Analgesic and Anti-inflammatory Drugs Quiz

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Questions and Answers

What is the primary mechanism of N-acetyl Cysteine (NAC) in treating acetaminophen toxicity?

Enhances renal excretion of acetaminophen through increased diuresis

Inhibits the absorption of acetaminophen in the gastrointestinal tract

Increases hepatic levels of glutathione to detoxify harmful metabolites (correct)

Directly neutralizes acetaminophen in the bloodstream

What is the maximum recommended dose of acetaminophen that could potentially be fatal?

25 g

10 g

15 g (correct)

20 g

Which combination of treatments is NOT considered effective for acetaminophen overdose?

Emesis using syrup of ipecac (correct)

Gastric lavage and supportive measures

Activated charcoal and MDAC after NAC

Intravenous fluids and renal dialysis

What is an essential step in the treatment of acetaminophen overdose regarding the timing of NAC administration?

Must be initiated within 1 hour of ingestion Signup and view all the answers

What is the role of liver function tests in the context of acetaminophen overdose?

To determine the extent of hepatic necrosis and damage Signup and view all the answers

What is the primary therapeutic action of acetaminophen?

Analgesic and antipyretic effects Signup and view all the answers

Which phase of acetaminophen poisoning is characterized by gastrointestinal symptoms?

Phase I Signup and view all the answers

In an overdose scenario, what happens to the conjugation pathways of acetaminophen?

They become saturated, increasing toxic metabolites. Signup and view all the answers

Which organ is primarily affected by the toxic action of acetaminophen?

Liver Signup and view all the answers

What clinical signs indicate Phase III of acetaminophen poisoning?

Liver failure and jaundice Signup and view all the answers

What is the main hazard associated with acetaminophen overdosing?

Liver damage Signup and view all the answers

What happens to glutathione levels during acetaminophen overdose?

They become depleted. Signup and view all the answers

What is the prognosis for acetaminophen poisoning after 7-10 days?

May show resolution of hepatic dysfunction. Signup and view all the answers

What is the predominant early acid-base disturbance in salicylate poisoning?

Respiratory alkalosis Signup and view all the answers

Which of the following is NOT a contributing factor to dehydration in metabolic disorders?

Excessive fluid intake Signup and view all the answers

In the context of salicylate poisoning, what is the fatal dose for adults?

390 mg/kg BW Signup and view all the answers

What treatment method is considered most effective for the elimination of salicylates from the gastrointestinal tract?

Whole bowel irrigation Signup and view all the answers

What is a common cause of death within the first 12-24 hours of salicylate poisoning?

Central respiratory failure Signup and view all the answers

Which laboratory investigation is primarily used to assess the severity of salicylate poisoning?

Blood salicylate level Signup and view all the answers

What electrolyte imbalance is commonly observed in patients with metabolic disorders related to salicylate toxicity?

Hypokalemia Signup and view all the answers

What supportive measure is essential in the management of salicylate poisoning?

Establishing airway, cardiovascular, and respiratory support Signup and view all the answers

What adverse effect on the gastrointestinal tract is commonly associated with salicylate poisoning?

Gastric erosion and ulceration Signup and view all the answers

Which of the following mechanisms of action is primarily responsible for the therapeutic effects of salicylates?

Inhibition of prostaglandin biosynthesis Signup and view all the answers

What is the typical clinical presentation of hypersensitivity reactions caused by salicylates?

Urticaria and skin rash Signup and view all the answers

How does salicylate poisoning affect prothrombin synthesis?

Increases prothrombin time Signup and view all the answers

Which of the following symptoms is most indicative of aspirin toxicity related to the central nervous system?

Excitability and delirium Signup and view all the answers

What renal complication is commonly associated with salicylate poisoning?

Renal tubular necrosis Signup and view all the answers

Which symptom is associated with salicylism, a condition resulting from high doses of salicylates?

High-pitched tinnitus Signup and view all the answers

In what way does salicylate poisoning lead to hyperthermia?

Uncoupling of oxidative phosphorylation Signup and view all the answers

Study Notes

Analgesic, Antipyretic and Anti-inflammatory Drugs

Salicylates are potentially life-threatening if ingested.
Common household aspirin is a major source of salicylate poisoning.
Available salicylate preparations include aspirin (acetyl salicylic acid), various cold preparations, and topical preparations like methyl salicylate (oil of wintergreen) and salicylic acid.

Salicylates - Conditions of Poisoning

Accidental: Children may ingest salicylates accidentally, sometimes mistaking an overdose of aspirin for a fever treatment. Elderly patients can experience chronic toxicity due to altered metabolic elimination.
Suicidal: Young adolescents may attempt suicide using salicylates, typically resulting in morbidity rather than mortality due to large fatal doses.

Salicylates - Mechanism of Action

Therapeutic: Therapeutic salicylate levels result in anti-inflammatory, analgesic, and antipyretic effects, primarily by inhibiting prostaglandin biosynthesis.
Toxic: Toxic action manifests in the gastrointestinal tract (GIT) with symptoms like burning mouth/throat pain, nausea, vomiting, gastric erosion, ulceration, and GIT bleeding, especially hematemesis.

