NCLEX-PN Pain Assessment and Management — Practice Questions

NASOGASTRIC TUBE FEEDING SAFETY: confirming tube placement BEFORE each feeding is a CRITICAL PATIENT SAFETY STEP. A misplaced tube (in the respiratory tract) with feeding infusion can cause ASPIRATION, PNEUMONIA, and potentially DEATH. TUBE PLACEMENT VERIFICATION: RECOMMENDED — ASPIRATION AND pH TESTING: aspirate gastric contents; gastric contents have pH < 5 (acidic); intestinal fluid is 6-8; respiratory fluid is >7; confirm pH before each feeding; AUSCULTATION OF AIR ('whoosh' test — inserting air and listening) is NOT RELIABLE as a primary confirmation method and should not be used as the sole method — bowel sounds can be transmitted to the respiratory tract; RADIOGRAPHY (X-RAY): GOLD STANDARD for initial placement confirmation — mandatory after initial NG tube insertion; visual confirmation of tube tip in the stomach; AFTER INITIAL X-RAY CONFIRMATION: subsequent checks before each feeding use pH and aspiration; CHECKING RESIDUAL: after confirming placement, aspirate to measure GASTRIC RESIDUAL VOLUME (GRV) — how much feeding remains from previous feeding; high residual (typically >250-500 mL, per facility policy) may indicate delayed gastric emptying; follow facility protocol (may hold feeding, notify RN, or continue feeding depending on clinical situation); replace aspirate to avoid losing gastric acid and electrolytes. ADDITIONAL SAFETY MEASURES: POSITION: elevate HOB 30-45° during feeding and 30 minutes after to reduce aspiration risk; RATE: start slowly, advance per orders; FLUSHING: flush tube with 30 mL water before and after feeding and medications; ASSESS for ASPIRATION SIGNS: coughing, choking, desaturation, respiratory distress. PN ROLE: verify placement per protocol; check residual; position client; administer feeding as ordered; monitor for complications; flush appropriately.

HYPONATREMIA is defined as serum sodium below 135 mEq/L. Normal: 135-145 mEq/L. A value of 125 mEq/L is SIGNIFICANTLY LOW. PATHOPHYSIOLOGY: sodium is the primary extracellular osmole; when sodium drops, serum osmolality drops; water moves by osmosis from the low-sodium ECF INTO cells (following osmotic gradient); BRAIN CELLS SWELL → neurological symptoms are the hallmark. CLINICAL MANIFESTATIONS based on severity and rate of onset: MILD (130-135 mEq/L): may be asymptomatic or have nausea, headache, malaise; MODERATE (125-130 mEq/L): headache, nausea, vomiting, lethargy, confusion, muscle cramps; SEVERE (<125 mEq/L): seizures, coma, respiratory arrest, death. RATE MATTERS: ACUTE hyponatremia (rapid drop) is more dangerous than chronic hyponatremia (brain has had time to adapt). CAUSES: HYPERVOLEMIC (too much water, normal sodium): heart failure, cirrhosis, nephrotic syndrome, SIADH; HYPOVOLEMIC (lost sodium and water, but more sodium than water): GI losses, diuretics, adrenal insufficiency; EUVOLEMIC: SIADH (syndrome of inappropriate antidiuretic hormone secretion — common cause; ADH causes water retention without sodium retention; causes: malignancy, CNS disorders, medications); water intoxication (rare). CONTRAST WITH HYPERNATREMIA (high sodium, >145 mEq/L): extreme thirst, dry mucous membranes, fever, decreased urine output, concentrated urine, confusion, seizures (cells shrink); treated with free water replacement. TREATMENT OF HYPONATREMIA: depends on cause and severity; mild-moderate: fluid restriction (for SIADH); replace sodium if depleted; CAUTION: correct SLOWLY (no more than 8-12 mEq/L per 24 hours) — rapid correction causes OSMOTIC DEMYELINATION SYNDROME (ODS, formerly central pontine myelinolysis) — irreversible brain damage. PN ROLE: monitor serum electrolytes; observe for neurological changes; report confusion or seizures immediately; measure I&O; implement fluid restriction if ordered.

