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The Pink Apothecary


It is a genuinely good question. Aren't we just supposed to count by fives and verify medication orders until our eyes bleed? I realize that some of you, med students, PA students, nursing students and even some P1-P2 pharmacy students may not have exposure to pharmacist positions where we are more clinical on the outpatient side. And hey, thats okay! But I'm going to open your eyes a little bit today to what we do in that setting. During my time at Penn Center, a primary care facility in west Philadelphia, I've taken blood pressures every day, multiple times a day. I don't take them for the practice or to double check anyone, I take them because our attendings and residents rely on us to take them. You may think this is a rarity, or something total bizarre, but I'm going to tell you why it works and what exactly we provide for our attendings and residents.

At Penn Center, pharmacists conduct "intervisit" care. Essentially our patients are scheduled to follow up with their primary care doctors every 6 months or so (less or more depending on their problems and stability). However, we all know the work burden of attendings and residents and we all know that sometimes 6 months is too long but you just can't fit people in any earlier. Schedules are backed up, and in most internal med practices this would be where you'd have to default to fitting in phone calls between patients or just trusting your patient to call if there is an emergent issue. At our practice, pharmacists fill that gap. We provide free appointments to our patients during the interim where the patient is waiting for their doctors appointment. So maybe we see them 2 months out, or a few weeks out. Either way, they're not waiting 6 months or more for their next contact with a healthcare provider.

What do we do during these appointments? We handle what we know best: the meds. Our pharmacists have built an extremely tight bond between the attendings and residents at our clinic so they trust us completely when it comes to managing, titrating and adding new medications for chronic diseases. They refer many of their patients to us for teachings, for med management, and sometimes when the patient is so complicated with their regimen that they really just need a second set of eyes. Typically we handle hypertension, and diabetes the most as far as chronic disease states.

For our hypertensive patients we conduct blood pressure tests so that we can properly titrate blood pressure medications. We order labs, we order meds, and we get things done in the interim so our docs can focus on their patient and other non-med related issues during their appointments. I had a patient the other day who popped in for a blood pressure check 3 weeks after seeing his PCP. His blood pressure had been mildly elevated when he last saw his PCP but they had stopped one of his blood pressure medications  because the patient admitted to being non-adherent to all of them. So in order to avoid dropping him too low when he became adherent, we dropped one. 3 weeks later I'm performing an intervisit blood pressure check and I get a blood pressure of 200/100. I panic (inwardly of course) and I go for his other arm to verify. 200/110. After doing a quick symptom evaluation and then leaving (running) to go get my preceptor, we discussed a plan to present to his PCP who happened to be on site. His PCP was extremely grateful he had told him to come in for a BP check with us, agreed with our plan, and we developed a plan to get our patient out of hypertensive urgency.

For our diabetics we do the same: order A1cs and titrate meds to optimize glycemic control as much as possible. We also do insulin and GLP-1 pen teachings so our patients being newly initiated on injectables have the best chance of lowering their A1c by properly administrating the drug to begin with. Our attendings and residents love us for this because there are so many different nuances between pens and they simply don't have time during their appointments to take the 30 minutes to make sure the patient REALLY gets it. We also utilize these appointments for diet and exercise counseling too. Many of our diabetic patients see us for weight management and are extremely grateful we can take the time to talk to them in depth about their lifestyles and what they can do to change that A1c. It takes time, and we have it, so we free up the doc's schedules to see their other high risk patients for issues pharmacy can't handle.

My particular rotation is unique in that my preceptor also handles our refugee patient population and their latent tuberculosis treatment. As you probably know, initiating and finishing LTBI treatment is vital to preventing conversion to active disease and avoiding multi-drug resistant TB development. We initiate, and monitor treatment to ensure that our patients are adherent and safe. In fact, after implementation of the pharmacist-run LTBI clinic, our LTBI treatment completion rate at Penn Center tripled to 94%. That is 11% higher than the goal completion rate set by the CDC!

Now some other questions you might have: why don't the med students handle it? We have 1-2 med students rotating into the clinic. They see their own patients either separate of, or with the residents. They too usually don't have time to dedicate to intervisit care, med teaching and titration between didactic seminars and their own patient load.

What about nurse practitioners? We actually have two great ones! And us doing these intervisit sessions frees them up for drop-in hours! So they handle all of our acute patients who need to be seen right away.

Our medical assistants? They are AMAZING. But hey, we have a ton of patients to see so they have a ton of blood sugar sticks to do, heights/weights to check, prescriptions to organize and rooming to figure out. Plus, when they don't have to do blood pressure they're able to converse with the patient and let us know the chief complaint before we even waltz into the room (and that is a godsend).

This model works. Our attendings and residents are extremely appreciative to have us around and they are constantly recommending their patients to make appointments with us. I've been told numerous times by docs during my six weeks at this center how valued we are as pharmacists. We lessen the burden by just doing what we've been trained to do. Again, this may seem totally weird if your only experience with pharmacists has been through CVS or the basement pharmacy in the hospital, but in ambulatory care this is the norm. Our scope of practice is expanding nationwide at a time where people need help accessing care. In every state we have the ability to immunize. In certain states we have the ability to prescribe medications, which expands public access to care. We are forming collaborative practices with physicians where we prescribe, manage and titrate in states like North Carolina. As students we participate in community outreach events just like other healthcare students do. We are no longer solely tied to our ability to manage product, we are a service based profession. Having us around improves patient safety, medication error rates, and clinical outcomes. As one of the pharmacists at our clinic would say, "we are pharmacists practicing at the top of our license".

So yeah, we carry stethoscopes and they aren't just for show, we're an integral part of the team.


September 15, 2017 No comments


I decided to take a break from doing my antibiotic series of brush letter pharm to do a review of our glucose lowering agents instead. This short review will cover mechanism of action, side effects, weight effects and A1c lowering of our 6 big classes: Biguanide, DPP-4, GLP-1 agonists, Meglitinides, Sulfonylureas and TZDs (side note, it is very difficult to find consistent reporting of A1c lowering of these agents, I did my best to report generally what I've seen in most literature). And before you ask, yes, I left out insulin on purpose. I'll cover that sometime in the future. Enjoy!

Biguanides: Metformin
oral agent

  • A1c lowering: 1-2%
  • MOA: decrease hepatic glucose output, decrease glucose absorption and enhance insulin sensitivity. Work better on fasting blood glucose levels (FBG).
  • Side effects: nausea, diarrhea, cramping, rare/life-threatening lactic acidosis esp. in patients with hepatic or renal impairment
  • Effects on weight: neutral/loss



Sulfonylureas: Glipizide, Glimepiride, Glyburide
oral agent
  • A1c lowering: 0.8-1%
  • MOA: increase insulin secretion from pancreatic beta cells by regulating ATP-sensitive K+ channels. Have effects on both fasting and post-prandial glucose (PPG).
  • Side effects: hypoglycemia, weight gain
  • Effects on weight: gain



Meglitinides: Repaglinide, Nateglinide
oral agent

  • A1c lowering: 0.7-1%
  • MOA: Regulate ATP-sensitive K+ channels on pancreatic beta cells to help improve insulin secretion (same MOA as sulfonylureas, different binding site). Reduces PPG more than FBG.
  • Side effects: hypoglycemia, weight gain
  • Effects on weight: gain



SGLT-2 Inhibitors: Canagliflozin, Empagliflozin, Dapagliflozin
oral agent

  • A1c lowering: 0.8-1%
  • MOA: inhibit SGLT-2 in the proximal tubule of the kidney which prevents reabsorption of glucose and subsequently causes glucose to be excreted from the body through urination
  • Side effects: hypotension, polyuria, yeast infections, UTIs
  • Weight: loss


DPP-4 Inhibitors: Sitagliptin, Saxagliptin, Linagliptin, Alogliptin
oral agent

  • A1c lowering: 0.5%
  • MOA: Inhibits DPP-4, enzyme that breaks down incretin hormone GLP-1. Potentiating action of GLP-1 leads to increased satiety, slowing of gastric emptying (therefore decreased appetite), and increased insulin secretion through glucose-dependent matters. Reduce PPG more so than FBG.
  • Side effects: nausea, otherwise generally well-tolerated
  • Effects on weight: neutral


GLP-1 receptor agonists: Exenatide, Liraglutide, Lixisenatide, Dulaglutide
injectable agent

  • A1c lowering: 0.8-1%
  • MOA: Potentiate the action of incretin hormone GLP-1 which leads to increased satiety, slowing of gastric emptying (therefore decreased appetite), and increased insulin secretion through glucose-dependent matters. Reduces PPG more than FBG.
  • Side effects: nausea, diarrhea, cramping
  • Effects on weight: loss



