NU 237 · NursingSection 5.8 · Digestive and endocrine disorders
Section 24 of 25
Diabetes mellitus and pancreatic islet tumours
Explain how the islets of Langerhans control blood glucose, how type 1, type 2 and gestational diabetes differ in cause, onset and treatment, how diabetes is diagnosed and how it damages the body, and what an insulinoma does — then apply this to recognising hyperglycaemia and hypoglycaemia at the bedside.
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Why this matters
Diabetes is one of the few diseases a nurse manages on every single shift, and almost every decision in that management comes down to one question: is the glucose too high or too low right now? The same insulin that keeps a patient well can make them unconscious within an hour if the dose, the meal and the activity do not match, and the same hyperglycaemia that looks harmless on a chart is quietly destroying retina, nerve and kidney over ten years. Once you can explain why a type 1 patient has no insulin at all while a type 2 patient has plenty of insulin that no longer works, the symptoms, the drugs and the teaching you give become predictable instead of memorised. This section also shows the opposite error: the islet tumour that pours out insulin and drives the glucose down.
What you need to know first
You need only everyday ideas: that food is turned into a sugar called glucose, that a hormone called insulin moves that glucose into cells, and that the pancreas lies behind the stomach. Insulin, beta cell, islet and insulin resistance are all defined below, so no previous endocrinology course is assumed.
Words to know (5)
Insulin
The hormone made by the beta cells of the pancreatic islets that moves glucose out of the blood and into cells, where it is used for energy or stored. After a meal, insulin rises so that glucose leaves the blood instead of accumulating in it.
Beta cell
The insulin-producing cell of the islet of Langerhans; when beta cells are destroyed, or cannot keep up with demand, diabetes appears. In type 1 diabetes the beta cells are destroyed, so no insulin can be made at all.
Insulin resistance
A state in which muscle, fat and liver cells respond poorly to insulin, so the pancreas must produce much more of it to move the same amount of glucose. A patient with visceral obesity may have a high insulin level and still a high glucose.
Hyperglycaemia and hypoglycaemia
Blood glucose above and below the normal range; a high glucose pulls water into the urine and damages vessels over years, while a low glucose starves the brain within minutes. A glucose of 2.6 mmol/L causes sweating and confusion, while 26 mmol/L causes thirst and heavy urination.
Insulinoma
An islet-cell tumour that secretes insulin when the body does not need it, so glucose is driven out of the blood and the brain is starved of fuel. A patient with an insulinoma may become confused before breakfast and recover within minutes of eating.
One idea at a timeIdea 1 / 7
In one sentence Insulin, released by the beta cells of the pancreatic islets, moves glucose out of the blood and into cells; diabetes is what happens when that movement fails.
The islets of Langerhans make the insulin that lets glucose into cells
Food is broken down into glucose, the body’s main energy supply. The pancreas contains the islets of Langerhans, small nests of cells that release their hormones straight into the bloodstream and therefore belong to the endocrine system. The beta cells of those islets make insulin, the hormone that lets glucose leave the blood and enter muscle, fat and liver cells, where it is burned for energy or stored.
Diabetes mellitus is the metabolic disorder that appears when this arrangement fails: glucose stays chronically high in the blood while the cells that need it are starved.
The old name describes the sign rather than the cause — mellitus means honey-sweet and refers to the sugar passed in the urine. What matters clinically is that the problem is never the sugar by itself but the missing or ineffective insulin, because every symptom and every treatment follows from that single fact.
For example
After a meal the glucose rises, the beta cells release insulin, glucose enters the cells and the blood level falls back. When insulin is missing, the same meal leaves the glucose high.
Pause and check yourself
In one sentence, what does insulin do, and what goes wrong in diabetes?
Show the answer
Insulin moves glucose from the blood into cells; in diabetes the insulin is missing or ineffective, so glucose accumulates in the blood while the cells are starved.
Read detailed explanations
Osmotic diuresis and the two hyperglycaemic crises
Glucose is freely filtered at the glomerulus, and the proximal tubule normally reclaims all of it. That reclamation has a ceiling: once the filtered load exceeds the transport capacity, which corresponds to a blood glucose of roughly 10 mmol/L (180 mg/dL), the remaining glucose stays in the tubular fluid and is excreted. Because glucose is an osmotically active solute, it holds water in the urine and drags sodium and potassium with it, producing an osmotic diuresis. This single mechanism explains the classic triad: polyuria from the solute load, polydipsia as the patient replaces the water lost, and dehydration with electrolyte depletion if the glucose stays high.
