Birthday Week...earthquakes, hurricanes, and cake

I'll jump right into it. 

Day VIII. I saw a few patients with one of the doctors during the first half of the day. Most of them were on antidepressants and antipsychotics, and psych medications are something I need to work on. Needless to say, I didn’t have too much input. However, one of the patients was on Paxil and was having trouble sleeping, so she was recommended from someone to take it at night. I brought this up again a few minutes later, and explained to her that it’s recommended to take the Paxil in the morning in order to get the effect during the day. The doctor seconded this as well, and added that she may not be sleeping well d/t not having the medication for the last week. So, I mostly listened to the doc’s recommendations regarding the prescription medications, and jumped in to ask about OTC products. Other than that, I’ve noticed a lot of patients here talk about having fibromyalgia, which I don’t know a lot about, so I read the Up To Date page for it.

• Fibromyalgia – unexplained chronic pain. In 2009, duloxetine (start with 20mg in AM, up to 60mg qday), milnacipran (start with 12.5mg x1, then BID x2 days, then 25mg BID x4days, then 50mg BID maintenance), and pregabalin (75mg BID) were the three medications approved for treatment of this disease. Some other TCA’s, SSRI’s, and SNRI’s have also been used. For patients with sleep issues on top of fibromyalgia, pregabalin or gabapentin is preferred, and for patients with exhaustion issues, duloxetine or milnacipran at breakfast is recommended. If going with a TCA, then amitriptyline 5-10mg starting is appropriate. TCAs, in general, may not be okay for the elderly d/t anticholinergic side effects (dry mouth, constipation, fluid retention, etc.). If contraindicated for a specific patient, then desipramine could be considered – it’s still a TCA, but with fewer anticholinergic effects. Some people believe fibromyalgia is a “bs” diagnosis…just putting together any unexplained chronic pain under an umbrella term.

Some things I learned (or relearned) today…

• The ACEI cough is not dose-dependent, and the onset can be from after the first dose all the way til months after therapy started (from CHEST)
• Birth control and antibiotics – makes birth control less effective, so always educate the patient about being extra careful, or using an extra form of protection while on the antibiotics.
• 5ml = 1 teaspoon – I know, I know…I should know this…
• Took some blood pressure readings – never quite got the hang of it, but practice makes perfect. I know pharmacists don’t generally take BP readings, but what’s the harm in having an extra skill?

Day IX. My Birthday!! The big 2-3 today, and also my golden birthday :). I got to work earlier, and brought a chocolate cheesecake! And then I went back to the kitchen where I found this amazing looking cake, made by my preceptor (pictured!). 

Amazingness!

And of course after I stopped taking pictures of the cake, I got to work ;). I took a look at the charts this morning, and noticed two patients were coming in for impacted cerumen and also iron deficiency, so I thought I’d look into the treatments for these.

• Impacted cerumen (ear wax) – this may be useful for community pharmacists especially. The causes are usually some kind of obstruction, narrowing of the ear canal, or cerumen overproduction. Treatments usually include cerumenolytics like mineral oil or hydrogen peroxide (the latter not generally for dry, irritated ears). If the cerumen has hardened, then carbamide peroxide (Debrox) is a good choice. Sig is 5-10 drops BID in the affected ear (tilt head for 3-5 minutes with a cotton ball in ear). This should be limited to 4 days, since a longer duration has shown to cause infection, irritation, or rash. Also, don’t recommend ear candling – AKA holding a narrow tube close to the opening of your ear with a flame at the other end. Ear wax = candle wax? Maybe, but let’s not get too carried away now.
• PO iron supplements – absorption of iron may be affected by anatacids (take 2 hours before or 4 hours after), quinolones, tetracycline, and general breakfast foods. It’s best absorbed as the ferrous salt in an acidic environment – maybe some ascorbic acid…OJ please!
• Ferrous fumarate – 106mg elemental iron in a 325mg tablet
• Ferrous sulfate – 65mg elemental iron in a 325mg tablet – cheapest
• Ferrous gluconate – 38mg elemental iron in a 325mg tablet
• So, iron content-wise: F>S>G…Forrest Shrimp Gump, or if you’re a fan of Pixar, then Fiona Shrek Gingerbread man. Take your pick! 

For iron deficiency anemia, 150-200mg elemental iron is recommended daily. For older adults, 10ml of ferrous sulfate elixir in a class of OJ should do the trick everyday. Results regarding improved feeling/energy should be seen in a week or so. Half of the Hgb deficit should be replenished in about a month, and then normal Hgb by 6-8 weeks. The duration of therapy varies between practitioners – some stopping therapy after Hgb is normal, others continuing it for 6 months. Also, iron can be used to treat pica – those who eat non-food items. Sometimes, this is due to iron deficiency, so they tend to eat things that contain iron. The following is a picture of what they found in a person’s body with pica. If a patient has pica d/t iron deficiency, then iron therapy should work quickly to treat this disease. 

