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Endocrine > The Endocrine Pancreas > Flashcards

The Endocrine Pancreas Flashcards

1
Q

What are the two theories that aim to explain what induces feelings of hunger / fullness? Brief explanation of each

A
  • Glucostatic Theory: food intake is determined by blood glucose concentration, as BG increases, feelings of satiety increase
  • Lipostatic Theory: food intake is determined by fat stores, as fat stores increase feelings of satiety increase
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2
Q

What are the three categories of energy output?

A
  • Cellular Work: transport / growth and repair / storage of energy
  • Mechanical Work: movement
  • Heat loss
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3
Q

What are anabolic and catabolic pathways? When do each of them occur?

A
  • Anabolic: build up, ingested nutrients supply body needs and rest is stored
  • Catabolic: Break down, reliance on body stores to provide energy
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4
Q

What does the brain need for energy?

A
  • The brain needs glucose

- Can use ketone bodies in times of starvation

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5
Q

How does the body restore low blood sugar to normal levels?

A
  • Glycogenolysis: breakdown od glycogen

- Gluconeogenesis: synthesis of glucose from other energy sources

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6
Q

What is the normal range for blood glucose?

When is a patient hypoglycaemic?

A
  • Normal: 4.2-6.3 mM (80-120 mg/dl)

- Hypo: <3 mM

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7
Q

What are the hormone producing cells of the pancreas? How much of the pancreas do they account for?

A
  • Islets of Langerhans

- 1% of pancreas, other 99% does digestion

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8
Q

What are the types of islet cells and what do they produce?

A
  • Alpha cells: produce glucagon
  • Beta cells: produce insulin
  • Delta cells: produce somatostatin (aka GHIH)
  • F cells: produce pancreatic polypeptide (function unknown)
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9
Q

Which metabolic processes does insulin initiate?

A
  • Glucose oxidation (so glucose can’t move back out of cells)
  • Glycogen synthesis
  • Fat synthesis
  • Protein synthesis
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10
Q

Which metabolic processes does glucagon initiate?

A
  • Glycogenolysis
  • Gluconeogenesis
  • Ketogenesis
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11
Q

Describe insulin synthesis and secretion from cells

A
  • Synthesized as preproinsulin, converted to proinsulin in ER
  • Proinsulin packaged into vesicles, where it gets cleaved to insulin + C peptide
  • Stored in that form until Beta cell activation & secretion
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12
Q

What stimulates insulin secretion?

A
  • Blood glucose concentration

- AA’s and FA’s also do but predominantly glc

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13
Q

How is excess glucose stored?

A
  • As glycogen in the liver and muscle

- As triacylglycerols (TAGs) in liver and adipose tissue

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14
Q

Describe the mechanism of insulin secretion by beta cells when blood glucose rises

A
  • Abundant glucose enters beta cells via GLUT-2 and metabolism increases
  • Beta cells have K channels that are sensitive to [ATP], K(ATP) channels, when glucose enters [ATP] increases
  • K(ATP) channels close due to high [ATP], intracellular [K] rises and cell depolarizes
  • Depolarization causes voltage dependent Ca channels to open, triggering insulin vesicle exocytosis into circulation
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15
Q

Which way does most of the K flow through K(ATP) channels and how does this work in the insulin release mechanism?

A
  • Net movement of K out of cell
  • When gates close, intracellular K increases, making the charge in the cell more positive, supplying the voltage for depolarization and Ca channel opening
  • When gates remain open the cell remains at a negative voltage due to outward flow of K
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16
Q

What hormones other than insulin lower blood glucose?

A

None

Insulin is the only hormone that lowers blood glucose

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17
Q

Explain how insulin causes insulin sensitive cells to take up more glucose?

A
  • Insulin binds tyrosine kinase receptors on cell surface
  • Causes mobilization of GLUT-4 transporters to cell membrane
  • More GLUT-4 transporters allows more glucose uptake
  • When insulin stimulation stops the GLUT-4 transporters return to the cytoplasmic pool
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18
Q

Why are most types of tissue NOT insulin dependent? How significant is it that muscle and fat are?

