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    Paracetamol Pharmacology and Toxicity

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    Harshini Chandrabose
    This document summarizes the pharmacology, uses, and toxicity of paracetamol. It notes that paracetamol is an analgesic-antipyretic with weak anti-inflammatory effects that acts primarily in the brain. It is well absorbed orally and metabolized in the liver before being excreted by the kidneys. Common uses include headaches, musculoskeletal pain, and fever reduction, especially in children. Toxicity occurs when very large doses overwhelm the liver's metabolic pathways, depleting glutathione and causing liver and kidney damage through reactive metabolites. Symptoms of toxicity can appear 12-24 hours after ingestion and recovery may take months.

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    Paracetamol Pharmacology and Toxicity

    Uploaded by

    Harshini Chandrabose
    22 views6 pages
    This document summarizes the pharmacology, uses, and toxicity of paracetamol. It notes that paracetamol is an analgesic-antipyretic with weak anti-inflammatory effects that acts primarily in the brain. It is well absorbed orally and metabolized in the liver before being excreted by the kidneys. Common uses include headaches, musculoskeletal pain, and fever reduction, especially in children. Toxicity occurs when very large doses overwhelm the liver's metabolic pathways, depleting glutathione and causing liver and kidney damage through reactive metabolites. Symptoms of toxicity can appear 12-24 hours after ingestion and recovery may take months.

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    This document summarizes the pharmacology, uses, and toxicity of paracetamol. It notes that paracetamol is an analgesic-antipyretic with weak anti-inflammatory effects that acts primarily in the brain. It is well absorbed orally and metabolized in the liver before being excreted by the kidneys. Common uses include headaches, musculoskeletal pain, and fever reduction, especially in children. Toxicity occurs when very large doses overwhelm the liver's metabolic pathways, depleting glutathione and causing liver and kidney damage through reactive metabolites. Symptoms of toxicity can appear 12-24 hours after ingestion and recovery may take months.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    22 views6 pages

    Paracetamol Pharmacology and Toxicity

    Uploaded by

    Harshini Chandrabose
    This document summarizes the pharmacology, uses, and toxicity of paracetamol. It notes that paracetamol is an analgesic-antipyretic with weak anti-inflammatory effects that acts primarily in the brain. It is well absorbed orally and metabolized in the liver before being excreted by the kidneys. Common uses include headaches, musculoskeletal pain, and fever reduction, especially in children. Toxicity occurs when very large doses overwhelm the liver's metabolic pathways, depleting glutathione and causing liver and kidney damage through reactive metabolites. Symptoms of toxicity can appear 12-24 hours after ingestion and recovery may take months.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
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    of 6

    Paracetamol Pharmacology

    and Toxicity
    Pharmacology
    ❖ Type : NSAIDS - Analgesic-antipyretics with poor anti-in ammatory action
    ❖ Action: It raises pain threshold, but has weak peripheral anti-in ammatory
    component. It is a poor inhibitor of PG synthesis in peripheral tissues, but more
    active on COX in the brain. The ability of paracetamol to inhibit COX-3 could also
    account for its analgesic- antipyretic action.
    ❖ Pharmacokinetics: Absorption: is well absorbed orally. Distribution: Equally in the
    body. Metabolism: Conjugation with glucuronic acid and sulfate in Liver.
    Excretion: By kidney. Plasma t1⁄2 is 2–3 hours. Effects after an oral dose last for 3–5
    hours.
    ❖ Adverse effects: Nausea and rashes occur occasionally, leukopenia is rare.

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    Uses
    ❖ Analgesic for headache, mild migraine, musculoskeletal pain, dysmenorrhoea,
    etc.
    ❖ It is one of the best drugs to be used as antipyretic, especially in children (no
    risk of Reye’s syndrome).
    ❖ Dose to dose it is equally ef cacious as aspirin for non-in ammatory conditions.
    ❖ Dose: 325–650 mg (children 10–15 mg/kg) 3–5 times a day.
    ❖ Paracetamol is not recommended in premature infants (< 2 kg) for fear of
    hepatotoxicity.
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    Toxicity
    ❖ The toxic dose is usually >200 mg/kg in children below 12-yr-old. Hepatic damage after
    paracetamol overdose usually begins at >150 mg/ kg.
    ❖ Mechanism of toxicity: When a very large dose of paracetamol is taken, glucuronidation capacity
    is saturated, hepatic glutathione is depleted and the metabolite (N-acetyl-p-benzoquinoneimine)
    binds covalently to proteins in liver cells (and renal tubules) causing necrosis.
    1. Stage I (12-24 hr): Nausea, vomiting and cold sweats
    2. Stage II (24-48 hr): Clinical recovery with biochemical evidence of hepatorenal injury
    3. Stage III (48-96 hr): Peak hepatotoxicity
    4. Stage IV (7-8 days): Recovery is heralded by return of consciousness and improvement in the
    hepatic function tests. Histological recovery may take up to 3 months.
    5. Death may occur within 2-7 days of ingestion.
    References:
    ❖ Essential Paediatrics Edition 8 by OP GHAI
    ❖ Essentials of Medical Pharmacology Seventh Edition by KD TRIPATHI
    Thankyou

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