Brainscape's Knowledge GenomeTM

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


See full index

Endocrine > Anti-Diabetic Medications in Type 2 Diabetes > Flashcards

Anti-Diabetic Medications in Type 2 Diabetes Flashcards

1
Q

What are the actions of insulin?

A

Induces glucose uptake and utilisation by cells
Promotes removal of glucose from blood
Promotes formation of glycogen and conversion of glucose into fat and adipose tissue
Stimulates amino acid uptake by cell and protein formation

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

What is type 2 diabetes?

A

State of insulin deficiency

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

What causes type 2 diabetes?

A

Resistance to insulin’s action at target tissues
Abnormal insulin secretion
Inappropriate liver gluconeogenesis
Obesity

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

What is the aim of non-pharmacological treatments for type 2 diabetes?

A

Optimise blood glucose and decreased possible complications

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

What is the first line treatment for type 2 diabetes?

A

Positive lifestyle changes = stop smoking, modify diet, maintain ideal body weight, exercise

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

What are the basics of drug treatment?

A

Insulin dependent = increasing insulin secretion

Insulin independent = slowing glucose absorption from kidneys and enhancing glucose excretion by kidneys

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

What are some insulin dependent drugs?

A

Sulphonylureas, incretin mimetics, glinides, DPP4-inhibitors

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

What are some insulin independent drugs?

A

Alpha glucosidase inhibitors, SGLT2 inhibitors

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

What is cellular energy status linked to?

A

Insulin secretion in pancreatic beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does elevation in blood glucose cause?

A

Increased diffusion of glucose into beta cells by GLUT 2 facilitated transport

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

What phosphorylates glucose once it enters the cell?

A

Glucokinase = glucose-6-phosphate then undergoes glycolysis in mitochondria, yielding ATP

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

What causes membrane depolarisation?

A

The closure of KATP channels due to the increased ATP/ADP ration within the cell

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

What does depolarisation of the cell membrane cause?

A

Opens voltage activated Ca2+ channels = increases intracellular Ca2+ which triggers insulin secretion

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

What are sulphonylureas?

A

Insulin secretagogues = require a functional mass of beta cells to be effective, efficacy may wane with time

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

What are some examples of sulphonylureas?

A

All contain sulphonylurea group = tolbutamide, glibenclamide, gliclazide, glipizide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do sulphonylureas work?

A

Displace the binding of ADG-Mg2+ from the SUR1 subunit = closes KATP channel and stimulates insulin release

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

What are some long and short acting sulphonylureas?

A

Long acting = glibenclamide, glipizide

Short acting = tolbutamide, gliclazide

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

What is a benefit of sulphonylureas?

A

Reduce microvascular complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do sulphonylureas cause hypoglycaemia?

A

By excess insulin secretion = associated with long acting agents, elderly patients, patients with reduced hepatic/renal disease and chronic kidney disease

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

When are sulphonylureas used as a first line treatment?

A

In patients intolerant to metformin, or with weight loss

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

How are sulphonylurease used as a second line treatment?

A

In conjunction with metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the third line use of sulphonylureas?

A

In conjunction with metformin and thiazolidinediones (or other drugs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why do sulphonylureas cause weight gain?

A

Anabolic effect of insulin is increased, appetite increased, urinary loss of glucose decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In what patients should long acting sulphonylureas be avoided?

A

In patients with renal impairment, the elderly and in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do glinides (meglinitinides) work?

A

Action similar to SUs but augmented by glycaemia = bind to SUR1 at distinct benzamido site close to KATP channel and trigger insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are some examples of glinides?

A

Lack sulphonylurea group = repaglinide, nateglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How are glinides administered?

A

Active orally = rapid onset (30-60mins)/offset (4hrs) kinetics and promote insulin secretion in response to meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the benefits of glinides?

A

Reduce postprandial blood glucose and are less likely to cause hypoglycaemia than long acting SUs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What drugs can glinides be used in conjunction with?

A

Metformin and thiazolidinediones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why is repaglinide safer than SUs in chronic kidney disease?

A

Subject mainly to hepatic metabolism

31
Q

In what situations should glinides be avoided?

A

In severe hepatic impairment, pregnancy and breastfeeding

32
Q

What is the incretin effect?

A

The insulin response to oral glucose is greater than the response to IV glucose

33
Q

What does the ingestion of food stimulate?

A

The release of GLP-1 from L cells in the ileum and GIP from K cells in the duodenum

34
Q

What are some effects for GLP-1 and GIP?

A

Both enhance insulin release from pancreatic beta cells and delay gastric emptying
GLP-1 decreases glucagon release from pancreatic alpha cells

35
Q

How do GLP=1 and GIP decrease blood glucose?

A

Enhance glucose uptake and utilisation, and decrease glucose production

36
Q

What effect does type 2 diabetes have on the incretin effect?

A

It reduces it

37
Q

What are some response triggered to restore in incretin effect?

A

Reduced breakdown of endogenous incretins

Administers exogenous analogues resistant to breakdown

38
Q

What enzyme rapidly stops the actions of GLP-1 and GIP?

A

DPP-4

39
Q

What is the action of gliptins (DPP-4 inhibitors)?