OPIOID-INDUCED RESPIRATORY DEPRESSION is the most dangerous immediate adverse effect of opioid medications. A respiratory rate of 8 breaths per minute (normal: 12-20) with deep sedation represents an ACUTE LIFE-THREATENING EMERGENCY. MECHANISM: opioids bind to mu receptors in the medullary respiratory center, depressing the respiratory drive; CO2 accumulates → hypercapnia → acidosis → respiratory arrest → cardiac arrest. RISK FACTORS for opioid respiratory depression: opioid-naïve patients (no tolerance); high doses; rapid dose escalation; concurrent CNS depressants (benzodiazepines, alcohol, other opioids); advanced age; underlying respiratory disease; renal or hepatic impairment; sleep apnea. IMMEDIATE ACTIONS for respiratory rate ≤8-10 with excessive sedation: ASSESS — stimulate the client (shout name, sternal rub); if responsive and breathing, monitor closely; if unresponsive or not breathing: CALL FOR HELP immediately; maintain AIRWAY (jaw thrust, head tilt-chin lift); OXYGEN; if no spontaneous breathing: VENTILATE; ADMINISTER NALOXONE (Narcan) per order or standing protocol: 0.4-2 mg IV (or IM/intranasal); onset 1-2 minutes; DURATION of naloxone is SHORTER than most opioids (30-60 minutes) — the opioid effect may return; REPEAT NALOXONE as needed; MONITOR continuously after naloxone. POST-NALOXONE: pain will return as opioid effect is reversed; document carefully; reassess need for opioid and adjust dose/frequency with provider. SEDATION SCALE: passive sedation scales (Pasero Opioid-Induced Sedation Scale, POSS) are used to guide opioid monitoring. COMMON BUT LESS URGENT OPIOID SIDE EFFECTS: CONSTIPATION (anticipate and prevent — start bowel regimen from day 1; use stimulant laxatives, not just stool softeners); NAUSEA (often transient); PRURITUS (especially with neuraxial opioids); URINARY RETENTION; MIOSIS (pupil constriction).

FASTING BLOOD GLUCOSE test measures blood glucose after an adequate fasting period and is used to: SCREEN for diabetes (fasting glucose ≥126 mg/dL on two separate occasions = diabetes); DIAGNOSE impaired fasting glucose (prediabetes: 100-125 mg/dL); MONITOR glycemic control in known diabetics (less commonly than A1c now, but still used). FASTING REQUIREMENTS: nothing to eat or drink (except WATER) for 8-12 hours before the test; water is allowed and encouraged (does not affect glucose; prevents dehydration which can concentrate the sample); no food, juice, coffee, milk, or caloric beverages; smoking may affect results (advise against). MEDICATION CONSIDERATIONS: most oral medications can be taken with a small sip of water unless specifically contraindicated; insulin-dependent diabetics should hold morning insulin dose UNLESS fasting glucose is known (hypoglycemia risk); specific instructions from the provider take precedence. COMMON LAB TESTS AND THEIR REQUIREMENTS: FASTING (nothing except water, 8-12 hours): blood glucose, HbA1c (no special requirements actually, but many labs draw it fasting), lipid panel, iron studies; NO SPECIAL PREP: CBC, electrolytes, BMP, CMP (though many labs prefer early morning); TIMED SAMPLES: cortisol (AM/PM), ACTH, morning cortisol best drawn 8 AM. PN ROLE: provide clear verbal AND written instructions; confirm the client understood (teach-back); document that instructions were given; confirm appointment time and location; advise the client to bring their glucose monitor if diabetic; if the client accidentally ate, inform the lab and the ordering provider before drawing — the fasting interpretation cannot be applied.

