Exocrine and Endocrine Pancreas

Question 1

What is the exocrine function of the pancreas?

Answer 1

Exocrine glands produce bicarbonate, amylase, protease and lipase enzymes which are released in ducts.

Question 2

What is the endocrine function of the pancreas?

Answer 2

It produces hormones in clusters called the islets of Langerhaan. Alpha cells produce glucagon, beta cells produce insulin, delta cells produce somatostatin and p (F) cells produce pancreatic polypeptides. These are released in ducts.

Question 3

What is the functional unit of the pancreas?

Answer 3

Acinar, which cluster together to form acinus. They release secretions into intercalacted ducts.

Question 4

What is the intercalated ducts?

Answer 4

Receive secretions from the exocrine glands of the acinus. It joins to a larger intercalated duct and forms an interlobular duct.

Question 5

Where is secretin produced?

Answer 5

In S cells of the duodenum which inhibits gastric acid secretion. It acts on the pancreatic duct cells to cause conversion of ATP-> cAMP for activation of basolateral K+ and Cl- channels to promote bicarbonate secretion.

Question 6

Where is bicarbonate synthesised?

Answer 6

In exocrine glands and released into intercalated ducts.

Question 7

What is the basal surface of a duct?

Answer 7

Facing the pancreatic blood supply. Contains the Na-H+ antiporter, Na+/K+ ATPase transporter and K+ channels.

Question 8

What is the apical surface of a duct?

Answer 8

Facing the lumen. Contains the HCO3- : CL- exchanger and Cl- channel.

Question 9

How does bicarbonate secretion occur?

Answer 9

Water and CO2 enter the cell and form H2CO3 by carbonic anydrase which disassociates into HCO3- and H+. HCO3- will undergo exchange with CL- on the apical surface which increases intracellular CL-. 3H+ will undergo exchange with 3Na+ on the basolateral surface. Rise in intracellular Na+ activates the Na+/K+ ATPase pump which increases intracellular K+. Secretin acts to cause conversion of ATP -> cAMP. This results in K+ channel and cAMP activated Cl- channel (CFTR) activation. There is great Cl- efflux which is recycled by the CL-/HC03- exchanger to cause bicarbonate secretion of HCO3-.

Question 10

What type of exchanger is the sodium-hydrogen pump?

Answer 10

Antiporter- 3 Na+ for 3H+

Question 11

What type of exchanger is the sodium-potassium pump?

Answer 11

ATP powered pump.

Question 12

What is the role of cholecystokinin?

Answer 12

Promotes the digestion of fats and proteins by acting on exocrine glands in ducts to release protease and amylase. It is released from pancreatic I cells.

Question 13

Where is cholecystokinin synthesised?

Answer 13

I cells of the pancreas.

Question 14

What is the role of secretin?

Answer 14

Released from S cells of the pancreas and duodenum. Acts on the ducts to promote bicarbonate secretion by activating cAMP signalling for CFTR activation which causes more HCO3- efflux. It is important in water homeostasis.

Question 15

How does cystic fibrosis occur?

Answer 15

Frameshift mutation of the CFTR gene which disrupts exocrine release of digestive enzymes and causes autodigestion of the pancreas.

Question 16

How can digestion in CFTR patients be aided?

Answer 16

Pancreatin medication containing amylase, starch and lipase with enteric coating

Question 17

What are the cells of the endocrine pancreas?

Answer 17

Alpha cells, beta cells, delta cells, pf cells, and epsirolein cells.

Question 18

What is the majority of the endocrine pancreas composed of?

Answer 18

Beta cells

Question 19

Which cell composes the least of the pancreas?

Answer 19

Delta cells and episorelin cells.

Question 20

Which hormones regulate appetite?

Answer 20

P(f) cells that produce pancreatic polypeptide and episorelin cells that produce ghrelin.

Question 21

What is the role of insulin?

Answer 21

Regulate blood glucose levels. It is released from beta cells and enters portal cells to stimulate glucose storage in the liver, muscles and adipose tissue.

