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MEH * > S7 Pancreas > Flashcards

S7 Pancreas Flashcards

1
Q

Where is the pancreas located?

A

Behind the stomach, on the left side of abdomen, with the duodenum on the right

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2
Q

What part of the gut does the pancreas develop from? And what is it’s blood supply?

A

The foregut

Coeliac trunk artery

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3
Q

What are the two main functions of the pancreas? Which is the major function?

A
  • exocrine - produces digestive enzymes that are secreted into the duodenum
  • endocrine - hormone production

Exocrine

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4
Q

What 7 polypeptide hormones are secreted by the pancreas?

A
  • insulin
  • glucagon
  • somatostatin
  • pancreatic polypeptide (PP)
  • ghrelin
  • gastrin
  • vasoactive intestinal peptide (VIP)
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5
Q

What cells secrete insulin and glucagon?

A

Beta cells and alpha cells

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6
Q

Which cells secrete somatostatin, PP, ghrelin and gastrin?

A

Delta cells, PP cells, e cells, G cells

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7
Q

What are the target tissues of insulin?

A

Liver, adipose and skeletal muscle

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8
Q

What are the target tissues of glucagon?

A

Liver and adipose

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9
Q

Which metabolic reactions do insulin and glucagon effect?

A

Insulin - carbs, lipids, proteins

Glucagon - carbs and lipids

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10
Q

Insulin and glucagon are either anabolic or catabolic, which is which?

A

Insulin - anabolic

Glucagon - catabolic

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11
Q

What is the normal plasma glucose range?

A

3.3-6mmol/L (UHL reference range)

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12
Q

What is the renal threshold for plasma glucose level? What occurs if this is reached?

A

10mmol/L then glycosuria occurs (glucose in urine)

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13
Q

Are insulin and glucagon water or lipid soluble? How does this mean it’s transported in the blood?

A

Water soluble

It dissolves in the plasma (no need for transport proteins)

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14
Q

What is the half life of insulin ad glucagon?

A

5 minutes

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15
Q

What is margination?

A

Movement of storage vesicles to the cell surface

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16
Q

What is exocytosis?

A

Fusion of vesicle with plasma membrane, releasing vesicle products out of cell

17
Q

How is insulin synthesised in beta cells?

A
  1. Pre-proinsulin is translated, signal cleavage occurs, proinuslin is folded (at rough ER)
  2. Proinsulin is transported to the Golgi
  3. Proinsulin is cleaved to produce insulin and C-peptide
18
Q

What is the structure of insulin?

A

A peptide with an alpha helix structure

  • two unbranched peptide chains, c-peptide between them
  • 3 disulphide bonds (increase stability of insulin)
19
Q

What are K(ATP) channels?

A

Channels in pancreatic beta cells that are sensitive to ATP - a high ATP concentration closes these channels, higher AMP opens them

20
Q

How does glucose stimulate insulin secretion?

A
  1. High plasma glucose levels. Glucose enters beta cells through GLUT2 transporters
  2. Glucose is then phosphorylated to glucose-6-phosphate by glucokinase and this enters the Krebs cycle and oxidative phosphorylation leading to a rise in the ATP/AMP ratio
  3. High ATP inhibits K(ATP) channels and reduces K+ effluent
  4. So the membrane depolarises causing Ca2+ channels to open, intracellular Ca2+ levels increase
  5. Ca2+ triggers exocytosis of insulin-containing granules
  6. Membrane is repolarised
21
Q

What does insulin do?

A
  • increase glucose uptake into target cells and glycogen synthesis via insertion of GLUT4 channels
  • inhibits breakdown of fatty acids
22
Q

What are the effects of insulin in the liver?

A
  • increases glycogen synthesis by stimulating glycogen formation and inhibit breakdown
  • inhibits breakdown of amino acids
23
Q

What are the effects of insulin in the muscles?

A

Increases uptake of amino acids which promotes protein synthesis

24
Q

What are the effects of insulin in adipose tissue?

A

Increases the storage of TAGs

25
Q

Why type of receptor is the insulin receptor?

A

Tyrosine kinase receptor

Has an alpha chain subunit (on exterior cell membrane) and a beta chain subunit (integral)

26
Q

How is glucagon synthesised and secreted?

A
  1. Synthesised in rough ER and then transported to Golgi
  2. Packaged into granules
  3. Margination
  4. Exocytosis
27
Q

When is glucagon secreted?

A

When there are low glucose levels in alpha cells

28
Q

What is the structure of glucagon?

A
  • one chain

* no disulphide bridges - so is flexible

29
Q

What are the effects of glucagon?

A
  • increase rate of glycogen breakdown in liver (glycogenolysis)
  • stimulates synthesis of glucose from amino acids (gluconeogenesis)
  • stimulates lipolysis to increase plasma fatty acid
30
Q

How is glucagon used clinically?

A

Used as an emergency medicine when a person with diabetes becomes hypoglycaemic and can’t take sugar orally

31
Q

How quick can insulin effects be?

A

Can be:

  • rapid (seconds) - a.a. and glucose uptake
  • intermediate (minutes)
  • delay (hours) - lipogenesis
32
Q

What is diabetes mellitus characterised by?

A
  • chronic hyperglycaemia

* leading to long term clinical complications

33
Q

How is diabetes mellitus diagnosed?

A
  • fasting blood test (plasma glucose conc over 7mM)
  • random blood test (plasma glucose conc over 11.1mM)
  • HbAc1
34
Q

What is type 1 diabetes mellitus caused by?

A

Absolute insulin deficiency due to autoimmune destruction of beta -cells

35
Q

What is type 2 diabetes mellitus caused by?

A

There’s normal secretion but relative peripheral insulin resistance due to defective insulin receptor mechanism (change in receptor no. and/or affinity), defective post-receptor events (tissues insensitive to insulin), excessive glucagon secretion

36
Q

How can an insulin deficiency arise?

A

Due to a mutation of the K(ATP) channel meaning channel is less sensitive to ATP (gain of function)

37
Q

What can insulin resistance result from?

A
  • genetic factors

* environmental factors e.g. obesity, sedentary lifestyle

38
Q

What happens if insulin resistance is present before a child is 12 years old?

A
  1. Beta cells manage to compensate by increasing the insulin production and maintains the normal blood glucose
  2. But then cells are unable to maintain the increased insulin production
  3. Beta-cell dysfunction leads to relative insulin deficiency

MEH * (22 decks)

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