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Endocrinology > The Endocrine Pancreas > Flashcards

The Endocrine Pancreas Flashcards

1
Q

Where is energy intake determined by the activity in?

A

Feeding centre

Satiety centre

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2
Q

What does the feeding centre promote?

A

Feelings of hunger and makes us want to eat

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3
Q

What does the satiety centre promote?

A

Feelings of fullness and stop us eating

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4
Q

Describe the glucostatic theory?

A

Food intake is determined by BG

As BG increases the drive to eat decreases

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5
Q

Describe the lipostatic theory?

A

Food intake is determined by fat stores

As fat stores increase the drive to eat decreases

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6
Q

What is leptin?

A

A peptide hormone released by adipose tissue to decrease feeding activity

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7
Q

What are the 3 categories of energy output?

A

Cellular work
Mechanical work
Heat loss

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8
Q

What is mechanical output?

A

Movement on large scale
Only part we can control
By skeletal muscle

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9
Q

What is metabolism?

A

Integration of all biochemical reaction in the body

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10
Q

What are the 3 elements of metabolism?

A

Extracting energy from nutrients in food
Storing that energy
Utilising that energy for work

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11
Q

What are anabolic pathways?

A

Pathways that build up using energy

Synthesis of larger molecules from smaller ones

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12
Q

What are catabolic pathways?

A

Pathways that break down releasing energy

Degradation of large molecules into smaller ones releasing energy

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13
Q

What is the absorptive state?

A

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

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14
Q

Is the absorptive state anabolic or catabolic?

A

Anabolic

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15
Q

What is the absorptive state dominated by?

A

Insulin

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16
Q

What is the fasted state?

A

Where we rely on body stores in our bodies to provide energy

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17
Q

Is the fasted state anabolic or catabolic?

A

Catabolic

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18
Q

What is the fasted stage dominated by?

A

Glucagon

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19
Q

What is glucose stored in the body in the form of?

A

Glycogen

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20
Q

What can the brain only use to provide energy?

A

Glucose

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21
Q

Why must we maintain BG in the fasted state?

A

To meet the brains requirements

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22
Q

Where is glycogen stored?

A

Liver

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23
Q

Where will glucose present in hyperglycaemia?

A

In the Urine

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24
Q

What occurs in the failure to maintain BG?

A

Hypoglycaemia

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25
Q

What is glycogenolysis?

A

The synthesis of glucose from glycogen

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26
Q

What is gluconeogenesis?

A

The synthesis of glucose from amino acids

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27
Q

What is the normal range of glucose conc.?

A

4.2-6.3 mM

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28
Q

What is considered hypoglycaemia?

A

<3mM

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29
Q

What are the 2 key endocrine hormones produced in the pancreas that are key for maintaining BG?

A

Insulin

Glucagon

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30
Q

What are the 2 broad components of the pancreas?

A

Endocrine

Exocrine

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31
Q

Where are endocrine hormone produced in the pancreas?

A

Islets of Langerhans

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32
Q

How does the pancreas release its exocrine chemicals?

A

Into ducts

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33
Q

What are the 4 types of islet cells?

A

Alpha
Beta
Delta
F cells

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34
Q

What do alpha islet cells produce?

A

Glucagon

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35
Q

What do beta islet cells produce?

A

Insulin

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36
Q

What do delta islet cells produce?

A

Somatostatin

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37
Q

What do F islet cells produce/?

A

Pancreatic polypeptide

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38
Q

What type of hormone is insulin?

A

Peptide

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39
Q

What does insulin stimulate?

A

Glc uptake by cells

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40
Q

How is insulin synthesised?

A

Synthesised as large preprohormone called preproinsulin
Converted to proinsulin in ER
Proinsulin is then packaged into vesicles
Within these is cleaved again to insulin and C peptide
Stored in this form until the B cell is activated and releases it

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41
Q

What is the major stimulus of insulin release?

A

Increase in BG conc.

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42
Q

Which is the only hormone to lower BG?

A

Insulin

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43
Q

Where is excess glucose stored?

A

In the liver as glycogen

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44
Q

What is excess Amino acids converted to?

