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endocrine system 1 > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

<p>What is energy intake determined by?</p>

A

Balance of activity in 2 hypothalamic centres

  1. feeding centre
  2. satiety centre
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2
Q

<p>What does the feeding centre promote?</p>

A

<p>Promotes feelings of hunger and drive to eat</p>

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3
Q

<p>What does the satiety centre promote?</p>

A

<p>Promotes feelings of fullness by suppressing the feeding centre
insulin sensitive</p>

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4
Q

<p>How is activity in the feeding and satiety centres controlled?</p>

A

<p>A complex balance of neural and chemical signals as well as the presence of nutrients in plasma</p>

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5
Q

<p>Glucostatic theory</p>

A

<p>Food intake is determined by blood glucoseas [BG] increases, the drive to eat decreases (- Feeding Centre; + Satiety centre)</p>

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6
Q

<p>Lipostatic theory</p>

A

<p>Food intake is determined by fat stores</p>

<p>as fat stores increase, the drive to eat decreases</p>

<p>(- feeding centre; + satiety centre)</p>

<p>leptin (peptide hormone) released by fat stores depress feeding activity</p>

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7
Q

<p>What are the 3 categories of energy output?</p>

A

cellular work

  • transporting molecules across membranes
  • growth and repair
  • storage of energy (eg. fat, glycogen, ATP synthesis)

mechanical work
- movement, either on large scale using muscle or intracellularly

heat loss

  • associated with cellular and mechanical work
  • accounts for half our energy output
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8
Q

<p>What is the only part of our energy output we can regulate voluntarily?</p>

A

<p>Mechanical work done by skeletal muscle</p>

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9
Q

<p>Metabolism</p>

A

<p>Integration of all biochemical reactions in the body</p>

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10
Q

<p>What are the 3 elements of metabolism?</p>

A

<p>- Extracting energy from nutrients in food</p>

<p>- Storing that energy</p>

<p>- Utilising that energy for work</p>

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11
Q

<p>Anabolic pathways</p>

A
  • build up
  • net effect is synthesis of large molecules from smaller ones
  • usually for storage purposes
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12
Q

<p>Catabolic pathways</p>

A
  • break down
  • net effect is degradation of large molecules into smaller ones
  • releasing energy for work
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13
Q

<p>What state do we enter after eating?</p>

A 
absorptive state (anabolic phase)
- ingested nutrients supply the energy needs of the body and excess is stored
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14
Q

<p>What state do we enter between meals and overnight?</p>

A

post-absorptive state/fasted state (catabolic phase)

- rely on body stores to provide energy

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15
Q

<p>What is meant by the brain being an obligatory glucose utiliser?</p>

A

<p>Most cells can use fats, carbohydrates or protein for energy but the brain can only use glucose</p>

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16
Q

<p>What affect does the brain have on the post-absorptive state?</p>

A

MUST maintain blood glucose concentration [BG] sufficient to meet the brain’s requirements.

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17
Q

<p>Why does hypoglycaemia occur?</p>

A

<p>failure to maintain [BG] sufficient to meet the brain's requirements</p>

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18
Q

<p>How is BG maintained?</p>

A

<p>Synthesising glucose from glycogen (glycogenolysis) or amino acids (gluconeogenesis)</p>

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19
Q

<p>Why does BG rise in diabetes?</p>

A

<p>In diabetes, glucose cannot be taken up by cells so BG rises and glucose is detected in the urine</p>

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20
Q

<p>What is the only structure to have access to BG when it falls below normal range?</p>

A

<p>Brain</p>

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21
Q

<p>What is the normal range of [BG]?</p>

A

<p>4.2-6.3 mM</p>

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22
Q

<p>When does hypoglycaemia occur?</p>

A

<p>[BG] <3mM</p>

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23
Q

<p>What 2 key endocrine hormones maintain [BG]?</p>

A

<p>-Insulin-Glucagon</p>

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24
Q

<p>What does 99% of the pancreas produce?</p>

A

NaHCO3

- operates as an exocrine gland releasing via ducts into the alimentary canal to support digestion

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25
Q

<p>What produces the endocrine hormones of the pancreas?</p>

A

<p>Islets of Langerhans</p>

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26
Q

<p>What are the 4 types of Islets of Langerhans?</p>

A
  • alpha cells
  • beta cells
  • delta cells
  • f cells
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27
Q

<p>What do the a cells produce?</p>

A

<p>Glucagon</p>

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28
Q

<p>What do the B cells produce?</p>

A

<p>Insulin</p>

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29
Q

<p>What do the delta cells produce?</p>

A

<p>Somatostatin</p>

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30
Q

<p>What do the F cells produce?</p>

A

<p>Pancreatic polypeptide ( function not really known, may help control of nutrient absorption)</p>

