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Therapeutics > Diabetes Mellitus- Treatment > Flashcards

Diabetes Mellitus- Treatment Flashcards

1
Q

How many people were estimated to be living with diabetes in 2021?

A

An estimated 537 million people were living with diabetes in 2021.

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2
Q

What is the expected number of people living with diabetes by 2045?

A

The number is expected to increase to 783 million people by 2045.

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3
Q

What major cardiovascular condition is diabetes associated with an increased risk of?

A

Diabetes is associated with an increased risk of atherosclerotic cardiovascular disease.

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4
Q

What is diabetes the leading cause of in terms of renal health?

A

Diabetes is the leading cause of renal failure.

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5
Q

How does diabetes affect vision health in adults?

A

Diabetes is the leading cause of adult blindness.

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6
Q

What serious limb-related complication is diabetes the leading cause of?

A

Diabetes is the leading cause of non-traumatic lower limb amputation.

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7
Q

Classification of diabetes

A
  1. Type 1 DM
  2. Type 2 DM
  3. Gestational diabetes
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8
Q

What is the primary characteristic of Type 1 DM?

A

The primary characteristic of Type 1 DM is the absence of insulin.

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9
Q

What causes the absence of insulin in Type 1 DM?

A

The absence of insulin is caused by the destruction of insulin-producing β cells in the pancreas.

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10
Q

What are the main characteristics of Type 2 DM?

A

Type 2 DM is characterized by decreased insulin secretion and insulin resistance.

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11
Q

What defines gestational diabetes?

A

Gestational diabetes is defined as any degree of glucose intolerance with onset during pregnancy that is not overt diabetes and resolves post-delivery.

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12
Q

Which class of drugs can induce diabetes through their effects on glucose metabolism?

A

Glucocorticoids
Thiazide diuretics
Atypical antipsychotics
Antiretroviral therapy (protease inhibitors)

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13
Q

How do glucocorticoids affect glucose metabolism?

A

Glucocorticoids can increase blood glucose levels, leading to potential glucose intolerance or diabetes.

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14
Q

What is the impact of thiazide diuretics on diabetes?

A

Thiazide diuretics can impair glucose metabolism and contribute to the development of diabetes.

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15
Q

How do atypical antipsychotics influence the risk of diabetes?

A

Atypical antipsychotics can cause weight gain and insulin resistance, increasing the risk of diabetes.

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16
Q

What effect does antiretroviral therapy, particularly protease inhibitors, have on diabetes risk?

A

Protease inhibitors in antiretroviral therapy can lead to insulin resistance and hyperglycemia, increasing the risk of diabetes.

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17
Q

What is insulin resistance in the context of Type 2 Diabetes?

A

In insulin resistance, normal amounts of insulin result in a subnormal insulin response by the body’s tissues.

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18
Q

How does the body initially compensate for insulin resistance?

A

The body compensates for insulin resistance by producing and releasing more insulin.

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19
Q

What is the “Starling curve of the pancreas” in relation to Type 2 Diabetes?

A

he “Starling curve of the pancreas” refers to the phenomenon where β-cells initially respond to insulin resistance by hypersecreting insulin, but over time, the ability to produce insulin declines as the β-cell mass becomes depleted.

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20
Q

What happens to β-cells during the progression of Type 2 Diabetes?

A

β-cells undergo hypersecretion of insulin due to insulin resistance, but as the disease progresses, the β-cell mass becomes depleted, leading to a decline in insulin secretion

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21
Q

How do hyperglycemia and lipid excess affect β-cells?

A

Hyperglycemia and lipid excess can be toxic to β-cells, contributing to their dysfunction and decline in insulin production.

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22
Q

What is metabolic syndrome?

A

Metabolic syndrome is a clustering of at least three out of five medical conditions: central obesity, hypertension, hyperglycemia, raised serum triglycerides, and low serum HDL.

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23
Q

What is the core clinical component of metabolic syndrome?

A

The core clinical component of metabolic syndrome is visceral/ectopic fat.

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24
Q

What is the core metabolic abnormality of metabolic syndrome?

A

The core metabolic abnormality of metabolic syndrome is insulin resistance.

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25
Q

What are the associated risks of metabolic syndrome?

