Clonazepam Pharmacology Podcast

On this podcast episode, I discuss clonazepam pharmacology, adverse effects, pharmacokinetics, and drug interactions.

Clonazepam is a benzodiazepine that enhances the activity of GABA which is an inhibitory neurotransmitter in the central nervous system.

It is important to try to avoid using benzodiazepines like clonazepam with opioids as it can increase the risk of respiratory depression and death.

Clonazepam is an intermediate-acting benzodiazepine that is only commercially available as an oral dosage form.

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Lurasidone Pharmacology

On this podcast episode, I discuss lurasidone pharmacology, adverse effects, and drug interactions.

CYP3A4 is an important enzyme in the breakdown of lurasidone. I discuss this further on this episode.

Lurasidone is best taken with food as this enhances absorption and helps improve drug concentrations.

Lurasidone tends to have a lower risk for metabolic syndrome compared to other antipsychotics which is a nice advantage.

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Desvenlafaxine Pharmacology

On this episode, I discuss desvenlafaxine pharmacology, adverse effects, pharmacokinetics, and drug interactions.

Desvenlafaxine is a serotonin and norepinephrine reuptake inhibitor that can be used for depression.

Renal elimination is an important method of deactivation of desvenlafaxine. Dose adjustments may be recommended as renal function drops below 50 mls/min.

Withdrawal syndrome due is a risk with desvenlafaxine as it has a significantly short half-life.

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Venlafaxine Pharmacology

In this episode, I discuss venlafaxine pharmacology, adverse effect, dose conversion of IR to ER, and drug interactions.

Venlafaxine is notorious for producing withdrawal symptoms when discontinued abruptly. I discuss these in detail on the podcast.

How significant is the interaction of venlafaxine with antiplatelet agents? I discuss that in this episode.

The onset of action is a critical education point that patients must be aware of as it takes some time for venlafaxine to work.

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Trihexyphenidyl (Artane) Pharmacology

On this episode, I breakdown trihexyphenidyl (Artane) pharmacology, adverse effects, and drug interactions.

Trihexyphenidyl is highly anticholinergic and can cause constipation, dry eyes, dry mouth, and urinary retention.

Dementia medications like donepezil can have their effects blunted by the use of trihexyphenidyl.

Trihexyphenidyl is an older anticholinergic that is rarely used for the management of EPS caused by antipsychotics.

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Duloxetine Pharmacology

On this episode, I discuss duloxetine pharmacology, adverse effects, and common drug interactions.

Duloxetine is an SNRI that is used for depression, anxiety, and various pain syndromes like neuropathy and fibromyalgia.

Duloxetine can inhibit CYP2D6 which can lead to higher concentrations of clozapine and propranolol and lower activity of tamoxifen.

CYP1A2 inhibitors like ciprofloxacin can raise concentrations of duloxetine leading to an increased potential for adverse effects.

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Amitriptyline Pharmacology

On this episode, I discuss amitriptyline pharmacology, adverse effects, and drug interactions.

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Quetiapine Pharmacology

On this episode, I discuss quetiapine pharmacology, adverse effects, pharmacokinetics, and drug interactions.

Quetiapine (Seroquel) is a medication seen a fair amount, particularly in the geriatric population where there is psychosis associated with dementia. It is classified as an antipsychotic. Mechanistically it’s going to block dopamine receptors, specifically D2. It also has some serotonin receptor blockade antagonism. It does have other activity as well from a mechanism of action standpoint. There is alpha-blocking activity potentially as well as an antihistamine/anticholinergic type of activity. Uses of this medication are schizophrenia, bipolar disorder with associated mania, miscellaneous psychotic disorders, and Parkinson’s type disease with psychosis. Off-label you may see it used for OCD, or augmentation for PTSD and depression.

There is a boxed warning of increased risk of mortality in elderly/dementia patients. As a class, antipsychotics have extrapyramidal symptoms, metabolic syndrome, anticholinergic activity, QTC prolongation, sexual dysfunction, hyperprolactinemia, neuroleptic malignant syndrome, sedation, fall risk, and potentially a drop in blood pressure as well. With quetiapine, it is important to recognize that antipsychotics can have varying degrees of how much these adverse effects happen and a lot of them are dose-dependent.

There are three important points in comparison to other antipsychotics. Quetiapine is not that great as far as metabolic syndrome risk goes. It’s in the middle of the other antipsychotics. Its extrapyramidal symptoms are better than most, which is why it’s used so often in Parkinson’s. Quetiapine tends to be more sedating than other antipsychotics. This can be helpful when patients are having psychosis worse in the evening or at night.

