NCLEX-PN Wound Care and Pain Management Practice Questions

RANGE-OF-MOTION EXERCISES maintain joint flexibility, prevent contractures, maintain muscle tone, improve circulation, and prevent complications of immobility. TYPES: PASSIVE ROM — nurse moves the client's joints through the range; used when client cannot participate (unconscious, complete paralysis, very weak); ACTIVE-ASSISTED ROM — nurse assists the client who can do some movement; ACTIVE ROM — client performs exercises independently; nurse provides instruction and encouragement. CORRECT TECHNIQUE: SUPPORT: hold the limb at the joint (above AND below) to stabilize and support the weight; SMOOTH AND SLOW: no jerky or rapid movements; FULL AVAILABLE RANGE: move the joint as far as it will comfortably go; STOP FOR PAIN: pain indicates possible injury or joint problem; stop, document, and report; WARMTH helps muscles and joints move more freely; some facilities encourage warm soaks prior to ROM; SEQUENCE: start at head and work down, or from proximal (closer to body) to distal (farther from body). FREQUENCY: typically 2-4 times per day; each joint 5-10 repetitions. ROM MOVEMENTS by joint type: HINGE JOINTS (elbow, knee) — flexion and extension; BALL-AND-SOCKET (shoulder, hip) — flexion, extension, abduction, adduction, rotation, circumduction; PIVOT (neck) — rotation; SADDLE (thumb) — wide variety of movements. CONTRACTURES: fixed joint deformity from muscle shortening due to prolonged immobility; prevention is key — far harder to reverse than to prevent; foot drop (plantar flexion contracture) prevented with foot board or splints and dorsiflexion ROM. PN ROLE: perform passive ROM, active-assisted ROM; document tolerance; report any pain, redness, swelling, decreased range; reinforce PT/OT instructions; educate family on ROM techniques.

PRESSURE INJURIES (formerly called pressure ulcers or decubitus ulcers) are localized areas of injury to the skin and/or underlying tissue, usually over a bony prominence, resulting from sustained pressure, shear, or friction. PATHOPHYSIOLOGY: pressure compresses capillaries, reducing blood flow; ischemia leads to tissue death; prolonged pressure (even low pressure over time) causes injury; highest-risk areas: sacrum/coccyx, heels, greater trochanter, ischial tuberosities, occiput, medial and lateral malleoli, elbows, scapulae. STAGING (NPUAP/EPUAP): STAGE 1: non-blanchable erythema of intact skin — early warning sign; STAGE 2: partial-thickness skin loss, shallow open ulcer with red/pink wound bed; STAGE 3: full-thickness skin loss, subcutaneous fat visible; STAGE 4: full-thickness tissue loss, bone, tendon, or muscle visible; UNSTAGEABLE: full-thickness but covered by slough/eschar; DEEP TISSUE INJURY: intact skin with discoloration/blood-filled blister. PRIMARY INTERVENTIONS: REPOSITIONING every 2 hours (or per individualized schedule based on tissue tolerance and patient condition); documentation of position changes; SKIN INSPECTION with each repositioning (especially bony prominences); KEEP SKIN CLEAN AND DRY: moisture (incontinence, sweat) dramatically increases skin breakdown; use moisture barriers (zinc oxide); MINIMIZE FRICTION AND SHEAR: use lift sheets for repositioning, not dragging; PRESSURE REDISTRIBUTION: specialty mattresses (foam, air-fluidized, low-air-loss); heel protectors; NUTRITION AND HYDRATION: protein critical for tissue repair (target adequate protein intake); adequate fluids; nutritional supplements if needed; BRADEN SCALE: most common standardized risk assessment tool (scores sensory perception, moisture, activity, mobility, nutrition, friction/shear; score ≤18 indicates risk).

DIGOXIN (Lanoxin) is a CARDIAC GLYCOSIDE used for: heart failure (positive inotrope — increases cardiac contractility); atrial fibrillation/flutter (rate control — increases AV node refractory period, slowing ventricular rate). MECHANISM: inhibits Na-K-ATPase pump → increased intracellular sodium → increased intracellular calcium → stronger cardiac contraction; also has vagotonic effects (slows SA and AV node). BEFORE EACH DOSE: APICAL PULSE FOR ONE FULL MINUTE — if below 60 bpm (bradycardia) in adults, HOLD THE DOSE and notify provider; per some protocols the parameter may be 50 or 55; in children the parameters vary by age. THERAPEUTIC RANGE: 0.5-2.0 ng/mL (the therapeutic range is narrow — easy to reach toxic levels). DIGOXIN TOXICITY SIGNS (EARLY): GI — anorexia, nausea, vomiting, diarrhea; NEUROLOGICAL — headache, fatigue, visual changes (classic: YELLOW-GREEN HALOS around lights, blurred vision, xanthopsia); CARDIAC — bradycardia, heart block, dysrhythmias (the most dangerous aspect — almost any dysrhythmia possible). FACTORS THAT INCREASE TOXICITY RISK: hypokalemia (low K+ makes the heart more sensitive to digoxin — monitor K+ levels, particularly in patients taking diuretics); hypomagnesemia; hypercalcemia; renal insufficiency (digoxin renally cleared); old age; drug interactions (amiodarone, verapamil, quinidine elevate digoxin levels). TREATMENT OF TOXICITY: DIGOXIN IMMUNE FAB (Digibind) — specific antidote; correct electrolytes; cardiac monitoring; supportive care. PN RESPONSIBILITIES: check apical rate before each dose; hold for bradycardia per parameters; report signs of toxicity immediately; monitor K+ levels; teach client to report nausea, vision changes, or slow pulse.

HEPARIN is an anticoagulant that works by activating antithrombin III, which in turn inhibits thrombin and factor Xa — interrupting the intrinsic and common coagulation pathways. MONITORING: IV HEPARIN is monitored with aPTT (activated partial thromboplastin time); normal aPTT = 25-40 seconds; THERAPEUTIC aPTT for heparin = 60-100 seconds (1.5-2.5 × control); aPTT is checked every 6 hours until stable, then daily. WARFARIN (Coumadin) is monitored with PT/INR (prothrombin time/International Normalized Ratio) — warfarin affects the extrinsic pathway (factor VII and others). PT/INR DOES NOT ACCURATELY REFLECT HEPARIN EFFECT. HEPARIN TOXICITY SIGNS: bleeding (easy bruising, petechiae, hematuria, melena, hemoptysis, intracranial bleeding); prolonged oozing from IV sites or skin punctures. ANTIDOTE: PROTAMINE SULFATE reverses heparin (1 mg protamine per 100 units of heparin); given slowly IV (can cause hypotension and anaphylaxis). HEPARIN-INDUCED THROMBOCYTOPENIA (HIT): IMMUNE-MEDIATED adverse reaction; paradoxically causes THROMBOSIS (not bleeding) despite low platelets; onset 5-10 days after starting heparin; PLATELET COUNT monitored to detect HIT (platelet drop >50% from baseline is suspicious); treatment: STOP heparin immediately, switch to non-heparin anticoagulant (argatroban, bivalirudin, fondaparinux). LOW MOLECULAR WEIGHT HEPARIN (LMWH — enoxaparin/Lovenox): monitored with anti-Xa level; does NOT require routine aPTT monitoring for most patients; subcutaneous injection; easier outpatient use. PN ROLE: monitor aPTT; assess for bleeding; hold pressure on IV sites; teach patient about bleeding precautions (soft toothbrush, electric razor, fall prevention); report any aPTT out of therapeutic range to RN immediately.

CARDIAC CATHETERIZATION via FEMORAL ARTERY ACCESS introduces a large catheter into the femoral artery. After removal, a small hole is left in a major artery — HEMORRHAGE and VASCULAR COMPLICATIONS are the primary post-procedure risks. PRIORITY POST-PROCEDURE ASSESSMENTS: SITE INSPECTION: bleeding (check directly and under the client — blood can pool under the client undetected); hematoma (expanding lump/discoloration at site — concerning if rapidly enlarging or causing neurovascular compromise); NOTE: femoral access requires the client to keep the leg STRAIGHT and LIMIT movement for the prescribed period (typically 2-6 hours depending on closure method); VASCULAR STATUS of the affected extremity: PULSES (dorsalis pedis and posterior tibial pulses distal to the site — check every 15 minutes initially); CIRCULATION: COLOR (pale = arterial occlusion; cyanotic = venous obstruction); TEMPERATURE (should be warm — cold = reduced perfusion); CAPILLARY REFILL (<3 seconds = adequate); SENSATION AND MOVEMENT (numbness, tingling, weakness = neurovascular compromise). FREQUENCY: typically every 15 minutes for the first hour, every 30 minutes for the next hour, then every hour. COMPLICATIONS TO DETECT: BLEEDING: may be external or internal (retroperitoneal hematoma — may not be visible but presents with flank/back pain, hypotension, tachycardia, dropping H&H); ARTERIAL OCCLUSION: absent or diminished distal pulse, pain, pallor, paresthesia, paralysis — 'the 5 P's of arterial occlusion'; PSEUDOANEURYSM: pulsatile mass at site; ARTERIOVENOUS FISTULA: palpable thrill at site; VASOVAGAL: hypotension, bradycardia, nausea. REPORT TO RN: any absent or diminishing distal pulse; expanding hematoma; bleeding that doesn't stop with pressure; hypotension or tachycardia; extremity pallor, cyanosis, or coldness.

HYPOKALEMIA is defined as serum potassium below 3.5 mEq/L. Normal range: 3.5-5.0 mEq/L. A level of 2.9 mEq/L is SIGNIFICANTLY LOW and clinically concerning. CLINICAL MANIFESTATIONS OF HYPOKALEMIA: CARDIAC: most dangerous; PVCs (premature ventricular contractions); U WAVES on ECG (prominent — a U wave following the T wave is a classic ECG sign of hypokalemia); flattened T waves; prolonged QU interval; progression to ventricular tachycardia or ventricular fibrillation if severe; MUSCLES: muscle weakness (legs first, ascending); muscle cramps; PARALYTIC ILEUS (lack of bowel sounds, abdominal distension, constipation); respiratory muscle weakness with very low K+; NEUROLOGICAL: fatigue, lethargy, confusion; RENAL: polyuria (paradoxically, hypokalemia impairs the kidney's ability to concentrate urine). CAUSES OF HYPOKALEMIA: loop and thiazide diuretics (most common); vomiting; nasogastric suction; diarrhea; sweating; poor dietary intake; increased renal excretion (hyperaldosteronism, Cushing's syndrome); alkalosis (K+ shifts into cells). TREATMENT: ORAL POTASSIUM REPLACEMENT (KCl tablets or liquid — better absorbed with food; GI irritating); IV POTASSIUM: NEVER push IV K+ directly — can cause cardiac arrest; dilute in IV fluids (typically no more than 10-20 mEq/hr via peripheral line; higher concentrations require central line); cardiac monitoring during IV K+ administration; DIETARY SOURCES: bananas, oranges, potatoes, leafy greens, tomatoes, beans. HYPERKALEMIA (contrast): K+ >5.0 mEq/L; PEAKED (TALL TENT) T WAVES on ECG; widened QRS; cardiac arrest risk; muscle weakness; causes: renal failure, ACE inhibitors, potassium-sparing diuretics, acidosis. PN ROLE: report abnormal K+ immediately; administer replacement per order; monitor ECG; assess for symptoms; teach dietary sources.

FLUID VOLUME EXCESS (FVE), also called hypervolemia or fluid overload, occurs when too much fluid is retained in the body. In HEART FAILURE, the failing heart cannot pump blood forward effectively; fluid backs up in the venous system and lungs. HALLMARK SIGNS OF FVE: PERIPHERAL EDEMA — dependent edema (ankles/feet when upright, sacrum when supine); PULMONARY EDEMA — crackles (rales) at lung bases; dyspnea; orthopnea (difficulty breathing when lying flat); paroxysmal nocturnal dyspnea; WEIGHT GAIN — 1 kg ≈ 1 liter of fluid; 2 kg in 2 days is significant (daily weight is the MOST SENSITIVE early indicator of fluid retention); ELEVATED BLOOD PRESSURE — from increased circulating volume; JUGULAR VEIN DISTENSION (JVD) — at 45° head of bed elevation, visible jugular pulsation >2 cm above sternal angle indicates elevated central venous pressure; FULL, BOUNDING PULSE — from increased cardiac output/volume; INCREASED URINE OUTPUT (if kidneys are responding) — or decreased if kidneys are failing; S3 HEART SOUND ('gallop') — associated with heart failure. CONTRAST WITH FLUID VOLUME DEFICIT (FVD/hypovolemia): poor skin turgor; dry mucous membranes; decreased urine output with concentrated urine; tachycardia; decreased BP (orthostatic hypotension); flat neck veins; dizziness; weight loss; weak thready pulse. NURSING INTERVENTIONS for FVE: MONITOR: daily weight (same time, same scale, same clothing), I&O, vital signs, lung sounds, edema; DIURETICS: furosemide (Lasix) most common loop diuretic; FLUID RESTRICTION as ordered; low SODIUM DIET (sodium promotes water retention); POSITION: semi-Fowler's or high-Fowler's for dyspnea; REPORT: rapid weight gain (>1 kg/day), worsening dyspnea or crackles.