A

Competitively inhibit DPP-4 = prolongs the actions of GLP-1 and GIP and increases plasma insulin

40
Q

How are gliptins used?

A

Only effective if insulin secretion is preserved
Usually in combination with SUs or metformin
Can be used as monotherapy

41
Q

What are some examples of gliptins?

A

Sitagliptin, saxagliptin, vildagliptin, linagliptin, alogliptin

42
Q

What are some features of sitagliptin?

A

Orally active, taken once daily, generally well tolerated, nausea is main adverse effect, no hypoglycaemia when used as monotherapy, weight neutral

43
Q

What are incretin analogues?

A

Peptides that mimic the action of GLP-1 but resist breakdown by DPP-4

44
Q

What are some examples on incretin analogues?

A

Extenatide, liraglutide

45
Q

What are incretin analogues agonists of?

A

G-protein coupled GLP-1 receptors = increase intracellular cAMP in pancreatic beta cells

46
Q

What are some effects of incretin analogues?

A

Stimulates insulin expression and release
Suppresses glucagon secretion, slows gastric emptying and decreases appetite
Cause modest weight loss and reduce hepatic fat accumulation

47
Q

How are incretin analogues administered?

A

Subcutaneously = extenatide twice daily, extenatide MR weekly, liraglutide once daily

48
Q

What are some adverse effects of incretin analogues?

A

May cause nausea and rarely pancreatitis (don’t cause hypoglycaemia)

49
Q

What is alpha glucosidase?

A

A brush border enzyme that breaks down starch and disaccharides to absorb glucose

50
Q

Why are alpha glucosidase inhibitors taken with meals?

A

To delay absorption of glucose and reduce postprandial increase in blood glucose

51
Q

What patients are given alpha glucosidase inhibitors?

A

Type 2 diabetics inadequately controlled by lifestyle measures or other drugs

52
Q

What are some side effects of alpha glucosidase inhibitors?

A

Flatulence, loose stools, diarrhoea, abdominal pain, bloating

53
Q

How effective are alpha glucosidase inhibitors?

A

Pose no risk of hypoglycaemia but improvement in glycaemic control is modest = infrequently used in UK

54
Q

What are some examples of alpha glucosidase inhibitors?

A

Acarbose, miglitol, voglibose

55
Q

What is the only drug that belongs to the biguamide drug family?

A

Metformin = first line agent for type 2 diabetes irrespective of obesity

56
Q

What is required for metformin to work?

A

Normal hepatic/renal function

57
Q

How does metformin work?

A

Reduces hepatic gluconeogenesis by stimulating AMPK

58
Q

How does metformin affect processes in the body?

A

Increases glucose uptake and utilisation by skeletal muscles, reduces carbohydrate absorption and increases fatty acid oxidation

59
Q

What are the desirable effects of metformin?

A

Reduces microvascular complications
Prevents hyperglycaemia but doesn’t cause hypoglycaemia
Causes weight loss

60
Q

How is metformin administered?

A

Suitable for oral administration and may be combined with other agents

61
Q

What are the side effects of metformin?

A

GI = diarrhoea, nausea, anorexia

Lactic acidosis = avoid use in patients with severe hepatic/renal disease, linked to excessive alcohol intake

62
Q

How do thiazolidinediones work?

A

Enhance insulin action at target tissues but don’t directly affect insulin secretion (ie reduce insulin resistance)

63
Q

What are thiazolidinediones?

A

Exogenous agonists of PPAR gamma, which associate with RXR

64
Q

Where is PPAR gamma mostly confined to?

A

Adipocytes

65
Q

What does the activated PPAR gamma-RXR complex act as?

A

Transcription factor that promotes the expression of genes encoding several proteins involved in insulin signalling and lipid metabolism

66
Q

What are the desirable effects of thiazolidinediones?

A

Promote fatty acid uptake and storage in adipocytes
Reduce hepatic glucose output and enhance peripheral glucose uptake
Don’t cause hypoglycaemia

67
Q

What are some examples of thiazolidinediones?

A

TZDs

Glitazones = ciglitazone, triglitazone, pioglitazone

68
Q

What are some adverse effects of thiazolidinediones?

A

Weight gain = linked to differentiation of pre-adipocytes
Fluid retention = TZDs promote Na+ reabsorption by kidneys
Ciglitazone/triglitazone cause hepatotoxicity
Increased incidence of bone fractures

69
Q

What are some features of pioglitazone?

A

Used in combination with metformin or SUs, only drug of glitazone class used as it doesn’t cause liver dysfunction

70
Q

Do SGLT2 inhibitors depend on insulin?

A

No

71
Q

How do SGLT2 inhibitors work?

A

Selectively block reabsorption of glucose by SGLT2 in the proximal tubule of the kidney nephron = deliberately causes glucosuria

72
Q

What are the benefits of SGLT2 inhibitors?

A

Decrease blood glucose with little risk of hypoglycaemia

Calorific loss and water accompanying glucose contributes to weight loss

73
Q

What are examples of SGLT2 inhibitors?

A

Dapagliflozin, canagliflozin, empagliflozin

Endocrine (42 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions