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On this episode, I discuss oxybutynin pharmacology, drug interactions, and adverse effects.
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On this episode, I will discuss glyburide pharmacology.
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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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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
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On this episode, I breakdown the pharmacology of hydrochlorothiazide including adverse effects, drug interactions, and other clinical pearls.
Hydrochlorothiazide has common brand names of Microzide, Hydrodiuril, and its common abbreviation is HCTZ. Extra caution should be taken with “HCTZ”; it may be mistaken for other abbreviations. Hydrochlorothiazide works pharmacologically by blocking the reabsorption of sodium in the distal tubule of the kidney. The result of the pharmacology of hydrochlorothiazide is increased water, sodium, and potassium excretion. Due to hydrochlorothiazide’s mechanism of action, it makes it advantageous when used for blood pressure, edema, and heart failure in addition to loop diuretics.
Hydrochlorothiazide’s adverse reactions are due to its pharmacology. Frequent urination should occur so, dosing hydrochlorothiazide at night should be avoided. Loss of electrolytes should also happen, and the risk for hypokalemia, hyponatremia, and hypomagnesemia increases. Other adverse reactions include the increased risk of dehydration, increased uric acid concentrations, and hypercalcemia. The risk for hypercalcemia is not as concerning in lower doses. There is a potential for a sulfonamide allergy. If the patient has had an anaphylactic reaction with a sulfonamide-containing medication, hydrochlorothiazide may want to be avoided, or at least a risk/benefit assessment should be done. Another potential adverse reaction is an increase in blood sugar, but that is not typically concerning at lower doses. Electrolytes, as well as creatinine clearance, should be monitored to make sure kidney function, and electrolyte levels remain stable.
Drug-drug interactions that can occur with hydrochlorothiazide are additive effects that may happen when taken with other medications. The risk for an unsafe drop in blood pressure may increase if it is taken with PDE inhibitors, Sinemet, or SGLT2 inhibitors. Hydrochlorothiazide should be avoided with Lithium, the risk for toxicity increases when the two are taken concurrently due to Lithium concentrations being increased. The risk of an AKI increases if it’s taken with NSAIDs, ACE inhibitors, or ARBs; increased monitoring is warranted. Topiramate may increase the risk for hypokalemia, while vitamin D and calcium supplements may increase the risk for hypercalcemia. Hyponatremia may be more likely to occur if it’s taken with SSRIs, carbamazepine, or oxcarbazepine. Hydrochlorothiazide may blunt the effect of allopurinol if it’s used for gout. Since blood sugar levels may be increased, hyperglycemia can occur, but it’s typically not clinically significant.
In cases of intolerability, or overdoses, the manifestations are extensions of hydrochlorothiazide’s adverse effect profile. Most commonly, electrolyte depletion and dehydration will occur.
Show notes provided by Chong Yol G Kim, PharmD Student.
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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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In the podcast this week, I talk about doxylamine pharmacology. Doxylamine is a first-generation antihistamine; it is commonly an active ingredient in night-time medications like Unisom, Nyquil, and Mucinex. The pharmacology of doxylamine is similar to other first-generation antihistamines, it competitively inhibits the binding of histamine at H1 receptors. Its main uses are as sleep aides, in cough-and-cold medications, but doxylamine has also been given with pyridoxine to treat nausea and vomiting during pregnancy.
Doxylamine’s adverse reactions are related to its anticholinergic properties, they include dry eyes, dry mouth, increased fall risk, sedation, urinary retention, constipation, and confusion. Contraindications include concurrent use with a monoamine oxidase inhibitor, known hypersensitivities, concomitant alcohol use, and if the patient has the following conditions: elevated intraocular pressure, narrow-angle glaucoma, asthma, peptic ulcer disease, urinary bladder neck obstruction, or gastric outlet obstruction. It is also a Beer’s list drug due to its anticholinergic effects. The normal dose in adults is 25 mg. In cases of overdosage, the most common manifestation is exacerbations of its anticholinergic effects. The major complications of an overdose include arrhythmia, respiratory failure, seizures, hyperthermia, rhabdomyolysis, and coma.
