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Metabolism, Endocrinology & Haematolgy > L13 & 14: Endocrine Pancreas & Diabetes > Flashcards

L13 & 14: Endocrine Pancreas & Diabetes Flashcards

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1
Q

The pancreas develops embryologically as an outgrowth of…?

A

Foregut

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2
Q

State the exocrine and endocrine function of the pancreas

A
  • Exocrine (99%): produces digestive enzymes and secretes them directly into duodenum via pancreatic duct
  • Endocrine (1%): hormone production from Islet of Lanerhans
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3
Q

Within an Islet of Langerhans, state where:

  • alpha
  • beta

…cells are found

A
  • Alpha cells: periphery
  • Beta cells: central

*Others are scattered and in smaller numbers

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4
Q

What cells, in Islet of Langerhans, secrete insulin?

A

Beta

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5
Q

What cells, in Islet of Langerhans, secrete glucagon?

A

Alpha

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6
Q

What cells, in Islet of Langerhans, secrete somatostatin?

A

Delta

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7
Q

What cells, in Islet of Langerhans, secrete pancreatic polypeptide?

A

PP cells

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8
Q

What cells, in Islet of Langerhans, secrete grehlin?

A

e cells

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9
Q

What cells, in Islet of Langerhans, secrete gastrin?

A

G cells

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10
Q

What cells, in Islet of Langerhans, secrete vasoactive intestinal peptide?

A

VIP cells

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11
Q

What does this image show?

A

Islet of Langerhans

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12
Q

State the role of:

  • Insulin
  • Glucagon
A
  • Insulin: lowers blood glucose levels
  • Glucagon: increase blood glucose levels
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13
Q

Are glucagon and insulin water or lipid solube?

A

Water. Travel in blood and then react with cell surface receptors on target cells. Receptor, with hormone bound, can then be internalised- hormone then inactivated.

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14
Q

What’s the half life of glucagon and insulin?

A

5 minutes

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15
Q

Which organ in body uses glucose at fastest rate?

A

Brain so it is very sensitve to changes in glucose concentration

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16
Q

What can high plasma glucose do to cells? (think about deformation)

A

Cause water to move out of cells so they shrivel

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17
Q

For insulin and glucagon, compare and contrast:

  • What state it says the body is in
  • Target tissues
  • Which ‘food groups’ it affects metabolism of
  • Anabolic or catabolic
A
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18
Q

State the expected plasma glucose concentrations when:

  • Normal
  • After a meal
  • Renal threshold
A
  • Normal: 3.3-6mmol/L
  • After meal: 7-8mmol/L
  • Renal threshold: 10mmol/L
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19
Q

What happens if plasma glucose is above renal threshold?

State two factors which can affect renal threshold

A

Kidneys excrete glucose in urine - glycosuria

  • Pregnancy decrease
  • Elderly increase
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20
Q

Insulin is anabolic and anti-gluconeogenic; what do we mean by anti-gluconeogenic?

A

Lower incorporation of pyruvate into gluconeogenesis but stimulates pyruvates incorporation into glycogen

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21
Q

Describe structure of insulin

A
  • Alpha helix
  • 2 unbranched polypeptides (A & B)
  • 2 disulphide bonds between A & B chains
  • 1 intrachain disulphide bond in A chain
  • C peptide between A & B chains
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22
Q

Is C peptide found in circulating insulin?

A

No as it is removed by golgi before secretion

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23
Q

Describe how insulin is produced and prepared for release in beta cells

A
  • Insulin sotred in secretory granules as crystalline zinc-insulin complex
  • Secretory vesicles contain equimolar amounts of insulin and C peptide
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24
Q

What can a measure of C peptide in plasma tell us?

A

Amount of endogenous insulin secreted (released in equimolar amounts)

