1. The Pancreas
Felicity Clark
Speciality Registrar
New Cross Hospital

2. Why is it important ?
 Pancreatitis
 Diabetes
 Common primary FRCA question

3. What you need to Know
 Exocrine Function
 Endocrine function
 Insulin
 Glucagon
 Somatostatin

4. Structure of the Pancreas
 Loblues
 2 types of parenchymal tissue
 Acinus (80%)
 Islets of Langherhans (2%)
 Blood vessels and ducts (15%)

5. Exocrine Pancreas
 Lumen of Acini produce pancreatic
secretions
 Accumulate in intralobular ducts
 Drain to the main pancreatic duct
 Drains directly into the duodenum

6. Exocrine Pancreas
 Control is via hormones
 gastrin, cholecystokinin and secretin
 secreted by cells in the stomach and
duodenum
 in response to distension and/or food

7. Exocrine Pancreas
 2 main classes of exocrine pancreatic secretions
 Bicarbonate ions – centroacinar cells – Secretin
 Neutralise acidic chyme
 Digestive enzymes – Basophilic cells –
Cholecystokinin
 Proteases – trypsinogen & chymotrypsinogen
 Pancreatic lipase
 Pancreatic amylase
 Secreted as inactive enzymes - zymogens
 Enteropeptidase activates

8. Endocrine Pancreas
 Islets of Langherhans
 Insulin
 Glucagon
 Somatostatin
 Pancreatic polypeptide

9. Insulin
 Anabolic
 51 amino acids
 pro- insulin – C peptide removed
 2 polypeptide chains – disulphide bridges
 Beta cells
 Binds to alpha sub unit of insulin receptor
 Autophosphorylation of tyrosine kinase
 Activates protein kinases
 Gene on short arm of chromosome 11

10. Effects of Insulin
 Carbohydrate metabolism
 Glucose uptake – liver /skeletal muscle
 Glycogen storage
 Glucose utilisation as energy source

11. Effects of Insulin
 Protein metabolism
 Stimulates amino acid uptake by cells
 Stimulates protein synthesis
 Inhibits Gluconeogenesis

12. Effects of Insulin
 Lipid metabolism
 Inhibits lipolysis
 Stimulates fatty acid synthesis from
glucose
 Stimulates glycerol synthesis
 Promotes carbohydrate metabolism /
sparing fat

13. Controlling factors - Insulin
 Secretion stimulated  Secretion inhibited
 Hyperglycaemia  Hypoglycaemia
 Amino acids  Beta blockers
 Beta agonists  alpha agonists
 Acetylcholine  Somatostatin
 Glucagon  Diazoxide
 Thiazides
 Volatiles

14. Insulin Deficiency
 Type 1 DM – Autoimmune
 Type 2 DM – Insulin resistance
 Secondary Diabetes –
 increased cortisol – cushings
 increased growth hormone
 increased glucagon

15. Insulin deficiency – think DKA
 Carbohydrate
 decreased glucose uptake
 Hyperglycaemia, Glycosuria
 Osmotic diuresis
 Protein
 Increased amino acids in plasma
 Nitrogen loss in urine
 Dehydration
 Ketoacidosis
 Respiratory alkalosis
 Coma
 Death

16. Insulin deficiency – think DKA
 Lipids
 increased Lipolysis
 Increased free fatty acids
 Ketogenesis
 Ketonuria

17. Insulin excess
 Insulinoma (rare)
 Iatrogenic (can measure C-peptide)
 Hypoglycaemia
 Tremor
 Sweating
 Tacchycardia
 Coma
 Death

18. Glucagon
 Catabolic
 29 amino acids
 Alpha cells
 Acts as a second messenger via cyclic
AMP
 Opposes insulin

19. Effects of Glucagon
 Carbohydrate Metabolism
 Increased Gluconeogenesis
 Increased glycogenolysis
 Glucose sparing – beta oxidation of fatty
acids for energy – ketone bodies

20. Effects of Glucagon
 Lipid Metabolism
 Stimulates Lipolysis
 Other effects
 Increases catecholamine production
 Direct positive inotrope

21. Controlling factors- Glucagon
 Secretion Stimulated  Secretion Inhibited
 hypoglycaemia  Hyperglycaemia
 increased amino acids  decreased amino
 beta agonists acids
 sepsis  increased free fatty
 stress acids
 trauma
 insulin
 somatostatin
 alpha agonists

22. Somatostatin
 delta cells
 hypothalamus
 also called growth hormone inhibiting
hormone
 inhibits insulin and glucagon release
 inhibits gastric acid production
 inhibits gallbladder contraction
 Neurotransmitter – SG - pain