NLE Endocrine & Metabolic Nursing — Diabetes Mellitus & Its ComplicationsSummary

Diabetes mellitus is a metabolic disorder characterized by hyperglycemia (elevated blood glucose) resulting from absolute or relative insulin deficiency, insulin resistance, or both. Insulin, secreted by pancreatic beta cells in the islets of Langerhans, facilitates glucose uptake into muscle and adipose tissue cells. When insulin is absent, insufficient, or ineffective, glucose accumulates in the bloodstream while cells are glucose-deprived, leading to the classic metabolic abnormalities and clinical manifestations. The disorder disrupts carbohydrate, fat, and protein metabolism, resulting in the characteristic 'three Ps': polyuria (excessive urination), polydipsia (excessive thirst), and polyphagia (excessive hunger), along with fatigue, weight loss (especially in Type 1), blurred vision, and impaired wound healing.

Type 1 DM results from autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency. The disease typically manifests in childhood or young adulthood (though can occur at any age) and accounts for 5–10% of all diabetes cases. Genetic predisposition (HLA associations) combined with environmental triggers (viral infections, dietary factors) initiate an autoimmune cascade in which the immune system mistakenly attacks insulin-producing cells. Patients are typically lean or normal weight and present with acute-onset symptoms (polyuria, polydipsia, weight loss, fatigue). Because beta cells are completely destroyed, patients have ZERO endogenous insulin production and are absolutely dependent on exogenous insulin for survival. Without insulin, Type 1 patients rapidly develop diabetic ketoacidosis (DKA) from uncontrolled lipolysis and ketone production. The disease is non-preventable (no lifestyle modification reverses autoimmune destruction, though tight glycemic control slows progression) and requires lifelong insulin therapy.

Type 2 DM develops from insulin resistance (cells do not respond normally to insulin signaling) combined with relative beta cell insufficiency (the pancreas cannot produce enough insulin to overcome the resistance). The disease accounts for 85–90% of all diabetes cases and is strongly associated with obesity, physical inactivity, and aging, though it is increasingly diagnosed in children and adolescents (linked to rising obesity rates globally and in the Philippines). Initially, the pancreas compensates by producing more insulin (hyperinsulinemia), and blood glucose may remain relatively normal. Over time, beta cells become exhausted and insulin production declines, leading to progressive hyperglycemia. Type 2 patients retain some endogenous insulin production, so they are at lower risk of DKA (though not immune, especially if severe illness or stress occurs). Instead, Type 2 patients are prone to hyperglycemic hyperosmolar nonketotic syndrome (HHNS), characterized by extreme hyperglycemia without significant ketosis. Type 2 can often be managed initially with lifestyle modification (weight loss, exercise, dietary changes) and oral agents, though many patients eventually require insulin (insulinization) as the disease progresses and beta cell function declines.

Diabetes diagnosis is based on four acceptable methods, each with specific thresholds established by the American Diabetes Association (ADA) and the Philippine Diabetes Association (PhDA). Fasting plasma glucose (FPG)—obtained after at least 8 hours without caloric intake—of ≥126 mg/dL confirms diabetes. Random (casual) plasma glucose ≥200 mg/dL with classic diabetic symptoms (polyuria, polydipsia, weight loss) also confirms diagnosis without need for repeat testing. The oral glucose tolerance test (OGTT), where the patient drinks 75 g of glucose and plasma glucose is measured 2 hours later, shows diabetes if the 2-hour value is ≥200 mg/dL. Hemoglobin A1c (HbA1c)—the percentage of hemoglobin molecules glycosylated by attachment of glucose—reflects average blood glucose over the preceding 2–3 months and is ≥6.5% in diabetes. HbA1c has the advantage of not requiring fasting and not being affected by acute illness, stress, or diurnal variation, making it increasingly used for diagnosis and monitoring. The prediabetic state is defined as FPG 100–125 mg/dL, 2-hour OGTT 140–199 mg/dL, or HbA1c 5.7–6.4%, presenting an opportunity for intervention to prevent progression to overt diabetes.

