This document provides an overview of hypoglycemia, including its definition as low blood glucose below 50 mg/dL, importance due to the brain's reliance on constant glucose supply, and symptoms ranging from adrenergic to neuroglycopenic effects. It describes the body's glucoregulatory systems that work to prevent and correct low blood sugar, including the release of glucagon, epinephrine, cortisol and growth hormone. Various causes of hypoglycemia are outlined, from insulin-induced in diabetes to other drug-related, critical illness, hormonal deficiency, tumor and genetic causes. The diagnosis involves considering history, symptoms and confirming a low blood glucose level, while treatment focuses on oral or IV glucose administration and

2. Overview of hypoglycemiaOverview of hypoglycemia
Defenition
Importance
Glucoregulatory system
Symptoms
Causes and Types
Diagnose
Treatment
Prevention

3. What is it?
Rate of glucose utilization exceed s the rate at wich glucose is
being produced.
• a blood glucose concentration below the fasting value( cutoff is 50
mg/dL.)

4. Why do we care about it?
 a medical emergency.
brain is completely dependent on blood glucose
Very low concentrations of plasma glucose (<20 or 30
mg/dL) cause severe CNS dysfunction.
The brain can not synthesize its own glucose; it requires a
continuous supply via arterial blood
As the plasma glucose concentration falls below the
physiologic range, blood-to-brain glucose transport
becomes insufficient for adequate brain energy metabolism
and functioning
It is, therefore, not surprising that the body has multiple
overlapping mechanisms to prevent or correct
hypoglycemia

5. Glucoregulatory systems
Two overlapping glucose-regulating
systems are activated by
hypoglycemia:
1) the islets of Langerhans, which
release glucagon
2) receptors in the hypothalamus,
which respond to abnormally low
concentrations of blood glucose.
The hypothalamic glucoreceptors can
trigger both the secretion of
epinephrine and release of ACTH
and GH by the anterior pituitary.
[ACTH increases cortisol synthesis
and secretion in the adrenal cortex]
Glucagon, epinephrine, cortisol, and
GH are each opposes the action of
insulin on glucose use.

6. Glucoregulatory systems
Insulin- inhibits glycogenolysis and
gluconeogenesisdecreased serum
glucose
Glucagon- promotes glycogenolysis and
gluconeogenesis
Epinephrine- limits utilization of
glucose by insulin-sensistive tissues
Growth hormone and cortisol have a
role during prolonged hypoglycemia

7. Symptoms of hypoglycemia
 The symptoms of can be divided into
two categories:
1) Adrenergic symptoms—anxiety,
palpitation, tremor, and sweating—
are mediated by epinephrine release
regulated by the hypothalamus in
response to hypoglycemia. Usually
adrenergic symptoms occur when
blood glucose levels fall abruptly.
2) Neuroglycopenia—the impaired
delivery of glucose to the brain—
results in impairment of brain
function, headache, confusion, slurred
speech, seizures, coma, and
death.Neuro glycopenic symptoms
often result from a gradual decline in
blood glucose, often to levels below 40
mg/dl.

8. Whipple’s Triad
Hypoglycemia is characterized by:
1)CNS symptoms, including confusion, aberrant
behavior, or coma
2)a simultaneous blood glucose level equal to or less
than 50 mg/dl
3)symptoms being resolved within minutes
following the administrationof glucose

9. What causes it?

10. Types of hypoglycemia
1). Insulin-induced hypoglycemia:
Hypoglycemia occurs frequently in patients with diabetes who are
receiving insulin treatment.
2). postprandial (reactive hypoglycemia):
It is caused by an exaggerated insulin release following a meal,
prompting transient hypoglycemia with mild adrenergic
symptoms. Drugs, antibodies to insulin or the insulin receptor,
inborn errors and reactive hypoglycemia (also referred to as
functional hypoglycemia),produce hypoglycemia in the
postprandial (fed) state.
3). Fasting hypoglycemia:
result from a reduction in the rate of glucose production by
hepatic glycogenolysis or gluconeogenesis Or result from increased
rate of
glucose use by the peripheral tissues due to overproduction of

