Hypoglycemia & Integration of Metabolic Pathways Flashcards
Whipple’s Triad
- Low plasma glucose
- Symptoms of hypo-g
- Resolution of symptoms w tx (food, glucose, glucagon, etc.)
Autonomic sx of Hypo-G
Diaphoresis Hunger Paresthesias Tremulousness Palpitations Anxiety
Neuroglycopenic sx of Hypo-G
Cogn impairment Visual changes Behavior changes Weakness Lethary Dizziness Seizures Coma
Counterregulatory hormone response to hypo-g <80
Dec insulin
Counterregulatory hormone response to hypo-g <65-670
Inc glucagon
inc epi
inc GH
Counterregulatory hormone response to hypo-g <55-60
Inc cortisol
Medications that cause hypo-g
Insulin & SU (inc glucose uptake regardless of plasma [glucose])
Beta-hydroxybutyrate
KB
Suggests insulin effect but does not distinguish between endo/exo insulin, or antibody
Causes w/ low insulin/effect will have _____ glycogen stores in response to hypo-g
depleted glycogen stores
Endogenous hyperinsulinism
SU use
Insulinoma
Exogenous hyperinsulinism
Insulin use
Insulinoma
Neuroendocrine tumor of pancreatic cells
Typically fasting hypo-g
Rare
Non-insulin mediated hypo-g
drugs EtOH Liver Dz Starvation Adrenal insufficiency Insulin-R mediated (IGF2, Insulin-R antibodies)
DKA characterized by:
hyperglycemia
Insulinoma causes low serum _____
Beta-OHB
EtOH metab generates high level of ____ & ____
NADH
Acetyl CoA
What contributes to both hypo-g & KA?
NADH
Gluconeogenesis
Pyruvate–> pyruvate carboxylase –> OAA –> PEPCK –> PEP –>-> F1,6BP –> F1,6bisPase –> F6P
Do NADH and/or Acetyl CoA affect gluconeogenesis, and if so, in what direction?
Neither affect it
Is thiamin required for glucose metab?
Yes, is a cofactor for PDH and TCA DH’s
Is B12 required for glucose metab?
No
What can cause excessive hepatic TG?
Excessive lipolysis
Excessive FA synth
Impaired FA ox
What normally happens to hepatic TG?
Released as VLDL