When you know a patient is taking doxylamine, it’s important to be cognizant of their occupation, as well as what other conditions they may have. For example, doxylamine should be used with caution in patients that drive heavy machinery due to its sedating properties. You might be able to tell if a patient’s experiencing an adverse reaction exacerbation if they begin having worsening dementia symptoms or increased urinary retention. Other indications include the use of artificial tears, or saliva, or increased complaints of constipation. To monitor for doxylamine, it’s important to monitor the patient’s tolerability. The onset of doxylamine is relatively quick as well, with a peak concentration within 2-4 hours.
For drug-drug interactions, CYP interactions aren’t as concerning as usual. The main interaction to consider when a patient is taking doxylamine is additive anticholinergic effects. Sedative effects can increase when benzodiazepines, skeletal muscle relaxants, opioids, or antihistamines are concurrently taken. Doxylamine can also counteract the usefulness of dementia or BPH medications due to its anticholinergic properties. There is also a risk of increased anticholinergic burden when taken with skeletal muscle relaxants or tricyclic antidepressants.
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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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Glipizide, or Glucotrol, is a sulfonylurea used for the treatment of Type 2 Diabetes. Pharmacologically, glipizide acts by stimulating beta-cells in the pancreas to release insulin. Specifically, glipizide will block the opening of ATP-sensitive potassium channels on the plasma membrane of beta-cells on the pancreas. The result of that is depolarization, which then causes stimulation of voltage-sensitive calcium channels, eventually causing the exocytosis of insulin. The increased insulin will then promote the storage of glucose, decreasing the amount of glucose in the blood.
Due to the pharmacology of glipizide, the concerning adverse drug reactions are hypoglycemia and weight gain. Other adverse drug reactions include diaphoresis, dizziness, syncope, nervousness, anxiety, tremors, and diarrhea. The contraindications include hypersensitivity, Type 1 Diabetes, and DKA. Glipizide is not used as often due to the risk of hypoglycemia and weight gain. Glipizide is usually dosed once daily, but it can be split up if the dose is escalated. There are differences in administration depending on the formulation. For immediate release formulations, glipizide should be taken 30 minutes before meals to ensure that absorption is stable. For extended formulations, it can be given with breakfast or any other meal.
Of all the sulfonylureas, glipizide is preferred in CKD. Other sulfonylureas, like glyburide, are not preferred due to a decrease in elimination that can result in dose accumulation. In geriatric populations, dosing is less aggressive to lessen the risk of any adverse drug reactions and more specifically hypoglycemia. There’s a risk of cross-reactivity with sulfonamide allergies, but the risk will vary and is low risk. If SJS occurs due to a sulfonamide-containing drug, glipizide likely wouldn’t be recommended.
The drug-drug interactions of glipizide include medications that can increase the risk of hypoglycemia, for example, medications like quinolone antibiotics and B-blockers can mask the symptoms of hypoglycemia. Other interactions include the type where it can counteract the effect of glipizide, for example, medications that can increase blood glucose levels like corticosteroids, antipsychotics such as olanzapine and clozapine, stimulants, and transplant medications like cyclosporine and tacrolimus. There are also CYP interactions that can impact glipizide since it’s metabolized by CYP2C9. More monitoring is warranted when medications that can inhibit CYP2C9, like fluconazole, and medications that can induce CYP2C9, like rifampin, are also given. In cases of overdose, hypoglycemia is most likely to occur. Correction of decreased glucose levels is necessary.
Show notes provided by Chong Yol G Kim, PharmD Student.
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On this episode of the Real Life Pharmacology Podcast, I discuss cetirizine pharmacology.
