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.0.0 RSP Endocrine > [1] Diabetes Mellitus > Flashcards

[1] Diabetes Mellitus Flashcards

1
Q

What is diabetes mellitus?

A

A group of metabolic disorders in which there are high blood sugar levels over a prolonged period.

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2
Q

What are the different types of diabetes mellitus?

A
  • Type 1
  • Type 2
  • Gestational diabetes
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3
Q

What is insulin?

A

The principle hormone that regulates the uptake of glucose from the blood into the most the cells of the body, especially the liver, adipose tissue, and muscle.

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4
Q

How does the body obtain glucose?

A
  • Intestinal absorption of food
  • Breakdown of glycogen
  • Gluconeogenesis
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5
Q

How can insulin influence the glucose balance in the body?

A
  • It can inhibit the process of gluconeogenesis or glycogenolysis
  • It can stimulate the transport of glucose into muscle and fat cells
  • It can stimulate the storage of glucose into muscle and fat ccells
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6
Q

What releases insulin?

A

Beta-cells in the islets of Langerhans in the pancreas

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7
Q

What is insulin released in response to?

A

Rising levels of blood glucose, typically after eating

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8
Q

How does lower glucose affect insulin release?

A

It reduces it

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9
Q

What is the role of glucagon?

A

It breaks down glycogen to glucose when there is low blood glucose

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10
Q

What will happen if the amount of insulin is insufficient, or if cells respond poorly to the effects of insulin due to insulin insensitivity?

A

Glucose will not be absorbed properly by body cells that require it, and will not be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements such as acidosis

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11
Q

What happens when glucose concentrations in the blood remains high over time?

A

They kidneys will reach a threshold of reabsorption whereby they can no longer reabsorb all of the glucose, and some will be excreted into the urine, producing glycosuria

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12
Q

How does glycosuria cause lead to the symptoms of dehydration and thirst?

A

It increases the osmotic pressure in the urine, and inhibits reabsorption of water by the kidney, resulting in increased urine production and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst

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13
Q

What is the cause of T1DM?

A

Unknown, however it is believed to involve a combination of genetic and environmental factors. The genetic predisposition is associated wtih the genetic markers HLA DR3 and HLA DR4.

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14
Q

What is the underlying pathophysiological mechanism in T1DM?

A

Destruction of insulin-producing ß-cells of the pancreatic islets, leading to insulin deficiency

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15
Q

What % of cases of T1DM are immune mediated in nature?

A

90%

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16
Q

What happens in immune-mediated T1DM?

A

T-cell mediated autoimmune attack leads to a loss of ß-cells, and therefore insulin

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17
Q

What is T2DM characterised by?

A

Insulin resistance, which may be combined with reduced insulin secretion

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18
Q

What is the proportion of insulin resistance to ß-cell dysfunction in T2DM?

A

It varies between individuals, with some having primarily resistance and very little defect in insulin secretion, and some the opposite

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19
Q

What causes type 2 diabetes mellitus?

A

Predominantly lifestyle factors and genetics, but a number of other health problems or medications can predispose to diabetes

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20
Q

What lifestyle factors are known to be involved in the development of T2DM?

A
  • Obesity and being overweight
  • Lack of physical activity
  • Poor diet, including high sugar, saturated fats, and trans fatty acid intake
  • Stress
  • Urbanisation
  • Smoking
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21
Q

How are genes involved in the development of diabetes mellitus?

A

Most cases of T2DM involve many genes, with each being a small contributor to the increased probability of the development of T2DM

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22
Q

What health conditions are associated with an increased risk of T2DM?

A
  • Acromegaly
  • Cushing’s syndrome
  • Hyperthyroidism
  • Pheochromocytoma
  • History of gestational diabetes
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23
Q

What medications can cause type 2 diabetes?

A
  • Thiazides
  • Glucocorticoids
  • Beta blockers
  • Atypical antipsychotics
  • Statins
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24
Q

What are the symptoms of diabetes mellitus?

