Pharmacology
Showing 40 of 40 topics
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ACE inhibitors and ARBs reduce blood pressure, proteinuria, heart-failure morbidity, and kidney/cardiovascular risk in selected patients, but they can raise creatinine and potassium. Check renal function and potassium before and after initiation or dose escalation, accept a modest hemodynamic creatinine rise when clinically stable, and investigate larger rises for volume depletion, renal-artery disease, NSAIDs, diuretics, obstruction, or acute illness rather than reflexively abandoning long-term RAAS blocka
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Extended-interval aminoglycoside dosing gives a large weight-based dose followed by a prolonged drug-free interval to exploit concentration-dependent bacterial killing and the post-antibiotic effect while limiting sustained renal exposure. It is appropriate only in selected patients with predictable pharmacokinetics and requires institution-specific nomogram use, renal monitoring, and careful exclusion of pregnancy, major renal instability, certain endocarditis regimens, dialysis, and other populations not
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Amiodarone is effective for selected atrial and ventricular arrhythmias but has an exceptionally broad toxicity profile because of its iodine content, tissue accumulation, very long half-life, and inhibition of CYP enzymes and P-glycoprotein. Long-term therapy requires baseline and periodic thyroid, hepatic, pulmonary, ocular, ECG, and interaction review, with urgent evaluation of new dyspnea/cough, thyroid symptoms, bradycardia, visual change, liver injury, or neurologic toxicity.
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Antibiotic-allergy management begins by defining the culprit drug and reaction phenotype. Low-risk historical labels can often be evaluated with direct challenge or a supervised graded test-dose pathway, while true immediate allergy may require an alternative agent or formal desensitization when the drug is essential. Desensitization creates temporary tolerance only and is generally inappropriate for severe delayed immune reactions such as SJS/TEN or DRESS.
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Switching an antibiotic from IV to oral therapy is appropriate when the patient is clinically improving, hemodynamically stable, able to absorb oral medication, and an active oral agent can achieve adequate exposure at the infection site. The decision depends on syndrome and source control rather than an arbitrary number of IV days; high-bioavailability agents can support early transition in many infections, while endocarditis, CNS infection, uncontrolled deep foci, severe immunocompromise, or organisms wit
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Obesity can alter antimicrobial volume of distribution, clearance, protein binding, and the probability of attaining pharmacokinetic/pharmacodynamic targets. There is no universal 'obesity adjustment': dosing must be drug-specific and incorporate infection severity, renal function, body-size metric, loading versus maintenance dose, infusion strategy, therapeutic drug monitoring, and toxicity risk.
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Antimicrobial de-escalation at roughly 48 to 72 hours is a structured reassessment of diagnosis, cultures, clinical trajectory, source control, organ function, and duration. The goal is to stop antibiotics when infection is unlikely, narrow broad empiric regimens to the most targeted active therapy, remove redundant coverage, transition to oral treatment when appropriate, and define the shortest evidence-based course without compromising treatment of a true serious infection.
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Antipsychotic safety monitoring should address both metabolic toxicity and cardiac repolarization risk. Before and during treatment, track weight/BMI, waist or cardiometabolic risk, blood pressure, glucose/A1C, lipids, movement symptoms, and agent-specific adverse effects; obtain ECG and electrolytes when QT risk is meaningful. Choice of drug should reflect the patient's psychiatric indication, prior response, obesity/diabetes risk, cardiac history, and interacting medications rather than assuming all antip
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Benzodiazepines should usually be tapered gradually after long-term use because abrupt discontinuation can cause rebound anxiety or insomnia, autonomic symptoms, delirium, seizures, and rarely life-threatening withdrawal. A safe taper is individualized to dose, duration, half-life, comorbidity, substance-use history, and withdrawal response, often beginning with reductions of roughly 5% to 10% at intervals of several weeks and slowing near the end when symptoms emerge.
