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ESA 5 - Pharmacology > Pharmacology of Oral Hypoglycaemic Agents > Flashcards

Pharmacology of Oral Hypoglycaemic Agents Flashcards

1
Q

What is blood glucose rises in diabetes due to?

A
  • An inability to produce insulin due to beta cell failure
  • Insulin resistance preventing insulin from working effectively, despite adequate insulin production
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2
Q

Why is diabetes considered to be a progressive disoder?

A

Beta cell function declines and there is a deteroration of glycaemic control

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3
Q

What effect does diabetes have on the risk of cardiovascular disease?

A

It increases it

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4
Q

What has caused the diabetes epidemic?

A

Environment, not genetics

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5
Q

What is the net change in glucose per day under normal glucose homeostasis?

A

0g/day

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6
Q

What is the average daily glucose input?

A

250g/day

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7
Q

What contributes to the net glucose input?

A
  • Dietary intake
  • Glucose production
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8
Q

How much glucose is taken in in the diet per day?

A

About 180g/day

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9
Q

How much glucose is produced by the body per day?

A

70g

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10
Q

By what processes does the body produce glucose?

A
  • Gluconeogenesis
  • Glycogenolysis
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11
Q

How much glucose does the body take up for its use per day?

A

250g

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12
Q

How much glucose does the brain take up for its use per day?

A

125g

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13
Q

How much glucose does the kidney filter per day?

A

About 180g

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14
Q

What happens to the glucose filtered by the kidney?

A

It reabsorbs and refilters it

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15
Q

How is glucose reabsorbed by the kidney?

A
  • 90% by SGLT2
  • Remaining glucose by SGLT1
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16
Q

How is type 1 diabetes treated?

A
  • Lifestyle
  • Insulin
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17
Q

How is type 2 diabetes treated?

A
  • Lifestyle
  • Non-insulin therapies
  • Insulin
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18
Q

What are the non-insulin therapies used in the treatment of type 2 diabetes?

A
  • Biguanides
  • Sulphonylureas
  • Thiazolidinediones
  • DPP4 inhibitors
  • alpha-Glucosidase inhibitors
  • SGLT2s
  • GLP1
  • Analogues
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19
Q

What do both type 1 and 2 diabetes require in their management?

A
  • Patient education
  • Ability to monitor results of therapy
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20
Q

Why is patient education required in diabetes?

A

Need to know how to self manage with regard to diet, exercise, and healthy living

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21
Q

Why is it important to consider the key challenges for patients with type 2 diabetes?

A

Because they are important in patient adherence and quality of life

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22
Q

What are the key challenges for patients with type 2 diabetes?

A
  • Weight gain, or fear of
  • Hypoglycaemia, or fear of
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23
Q

Why is weight gain a key challenge for patients with type 2 diabetes?

A

Insulin is an anabolic hormone, and so builds up protein and lays down fat

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24
Q

How are newer drugs reducing the problem of weight gain in patients with diabetes?

A

Newer drugs are weight neutral, or promote weight loss

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25
Q

What is the result of patients fearing hypoglycaemia?

A

Patients often run a little higher to prevent hypoglycaemic episodes

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26
Q

Why is hypoglycaemia a potential problem for patients with type 2 diabetes?

A

Excessive stimulation of beta-cells can cause increased insulin, and so reduced blood glucose

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27
Q

When is insulin-induced hypoglycaemia especially common?

A
  • Between meals and overnight
  • In elderly
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28
Q

What is the NICE HbA1c target in type 2 diabetes?

A

6.5-7.5%

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29
Q

What % of type 2 diabetics achieve the NICE HbA1c target?

A

<50%

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30
Q

How should diabetes be treated if the HbA1c is 6.5%?

A

Using diet and first 2 treatment steps

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31
Q

What should be done if the HbA1c is above 7.5% in patients with diabetes?

A

Go beyond the first 2 treatment steps, unless at risk of severe hypoglycaemia

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32
Q

What is the action of metformin?

