NLE Endocrine & Metabolic Nursing — Diabetes Mellitus & Its ComplicationsRevision Notes

Exam Tips

• NLE scenario tip: If the stem says 'young, lean, prone to DKA, needs insulin' → Type 1 DM.
• If the stem says 'older, overweight Filipino, managed with oral agents, developed confusion without ketones' → Type 2 DM, suspect HHNS.
• The 3 Ps mnemonic: 'Poly-U, Poly-D, Poly-P' — Urination, Drinking, Eating (all 'poly' = too much).
• Gestational DM is covered in NCM 103 (Maternal and Child Nursing) — expect cross-topic questions.

Key Points

• Diabetes is a disorder of glucose metabolism caused by absolute insulin deficiency, insulin resistance, or both.
• Insulin is produced by pancreatic beta cells and moves glucose INTO cells; without it, glucose remains in the blood (hyperglycemia) while cells 'starve.'
• TYPE 1 DM: Autoimmune destruction of beta cells → ABSOLUTE insulin deficiency. Onset usually in young/lean individuals. ALWAYS requires insulin. Prone to DKA.
• TYPE 2 DM: Insulin resistance + relative deficiency. Usually older or overweight patients (but increasing in younger Filipinos). Managed initially with diet/oral agents, eventually may need insulin. Prone to HHNS.
• Gestational DM: Glucose intolerance recognized during pregnancy — monitor with OGTT.
• Classic manifestations — the 3 Ps: POLYURIA (excess urination), POLYDIPSIA (excess thirst), POLYPHAGIA (excess hunger) — plus fatigue, weight loss, blurred vision, slow healing, and recurrent infections.
• Pre-diabetes: Fasting glucose 100–125 mg/dL (impaired fasting glucose) or A1c 5.7–6.4% — at high risk of progressing to Type 2 DM.

Definitions

Section Title

Pathophysiology & Types of Diabetes Mellitus

Common Mistakes

• Confusing Type 1 and Type 2: Remember — Type 1 is ABSOLUTE deficiency (autoimmune), ALWAYS needs insulin, and is prone to DKA. Type 2 is RELATIVE deficiency (resistance), initially managed without insulin, and prone to HHNS.
• Assuming all obese or older patients have Type 2 — Type 1 can occur at any age.
• Forgetting that gestational DM requires OGTT screening at 24–28 weeks of pregnancy.
• Missing the 4th 'P' — weight loss (from fat and muscle breakdown) which is especially prominent in Type 1.

Formulas

Exam Tips

• Memorize the 'magic numbers': 70–100 (normal FPG), 126 (DM FPG cutoff), 200 (random/OGTT cutoff), 6.5% (A1c diagnosis), <7% (A1c target).
• NLE item pattern: 'Which value confirms a diagnosis of DM?' → FPG ≥126 mg/dL confirmed on two occasions, OR A1c ≥6.5%, OR random ≥200 with symptoms.
• A1c is NOT used in pregnancy — use OGTT for gestational DM screening.
• The 2-hour OGTT cutoff for pre-diabetes is 140–199 mg/dL — know the range, not just the DM cutoff.

Key Points

• FASTING PLASMA GLUCOSE (FPG): Normal = 70–100 mg/dL; Pre-diabetes = 100–125 mg/dL; Diabetes = ≥126 mg/dL (confirmed on 2 separate occasions).
• RANDOM/CASUAL PLASMA GLUCOSE: Diabetes = ≥200 mg/dL WITH classic symptoms (polyuria, polydipsia, weight loss).
• ORAL GLUCOSE TOLERANCE TEST (OGTT, 2-hour): Diabetes = ≥200 mg/dL at 2 hours; Pre-diabetes = 140–199 mg/dL.
• HbA1c (GLYCOSYLATED HEMOGLOBIN): Normal = <5.7%; Pre-diabetes = 5.7–6.4%; Diabetes = ≥6.5%. Treatment TARGET = <7%. Reflects average blood glucose over the PAST 2–3 MONTHS.
• HbA1c is NOT affected by daily glucose fluctuations — it gives the 'big picture' of glycemic control over months.
• A single abnormal value must be confirmed by REPEAT TESTING on a different day (unless symptoms + random glucose ≥200 mg/dL).

