DM: Hypoglycemia

Question 1

What is the Whipple’s triad?

Answer 1

1. Symptoms consistent with hypoglycemia
2. Low plasma glucose concentration measured with a precise method
3. Relief of symptoms the after plasma glucose level is raised

Question 2

Lower limit of fasting plasma glucose concentration

Answer 2

~70 mg/dL

Question 3

Duration of fasting in which hepatic glycogen stores are usually sufficient to maintain plasma glucose levels

Answer 3

~8 hours

Question 4

What is the first defense against hypogclyemia?

Answer 4

Decrease in insulin secretion (primary glucose regulatory factor)

Question 5

What are the primary counterregulatory hormones?

Answer 5

Glucagon and epinephrine

Question 6

True or False: Cortisol and growth hormone play a role in the defense against acute hypoglycemia.

Answer 6

False. They are able to support glucose production and restrict glucose utilization to a limited amount (~20% compared to epinephrine).

Question 7

What is the second defense against hypoglycemia?

Answer 7

Increased glucagon

Question 8

What is the third defense against hypoglycemia?

Answer 8

Increased epinephrine

Question 9

Hypoglycemia unawareness is reversible by as little as _____ weeks of scrupulous avoidance of hypoglycemia in most affected patients.

Answer 9

2-3 weeks

Question 10

How does alcohol intake cause hypoglycemia?

Answer 10

Alcohol blocks gluconeogenesis

Question 11

How does sepsis cause hypoglycemia?

Answer 11

Increased glucose utilization is induced by cytokine production in macrophage-rich tissues such as the liver, spleen, and lung.

Question 12

TRUE OR FALSE: Cortisol and growth hormone are critical in the prevention of hypoglycemia.

Answer 12

False

Question 13

What is the mechanism of hypoglycemia in patients with non-beta-cell tumors?

Answer 13

Overproduction of an incompletely processed form of insulin-like growth factor II (“big IGF-II”)

Question 14

What is the mechanism of hypoglycemia in patients with primary beta cell disorder or with intake of insulin secretagogue?

Answer 14

Failure of insulin secretion to fall to very low levels during hypoglceymia

Question 15

Critical diagnostic findings in endogenous hyperinsulinism

Answer 15

Plasma insulin >=3 uU/mL
Plasma C-peptide >=0.6 ng/mL
Plasma proinsulin >=5 pmol/L

-When plasma glucose <55 mg/dL + symptoms of hypogclyemia

(Insulin, C-peptide, and proinsulin levels are inappropriately high in the setting of a low plasma glucose concentration)

Question 16

What indicates increased insulin (or IGF) action after IV administration of glucagon? (level of B-hydroxybutyrate and glucose)

Answer 16

Low plasma beta-hydroxybutyrate concentration and an increment in plasma glucose level

Question 17

What is nesidioblastosis?

Answer 17

It refers to diffuse islet involvement with beta cell hypertrophy, and sometimes hyperplasia, which leads to fasting endogenous hyperinsulinemic hypoglycemia

Question 18

What is the term used to denote patients with diffuse beta cell hypertrophy and develops postprandial hypoglycemia?

Answer 18

Noninsulinoma pancreatogenous hypoglycemia

Question 19

Which drugs can be given to treat hypoglycemia in patients with inoperable insulinomas?

Answer 19

Diazoxide (potassium channel activator that inhibits insulin secretion)
Octreotide (somatostatin analogue)
Everolimus (mammalian target of rapamycin inhibitor)

Question 20

What causes pseudohypoglycemia?

Answer 20

Continued glucose metabolism by the formed elements of the blood ex vivo, particularly in the presence of leukocytosis, erythrocytosis, or thrombocytosis, or with delayed separation of the serum from the formed elements

Question 21

Which inborn errors of metabolism cause fasting hypoglycemia?

Answer 21

1) disorders of glycogenolysis:

glycogen storage disease
types 0
I - high lactate before meals, high triglycerides
III - low lactate after meals, high triglycerides, high ketones
IV
Fanconi-Bickel syndrome

2) defects in fatty acid oxidation (carnitine cycle, fatty acid beta oxidation, electron transfer, ketogenesis)
3) defects in gluconeogenesis (fructose-1, 6-bisphosphatase)

Question 22

Which inborn errors of metabolism cause postprandial hypoglycemia?

Answer 22

1) glucokinase, SUR1, and Kir6.2 potassium channel mutations
2) congenital disorders of glycosylation
3) inherited fructose intolerance

Question 23

Which inborn errors of metabolism cause exercise-induced hypoglycemia?

Answer 23

Increased activity of monocarboxylate transporter 1 in beta cells which causes hyperinsulinemia

Question 24

What is the reasonable initial dose of glucose in a person with acute hypoglycemia?

Answer 24

15-20 g of glucose