In which way is Tolsura (Itraconazole) different from Sporanox (Itraconazole)?
a. Different dosing frequency b. Less side effects c. Different indication d. Different dosage form e. No difference
In which way is Tolsura (Itraconazole) different from Sporanox (Itraconazole)?
a. Different dosing frequency b. Less side effects c. Different indication d. Different dosage form e. No difference
Answer: (c) different indication.
Tolsura (itraconazole capsules) and Sporanox (itraconazole) are azole antifungals used to treat different types of infections. Tolsura is used to treat blastomycosis, pulmonary and extrapulmonary; histoplasmosis, including chronic cavitary pulmonary disease and disseminated, non-meningeal histoplasmosis; and aspergillosis, pulmonary and extrapulmonary, in patients who are intolerant of or who are refractory to amphotericin B therapy.
Sporanox is used to treat fungal infections of the lungs, mouth or throat, toenails, or fingernails.
The dose of Tolsura to treat blastomycosis and histoplasmosis is 130 mg to 260 mg daily. The dose of Tolsura to treat aspergillosis is 130 mg to 260 mg daily.
Dosage of Sporanox depends upon the condition for which it is being used to treat.
Side effects of Tolsura and Sporanox that are similar include nausea, vomiting, skin rash, headache, diarrhea, itching, and dizziness.
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A 35-year-old man who is a regular patient of yours comes to your pharmacy counter with a new prescription. His shoulders appear tense and his eyebrows are knit tightly.
He says to you, "I can't believe I have to fill another prescription today. I was just in three weeks ago and spent $75 dollars on some fancy new medication that didn't do a darn thing!" What might be an appropriate active listening response to this patient?
a. It must be very frustrating to have to try something new.
b. It's too bad we can't take a prescription back for a refund.
c. I can provide you with a smaller quantity this time.
d. Your doctor is trying to find the best medication for you.
A 35-year-old man who is a regular patient of yours comes to your pharmacy counter with a new prescription. His shoulders appear tense and his eyebrows are knit tightly.
He says to you, "I can't believe I have to fill another prescription today. I was just in three weeks ago and spent $75 dollars on some fancy new medication that didn't do a darn thing!" What might be an appropriate active listening response to this patient?
a. It must be very frustrating to have to try something new.
b. It's too bad we can't take a prescription back for a refund.
c. I can provide you with a smaller quantity this time.
d. Your doctor is trying to find the best medication for you.
Answer (a). It must be very frustrating to have to try something new. Answer "b" does not acknowledge the patient's feelings; answer "c" moves to finding a solution without acknowledging the patient's feelings and "d" is placating.
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Which of the following information is/are TRUE ABOUT Naloxone? [Select All That Apply].
a. Naloxone hydrochloride is a pure opioid antagonist that competitively binds to μ-opioid receptors only when opioids are present.
b. No tolerance or dependence is associated with naloxone use
c. When comparing the μ-opioid receptor affinity of naloxone with that of most opioids, including heroin, naloxone has a greater affinity to bind to the receptor site.
d. Naloxone has a short duration of activity about 30 to 90 minutes.
Which of the following information is/are TRUE ABOUT Naloxone? [Select All That Apply].
a. Naloxone hydrochloride is a pure opioid antagonist that competitively binds to μ-opioid receptors only when opioids are present.
b. No tolerance or dependence is associated with naloxone use
c. When comparing the μ-opioid receptor affinity of naloxone with that of most opioids, including heroin, naloxone has a greater affinity to bind to the receptor site.
d. Naloxone has a short duration of activity about 30 to 90 minutes.
Answer: (a, b, c and d). Naloxone was patented in 1961, was first approved by the Food and Drug Administration (FDA) in 1971, and is currently on the World Health Organization's List of Essential Medicines.
Naloxone hydrochloride is a pure opioid antagonist that competitively binds to μ-opioid receptors only when opioids are present and bound at the receptor site. Naloxone demonstrates no effect on mu, kappa, or delta receptors in a person who has not taken opioids. No tolerance or dependence is associated with naloxone use.
