Moxifloxacin is a fourth-generation fluoroquinolone that works by inhibiting bacterial DNA gyrase and topoisomerase IV—two enzymes essential for DNA replication, repair, and transcription. By blocking both targets, it provides broad-spectrum activity against gram-positive, gram-negative, and atypical pathogens. Its enhanced gram-positive coverage, especially against Streptococcus pneumoniae, distinguishes it from earlier fluoroquinolones like ciprofloxacin.

Pharmacokinetically, moxifloxacin has excellent oral bioavailability, meaning the PO and IV doses are essentially interchangeable. It distributes well into tissues like the lungs and sinuses, making it a frequent choice for respiratory infections. With a long half-life of about 12 hours, once-daily dosing is standard.

Adverse effects are similar to the fluoroquinolone class, with concerns including tendonitis and tendon rupture, QT interval prolongation, CNS effects like confusion or agitation—particularly in older adults—and the risk of peripheral neuropathy. Moxifloxacin is especially notable for a higher propensity toward QT prolongation compared with some of its peers, making it important to avoid in patients with existing QT issues or those taking other QT-prolonging medications.

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On this episode of the Real Life Pharmacology Podcast, I cover albuterol pharmacology, adverse effects, and a rare indication for this classic respiratory medication.

Albuterol is a short-acting beta-2 adrenergic agonist (SABA) that works by stimulating beta-2 receptors in the bronchial smooth muscle. This stimulation activates adenylate cyclase, increases cyclic AMP, and leads to relaxation of airway smooth muscle. The end result is rapid bronchodilation, making albuterol effective for quick relief of acute bronchospasm in conditions such as asthma and COPD.

Common adverse effects occur due to both beta-2 and some unintended beta-1 receptor stimulation. Patients may experience tremors, nervousness, headache, or tachycardia. Higher doses or frequent use can lead to hypokalemia because beta-2 stimulation drives potassium into cells. Some individuals may also report palpitations or feelings of anxiety. These effects are generally mild and transient but can be more pronounced in older adults, those with cardiovascular disease, or when albuterol is used excessively.

Albuterol has several clinically relevant drug interactions. Concomitant use with non-selective beta-blockers (such as propranolol) can blunt its bronchodilatory effect and may precipitate bronchospasm in susceptible individuals. Using albuterol with other sympathomimetics can enhance cardiovascular stimulation, increasing the risk of tachycardia or hypertension. Diuretics, especially loop or thiazide types, may compound albuterol-induced hypokalemia. Additionally, monoamine oxidase inhibitors (MAOIs) or tricyclic antidepressants can potentiate the effects of albuterol and increase the risk of cardiovascular adverse reactions.

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Glycopyrrolate is an anticholinergic medication commonly used to reduce excessive secretions, particularly in palliative care, postoperative settings, and certain neurologic conditions. It works by blocking acetylcholine at muscarinic receptors, which decreases salivary and respiratory secretions. Clinically, glycopyrrolate is often used to manage terminal respiratory secretions (“death rattle”).

Adverse effects of glycopyrrolate are primarily related to its anticholinergic properties. These may include dry mouth, constipation, urinary retention, blurred vision, tachycardia, and decreased sweating. While it has fewer central effects than agents like scopolamine, caution is still warranted in patients with glaucoma, gastrointestinal obstruction, or significant urinary retention risk. Monitoring hydration and bowel function is important, especially in elderly or frail patients.

Dosing strategies depend on the clinical need. In palliative care, low doses may be given subcutaneously or intravenously every 4–6 hours as needed, while oral dosing is common for chronic sialorrhea.

Clinicians should consider the patient’s overall medication burden, as cumulative anticholinergic load can worsen cognitive impairment and contribute to falls or constipation. I discuss drug interactions and other commonly used medications that may contribute to anticholinergic burden.

