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Year 2 Diabetes & Endocrinology (JK) > The endocrine pancreas 1+2 > Flashcards

The endocrine pancreas 1+2 Flashcards

1
Q

Body energy = energy intake - ?

A

energy output

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2
Q

the 2 hypothalamic centres which determine energy intake

A

feeding centre

satiety centre

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3
Q

Feeding centre

A

promotes feeling of hunger and drive to eat

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4
Q

satiety centre

A

promotes feeling of fullness by suppressing the feeding centre

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5
Q

What 3 things control activity in the 2 hypothalamic centres which determine energy intake?

A

neural signals
chemical signals
presence of chemicals in the plasma

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6
Q

What is the glucostatic theory?

A

food intake is determined by blood glucose

as BG increases, drive to eat decreases, inhibit feeding centre and stimulate satiety centre

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7
Q

What is the lipostatic theory?

A

food intake is determined by fat stores

as they increase, drive to eat decreases, inhibit feeding centre and stimulate satiety centre

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8
Q

What hormone is linked to the lipostatic theory and what is its function?

A

Leptin

peptide hormone which is released by fat stores which depresses feeding activity

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9
Q

What will occur if these 2 hypothalamic centres are disrupted? What are other common causes of this?

A

obesity

more often due to just eating too much and not exercising enough

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10
Q

What are the 3 types of energy output

A

cellular work
mechanical work
heat loss

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11
Q

What is the only part of our energy output which we can regulate?

A

mechanical work - large scale eg muscle

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12
Q

Define metabolism

A

integration of all biochemical reactions in the body

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13
Q

The 3 parts of metabolism are

A

extracting energy from food
using that energy
storing energy

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14
Q

Is catabolism or anabolism linked to storage?

A

anabolism

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15
Q

What is the absorptive state?

A

after eating - ingested nutrients supply energy needs and excess is stored

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16
Q

Is the absorptive state anabolic or catabolic phase?

A

anabolic

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17
Q

What is the post-absorptive state?

A

between meals/overnight pool of nutrients in plasma decreases - fasted state

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18
Q

Is the post-absorptive state anabolic or catabolic phase?

A

catabolic

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19
Q

What organ is named as the main obligatory glucose utiliser?

A

brain

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20
Q

What other energy source can the brain use and when?

A

ketone bodies

starvation

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21
Q

What happens if in the post-absorptive state, Bg is not maintained?

A

hypoglycaemia

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22
Q

How is BG maintained in the post - absorptive state?

A

gluconeogenesis and glycogenolysis

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23
Q

What is gluconeogenesis?

A

make new glucose from amino acids

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24
Q

What is glycogenolysis?

A

making glucose from glycogen

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25
Q

Normal [BG]?

A

5mM

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26
Q

Hypoglycaemia [BG]?

A

< 3mM

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27
Q

What 2 hormones tightly regulate [BG]?

A

insulin and glucagon

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28
Q

Where are the 2 endocrine hormones produced in the pancreas and what % of the pancreas is endocrine?

A

islets of Langerhans

1%

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29
Q

What is the blood supply to the islets of Langerhans?

A

copious

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30
Q

4 types of islets of Langerhans and what they produce

A 
alpha = glucagon 
beta = insulin 
delta = somatostatin 
F = pancreatic polypeptide
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31
Q

What Is insulin?

A

A peptide hormone secreted by pancreatic beta cells which stimulates glucose uptake by cells

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32
Q

What are the different molecules names in the formation of insulin?

A

preproinsulin
proinsulin
insulin and c peptide

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33
Q

How is insulin stored?

A

in a vesicle as insulin and c peptide until activated

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34
Q

What is the major stimulus for insulin secretion?

A

[BG] increase

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35
Q

What is the only hormone which can lower [BG]?

A

insulin

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36
Q

What state (absorptive or post-absorptive) does insulin dominate?

A

absorptive

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37
Q

Why do most cells use glucose as energy source during the absorptive state?

A

Easy to metabolise

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38
Q

How is excess glucose stored? (2 ways)

A

glycogen in liver and muscle

TAG in adipose tissue and liver

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39
Q

What happens to excess amino acids?