A

Metabolic syndrome is associated with a high risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM).

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26
Q

What is thought to cause metabolic syndrome?

A

Metabolic syndrome is thought to be caused by an underlying disorder of energy utilization and storage, with complex and partially understood pathophysiology

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27
Q

What are common characteristics of patients with metabolic syndrome?

A

Most patients are older, obese, sedentary, and have a degree of insulin resistance.

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28
Q

What are some important risk factors for metabolic syndrome?

A

Important risk factors include diet (especially sugar-sweetened beverages), genetics, aging, sedentary behavior, disrupted chronobiology/sleep, mood disorders/psychotropic medication use, excessive alcohol use, and chronic stress.

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29
Q

How does central obesity relate to metabolic syndrome?

A

Central obesity, indicated by high waist circumference, is both a sign and a cause of metabolic syndrome, contributing to insulin resistance.

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30
Q

What happens when there is a mismatch between energy intake and physical activity?

A

A mismatch between continuous energy intake and insufficient physical activity leads to a backlog of mitochondrial oxidation products, resulting in mitochondrial dysfunction and insulin resistance.

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31
Q

Can normal-weight individuals have metabolic syndrome?

A

Yes, patients of normal weight can also be insulin-resistant and have metabolic syndrome.

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32
Q

What markers are often increased in metabolic syndrome?

A

Markers of systemic inflammation, such as C-reactive protein (CRP), are often increased in metabolic syndrome.

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33
Q

How does chronic stress contribute to metabolic syndrome?

A

Chronic stress leads to HPA-axis dysfunction, raising cortisol levels, hyperglycemia, and hyperinsulinemia, which contribute to metabolic syndrome.

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34
Q

Complications and comorbidities associated with diabetes

A

macrovascular
microvascular

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35
Q

Macrovascular

A

Ischemic stroke
Myocardial infarction
Peripheral arterial disease

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36
Q

Microvascular

A

Retinopathy
Nephropathy
Neuropathy

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37
Q

Major causes of death

A

Cardiovascular (70%)
Renal failure (10%)

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38
Q

What lifestyle modifications are recommended for managing complications and comorbidities of diabetes?

A

Recommended lifestyle modifications include diet (referral to a dietician), smoking cessation, physical exercise, and stress reduction.

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39
Q

What comorbidities should be treated pharmacologically in diabetic patients?

A

Dyslipidemia and hypertension should be treated pharmacologically in diabetic patients.

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40
Q

What is primary cardiovascular prevention?

A

Primary prevention aims to prevent cardiovascular events in patients at high risk but without any previous history of such events.

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41
Q

What is secondary cardiovascular prevention?

A

Secondary prevention aims to prevent further events in patients with a history of cardiovascular disease.

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42
Q

When is secondary prevention with statin and aspirin indicated in diabetic patients

A

Secondary prevention with statin and aspirin is indicated in all diabetics following a cardiovascular event, if there are no contraindications.

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43
Q

Is primary prevention with statins and aspirin indicated for all diabetics?

A

No, primary prevention with statins is not indicated for all diabetics as the benefits may not always outweigh the risks. Aspirin is only indicated as secondary prevention.

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44
Q

For which diabetic patients is statin therapy recommended according to PHC EML 2020?

A

Statin therapy is recommended for all type 2 diabetic patients who:

  • Are over 40 years of age,
  • Have had diabetes for over 10 years,
  • Have chronic kidney disease (eGFR < 60 mL/minute),
  • Have type 1 diabetes with microalbuminuria.
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45
Q

When is aspirin indicated in diabetic patients?

A

Aspirin is indicated only for secondary prevention following a cardiovascular event in diabetic patients.

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46
Q

Why is it important to specify treatment targets when initiating diabetes therapy?

A

Specifying treatment targets helps determine both the initial regimen choice and the escalation of treatment based on the patient’s profile.

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47
Q

What is typically used to monitor control in diabetic patients?

A

HbA1c is typically used to monitor control in diabetic patients.

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48
Q

How does a 1% drop in HbA1c affect diabetes outcomes?

A

Every 1% drop in HbA1c is associated with improved outcomes over the long term, with no threshold effect.