SEVERE HYPOGLYCEMIA (blood glucose <54 mg/dL with impaired consciousness) is a MEDICAL EMERGENCY. An unconscious client with a blood glucose of 38 mg/dL requires immediate treatment. PRIORITY TREATMENT: IV ACCESS AVAILABLE: 50% DEXTROSE (D50W) — 25 grams (50 mL) IV push is standard treatment for severe hypoglycemia with IV access; glucose is administered directly into the bloodstream for rapid correction; blood glucose typically rises within 5-10 minutes; NO IV ACCESS (or if IV is delayed): GLUCAGON — 1 mg IM or SubQ (kit given to family for home use); mechanism: stimulates liver to release stored glucose (glycogenolysis and gluconeogenesis); takes 15-20 minutes to work; less effective with alcohol intoxication or prolonged fasting (depleted glycogen stores); INTRANASAL GLUCAGON (Baqsimi): 3 mg — newer delivery method; easier to administer. DO NOT give oral glucose (juice, glucose tablets) to an UNCONSCIOUS client — aspiration risk. AFTER REGAINING CONSCIOUSNESS: give a complex carbohydrate snack; monitor blood glucose frequently; assess for the CAUSE of hypoglycemia (missed meal, too much insulin, increased exercise, vomiting). INSULIN SHOULD NEVER BE GIVEN — insulin lowers glucose further; would be fatal. HYPOGLYCEMIA CAUSES in diabetes: too much insulin or oral antidiabetic medication; missed or delayed meals; increased physical activity without adjusting medication or intake; alcohol consumption; liver or kidney disease affecting drug clearance. CLINICAL MANIFESTATIONS: MILD (BS 54-69): adrenergic — diaphoresis, shakiness, palpitations, hunger, pallor, anxiety; MODERATE: neuroglycopenic — confusion, difficulty concentrating, headache, visual changes; SEVERE: seizures, loss of consciousness, coma. RULE OF 15 for conscious clients with mild hypoglycemia: 15g fast carbs, wait 15 min, recheck.

CATHETER-ASSOCIATED URINARY TRACT INFECTION (CAUTI) is the most common healthcare-associated infection (HAI) in hospitals. Every day an indwelling urinary catheter is in place increases infection risk by 3-7%. CAUTI PREVENTION is a major patient safety priority. APPROPRIATE INDICATIONS FOR INDWELLING URINARY CATHETERS: urinary retention that doesn't respond to other management; accurate I&O monitoring in critically ill clients; perioperative use for specific surgeries; wound healing in sacral/perineal wounds where urine would compromise healing; hospice/end-of-life comfort; urological procedures; neurogenic bladder (selected cases). NOT APPROPRIATE indications: incontinence for CONVENIENCE (of staff or client); prolonged post-operative use without clinical need; avoiding repositioning. ALTERNATIVES TO CATHETERIZATION FOR INCONTINENCE: SCHEDULED TOILETING (every 2-4 hours); PROMPTED VOIDING; BLADDER TRAINING; EXTERNAL CONDOM CATHETER (for male patients); ABSORBENT PADS/BRIEFS; SKIN PROTECTION (moisture barriers to prevent skin breakdown from moisture — valid concern but doesn't require catheter); PELVIC FLOOR EXERCISES (Kegel exercises, though less applicable in acute illness). IF CATHETER IS GENUINELY INDICATED: use SMALLEST POSSIBLE CATHETER (less trauma); maintain CLOSED STERILE DRAINAGE SYSTEM; keep urine drainage bag BELOW BLADDER LEVEL (prevents reflux); empty bag when 2/3 full; assess daily for continued need; REMOVE AS SOON AS POSSIBLE (each additional day increases risk). CAUTI SIGNS: fever without other source, suprapubic tenderness, cloudy or foul-smelling urine (though these alone don't diagnose CAUTI), burning urination when catheter is removed.