Insulin is available in four major categories based on speed of action: (1) Rapid-acting insulins (lispro, aspart, glulisine) have onset ~15 minutes, peak ~30 minutes to 1.5 hours, and duration ~3–4 hours; they appear clear in the vial and are given immediately before or with meals to cover postprandial (after-meal) glucose rises. (2) Short-acting (regular) insulin has onset ~30 minutes to 1 hour, peak ~2–4 hours, and duration ~5–8 hours; it is also clear and is the ONLY insulin formulation that can be given intravenously (critical for DKA/HHNS management). (3) Intermediate-acting (NPH—Neutral Protamine Hagedorn) insulin has onset ~1–2 hours, peak ~6–12 hours, and duration ~12–18 hours; it appears cloudy due to suspension of zinc and protamine, requiring gentle rolling (NOT shaking) before use, and is never mixed with long-acting insulins. (4) Long-acting insulins (glargine, detemir, degludec) have onset ~1–2 hours, are peakless (no pronounced peak—providing steady basal coverage), and duration ~24 hours or longer; they appear clear and must NEVER be mixed with any other insulin. The peak is the time of maximum insulin activity and therefore highest risk for hypoglycemia; knowing when an insulin peaks tells the nurse when to monitor most closely for hypoglycemic symptoms (shakiness, sweating, tachycardia, confusion, loss of consciousness) and when to ensure the patient has eaten.

Safe insulin administration requires strict aseptic technique and understanding of mixing protocols. When two insulins are to be given together, the order of drawing is critical: CLEAR BEFORE CLOUDY. This means first injecting air into the cloudy (NPH) vial to prevent a vacuum, then injecting air into the clear (regular or rapid-acting) vial, then withdrawing the desired amount of clear insulin, then withdrawing the NPH. This sequence prevents contaminating the clear insulin vial with intermediate insulin, which would alter its pharmacology. Insulin should be stored in the refrigerator (36–46°F / 2–8°C) when unopened; once in use, it can be kept at room temperature (up to 86°F / 30°C) for 28 days (varies by insulin type—always check the package insert). Injection sites should be rotated within one anatomic region (abdomen, thighs, upper arms, buttocks) to prevent lipohypertrophy (hypertrophied fatty tissue from repeated injections at the same spot), which alters insulin absorption and causes unpredictable glucose control. The abdomen is preferred because it provides the fastest and most consistent absorption. Patients should be taught to inject at a 90-degree angle (45 degrees if thin), to avoid rubbing after injection, and to keep records of injection sites to ensure proper rotation. Under RA 9173, nurses have the responsibility to teach patients proper injection technique and ensure competency before discharge.

Type 2 diabetes management typically begins with lifestyle modification (diet, exercise, weight loss) and oral agents, with insulin added later if needed (insulinization). Major classes include: (1) Biguanides (metformin), first-line agents that decrease hepatic glucose output and improve peripheral insulin sensitivity; metformin does NOT cause hypoglycemia when used alone, is weight-neutral, and is well-tolerated but carries risk of lactic acidosis (rare) in renal impairment and must be held perioperatively or around contrast dye administration. (2) Sulfonylureas (glipizide, glyburide, glimepiride) and meglitinides (repaglinide, nateglinide) stimulate pancreatic insulin secretion and carry hypoglycemia risk; sulfonylureas also cause weight gain and have potential disulfiram-like reactions with alcohol. (3) Thiazolidinediones (pioglitazone) improve insulin sensitivity but cause fluid retention (contraindicated in heart failure), weight gain, and hepatotoxicity. (4) Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin) enhance GLP-1 and GIP, promoting insulin secretion; they have low hypoglycemia risk and are weight-neutral. (5) Sodium-glucose cotransporter 2 (SGLT2) inhibitors (empagliflozin, dapagliflozin, canagliflozin) promote glucose excretion in urine; they lower glucose, weight, and blood pressure but increase risk of genital/urinary tract infections and euglycemic DKA (DKA with only mildly elevated glucose, hard to recognize). (6) Glucagon-like peptide-1 (GLP-1) receptor agonists (exenatide, liraglutide, semaglutide) are injectables that promote weight loss, lower glucose, and reduce cardiovascular events but commonly cause nausea and GI upset. Each agent has specific contraindications, side effects, and monitoring requirements that must be understood for safe prescription and patient counseling.