Definitions

Section Title

Diagnostic Values — Memorize These Numbers

Common Mistakes

• Confusing diagnostic cutoffs: FPG ≥126 for DM (NOT 120 or 130), A1c ≥6.5% for DM (NOT 7%).
• Thinking the A1c target IS the diagnostic cutoff — A1c ≥6.5% = diagnosis; A1c <7% = treatment TARGET for already-diagnosed patients.
• Forgetting that one abnormal lab result (except symptoms + random ≥200) must be REPEATED to confirm diagnosis.
• HbA1c can be falsely LOW in hemolytic anemia (RBC lifespan shortened) and falsely HIGH in iron deficiency anemia.

Exam Tips

• The NLE will ask: 'Which insulin can be given IV?' → ONLY REGULAR (short-acting) insulin.
• Memory trick for appearance: 'NPH is Not Pure and Hazy' → NPH is CLOUDY. All others are CLEAR.
• Memory trick for peak: 'Regular peaks at Regular meal time' → 2–4 hours after injection (regular mealtime). NPH peaks 6–12 hours later — think of it as the 'midnight risk.'
• Mixing insulin sequence: AIR into NPH → AIR into Regular → WITHDRAW Regular → WITHDRAW NPH. Mnemonic: 'AARN' — Air-Air-Regular-NPH.
• Glargine mnemonic: 'Glargine = Gentle and Flat' — no peak, given once daily, never mixed.
• For NLE: The abdomen has the FASTEST and most CONSISTENT insulin absorption.

Key Points

• PEAK = the time of HIGHEST HYPOGLYCEMIA RISK. Knowing the peak tells you when to feed the patient and when to monitor most carefully.
• RAPID-ACTING (lispro, aspart, glulisine): Onset ~15 min | Peak ~30 min–1.5 hr | Duration 3–4 hr | Appearance: CLEAR. Given WITH or just BEFORE a meal — food must be ready.
• SHORT-ACTING (Regular): Onset ~30 min–1 hr | Peak ~2–4 hr | Duration 5–8 hr | Appearance: CLEAR. The ONLY insulin given INTRAVENOUSLY (used in DKA/HHNS drips).
• INTERMEDIATE-ACTING (NPH): Onset 1–2 hr | Peak ~6–12 hr | Duration 12–18 hr | Appearance: CLOUDY. Roll gently — do NOT shake.
• LONG-ACTING (glargine/Lantus, detemir): Onset ~1 hr | Peak: PEAKLESS (no significant peak) | Duration ~24 hr | Appearance: CLEAR. NEVER mixed with other insulins. Provides 'basal' coverage.
• MIXING RULE — 'Clear before Cloudy': Draw up REGULAR (clear) FIRST, then NPH (cloudy). Air injection: inject air into NPH vial first (cloudy), then air into regular vial, then withdraw regular, then NPH.
• Injection sites — fastest absorption: ABDOMEN > arm > thigh > buttock. Rotate sites within one area to prevent lipohypertrophy.
• Store open/in-use vial at room temperature (up to 30 days); unopened insulin vials stored in the refrigerator (NOT frozen).
• NPH is cloudy because it contains protamine — gently ROLL (not shake) the vial to resuspend.

Definitions

Section Title

Insulin — Types, Onset, Peak, Duration (The Most Tested Table)

Common Mistakes

• CRITICAL ERROR: Giving rapid-acting insulin and then delaying the meal — the patient will become hypoglycemic. Food MUST be ready BEFORE administering rapid-acting insulin.
• Mixing glargine with regular insulin — NEVER DO THIS. Glargine is incompatible with all other insulins.
• Drawing up NPH (cloudy) before regular (clear) — this contaminates the regular vial with NPH. Always CLEAR BEFORE CLOUDY.
• Shaking NPH — this causes bubbles and incorrect dosing. GENTLY ROLL to resuspend.
• Assuming NPH can be given IV — ONLY REGULAR INSULIN is given IV. All other insulins are subcutaneous.
• Forgetting that NPH peaks at 6–12 hours — if given at 8 PM, peak is 2–8 AM (nighttime hypoglycemia risk → Somogyi effect).