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31
Q

<p>How many islets are there scattered throughout the pancreas?</p>

A

<p>1-2 million each with a copious blood supply</p>

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32
Q

<p>What does control of BG depend on?</p>

A

<p>Balance between insulin and glucagon</p>

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33
Q

<p>What state does insulin dominate?</p>

A

<p>Fed state</p>

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34
Q

<p>What state does glucagon dominate?</p>

A

<p>Fasted state</p>

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35
Q

<p>What does an increase in insulin result in?</p>

A

<p>- Increased glucose oxidation</p>

<p>- Increased glycogen synthesis</p>

<p>- Increased fat synthesis</p>

<p>- Increased protein synthesis</p>

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36
Q

<p>What does an increase in glucagon result in?</p>

A

<p>- Increased glycogenolysis</p>

<p>- Increased gluconeogenesis</p>

<p>- Increased ketogenesis</p>

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37
Q

<p>What is insulin?</p>

A

<p>Peptide hormone produced by pancreatic B cells</p>

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38
Q

<p>What does insulin stimulate?</p>

A

<p>Glucose uptake by cells</p>

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39
Q

<p>How is insulin synthesised?</p>

A

as a large preprohormone (preproinsulin) then converted to proinsulin in the ER

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40
Q

<p>How does proinsulin become insulin?</p>

A

proinsulinpackaged as granules in secretory vesicles and cleaved to give insulin and C-peptide
(stored in this form until the beta cell is activated and secretion occurs)

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41
Q

<p>What enters the blood from the GIT during the absorptive state?</p>

A

<p>- glucose</p>

<p>- amino acids (aa)</p>

<p>- fatty acids</p>

<p>both glucose and aa’s stimulate insulin secretion but the major stimulus is blood glucose concentration</p>

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42
Q

<p>What is the only hormone which lowers BG?</p>

A

<p>Insulin</p>

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43
Q

<p>What happens to excess glucose during the absorptive state?</p>

A

stored as glycogen in liver and muscleor triacylglycerols (TAG) in liver and adipose tissue

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44
Q

<p>What are amino acids used to do?</p>

A

<p>to make new proteins converted to fat (in excess)</p>

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45
Q

<p>How are fatty acids stored?</p>

A

<p>Fatty acids are stored in the form of triglycerides in adipose tissue and liver</p>

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46
Q

<p>What special channel do B cells possess?</p>

A

<p>KATP channel- specific type of K+ ion channel that is sensitive to the [ATP] within the cell</p>

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47
Q

<p>How does glucose enter cells when it is abundant?</p>

A

<p>glucose transport proteins (GLUT) and metabolism increases</p>

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48
Q

<p>Once glucose enters the cell and increases metabolism what happens?</p>

A
  • increases [ATP] within the cell causing the KATP channel to close
  • intracellular [K+ ] rises, depolarising the cell
  • voltage-dependent Ca2+ channels open and trigger insulin vesicle exocytosis into the circulation
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49
Q

<p>How does low [BG] prevent insulin being secreted?</p>

A
  • [ATP] is low so KATP channels are open
  • K+ ions flow out removing +ve charge from the cell and hyperpolarizing it,
  • voltage-gated Ca2+ channels remain closed and insulin is not secreted
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50
Q

<p>What is the primary action of insulin?</p>

A

binds to tyrosine kinase receptors on the cell membrane of insulin-sensitive tissues (muscle and adipose tissue) to increase glucose uptake by these tissues

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51
Q

<p>What does insulin stimulate with regards to GLUT4?</p>

A

mobilization ofGLUT-4 which reside in cytoplasm of muscle and adipose cells

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52
Q

<p>What happens to GLUT4 after being stimulated by insulin?</p>

A

<p>GLUT4 migrates to the membrane andtransports glucose into the cell</p>

<p>When insulin stimulation stops, the GLUT-4 transporters return to the cytoplasmic pool.</p>

53
Q

<p>What is the glucose taken up by cells primarily used for?</p>

A

<p>used for energy.</p>

54
Q

<p>What are the only insulin sensitive tissues?</p>

A

<p>Muscle and fat</p>

55
Q

<p>What percentage of the body do muscle and fat make up?</p>

A

<p>-Muscle ~40%-Fat ~20-25%</p>

56
Q

<p>How is glucose taken up in tissues other than muscle and fat?</p>

A

<p>via GLUT-transporterswhich are notinsulin-dependent</p>

<p>(GLUT-1, GLUT-2, GLUT-3)</p>

57
Q

<p>What do GLUT 1,3 and 2 facilitate the movement of?</p>

A

glucose
GLUT-1: brain, kidney and red blood cells
GLUT-2: beta cells of pancreas and liver
GLUT-3: Similar to GLUT-1

