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Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

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Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
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Phase II Reactions: Acetylation Reactions01:24

Phase II Reactions: Acetylation Reactions

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Acetylation, a phase II biotransformation reaction, introduces an acetyl group to drugs or their metabolites. Acetyltransferase enzymes facilitate this reaction, which resembles α-amino acid conjugation due to the addition of a functional group to the drug molecule.
The substrates for acetylation are typically drugs or their metabolites with an amino, sulfonamide, or hydrazine functional group. Acetylation can occur at several points in the drug molecule, including primary, secondary, and...
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Hepatic Drug Excretion: Enterohepatic Cycling01:17

Hepatic Drug Excretion: Enterohepatic Cycling

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Enterohepatic cycling involves the active secretion of drugs and their metabolites into the bile via transporters in the canalicular membrane of hepatocytes. This secretion is an integral part of the digestive process, releasing these substances into the gastrointestinal (GI) tract.
Post-release drugs and metabolites can be reabsorbed into the body from the intestine. For conjugated metabolites like glucuronides, reabsorption requires enzymatic hydrolysis by intestinal microflora. This...
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Hepatitis01:25

Hepatitis

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Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver.
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Hepatic Encephalopathy01:29

Hepatic Encephalopathy

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DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic...
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Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

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Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
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Related Experiment Video

Updated: May 7, 2026

Creation of Reversible Cholestatic Rat Model
09:39

Creation of Reversible Cholestatic Rat Model

Published on: May 22, 2011

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Reversible cholestatic hepatitis caused by acetohexamide.

J M Rank1, R C Olson

  • 1University of Minnesota Hospital, Minneapolis.

Gastroenterology
|June 1, 1989
PubMed
Summary

Acetohexamide use can cause cholestatic hepatitis with eosinophilia. Discontinuing the drug led to rapid recovery, normalizing liver function and eosinophil counts.

Area of Science:

  • Hepatology
  • Clinical Pharmacology

Background:

  • Drug-induced liver injury (DILI) is a significant concern in clinical practice.
  • Cholestatic hepatitis is a pattern of liver damage characterized by impaired bile flow.
  • Eosinophilia, an increase in eosinophils, can be associated with various conditions, including drug reactions.

Observation:

  • A patient developed acute cholestatic hepatitis and jaundice, accompanied by fever and elevated eosinophil levels in the blood and liver.
  • The patient had been taking acetohexamide, an oral hypoglycemic agent, for 1.5 years.
  • Symptoms appeared acutely after a prolonged period of drug exposure.

Findings:

  • Discontinuation of acetohexamide resulted in the complete resolution of liver damage.
  • Liver enzymes, bilirubin levels, and peripheral eosinophil counts promptly normalized after drug withdrawal.

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  • Histopathological evidence of hepatic eosinophilia also resolved.
  • Implications:

    • This case highlights acetohexamide as a potential cause of drug-induced cholestatic hepatitis with eosinophilia.
    • Early recognition and drug discontinuation are crucial for favorable outcomes in DILI.
    • Monitoring liver function and eosinophil counts may be warranted in patients on long-term acetohexamide therapy.