A
  • Polydipsia
  • Polyuria
  • Fatigue
  • Weight loss and loss of muscle bulk
  • Thrush
  • Blurred vision
  • Slow healing of cuts and grazes
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25
Q

How do people with type 1 diabetes mellitus sometimes present?

A

With diabetic ketoacidosis

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26
Q

Describe the onset of T1DM

A

The symptoms can develop very quickly, over a few days or weeks, especially in children. In adults, they are more likely to take a few months to develop

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27
Q

Describe the onset of T2DM

A

They develop slowly, and don’t necessarily make the person feel unwell, so the person may not realise they have it for a long time

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28
Q

What is a diagnosis of diabetes mellitus made on?

A

The basis of a high plasma glucose

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29
Q

What are the diagnostic criteria for diabetes mellitus?

A
  • Random venous plasma glucose >11.1mmol/L
  • Fasting plasma glucose concentration >7.0mmol/L (whole blood >6.1mmol/L)
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30
Q

When can a diagnosis of diabetes not be made on the basis of a single glucose measurement?

A

When there are no symptoms, as is often the case in T2DM

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31
Q

What confirms a diagnosis of diabetes when there is a single reading of raised plasma glucose but no symptoms?

A

At least 1 additional glucose test result on another day with a value in the diabetic range

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32
Q

Why is it important to get at least two readings of raised plasma glucose when diagnosing diabetes with no symptoms?

A

Because a diagnosis of diabetes has important legal and medical implications for the patient

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33
Q

What should a person newly diagnosed with type 1 diabetes develop?

A

An individual care plan

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34
Q

Who does the individual care plan in type 1 diabetes need to be jointly agreed between?

A

The patient and the doctor

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35
Q

How should the individual care plan for a patient with type 1 diabetes develop over time?

A

It should be reviewed and modified annually

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36
Q

What should be taken into account when reviewing and modifying the individual care plan in diabetes mellitus?

A

Changes in the person’s wishes, circumstances, and medical findings

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37
Q

What should the individual care plan in type 1 diabetes involve?

A
  • Education, involving nutritional advice
  • Insulin therapy
  • Self-monitoring
  • Hypoglycaemia avoidance and monitoring
  • Other elements
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38
Q

Why is it important to offer dietary advice to those with type 1 diabetes mellitus?

A

So they can adequately manage their blood glucose, as well as their weight and cardiovascular risk

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39
Q

What programmes should be made available to patients with type 1 diabetes, regarding dietary management?

A

Programmes that will allow them to make optimal choices about the variety of foods they eat, and change their insulin dose to mimic as far as possible the physiological response

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40
Q

What should any nutritional information given to a patient with T1DM take into account?

A
  • Any personal and cultural needs
  • Associated features of diabetes, such as obesity or being underweight, hypertension, and renal failure
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41
Q

How often should HbA1c levels be monitored in adults with type 1 diabetes?

A

Every 3-6 months

You should consider measuring more often if the glucose control is suspected to be changing rapidly

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42
Q

What is the target HbA1c in diabetes mellitus?

A

6.5%, however an individualised target can be made

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43
Q

Why is a target HbA1c of 6.5% given?

A

To minimise the risk of long-term vascular complications

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44
Q

What might an individualised HbA1c target take into account?

A
  • Daily activities
  • Likelihood of complications
  • Co-morbidities
  • Occupation
  • History of hypoglycaemia
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45
Q

What blood glucose level should be aimed for in T1DM?

A

Fasting plasma glucose level of 5-7mmol/L on walking, and a plasma glucose of 4-7mmol/L before meals at other times of the day

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46
Q

How often should patients with T1DM self-monitor their glucose levels?

A

At least 4 times a day, including before each meal and before bed.