Hypoglycemia (blood glucose <70 mg/dL, though symptoms may appear at slightly higher levels in patients with longstanding diabetes or poor glycemic control) is the most common acute diabetic emergency and results from excessive insulin or oral agent relative to carbohydrate intake, physical activity, or both. Symptoms develop rapidly and are caused by sympathetic (adrenergic) activation and cerebral glucose deprivation. The mnemonic 'COLD AND CLAMMY—NEED SOME CANDY' captures the classic presentation: shakiness/tremor, sweating/diaphoresis, tachycardia/palpitations, hunger, anxiety, pallor, and nervousness. As hypoglycemia worsens and the brain becomes more deprived, neuroglycemic symptoms emerge: confusion, slurred speech, blurred vision, difficulty concentrating, headache, and if untreated, seizures and loss of consciousness/coma. Hypoglycemia unawareness (loss of warning symptoms) occurs in patients with long-standing diabetes or frequent hypoglycemic episodes and is particularly dangerous because the patient may progress rapidly to severe hypoglycemia without realizing it. Management follows the 'Rule of 15': if the patient is conscious and able to swallow, administer 15 grams of FAST-ACTING carbohydrate (examples: ½ cup fruit juice or regular soda, 3–4 glucose tablets, 1 tablespoon honey, 5–6 hard candies), WAIT 15 minutes, recheck blood glucose, and if still <70 mg/dL, repeat the 15-gram dose. Once glucose is back to normal, the patient should eat a longer-acting snack or meal (carbohydrate plus protein) to prevent recurrence. If the patient is UNCONSCIOUS, SEIZING, or UNABLE TO SWALLOW, nothing should be given by mouth (risk of aspiration); in hospital, IV dextrose (D50—50% dextrose solution) should be given rapidly; out of hospital, intramuscular or subcutaneous glucagon (1 mg) is administered to mobilize hepatic glucose stores. Family members and caregivers must be taught when and how to use glucagon emergency kits.

DKA is a life-threatening acute hyperglycemic emergency that occurs primarily in Type 1 diabetics (though can occur in Type 2 with severe illness) and results from absolute or near-absolute insulin deficiency. Without insulin, the body cannot utilize glucose for energy; instead, it shifts to rapid fat catabolism (lipolysis), producing ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) faster than they can be metabolized, leading to metabolic ACIDOSIS. The typical precipitating factors include missed insulin doses, new-onset Type 1 DM, infection (UTI, pneumonia, sepsis—the most common trigger), acute illness (MI, stroke), trauma, surgery, or emotional stress. Onset is rapid (hours). Biochemical findings include: plasma glucose usually >250 mg/dL (often 300–600), ELEVATED KETONES in blood and urine (the defining feature), metabolic ACIDOSIS (arterial pH <7.35, bicarbonate <18 mEq/L), low pCO2 (respiratory compensation), elevated anion gap, elevated serum osmolality, and variable potassium (see below—the potassium paradox). Clinical presentation includes Kussmaul respirations (deep, rapid, regular breathing to blow off CO2 as respiratory compensation for acidosis), fruity-smelling breath (from acetone—like nail polish remover), nausea, vomiting, abdominal pain (can mimic surgical abdomen), dehydration (from osmotic diuresis), weakness, fatigue, and altered mental status (restlessness, confusion, lethargy, coma in severe cases). The mortality rate, though much lower with modern intensive care, remains 1–5% if not recognized and treated promptly.