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49
Q

What is the relationship between HbA1c levels and the risk of microvascular complications?

A

At HbA1c levels below 7%, the risk for microvascular complications is low, and the incremental benefit of lowering HbA1c further has diminishing returns but increased risk of hypoglycemia.

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50
Q

What HbA1c target is appropriate for most diabetic patients?

A

For most patients, a target HbA1c of 7% is appropriate.

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51
Q

For which patients might a tighter HbA1c control target be appropriate?

A

A tighter control with HbA1c below 6.5% might be appropriate for younger patients without comorbidities, newly diagnosed patients, and those without established macrovascular disease (although there is a greater risk for hypoglycemia).

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52
Q

For which patients might a looser HbA1c target of 7-8% be more appropriate?

A

A looser HbA1c target of 7-8% may be more appropriate for older patients, those with multiple comorbidities or existing complications, those with short life expectancy, and those with limited support.

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53
Q

What is the “legacy effect” in diabetes treatment?

A

The “legacy effect” refers to the long-term benefit associated with a period of early intensive glucose control, where treatment arms treated with intensive glucose control early in the disease course demonstrated a reduction in the risk of long-term complications even after blood glucose levels increased and became comparable to those treated with conventional glucose control.

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54
Q

What monitoring steps are required at every visit for patients with diabetes or related chronic conditions?

A
  • Finger-prick blood glucose.
  • Weight and BMI calculation.
  • Waist circumference measurement.
  • Blood pressure measurement
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55
Q

What tests are conducted at baseline for patients with diabetes or related chronic conditions?

A
  • Serum creatinine concentration and calculation of eGFR.
  • Serum potassium concentration if on ACE-inhibitor or eGFR <30 mL/minute.
  • Urine protein by dipstick:
    –>If dipstick negative, request ACR (Albumin-Creatinine Ratio), unless already on an ACE-inhibitor. Microalbuminuria:
    –>Men: 2.5 to 25 mg/mmol
    –>Women: 3.5 to 35 mg/mmol
    –>If dipstick positive, follow guidelines for diabetic kidney disease.
  • Blood lipids: fasting total cholesterol, triglycerides, HDL, and LDL cholesterol.
  • Foot examination.
  • Eye examination for retinopathy.
  • Waist circumference measurement.
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56
Q

How frequently should HbA1c be measured?

A

6-monthly in patients meeting treatment goals
.
3-monthly in patients with sub-optimal control or if therapy has changed, until stable.

Note: Monitoring HbA1c implies active clinical management if levels are sub-optimal.

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57
Q

What tests should be conducted annually for patients with diabetes or related chronic conditions?

A

– Serum creatinine concentration and calculation of eGFR.
– Serum potassium concentration if on ACE-inhibitor/eGFR <30 mL/minute.
– Urine protein by dipstick:
—>If dipstick negative, request ACR, unless already on an ACE-inhibitor. Microalbuminuria:
—–»Men: 2.5 to 25 mg/mmol
—–»Women: 3.5 to 35 mg/mmol
–>If dipstick positive, follow guidelines for diabetic kidney disease.
- Eye examination for retinopathy.
- Foot examination.
- Assessment for peripheral neuropathy.
- Oral and dental examination.
- Assessment for macrovascular disease.
- Resting ECG.

58
Q

Non- glycemic targets

A

BMI<= 25kg/ m2

BP<= 140/90 and >=120/70 mmHg

59
Q

General non- pharmacological measures

A
  1. Lifestyle modification, including self- care practices
  2. Refer to a dietician if available for annual follow up
  3. Refer to a support group if available
  4. Education about diabetes and its complications
  5. Increased regular physical activity, aim for 30 minutes 5 times a week
  6. Appropriate weight loos if weight exceeds ideal weight
  7. Discourage smoking
  8. Moderate or no alcohol intake (<= standard drinks per day for males and females)
  9. Education about foot care
  10. All patients should wear a notification bracelet
60
Q

What is the role of normal physiologic insulin secretion?

A

Normal physiologic insulin secretion regulates blood glucose levels by releasing insulin in response to food intake and maintaining a base level of insulin to manage overall glycemic control.

61
Q

When does insulin peak in the body?