Two acute syndromes follow from the same starting point but differ in the insulin that remains. In diabetic ketoacidosis, insulin is absent, so lipolysis is unrestrained and free fatty acids reach the liver faster than they can be oxidised; the liver converts them by ketogenesis into beta-hydroxybutyrate and acetoacetate, two strong organic acids. The result is a metabolic acidosis with a raised anion gap, sometimes with the glucose only moderately raised, and the patient compensates with deep, sighing Kussmaul respirations.
In the hyperosmolar hyperglycaemic state, usually in older patients with type 2 diabetes, enough insulin remains to suppress ketogenesis but not enough to control the glucose, so values above 30 mmol/L (540 mg/dL) develop with extreme hyperosmolality, profound dehydration and altered consciousness, and the mortality is higher than in ketoacidosis.
Both are precipitated by something else — a chest or urinary infection, myocardial infarction, stroke, steroids or missed treatment — so the nurse treats the glucose while hunting the trigger. Fluids come first, insulin follows, and potassium is monitored closely because insulin shifts it into cells and can cause a fatal fall.
Hypoglycaemia: the counter-regulatory response and the Rule of 15
A falling glucose is a threat to the brain, which cannot store fuel, so the body defends itself with a counter-regulatory response. Glucose sensors detect the fall and the alpha cells release glucagon, which tells the liver to break down glycogen and to manufacture new glucose; at the same time the sympathoadrenal system releases epinephrine, which produces the early warning signs — sweating, tremor, palpitations, hunger and anxiety. When the fall continues, the brain itself is affected and the symptoms change to confusion, drowsiness, slurred speech, abnormal behaviour, seizures and coma. These neuroglycopenic features are the dangerous ones, because a patient who is confused may be mistaken for drunk, tired or mentally unwell instead of hypoglycaemic. In long-standing type 1 diabetes the glucagon and epinephrine responses become blunted, so the early warning signs disappear; this is hypoglycaemia unawareness, and it removes the very safety system that usually prompts the patient to eat.
Hypoglycaemia is generally defined below 4.0 mmol/L and is treated with the Rule of 15: give 15 to 20 grams of fast-acting carbohydrate, wait 15 minutes, recheck the glucose, and repeat until it is above 4.0 mmol/L, then give a longer-acting carbohydrate with protein to prevent recurrence. A patient who is unconscious is never given anything by mouth, because of the risk of aspiration; treatment is intravenous glucose or intramuscular glucagon.
Two patterns are often confused at the bedside. The Somogyi effect is rebound hyperglycaemia after unrecognised nocturnal hypoglycaemia, while the dawn phenomenon is a morning rise driven by growth hormone and cortisol. Distinguishing them matters because one calls for less evening insulin and the other for more, so the nurse reviews the overnight glucose pattern and the cause of each episode — a missed meal, unusual exercise or the wrong dose.
Insulinoma: the Whipple triad and the supervised fast
An insulinoma is a tumour of the beta cells that secretes insulin independently of the blood glucose. The clinical problem is not a high glucose but a low one, and the classic description is the Whipple triad: symptoms consistent with hypoglycaemia, a documented low plasma glucose at the time of the symptoms, and relief of the symptoms when the glucose is raised. All three parts must be present, because each one alone is misleading; a patient who feels better after eating may simply have skipped lunch. An oral glucose tolerance test is not the diagnostic starting point for suspected insulinoma. If a spontaneous hypoglycaemic episode cannot be sampled, a supervised fast of up to 72 hours in hospital may be used, with glucose, insulin, C-peptide and proinsulin measured at the moment the patient becomes symptomatic and the glucose falls.
The interpretation is the key step. During documented hypoglycaemia, inappropriately unsuppressed insulin with C-peptide and proinsulin supports endogenous hyperinsulinism. This does not by itself prove an insulinoma: insulin secretagogues such as sulfonylureas must be excluded by drug testing and clinical assessment. By contrast, a patient who has injected too much insulin has a high insulin level with a suppressed C-peptide, because injected insulin does not come with C-peptide.
Once the biochemistry is confirmed, imaging — computed tomography, magnetic resonance imaging or endoscopic ultrasound — is used to locate the tumour before surgery, though small tumours can be missed. Treatment is surgical, by enucleation of a single lesion or by distal pancreatectomy when the tail and part of the body must be removed.
After surgery the nurse watches for two opposite problems: transient hyperglycaemia while the remaining beta cells adjust, and persisting hypoglycaemia if tumour tissue remains. Non-functioning islet tumours belong to the same family and are managed for their size and pressure effects rather than for hormone excess.
Explore the diagram
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Insulin, its failure and its excess
Insulin is the link between the blood and the cell. At the top, the normal route: the beta cells of the islet of Langerhans release insulin, and glucose leaves the blood to enter the cells. Below it, the two ways that link breaks — no insulin in type 1, ineffective insulin in type 2 — and the tumour that adds too much insulin instead of too little.
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01 / 5Islet of Langerhans: the beta cell and insulin
If the drawing is wider than this panel, scroll it sideways. Labels stay readable; the numbered explanations below show the same ideas.
Islet of Langerhans: the beta cell and insulin
The islets are small nests of endocrine cells scattered through the pancreas, and they release their hormones straight into the blood rather than into a duct. Their beta cells make insulin. It promotes glucose uptake in muscle and fat, supports energy storage and reduces glucose production by the liver. Losing beta cells therefore disrupts glucose regulation and raises blood glucose; it does not stop glucose entering every tissue.
Schematic comparison, not anatomical: the pancreas is not drawn and the cells are represented as boxes. The two diabetes types are separated for clarity, although real patients may have features of both, and raised glucose first recognised in pregnancy requires classification before treatment.
Key points to remember
✓The islets of Langerhans release insulin from their beta cells; insulin moves glucose from blood into cells, and diabetes mellitus is chronic hyperglycaemia caused by insulin that is missing or ineffective.
✓Type 1 is an autoimmune destruction of the beta cells by T lymphocytes and macrophages, causing absolute insulin deficiency, fast onset, weight loss, thirst and heavy urination, and a lifelong need for insulin.
✓Type 2 combines insulin resistance with a beta-cell output that cannot keep up; it makes up 80 to 90% of cases, is linked to visceral obesity, hypertension, dyslipidaemia, family history and inactivity, and has a slow, often silent onset.
✓Diagnosis uses a fasting plasma glucose of 7.0 mmol/L (126 mg/dL) or more, a two-hour post-load value of 11.1 mmol/L (200 mg/dL) or more, or a random value of 11.1 mmol/L with classic symptoms.
✓Long-standing hyperglycaemia causes retinopathy, neuropathy and nephropathy, treatment can cause hypoglycaemia, and an insulinoma does the opposite of diabetes by pouring out insulin and driving the glucose down.
Go deeper
Worked example
A 55-year-old man with a foot ulcer and a glucose of 18 mmol/L. A 55-year-old man comes to the clinic with a small ulcer on his right foot that has not healed for three weeks. He mentions that for several months he has been drinking and passing urine much more than usual, and that he has lost four kilograms without trying. He weighs 104 kg, his waist is large and his blood pressure is 152/92 mmHg. A random plasma glucose is 18 mmol/L (324 mg/dL), and the urine dipstick is positive for glucose and negative for ketones.
Recognise the hyperglycaemic picture. Thirst, heavy urination, weight loss, an ulcer that will not heal and glucose in the urine are the classic signs of a glucose that has been high for months. The glucose is above the kidney’s reabsorption capacity, which is why sugar has spilled into the urine.
Decide which diabetes fits. A slow onset over months, visceral obesity, hypertension, older age and no ketones all point to type 2 diabetes, in which the pancreas still makes some insulin and compensates for insulin resistance until it can no longer keep up. The absence of ketones supports type 2 but never completely excludes type 1, so the whole picture is used, not one result.
Confirm the diagnosis properly. A random glucose of 18 mmol/L with thirst and polyuria is already diagnostic. If the history were less clear, the next step would be a fasting plasma glucose of 7.0 mmol/L or more, confirmed on a second occasion, or a two-hour value of 11.1 mmol/L or more on a 75 g oral glucose tolerance test.
Screen for the complications that years of high glucose have already caused. The feet are examined for protective sensation, pulses, skin changes and infection; the eyes for retinopathy; the urine for protein; and the blood pressure and lipids are recorded because they multiply the vascular risk. This ulcer is not a small local problem but the visible end of a systemic process.
Plan the nursing care around what the patient must do at home. Teaching covers blood glucose monitoring and when to check, food choices and portion sizes rather than forbidden foods, the correct timing and technique of the prescribed medicines, daily foot inspection, and the signs of both hyperglycaemia and hypoglycaemia with what to do about each. The plan is negotiated, because a diet and injection schedule he cannot follow will fail no matter how right the prescription is.
The ulcer is not the disease; it is the visible end of a process that began years earlier, when insulin resistance started to raise a glucose nobody was measuring. The glucose result tells you the diagnosis, but the examination tells you the cost: feet, eyes, kidneys, vessels and blood pressure all have to be assessed together, because they fail at the same time and for the same reason. The nurse’s job is to confirm the picture with the right tests, treat the foot without delay, and then build a management plan the patient can actually carry out, since the complications that matter are prevented over years, not in one consultation.