HHNS (also called HHS—hyperglycemic hyperosmolar state) is an acute hyperglycemic emergency that occurs primarily in Type 2 diabetics, particularly older patients, and results from severe hyperglycemia and profound dehydration WITHOUT significant ketosis or acidosis. The pathophysiology involves enough endogenous insulin to suppress lipolysis and ketone formation but insufficient insulin to control hyperglycemia. The severe hyperglycemia (often >600 mg/dL, sometimes exceeding 1,000 mg/dL—much higher than DKA) creates a powerful osmotic diuresis, pulling massive amounts of fluid from intracellular and interstitial compartments into the vascular space and then into the urine, resulting in profound dehydration (often 5–10 liters of fluid loss versus 2–3 liters in DKA). Common triggers include infection (pneumonia, UTI, sepsis), acute illness (MI, stroke), medication non-adherence, and in elderly patients, inadequate access to water or confusion affecting fluid intake. Onset is gradual (days), allowing time for more severe dehydration to develop. Biochemical findings include: extreme hyperglycemia (>600, often >800–1,000 mg/dL), VERY HIGH serum osmolality (>320 mOsm/kg; normal ~285–295), MINIMAL or NO ketosis (no significant ketonemia; maybe small amounts of urine ketones), NORMAL or NEAR-NORMAL pH (no acidosis—this is key), and varying potassium. Clinical presentation includes severe dehydration signs (sunken eyes, poor skin turgor, dry mucous membranes, tachycardia, hypotension), marked neurologic changes (lethargy, confusion, seizures, stroke-like symptoms, coma—worse than DKA because of higher osmolality), and absence of Kussmaul respirations or fruity breath (no ketosis). HHNS carries higher mortality (~5–15%) than DKA, particularly in elderly patients, and recovery is often slower.

Management of both DKA and HHNS follows the same priority sequence, with fluid resuscitation first, insulin second, and careful electrolyte (especially potassium) monitoring throughout. Step 1: IV FLUIDS—the priority. Both conditions feature profound dehydration; aggressive IV rehydration with 0.9% normal saline (isotonic, does not cause cerebral edema) is begun immediately. The first liter may be given rapidly (500 mL in 15–30 minutes if hemodynamically compromised) to restore perfusion; subsequent fluids are given more slowly, with rate adjusted based on vital signs, renal function, and fluid status. Fluid alone often reduces glucose by 25–30% through dilution and improved renal perfusion, improving glomerular filtration of glucose. Step 2: REGULAR INSULIN IV—started once fluids are underway. A typical protocol is an initial bolus of 0.1 units/kg IV, followed by continuous infusion of 0.05–0.1 units/kg/hour; the rate is adjusted to reduce glucose by ~50–100 mg/dL/hour (too-rapid correction risks cerebral edema, especially in children). Regular insulin is the ONLY insulin given IV because it has rapid onset and is the only form compatible with IV lines. Once glucose reaches 200–250 mg/dL, dextrose (D5 or D10) is ADDED to the IV fluids to allow continued insulin infusion (preventing hyperglycemia and hypokalemia) while insulin clears remaining ketones. Step 3: POTASSIUM—the classic NLE trap. Here is the critical concept: At presentation in DKA, TOTAL BODY POTASSIUM IS DEPLETED (from osmotic diuresis and acidosis-driven urinary losses), BUT the serum potassium may initially appear NORMAL or EVEN HIGH because acidosis drives potassium OUT OF cells into the serum (a buffering mechanism). The student's instinct is 'high K = do not give K,' which is exactly WRONG. Once insulin and fluids are administered, insulin drives glucose and potassium BACK INTO cells, and fluids dilute the serum potassium, causing a dramatic drop in serum K toward hypokalemia. Severe hypokalemia causes fatal arrhythmias (asystole, VF). The correct protocol is: (1) Check initial K level; (2) If K is HIGH, do NOT give K, monitor closely; (3) Once K drops to NORMAL (3.5–5 mEq/L) or LOW range, START K replacement (20–40 mEq/hour in IV fluids, adjusted based on repeat labs every 2–4 hours); (4) Monitor continuous ECG and check K levels frequently (every 1–2 hours initially); (5) Insulin should NOT be given if K is dangerously low (<2.5 mEq/L) without concurrent potassium replacement, because insulin will drive it lower. Step 4: Address the PRECIPITATING CAUSE—most commonly infection; antibiotics, source control, and supportive care are essential. Step 5: BICARBONATE—generally NOT given unless pH is <6.9 (because as insulin lowers glucose and fluids dilute ketones, the acidosis resolves naturally); bicarbonate can paradoxically worsen outcomes and cause hypokalemia.