Cetirizine, commonly known as Zyrtec, is a 2nd generation antihistamine. Compared to 1st generation antihistamines, like diphenhydramine and chlorpheniramine, 2nd generation antihistamines have fewer anticholinergic effects. Pharmacologically, cetirizine works by selectively blocking histamine from binding to the H1 receptor. The uses for cetirizine are allergic rhinitis, itching, and sometimes acute allergic reactions. Commonly, cetirizine is dosed at 10 mg daily, and can even be escalated to 10 mg twice daily in rare situations. In adults 77 years old and older, the manufacturer recommended dose tops out at 5 mg daily. There are also liquid and chewable formulations for children.
The adverse drug reactions cetirizine are mostly dose-dependent and related to its pharmacology. Out of all of the 2nd generation antihistamines, like fexofenadine and loratadine, cetirizine is the most sedating. Other adverse drug reactions related to its anticholinergic effects are urinary retention, constipation, confusion, fatigue, and dizziness. Lab monitoring is not necessary when taking cetirizine. It is important to monitor the adverse drug reactions when taking cetirizine, as well as improvement in the signs and symptoms of what it’s used for.
Cetirizine does not undergo metabolism through liver CYP enzymes, so drug-drug interactions involving those enzymes are uncommon. The interactions that are concerning are additive effects of cetirizine’s adverse drug reactions. Drowsiness can be compounded when cetirizine is taken with opioids, sleep medications, alcohol, or other older anticholinergics with sedative effects. There is also a risk of an increased anticholinergic burden when taking medications like Cogentin, oxybutynin, TCAs, and inhaled anticholinergics.
The manifestation of overdoses will vary depending on age. In adults, the most common observation made was sedation and somnolence. In children, restlessness and irritability were observed initially, then drowsiness. Cetirizine is not removed by dialysis. When treating overdoses, the symptoms that manifest should be treated.
Show notes provided by Chong Yol G Kim, PharmD Student.
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Folic acid is a water-soluble vitamin; compared to fat-soluble vitamins, accumulation is not as much of an issue. It is responsible for the formation of coenzymes, DNA synthesis, erythropoiesis, and certain metabolic processes. Due to the mechanism of folic acid, if there is a deficiency present, anemia can manifest. Although the recommended dietary intake is 0.2 mg, supplementation may be necessary. Some situations where supplementation may be desired are prevention of neural tube defects in pregnancy, patients suffering from alcohol abuse disorder, bariatric surgery patients, and certain types of GI disorders where malabsorption may be present. If a patient is taking certain medications folic acid supplementation may be necessary as well. Notable drugs where a patient may require folic acid include methotrexate and phenytoin.
The dosages used most often when supplementing folic acid are in the 1-5 mg range, and most of the time it will be 1 mg. Folic acid has a relatively safe adverse drug reaction profile. Some possible adverse drug reactions are flushing, malaise, erythema, skin rash, and hypersensitivity reactions. Although uncommon, the chance for an adverse drug reaction occurring increases as the dose increases. For monitoring folic acid, the normal levels can vary between 2-20 ng/mL, but they can vary based upon the lab. A type of anemia that can manifest with a folic acid deficiency is megaloblastic anemia. When assessing megaloblastic anemia, vitamin B12 levels should also be assessed.
Folic acid levels can be impacted by phenytoin, methotrexate, trimethoprim and sulfamethoxazole, sulfasalazine, triamterene, and alcohol. When a patient is only taking trimethoprim and sulfamethoxazole for acute treatment of a UTI, folic acid levels aren’t as concerning. Whenever it changes from acute treatment to prophylaxis, folic acid levels should be monitored more closely. Theoretically, folic acid can lower concentrations of phenytoin, and phenobarbital, so closer monitoring may be warranted.
Show notes provided by Chong Yol G Kim, PharmD Student.
Be sure to check out our free Top 200 study guide – a 31 page PDF that is yours for FREE!
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