A

converted to fat

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40
Q

What happens to excess fatty acids?

A

TAG in liver and adipose tissue

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41
Q

What specific ion channels do beta cells have and what are they sensitive to?

A

K+

[ATP]

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42
Q

How do K+ ion channels in beta cells work to release insulin ultimately?

A 
glucose enters through GLUT after a meal 
metabolism and [ATP] increases
K-ATP closes and cell depolarises 
voltage dependent calcium channels open 
calcium causes exocytosis of insulin
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43
Q

What receptors does insulin bind to and on what kind of tissues?

A

tyrosine kinase

insulin sensitive –> muscle and fat

44
Q

Insulin stimulates the mobilisation of what kind of transporters?

A

GLUT-4

45
Q

Where do GLUT-4 transporters live?

A

cytoplasm of unactivated muscle and adipose tissue

46
Q

GLUT-1 transports…

A

basal glucose uptake into many tissues eg brain, RBC, kidney

47
Q

Where are GLUT-2 transporters found?

A

b cells of pancreas and liver

48
Q

What are the 3 GLUT non insulin dependent receptors?

A

1.2.3

49
Q

Is the liver insulin sensitive?

A

no

50
Q

What GLUT receptors does the liver use?

A

GLUT 2

51
Q

How does insulin effect glucose transport into the liver?

A

glucose enters down concentration gradient

glucose transport into hepatocytes is enhanced by insulin status

52
Q

Why does insulin have an effect on glucose transport into liver?

A

hexokinase enzyme lowers [glucose] in the cell and forms a concentration gradient in favour of glucose entering into the hepatocytes

53
Q

List some other anabolic functions of insulin

A 
glycogen synthesis in muscle and liver 
amino acid uptake into muscle 
protein synthesis 
TAG synthesis in adipocytes and liver 
inhibits gluconeogenic enzymes
54
Q

List 2 other actions of insulin which are due to activation of multiple transducer pathways

A

permissive effect on HGH

promotes K+ entry into cells

55
Q

Insulin half-life and what is it degraded by?

A

5 mins

liver and kidneys

56
Q

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

A

endocytosed

destroyed by insulin protease

57
Q

Stimuli which increase insulin release

A 
increase [BG]
glucagon 
vagal nerve activity 
increased amino acids in plasma 
incretin hormones eg CCK
58
Q

Stimuli which inhibit insulin release

A

decreased [BG]
somatostatin
stress eg infection
sympathetic alpha 2 effects

59
Q

Why does glucagon increase insulin release?

A

insulin required to take up glucose created via gluconeogenesis stimulated by glucagon

60
Q

Why does vagal activity increase insulin release and discuss iv vs oral glucose

A

parasympathetic - GI hormones
incretin hormones increase insulin
oral glucose better due to direct effect + incretin hormones and vagal stimulation of B cells

61
Q

What is glucagon?

A

peptide hormone produced by alpha cells of the pancreatic islets and is a glucose mobilising hormone

62
Q

What organ does glucagon primarily act upon?

A

liver

63
Q

Half life of glucagon and what is it degraded by?

A

5-10 mins

liver

64
Q

What 4 hormones make up the glucose counter regulatory system?

A

glucagon
HGH
cortisol
epinephrine

65
Q

When is glucagon most active?

A

post-absorptive state

66
Q

Receptors for glucagon?

A

GPCR to adenylate cyclase/cAMP

67
Q

When glucagon receptors are activated what happens?

A

phosphorylate specific liver enzymes

68
Q

3 consequences of phosphorylation of specific liver enzymes

A

increased gluconeogenesis
increased glucogenolysis
formation of ketones from FA

69
Q

What is the net result of glucagon action on the liver enzymes?

A

increased [BG]

70
Q

What is the pattern of glucagon secretion and when does this increase?

A

constant

when [BG] < 5.6mM

71
Q

Why do amino acids also stimulate glucagon aswell as insulin release?

A

adaption for high protein meal

prevent hypoglycaemia

72
Q

How is glucose spared for the brain in the post absorptive state?