Microvascular complications (affecting small blood vessels and tissues) are primarily caused by hyperglycemia-induced oxidative stress, basement membrane thickening, and sorbitol pathway activation. These complications are largely PREVENTABLE or SLOWED by tight glycemic control and aggressive management of hypertension and dyslipidemia. (1) Diabetic Retinopathy: hyperglycemia damages retinal capillary endothelium, causing microaneurysms, hemorrhages, hard exudates, and eventually retinal detachment and neovascularization (proliferative retinopathy). It is the leading cause of adult vision loss/blindness in developed countries and a growing problem in the Philippines. Early stages are asymptomatic; advanced disease causes blurred vision, floaters, and vision loss. Prevention and early detection require annual dilated retinal exams and tight glucose and blood pressure control; laser photocoagulation can prevent vision loss if caught early. (2) Diabetic Nephropathy: glomerular basement membrane thickening and nodular glomerulosclerosis (Kimmelstiel-Wilson lesions) damage the kidneys, leading to proteinuria (microalbuminuria initially, then overt proteinuria), declining GFR, and eventual end-stage renal disease (ESRD). Nephropathy is the leading cause of ESRD and dialysis need in developed nations. Early detection requires regular urine microalbumin screening; ACE inhibitors and ARBs slow progression significantly (renal protective effect beyond blood pressure lowering) and are first-line antihypertensives in diabetics. (3) Diabetic Neuropathy: hyperglycemia damages peripheral nerves (peripheral neuropathy) and autonomic nerves (autonomic neuropathy), causing loss of protective sensation (especially in feet), paresthesias, numbness, tingling, and pain. Autonomic involvement causes gastroparesis (delayed gastric emptying), orthostatic hypotension, and silent ischemia (MI without chest pain). The combination of neuropathy (loss of protective sensation) + poor circulation + infection vulnerability creates the perfect storm for foot ulceration and amputation—the single most common reason for lower-limb amputation in diabetics. Tight glucose control, regular foot exams, and proper foot care (daily inspection, proper footwear, no heating pads, early treatment of wounds) are essential preventive measures.

Macrovascular complications (atherosclerotic disease of large blood vessels) result from chronic hyperglycemia, hypertension, dyslipidemia, and increased inflammation and thrombosis. Diabetes is considered a coronary artery disease equivalent, meaning a diabetic without prior MI has the same risk of future MI as a non-diabetic with prior MI—reflecting the aggressive atherosclerosis in diabetes. (1) Coronary Artery Disease (CAD): diabetics develop MI at younger ages, more frequently, and with worse outcomes than non-diabetics; diabetics also have higher rates of silent MI (painless, detected only on ECG) due to autonomic neuropathy affecting pain perception. (2) Cerebrovascular Disease: diabetes increases stroke risk 2–4-fold; strokes are often more severe and have worse prognosis in diabetics. (3) Peripheral Arterial Disease (PAD): narrowing of arteries to the legs causes claudication (leg pain with walking), poor wound healing, and increased amputation risk, especially combined with diabetic neuropathy. Cardiovascular disease (combined CAD, stroke, PAD) is the LEADING CAUSE OF DEATH in diabetics, accounting for >60% of mortality. Prevention requires tight glucose control, aggressive hypertension management (target <130/80 mmHg in diabetics per current guidelines), lipid management (statin therapy is recommended for most adults with diabetes), antiplatelet therapy (aspirin), smoking cessation, and regular exercise. Unlike microvascular disease, macrovascular disease is not fully reversible with glucose control alone but is slowed significantly.