11. Types of hypoglycemia
4). Hypoglycemia and alcohol intoxication:
Alcohol concumption can inhibit hepatic gluconeogenesis and increase
glycogen phosphorylase activity, depleting hepatic glycogen stores and
resulting In hypoglycemia. The metabolism of ethanol results in a
massive increase in the concentration of cytosolicNADH in the liver.
The ethanol-mediated increase in NADH causes
the intermediates of gluconeogenesis to be diverted into alternate
reaction pathways, resulting in decreased synthesis of glucose.
5). Drugs :
Drugs are the most prevalent cause, and many, including
propranolol, salicylates,and disopyramide, produce
hypoglycemia.(sulfonylureas, insulin, …)

12. Types of hypoglycemia
6) Critical illness:
Hepatic failure, Renal failure, Cardiac failure, Sepsis,
Malnutrition
7) Hormonal Deficiencies:
Glucagon, Epinephrine, Cortisol, Growyh Hormone
8) Endogenous Hyperinsulinism:
Pancratic beta cell disorder, Tumor(insulinoma)
9) Autoimmune Hypoglycemia:
Insulin antibodies, insulin receptor antibodies

13. Types of hypoglycemia
10) Non–islet cell tumor hypoglycemia (NICTH):
The diagnosis of NICTH can usually be made by the presence of fasting
hypoglycemia, low insulin, proinsulin, and C-peptide levels, an elevated
IGF-II–to–IGF-I ratio, and low growth hormone and
β-hydroxybutyrate levels.
11) Hypoglycemia of Infancy and Childhood:
Neonatal blood glucose concentrations are much lower than those of
adults (mean, <35 mg/ L) and decline shortly after birth when liver
glycogen stores are deplete .
causes: (1) prematurity, (2) maternal diabetes, (3) gestational
diabetes mellitus (GDM), and (4) maternal toxemia.
12) Alimentary hypoglycemia:
Alimentary hypoglycemia presents 2 hrs after a meal
13) Idiopatic postprandial Hypoglycemia

14. Types of hypoglycemia
Defects in fatty acid oxidation also result in
hypoglycemia.
Jamaican vomting disorder also can lead to death
because of severe hypoglycemia.( by Hypoglycin
toxin)

15. Diagnosis
History
Drug use, infection, illness (hepatic, renal, cardiac),
surgeries
ECG, CXR

16. Laboratory tests
Blood sugar be tested at the same time a person is
experience ing hypoglycemic symptoms.(best test)
Insulin levels : elevated level and low blood sugar
 Insulinoma
OGTT : reactive hypoglycemia. Performed test for 5
hours while simultaneously testing glucose and
insulin levels. To be meaningful, low blood sugar
(<50 mg/dl) during the test should be accompanied
by typical symptoms.( Now realize that OGTT can
actually trigger hypoglycemic symptoms in people
with no signs of disorder)

17. Laboratory tests
72-hour fasting plasma glucose : most reliable
diagnostic test for evaluation of fasting hypoglycemia.
Continue fast for as long as 72 hours or until
symptoms develop in the presence of hypoglycemia.
Obtain simultaneous insulin levels every 6 hours,
when glucose is low and when symptoms develop.
Also measure beta-hydroxybutyrate serum level.
C-peptide levels : C-peptide levels are elevated in
Insulinoma, normal or low with exogenous insulin,
and evelated with oral sulfonyureas.

18. Laboratory tests
Proinsulin : 1) beta cell tumor 2) Familial
hyperinsulinism
Cortisol : measure adrenal insuffiency

19. Diagnosis
Differential
Neurologic: seizure disorder
Drug/alcohol intoxication
Psychosis, depression

20. Treatment
Glucose
Oral consumption of glucose in the conscious patient
IV dextrose: 5-20% solutions, 50% ampules
Subcutaneous or intramuscular injection of
glucagon
Monitor glucose q 2-4 hours
If adrenal insufficiency, administer 100 mg
hydrocortisone & 1 mg glucagon

21. Prevention
Treatment of underlying problem
Eliminate/reduce offending drug
Treat infection
Frequent feedings, avoidance of fasting

22. Thanks