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On this episode, I discuss gemfibrozil pharmacology, adverse effects, and important drug interactions.
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On this episode, I discuss trospium pharmacology, adverse effects, and important drug interactions you should know.
Trospium chloride (Sanctura) is a bladder antimuscarinic or anticholinergic. It blocks the action of acetylcholine in bladder smooth muscle. It is used for urinary frequency and overactive bladder. The immediate-release formulation is taken twice a day. There is an extended-release version that is more expensive.
As its classification suggests it is going to have anticholinergic effects that include dry eyes, dry mouth, constipation, urinary retention, GI tract slowing down, CNS sedation, and increased risk of falls. Compared to older bladder anticholinergics such as oxybutynin or tolterodine there is less CNS penetration. Hopefully, this will cause the patient to experience fewer CNS side effects. A downside to this being a newer medication is that it costs more.
Trospium is on the BEERS list. Look for medications started after the trospium that indicate anticholinergic side effects such as saliva substitutes, an increase in BPH medications, artificial tears, or constipation medications.
It should be administered on an empty stomach as food can block absorption. If the patient is currently taking it with food and seeing results there is no need to change how they are taking it.
Trospium is not metabolized by CYP enzymes minimizing drug interactions. Most interactions occur because of additive effects. Avoid using it with other medications on the BEERS list, especially other anticholinergic medications. Be cautious using other medications with sedative effects and CNS depression (benzodiazepines, sleep medications, opioids, alcohol) as they may have additive effects.
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On this episode, I discuss propranolol pharmacology, adverse reactions, and important drug interactions you should know.
Propranolol (Inderal) is a non-selective beta-blocker. There are many indications for it including hypertension, tachycardia, atrial fibrillation, post-MI, chronic stable angina, essential tremors, migraine prophylaxis, esophageal varices, performance anxiety disorder, lithium-induced tremor, psychotic induced akathisia, and thyroid storm.
Propranolol blocks beta-1 receptors that are commonly referred to as the cardiac receptors and beta-2 receptors that are in the lungs. Albuterol is a beta-2 agonist meaning that propranolol can block its effects. This may lead to bronchospasms and worsening of respiratory conditions. This is one of the major issues when using a non-selective beta-blocker vs a selective one.
Other adverse effects include a drop in blood pressure and pulse. Fatigue is also seen in many geriatric patients so it is important to be titrating them up slowly. If you notice patients increasing caffeine intake, starting a stimulant, or experiencing new depression symptoms that can be a sign of fatigue. Sexual dysfunction has also been seen in patients taking propranolol. Propranolol may mask symptoms of hypoglycemia. Closely monitor patients that are taking insulin and/or sulfonylureas. Abrupt discontinuation can increase the risk for acute coronary syndromes, especially if the patient is already at risk. Make sure that the medication is taken consistently and there aren’t periods of multiple missed doses.
Propranolol comes in multiple dosage forms that have been mixed up. When dispensing or administering take extra caution that the medication is correct.
Propranolol is a weak CYP1A2 inhibitor that could increase concentrations of tizanidine or theophylline. Propranolol also gets broken down by CYP1A2. Medications that inhibit this enzyme can increase the concentration of propranolol. Examples of these are ciprofloxacin and fluvoxamine. Inducers of CYP1A2 can reduce concentrations. These are rifampin, carbamazepine, and phenobarbital. A unique CYP1A2 inducer is smoking tobacco. Medications can cause additive effects when it comes to blood pressure and pulse. Be careful with any blood pressure-lowering medications including antihypertensives, PDE5 inhibitors (sildenafil), and Parkinson’s medications (Sinemet). Drugs that can lower pulse include centrally acting alpha 2 antagonists (clonidine) and acetylcholinesterase inhibitors (donepezil, rivastigmine).
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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
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On this episode, I discuss oxybutynin pharmacology, drug interactions, and adverse effects.
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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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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
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On this episode, I discuss torsemide pharmacology, adverse effects, drug interactions and pharmacokinetics. Torsemide is commonly known as Demadex. It is a loop diuretic, and like other loop diuretics, it acts by inhibiting the reabsorption of Na+ and Cl- in the ascending loop of Henle. What results is a decrease in the reabsorption of water, causing a loss of electrolytes as well as water. The pharmacology of torsemide makes it useful in cases of heart failure, cirrhosis, or hypertension. Torsemide, and other loop diuretics, can also be a part of the prescribing cascade. For example, pregabalin and gabapentin, along with amlodipine and pioglitazone can cause or worsen edema, resulting in a new prescription of torsemide.
Torsemide is typically initially dosed between 5-20 mg, depending on the use. If the indication isn’t very severe it might be dosed lower, between 5-10 mg, or higher if it’s a more severe indication starting at 20 mg and titrated up. It should be cautioned in patients with a history of dehydration and renal failure, and it is contraindicated in cases of anuria, hepatic coma, and hypersensitivity. It may sometimes be necessary to be converted to furosemide or bumetanide, or torsemide from the other two. The conversion is, 20 mg of torsemide is equivalent to 40 mg of oral furosemide, which is equivalent to 1 mg bumetanide.
The adverse effects go hand-in-hand with its pharmacology, these include dehydration, increased urination, increased risk of acute renal failure, electrolyte imbalances, and ototoxicity. Also related to the pharmacology of torsemide, electrolytes, renal function, as well as blood pressure should be monitored. Kinetics may vary depending on what loop diuretic it is. It is generally more consistent with furosemide, but torsemide can sometimes have less variability as well as a longer half-life in comparison.
