Real Life Pharmacology - Pharmacology Education for Health Care Professionals

Available Episodes

5 of 392

Solifenacin Pharmacology
Solifenacin is a bladder antimuscarinic medication most commonly used for overactive bladder (OAB) with symptoms of urinary frequency, urgency, and urge incontinence. Like other agents in its class, understanding the pharmacology can help anticipate potential side effects, drug interactions, and downstream prescribing problems. Mechanism of Action Solifenacin selectively blocks muscarinic M3 receptors in the bladder detrusor muscle. Inhibiting these receptors reduces involuntary bladder contractions, increases bladder capacity, and delays the urge to void. While M3 selectivity may theoretically reduce side effects compared to nonselective antimuscarinics, in clinical practice, many anticholinergic effects still occur. Adverse Effects Because muscarinic receptors are present throughout the body, solifenacin can lead to a range of anticholinergic adverse effects: Dry mouth – among the most common, can be significant enough to cause dental issues with long-term use. Constipation – especially problematic in older adults; severe cases may require hospitalization. Blurred vision – due to impaired accommodation. Cognitive impairment – increased risk in older adults, particularly with cumulative anticholinergic burden. Urinary retention – paradoxical worsening in patients with bladder outlet obstruction. Drug Interactions CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin, ritonavir) can increase solifenacin plasma concentrations, raising the risk of side effects. Other anticholinergics (e.g., diphenhydramine, tricyclic antidepressants, other bladder antimuscarinics) can result in additive toxicity and higher anticholinergic burden. QT-prolonging drugs (e.g., amiodarone, certain fluoroquinolones) may have additive cardiac risk since solifenacin has been associated with QT prolongation in rare cases. Prescribing Cascade Examples Constipation → Laxative initiation – A patient starts solifenacin for OAB and develops severe constipation, leading to chronic use of stimulant laxatives like senna or bisacodyl. Dry mouth → Mouth rinse prescription – Dry mouth is treated with saliva substitutes or prescription rinses, instead of reassessing the anticholinergic therapy. Cognitive decline → Donepezil initiation – In older adults, cognitive impairment may be mistaken for dementia progression, leading to cholinesterase inhibitor prescribing—directly counteracting the anticholinergic effects of solifenacin. Solifenacin can be an effective treatment for OAB, but the risk of adverse effects and prescribing cascades—especially in older adults—cannot be ignored. Healthcare professionals should regularly review the indication, monitor for anticholinergic burden, and look for opportunities to deprescribe when appropriate.
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Itraconazole Pharmacology
In this episode, we break down itraconazole—a potent antifungal with a lot of baggage. If you’re a pharmacist, clinician, or student who needs to understand how this drug works and why it can be tricky to use, this episode is for you. We start with the basics. Itraconazole blocks 14α-demethylase, an enzyme fungi need to make their cell membranes. That disruption kills or slows the fungus. It works against tough bugs like Aspergillus, Histoplasma, and Blastomyces, plus common skin infections. Side effects? Nausea, liver enzyme elevations, and more seriously, heart failure. Yes, itraconazole has a black box warning for worsening or causing congestive heart failure. If your patient has heart issues, think twice. Drug interactions are everywhere. Itraconazole is a strong CYP3A4 inhibitor. It can raise levels of drugs like statins, benzos, calcium channel blockers, and immunosuppressants—sometimes to dangerous levels. Don’t co-prescribe without checking.
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Levomilnacipran Pharmacology
In this episode of our pharmacology podcast, we take a deep dive into the pharmacology of levomilnacipran (Fetzima), a unique serotonin-norepinephrine reuptake inhibitor (SNRI) approved for the treatment of major depressive disorder (MDD) in adults. Designed for pharmacy students, clinicians, and anyone interested in psychopharmacology, this episode breaks down what makes levomilnacipran different from other antidepressants and how to use it effectively in clinical practice. We explore levomilnacipran's mechanism of action, which features a greater affinity for norepinephrine reuptake inhibition compared to serotonin—an uncommon trait among SNRIs. This pharmacologic profile gives it a distinctive effect on energy, motivation, and physical symptoms of depression. Listeners will also learn about its pharmacokinetics, including once-daily dosing, renal elimination, and metabolism via the CYP3A4 pathway—making drug interactions an important consideration. The episode also covers levomilnacipran side effects, including common adverse reactions like nausea, dry mouth, constipation, and increased heart rate or blood pressure. We'll also highlight rare but serious risks like serotonin syndrome and urinary hesitation. Because levomilnacipran drug interactions can impact safety and efficacy, we review important combinations to avoid, such as CYP3A4 inhibitors (e.g., ketoconazole), serotonergic drugs, and blood pressure-altering agents. For pharmacists and prescribers, this is a key segment to help guide safer medication use and monitoring. Finally, we wrap up with clinical pearls for starting, titrating, and monitoring levomilnacipran therapy—including renal dose adjustments and differences with duloxetine. Whether you're studying for boards or optimizing your patient’s antidepressant regimen, this episode delivers a concise, evidence-based overview of levomilnacipran pharmacology in a digestible, podcast-friendly format.
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Asenapine Pharmacology
Asenapine is an atypical antipsychotic that acts as an antagonist at multiple receptors, including dopamine D2 and serotonin 5-HT2A, contributing to its antipsychotic and mood-stabilizing effects. Adverse effects of asenapine include somnolence, dizziness, and extrapyramidal symptoms. Because asenapine is significantly metabolized by CYP1A2, inhibitors or inducers of these enzymes can affect its plasma concentrations. Co-administration with other CNS depressants may increase the risk of sedation and impaired cognitive or motor function. Asenapine can prolong the QT interval, so caution is advised when used with other medications that affect cardiac conduction.
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Loxapine Pharmacology
Loxapine is a first-generation (typical) antipsychotic with dopamine D2 receptor antagonism as its primary mechanism, though it also has affinity for serotonin 5-HT2A receptors, making its pharmacology somewhat atypical. Loxapine is available in multiple formulations, including oral capsules and an inhalation powder, the latter approved specifically for acute agitation in patients with schizophrenia or bipolar I disorder. Sedation and extrapyramidal symptoms (EPS), including dystonia, akathisia, and parkinsonism, are common adverse effects due to its potent dopamine blockade in the nigrostriatal pathway. Orthostatic hypotension can occur with loxapine due to its alpha-1 adrenergic blockade, requiring monitoring in elderly patients or those on antihypertensives.
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