Post-operative fever has a timing-based differential using the '5 W's' mnemonic: WIND (POD 1-2): ATELECTASIS — partial alveolar collapse from splinting (guarding breathing to avoid pain), anesthesia effects, and secretion retention; causes fever due to inflammatory response; TREATED with: ambulation, deep breathing exercises, incentive spirometry (IS), coughing, adequate pain control so client CAN breathe deeply; WATER (POD 3-5): URINARY TRACT INFECTION — from Foley catheter; increased urinary frequency, urgency, dysuria, cloudy urine; prevent with early Foley removal; WOUND (POD 5-7): WOUND INFECTION — surgical site infection; redness, warmth, swelling, purulent drainage; WALKING (POD 5+): DEEP VEIN THROMBOSIS (DVT)/PULMONARY EMBOLISM — calf pain, swelling, tachycardia, dyspnea; prevent with early ambulation, SCDs, anticoagulants; WONDER DRUGS (any time): DRUG FEVER — particularly from medications like antibiotics, phenytoin, allopurinol; diagnosis of exclusion. INCENTIVE SPIROMETRY (IS): device that provides visual feedback on inspiratory effort; goal is maximum sustained inspiration; hold breath at peak for 2-3 seconds; typical post-op goal: 10-15 breaths per hour while awake; must be used CORRECTLY — slow, deep breath; many clients use it incorrectly as a blowing (expiratory) device when it requires INHALATION. PN ROLE: teach and reinforce IS use pre-operatively (before surgery — better compliance than teaching when in pain); encourage early ambulation (most powerful preventive measure for multiple complications); assess lung sounds for crackles; administer antipyretics and analgesics as ordered; document and report persistent or high fever.

METFORMIN (Glucophage) is the FIRST-LINE oral medication for type 2 diabetes. MECHANISM: decreases hepatic glucose production (gluconeogenesis); increases insulin sensitivity in peripheral tissues; mild GI effects slow glucose absorption. CRITICAL PATIENT EDUCATION — CONTRAST DYE: Metformin + iodinated IV contrast can cause LACTIC ACIDOSIS — a rare but potentially fatal complication. PROTOCOL: HOLD METFORMIN before any procedure requiring IV iodinated contrast (CT scans, cardiac catheterization, angiography); restart ONLY after kidney function confirmed adequate (typically 48 hours after procedure with normal serum creatinine). The risk is related to metformin's renal clearance — if contrast causes acute kidney injury, metformin accumulates. LACTIC ACIDOSIS WARNING SIGNS: nausea, vomiting, abdominal pain, fatigue, muscle pain, rapid breathing (Kussmaul respirations), dizziness — report immediately. ADDITIONAL TEACHING POINTS: (1) TAKE WITH FOOD: metformin is taken WITH meals to reduce GI side effects (nausea, diarrhea, abdominal cramping — most common side effects, usually improve over time); (2) DOES NOT CAUSE HYPOGLYCEMIA alone — unlike sulfonylureas and insulin, metformin does not stimulate insulin secretion and does NOT typically cause hypoglycemia when used as monotherapy; (3) HOLD BEFORE SURGERY: general anesthesia and NPO status can affect kidney function; (4) CONTRAINDICATIONS: renal impairment (eGFR <30 mL/min contraindicated; use caution and possibly reduce dose at eGFR 30-45); hepatic impairment; heart failure requiring treatment; (5) SIDE EFFECT — vitamin B12 deficiency with long-term use; periodically check B12. PN ROLE: educate on contrast dye holding; teach to take with food; reinforce hypoglycemia is NOT typically expected from metformin alone; instruct to report unusual fatigue, muscle aches, or breathing difficulty.

OXYGEN THERAPY IN COPD requires special consideration. NORMAL PHYSIOLOGY: the primary drive to breathe is a RISE IN CO2 (CO2 chemoreceptors are the dominant stimulus). COPD HYPOXIC DRIVE: some patients with SEVERE CHRONIC COPD retain CO2 chronically (hypercapnia); their CO2 receptors have adapted ('reset') to high CO2; in these patients, the HYPOXIC DRIVE (low O2 stimulating breathing) becomes relatively more important. RISK OF HIGH O2: in HYPERCAPNIC COPD patients, giving HIGH-FLOW OXYGEN can: suppress the hypoxic drive → decreased respiratory rate → CO2 retention worsens → possible CO2 narcosis (confusion, somnolence) → respiratory failure. CURRENT EVIDENCE: the 'hypoxic drive' theory is somewhat simplified; contemporary evidence emphasizes that excessive O2 in COPD also causes: HALDANE EFFECT (oxyhemoglobin shifts, releasing CO2); V/Q mismatch changes. CLINICAL PRACTICE: target SpO2 of 88-92% for known or suspected hypercapnic COPD patients receiving supplemental oxygen; use lowest flow that achieves this target; adjust based on clinical response and ABG results; MONITOR for DROWSINESS, CONFUSION, DECREASED RESPIRATORY RATE — may indicate CO2 buildup; titrate down if this occurs; do NOT withhold O2 from a hypoxic client — hypoxia is still dangerous; balance is key. CONTRAINDICATION IS FALSE: O2 is NOT contraindicated in COPD; it is simply managed carefully. PN ROLE: administer oxygen as ordered; apply and use SpO2 monitoring; document O2 flow rate and SpO2; report drowsiness, decreased respiratory rate, SpO2 outside target range to RN; titrate within ordered parameters.