In some scenarios, the patient should monitor their glucose up to 10 times a day

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47
Q

Give 3 examples of when a person might need to self-monitor their glucose levels up to 10 times a day

A
  • If they are ill
  • If there is an increased frequency of hypoglycaemic episodes
  • If they are undertaking strenuous exercise
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48
Q

Is continuous blood glucose monitored used in T1DM?

A

It is not routinely offered, however is an option in certain circumstances

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49
Q

When might continuous blood glucose monitoring be used in T1DM?

A
  • More than one episode per year of severe hypoglycaemia with no obvious cause
  • Complete loss of awareness of hypoglycaemia
  • Extreme fear of hypoglycaemia
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50
Q

What kind of hormone in insulin?

A

Polypeptide

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51
Q

What does insulin consist of structurally?

A

Two peptide chains that are connected by disulphide bonds

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52
Q

How is insulin produced?

A

It is synthesised as the pre-cursor proinsulin, and then undergoes proteolytic cleavage to form insulin and C-peptide, both of which are secreted from the ß-cells of the pancreas

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53
Q

What is the secretion of insulin controlled by?

A

Plasma glucose levels

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54
Q

Why is exogenous insulin administered in T1DM?

A

To replace absent insulin secretion

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55
Q

What are the 6 main categories of exogenous insulin?

A
  • Ultrafast acting
  • Rapid acting
  • Short acting
  • Intermediate acting
  • Long acting
  • Very long acting
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56
Q

Give an example of ultrafast acting insulin

A

FiAsp

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57
Q

Give 3 examples of rapid acting insulins

A
  • Humalog
  • Novorapid
  • Apidra
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58
Q

What is the onset of action of short-acting insulin?

A

5-15 minutes

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59
Q

When does the action of rapid acting insulin peak?

A

At about 60 minutes

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60
Q

What is the duration of action of rapid acting insulin?

A

4-6 hours

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61
Q

When is rapid acting insulin injected?

A

Just before eating

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62
Q

Give two examples of short acting insulins

A
  • Actrapid
  • Humulin S
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63
Q

What is the onset of action of short acting insulins?

A

30-60 minutes

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64
Q

When does the action of short acting insulin peak?

A

2-3 hours

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65
Q

What is the duration of action of short acting insulin?

A

8-10 hours

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66
Q

When is short acting insulin injected?

A

15-30 minutes before eating

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67
Q

What is the problem with short acting insulin?

A

Because it is only injected 15-30 minutes before eating, but doesn’t peak for 2-3 hours, the person will have very high glucose after the meal, which can increase the risk of long-term complications over time

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68
Q

Give 3 examples of intermediate acting insulins

A
  • Insulatard
  • Humulin I
  • Insuman Basal
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69
Q

What is the onset of action of intermediate acting insulin?

A

Slower 2-4 hours

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70
Q

When does the action of intermediate acting insulin peak?

A

4-8 hours

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71
Q

What is the duration of action of intermediate acting insulins?

A

12-20 hours

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72
Q

What is the purpose of intermediate acting insulin?

A

They cover between meals and overnight

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73
Q

Give an example of a long acting insulin

A

Glargine

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74
Q

What is the onset of action of glargine?

A

2-6 hours

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75
Q

What is the duration of action of glargine?

A

24 hours

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76
Q

Give an example of a very long acting insulin

A

Degludec

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77
Q

What is the duration of action of degludec?

A

50+ hours

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78
Q

What are the adverse effects of insulin?

A
  • Hypoglycaemia
  • Weight gain
  • Local injection site reactions
  • Lipodystrophy
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79
Q

How can the risk of lipodystrophy with insulin injections be minimised?

A

By changing the injection site

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80
Q

How is human insulin produced?

A

By recombinant DNA technology, using strains of E. Coli or yeast that are genetically modified to contain the gene for human insulin

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81
Q

What produces insulin with different pharmacokinetic properties?

