Diabetes drugs & NICE pathways flashcards
27 high-yield MRCP Part 1 cards from the Intellect Medicos Endocrinology & Diabetes course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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Under the 2026 NICE NG28 update, what is first-line drug treatment for type 2 diabetes with no relevant comorbidities?
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Modified-release metformin AND an SGLT-2 inhibitor.
Why? SGLT-2 inhibitors add cardiovascular and renal protection. If metformin is contraindicated or not tolerated, offer an SGLT-2 inhibitor alone.
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Why does NICE now recommend modified-release rather than standard-release metformin?
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Similar glucose-lowering with fewer gastrointestinal side effects (and possibly better adherence).
Why? Standard-release can still be used if the person needs to crush tablets or use a liquid, or already tolerates it.
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In type 2 diabetes with no comorbidities, which drug class does NICE add next if metformin plus an SGLT-2 inhibitor is not enough?
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A DPP-4 inhibitor.
Why? If that is not tolerated or not effective, use a sulfonylurea, pioglitazone or insulin-based treatment.
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Which additional drug does NICE offer from the start for type 2 diabetes with established atherosclerotic cardiovascular disease?
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Subcutaneous semaglutide once weekly (up to 1 mg), with MR metformin and an SGLT-2 inhibitor.
Why? Semaglutide has proven cardiovascular benefit; tirzepatide lacked evidence in this group.
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What does NICE offer for type 2 diabetes with CKD and eGFR 20–30 mL/min/1.73m²?
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Dapagliflozin or empagliflozin plus a DPP-4 inhibitor.
Why? Metformin is not started below eGFR 30. Below eGFR 20, consider a DPP-4 inhibitor alone, then pioglitazone or insulin.
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In type 2 diabetes with obesity, what does NICE consider as the first additional treatment if metformin plus an SGLT-2 inhibitor is not enough?
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A GLP-1 receptor agonist or tirzepatide.
Why? Add it after at least 3 months of initial therapy if more glucose lowering is needed. If these are unsuitable, add a DPP-4 inhibitor instead.
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For early-onset type 2 diabetes (diagnosed before age 40), what does NICE suggest considering alongside metformin and an SGLT-2 inhibitor from the start?
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A GLP-1 receptor agonist or tirzepatide.
Why? Early-onset type 2 diabetes is aggressive, with high lifetime complication risk.
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A frail older person with type 2 diabetes cannot take metformin, and their frailty puts them at risk from an SGLT-2 inhibitor. What does NICE suggest instead?
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DPP-4 inhibitor monotherapy.
Why? In frailty NICE offers modified-release metformin, and an SGLT-2 inhibitor only if frailty does not put the person at risk (e.g. volume depletion, hypotension). A DPP-4 inhibitor is also the first add-on if more treatment is needed.
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In type 2 diabetes on an initial regimen that does not cause hypoglycaemia (e.g. metformin plus an SGLT-2 inhibitor), what HbA1c target applies, and at what level is treatment intensified?
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Target 48 mmol/mol (6.5%); intensify if it rises to 58 mmol/mol (7.5%) or higher, then aim for 53 mmol/mol (7.0%).
Why? If the person takes a medicine that can cause hypoglycaemia (e.g. a sulfonylurea), the target is 53 mmol/mol (7.0%). Targets are agreed individually and may be relaxed in older or frail people.
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What is the main mechanism of action of metformin?
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It reduces hepatic gluconeogenesis and increases insulin sensitivity.
Why? It does not stimulate insulin release, so it does not cause hypoglycaemia or weight gain.
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Which vitamin deficiency is linked to long-term metformin use?
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Vitamin B12 deficiency.
Why? The MHRA (2022) advises testing B12 if deficiency is suspected (e.g. new neuropathy or megaloblastic anaemia) and considering periodic monitoring in people with risk factors.
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Below which eGFR should metformin not be used?
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eGFR below 30 mL/min/1.73m² (reduce the dose if below 45).
Why? Metformin is renally cleared; accumulation increases lactic acidosis risk. It should also be withheld in sepsis, dehydration and acute hypoxic states.
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What is the mechanism of action of sulfonylureas?
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They close ATP-sensitive potassium channels on beta cells, causing depolarisation and insulin release.
Why? They are insulin secretagogues, so they work only if beta cells still function.
