Real Life Pharmacology - Pharmacology Education for Health Care Professionals

Available Episodes

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Ciprofloxacin Pharmacology Podcast
On this podcast, I cover ciprofloxacin pharmacology. Ciprofloxacin is one of the most widely recognized fluoroquinolone antibiotics and has been on the market for decades. Because of its broad utility, it often comes up in practice, but it also carries significant adverse effect concerns and boxed warnings that pharmacists and prescribers need to keep in mind. From a pharmacology standpoint, ciprofloxacin works by inhibiting bacterial DNA gyrase and topoisomerase IV, enzymes that are essential for bacterial DNA replication, transcription, and repair. This action gives ciprofloxacin bactericidal activity against a variety of gram-negative organisms, including E. coli, Klebsiella, Enterobacter, and Pseudomonas aeruginosa. It also has some gram-positive activity, though it is generally not the best choice for strep infections. Ciprofloxacin comes in multiple dosage forms, including oral tablets, oral suspension, and intravenous formulations, which makes it flexible across care settings. I discuss the conversion of IV and PO formulations. Pharmacokinetics are important to consider. Ciprofloxacin is primarily renally eliminated, so dose adjustments are necessary in patients with impaired kidney function. Distribution into tissues is generally good, but it has limited activity in the lungs against Streptococcus pneumoniae, which is why it is not a first-line option for community-acquired pneumonia. Adverse effects are a major concern. The fluoroquinolone class carries multiple boxed warnings. Ciprofloxacin has been associated with tendon rupture, peripheral neuropathy, CNS effects such as agitation or seizures, and exacerbation of myasthenia gravis. More recent warnings include the risk for aortic aneurysm and hypoglycemia or hyperglycemia, particularly in older adults or those with comorbidities. On top of these boxed warnings, ciprofloxacin can also prolong the QT interval and cause GI upset. Drug interactions are another big factor in practice. Ciprofloxacin is a CYP1A2 inhibitor, which can raise levels of drugs like theophylline, tizanidine, and clozapine. It also interacts with polyvalent cations such as calcium, magnesium, iron, and aluminum, which can dramatically reduce its absorption—sometimes by more than 50%. This is a common reason for treatment failure if counseling isn’t provided. From a dosing perspective, ciprofloxacin is usually given 250–750 mg orally twice daily or 400 mg IV every 8–12 hours depending on the indication and severity of infection. Renal dosing adjustments are needed as kidney function declines. In summary, ciprofloxacin is a powerful antibiotic when used appropriately. It remains an option for urinary tract infections, complicated intra-abdominal infections, and some cases of hospital-acquired pneumonia, but its use must be balanced with the potential for significant adverse effects and interactions. For pharmacists, educating patients on drug interactions, counseling about boxed warnings, and ensuring correct dosing in renal impairment are some of the most valuable interventions when ciprofloxacin shows up on a medication list.
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Vilazodone Pharmacology
Vilazodone (brand name Viibryd) is an antidepressant with a unique pharmacologic profile compared to most other agents in the SSRI class. While not a first-line choice for every patient, understanding its mechanism, adverse effects, and interaction profile is essential for optimizing therapy and preventing downstream prescribing problems. Mechanism of ActionVilazodone is classified as a selective serotonin reuptake inhibitor (SSRI) and a partial agonist at the 5-HT1A receptor. The SSRI activity increases synaptic serotonin by blocking the serotonin transporter, while partial agonism at 5-HT1A receptors may contribute to antidepressant effects and potentially reduce certain SSRI-associated adverse effects (though clinical evidence for this benefit is mixed). Adverse Effects GI effects – diarrhea, nausea, and vomiting are frequent early in therapy. Taking the medication with food can help minimize these. Insomnia – often dose-related; morning dosing may help. Sexual dysfunction – may be slightly lower than with some SSRIs but still present. Serotonin syndrome – rare but serious, particularly if combined with other serotonergic drugs. Discontinuation syndrome – abrupt cessation can lead to dizziness, irritability, and flu-like symptoms. Drug InteractionsVilazodone is primarily metabolized by CYP3A4. This means: CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin, ritonavir) can increase vilazodone concentrations, potentially worsening side effects—dose reductions may be required. CYP3A4 inducers (e.g., carbamazepine, rifampin, St. John’s Wort) can lower drug levels, reducing effectiveness. Other serotonergic agents (e.g., triptans, SNRIs, MAOIs, tramadol, linezolid) increase the risk of serotonin syndrome. Antiplatelets and anticoagulants – SSRIs can impair platelet aggregation, increasing bleeding risk when combined with aspirin, NSAIDs, or warfarin. Prescribing Cascade ExamplesVilazodone’s adverse effects can easily lead to unnecessary prescriptions if side effects aren’t recognized: GI upset → Acid suppression therapy – Diarrhea or nausea prompts the addition of proton pump inhibitors or antiemetics, instead of adjusting vilazodone dose or timing. Insomnia → Hypnotic initiation – Trouble sleeping results in adding zolpidem or trazodone, without reassessing morning dosing or vilazodone’s role. Sexual dysfunction → PDE5 inhibitor prescription – Erectile dysfunction leads to sildenafil use, when the root cause is vilazodone’s serotonergic activity. Vilazodone’s combination of SSRI and 5-HT1A partial agonist activity makes it somewhat distinct, but its side effect profile and interactions require the same careful monitoring as other antidepressants. Healthcare professionals can play a key role in catching early signs of adverse effects, preventing prescribing cascades, and ensuring drug–drug interactions are managed appropriately.
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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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