A

Modification of the amino acid sequence of human insulin

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82
Q

What factors can affect the onset and duration of various insulin preparations?

A
  • Dose
  • Injection site
  • Temperature
  • Blood supply
  • Physical activity
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83
Q

Why can insulin not be taken orally?

A

As it is a polypeptide, and therefore would be degenerated in the GI tract

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84
Q

How is insulin administered?

A

Normally subcutaneously, but can be given IV in hyperglycaemic emergencies

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85
Q

What are insulin pumps also known as?

A

Subcutaneous insulin infusion

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86
Q

How do insulin pumps deliver insulin?

A

They deliver a basal rate of insulin

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87
Q

Does the patient ever need to inject insulin if they have an insulin pump?

A

Yes, they inject a bolus of insulin to cover mealtimes

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88
Q

What is the advantage of insulin pumps?

A

They are more convenient for the patient, as they eliminate the need for multiple daily injections

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89
Q

When are insulin pumps recommended as a treatment option?

A

For adults or children 12 years or older with type 1 diabetes mellitus, providing that attempts to achieve target HbA1c with multiple daily injections result in the person experiencing disabling hypoglycaemia, or HbA1c levels remain high (8.5% or above) despite a high level of care

90
Q

What factors should be considered in adults with erratic and unpredictable glucose control in T1DM on a previously optimised insulin regime?

A
  • Injection technique
  • Injection sites
  • Self-monitoring skills
  • Knowledge and self-management skills
  • Nature of lifestyle
  • Psychological and psychosocial difficulties
  • Possible organic causes
91
Q

What needs to be considered when adopting an individualised approach to a patient with T2DM?

A
  • Needs and circumstances
  • Personal preferences
  • Co-morbidities
  • Risks from polypharmacy
  • Ability to benefit from long-term interventions due to life expectancy
92
Q

Who should be offered structured education in T2DM

A

Patients and/or their family members/carers

93
Q

When should education be offered in T2DM?

A

At/around the time of diagnosis, with annual reinforcement and review

94
Q

How should education be provided in T2DM?

A

Group education programmes should be offered as the preferred option, however you should also provide an alternative of equal standard to those unwilling or unable to participate in groups

95
Q

What should nutritional advice given in T2DM be sensitive to?

A

A person’s needs, culture and beliefs, and willingness to change

96
Q

What dietary advice should be given in T2DM?

A

Emphasis on the need for healthy balanced eating, encouraging;

  • High-fibre, low-glycaemic index sources of carbohydrates, such as fruit, vegetables, wholegrains and pulses
  • Low-fat dairy products and oily fish
  • Control intake of foods containing saturated and trans-fatty acids
97
Q

What initial weight loss target should be set for those with diabetes who are overweight?

A

Body weight loss of 5-10%

98
Q

Other than healthy eating, how else should T2DM be patients be advised to keep healthy?

A

Keep as active as possible

99
Q

How often should HbA1c be measured for adults with T2DM?

A

At 3-6 montly intervals, until stable on unchanging therapy, and then 6-montly intervals

100
Q

How should T2DM patients be involved in their management, regarding HbA1c?

A

They should be involved in decisions about their HbA1c target, and encouraged to achieve and maintain their target

101
Q

When should patients not be encouraged to achieve and maintain their target?

A
  • If it resulting in any adverse effects, including hypoglycaemia
  • If their efforts to achieve the target impairs their quality of life
102
Q

What is the HbA1c target for adults with T2DM managed by lifestyle and diet alone, or combined with a single drug?

A

6.5%

103
Q

What HbA1c should be aimed for in T2DM patients on a drug associated with hypoglycaemia?

A

7%

104
Q

What should be done if HbA1c levels are not adequately controlled by a single drug, and rise to 7.5% or higher in a T2DM patient?

A
  • Reinforce advice about lifestyle, diet, and drug adherence
  • Support the person in achieving a goal of 7% or lower
  • Intensify the drug treatment
105
Q

When can you consider relaxing the HbA1c target for T2DM?

A

On a case-by-case benefit, particularly for those who are older or frail

106
Q

Why might you consider relaxing the HbA1c target in those who are older and frail?

A
  • They are unlikely to achieve longer-term risk reduction benefits due to shorter life expectancy
  • They are more likely to have severe consequences as a result of hypoglycaemia, e.g. they are at risk of falling, they have decreased awareness of hypoglycaemia, or they drive/operate machinery as part of their job
  • Intensive management is inappropriate, for example those with significant co-morbidities
107
Q

When is blood glucose monitored offered in T2DM?

A

It is not routinely offered, unless;

  • They are on insulin
  • There is evidence of hypoglycaemic episodes
  • The person is on oral medication that may increase their risk of hypoglycaemia while driving or operating machinery
  • The person is pregnant, or planning to become pregnant
  • It is only intended as short-term monitoring when starting treatment with oral or IV corticosteroids
108
Q

When are oral hypoglycaemics offered to patients with type 2 diabetes?

A

When their diabetes is not being well controlled with diet

109
Q

Which T2DM patients are most likely to respond well to oral agents?

A

Those who have developed diabetes after the age of 40, and have had it for less than 5 years

110
Q

What might T2DM patients require, in terms of oral agents?

A

They may require a combination of oral agents, with or without insulin

111
Q

What oral agent is first line in T2DM?

A

Metformin

112
Q

What can be used as a monotherapy if metformin is contraindicated or not tolerated?

A
  • DPP-4 inhibitors
  • Pioglitazones
  • Sulfonylurea
113
Q

When might treatment with SGLT-2 inhibitors be appropriate in T2DM?

A

In the treatment of some adults, if metformin is contraindicated or not tolerated

114
Q

What is done if drug treatment with metformin has not continued to control HbA1c adequately?

A

Consider dual therapy with DPP-4 inhibitors, pioglitazones, or sulphonylureas - this is called the first intensification

115
Q

What is done if the first intensification of anti-diabetes medication is still ineffective?

A

You need to progress to the second intensification, which can be treatment with 3 non-insulin anti-hyperglycaemics (triple therapy), or any treatment combination containing insulin.

116
Q

What might be included in triple therapy?

A
  • Metformin, a DPP-4 inhibitor, and sulphonylurea
  • Metformin, pioglitazone, sulponylurea
117
Q

What class of drug is metformin in?

A

Biguanide

118
Q

What kind of anti-hyperglycaemic is metformin classified as?

A

An insulin sensitiser

119
Q

Why is metformin classified as an insulin sensitiser?

A

As it increases glucose uptake and use by target tissues, therefore decreasing insulin resistance

120
Q

Is metformin used alone or in combination with other agents?

A

It can either be used alone, or in combination with other oral agents or insulin

121
Q

What is the main mechanism of action of metformin?

A

The reduction of hepatic gluconeogenesis.

122
Q

Why does the reduction of hepatic gluconeogenesis help in diabetes?

A

Because excess glucose is produced by the liver, which is a major source of hyperglycaemia in type 2 diabetes, accounting for the high fasting blood glucose

123
Q

What are the secondary mechanisms of action of metformin?

A
  • Slows intestinal absorption of sugars
  • Improves peripheral glucose uptake and utilisation
124
Q

Does metformin cause weight loss or weight gain?

A

Weight loss

125
Q

Why might metformin cause weight loss?

A

Because it causes a loss of appetite

126
Q

How does the risk of hypoglycaemia with metformin compare to other oral agents?

A

It is much lower

127
Q

Why is the risk of hypoglycaemia much lower with metformin than other agents?

A

Because it does not promote insulin secretion, and therefore hyperinsulinaemia is not a problem

128
Q

What are the adverse effects of metformin?

