Pharmacological Therapies: Practice Questions & Explanations

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.

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.

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).

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.

FUROSEMIDE (LASIX) is a LOOP DIURETIC — it inhibits sodium and chloride reabsorption in the Loop of Henle, resulting in increased excretion of: water (the desired diuretic effect); sodium; chloride; POTASSIUM (the most clinically important side effect); magnesium; calcium; hydrogen ions.

Hypokalemia risk: Every loop diuretic dose causes some potassium loss; at therapeutic doses for fluid overload (40-120 mg/day for furosemide), hypokalemia is common and can be severe; symptoms: muscle weakness, fatigue, leg cramps, cardiac dysrhythmias (PVCs, atrial fibrillation, life-threatening arrhythmias); ECG changes: U waves, flat T waves; dangerous at levels below 3.0 mEq/L.

Nursing interventions: Check potassium before administration; hold and notify provider if K+ below 3.5 mEq/L (per facility policy — some protocols hold at <3.0); supplement potassium per order (oral KCl with food; IV KCl if severe — never rapid IV push); encourage dietary potassium (bananas, oranges, leafy greens, potatoes); monitor for hypokalemia symptoms; educate client to report muscle cramps, weakness, palpitations.

Additional monitoring: Daily weight (most sensitive early indicator of fluid balance); I&O; vital signs; skin turgor; lung sounds; electrolytes (sodium, magnesium, BUN, creatinine in addition to potassium); ototoxicity risk with rapid IV administration of large doses.

Metformin patient teaching priorities:

With food: Taking with meals significantly reduces GI side effects (nausea, diarrhea, abdominal discomfort) that cause many patients to discontinue.

Lactic acidosis: Rare but serious adverse effect; early symptoms: unusual muscle pain, weakness, difficulty breathing, stomach discomfort, dizziness, unusual sleepiness; risk increased with renal impairment — metformin is contraindicated with eGFR below 30.

Contrast/surgery hold: Metformin must be HELD 48 hours before IV contrast (risk of contrast-induced nephropathy with metformin = increased lactic acidosis risk) and any major surgery; resume after renal function confirmed normal 48 hours post-procedure.

Hypoglycemia: Metformin alone does NOT cause hypoglycemia (it reduces hepatic glucose production without stimulating insulin release) — this distinguishes it from sulfonylureas.

Monitoring: BMP/CMP for renal function monitoring; HbA1c every 3-6 months.

RED MAN SYNDROME (vancomycin-related):

Mechanism: NOT an allergic reaction — it is a direct mast cell degranulation triggered by too-rapid infusion; the faster the infusion, the more histamine release.

Presentation: Facial flushing/erythema; neck and chest redness ('red man' distribution); hypotension; pruritus (itching); can progress to bronchospasm and hypotension if severe.

Timing: Typically occurs during infusion or within 30-60 minutes of starting.

Treatment: STOP or SLOW the infusion immediately; diphenhydramine (Benadryl) IV or IM; once reaction resolves, restart at a SLOWER rate; the standard recommendation is to infuse vancomycin at NO FASTER than 10-15 mg/min (typically 1g over at least 60 minutes, preferably 90 minutes).

Distinguish from true allergy: True allergy to vancomycin exists but is much less common; anaphylaxis would show urticaria, angioedema, bronchospasm — treat with epinephrine; the distribution and timing pattern distinguishes Red Man Syndrome from true allergy.

HEPARIN MONITORING with aPTT:

Therapeutic range: For anticoagulation (treatment of VTE, PE, atrial fibrillation), aPTT target is typically 60-100 seconds (1.5-2.5× normal); this range varies by indication and institution protocol; SUPRATHERAPEUTIC (>100 seconds): Excessive anticoagulation — HIGH BLEEDING RISK.

Nursing actions: Hold or reduce the infusion per heparin protocol; notify RN and/or provider for orders; assess for bleeding (check IV sites, urine color, stool, neurological status, vital signs); anticipate order to repeat aPTT after adjustment; HEPARIN REVERSAL if major bleeding: protamine sulfate (antidote).

Monitoring frequency: aPTT checked every 6 hours until stable in therapeutic range, then every 12-24 hours.

Pn scope: Monitor aPTT results; identify values outside parameters; report to RN; implement protocol-driven adjustments per orders; never independently adjust heparin without an order or protocol.

SUPRATHERAPEUTIC INR (4.8 vs target 2-3): This represents excessive anticoagulation — significantly increased bleeding risk.

Assessment priorities: Urine colour (haematuria); stool colour/occult blood (GI bleed); skin for excessive bruising or haematomas; neurological status (headache, confusion, focal deficits = possible intracranial haemorrhage); injection/IV sites for prolonged bleeding.

Critical: Any neurological change + supratherapeutic INR = possible intracranial bleed = IMMEDIATE emergency response.

Nursing actions: Do not administer the next warfarin dose; notify RN/provider with INR value; anticipate: hold warfarin; possibly vitamin K administration; possible fresh frozen plasma if active major bleeding.

Follow-up: Repeat INR; dietary review (increased vitamin K intake?); medication interactions (new antibiotics, NSAIDs).

Pn scope: Assess for bleeding, hold warfarin, notify — do not independently administer vitamin K without order.

IV site complications:

Phlebitis: Inflammation of the vein wall — redness, warmth, pain, and a palpable cord along the vein; can be caused by mechanical trauma, chemical irritation from medications, or infection.

Infiltration: IV catheter has displaced from the vein — fluid infusing into surrounding tissue; swelling, pallor, cool skin, pain.

Extravasation: Infiltration of vesicant (tissue-damaging) medication — more serious; requires specific antidote in some cases.

Immediate action: Stop the infusion; remove the IV catheter; do NOT continue infusing through a compromised site.

Treatment: Elevate the extremity; warm compress for phlebitis; cold or warm compress per policy for infiltration (depends on infiltrated substance); document the complication; notify RN for assessment and orders.

Vesicant extravasation: Some chemotherapy agents and vasopressors require specific antidotes (hyaluronidase for some agents, phentolamine for norepinephrine extravasation) — report immediately.

Pre-furosemide assessment:

Potassium: Most critical — loop diuretics (furosemide, torsemide, bumetanide) block Na-K-Cl co-transporter in the loop of Henle; significant potassium loss with every dose; hold and notify if K+ < 3.0-3.5 mEq/L (facility-specific threshold).

Blood pressure: Hold if hypotensive per orders — diuresis on an already volume-depleted patient worsens hypotension, tachycardia, and possibly syncope.

Urine output: Anuria (no urine) contraindicates furosemide — there is nothing to diurese.

Renal function: BUN/creatinine — severe renal impairment changes dosing.

Allergies: Cross-reactivity with sulphonamide allergy (controversial — check facility policy).

Hearing: Furosemide is ototoxic, especially with high IV doses or co-administration of aminoglycosides — inquire about hearing symptoms.

Weight: Daily weights are the best measure of fluid loss/gain in patients on diuretics; establish baseline before first dose.

OXYGEN THERAPY IN COPD — RATIONALE: Clients with chronic CO2 retention (type 2 respiratory failure) may rely partly on hypoxaemia to drive respiration (hypoxic drive); high-flow O2 can blunt this drive, causing hypoventilation and CO2 retention; TARGET SpO2 in COPD: 88-92% (NOT 95-100% as in normal patients);

Current evidence: The 'hypoxic drive' concern is real but somewhat overstated; high-flow O2 also causes V/Q mismatch effects in COPD; the clinical consensus remains: use the lowest effective O2 to achieve SpO2 88-92%.

What to do: Return to prescribed 2 L/min; assess SpO2, respiratory rate, work of breathing, level of consciousness (CO2 narcosis signs: somnolence, confusion, decreased respiratory effort); notify RN with assessment findings; the client's dyspnoea needs investigation (infection, bronchospasm, anxiety, other cause); do not leave the client without assessing the reason for discomfort.

Patient education: Explain the reason for specific O2 settings in COPD.

Warfarin monitoring: INR (International Normalized Ratio) is the standardized PT measurement for warfarin.

Therapeutic ranges: Most indications (atrial fibrillation, DVT/PE treatment): 2.0-3.0; Mechanical heart valves: 2.5-3.5.

INR above range: Excessive anticoagulation, bleeding risk — hold warfarin, possible vitamin K (antidote).

INR below range: Insufficient anticoagulation, clot risk.