For drug-drug interactions, additive effects are the main concern. When combined with Sinemet or PDE inhibitors, there may be an unsafe drop in blood pressure. If it’s combined with SGLT2 inhibitors there can be increased diuresis. There can also be an increased risk of renal issues when taken with an NSAID, ACE inhibitors, or ARBs; if an NSAID is necessary, the dose or duration should be limited, and the kidney function should be monitored. The risk for ototoxicity increases when taken with aminoglycosides, and drugs that can cause edema should be monitored.
The main signs and symptoms of intolerance, or overdose, are extensions of its adverse effects and are related to its pharmacology. Commonly, it will be dehydration, hypotension, or symptoms of either. When treating overdoses, symptomatic relief is necessary; it is commonly achieved by fluid and electrolyte replacement.
Show notes provided by Chong Yol G Kim, PharmD Student.
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On this episode, I breakdown the sacubitril valsartan pharmacology.
The drug for this week is the combination drug sacubitril/valsartan, also known as Entresto. Entresto has a novel dual mechanism of action to treat HFrEF. Sacubitril, currently, is the only FDA-approved medication that is a neprilysin inhibitor. For background, neprilysin is an enzyme that breaks down natriuretic peptides. The inhibition of neprilysin results in an increase in natriuretic peptides, which causes vasodilation, fluid loss, and a decrease in blood pressure. Valsartan is an angiotensin II receptor blocker; it prevents angiotensin II from binding to AT1 to reduce blood pressure by reducing vasoconstriction, synthesis, and release of aldosterone and ADH, cardiac remodeling, and renal reabsorption of sodium. The unique pharmacology of Entresto makes it advantageous to use in HFrEF and is even now one of the preferred agents.
Common adverse reactions that occur when taking Entresto are related to its dual mechanism pharmacology. The most common adverse reactions of Entresto are hyperkalemia, angioedema, hypotension, and renal impairment. Entresto is contraindicated in pregnancy due to fetotoxicity; it requires a 36 hour washout period when transitioning from an ACE inhibitor due to the increased risk of angioedema.
Entresto is initially dosed at 24/26 mg twice a day if the patient is on a low dose ACE inhibitor/ARB, or if the patient has not taken anything. If a patient is taking over 10 mg of enalapril equivalents a day or 160 mg of valsartan equivalents a day, then the preferred initial dose is 49/51 mg twice a day. Regardless of initial dosing, the target dose is 97/103 mg twice a day. In cases of severe renal impairment, or moderate hepatic impairment, the initial dosing should start at 24/26 twice a day; titration remains the same.
The pharmacology of Entresto leaves room for many potential drug-drug interactions. There’s a risk of duplicate therapy with other ACE inhibitors or ARBs. An exacerbation of adverse drug reactions can also occur when taking medications that can lower blood pressure, like Sinemet, or medications that can increase the risk for hyperkalemia, like trimethoprim, and spironolactone, or medications that can increase the risk of renal impairment, like NSAIDs. Entresto has also been shown to increase the risk of lithium toxicity.
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Show notes provided by Chong Yol G Kim, PharmD Student.
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I cover melatonin pharmacology on this episode of the Real Life Pharmacology Podcast.
Melatonin, commonly taken by patients for insomnia, is an endogenous hormone produced by the pineal gland. It is an over-the-counter supplement available in dosage forms such as liquid drops, gummies, and tablets. The pharmacology of melatonin is primarily through the activation of melatonin receptors in the suprachiasmatic nucleus; it is also a derivative of L-tryptophan. The production and secretion of melatonin is stimulated by darkness and is inhibited by light. Melatonin concentrations are also shown to vary with age. Its production primarily begins between months 3-4 post-birth, and it peaks between years 1-3. The production and secretion decrease with age and can play a role in insomnia in adults. The doses of melatonin can vary but is commonly found in 1 mg, 3 mg, 5 mg, and 10 mg. Although it is usually taken in higher doses, doses between 0.1-0.5 mg may be adequate.
Certain things need to be taken into consideration when a patient is taking melatonin. Some of the things that should be taken into consideration are if it works as it’s expected to or if the patient is already on stimulating medications that can cause insomnia. If the patient is taking other medications like zolpidem, trazodone, or mirtazapine, melatonin may not be needed. Other things that should be taken into consideration are if the patient tolerates melatonin well and if a lower dose of melatonin can be used. Melatonin is commonly well-tolerated, but it can occasionally cause CNS issues at higher doses such as oversedation, cognitive impairment. It can even cause hyperprolactinemia that can cause sexual dysfunction, fertility risk, lactation, and is associated with lower bone mineral density.
Common adverse drug reactions associated with the pharmacology of melatonin are headache, CNS depression, irritability, and daytime sedation. With long-term use, melatonin can cause suppression of the hypothalamic-pituitary axis. Melatonin is primarily metabolized by CYP1A2, CYP2C9, and CYP2C19. The concentration and efficacy of melatonin can potentially be impacted by medications that induce or inhibit the CYP enzyme system, such as propranolol, calcium-channel blockers, and others. Interactions of melatonin that are not CYP mediated are additive effects when taken with other sedatives, caffeine, and ethanol that can reduce the efficacy of melatonin, or other medications that can increase the risk of adverse drug reactions.
Melatonin is regulated by the FDA as a dietary supplement, and not as a medication. Toxicology studies are limited.
Show notes provided by Chong Yol G Kim, PharmD Student.
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On this episode, I discuss ketamine pharmacology.
Ketamine is primarily broken down by CYP2B6 which fortunately does not have a lot of common medications that can interfere with its action.
Ketamine can cause psychiatric type adverse effects such as hallucinations, nightmares, and vivid dreams.
At lower to moderate dosages, ketamine does have some mild sympathetic activity which can raise blood pressure and heart rate.
I discuss important drug interactions on the podcast, be sure to check out my latest project which is a 200+ page book on managing drug interactions in primary care.
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