Exam Tips

• NLE pattern: 'Before the patient undergoes CT scan with contrast, which medication should the nurse instruct the patient to HOLD?' → Metformin.
• Drug ending memory trick: '-FLOZIN = FLUSHES glucose out through urine' (SGLT2 inhibitors). '-TIDE = TIDES back insulin release with meals' (GLP-1 agonists).
• Sulfonylureas = 'Sulfa = Sugar release' → hypoglycemia risk — always teach patients signs of hypoglycemia.
• The NLE frequently pairs metformin with contrast dye — always hold metformin 24–48 hours before and after contrast administration, restarted only after renal function confirmed adequate.

Key Points

• METFORMIN (Biguanide) — FIRST-LINE for Type 2 DM: Decreases hepatic glucose output and improves insulin sensitivity. Does NOT cause hypoglycemia by itself. Risk: LACTIC ACIDOSIS — HOLD before contrast dye studies and in renal impairment. Take WITH food to reduce GI upset.
• SULFONYLUREAS (glipizide, glyburide, glimepiride): Stimulate pancreatic insulin secretion → HYPOGLYCEMIA RISK + weight gain. Caution with alcohol (disulfiram-like reaction). Teach patients about hypoglycemia signs.
• MEGLITINIDES (repaglinide, nateglinide): Rapid, short-acting insulin secretagogues. TAKE WITH MEALS — SKIP THE DOSE IF SKIPPING THE MEAL (to prevent hypoglycemia).
• THIAZOLIDINEDIONES/TZDs (pioglitazone): Improve insulin sensitivity. Causes FLUID RETENTION — avoid in heart failure patients. Also: weight gain and hepatotoxicity — monitor liver enzymes.
• DPP-4 INHIBITORS (sitagliptin, '-gliptin'): Increase incretin levels to stimulate insulin and reduce glucagon. Generally well-tolerated; low hypoglycemia risk.
• SGLT2 INHIBITORS (empagliflozin, dapagliflozin — endings in '-gliflozin'): Block glucose reabsorption in kidneys → glucose excreted in urine. Risk: GENITAL/URINARY TRACT INFECTIONS (glucosuria promotes bacterial growth) and EUGLYCEMIC DKA.
• GLP-1 RECEPTOR AGONISTS (liraglutide, semaglutide, exenatide — endings in '-tide'): Injectable agents; promote insulin secretion, suppress glucagon, slow gastric emptying, and promote weight loss. Common GI side effects (nausea, vomiting).
• ACE inhibitors and ARBs are protective against diabetic nephropathy — used even without hypertension in diabetic patients with microalbuminuria.

Definitions

Section Title

Oral & Non-Insulin Antidiabetic Agents (Type 2 DM)

Common Mistakes

• Saying metformin causes hypoglycemia — it does NOT cause hypoglycemia when used ALONE (only when combined with insulin/sulfonylureas).
• Giving pioglitazone to a patient with heart failure — TZDs cause fluid retention, which can exacerbate heart failure.
• Forgetting to HOLD METFORMIN before CT scans with contrast — risk of lactic acidosis from reduced renal clearance.
• Not teaching meglitinide patients to SKIP the dose if they skip a meal — this is a critical patient safety teaching point.
• Confusing drug endings: '-gliflozin' = SGLT2 inhibitors; '-gliptin' = DPP-4 inhibitors; '-tide' = GLP-1 agonists.