Contents of someone's stomach with pica

 

 Day X. Day after my birthday…not as exciting, but there was still cheesecake and cake left over ;). We had a patient come in today wanting more Ambien for sleep. She started off with just 1 pill a week, and now is up to 3 pills a week. It’s not recommended to take this long-term, so we discussed some alternatives with her. We ended up putting her on trazodone – since it’s shown to be okay long-term, it’s not too expensive, and there’s low abuse potential. She was a little bit resistant at first, but left willing to try it out. As for sleep medications in general…

• Benzos – triazolam is short acting, and flurazepam and quazepam are long acting (others are intermediate).
• The “Z’s” – Zaleplon is good for sleep initiation since it’s short acting, zolpidem is also good for sleep initiation, and zolpidem ER & eszopiclone are for sleep maintenance. The latter two are brand only.
• Ramelteon – is a melatonin agonist (brand only) and is good for sleep initiation. It’s the only sedative-hypnotic that isn’t controlled. 8mg PO QHS.
• Antidepressants – amitriptyline 5-10mg at night, trazodone 50mg at night, and doxepin 3-6 mg at night (longer acting).

Day XI. We got a call today from one of our patients about whether or not she can use the Miacalcin (calcitonin-salmon) Nasal Spray that she got in the mail. It’s supposed to be refrigerated prior to opening, and then after opening, it can be in room temperature for 35 days. She had been receiving the Miacalcin via mail order, but it’s always been sent with an ice pack or something. This time, however, it wasn’t chilled. The question is…can she still use it? She emailed the company, and the response she received was something along the following, “The product must be refrigerated prior to opening. There was a study done by Rutgers in 2002 that showed that Miacalcin Nasal Spray retained its potency even in 40’C (about 104’F) for 3 days, so that her product should be fine.” Doesn’t the latter sentence kinda contraindicate the first one? Anyway, so I pulled up the study, and sure enough…the researchers studied 55 vials of Miacalcin Nasal Spray in 20’C, 40’C, and 60’C for 3 days. The vials in the first two temperatures retained about 97-99% of the potency (60’C was too hot, however). The patient also asked her pharmacist and he said that the manufacturers send the product without ice packs, so it should be okay. I actually called the manufacturer myself and asked them about it. She said she’d have to call me back after discussing it with the shipping department. So what she found out was that they do send it to pharmacies without ice packs, but it’s overnight shipping, and they expect the pharmacies to refrigerate the product right away. She said she can’t say anything about the mail order company, since it’s not as controlled – we don’t know if it was an overnight shipment, how long it was sitting outside of the patient’s house, whether or not she put it in the refrigerator right after, etc. My opinion on this issue was that if she found it on her door step in the morning, and put it in the fridge right after…then it’s fine to take.

Day XII. Spent most of the day looking into residency programs…I’m thinking North Carolina and some of the surrounding states, California possibly, and Florida. Maybe Chicago and Michigan, but I don’t know about the weather. One of the doctors is off today, and the other one I usually work with has a half day, so today will be fairly slow! Anyway, a lot of weird things have been happening lately, like an unexpected earthquake in Virginia (aftershocks felt in NC), and also a huge hurricane warning…Hurricane Irene. I don’t know if it’s just me, but it seems like more people have been coming in this week about their anxiety. So the point is I was asked a lot of unexpected questions about anxiety today that I didn’t know the answers to. So, of course, I read about it in hopes that I’ll be more prepared next time.

• First line: SSRI’s (paroxetine, sertraline, citalopram, and escitalopram studied…but others used too) and SNRI’s. Studies have shown that these medications work for 6 months, but clinical experience has shown much longer. So, I’ve listed a few interesting characteristics about some of these antidepressants used for anxiety. Now THIS is the stuff we need to memorize. You know that drugs like paroxetine, sertraline, and citalopram are SSRIs? Good for you. You know that SSRIs increase serotonin levels in the synaptic cleft? Good for you. Being able to recall the following information when making recommendations is where the money is at…this is how pharmacists can be seen as knowledge workers.
• Fluoxetine – long half life, no tapering off necessary, but also takes a while to see effects.
• Paroxetine – some week anticholinergic effects (from my previous post, this is also the SSRI associated with weight gain), and most notorious for sexual dysfunction of the SSRIs.
• Sertraline – GI symptoms have been seen.
• Venlafaxine – some GI symptoms, may increase BP at 100-300mg/day doses
• Duloxetine – good for when patient also has diabetic neuropathy.
• Mirtazapine (different class of antidepressant) – less sexual dysfunction, increased weight associated.

It’s these little differences that are good to know – then you are able to help guide individualized therapy.  With respect to duloxetine and venlafaxine (SNRIs), the common side effects include nausea, dizziness, insomnia, sedation, constipation, and sweating.

