Exam 2 · Week 6 · Standalone study page
M6 · Diabetes
This page keeps all of the original course information, while reducing the decision to one module: glucose emergencies, insulin and complication prevention.
▸M6DiabetesWeek 6
💡 The one idea
Hypoglycemia kills in minutes. Hyperglycemia kills over hours. When a diabetic patient changes behavior, confusion or shakiness, check the glucose first — treat low before high.
⭐ The Rule of 15
15 g of fast carbohydrate → wait 15 minutes → recheck. Repeat until above 70, then give a snack with protein.
15 g looks like: 4 oz juice 3 glucose tabs 1 tbsp honey
If the patient is unconscious or cannot swallow, nothing goes in the mouth. IM glucagon or IV dextrose.
| DKA | HHS / HHNS | |
|---|---|---|
| Diabetes type | Usually type 1 | Usually type 2 |
| Onset | Hours to a day — fast | Days to weeks — slow |
| Glucose | >250 | >600, often far higher |
| Ketones | Present — large | Absent / minimal |
| pH | <7.35 acidotic | Normal |
| Breathing | Kussmaul, fruity breath | Normal |
| Mental state | Alert → drowsy | Profound confusion, seizures |
| Mortality | Lower | Higher |
💧 Treatment order — identical for both
Fluids come before insulin. Insulin drives potassium into cells and can drop it dangerously.
Add dextrose once glucose reaches ~250 so the drip can continue clearing ketones without going hypoglycemic.
| Insulin | Onset | Peak | Duration |
|---|---|---|---|
| Lispro / aspart (rapid) | 15 min | 1 h | 3–4 h |
| Regular (short) | 30 min | 2–3 h | 5–8 h |
| NPH (intermediate) | 1–2 h | 4–12 h | 12–18 h |
| Glargine (long) | 1–2 h | No peak | ~24 h |
Peak time is when hypoglycemia happens. That is the only reason the exam asks you to memorize these. Glargine is never mixed with another insulin. When mixing NPH and regular: clear before cloudy.
⭐ High-yield — what the exam actually asks
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- Type 1: autoimmune beta-cell destruction, absolute deficiency, thinner, younger, prone to DKA. Type 2: insulin resistance, obesity-associated, prone to HHS.
- Insulin: rapid (lispro, aspart)
15 minbefore meals, onset ~15 min, peak1–3 hr— watch for hypoglycemia at the peak. Regular is the only IV insulin. Long-acting (glargine, detemir) has no peak and is never mixed. - Rapid-acting may be mixed with intermediate (NPH). Nothing mixes with glargine.
- Metformin cuts hepatic glucose production; GI upset, rare lactic acidosis. Sulfonylureas (glipizide) cause hypoglycemia.
- Hypoglycemia, conscious:
15 gfast carb, recheck in15 min. Unconscious: glucagon or IV dextrose. Signs: shaky, sweaty, tachycardic, confused, headache.
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- DKA (Type 1): ketones positive, fruity breath, Kussmaul respirations, acidotic pH, N/V, faster onset, glucose lower than HHS. HHS (Type 2): no ketones, normal pH, no N/V, much higher glucose, slow insidious onset.
- Both crises: IV fluids first, then a regular insulin drip. Never subQ insulin in a crisis. Replace potassium.
- Sick day rules: keep taking insulin even if not eating, glucose
q2–4 hr, ketones if Type 1, hydrate, call if glucose>250and not falling or if ill more than 2 days. - A1C goal
<7%(ideal 6.5%); non-diabetic ~5.6–5.7%. Rotate injection sites or lipodystrophy wrecks absorption. - Complications: microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (CAD, stroke, PAD).
🎧 From the LSC exam-prep recording
What the faculty actually said in the review session for this week — their numbers, their worked calculations, their priority rulings. On an exam, this beats the textbook.
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- DKA vs HHS as they framed it: DKA is type 1, presents within ~24 h because they are so sick, with Kussmaul breathing, fruity breath, metabolic acidosis, abdominal pain and vomiting. HHS is type 2, sits at home for days, glucose 500–800, profound dehydration, and much more prominent mental-status change — up to paralysis — with no acidosis.
- Why DKA gets the GI symptoms: no insulin → the body burns fat → the pH falls, and the gut hates a low pH. Fruity breath, Kussmaul and the acidosis all come from the same place, which is why HHS has none of them.
- In severe hyperglycemia the first assessment is dehydration — that is circulation. Ahead of a fingerstick, ahead of level of consciousness. Glucose is not part of A-B-C-D, and confusion is D.
- Complications split two ways: microvascular = eyes, kidneys, nerves (retinopathy, nephropathy, neuropathy); macrovascular = brain, heart, limbs (stroke, MI, peripheral arterial disease). Their warning: nerve damage is permanent — good control from here does not bring it back.