Formulas

Exam Tips

• NLE memory trick: 'Cold and Clammy = Need Some Candy' (hypoglycemia — sweating, cool skin). 'Hot and Dry = Sugar High' (hyperglycemia — warm, flushed, dry skin).
• NLE priority question pattern: 'Which is the PRIORITY action for a conscious patient with blood glucose of 52 mg/dL?' → Give 15 g fast-acting carbohydrate (Rule of 15).
• 'What should the nurse do FIRST for an unconscious diabetic patient?' → Establish IV access and give D50W (or call for glucagon if no IV).
• Rapid-acting insulin peak (30 min–1.5 hr) and NPH peak (6–12 hr) are the most common times for hypoglycemia — time assessments to these windows.
• In Philippine community health settings (Barangay Health Centers), glucagon IM may be the only available option — know both hospital and community management.

Key Points

• HYPOGLYCEMIA: Blood glucose < 70 mg/dL. The most common acute diabetic emergency.
• CAUSES: Too much insulin or oral agents, skipped/delayed meals, unusual physical activity, alcohol intake.
• ONSET: RAPID (minutes to hours) — compare with hyperglycemic emergencies which develop over hours to days.
• SIGNS — 'Cold and Clammy — Need Some Candy': EARLY (adrenergic): shakiness/tremors, diaphoresis (sweating), tachycardia, palpitations, hunger, pallor, anxiety. LATE (neuroglycopenic — brain deprived of glucose): confusion, slurred speech, blurred vision, inability to concentrate, seizures, loss of consciousness, coma.
• RULE OF 15 (Conscious Patient): Give 15 g of FAST-ACTING carbohydrate → RECHECK in 15 minutes → if still <70 mg/dL, REPEAT 15 g carbs → once normalized, give a longer-acting snack (protein + carb) or meal.
• 15 g fast-acting carbs = ½ cup (120 mL) fruit juice or regular soda, 3–4 glucose tablets, 1 tablespoon sugar dissolved in water.
• UNCONSCIOUS PATIENT or cannot swallow: IV DEXTROSE 50% (D50W) in the hospital setting. OR Glucagon IM/subcutaneous in the community setting. NEVER give anything by mouth to an unconscious patient (aspiration risk).
• Glucagon stimulates the liver to release glycogen stores → raises blood glucose.
• After recovery from hypoglycemia: Investigate and address the CAUSE (insulin dose adjustment, meal timing, activity level).

Definitions

Section Title

Acute Complications — Hypoglycemia

Common Mistakes

• CRITICAL: Giving oral fluids or food to an unconscious/drowsy patient — this causes ASPIRATION. Unconscious hypoglycemic patients need IV D50 or IM glucagon.
• Giving a sugary drink and not rechecking in 15 minutes — the Rule of 15 requires both the 15 g AND the 15-minute recheck.
• Not following up with a longer-acting snack after treating hypoglycemia — glucose will drop again without a protein + complex carb snack.
• Confusing cold/clammy (hypoglycemia) with hot/flushed (hyperglycemia): 'Cold and clammy = low (candy); Hot and dry = high (sky).'
• Forgetting that unconscious patients need D50 FIRST — do not attempt oral feeding.

Exam Tips

• NLE priority question: 'What is the PRIORITY intervention for a patient in DKA?' → IV normal saline (fluid resuscitation FIRST — before insulin).
• DKA vs. HHNS quick differentiator: KETONES + ACIDOSIS = DKA; NO ketones + extreme hyperglycemia + high osmolality = HHNS.
• Potassium trap mnemonic: 'Acidosis PUSHES K OUT; Insulin PULLS K IN.' Watch for K to drop when insulin starts.
• ECG changes of hypokalemia: flattened T waves, U waves, widened QRS — report these immediately in DKA treatment.
• Fruity breath = ketones = DKA — Kussmaul breathing = DKA. Neither is present in HHNS.
• Glucose target to add dextrose: 200–250 mg/dL. This number is commonly tested in NLE.