• Second line – TCAs. Imipramine is a TCA that has been shown to be efficacious for anxiety. However, TCAs are generally chosen as second line due to the cardiotoxic and anticholinergic effects seen with TCAs.
• Second line – Benzos. Short term benzo use is fine, but long-term is not recommended d/t dependence issues. If a patient is not responding to antidepressants, and benzos are working – then long term use can be considered IF they can maintain a low dose over time. However, if they are increasing their dose, then that could be a sign of tolerance (and long term use is contraindicated). Generally, benzos have a faster onset than antidepressants.
• Second line – buspirone. A few things about this medication – time to onset is about 4 weeks, much like the antidepressants, and has a weaker anxiolytic effect than the benzos. I would recommend trying this if the above classes don’t work.
• Second line – pregabalin. It’s approved for anxiety in Europe, but not in the US (yet?). Dependence is possible with this medication, but to a lesser extent than the benzos.
• Others to try if absolutely nothing seems to help: quetiapine, tiagabine, hydroxyzine.

Overall this week was interesting! I mean, with an earthquake on your birthday and a hurricane on its way, that's kind of an understatement.

Fake it 'til ya make it

I’m happy to say that I had a fulfilling week.

Day V (Wednesday):

• Pt. #1 was a newly diagnosed diabetic, and I was asked to be at the counseling session not only for his diabetic medications, but also his others. His medications included: losartan/HCTZ, ASA 81, Vitamind D, MVI, Simvastatin 40mg/ amlodipine 5mg, Jalyn (dunasteride and tamsulosin), fish oil, starting metformin (500mg once a day). The question I was asked was when to take metformin. My answer was that the important thing is to take it with food, so it can be taken whenever you’re used to taking your other medications, as long as it’s with food. He also asked about some stomach upset he was experiencing after taking his metformin, but also after eating some nice fried chicken. I wanted to find out if he experienced the GI symptoms any other time he had taken the metformin (since it is a common ADR), and he said no. So, my thoughts were that it may not have been the metformin, and to continue taking it. I was asked, from his wife, about changes in the ability to taste with warfarin. I had NO idea, but my reply was, “I haven’t heard of that side effect specifically, but it may be a rare one that researchers found in their studies.”
• So this is what inspired the title of this post. As upcoming new, young Pharm.D’s (or any field for that matter), it may be a challenge to gain respect from patients d/t lack of experience. The second you show a slight bit of uncertainty in your response, you’ve lost their confidence in you. And I don’t mean you always have to have an answer, or make up anything (definitely not the latter). Either respond confidently if you DO know the answer or confidently say, “I learned that in pharmacy school, but would like to brush up on the details before giving you an answer.” The problem that I have is if I actually do know an answer to a question, I feel like I need to know exactly which study showed that conclusion (which I don’t usually know), so that prevents me from sounding confident. Just say what you learned with confidence, even if you don’t feel 100% confident – it comes with practice, and you KNOW this stuff. I’ve used some from of the word “confident” about 6 times in this paragraph – just trying to drive home a point.
• Patient #2 wanted to go over her medications – Lipitor, PPI, DM medications, metroprolol, temazepam PRN, losartan. Her chief complain was being tired all the time and muscle pain. Her Lipitor was going to be D/C’d, so I explained that this will help with the muscle pain. I also told the doctor later that losartan has been shown to be associated with myopathy…and that may be something to consider if she shows up with her next appointment with the same complaint. This patient was 90 y/o, so I wanted to know if she knew her S/S of hypoglycemia to prevent a devastating fall. She also told me about some arthritic pain in her joints and that she takes Tylenol for that. I explained the difference between NSAIDs and Tylenol as far as anti-inflammatory properties are concerned, so hopefully this will help her pain a little bit.
• Some of the patients have specialists who change their medications around for one reason or another, and the family doctor here was just wondering the reason behind some of the changes. For the first one – the specialist had changed a patient’s sertraline to another antidepressant d/t risk of bleeding. I hadn’t heard of this before, and didn’t have much information about the patient, but apparently SSRIs have an anti-platelet effect. So, I thought this might be the cause of this change. The other one – a patient was on Multaq, Wellbutrin, and metroprolol. I did a drug-interactions check on these three before, and didn’t see anything major, except for the possibility of increased metoprolol levels in the body d/t hepatic enzyme inhibition. Well, turns out that he eventually got switched to atenolol, and it’s likely because atenolol is not hepatically metabolized!

Day VI.

• Patient #1. She had triglycerides > 1200. She was on Tricor (fenofibrate) last year, and decided to stop taking her medication. I did some research on fibrates for cholesterol, and here’s what I learned:
• Fenofibrate and gemfibrozil can decrease TGs by 20-50%. Gemfibrozil increases muscle toxicity if given concomitantly with a statin, but fenofibrate does not. (As a side note, pravastatin, fluvastatin, and rosuvastatin are not metabolized by CYP3A4). Dose for Tricor is 54-160mg once a day, and gemfibrozil is 600mg BID. Both must be taken 30 minutes before meals to have the maximum effect.

              Anyway, I was consistent with the open-ended questions, and finally got out of her that she takes all of her medications every other day (Thanks Drs. Apgar and Herrier). So we discussed her concerns, and how high doses and overdoses of medications are the things usually associated with kidney and liver dysfunction, and not the doses she was on.

