Endocrine pancreas 2 - Glucagon Flashcards

1
Q

define incretin hormones?

A

hormones released by GI tract during digestion - e.g. gastrin, secretin etc.

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2
Q

what is glucagon?

A

peptide hormone produced by alpha cells

also a GLC-mobilising hormone

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3
Q

glucagon 1y action?

A

raise BG

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4
Q

half-life of glucagon?

A

5-10 mins, degraded by liver

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5
Q

what is the Glucose counter-regulatory control system and when is it most active?

A
system involving:
-glucagon
-epinephrine
-cortisol
-GH (growth)
...which opposes insulin
most active during post-absorptive state
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6
Q

how does glucagon increase BG?

A

1) increase glycogenolysis
2) increase gluconeogenesis
3) forms ketones from fatty acids (starvation/diabetes)

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7
Q

why is it important that amino acids stimulate both insulin and glucagon?

A

increase in amino acids (e.g. protein-heavy meal) increases secretion of insulin and uptake of GLC into cells -
need glucagon to balance this as not enough GLC would be present for brain - leading to HYPOGLYCAEMIA

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8
Q

Stimuli that promote glucagon release?

A
BG < 5mM
increased amino acid conc.
sympathetic innervation and epinephrine 
cortisol
stress
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9
Q

Stimuli that inhibit glucagon release?

A
GLC
FFA (free fatty acids)
ketones
insulin 
somatostatin
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10
Q

result of increase sympathetic innervation?

A

increases glucagon and epinephrine, decreases insulin

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11
Q

result of increase parasympathetic innervation?

A

increases insulin (and a little glucagon) and epinephrine

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12
Q

role of somatostatin?

A

to (gradually) inhibit activity of GI tract - slows down movement and absorption

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13
Q

what can somatostatin treat?

A

life threatening diarrhoea

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14
Q

effects of exercise on BG?

A

insulin-independent increase in the number of GLUT-4 transporters
insulin sensitivity of muscle increases
entry of GLC into muscles increases

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15
Q

how to GLC get into active and non-active muscle cells?

A

active:
GLUT4s migrate to membrane without insulin dog GLC uptake is independent
also increases muscle’s sensitivity to insulin

non-active:
insulin binds to receptor THEREFORE GLUT4s go to cell membrane

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16
Q

what happens during starvation?

A

brain and muscles use ketone bodies (converted from excess FAs),
most other tissues use the FAs

17
Q

how does the brain use ketones?

A

only works if pancreas is functioning properly as ketone body uptake is insulin dependent

18
Q

why is starvation dangerous for diabetics?

A

diabetics cannot produce enough insulin therefore ketone cannot be used by brain - results in LIFE THREATENING KETOACIDOSIS

19
Q

pH of ketoacidosis?

A

<7.1

20
Q

how to detect hyperglycaemia?

A

glucose tolerance test -

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

21
Q

diabetic complications of hyperglycaemia?

A

retinopathy
neuropathy
nephropathy
CVD