The reversal of opioid toxicity with naloxone is dose dependent. Individuals who have used a particularly potent opioid (e.g., fentanyl), have high concentration of opioids in their system, or have used a long-acting opioid may require more frequent and/or larger doses of naloxone to reverse symptoms.
When comparing the μ-opioid receptor affinity of naloxone with that of most opioids, including heroin, naloxone has a greater affinity to bind to the receptor site. This mechanism allows naloxone to remove the opioid from the receptor site and then bind it more securely. When this occurs, respiratory depression resolves partially or fully (depending on the amount, form, and route of opioids taken), hypotension resolves, and CNS depression abates.
Depending on the type of opioid used, the individual may be at risk for experiencing rebound opioid toxicity and/or acute respiratory depression because of the short duration of activity of naloxone (i.e., 30-90 minutes).
This effect most often occurs when an individual has taken a long-acting opioid such as methadone or extended-release oxycodone. Naloxone's short duration of action is an important reason to convey to patients that receiving emergency medical care for an opioid overdose is important, even if the person has responded to the naloxone.
Naloxone is not effective in treating overdoses of non-opioid prescription medicines like benzodiazepines or barbiturates. It also is not effective in overdoses with stimulants, such as cocaine and amphetamines, or other non-opioid illicit drugs such as MDMA (Ecstasy, Molly), GHB (G), or ketamine (Special K). However, a polysubstance overdose that includes opioids warrants the use of naloxone.
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Which of the following information is/are TRUE ABOUT Essential Fatty Acids? [Select ALL That Apply]
a. Linoleic and alpha-linolenic are essential fatty acids. b. Arachidonic acid is classified as 'conditionally essential' fatty acid. c. Ideally, in the diet, the ratio of omega-6 to omega-3 fatty acids should be between 1:1 and 4:1. d. Excessive intake of omega-6 fatty acids can cause the deficiency of omega-3 fatty acids.
Which of the following information is/are TRUE ABOUT Essential Fatty Acids? [Select ALL That Apply]
a. Linoleic and alpha-linolenic are essential fatty acids. b. Arachidonic acid is classified as 'conditionally essential' fatty acid. c. Ideally, in the diet, the ratio of omega-6 to omega-3 fatty acids should be between 1:1 and 4:1. d. Excessive intake of omega-6 fatty acids can cause the deficiency of omega-3 fatty acids.
Answer (a, b, c and d). Essential fatty acids, or EFAs, are fatty acids that humans and other animals must ingest because the body requires them for good health but cannot synthesize them.
Only two fatty acids are known to be essential for humans: alpha-linolenic acid (an omega-3 fatty acid) and linoleic acid (an omega-6 fatty acid). Some other fatty acids are sometimes classified as "conditionally essential," meaning that they can become essential under some developmental or disease conditions; examples include docosahexaenoic acid and gamma-linolenic acid.
It is not only important to incorporate good sources of omega-3 and omega-6s in a diet, but also consume these fatty acids in the proper ratio. Omega-6 fatty acids compete with omega-3 fatty acids for use in the body, and therefore excessive intake of omega-6 fatty acids can inhibit the use of omega-3 fatty acids by the body.
Ideally, the ratio of omega-6 to omega-3 fatty acids should be between 1:1 and 4:1. Instead, most Americans consume these fatty acids at a ratio of omega-6: omega-3 between 10:1 and 25:1, and are consequently unable to reap the benefits of omega-3s.
This imbalance is due to a reliance on processed foods and oils, which are now common in the Western diet. To combat this issue it is necessary to eat a low-fat diet with minimal processed foods and with naturally occurring omega-3 fatty acids. A lower omega-6: omega-3 ratio is desirable for reducing the risk of many chronic diseases.
Arachidonic acid is not one of the essential fatty acids. However, it does become essential if there is a deficiency in linoleic acid or if there is an inability to convert linoleic acid to arachidonic acid.
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A List of Drugs with Their Normal Therapeutic Concentrations.
A List of Drugs with Their Normal Therapeutic Concentrations.