• Pt. #2 – only issue with him was lots of hypoglycemic events with his diabetes. My first question to the doctor was whether the patient was whether the patient was on a sulfonylurea, which he wasn’t sure about. So we go in to see the patient, and he’s on glimepiride BID (which is odd). We switch him over to once a day dosing, and all eyes are on me when asked what time he should take it during the day. I say (with confidence, continuing with this post’s theme) “I would like you to take it in the morning with your first meal…” which is actually something I had looked up a couple days ago.

I also looked into a few things for the doctors today, which was beneficial for both of us…

• She wanted a refresher on the potency of the different IM steroid injections. Low potency: cortisone and hydrocortisone. Intermediate potency: methylprednisone, prednisolone, prednisone, triamcinolone. High potency: betamethasone and dexamethasone. The more soluble a drug is, the shorter acting it is. The more insoluble, the longer acting – but also associated with more irritation. Sometimes, a clinician will want to have a mixture of long and short acting to get the benefit of the longer acting steroid but with less irritation.
• I also looked into twice a week statin dosing for patients who need the drug but can’t tolerate it everyday. There was a study published in the American Journal of Cardiology in 2008 that looked at Crestor twice weekly. There was improvement over 8 weeks with twice a week dosing, regardless of whether or not the patients were taking baseline anticholesterol medications from different classes. Crestor and Lipitor have been looked into for less frequent dosing d/t their long half lives (19 hours and 14 hours, respectively). However, my question is why not pravastatin? Its half life is 77 hours.
• Weight gain associated with SSRIs. According to UpToDate, fluoxetine is the most notorious for this, and paroxetine is the least associated with weight gain.
• Going back to the beta blocker discussion from the previous post, some BBs have ISA (intrinsic sympathomimetic activity) – both agonist and antagonist at the beta adrenergic receptors. This allows these beta blockers to be indicated for excessive bradycardia – pindolol, penbutolol, and acebutolol.

Day VII.

• Pt. #1. 59 y/o male comes in with hypertension and elevated triglycerides (400), history of drinking, and gout. Medications include: lisinopril, ASA 81mg BID, OTC niacin, simvastatin 80mg, colchicine QOD. He was in for his elevated triglycerides and muscle pain. Now let me warn you – I wasn’t too happy with all the recommendations I gave or didn’t give for this patient after he had already left. First of all, of course his simvastatin dose had to be decreased to 40mg d/t FDA regulations, so that’s fine. He was taking his colchicine every other day d/t muscle pain – this helped with the muscle pain and still controlled the gout flare ups. With respect to this, the muscle pain could have been just the statin or a combination of both of these drugs, it’s hard to tell. So we’re just going to see how he does on the QOD colchicine and lowered statin dose. ALSO, speaking of colchicine, the patient mentioned that Colcrys was fairly expensive, so the doctor said it came as a generic and seconded that with me. So right on the spot, I wanted to check the price difference between the two…and they both came out to the same $$. Consequently, I googled it (I love my iPhone!), and turns out the generic colchicine oral tablets were stopped in 2009 so the company could have exclusive marketing with Colcrys for 3 years! While the doctor did his examination, I asked if he took any OTC pain medications – just Aleve (I wanted to make sure he wasn’t taking APAP d/t his drinking issues). When asked what I thought of Niaspan vs. Tricor for his elevated TGs, I said both are good drugs for elevated TGs, but Tricor has been associated with a great drop in TG levels. The doctor still wanted to go with Niaspan, however. In retrospect, I would’ve stated the actual %decrease in TGs with both these drugs (15-25% with Niaspan and 20-50% with Tricor). At least I know this now though! Then we got to his ASA 81mg BID regimen. He had no history of an MI or stents, so we recommended going back down to 81mg a day. In retrospect, I wish I had recommended 325mg ASA before the niacin – to kill two birds with one stone. I didn’t though, but will pay more attention to this next time.
• I was also asked to counsel a patient with a PhD in pharmacology – haha. It actually went well though, and I could answer his questions. He was wondering when to take Synthroid, and why he had to take it at a certain time. I explained that the absorption of Synthroid is fairly erratic (40-80%), and that taking it with food may decrease the absorption even more. So, I recommended taking it right when he woke up, 30 minutes before breakfast. Also, if a patient were also taking calcium and iron, then I’d recommend separating these two from the Synthroid by about 2 hours.
• Another thing I was asked to look up was sexual dysfunction with lisinopril/HCTZ combo. A few of the doctor’s patients actually complained about this side effect when put on this medication. This ADR, I believe, is attributed to the HCTZ.

Here’s me, ready for another week!

First, and Second, Impressions

I got spoiled with CPRS and Vista – the two computer programs used in the VA hospital system. I didn’t realize it then, but they are amazing! Anyone with access to patient information can get a patient’s lab values, current medications, outpatient medications…and can go back years and years. It’s a great system for excellent communication between nurses, doctors, pharmacists, and specialists. Okay I’m getting to my point…so I walk into my current rotation site for the first time last week (I’m at an outpatient clinic). I get my login username and password and sit down at my computer, ready review charts. I log in, and the only thing my log in is good for is to get the schedule of patients for the day. Where do I find all the labs? What about the medications and past medical history and chief complaint??

