Hypoglycaemia

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Hypoglycaemia

• Dr. Essam H. Jiffri

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INTRODUCTION

• -Hypoglycaemia is defined as a fasting venous
  whole-blood glucose level of less
• than 2.2 mmol/L (plasma glucose lt2.5 mmo1/l),
  when measured by a
• glucose-specific ( enzymatic) method.
• -Hypoglycaemia is dangerous because glucose is a
  vital primary fuel for the brain.

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INTRODUCTION

• -Deficiency produces disordered function and, if
  prolonged or severe, can cause tissue damage
  or death.
• -In fasting, the brain still has an energy
  requirement equivalent to 80 g glucose 24/h,
• which cannot be provided by NEFA, the
  immediately available alternative fuel.
• -The brain can utilize ketone bodies but these
  are not produced rapidly enough to protect
  against acute hypoglycaemia.

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Clinical Features

• -Symptoms fall into two main categories
• -In early acute hypoglycaemia include
  nervousness, weakness, headache, sweating,
  dizziness, tremor, tachycardia, palpitations,
  anxiety and hunger).

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Clinical Features

• -Those caused by dysfunction of the central
  nervous system (neuroglycopaenia),
• include visual symptoms, headache, blunted
  mental, loss of motor function, confusion,
  abnormal behavior and loss of consciousness.

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Causes

• -It has been traditional to classify
  hypoglycaemia as conditions that produce low
  blood glucose levels during fasting.
• -An alternative approach is based on the
  pathophysiology of hypoglycaemia, particularly
  reduced gluconeogenesis and increased utilization
  of glucose.

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Causes
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CAUSES

• I-Decreased Output of Glucose
• -Hypoglycaemia may result from impaired
  glycogenolysis or reduced gluconeogenesis.
• -Gluconeogenesis may be impaired because of
  reduced formation from amino acids
• and glycerol.

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I-Decreased Output of Glucose

• Liver Disease
• -Hypoglycaemia might be expected to be a
  complication of liver disease because
• of the role of this organ in gluconeogenesis
• Alcohol Abuse
• -Alcohol inhibits gluconeogenesis following
  alcohol ingestion.

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I-Decreased Output of Glucose

• Inherited Metabolic Disorders
• - Endocrine Disease
• -Deficiency of counter-regulatory hormones is
  common cause of hypoglycaemia.
• -It occurs in cortisol deficiency, due either to
• primary adrenal failure or
• secondary to adrenocorticotrophic hormone (ACTH)
  deficiency
• -In growth hormone deficiency.
• -Impaired gluconeogenesis is the most likely
  reason.

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CAUSES

• 2-lncreased Glucose Utilization
• Reduced Fat Stores Low
• -Fat stores allow only limited ketogenesis and
  this may contribute to hypoglycaemia
• in premature infants and in malnutrition.

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2-lncreased Glucose Utilization

• Decreased Ketone Body Production
• -Continued utilization of glucose by the brain
  can cause hypoglycaemia when the
• production of ketone bodies is defective.

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2-lncreased Glucose Utilization

• Impaired Fatty Acid Oxidation Activated
• -Long-chain fatty acids are transported by
  carnitine into mitochondria for oxidation,
• this being facilitated by two carnitine
  acyltransferases, deficiency or inactivity of one
  of these enzymes may cause impaired oxidation of
  long-chain fatty acids.

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CAUSES

• 3-Decreased Output and Increased Utilization of
  Glucose
• Insulin
• -Insulin reduces blood glucose acutely, mainly by
  increasing cellular uptake and
• utilization therefore excess administration
  causes hypoglycaemia.
• -Hyperinsulinaemia may also result from
  inappropriate endogenous production.

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3-Decreased Output and Increased Utilization of
Glucose

• Insulin
• -Insulinomas, which are common causes of
  hypoglycaemia in adults, are tumours of
  pancreatic beta cells.
• -Nesiodioblastosis is a diffuse increase in
  pancreatic endocrine cells and is an
• important cause of hypoglycaemia in infancy.

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3-Decreased Output and Increased Utilization of
Glucose

• Sulphonylureas
• - Sulphonylureas increase glucose-stimulated
  insulin release and hypoglycaemia is the most
  commonly observed side-effect.

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3-Decreased Output and Increased Utilization of
Glucose

• Nonpancreatic Tumour
• - Some nonpancreatic tumours, particularly
  primary liver carcinomas, occasionally
• cause hypoglycaemia.

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3-Decreased Output and Increased Utilization of
Glucose

• Postgastrectomy
• - Hypoglycaemia is 2h after a meal rich in
  carbohydrate is common in patients with
• a partial gastrectomy.
• - It occurs because of rapid passage of sugar
  into the small intestine and enhanced release of
  enteric hormones which augment glucose-stimulated
  insulin release, this excess release of insulin
  causes hypoglycaemia.

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Investigation of Hypoglycaemia in Adults

• - Once the diagnosis is considered blood glucose
  and insulin should be measured after an overnight
  fast hypoglycaemia with inappropriately high
  insulin levels is being demonstrated by such a
  protocol in over 90 of cases of insulinoma.

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Investigation of Hypoglycaemia in Adults

• - For some patients an extended fast of up to 72
  h is needed, and glucose and insulin
  concentration should be determined every 4-6h, or
  when the patient has symptoms.
• - Hypoglycaemia due to non-islet cell tumours is
  usually very severe and tuomours may be detected
  by physical examination or imaging techniques.

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Hypoglacaemia in Infancy and Childhood

• Hypoglycaemia often occurs at birth, as normal
  blood control is established after a few days of
  birth.

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Investigation of Hypoglacaemia in Infancy and
Childhood

• - minimum investigations are
• - blood glucose
• - serum insulin, and
• - blood or urinary ketone bodies.
• - It may be necessary to estimate
• - Growth hormone
• - Cortisol
• - NEFA, and
• - Other intermediary metabolites

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Hypoglacaemia in Infancy and Childhood

• Most neonates with persistent hypoglycaemia have
  hyperinsulinism due to
• -Deficiency of counter-regulatory hormone, or
• -An enzyme deficiency affecting gluconeogenisis
  or glycogenolysis.
• - In older children hyperinsulinism, growth
  hormone or cortisol deficiency are important
  cause.