Patient education: Maintain consistent vitamin K intake (don't suddenly increase/decrease leafy greens — vitamin K antagonizes warfarin); avoid alcohol; report signs of bleeding; many drug interactions.

Contrast: aPTT monitors HEPARIN (not warfarin); platelet count monitors for thrombocytopenia. The classic NCLEX confusion is warfarin/INR vs heparin/aPTT — memorize: 'WARfarin = INR; heparin = PTT.'.

Digoxin administration safety:

Assess apical pulse: Count the apical heart rate for ONE FULL MINUTE before each dose.

Hold and notify: If apical HR < 60 bpm in adults (< 70 in children, < 90-110 in infants depending on protocol).

Why: Digoxin has negative chronotropic effect (slows heart rate) — giving it to a bradycardic patient can cause dangerous further slowing or heart block.

Digoxin toxicity signs: Bradycardia, nausea/vomiting, anorexia, visual disturbances (yellow-green halos, blurred vision), confusion, dysrhythmias.

Therapeutic level: 0.5-2.0 ng/mL (toxicity often > 2.0); RISK FACTORS for toxicity: hypokalemia (low potassium increases digoxin binding and toxicity), renal impairment, advanced age.

Antidote: Digoxin immune Fab (Digibind) for severe toxicity.

LPN role: Always check apical pulse before digoxin; report bradycardia and toxicity signs immediately.

OPIOID SAFETY — RESPIRATORY DEPRESSION: The most dangerous opioid adverse effect is respiratory depression — opioids suppress the brainstem respiratory drive.

Priority assessments: Respiratory rate (hold and notify if < 12/min in adults); Sedation level (use a sedation scale — increasing sedation precedes respiratory depression); oxygen saturation.

Assess before: Establish baseline RR and sedation.

Assess after: Peak effect timing — IV opioids 15-30 min, oral 60 min.

Progression: Sedation increases BEFORE respiratory rate drops — a sedated patient who is hard to arouse is a warning sign even if RR is still normal.

Antidote: Naloxone (Narcan) reverses opioid respiratory depression — should be available.

Additional monitoring: Constipation (give stool softeners prophylactically); orthostatic hypotension; nausea; urinary retention; LPN role: assess respiratory status before/after, monitor sedation, hold and notify for RR < 12, have naloxone accessible.

ACE INHIBITOR SIDE EFFECTS (drugs ending in '-pril': lisinopril, enalapril, ramipril):

Dry cough: Persistent, non-productive cough occurs in 5-20% of patients due to bradykinin accumulation; often requires switching to an ARB (angiotensin receptor blocker, '-sartan' drugs) which doesn't cause cough.

Angioedema: Rare but life-threatening — swelling of face, lips, tongue, throat; can obstruct the airway; MEDICAL EMERGENCY requiring immediate discontinuation and treatment.

Hyperkalemia: ACE inhibitors raise potassium — monitor levels, caution with potassium supplements/salt substitutes.

Hypotension: Especially first-dose.

First-dose: monitor for orthostatic hypotension.

Renal: Monitor kidney function (can worsen in renal artery stenosis).

Teratogenic: Contraindicated in pregnancy.

Patient education: Report persistent cough, any facial/throat swelling immediately, dizziness; rise slowly; avoid salt substitutes (potassium); LPN role: teach side effects, monitor BP and potassium, report cough and angioedema.

VENTROGLUTEAL SITE — THE PREFERRED IM SITE:

Location: Place the palm on the greater trochanter, index finger on the anterior superior iliac spine, middle finger toward the iliac crest, inject in the V between fingers.

Advantages: Free of major nerves and blood vessels — notably AWAY from the SCIATIC NERVE (the danger of the older dorsogluteal site); thick gluteus medius and minimus muscle; safe for adults and children > 7 months; accommodates up to 3 mL; DORSOGLUTEAL (older site, now discouraged): Risk of sciatic nerve injury and inadvertent intravascular injection; no longer recommended as first choice.

Other im sites: Deltoid (small volume ≤1 mL, vaccines); vastus lateralis (preferred for infants, large muscle).

Im technique: 90-degree angle, appropriate needle length for muscle depth, aspiration is no longer routinely recommended for vaccines (CDC guidance) but may be used per facility policy for other IM meds; LPN role: select the safest site, use correct technique, rotate sites.