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Endocrine System > The Endocrine Pancreas 2 > Flashcards

The Endocrine Pancreas 2 Flashcards

1
Q

What class of hormone is glucagon?

A

Peptide hormone

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2
Q

What is the primary function of glucagon?

A

Raise blood glucose, it is a glucose mobilising hormone that mainly acts on the liver

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3
Q

What is the plasma half life of glucagon?

A

5-10 minutes

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4
Q

Where is glucagon mainly degraded?

A

In the liver

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5
Q

What system does glucagon form part of, which opposes the actions of insulin?

A

Glucose counter-regulatory control system

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6
Q

What does the glucose counter regulatory control system consist of?

A

Glucagon

Epinephrine

Cortisol

Growth hormone

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7
Q

Is glucagon most active in the absorptive or post-absorptive state?

A

Post-absorptive state

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8
Q

What kind of receptors are glucagon receptors?

A

G-protein coupled receptors linked with adenylate cyclase/cAMO system

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9
Q

What does the activation of glucagon receptors cause?

A

Increased glycogenolysis

Increased gluconeogenesis

Formation of ketones from fatty acids (lipolysis)

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10
Q

What effect does increased blood glucose have on insulin and glucagon?

A

Increased insulin secretion

Decreased glucagon secretion

Decreased blood glucose has the opposite effects

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11
Q

How do amino acids impact the release of insulin and glucagon?

A

Stimulates the release of both, which is an adaptation to adjust for the composition of a meal very high in protein

If not for this effect on glucagon then the insulin stimulating effects would result in very low [BG]

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12
Q

What is meant by obligatory glucose user?

A

Endocrine system ensures there is enough glucose circulating to supply the needs of the brain

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13
Q

Other than the brain, what can tissues use when glucose is not available?

A

Free fatty acids and ketones to produce energy

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14
Q

What are examples of stimuli that promotes glucagon release?

A
  • Low [BG] (<5mM)
  • High [amino acid]
    • Prevents hypoglycaemia following insulin response to amino acids
  • Sympathetic innervation and epinephrine, b2 effect
  • Cortisol
  • Stress
    • Such as exercise, infection
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15
Q

What are examples of stimuli that inhibits glucagon release?

A
  • Glucose
  • Free fatty acids (FFA) and ketones
  • Insulin
    • Fails in diabetes so glucagon levels rise despite high [BG]
  • Somatostatin
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16
Q

How does parasympathetic activity (vagus nerve) impact Islet cells?

A

Increases insulin and to a lesser extent increases glucagon, in association with the anticipatory phase of digestion

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17
Q

How does sympathetic activity impact Islet cells?

A

Promote glucose mobilisation, so increased glucagon, increased epiniphrine and inhibition of insulin, all appropriate for fight or flight response

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18
Q

Give a summar of glucose counter regulatory controls for:

muscle glycogenolysis

liver glycogenolysis

gluconeogenesis

inhibition of glucose uptake

lipolysis

protein catabolism

A
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19
Q

What class of hormone is somatostain?

A

Peptide hormone

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20
Q

What is somatostatin produced by?

A

D cells of the pancreas

Hypothalamus

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21
Q

What is somatostatin also known as?

A

Growth hormone inhibiting hormone (GHIH)

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22
Q

Wjhat is the main action of somatostatin?

A

To inhibit activity in GI tract, slow down absorption of nutrients to prevent exaggerated peaks in plasma concentration

23
Q

What can synthetic somatostatin (SS) be used for clinically?

A

To help patients with life-threatening diarrhoea associated with gut or pancreatic tumours

24
Q

What effect does somatostain have on insulin and glucose?