- Type 1 vs type 2 vs DI, their matrix: the three Ps belong to both diabetes types. DI has polyuria and polydipsia but no polyphagia — it is an ADH problem, nothing to do with glucose. Autoimmune beta-cell destruction + lifelong insulin + DKA risk = type 1. Obesity, insulin resistance, oral agents and HHS = type 2.
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- NPH is the only intermediate insulin: onset 1–2 h, peak 6–8 h → snack at 8 hours, when the hypoglycemia risk is highest. Cloudy is normal — it looks like skim milk. Roll it, never shake; insulin is a protein and briskly shaking it foams.
- Their rule for every insulin: the onset tells you when she should eat, the peak tells you when she is most likely to go low.
- Lispro and aspart work in 15 minutes → give immediately before the meal. Not 30 minutes ahead — she will be hypoglycemic before the tray arrives — and do not hold it until after she eats, and do not wait to mix it with the NPH.
- The common regimen to recognize: rapid-acting before every meal + a long-acting basal for 24-hour background insulin, because a failed pancreas makes none.
- Hypoglycemia at 58 mg/dL: awake → 4–6 oz of juice. Unconscious → 50 mL of D50 IV, or IM glucagon when there is no line, which is what EMS gives. Not water, not skim milk, not oral carbohydrate in an unconscious client.
- Their mnemonic for reading it without a glucose value: "Cool and clammy, give them candy. Dry and hot, insulin shot."
- Sliding scale is ACHS — before each of the three meals plus bedtime, four checks — and it is always regular insulin, never a long-acting one. Under 150 usually means no coverage. If a type 1 client says a dose will tank her, you may document "given 4, refused 4" — do not override her knowledge of her own body.
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- Metformin, their SATA: take it with meals (notorious for GI upset), watch for lactic acidosis — the nasty one, and the slide that called it "rare but not serious" is wrong, it is rare and serious — hold it 48 h before IV contrast, and report a persistent metallic taste. It does not drop glucose in 2–3 hours (it works on insulin resistance) and it does not cause weight gain — it tends to cause weight loss.
- Metformin carries no hypoglycemia risk — it does not make the pancreas secrete insulin. Sulfonylureas do, so they can.
- Sulfonylureas (glyburide, glipizide): hypoglycemia, weight gain, increased appetite, photosensitivity, allergic reaction — and a sulfa cross-allergy. Not hyponatremia, not constipation, not bradycardia. Their explicit advice on that item: if you cannot name the mechanism, do not pick it.
- Why sulfonylureas and insulin both cause weight gain: they drive sugar into cells, blood glucose falls, and the body answers by making her hungry.
- The diabetic plate method: 50% non-starchy vegetables and fruit, 25% lean protein, 25% grains, plus a glass of dairy. Their best meal was black bean chili with brown rice and spinach — protein, fiber, low glycemic index, no saturated fat. The cheeseburger's whole-wheat bun was bait.
- Nutrition teaching: consistent amounts of carbohydrate at regular times. Not "avoid all carbohydrates", not "only sugar-free foods", not "skip meals as long as I take my insulin." Type 1 clients can eat sugar — they cover it with insulin.
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- Sick-day rule they guarantee will be tested: keep taking your insulin and monitor frequently. Never skip it, never halve it, never take "only rapid-acting." If she cannot keep anything down at all, she comes to hospital — she is heading for DKA.
- Exercise: hold it if glucose is over 250 with ketones — exercising then pushes a near-DKA into a real one. Check before and after, carry fast-acting carbohydrate, and never skip insulin before a run.
- DKA drip set: hourly glucose · replace potassium as soon as it is normal and falling · swap to a D5-containing fluid at glucose 250 so the drop is not fast enough to cause cerebral edema · bicarbonate only if pH under 7.0. Their trend case ran K 5.8 → 4.2 → 3.5 with bicarb 12 → 16 → 20, and the answer was give potassium.
- Why the potassium moves: acidosis drives H⁺ into the cells and kicks potassium out, so they arrive hyperkalemic. Insulin then drives potassium back in — which is why a normal-and-falling K is the moment to replace it, not later.
- Diabetic neuropathy findings only: burning feet, reduced light touch, lost vibration sense in the toes, and gastroparesis (peristalsis needs nerves). Blurred vision and floaters are retinopathy; proteinuria is nephropathy.
- Calc: insulin 0.1 units/kg/hr, 165 lb = 75 kg, supplied 100 units/100 mL → 7.5, rounded to
8 mL/hr.
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- Two stem-reading rules they drilled: "indicates an understanding" means you are hunting a TRUE statement; "needs further teaching" means you are hunting a FALSE one. Write which one at the top of the whiteboard, because by option 4 your brain has flipped.
- Watch only, always, never. Medicine is rarely that absolute, so those options usually lose. And two options that say almost the same thing are usually both wrong — they cannot both be right.
⚠️ Exam traps
- Hypoglycemia outranks a very high glucose in acuity — she can lose consciousness fast.
- Ketones are the single cleanest DKA/HHS discriminator.
⚠️ What it turns into — the complication for each one
The disorder cards below run definition, causes, signs, diagnostics, management and nursing. This is the part they do not have, and it is where the exam lives: so what happens if this is missed or left? Two emergencies at the acute end and a long list of vessel damage at the chronic end. Hypoglycaemia kills faster than hyperglycaemia — treat it first, ask afterwards.
| Disorder | What it turns into |
|---|---|
| Type 1 diabetes mellitus | DKA as the first presentation or after a missed dose or an illness, hypoglycaemia from insulin, and every chronic complication below over time |
| Type 2 diabetes mellitus | HHS, and the chronic vascular disease that is often already present at diagnosis. Silent myocardial infarction, because neuropathy blunts the chest pain |
| Diabetic ketoacidosis | Cerebral edema if the glucose is dropped too fast — the reason for a controlled correction. Hypokalaemia once insulin drives potassium into the cells, causing arrhythmia. Shock and coma |
| Hyperglycemic hyperosmolar state | Extreme dehydration, thrombosis from the hyperviscosity, seizures and coma. Mortality is higher than DKA, and it creeps up over days in an older adult |
| Hypoglycemia | Seizures, coma, permanent brain injury, falls and fractures, road traffic collisions, death. Hypoglycaemia unawareness after repeated episodes removes the warning symptoms |
| Chronic complications of diabetes | Retinopathy and blindness. Nephropathy to end-stage renal disease. Neuropathy leading to foot ulcer and amputation, and gastroparesis. Coronary disease, stroke and peripheral arterial disease |
💉 Diabetes, section by section
The two types, the three acute emergencies and the long-term damage. Same six sections every time, so the part you want is always in the same place.
Type 1 Diabetes MellitusInsulin alwaysOpenClose
Definition and Overview
An autoimmune destruction of the beta cells of the pancreas, so the body makes no insulin at all. Without insulin, glucose cannot get into cells; it piles up in the blood while the cells starve and burn fat instead, producing ketones. People with type 1 need exogenous insulin to stay alive — it is not a lifestyle matter and it is never optional.
Causes and Risk Factors
Genetic susceptibility plus an environmental trigger, often a viral illness. Family history, and other autoimmune conditions in the person or the family — thyroid disease, celiac disease, Addison disease. Onset is usually before age 30 but can happen at any age.
Clinical Manifestations
The classic three: polyuria, polydipsia and polyphagia — peeing, drinking and eating — with weight loss despite eating, fatigue, blurred vision and slow healing. Onset is abrupt, often over days to weeks, and for many people the first presentation is diabetic ketoacidosis, not a routine blood test.
Assessment and Diagnostic Findings
Diagnosis on any one of: fasting glucose ≥126 mg/dL, 2-hour OGTT ≥200, A1C ≥6.5%, or a random glucose ≥200 with classic symptoms. Autoantibodies and a low C-peptide confirm type 1 rather than type 2. Ongoing: A1C every 3 months, target under 7% for most adults, self-monitored glucose or continuous glucose monitoring, annual dilated eye examination, urine albumin-to-creatinine ratio, creatinine, lipids, blood pressure and a comprehensive foot examination at every visit.
Medical Management
Insulin, matched to carbohydrate and activity. Usually a basal–bolus regimen — a long-acting basal insulin once or twice daily plus rapid-acting insulin with meals and for correction — or an insulin pump. Carbohydrate counting and an insulin-to-carbohydrate ratio. Nutrition therapy, regular activity, and treatment of blood pressure and lipids to protect the heart and kidneys.
Nursing Management and Client Education
Teach injection technique and site rotation within one area to avoid lipohypertrophy, which makes absorption erratic. The abdomen absorbs fastest, then the arm, thigh and buttock, and exercise speeds absorption from the limb being used. When mixing insulins, draw up the clear regular insulin before the cloudy NPH — and never mix or dilute a long-acting insulin such as glargine at all. Unopened insulin lives in the fridge; the vial or pen in use can stay at room temperature for about 28 days. Teach the signs of hypoglycaemia and the 15/15 rule, and to carry fast-acting carbohydrate everywhere. Teach sick-day rules: keep taking insulin even when not eating, check glucose and ketones more often, and drink fluids — stopping insulin during illness is what causes DKA. Daily foot checks with a mirror, never barefoot, and medical identification.
Type 2 Diabetes MellitusOpenClose
Definition and Overview
The body still makes insulin, but the tissues resist it and the pancreas gradually cannot make enough to overcome that resistance. Because some insulin is present, fat is not broken down the same way, so ketoacidosis is uncommon — the emergency of type 2 is the hyperosmolar state instead. It accounts for the large majority of diabetes.
Causes and Risk Factors
Overweight and obesity, especially central obesity, and physical inactivity, plus age over 35, family history, gestational diabetes or a baby over 9 lb, polycystic ovary syndrome, hypertension, dyslipidaemia, and being of African, Hispanic, Native American, Asian or Pacific Islander ancestry. Prediabetes — A1C 5.7–6.4% — is the warning stage, and it is reversible.
Clinical Manifestations
Onset is gradual and often silent for years. Fatigue, blurred vision, recurrent infections (skin, urinary, vaginal candidiasis), slow-healing wounds, numbness or tingling in the feet, and acanthosis nigricans — velvety dark skin in the neck folds and axillae. The classic polyuria and polydipsia appear later, if at all. Many people are diagnosed only when a complication — a foot ulcer, retinopathy, a heart attack — brings them in.
Assessment and Diagnostic Findings
Same diagnostic thresholds as type 1: fasting ≥126, OGTT ≥200, A1C ≥6.5%, or random ≥200 with symptoms. Screen every adult from 35, and earlier with risk factors. Monitoring is the same package — A1C, self-monitoring, annual dilated eye examination, urine albumin, renal function, lipids, blood pressure and foot examination at every visit, with monofilament testing for sensation.
Medical Management
Nutrition, weight loss and activity are first-line and remain the foundation — about 150 minutes of moderate activity a week, and a modest weight loss produces a disproportionate improvement. Metformin is usually the first drug. Then, by comorbidity, GLP-1 receptor agonists and SGLT2 inhibitors, which also protect the heart and kidneys, plus sulfonylureas, DPP-4 inhibitors and eventually insulin. Bariatric surgery for selected clients. Statins and blood pressure control are part of the diabetes treatment, not separate from it.
Nursing Management and Client Education
Teach that this is progressive — needing insulin later is the disease advancing, not a personal failure, and clients hear it as failure unless you say so. Go through drug specifics: metformin causes GI upset that settles, and is held before and for 48 hours after iodinated contrast because of lactic acidosis risk; sulfonylureas cause hypoglycaemia; SGLT2 inhibitors cause genital yeast infections and need good fluid intake; GLP-1 agonists cause nausea and are injected. Plate-method meal planning, label reading, and consistent carbohydrate. Exercise lowers glucose — check before, carry carbohydrate, and do not exercise if glucose is over 250 with ketones. Daily foot inspection, properly fitting shoes, never barefoot and never a heating pad on the feet, and a podiatrist for nails. Annual influenza and pneumococcal vaccination. Smoking cessation.
Diabetic KetoacidosisEmergencyOpenClose
Definition and Overview
An emergency of absolute insulin deficiency, so cells burn fat and the resulting ketones make the blood acidotic. The triad is hyperglycaemia, ketosis and metabolic acidosis, with an osmotic diuresis that produces profound dehydration. It is mainly a complication of type 1 and develops over hours to a day or two.
Causes and Risk Factors
Infection or another acute illness is the commonest trigger, then missed or omitted insulin (including a pump failure), a new diagnosis of type 1, surgery, trauma, myocardial infarction, pregnancy, corticosteroids and SGLT2 inhibitors — the last of which can produce DKA with a near-normal glucose.
Clinical Manifestations
Glucose usually >250 mg/dL, arterial pH <7.30, bicarbonate <18, and ketones in blood and urine. Kussmaul respirations — deep, rapid breathing blowing off CO2 — and a fruity, acetone breath. Polyuria and polydipsia, then dehydration: dry mucous membranes, poor turgor, tachycardia, hypotension. Nausea, vomiting and abdominal pain. Confusion progressing to coma. Serum potassium is often normal or high on arrival even though total body potassium is depleted — and it will crash once insulin starts.
Assessment and Diagnostic Findings
Point-of-care glucose, ABGs or venous gas, serum and urine ketones, and a full metabolic panel with the anion gap. Follow potassium hourly at the start — it is the number that will hurt the client. CBC, cultures and a chest x-ray to find the trigger, ECG for hyperkalaemia and ischemia, hourly glucose, hourly urine output, and neurological status. Watch the anion gap: the gap closing, not the glucose falling, is what tells you the DKA has resolved.
Medical Management
Three things at once. Fluids first — isotonic normal saline, large volumes, switching to half-normal saline once the pressure is restored, and to a dextrose-containing fluid when glucose reaches about 200–250 mg/dL so the infusion can continue without hypoglycaemia. A continuous IV infusion of regular insulin, the only insulin given intravenously. Potassium replacement, started before or with the insulin unless potassium is above 5.3. Bicarbonate only for severe acidosis. Treat the trigger.
Nursing Management and Client Education
Fluids, insulin and potassium — and hold the insulin if the potassium is below 3.3 mmol/L until it is replaced, because insulin drives potassium into cells and can stop the heart. Continuous cardiac monitoring while potassium is running. Hourly glucose and neurological checks; strict hourly intake and output. Bring the glucose down slowly — too fast a fall risks cerebral edema, especially in children. Keep the client nil by mouth while vomiting, and overlap subcutaneous insulin with the infusion for at least an hour before stopping the drip. Then teach, because most DKA is preventable: sick-day rules, never stopping insulin, checking ketones when glucose is over 240 or during illness, and when to call. If the trigger was cost or access, say so and get social work involved.
