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Sem 2 - MEH > The Endocrine Pancreas > Flashcards

The Endocrine Pancreas Flashcards

1
Q

What tissue does the pancreas come from?

A

It is a foregut stucture (coeliac truck).

The pancreas is a large gland

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2
Q

What are the two functions of the pancreas?

A

Exocrine: Produces digestive enzymes secreted directly into duodenum

  • Exocrine function form the bulk of the gland. - Alkaline secretion via pancretic duct into duodenum

Endocrine: Hormone production and secretion

  • From islets of langerhans

Only 1% of the pancreas is endocrine tissue, the other 99% is exocrine tissue.

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3
Q

Exocrine v endocrine tissue in pancreas

A

Exocrine - ducts

Endocrine - diffuse into blood

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4
Q

What polypeptide hormones are secreted by pancreas?

A
  • Insulin - B-cells
  • Glucagon - A-cells
  • Somatostatin - delta-cells
  • Panreatic polypeptide (PP) - PP cells
  • Ghrelin - e cells
  • Gastrin - G cells
  • Vasoactive intestinal peptide - VIP cells

All of these hormones are associated with a particular type of cell in the pancreas.

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5
Q

How is plasma glucose controlled?

A

Using a feedback system.

Insulin: Lowers blood glucose. - Cells to take up glucose and liver to produce glycogen.

Glucagon: Raises blood glucose.

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6
Q

What are the actions of Insulin and Glucagon?

(signal, target tissue, affects on metabolism, actions)

A
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7
Q

Why is it important that blood glucose remains constant?

A
  • Brain uses glucose at fastest rate in the body
    • Relies on blood
      • Sensitive to falls in glucose
      • or rise = increased osmolarity
      • Circulation glucose needs to be controlled
  • Normally 3.3-6 mmol/L (UHL reference range)
  • After a mean 7-8 mmol/L
  • Renal threshold = 10mmol/L (threshold at which glucose gets into the urine)
    • Glucosuria
      • Pregancy, the renal threshold decreases
      • Elderly, the renal threshold increases
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8
Q

What are the properties of insulin and glucagon?

A
  • Water soluble hormones:
    • Carried dissolved in plasma - no special transport proteins
    • Short half life - 5 mins
    • Interact with cell surface receptors on target cells
    • Receptor with hormone bound can be internalised - inactivation
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9
Q

Properties of insulin

A
  • Action (favours storage) it is the hormone of energy storage
  • Is anti-gluconeogenic - At high dose, it lowers incorporation of pyruvate - into blood glucose, but also stimulated its incorporation into liver glycogen.
  • Insulin is anabolic
    • Anti-gluconeogenic
    • Anto-lipolytic and anti-ketogenic
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10
Q

What is the structure of insulin?

A
  • Insulin is a big peptide with an alpha structure - 3 bits
  • Consists of two un-branched peptide chains which are connected by 2 disulphide bridges. This ensures stability (hold chains together)
    • 51 amino acids
    • 2 polypeptide chains
    • A = 21, B = 30
    • 2 disulphide bridges = rigid structure
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11
Q

How is insulin synthesised?

A
  1. Pre-pro insulin translation signal cleavage, proinsulin folding
  2. Proinsulin is transported to golgi
  3. Proinsulin is cleaved to produce insulin and C-peptide
  4. Both Insulin and C-peptide in vesicle. They marginate to surface of pancreasic B cell where all cuddle together
  5. Only when there is a signal from Ca2+ will these vesicles fuse with the cell membrane and secrete contents.
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12
Q

What are KATP channels?

A

These are channels that are regulated by ATP / ADP

  • Glucose closes KATP channels in pancreatic beta-cells
  • Metabolic inhibition reopens KATP channels
  • Cell attached patch recordings, high external K, -60mV
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13
Q

How are KATP channels and insulin secretion linked?

A
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14
Q

What does insulin do?

A

Increases glucose uptake into target cells and glycogen synthesis (insertion of GLUT4 channel)

  • In the liver, it increases glycgen synthesis by stimulating glycogen formating and by inhibiting breakdown
  • In muscles it increases uptake of AA promoting protein synthesis
  • In liver inhibits breakdown of AA
  • In adipose tissue increases storage of triglycerides

​Inhibits breakdown of fatty acids.

