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104 Theme 2 - Liver and Metabolism > Hypoglycaemia > Flashcards

Hypoglycaemia Flashcards

1
Q

What is hypoglycaemia?

A
  • Defined as a blood glucose level of below 4 mM (72 mg/dL)
  • Symptoms may develop at higher levels if there is rapid fall of previously elevated levels, although some individuals may show no effects even below 4 mM
  • A rapid fall in blood glucose may produce a phase of sweating, tachycardia and agitation due to activation of the sympathetic nervous system and release of adrenaline & glucagon
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2
Q

What are the symptoms of hypoglycaemia?

A
  • Symptoms: equivalent to cerebral anoxia and may include moodiness, faintness, numbness in arms and hands, blurred vision, confusion, memory loss, dizziness or lethargy that may progress to coma
  • Serious consequences of hypoglycaemia relate to effects on the brain – loss of cognitive function, seizures and coma
  • Loss of consciousness occurs at blood glucose levels of 2.5 mM (45 mg/dL)
  • Rapid restoration of blood glucose (by i.v. glucose or injection of glucagon) is essential and prolonged or repeated hypoglycaemia may result in permanent brain damage
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3
Q
A
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4
Q

What are the causes of hypoglycaemia?

A

Hypoglycaemia in healthy individuals is normally mild and may be due to fasting or exercise.

Other causes of hypoglycaemia include:

  • Hypernatraemia (e.g. diabetes insipidus)
  • Hypovolaemia from vomiting, dehydration, etc.
  • Pathologies such as adrenal insufficiency
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5
Q

What causes alcohol induced hypoglycaemia?

A
  • Develops several hours after alcohol ingestion
  • Occurs on depletion of glycogen stores when blood glucose is reliant on hepatic gluconeogenesis
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6
Q

What do alcohol induced hypoglycaemia cause?

A
  • In the short-term (24 hours): consumption of alcohol places additional stresses on gluconeogenesis, as alcohol is metabolised primarily in the liver by an unregulated process
  • In the long-term (years): gluconeogenesis may also be decreased by liver damage and reduced muscle mass (longer term)
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7
Q

How does metabolism of alcohol work?

A
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8
Q

What are the metabolic consequences of alcohol metabolism?

A
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9
Q

What are the symptoms of alcohol-induced hypoglycaemia?

A

Occurs as a result of ethanol ingestion when blood glucose levels are reliant on gluconeogenesis e.g. 12-24 hours after a meal when glycogen stores are depleted.

  • Fall in blood glucose leads to a stress response (rapid heart beat, clammy skin), in an effort to enhance the stimulation of gluconeogenesis by combined action of glucagon and adrenaline
  • Rapid breathing is a physiologic response to metabolic acidosis, resulting from excess of lactic acid
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10
Q

What are the effects of long term alcohol metabolism on lipid metabolism?

A
  • High levels of NADH inhibit fatty acid oxidation; instead the excess NADH signals that conditions are right for fatty acid synthesis
  • TGs accumulate in the liver causing a condition known as ‘fatty liver’. Also exported as VLDL.
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11
Q

Fatty liver disease can progress over time in 3 stages…

A
  1. The liver becomes inflamed causing damage to the liver tissue (also known as steatohepatitis).
  2. Scar tissue forms at sites of damage (known as fibrosis).
  3. Extensive scar tissue replaces healthy tissue (known as cirrhosis of the liver).
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12
Q

What are the effects of long term alcohol metabolism on effects on efficiency of ethanol metabolism?

A

Acetate produced from EtOH can be converted into acetyl-CoA

BUT further processing of acetyl-CoA in TCA cycle prevented because high levels of NADH inhibits both citrate synthase and α-ketoglutarate dehydrogenase

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13
Q

Accumulation of acetyl CoA has two consequences…

A
  1. Production of ketone bodies which are released into the blood and exacerbates the already acidic conditions resulting from high lactate levels
  2. Processing of acetate in the liver becomes inefficient, leading to build-up of acetaldehyde, which is highly toxic
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14
Q

What is Alcohol-induced hepatomegaly?

A

Alcohol-induced hepatomegaly (enlarged liver)

  • Alcohol consumption decreases the activity of the proteosome
  • Leads to accumulation of protein, which causes enlargement of the liver
  • Decreased proteosome activity also increases oxidative stress

*Note: this is just one reason why the liver could be enlarged

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15
Q

What is Alcohol-induced thiamine (vitamin B1) deficiency?

A
  • People with chronic alcoholism frequently have deficient intakes of micronutrients (e.g. vitamins B1, A, C, E and folate) and minerals (e.g. zinc and selenium).
  • 50% of alcoholics with liver disease will have thiamine deficiency (B1)
  • Symptoms include anorexia, irritability, and difficulties with short-term memory
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16
Q

What are the causes of Alcohol-induced thiamine (vitamin B1) deficiency?

A
  • Malnourishment
  • Ethanol interferes with GI absorption
  • Hepatic dysfunction, which hinders storage and activation to thiamine pyrophosphate
17
Q

________ is a cofactor for many enzymes

A

Thiamine is a cofactor for many enzymes

18
Q

Thiamine has a half life of _______ days, therefore deficiency can occur rapidly during depletion

A

Thiamine has a half life of 10-20 days, therefore deficiency can occur rapidly during depletion

19
Q

What are glycogen storage diseases?

A
  • Inherited diseases in which the stores of glycogen are affected by defects in either the enzymes of synthesis or degradation of glycogen.
  • Many different types depending on which enzyme is affected
  • They are all autosomal recessive except for type IX which is sex-linked
  • All result in the production of an abnormal amount or abnormal type of glycogen
20
Q

What are the types of glycogen storage diseases?

