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2 MEH > 13 Endocrine Pancreas > Flashcards

13 Endocrine Pancreas Flashcards

1
Q

Where does the pancreas sit in the body?

A
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2
Q

How does the pancreas develop?

A

=Large gland

=Outgrowth of foregut (embryologically)

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3
Q

What are the 2 functions of the pancreas?

A
  1. Exocrine: Produce digestive enzymes secreted directly into duodenum- alkaline secretions via pancreatic duct to duodenum
  2. Endocrine: Hormone production- from islets of Langerhans
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4
Q

What % of the pancreas as a whole is exocrine and what % is endocrine?

A

Endocrine= 1%

Exocrine= 99%

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5
Q

What are the arrows in the following diagram showing?

A

Islets of langerhans

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6
Q

Describe the blood supply to the Islets of Langerhans.

A

Blood supply= in close proximity

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7
Q

Name the 7 polypeptide hormones secreted by the pancreas and the islet cells that release them:

A
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8
Q

Complete the missing gaps in the following table:

A
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9
Q

Name a tissue that is very sensitive to plasma glucose.

A

The brain

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10
Q

What levels should glucose be at?

A

Normal: 3.3-6 mmol/L

After a meal: 7-8 mmol/L

Renal threshold: 10 mmol/L

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11
Q

How would a patients urine be described if the renal threshold was exceeded?

A

Glycosuria

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12
Q

How are insulin and glucogon carried in the blood?

A

Water soluble hormones- carried dissolved in plasma

Short half-life: 5mins

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13
Q

How do insulin and glucagon carry out their function?

A
  1. Interact with cell surface receptors on target cells
  2. Receptor with hormone bone can be internalised- inactivation
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14
Q

Why is insulin ‘anti-gluconeogenic’?

(it is also anti-lipolytic and anti-ketogenic)

A
  1. At high dosage
  2. –> lowers incorporation of pyruvate into blood glucose
  3. –> stimulates pyruvates incorporation into liver glycogen
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15
Q

What is the polypeptide structure of insulin?

A

Big peptide with alpha helix structure

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16
Q

What’s the pathway of insulin from rER to exit the cell?

A
  1. Pre-proinsulin translation, signal cleavage, proinsulin folding
  2. Proinsulin transported to golgi
  3. Proinsulin cleaved to produce insulin and C-peptide
  4. Secretory granule formation
17
Q

How are KATP channels regulated by metabolism?

A
  • Metabolism high:
    • KATP channels shut
    • Insulin secretion
  • Metabolism low:
    • opens KATP channels
    • NO insulin secreted
18
Q

What does insulin do?

A

Increases glucose uptake into target cells and glycogen synthesis in:

  • Liver
    • stimulate glycogen formation and inhibit its breakdown
    • inhibits breakdown of amino acids
  • Muscles
    • increases uptake of amino acids promoting protein synthesis
  • Adipose tissue
    • increases storage of tryglycerides
19
Q

Describe the insulin receptor.

A
  1. On cell surfaces
  2. dimer
  3. 2 identical subunits span cell membrane
  4. alpha chain on exterior
  5. beta chain on interior
20
Q

Through what channel is glucose taken up into target cells?

A

Glut 4 channel

21
Q

What are the functions of glucagon?

A
  1. Raise blood glucose levels
    1. Glycogenolytic
    2. Gluconeogenic
  2. Mobilises energy release
    1. Lipolytic
    2. Ketogenic
22
Q

What triggers glucagon to be released?

A

Low glucose levels in alpha cells

23
Q

How is glucagon synthesised and secreted?

A
  1. Synthesised in rER in alpha cells
  2. Transported to Golgi
  3. Packaged in granules
  4. Margination- storage vesicles (granules) move to cell surface
  5. Exocytosis- fusion of vesicle membrane with plasma membrane- release contents
24
Q

Why does glucagon have a simpler synthesis than insulin?

A

Larger precursor molecule

25
Q

What effects does glucagon have in the body?

(primarily liver)

A
  • Liver
    • increases glycogenlysis- rate of glycogen breakdown
    • stimulates pathway synthesis of glucose from amino acids (Gluconeolysis)
  • Stimulate lipolysis-
    • increase plasma fatty acid

NET EFFECT= rise in blood glucose levels

26
Q

When might glucose be given clinically?

A

Diabetic:

  • Experiencing hypoglycaemia
  • Cannot take sugar orally
27
Q

If the insulin levels are abnormal (too high or too low) what does it cause?

A

High- hypoglycaemia

Low- hyperglycaemia (diabetes mellitus)

28
Q

If the glucagon levels are abnormal (too high or too low) what does it cause?

A

High: makes diabetes worse

Low: may contribute to hypoglycaemia

29
Q

What is diabetes mellititus?

A
  • Group of metabolic diseases
  • Affects >2% of population (UK)
    • Chronic hyperglycaemia
      • Causing long-term clinical complications
    • Associated w./ glycosuria
30
Q

How do we diagnose diabetes?

A

Venous plasma glucose concentration

31
Q

A patient may be diagnosed as diabetic if their blood glucose levels are outside of what range?

A
32
Q

What causes Type 1 diabetes?

A

(Absolute immune deficiency)

  • Autoimmune destruction of Pancreatic Beta-cells can be:
    • ABSOLUTE: cells destroyed
    • RELATIVE: secretory response of cells abnormally slow or small- defective beta cells/beta cell loss
33
Q

What happens to the KATP channels in an insulin deficiency?

A

They become less ATP sensitive

34
Q

What causes (at the cellular level) Type 2 diabetes?

A

Normal secretion but relative peripheral insulin resistance:

  • Defective insulin receptor mechanism
      • change in receptor number
      • change in receptor affinity
  • Defective post receptor events
  • Excessive/inappropriate glucogon secretion
35
Q

What are the main sites of glucose utilisation which would show decreased response to circulating insulin?

A

Adipose

Liver

Skeletal

36
Q

Outline how a person develops insulin resistance in 3 steps:

A
  1. Beta cells compensate for inital hyperglycaemia by increasing insulin production- normal blood glucose maintained
  2. Beta cells unable to maintain insulin production- impaired glucose tolerance
  3. Beta cell dysfunction- causes relative insulin deficiency
37
Q

Complete the table with either a + or -

A
38
Q

Complete the table with either a +or -

A

2 MEH (18 decks)

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