Hypoglycemia UMY
Hypoglycemia UMY
Hypoglycemia UMY
Hypoglycemia
Hepatic Failure
Decreased glycogenolysis
Decresed gluconeogenesis
Large functional reserve,( 20% func required to prevent
hypoglycemia)
Genetic defects in glycometabolic pathways
Finally, compromised drug metabolism (tolbutamide, glyburide,
glipizide )
Endocrinopathies
Glucagon deficiency
Treatment of Choice
Enucleation
Recurrence at 10 yrs is 6% and 20 yrs is 10%
Insulinoma
Treatment:
• Surgical resection
• Diazoxide
• Octreotide
• Inteferon alpha
• Malignant:
• Octreotide-idium 111
• Chemo: streptozozin, doxorubicin
Islet Hyperplasia
Anti-insulin antibody
autoantibodies against insulin bind free circulating plasma insulin
when its concentration is high and release insulin when the
concentration of free plasma insulin drops.
Release of insulin at inappropriate times can cause hypoglycemia.
Symptoms
Adrenergic Symptoms
usually seen early with a rapid decline in blood glucose and include
tachycardia, tachypnea, vomiting, and diaphoresis
Neuroglycopenic
usually associated with slower or prolonged hypoglycemia, include
poor feeding, altered mental status, lethargy, and seizures
Definition of Hypoglycemia
1. Development of neurogenic or neuroglycopenic symptoms
• Moderate
– Autonomic and neuroglycopenic symptoms
– Individual is able to self-treat
• Severe
– Requires the assistance of another person
– Unconsciousness may occur
– Plasma glucose is typically <2.8 mmol/L
Response to Hypoglycemia
Pathophysiology
disruption of controlled gastric emptying
decreased transit time
rapid elevation in plasma glucose that triggers
exaggerated insulin response.
abnormal insulin then causes a precipitous drop in blood
glucose
Partial Remission or Honeymoon
Phase
In approximately 60-80 % of children & adolescents,
insulin requirements decrease transiently following
initiation of treatment
Most studies define partial remission phase as that
when the patient requires < 0.5 units of insulin/ kg
body weight/ day and has HbA1c <7%
The partial remission phase commences within days
or weeks of the start of insulin therapy & may last for
weeks to months
Frequent hypoglycemia attacks happen in this period
During this phase blood glucose levels are frequently
stable within the normal range, despite fluctuations in
diet and exercise
As low dose subcutaneous insulin therapy does not
prolong residual beta cell function
Somogyi Phenomenon
May also occur when patients are switched to intensive insulin regimens.
Principles of therapy
CONFIRM
severe
Adolescence Elderly
Children unable to detect and/or Poor health literacy, Food
treat mild hypoglycemia insecurity
A1C <6.0% Increased A1C
Long duration of diabetes Duration of insulin therapy
Prior episode of severe Severe cognitive impairment
hypoglycemia
Hypoglycemia unawareness Renal impairment
Autonomic neuropathy Neuropathy
Treatment of SEVERE Hypoglycemia
in Conscious Person
1. Treat with oral “fast sugar” (simple carbohydrate)
(20 g) to relieve symptoms
Comment — This is a classic case of insulinoma. The patient was healthy but had episodes of
neuroglycopenia. Whipple's triad (symptoms of hypoglycemia, low serum glucose concentrations at the
same time, and relief of symptoms by glucose administration) was satisfied. That the hypoglycemia was
caused by endogenous insulin was confirmed by the high serum insulin, C-peptide and proinsulin
concentrations, and supported by the low serum beta-hydroxybutyrate concentration and the small rise in
serum glucose after intravenous glucagon administration.
CASE 2 — A 27-year-old man was referred by his local physician for evaluation of
hypoglycemia found incidentally during a work-up for peptic ulcer disease.
Past medical history included gastric by pass surgery for morbid obesity 2
years ago. During the last four months, he had several episodes of weakness
and feeling "shaky inside" late in the evening. During the night he would
periodically drink soda. When symptomatic, reflectance meter blood glucose
values measured by the patient using equipment purchased for his seven-year-
old daughter (diagnosed with type 1 diabetes one year earlier) had been in the
range of 40 to 50 mg/dL (2.2 to 2.8 mmol/L). Serum values after an overnight
fast were:
Glucose - 36 mg/dL (2.0 mmol/L)
Insulin - 140 microU/mL (840 pmol/L)
C-peptide - <33 pmol/L(0.03-1nmol/L)
Proinsulin - 0.9 pmol/L(2-31 pmol/L)
The low serum C-peptide and proinsulin values indicate that the hyperinsulinemia
(140 microU/mL (840 pmol/L)) was due to exogenous insulin administration.
CASE 8 — A 76-year-old woman was referred for the evaluation of postprandial adrenergic
symptoms with occasional visual changes. There was one episode of confusion while on a
telephone call to her daughter. During an episode of light headedness, sweating, weakness and
irritability two hours after breakfast (which occurred while under observation), serum values were
as follows:
Glucose 51 mg/dl (2.8 mmol/L)
Insulin 6.4 microU/mL (45.9 pmol/L)
C-peptide 2.6 ng/mL (858 pmol/L)
Betahydroxybutyrate 0.1 mmol/L
Glucose increase after glucagon 46 mg/dL (2.6 mmol/L)
Sulfonylurea negative
A mixed meal test was performed because of the presence of postprandial symptoms
accompanied by biochemical evidence of insulin-mediated hypoglycemia. Biochemical testing 180
minutes after a mixed meal revealed the following:
Glucose 43 mg/dl (2.4 mmol/L)
Insulin 22.0 microU/ml (157.8 pmol/L)
C-peptide 4.7 ng/ml (1551 pmol/L)