Salicylates - Other Toxic Effects

Hematology: Bleeding tendencies due to inhibition of prothrombin synthesis (prothrombin time) and platelet function (increased bleeding time).
Hypersensitivity (Allergy): Symptoms like urticaria (skin rash), bronchial asthma, and angioneurotic edema.
Central Nervous System (CNS): Central stimulation, restlessness, excitability, delirium, and convulsions (due to increased CO2). Coma in severe cases, due to vasomotor and respiratory center inhibition.
Kidney: Renal compromise due to direct aspirin-induced renal tubular necrosis (leading to uremia), and indirect effects like decreased renal perfusion due to dehydration.
Hyperthermia: Occurs due to oxidative phosphorylation uncoupling, and subsequent increased cellular metabolic rate, associated with sweating and vomiting. Dehydration can also occur.
Salicylism: High-pitched tinnitus, vertigo, and deafness may occur with therapeutic or toxic doses, due to 8th cranial nerve involvement. This is usually reversible.
Liver: May show mild liver necrosis.
Metabolic Disorders: Initially, there's a short period of hyperglycemia (due to glycolysis). Later, hypoglycemia occurs due to glycogen depletion.
Fluid and Electrolyte Disturbances: Dehydration occurs due to increased metabolic rate and hyperthermia (sweating). Vomiting and hyperventilation contribute to this. Hypokalemia might happen due to potassium loss in urine.
Acid-base Imbalance: Respiratory alkalosis is the main manifestation. Increased CNS and respiratory center stimulation leads to increased rate/depth of respiration, reduced plasma CO2, reduced carbonic acid, and increased HCO3/H2CO3 ratio; leading to an elevated blood pH.

Salicylates - Fatal Dose and Causes of Death

Fatal Dose: 390 mg/kg body weight (BW). (A typical aspirin tablet contains 320 mg acetyl salicylic acid; 60-70 tablets would be fatal.)
Fatal Serum Level: >100 mg %.
Early (12-24 hrs): Central respiratory failure and cardiac arrhythmias (acidosis).
Delayed (few days): Renal failure and hemorrhage.

Salicylates - Investigations

Blood salicylate levels to assess poisoning severity (not immediately)
Coagulation profile (prothrombin time/concentration and bleeding time)
Arterial pH, CO2, HCO3, and potassium (K) to assess acid-base balance.
Kidney and liver function tests.
X-ray to possibly visualize aspirin concretions in the stomach.

Salicylates - Treatment

Supportive measures (ABCs: Airway, Breathing, Circulation) - establish adequate airway, cardiovascular, and respiratory support.
GIT decontamination (e.g., emesis, gastric lavage, activated charcoal). Saline cathartics may aid in elimination from GIT.
Excretion of the poison (forced alkaline diuresis for moderate toxicity; hemodialysis for severe cases and/or renal dysfunction)

Paracetamol (Acetaminophen) - Introduction

Acetaminophen (APAP) is a coal tar analgesic, a major active metabolite of phenacetin and acetanilide.
It is a common cause of poisoning.

Paracetamol - Conditions of Poisoning

Accidental: Especially common in children.
Suicidal: Rare.

Paracetamol - Mechanism of Action (Toxic effect)

Therapeutic: Similar to aspirin concerning analgesic and antipyretic properties by inhibiting central prostaglandin (PG) synthesis. Anti-inflammatory effects of APAP are relatively weak.
Toxic (Liver): The main hazard of APAP overdose is liver damage. Excess APAP saturates the conjugation pathways causing an increase in toxic metabolite, overwhelming the glutathione detoxification mechanism (which depletes glutathione stores). The toxic metabolite then binds to -SH groups of hepatic cellular proteins, leading to centrilobular necrosis.

Paracetamol - Toxic Effects (Other)

Kidneys: Tubular necrosis.

Paracetamol - Clinical Presentations

Phase 1 (0.5-24 hrs): GIT symptoms (malaise, diaphoresis, nausea, vomiting, drowsiness).
Phase 2 (24-72 hrs): Recovery or apparent recovery with blood chemistry changes (pain/tenderness in the right hypochondrium; altered liver function tests, increased serum enzymes (AST, ALT, LDH), bilirubin; prolonged prothrombin time).
Phase 3 (72-96 hrs): Fulminant liver failure (jaundice, coagulation defects, encephalopathy, altered consciousness). This phase is potentially reversible if treated rapidly.
Phase 4 (7-10 days): Recovery- resolution of hepatic dysfunction and complete recovery within 3-6 months, unless severe multi-organ failure occurs.

Paracetamol - Fatal Dose and Causes of Death

Fatal Dose: 15 g (a tablet typically contains 325-500 mg)
Causes of death vary depending on the severity and time interval following the overdose.

Paracetamol - Investigations

Serum APAP level to assess toxicity.
Liver function tests and prothrombin time.
Kidney function tests.

Paracetamol - Treatment

Supportive measures (ABCs).
GIT decontamination (e.g., emesis, gastric lavage, activated charcoal)
Prevent absorption (activated charcoal, MDAC)
Excretion (hemodialysis for renal failure)
Specific antidote: N-acetylcysteine (NAC). It is the only proven method to prevent hepatic necrosis. Initial high dose followed by maintenance doses. Other possible antidotes such as cimetidine or methionine are not proven to be as effective as NAC.
Symptomatic treatment (e.g., liver support with dextrose, sorbitol).

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Description

Test your knowledge on analgesic, antipyretic, and anti-inflammatory drugs, focusing on salicylates such as aspirin. Understand the potential poisoning risks and the mechanisms through which these medications operate. This quiz covers both therapeutic uses and conditions of toxicity related to salicylates.