Term
| In what way is micromedex more useful than Efacts? |
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Definition
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Term
| When does Oklahoma Law say a PDR shall be performed? |
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Definition
| When deemded appropriate or when required by law or rule |
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Term
| Give examples of when therapeutic duplication is okay? |
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Definition
beta-blocker & ca-channel blocker long-acting & short-acting formulations of a drug |
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Term
| Give examples of clinical misuse |
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Definition
Using a medication for the wrong indication Using a medication to treat a side effect of another medication (eg, treating acid reflux w/ a med, when the reflux is being caused by their Ca-channel blocker.) |
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Term
What are some typical anti-cholinergic effects? Hint: go from head to toes |
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Definition
| drowsiness, confusion (elderly), lack of accomodation, dry mouth, increased HR, decreased motility, decreased urination |
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Term
| What are some typical adverse effects of beta agonists? |
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Definition
| HTN, increased HR, tremor |
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Term
| What PDR elements would you think about for Combivent? |
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Definition
Overutilization Underutilization Therapeutic duplication - It could be appropriate to have albuterol in addition to combivent as long as a pt is alternating their use & didn't use the albuterol too often; you want to make sure the pt is not exceeding the max dose. |
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Term
| How much carbidopa do we need to tie up dopa decarboxylase in the circulation? |
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Definition
75mg of carbidopa is required so that L-dopa can make it to the CNS |
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Term
T or F Sudafed could cause rebound congestion if overused |
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Definition
| False, rebound congestion is usually the result of overuse of topical agents. So, we should only limit our use to 3 days for topical agents. |
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Term
| Why is compliance essential for catapress/catapress TTS? |
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Definition
| If central outflow is inhibited, peripheral beta receptors will up-regulate b/c of the inactivity. If the pt abruptly stops taking clonidine, there will be excessive stimulation of beta receptors, & the pt will experience rebound HTN. |
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Term
How long does it take Tegretol (carbamazepine) suspension to peak? Tablets? What happens if you eat food w/ tegretol tablets? Suspension? Sustained-release tablets? |
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Definition
suspension - 1.5hr; tablet - 4 to 6 hrs Pts should take tegretol susp w/ food to decrease the peak and side effects. If tablets are taken w/ food, absorption will increase. If SR form is taken w/ food, nothing happens. So, it's safe to tell pts to eat food no matter what the form of tegretol. |
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Term
T or F the peak level of standard release Sinemet is higher than the therapeutic concentration |
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Definition
| T, so the pt should take it w/ food. |
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Term
Should metoprolol be taken w/ food? Why or why not? |
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Definition
| Metoprolol should be taken w/ food, b/c the food can increase the absorption & / or bioavailability. It's possible that it decreases first-pass elimination when given w/ food, but this is not certain. Whatever the reason, the overall bioavailability of metoprolol is increased when taken w/ food. |
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Term
| Should pts take flomax w/ food? Why or Why not? |
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Definition
| Pts should take flomax 30 min after the same meal everyday. This can prevent side effects such as orthostatic hypotension and dizziness. The food lowers the peak level, but the AUC stays the same. |
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Term
Out of tegretol, sinemet, metoprolol, flomax, coreg, and accolate, which meds have concentration related side effects? Which medication should not be taken w/ food? Why? Which of the meds are IR tabs that should be taken w/ food? |
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Definition
Tegretol, sinemet, flomax & coreg. Accolate should be taken on an empty stomach, b/c absorption can be decreased by 40% if taken w/ food. Flomax and coreg |
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Term
| Should coreg be taken w/ food? Why or why not? |
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Definition
| Coreg should be taken w/ food to lower peak levels & prevent side effects such as hypotension & dizziness. |
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Term
| What therapeutic uses does epinephrine have? Phenylephrine? |
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Definition
epi - anaphylactic rxns, cardiac arrest, local anesthetics (vasoconstriction) phe - nasal decongestant, mydriatic, vasopressor |
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Term
Device-wise, what are some differences b/w spiriva and foradil? |
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Definition
| W/ spiriva, there's a window that you can look through to see if you got all of the dose. Spiriva has 1 button to puncture the capsule; foradil has 2 buttons. |
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Term
What side effect do most alpha-1 antagonists have in common? What pt information is important to give to people taking these medications for the first time? Why is adherence important? |
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Definition
| Dizziness due to vasodilation; take the medicine at night b/c of 1st dose hypotension. Adherence is also important, b/c reapeated administration causes desensitization. So, the dosing is titrated up. If a pt stops taking this med, & then takes the larger dose, bp will go way down. |
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Term
| What's the difference b/w albuterol and xopenex (levalbuterol)? |
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Definition
| Albuterol is the R and S isomer; xopenex is just the R isomer. |
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Term
| What's the difference b/w xopenex solution and xopenex concentrate? |
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Definition
Xopenex solutions come pre-diluted in 0.31, 0.63, and 1.25 mg/3ml. Xopenex concentrate has to be diluted. It comes in a 1.25 mg/0.5ml strength. So, we want to be sure to get the right dose. |
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Term
How is the nebulizer advantageous? |
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Definition
It allows people who are uncoordinated and people who can’t take deep breaths to get all of the medicine. So, there’s essentially no technique-dependence. |
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Term
| What are the beta-1 blockers? |
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Definition
