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

The Endocrine Pancreas 1&2 Flashcards

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
Q

What is the effect on the cell, in relation to the K ATP channels and voltaic changes, when the BG is low?

A

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

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26
Q

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?

A

Muscle and adipose tissue

Tyrosine kinase receptors

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27
Q

What is the glucose transporter that insulin stimulates? Is it a specific receptor?

A

GLUT-4

Yes

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28
Q

Do tissues other than muscle and fat require insulin to uptake glucose?

A

No

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29
Q

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?

A

GLUT-1 & GLUT-3 - basal glucose uptake in many tissues including brain, kidney, RBCs
GLUT-2- Beta cells of pancreas and liver

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30
Q

How does glucose enter the tissues of the liver?

A

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
Q

Although insulin has no direct effect on the liver, how can it indirectly affect the organ? How does this happen?

A

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
Q

What effect does insulin have on glycogen synthesis pin muscle and liver?

A

Increases it and also inhibits glycogen phosphorylase

33
Q

What effect does insulin have on amino acid uptake in muscle?

A

Increases it, promoting protein synthesis

34
Q

What effect does insulin have on protein synthesis?

A

Increases it

35
Q

What is the half-life of insulin?

A

Around 5 minutes

36
Q

Where is insulin primarily degraded?

A

Liver and kidneys

37
Q

What are the five stimuli which stimulate insulin release?

A 
Increased BG
Increased amino acids in the plasma
Glucagon
Other incretin hormones e.g. gastrin, secretin, CCK, GLP-1, GIP
Vagal nerve activity
38
Q

What stimuli inhibit insulin release?

A

Low BG
Somatostatin (GHIH)
Sympathetic alpha 2 effects
Stress e.g. exercise and hypoxia

39
Q

What nerve stimulation prompts insulin release?

A

Vagal nerve

40
Q

What is the difference in insulin response to glucose administered i.v compared with oral administration?

A

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
Q

Which BG hormone dominates in the fed state? (carbohydrate breakdown) What effects are seen?

A

Insulin

Increased glucose oxidation
Increased glycogen synthesis
Increased fat synthesis
Increased protein synthesis

42
Q

Which BG hormone dominates in the fasting state? (fat breakdown) What effects are seen?

A

Glucagon

Increased glycogenolysis
Increased gluconeogenesis
Increased ketogenesis

43
Q

What type of hormone is glucagon?

A

Linear peptide hormone

44
Q

Where is glucagon produced?

A

Alpha cells of the pancreatic islet cells

45
Q

What is the primary purpose of glucagon?

A

To raise BG

46
Q

What is the plasma half-life of glucagon?

A

5-10 mins

47
Q

The action of which hormone does glucagon primarily oppose?

A

Insulin

48
Q

What type of receptors are glucagon receptors?

A

G-protein receptors

49
Q

What system are glucagon receptors linked to? What is the function of this system?

A

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
Q

What is the level go BG at which the secretion go glucagon increases dramatically? How does this compare with the average BG range?

A
51
Q

Why is it important that amino acids stimulate glucagon release?

A

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
Q

Summarise the effects of a change in BG on insulin and glucagon release

A

Increased BG -> increased insulin and decreased glucagon
Decreased BG -> decreased insulin and increased glucagon

Opposite effects

53
Q

What effects do amino acids in the plasma have on insulin and glucagon?

A

They stimulate the release of both insulin and glucagon, this is an adaptation to compensate for the high protein content of carnivorous diets

54
Q

What stimulate glucagon release?

A 
Low BG
High amino acids
Sympathetic innervation and epinephrine
Cortisol
Stress
55
Q

What inhibits glucagon release?

A

Glucose
FFA and ketones
Insulin
Somatostatin

56
Q

What type of hormone is somatostatin?

A

Peptide hormone

57
Q

Where is somatostatin produced?

A

D-cells of the pancreas

58
Q

What is the main function of somatostatin?

A

To inhibit activity in the GI tract

59
Q

What is the effect of activity on the entry of glucose into skeletal muscle?

A

It is increased, even in the absence of insulin

60
Q

What happens the the insulin sensitivity of muscle during exercise?

A

It increases

61
Q

How does glucose entry into active muscle cells differ from that of non-active muscle cells?

A

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
Q

What is the body’s response to starvation?

A

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
Q

What is diabetes mellitus?

A

Loss of control of BG levels

64
Q

Outline the pathology of Type 1 DM

A

Autoimmune destruction of the pancreatic Beta cella destroys ability to produce insulin and compromises patients ability to absorb glucose from the plasma

65
Q

What percentage of type 1 DM patients are insulin dependant?

A

10%

66
Q

Why can ketoacidosis occur in type 1 DM?

A

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
Q

Outline the pathology of Type II DM

A

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
Q

Outline the treatment for type II DM

A

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
Q

Although there is elevated BG in both type 1 and 2 DM, what is the issue which causes each type?

A

Type 1 is caused by inadequate inulin release

Type 2 is caused by inadequate tissue response

70
Q

What is the general diagnostic criterion for DM?

A

Hyperglycaemia

71
Q

What is the test for BG?

A

Glucose Tolerance Test

72
Q

Can the glucose tolerance test distinguish between type I and II DM?

A

No

73
Q

What are some common serious diabetic complications?

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular disease

Diabetes & Endocrinology (18 decks)

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