TZDs: pioglitazone, rosiglitazone
oral agent
  • A1c lowering:1-1.25%
  • MOA: inhibits PPAR-y which encourages storage of fatty acids and utilization of glucose. Enhances insulin sensitivity. Works on both FBG and PPG levels.
  • Side effects: fluid retention (can lead to acute decompensated HF), fractures
  • Effects on weight: gain



September 03, 2017 No comments



Hello pharmacy friends! As I go through my APPE year, I'm growing my arsenal of easy-to-access and usable resources. One great way I've found to do this is to create pocket cards! Pocket cards are small info sheets able to be printed out and kept in your white coat pocket! For each rotation I've been on I create a few for the disease states I see most frequently. I've had some friends ask if I could share them, so I am going to compile them all here in one post, organized by subject!

Disclaimer: these are by NO means an exhaustive resource. Each card was created using the most up-to-date guidelines I could find, and as always guidelines are subject to change and are not applicable to each and every patient. These are just meant to serve as a basic resource. All of these were created by myself, so if you'd like to share feel free but please credit my blog if you plan on advertising them somewhere!


Infectious Disease

Abx Spectrums


Tuberculosis 





Community-Acquired Pneumonia




Diabetes and Endocrinology

Estimated Plasma Glucose per A1c levels
This calculator from the ADA is also a great resource for calculating this on the fly: https://professional.diabetes.org/diapro/glucose_calc

September 02, 2017 No comments



Fact: I did not appreciate how important clinical trials would become in my every day life as an APPE student when I first took a biostatistics class during P1 year. Our ability to analyze and evaluate data from clinical trials is critical to providing evidence-based recommendations to our healthcare team. Although guidelines are also a great source of information, your preceptors will soon expect you know the landmark trials that set the foundation for the guidelines. When I first got out onto rotation I had no idea where to look for these landmark trials, so I asked, I googled, and I compiled. Now I have a pretty hefty dropbox filled with landmark trials relevant to each rotation I've been on! Since I'm currently on primary care, I figured I'd list some of the landmark trials we talk about the most and use the most in our every day practice.

Disclaimer: this is by no means totally comprehensive. I am very aware there are more trials than just these. These were picked at random and also listed at random. Also, I've tried not to enter in my own opinion because if I did I'd probably have a novel on my hands here.

1. SPRINT (2015)
Investigated if intensive BP control (target SBP <120 mmHg) in patients at high risk for CVD (without a history of stroke or diabetes) yielded CV outcomes superior to standard BP control (135-139 mmHg)

Primary end point: composite outcome of MI, ACS without MI, stroke, CV death and acute HF

Outcome: the trial was stopped after 3 years after an interim analysis showed superiority of intensive BP control compared to standard BP control. For the primary end point: 5.2% vs. 6.8%; P<0.001; NNT 63. There were more ADE (hypotension, syncope and AKI) observed in the intensive BP control arm.

2. ACCORD (2008) AND ACCORD-BP (2010)
Accord
Investigated whether intensive HbA1c goals (<6%) in patients with T2DM and baseline HbA1c >7.5% reduces the risk of CV events compared to standard HbA1c goals (7-7.9%)

Primary end point: annual rate of nonfatal MI or nonfatal stroke or CV death

Outcome: There was no difference in the primary end point between the two arms (2.11% vs. 2.29%; HR 0.90; 95% CI 0.78-1.04; P=0.16). The trial was stopped early (after 3.7 yrs) due to the observed increase in all cause mortality (NNH=370) and CV mortality. Now we only recommend intensive HbA1c lowering in certain populations.

Accord-BP
Does intensive BP control (SBP <120 mmHg) reduce the rates CV events when compared to the standard BP control (SBP <140 mmHg) in patients with T2DM and at high risk for CV events.

Primary end point: annual rate of nonfatal MI, nonfatal stroke or CV death

Outcome: There was no difference between the two study arms (1.87% vs. 2.09%; HR 0.88; 95% CI 0.73-1.06; P=0.20). JNC8 subsequently used this to determine their goal for diabetics (<140/90 mmHg). The intensive BP control arm did experience more side effects and were on more HTN medications compared to standard control (NNH 49).

3. IMPROVE-IT (2015)
Investigated whether the combination of ezetimibe and simvastatin reduces a composite CV outcome in patients with recent ACS compared to simvastatin monotherapy.

