Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Diabetes > Flashcards

Diabetes Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the main modulators of blood glucose?

A

Insulin

Glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What activates insulin release?

A

Glucose

Increases ATP concentration inside B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the role of glucagon in glucose control

A

Increases concentration of glucose in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What processes do glucagon trigger that increase blood glucose concentration?

A

Glycogenolysis

Gluconeogenesis

Inhibition of glycogen synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the two types of diabetes?

A

Type I

Type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathogenesis of type I diabetes

A

B cells are destroyed in an autoimmune process

Insulin replacement therapy is essential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathogenesis of type II diabetes

A

Individuals are resistant to insulin

Fails to secrete sufficient hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Conditions caused by damage to blood vessels due to diabetes mellitus

A

Retinopathy

Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does glycosuria and osmotic diuresis present?

A

Thirst

Polydypsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What causes death in diabetes?

A

Ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does ketoacidosis cause death?

A

Lipid metabolism causes the formation of ketones which decreases the pH

Leads to heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

10 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Subcutaneous injection

Insulin hexamer

Protamine

Insulin glargine

Insulin analogues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why can’t insulin be given by mouth?

A

Due to the proteolytic action of digestive enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How can an insulin hexamer be produced?

A

Bind insulin to zinc/other ionic metals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why does insulin hexamer have a longer half-life?

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?

A

Hans

23
Q

What is protamine?

A

Postively charged nuclear protein

24
Q

How does protamine increase the half-life of insulin?

A

Clusters hexamers together

25
Q

How long is the half-life of insulin using protamine?

A

8-9 hours

26
Q

What is the name of protamine insulin?

A

NPH

Nuclear protamine Hans

27
Q

What was the importance of NPH?

A

Meant the patient would survive the night

28
Q

What technology allows for insulin glargine to be formed?

A

Recombinant technology

29
Q

What are the distinguishing features of insulin glargine?

A

Long acting form

Peak-less

30
Q

How does insulin glargine synthesis not lead to changes in insulin action?

A

Changing the amino acids in the insulin structure changes its activity

But insulin glargine is formed through changing the ends

31
Q

Describe the process of making insulin glargine

A

One aspargine and two arginine molecules are added to the ends

This makes it less soluble

32
Q

How does insulin glargine have a longer half-life?

A

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
Q

What are insulin analogues?

A

Changes the structure of insulin

34
Q

Two insulin analogues

A

Insulin detemir

Insulin lispro

35
Q

How is insulin determir formed?

A

Fatty acid is bound to the lysine amino acid at position B29

36
Q

How does insulin detemir increase the half-life of insulin?

A

B29 amino acid binds to albumin

Insulin slowly dissociates from this complex

37
Q

How is insulin lispro formed?

A

Lysine and proline residues on the C-terminal end of the B-chain are reversed

38
Q

When is insulin lispro used?

A

When insulin is required quickly

Through blocking the formation of insulin dimers and hexamers

Prevents hypoglycemia

39
Q

Insulin forms used for long-term action

A

Insulin glargine

Insulin detemir

40
Q

Insulin form used for quick effect

A

Insulin lispro

41
Q

What are the two main targets of therapy for diabetes?

A

Increasing insulin concentration

Increasing insulin secretion

42
Q

Drugs increasing insulin secretion

A

Sulphonylureas

Metformin

Acarbose

43
Q

On which patients are sulphonylureas effective?

A

Patients with some functioning B cells

44
Q

How do sulphonylureas work?

A

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
Q

How does metformin work?

A

Increases glucose uptake into tissues

Inhibits gluconeogenesis

46
Q

How does acarbose work?

A

Inhibits a-glucosidase

Delaying the carbohydrate absorption and reducing the rise in blood glucose that follows a meal

47
Q

What is the best treatment for type II diabetes?

A

Exercise

Reversible condition

48
Q

Why does ingestion of glucose cause increased insulin release than intravenous injection of glucose?

A

Autonomic system activation following smell and chewing activates neuroendocrine cells

Secrete peptide GLP1

GLP1 blocks K-ATP channels and increases insulin secretion

49
Q

What are newer hypoglycemic drugs like?

A

Oral forms

50
Q

Examples of newer oral hypoglycemic drugs

A

Meglitinides - block KATP

Thiozolidines - slow decrease in glucose by binding to transcription factor receptor

Pharmacology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions