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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

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2
Q

What is type 2 diabetes?

A

State of insulin deficiency

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3
Q

What causes type 2 diabetes?

A

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

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4
Q

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

A

Optimise blood glucose and decreased possible complications

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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

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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

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7
Q

What are some insulin dependent drugs?

A

Sulphonylureas, incretin mimetics, glinides, DPP4-inhibitors

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8
Q

What are some insulin independent drugs?

A

Alpha glucosidase inhibitors, SGLT2 inhibitors

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9
Q

What is cellular energy status linked to?

A

Insulin secretion in pancreatic beta cells

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10
Q

What does elevation in blood glucose cause?

A

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

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11
Q

What phosphorylates glucose once it enters the cell?

A

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

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12
Q

What causes membrane depolarisation?

A

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

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13
Q

What does depolarisation of the cell membrane cause?

A

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

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14
Q

What are sulphonylureas?

A

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

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15
Q

What are some examples of sulphonylureas?

A

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

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16
Q

How do sulphonylureas work?

A

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

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17
Q

What are some long and short acting sulphonylureas?

A

Long acting = glibenclamide, glipizide

Short acting = tolbutamide, gliclazide

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18
Q

What is a benefit of sulphonylureas?

A

Reduce microvascular complications

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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

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20
Q

When are sulphonylureas used as a first line treatment?

A

In patients intolerant to metformin, or with weight loss

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21
Q

How are sulphonylurease used as a second line treatment?

A

In conjunction with metformin

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22
Q

What is the third line use of sulphonylureas?

A

In conjunction with metformin and thiazolidinediones (or other drugs)

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23
Q

Why do sulphonylureas cause weight gain?

A

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

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24
Q

In what patients should long acting sulphonylureas be avoided?