A

Mainly gastrointestinal, inlcuding nausea, vomiting, diarrhoea, and abdominal pain

129
Q

What minimises the risk of adverse effects with metformin?

A

Gradually increasing the dose over several weeks

130
Q

What can be done if GI side effects are experienced with standard release metformin?

A

Consider a trial of modified-release metformin

131
Q

What effect might long-term use of metformin have?

A

May interfere with vitamin B12 absorption

132
Q

In what conditions is metformin contraindicated?

A
  • Acute MI
  • Exacerbation of heart failure
  • Sepsis, or other disorders that can cause acute kidney failure
133
Q

Who should metformin be caused with caution in?

A
  • Patients over 80 years of age
  • Those with heart failure
  • Alcohol abuse
134
Q

When should metformin be temporarily discontinued?

A

In patients undergoing procedures requiring IV radiographic contrast

135
Q

At what eGFR should metformin be stopped?

A

Below 30ml/min

136
Q

Why should metformin be stopped at eGFRs below 30ml/min?

A

Due to the risk of lactic acidosis

137
Q

Regarding renal function, what caution should be taken with metformin?

A

Caution in prescribing metformin for those at risk of sudden deterioration of kidney function, and those at risk of eGFR falling below 45ml/min

138
Q

Is metformin absorbed well after oral administration?

A

Yes

139
Q

Is metformin bound to serum proteins?

A

No

140
Q

Is metformin metabolised?

A

No

141
Q

How is metformin excreted?

A

Via the urine

142
Q

Give three examples of DPP-4 inhibitors

A
  • Alogliptin
  • Linagliptin
  • Sitagliptin
143
Q

What is the mechanism of action of DPP-4 inhibitors?

A

They inhibit the enzyme DPP-4, which is responsible for the inactivation of incretin hormones such as GLP-1. Prolonging the activity of these hormones increases insulin release in response to meals, and reduces inappropriate secretion of glucagon

144
Q

Do DPP-4 inhibitors cause weight loss or weight gain?

A

Neither, they are weight neutral as do not affect satiety

145
Q

What are the adverse effects of DPP-4 inhibitors?

A

In general, they are well tolerated. The most common adverse effects are nasopharyngitis and headache.

Pancreatitis can occur, although this is infrequent

146
Q

Are DPP-4 inhibitors well absorbed after oral administration?

A

Yes

147
Q

Does food affect the absorption of DPP-4 inhibitors?

A

No

148
Q

How are DPP-4 inhibitors metabolised?

A

Saxagliptin is metabolised by enzymes in the CYP450 system

Alogliptin and sitagliptin are excreted mostly uncharged

149
Q

How is alogliptin and sitalgliptin excreted?

A

In the urine

150
Q

How is linagliptin elimited?

A

Mainly by the enterohepatic system

151
Q

Which DPP-4 inhibitors require dosage adjustments in renal impairment?

A

All apart from linagliptin

152
Q

What kind of oral anti-hyperglycaemics are the thiazolidinediones?

A

Insulin sensitisers

153
Q

What is required for the action of thiazolidinediones?

A

The presence of some insulin

154
Q

Give two examples of thiazodinediones

A
  • Pioglitazone
  • Rosiglitazone
155
Q

Is there a risk of hyperinsulinaemia with thiazolidinediones?

A

No, because they do not promote insulin release from ß-cells

156
Q

What is the mechanism of action of thiazolidinediones?

A

They lower insulin resistance by acting as agonists for the PPAR-gamma (which is a type of receptor). Activation of this receptor regulates the transcription of several insulin-responsive genes, resulting in an increased insulin sensitivity in adipose tissue, liver, and skeletal muscle

157
Q

What are the adverse effects of thiazolidinediones?

A
  • Soem reported cases of liver toxicity
  • Weight gain
  • Associated with osteopenia
  • May increase the risk of bladder cancer
158
Q

What is the result of a few cases of liver toxicity being reported with thiazolidinediones?

