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Y2 - Endocrine > Diabetes Medication > Flashcards

Diabetes Medication Flashcards

1
Q

What is the mechanism of metformin?

A

Inhibits the mitochondrial respiratory chain to cause a decrease in ATP which decreases hepatic glucose production to lower glucose levels
Increases gut glucose utilisation and metabolism

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2
Q

Where does metformin act?

A

Hydrophilic so requires active transport by organic cation transporters to be taken into the intestines, liver and kidney

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3
Q

Is metformin insulin dependent or independent?

A

Insulin independent

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4
Q

What are the clinical benefits of metformin?

A

Lowers glucose levels
Weight neutral or negative
Cheap

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5
Q

What is the usual dose of metformin?

A

500mg bd

Max dose 1g bd

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6
Q

What are the side effects of metformin?

A 
GI intolerance (diarrhoea, bloating, abode pain, dyspepsia, metallic taste in mouth)
Metformin associated lactic acidosis
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7
Q

What should be done if a patient on metformin has GI side effects?

A

Reduce to 500mg od and increase slowly

Or use a modified release formulation

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8
Q

What should be done if a patient on metformin develops metformin associated lactic acidosis?

A

Max dose 1g daily if eGFR <45

Metformin contraindicated if eGFR <30

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9
Q

Does metformin have an effect on CVD?

A

Large sustained benefit on CV mortality

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10
Q

When is metformin prescribed?

A

First line for all diabetic patients

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11
Q

What are examples of sulphonylureas?

A

Gliclazide (most common)

Glipizide

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12
Q

What is the mechanism of action of sulphonylureas?

A

Bind to KATP channels of pancreatic beta cells, causing channels to close
This causes depolarisation, calcium channels open and insulin secretion increases

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13
Q

Is the mechanism of sulphonylureas glucose independent or dependent?

A

Independent - can cause insulin secretion even when glucose is not increased

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14
Q

What type of drug are sulphonylureas?

A

Insulin secretagogues

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15
Q

What are the clinical benefits of sulphonylureas?

A

Potent glucose lowering

Cheap

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16
Q

What are the side effects of sulphonylureas?

A

Increased risk of hypoglycaemia

Weight gain

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17
Q

Do sulphonylureas have an effect on CVD?

A

May increase risk but unsure, doesn’t decrease risk

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18
Q

Which patients are most at risk of hypoglycaemia on sulphonylureas?

A

Elderly
Patients who have had diabetes for a long time
High creatine
Lower HbA1c (esp <50mmol/mol)

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19
Q

For which occupations would hypoglycaemia be a risk?

A

Driving

Working up ladders

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20
Q

When are sulphonylureas prescribed?

A

2nd line after metformin, especially if cost is a major consideration

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21
Q

What is the mechanism of thiazolidinediones (TZDs)

A

Act mainly on adipocytes to increase differentiation from pre-adipocytes to mature adipocytes, increasing subcutaneous fat mass by taking fat from liver and muscle to reduce lipo-toxicity
This increases insulin sensitivity

22
Q

What are examples of TZDs?

A

Pioglitazones

23
Q

What are the clinical benefits of TZDs?

A

Reduce glucose levels
Especially potent in obese women
Reduce blood pressure
Very cheap

24
Q

What are the side effects of TZDs?

A

Weight gain
Fluid retention (peripheral oedema)
Increase in risk of cardiac failure (but risk is v low in young people so doesn’t make much difference)
Fracture risk

25
Q

Do TZDs have an effect on CVD?

A

Probably reduces CV risk

26
Q

When are TZDs prescribed?

A

2nd line where cost is a major consideration or if there is a need to minimise hypoglycaemia
Not used in over 65s or patients with heart problems
Best for younger, obese, insulin resistance patients

27
Q

Which drugs use the incretin effect?

A

DPP4 inhibitors

GLP-1 receptor agonists

28
Q

What is the incretin effect?

