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MEH > Lecture 13 > Flashcards

Lecture 13 Flashcards

1
Q

Where is the pancreas found?

A

Behind the stomach

  • overlays aorta and portal vein
  • fits into a curve of the duodenum
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2
Q

What is the shape of the pancreas?

A

‘Fish like’

Head > Body > Tail

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3
Q

What are the regions of the GI tract?

A

Foregut: Supplied by blood from coeliac trunk- branch off aorta (closest to head)
Midgut: Supplied by blood from the SMA- Superior mesenteric artery (middle)
Hindgut: Supplied by blood from IMA- Inferior mesenteric artery (end)

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4
Q

Where does the pancreas originate from?

A

Outgrowth of the foregut

-supplied by coeliac trunk

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5
Q

What are the 2 functions of the pancreas?

A
  • produces digestive enzymes secreted directly into duodenum/alkaline secretion into duodenum (exocrine secretion)
  • hormone production from islets of langerhans (endocrine action)
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6
Q

What is the ratio of endocrine to exocrine tissue in the pancreas?

A

1% endocrine

99% exocrine

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7
Q

What is exocrine tissue near to?

A

Blood supply

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8
Q

What are some polypeptide hormones secreted by the pancreas and where are they made?

A
  • insulin (beta cells)
  • glucagon (alpha cells)
  • somatostatin (delta cells)
  • pancreatic polypeptide (PP cells)
  • ghrelin (epsilon cells)
  • gastrin (G cells)
  • vasoactive intestinal peptide (VIP cells)
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9
Q

What is the overall role of insulin and glucagon?

A

Regulation of metabolism of carbohydrates, proteins, and fats

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10
Q

What is the distribution of cells in human islet?

A

Heterogenous

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11
Q

What happens if plasma glucose goes too high/low?

A

Osmotic effect- causes shrinking of cells (high)

Run out of energy (low)

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12
Q

Why does glucose need to be regulated?

A

Because if not there would be pulsatile additions of glucose to plasma
-don’t want it to spike up and down

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13
Q

What is the function of insulin and glucagon specifically?

A

Insulin- lowers blood glucose levels (stimulated by high plasma glucose, causes cells to remove glucose from plasma and store it)
Glucagon- raises blood glucose levels (stimulated by low plasma glucose, causes cells to break down stores into glucose and release those stores)

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14
Q

What are the similarities between insulin and glucose?

A

Insulin
-signalled by feeding
-target tissues are liver, adipose tissue, skeletal muscle
-remove glucose from plasma and storing it (to make carbohydrates, lipids, proteins = ANABOLIC)
Glucagon
-signalled by fasting
-target tissues are liver and adipose tissue
-break down carbohydrates/lipids (CATABOLIC)

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15
Q

What area of the body uses up glucose most quickly?

A

Brain

  • as it relies on blood
  • sensitive to rise/fall in glucose, don’t want cells in brain to shrink due to high osmolality
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16
Q

What is the normal plasma glucose level before and after a meal?

A

3.3-6 mmol/L

After a meal 7-8 mmol/L

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17
Q

What is the renal threshold?

A

Point at which tissues in the kidney can’t deal with amount of glucose in the plasma.
Too much glucose to reabsorb (normally kidneys reabsorb all of glucose)
= glucose appears in urine
10 mmol/L

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18
Q

What is glycosuria?

A

Excretion of glucose in the urine.

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19
Q

When does glycosuria occur in a healthy individual?

A

During pregnancy

-the renal threshold is lowered

20
Q

What happens to the renal threshold in elderly?

A

Increases

21
Q

What are some properties of insulin/glucagon?

A
  • water soluble (dissolved in plasma-no special transport proteins)
  • short half lives (5 mins from release to destruction)
  • interact with cell surface receptors in target cells
  • destroy insulin/glucagon by making an internalised/inactivated receptor
22
Q

What is gluconeogenesis?

A

Constructing glucose from smaller units

23
Q

What does insulin have effects on?

A

Carbohydrate/protein/lipid metabolism

24
Q

What do islets of langerhans look like?

A

Spherical structures scattered through the exocrine tissue

25
Q

How do cells in the islets of langerhans store their hormones?

A

Intracellularly in membrane-limited vesicles: storage granules

26
Q

What do Beta/alpha cells have as a structural adaptation?

A 
Extensive RER
Well defined Golgi apparatus 
Many mitochondria 
Well defined system of microtubules and microfilaments 
(Synthesis of proteins)
27
Q

What is the structure of insulin?

A

2 unbranched polypeptide chains linked covalently by 3 disulphides bridges

28
Q

How is insulin synthesised?

