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Endocrine- Diabetes > Type 2 Diabetes Treatments > Flashcards

Type 2 Diabetes Treatments Flashcards

1
Q

What is the main aim of treatment in type 2 diabetes?

A

Reduce the risk of microvascular complications

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2
Q

The KATP channel involved in insulin secretion is an octomeric complex composed of what?

A

4 potassium inward rectifier (Kir) 6.2 subunits // 4 sulphonylurea receptor (SUR) 1 subunits

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3
Q

In the KATP channel involved in insulin secretion, what forms the potassium selective ion channel?

A

Tetramer of Kir 6.2 subunits

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4
Q

In the KATP channel involved in insulin secretion, what regulates potassium channel activity?

A

SUR1 subunits

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5
Q

Where does ATP bind to the KATP channel involved in insulin secretion?

A

Each of the Kir 6.2 subunits

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6
Q

What happens in the KATP channel involved in insulin secretion, to maintain the resting potential of the beta cell and inhibit insulin secretion until ATP is bound?

A

ADP-Mg++ binds to the SUR1 subunits to keep the channel open

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7
Q

Which type 2 diabetes drugs have their action at the KATP channel which regulates insulin secretion?

A

Sulphonylureas

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8
Q

What type of drug is a biguanide?

A

Metformin

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9
Q

What is the 1st line agent for type 2 diabetes?

A

Metformin

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10
Q

In what dosages is metformin available?

A

500mg, 850mg, 1g

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11
Q

Metformin should usually be started on what dose?

A

500mg once or twice daily

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12
Q

There is little evidence for taking more than how much metformin daily?

A

1g

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13
Q

Where does metformin act? What is its role there?

A

Liver // Lower glucose production

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14
Q

How does metformin lower glucose production at the liver?

A

Decrease hepatic gluconeogenesis // Increase peripheral glucose uptake

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15
Q

What are some other functions that metformin is said to have?

A

Reduced absorption of glucose from the gut // Enhanced anaerobic glycolysis

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16
Q

How effective is metformin at hyperglycaemia management?

A

Reduces HbA1c by 15-20mmol/l by lowering insulin resistance

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17
Q

How likely is metformin to cause hypoglycaemia?

A

Very unlikely (when used as monotherapy)

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18
Q

What effect does metformin have on weight?

A

Weight loss (suppresses appetite)

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19
Q

Does metformin prevent microvascular complications?

A

Yes

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20
Q

What is the only drug to prevent macrovascular complications of type 2 diabetes?

A

Metformin

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21
Q

Is metformin safe in pregnancy?

A

Yes

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22
Q

What are some minor effects of metformin which may contribute to its ability to decrease risk of macrovascular complications?

A

Reduces triglycerides and LDL, minor reduction in BP

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23
Q

What other conditions can metformin be used in?

A

PCOS and NAFLD

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24
Q

Where are the main metformin side effects? Give examples.

A

GI tract: anorexia, nausea, vomiting, diarrhoea, abdominal pain, taste disturbance

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25
Q

How common are GI side effects from metformin? How often can people not tolerate them?

A

25% will have side effects, 5% will be intolerable

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26
Q

Metformin can interfere with the absorption of which vitamins?

A

B12 and folic acid

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27
Q

What are some very rare side effects of metformin?

A

Lactic acidosis, liver failure, rash

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28
Q

When may lactic acidosis occur in a patient on metformin?

A

Co-existing renal failure or acute illness

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29
Q

How can adverse effects of metformin be reduced?

A

Slow release formulations and start low go slow methods

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30
Q

Does metformin cause renal toxicity?

A

Not directly, only if there is underlying renal disease

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31
Q

With regards to renal toxicity, when should metformin be stopped?

A

If eGFR < 30ml/min // Serum creatinine > 150macromol/l

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32
Q

If a patient is on metformin and their eGFR is between 30-45ml/min, what should be done?

A

Halved dose

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33
Q

When should metformin be temporarily withheld?

A

If a patient is getting IV contrast

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34
Q

If a patient is on metformin and is acutely unwell or having elective surgery, what should they be put on instead?

A

Insulin

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35
Q

With regards to liver toxicity, when should metformin be stopped?

A

If there is advanced cirrhosis/liver failure // Risk of lactic acidosis e.g. encephalopathy or alcohol excess

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36
Q

When are sulphonylureas used as treatment for type 1 diabetes?

