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Reproductive and Endocrine > Pancreas > Flashcards

Pancreas Flashcards

1
Q

Why does a pancreas dissected out of a mouse have to be speedily placed into fluid which inactivates the enzymes?

A

The pancreas rapidly digests itself when removed.

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2
Q

What is the tail of the pancreas associated with, and what is the head of the pancreas associated with?

A 
Tail = spleen
Head = duodenum
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3
Q

What are the two divisions of the pancreas?

A

Exocrine (majority of pancreas) and endocrine (lighter staining)

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4
Q

What are the three parts of the exocrine pancreas?

A

Acinus
Intercalated duct - leads from acinus to striated duct
Striated duct - connects intercalated duct to intralobular duct

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5
Q

What is the function of the intercalated ducts of the exocrine pancreas?

A

To secrete bicarbonate which acts as a buffer to increase the pH so the enzymes in the duodenum can work.

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6
Q

What is the function of the exocrine pancreas?

A

To secrete bicarbonate, enzymes, zymogens, and this is controlled by CCK and secretin (which are stimulated by the parasympathetic vagus nerve).

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7
Q

Where is CCK secreted and what is its function in the exocrine pancreas?

A

Secreted by I cells in the duodenum in response to chyme. CCK helps digestion of fats, proteins and carbohydrates by acting on the cells of the acinus to stimulate secretion of digestive enzymes.

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8
Q

Where is secretin secreted, and what is its function in the exocrine pancreas?

A

Secreted by S cells in the duodenum. Secretin acts on the intercalated ductal cells to stimulate secretion of bicarbonate ions.

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9
Q

How does secretin cause the cells of the intercalated duct to secrete bicarbonate ions?

A

1) Secretin causes an increase in intracellular production of cAMP
2) The increase in cAMP activates K+ and Cl- channels to open
3) K+ diffuses down a concentration gradient out of the cell, which causes Cl- to diffuse out of the cell through CFTR down an electrical gradient
4) Carbon dioxide and water from carbonic acid in the cell which then dissociated to H+ and HCO3- ions
5) There is a concentration gradient fro Na+ into the cell, so the Na+/H+ exchanger pumps H+ out of the cell which causes HCO3- to accumulate inside the cell
6) The Cl-/HCO3- exchanger pumps HCO3- out of the cell and lets Cl- flow back in

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10
Q

Which organs are affected by cystic fibrosis?

A

Lungs, liver, pancreas, intestine

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11
Q

How does cystic fibrosis lead to the development of fibrotic scar tissue (fibrosis) in the pancreas, and why is this a problem?

A

The frameshift mutation in the CFTR gene leads to abnormal Na+ and Cl- transport across the membrane so that a thick sticky mucus is produced. This blocks the exocrine movement of digestive enzymes, and causes the enzymes to stay in the pancreas and rapidly begin to digest the pancreas itself. This is what causes fibrotic scar tissue to develop, and leaves the tissue non-functional.

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12
Q

What is the drug called that orally administers pancreatic enzymes (lipase, protease, amylase) in an enteric coating to aid digestion?

A

Pancreatin.

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13
Q

What are the five types of cells in the Islet of Langerhans, and what do they secrete?

A

1) Alpha cells - glucagon
2) Beta cells - insulin
3) Delta cells - somatostatin
4) Epsilon cells - ghrelin
5) Pancreatic polypeptide secreting cells - PP

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14
Q

Where in the Islet of Langerhans do you find alpha cells?

A

Around the periphery

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15
Q

Where in the Islet of Langerhans do you find beta cells?

A

In the middle, making up the majority of the islet

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16
Q

Where in the Islet of Langerhans do you find delta cells?

A

Sporadically throughout the islet

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17
Q

Where in the Islet of Langerhans do you find epsilon cells?

A

Sporadically on the periphery

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18
Q

Where does insulin go when it is released from beta cells?

A

It is pushed into the hepatic portal vein and goes to the liver, which is the prime target organ.

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19
Q

What are the two forms that insulin exists in?

A

1) Monomeric - active form, made up of an alpha chain and beta chain linked by disulphide bridges, easily transported through membranes but only a short half life (6 minutes)
2) Hexameric - storage form made up of six monomers around a central zinc atom linked by histidine bonds, long half life but slow diffusion rate

20
Q

What are the three stages in insulin synthesis?

A

1) Preproinsulin formed, which is comprised of an alpha chain then connecting sequence then beta chain then signal peptide which targets polypeptide chain to rough endoplasmic reticulum.
2) Signal peptide cleaved to leave proinsulin. Proinsulin folds into a spiral and alpha and beta chain are linked by disulphide bridges.
3) Enteropeptidases in the Golgi body release the central C-peptide to leave insulin in its active form.

21
Q

What level can be measured in the blood to detect how well someone’s body is synthesising insulin?

A

C-peptide

22
Q

How is insulin secretion from a beta cell stimulated?

A

Glucose enters beta cell through Glut 2 channel. This allows ATP to be synthesised inside the cell.
ATP causes K+ channel to be blocked, so K+ does not leak out of cell and cell becomes depolarised.
Depolarisation activates the voltage-gated Ca2+ channels so Ca2+ diffuses into the cell.
Ca2+ influx stimulates constitutive secretion of the insulin granules.