A
  • Because other tissues use different GLUT transporters that do not depend on insulin for recruitment to the cell membrane
  • Fat 20-25% BW, muscle about 40% - it’s significant
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19
Q

What types of GLUT transporters are found on different cell types?

A
  • GLUT 1 & 3: basal glucose uptake in many tissues (eg. brain, kidneys and RBC)
  • GLUT 2: Beta cells of pancreas and liver
  • GLUT 4: muscle and adipose tissue
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20
Q

Is glucose transport into the liver insulin dependent?

A
  • No, uses GLUT 2 transporters so glucose moves with concentration gradient

Glucose transport in the liver is affected by insulin though………..

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21
Q

How does insulin affect glucose transport in liver cells?

A
  • If insulin is bound, hexokinase is activated, phosphorylates glucose so it can’t move out via GLUT 2 and creates a concentration gradient favouring glucose movement into the cell
  • If insulin is not bound the liver synthesizes glucose via glycogenolysis and gluconeogenesis, creating a high intracellular [glc] so glucose moves out of the cell
22
Q

Additional mechanisms of insulin? (basically just list them all actually)

A
  • Stimulates glycogen synthase, inhibits glycogen phosphorylase
  • Increases AA uptake and therefore protein synthesis, inhibits proteolysis
  • Increases TAG synthesis in fat & liver, inhibits lipolysis
  • Inhibits gluconeogenesis
  • Promotes K ion entry into cells by stimulating Na/K ATPase. important clinically
23
Q

What is the approximate half life of insulin?

What happens once insulin action is complete?

A
  • 5 minutes

- Insulin bound receptors are internalized by endocytosis and destroyed by insulin protease (some recycled)

24
Q

List the stimuli that promote insulin secretion

A
  • Increased blood glucose
  • Increased [AA] in plasma
  • Glucagon (insulin is required to uptake glucose synthesized by gluconeogenesis)
  • Other hormones controlling GI secretion (gastrin / secretin / CCK / GLP-1 / GIP)
  • Vagal tone
25
Q

List the stimuli that inhibit insulin secretion

A
  • Low blood glucose
  • Somatostatin (GHIH)
  • Sympathetic (alpha 2) effects
  • Stress (eg. hypoxia)
26
Q

Why is insulin response to IV glucose less than it is to orally consumed glucose?

A
  • Because orally consuming glucose causes vagal stimulation of insulin release as well as the effect of raised blood glucose on insulin release
  • Vagus also stimulates release of other GI hormones that can also stimulate insulin release
27
Q

What is the main function of glucagon? What is its main target?

A
  • Raise blood glucose concentration

- Acts mainly on the liver

28
Q

Plasma half life of glucagon? Where is it degraded?

A
  • 5-10mins plasma half life

- Mainly degraded by liver

29
Q

What hormones are involved in the glucose counter-regulatory control system?

A
  • Insulin
  • Glucagon
  • Epinephrine
  • GH
  • cortisol
30
Q

What type of receptor does glucagon act on?

A
  • G Protein Coupled Receptor linked to the adenylate cyclase / cAMP system
31
Q

What processes are initiated in liver cells when glycogen is bound?

A
  • Increased glycogenolysis
  • Increased gluconeogenesis (substrates: AA’s and glycerol - from lipolysis)
  • Formation of ketones from Fatty Acids (lipolysis)
32
Q

What effect do amino acids have on the secretion of insulin and glucagon?
Why is this?

A
  • AA’s stimulate both insulin and glucagon release
  • Adaptation to maintain blood glucose in carnivores. If you eat a high protein, low carb meal and only insulin was released then blood glucose would drop very low. Since glucagon is also released blood glucose is maintained so there I available energy for the brain and other tissues
33
Q

List the stimuli that promote glucagon release

A
  • Low blood glucose
  • AA’s in plasma
  • Sympathetic innervation and epinephrine
  • Cortisol
  • Stress / exercise / infection
34
Q

List the stimuli that inhibit glucagon release

A
  • High blood glucose
  • Free Fatty Acids and Ketones
  • Insulin
  • Somatostatin
35
Q

Effect of parasympathetic innervation on insulin and glucagon release? What nerve is this via?

