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 Episolon-

• Function- Dual system- Exocrine and Endocrine

Structure-

• Normal vs Abnormal (Diabetes)

• Normal
 o Sugar molecule how it looks like from the beginning

 Simple sugar

o Metabolism- breakdown of glucose molecule to energy

 Release from 1 molecule of glucose to produce

ATP

• Process. What cells really contribute?

o Mitochondria main cells

o Hepatocytes

o Krebs Cycle, Calvin Cycle, Cori Cycle, 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.

o Cycles mentioned above. Know main enzymes that are

involved.

How does pancreas sense that there is food coming….how does it

prepare..pancreatic juice?

• The I cell and S cell –

o CCK

• If it wasn’t diabetes it could have been

o Pancreatic Cancer- death sentence

-Pancreas (main function of this case)

-Graphs- Glucose levels from fasting

Eating over 24 hours

All graphs pertaining to glucose levels…

o
 Definition of Diabetic Ketoacidosis
The most severe and life threatening complication of
poorly controlled type 1 diabetes is diabetic ketoacidosis
(DKA). DKA is characterized by metabolic acidosis,
hyperglycemia and hyperketonemia. Diagnosis of DKA is
accomplished by detection of hyperketonemia and
metabolic acidosis (as measured by the anion gap) in the
presence of hyperglycemia.
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. The anion gap therefore, represents an
artificial assessment of the unmeasured ions in plasma.
Calculation of the anion gap involves sodium (Na+),
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. The anion gap will
increase when the concentration of plasma K+, Ca2+, or
Mg2+ is decreased, when organic ions such as lactate are
increased (or foreign anions accumulate), or when the
concentration or charge of plasma proteins increases.
Normal anion gap is between 8mEq/L and 12mEq/L and a
higher number is diagnostic of metabolic acidosis. Rapid
and aggressive treatment is necessary as the metabolic
acidosis will result in cerebral edema and coma eventually
leading to death.
The hyperketonemia in DKA is the result of insulin
deficiency and unregulated glucagon secretion from α-
cells of the pancreas. Circulating glucagon stimulates the
 adipose tissue to release fatty acids stored in triglycerides.
The free fatty acids enter the circulation and are taken up
primarily by the liver where they undergo fatty acid
oxidation to acetylCoA. Normally, acetyl CoA is completely
oxidized to CO2 and water in the TCA cycle. However, the
level of fatty acid oxidation is in excess of the livers' ability
to fully oxidize the excess acetyl CoA and, thus, the
compound is diverted into the ketogenesis pathway. The
ketones (ketone bodies) are β-hydroxybutyrate and
acetoacetate with β-hydroxybutyrate being the most
abundant. Acetoacetate will spontaneously (non-
enzymatic) decarboxylate to acetone. Acetone is volatile
and is released from the lungs giving the characteristic
sweet smell to the breath of someone with
hyperketonemia. The ketones are released into the
circulation and because they are acidic lower the pH of the
blood resulting in metabolic acidosis.
Insulin deficiency also causes increased triglyceride and
protein metabolism in skeletal muscle. This leads to
increased release of glycerol (from triglyceride metabolism)
and alanine (from protein metabolism) to the circulation.
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. The increased
rate of glucose production in the liver, coupled with the
glucagon-mediated inhibition of glucose storage into
glycogen results in the increased glucose release from the
liver and consequent hyperglycemia. The resultant
hyperglycemia produces an osmotic diuresis that leads to
loss of water and electrolytes in the urine. The ketones are
also excreted in the urine and this results in an obligatory
loss of Na+ and K+. The loss in K+ is large, sometimes
exceeding 300 mEq/L/24 h. Initial serum K+ is typically
normal or elevated because of the extracellular migration of
K+ in response to the metabolic acidosis. The level of K+ will
fall further during treatment as insulin therapy drives K+ into

The Pancreas
The secretions of the pancreas, called pancreatic juice, include various
enzymes, including pancreatic amylase (digestion of starch), trypsin,
carboxypepiydase, and chymotrypsin (proteases), as well as
pancreatic lipase (digestion of fats). Sodium bicarbonate is also
produced, making the pancreatic juice alkaline. An alkaline solution
neutralizes the HCl in the chyme and provides an optimal environment
for the action of these enzymes.

Pancreatic juice is produced in clusters of exocrine cells called acini.

The remaining cells in the pancreas (about 1 percent of the total) also
form clusters (islets of Langerhans). These are the endocrine cells that
produce the hormones insulin, glucagon, somatostatin, and pancreatic
polypeptide.
Pancreatic juice collects in small ducts that merge to form two large
ducts. The main pancreatic duct (duct of Wirsung) exits the pancreas
and merges with the common bile duct from the liver and gallbladder.
This combined duct, called the hepatopancreatic ampulla (ampulla of
Vater), then enters the duodenum. A smaller, second duct that exits
the pancreas, the accessory pancreatic duct (duct of Santorini), joins
the duodenum directly.