Key Points

• DKA (Diabetic Ketoacidosis) — MOSTLY TYPE 1 DM: Absolute insulin lack → fat breakdown → KETONES produced → METABOLIC ACIDOSIS. Onset: hours. Triggered by: missed insulin, infection, illness, stress.
• DKA SIGNS: Blood glucose usually >250 mg/dL (300–600 range); KETONES in blood and urine; ACIDOSIS (pH <7.35, low bicarbonate/HCO3); KUSSMAUL RESPIRATIONS (deep, rapid breathing — compensating by blowing off CO2); FRUITY/ACETONE BREATH; nausea/vomiting/abdominal pain; dehydration; altered mental status.
• HHNS/HHS (Hyperglycemic Hyperosmolar Nonketotic Syndrome) — TYPE 2 DM (older patients): Enough residual insulin to prevent ketosis, but NOT enough to prevent extreme hyperglycemia and profound dehydration. Onset: DAYS (slower). Higher mortality than DKA.
• HHNS SIGNS: Blood glucose VERY HIGH (>600, often >800–1,000 mg/dL); PROFOUND dehydration; HIGH serum osmolality (>320 mOsm/kg); SEVERE neurologic changes (lethargy, seizures, coma); NO significant ketones; pH near NORMAL; NO Kussmaul breathing.
• KEY DIFFERENCE MEMORY: DKA = 'KETO-ACIDOSIS' (ketones + acid + Kussmaul); HHNS = 'HYPER-OSMOLAR' (extreme high glucose + extreme dehydration, no ketones).
• DKA/HHNS MANAGEMENT — SAME PRIORITY ORDER: (1) IV NORMAL SALINE (0.9%) FIRST — correct dehydration. (2) REGULAR INSULIN IV drip — lower glucose gradually. (3) POTASSIUM — monitor and replace. (4) Add DEXTROSE when glucose reaches ~200–250 mg/dL. (5) Treat the PRECIPITATING CAUSE.
• POTASSIUM TRAP (Most Important NLE Trap): In DKA, total body K is DEPLETED. But serum K may appear NORMAL or HIGH initially because acidosis + insulin lack push K OUT of cells. When you give INSULIN + IV fluids → K shifts back INTO cells → SERUM K DROPS RAPIDLY → HYPOKALEMIA → FATAL ARRHYTHMIAS. ALWAYS monitor K and ECG. Replace K in IV fluids once level is normal-to-low AND urine output is adequate. DO NOT START INSULIN if K is dangerously low (<3.3 mEq/L) without first replacing K.
• Add DEXTROSE (D5 solution) to IV fluids when glucose reaches 200–250 mg/dL — this allows the insulin drip to continue clearing ketones (DKA) without causing hypoglycemia or cerebral edema (especially dangerous in children).

Definitions

Section Title

Acute Complications — DKA vs. HHNS (The Classic NLE Comparison)

Common Mistakes

• Giving insulin in DKA without first checking and replacing potassium — if K is <3.3 mEq/L, hold insulin and replace K first.
• Thinking HHNS patients have acidosis — they do NOT have significant ketosis or acidosis. pH is near normal.
• Choosing D5W or D10W as the FIRST fluid in DKA/HHNS — the FIRST fluid is ALWAYS 0.9% Normal Saline (isotonic, restores volume).
• Not adding dextrose to IV fluids when glucose drops to 200–250 mg/dL — this risks hypoglycemia and prevents continued ketone clearance.
• Thinking HHNS is less dangerous — HHNS has a HIGHER MORTALITY than DKA due to the extreme dehydration and older patient population.

Exam Tips

• NLE question: 'Which complication is the LEADING CAUSE OF ADULT BLINDNESS?' → Diabetic retinopathy. 'Leading cause of ESRD?' → Diabetic nephropathy. 'Leading cause of DEATH in DM?' → Cardiovascular disease.
• Foot care NLE priority: 'What is the most important nursing instruction for a patient with diabetic neuropathy?' → Inspect feet daily, wear closed shoes, NEVER barefoot, never use heating pads.
• Peripheral neuropathy = loss of protective sensation → foot ulcers → amputation. This chain is the basis of preventive foot care teaching.
• Autonomic neuropathy causes SILENT MI — warn diabetic patients that they may not feel typical chest pain during a heart attack.
• The 3 microvascular complications (the 3 Rs): Retinopathy, Renal (nephropathy), and 'Reuropathy' (neuropathy) — all prevented by tight glucose control.