A

lower insulin
muscle and fat cannot readily access glucose
glucose sparing for brain

73
Q

Stimuli that promote glucagon release

A 
low [BG]
amino acids in plasma 
sympathetic innervation and epinephrine, B2 effect
cortisol 
stress
74
Q

Stimuli that inhibit glucagon release

A

insulin
glucose
somatostatin
FFA and ketones

75
Q

Parasympathetic effect on islet cells

A

increase insulin, to a less degree glucagon

vagus - anticipatory phase of digestion

76
Q

Sympathetic effect on islet cells

A

increase glucose mobilisation

increase glucagon and epinephrine and inhibit insulin

77
Q

What is somatostatin?

A

peptide hormone produced by D cells in pancreas and hypothalamus , also known as GHIH.

78
Q

How does somatostatin act?

A

slow down absorption in Gi tract to prevent surges

prevents glucagon and insulin

79
Q

How can somatostatin be used clinically (GI)

A

diarrhoea and tumours who have symptoms of diabetes

80
Q

What does exercise do to glucose uptake?

A

increase in muscle without insulin being present by increasing insulin sensitivity of muscle

81
Q

What happens with GLUT-4 receptors and what are long term effects of exercise?

A

increase in number and migrate to cell surface without insulin
effect persists and long term effects if regular exercise

82
Q

How are ketone bodies formed?

A

in starvation FFA are formed from adipose tissue and make ketone bodies by conversion in the liver

83
Q

What 2 parts of the body are ketone bodies used by?

A

brain and muscle

84
Q

Benefit of ketone bodies

A

spares the protein which would be broken down in starvation

85
Q

What is diabetes mellitus?

A

loss of control of blood glucose levels

86
Q

What is type 1/IDDM diabetes?

A

autoimmune destruction of the pancreatic b cells

destroys ability to produce insulin and compromises ability to absorb glucose

87
Q

Treatment of type 1 diabetes

A

need insulin injections every day

88
Q

What is ketoacidosis?

A

similar to starvation - lack of access to nutrients

lack of insulin depresses ketone body uptake

89
Q

Harm of ketoacidosis

A

build up in blood - acidic

life threatening and death

90
Q

2 ways ketones are detectable

A

urine

acetone breath

91
Q

What is type 2 diabetes?

A

insulin resistance of peripheral tissues and fat and muscle no longer respond to normal insulin levels

92
Q

2 reasons why fat and muscle no longer respond to insulin

A

reduced number of receptors

abnormal response of insulin receptors

93
Q

What happens to b cells in type 2 diabetes?

A

nothing - still intact

may even be hyperinsulinaemia

94
Q

What is type 2 diabetes associated with?

A

obesity, diet, exercise

95
Q

Usual age for type 2 diabetes

A

> 40 but decreasing

96
Q

Treatment of type 2 diabetes

A

diet and exercise
oral hypoglycaemic drugs eg metformin
sulphonylureas

97
Q

Why can type 2 diabetes treatments not be used in type 1?

A

requires functioning b cells

98
Q

Diagnostic criteria for diabetes

A

hyperglycaemia

99
Q

What test is done to diagnose diabetes?

A

glucose tolerance test

100
Q

Why is [BG] increased in type 1 and type 2 diabetes?

A

type 1 - inadequate insulin release

type 2 - inadequate tissue response

101
Q

Briefly describe how a glucose tolerance test would be done

A

patient ingests glucose after fasting
[BG] should return to fasting in an hour
if not returned by 2 hours is diabetic

102
Q

How to convert to mM from mg/dl?

A

divide by 18

103
Q

Why are there risks associated with hyperglycaemia?

A

glucose is a highly reactive molecule

104
Q

4 hyperglycaemia complications

A

retinopathy
neuropathy
nephropathy
CVD

105
Q

Who is especially at risk of diabetic hypoglycaemia?

A

type 1 on exogenous insulin

106
Q

How is hypoglycaemia staged?

A

changes in [BG]

Year 2 Diabetes & Endocrinology (JK) (24 decks)

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