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Beta blockers reduce sympathetic heart-rate and contractility effects and are foundational for HFrEF with evidence-based agents, post-MI/ischemic disease in selected patients, arrhythmia rate control, and other specific indications. They are not interchangeable and are not universal first-line therapy for uncomplicated hypertension. Start low and titrate according to indication, heart rate, blood pressure, congestion, conduction disease, bronchospasm risk, and symptoms; abrupt withdrawal can cause rebound t
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Clarify reported penicillin allergy, understand side chain cross reactivity, and consider test dose or allergy referral to expand options.
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Dihydropyridine calcium-channel blockers such as amlodipine primarily vasodilate and lower blood pressure, while nondihydropyridines verapamil and diltiazem also slow AV nodal conduction and reduce contractility. This distinction determines use and toxicity: DHPs commonly cause edema and flushing; non-DHPs can cause bradycardia, heart block, constipation, drug interactions, and worsening HFrEF.
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Current C. difficile treatment favors fidaxomicin over a standard course of oral vancomycin for many initial and recurrent nonfulminant episodes when resources permit, while oral vancomycin remains an acceptable alternative. Fulminant disease requires high-dose oral or nasogastric vancomycin plus IV metronidazole, rectal vancomycin when ileus prevents delivery, early surgical consultation, and aggressive supportive care; recurrence prevention includes minimizing unnecessary antibiotics and considering bezlo
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Digoxin has a narrow therapeutic window and serum concentrations must be interpreted in relation to dose timing, kidney function, indication, electrolytes, symptoms, and interacting medications. Toxicity can cause nausea, anorexia, confusion, visual disturbance, bradyarrhythmias, AV block, atrial tachycardia with block, or ventricular arrhythmias. Severe toxicity with life-threatening arrhythmia, hemodynamic instability, or significant hyperkalemia is treated with digoxin immune Fab.
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Direct oral anticoagulant dosing must be matched to the exact indication, renal function, age, body size, hepatic function, and interacting P-glycoprotein/CYP3A4 drugs. Dose-reduction rules are not interchangeable among apixaban, rivaroxaban, edoxaban, and dabigatran, and underdosing without a labeled indication can increase thromboembolism while overdosing in impaired clearance increases bleeding.
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Fluoroquinolones can be highly effective oral and IV antibiotics, but their use is limited by potentially serious adverse effects including tendinopathy and tendon rupture, peripheral neuropathy, CNS effects, dysglycemia, QT prolongation, C. difficile infection, and an FDA warning about aortic aneurysm or dissection risk in susceptible patients. Prescribe them when the expected infectious benefit outweighs these risks and when safer effective alternatives are not preferable.
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Gabapentin and pregabalin require renal dose adjustment and can cause dizziness, ataxia, sedation, edema, and clinically important respiratory depression when combined with opioids or other CNS depressants, especially in older adults or patients with lung disease. They also have misuse and dependence potential in some populations. Prescribe them for a clear indication, titrate gradually, reassess functional benefit, and taper rather than abruptly stopping high-dose or long-term therapy.
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Estimate pretest probability with the 4T score, stop all heparin if intermediate or high probability, and start a non heparin anticoagulant.
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Inhaled corticosteroids are the foundation of anti-inflammatory asthma therapy and should be delivered as part of an ICS-containing regimen rather than leaving patients reliant on short-acting bronchodilator alone. Effectiveness depends on correct device technique, adherence, an appropriate step for symptom and exacerbation risk, and repeated reassessment. Local adverse effects can be reduced with technique, spacer use for compatible pressurized metered-dose inhalers, and mouth rinsing.
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Outpatient insulin titration should match the patient's glucose pattern rather than increasing every dose at once. Basal insulin primarily targets fasting glucose, while prandial insulin targets meal-related excursions. Safe basal-bolus care combines an individualized glycemic goal, small protocolized dose changes every few days, hypoglycemia prevention, injection and sensor technique, sick-day rules, and ongoing reassessment for whether noninsulin agents can simplify the regimen.
