Hypoglycemia Flashcards
When does hypoglycemia occur?
Glucose utilization exceeds production
What tissue is absolutely dependent on glucose? What does it use when glucose not available?
Brain needs glucose, but uses ketones in absence
What are main tissues of glucose use?
Brain, muscle, RBC/WBC, renal medulla
Sources of glucose (3)
Ingestion
Gluconeogenesis: long term
Glycogenolysis: exhausted 24-36 hr
Fasting hormonal response on glucose utilization: What are effects of insulin, glucagon, epinephrine, cortisol, growth hormone?
Insulin: Suppresses all glucose utilization
Glucagon: Glycogenolysis, gluconeogenesis
Epinephrine: Glycogenolysis, lipolysis, ketogenesis
Cortisol: gluconeogenesis
GH: lipolysis
What happens with decrease in insulin?
Increase in fatty acids and ketone generation
At what plasma glucose are symptoms noticeable? Is it above or below levels for hormonal secretion
50-55mg/dL
This is below levels for hormonal secretion
Whipple’s Triad
Symptoms/signs compatible with hypoglycemia
Low plasma glucose
Resolution of symptoms/signs when plasma glucose restored to normal
Neurogenic symptoms of hypoglycemia: Adrenergic (3) and Cholinergic (3)
Result of sympathetic nervous discharge in response to hypoglycemia
Adrenergic: palpitations, tremor, anxiety
Cholinergic: sweating, hunger, paresthesis
Neuroglycopenic Symptoms (big list)
Result of failure of brain function
Confusion, dizziness, fatigue, inability to concentrate, blurred vision, headache, focal neurological signs, loss of consciousness, seizures, depressed respiration, death
Which symptoms come first?
Neurogenic precede neuroglycopenic symptoms
What is the impact of previous episodes of hypoglycemia? (2)
Attenuate adrenergic response
Hypoglycemia-associated autonomic failure
What are 3 broad categories of fasting hypoglycemia?
- Insulin-mediated (too much insulin) (4)
- Failure of counter-regulation (too little counter) (2)
- Congenital error of metabolism (3)
What is most common cause (broad) of persistent hypoglycemia? Is the specific cause different for adults vs. children?
Most common cause is hyperinsulinemia
For adults most likely due to insulinoma
For children, most likely due to congenital hyperinsulinism
What are diagnostic criteria for hyperinsulinemic hypoglycemia? (5)
Hyperinsulinemia High C-peptide Hypofattyacidemia Hypoketonemia Glycemic response to glucagon
Are insulinomas big or small? Usually benign or malignant? Where are they located?
Typically small and benign.
Usually located in pancreas
What are ectopic locations for insulinomas? (5)
Duodenum, Meckel’s diverticulum, bile duct, ovary, omentum
Biochemical profile of insulinomas (3)
Elevated insulin, proinsulin (25% of circulating insulin) and C-peptide
How are insulinomas treated?
Surgical resection
What congenital syndrome is associated with congenital hyperinsulinism?
Beck with Wiedemann syndrome
What is classic presentation of congenital hyperinsulinism? (3)
Severe neonatal hypoglycemia
Large birth weight
High glucose requirements
Diffuse vs. Focal hyperinsulinism Treatment
Focal: remove affected area
Diffuse: need to use therapy
Pharmacological Treatment for hyperinsulinemic hypoglycemia: Diazoxide–MOA and AE
Activates ATP-dependent K channel
Side effects: fluid retention, hypertrichosis
Pharmacological treatment for hyperinsulinemic hypoglycemia: Octreotide–MOA and AE
Activates ATP dependent K channel, affects intracellular translocation of Ca, direct inhibition of insulin secretion
Tachyphylaxis, suppression of GH/TSH/ACTH, GI side effects, necrotizing enterocolitis
Categories of Autoimmune hypoglycemia
Bind to insulin receptor: agonists (hypoglycemia) or antagonists (hyperglycemia)
Insulin antibodies (hirata’s disease): fasting hypoglycemia
GH/Cortisol Deficiency: Clues (3)
Midline defect, microphallus, cholestatic liver disease
GH/Cortisol deficiency: treatment (2)
Shorten fasting, hormone replacement
Critical samples in GH/cortisol deficiency:
Ketone pattern
G6Pase deficiency: Clinical (2)
Impaired gluconeogenesis/glycogenolysis
Failure to thrive, hepatomegaly
G6Pase deficiency: Labs (3) and test (1)
Hyperlacticacidemia, hyptertriglyceridemia, hyperuricemia
Lack of glycemic response to fed glucagon stimulation test
G6Pase deficiency: Treatment (4)
Frequent carb-rich meals
Intragastric dextrose
Uncooked cornstarch
No lactose/fructose
G6Pase deficiency: Types
Glycogen storage disease 1a
Glycogen storage 1b (10%): added neutropenia
F1,6BP deficiency: Clinical signs and trigger
Attacks of acidemia, hyperlacticacidemia, hyperuricemia
Triggered by fasting/fructose
F1,6BP deficiency: Rx (2)
Limit fasting to less than 8-12 hours
No fructose/sucrose
Glycogen Debrancher Deficiency (GSD type 3): Clinical signs (3)
Failure to thrive, hepatomegaly, muscle weakness
Glycogen Debrancher Deficiency (GSD type 3): labs
Impaired glycogenolysis: hyperketonemia
Glycogen Debrancher Deficiency (GSD type 3): Rx (3)
Frequent low carb feeds
Intragastric dextrose
Uncooked cornstarch
Late symptoms of Glycogen Debrancher Deficiency (GSD type 3) (2)
Cardiomyopathy
Myopathy
Medium Chain Acyl-CoA Dehydrogenase Deficiency–FAO defect: Signs (2)
Hypoketotic hypoglycemia
Mimics Reye’s syndrome
Medium Chain Acyl-CoA Dehydrogenase Deficiency–FAO defect: Rx (1)
Limit fasting to less than 12 hours
Hypoglycemia due to drugs (4)
Sulfonylureas
Salicylate OD
Beta-adrenergic blocking agents (no adrenergic warning signs, HHS pattern)
Pentamidine for pneumocystis
What substance can stimulate hypoglycemia in fasting state? How does it do this?
Alcohol; by using NDH
DDX of Hypoglycemia based on critical sample
See chart! Know chart!
