Physiology of Pancreas Flashcards Preview

SF3-EXAM 4 (CAMELITA) > Physiology of Pancreas > Flashcards

Flashcards in Physiology of Pancreas Deck (36)
Loading flashcards...

Which hormones are released during the fasting state?

  • Glucagon
  • Catecholamines
  • Cortisol (supplementary if the first two don't get the job done)
  • Growth hormone (supplementary if the first two don't get the job done)


What are the sources of control of the synthesis and secretion of islet hormones?

  • Humoral communication
    • ​Blood supply of the islet course otuward from the center toward the periphery, carrying glucose and other secretagogues
  • Cell-cell communication
    • Cells within an islet connect with one another and communicate through gap junctions
  • Neural communication
    • Islets are innervated by the sympathetic and parasympathetic divisions of the ANS


Products of alpha cells

  • Glucagon (20% of islet cells located near periphery)


Products of beta cells

  • Insulin-60-75% of islet cells located mainly in the center
  • Amylin


Products of delta cells

  • Somatostatin- 5% of islet cells interspersed between the alpha and beta cells


Products of F cells

Pancreatic polypeptide


Insulin is encoded by a single gene on Chromosome ___.



Insulin synthesis and secretion is stimulated when islets are exposed to glucose. What are the components of the secretory granules that secrete insulin?

Insulin, C peptide and a small amount of proinsulin

NOTE: The half-life of insulin is approximately 5 mins


What are the mechanism by which insulin beinds to it's cell receptors?

1. Insulin binds to specific receptor tyrosine kinase on the plasma membrane

2. Insulin recept can phosphorylate both itself and other intracellular substrate at tyrosine kinase residues

3. insulin is able to transmit its signal across the plasma membrane of insulin target tissues


Approximately 60% of insulin that enters into the portal vein is removed by the _____.


NOTE: C-peptide is not extracted by the liver, but is excreted by the kidneys. This is important diagnostically. C-peptide is not harmed by the liver, so it makes it out of circulation in the exact amount that the beta cells synthesized it. 


High C-peptide levels are diagnostic of __________.



When is glucose response to insulin maximal?

When only approximately 5% of the receptors are occupied


What effect does insulin have at the liver?


Glycogen synthesis


Protein Metabolism


The biggest issue with diabetes is the inability of ______ to take up glucose.

Skeletal muscle


Function of insulin at skeletal muscle

  • Increases GLUT4 translocation
  • Increases glycogen synthesis
  • Increase glycolysis
  • Increases protein synthesis and slows protein degradation
  • Increases triglycerides


Function of insulin at adipocytes

  • Increase GLUT4 transporters
  • Increase glycolysis
    • Increase in a-glycerol phosphate
    • Increase in acteyl CoA
    • Increase in FA synthesis
  • Increase triglycerides
    • Increase LPL
    • Inhibits hormone sensitive lipase


How does glucose stimulate the release of insulin?

1. Glucose enters the β-cells through the glucose transporters, GLUT2.

2.The glucose that enters the β-cell is phosphorylated to glucose-6-phosphate by glucokinase

3. Glucose-6-phosphate enters glycolytic pathway, leading to a rise in the ATP:ADP ratio within the cell.

4. An increased intracellular ATP:ADP ratio closes the ATP-sensitive potassium channel.

5. Upon depolarization, voltage-gated calcium ion (Ca2+) channels open, allowing calcium ions to move into the cell by facilitated diffusion.

6. The significantly increased amount of calcium ions in the cells' cytoplasm causes the release into the blood of previously synthesized insulin, which has been stored in intracellular secretory vesicles.


Aside from glucose, what other factors stimulate the release of insulin?

  • FFAs
  • Amino acids
  • Sulfonyurea drugs
  • Epinephrine and norepinephrine


A healthy person will have a spike of insulin within ____ minutes of eating.


*There's a drop and then another slight increase of insulin within 120 minutes of eating. This 2nd peak is caused by reload of beta cells, which are synthesizing more insulin


What is the one time in which glucagon and insulin work together?

When amino acids levels are high


________ mg/dL of glucose is the "magic mark" where glucagon is shut down and insulin begins to rise.



When do growth hormone and cortisol come into play with regard to hypoglycemia?

When fasting for 2 or more days

NOTE: The kidneys can also produce glucose by gluconeogenesis in cases of prolonged fasting. 

REMEBER: Glucagon and epinephrine are the first hormones to kick in when blood glucose is low. Cortisol and GH supplement them


Type I DM

  • Diabetes B- cell destruction
    • Immmune-mediated
    • Idiopathic

NOTE: Autoantibodies are formed against islet cell cell autoantibodies, insulin, and GAD65


Type II DM

  • Progressive insulin secretory defect
    • Gestational diabetes mellitus (3rd trimester of preganancy)
    • MODY
    • Disease of the exocrine pancreas (cystic fibrosis)
    • Drug or chemical induced diabetes


What are the general signs and symptoms of DM?

  • Polyrua, nocturia, polydipsia
  • Weight loss, sometimes with polyphagia
  • Blurred vision
  • Impairment of growth
  • Susceptibility to certain infections
  • Hyperglygemia with keto acidosis
  • Hyperglycemic Hyperosmolar syndrome

NOTE: Ketoacidosis is generally associated with Type I. Type II is associated with hyperosmolar hyperglycemic syndrome (HHS).


________ cell loss to a certain degree triggers Type I DM.


NOTE: Immunologic trigger can lead to diabetes in people with genetic predisposition to it. When an immunologic trigger you can see beta cell numbers steadily dropping.


What are the metabolic consequences of insulin deficiency?

  • Increased blood glucose concentration
  • Increased blood FFA and ketoacid concentration- fat depletion
  • Increased blood amino acid concentration- protein depletion


What are the consquences of DM Type I on fluids and electrolytes?

  • Metabolic acidosis
  • Glycosuria and osmotic diuresis
  • Increased plasma osmolality
  • Hyperphagia
  • Polydipsia
  • Hypovolemia and hypotension
  • Coma and death



Refers to any of several hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production.

NOTE: Genes affected are HNF-4a, HNF-1a, IPF-1, HNF-1B, NeuroD1


Contrast MODY from DM II


  • Nonobese
  • Monogenic
  • Metabolic syndrome absent


  • Obese
  • Polygenic
  • Metabolic syndrome present