A
  • Family of inborn errors of metabolism with overall frequency of 1:20000-1:40000 births.
  • May affect any of the enzymes involved in glycogen synthesis and breakdown e.g.
21
Q

Label the corresponding glycogen storage disease for each number

A
22
Q

What are the glycogen storage diseases 1-3?

A

Type I. von Gierke’s disease

•Affects mainly the liver and kidneys caused by a deficiency in glucose 6-phosphatase

Type II. Pompe’s disease

•A deficiency of a-1,4 glucosidase activity in the lysosomes. Can be one of the most devastating of the glycogen storage diseases. Causes death by cardiorespiratory failure

Type III Cori’s disease

•The amylo 1,6 glucosidase (de-branching enzyme) is deficient. Unable to break down glycogen, resulting in hypoglycaemia. Strangely, symptoms often disappear at puberty.

23
Q

What are the glycogen storage diseases 4-5?

A

Type IV Andersen’s disease

•One of the most severe of these diseases. Liver glycogen in normal amounts but comprises long unbranched chains that have low solubility. Sufferers seldom live beyond five years.

Type V. McArdle’s syndrome

•Affects muscle glycogen phosphorylase (liver enzyme is normal). Muscle cannot break down glycogen (which accumulates)

Sufferers have a low tolerance to exercise and fatigue easily, with painful muscle cramps after exercise. Otherwise they have a normal life-span

24
Q

What is the most common glycogen storage disease?

A

Type 1 GSD: Von Gierke’s Disease

•Most common GSD – 25% OF GSDs

25
Q

What causes Type 1 GSD: Von Gierke’s Disease?

A
  • Lack of glucose-6-phosphatase means that glucose cannot be exported from the liver.
  • Results in high levels of G-6-P in the liver & kidney
  • Glucose-6-phosphate is metabolized to lactic acid or converted to glycogen or lipid
26
Q

What are the symptoms of Type 1 GSD: Von Gierke’s Disease?

A

•Symptoms appear when intervals between feeds increases and infants sleep through the night, or when illness prevents normal feeding routine.

27
Q

What is the Management and treatment of Von Gierke’s Disease?

A
  • Aim of treatment is to correct hypoglycaemia and maintain normoglycaemia
  • Young infants can be fed glucose through nasogastric tubes while older children are fed glucose drinks at 2-3 hour intervals night and day to prevent fall in blood glucose and cerebral damage
  • Uncooked cornstarch may be used to prolong period between feeds.
  • Restrict dietary lipids
  • Liver transplant
28
Q

What is the result of the pathogenesis of Von Gierke’s Disease?

A
  • Abnormal levels of glycogen accumulation in the liver and kidney – causing enlargement of the liver and kidneys
  • Increased glycolysis leading to lactic acidosis
  • Increased fatty acid, TG and VLDL synthesis and excretion.
29
Q

What is the effect of Von Gierke’s disease on metabolism?

A
  • Body attempts to compensate for hypoglycaemia by releasing glucagon (hyperglucagonaemia) and adrenaline resulting in mobilisation of fat stores and release of fatty acids.
  • Conversion of fatty acids to TGs and VLDL in the liver resulting in accumulation of fat in liver and hyperlipidaemia. May lead to hepatomas. Accumulation of fat in cheeks and buttocks.
  • Patients suffer with enlarged livers and/or kidneys, stunted growth, severe tendencies to hypoglycaemia (convulsions), hyperlactaemia and hyperlipidemia.
  • May also have hyperuricaemia as a result of hyperlactaemia as lactic acid in the blood competes for kidney transport mechanisms
30
Q
  1. Briefly explain why gluconeogenesis is inhibited during the oxidation of alcohol
A

Answer: Alcohol metabolism results in the production of large quantities of NADH within the liver which increases the NADH:NAD+ ratio.

  • This results in the conversion of pyruvate to lactate, oxaloacetate to malate and dihydroxyacetone to glycerol-3-phosphate
  • These reactions deplete the liver of the metabolites required for gluconeogenesis.
31
Q
  1. Under what conditions is alcohol-induced hypoglycaemia likely to be a problem?
A

Answer: in the short term when glycogen stores are depleted and unable to maintain blood glucose therefore relying on gluconeogenesis

•in the long term when liver gluconeogenesis is compromised e.g. when the liver is damaged due to excessive alcohol consumption or there is reduced muscle mass due to poor nutrition.

32
Q
  1. In addition to alterations in gluconeogenesis and thiamine deficiency, name one other consequence of ingestion of large amounts of alcohol within the liver
A

Answer: Generation of fatty liver due to excessive production of acetate which can be converted to triacylglycerol.

  • Oxidant stress leading to lipid peroxidation and fibrosis
  • Free radical attack on DNA in nucleus and mitochondria causing deletions and mutations
33
Q
  1. Briefly explain why alcoholism can result in a thiamine deficiency
A

Answers: Ethanol interferes with GI absorption

Hepatic dysfunction hinders storage and activation of the thiamine

Malnourishment. And lack of thiamine in the diet

34
Q
  1. Which hormones are increased in Von Gierke’s disease? Why are these hormones increased?
A

Answers: Glucagon and adrenalin

Produced in response to the hypoglycaemia that occurs as a result of the lack of glucose export from the liver

35
Q
  1. What are the effects of Von Gierke’s disease on lipid metabolism?
A

Answers: Lipid mobilisation from the adipose tissue is increased under the influence of adrenalin and glucagon

Increased synthesis of TGs and VLDL in the liver due to excess of metabolic fuel (excess of glucose-6-phosphate and fatty acids)

This results in increased blood lipid levels and increased storage of lipids in the liver

104 Theme 2 - Liver and Metabolism (15 decks)

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