Metabolic syndrome is something to worry about more in younger patients. The long-term risk of diabetes and hyperlipidemia is going to be a lot higher for them than an 80-year-old using a low dose for dementia-related aggression.

3A4 is a pathway of breakdown for quetiapine drug interactions. With larger food intakes absorption can increase about 15% to 25% and that’s in the area under the curve. This is not something to be very concerned about unless patients change the way they take it. 

Quetiapine’s drug interactions are mostly additive effects. Watch out for other sedative drugs such as alcohol, opioids, and benzodiazepines. The same goes for drugs causing QT prolongation. Quetiapine has alpha-blocking activity and an added effect on patients with borderline low blood pressure or at risk for falls. It also mechanistically has a potential antihistamine burden that can play a role in adding on to anticholinergic effects. Then lastly it is metabolized partly by CYP3A4 so there is some potential there for drug interactions. Classic enzyme inducers are St. John’s Wort and carbamazepine which would lower the concentration of quetiapine.

Eric Christianson, PharmD, BCPS, BCGP

Information for the podcast is obtained from various sources including the Highly Rated Flippin’ Pharmacology Flashcards which you can find on Amazon by clicking here!

Fluvoxamine Pharmacology

On this episode, I discuss fluvoxamine pharmacology, adverse effects, and most importantly, drug interactions.

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Zaleplon Pharmacology

On this episode, I discuss the pharmacology of zaleplon including side effects, drug interactions, and important clinical pearls.

Zaleplon is a non-benzodiazepine sleep aide commonly known as Sonata. It is commonly used for sedation and the management of insomnia. Zaleplon is a controlled medication, with a high risk for dependence, and because of that, it is best used to treat short-term insomnia. The pharmacology of zaleplon is similar to other sleep aids like Ambien, and Lunesta; they all have an impact on GABA. Specifically, zaleplon regulates the GABABZ receptor. The GABABZ receptor has been shown to be responsible for the pharmacological properties of benzodiazepines which produce sedative, anxiolytic, relaxant, and anticonvulsive effects. For pharmacokinetics, zaleplon has a general onset of action around 30-60 minutes, because of that it is best dosed closer to bedtime. 

For sedatives, and other drugs similar to zaleplon, it is generally better to start at lower doses in geriatrics and smaller patients. The commonly accepted dosing is between 5-20 mg, but it is best to use non-pharmacological therapies, instead of pharmacological whenever possible. The most common side effect that may be experienced with zaleplon is next-day sedation, also known as hangover sedation. Loss of mental clarity, dizziness, and confusion may also be present. Serious side effects of taking zaleplon are abnormal sleep behaviors, which it carries a US boxed warning for, and risk of dependence. Zaleplon is also on Beer’s list because of the increased risk of falls, delirium, and increased complications while driving due to sedation and lethargy. 

When a sedative is first prescribed, it’s important to first look at the other medications a patient may be taking to see if that’s what may be causing insomnia. For example, a diuretic administered at night can cause excessive urination that can lead to insomnia. The addition of stimulants too late in the day can also cause that, and similarly, lifestyle changes like increased intake of caffeine can increase the risk for insomnia as well. 

Most of the drug-drug interactions that zaleplon has are due to additive depressive effects. Examples include alcohol, opioids, older antihistamines, trazodone, or any medication that can cause sedation. There is also a smaller risk for CYP3A4 interaction. Concurrent administration of an inducer, like St. John’s Wort, or carbamazepine, can lower the concentrations of zaleplon. Likewise, inhibitors may increase concentrations.

In cases of overdose, the signs and symptoms that will most likely precipitate are exaggerations of zaleplon’s adverse effects. The manifestations of CNS depression can range from drowsiness to coma. More mild cases might have drowsiness, confusion, and lethargy; while more serious cases may have ataxia, hypotonia, hypotension, respiratory depression, coma, and death. To treat a zaleplon overdose, symptomatic and supportive measures are necessary along with gastric lavage. Animal studies suggest that flumazenil is an antidote as an antagonist to zaleplon, but there is no human data. With proper treatment, recoveries have been made with overdoses greater than 200 mg. In instances where the outcome was fatal, it was most often associated with the use of additional CNS depressants.

Show notes provided by Chong Yol G Kim, PharmD Student.

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Resources

Paragraph 1: taken from podcast, also taken from https://go.drugbank.com/drugs/DB00962#pharmacodynamics

Paragraph 2: taken from podcast

Paragraph 3: taken from podcast

Paragraph 4: taken from podcast

Paragraph 5: taken from FDA label