252. The pancreas Flashcards

1
Q

How is feeding and hunger controlled?

A

Two centres in the hypothalmus: Feeding centre and satiety centre.

Glucostatic theory- these centres respond to blood glucose levels.

Lipostatic theory- these centres respond to fat stores

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2
Q

What hormone is released by fat stores to decrease feeding activity?

A

Leptin

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3
Q

What are the three ways we consume energy?

A

Cellular work
Mechanical work
Heat loss

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4
Q

If most cells can use fats, carbs or protein as an energy source why do we need a constant blood glucose level?

A

The brain is an obligitory glucose user. I.e. it can only use glucose for energy.

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5
Q

What are the normal ranges of blood glucose?

When does hypoglyceamia occur?

A

4.2-6.3mM (5 is useful)

Hypoglyceamia<3mM

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6
Q

What are the four cells found in the islets of langherhan?

A

Alpha cells produce glucagon
Beta cells produce insulin
Delta cells produce somatostatin
F cells produce pancreatic polypeptide (function not known)

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7
Q

How is insulin released into the bloodstream?

A

Beta cells uptake glucose causing potassium channels to close. The intracellular rise in potassium leads too ca channels opening, releasing insulin.

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8
Q

How does insulin work?

A

Only hormone that can lower blood sugar. Causes glut-4 transporters in muscle and adipose tissue to be expressed in response to insulin

This causes glucose to be taken into the cell.

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9
Q

What other actions does insulin have?

A

Increases glycogen synthesis in muscle and liver. Stimulates glycogen synthase and inhibits glycogen phosphorylase

Increases amino acid uptake into muscle

Increases protein synthesis and inhibits proteolysis

increases triacylglycerol synthesis in adipocytes and liver

inhibits the enzymes of gluconeogenesis in the liver

Promotes potassium ion entry into cells

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10
Q

What stimuli cause insulin to be released?

A

increased BG
Increased amino acids in plasma
Glucagon
other incretin hormones e.g. Gastrin, secretin, CCK, GLP-1, GIP

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11
Q

What stimuli cause insulin to be inhibited?

A

Low BG
Somatostatin
Sympathetic effects
Stress e.g. hypoxia

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12
Q

Why does oral glucose have more of an affect that IV?

A

The vagus nerve controls insulin release and so it will cause an added affect when glucose is delivered via the GI tract

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13
Q

Glucagon is released in response to decreasing plasma glucose. How does it work to increase plasma glucose

A

Increased glycogenolysis
Increased gluconeogenesis
Formation of ketones from fatty acids

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14
Q

How do amino acids affect insulin and glucagon?

A

Cause release of both. This allows insulin to utilise amino acids for protein synthesis yet glucagon stops hypoglyceamia from occurring due to this

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15
Q

What stimulus promote glucagon release?

A
Low BG
High amino acid concentration
Sympathetic innervation
Cortisol
Stress e.g. exercise/infection
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16
Q

What stimulus inhibit glucagon?

A

Glucose
FFA and ketones
Insulin
Somatostatin

17
Q

What are the counter-regulatory hormones?

A

Glucagon
Epinepherine
Cortisol
Growth hormone

Somatostatin, not counter insulin but suppresses insulin and glucagon release

18
Q

What is the role of somatostatin?

A

Inhibits activity in the GI tract. Idea is to slow down absorption of nutrients to stop exaggerated peaks in plasma concentrations

19
Q

How does exercise affect glucose uptake?

A

In active muscle GLUT-4 transporters migrate to the membrane without insulin being present.

Exercise increases insulin sensitivity

20
Q

What occurs in starvation?

A

Body relies on stores for energy. FFA’s aer readily converted into ketones which provides an additional source for muscle and brain.

This spares protein which is broken down last

21
Q

What is the treatment for diabetes type II?

A

LIFESTYLE CHANGES

Metformin
Sulphonylureas
Insulin?

22
Q

Explain the process of a glucose tolerance test.

A

Patient ingests glucose after fasting.
Should be normal after 1 hour
If still high after 2 hours, this indicates diabetes

23
Q

What are the complications of persistent hyperglyceamia?

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular disease