58
Q

<p>How does the liver take up glucose?</p>

A

GLUT 2 transporterswhich are insulin independent

59
Q

<p>How does glucose enter the liver?</p>

A

<p>Down a concentration gradient</p>

60
Q

<p>In terms of glucose transport, what affect does insulin have on the liver?</p>

A

no direct effect on the liver

glucose transport into hepatocytes is affected by insulin status

61
Q

<p>Why does the liver take up glucose in the fed state?</p>

A

insulin activates hexokinase which lowers [glucose]ic creating a gradient favouring glucose movement into the cells

62
Q

<p>What does liver do in the fasted state?</p>

A

synthesises glucose via glycogenolysis and gluconeogenesis

increasing [glucose]ic creating a gradient favouring glucose movement out of the cells into the blood

63
Q

<p>What anabolic actions does insulin have?</p>

A
  • increases glycogen synthesis in muscle and liver: stimulates glycogen synthase and inhibits glycogen phosphorylase
  • increases amino acid uptake: increases protein synthesis and inhibits proteolysis
  • increases triacylglycerol synthesis in adipocytes and liver: stimulates lipogenesis and inhibits lipolysis
  • inhibits the enzymes of gluconeogenesis in the liver
64
Q

<p>Other than its effect on glucose and its anabolic actions, what other 2 actions does insulin have on the body?</p>

A

<p>-permissive effect on Growth Hormone</p>

<p>- promotes K+ ion entry into cells by stimulating Na+/K+ ATPase. (very important clinically)</p>

65
Q

<p>Why are the additional actions of glucose possible?</p>

A

activation of multiple signal transduction pathways associated with the Insulin Receptor

66
Q

<p>What is the half-life of insulin?</p>

A

<p>~5 minutes</p>

<p>degraded principally in liver and kidneys</p>

67
Q

<p>What happens once insulin action is complete?</p>

A

insulin-bound receptors internalised by endocytosis and destroyed by insulin protease (some recycled)

68
Q

<p>Give examples of stimuli which increase insulin release.</p>

A
  • increased [BG]
  • increased [amino acids]plasma
  • glucagon (insulin required to take up glucose created via gluconeogenesis stimulated by glucagon)
  • incretin hormones controlling GI secretion and motility (gastrin, secretin, CCK, GLP-1, GIP)
  • vagal nerve activity
69
Q

<p>Give examples of stimuli which inhibit insulin release?</p>

A

<p>- Low [BG]</p>

<p>- Somatostatin (GHIH)</p>

<p>- Sympathetic a2 effects</p>

<p>-Stress eghypoxia</p>

70
Q

<p>Why is the insulin response to anIV glucose load less than that of an equivalent oral load?</p>

A

oral load increases insulin by direct effect on B cells and vagal stimulation on B cells (plus incretin effects)

71
Q

<p>What is glucagon?</p>

A

peptide hormone produced by a-cells of the pancreatic islet cells

72
Q

<p>What is the primary purpose of glucagon?</p>

A

<p>to raise blood glucose</p>

<p>It is a glucose-mobilizing hormone, acting mainly on the liver</p>

73
Q

<p>What is the half-life of glucagon?</p>

A

<p>Plasma half-life 5-10mins, degraded mainly by liver</p>

74
Q

<p>When is glucagon most active?</p>

A

<p>Post-absorptive state</p>

75
Q

<p>What hormones make up the glucose counter-regulatory control system?</p>

A

<p>- Epinephrine</p>

<p>- Cortisol</p>

<p>-GH</p>

<p>- Glucagon</p>

76
Q

<p>What are the glucagon receptors?</p>

A

G-protein coupled receptors linked to the adenylate cyclase/cAMP system

77
Q

<p>What do the glucagon receptors do when activated?</p>

A

<p>phosphorylate specific liver enzymes</p>

78
Q

<p>What does phosphorylation of specific liver enzymes by glucagon receptors result in?</p>

A

<p>- Increase glycogenolysis</p>

<p>- Increase gluconeogenesis (substrates: aa’s and glycerol (lipolysis))</p>

<p>- Formation of ketones from fatty acids (lipolysis)</p>

79
Q

<p>What is the net result of activation of glucagon receptors?</p>

A

<p>Elevated [BG]</p>

80
Q

<p>Describe the rate of secretion of glucagon?</p>

A

<p>relatively constant</p>

<p>although secretion increases dramatically when [BG] < 5.6mM (normal [BG] 4.2-6.3mM)</p>