Key Points

• MICROVASCULAR (small vessel disease) — PREVENTED by TIGHT GLUCOSE CONTROL: Retinopathy, Nephropathy, Neuropathy (peripheral and autonomic).
• RETINOPATHY: Damage to retinal blood vessels → leading cause of ADULT BLINDNESS in the Philippines. Annual eye exam (fundoscopic exam by ophthalmologist) is standard care. Laser therapy used for proliferative retinopathy.
• NEPHROPATHY: Damage to glomerular capillaries → leading cause of END-STAGE RENAL DISEASE (ESRD) requiring dialysis. FIRST SIGN = microalbuminuria (protein in urine). ACE inhibitors or ARBs are RENOPROTECTIVE — given even without hypertension in diabetic patients with microalbuminuria.
• NEUROPATHY: PERIPHERAL neuropathy: numbness, tingling, burning pain, loss of PROTECTIVE SENSATION in feet/hands (glove-and-stocking distribution) → cannot feel pain from wounds → FOOT ULCERS → GANGRENE → AMPUTATION. AUTONOMIC neuropathy: gastroparesis (delayed gastric emptying, erratic glucose absorption), orthostatic hypotension, and silent MI (cannot feel chest pain).
• MACROVASCULAR (large vessel disease): Coronary artery disease (CAD), cerebrovascular accident (stroke), and peripheral vascular disease (PVD). CARDIOVASCULAR DISEASE IS THE LEADING CAUSE OF DEATH IN DIABETES.
• FOOT CARE — A Major NLE Emphasis: Inspect feet DAILY (use a mirror for the sole). Wash feet in warm (not hot) water and DRY THOROUGHLY (especially between toes). Wear proper CLOSED-TOE SHOES — NEVER go barefoot. Cut toenails STRAIGHT ACROSS. NEVER use heating pads, hot water bottles, or electric blankets (neuropathy masks burns). Avoid ill-fitting shoes. Report any wound, blister, or redness immediately.
• Peripheral vascular disease signs: intermittent claudication, absent peripheral pulses, cool/pale extremities, delayed capillary refill — amputation risk if untreated.
• Autonomic neuropathy → silent MI: Diabetic patients may have a myocardial infarction WITHOUT chest pain (angina equivalent) — atypical symptoms like sudden dyspnea, fatigue, jaw/arm pain, or diaphoresis may be the only signs.

Definitions

Section Title

Long-Term Complications of Diabetes

Common Mistakes

• Thinking macrovascular complications (heart disease) are less important — CARDIOVASCULAR DISEASE is the #1 cause of death in diabetic patients.
• Telling patients to use heating pads or hot water soaks for foot pain — neuropathy prevents them from sensing burns.
• Not teaching patients to cut nails straight across — curved cutting causes ingrown nails and infections.
• Forgetting that silent MI is possible in diabetic patients — always assess for atypical MI symptoms (dyspnea, fatigue, diaphoresis) rather than expecting classic chest pain.
• Not starting ACE inhibitors/ARBs at microalbuminuria stage — waiting until overt proteinuria misses the protective window.

Exam Tips

• NLE question pattern: 'A diabetic patient has consistently high morning glucose readings. What is the PRIORITY nursing action?' → Check blood glucose at 2–3 AM to differentiate Somogyi from Dawn phenomenon.
• Somogyi = 'So-MOGYI-low at night' → 3 AM glucose is LOW → REDUCE evening insulin.
• Dawn = 'The Dawn rises NORMALLY' → 3 AM glucose is NORMAL/HIGH → INCREASE insulin.
• Both are high in the morning — the 3 AM check is the clinical tool to tell them apart. This is the NLE trick question.