Bisoprolol & Betaxolol Atenolol Metoprolol Acebutolol |
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Term
| What are the non-selective beta blockers? |
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Definition
Timolol Propranolol Nadolol |
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Term
If a beta-blocker has ISA activity, what does it do? What are the beta-blockers that have ISA (intrinsic sympathomimetic activity)? |
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Definition
It's a beta-blocker, but it still has some low-level agonist activity. These drugs are used for pts who get severe bradycardia from regular beta-blockers. Carteolol Acebutolol Pindolol Penbutolol (these are all non-selective except for acebutolol) |
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Term
| What are the class adverse effects of beta-blockers? |
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Definition
| decreased HR; a person is unable to increase CO w/ exercise which means they can't raise HR -this leads to exercise-induced fatigue; fatigue may also occur at rest; some CNS effects like drowsiness; if the dose is high enough, a beta-1 antagonist could antagonize beta-2 receptors and cause breathing problems. |
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Term
| Why is adherence important for metoprolol? |
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Definition
| If you all of a sudden stop taking it, you're receptors will be super-sensitive and adrenaline will bind and raise HR and increase BP. |
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Term
| Which has more CNS adverse effects: atenolol or metoprolol? Why? |
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Definition
| Metoprolol has more CNS adverse effects than atenolol, b/c metoprolol is more lipophilic. |
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Term
T or F Timolol could be given to an asthmatic since it's just an eye drop |
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Definition
| False, even though it's opthalmic, it shouldn't be given to pts w/ respiratory problems - use betoptic instead. |
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Term
Why is it that not all drug interactions are the same b/w beta blockers and ca channel blockers? |
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Definition
This is b/c some Ca channel blockers are non-dihydropyridine agents (ie, Verapamil & diltiazem) & some are dihydropyridine agents (eg, amlodipine). The nondiihydropyridine agents are more problematic. |
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Term
Give an example of additive pharmacology |
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Definition
| Additive pharmacology occurs when beta-blockers and ca channel blockers interact. Essentially, all of the drugs' mechanisms occur to a greater effect (ie, additive hypotension & bradycardia, negative inotropic effects, & slowed AV conduction). |
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Term
Give an example of when the additive pharmacology of a beta-blocker and ca channel blocker would be therapeutic? |
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Definition
| In Afib, there is rapid uncoordinated firing of the SA node, and the AV node is being overstimulated. Sometimes, people w/ Afib can get a HR of over 100, & that's when it can become symptomatic. The additive effect of a beta-blocker and ca channel blocker can slow the AV conduction. |
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Term
When would a drug-drug interaction be probelmatic b/w a beta-blocker and ca channel blocker? When would it not be problematic? |
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Definition
Beta blocker + verapamil = a problem for negative inotropic effects & slowed AV conduction. Beta blocker + diltiazem = still a problem, but not as bad as verapamil. Beta blocker + dihydropyridine = not a problem for negative inotropic effects & slowed AV conduction, but would be a problem for additive hypotension (this is b/c the dihydropyridines cause peripheral vasodilation rather than directly effecting the heart). |
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Term
What are 2 risk factors for interactions b/w beta-blockers and ca channel blockers? |
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Definition
| Higher dosage regimens & existing left ventricular dysfunction (ventricles aren't pumping hard enough). |
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Term
| How could you monitor a CV drug interaction? |
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Definition
You could check the pt's pulse rate & BP (objective measures). You could also ask if the pt is feeling dizziness, dyspnea, or lethargy/fatigue (subjective measures). |
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Term
| How does an ACE inhibitor work? Knowing this, what interaction could occur b/w an ACE inhibitor and a potassium sparing diuretic (triamterene, aldactone)? |
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Definition
Normally angiotensin II stimulates aldosterone release. Aldosterone causes Na retention & K excretion. An ACE inhibitor would inhibit production of angiotensin II, cause Na excretion & K retention. So, [K] is elevated in the blood. Dyazide contains the K-sparing diuretic, triamterene. If triamterene was also increasing [K], hyperkalemia could occur. However, dyazide also contains HCTZ, which helps to get rid of some potassium. So, this interaction isn't as severe for everyone, b/c people w/ healthy kidneys can secrete any extra potassium. |
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Term
| Give instances when you would be concerned about a possible rxn between an ACE inhibitor and a potassium sparing diuretic? |
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Definition
| Someone w/ kidney disease wouldn't be able to excrete this excess potassium. Also, someone w/ CHF: CHF pts have more aldosterone effect; reversal of this w/ an ACE inhibitor would lead to a higher potassium level than normal. Another risk factor would be dose: higher dose could lead to higher potassium reabsorption. |
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Term
T or F Anyone who is on a combo of ACE inhibitor and K-sparing diuretic should have their [K] levels checked. |
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Definition
| True, they should have them checked w/in a week. If they have risk factors, they should be checked earlier than a week. |
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Term
If someone is already on a diuretic & they have been given an ACE inhibitor, what could happen? Explain. Is it a problem is a diuretic is added to an ACE inhibitor? |
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Definition
| When someone is on a diuretic, their kidneys are trying to compensate for all of the Na and water being lost (due to the diuretic) by activating angiotensin II and secreting aldosterone. If an ACE inhibitor is added to the diuretic, it would inhibit angiotensin II (which was vasoconstricting), & the pt could experience 1st dose hypotension. They could become dizzy and pass out. It's not too big of a deal if someone is already on an ACE inhibitor and they have been given a diuretic. |
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Term
Explain the drug-drug interaction b/w diltiazem and simvastatin. |
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Definition
| Simvastatin is normally metabolized by the CYP 450 enzyme, 3A4. Diltiazem inhibits this enzyme. The increased simvastatin plasma level can increase the risk of myopathy. It's more of a problem when diltiazem is added to simvastatin. |
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