A

Insulin peaks immediately after meals, which is known as “prandial” insulin secretion

62
Q

What is the purpose of “basal” insulin?

A

“Basal” insulin is the constant, background level of insulin that is always available to manage glucose levels between meals and overnight.

63
Q

Why is a constant supply of basal insulin important?

A

A constant supply of basal insulin is essential to maintain overall glycemic control by suppressing hepatic glucose production and managing blood glucose levels between meals and overnight.

64
Q

How does basal insulin secretion function throughout the day?

A

Basal insulin secretion occurs continuously, maintaining a nearly constant level throughout the day. It is not suitable for handling post-meal glucose increases.

65
Q

What percentage of daily insulin requirements does basal insulin provide?

A

Basal insulin provides about 50% of the daily insulin requirements.

66
Q

When does postprandial insulin secretion occur?

A

Postprandial insulin secretion occurs in response to food intake.

67
Q

What is the function of postprandial insulin?

A

Postprandial insulin helps control hyperglycemia after meals and provides the remaining 50% of the daily insulin requirement.

68
Q

How does postprandial insulin contribute to overall insulin needs?

A

Postprandial insulin contributes by managing glucose spikes after eating, thus covering the other 50% of daily insulin requirements that basal insulin does not.

69
Q

What is the primary goal of insulin therapy?

A

The primary goal of insulin therapy is to improve glycemic control in patients with diabetes.

70
Q

What is a common side effect of insulin therapy?

A

Hypoglycemia is the most common side effect of insulin therapy.

71
Q

How should an insulin regimen be designed?

A

An insulin regimen should closely mimic normal physiologic insulin secretion patterns to manage blood glucose levels effectively

72
Q

What is the challenge in managing insulin therapy?

A

The challenge is balancing potential hyperglycemia with potential hypoglycemia, aiming for optimal glycemic control without causing adverse effects

73
Q

Is insulin therapy used for type 1 diabetes mellitus (DM)?

A

Yes, insulin is the sole therapy for type 1 DM

74
Q

When is insulin therapy used for type 2 diabetes mellitus (DM)?

A

Insulin therapy is used in type 2 DM when the condition is poorly controlled with diet and oral agents, either as combination therapy or monotherapy.

75
Q

Why is insulin administered subcutaneously or intravenously rather than orally?

A

Insulin is a protein that gets degraded in the gastrointestinal system if taken orally, so it is administered subcutaneously or intravenously to ensure its efficacy.

76
Q

Long acting basal insulin

A

detemir or glargine

77
Q

Intermediate acting insulin-

A

Humulin N or protaphane

78
Q

Ultrafast acting insulin

A

lispro

79
Q

Fast acting insulin

A

Actrapid

80
Q

Biphasic (analog)

A

Humalog

81
Q

Biphasic (human)

A

actraphane

82
Q

How do various insulin preparations differ from one another?

A

Various insulin preparations differ by their rate of absorption from subcutaneous tissue, which affects their onset and duration of action.

83
Q

What factors can influence the absorption rate of insulin?

A

Absorption rate can be influenced by the site of injection, temperature, physical activity following injection, and whether insulin is bound to protamine or zinc salts.

84
Q

What types of insulin were used prior to the 1980s?

A

Before the 1980s, diabetes was treated with animal insulins derived from (porcine) pigs or (bovine) cows.

85
Q

How is human insulin currently produced and what are its types?

A

Human insulin is synthetically made in laboratories using genetically engineered bacteria. It is available in two forms: Actrapid (regular or fast-acting) and Protophane (intermediate-acting, sometimes referred to as NPH, which has protamine added to delay absorption).

86
Q

What is a key benefit of human insulins compared to insulin analogs?

A

A key benefit of human insulins over analogs is their lower cost.

87
Q

What issue can occur with both human and animal insulins when injected?

A

Human and animal insulins can clump together when injected, which can lead to slowed, sporadic, and unpredictable absorption rates.

88
Q

How are insulin analogs different from human insulins?

A

Insulin analogs are also made in laboratories but undergo additional modifications to reduce clumping and achieve more predictable absorption. They can be engineered to have faster onset and longer duration of action.

89
Q

What advantage do insulin analogs have over human insulins?

