Hypoglycemia

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Introduction

 

Hypoglycemia is characterized by three things:

Temporary hypoglycemia can cause cerebral dysfunction, and prolonged hypoglycemia can cause death. The body thus has overlapping mechanisms to prevent or correct hypoglycemia. The most notable are elevations of glucagon and epinephrine, together with a decrease in insulin.

 

 

The Case of...

a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.

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Causes and Risk Factors

Ketotic

Non-Ketotic

dec. intake

  • starvation
  • emesis

non-ketotic

  • endogenous - insulinoma
  • GDM affecting mother
  • exogenous - oral hypoglycemics

 

Insulin-Induced Hypoglycemia
Hypoglycemia frequently occurs in patients receiving intensive insulin treatment.If patients are consious, oral administration of carbohydrate is used. In unconsious patients, intramuscular administration of glucagon is used.

 

Postprandial Hypoglycemia
Exaggerated insulin release can follow a meal, triggering hypoglycemia with mild adrenergic symptoms. For this reason, it is recommended to eat frequent small meals.

 

Fasting Hypoglycemia
Fasting hypoglycemia tends to produce neuroglycopenic symptoms and may result from decreased liver production of glucose, ie in patients with liver damage. It may also reult from increased peripheral glucose use, often due to increased insulin levels due to a pancreatic tumour.

 

Hypoglycemia and Alcohol
Ethanol is oxidized first to acetaldehyde by alcohol dehydrogenase, then to acetate by aldehyde dehydrogenase. These reactions reduce NAD+, producing large amounts of NADH. This favours the reduction of pyruvate to lactate and of oxaloacetate to malate, two important intermediates in gluconeogenesis. This decreased glucose synthesis can cause hypoglycemia, especially in people who have depleted their stores of glycogen. Hypoglycemia can produce many of the symptoms of alcohol intoxication, such as agitation, impaired judgment, and surliness.

 

Patients who use insulin as a part of intensive therapy are at increased risk of hypoglycemia several hours after drinking alcohol.

 

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Pathophysiology

Glucagon and epinephrine are the most important immediate responders to hypoglycemia. Epinephrine is not normally essential, but in Type I diabetes, where glucagon secretion is impaired, epinephrine becomes critical.

 

 

Cortisol and growth hormone are less important in short-term maintenance of blood glucose but do play a role in long-term management of glucose metabolism.

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Signs and Symptoms

  • history
  • physical exam

History

Symptoms of hypoglycemia can be divided into two categories.

Adrenergic Symptoms
Adrenergic symptoms are mediated by epinephrine release due to hypoglycemia sensing of the hypothalamus. These include anxiety, palpitations, tremors, and sweating. These symptoms usually occur when blood glucose levels fall abruptly.

Neuroglycopenic Symptoms
Neuroglycopenia is the impaired delivery of glucose to the brain, and results in headache, confusion, slurred speech, seizures, coma, and death. These symptoms often result from a gradual decline in blood glucose which does not trigger epinephrine response.

Physical Exam

 

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Investigations

  • lab investigations
  • diagnostic imaging

Lab Investigations

Diagnostic Imaging

 

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Differential Diagnosis

 

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Treatments

ABCs and vitals

serum blood glucose

critical samples

Mild-moderate

BG <4 mmol/L: 15g carbohydrate

BG<2.2 mmol/L: 20g carbohydrate

severe and unconscious: unable to drink

 

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Consequences and Course

 

 

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Resources and References

 

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Topic Development

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