A

In patients with renal impairment, the elderly and in pregnancy

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25
How do glinides (meglinitinides) work?
Action similar to SUs but augmented by glycaemia = bind to SUR1 at distinct benzamido site close to KATP channel and trigger insulin release
26
What are some examples of glinides?
Lack sulphonylurea group = repaglinide, nateglinide
27
How are glinides administered?
Active orally = rapid onset (30-60mins)/offset (4hrs) kinetics and promote insulin secretion in response to meals
28
What are the benefits of glinides?
Reduce postprandial blood glucose and are less likely to cause hypoglycaemia than long acting SUs
29
What drugs can glinides be used in conjunction with?
Metformin and thiazolidinediones
30
Why is repaglinide safer than SUs in chronic kidney disease?
Subject mainly to hepatic metabolism
31
In what situations should glinides be avoided?
In severe hepatic impairment, pregnancy and breastfeeding
32
What is the incretin effect?
The insulin response to oral glucose is greater than the response to IV glucose
33
What does the ingestion of food stimulate?
The release of GLP-1 from L cells in the ileum and GIP from K cells in the duodenum
34
What are some effects for GLP-1 and GIP?
Both enhance insulin release from pancreatic beta cells and delay gastric emptying GLP-1 decreases glucagon release from pancreatic alpha cells
35
How do GLP=1 and GIP decrease blood glucose?
Enhance glucose uptake and utilisation, and decrease glucose production
36
What effect does type 2 diabetes have on the incretin effect?
It reduces it
37
What are some response triggered to restore in incretin effect?
Reduced breakdown of endogenous incretins | Administers exogenous analogues resistant to breakdown
38
What enzyme rapidly stops the actions of GLP-1 and GIP?
DPP-4
39
What is the action of gliptins (DPP-4 inhibitors)?
Competitively inhibit DPP-4 = prolongs the actions of GLP-1 and GIP and increases plasma insulin
40
How are gliptins used?
Only effective if insulin secretion is preserved Usually in combination with SUs or metformin Can be used as monotherapy
41
What are some examples of gliptins?
Sitagliptin, saxagliptin, vildagliptin, linagliptin, alogliptin
42
What are some features of sitagliptin?
Orally active, taken once daily, generally well tolerated, nausea is main adverse effect, no hypoglycaemia when used as monotherapy, weight neutral
43
What are incretin analogues?
Peptides that mimic the action of GLP-1 but resist breakdown by DPP-4
44
What are some examples on incretin analogues?
Extenatide, liraglutide
45
What are incretin analogues agonists of?
G-protein coupled GLP-1 receptors = increase intracellular cAMP in pancreatic beta cells
46
What are some effects of incretin analogues?
Stimulates insulin expression and release Suppresses glucagon secretion, slows gastric emptying and decreases appetite Cause modest weight loss and reduce hepatic fat accumulation
47
How are incretin analogues administered?
Subcutaneously = extenatide twice daily, extenatide MR weekly, liraglutide once daily
48
What are some adverse effects of incretin analogues?
May cause nausea and rarely pancreatitis (don't cause hypoglycaemia)
49
What is alpha glucosidase?
A brush border enzyme that breaks down starch and disaccharides to absorb glucose
50
Why are alpha glucosidase inhibitors taken with meals?
To delay absorption of glucose and reduce postprandial increase in blood glucose
51
What patients are given alpha glucosidase inhibitors?
Type 2 diabetics inadequately controlled by lifestyle measures or other drugs
52
What are some side effects of alpha glucosidase inhibitors?
Flatulence, loose stools, diarrhoea, abdominal pain, bloating
53
How effective are alpha glucosidase inhibitors?
Pose no risk of hypoglycaemia but improvement in glycaemic control is modest = infrequently used in UK
54
What are some examples of alpha glucosidase inhibitors?
Acarbose, miglitol, voglibose
55
What is the only drug that belongs to the biguamide drug family?
Metformin = first line agent for type 2 diabetes irrespective of obesity
56
What is required for metformin to work?
Normal hepatic/renal function
57
How does metformin work?
Reduces hepatic gluconeogenesis by stimulating AMPK
58
How does metformin affect processes in the body?
Increases glucose uptake and utilisation by skeletal muscles, reduces carbohydrate absorption and increases fatty acid oxidation
59
What are the desirable effects of metformin?
Reduces microvascular complications Prevents hyperglycaemia but doesn't cause hypoglycaemia Causes weight loss
60
How is metformin administered?
Suitable for oral administration and may be combined with other agents
61
What are the side effects of metformin?
GI = diarrhoea, nausea, anorexia | Lactic acidosis = avoid use in patients with severe hepatic/renal disease, linked to excessive alcohol intake
62
How do thiazolidinediones work?
Enhance insulin action at target tissues but don't directly affect insulin secretion (ie reduce insulin resistance)
63
What are thiazolidinediones?
Exogenous agonists of PPAR gamma, which associate with RXR
64
Where is PPAR gamma mostly confined to?
Adipocytes
65
What does the activated PPAR gamma-RXR complex act as?
Transcription factor that promotes the expression of genes encoding several proteins involved in insulin signalling and lipid metabolism
66
What are the desirable effects of thiazolidinediones?
Promote fatty acid uptake and storage in adipocytes Reduce hepatic glucose output and enhance peripheral glucose uptake Don't cause hypoglycaemia
67
What are some examples of thiazolidinediones?
TZDs | Glitazones = ciglitazone, triglitazone, pioglitazone
68
What are some adverse effects of thiazolidinediones?
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
What are some features of pioglitazone?
Used in combination with metformin or SUs, only drug of glitazone class used as it doesn't cause liver dysfunction
70
Do SGLT2 inhibitors depend on insulin?
No
71
How do SGLT2 inhibitors work?
Selectively block reabsorption of glucose by SGLT2 in the proximal tubule of the kidney nephron = deliberately causes glucosuria
72
What are the benefits of SGLT2 inhibitors?
Decrease blood glucose with little risk of hypoglycaemia | Calorific loss and water accompanying glucose contributes to weight loss
73
What are examples of SGLT2 inhibitors?
Dapagliflozin, canagliflozin, empagliflozin

Endocrine (42 decks)

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