CSB601 Chap.8 Diabetes Pharmacotherapy and Adherence
Diabetes Pharmacotherapy and Adherence
Mechanism decides the medicine
This chapter follows the Week 6 diabetes material. Type 1 diabetes is absolute insulin deficiency and needs basal and bolus insulin replacement; type 2 combines insulin resistance with progressive beta-cell failure and is managed stepwise, starting with metformin.
Each add-on class acts on a different defect, from urinary glucose loss to incretin signalling and glucose-independent insulin release.
Harm and adherence shape the plan
Choice is never driven by glucose alone.
Cardiovascular disease, heart failure, kidney disease, weight and hypoglycaemia risk all move particular classes forward or back, and a regimen only works if the person can take it consistently alongside diet and activity changes.
What this chapter covers
- 01
Type 1 Versus Type 2 Defects
- 02
Metformin as First-Line Therapy
- 03
Incretin and SGLT2 Mechanisms
- 04
Sulfonylureas and Hypoglycaemia Risk
- 05
Comorbidity-Led Add-On Choice
- 06
Adherence Barriers and Interventions
Worked example · free
Rising readings after a lifestyle lapse
- 2Adherence: ask about missed, extra or irregular doses since the roster change, then about diet and activity; both drug and non-drug factors can raise readings without any drug failing.
- 2Lifestyle: diet, physical activity and weight management improve insulin sensitivity, so a diabetes educator plan for shift work is part of treatment.
- 2Add-on: with chronic kidney disease, an SGLT2 inhibitor is prioritised because it lowers glucose and reduces cardiovascular and renal risk.
Key terms
- Basal-Bolus Regimen
- An insulin plan pairing a long-acting basal insulin for fasting glucose with mealtime bolus insulin for postprandial glucose.
- Relative Insulin Deficiency
- The type 2 state in which insulin is still produced but is insufficient for the degree of insulin resistance.
- Incretin
- A gut hormone signal that raises glucose-dependent insulin secretion, the pathway used by GLP-1 agonists and DPP-4 inhibitors.
- Hepatic Glucose Output
- Glucose released by the liver, which metformin reduces and which drives high fasting glucose in type 2 diabetes.
Diabetes Pharmacotherapy and Adherence FAQ
Why does a sulfonylurea cause hypoglycaemia when metformin alone does not?
Sulfonylureas stimulate insulin secretion regardless of the blood glucose level, so a missed meal or extra exercise leaves insulin working with little glucose available. Metformin reduces liver glucose production and improves sensitivity without forcing insulin release.
In older adults, guidance on medicines to use with caution names gliclazide, glipizide and glibenclamide for exactly this reason, so a falls or confusion history should prompt a review.
Which diabetes medicines are linked with weight loss and which with weight gain?
The pre-workshop reading links GLP-1 receptor agonists with weight loss and cardiovascular benefit. Sulfonylureas are linked with weight gain alongside their hypoglycaemia risk, which matters for patients already above a healthy weight. DPP-4 inhibitors give modest glucose lowering with a low hypoglycaemia risk, and SGLT2 inhibitors are valued mainly for cardiovascular and renal protection.
When is insulin used in type 2 diabetes?
Insulin is started once tablets and other non-insulin options no longer hold glucose at target, and it is often started as a basal insulin. In type 1 diabetes, by contrast, insulin is needed from diagnosis for survival. Whatever the type, insulin dosing has to match food intake, physical activity and illness, and hypoglycaemia is the main risk to counsel on.
Why is HbA1c monitored as well as finger-prick readings?
The reading lists blood glucose, HbA1c and ketones as monitoring tools, and study guide cases ask you to interpret both. Treat HbA1c as a separate measure of control alongside the meter readings. When a question supplies a target, use that figure in your answer. Ketone testing is added when indicated, which the reading discusses under insulin replacement in type 1 diabetes.
Exam move
Start with a one-page map of glucose regulation: beta-cell secretion, insulin action in liver, muscle and fat, and hepatic glucose output. Place each drug class on the organ it targets and write its mechanism in five words or fewer. Next, build a comparison grid of hypoglycaemia risk, weight effect and organ benefit, filling only the cells you can support from the reading, so you notice where a claim would be unsupported.
Practise two classic explanations aloud: why type 1 needs insulin from the start, and why metformin alone does not cause hypoglycaemia. For adherence, list drug factors and non-drug factors in separate columns for any case you meet, then attach one intervention and one team member to each. Finish with short cases where the comorbidity, not the glucose reading, decides the add-on.
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