Primary end point: composite end point of CV mortality, nonfatal stroke or major CV event

Outcome: The combination of ezetimibe and simvastatin significantly reduced the rate of the composite primary end point (34.7% vs. 32.7%; P=0.016; NNT 50), but was most likely led by reductions seen in MI and stroke. The addition of ezetimibe to simvastatin provides about a 23-25% reduction in LDL-C. This trial hasn't changed practice very much, also worth noting the AAR was 2%.

4. UKPDS 34 (1998)
Investigated whether metformin reduces DM-related complications and all cause mortality when compared to other intensive agents and diet changes in newly diagnosed T2DM patients who are also overweight.

3 arms included metformin vs. diet vs. intensive treatment (chlorpropamide, glibenclamide or insulin)

Primary end point: all cause mortality, DM-specific mortality and DM-specific end points

Outcome: Metformin was associated with a reduction in all cause mortality DM related complications when compared to the other two arms but metformin vs. diet was the primary analysis. This trial is why we use metformin first line for newly diagnosed T2DM patients.

5. ACCOMPLISH (2008)
This trial compared the ability of benazepril/amlodipine vs. benazepril/HCTZ to reduce CV events in hypertensive patients at risk for CV complications.

Primary end point: composite of CV mortality, nonfatal MI, nonfatal CVA, UA, coronary revascularization or resuscitation after cardiac arrest

Outcome: Benazepril/amlodipine was associated with a reduction in the composite primary end point (9.6% vs. 11.8%; HR 0.80; 95% CI 0.72-0.90; P<0.001). Consider that they used HCTZ vs. Chlorthalidone for their diuretic (HCTZ is shorter acting and may be worse when it comes to 24 hour BP control).

6. SMART (2006)
Investigated whether use of a long-acting beta2 agonist (LABAs) in asthmatics increases mortality and other respiratory related ADE.

Primary end point: respiratory-related death or life-threatening events

Outcome: there was no difference found between the two arms for the primary composite end point. Importantly, there were increases observed in the following secondary outcomes: asthma-related deaths or life-threatening events, death from asthma and respiratory related death. These outcomes were more pronounced in subgroup analyses for African Americans and those not using corticosteroid inhalers. Because of this trial, LABAs are added to ICS in step 3 of asthma treatment, and they have a black box warning for asthma-related death.


7. EMPA-REG OUTCOME (2015)
Compared empagliflozin 10mg and 25mg to placebo in reducing composite end point CV event outcome in patients with T2DM at risk for CV events.

Primary end point: composite CV mortality, nonfatal MI or nonfatal stroke

Outcome: Reduction in the primary end point was observed with empagliflozin (10.5% vs. 12.1%; P=0.04). There was also an observed reduction in all-cause mortality and CV mortality. A1c reduction with empagliflozin was about 0.5%. Worth noting that the empagliflozin dose groups were pooled in the analysis.


8. LEADER (2016)
Investigated whether liraglutide reduced composite CV end point in T2DM patients at risk for CV events compared to placebo

Primary end point: composite of first occurrence of CV mortality, nonfatal stroke, or nonfatal MI

Outcomes: liraglutide achieved reduction in the primary end point (13.0% vs. 14.9%; HR 0.87; 95% CI 0.78 -0.97; P<0.001) and also showed statistical significance in the all-cause mortality analysis. Unfortunately, only modest reductions in HbA1c were observed and no one achieved an A1c <7%.

9. HOPE (2000) AND MICRO-HOPE
Hope
Investigated whether Ramipril reduces the rate of CV events with patients who have multiple CV risk factors but not heart failure.

Primary end point: composite of MI, stroke, and CV death

Outcomes: Ramipril signficantly lowered the rate of the composite primary end point (14.0% vs. 17.8%; HR 0.78; 95% CI 0.70-0.86; P<0.001; NNT 27). Benefits were seen in all sub group analyses, and there was a statistically significant reduction observed in all-cause mortality.

The MICRO-HOPE substudy investigated the effects of Ramipril on microvascular complications in T2DM such as microalbuminuria and nephropathy. Ramipril was found to also prevent overt nephropathy and have renoprotective effects.

10. HEART PROTECTION STUDY (2002)
Investigated whether simvastatin would reduce CV mortality and morbidity in those at high risk for CVD

Primary end point: All cause mortality, CV mortality, coronary mortality, vascular and non-vascular mortality

Outcomes: The reduction in all cause mortality caused by the simvastatin group was statistically significant (P=0.0003) vs. placebo, and there were benefits seen in coronary and vascular mortality. Essentially there was no LDL-C threshold where they didn't see a benefit, and effect did not differ based on baseline cholesterol.