Key Points

• Both cause MORNING HYPERGLYCEMIA — but have OPPOSITE causes and opposite treatment.
• SOMOGYI PHENOMENON ('Rebound Hyperglycemia'): Nighttime HYPOGLYCEMIA (from too much evening insulin) → body releases counter-regulatory hormones (glucagon, epinephrine, cortisol) → REBOUND morning hyperglycemia. Patient may have nighttime sweats, nightmares, or headaches on waking.
• Somogyi DIAGNOSIS: Check blood glucose at 2–3 AM — it will be LOW (hypoglycemia during the night).
• Somogyi TREATMENT: REDUCE the evening insulin dose OR add a bedtime snack to prevent nocturnal hypoglycemia.
• DAWN PHENOMENON: Morning hyperglycemia from a NORMAL early-morning physiological surge of counter-regulatory hormones (growth hormone, cortisol, glucagon) — WITHOUT prior nighttime hypoglycemia.
• Dawn Phenomenon DIAGNOSIS: Check blood glucose at 2–3 AM — it will be NORMAL or ELEVATED (no nocturnal hypoglycemia).
• Dawn Phenomenon TREATMENT: ADJUST or INCREASE insulin dose (often the evening or basal insulin), or change the timing of insulin administration.
• KEY MEMORY: Somogyi = LOW at 3 AM → REDUCE insulin. Dawn = NORMAL/HIGH at 3 AM → INCREASE insulin.

Definitions

Section Title

Somogyi Phenomenon vs. Dawn Phenomenon — Morning Glucose Puzzles

Common Mistakes

• Increasing insulin for Somogyi effect — this makes it worse by increasing nocturnal hypoglycemia. Always check 3 AM glucose FIRST.
• Confusing the two: Remember — the ONLY way to differentiate is a 3 AM blood glucose check.
• Not teaching patients to check their 3 AM glucose when morning hyperglycemia cannot be explained by diet or daytime insulin.

Exam Tips

• NLE scenario: 'A Type 1 DM patient has flu and is not eating. Should she take her insulin?' → YES. Illness raises glucose; insulin is never omitted.
• Sick-day management is often tested in community health and home care nursing contexts — relevant to Philippines' barangay-level health education.
• Annual preventive exams (eye, foot, kidney) are NLE favorites for chronic disease management questions.

Key Points

• NEVER OMIT INSULIN when sick — illness (infection, fever) raises blood glucose even if the patient is not eating. Insulin requirements actually INCREASE during illness.
• SICK-DAY RULES: Monitor blood glucose every 4 hours. Check urine/blood ketones if glucose >240 mg/dL. Maintain fluid intake (non-sugar fluids if glucose is high; regular fluids if glucose is normal). Take 10–15 g carbohydrates every 1–2 hours if not eating regular meals.
• KNOW WHEN TO CALL THE PROVIDER: Glucose persistently >240 mg/dL, moderate-to-large ketones, vomiting (cannot hold fluids), altered consciousness, fever >38.5°C lasting >24 hours.
• EXERCISE: Lowers blood glucose — may need to REDUCE insulin dose or eat extra carbohydrates before exercise. Check glucose before, during (if prolonged), and after exercise. Exercise is generally recommended but should be individualized.
• BLOOD GLUCOSE MONITORING: Regular self-monitoring is essential. Target fasting glucose typically 80–130 mg/dL; 2-hour post-meal <180 mg/dL.
• DIET: Carbohydrate-consistent diet; three meals per day at regular times with healthy snacks as needed; limit refined sugars and saturated fats; high fiber diet recommended.
• HbA1c checks every 3 months if not at goal, every 6 months if at goal (<7%).
• Annual foot exam, annual eye exam, annual microalbuminuria check — key Philippine PhilHealth-covered preventive services for diabetic patients.

Definitions

Section Title

Diabetic Self-Management & Sick-Day Rules

Common Mistakes

• Telling a sick Type 1 patient to stop insulin because they are not eating — NEVER omit insulin during illness.
• Not checking ketones when glucose is elevated during illness — this is an early warning sign of developing DKA.
• Not individualizing exercise plans — patients must check glucose before exercise and carry fast-acting carbohydrates.