A

Periodic monitoring of liver function is recommended

159
Q

Why might weight gain occur with thiazolidinediones?

A

Becasue they increase subcutaneous fat and fluid retention

160
Q

Other than weight gain, what effect can increased fluid retention caused by thiazolidinediones have?

A

Can worsen heart failure, therefore they should be avoided in severe heart failure

161
Q

What can osteopenia cause?

A

Increased fracture risk

162
Q

Are thiazolidinediones well absorbed after oral administration?

A

Yes

163
Q

Are thiazolidinediones bound to serum albumin?

A

Yes, extensively

164
Q

How are thiazolidinediones metabolised?

A

Metabolised extensively by CYP450 enzymes

165
Q

How is pioglitazone eliminiated?

A

The majority of active drug and metabolite are excreted in bile and eliminated in faeces. Renal elimination is negligible

166
Q

How is rosiglitazone excreted?

A

Primarily in urine

167
Q

Is dosage adjustment of thiazolidinediones required in renal impairment?

A

No

168
Q

What kind of oral hyperglycaemics are sulphonylureas?

A

Insulin secretagouges

169
Q

Why are sulphonylureas classified as insulin secretagouges?

A

Because they promote insulin release from ß-cells of the pancreas

170
Q

What is the most importants sulphonylurea?

A

Gliclazide

171
Q

What is the main mechanism of action of sulphonylureas?

A

Stimulation of insulin release from ß-cells in the pancreas by blocking ATP-sensitivie potassium channels, which results in depolarisation, calcium influx, and insulin exocytosis

172
Q

What are the other mechanisms of action of sulphonylureas?

A
  • Reduction in hepatic glucose production
  • Increase peripheral insulin sensitivity
173
Q

What are the major adverse effects of sulphonylureas?

A
  • Weight gain
  • Hyperinsulinaemia and hypoglycaemia
174
Q

When is caution required in sulphonylureas?

A

In hepatic or renal insufficiency

175
Q

Why is caution required with sulphonylureas in hepatic and renal insufficiency?

A

Due to the risk of accumulation

176
Q

How are sulphonylureas administered?

A

Orally

177
Q

How are sulphonylureas metabolised?

A

By the liver

178
Q

How are sulphonylureas excreted?

A

In urine and faeces

179
Q

What is the duration of action of sulphonylureas?

A

12-24 hours

180
Q

Give 2 examples of SGLT2 inhibitors?

A
  • Canaglifoxin
  • Dapaglifozin
181
Q

What is the mechanism of action of SGLT2 inhibitors?

A

The sodium-glucose-cotransporter is responsible for absorbing filtered glucose in the tubular lumen of the kidney. It inhibits this, reducing reabsorption of glucose, increasing urinary glucose excretion, and lowering blood glucose

182
Q

What are the adverse effects of SGLT2 inhibitors?

A
  • Female general mycotic infections, for example vulvovaginal candidiasis, urinary tract infections, and urinary frequency
  • Hypotension, particularly in elderly or patients on diuretics
183
Q

When are SGLT2 inhibitors administered?

A

One daily, in morning

184
Q

How are SGLT2 inhibitors excreted?

A

Primarily via the faeces, however some of the dose is renally eliminated

185
Q

What is the result of some of the dose of SGLT2 being renall eliminated?

A

They should be avoided in renal impairmetn

186
Q

What kind of oral anti-hyperglycaemics are meglitinides?

A

Insulin secretagogues

187
Q

What is the mechanism of action of meglitinides?

A

They stimulate insulin production by binding to a distinct site on the ß-cell, closing ATP-sensitive potassium channels, and initiating a series of reactions that result in the release of insulin

188
Q

Describe the onset of action of meglitinides

A

Rapid

189
Q

Describe the duration of action of meglitinides

A

Short

190
Q

When are meglitinides particularly effective?

A

In the early release of insulin that occurs after a meal

191
Q

What are the adverse effects of meglitinides?