Hyperglycemic Hyperosmolar StateEmergencyOpenClose
Definition and Overview
The type 2 emergency. Enough insulin is present to prevent ketosis, but not enough to control glucose, so it climbs enormously — often over 600 mg/dL — and drags water out of the cells and out of the body through the kidneys. The result is extreme hyperglycaemia and profound dehydration with a very high serum osmolality, and little or no ketosis or acidosis. It develops slowly, over days to weeks, and carries a higher mortality than DKA.
Causes and Risk Factors
Typically an older adult with type 2 diabetes, often undiagnosed, who cannot get to fluids — because of dementia, immobility, a stroke or living alone. Triggered by infection (pneumonia and urinary infection most often), acute illness, corticosteroids, thiazide diuretics, dialysis, tube feeding, or new-onset diabetes.
Clinical Manifestations
Glucose over 600 mg/dL, serum osmolality over 320 mOsm/kg, pH above 7.30, bicarbonate above 18, and minimal or absent ketones. Severe dehydration: dry mucous membranes, sunken eyes, poor turgor, tachycardia, hypotension. The presentation is dominated by neurological change — confusion, lethargy, seizures, focal deficits that mimic a stroke, and coma. There is no Kussmaul breathing and no fruity breath — the absence of those does not mean the client is less sick.
Assessment and Diagnostic Findings
Glucose, serum osmolality, full metabolic panel, ABGs and ketones to distinguish it from DKA. Serum sodium needs correcting for the glucose. Look hard for the precipitating infection: cultures, chest x-ray, urinalysis. Continuous neurological assessment, hourly glucose and urine output, cardiac monitoring, and daily weight. Fluid deficits here are often 8–12 liters.
Medical Management
Fluid replacement is the priority and the mainstay — isotonic saline first, then hypotonic fluid, replacing the deficit gradually over 24–48 hours. Insulin infusion at a lower rate than in DKA, added once fluids are running, with dextrose added as glucose approaches 250–300. Potassium replacement as levels fall. Treat the precipitating illness. Prophylactic anticoagulation, because the hyperosmolar blood clots.
Nursing Management and Client Education
Correct it slowly. Dropping glucose or sodium too quickly causes cerebral edema, and this client is already neurologically impaired. Hourly neurological checks and glucose, strict intake and output, continuous cardiac monitoring, and careful listening to the lungs, since these clients are often old with cardiac or renal disease and can be tipped into fluid overload. Prevention is largely social: identify who cannot reach a drink, who lives alone, who has no one checking on them. Teach the family to offer fluids during any illness, to check glucose more often when unwell, and to call early for confusion — confusion in an older adult with diabetes is a reason to check a glucose, every time.
HypoglycemiaTreat it nowOpenClose
🖼️ InfographicsInsulin & Patient Education
Definition and Overview
A blood glucose below 70 mg/dL. It is the most common acute complication of diabetes treatment and, unlike hyperglycaemia, it can kill within minutes, because the brain has no stored fuel. Severe hypoglycaemia is any episode needing another person's help.
Causes and Risk Factors
Too much insulin or sulfonylurea, too little food, or more activity than usual — and often all three together. Also alcohol without food, weight loss, vomiting, kidney impairment slowing drug clearance, an injection into a site about to be exercised, and a dose given without checking that the meal actually arrived. Hypoglycaemia unawareness — losing the warning symptoms after many episodes, or with beta blockers or autonomic neuropathy — is what makes it dangerous.
Clinical Manifestations
Adrenergic first: shaky, sweaty, pale, palpitations, anxious, hungry. Then neuroglycopenic: confusion, difficulty concentrating, slurred speech, blurred vision, irritability or uncharacteristic behavior, drowsiness, seizure and coma. Beta blockers mask everything except the sweating, so in a client on a beta blocker, diaphoresis with confusion is hypoglycaemia until proven otherwise. At night it shows as nightmares, sweating and a headache on waking.
Assessment and Diagnostic Findings
Check a fingerstick glucose whenever a client with diabetes behaves oddly — new confusion, aggression, drowsiness or a fall. Whipple's triad confirms it: symptoms, a low measured glucose, and relief when it is corrected. Review the insulin or sulfonylurea doses, meal timing, activity and alcohol against the pattern of the lows, and look at the continuous glucose monitor download if there is one.
Medical Management
Conscious and able to swallow: the 15/15 rule — 15 g of fast-acting carbohydrate, recheck in 15 minutes, and repeat until the glucose is above 70, then give a snack or meal containing protein and complex carbohydrate. Fifteen grams is 4 ounces of juice or regular soda, 3 to 4 glucose tablets, or a tablespoon of honey. Unconscious or unable to swallow: 50% dextrose intravenously, or glucagon intramuscularly, subcutaneously or intranasally if there is no IV access. Sulfonylurea-induced hypoglycaemia needs prolonged observation because it recurs.