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25
Following synthesis and storage of insulin in secretory granules in B cells; describe how insulin is released in response to high plasma glucose Contrast this to why insulin is not released when plasma glucose is low
26
What receptor family does insulin receptor belong to?
Tyrosine kinase receptor family
27
What is the effect of insulin binding to its receptor on target cell?
Insertion of Glut 4 channel into target plasma membranes which then increases uptake of glucose
28
Explain the main actions of insulin on carbohydrate, protein and lipid metabolism in terms of what insulin decreases and what it increases
29
Describe the structure of glucagon
One polypeptide chain with no disulfide bonds
30
Describe the synthesis of glucagon
Large precursor molecule which undergoes post-translational processing to produce active form. Synthesised in ER and transported to golgi then packaged in vesicles.
31
State the 2 major actions of glucagon
* **Liver:** increase rate of glycogen breakdown, gluconeogenesis, ketogenesis * **Adipose:** stimulate lipolysis
32
What kind of receptor is glucagon receptor?
GPCR
33
Describe what happens when glucagon binds to glucagon receptor
* Binding activates adenylyl cyclase * Increases cAMP * Activates protein kinase A * PKA phosphorylates and activates enzymes in target cells
34
When is glucagon used instead of sugar?
In emergency hypo as patient cannot take sugar orally
35
What is diabetes mellitus?
Group of metabolic disorders charcterised by chronic hyperglycaemia due to insulin deficiency, insulin resitance or both
36
Describe what T1DM is
Insulin deficiency due to autoimmune destrution of most, or all, or B cells: * _Absolute:_ all B cells destroyed * _Relative:_ secretory response of B cells is abnormally slow or failure to secrete adequete amounts of insulin *\*Thought that KATP channels are less sensitive to ATP*
37
Describe the genetic predisposition of T1DM
* Associated with HLA DR3 and HLA DR4 * Likely that genetic predisposition interacts with environmental trigger resulting in produciton of killer lymphocytes, macrophages and antibodies that destroy B cells
38
Describe typical T1DM presentation
* Polyuria * Polydipsia * Weight loss * High plasma glucose * Common in lean, young who may have had viral infection
39
Why do you get polyuria in diabetes?
Glucose exceeds renal threshold. Kidneys can't reabsorb all glucose as there is too much hence extra glucose remains in nephron tubule increased osmotic load on nephron so less water absorbed to maintain isomotic conditions
40
How do you treat T1DM
* Exogenous insulin via subcutaneous injection * Education * Diet & exercise
41
What is T2DM?
Normal secretion of insulin but relative peripheral insulin resistance which may be due to: * Defective insulin receptor mechanism *(change in affinity or number)* * Defective post-receptor events *(e.g. tissues insensitive to insulin)* * Excessive inappropriate glucagon secretion
42
What is associated with T2DM?
* Genetics * Sedentary lifestyle * Obesity
43
Describe the typical T2DM presentation
* Polyuria * Polydipsia * Glycosuria * High plasma glucose * Lack of energy * Persistent infections * Slow healing * Visual problems ## Footnote *\*Often older and have central obesity*
44
Describe how insulin resistance in the young can lead to overt T2DM
Insulin resistance present at least 12 years before onset of hyperglycaemia and development of T2DM. 1. Initially, beta cells compensate by increasing insulin production 2. Beta cells unable to maintain this leading to impaired glucose tolerance 3. Beta cell dysfunction leads to relative insulin deficiency
45
How do you treat T2DM?
* Diet * Lifestyele * Education * Tablets *(non-insulin therapies which increase sensitivity or production e.g. sulphonylureas)*
46
State 4 tests, and results, which can diagnose diabetes
* Fasting glucose (\>7mmol/L) * Oral glucose test (\>11.1mmol/L 2 hours after 75g of oral glucose) * Random (\>11.1mmol/L) * HbA1c ## Footnote *\*Need symptoms and one abnormal test, or 2 abnormal tests if asymptomatic*
47
Explain the sequences of events leading to ketoacidosis in a type 1 diabetic (more common T1DM)
* Glucose not being taken up by ells do lack of insulin * Lots of B oxidation of fatty acids (lipolysis) to provide energy for cells * Lipolysis produces lots of ketone bodies * H+ associated with ketone bodies causes metabolic acidosis/ketoacidosis * MUST test for ketones in blood and urine
48
What are the symptoms of ketoacidosis?
* Hyperventilation * Nausea * Vomitting * Dehydration * Abdominal pain
49
Define hyperglycaemia and hypoglycaemia
* Hyperglycaemia: elevated plasma glucose * Hypoglycaemia: low plasma glucose
50
Describe the effect of persistent hyperglycaemia (2)
* Upatake of glucose into some tissues e.g. neves, eyes & kidneys doens't require insulin so intracelluar glucose concentration increases. It is then **metabolised by aldose reductase**, **reducing NADPH levels**, leading to increased disulfide bond formation which can **alter protein structure and function**. Reaction also produces sorbitol which can cause osmotic damage * **Glycation of plasma proteins** can alter structure and function
51
State symptoms and signs of hypoglycaemia
* Seizures * Unconsciousness * Weakness * Slurred speech *\*NOTE: signs/symptoms of hyperglycaemia is like presentation of diabetes*
52
State some microvascular and macrovascular complications of diabetes
53
What is metabolic syndrome
A group of symptoms inlcduing insulin resistance, dyslipidaemia, glucose intolerance and hypertension associated with central adiposity. All are risk factors associated with cardiovascular disease
54
When enzyme cleaves C peptide in proinsulin?
Convertase 1 & 2
55
C peptide has a longer half life and is more stable in blood than insulin- true or false
True
56
State the main glucose transporter in pancreatic cells and hepatocytes
Glut 2 Bidirectional and not regulated by insulin
57
Metformin is often given to T2DM patients; what does it do?
Decreases gluconeogenesis
58
Explain what happens in diabetic eye disease
Visual problems due to: * Osmotic effects of glucose (glaucooma) and cateracts * Diabetic retinopathy due to damaged blood vessels in retina leaking and forming protein exudates on retina or rupturign and bleeding into eye. New vessels may form, proliferative retinopathy, but are weak and easily bleed
59
Explain what happens in diabetic kidney disease (nephropathy)
* Damage to glomeruli * Poor blood supply * Damage from infections of UTIs * Early sign is increase in protein in urine (microalbuminuria)
60
How is HbA1c formed and what does it give an indication of? What are general values to expect?
Glucose in blood reacts with terminal valine of Hb to produce glycated Hb. % of Hb that is glycated gives indicator of how effectie blood glucose control has been in past 2-3 months. Normal: 4-6% Poorly controlled: \>10%

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