A
  • Decreases insulin resistance, leading to increased glucose utilisation by tissues
  • Decreases hepatic glucose production
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33
Q

What are the advantages of metformin?

A
  • Limits weight gain
  • Decreases incidence of CVS events
  • Can be combined with all other diabetes medications
  • Cheap
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34
Q

Who is offered metformin?

A

All patients presenting with type II diabetes without contraindications

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35
Q

What should be done if control of diabetes is not sufficient on metformin?

A

The patient should be left on metformin, and other medications should be added

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36
Q

What effect does metformin have when it is given with insulin?

A

It allows better control with lower doses of insulin when used in conjunction with metformin

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37
Q

What are the problems with metformin?

A
  • Side effects
  • Rarely, lactic acidosis
  • Uncommonly, vitamin B12 deficiency
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38
Q

What are the side effects of metformin?

A
  • Nausea
  • Vomiting
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39
Q

What should be done when a patient on metformin develops side effects?

A

Should stop the medication, and try modified release preperation

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40
Q

How can metformin cause vitamin B12 deficiency?

A

It can interfere with B12 absorption at the terminal ileum

41
Q

What are the contraindications for metformin?

A
  • Renal failure
  • Cardiac failure
  • Respiratory failure
  • Liver failure
42
Q

At what GFR should metformin not be given?

A

<30ml/min

43
Q

Why should metformin not be given in renal failure?

A

Risk of accumulation and lactoacidosis

44
Q

What is the action of sulphonylureas?

A

Stimulate beta cells to release insulin by attaching to a receptor on the beta cell

45
Q

What are the advantages of sulphonylureas?

A
  • Decreased microvascular risk
  • Low cost
46
Q

What are the problems with sulphonylureas?

A
  • Weight gain
  • Hypoglycaemia
47
Q

What are the two most commonly used sulphonylureas?

A
  • Gliclazide
  • Glimepiride
48
Q

What are the possible formations of gliclazide?

A

Standard or slow release

49
Q

In what special situation can gliclazide be used?

A

In renal impairment

50
Q

Why can gliclazide be used in renal impairment?

A

As it is metabolised hepatically

51
Q

How is acarbose unique?

A

It is the only alpha-glucosidase inhibitor available

52
Q

What is the action of acarbose?

A

It inhibits the breakdown of carbohydrates to glucose in the bowel by blocking the action of the enzyme alpha-Glucosidase

53
Q

What are the side effects of acarbose?

A
  • Flatulence
  • Loose stools
  • Diarrhoea
54
Q

Why is acarbose rarely, if ever, used nowadays?

A

It is not very effective

55
Q

By how much can acarbose reduce HbA1c?

A

0.5%

56
Q

What is the mechanism of action of glitazones?

A

Binds to and activates one or more peroxisome proliferator activated receptors, which increases insulin sensitivity in muscle and adipose tissue, and decreases hepatic glucose output

57
Q

What are the advantages of glitazones?

A

Can be used in combination with other oral agents

58
Q

Give two examples of glitazones

A
  • Rosiglitazone
  • Pioglitazone
59
Q

Why is rosiglitazone no longer used?

A

Due to cardiovascular concerns

60
Q

Is pioglitazone still used?

A

Yes, but there are concerns

61
Q

What are the concerns regarding pioglitazone?

A
  • Weight gain
  • Fluid retention
  • Heart failure
  • Bone metabolism
  • Bladder cancer
62
Q

What are the concerns regarding pioglitazone and bone metabolism?

A

Increased risk of fractures due to exacerbation of oesteoporosis, especially in elderly women

63
Q

What is high glucose in type 2 diabtes due to?

A

Insufficient insulin release, and over production of glucagon

64
Q

What does GLP-1 therapy do?

A

It increases insulin secretion from beta cells, and decreases production of glucagon from alpha cells

65
Q

What is GLP-1 released from?

A

Intestinal L cells

66
Q

What does GLP-1 act on physiologically?