A

Insulin analogs generally have a more predictable absorption profile and can be modified for a faster onset and longer duration of action compared to human insulins.

90
Q

What is the onset, peak, and duration of action for short-acting insulin (regular human insulin)?

A

Onset of Action: 30 minutes
Peak Action: 2 – 5 hours
Duration of Action: 5 – 8 hours

91
Q

When is short-acting insulin usually administered and why?

A

Short-acting insulin is usually given 30 minutes before meals to manage postprandial blood glucose levels effectively.

92
Q

What are the characteristics of intermediate-acting insulin (NPH)?

A

Onset of Action: 1 – 3 hours
Peak Action: 6 – 12 hours
Duration of Action: 16 – 24 hours

93
Q

When is intermediate-acting insulin typically administered?

A

Intermediate-acting insulin is usually given at night, not later than 22:00, to manage overnight blood glucose levels and provide basal insulin coverage.

94
Q

What is biphasic insulin and how is it administered?

A

Biphasic insulin is a mixture of regular human insulin and intermediate-acting insulin in varying proportions (e.g., 30/70, which contains 30% regular insulin and 70% intermediate-acting insulin). It is usually given twice daily.

95
Q

What are the onset, peak, and duration of action for biphasic insulin?

A

Onset of Action: 30 minutes
Peak Action: 2 – 12 hours
Duration of Action: 16 – 24 hours

96
Q

How are all patients with type 1 diabetes managed?

A

All patients with type 1 diabetes are managed with insulin.

97
Q

What are the two main insulin regimens used for managing type 1 diabetes?

A

The two main insulin regimens are the Basal-Bolus regimen and the Biphasic/Pre-mixed insulin regimen.

98
Q

What is the Basal-Bolus insulin regimen?

A

The Basal-Bolus regimen involves using a combination of intermediate-acting insulin (for basal coverage) and short-acting insulin (for bolus coverage). It includes administering short-acting insulin before meals and intermediate-acting insulin at bedtime (not later than 22:00).

99
Q

What is the initial total insulin dose for a patient using the Basal-Bolus regimen?

A

The initial total insulin dose is 0.6 units/kg body weight.

100
Q

How is the total insulin dose divided in the Basal-Bolus regimen?

A

The total insulin dose is divided into:

  • 40-50% as basal insulin
  • The remaining amount as bolus insulin, split equally before each meal
101
Q

How should insulin doses be adjusted in the Basal-Bolus regimen?

A

Insulin doses should be adjusted on an individual basis according to the patient’s specific needs and response.

102
Q

What is the Premixed Insulin regimen and when is it typically used?

A

The Premixed Insulin regimen involves using a mixture of intermediate- or short-acting insulin twice daily. It is a practical option for patients who cannot monitor their blood glucose frequently and provides adequate control when used with at least daily blood glucose monitoring.

103
Q

Indications for insulin therapy in type 2 DM

A
  • inability to control blood glucose pharmacologically i.e. combination/ substitution insulin therapy
  • temporary use for major stress e.g. surgery, medical illness
  • severe kidney or liver disease
  • pregnancy e
104
Q

Advice before insulin initiation in type 2 DM

A
  • At initiation of inulin therapy, give appropriate advice on self blood glucose monitoring (SGBM) and diet
  • it is advisable to maintain all patients on metformin once therapy with insulin has been initiated
105
Q

May consider using insulin in first line therapy at diagnosis in Type 2 diabetes if:

A
  • Marked weight loss (catabolism)
  • FPG > 14 mmol/L or random glucose > 16.7 mmol/L
  • HbA1C > 11%
  • Ketonuria or ketoacidosis
106
Q

Insulin is less desirable, and may be avoided, in type 2 diabetics in following situations:

A
  • Insulin allergy
    Failure or inability to master injections or self titration
  • Frequent or severe hypoglycemia despite multiple dosage adjustments
  • Circumstances where risk of severe hypoglycaemia and or its consequences are significant (workers with rotating shifts, truck or bus drivers)
  • Obesity related morbidity which has worsening or likely to worsen significantly with weight gain from insulin therapy
107
Q

Regimens to choose from in type 2 DM

A
  1. add on
  2. biphasic/ premixed
  3. basal bolus
108
Q

Importantly, insulin therapy is associated with:

A
  • Weight gain (3 – 5 kg)
  • Local skin reactions.
  • Risk of hypoglycemia with monotherapy, even greater when paired with sulphonylurea (so typically we advise stopping the sulfonylurea when adding insulin on to oral diabetic therapy).
109
Q

Counselling the patient

A
  1. Injection technique and sites
  2. Insulin storage:
    Keep stock in fridge; room temp if in use
  3. Recognition and treatment of complications:
    Eg. Lipohypertrophy, lipoatrophy, hypoglycemia, DKA
  4. In visually impaired patients and arthritic patients, prefilled pens and cartridges
110
Q

What are secretagogues and which class of drugs do they belong to?

A

Secretagogues are drugs that stimulate insulin production. They belong to the class of drugs known as sulphonylureas.

111
Q

How do sulphonylureas help in managing diabetes?

A

Sulphonylureas help manage diabetes by stimulating the pancreas to produce more insulin, thereby lowering blood glucose level

112
Q

What is the role of biguanides in diabetes management?

A

Biguanides, such as metformin, reduce hepatic glucose production and enhance peripheral glucose uptake, helping to lower blood glucose levels.

113
Q

How does metformin work in the body?

A

Metformin works by decreasing the amount of glucose produced by the liver (hepatic glucose production) and improving the body’s sensitivity to insulin, leading to better glucose uptake by peripheral tissues

114
Q

What are the main effects of biguanides on glucose metabolism?

A

Biguanides primarily reduce hepatic glucose production and enhance peripheral glucose uptake, contributing to improved overall glucose control.

115
Q

Examples of biguanides

A

Metformin

116
Q

Examples of sulfonylureas

A

Glimepiride,
gliclazide,
glibenclamide

117
Q

How does metformin lower blood glucose levels?

A

Metformin lowers blood glucose levels by:

  1. Reducing hepatic gluconeogenesis and glycogenolysis, which overall decreases glucose production.
  2. Improving insulin resistance by enhancing insulin-mediated glucose uptake in skeletal muscle through the phosphorylation of GLUT4, thereby increasing its sensitivity to insulin.
  3. Decreasing carbohydrate absorption from the gastrointestinal tract.
  4. Lowering triglyceride and total cholesterol levels, while raising HDL cholesterol.
  5. Being weight neutral or associated with modest weight loss and not causing hypoglycemia (no risk of severe hypoglycemia when used alone).
118
Q

What are the additional benefits of metformin beyond glucose control?

A

Metformin is associated with a mortality benefit, reducing all-cause mortality, diabetes-related mortality, and the risk of myocardial infarction.

119
Q

Why is metformin indicated as a first-line treatment for type 2 diabetes?

A

Metformin is indicated as a first-line treatment for type 2 diabetes due to its beneficial effects, including its ability to improve insulin sensitivity, lower glucose production, and manage lipid levels. Additionally, it does not enhance lipogenesis (unlike insulin) and is unlikely to cause hypoglycemia.

120
Q

What is the initial dosing regimen for metformin?

A

The initial dosing regimen for metformin is 500 mg once or twice daily, or 850 mg once or twice daily, taken with meals.

121
Q

How should the dose of metformin be adjusted over time?

A

The dose should be increased every 5-7 days, up to a maximum of 2000 mg/day, based on gastrointestinal (GIT) side effects.

122
Q

What is the preferred formulation of metformin for patients with severe GIT side effects?

A

The extended-release formulation of metformin is preferred for patients with severe GIT side effects.

123
Q

What is the recommended maximum dose of metformin for patients with an eGFR < 45?

A

For patients with an eGFR < 45, the maximum recommended dose of metformin is 500 mg twice daily, with careful consideration of the risk-benefit ratio.

124
Q

What is the dosing recommendation for metformin in patients with an eGFR < 30?

A

Metformin is contraindicated in patients with an eGFR < 30.

125
Q

What should be considered when prescribing metformin in combination with dolutegravir?

A

When metformin is used with dolutegravir, the maximum recommended dose of metformin is 500 mg twice daily.

126
Q

What are the common gastrointestinal (GIT) side effects of metformin, and how prevalent are they?