Nursing Management and Client Education
Never put food or fluid in the mouth of a client who is not fully awake — give glucagon or IV dextrose instead. Do not treat with chocolate, ice cream or anything containing fat — the fat slows absorption exactly when speed is the point. Turn the client on their side after glucagon; it commonly causes vomiting. Recheck, document, and then work out why, because an unexplained low will happen again. Teach the client and the family the 15/15 rule, to carry fast carbohydrate at all times, and how to give glucagon — the family needs to have practiced it before the night they need it. Medical identification. Teach that alcohol on an empty stomach causes lows hours later, and that a low while driving means pulling over and treating before going on.
Chronic Complications of DiabetesOpenClose
Definition and Overview
The long-term damage of sustained hyperglycaemia, in two categories. Microvascular — small vessels — gives retinopathy, nephropathy and neuropathy. Macrovascular — large vessels — gives coronary artery disease, stroke and peripheral arterial disease. Cardiovascular disease is what most people with diabetes actually die of.
Causes and Risk Factors
Duration of diabetes and cumulative glycaemic control are the two biggest factors, which is what the A1C is really measuring. Then hypertension, smoking, dyslipidaemia, obesity, albuminuria and genetic susceptibility. Neuropathy and foot ulceration are made far more likely by any loss of protective sensation.
Clinical Manifestations
Retinopathy: often no symptoms until sight is lost — then floaters, blurring, dark spots. Nephropathy: silent, detected as albuminuria long before creatinine moves. Peripheral neuropathy: burning, tingling or numbness in a stocking-and-glove distribution, worse at night, progressing to loss of sensation. Autonomic neuropathy: gastroparesis with early satiety, bloating and erratic glucose; orthostatic hypotension; erectile dysfunction; a resting tachycardia; and a silent myocardial infarction — a heart attack with no chest pain, presenting as breathlessness, fatigue or confusion. Peripheral arterial disease: intermittent claudication, cool feet, absent pulses, hair loss, and ulcers that will not heal.
Assessment and Diagnostic Findings
Annual dilated retinal examination. Annual urine albumin-to-creatinine ratio and estimated GFR. Comprehensive foot examination at every visit, with a 10 g monofilament to test protective sensation and palpation of pedal pulses. Lipids and blood pressure every visit. A1C every 3 to 6 months. Ask directly about erectile dysfunction, bloating and dizziness on standing — clients rarely volunteer these.
Medical Management
Glycaemic control is prevention, and it works — tight control markedly reduces microvascular disease. Blood pressure to target with an ACE inhibitor or ARB, which also protects the kidney. Statins for cardiovascular risk. SGLT2 inhibitors and GLP-1 agonists where kidney or heart disease is present. Laser photocoagulation or anti-VEGF injections for retinopathy. Gabapentin, pregabalin or duloxetine for painful neuropathy. Revascularisation for critical limb ischemia; dialysis or transplant for end-stage kidney disease.
Nursing Management and Client Education
Foot care is the teaching that prevents amputations. Inspect the feet daily, using a mirror or asking someone if eyesight is poor; wash in lukewarm water tested with the elbow or a thermometer, and dry between the toes; moisturise the foot but not between the toes; cut nails straight across or have a podiatrist do it; never go barefoot, never use a heating pad or hot water bottle on the feet, and never treat a corn or callus yourself. Shoes checked inside before putting them on. Report any break in the skin the same day. Keep the annual eye and kidney checks even when nothing hurts — both are silent. Stop smoking. And name the silent heart attack out loud: teach that unusual fatigue, breathlessness or indigestion needs urgent attention even without chest pain.
🧠 Mind maps 1
One per disorder, built from the structure of your ATI chapter.
🎯 Who gets it
- DKA risk: undiagnosed or untreated type 1 diabetes, or skipping insulin doses.
- A missed or too-low insulin dose can trigger DKA.
- Illness or emotional stress raises insulin demand through faster carbohydrate metabolism.
- Infection is the most common trigger of DKA.
👀 What you see
- Polyuria: osmotic diuresis from hyperglycemia leads to excess urine output.
- Polydipsia: fluid loss from diuresis triggers excessive thirst and dehydration.
- Polyphagia: cells can't use glucose, so hunger increases despite eating.
- Weight loss occurs as the body breaks down fat cells can't use.
🧪 What confirms it
- DKA blood glucose typically exceeds
250 mg/dL, sometimes reaching800 mg/dLor higher. - HHS blood glucose exceeds
600 mg/dL. - DKA sodium can run low or normal, shifting with hyperglycemia, dehydration, and fluid changes.
- DKA potassium starts high as it leaves cells, then drops after fluids and insulin.
🩺 What you do
- Recheck vital signs at
15-minintervals initially, tapering toevery 4 hronce the client stabilizes. - Always treat the underlying cause, most often infection.
