Alcohol Metabolism and Liver Disease

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Questions and Answers

What percentage of absorbed lead remains in the blood after exposure?

  • 50-60%
  • 15-20%
  • 5-10% (correct)
  • 80-85%

Which of the following conditions is linked to chronic arsenic exposure?

  • Radiodense deposits in epiphyses
  • Microcytic hypochromic anemia
  • Basophilic stippling
  • Hyperpigmentation and hyperkeratosis (correct)

Which symptom is NOT characteristic of lead poisoning?

  • Abdominal pain
  • Encephalopathy
  • Memory loss
  • Cerebral palsy (correct)

Which pathologic feature is associated with lead poisoning in the blood?

<p>Basophilic stippling (A)</p> Signup and view all the answers

What primary disease results from fetal exposure to mercury?

<p>Minamata disease (C)</p> Signup and view all the answers

At which blood alcohol level is a person likely to experience slurred speech and poor judgment?

<p>200 mg/dL (C)</p> Signup and view all the answers

Which of the following statements about blood alcohol levels and their effects is accurate?

<p>200 mg/dL correlates with irritability and motor incoordination. (B)</p> Signup and view all the answers

Which process is primarily responsible for metabolizing ethanol in the body?

<p>Oxidation of ethanol to acetaldehyde (B)</p> Signup and view all the answers

What is the consequence of prolonged high blood alcohol levels on cognitive functions?

<p>Significant decrease in cognitive functions (B)</p> Signup and view all the answers

What blood alcohol concentration is often categorized as light coma and depressed vital signs?

<p>300 mg/dL (C)</p> Signup and view all the answers

Which of the following is most likely a result of acute ethanol consumption at high levels?

<p>Risk of death (C)</p> Signup and view all the answers

What condition can result from the oxidation of ethanol to acetaldehyde?

<p>Asian flush syndrome (C)</p> Signup and view all the answers

What effect does a blood alcohol level of 80 mg/dL generally have on motor performance?

<p>Mild decrease in performance (A)</p> Signup and view all the answers

What biochemical change primarily leads to fatty change in the liver due to alcohol consumption?

<p>Excess NADH over NAD stimulates lipid biosynthesis (B)</p> Signup and view all the answers

Which syndrome is primarily associated with thiamine (Vit B1) deficiency due to alcohol abuse?

<p>Wernicke syndrome (B)</p> Signup and view all the answers

What is a major consequence of acetaldehyde formation in individuals abusing alcohol?

<p>Impaired microtubule function (A)</p> Signup and view all the answers

Which organ system is NOT typically affected by ethanol toxicity?

<p>Integumentary system (B)</p> Signup and view all the answers

In the chronic consumption of alcohol, which of the following is a primary mechanism of alcoholic liver disease?

<p>Increased oxidative stress (D)</p> Signup and view all the answers

Which nutritional deficiency is strongly associated with Korsakoff syndrome in chronic alcoholics?

<p>Thiamine deficiency (D)</p> Signup and view all the answers

What is a typical lesion in the nervous system caused by chronic alcohol consumption?

<p>Wernicke syndrome (A)</p> Signup and view all the answers

What condition may result from the toxic effects of alcohol on the gastrointestinal tract?

<p>Pancreatitis (B)</p> Signup and view all the answers

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Study Notes

Alcohol Metabolism and Effects

  • Alcohol dehydrogenase (ADH) oxidation occurs in the cytosol.
  • Cytochrome P-450 system, particularly CYP2E1 isoform, is located in the endoplasmic reticulum (ER).
  • Catalase is found in peroxisomes, aiding in alcohol oxidation.
  • Aldehyde dehydrogenase (ALDH) oxidizes acetaldehyde in mitochondria.

Alcohol and the Liver

  • Fatty change affects over 90% of chronic alcohol drinkers, leading to fatty liver.
  • Alcoholic hepatitis occurs in 10-15% of alcoholics.
  • Alcoholic cirrhosis is a severe liver disease due to prolonged alcohol intake.

Biochemical Effects of Fatty Change

  • Increased catabolism of fat in peripheral tissues and elevated delivery of free fatty acids to the liver.
  • An excess of NADH stimulates lipid biosynthesis.
  • Mitochondrial fatty acid oxidation is reduced.
  • Acetaldehyde binds to tubulin, impairing microtubule function and reducing lipoprotein transport from the liver.
  • Wernicke syndrome arises from thiamine (Vitamin B1) deficiency.
  • Korsakoff syndrome features memory loss and confabulation.
  • Cerebellar degeneration and peripheral neuropathy can also be attributed to thiamine deficiency.

Mechanisms of Disease from Ethanol Abuse

  • Liver Lesions: Fatty change, acute hepatitis, and cirrhosis caused by toxicity.
  • Nervous System: Wernicke syndrome (thiamine deficiency), Korsakoff syndrome (toxic effects), cerebellar degeneration (nutritional deficiency), and peripheral neuropathy (thiamine deficiency).
  • Cardiovascular System: Alcohol can lead to cardiomyopathy and hypertension due to toxicity.
  • Gastrointestinal Tract: Alcohol causes gastritis and pancreatitis through toxic effects.
  • Skeletal Muscle: Rhabdomyolysis is also induced by toxicity.
  • Reproductive System: Alcohol consumption can lead to testicular atrophy.

Effects of Blood Alcohol Levels

  • Blood alcohol level of 20 mg/dL results in decreased inhibitions and mild intoxication.
  • At 80 mg/dL, complex cognitive functions and motor performance decrease markedly.
  • A level of 200 mg/dL shows slurred speech, motor incoordination, irritability, and poor judgment.
  • At 300 mg/dL, light coma may occur alongside depressed vital signs.
  • A blood level of 400 mg/dL can result in death.

Lead Toxicity

  • Common sources include lead-contaminated air, food, old house paints, soil, and gasoline.
  • 80-85% of absorbed lead accumulates in bone and developing teeth.
  • Blood shows microcytic hypochromic anemia and basophilic stippling as pathologic features.
  • Nervous system effects include memory loss and encephalopathy.
  • Gastrointestinal symptoms include abdominal pain, while kidney effects present as chronic tubulointerstitial disease.

Mercury Exposure

  • Minamata disease is a severe outcome of mercury exposure, leading to cerebral palsy, deafness, blindness, and significant CNS defects during fetal development.

Arsenic Toxicity

  • Acute exposure results in central nervous system damage, often progressing to death by disrupting mitochondrial oxidative phosphorylation.
  • Chronic exposure leads to skin hyperpigmentation and hyperkeratosis.

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