A

1st line in underweight type 2 diabetics, or those intolerant to metformin // 2nd line as an add on to metformin

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37
Q

Chlopropramide and tolbutamide are examples of what?

A

1st generation sulphonylureas (rarely used now)

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38
Q

2nd generation sulphonylureas are used in practice now. Give 2 examples? Why are these better than 1st generation?

A

Gliclazide, glibenclamide // Shorter acting

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39
Q

What is the time taken until peak release of insulin, following a sulphonylurea?

A

1-2 hours

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40
Q

What is the dosage of gliclazide?

A

40mg od - 160mg bd

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41
Q

What is the dosage of glibenclamide?

A

5mg - 15mg od

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42
Q

What must still be functioning in order for sulphonylureas to work?

A

Beta cells

43
Q

How do sulphonylureas work?

A

Displace the binding of ADP-Mg++ from the SUR1 subunit thus closing the beta cell KATP channel to depolarise the cell and increase insulin secretion

44
Q

Is there a risk of hypoglycaemia with sulphonylureas?

A

Yes

45
Q

How effective are sulphonylureas at hyperglycaemia management?

A

15-20mmol/mol decrease in HbA1c by increasing insulin secretion and rapid reduction in hyperglycaemia

46
Q

Which type(s) of complications do sulphonylureas prevent?

A

Microvascular only

47
Q

Who should sulphonylureas be given with care in, because of the risk of hypoglycaemia?

A

Elderly/frail, alcohol excess, liver disease

48
Q

What effect do sulphonylureas have on weight?

A

Weight gain

49
Q

Apart from hypoglycaemia, what are some side effects of sulphonylureas?

A

GI upset, headache (rarely hypersensitivity and liver dysfunction)

50
Q

When should sulphonylureas be avoided?

A

Hepatic or renal failure, pregnancy

51
Q

What other drugs will impede the actions of biguanides and sulphonylureas due to their own effects on insulin action?

A

Corticosteroids and thiazides

52
Q

What type of drug are thiazolidinediones?

A

PPAR gamma agonists

53
Q

What is the only available thiazolidinedione agent?

A

Pioglitazone 15-45mg once daily

54
Q

What is PPAR gamma?

A

A nuclear receptor which is found predominantly in adipose tissue, but also in skeletal muscle and liver

55
Q

How are thiazolidinediones taken into a cell? What do they bind with?

A

They are lipophilic and readily enter cells // Bind with PPAR gamma with high affinity

56
Q

Thiazolidinediones acting on PPAR gamma has what effect?

A

Transcription of genes which encode lipoprotein lipase, fatty acid transport proteins, fatty acid CoA synthase and GLUT4

57
Q

What is the role of lipoprotein lipase?

A

Hydrolyses the breakdown of lipids in lipoproteins into fatty acids and glycerol

58
Q

Deficiency of lipoprotein lipase leads to what?

A

Hypertriglyceridaemia

59
Q

What is the overall action of pioglitazone?

A

Enhance the action of insulin at target tissues

60
Q

What effect do thiazolinediones have on hyperglycaemia management?

A

Reduces HbA1c by 15-20mmol/mol by increasing insulin sensitivity

61
Q

What effect do thiazolinediones have on fatty acids?

A

Increase uptake and storage in adipocytes, rather than the skeletal muscle and liver

62
Q

Do thiazolinediones cause hypoglycaemia?

A

Not unless used in combination with sulphonylureas

63
Q

Do thiozolinediones prevent complications?

A

No (improvement in microalbuminaemia though)

64
Q

What cardiac effect do thiazolinediones have?

A

Big risk of worsening heart failure due to fluid retention (in those with PRE-EXISTING heart failure)

65
Q

Are thiazolinediones hepatotoxic?

A

Yes

66
Q

What effect will thiazolinediones have on weight? Why?

A

Increase- increased subcutaneous fat and fluid retention

67
Q

Who are thiazolinediones not recommended in and why?

A

Those over the age of 65 due to increased risk of hip fractures

68
Q

Which two types of diabetes drugs act on the incretin pathway?

A

DPP-IV inhibitors and GLP-1 agonists

69
Q

What happens to the incretin effect in type 2 diabetes?

A

It is reduced

70
Q

Drugs involving the incretin effect will only work if there is what?

A

Some degree of insulin production present

71
Q

GIP is one of the hormones involved in the incretin effect. Where is it secreted from? In response to what?

