CLINICAL CHEMIISTRY (MT 305) CARBOHYDRATE LECTURE ONE

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CLINICAL CHEMIISTRY (MT 305) CARBOHYDRATE LECTURE ONE Powered By Docstoc
					    Hypoglycaemia


     Dr. Essam H. Jiffri



1
           INTRODUCTION

-Hypoglycaemia is defined as a fasting
  venous whole-blood glucose level of less
  than 2.2 mmol/L (plasma glucose <2.5
  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
22
     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.
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