WARFARIN (Coumadin) is a VITAMIN K ANTAGONIST anticoagulant — it works by blocking the vitamin K-dependent clotting factors (II, VII, IX, X) and the anticoagulant proteins C and S. VITAMIN K INTERACTION: Vitamin K REVERSES warfarin's anticoagulant effect by providing the substrate for clotting factor synthesis. High Vitamin K intake → more clotting factors activated → lower INR (subtherapeutic, increased clot risk); Low Vitamin K intake → fewer clotting factors → higher INR (supratherapeutic, increased bleeding risk). KEY TEACHING POINT: Patients on warfarin do NOT need to ELIMINATE vitamin K foods — they need to be CONSISTENT in their intake. Sudden changes (starting a diet high in leafy greens, or stopping a diet high in leafy greens) will destabilize INR. HIGH VITAMIN K FOODS: kale, spinach, collard greens, Swiss chard, broccoli, Brussels sprouts, green onions, parsley. MONITORING: INR (International Normalized Ratio) is monitored regularly; THERAPEUTIC INR: 2.0-3.0 for most indications (DVT, PE, atrial fiib, mechanical heart valves require 2.5-3.5); ANTIDOTE: Vitamin K (phytonadione) — reverses warfarin; for serious bleeding: fresh frozen plasma (FFP) or 4-factor PCC (prothrombin complex concentrate) for faster reversal. DRUG INTERACTIONS: warfarin has MANY interactions; drugs that INCREASE INR (bleeding risk): antibiotics (especially broad-spectrum, disrupt gut bacteria that produce Vitamin K), NSAIDs, cimetidine, amiodarone, statins; drugs that DECREASE INR (clot risk): rifampin, barbiturates (enzyme inducers), cholestyramine (binds warfarin in gut). BRIDGING: hospitalized patients on warfarin may need IV heparin while warfarin is being adjusted or held for procedures. PN TEACHING: take warfarin at the SAME TIME each day; never skip or double-up doses; notify provider of any new medication (OTC or prescription); wear a medical alert bracelet; avoid activities with high bleeding risk; call provider if INR is out of range.

HYPERCALCEMIA is defined as serum calcium >10.5 mg/dL. Normal: 8.5-10.5 mg/dL. A level of 12.5 mg/dL is significantly elevated. CLINICAL MNEMONIC for hypercalcemia: 'BONES, GROANS, MOANS, AND STONES': BONES: bone pain and pathological fractures — calcium is being leached from bones (especially in malignancy or hyperparathyroidism); GROANS: GI symptoms — nausea, vomiting, anorexia, CONSTIPATION (calcium decreases GI motility), abdominal pain; MOANS: neuropsychiatric — confusion, depression, psychosis, altered mental status, DECREASED DEEP TENDON REFLEXES (calcium stabilizes nerve membranes, reducing excitability), muscle weakness, fatigue, lethargy; STONES: kidney stones (calcium oxalate or calcium phosphate) — polyuria, nephrolithiasis, nephrocalcinosis. CARDIAC EFFECTS: shortened QT interval on ECG (calcium shortens repolarization); dysrhythmias in severe cases. CONTRAST WITH HYPOCALCEMIA: TETANY (muscle spasms, cramping); POSITIVE TROUSSEAU'S SIGN (carpal spasm when BP cuff inflated above systolic for 3 minutes); POSITIVE CHVOSTEK'S SIGN (facial muscle twitch when tapping the facial nerve anterior to the ear); PARESTHESIAS (perioral, fingertips); SEIZURES; INCREASED DEEP TENDON REFLEXES; PROLONGED QT INTERVAL on ECG. CAUSES OF HYPERCALCEMIA: MALIGNANCY (most common in hospitalized patients — bone metastases, PTH-related protein secretion); PRIMARY HYPERPARATHYROIDISM (most common cause overall in outpatients); vitamin D toxicity; prolonged immobilization; thiazide diuretics; sarcoidosis; milk-alkali syndrome. TREATMENT: IV NORMAL SALINE (first-line — hydration promotes renal calcium excretion); FUROSEMIDE (after adequate hydration — promotes calciuresis); BISPHOSPHONATES (for malignancy-associated hypercalcemia); CALCITONIN (rapid but temporary); CORTICOSTEROIDS (for vitamin D-related causes, sarcoidosis); DIALYSIS (severe refractory cases). PN ROLE: monitor for symptoms; hydration; fall risk (weakness, confusion); educate on adequate hydration; report severe symptoms or rapidly rising values.