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15
Q

What is glucagon?

A

Hormone that opposes insulin

  • Acts to raise blood glucose levels
  • It is glycogenolytic
  • Gluconeogenic
  • Lipolytic
  • Ketogenic

It mobilises energy release

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16
Q

How do a cells synthesises and secrete glucagon?

A
  • Glucagon is secreted by a-cells
  • Secreted due to low glucose levels in a-cells
  • Synthesized in rough ER transported to Golgi
  • Packed in granules
  • Effect mainly in the liver
  • Granules move to cell surface
    • Margination - movement of storage vesicles to cell surface
    • Exocytosis - fusion of vesicel membrane with palsma membrane with the release of vesicle contents
17
Q

What is the structure of glucagon?

A
  • 29 AA in one polyppetide chain
  • No disulphide bridges = Flexible structure
  • Simpler synthesis
18
Q

What effect does glucagon have?

A
  • In the liver, it increases the rate of glycogen breakdown (glycogenolysis)
  • Stimulates the pathway for synthesis of glucose from AA (glucoseneogenesis)
  • Net effect is a rise in blood glucose levels
  • Stimulates lipolysis to increase plasma fatty acid
19
Q

Why is glucagon clinically important?

A

Glucagon in emergency medicine is used when a person with diabetes is experiencing hypoglycaemia and cannot take sugar orally

20
Q

In what stages of carbohydrate metabolism are insulin and glucagon stimulated?

A
21
Q

In what stages of lipid metabolism are insulin and glucagon produced?

A
22
Q

In what stages of amino acid metabolism are insulin and glucagon secreted?

A
23
Q

What is it called if Insulin is high / low?

A

High insulin = Hypoglycaemia

Low insulin = Hyperglycaemia -Diabetes mellitus

24
Q

What happens if glucagon levels are high / low?

A

High glucagon = Makes diabetes worse

Low glucagon = May contribute to hypoglycaemia

25
Q

How do you know if you have disorders of blood glucose?

A
  • Diabetes mellitis
    • Mellitus (L) = honeysweet
  • Group of metabolic diseases
  • Affect over 2% of population in UK
  • Characteried by:
    • Chronic hyperglycaemia (prolonged elevation of blood glucose)
    • Leading to long-term clinical complications
  • Associated with elevated glucose levels in urine.
26
Q

How do you diagnose diabetes mellitus?

A

Diagnosis basis of venous plasma glucose concentration:

  • Normal range is 3.3-6mmol/L plasma glucose
  • Fasting: over 7mM
  • Random: Over 11.1 mM
27
Q

Causes of type 1 diabetes?

A

Asolute insulin deficiency (Autoimmune destruction of pancreatic b-cells)

  • Absolute - pancreatic b-cells destroyed
  • Relative - secretory response of b-cells is abnormaly slow or small (insulin -deficiency - failure to secrete adequate amounts of insulin from b-cells or b-cell loss)
  • Explaied by a gain of function mutation in Kir6.2 - this mutations makes the KATP channels less ATP sensitve
28
Q

What causes type 2 diabetes?

A

Normal (?) secretion by relative peripheral insulin resistance

  • Defective insulin receptor mechanism - change in receptor number and/or affinity
  • Defective post-receptor events
    • Insulin resistance - tissues become insensitive to insulin
  • Or excessive or inapproproate glucagon secretion.
29
Q

Insulin resistance

A

Main site of glucose utilisation (adipose, liver and skeletal muscle) show decreased response to normal circulating concentrations of insulin

Affects:

  • 25% og general population
  • 92% of patients wiht type 2 diabetes

Results from combination of:

  • Genetic factors
  • Environmental factors including:
    • Obesity
    • Sedentary lifestyle
30
Q

What happens if there is insulin resistance in the young?

A
  • Insulin resistance present before (12+years) onset of hyperglycaemia and development of overt type 2 diabetes
  • Initially:
    • B cells compensate by increasing insulin production - maintain normal blood glucose
  • Eventually:
    • B-cells unable to maintain increased insulin production - impaired glucose tolerance
  • Finally:
    • B-cell dysfunction leads to relative insulin deficiency - overy type 2 diabetes

Sem 2 - MEH (22 decks)

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