A

Secreted from endocrine K cells, in response to absorbable carbohydrates and lipids (hence increased after meals)

72
Q

What action does GIP have in response to meals?

A

It binds with its receptor on the beta cells to increase cAMP and produce insulin

73
Q

Where is GLP-1 expressed?

A

Pancreatic alpha cells and L cells of intestinal mucosa

74
Q

The secretion of GLP-1 throughout the day is correlated with what?

A

Secretion of insulin

75
Q

What is the function of GLP-1?

A

Binds to GPCRs on the beta cell to increase cAMP and release insulin. Also decreases glucagon so there is decreased glucose production.

76
Q

Delayed gastric emptying is an action of which drugs? What is the advantage of this?

A

DDP-IV inhibitors and GLP-1 agonists, it means not as much CHO needs broken down at once

77
Q

GLP-1 is metabolised by what?

A

DDP-IV

78
Q

Do drugs acting on the incretin pathway cause hypos? Why/why not?

A

No- when glucose is in a normal range, incretin drugs do not bind

79
Q

Give 2 examples of GLP-1 receptor agonist?

A

Exenatide and liraglutide

80
Q

Which GLP-1 agonist drug has a shorter half life?

A

Exenatide

81
Q

How often and how are GLP-1 agonists taken?

A

Exenatide = twice daily SC injection, liraglutide = once daily SC injection

82
Q

What are the actions of GLP-1 agonists?

A

Increase insulin secretion from pancreas // decrease glucagon secretion // increase insulin sensitivity

83
Q

What effect do GLP-1 agonists have on weight? Why?

A

Weight loss- acts on the hypothalamus to reduce appetite

84
Q

What are the adverse effects of GLP-1 agonists?

A

Nausea (usually resolves), injections, potential pancreatic cancer/pancreatitis

85
Q

What do all DDP-IV inhibitor drug names end in?

A

Gliptin

86
Q

How are DDP-IV inhibitors administered? How often?

A

Once daily oral

87
Q

DDP-IV inhibitors are usually used in combination with which other drugs? Can they be used as mono therapy?

A

Metformin and thiazolinediones // They can but not common

88
Q

What is the action of DDP-IV inhibitors?

A

Increase the action of GLP-1, promote insulin secretion from the pancreas

89
Q

What effect do DDP-IV inhibitors have on weight?

A

Neural

90
Q

Which drug which acts on the incretin pathway has the biggest decrease in HbA1c?

A

GLP-1 agonists

91
Q

Give 2 examples of SGLT2 inhibitors?

A

Canagliflozin, empagliflozin

92
Q

What is the mechanism of action of SGLT2 inhibitors?

A

Selectively block the reabsorption of glucose by the SGLT2 transporter in the proximal tubule to deliberately cause glycosuria

93
Q

Do SGLT2 inhibitors have a risk of hypoglycaemia?

A

No

94
Q

What effect do SGLT2 inhibitors have on weight?

A

Weight loss (because you pee out the sugar i.e. calories)

95
Q

Is the action of SGLT2 inhibitors dependent on insulin?

A

No

96
Q

Apart from reduction in blood glucose, what are some other positive effects of SGLT2 inhibitors?

A

Reduces CV risk and hospitalisation for heart failure, beneficial for most renal outcomes

97
Q

What are some adverse effects of SGLT2 inhibitors?

A

Thrush, and increased risk of UTIs

98
Q

Who do SGLT2 inhibitors not work in?

A

Those with an eGFR < 60

99
Q

Which type 2 diabetics receive insulin?

A

Those who fail on non-insulin therapies

100
Q

What type of insulin is used in type 2 diabetes? What treatment is this added onto?

A

Intermediate acting insulin once daily, with metformin +/- sulphonylurea

101
Q

What type of insulin (i.e. human or analogue) is used in type 2 diabetes?

A

Human

102
Q

Is there an upper limit to the amount of insulin that can be given to a type 2 diabetic?

A

No, keep going until sugars are back to normal

103
Q

What are some side effects of insulin treatment?

A

Hypo/hyperglycaemia, local reaction at injection site, loss of fatty tissue at injection site, insulin resistance

104
Q

What should happen to insulin dose in a patient with renal failure?

A

Decreased (as it will take longer to be excreted)

Endocrine- Diabetes (11 decks)

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