Welcome to today’s episode, where we’re diving into the world of nitrate medications—one of the cornerstone therapies in cardiovascular care. Whether you’re a pharmacist, nurse, med student, or just curious about how medications keep the heart happy, nitrates are fascinating because of their unique mechanism and versatile clinical uses.

Nitrates work by releasing nitric oxide, a powerful molecule that relaxes smooth muscle and dilates blood vessels. This vasodilation primarily reduces venous return to the heart, lowering preload and myocardial oxygen demand, and at higher doses, can also decrease afterload. For patients with angina, this means less chest pain, improved exercise tolerance, and better quality of life.

In this episode, we’ll cover the most commonly used nitrates—from sublingual nitroglycerin for rapid relief of acute angina, to isosorbide dinitrate and mononitrate for chronic management. We’ll discuss how their formulations, onset, and duration of action affect clinical use, and why concepts like tolerance and nitrate-free intervals are critical to understand.

We’ll also explore important drug interactions, including why combining nitrates with PDE5 inhibitors can be dangerous, and highlight practical tips for patient counseling and monitoring. By the end of this episode, you’ll have a clear picture of how and when nitrates are used, and the key pearls every clinician should know to maximize benefit while minimizing risk.

So whether you’re reviewing for boards, prepping for clinical rotations, or just brushing up on cardiovascular pharmacology, stay tuned—we’re about to break down nitrates in a way that’s simple, practical, and memorable.

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Alprazolam is a short-acting benzodiazepine that enhances the inhibitory effects of gamma-aminobutyric acid (GABA) at the GABA-A receptor. Clinically, this results in anxiolytic, sedative, muscle-relaxant, and anticonvulsant effects.

After oral administration, alprazolam is rapidly absorbed, with onset of action typically within 30–60 minutes. It undergoes extensive hepatic metabolism primarily via CYP3A4 to inactive metabolites, and has an elimination half-life of approximately 11 hours, which may be prolonged in elderly patients or those with hepatic impairment.

Common adverse effects include sedation, dizziness, impaired coordination, and cognitive slowing. More serious risks include respiratory depression, especially when combined with opioids, alcohol, or other CNS depressants.

Clinically, alprazolam should be used at the lowest effective dose for the shortest possible duration. Abrupt discontinuation should be avoided; gradual tapering is essential to reduce withdrawal risk. It is a controlled substance that carries the risk of addiction and dependence.

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Pimavanserin is an atypical antipsychotic approved for the treatment of hallucinations and delusions associated with Parkinson’s disease psychosis. Unlike traditional antipsychotics, it does not block dopamine receptors, making it a unique option for patients with Parkinson’s disease who are highly sensitive to dopamine antagonism.

Pimavanserin works primarily as a selective serotonin 5-HT2A inverse agonist and antagonist, with minor activity at 5-HT2C receptors. This dopamine-sparing effect is the key reason it does not worsen motor symptoms in Parkinson’s disease.

The most commonly reported side effects include peripheral edema, nausea, confusion, and hallucinations. QT interval prolongation is a clinically important concern, especially in patients with existing cardiac risk factors. Somnolence may occur but is generally less prominent compared with dopamine-blocking antipsychotics.

Pimavanserin carries a boxed warning for increased mortality in elderly patients with dementia-related psychosis, consistent with other antipsychotics. It should not be used in patients with known QT prolongation, a history of ventricular arrhythmias, or in combination with other QT-prolonging agents when possible.

Strong CYP3A4 inhibitors, such as ketoconazole or clarithromycin, can significantly increase pimavanserin concentrations and require dose reduction. Strong CYP3A4 inducers, such as rifampin or carbamazepine, may reduce efficacy and should generally be avoided. Additive QT prolongation may occur when combined with other QT-prolonging medications, including certain antiarrhythmics, fluoroquinolones, and macrolide antibiotics.

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