A

Fat

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45
Q

What are amino acids used to make?

A

Proteins

46
Q

What are FA stored in the form of in adipose tissue and the liver?

A

TAG

47
Q

Describe the activation of beta cells to secrete insulin by glucose

A

High glucose in the blood
Enters the beta cell through GLUT transporter
ATP increases
Katp channels close
Cell depolarises and calcium channels open
Ca2+ entry acts as an intracellular signal
Ca2+ signal triggers exocytosis and insulin is secreted

48
Q

Describe the effect of low BG on beta cell activation

A 
BG is low 
ATP in the cell remains low 
Katp channels remain close so K+ ions flow out hyperpolarising the cell 
Ca2+ channels remain closed
Insulin is not exocytoses
49
Q

Where does insulin bind?

A

To tyrosine kinase receptors on the cell membrane of insulin sensitive tissue

50
Q

What is the effect of insulin binding to target cells?

A

Increase glucose uptake by these cells

51
Q

What does insulin stimulate the mobilization of in the cekk?

A

GLUT-4 channels which reside in the cytoplasm of unstimulated muscle and adipose cells

52
Q

What is the action of GLUT4 transporters hen activated?

A

Migrate to the cell membrane

Then able to transport glucose into the cell

53
Q

What happens to GLUT4 transporters when insulin stimulation stops?

A

It returns to the cytoplasmic pool

54
Q

Which tissues are insulin sensitive?

A

Only muscle and fat

55
Q

In tissue other than muscle and fat how is glucose taken up?

A

Uptake is via other GLUT transporters which are not insulin dependent

56
Q

Is the liver an insulin sensitive tissue?

A

No

57
Q

How does the liver take up glucose?

A

By GLUT 2 transporters which are insulin independent

Down a concentration gradient

58
Q

How does the presence of insulin affect glucose uptake in the liver?

A

Enhances the uptake of glucose by the liver

59
Q

In the fasted state what does the liver do to increase blood Glc?

A

The liver synthesises glucose via glycogenolysis and gluconeogenesis

60
Q

What are some additional actions of glucose?

A

Increases glycogen synthesis

Increases AA uptake into muscle promoting protein synthesis

Increases protein synthesis and inhibits proteolysis

Increases TAG synthesis in adipocytes and liver

Inhibits the enzymes of gluconeogenesis in the liver

Has a permissive effect on GH

Promotes K+ entry into the cell by stimulating the Na+/K+ ATPase

61
Q

What is the half life of insulin?

A

5 minutes

62
Q

What happens to insulin bound receptors when insulin action is complete?

A

They internalise by endocytosis and are destroyed

- some are recycled

63
Q

Which stimuli increase insulin release

A 
Increased BG
Increased AA 
Glucagon (insulin is required to take up the glucose that is released by glucagon)
Other hormones controlling GI secretion 
e.g CCK
Vagal nerve activity
64
Q

Which stimuli inhibit insulin secretion?

A

Low BG
Somatostatin
Sympathetic alpha effects
Stress

65
Q

What does vagal activity stimulate the release of?

A

Major GI hormones

And insulin

66
Q

Why is the insulin response to IV glucose less than the equivalent amount of glucose administered orally?

A

Because oral loading of the same dose increases amount of BG both by direct effect on Beta cells and by vagal stimulation of beta cells

67
Q

Where is glucagon produced?

A

Alpha islet cells

68
Q

What is the primary purpose of glucagon?

A

To raise BG

69
Q

Where does glucagon mainly act?

A

On the liver

70
Q

What does glucagon have the opposite action to?

A

Insulin

71
Q

When is glucagon most active?

A

In the post-absorptive state

72
Q

What type of receptors are glucagon receptors?

A

G couple receptors

73
Q

What is the effect of glucagon binding to its receptor?

A

Phosphorylation chain is activated leading to:

  1. Increased glycogenolysis 2.increased gluconeogenesis (substrates: aa’s and glycerol (lipolysis))
  2. formation of ketones from fatty acids (lipolysis)
74
Q

Where does glycogenolysis, gluconeogenesis and lipolysis occur?