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Bisacodyl, commonly known by the brand name Dulcolax, is a stimulant laxative widely used for short-term relief of constipation and bowel preparation before procedures. It works by directly stimulating the enteric nerves in the colon, increasing peristalsis, and promoting bowel evacuation.

Mechanism of Action:
Bisacodyl acts primarily on the large intestine. It stimulates intestinal smooth muscle and alters water and electrolyte transport, increasing fluid accumulation in the bowel and triggering defecation. The result is a bowel movement typically within 6–12 hours orally or within 15–60 minutes when given rectally.

Dosage Forms and Dosing:
Bisacodyl is available as oral tablets (5 mg) and rectal suppositories (10 mg). Typical adult dosing is 5–15 mg by mouth once daily or 10 mg rectally as needed. It’s often used for acute constipation, bowel prep, or to prevent straining in specific medical situations.

Adverse Effects:
Common side effects include abdominal cramping, diarrhea, and nausea. Chronic or excessive use may lead to electrolyte imbalances, dehydration, and laxative dependence.

Drug Interactions and Monitoring:
Concurrent use with antacids, proton pump inhibitors, or milk may cause premature dissolution of enteric-coated tablets, leading to gastric irritation. Monitoring for bowel regularity, hydration status, and signs of electrolyte imbalance is important—especially in elderly or debilitated patients.

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On this podcast episode, I cover fludrocortisone. Fludrocortisone is a synthetic corticosteroid with potent mineralocorticoid activity and minimal glucocorticoid effects. It works primarily by promoting sodium reabsorption and potassium excretion in the distal renal tubules, leading to increased water retention and expansion of extracellular fluid volume. This pharmacologic action helps maintain blood pressure and electrolyte balance.

Fludrocortisone is most commonly indicated for the treatment of adrenocortical insufficiency, such as Addison’s disease, and for managing orthostatic hypotension by enhancing vascular tone and volume status.

Adverse effects are typically related to its mineralocorticoid potency and may include hypertension, edema, hypokalemia, and weight gain. Long-term use can also lead to complications such as heart failure exacerbation, osteoporosis, and mood changes. Because of its sodium-retaining effects, careful monitoring of blood pressure, electrolytes, and signs of fluid overload is recommended during therapy.

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One of the most important yet often overlooked concepts in pharmacology is the prescribing cascade. It occurs when a new medication is prescribed to treat a side effect caused by another drug, without realizing that the first medication is the root cause. This leads to a chain reaction of additional prescriptions, unnecessary complexity, and often, new adverse effects.

Prescribing cascades can sneak up on even the most careful clinicians. A patient develops a new symptom after starting a medication—perhaps swelling, dizziness, or urinary changes—and instead of identifying the drug as the culprit, another medication is added to manage the symptom. Over time, this cycle contributes to polypharmacy, drug interactions, and reduced quality of life.

These cascades are particularly concerning in older adults, where multiple comorbidities and high medication counts make it easy for adverse effects to be misinterpreted as new conditions. But they can occur at any age and in any clinical setting.

The key to preventing prescribing cascades is maintaining a critical mindset:

Recognizing and interrupting the prescribing cascade is one of the simplest and most impactful ways we can improve medication safety. In this podcast, I share some of my favorite real-world examples that illustrate just how easily these cascades can happen.

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Airsupra is a combination inhaler that contains albuterol and budesonide, approved for as-needed use in adults with asthma. It represents the first rescue inhaler to combine a short-acting beta-2 agonist (SABA) with an inhaled corticosteroid (ICS) in a single device. The albuterol component provides rapid bronchodilation by relaxing airway smooth muscle, while budesonide works to reduce airway inflammation and mucus production. This dual mechanism allows Airsupra to not only relieve acute bronchoconstriction but also address the underlying inflammatory process that contributes to asthma exacerbations.

Clinically, Airsupra is indicated for as-needed treatment or prevention of bronchoconstriction in adults with asthma, but it is not approved for COPD. The typical dosing is two inhalations as needed, with a maximum of six doses (12 inhalations) in a 24-hour period.

The rationale for its use aligns with recent asthma guideline updates, which emphasize minimizing SABA-only use because it fails to address inflammation and may contribute to worse outcomes over time.

Common adverse effects include tremor, nervousness, tachycardia, and hypokalemia from albuterol, as well as oral thrush and hoarseness from budesonide. Patients should rinse and spit after each use to reduce the risk of oral candidiasis.

Drug interactions can occur with non-selective beta-blockers, which may blunt albuterol’s effects. CYP3A4 also plays a role in budesonide metabolism. Systemic absorption typically isn’t too much of an issue with infrequent use.

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In this episode of Real Life Pharmacology, we take a deep dive into daptomycin, a lipopeptide antibiotic primarily used for serious Gram-positive infections, including MRSA and VRE. Daptomycin works by binding to bacterial cell membranes in a calcium-dependent manner, causing rapid depolarization and cell death.

One key limitation is that daptomycin should never be used for pneumonia because pulmonary surfactant inactivates the drug. Clinically, it’s often reserved for bacteremia, endocarditis, or complicated skin and soft tissue infections.

From a pharmacokinetic standpoint, daptomycin is given intravenously and primarily eliminated unchanged by the kidneys, so dose adjustments are necessary in renal impairment.

Monitoring creatine kinase (CK) levels is crucial, as one of the major adverse effects is myopathy and, rarely, rhabdomyolysis. Patients on statins have a higher risk of muscle toxicity, and clinicians should consider holding or monitoring statin therapy closely.

Eosinophilic pneumonia is another rare but serious adverse reaction that can develop after prolonged therapy. Daptomycin has minimal drug interactions, making it an appealing option when other agents pose risks. Overall, it’s a powerful antibiotic when used appropriately, but requires careful monitoring for muscle and respiratory-related side effects.

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Cefepime is a fourth-generation cephalosporin antibiotic with broad-spectrum activity against both gram-positive and gram-negative organisms, including Pseudomonas aeruginosa. It works by inhibiting bacterial cell wall synthesis through binding to penicillin-binding proteins, leading to cell lysis and death.

Clinically, cefepime is commonly used in hospital settings for serious infections such as pneumonia, febrile neutropenia, urinary tract infections, skin infections, and intra-abdominal infections. It’s typically administered intravenously, with doses often ranging from 1 to 2 grams every 8 to 12 hours depending on the indication and renal function.

From a pharmacokinetic standpoint, cefepime is primarily renally eliminated, so dose adjustments are required in patients with impaired kidney function. Failure to reduce the dose appropriately can lead to neurotoxicity — one of the key adverse effects associated with cefepime — manifesting as encephalopathy, confusion, myoclonus, or seizures, particularly in elderly or renally impaired patients.

Common side effects include gastrointestinal upset and rash. Cefepime has relatively limited drug interactions, though concurrent nephrotoxic agents can increase the risk of renal injury.

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Midodrine is an oral alpha-1 agonist most commonly used for the treatment of symptomatic orthostatic hypotension. Its mechanism of action is through peripheral vasoconstriction, which helps increase blood pressure. Because of its short duration of action, it is typically dosed three times daily, with the last dose recommended in the late afternoon to reduce the risk of hypertension at night.

Clinically, midodrine is often considered when non-pharmacologic strategies for orthostatic hypotension (such as increased salt/fluid intake, compression stockings, or physical counter-maneuvers) are not enough. Pharmacists should also be aware of prescribing cascades—such as urinary retention leading to tamsulosin initiation—that can arise when midodrine is used.

Midodrine is generally not metabolized through cytochrome P450 pathways, so significant drug–drug interactions are less common. However, caution should be exercised with other agents that can raise blood pressure (like decongestants) or slow the heart rate (such as beta-blockers). Monitoring parameters include blood pressure, pulse, symptoms of urinary retention, and the patient’s overall response to therapy.

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