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Pharmacology > Diabetes > Flashcards

Diabetes Flashcards

(50 cards)

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1
Q

Describe the different cells making up the Islet of Langerhans and their function

A

A cells = glucagon

B cells = insulin

D cells = somatostatin

PP cells = pancreatic polypeptide

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2
Q

What are the main modulators of blood glucose?

A

Insulin

Glucagon

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3
Q

Describe the role of insulin in blood glucose control

A

Decreases blood glucose concentration

Metabolism of carbohydrates, fats and proteins

Synthesises enzymes involved in glucose metabolism

Activation of RAS -> activation of MAP kinases -> DNA transcription -> RNA production -> enzyme synthesis

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4
Q

What activates insulin release?

A

Glucose

Increases ATP concentration inside B cells

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5
Q

Describe the role of glucagon in glucose control

A

Increases concentration of glucose in the blood

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6
Q

What processes do glucagon trigger that increase blood glucose concentration?

A

Glycogenolysis

Gluconeogenesis

Inhibition of glycogen synthesis

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7
Q

What are the two types of diabetes?

A

Type I

Type II

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8
Q

Pathogenesis of type I diabetes

A

B cells are destroyed in an autoimmune process

Insulin replacement therapy is essential

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9
Q

Pathogenesis of type II diabetes

A

Individuals are resistant to insulin

Fails to secrete sufficient hormone

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10
Q

Symptoms of type II diabetes

A

Wasting due to increased protein breakdown

Ketoacidosis due to increased fat metabolism

Osmotic diuresis due to decreased utilisation of glucose

Damage to blood vesels

Neuropathy

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11
Q

Conditions caused by damage to blood vessels due to diabetes mellitus

A

Retinopathy

Nephropathy

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12
Q

How does glycosuria and osmotic diuresis present?

A

Thirst

Polydypsia

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13
Q

What causes death in diabetes?

A

Ketoacidosis

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14
Q

How does ketoacidosis cause death?

A

Lipid metabolism causes the formation of ketones which decreases the pH

Leads to heart failure

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15
Q

What is the half-life of insulin following intravenous injection?

A

10 minutes

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16
Q

Why is the intravenous route of insulin administration inconvenient?

A

Short half-life

Constant injections are required to maintain a relatively high concentration in the body

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17
Q

What are ways to prolong the half-life of insulin?

A

Subcutaneous injection

Insulin hexamer

Protamine

Insulin glargine

Insulin analogues

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18
Q

Why can’t insulin be given by mouth?

A

Due to the proteolytic action of digestive enzymes

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19
Q

How much longer is the half-life of insulin following subcutaneous injection instead of intravenous injection?

A

From 10 minutes to 2-4 hours

Travels into the blood slower

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20
Q

How can an insulin hexamer be produced?

A

Bind insulin to zinc/other ionic metals

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21
Q

Why does insulin hexamer have a longer half-life?

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A

Cannot diffuse as easily into the bloodstream

The molecule has to break down into simpler monomers to allow for appropriate diffusion

The breakdown prolongs the half-life of insulin

22
Q

Who came up with the idea of using protamine to modify insulin’s half-life?

23
Q

What is protamine?

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A

Postively charged nuclear protein

24
Q

How does protamine increase the half-life of insulin?

Study These Flashcards
A

Clusters hexamers together

25
How long is the half-life of insulin using protamine?
8-9 hours
26
What is the name of protamine insulin?
NPH Nuclear protamine Hans
27
What was the importance of NPH?
Meant the patient would survive the night
28
What technology allows for insulin glargine to be formed?
Recombinant technology
29
What are the distinguishing features of insulin glargine?
Long acting form Peak-less
30
How does insulin glargine synthesis not lead to changes in insulin action?
Changing the amino acids in the insulin structure changes its activity But insulin glargine is formed through changing the ends
31
Describe the process of making insulin glargine
One aspargine and two arginine molecules are added to the ends This makes it less soluble
32
How does insulin glargine have a longer half-life?
Less soluble in physiologic pH Through changing the pKa The insulin therefore acts as a crystal in the body and does not dissolve Injected once a day
33
What are insulin analogues?
Changes the structure of insulin
34
Two insulin analogues
Insulin detemir Insulin lispro
35
How is insulin determir formed?
Fatty acid is bound to the lysine amino acid at position B29
36
How does insulin detemir increase the half-life of insulin?
B29 amino acid binds to albumin Insulin slowly dissociates from this complex
37
How is insulin lispro formed?
Lysine and proline residues on the C-terminal end of the B-chain are reversed
38
When is insulin lispro used?
When insulin is required quickly Through blocking the formation of insulin dimers and hexamers Prevents hypoglycemia
39
Insulin forms used for long-term action
Insulin glargine Insulin detemir
40
Insulin form used for quick effect
Insulin lispro
41
What are the two main targets of therapy for diabetes?
Increasing insulin concentration Increasing insulin secretion
42
Drugs increasing insulin secretion
Sulphonylureas Metformin Acarbose
43
On which patients are sulphonylureas effective?
Patients with some functioning B cells
44
How do sulphonylureas work?
Mimics the action of glucose 1. Glucose enters beta cells 2. Converts into ATP 3. ATP blocks K-ATP channels 4. Calcium enters and causes insulin release Blocks K-ATP channels
45
How does metformin work?
Increases glucose uptake into tissues Inhibits gluconeogenesis
46
How does acarbose work?
Inhibits a-glucosidase Delaying the carbohydrate absorption and reducing the rise in blood glucose that follows a meal
47
What is the best treatment for type II diabetes?
Exercise Reversible condition
48
Why does ingestion of glucose cause increased insulin release than intravenous injection of glucose?
Autonomic system activation following smell and chewing activates neuroendocrine cells Secrete peptide GLP1 GLP1 blocks K-ATP channels and increases insulin secretion
49
What are newer hypoglycemic drugs like?
Oral forms
50
Examples of newer oral hypoglycemic drugs
Meglitinides - block KATP Thiozolidines - slow decrease in glucose by binding to transcription factor receptor

Pharmacology (13 decks)

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