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Linezolid has reversible monoamine-oxidase inhibitory activity and can precipitate serotonin toxicity when combined with serotonergic medications, although the absolute risk is low in many necessary treatment situations. Management requires medication reconciliation, assessment of the urgency and alternatives for both the antibiotic and serotonergic drug, symptom monitoring for clonus/hyperreflexia/autonomic instability, and attention to linezolid's other toxicities such as cytopenias, neuropathy, optic neu
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Lithium requires baseline and periodic monitoring of serum trough concentration, kidney function, thyroid function, calcium, pregnancy status when relevant, and interacting medications. Toxicity risk rises with dehydration, sodium depletion, CKD, NSAIDs, thiazides, ACE inhibitors, ARBs, and dose changes. New tremor, ataxia, dysarthria, vomiting, confusion, or neurologic slowing should prompt an urgent level and renal assessment; severe neurotoxicity may require hemodialysis.
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Recognize CNS and cardiovascular toxicity after local anesthetic exposure; stop injection, manage airway and seizures, and initiate lipid emulsion therapy.
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Macrolides, particularly erythromycin and clarithromycin and to a lesser degree azithromycin, can contribute to QT prolongation and clinically important drug interactions. Safe use requires review of baseline torsades risk, electrolytes, concomitant QT-prolonging medications, CYP3A4 and P-glycoprotein interactions, hepatic function, and whether a nonmacrolide alternative can provide equivalent antimicrobial benefit.
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Low-dose methotrexate for inflammatory disease is usually taken once weekly, not daily. Daily administration errors can cause fatal mucositis, pancytopenia, sepsis, and organ injury. Safe therapy requires a clearly labeled weekly schedule, folic acid supplementation, baseline and periodic CBC, liver tests, and renal function, plus medication-interaction, pregnancy, infection, alcohol/liver-risk, and pulmonary-symptom review.
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Rigidity, hyperthermia, and autonomic instability after dopamine blockade; stop triggers, give supportive care, and consider dantrolene or bromocriptine.
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Neuromuscular blocking agents produce skeletal muscle paralysis but provide no sedation, analgesia, or amnesia. Succinylcholine and rocuronium are common rapid-sequence agents; selection depends on contraindications, expected airway course, organ function, and reversibility. In the ICU, continuous paralysis is reserved for selected indications and requires reliable analgesia/sedation, ventilatory support, quantitative or clinical neuromuscular monitoring, eye and skin protection, thrombosis prevention, and
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Safe outpatient opioid prescribing begins with defining a functional treatment goal, using nonopioid therapies when effective, prescribing the lowest effective dose for the shortest necessary duration, checking medication and substance-use risks, avoiding hazardous sedative combinations when possible, and offering naloxone to patients at increased overdose risk. Long-term therapy requires periodic reassessment of pain, function, adverse effects, controlled-substance data, toxicology when appropriate, and wh
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P-glycoprotein and CYP3A4 interactions can markedly alter exposure to many anticoagulants, antiarrhythmics, immunosuppressants, anticonvulsants, statins, and other drugs. Strong inhibitors increase substrate concentrations and toxicity risk, while strong inducers lower exposure and can cause treatment failure. Interaction management should identify the exact substrate, inhibitor/inducer strength, route, duration, organ function, and whether the product labeling recommends avoidance, dose adjustment, or moni
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Extended-infusion piperacillin-tazobactam prolongs the fraction of the dosing interval during which free drug concentrations remain above the pathogen MIC, the pharmacodynamic exposure most associated with beta-lactam efficacy. Implementation requires a validated dose and infusion duration, renal-adjustment strategy, compatible IV access, stability guidance, timely first-dose delivery in severe infection, and stewardship review once cultures permit narrowing.
