Hypoglycemia Flashcards
Nesidioblastosis
medical term for hyperinsulinemic hypoglycemia attributed to excessive function of pancreatic beta cells with an abnormal microscopic appearance. The term was coined in the first half of the 20th century. The abnormal histologic aspects of the tissue included the presence of islet cell enlargement, islet cell dysplasia, beta cells budding from ductal epithelium, and islets in apposition to ducts.
Geoffrey J. Service,
Well known endocrinologist / hypoglycemia is the field
Nesidioblastosis in NEJM
Causes of Hypoglycemia
Hypoglycemia in diabetes
Hypoglycemia in patients without diabetes
- Drugs
- Critical illness
- Malnourishment
- Cortisol deficiency
- Nonislet cell tumors
- Endogenous hyperinsulinism
- Accidental, surreptitious, or malicious hypoglycemia
Drugs
Insulin/sulfonylureas/meglitinides
Alcohol, may also cause hypoglycemia.
The drugs MC cause hypoglycemia were quinolones, pentamidine, quinine, beta blockers, angiotensin-converting enzyme inhibitors, and IGF-1.
Ethanol inhibits gluconeogenesis but not glycogenolysis. Thus, alcohol-induced hypoglycemia typically follows a several day alcohol binge
Cocain abuse
Critical illness
Sepsis is a relatively common cause of hypoglycemia Hypoglycemia develops when the body cant keep up with cytokine activity + cytokine induced inhibition of gluconeogenesis in the setting of glycogen depletion Chronic kidney disease involves impaired gluconeogenesis, reduced renal clearance of insulin, and reduced renal glucose production. In severe liver failure, gluconeogenesis is also impaired.
In tropical countries where malaria is endemic, hypoglycemia can result from malaria, its treatment, or both
Endogenous hyperinsulinism
Hyperinsulinemic hypoglycemia occurs when there is a failure of insulin secretion to fall to very low rates as plasma glucose concentrations fall to hypoglycemic levels; hypoglycemia is the result of low rates of glucose production rather than high rates of glucose utilization.
Endogenous hyperinsulinism is more likely in an otherwise overtly well individual with no clinical clues to the common causes of hypoglycemia. In adults, hypoglycemia due to endogenous hyperinsulinism can be caused by the following (table 1):
■A beta cell secretagogue, such as a sulfonylurea
■A beta cell tumor (see “Insulinoma”)
■A functional beta cell disorder, often termed nesidioblastosis, that can occur as a feature of the non insulinoma pancreatogenous hypoglycemia syndrome (NIPHS) or of post-gastric bypass hypoglycemia (see “Noninsulinoma pancreatogenous hypoglycemia syndrome”)
■Insulin autoimmune hypoglycemia
LABS hypoglycemia
■Glucose
■Insulin
■C-peptide
■Beta-hydroxybutyrate
■Proinsulin
■Sulfonylurea and meglitinide screen
Hypoglycemia what labs mean
■Glucose
■Insulin
■C-peptide
■Beta-hydroxybutyrate
■Proinsulin
■Sulfonylurea and meglitinide screen
Plasma insulin: concentration of 3 microU/mL (20.8 pmol/L) by immunochemiluminometric assay (ICMA) when bg< 55 mg/dL (3.0 mmol/L) consistent with hyperinsulinemia (eg, insulinoma).
Plasma C-peptide Plasma distinguishes endogenous from exogenous hyperinsulinemia.- concentration of 0.2 nmol/L (200 pmol/L or 0.6 ng/mL) is normal. For plasma proinsulin, the diagnostic criterion for insulinoma is 5 pmol/L or greater
Plasma beta-hydroxybutyrate — Because of the antiketogenic effect of insulin, plasma beta-hydroxybutyrate (BHOB) concentrations are lower in insulinoma patients than in normal subjects. All patients with insulinoma had plasma BHOB values of 2.7 mmol/L or less at the end of the fast
The plasma BHOB value, as well as the glucose response to glucagon, can be used to confirm the diagnosis in patients in whom the insulin and C-peptide values are in the borderline range (eg, plasma insulin concentration of <3 microU/mL [20.8 pmol/L], C-peptide <0.2 nmol/L [0.6 ng/mL]) or to indicate the action of an insulin-like factor.
Glycemic response to glucagon — Insulin is antiglycogenolytic and hyperinsulinemia permits retention of glycogen within the liver. As a result, patients with insulin-mediated hypoglycemia respond to 1 mg of intravenous glucagon (a potent glycogenolytic agent) by releasing glucose. Normal subjects will have released virtually all glucose from the liver at the end of the 72-hour fast and cannot therefore respond as vigorously to intravenous glucagon as a patient with an insulinoma. At the end of the fast, patients with an insulinoma have an increase in plasma glucose of 25 mg/dL (1.4 mmol/L) or more in 20 to 30 minutes, whereas normal subjects have a smaller increment (figure 5).
Arterial calcium stimulation
— A selective arterial calcium stimulation test with hepatic venous sampling can be performed to distinguish between a focal abnormality (insulinoma) and a diffuse process (islet cell hypertrophy/nesidioblastosis). We reserve this test for complex cases of endogenous hyperinsulinemic hypoglycemia and negative radiologic localization studies.
This test involves selective injection of calcium gluconate into the gastroduodenal, splenic, and superior mesenteric arteries with subsequent sampling of the hepatic venous effluent for insulin. A positive result is a doubling or tripling of basal insulin concentrations. The increase in insulin occurs in samples from the artery supplying the region with hyperfunctioning islets, either an insulinoma or islet hypertrophy, which facilitates operative localization.
In patients with insulinoma, the response is positive in one artery alone unless the tumor resides in an area fed by two arteries, or the patient has multiple insulinomas scattered throughout the pancreas (table 5). In contrast, in patients with islet cell hypertrophy, positive responses are usually but not always observed after injection of multiple arteries. (See “Noninsulinoma pancreatogenous hypoglycemia syndrome”, section on ‘Localization studies’ and “Diagnostic dilemmas in hypoglycemia: Illustrative cases”.)