<p>Nevertheless the ratio to insulin is more significant than actual concentration.</p>

81
Q

<p>What do amino acids in the plasma stimulate the release of?</p>

A

<p>release of both insulin and glucagon.</p>

82
Q

<p>Why is important for amino acids to stimulate both insulin and glucagon?</p>

A

<p>insulinstimulating effects of amino acids resultin very low [BG] and iscounteracted by glucose mobilizing effects of glucagon</p>

83
Q

<p>What can other tissues use as energy sources instead of glucose?</p>

A

<p>FFAs and ketones to produce energy</p>

84
Q

<p>Why is there glucose sparing for obligatory glucose users in the post-absorptive state?</p>

A

lower insulin levels mean a large mass of tissue (muscle and fat)cannot readily access glucose

85
Q

<p>Give examples of stimuli that promote glucagon release?</p>

A

<p>- Low [BG]</p>

<p>- High [amino acids]: prevents hypoglycaemia following insulin release</p>

<p>- Sympathetic innervation and epinephrine, B2 effect</p>

<p>- Cortisol</p>

<p>- Stress e.g. exercise, infection</p>

86
Q

<p>Give examples of stimuli that inhibit glucagon release?</p>

A

<p>- Glucose</p>

<p>- Free fatty acids (FFA) and ketones</p>

<p>- Insulin (fails in diabetes so glucagon levels rise despite high [BG)</p>

<p>- Somatostatin</p>

87
Q

<p>What effects does the parasympathetic system have on insulin and glucagon release?</p>

A

<p>- increase in insulin</p>

<p>- increase in glucagon (to a lesser extent)</p>

<p>in association with the anticipatory phase of digestion.</p>

88
Q

<p>What effect does the sympathetic system have on insulin and glucagon?</p>

A

<p>- increased glucagon (promotes glucose mobilization)</p>

<p>- increased epinephrine</p>

<p>- inhibition of insulin</p>

89
Q

<p>What is somatostatin?</p>

A

a peptide hormone secreted by D-cells of the pancreas (and hypothalamus aka GHIH)

90
Q

<p>What is the main pancreatic action of somatostatin?</p>

A

<p>Inhibit activity in the GIT</p>

91
Q

<p>What is the function of SS in inhibiting the GIT?</p>

A

<p>slow down absorption of nutrients to prevent exaggerated peaks in plasma concentrations</p>

92
Q

<p>Why may synthetic somatostatin be used clinically?</p>

A

<p>to help patients with life-threatening diarrhoea associated with gut or pancreatic tumours</p>

93
Q

<p>What do patients with SS secreting tumours often develop?</p>

A

<p>symptoms of diabetes which disappear when the tumour is removed.</p>

94
Q

<p>Although SS is not a counter regulatory hormone, what effect does it have on both insulin and glucagon?</p>

A

<p>It strongly suppresses the release of both insulin and glucagon in a paracrine fashion</p>

95
Q

<p>What does GHIH inhibit release of from the anterior pituitary?</p>

A

<p>GH</p>

96
Q

<p>What is increased during exercise even in the absence of insulin?</p>

A

<p>Entry of glucose into skeletal muscle is increased</p>

97
Q

<p>What effect does exercise have on [BG]?</p>

A

increases the insulin sensitivity of muscle causes an insulin-independent increase in the number of GLUT-4 transporters incorporated into the muscle membrane

98
Q

<p>What can regular exercise produce?</p>

A

<p>prolonged increases in insulin sensitivity</p>

99
Q

<p>How does glucose enter the cell in non-active muscle?</p>

A

<p>insulin binds to its receptor=(glucose transporters)GLUT4migratesto the cell membraneallowing glucose to enter.</p>

100
Q

<p>How does glucose enter the cell in active muscle?</p>

A

GLUT4 transporters migrate to the membrane

- exercise causes glucose uptake independently of insulin andincrease insensitivity of the muscle to insulin

101
Q

<p>What does the body rely on when nutrients are scarce?</p>

A

<p>Stores for energy</p>

102
Q

<p>What happens to the brain after a period of starvation?</p>

A

<p>Brain adapts to be able to use ketones</p>

103
Q

<p>How are stores used during starvation?</p>

A

<p>Adipose tissue is broken down and fatty acids are released</p>

104
Q

<p>Why are spare FFAs converted to ketones and used by the brain in starvation?</p>