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Proton pump inhibitors are highly effective for peptic ulcer disease, erosive esophagitis, upper-GI bleeding risk, Barrett-related indications, and other acid-mediated disorders, but many patients remain on them after the original indication ends. Deprescribing is appropriate when no ongoing indication exists, using dose reduction, on-demand therapy, or discontinuation while anticipating transient rebound acid hypersecretion. Long-term associations should be discussed in proportion to evidence rather than u
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Modern ICU sedation emphasizes analgesia-first assessment, the lightest effective sedation target, validated pain and sedation scales, daily reassessment, delirium prevention, sleep support, and early mobility. For mechanically ventilated adults in whom light sedation or delirium reduction is a high priority, current SCCM guidance conditionally favors dexmedetomidine over propofol; drug choice must still reflect hemodynamics, ventilation needs, neurologic goals, and procedural requirements.
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Triad of altered mental status, autonomic instability, and neuromuscular hyperactivity after serotonergic drugs; stop agents, give benzodiazepines, and consider cyproheptadine.
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Statin-associated symptoms should be evaluated systematically because many patients can tolerate a different statin, lower or intermittent dose, or combination therapy. Confirm the indication and cardiovascular-risk benefit, exclude hypothyroidism and interacting drugs when appropriate, measure CK for severe muscle symptoms rather than routinely, and distinguish benign myalgia from myopathy or rhabdomyolysis. Drug interactions are most important with CYP3A4-metabolized statins and strong inhibitors.
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Thiazide and thiazide-like diuretics are effective antihypertensives but can cause hyponatremia, hypokalemia, hypomagnesemia, hyperuricemia, glucose changes, and volume depletion. Electrolyte risk is greatest in older adults, low-body-mass patients, high water intake, low solute intake, CKD, and combination with SSRIs or other hyponatremia-promoting drugs; check sodium and potassium after initiation or dose escalation in susceptible patients.
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Trimethoprim-sulfamethoxazole requires indication-specific renal dose adjustment and can cause clinically important hyperkalemia because trimethoprim reduces distal renal potassium secretion. It may also raise serum creatinine by inhibiting tubular creatinine secretion without a true fall in GFR. Risk is greatest with CKD, older age, high-dose therapy, ACE inhibitors, ARBs, potassium-sparing diuretics, and other potassium-raising drugs, so baseline and follow-up renal function and potassium should be matche
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Valproate therapy can cause hepatotoxicity, thrombocytopenia, pancreatitis, hyperammonemic encephalopathy, weight/metabolic effects, and major fetal harm. Monitor CBC/platelets and liver tests at baseline and during therapy based on clinical risk, check ammonia when unexplained lethargy or mental-status change occurs rather than as routine screening, and review pregnancy potential, drug interactions, and dose-related adverse effects at every visit.
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Vancomycin monitoring for serious methicillin-resistant Staphylococcus aureus infections should target an AUC24/MIC exposure, commonly 400 to 600 when MIC is assumed to be 1 mg/L, rather than using trough concentration alone as the primary target. Safe dosing integrates body size, kidney function, illness severity, indication, measured concentrations, Bayesian or first-order pharmacokinetic methods, and prompt dose adjustment when renal function or volume status changes.
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Vasopressors restore perfusion pressure when hypotension persists despite appropriate evaluation and fluid resuscitation. In septic shock, norepinephrine is the preferred first-line agent; vasopressin is commonly added when norepinephrine requirements escalate, and epinephrine can be added when pressure remains inadequate. Drug choice should follow shock physiology, rhythm, cardiac function, access, and response rather than a fixed sequence for every cause of shock.
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Warfarin initiation requires a clear indication, INR target, interaction and bleeding review, and a plan for early INR checks. Parenteral bridging is required when treating acute VTE because warfarin initially reduces protein C/S before fully suppressing procoagulant factors, but bridging is not routinely needed for every atrial-fibrillation initiation or perioperative interruption. Dose changes should follow INR trend and total weekly dose, with extra monitoring after interacting medications, illness, diet
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