A
  • pre-proinsulin (singe chain polypeptide) synthesised on ribosomes of RER
  • ‘pre’ part is the signal peptide ensuring the protein enters cisternal space of RER
  • signal peptide is removed once it enters the RER
  • remaining proinsulin folds to ensure correct alignments of cysteine residues so the correct disulphide bonds form
  • proinsulin is transported to trans-Golgi apparatus and packed into storage vesicles
  • proteolysis removes C-peptide from near middle of chain
  • breaking the chain into 2 chains held together by disulphide bonds
  • storage vesicles contain both insulin and C-peptide in equimolar amounts
  • entire contents of the vesicle are released during secretion
29
Q

How do you monitor endogenous insulin secretion?

A

Level of C-peptide in the blood (as it is released with insulin in equimolar amounts)

30
Q

What type of receptor is the insulin receptor?

A

Tyrosine kinase receptor

31
Q

What are the major actions of insulin on carbohydrate/lipid/amino acid metabolism?

A
  • increases glucose transport into adipose tissue and skeletal muscle via GLUT4 channels
  • increases glycogenesis and decreases glycogenolysis in liver and muscle
  • decrease gluconeogenesis in liver
  • in muscles increases uptake of AA’s, promoting protein synthesis
  • in liver it inhibits breakdown of AA’s
  • in adipose tissue it increases storage of triglycerides
  • inhibits breakdown of fatty acids
32
Q

What is the action of insulin?

A

Hormone of energy storage

  • anabolic
  • anti-gluconeogenic
  • anti-lipolytic
  • anti-ketogenic
33
Q

What are KATP channels?

A

ATP sensitive K+ channel senses metabolic changes in pancreatic beta cells.

  • glucose closes KATP channels
  • when KATP channels open, beta cells hyperpolarise (K+ leaves) and insulin secretion is suppressed
34
Q

When do KATP channels open?

A
  • metabolism is low (low ATP, high ADP)
  • no insulin secreted
  • calcium channels closed
35
Q

When do KATP channels close?

A
  • metabolism is high (high ATP, low ADP)
  • insulin secreted
  • calcium channels open so moves into beta cell causing exocytosis of vesicles containing insulin
36
Q

What is the structure of an insulin receptor?

A

Dimer: 2 identical subunits spanning the membrane

  • each subunit made from and alpha and a beta chain connected by a disulphide bond
  • alpha chain: exterior
  • beta chain: interior and spans membrane
37
Q

Give a brief overview of the uptake and metabolism of insulin:

A
  • insulin binds to insulin receptor
  • glucose floods in through GLUT4 transporter
  • glucose either converted to glycogen, or broken down into pyruvate
  • pyruvate goes on to make fatty acids via acetyl coA
38
Q

What does glucagon act to do?

A

Oppose insulin

  • raise blood glucose levels (mobilises energy release)
  • glycogenolytic
  • gluconeogenic
  • lipolytic
  • ketogenic
39
Q

How is glucagon synthesised and secreted?

A
  • synthesized in RER transported to golgi
  • packaged in granules
  • secreted by alpha cells due to low glucose levels
  • mainly effects the liver (glycogen stored)
  • granules move to surface via margination and released by exocytosis
40
Q

What is margination and exocytosis?

A

Margination: movement of storage vesicles to cell surface
Exocytosis: fusion of vesicle membrane with plasma membrane releasing its contents

41
Q

What is the structure of glucagon?

A

No disulphide bridges so is flexible

42
Q

How is glucagon synthesised?

A
  • large precursor molecule (pre-proglucagon)

- post translational processing to produce active molecule

43
Q

What are the effects of glucagon?

A

Glycogenolysis: liver increases glycogen breakdown
Gluconeogenesis: stimulates synthesis of glucose from AA’s
Stimulates lipolysis: increases plasma fatty acid
=rise in plasma glucose levels

44
Q

When is glucose used in emergency medicine?

A

When a person with diabetes is experiencing hypoglycaemia and cannot take sugar orally

45
Q

What is it called when there are abnormal insulin levels and how does high/low levels of glucagon affect it?

A

Hypoglycaemia: high insulin levels
-low levels of glucagon can contribute to hypoglycaemia
Hyperglycaemia: low insulin levels (diabetes mellitus)
-high levels of glucagon makes diabetes worse

46
Q

What happens to KATP channels in diabetes?

A

They become ATP insensitive

47
Q

How does glucagon act upon its receptor?

A
  • binds to specific receptor on membrane
  • receptor is GPCR
  • binding activates adenylate cyclase, increasing cAMP, activating PKA, which phosphorylates many enzymes

MEH (22 decks)

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