A

In the liver

75
Q

When does glucagon release increase dramatically?

A

When Bg <5.6 mM

76
Q

What else are a potent stimulus for glucagon secretion?

A

Amino acids

77
Q

What is the effect of increases BG on insulin and glucagon?

A

Increased insulin

Decreased glucagon

78
Q

What is the effect of decreased Bg on glucagon and insulin?

A

Increases glucagon

Decreases insulin

79
Q

Do amino acids stimulate the release of insulin or glucagon?

A

Both

80
Q

Which stimuli promote glucagon release?

A 
Low Bg
High AA 
Sympathetic innervation 
Cortisol 
Stress
81
Q

Which stimuli inhibit glucagon release?

A

Glucose
Free FA and ketones
Insulin
Somatostatin

82
Q

Why is insulin and glucagon released with high AA?

A

To counteract blood glucose getting to low with the effects of insulin

83
Q

What is the effect of parasympathetic activity (vagal) on insulin?

A

Increases the release of insulin

Rest and digest `

84
Q

What is the effect of sympathetic activity on insulin?

A

Inhibits insulin

Increases glucagon - promoting glucose mobilisation

85
Q

What type of hormone is somatostatin?

A

Peptide

86
Q

Which cells secrete somatostatin?

A

Delta islet cells

87
Q

What is the pain pancreatic action of somatostatin?

A

To inhibit the activity in the GI tract

88
Q

What is the effect of somatostatin on insulin and glucagon?

A

To suppress the release of both

89
Q

Is SS a counter regulatory hormone in the control of Bg?

A

No

90
Q

What is the effect of exercise on Bg?

A

The entry of glucose into skeletal muscle is increased

91
Q

How does exercise decrease BG?

A

Increases the sensitivity of insulin receptors

Causes insulin independent increase in GLUT 4 transporters art the membrane

92
Q

Describe glucose intake in an active muscle?

A

GLUT 4 transporters can migrate to the membrane without insulin being present
Increasing glucose uptake

93
Q

After a period of starvation how does the brain adapt to get energy?

A

It adapts to be able to use ketones

94
Q

What happens to tissue during starvation?

A

FFA can be released and used by most tissues to produce energy

95
Q

Broadly what is DM?

A

Loss of control of BG levels

96
Q

What are the 2 types of DM?

A

Type I

Type II

97
Q

What is the pathophysiology of type I DM?

A

Autoimmune destruction of Beta cells destroy the ability of the pancreas to produce insulin

98
Q

What is the treatment for type I diabetes?

A

Insulin injection

99
Q

What type of need to type I DM patients have for insulin?

A

Absolute need

100
Q

What is ketoacidosis in type I DM?

A

DKA occurs when the body has insufficient insulin to allow enough glucose to enter cells
The body switches to burning fatty acids and producing acidic ketone bodies.
This can quickly lead to life threatening acidosis

101
Q

What is the pathophysiology of type II DM?

A

Peripheral tissues become insensitive to insulin

Insulin resistance

102
Q

What can cause a decrease in response to insulin in type II DM?

A

Due to abnormal response of insulin receptors

Or a reduction in their number

103
Q

What is type II DM commonly associated with?

A

Obesity

104
Q

What is the initial treatment for Type II?

A

Exercise and diet change

Oral hypoglycaemic drugs

105
Q

What are the 2 main oral hypoglycaemic drugs administered?

A

Metformin

Sulphonylureas

106
Q

What does oral hypoglycaemic drugs require?

A

Functioning beta cells

107
Q

What is hyperglycaemia?

A

Elevated BG

108
Q

What is the diagnostic criteria for DM?

A

Hyperglycaemia

109
Q

What is the first test for DM?

A

Glucose tolerance test

110
Q

What is indicative of DM in a GTT?

A

BG is still elevated after 2 hours

111
Q

What are some of the long term consequences of hyperglycaemia?

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular Disease (due to atherosclerosis)

112
Q

What can the end stage complication of hypoglycaemia be?

A

Hypo coma

Death

Endocrinology (19 decks)

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