You are on page 1of 5

Pancreas: Where did it come from? Layer?

• Anatomy- Gland o 3 parts  head, body, tail

o 2 major ducts    Duct of warsum Duct of Santori Ampulla of Vater

o Histology  Islets of Langerhans • Alpha, beta, delta, epsilon o Alpha-Glucagon-Helps break down glycogen. How does this relate to insulin…know relationship. o Beta-Insulin- To aid entry of glucose into cell o Delta- Somatostatin-Controls the level of secretion of insulin and glucagon. The “puppeteer” of the two above. o Episolono • Function- Dual system- Exocrine and Endocrine o Structure-

• •

Normal vs Abnormal (Diabetes) Normal

breakdown of glucose molecule to energy  Release from 1 molecule of glucose to produce ATP • Process. o Cycles mentioned above. Know main enzymes that are involved.pancreatic juice? • The I cell and S cell – o CCK • If it wasn’t diabetes it could have been o Pancreatic Cancer.how does it prepare. Calvin Cycle..Glucose levels from fasting Eating over 24 hours All graphs pertaining to glucose levels… o .o Sugar molecule how it looks like from the beginning  Simple sugar o Metabolism. What cells really contribute? o Mitochondria main cells o Hepatocytes o Krebs Cycle. Cori Cycle. How does pancreas sense that there is food coming…. Glycolysis…  Energy comes from these how? • Think of different ways that glucose is broken down and how many default systems are out there to reach end result.death sentence -Pancreas (main function of this case) -Graphs.

The hyperketonemia in DKA is the result of insulin deficiency and unregulated glucagon secretion from αcells of the pancreas. The anion gap refers to the difference between the concentration of cations other than sodium and the concentration of anions other than chloride and bicarbonate. DKA is characterized by metabolic acidosis.Definition of Diabetic Ketoacidosis The most severe and life threatening complication of poorly controlled type 1 diabetes is diabetic ketoacidosis (DKA). Ca2+. or when the concentration or charge of plasma proteins increases. when organic ions such as lactate are increased (or foreign anions accumulate). or Mg2+ is decreased. Normal anion gap is between 8mEq/L and 12mEq/L and a higher number is diagnostic of metabolic acidosis. represents an artificial assessment of the unmeasured ions in plasma. Circulating glucagon stimulates the . Diagnosis of DKA is accomplished by detection of hyperketonemia and metabolic acidosis (as measured by the anion gap) in the presence of hyperglycemia. Calculation of the anion gap involves sodium (Na+). hyperglycemia and hyperketonemia. The anion gap will increase when the concentration of plasma K+. The anion gap therefore. Rapid and aggressive treatment is necessary as the metabolic acidosis will result in cerebral edema and coma eventually leading to death. chloride (Cl–) and bicarbonate (HCO3–) measurements and it is defined as [Na+ – (Cl– + HCO3–)] where the sodium and chloride concentrations are measured as mEq/L and the bicarbonate concentration is mmol/L.

However. thus. The ketones are also excreted in the urine and this results in an obligatory loss of Na+ and K+. The increased rate of glucose production in the liver. Initial serum K+ is typically normal or elevated because of the extracellular migration of . The ketones (ketone bodies) are β-hydroxybutyrate and acetoacetate with β-hydroxybutyrate being the most abundant. the level of fatty acid oxidation is in excess of the livers' ability to fully oxidize the excess acetyl CoA and. Insulin deficiency also causes increased triglyceride and protein metabolism in skeletal muscle. The loss in K+ is large. Acetone is volatile and is released from the lungs giving the characteristic sweet smell to the breath of someone with hyperketonemia. These substances then enter the liver where they are used as substrates for gluconeogenesis which is enhanced in the absence of insulin and the elevated glucagon. coupled with the glucagon-mediated inhibition of glucose storage into glycogen results in the increased glucose release from the liver and consequent hyperglycemia.adipose tissue to release fatty acids stored in triglycerides. This leads to increased release of glycerol (from triglyceride metabolism) and alanine (from protein metabolism) to the circulation. Normally. The free fatty acids enter the circulation and are taken up primarily by the liver where they undergo fatty acid oxidation to acetylCoA. sometimes exceeding 300 mEq/L/24 h. acetyl CoA is completely oxidized to CO2 and water in the TCA cycle. The ketones are released into the circulation and because they are acidic lower the pH of the blood resulting in metabolic acidosis. The resultant hyperglycemia produces an osmotic diuresis that leads to loss of water and electrolytes in the urine. Acetoacetate will spontaneously (nonenzymatic) decarboxylate to acetone. the compound is diverted into the ketogenesis pathway.

the accessory pancreatic duct (duct of Santorini). The remaining cells in the pancreas (about 1 percent of the total) also form clusters (islets of Langerhans). and chymotrypsin (proteases). called the hepatopancreatic ampulla (ampulla of Vater). An alkaline solution neutralizes the HCl in the chyme and provides an optimal environment for the action of these enzymes. These are the endocrine cells that produce the hormones insulin. . somatostatin. second duct that exits the pancreas. glucagon. Sodium bicarbonate is also produced. The level of K+ will fall further during treatment as insulin therapy drives K+ into The Pancreas The secretions of the pancreas. then enters the duodenum. Pancreatic juice is produced in clusters of exocrine cells called acini. include various enzymes. carboxypepiydase. including pancreatic amylase (digestion of starch). called pancreatic juice. This combined duct. trypsin. The main pancreatic duct (duct of Wirsung) exits the pancreas and merges with the common bile duct from the liver and gallbladder. joins the duodenum directly. making the pancreatic juice alkaline. Pancreatic juice collects in small ducts that merge to form two large ducts. and pancreatic polypeptide.K+ in response to the metabolic acidosis. as well as pancreatic lipase (digestion of fats). A smaller.