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Diabetes & Endocrinology > The Endocrine Pancreas 1&2 > Flashcards

The Endocrine Pancreas 1&2 Flashcards

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1
Q

What is the feeding centre, one of the two hypothalamic centres?

A

Promotes feelings of hunger and a drive to eat

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2
Q

What is the satiety centre, one of the two hypothalamic centres determining food intake?

A

Promotes feelings of fullness by suppressing the feeding centre

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3
Q

What is glucostatic theory?

A

That food intake is determined by glucose and that the feeding centre activity dominates when glucose levels fall, whilst activity in the satiety centre is suppressed

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4
Q

What is lipostatic theory?

A

That food intake is determined by fat stores and as fat stores increase activity in the satiety centre becomes dominant and decreases eating. As the stores diminish the satiety centre is suppressed and the drive to eat increases via enhanced activity in the feeding centre. Leptin is a peptide hormone released by fat stores which depresses feeding activity. Obesity results from disruption of these pathways

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5
Q

What are the three categories of energy output?

A

Cellular work

Mechanical work

Heat loss

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6
Q

What type of metabolic phase is the absorptive state entered into after eating? What occurs in this phase?

A

Anabolic, ingested nutrients supply the energy needs of the body and excess is stored

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7
Q

What type of metabolic phase is the post-absorptive phase entered into after eating? What occurs in this phase?

A

Catabolic, body stores are relied upon to provide energy

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8
Q

What key organ is an ‘obligatory glucose user’? Can the brain use energy sources other than glucose in normal metabolism?

A

The brain

No

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9
Q

What is hypoglycaemia? What are the eventual complications?

A

Low blood glucose levels, coma and death

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10
Q

What is glycogenolysis?

A

Synthesising glucose from glycogen

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11
Q

What is gluconeogenesis?

A

Synthesising glucose from amino acids

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12
Q

What is the normal rage for blood glucose?

A

4.2-6.3mM

Think 5mM

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13
Q

What level of blood glucose indicates hypoglycaemia?

A
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14
Q

What are the two key endocrine hormones which maintain BG? Where are they produced?

A

Insulin, glucagon

Pancreas

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15
Q

What percentage of the pancreas has endocrine function?

A

1%

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16
Q

Where in the pancreas are the endocrine hormones produced?

A

Islets of Langerhans

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17
Q

What are the four types of islet cells found in the pancreas? What does each cell type produce?

A

Alpha cells - glucagon
Beta cells - insulin
Delta cells - somatostatin
F cells - pancreatic polypeptide (function not understood)

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18
Q

Which of the two pancreatic hormones dominates in a fed state and which dominates in a fasted state?

A

In a fed state insulin dominates and in a fasted state glucagon dominates

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19
Q

What cells of the pancreas produce insulin?

A

Beta cells

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20
Q

What is the major stimulus for insulin secretion? Give two other stimuli

A

Blood glucose concentration

Glucose
Amino acids

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21
Q

What is the only hormone that lowers blood glucose?

A

Insulin

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22
Q

In what two forms can excess of glucose be stored in? Where?

A

Glycogen - liver and muscle

Triacylglycerols (TAGs) - liver and adipose tissue

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23
Q

What type of channel is present in Beta cells that is sensitive to the ATP within the cell?

A

K+ ion channel

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24
Q

What is the response of the K+ ion in pancreatic islet Beta cells when glucose is abundant and it enters the cell, increasing metabolism? What transport mechanism does the glucose enter the cell by? What effect is there on the intracellular levels of K+ and what is the result of this for the cell?

A

The K ATP channel closes. The GLUT transport proteins. The intracellular K+ rises and the cell depolarises. Voltage-dependant CA2+ channels open, triggering insulin vesicle exocytosis into the circulation