…Ten minutes later, you would’ve found me sitting about ten feet away from my computer, physically flipping through papers to find all this information. I know paper charts are the norm in most outpatient clinics, but after being at the VA for three months (and as my first clinical experience), it just seemed so archaic to me. I guess this was my first experience with “culture shock.” So in a nutshell, I’m really liking this place…I’m learning a lot in general – not just about pharmacy, but about adjusting to different perceptions and settings in the health care world. I’m also learning about myself – things I like and dislike (and am working on changing!). To organize this a little bit, I’ll discuss my first 4 days (which includes today) at my new rotation site.

Day 1. I walked into the clinic at 8:00. I was introduced to everyone else (who already knew a pharmacy student from AZ was coming!), and took a tour of the clinic – which is a beautiful facility, complete with a decked out kitchen/gym/dance room (!)/patient rooms/offices. Then I sit down in one of the offices, and talk to the nurses for a little bit. Some of the first questions I was asked, which caught me off guard – “So, what exactly are they going to have you do here? You know, we take the medication histories as nurses, and don’t really need a pharmacist.” And after I talked about how I was certified to give immunizations, they turn to each other and say, “I can’t believe they’re having pharmacists stick people.” At this point, I’m feeling a little uneasy since they have no clue what I’ll be doing for the next 6 weeks, and some slight negativity toward pharmacy. 12:00pm rolls around, and I still haven’t met my preceptor. She is THE nicest lady in the world, and just didn’t realize I was there already. Anyway, my first task for the day was to go to the airport with the doctor and give a combined talk about women’s health to a group of women. Uhhh, our women’s health lecture was a year ago, and all I remembered was that progestin requires an intact uterus, oh and estrogen = breast cancer? Needless to say, I researched as much as I could for the hour I had. I looked up a few things I thought I’d be asked about…

• The HCG diet – HCG is a hormone that is released during pregnancy that allows fat stores be available for energy use. So, with a couple drops of this per day (with the restricted 500 calorie/day diet), you’re using up those calories quickly and then getting into your fat stores even more quickly with the help of the HCG. With this diet, they claim you lose 1-2 lbs a day (comes in 26 or 40 day kits).
• Osteoporosis – nonpharmacologic therapy includes diet with calcium and vitamin D, exercise, stop smoking, **long term glucocorticoid and PPI use**. Basic drug therapy would be bisphosphonates – risedronate 5mg/day, 35mg/weekly, or 150mg/month. Another option is alendronate 10mg/day or 70mg/weekly. Another class of drugs is raloxifene, which has a decreased risk of breast CA compared to estrogen, but an increased thrombus risk. Important counseling point with bisphosphonates is to stand up for 30 minutes after taking the oral form.
• Post menopause – Estrogen is an option, but with the risk of breast CA down the road, coronary heart disease, previous thrombotic events, stroke. The Women’s Health Initiative study is what is often cited with respect to this topic. If hormone therapy is started, the lowest possible and effective dose should be used. After 2-3 years, see if the patient can D/C it (40-50% stop therapy in one year, 65-75% stop in within 2 years).
• And that’s about all I got to J. Not a lot, but when I got to the conference, I found myself able to answer a lot of the questions the women asked. Some asked about diabetes control (I discussed goal levels, different types of insulin and oral medications), best OTC medication for pain (NSAIDs having the anti-inflammatory effect unlike APAP, maximum doses, underlying kidney/liver dysfunction, history of gastric ulcers, etc.), and other questions. I had a great time!

When I got back to the clinic, I was back to sitting at my desk. I was given a couple of patients to look over, but didn’t get to talk to any patients about their medications. As I was going through the patient med lists, I realized there were a lot of brand names that I didn’t know, especially considering I didn’t work through pharmacy school. Some I learned include (and I’m including this, since the NAPLEX doesn’t differentiate between brand and generic names now):

• Nuvigil (armodafinil) – for narcolepsy
• Savella (milnacipran) – fibromyalgia
• Mirapex (pramipexole) – RLS
• Lyrica (pregabalin) – fibromyalgia
• Paxil (paroxetine) – depression
• Cymbalta (duloxetine) – depression, fibromyalgia, anxiety

The rest of the day was spent looking things up, and just waiting til 5:00pm, honestly.

Day II. If I thought the day before was slow, boy was I in for a treat on Day II. Let’s just say my phone was charged 100% at 9:00am, and by 2:00pm I was at 0%. After the first couple hours though, I told myself I would make the best use of my time, and to be thankful for any down time at all. I also reminded myself that my experience will be what I make it, and that they had never had a pharmacy student before, so I had to be proactive about things. I told myself I would make the best of the day, and tell them exactly what I wanted to do the next week. What does making the ‘best of the day’ mean to me?

• Looking up all the residency programs that I’d be interested in North Carolina. My preceptor said she knows a lot of the hospital pharmacists here, and would take me to see them personally, so I decided to make a list of the pharmacists who do take students in for residencies.
• Matched AIC levels to average glucose levels – for example, if a patient’s AIC is 6%, then his/her average glucose was 120 for the last 3 months. As the AIC level goes up in increments of 1%, the glucose goes up by 30’s…7% ~ 150, 8% ~ 180, etc.
• Read the news!