A
  • Brain
  • Stomach
  • Pancreas
  • Liver
  • Muscle
67
Q

What effect does GLP-1 have on the brain?

A

It increases satiety, and therefore decreases food intake

68
Q

What is the end effect of GLP-1 action on the brain?

A

Causes patients to loose weight

69
Q

What effect does GLP-1 have on the stomach?

A

Decreases gastric emptying

70
Q

What effect does GLP-1 have on the pancreas?

A
  • Increases inuslin secretion
  • Decreases glucagon secretin
  • Increases insulin biosynthesis
71
Q

What effect does GLP-1 have on liver?

A

Indirectly decreases glucose production

72
Q

What effect does GLP-1 have on muscles?

A

It indirectly increases glucose uptake

73
Q

What are the types of GLP-1 therapies?

A
  • Oral preparations
  • Injectables
74
Q

What are the oral preparations of GLP-1 therapies known as?

A

DDP-4 inhibitors, or gliptins

75
Q

What is the mechanism of action of gliptins?

A

Protect the native GLP-1 from inactivation by DPP-4, and therefore increases postprandial active GLP-1 concentrations

76
Q

Give 4 examples of gliptins

A
  • Sitagliptin
  • Vildagliptin
  • Saxagliptin
  • Linagliptin
77
Q

What are the advantages of gliptins?

A
  • Low risk of hypoglycaemia
  • Weight neutral, or promote weight loss
78
Q

What are the problems with gliptin therapy?

A
  • GI symptoms
  • Possible increased risk of pancreatitis
  • Only a modest HbA1c reduction
  • High cost
79
Q

How much does gliptin therapy cost?

A

£30 a month

80
Q

What are the injectable GLP-1 therapies known as?

A

GLP-1 receptor agonists

81
Q

What is the mechanism of action of GLP-1 receptor agonists?

A

They mimic the nature of native GLP-1

82
Q

What are the advantages of GLP-1 receptor agonists?

A
  • Low risk of hypoglycaemia
  • Generally perceived to be safe and well tolerated agents
83
Q

Do GLP-1 receptor agonists cause pancreatitis?

A

Despite concerns, NICE and the FDA found no evidence of pancreatitis in reported studies

84
Q

What are the problems with GLP-1 receptor agonists?

A
  • Side effects
    Ocassionally painful to inject
85
Q

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

A
  • Nausea
  • Loose stools/diarrhoea
  • Gastro-oesophageal reflux
86
Q

Why are GLP-1 receptor agonists ocasionally painful to inject?

A

Because it is an acidic solution

87
Q

What are the contraindiciations for treatment with GLP-1 receptor agonists?

A
  • eGFR <30ml/min
  • Organ failure
88
Q

What should be used instead of GLP-1 receptor agonists in organ failure?

A

An agent with a more predictable metabolism, e.g. insulin

89
Q

Give two examples of GLP-1 receptor agonists

A
  • Exanatide
  • Liraglutide
90
Q

How often is exanatide taken?

A

Twice daily, or once weekly

91
Q

Give an example of a sodium-glucose co-transporter 2 inhibitor

A

Glifozin

92
Q

What approach does glifozin take to remove excess glucose?

A

A novel insulin-independant approach

93
Q

Who can glifozin be used in?

A

Patients with type 2 diabetes, as an add on therapy

Not currently prescribed for type 1, but trials ongoing

94
Q

What are the side effects of glifozin?

A
  • Increased risk of lower urinary tract symptoms
  • Polyuria
95
Q

In what % of men and women on glifozin do genital or urinary tract infections occur?

A
  • 5% of women
  • 1% of men
96
Q

What action should be taken if a patient on glifozin presents with a genital or urinary tract infection?

A

If it happens once, treat the condition. If it happens again, stop the drug

97
Q

How much extra urine is produced due to glifozin treatment?

A

Up to 350ml/day

98
Q

Give three examples of glifozins?

A
  • Dapagliflozin
  • Canaglifozin
  • Empaglifozin

ESA 5 - Pharmacology (28 decks)

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