Diabetic foot complications are among the most preventable yet most common causes of disability and amputation in diabetes. The pathophysiology involves neuropathy (loss of protective sensation, preventing the patient from feeling foot injuries), peripheral vascular disease (poor circulation preventing healing), and increased infection risk (from hyperglycemia impairing immune function). A simple blister, callus, or nail cut that a non-diabetic would barely notice can become an ulcer, become infected, and progress to amputation in a diabetic. Prevention requires a comprehensive foot care regimen that patients and families must understand and practice daily. Key components: (1) DAILY INSPECTION: Patients must inspect feet (including between toes, soles, and heels) daily, looking for redness, swelling, blisters, cracks, cuts, or calluses; patients with poor vision or mobility should ask family to inspect or use a mirror; early detection prevents progression. (2) PROPER HYGIENE: Feet should be washed daily with warm (not hot—neuropathy prevents heat sensation, risking burns) water and mild soap, then carefully dried, especially between toes (moisture promotes fungal infections). (3) FOOTWEAR: Shoes must be closed-toe (protecting feet from trauma), properly fitted (not tight, no rubbing), and broken in gradually; custom orthotics may be needed for high-risk feet; patients must NEVER walk barefoot, even at home. (4) NAIL CARE: Nails should be cut STRAIGHT ACROSS (not curved, which can cause ingrown nails) and at an appropriate length; if vision or dexterity is limited, a family member or podiatrist should trim nails (do not use razors or sharp instruments). (5) ABSOLUTE CONTRAINDICATIONS: NEVER use heating pads, hot water bottles, or hot baths/soaks on diabetic feet (neuropathy prevents heat sensation, risking severe burns); this is a crucial safety teaching point. (6) CALLUS AND CORN MANAGEMENT: avoid commercial callus removers or 'corn plasters' (risk of ulceration); use gentle pumice if needed; see a podiatrist for professional management. (7) EARLY TREATMENT: Any wound, blister, rash, or infection should be reported to the provider immediately; delays can lead to progression. (8) REGULAR PROFESSIONAL EXAMS: Annual or more frequent foot exams by a provider experienced in diabetic foot care, including sensory testing (monofilament test), vascular assessment, and screening for ulcer risk.

Two distinct causes of morning hyperglycemia in insulin-treated diabetics are frequently confused; understanding the difference is essential because the treatment is opposite. (1) Somogyi Phenomenon (Waning Phenomenon): nocturnal hypoglycemia triggers a rebound hyperglycemia from counter-regulatory hormone release (glucagon, epinephrine, cortisol). The patient has a low blood glucose in the middle of the night (e.g., 2–3 a.m.), which stimulates counter-regulatory hormones, causing morning hyperglycemia. The treatment is to REDUCE the evening insulin dose or ADD a bedtime carbohydrate snack to prevent the nocturnal low. (2) Dawn Phenomenon: early-morning hyperglycemia results from normal early-morning hormone surge (cortisol, growth hormone, glucagon) stimulating hepatic glucose production; it is NOT preceded by nocturnal hypoglycemia. The glucose at 2–3 a.m. is normal or even high, but morning glucose is high simply due to the natural hormone surge. The treatment is to INCREASE or ADJUST the timing of evening insulin (or use a longer-acting basal insulin) to cover the early-morning surge. Differentiation is simple: CHECK THE 2–3 A.M. GLUCOSE. If low → Somogyi phenomenon (reduce evening insulin). If normal/high → Dawn phenomenon (increase evening insulin).