I’m the type of person who likes to feel useful and have a purpose. To be honest, this isn’t exactly what I was feeling at this point, so I felt a little bit defeated at the end of the day. However, I also went into Day II with a negative mindset. So, I talked to the doctors about how I would like to see the patients with them, and have their medication list before-hand so I can make any relevant drug therapy recommendations. I also discussed how in pharmacy school, we’re trained to read and evaluate the literature, and make evidence-based recommendations, so to use that for the 5-6 weeks that I’m here. In response, one of the doctors said, “okay, let’s plan then,” and pulled up his patient list for Monday. If you’re proactive, others around you will notice and reciprocate.

Day III. I went into work on Monday with a good feeling. I got to my desk, put on my white coat, set up my laptop, and went up to the front desk to ask for specific patient charts. I wasn’t told to do this, or really given formal permission, but I started setting up my own morning routine.

• Patient #1. 65 y/o male with PMH of hyperlipidemia, CKDIII, uncontrolled diabetes, hypertension, 8 stents, possible CHF (he hadn’t been to use cardiologist in about 4 years). His CC was his DM, and the need for more test strips. Medications included: simvastatin 80mg (just increased in May), Novolin 70/30, lisinopril/HCTZ 20/12/5 BID, amlodipine 10mg, ASA 325BID, plavix 75mg, coreg 25mg BID, lasix 80mg qday, vitamin C. He is extremely noncompliant, always making excuses for not eating well and exercising, money is very tight (only takes plavix when he can afford it).
• My recommendations: Decrease his simvastatin to 20mg/day…which is consistent with the new FDA guidelines from June that state max dose of simvastatin is 20mg/day if also on amlodipine. I suggested this only after checking his lipid panel and seeing that it was fairly well controlled: TC – 168, TG – 165, LDL – 93, HDL – 43. Also, his ASA dose was weird, but I wanted to see if there was a valid reason for this dose. I asked him if he takes ASA, and he said he took 325 BID. After that, I asked him if any of his doctors recommended this specific dose, and his response was that he wasn’t sure but he’s been doing it for years. I mentioned this to his doctor, and we both decided that he may be compensating for not taking his Plavix regularly. Considering this patient’s situation, compliance history, and unwillingness to cooperate (myself and the manager of the clinic/CDE tried talking to him for 2 hours today), we decided not to change anything except for his insulin and simvastatin dose.
• Patient #2, I don’t have her medications written down, but it was a 1 on 1 session. The doctor was changing a few of her medications, and wanted some clarification as to why. She was a diabetic patient taking HCTZ for her HTN. She noticed that every time she took HCTZ, her blood sugars would go up, and if she stopped the diuretic then she’d experience edema. So, I explained that a side effect of HCTZ in some patients is the elevated blood glucose, and that she would be switched to another HTN drug. We also went over her inhaler technique (with spacer) and any other questions she had.

I looked up a few things today…a patient came in saying that his blood sugars are always high in the morning. I was asked to explain the Somogyi and Dawn effects to the patient, but I had to admit I had no clue what these were. But, if asked again, I could totally do it J

• Dawn Phenomenon: elevated growth hormone, catecholamines, cortisol released in the early morning for everyone in response to lower glucose levels in the body than usual. This is okay for non-diabetics, but for diabetic patients who don’t have enough insulin, this could lead to hyperglycemia…enough to block the effects of the last dose of insulin. Some recommendations could be to decrease carbs at night time or eat in the morning to turn off the hormone cycle.
• Somogyi Effect: This usually happens post long-acting insulin – when it’s working too strongly at the wrong time. So, the hormones in the body could detect low sugars and kick in to signal the liver to release glucose. A way to differentiate between the two is to check sugars at 2-3am. If blood sugar is high, then it’s a Dawn Phenomenon, if it’s low, then it’s due to the Somogyi effect.

I also got asked for my starting dose of gabapentin for DM neuropathy. I said 300mg a day and titrate up to TID if renal function is okay, and that the max dose is 3600mg/day. And that’s how I ended my Monday!

Day IV: Came in, looked up the patients!

• Patient #1: 80y/o male with GERD, HTN, HLD, BPH, Depression. His medications: ranitidine 150mg qday, fenofibrate 160mg qday, pantoprazole 40mg qday, citalopram 20mg qday, flomax 0.4mg qday, metoprolol ER 50mg qday.
• My recommendations: If his GERD symptoms aren’t severe, then stop the pantoprazole and continue the ranitidine. Add back the PPI if absolutely necessary. If his BPH sx aren’t better, then consider changing the flomax to terazosin or prazosin…this actually ended up being the case. That was all for him – his BP was great (128/84), cholesterol was fine.
• Patient #2: 60 y/o female with HTN, HLD, and renal issues. Medications include Toprol XL 100mg, simvastatin 40mg, and amlodipine 2.5mg.
• My recommendations included decreasing the simvastatin dose to 20mg d/t the amlodipine. Also, she mentioned that she would sometimes feel her ankles swelling up, but it would go away and wasn’t painful – and I attributed this to the CCB which acts by peripheral vasodilation.

