Senna Pharmacology

Senna is a stimulant laxative. Its pharmacological activity comes from natural compounds called sennosides. Metabolites act locally in the colon to stimulate peristalsis, thereby accelerating bowel movements. While osmotic laxatives are generally considered first-line laxative agents, this makes senna a useful alternative for the short-term treatment of constipation. The pharmacokinetics of senna are unique in that its onset of action typically takes 6 to 12 hours after oral administration, reflecting the time required for colonic bacteria to metabolize sennosides into active compounds. This delayed onset makes senna better suited for bedtime dosing when overnight relief is desired. Although senna is effective, its use carries potential adverse effects. Common side effects include abdominal cramping, diarrhea, and, rarely, electrolyte disturbances such as hypokalemia. Chronic or excessive use can lead to dependency and possibly melanosis coli, a benign but visible pigmentation of the colon lining. Drug interactions may occur, particularly with medications affected by potassium levels, such as digoxin or diuretics. For these reasons, senna is generally recommended for short-term use, with emphasis on evaluating underlying causes of constipation before long-term therapy is considered.

Revefenacin (brand name Yupelri) is a long-acting muscarinic antagonist (LAMA) used for the maintenance treatment of chronic obstructive pulmonary disease (COPD). It works by blocking muscarinic receptors, particularly the M3 subtype, in airway smooth muscle. This antagonism reduces cholinergic bronchoconstriction and leads to sustained bronchodilation. Unlike short-acting anticholinergics such as ipratropium, revefenacin provides 24-hour bronchodilation with once-daily dosing. One of the distinguishing features of revefenacin is that it is the first nebulized LAMA approved for COPD maintenance therapy. Many patients with advanced COPD, physical limitations, or difficulty using handheld inhalers benefit from a nebulized formulation, as it allows medication delivery without requiring hand-breath coordination or a forceful inhalation. This makes it a useful option for patients with poor inhaler technique or those transitioning from hospital care. Pharmacokinetically, revefenacin is delivered via nebulization, with peak effects typically observed within a couple of hours. Importantly, systemic absorption is relatively low, but elderly patients or those with hepatic impairment may be more susceptible to anticholinergic side effects. Clinically, revefenacin improves lung function, reduces COPD symptoms, and can decrease exacerbation frequency. Common adverse effects include cough, dry mouth, constipation, and urinary retention. Caution is advised in patients with narrow-angle glaucoma or prostatic hyperplasia due to its antimuscarinic properties. Revefenacin is not intended for acute bronchospasm or rescue therapy—it is strictly for long-term, once-daily maintenance.

Desmopressin is a synthetic analog of vasopressin, also known as antidiuretic hormone (ADH). It works by mimicking the action of natural ADH on the kidneys, primarily increasing water reabsorption in the collecting ducts. This effect reduces urine production and helps concentrate the urine. Because of this mechanism, desmopressin is commonly used in conditions like diabetes insipidus, nocturnal enuresis (bedwetting), and sometimes for nocturia in adults. It also has a role in certain bleeding disorders, such as mild hemophilia A and von Willebrand disease, since it can increase plasma levels of factor VIII and von Willebrand factor. In this podcast, we will explore desmopressin pharmacology and much more. Desmopressin is available in several dosage forms, including oral tablets, intranasal spray, and injectable formulations. The choice depends on the indication and patient-specific factors such as age, convenience, or the need for rapid effect. Adverse effects of desmopressin are largely related to water balance. Because it reduces urine output, patients are at risk for water retention and hyponatremia, which can lead to headaches, confusion, seizures, or in severe cases, coma. Monitoring sodium levels is especially important in elderly patients and those taking other medications that can affect fluid or electrolyte balance. Clinicians also need to be mindful of drug interactions. Medications that increase the risk of hyponatremia, such as SSRIs, carbamazepine, or certain diuretics, may enhance desmopressin’s adverse effects. Conversely, drugs that blunt its activity can reduce effectiveness. Careful monitoring and patient education are key parts of safe use.

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.

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.

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.

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.

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.

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.

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.