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D&E Physiology > The Endocrine Pancreas 2 > Flashcards

The Endocrine Pancreas 2 Flashcards

1
Q

What type of hormone is glucagon?

A

Peptide hormone

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2
Q

Where is glucagon made?

A

alpha cells in pancreatic islets

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3
Q

What is the role of glucagon?

A

Raise blood glucose

Glucose-mobilising hormone

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4
Q

Glucagon acts on what?

A

The liver

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5
Q

What is the half life of glucagon?

A

5-10mins

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6
Q

What hormones make up the counter-regulatory control system for glucose?

A

Glucagon
Epinephrine
Cortisol
GH

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7
Q

When is glucagon most active?

A

Fasted state

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8
Q

Glucagon binds to what?

A

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

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9
Q

What happens when glucagon binds to G-protein coupled receptors?

A

Phosphorylation of specific liver enzymes

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10
Q

What is the effect of the Phosphorylation of specific liver enzymes by glucagon?

A

Increased Glycogenolysis
Increased gluconeogenesis
Formation of ketones from FAs (lipolysis)

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11
Q

What happens to Liver glycogen in the presence of glucagon?

A

Conversion of glycogen to glucose

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12
Q

What happens to lipids in adipose tissue in the presence of glucagon?

A

Lipids become free fatty acids and glycerol

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13
Q

What happens to muscle cells in a low [Glucose] environment?

A

Use of glycogen

FAs/Breakdown of proteins to amino acids for energy

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14
Q

What can the brain use for energy?

A

Glucose

Ketone bodies

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15
Q

Glycogen is converted into what in muscles/

A

Pyruvate/lactate –> Glucose (gluconeogenesis)

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16
Q

Amino acids in the plasma stimulate what?

A

Increased insulin and glucagon

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17
Q

What is the benefit of a high protein meal with little carbohydrate stimulating Insulin AND glucagon?

A

Prevents hypoglycaemia following insulin release in response to aa.

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18
Q

Stimuli that promote glucagon release?

A

Low [BG] (<5mM)
High [amino acids] .
sympathetic innervation and epinephrine, beta2 effect
Cortisol
Stress e.g. exercise, infection

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19
Q

Stimuli that inhibit glucagon release?

A

Glucose
FFAs and Ketones
Insulin
Somatostatin

20
Q

What effect does increased parasympathetic (vagal) activity have on islet cells?

A

Increased insulin
(somewhat) increased glucagon
ANTICIPATORY DIGESTION

21
Q

What effect does increased sympathetic activity have on islet cells?

A

Increased glucose mobilisation
Increased Glucagon, epinephrine
Inhibited insulin

22
Q

Where is somatostatin secreted from?

A

D-cells (pancreas)

Hypothalamus

23
Q

What is the pancreatic action of somatostatin?

A

Inhibit GIT activity
Slow down absorption of nutrients
Prevent peaks in plasma concentrations

24
Q

What is a use of synthetic somatostatin?

A

Treating life threatening diarrhoea associated with gut/pancreatic tumours

25
Q

What is the paracrine effect of somatostatin?

A

Suppress release of glucagon and insulin

26
Q

What is the effect of somatostatin on the anterior pituitary?

A

Inhibits secretion of GH

27
Q

What is the other name of somatostatin?

A

GHIH - Growth Hormone Inhibiting Hormone

28
Q

What causes a stimulation of somatostatin release?

A

↑[aa]plasma

↑[Glucose]plasma

29
Q

How is entry of glucose into muscle increased during exercise?

A

Increased insulin sensitivity

Insulin-independent ↑ in number of Glut-4 transporters

30
Q

How long does increased insulin sensitivity last after exercise?

A

Several hours

31
Q

How does the brain adapt in starvation?

A

Adapts to use ketones for energy

32
Q

How are nutrients provided in starvation?

A

Adipose tissue is broken down into fatty acids

Fatty acids -> Ketones

33
Q

Which store is depleted last in starvation? Why?

A

Protein - weakening, makes person vulnerable to infection

34
Q

What is the cause of T1DM?

A

Autoimmune destruction of pancreatic beta cells

35
Q

Why does diabetes cause ketoacidosis?

A

Lack of insulin depresses the uptake of ketone bodies, which are acidic

36
Q

What is considered an acid blood pH?

A

ph<7.1

37
Q

Why do tissues no longer respond normal levels of insulin in T2DM?

A

Abnormal response of insulin receptors

Reduction in insulin receptor numbers

38
Q

Typical risk factors for T2DM?

A

Obesity
>40yrs
High sugar/fat diet

39
Q

What is the initial treatment for T2DM?

A

Exercise

Dietary change

40
Q

What is the first line therapy for T2DM?

A

Metformin (oral hypoglycaemic drugs)

41
Q

How does Metformin work?

A

Inhibit hepatic gluconeogenesis

Antagonise glucagon action

42
Q

How do Sulphonylureas work?

A

Close Katp in B cells

Stimulate Ca2+ entry and insulin secretion

43
Q

What is the diagnostic test for DM?

A

Glucose tolerance test
Ingest glucose after fasting [BG] is measured
Elevation after 2hrs indicates DM

44
Q

What are the most common diabetes complications?

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular disease

45
Q

Coma appears at what [BG] levels?

A

1.7mM

46
Q

Death occurs at what hypoglycaemia [BG]?

A

0.6mM

47
Q

At what [BG] is cortisol secreted?

A

3.2mM

D&E Physiology (10 decks)

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