Common misconception
Many beginners believe that diabetes is caused by eating sugar and can be cured by cutting it out. Blood glucose is controlled by insulin, not by willpower over a sweet tooth: type 1 destroys the beta cells, type 2 combines insulin resistance with a failing insulin supply, and neither is caused by a single food. Avoiding sugar may improve the numbers for a while, but it does not restore insulin secretion, so a person with type 1 can never stop insulin and a person with type 2 still needs monitoring, medication and follow-up. The opposite mistake is just as common: because a low glucose is treated with sugar, patients sometimes assume that sweets are a medicine and take them when the glucose is high.
Check your reasoning
Two patients arrive with a glucose of 20 mmol/L. One is a thin 19-year-old who has been vomiting and is breathing deeply and rapidly; the other is a 68-year-old with a chest infection, profound thirst and no vomiting. Using the mechanisms in this section, explain why these two are not managed in the same way.
Reveal an answer
The young patient has almost no insulin, so the brake on fat breakdown is gone: free fatty acids are converted into ketone acids and the picture is diabetic ketoacidosis, with a raised anion gap, deep sighing breathing and vomiting. The older patient still makes enough insulin to suppress ketone production but not enough to control the glucose, so the glucose climbs much higher and the dominant problem is extreme dehydration and hyperosmolality without significant ketones. Both need fluids first, then insulin, and both need potassium watched closely and the precipitating cause found — here the chest infection — but the ketoacidotic patient needs acid and ketone monitoring that the other does not.
Where this comes from
Endocrine Disorders lecture notes (supplied), Level 200 nursing · “Pancreatic islet tumors”, lines 788–835: the islets of Langerhans as endocrine tissue, insulinoma and non-functioning islet cell cancer, hypoglycaemia with weakness, mental confusion and seizures, the notes’ five-hour glucose tolerance test (corrected below), surgical removal with pancreatectomy and glucose administration, and the pre- and post-operative nursing priorities; “Diabetes Mellitus (DM)”, lines 837–987: the definition of diabetes mellitus, type 1 and type 2 features, gestational diabetes, diagnostic glucose values, the autoimmune and insulin-resistance pathophysiology, treatment for each type, complications and nursing intervention.
Beyond the supplied notes: corrections and standard diabetes knowledge · the notes state that type 1 occurs “in about 10% of the population”; this is corrected to roughly 5 to 10% of all people with diabetes. The notes require a fasting plasma glucose of 126 mg/dL “on three different tests”; standard practice confirms an abnormal fasting value on a second occasion and accepts a single value when classic symptoms are present. The notes describe an amylin analogue that “causes glucose to enter the bloodstream slowly”; amylin analogues slow gastric emptying and blunt the post-meal glucose rise. The ketosis-prone presentation of type 1, diabetic ketoacidosis and the hyperosmolar hyperglycaemic state, the anion gap, Kussmaul respirations, HbA1c, the Rule of 15 for hypoglycaemia, the Somogyi effect and the dawn phenomenon, and the Whipple triad, C-peptide and 72-hour fast for insulinoma are standard knowledge added because the supplied notes do not cover them.
WHO pregnancy hyperglycaemia classification and NICE NG3 diabetes in pregnancy · correction of the blanket gestational-diabetes definition and oral-drug avoidance. WHO distinguishes gestational diabetes from overt diabetes first detected in pregnancy; NICE NG3 recommendations 1.2.18–1.2.22 allow metformin and specify insulin indications. https://www.ncbi.nlm.nih.gov/books/NBK169020/ ; https://www.nice.org.uk/guidance/ng3/chapter/recommendations
Endocrine Society — Evaluation and Management of Adult Hypoglycemic Disorders · correction of the five-hour oral glucose tolerance test for suspected insulinoma. Diagnose endogenous hyperinsulinism using samples during hypoglycaemia, with a medically supervised fast up to 72 hours when needed, and exclude insulin secretagogues before attributing it to insulinoma. https://academic.oup.com/jcem/article/94/3/709/2596247
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About this course and its sources
The urinary and endocrine lessons build on the supplied Level 200 nursing notes (course instructor Bakume Jessey). Disease mechanisms, blood, lymphatic, cardiovascular and digestive lessons use cited external references. Diagrams are original educational schematics. Sections that go beyond the supplied notes say so in their sources. Specialist clinical and French-language editorial review remain pending.