Amikacin: 15 to 25 mcg/mL Aminophylline: 10 to 20 mcg/mL Amitriptyline: 120 to 150 ng/mL Carbamazepine: 5 to 12 mcg/mL Cyclosporine: 100 to 400 ng/mL (12 hours after dose) Desipramine: 150 to 300 ng/mL Digoxin: 0.8 to 2.0 ng/mL Disopyramide: 2 to 5 mcg/mL Ethosuximide: 40 to 100 mcg/mL Flecainide: 0.2 to 1.0 mcg/mL Gentamicin: 5 to 10 mcg/mL Imipramine: 150 to 300 ng/mL Kanamycin: 20 to 25 mcg/mL Lidocaine: 1.5 to 5.0 mcg/mL Lithium: 0.8 to 1.2 mEq/L Methotrexate: varies with use Nortriptyline: 50 to 150 ng/mL Phenobarbital: 10 to 30 mcg/mL Phenytoin: 10 to 20 mcg/mL Primidone: 5 to 12 mcg/mL Procainamide: 4 to 10 mcg/mL Quinidine: 2 to 5 mcg/mL Salicylate: varies with use Sirolimus: 4 to 20 ng/mL (12 hours after dose; varies with use) Tacrolimus: 5 to 15 ng/mL (12 hours after dose) Theophylline: 10 to 20 mcg/mL Tobramycin: 5 to 10 mcg/mL Valproic acid: 50 to 100 mcg/mL
Which of the following information is TRUE ABOUT Tall Man Letters? [Select All that apply].
a. Several studies have shown that highlighting sections of words using tall man lettering can make similar drug names easier to distinguish.
b. The Institute for Safe Medication Practices (ISMP), the FDA, The Joint Commission, and other safety-conscious organizations such as the National Association of Boards of Pharmacy (NABP) have promoted the use of tall man letters as one means of reducing confusion between similar drug names.
c. Nearly all of surveyed (87%) conducted by ISMP for Tall Man Letters felt that the use of tall man letters by the medical product industry helped to reduce errors in drug selection.
d. Approximately 50% of all survey respondents reported using tall man letters in conjunction with pharmacy-generated product and shelf labels, computer screens, and medication administration records.
e. Use of the tall man letters on computer-generated pharmacy labels was the most prevalent and was considered to be most effective, whereas use of the letters on preprinted order forms was among the least prevalent and was considered to be least effective.
Which of the following information is TRUE ABOUT Tall Man Letters? [Select All that apply].
a. Several studies have shown that highlighting sections of words using tall man lettering can make similar drug names easier to distinguish.
b. The Institute for Safe Medication Practices (ISMP), the FDA, The Joint Commission, and other safety-conscious organizations such as the National Association of Boards of Pharmacy (NABP) have promoted the use of tall man letters as one means of reducing confusion between similar drug names.
c. Nearly all of surveyed (87%) conducted by ISMP for Tall Man Letters felt that the use of tall man letters by the medical product industry helped to reduce errors in drug selection.
d. Approximately 50% of all survey respondents reported using tall man letters in conjunction with pharmacy-generated product and shelf labels, computer screens, and medication administration records.
e. Use of the tall man letters on computer-generated pharmacy labels was the most prevalent and was considered to be most effective, whereas use of the letters on preprinted order forms was among the least prevalent and was considered to be least effective.
Answer: (a,b,c,d and e). Tall man (uppercase) letters are used within a drug name to highlight its primary dissimilarities and help to differentiate look-alike names. Several studies have shown that highlighting sections of words using tall man lettering can make similar drug names easier to distinguish, and fewer errors are made when tall man letters are used to differentiate products with look-alike names.
The Institute for Safe Medication Practices (ISMP), the FDA, The Joint Commission, and other safety-conscious organizations such as the National Association of Boards of Pharmacy (NABP) have promoted the use of tall man letters as one means of reducing confusion between similar drug names.
From a survey conducted by the ISMP in 2008, most respondents appeared to agree. Nearly all of those surveyed (87%) felt that the use of tall man letters by the medical product industry helped to reduce errors in drug selection, and two-thirds (64%) reported that tall man lettering actually prevented them from dispensing or administering the wrong medication.
