Endocrine Module 2- Section 1-Pancreas Flashcards
pancreas
endocrine and exocrine fxn
endocrine fxn consists of islets cells-alpha, beta, delta
alpha-glucagon
beta-insulin
delta-somatostatin
Glucagon Function
prevents hypoglycemia, increases blood glucose levels
catabolic and mobilizes fuel
Glucagon Target Cells
liver-glycogenolysis (break down glycogen), glucogenesis (glucose formation)
Fat tissue- lypolysis
Muscle-proteolysis (for amino acid release)
In response to hyporglycemia-glucagon trying to make fuel
Factors that stimulate glucagon secretion
hypoglycemia, exercise, stress, fasting
Factors that inhibit glucagon secretions
hyperglycemia
Amylin
co-secreated with insulin during feeding. Supress glucagon
Insulin-Function
prevents hyperglycemia, promotes “metabolic fuel” storage
decrease blood glucose levels, decrease blood levels if amino acid concentrations and FFA/ketons, decrease serum potassium uptake into cells
Insulin target-Liver
increased glucose uptake, formation of glycogen, lipid/protein synthesis
decreased ketogenesis, glycogenolysis
Insulin target- muscle
increased glucose uptake, formation of glycogen, amino acid uptake, protein synth
decreased glycogenolysis
Insulin Target- adipose tissue
Increased- glucose uptake, glucose to form glycerol phosphate, fat storage
Decreased-lypolysis
Factors that stimulate nsulin secretions
hyperglycemia
increased serum levels of FFA, amino acids
GI/digestive hormones
parasympathetic stimulation of pancreatic beta cells
Factors that inhibit insulin secretion
hypoglycemia, negative feedback loop (increased insulin levels)
sympathetic simulation of pancreatic beta cells
prostaglandins (PGE2)
Insulin Sensitivity
body can down or up regulate insulin receptors
excessive insulin will decrease number of insulin receptors
DM Type 1
insulin insufficiency d/t result of pancreatic destruction of beta cells islets of langerhans
Hyperglycemia–cells unable to take up glucose from blood
Hyperlipidemia–lack of insulin is inhibitory to fat storage, athersclerotic changes in BV
Increased Ketone Bodies/ketoacidosis- ketones formed from increased FFA metabolism in liver
Catabolic Affect on muscle mass (attempt to mobilize amino acids for fuel)
Insulin Shock
hypoglycemia
excessive insulin administration, increased physcial activity, poor glucose monitoring
will see hunger, sweating, irritability