A

Can casue hypoglycaemia and weight gain, however incidence is less than with sulphonylureas

192
Q

What effect do drug interactions have on the action of meglitinides?

A

May increase or decrease it’s action, so caution with polypharmacy

193
Q

What other oral anti-hyperglycaemic should meglitinides not be used with?

A

Sulphonylureas

194
Q

Why should meglitinides not be used in combination with sulphonylureas?

A

Due to their overlapping mechanisms of action, which could cause hypoglycaemia

195
Q

How are meglitinides administered?

A

Orally

196
Q

When should meglitinides be administered?

A

Prior to a meal

197
Q

Are meglitinides well absorbed after oral administration?

A

Yes

198
Q

How are meglitinides metabolised?

A

By CYP450 in the liver

199
Q

How are meglitinides excreted?

A

Through bile

200
Q

Give two examples of alpha-glucosidase inhibitors

A
  • Acarbose
  • Miglitol
201
Q

Where are alpha-glucosidase enzymes normally located?

A

In the intestinal brush border

202
Q

What do alpha-glucosidase enzymes do?

A

Break down carbohydrates into glucose and simple sugars that can be absorbed

203
Q

What is the mechanism of action of alpha-glucosidase inhibitors?

A

They reversibly inhibit the alpha-glucosidase enzymes, and so delay the digestion of carbohydrates if taken at the start of a meal, resulting in a lower post-prandial glucose level

204
Q

Do alpha-glucosidase inhibitors cause hypoglycaemia?

A

Not if used in a monotherapy, however can if used with other agents such as insulin

205
Q

Why do alpha-glucosidase inhibitors not cause hypoglycaemia when used as a monotherapy?

A

Because they do not stimulate insulin release or increase insulin sensitivity

206
Q

What are the adverse effects of alpha-glucosidase inhibitors?

A
  • Flatulence
  • Diarrhoea
  • Abdominal cramping
207
Q

What are the contraindications for the use of alpha-glucosidase inhibitors?

A
  • Inflammatory bowel disease
  • Colonic uleration
  • Intestinal obstruction
208
Q

Is acarbose well absorbed after oral administration?

A

No, it is poorly absorbed

209
Q

How is acarbose elimiated?

A

It is metabolised by intestinal bacteria, and some of the metabolites are absorbed and excreted into urine

210
Q

Is miglotol well absorbed after oral administration?

A

Yes, very well

211
Q

Does miglotol have systemic effects?

A

No

212
Q

How is miglotol excreted?

A

By the kidney

213
Q

Give 2 examples of GLP-1 analogues

A
  • Exanatide
  • Liraglutide
214
Q

What is the mechanism of action of GLP-1 analogues?

A

They increase glucose dependant insulin release, decrease secretion of glucose, slows gastric emptying, and increases satiety

215
Q

Do GLP-1 analogues cause weight loss or weight gain?

A

They can cause weight loss

216
Q

What are the adverse effects of GLP-1 analogues?

A

There is a risk of pancreatitis

217
Q

How are GLP-1 analogues administered?

A

Injection

218
Q

When should exanatide be injected?

A

At least twice daily, at least 60 minutes before morning and evening meals.

219
Q

How often should extended release exanatide be injected?

A

Once weekly

220
Q

When should liraglutide be injected?

A

Once-daily, irrespective of meals

221
Q

What are the acute complications of diabetes mellitus?

A
  • Diabetic ketoacidosis
  • Hyperosmolar hyperglycaemic state
  • Hypoglycaemia
222
Q

What are the chronic complications of diabetes mellitus?

A
  • Cardiovascular disease
  • Diabetic nephropathy
  • Diabetic retinopathy and diabetic eye problems
  • Diabetic neuropathy
  • Diabetic foot and leg
  • Frequent, recurrent, and persistent infections

.0.0 RSP Endocrine (18 decks)

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