A fully alphabetized list of drug names with tall man lettering can be found at www.ismp.org/Tools/tallmanletters.pdf.
TallMan Letter
Approximately 50% of all survey respondents reported using tall man letters in conjunction with pharmacy-generated product and shelf labels, computer screens, and medication administration records. Half to three-quarters of respondents who used tall man letters with look-alike drug name pairs felt that this strategy was effective in reducing the risk of errors, depending on where it was used.
Use of the tall man letters on computer-generated pharmacy labels was the most prevalent and was considered to be most effective, whereas use of the letters on preprinted order forms was among the least prevalent and was considered to be least effective. In general, between one-quarter and one-third of respondents were undecided about the effectiveness of tall man letters, but very few reported that the letters were wholly ineffective in reducing the risk of errors. The use of tall man letters was less widely reported for drugs listed on prescriber order entry screens and smart pump libraries.
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Which of the following statements correctly describes the mechanism of action of Invokana (Canagliflozin)?
a. Increase insulin sensitivity towards blood glucose. b. Stimulates insulin release from functioning beta cells of pancreas. c. Delayed the absorption of glucose from gut to blood. d. Increase gluconeogenesis in the liver. e. Increase excretion of glucose through kidney.
Which of the following statements correctly describes the mechanism of action of Invokana (Canagliflozin)?
a. Increase insulin sensitivity towards blood glucose. b. Stimulates insulin release from functioning beta cells of pancreas. c. Delayed the absorption of glucose from gut to blood. d. Increase gluconeogenesis in the liver. e. Increase excretion of glucose through kidney.
Answer: (e). Sodium-glucose co-transporter 2 (SGLT2), expressed in the proximal renal tubules, is responsible for the majority of the reabsorption of filtered glucose from the tubular lumen. Canagliflozin is an inhibitor of SGLT2. By inhibiting SGLT2, Canagliflozin reduces reabsorption of filtered glucose and lowers the renal threshold for glucose (RTG), and thereby increases urinary glucose excretion (UGE).
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Which of the following drugs interacts with Invokana (Canagliflozin)? [SELECT All THAT APPLY]
a. Digoxin b. Rifampin c. Ketoconazole d. Trazodone e. Tramadol
Which of the following drugs interacts with Invokana (Canagliflozin)? [SELECT All THAT APPLY]
a. Digoxin b. Rifampin c. Ketoconazole d. Trazodone e. Tramadol
Answer: (a and b). Co-administration of Canagliflozin with rifampin, a nonselective inducer of several UGT enzymes, including UGT1A9, UGT2B4, decreased Canagliflozin area under the curve (AUC) by 51%. This decrease in exposure to Canagliflozin may decrease efficacy.
If an inducer of these UGTs (e.g., rifampin, phenytoin, phenobarbital, ritonavir) must be co-administered with Invokana (Canagliflozin) (Canagliflozin), consider increasing the dose to 300 mg once daily if patients are currently tolerating Invokana (Canagliflozin) 100 mg once daily, have an eGFR greater than 60 mL/min/1.73 m2, and require additional glycemic control.
Consider other antihyperglycemic therapy in patients with an eGFR of 45 to less than 60 mL/min/1.73 m2 receiving concurrent therapy with a UGT inducer and require additional glycemic control.
There was an increase in the AUC and mean peak drug concentration (Cmax) of digoxin (20% and 36%, respectively) when co-administered with Invokana (Canagliflozin) 300 mg. Patients taking Invokana (Canagliflozin) with concomitant digoxin should be monitored appropriately.
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Which of the following information is TRUE about Invokana (Canagliflozin)? [SELECT ALL THAT APPLY]
a. The 300-mg dose of Invokana is proven to show greater A1C reductions than Januvia. b. It is a once-daily pill that works around the clock. c. It is not for weight loss, but may help a patient to lose weight-on average 3%. d. In most clinical trials, the majority of people taking Invokana reached an A1C goal of less than 7%. e. The most common side effect associated with the use of Invokana is hypoglycemia.