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What are the two commonest adverse effects of sulfonylureas?
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Hypoglycaemia (worse with long-acting agents) and weight gain.
Why? Rarer effects include SIADH, cholestatic liver injury, bone marrow suppression and haemolysis in G6PD deficiency.
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What is the mechanism of action of pioglitazone?
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PPAR-gamma agonist, reducing peripheral insulin resistance.
Why? It increases insulin sensitivity in fat and muscle.
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In which cardiac condition is pioglitazone contraindicated, and why?
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Heart failure — it causes fluid retention.
Why? Fluid retention occurs in about 10% and is worse with insulin. Other effects include weight gain and fractures.
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Which cancer is associated with pioglitazone?
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Bladder cancer.
Why? Avoid it in active or previous bladder cancer and in uninvestigated haematuria.
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How do GLP-1 receptor agonists (e.g. semaglutide, liraglutide) lower glucose?
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They increase glucose-dependent insulin secretion, suppress glucagon, slow gastric emptying and reduce appetite.
Why? They usually cause weight loss and carry a low hypoglycaemia risk on their own.
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Which serious adverse effect of GLP-1 receptor agonists should prompt stopping the drug if severe abdominal pain occurs?
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Acute pancreatitis.
Why? GI side effects (nausea, vomiting, diarrhoea) are common.
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According to the MHRA (2025), what contraceptive advice applies to women starting tirzepatide?
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Use a non-oral method (or add a barrier method) for 4 weeks after starting and after each dose increase.
Why? Tirzepatide may reduce oral contraceptive absorption in people living with overweight or obesity. GLP-1 medicines should not be used in pregnancy or breastfeeding; stop tirzepatide at least 1 month before trying to conceive.
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What is the mechanism of action of DPP-4 inhibitors (gliptins)?
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They block breakdown of endogenous incretins (GLP-1 and GIP), increasing insulin and reducing glucagon.
Why? They are oral, weight-neutral and low risk for hypoglycaemia — useful in older people or those at risk from hypos.
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What is the mechanism of action of SGLT-2 inhibitors (gliflozins)?
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They inhibit the sodium–glucose co-transporter 2 in the proximal convoluted tubule, causing glycosuria.
Why? Effects: weight loss, lower blood pressure (sodium loss) and cardiovascular and renal benefit.
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A man with type 2 diabetes on dapagliflozin is unwell with vomiting after surgery. Glucose is 9 mmol/L, pH 7.15 and blood ketones 5.2 mmol/L. What is the diagnosis?
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Euglycaemic diabetic ketoacidosis caused by the SGLT-2 inhibitor.
Why? Glycosuria keeps glucose near normal while ketones rise. Interrupt SGLT-2 inhibitors during acute serious illness and around major surgery, check blood ketones, and restart once ketones are normal and the patient is stable.
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Which rare but serious genital infection has the MHRA linked to SGLT-2 inhibitors?
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Fournier's gangrene (necrotising fasciitis of the perineum).
Why? Glycosuria predisposes to urinary and genital infections, which are common.
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How does insulin glargine achieve its long, flat action profile?
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It precipitates in subcutaneous tissue and is slowly released.
Why? Detemir prolongs action by binding albumin; degludec forms multi-hexamer chains. Long-acting analogues cause less nocturnal hypoglycaemia than NPH (isophane).
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What is the standard insulin regimen for type 1 diabetes?
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Basal–bolus (multiple daily injections): long-acting basal insulin plus rapid-acting insulin with meals.
Why? It best mimics physiological insulin secretion and allows flexible dosing. Twice-daily premixed is less flexible with more hypoglycaemia.
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During Ramadan, how should a patient split their metformin dose?
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One-third before sunrise (suhoor) and two-thirds after sunset (iftar).
Why? The larger dose goes with the larger meal. Pioglitazone needs no dose change; once-daily sulfonylureas are taken after sunset.
More Endocrinology & Diabetes topics
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- Cushing's & adrenal insufficiency
- Aldosterone, CAH & phaeochromocytoma
- Thyroid physiology, TFTs & hypothyroidism
- Hyperthyroidism & thyroid cancer
- Pituitary: prolactin, GH & hypopituitarism
- Reproductive endocrinology
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- DKA, HHS & hypoglycaemia
- Calcium, parathyroid & MEN
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