A

<p>FFA’s can be readily used by most tissues to produce energy and liver will convert excess to ketone bodies which provides an additional source for muscle and brain!</p>

105
Q

<p>Diabetes mellitus</p>

A

<p>Loss of control of blood glucose levels</p>

106
Q

<p>How does T1DM occur?</p>

A

<p>autoimmune destruction of the pancreatic B-cells destroys ability to produce insulin</p>

<p>compromises patients ability to absorb glucose from the plasma</p>

<p>10% of diabetic patients are insulin-dependent</p>

107
Q

<p>What is another name for T1DM?</p>

A

<p>Insulin dependent diabetes mellitus (IDDM)</p>

108
Q

<p>What can untreated T1DM lead to?</p>

A

starvation and death

109
Q

<p>What do T1DM have an absolute need for?</p>

A

<p>Insulin</p>

110
Q

<p>How does ketoacidosis occur in T1DM?</p>

A

<p>a lack of insulin depresses ketone body uptake.</p>

<p>build up rapidly in the plasma and because they are acidic create life threatening acidosis (ketoacidosis or ketosis)</p>

<p>with plasma pH < 7.1. Death will occur within hours if untreated.</p>

111
Q

<p>How are ketones detectable?</p>

A

<p>In urine and produce distinctive acetone smell to breath</p>

112
Q

<p>What is another name for T2DM?</p>

A

<p>Non-insulin dependent diabetes mellitus (NIDDM)</p>

113
Q

<p>How does T2DM occur?</p>

A

<p>peripheral tissues become insensitive to insulin = insulin resistance</p>

<p>due toan abnormal response/reductionof insulin receptors</p>

114
Q

<p>What may B cells be in T2DM?</p>

A

<p>Hyperinsulinaemia</p>

115
Q

<p>What is T2DM typically associated with?</p>

A

<p>Obesity</p>

116
Q

<p>When does T2DM usually occur?</p>

A

<p>>40 years</p>

117
Q

<p>What is initial treatment of T2DM aimed at?</p>

A

<p>restore insulin sensitivity of tissues with exercise and dietary change</p>

118
Q

<p>What treatment options are there for T2DM?</p>

A

<p>- Lifestyle changes</p>

<p>- Metformin</p>

<p>- Sulfonylureas</p>

<p>- Other oral hypoglycaemic drugs</p>

<p>- Insulin</p>

119
Q

<p>What does metformin do?</p>

A

<p>Inhibits hepatic gluconeogenesis and antagonises action of glucagon</p>

120
Q

<p>What do sulfonylureas do?</p>

A

close the KATP in B cells and therefore stimulate Ca2+ entry and insulin secretion

121
Q

<p>Why is [BG] elevated in T1DM?</p>

A

<p>Inadequate insulin release increase [BG]</p>

122
Q

<p>Why is [BG] elevated in T2DM?</p>

A

<p>Inadequate tissue response increase[BG]</p>

123
Q

<p>What is the diagnostic criteria for diabetes?</p>

A

<p>Hyperglycaemia</p>

124
Q

<p>What test is performed to diagnose diabete1s?</p>

A

<p>Oral glucose tolerance test</p>

125
Q

<p>How is the OGTT carried out?</p>

A

patient ingests glucose load after fasting and [BG] measured. elevation after 2 hours is indicative of diabetes

([BG] will normally return to fasting levels within an hour)

(does not distinguish Type I from II)

126
Q

<p>What diabetic complications can occur?</p>

A

<p>- Retinopathy</p>

<p>- Neuropathy</p>

<p>- Nephropathy</p>

<p>- Cardiovascular disease</p>

127
Q

<p>Who is hypoglycaemic a particular problem in?</p>

A

<p>Type 1 patients</p>

128
Q

<p>What are the stages of hypoglycaemia?</p>

A

<p>- 4.6mM [BG]: Inhibition of insulin secretion</p>

<p>- 3.8mM [BG]: Glucagon, epinephrine and GH secretion</p>

<p>- 3.2mM [BG]: Cortisol secreted</p>

<p>- 2.8mm [BG]: Cognitive dysfunction</p>

<p>- 2.2mM [BG]: Lethargy</p>

<p>- 1.7mM [BG]: Coma</p>

<p>- 1.1mM [BG]: Convulsions</p>

<p>- 0.6mM [BG]: Permanent brain damage and death</p>

129
Q

<p>What is leptin?</p>

A

peptide hormone released by fat stores which depresses feeding activity

endocrine system 1 (25 decks)

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