A
  • Vagus
  • Increases insulin secretion
  • Increases glucagon secretion to a lesser extent, in association with the anticipatory phase of digestion
36
Q

Effect of sympathetic innervation on insulin and glucagon release?

A
  • Increases glucagon and epinephrine secretion
  • Inhibits insulin

Want mobilization of glucose for fight or flight response

37
Q

Where is somatostatin secreted from? What is its main pancreatic action??

A
  • D-cells of the pancreas and the hypothalamus (aka GHIH)

- Main pancreatic action is to slow GI absorption of nutrients to prevent spikes in plasma concentrations

38
Q

Actions of somatostatin?

A
  • Inhibit insulin and glucagon release in a paracrine fashion
  • Inhibit GI tract activity
  • Inhibit secretion of GH from anterior pituitary
39
Q

What promotes the release of somatostatin?

A
  • Elevated plasma AA’s

- Elevated blood glucose

40
Q

What is the effect of exercise on blood glucose and why?

A
  • Exercise causes insulin independent recruitment of GLUT-4 transporters to the cell surfaces of skeletal muscle. It also increases insulin sensitivity of these cells
  • Effects last for hours, and regular exercise can cause prolonged increases in insulin sensitivity
  • Therefore would cause blood glucose to decrease
41
Q

What happens when starvation is entered and glucagon stores are depleted?

A
  • Adipose tissue broken down into Free Fatty Acids
  • FFA’s can be used by most of the body for energy
  • Liver converts FFA’s to ketone bodies that the brain can use in periods of starvation
42
Q

When fat stores are depleted in starvation what is the last energy store to be used?

A
  • Protein
  • When adipose is used up protein can be broken down to provide substrates for gluconeogenesis
  • Breaking down bodies own protein is very weakening, makes you vulnerable to infection
43
Q

What is type 1 diabetes also known as?

Describe the pathophysiology of type 1 diabetes mellitus

A
  • Insulin Dependent Diabetes Mellitus (IDDM)
  • Autoimmune destruction of pancreatic beta cells results in inability to produce insulin. Results in starvation, ketoacidosis and death if untreated
44
Q

Treatment of type 1 diabetes?

A
  • Injected insulin

Peptide hormones can’t be taken orally

45
Q

Describe how ketoacidosis occurs in diabetes. How does this lead to death?

A
  • Diabetes means can’t access nutrients being consumed, so body goes into starvation and begins to produce ketone bodies as a energy source for the brain
  • Lack of insulin causes depression of ketone body uptake, results in buildup of ketone bodies in plasma
  • ketones are acidic and cause pH < 7.1 in the plasma, which is fatal within hours if untreated
46
Q

What is type 2 diabetes also known as?

Describe the pathophysiology of type 2 diabetes mellitus

A
  • Non-Insulin Dependent Diabetes Mellitus (NIDDM)
  • Peripheral tissues become insensitive to insulin (insulin resistance), due to either abnormal receptor response or reduction in receptor number
  • Beta cells remain in-tact and there may even be hyperinsulinaemia
47
Q

Causes / risk factors for type 2 diabetes? When does it usually present?

A
  • Obesity, high sugar and animal fat diets with low exercise are risk factors
  • Usually presents at >40yrs, but age of onset decreasing
48
Q

Why is blood glucose raised in type 1 and type 2 diabetes?

A
  • Type 1: inadequate insulin production

- Type 2: inadequate tissue response

49
Q

How does a glucose tolerance test work? What does it diagnose?

A
  1. Fasting blood glucose measured
  2. Patient consumes some glucose
  3. Glucose should be back to fasting baseline after an hour, if after 2 hours still elevated indicates diabetes
  • Diagnoses diabetes, doesn’t distinguish between type 1 and 2
50
Q

How to convert mg/dl (US units) to mM?

A

Divide by 18

MW of glucose is 180 and mM is per litre

51
Q

What is the effect of diabetes on blood glucose? Possible complications due to this?

A
  • Hyperglycaemia

Leads to:

  • Retinopathy
  • Neuropathy
  • Nephropathy
  • CVS disease

Endocrine (30 decks)

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