Question 22

What is the hexameric form?

Answer 22

Insulin in its storage form. It has a central zinc ion surrounded by 6 insulin molecules linked by hexatidine bonds. It has a slow diffusing capacity.

Question 23

What is the monomeric form?

Answer 23

Insulin in its active form which is a single alpha and beta chain joined by disulphide bonds. It has a T12 of=6mins and has a fast diffusing capacity.

Question 24

How is insulin synthesised?

Answer 24

It exists as a single 24 amino acid long polypeptide chain with alpha and beta joined by connecting bridge. It is preporinsulin. It releases a 24 amino acid singal to cause it to move to Golgi apparatus. Here, it is converted from preproinsulin-> proinsulin. This enters the transgolgi network and undergoes change and modification into mature insulin in the hexameric store awaiting metabolic or vagal nerve stimulation.

Question 25

How is insulin secreted?

Answer 25

High glucose levels activates the GLUT2 pump for glucose uptake. It is metabolised and releases phosphate and enters glycolysis to synthesis ATP in beta cells. This activates the ATP Na+/K+ sensitive channel and causes depolarisation and rise in intracellular K+. Depolarisation causes activation voltage gated Ca2+ to act on hexameric insulin stores to ->monomeric insulin stores and exocytosis for release into bloodstream.

Question 26

What is the structure of insulin receptor?

Answer 26

Consists of alpha and beta subunit joined by disulphide bond. Alpha subunit is hwere insulin binds. Beta subunit is transmembrnae and contains tyrosine kinase for phosphorylation inf the insulin receptor substrates 1, 2, 3 and 4.

Question 27

What is the mechanism of insulin action?

Answer 27

Insulin acts on the alpha subunit. Causes signalling for reducing lipid and portein metabolism and affects growth and phosphorylation of the insulin receptor substrate 1 specifically which recruits GLUT4 to move to cell membrane for uptake of glucose.

Question 28

What happens to glucose?

Answer 28

Majority of glucose is stored; 35% is oxidised into CO.

Question 29

What are anabolic effects of insulin?

Answer 29

Promotes anabolism for storage via glycogenolysis.

Question 30

What are the catabolic effects of insulin?

Answer 30

Reduces catabolism.

Question 31

Where does glucose homeostasis occur?

Answer 31

In the liver hepatic where there is gluconeogenesis of porteins and fat

Question 32

Where is the majority of glucose stored?

Answer 32

Liver glycogen stores.

Question 33

Where is the majority of glucose used?

Answer 33

In the brain which lacks any GLUT transporters and no insulin action so it uses all glucoses that it receives because it cannot be stored.

Question 34

What are faculative glucose consumers?

Answer 34

All the organs and tissues of the body excluding the brain which can respond to insulin to regulate glucose use.

Question 35

How is glycogen synthesised?

Answer 35

Single polysaccharide chain which is a store of glucose in the liver.

Question 36

How is glucagon synthesised in the pancreas?

Answer 36

29 amino acid polyepptide non steroid hormone. From pro-glucagon -> glucagon by action of proprotein convertase 2 enzyme in alpha cells.

Question 37

How is glucagon synthesised in the intestine?

Answer 37

From pro-glucagon -> lower intestinal cells of jejunum and ileum GLP1 (incretin), GLP2 and ILP-2 (insulin like peptide) in L cells of the intestine. In K cells in the duodenum and upper jejunum, it produces GIP.

Question 38

What is glucagon-like peptide one?

Answer 38

Synthesised from por-glucagon by L cells in the intestines. It is an incretin. Reduces inflammation, increases kidney Na+ excretion and increases cardiac function and v=protection and reduces fatty acid metabolism and inflammation.

Question 39

What is the effect of incretin?

Answer 39

Promotes insulin and inhibits glucagon release. It acts on the hypothalamus to reduce appetite, slows gastric emptying. It reduces hepatic glucose output via reducing glycogenolysis.