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The Patient Y3 semester 1 > Pancreas & Insulin Therapies: Hyperglycaemia and Hypoglycaemia > Flashcards

Pancreas & Insulin Therapies: Hyperglycaemia and Hypoglycaemia Flashcards

1
Q

How does glucose provide energy?

A
  • Ubiquitous energy source
  • Glycogen is ‘stored’ reservoir’ of glucose. Excess glucose converted to glycogen and stored in the liver.
  • CNS cannot substitute glucose; delivery is therefore critical
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2
Q

What is the value for hypoglycaemia?

A

Hypoglycaemia <2.5mmol/L

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3
Q

What is the value for hyperglycaemia?

A

> 10mmol/L, sustained

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4
Q

Values for normoglycemia?

A
  • Normoglycaemia 3-5mmol/L healthy fasting value,

* Normoglycaemia 7-8mmol/L healthy post-prandial/eating

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5
Q

The Homeostasis of Hyperglycaemia?

A
  • Insulin is the principle hormone that is detected when blood sugar levels rise.
  • Detected by the insulin secreting cells In the pancreas.
  • Increases in blood sugar levels caused by food intake but you will also convert glycogen into glucose and also fatty acids and amino acids into glucose precursors in the liver (endogenous glucose production)
  • I.e. if you skip breakfast, you will use glycogen stores up.
  • Insulin acts on numerous tissues to bring blood sugar levels back down to restore the homeostatic loop (negative feedback).
  • Drugs can act on insulin release or insulin action.
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6
Q

The Homeostasis of Hypoglycaemia

A
  • Fasting overnight fast
  • Fall in blood glucose - hypoglycaemia (psychological trigger)
  • Glucagon release: pancreatic alpha cells
  • Endogenous glucose production: liver, muscle, adipocytes
  • Raises blood glucose
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7
Q

Where Is the principle site for gluconeogenesis and glycogenolysis?

A

The liver.

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8
Q

Biogenesis of insulin:

A
  • Protein Hormone
  • Derived from proinsulin (gene that insulin is produced from)
  • 23 amino acids are removed (C-peptide)
  • C peptide is used in therapy as It has a longer half life
  • Synthesised in β-cells (islets of Langerhans)
  • Located in β-cell secretory granules
  • Granules crystallised around zinc (zinc provides the network that allows the crystals of insulin to form)
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9
Q

How does forming insulin with zinc improve formulation?

A

Longer lasting shelf life

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10
Q

Where are the islets of langerhans located?

A

Located in the pancreas.

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11
Q

What are the 5 different cells in the islet?

A
  • B cells
  • Alpha cells
  • S cells
  • E cells
  • PP cells
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12
Q

Where are the islets of langerhans distributed?

A
  • Islets of Langerhans highly vascularised
  • Distributed throughout the pancreas each one with their own blood supply
  • Evolutionally conserved structure throughout the species
  • As a result of the rich blood supply, the islets are constantly informed about the circulating concentrations of glucose
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13
Q

What is the purpose of B cells?

A

Release insulin

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14
Q

What is the purpose of Alpha cells?

A

Release glucagon

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15
Q

What do δ-cells do?

A

Release somatostatin

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16
Q

What do ε-cells do?

A

Release ghrelin

17
Q

What do PP cells do?

A

release pancreatic polypeptide

18
Q

Control of Insulin Release by Glucose: (insulin secretagogue)

A

Food intake –> Digestion –> Glucose –> Glucose uptake by islet B cells –> K channels close, depolarisation –> Ca2+ influx –> insulin release

19
Q

Control of Insulin Release by Glucose: (insulin action) (GLP 1)

A

Food intake -> Digestion –> Release of gut hormones inc GLP-1 (only occurs if glucose is being digested) –> Rise in serum GLP-1 –> Activation on the GLP 1 receptor on islet B cells –> cell signalling –> insulin release

20
Q

How Does Insulin Lower Blood Sugar?

A
  • Insulin binds to insulin receptor
  • Receptor is very different to most receptors as it has endogenous kinase activity
  • Receptor switches on and becomes active
  • The intrinsic kinase activity sets off a cascade of other cell signalling mechanism
  • Most important pathway – switches on transporters in the cell membrane and causes the appearance of new transporters (glut 4) in the membrane.
  • When it becomes activated, glucose enters the cell by facilitated diffusion down its conc gradient and lowers blood sugar levels .
21
Q

What Does Insulin Do?

A 
Promotes Hypoglycaemia 
• Increases the transport of glucose into cells
• Converts glucose to glycogen
• Decreases glycogen breakdown
• Increase fat stores
• Increase protein production
22
Q

The Endocrine Actions of Insulin Are Anabolic. True or false?

A

True

23
Q

What is diabetes Mellitus:

A

“Diabetes is a chronic disease, which occurs when the pancreas does not produce enough insulin, or when the body cannot effectively use the insulin it produces. This leads to an increased concentration of glucose in the blood (hyperglycaemia)”.

Cannot be cured but it can be managed…

24
Q

What is type 1 diabetes?

A

Type 1 diabetes is a disease of the beta cells, beta cells are destroyed so insulin can’t be produced.

25
Q

What is type 2 diabetes?

A

Islets also become problematic with type 2 diabetes as the beta cells fail overtime and unfortunately the alpha cells become more active = hyperglycaemia

26
Q

How does obesity cause type 2 diabetes?

A

insulin doesn’t act the way its supposed to and tissues become insensitive to it.

27
Q

Non medical causes of hypoglycaemia?

A

inadequate, irregular food intake; insulin overdose; sulphonylurea overdose

28
Q

Medical causes of hypoglycaemia?

A

insulinoma; hyperinsulinism; T1DM (nocturnal); post gastric-bypass hypoglycaemia; transient neonatal hypoglycaemia

29
Q

Symptoms of hypoglycaemia?

A
  • Autonomic Symptoms: hunger, sweating, shaking, increased heart rate, headache, nausea
  • Neuroglycopaenic Symptoms: confusion, drowsiness, odd behaviour, incoherent speech, poor co-ordination
  • Hypoglycaemic Coma
  • Death
30
Q

Hyperglycaemia-Inducing Therapies 1:

Glucagon Therapy

A
  • First-aid treatment for severe hypoglycaemia when oral glucose is not possible or desired
  • Route: injection (i.m.; i.v.; s.c.)
  • Must be reconstituted prior to use
  • Acutely raises plasma glucose levels
  • Side effects: headache and nausea
31
Q 
Hyperglycaemia-Inducing Therapies 2:
Diazoxide Therapy (Eudemine®, Proglycem) – insulinomas how do they work?
A
  • Oral administration
  • Reverses the action of glucose on the β-cell
  • Doesn’t cause a depolarisation causes a hyperpolarisation, stops calcium coming in and stops insulin being released.

Side effects:
• anorexia, nausea, vomiting, hypotension, oedema, tachycardia, arrhythmias, hypertrichosis on prolonged treatment

The Patient Y3 semester 1 (17 decks)

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