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    Alcoholism

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    medkyuti Qt
    The document discusses alcoholism, liver cirrhosis, and systemic carnitine deficiency. It provides details on: 1) The physiological effects of alcohol intoxication on the brain and the mechanism behind alcoholics developing hypoglycemia. 2) The mechanism behind hepatic encephalopathy and hepatic coma in liver cirrhosis, which involves high ammonia levels damaging the central nervous system. 3) The genetic basis and biochemical effects of systemic carnitine deficiency, which is caused by mutations preventing carnitine transport and leading to defective fatty acid oxidation and hypoglycemia during fasting.

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    Alcoholism

    Uploaded by

    medkyuti Qt
    18 views2 pages
    The document discusses alcoholism, liver cirrhosis, and systemic carnitine deficiency. It provides details on: 1) The physiological effects of alcohol intoxication on the brain and the mechanism behind alcoholics developing hypoglycemia. 2) The mechanism behind hepatic encephalopathy and hepatic coma in liver cirrhosis, which involves high ammonia levels damaging the central nervous system. 3) The genetic basis and biochemical effects of systemic carnitine deficiency, which is caused by mutations preventing carnitine transport and leading to defective fatty acid oxidation and hypoglycemia during fasting.

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    The document discusses alcoholism, liver cirrhosis, and systemic carnitine deficiency. It provides details on: 1) The physiological effects of alcohol intoxication on the brain and the mechanism behind alcoholics developing hypoglycemia. 2) The mechanism behind hepatic encephalopathy and hepatic coma in liver cirrhosis, which involves high ammonia levels damaging the central nervous system. 3) The genetic basis and biochemical effects of systemic carnitine deficiency, which is caused by mutations preventing carnitine transport and leading to defective fatty acid oxidation and hypoglycemia during fasting.

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    18 views2 pages

    Alcoholism

    Uploaded by

    medkyuti Qt
    The document discusses alcoholism, liver cirrhosis, and systemic carnitine deficiency. It provides details on: 1) The physiological effects of alcohol intoxication on the brain and the mechanism behind alcoholics developing hypoglycemia. 2) The mechanism behind hepatic encephalopathy and hepatic coma in liver cirrhosis, which involves high ammonia levels damaging the central nervous system. 3) The genetic basis and biochemical effects of systemic carnitine deficiency, which is caused by mutations preventing carnitine transport and leading to defective fatty acid oxidation and hypoglycemia during fasting.

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    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    of 2

    Alcoholism & Liver Cirrhosis Guide Questions:

    1. What causes inebriation after alcohol ingestion? 


    - Inebriation is synonymous with alcohol intoxication, which is the negative behavior and
    physical effects after overconsumption of alcohol or ethanol. This is a physiologic state
    wherein it is induced by alcohol consumption. As we all know, ethanol or alcohol is an
    inhibitory neurotransmitter and it is believed that it mimics GABA’s effect in the brain, thus,
    reducing signal flow in the brain. It also facilitates the operation of inhibitory
    neurotransmitters like GABA. That is why this dual effect makes it harder for the brain to do
    its normal function.

    2. Why are alcoholics susceptible to the development of hypoglycemia?


    - When alcohol is consumed, it can inhibit the liver’s ability to release glucose into the blood.
    When gluconeogenesis is inhibited, it would eventually leads to hypoglycemia. As we all
    know that too much NADH would favor lactic acid production, hence, pyruvate is directed to
    undergo anaerobic glycolysis pathways, depleting all pyruvate and none would enter the
    Kreb’s cycle, resulting in absence of ATP production.

    3. What is the mechanism behind the development of hepatic coma in liver cirrhosis?         
    - Hepatic encephalopathy is the impairment of brain function as a result of liver cirrhosis.
    This impairment affects behavior, mood, speech, and sleep cycle. Hyperammonaemia plays
    the important role in the pathogenesis of Hepatic encephalopathy. The brain-blood barrier
    disturbances, changes in neurotransmission, neuroinflammation, oxidative stress, and
    benzodiazepine pathway abnormalities are considered to be involved in the development of
    Hepatic encephalopathy.
    - Hepatic encephalopathy has 4 stages wherein it can lead to hepatic coma when left
    untreated. High ammonia levels are toxic to the central nervous system which is why hepatic
    encephalopathy may further lead to hepatic coma.
    Systemic Carnitine Deficiency Guide Questions:

    1. What is the genetic basis for ”systemic carnitine deficiency” (SCD)?

    - Systemic Carnitine Deficiency is an autosomal recessive disorder that prevents the body from
    utilizing fats for energy production during the fasting state.  

    - This disorder is caused by a mutation in the SLC22A5 gene wherein this gene is one that
    provides instructions for making a protein called OCTN2 that is found in the heart, liver, muscles,
    kidneys, and other tissues. This protein is positioned within the cell membrane and it is important
    because it transports carnation into the cell. Once this gene is mutated, this can result in the
    improper transfer of carnitine across the cell membrane resulting in urinary carnitine wasting
    which will lead to a low plasma level of carnitine and decreased intracellular carnitine
    accumulation. Hence, it impairs the entry of long-chain fatty acids into the mitochondrial matrix.
    According to Li et al, there are approximately half of the missense mutations while the other half
    are composed of splice site, nonsense, and deletion or insertion mutations, which results in
    dysfunctional OCTN2 gene product and decreased carnitine transport in various tissues.

    2. What is the biochemical basis for the outstanding manifestations of patients with SCD?

    * During periods of fasting, our body’s predominant source of energy production is fatty acids. In
    patients with Systemic Carnitine Deficiency, there is deficient carnitine, thus, it will result in
    defective fatty acid oxidation. When fat cannot be utilized, glucose is consumed without
    regeneration via gluconeogenesis resulting in hypoglycemia. In addition to that, there will be
    released fat from adipose tissue which will result in the accumulation of fats in the liver, skeletal
    muscle, and heart resulting in hepatic steatosis and myopathy.

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