When diabetic patients become ill (from infection, surgery, trauma, or other acute illness), blood glucose typically rises even if food intake decreases, because illness increases counter-regulatory hormones (cortisol, catecholamines, glucagon) and inflammatory cytokines. A critical teaching point is that patients must NEVER omit insulin during illness, even if they are not eating—this is a common and dangerous mistake. Sick-day management includes: (1) CONTINUE INSULIN: Take the usual insulin dose (or even slightly more) despite reduced eating; the illness itself raises glucose. (2) INCREASE MONITORING: Check blood glucose more frequently (every 2–4 hours) and test for ketones if glucose is elevated (to detect early DKA); this is especially important for Type 1 patients. (3) MAINTAIN HYDRATION AND CARBOHYDRATES: If food cannot be tolerated, take frequent small amounts of liquids containing carbohydrates (juice, regular soda, clear broth, gelatin) to prevent both dehydration and hypoglycemia. (4) NOTIFY PROVIDER: Contact the healthcare provider if glucose remains elevated (>240 mg/dL), ketones are present, vomiting persists, or symptoms worsen—these may indicate DKA development. (5) REST: Allow adequate rest to facilitate recovery. General self-management education (outside of sick days) includes carbohydrate-consistent diet (understanding portion sizes and carb counting), regular moderate exercise (understanding hypoglycemia risk and need to adjust insulin/carbs around activity), regular home glucose monitoring, understanding medication regimens and side effects, recognizing hypoglycemic symptoms, and achieving A1c targets (<7% for most adults, individualized based on age and complications). Patient education is the cornerstone of diabetes management and is a key nursing responsibility under RA 9173; nurses must assess literacy, language, and cultural factors affecting learning and provide education appropriate to the patient's level.

The nursing process in diabetes care applies NANDA International nursing diagnoses to identify patient problems and develop individualized care plans. Common diabetes diagnoses include: (1) Ineffective Health Maintenance r/t (related to) insufficient knowledge regarding diabetes self-management; (2) Unbalanced Nutrition: More Than Body Requirements r/t lack of knowledge about balanced diet and portion control (Type 2); (3) Impaired Physical Mobility r/t complications (neuropathy, vision loss, CVA); (4) Risk for Imbalanced Fluid Volume r/t osmotic diuresis (in DKA/HHNS); (5) Acute Confusion r/t hypoglycemia or hyperglycemia (DKA/HHNS); (6) Risk for Infection r/t hyperglycemia-impaired immunity; (7) Risk for Peripheral Neurovascular Dysfunction r/t neuropathy and vascular disease; (8) Deficient Knowledge r/t insulin administration, medications, self-monitoring, foot care; (9) Fatigue r/t hyperglycemia and metabolic changes; (10) Powerlessness r/t chronic disease management; (11) Anxiety r/t newly diagnosed diabetes or fear of complications. Nursing interventions are prioritized using Maslow's hierarchy: physiologic needs (stabilizing acute crises like DKA, treating hypoglycemia, ensuring nutrition/hydration) → safety needs (preventing infection, foot ulcers, teaching fall prevention) → love/belonging → esteem → self-actualization (patient empowerment through education and support). For each diagnosis, specific interventions are tailored to the patient's age, type of diabetes, complications, literacy, and social support.

The Nursing Act of the Philippines (Republic Act 9173) defines the scope of nursing practice, including the roles and responsibilities of nurses in chronic disease management such as diabetes. Under RA 9173, registered nurses (RNs) provide direct patient care, health teaching, and health counseling. In diabetes management, the nurse's role includes: (1) Assessment: conducting comprehensive health histories, assessing for diabetic symptoms and complications, performing physical exams; (2) Diagnosis: applying the nursing process to identify patient problems using NANDA diagnoses; (3) Planning: developing individualized care plans with patient/family input; (4) Implementation: administering medications (including insulin), performing wound care, monitoring glucose, teaching self-management, providing emotional support, coordinating referrals; (5) Evaluation: assessing patient progress toward goals and adjusting interventions. The National Competency-Based Curriculum for Nursing (NCM) establishes competencies expected of nurses working in various healthcare levels—from NCM Level 1 (basic community-based care in rural health units) to NCM Level 3 (tertiary/specialty nursing in hospitals). In diabetes care, nurses at all levels must understand pathophysiology, recognize complications, administer medications safely, provide patient education, and collaborate with physicians and allied professionals. The Philippine healthcare delivery system includes primary health centers (PHCs) serving rural communities, city health centers, district hospitals, and tertiary institutions; nurses in each setting must adapt diabetes care to available resources (e.g., in rural areas, nurses may manage stable diabetes with minimal physician oversight; in tertiary centers, nurses collaborate in intensive care of acute crises). Adherence to evidence-based guidelines (Philippine Clinical Practice Guidelines, ADA standards), infection control, and professional ethics are foundational.