A

Insulin secretion is higher after oral glucose than after IV glucose
This is because substances called incretins are released when glucose is absorbed in the gut
Incretins increase insulin secretion

29
Q

What are examples of incretins?

A

GIP

GLP-1

30
Q

What are incretins broken down by?

A

DPP4

31
Q

How do incretins increase insulin secretion?

A

After the triggering pathway has started insulin secretion incretins act via G-protein coupled GLP-1/GIP receptors to increase cAMP
This closes the KATP channel, increases calcium influx and increases insulin secretion

32
Q

What is the benefit of incretin-like drugs compared to sulphonylureas?

A

Sulphonylureas can increase insulin even when there is no glucose leading to hypoglycaemia
Incretin-like drugs can only act after glucose has initiated insulin secretion so do not cause hypoglycaemia

33
Q

What is the mechanism of DPP4 inhibitors?

A

Inhibit breakdown of GLP-1 and GIP by inhibiting DPP4

This augments the incretin effect and increases insulin secretion without causing hypoglycaemia

34
Q

What are examples of DPP4 inhibitors?

A

Sitagliptin
Alogliptin
Saxagliptin

35
Q

What are the clinical benefits of DPP4 inhibitors?

A 
Glucose lowering (but weak)
Weight neutral
36
Q

What are the side effects of DPP4 inhibitors?

A

Minimal, generally well tolerated

Possible increased risk of pancreatitis

37
Q

Do DPP4 inhibitors have an effect on CVD?

A

Unsure - mixed results

38
Q

What is the mechanism of GLP-1 receptor agonists?

A

These are GLP-1 molecules modified to avoid breakdown by DPP4
Act in the same way as GLP-1 to increase insulin secretion
Lower glucagon

39
Q

What are the clinical benefits of GLP-1 receptor agonists?

A

Potent glucose reduction
Weight loss
Blood pressure reduction

40
Q

What are the side effects of GLP-1 receptor agonists?

A

Nausea and vomiting (often improves after about 6 weeks)

Small increase in gallstones

41
Q

Do GLP-1 receptor agonists have an effect on CVD?

A

Reduce risk

42
Q

Do GLP-1 receptor agonists have an effect on renal disease?

A

Reduction in new onset macroalbuminmemia but no impact in eGFR decline

43
Q

When are GLP-1 agonists prescribed?

A

Given with metformin for patients at high risk of CVD or kidney disease or for patients who want to lose weight

44
Q

When are DPP4 inhibitors prescribed?

A

2nd line for people with no risk factors

45
Q

What is the mechanism of SGLT2 inhibitors?

A

In most people glucose is filtered into kidney tubules and glucose transporters (SGLT) absorb all the glucose
SGLT2 inhibitors decrease uptake of sugar and increase renal glucose loss - so basically make you pee sugar

46
Q

What indirect effects do SGLT2 inhibitors have?

A

Glucose reduction
Renal protection
Reduction in insulin and increase in glucagon
Increase in lipolysis, increase in free fatty acids, increase in ketone body production
Cardiac benefit but can increase ketosis and risk of ketoacidosis

47
Q

What are the clinical benefits of SGLT2 inhibitors?

A

Moderate efficacy

Blood pressure reduction

48
Q

What are examples of SGLT2 inhibitors?

A

Dapagliflozin
Canagliflozin
Empagliflozin

49
Q

What are the side effects of SGLT2 inhibitors?

A

Thrush - secondary to glycosuria
Fournier gangrene
Hypovolaemia and hypotension
Diabetic ketoacidosis

50
Q

Do SGLT2 inhibitors have an effect on CVD?

A

Large CV benefit

51
Q

Do SGLT2 inhibitors have an effect on renal outcomes?

A

Beneficial effect

52
Q

When are SGLT2 inhibitors prescribed?

A

2nd line for patients at high risk for CV or renal disesae

Y2 - Endocrine (9 decks)

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