Which of the following information is TRUE about Invokana (Canagliflozin)? [SELECT ALL THAT APPLY]
a. The 300-mg dose of Invokana is proven to show greater A1C reductions than Januvia. b. It is a once-daily pill that works around the clock. c. It is not for weight loss, but may help a patient to lose weight-on average 3%. d. In most clinical trials, the majority of people taking Invokana reached an A1C goal of less than 7%. e. The most common side effect associated with the use of Invokana is hypoglycemia.
Answer: (a,b,c, and d). Invokana (Canagliflozin) is a sodium-glucose co-transporter 2 (SGLT2) inhibitor indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.
The recommended starting dose is 100 mg once daily, taken before the first meal of the day. Dose can be increased to 300 mg once daily in patients tolerating Invokana (Canagliflozin) 100 mg once daily who have an eGFR of 60 mL/min/1.73 m2 or greater and require additional glycemic control.
Invokana (Canagliflozin) is limited to 100 mg once daily in patients who have an eGFR of 45 to less than 60 mL/min/1.73 m2. Assess renal function before initiating Invokana (Canagliflozin). Do not initiate Invokana (Canagliflozin) if eGFR is below 45 mL/min/1.73 m2. Discontinue Invokana (Canagliflozin) if eGFR falls persistently below 45 mL/min/1.73 m2.
It can increase the risk of hypoglycemia when combined with insulin or an insulin secretagogue. A lower dose of insulin or insulin secretagogue may be required to minimize the risk of hypoglycemia when used in combination with Invokana (Canagliflozin).
It causes intravascular volume contraction. Symptomatic hypotension can occur after initiating Invokana (Canagliflozin), particularly in patients with impaired renal function (eGFR <60 mL/min/1.73 m2), elderly patients, patients on either diuretics or medications that interfere with the renin‐angiotensin‐aldosterone system, or patients with low systolic blood pressure.
The most common side effects of Invokana (Canagliflozin) include genital yeast infections, urinary tract infection, and changes in urination.
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After completing the therapy, H. pylori follow-up status testing shall be done within what time frame to ensure H. Pylori has been completely eradicated?
a. 7 days b. 72 hours c. 4 weeks d. 6 months e. a month
After completing the therapy, H. pylori follow-up status testing shall be done within what time frame to ensure H. Pylori has been completely eradicated?
a. 7 days b. 72 hours c. 4 weeks d. 6 months e. a month
Answer: (c) Before the seriousness of H. pylori infections was fully appreciated and when it was still believed that H. pylori eradication therapy could routinely cure more than 90% of patients, confirmation of cure testing was not routinely recommended.
Although confirmation for cure testing is currently considered the standard of care, preferably with noninvasive tests such as the stool antigen or a urea breath test, it is often not done.
Post eradication testing is not only useful to confirm H. pylori eradication but also serves to alert the clinician when resistance begins to undermine their locally effective current regimens. In this issue of Clinical Gastroenterology and Hepatology, Gatta et al report a pilot study suggesting that it may be possible to accurately assess cure using changes in serum pepsinogen II levels.
A positive urea breath test (UBT), histology, culture, or rapid urease test (RUT) any time after therapy is considered as evidence of treatment failure. However, it has been recommended that posttreatment testing be delayed for at least 4 weeks after the end of therapy.
This recommendation is based on the fact that it takes time for any remaining bacteria to recover and repopulate the stomach in sufficient numbers to be detected reliably. By 4 weeks, the accuracy of a negative test is in the range of 98% to 100%.
There is little or no gain by repeating negative tests to ensure success (e.g, 2 negative urea breath tests) as a second urea breath test has not shown an increase in accuracy and adds an incremental cost with little clinical benefit.
One caveat among available noninvasive tests is that when using the stool antigen to assess outcome, it may be best to increase the interval from 4 to 6 or 8 weeks to ensure that a positive result is not false positive.
The available data show that the stool antigen tests that use monoclonal anti-H. pylori antibodies are more reliable than polyclonal stool antigen tests and monoclonal antibody-based stool antigen tests are recommended.
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