A

It is not a counter regulatory hormone in the control of blood glucose

But it does strongly suppress the release of both insulin and glucagon in a paracrine fashion

25
What effect does somatostain have on growth hormone?
Inhibits its release from anterior pituitary
26
What can disruption of the steady state be caused by?
Exercise Starvatopm Diabetes
27
How does exercise affect the entry of glucose into skeletal muscle?
Entry of glucose into skeletal muscle is increased during exercise, even in the absence of insulin
28
How does exercise impact the insulin sensitivity of a muscle?
Increases it and causes an intulin-independent increase in the number of GLUT-4 transporters incorporated into muscle membrane
29
What is the difference in migration of GLUT-4 transporters during exercise and when not exercising?
When not exercising, requires insulin to activate When exercising, can migrate to membrane without insulin being present
30
How does the body get energy during starvation?
When nutrients are scarce the body relies on stores for energy, adipose tissue is broken down and fatty acids are released FFA can be used by most tissues to produce energy and liver will convert excess to ketone bodies which provide additional source of energy for brain and muscles
31
Why does the brain adapt after a period of starvation to use ketones?
To save proteins that would otherwise be broken down to provide gluconeogenic substrates
32
Can be brain always use ketones as fuel?
No, it needs to adapt to be able to use them - which it does after a period of starvation
33
Why are proteins of the body the last store to be depleted in starvation?
It is very weakening and leaves you vulnerable to infection
34
What are the 2 main forms of diabetes?
Type 1 Type 2
35
What is type 1 diabetes also known as?
Insulin dependent diabetes mellitus (IDDM)
36
What does IDDM stand for?
Insulin dependent diabetes mellitus
37
What is type 1 diabetes?
Autoimmune destruction of pancreatic B cells meaning loss of ability to produce insulin and compromises ability to absorb glucose from plasma
38
What percentage of diabetic patients have type 1 diabetes?
10%
39
Why do type 1 diabetics take daily injections and not an oral tablet?
Peptide hormones cannot be given orally
40
What would happen to a type 1 diabetic who did not take insulin injections?
Excessively wasted, develop keoacidosis, coma and die
41
What is a consequence of the body thinking it is starving in diabetes?
Liver produces glucose which makes the problem worse
42
Why does ketoacidosis occur in diabetes?
Normally, when nutrients are scarce the body relies on stores for energy (adipose tissue broken down and free fatty acids release) However, in poorly controlled insulin dependent diabetes a lack of insulin depresses ketone body uptake so they build up rapidly in the plasma and because they are acidic create life threatening acidosis (ketoacidosis or ketosis) with plasma pH \< 7.1
43
What are indicators of ketoacidosis?
Ketones are detectable in urine and produce distinctive acetone smell to breath
44
What is type 2 diabetes also called?
Non-insulin dependent diabetes mellitus (NIDDM)
45
What does NIDDM stand for?
Non-insulin dependent diabetes mellitus
46
What happens in type 2 diabetes?
Peripheral tissues become insensitive to insulin (called insulin resistance) Muscle and fat can no longer respond to normal levels of insulin, either due to abnormal response of insulin receptors or a reduction in their number B cells remain intact (may even be insulinaemia)
47
What percentage of diabetics are type 2?
90%
48
What is type 2 diabetes typically associated with?
Obesity and usually appears \>40 years but age is decreasing
49
What is the treatment for type 2 diabetes?
1) Initial tretment is aimed at trying to restore insulin sensitivity of tissues with exercise and dietary changes 2) If this fails, oral hypoglycaemic drugs will be used 3) Eventually end up taking insulin
50
What is a glucose tolerance test?
Patient ingests glucose load after fasting [BG] measured [BG] will normally return to fasting levels within an hour, elevatin after 2 hours is indicative of diabetes
51
Can a glucose tolerance test distinguish type 1 from type 2 diabetes?
No, it cannot
52
What are examples of diabetic complications?
Retinopathy Neuropathy Nephropathy Cardiovascular disease
53
What are complications of hypoglycaemia in diabetes?
Cognitive dysfunction Lethargy Coma Convulsions Permanent brain damage and death

Endocrine System (26 decks)

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