A CLIENT WITH TRACHEOSTOMY reporting inability to breathe is a RESPIRATORY EMERGENCY. Never leave the client alone during a tracheostomy emergency. IMMEDIATE ASSESSMENT AND ACTIONS: STAY WITH CLIENT and CALL FOR HELP (call code/emergency team, call RN and provider); ASSESS AIRWAY: look-listen-feel at the tracheostomy opening; ASSESS TUBE POSITION: is the tube in the correct position or has it been displaced (dislodged, obstruction)? OBSTRUCTION WITH MUCUS PLUG (most common cause): suction the tracheostomy immediately using sterile technique (inner cannula, suction through tube); can also attempt to IRRIGATE with 1-2 mL normal saline (now less recommended but still used acutely); INNER CANNULA: remove and clean or replace disposable inner cannula — this can rapidly relieve blockage; TUBE DISLODGEMENT: if tube has come out or is clearly out of the trachea: keep stoma open; position: hyperextend the neck to open the stoma; use an obturator to re-insert same tube if available; OR use 10% smaller tube if same size won't go in easily; EMERGENCY SUPPLIES that must be AT BEDSIDE for every tracheostomy patient: tracheostomy tube of SAME SIZE AND ONE SIZE SMALLER, obturator (used for reinsertion), bag-valve mask (Ambu bag) that fits tracheostomy, suction supplies, extra inner cannula, emergency tracheostomy tray; BAG-VALVE MASK VENTILATION through tracheostomy if client is not breathing; OXYGEN: ensure 100% O2 during emergency. PN ROLE: recognize the emergency; call for help; initiate airway management within scope; have emergency supplies organized at bedside; document. ONGOING CARE: tracheostomy care every 8 hours or per protocol (clean stoma, change inner cannula, change ties when loose/soiled, assess for complications).

CHRONIC PAIN management has evolved significantly with recognition that pain is complex — involving biological, psychological, and social factors (the biopsychosocial model). EVIDENCE-BASED NON-PHARMACOLOGICAL APPROACHES: COGNITIVE-BEHAVIORAL THERAPY (CBT) for pain: most evidence-based psychological approach; addresses catastrophizing, maladaptive thoughts, pain behaviors; improves functioning and quality of life even when pain intensity doesn't fully resolve; MINDFULNESS-BASED STRESS REDUCTION (MBSR): meditation-based approach; reduces pain-related distress; PHYSICAL THERAPY AND EXERCISE: counterintuitive but movement is generally beneficial for most chronic pain (including low back pain); reduces deconditioning and muscle atrophy; HEAT THERAPY: increases blood flow, relaxes muscles; for chronic muscle pain; not for acute inflammation; COLD THERAPY (CRYOTHERAPY): reduces inflammation and acute pain; numbs area; for acute injuries or inflammatory conditions; TENS (Transcutaneous Electrical Nerve Stimulation): low-level electrical current modulates pain signals; evidence moderate; useful adjunct; MASSAGE: reduces muscle tension; improves mood; evidence for some chronic pain types; BIOFEEDBACK: teaches physiological self-regulation; ACUPUNCTURE: evidence for some pain conditions (low back pain, osteoarthritis, headache); DISTRACTION: music therapy, guided imagery, virtual reality (newer, emerging evidence); POSITIONING AND ASSISTIVE DEVICES: proper positioning, orthotic devices for joint pain. MULTIMODAL ANALGESIA: the current standard of care combines multiple approaches (pharmacological and non-pharmacological) at lower doses to achieve pain control while minimizing side effects of any single approach. PN ROLE: teach and implement non-pharmacological measures; assess pain with validated tools (0-10 numeric, FACES, FLACC for children); document pain assessment and response to interventions; advocate for adequate pain management; avoid stigmatizing chronic pain patients.