- Give isotonic fluids; the client may need
6 to 9 Lin24 hrto replace half the deficit. - Watch older adults closely for fluid overload risk (heart failure, pulmonary complications).
💬 What you teach
- Wear a medical alert bracelet identifying your diabetes diagnosis.
- Take steps to prevent dehydration and future hyperglycemic crises.
- Drink
2 to 3 L/dayof fluids from food, beverages, and water unless restricted.
Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.
🎥 Lecture recordings 2
Tap a card to open that recording in Google Drive. The same list lives in the lecture library.
All NUR 258 recordings →🖼️ Infographics 11
Tap a card to open the matching graphics in your infographic library.
📄 Simple Nursing handouts for this module — 3 of them, straight from your Drive.
📋 Active Learning Templates 1
One per disorder. Every row is filled from that section of the ATI chapter — print it, cover the right, rebuild it.
📋 Complications of Diabetes Mellitus (DKA and HHS)6 parts
🖼️ InfographicsDKA vs HHNS
Filled from ATI chapter 83, row by row from that chapter’s own sections — 12 of 12 rows have content.
🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
- DKA is a rapid, life-threatening emergency in type 1 (sometimes type 2) diabetes marked by hyperglycemia above 250 mg/dL, ketosis, and acidosis; HHS is a slower-onset crisis with glucose above 600 mg/dL, severe dehydration, and no ketosis.
Health Promotion & Disease Prevention
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Sick-day rules taught before the first illness. Never stop insulin because you are not eating — illness raises glucose without food, and stopping insulin is how people arrive in DKA.
- Check glucose every
3–4 hourswhen unwell, and ketones if glucose is above about240 mg/dLor vomiting. - Fluid hourly; carbohydrate as liquid if solid food is not possible.
- Know when to call: vomiting beyond a few hours, moderate or large ketones, or glucose that will not come down.
- Annual influenza vaccination and prompt treatment of infection — infection is the commonest trigger for both.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
- DKA risk: undiagnosed or untreated type 1 diabetes, or skipping insulin doses.
- A missed or too-low insulin dose can trigger DKA.
- Illness or emotional stress raises insulin demand through faster carbohydrate metabolism.
- Infection is the most common trigger of DKA.
- High cortisol, glucagon, and epinephrine boost glucose production and blunt insulin's effect.
- HHS risk: severe hyperglycemia causes sustained osmotic diuresis from too little insulin.
- In HHS, enough insulin remains to block ketosis but not to control glucose.
- Poor fluid intake or kidney function worsens hyperosmolarity and dehydration in HHS.
Assessment — Expected Findings
- Polyuria: osmotic diuresis from hyperglycemia leads to excess urine output.
- Polydipsia: fluid loss from diuresis triggers excessive thirst and dehydration.
- Polyphagia: cells can't use glucose, so hunger increases despite eating.
- Weight loss occurs as the body breaks down fat cells can't use.
- GI symptoms (nausea, vomiting, abdominal pain) stem from ketosis and acidosis.
- Blurred vision, headache, and weakness result from fluid volume depletion.
- Hypotension results from dehydration caused by osmotic diuresis.
- A fruity breath odor comes from ketone buildup in the blood.
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
- DKA blood glucose typically exceeds
250 mg/dL, sometimes reaching800 mg/dLor higher. - HHS blood glucose exceeds
600 mg/dL. - DKA sodium can run low or normal, shifting with hyperglycemia, dehydration, and fluid changes.
- DKA potassium starts high as it leaves cells, then drops after fluids and insulin.
- HHS sodium is usually normal or low, shifting with dehydration and osmotic fluid changes.
Diagnostic Procedures
From this module — built from the notes above on this page, not a section of the ATI chapter.
- DKA: glucose usually
>250 mg/dL, pH <7.35, bicarbonate low, ketones present, anion gap raised. - HHS: glucose often
>600 mg/dL, serum osmolality >320, little or no ketosis, pH near normal. - DKA is acidosis. HHS is dehydration. That is the whole distinction, and it decides the emphasis of treatment.
- ECG for potassium effects; look for the trigger — infection, missed insulin, myocardial infarction.
- Kussmaul respirations and a fruity breath belong to DKA, not HHS.
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
- Recheck vital signs at
15-minintervals initially, tapering toevery 4 hronce the client stabilizes. - Always treat the underlying cause, most often infection.
- Give isotonic fluids; the client may need
6 to 9 Lin24 hrto replace half the deficit. - Watch older adults closely for fluid overload risk (heart failure, pulmonary complications).
- Start rapid
0.9%sodium chloride for1 to 3 hr, switching to0.45%if sodium is elevated. - Add dextrose to IV fluids when glucose falls to
200 mg/dLin DKA or250 mg/dLin HHS. - Use IV insulin, not subcutaneous, for moderate to severe DKA.
- Give regular insulin
0.1 unit/kgIV bolus, then infuse at0.05 unit/kg/hr. - Check glucose hourly; target glucose under
200 mg/dL, pH over7.3, bicarbonate over15 mEq/L.