A

Common GIT side effects of metformin include diarrhea, nausea, vomiting, cramping, and bloating. These effects occur in 20-30% of patients and are not dose-dependent.

127
Q

How can the tolerability of metformin be improved for patients with gastrointestinal side effects?

A

Switching to the extended-release formulation of metformin can improve gastrointestinal tolerability.

128
Q

How common is lactic acidosis with metformin use, and in which patients is it a greater concern?

A

Lactic acidosis is rare with metformin use. It is of greater concern in patients at very high risk, including those with severe heart, lung, liver, renal (eGFR < 30), or peripheral vascular disease. The condition may be due to the inhibition of gluconeogenesis, leading to increased lactate levels.

129
Q

What is the potential effect of metformin on vitamin B12 levels, and how should this be monitored?

A

Metformin can cause vitamin B12 deficiency in 7-30% of long-term users, though the exact mechanism is not known. Vitamin B12 levels should be checked if patients present with peripheral neuropathy or anemia

130
Q

What are the weight and hypoglycemia effects of metformin?

A

Metformin is weight neutral and does not cause hypoglycemia.

131
Q

What is the primary mechanism of action of sulphonylureas?

A

ulphonylureas stimulate insulin secretion from pancreatic beta cells by binding to the sulphonylurea receptor on the ATP-sensitive potassium (KATP) channel on pancreatic beta cells, leading to membrane depolarization, calcium influx, and exocytosis of stored insulin.

132
Q

What additional actions do sulphonylureas have beyond stimulating insulin secretion?

A

Beyond stimulating insulin secretion, sulphonylureas:

  • Increase peripheral insulin sensitivity
  • Reduce glucagon release
133
Q

Why do sulphonylureas require residual beta cell function to be effective?

A

Sulphonylureas require residual beta cell function because their mechanism of action relies on stimulating insulin secretion from functioning beta cells.

134
Q

How do sulphonylureas affect insulin release in relation to blood glucose levels?

A

Sulphonylureas cause insulin release regardless of blood glucose levels, meaning they stimulate insulin secretion even when blood glucose is normal or low

135
Q

How do sulphonylureas interact with the ATP-sensitive potassium (KATP) channel on pancreatic beta cells?

A

Sulphonylureas bind to the sulphonylurea receptor on the KATP channel, causing the channel to close. This leads to membrane depolarization, calcium influx, and the exocytosis of stored insulin

136
Q

What is the initial dosing and maximum dose for glimepiride?

A

For glimepiride:

Initial dose: 1 mg daily

Titrate: Increase by 1 mg increments at weekly intervals

Maximum dose: 4 mg daily

137
Q

How should glibenclamide be dosed, and what is the maximum daily dose?

A

For glibenclamide:

Initial dose: 2.5 mg daily

Titrate: Increase weekly to a maximum of 15 mg daily

Doses ≥10 mg per day: Should be divided into multiple doses

138
Q

What is the dosing regimen for gliclazide, including the modified-release (MR) formulation?

A

For gliclazide:

Regular formulation: 40-80 mg daily orally, adjusted according to response, with a maximum of 320 mg/day in divided doses

Modified-release (MR) formulation: 30 mg once daily, increased monthly according to response, with a maximum of 120 mg/day

139
Q

What are the cautions associated with sulphonylureas in terms of renal and hepatic impairment, and pregnancy?

A

Sulphonylureas should be used with caution:

Renal impairment: Avoid in patients with eGFR < 60

Hepatic impairment: Contraindicated in severe hepatic impairment

Pregnancy: Contraindicated during pregnancy

140
Q

What is the risk of severe hypoglycemia with sulphonylureas?

A

Severe hypoglycemia occurs in 0.2-0.4 cases per 1000 patient-years with sulphonylureas.

141
Q

What are the risk factors for hypoglycemia in patients taking sulphonylureas?

A

Risk factors for hypoglycemia with sulphonylureas include:

Renal impairment
Elderly patients
Irregular meal schedule
Combination therapy with insulin

142
Q

What is a common non-hypoglycemic adverse effect of sulphonylureas?

A

A common non-hypoglycemic adverse effect of sulphonylureas is weight gain.

Therapeutics (15 decks)

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