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25
What is the effect on the cell, in relation to the K ATP channels and voltaic changes, when the BG is low?
The glucose is low so the K ATP channels are open so K+ flows out removing positive charge forms he cell and hyperpolarizing it, so that the voltage gated Ca2+ channels remain closed and insulin is not secreted
26
What are the two types of insulin sensitive tissue? What type of receptors not he surface of the cells of these tissues does insulin bind to?
Muscle and adipose tissue | Tyrosine kinase receptors
27
What is the glucose transporter that insulin stimulates? Is it a specific receptor?
GLUT-4 | Yes
28
Do tissues other than muscle and fat require insulin to uptake glucose?
No
29
In tissues other than muscle and fat, where GLUT-4 is used to uptake glucose, where insulin is not required to uptake glucose, which transporters are used?
GLUT-1 & GLUT-3 - basal glucose uptake in many tissues including brain, kidney, RBCs GLUT-2- Beta cells of pancreas and liver
30
How does glucose enter the tissues of the liver?
Being neither muscle nor fat, the liver does not require the action of insulin to allow it to uptake glucose, and instead used the GLUT-2 transporter which allows glucose to enter via a concentration gradient
31
Although insulin has no direct effect on the liver, how can it indirectly affect the organ? How does this happen?
Glucose transport into hepatocytes is affected by insulin status - in a fed state the liver is able to take up glucose because insulin activates hexokinase and lowers the intracellular glucose, creating a concentration gradient which favours glucose movement into the cells In a fasted state, liver synthesises glucose via gluconeogenesis, increasing intracellular glucose concentration which creates a gradient which favours glucose movement out of the cells into the blood
32
What effect does insulin have on glycogen synthesis pin muscle and liver?
Increases it and also inhibits glycogen phosphorylase
33
What effect does insulin have on amino acid uptake in muscle?
Increases it, promoting protein synthesis
34
What effect does insulin have on protein synthesis?
Increases it
35
What is the half-life of insulin?
Around 5 minutes
36
Where is insulin primarily degraded?
Liver and kidneys
37
What are the five stimuli which stimulate insulin release?
``` Increased BG Increased amino acids in the plasma Glucagon Other incretin hormones e.g. gastrin, secretin, CCK, GLP-1, GIP Vagal nerve activity ```
38
What stimuli inhibit insulin release?
Low BG Somatostatin (GHIH) Sympathetic alpha 2 effects Stress e.g. exercise and hypoxia
39
What nerve stimulation prompts insulin release?
Vagal nerve
40
What is the difference in insulin response to glucose administered i.v compared with oral administration?
The insulin response to iv insulin is lower because there is not the vagal stimulation of the release that would be present if the insulin was in the stomach (vagus stimulates GI hormone release including insulin)
41
Which BG hormone dominates in the fed state? (carbohydrate breakdown) What effects are seen?
Insulin Increased glucose oxidation Increased glycogen synthesis Increased fat synthesis Increased protein synthesis
42
Which BG hormone dominates in the fasting state? (fat breakdown) What effects are seen?
Glucagon Increased glycogenolysis Increased gluconeogenesis Increased ketogenesis
43
What type of hormone is glucagon?
Linear peptide hormone
44
Where is glucagon produced?
Alpha cells of the pancreatic islet cells
45
What is the primary purpose of glucagon?
To raise BG
46
What is the plasma half-life of glucagon?
5-10 mins
47
The action of which hormone does glucagon primarily oppose?
Insulin
48
What type of receptors are glucagon receptors?
G-protein receptors
49
What system are glucagon receptors linked to? What is the function of this system?
Adenylate cyclase/cAMP system Phosphorylates specific liver enzymes which increase glycogenolysis, increase gluconeogenesis and lipolysis - formation of ketones from amino acids Net result is elevated BG
50
What is the level go BG at which the secretion go glucagon increases dramatically? How does this compare with the average BG range?
51
Why is it important that amino acids stimulate glucagon release?
Otherwise hypoglycaemia would result, as amino acids stimulate insulin release, which if there were no glucagon, would stimulate glucose uptake into the cells and thereby dramatically lowering BG
52
Summarise the effects of a change in BG on insulin and glucagon release
Increased BG -> increased insulin and decreased glucagon Decreased BG -> decreased insulin and increased glucagon Opposite effects
53
What effects do amino acids in the plasma have on insulin and glucagon?
They stimulate the release of both insulin and glucagon, this is an adaptation to compensate for the high protein content of carnivorous diets
54
What stimulate glucagon release?
``` Low BG High amino acids Sympathetic innervation and epinephrine Cortisol Stress ```
55
What inhibits glucagon release?
Glucose FFA and ketones Insulin Somatostatin
56
What type of hormone is somatostatin?
Peptide hormone
57
Where is somatostatin produced?
D-cells of the pancreas
58
What is the main function of somatostatin?
To inhibit activity in the GI tract
59
What is the effect of activity on the entry of glucose into skeletal muscle?
It is increased, even in the absence of insulin
60
What happens the the insulin sensitivity of muscle during exercise?
It increases
61
How does glucose entry into active muscle cells differ from that of non-active muscle cells?
In non-active muscle insulin binds to its receptor, allowing GLUT4 to migrate to the cell membrane and permit entry of glucose In the active muscle cell, GLUT4 transporters can move to the cell membrane without the presence of insulin
62
What is the body's response to starvation?
Adipose tissues are broken down and fatty acids released. The liver converts excess to ketones which provide an additional source for muscle and BRAIN-after a period of starvation the brain adapts to use ketones as an energy source - this preserves proteins to ward against the vulnerability to infection and the weakness that protein breakdown causes
63
What is diabetes mellitus?
Loss of control of BG levels
64
Outline the pathology of Type 1 DM
Autoimmune destruction of the pancreatic Beta cella destroys ability to produce insulin and compromises patients ability to absorb glucose from the plasma
65
What percentage of type 1 DM patients are insulin dependant?
10%
66
Why can ketoacidosis occur in type 1 DM?
When poorly controlled, the lack of insulin depress ketone body uptake, this leads to an excess of ketones in the plasma and because they are acidic they lead to a life threatening ketoacidosis with plasma pH
67
Outline the pathology of Type II DM
Peripheral tissues become insensitive to insulin = insulin resistance Muscle and fat no longer respond to the normal levels of insulin, either due to an abnormal response of tissue insulin receptors or a reduction receptor numbers Beta cells remain intact and appear normal, and there may even be hyperinsulinaemia
68
Outline the treatment for type II DM
Initial treatment aims to restore tissue sensitivity with diet and exercise changes to try to prevent development into mature type 2 dm Beyond this hypoglycaemic drugs will be used, commonly metformin Eventually many type 2 patients end up taking insulin to prevent hyperglycaemia
69
Although there is elevated BG in both type 1 and 2 DM, what is the issue which causes each type?
Type 1 is caused by inadequate inulin release Type 2 is caused by inadequate tissue response
70
What is the general diagnostic criterion for DM?
Hyperglycaemia
71
What is the test for BG?
Glucose Tolerance Test
72
Can the glucose tolerance test distinguish between type I and II DM?
No
73
What are some common serious diabetic complications?
Retinopathy Neuropathy Nephropathy Cardiovascular disease

Diabetes & Endocrinology (18 decks)

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