Medications
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Isotonic fluid first — both are profoundly volume depleted, HHS more so.
- Regular insulin by continuous IV infusion — only regular insulin is given intravenously.
- Potassium before or with the insulin once it is not high and urine is flowing. Insulin drives potassium into cells and can drop it dangerously.
- Add dextrose when glucose reaches about
200–250 mg/dLso the infusion can continue clearing ketones without hypoglycemia. - Bicarbonate only for severe acidosis; it is not routine.
Therapeutic Procedures
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Hourly glucose, and electrolytes every
2–4 hours; strict intake and output. - Continuous cardiac monitoring while potassium is shifting.
- Overlap the subcutaneous insulin with the infusion by
1–2 hoursbefore stopping it, or the ketosis returns. - Correct glucose gradually — too fast risks cerebral edema, particularly in the young.
- Treat the precipitating cause, or it happens again next week.
💬 Around the patientClient Education · Interprofessional Care
Client Education
- Wear a medical alert bracelet identifying your diabetes diagnosis.
- Take steps to prevent dehydration and future hyperglycemic crises.
- Drink
2 to 3 L/dayof fluids from food, beverages, and water unless restricted. - If glucose runs low, drink liquids that contain sugar.
- Check glucose every
2 to 4 hrduring illness, and keep taking insulin. - Check urine for ketones whenever glucose exceeds
240 mg/dL. - Drink carbohydrate- and electrolyte-containing fluids, like sports drinks, if solid food isn't tolerated.
Interprofessional Care
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Provider or intensivist for the insulin and fluid protocol.
- Diabetes educator before discharge — an admission for DKA is a teaching failure until proven otherwise.
- Pharmacist for infusion concentrations and the transition to subcutaneous insulin.
- Dietitian and social work — cost of insulin and supplies is a common and unspoken cause of missed doses.
⚠️ What goes wrongComplications
Complications
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Hypokalemia during treatment — the commonest serious complication, and the reason potassium is checked before insulin.
- Cerebral edema from correcting glucose or sodium too quickly. Headache and falling consciousness during treatment is the warning.
- Hypoglycemia if dextrose is not added in time.
- Fluid overload, especially in older clients and in HHS.
- Thrombosis — HHS is a hyperviscous, hypercoagulable state.
📝 Notes & key concepts
The lines from this module that carry a number, a dose or an absolute rule — the ones that decide questions. Everything else is on the cards above.
- Type 1: autoimmune beta-cell destruction, absolute deficiency, thinner, younger, prone to DKA. Type 2: insulin resistance, obesity-associated, prone to HHS.
- Insulin: rapid (lispro, aspart)
15 minbefore meals, onset ~15 min, peak1–3 hr— watch for hypoglycemia at the peak. Regular is the only IV insulin. Long-acting (glargine, detemir) has no peak and is never mixed. - Hypoglycemia, conscious:
15 gfast carb, recheck in15 min. Unconscious: glucagon or IV dextrose. Signs: shaky, sweaty, tachycardic, confused, headache. - DKA (Type 1): ketones positive, fruity breath, Kussmaul respirations, acidotic pH, N/V, faster onset, glucose lower than HHS. HHS (Type 2): no ketones, normal pH, no N/V, much higher glucose, slow insidious onset.
- Both crises: IV fluids first, then a regular insulin drip. Never subQ insulin in a crisis. Replace potassium.
- Sick day rules: keep taking insulin even if not eating, glucose
q2–4 hr, ketones if Type 1, hydrate, call if glucose>250and not falling or if ill more than 2 days. - A1C goal
<7%(ideal 6.5%); non-diabetic ~5.6–5.7%. Rotate injection sites or lipodystrophy wrecks absorption. - DKA vs HHS as they framed it: DKA is type 1, presents within ~24 h, Kussmaul, fruity odor, acidosis, abdominal pain and vomiting. HHS is type 2, sits at home for days, glucose
500–800, profound dehydration, much more prominent neuro and mental status change (up to paralysis), no acidosis. - In severe hyperglycemia the first assessment is dehydration — circulation. Ahead of a fingerstick, ahead of LOC, because glucose is not A-B-C-D.
- NPH is the only intermediate insulin: onset 1–2 h, peak 6–8 h → snack at 8 hours. Cloudy is normal. Roll it, never shake — protein foams.
- Lispro and aspart work in 15 minutes → give immediately before the meal, never 30 minutes ahead.
- Hypoglycemia at 58 mg/dL: awake → 4–6 oz juice. Unconscious → 50 mL of D50 IV.
- Sick-day rule they guarantee will be tested: keep taking insulin. Monitor frequently. Never skip it, never halve it.
- Exercise: hold it if glucose
>250with ketones, carry fast-acting carbohydrate, never skip insulin before a run.
🎯 Module quiz
Questions for this module. They also feed the Mega Quiz.
Nothing here yet — drop it in when you have it