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Study Notes
Clinical Toxicology - Salicylates
- Aspirin poisoning affects people of all ages
- Children are more susceptible to accidental ingestion
- Adult salicylate toxicity is often due to chronic misuse or intentional large doses
- Children are at greatest risk for severe complications after salicylate poisoning
Mechanism of Salicylate Toxicity
- CNS stimulation occurs with salicylate intoxication
- Respiratory center stimulation can occur indirectly by increasing PCO2 production, enhancing oxygen consumption, leading to hyperthermia and hyperpnea
- Respiratory center stimulation can also occur directly by increasing respiration depth and rate, resulting in decreased plasma CO2 (alkalosis)
- Kidneys attempt to compensate for acid-base imbalances by excreting more bicarbonate and retaining non-bicarbonate anions, which leads to metabolic acidosis
- Salicylate toxicity also uncouples oxidative phosphorylation, reducing ATP production, and causing metabolic acidosis, leading to increased glycolysis
Salicylate Toxicity - Continued
- Body utilizes glycogen stores, then shifts to lipid metabolism, leading to increased free fatty acids and ketone bodies, potentially causing ketoacidosis
- Amino acid metabolism is inhibited, leading to amino acid accumulation
- Salicylates interfere with normal blood glucose levels, eventually depleting glucose stores and resulting in hypoglycemia
- High doses of salicylates lead to a switch from first-order to zero-order kinetics in metabolism with a constant degradation rate, regardless of dose, resulting in higher serum and tissue salicylate concentrations particularly in the CNS
Characteristics of Salicylate Poisoning
- Symptoms can include nausea, vomiting, tinnitus, headache, hyperpnea, neurologic abnormalities (confusion, hyperactivity, slurred speech, and convulsions), decreased PCO2, and respiratory alkalosis
Management of Salicylate Poisoning
- Removal of aspirin from the gastrointestinal tract is a primary step
- Correct metabolic acidosis, dehydration, hyperthermia, hypoglycemia, and hypokalemia are necessary
- Gastric decontamination, like emesis, is effective in children for removing toxins
Management of Salicylate Poisoning - Continued
- Dehydration is common and oral fluid replacement is essential, potentially transitioning to parenteral fluids in moderate to severe cases of toxicity
- Sodium bicarbonate is used to correct metabolic acidosis and alkalinize urine, enhancing salicylate excretion by the kidneys
- Potassium chloride is used to correct hypokalemia and prevent alkalosis from sodium bicarbonate administration
- Fever can be reduced with cold or tepid water
- Other symptomatic treatments include diazepam for seizures, calcium supplements for hypocalcemic tetany, and vitamin K for coagulation defects
Ibuprofen
- Ibuprofen is generally considered safe
- Rapidly metabolized after absorption with a short elimination half-life (approximately 2 hours)
- A single therapeutic dose is completely eliminated within 24 hours
- Acute overdose does not prolong the elimination half-life
- Acute renal failure may result from decreased production of intra-renal prostaglandins, decreasing renal blood flow and glomerular filtration rate
- Symptoms are minimal and manifest through gastrointestinal upset, such as nausea and vomiting
- Drowsiness, lethargy, or mild coma may occur but resolve within 24 hours even with high doses
- Treatment involves basic poison management, including supportive, symptomatic care
Vitamins
- Accidental vitamin poisoning, particularly in children under five, is a major concern
- Similar toxicity in adults has been observed, with reports increasing following the introduction of high doses
- With fat-soluble vitamins (A and D), toxicity manifestations are common
- Water-soluble vitamins (B-complex and vitamin C) generally cause minor adverse reactions, with the exception of vitamin C, which can cause renal toxicity.
- Vitamin K is rarely associated with toxicity, as it's often not included in over-the-counter products
Vitamin A
- Hypervitaminosis A can occur with large doses, potentially causing skin and other serious concerns
- Large doses during pregnancy can be teratogenic causing birth defects
- Toxicity causes protein saturation leading to degradation of cellular membranes.
- Vitamin A is primarily stored in hepatocytes. Large doses can be absorbed by Ito cells leading to fibroblast formation and hepatic pathology
Vitamin D
- Vitamin D is the most toxic of the vitamins
- Toxicity results in elevated plasma calcium levels and associated issues
- Chronic use can lead to the deposition of calcium in soft tissues, especially the kidneys and heart, significant for renal function and cardiac rhythm disturbances
- Treatment involves stopping vitamin intake, reducing calcium intake, administering glucocorticoids, and increasing fluid intake
Other Vitamins
- Vitamin K is not commonly a cause of toxicity, as it is rarely present in over-the-counter products
- Vitamin E has a low toxicity profile. Megadoses can cause headache, nausea, fatigue, dizziness, and vision problems
- Vitamin C toxicity is not common, but high doses can overwhelm pathways and lead to adverse effects
- Vitamin B1 (thiamine) toxicity is now less common with decreased use of parenteral forms, and symptoms range from nervousness, convulsions, and muscle weakness. Niacin (vitamin B3) use in high quantities leads to flushing and pruritus but more intense toxicity was noted in dosages greater than 30 g
- Vitamin B6 (pyridoxine) has rarely been associated with toxicity, typically due to a deficiency state
- Vitamin B12 (cyanocobalamin) can, in rarer cases, cause allergic reactions in individuals sensitive to injectable products
- Folic acid may lead to increased seizure frequency in epileptic patients.
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Description
This quiz covers the clinical aspects of salicylate toxicity, focusing on the effects of aspirin poisoning across different age groups. It discusses the mechanisms behind salicylate toxicity and the body's response, including the impact on the central nervous system and respiratory functions. Gain insights into the risks and complications associated with both accidental and intentional salicylate ingestion.