I also looked up things I’ve been meaning to look into again…

• Selective beta blockers: metoprolol, esmolol, bisoprolol, atenolol. Nonselective beta blockers: propranolol, timolol, nadolol. Beta and alpha blockers: carvedilol, labetolol
• If using simvastatin with verapamil, diltiazem, and amiodarone, the maximum simva dose is 10mg. If using simvastatin with amlodipine and ranolazine, the max simva dose is 20mg.
• Simvastatin 80 mg = rosuvastatin 10mg, atorvastatin 40mg

All in all, I do feel like I’m getting something from this rotation site and am happy I’m here. I’m also glad that I waited a few days to write about this site. This post would have been completely different if I had based it on my first impressions.

AZ to NC: Rotation #4

As promised, here's a summary of the road trip from Arizona to North Carolina for my 4th rotation...!

Starting in Arizona

 

 

 

 

 

 

On to Utah

Hiked this in Zion - Utah

Next, Colorado

Awesome hike - Boulder, CO

Cute independent in CO

Through Kansas

Went to the top of the Arch in Missouri

Through Indiana

Guess where! Yup, Kentucky

Virginia, and West Virginia too

And finally made it!

Yum :)

That sums it up in a dozen shots...pictures don't do justice for some of the places we saw, however. Anyway, after getting settled in, I started my rotation at the clinic a few days ago. My thoughts and opinions are all over the place right now, so I'll wait a couple more days to discuss my current site :).

Are you a "pull & pray" kinda guy, or "fill & pull?"

This is my final post regarding my first two rotations (both at the same place). I learned so much these last three months, and cannot thank my preceptors enough! I had a wonderful, challenging experience, and have high standards going into my next rotations. Speaking of my next rotation, I begin #4 (I did an early one last summer), tomorrow in a family clinic in Raleigh, North Carolina. As I've mentioned before, this clinic does not have a pharmacist working there, and I will be their first "taste" of how useful a pharmacist can be, so the pressure is ON!  I'm not yet sure what I'll be doing there, but I hope to incorporate myself well into their system by next week. I road tripped from Arizona to North Carolina for this rotation, and will have pictures of the road trip on a subsequent post (I know, not quite pharmacy-related, but the road trip took me to my next rotation site, so it's still fairly relevant) ;)!

Renal

So there’s a saying at the hospital when talking about removing a patient’s catheter. You can either fill and pull, or pull and pray. If you pull the catheter without doing anything, then you’ll end up praying that the patient is able to urinate completely on his own. However, if you fill the bladder (leaving some air on top) prior to pulling the catheter, then you’ll know if the patient empties his entire bladder, since he/she will feel the air bubble come out while urinating. I thought this was interesting, so I thought I’d share! Also, if a patient is losing potassium due to any reason, for example, diuretics, then replenish with 10mEq KCl per 0.1 drop from 4.0 in potassium. The dose for acetylcysteine in contrast-induced nephropathy is 600-1200mg BID for 2 days prior to contrast use.

Infectious

For disseminated cocci, ketoconazole is the only one with FDA approval. Itraconazole and fluconazole have been shown to be effective in prospective trials. They seem to have the same efficacy, except itraconazole 200mg/day is better than fluconazole 400mg/day for skeletal lesions. Fluconazole can increase QT interval, while itraconazole does not. Both, however, are hepatotoxic. The treatment for diverticulitis (e.coli and b. fragilis) is either Unasyn 3g q6h, zosyn 3.375mg q6h, or metronidazole 500mg q8-12h + ceftriaxone 1-2g q24h. We also discussed vancomycin nomograms a few times, and I finally found a nomogram that I liked. There are so many out there, and even the experts don’t seem to agree sometimes. So, it’s just a matter of which one works best for your practice. Here’s the link to the one I found: http://www.venturafamilymed.org/Documents/Vancomycin%20Dosing.pdf.

Heart

We reviewed AV blocks one afternoon…

• First degree AV block: prolonged PR interval of greater than 0.20 seconds.
• Second degree AV block
• Type 1 (Mobitz 1 or Wenckebach): PR interval gets longer and longer, and then a beat is dropped.
• Type 2 (Mobitz 2 or Hay): PR interval stays the same and then suddenly drops.
• Third degree AV block: the atria and ventricles are both functioning, but they’re not communicating with each other. This is also a complete block.

P waves are in relation to the atria, and the QRS complexes are in relation to the ventricles. Switching gears…if a patient has severe CHF or has proteinuria, the ARB + ACEI combination could be considered.

Labs

Parathyroid hormone (PTH) goals depend on renal function…

CKD Stages IV and V: 150-300

CKD Stage III: 35-70

Much of the final days of this rotation was repetition of what I had seen in prior weeks - which was great, because I feel like it's been engrained into my head. I cannot say it enough - I had a wonderful experience here.

