Hypoglycemia

Question 1

HORMONAL RESPONSES TO HYPOGLYCEMIA

Answer 1

• decrease insulin (immediate)
• increase glucagon (minutes)
• increase catecholamines
• increase GH
• increase carticosteroids (slow)

Question 2

AUTONOMIC SYMPTOMS OF

HYPOGLYCEMIA

Answer 2

Adrenergic:

• Tremor
• Palpitations
• Anxiety

Cholinergic:

• Diaphoresis
• Hunger
• Paresthesias

Question 3

NEUROGLYCOPENIC SYMPTOMS OF

HYPOGLYCEMIA

Answer 3

• Sensations of warmth, weakness, fatigue
• Difficulty thinking, confusion
• Changes in affect, behavior
• Difficulty speaking
• Blurred vision
• Amnesia
• Seizures
• Coma
• Death

Question 4

HYPOGLYCEMIC UNAWARENESS

Answer 4

• occurs in setting of repeated episodes of hypoglycemia
• Downward shift in the threshold for the
  counter-regulatory hormone response to
  hypoglycemia resulting in the loss of
  autonomic warning symptoms prior to
  the onset of cerebral dysfunction

Question 5

RISK FACTORS OF SEVERE

HYPOGLYCEMIA IN TYPE 1 DIABETES

Answer 5

• Intensive control, lower HbA1C
  • Previous severe hypoglycemia
  • Absent insulin secretion
  • Hypoglycemic unawareness

Question 6

GLUCAGON

Answer 6

• Inc. glycogenolysis
  I- nc. gluconeogenesis
• Antagonize hepatic actions of insulin

Question 7

WHIPPLE’S TRIAD

Answer 7

• used to evaluate whether someone has INSULINOMA
  1. Symptoms consistent with hypoglycemia
  2. Low plasma glucose
  3. Symptoms relieved promptly when glucose is returned to normal

Question 8

REACTIVE HYPOGLYCEMIA

Answer 8

• Clincal features: Post-prandial (after-meal) autonomic symptoms
• thought to represent a consequence of excessive insulin release triggered by the carbohydrate meal, but continuing past the digestion and disposal of the glucose derived from the meal
• Whipple’s triad frequently is not fulfilled

** Oral glucose challenge (OGTT) is a poor
diagnostic test for reactive hypoglycemia

Question 9

Alcohol-induced Hypoglycemia

Answer 9

• Usual history is moderate to excessive EtOH consumption with little or no food during the previous 6 to 36 hours.
• Mechanism: Inhibition of hepatic gluconeogenesis.
• Hepatic glycogenolysis is not impaired, hence patients typically do not present until hepatic glycogen store have been exhausted
• Patients typically are comatose at
  presentation.