23
Q

What is the insulin receptor comprised of?

A

1) Two alpha subunits which are extracellular (sit on the cell membrane) and are bound together by disulphide bridges. They have the insulin binding site.
2) Two beta subunits which traverse the cell membrane and have tyrosine kinase domains.

24
Q

What does insulin activating the insulin receptor lead to?

A

Phosphorylation of insulin receptor substrates (of which there are 4 types).

25
Q

What is the result of phosphorylation of IRS-1 in muscle and adipose tissue?

A

The vesicle containing GLUT-4 moves to the cell surface and inserts into the plasma membrane. GLUT-4 then functions as a high-affinity receptor and takes up glucose into the cell for storage.

26
Q

What are some of the effects of insulin?

A

Increased uptake of glucose by muscle, adipose tissue, liver.
Increased glycogenesis in the liver and muscle, increased lipogenesis in adipose tissue.
Increased cholesterol synthesis in the liver.
Increased amino acid uptake and protein synthesis.
Decreased glycogenolysis, gluconeogensis, ketogenesis, lipolysis, proteolysis.

27
Q

What is the principle organ of glucose homeostasis?

A

The liver

28
Q

About 200g of glucose is produced and utilised each day, where is the majority of this derived from and where can it be derived from if there is liver failure or a great demand for glucose?

A

Majority from gluconeogenesis and glycogenolysis in the liver.
Can be derived from gluconeogenesis in the kidney if needed.

29
Q

What are the two types of glucose uptake demonstrated by the brain and other tissues (e.g muscles)?

A

Brain = obligatory glucose uptake, not controlled by insulin

Other tissues = facultative glucose uptake, responsive to insulin levels

30
Q

What is the Oral Glucose Tolerance Test, and what are two outcomes that can be found?

A

The person drinks glucose and then their blood glucose is tested 2 hours later.
The person may have Impaired Glucose Tolerance, or Impaired Fasting Glucose.

31
Q

What is the Insulin Tolerance Test?

A

Assesses function of the pituitary gland.
Insulin is injected intravenously to induce hypoglycaemia. Levels of ACTH and GH are measured in the blood, they should have increased due to the stress response. ACTH causes release of cortisol, cortical and and GH counter-regulate the action of insulin.

32
Q

What is glycogen converted to in glycogenolysis?

A

Glycogen -> glucose-1-phosphate -> glucose-6-phosphate

Glucose-6-phosphate enters the glycolytic pathway and is dephosphorylated and converted to glucose.

33
Q

How is glucagon synthesised in alpha cells?

A

The enzyme Proprotein Convertase-2 cleaves proglucagon to produce glucagon.
(Proglucagon can be cleaved in intestinal L cells to form other products: GLP-1, GLP-2, IP-1)

34
Q

What effect does insulin have on glucagon secretion?

A

Insulin directly inhibits glucagon secretion.

35
Q

What are the actions of glucagon?

A

Glucagon acts on the liver to increase glycogenolysis, gluconeogenesis, lipolysis, proteolysis, ketogenesis.
Glucagon also acts on adipose tissue to increase lipolysis and decrease lipogenesis.

36
Q

What are the effects of GLP-1?

A

Reduces appetite by acting on the hypothalamus.
Reduces gastric emptying.
Suppresses glucagon secretion by alpha cells.
Stimulates insulin secretion by beta cells.

37
Q

What is the role of GLP-1 in the new combinatorial therapy proposed for type 1 diabetes?

A

Traces of C-peptide found in the blood of people with type 1 diabetes suggests the existence of Micro-Insulin Secreting Beta Cells which escape destruction because they don’t produce enough insulin to attract an immune response. Giving the person GLP-1 as well as insulin could increase the endogenous insulin secretion from the micro-insulin secreting beta cells.

38
Q

What are some of the effects of GLP-1 agonists?

A

Anti-inflammation
Increased intestinal growth
Decreased lipoprotein synthesis by intestine
Increased glucose utilisation by the heart
Cardioprotective and vasoprotective effects
Increased Na+ excretion by the kidney
Reduced appetite
Increased secretion of somatostatin and insulin, decreased secretion of glucagon

39
Q

What are the two things somatostatin is classed as?

A

A neuropeptide, and a gastric peptide.

40
Q

What are the effects of somatostatin?

A

Inhibits secretion of glucagon and insulin and secretions from the exocrine pancreas. Works to dampen everything down and return to basal levels after you’ve eaten and digested your food.

41
Q

How does HbA1c work as a measure of blood glucose level?

A

It measures glycosylated haemoglobin. Excess glucose in the blood will bind to haemoglobin in red blood cells and will not dissociate again. Since red blood cells last 120 days, HbA1c can look at your blood glucose level over the past 6-8 weeks.

42
Q

What is normal HbA1c?

A
43
Q

What is the desirable HbA1c for diabetics?

A

48mmol/mol (6.5%)

44
Q

What HbA1c indicates prediabetes?

A

42 - 47mmol/mol (6 - 6.4%)

45
Q

What is the key intermediate in gluconeogenesis?

A

Glucose-6-phosphate

Reproductive and Endocrine (11 decks)

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