"I don't know, but I'll get back to you." Part 2

After about a month and a half into my rotation, I felt pretty confident about the recommendations I was making, and my everyday routine. However, I continued to learn that I knew only a fraction of what was out there. Here is my second "edition" of questions I initially did not know the answer to.

1. What will 1 unit of platelets do for a patient? Increase the platelet count by 30-50K.

2. What could you use as a cathartic (diuretic) in a patient with CHF and a history of heavy alcohol abuse? lactulose! 

3. When can you start different oral diabetic agents after using imagine that requires contrast? You can use glipizide right after contrast, but with metformin you have to wait 2 days after contrast. 

4. What should you monitor when giving valproate? LFTs

5. How should you dose alpha blockers? These are the 'zosins, and they should be titrated up d/t orthostatic hypotension. For example, with terazosin, you could do 2mg x 1 week, 4mg x 1 week, and 6mg indefinitely.

6. What is the dose of ceftazidime for pseudomonas UTI? You could do 1g q8h, or 1g BID for renal dysfunction. 

7. What can cephalosporins cause? Elevated transaminases.

8. What bugs can cause culture-negative endocarditis? HACEK - H. aprophilus, Actinobacillus, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae. 

9. What is the maximum gabapentin dose? 3600mg/day.

10. What lab value is indicative of jaundice? bilirubin >4. 

11. What are you worried about in a patient with FEV1 < 1.0? You're worried about CO2 retention when you're replenishing O2.

Recommendations: I noticed that a patient was not being started on an ACEI post MI, and when I looked into it, the patient had an ACEI allergy. So, I recommended trying losartan instead. I also started a patient on ASA 81mg, since I saw that he wasn't on it and had a history of drug-eluting stents. I also recommended that a patient be started on calcium and vitamin D supplements, since the patient was on chronic prednisone therapy for his COPD.

Two's Company, Three's a Crowd

I had mentioned needing a topic for my second management conference presentation a few weeks ago. I got some great suggestions; however, a patient's drug therapy choices caught my attention a couple weeks ago. I'll go ahead and summarize my power point that I presented. I thought I would have some clear-cut conclusions at the end of my literature search; however, I ended up with more questions than answers. I'm learning that this is the case a lot of the time in the health care field.

Title: "Safety and efficacy of triple antithrombotic therapy in post-PCI stent patients who require long term anticoagulant therapy."

Background: Standard of practice post-stent: ASA + clopidogrel to prevent stent thrombosis. Standard of practice for mechanical heart valve, DVT, atrial fibrillation: oral anticoagulation (warfarin) to prevent stroke. Basically, the ASA-clopidogrel combination is less effective in preventing stroke than warfarin, and warfarin alone is not enough to prevent stent thrombosis. Okay, so why not just use all three medications to prevent stent thrombosis and stroke? Increased bleeding risk, obviously! We have a problem here, don't we?

Patient case:  67 y/o male with chief complaint of chest pain. Troponin of 0.8 x 1, so sent to the cath lab and received drug-eluting stents for STEMI. The attending on our team was considering warfarin for a thrombus prophylaxis s/p MI (d/t possible blood pooling in the left ventricle). The patient already needs ASA + clopidogrel for his stents - is this patient a candidate for warfarin as well?

Literature review: I found that the quality of literature on this topic was poor; however, I was able to make some conclusions from the studies that I chose to look at. I chose certain studies because they looked at both the efficacy of triple antithrombotic therapy (ability to prevent stent thrombosis and stroke) as well as safety of triple therapy (incidence of bleeding).The three studies I looked at were by: Karjalainen et al., Rossini et al., and Sarafoff et al.

Conclusions: 1) In patients with an indication for warfarin that isn't a mechanical mitral valve, aim for lower INR goals (2.0-2.5). 2) ASA + warfarin combination may lead to higher rates of stent rethrombosis (this was statistically significant in a couple of the trials) than other antithrombotic therapies. 3) Post-stent patients with an indication for warfarin may benefit from warfarin + clopidogrel therapy. 4) bare metal stents may be considered over drug-eluting stents for patients with a compelling indication for oral anticoagulation (BMS require a shorter clopidogrel duration ~1month).

Things to consider for this topic: What is the indication for warfarin? - most studies were done on atrial fibrillation patients. What is the CHADS2 score? - does it make a difference if the score is 1 vs 6? What type of stent does the patient have? - drug eluting vs. bare metal. Does the patient have a history of bleeds? What dose of ASA is appropriate for the patient? Should gastroprotectants be used to minimize bleeding risks?

Patient follow up: The patient was discharged on ASA + clopidogrel, without warfarin. The patient did not seem reliable in following up with the anticoagulation clinic and we believed his risk of bleeding would exceed the benefit of the addition of warfarin.

There is a future study coming out that compares warfarin + clopidogrel with warfarin + ASA + clopidogrel. The end points will be bleeds and major adverse cardiac events (MACE). This will be a study worth reading, especially because it's a prospective, randomized trial.

At first, this topic wasn't the most fulfilling to look into because of the lack of answers; however, I thought it was worth my time, since I now know the appropriate questions to ask about the patient before making any recommendations!