11. CANVAS (2017)
Studied whether canagliflozin lowered the risk of CV events compared to placebo in patients with T2DM at high risk for developing CV events?

Primary end point: composite of CV mortality, nonfatal MI, nonfatal stroke

Outcomes: canagliflozin significantly reduced the rate of CV death and nonfatal CV events. There were also benefits seen in renal protection. Investigators saw a similar rate of reduction in HbA1c compared to empagliflozin (0.5%) but weirdly enough, canagliflozin was associated with an increased risk of amputation in this study.


12. TORCH (2007)
Investigated the ability of salmaterol/fluticasone combination therapy to reduce mortality in patients with COPD

Primary end point: All-cause mortality at 3 years and COPD-related mortality at 3 years

Outcomes: combination therapy slowed lung function decline, improved quality of life, and reduced exacerbations and hospitalizations. However the combo arm did not achieve statistical significance with the primary end point, despite there being a trend in reduction (P=0.052).

13. WISDOM (2014)
This study investigated whether you could safely taper inhaled corticosteroids off in severe COPD patients with stable symptoms who were on triple therapy (tiotropium, fluticasone and salmaterol).

Primary end point: time to first COPD exacerbation in the first 12mo after ICS withdrawal

Outcomes: ICS withdrawal does not increase the risk of COPD exacerbation and is generally safe. Basically this trial concluded that we have to weigh the risk with each patient. We don't know the long term benefits of withdrawing ICS but we do know they increase the risk for pneumonia, and they may also slow FEV1 decline. So assess on a patient-by-patient basis.

14. ALLHAT (2002)
This trial compared chlorthalidone, lisinopril and amlodpine in reducing CV events in patients with HTN

Primary end point: Fatal CAD or nonfatal MI at 6 years

Outcomes: Chlorthalidone emerged from underdog to super star. Compared to amlodipine it reduced the incidence of CHF, and compared to lisinopril it decreased the incidence of CAD, stroke, CHF and angina. Essentially this is where JNC8 got their first line agents. Alpha-antagonist doxazosin was dropped from this when they found it increased CHF compared to chlorthalidone.

15. JUPITER (2008)
Investigated whether rosuvastatin decreased the rate of CV events in patients with normal LDL-C and elevated CRP.

Primary end point: First major CV event (its a composite of a lot of CV outcomes)

Outcomes: Rosuvastatin reduced LDL-C, CRP and also the incidence of major CV events. However, the trial is widely criticized for being stopped early.


August 26, 2017 No comments




The Beginning
When I was 9 years old, I had a small accident that required a few stitches over my eyebrow. I was sitting in the CHOP emergency waiting room with my parents, anxiously shuffling around while holding a bloody towel over the wound. My dad prepared me for what to expect, as all good doctors should, "now, they're going to use a needle to numb the area that they'll put stitches on". I was never afraid of needles, but I was quite aware about how much pain I could be in from a needle to the face compared with a needle to the arm. Hours later we funneled into one of the patient rooms and the pediatric ER doc came in with a gel. Lidocaine gel. He explained that this would numb the area and that I'd feel a little pressure but no pain. "No pain?!" "No pain.". It was incredulous to me. I was ecstatic, and I felt no pain.

A few weeks later I'd enter into the 3rd grade and write an essay on the wonders of lidocaine gel. I'd subsequently forget about that essay, and rediscover it during the first week of my P1 year as my family packed up our home and moved. Discovering this essay was the proof I needed that starting pharmacy school was the right decision for me. Looking back, I realize I had a larger body of proof in the total history of my love for medicine. 

My parents are in the medical field. My dad is a kidney doctor, my mom is a critical care nurse. Medicine was everywhere for me growing up. We had pantries full of it. I knew the appropriate dose of ibuprofen to take at 7 yrs old. I knew what a code meant, what dialysis consisted of, and I knew what my parents did was AWESOME. However, there was still a lot I had to learn, and most dinner conversations were filled with medical terms that kept my mind spinning for days. I wanted to understand my parent's secret coded language. I wanted to know why people got sick and I wanted to know how these magic drugs worked to help sickness. 

My secondary source of inspiration was my science teachers. I never thought of myself as a scientist or even a science person growing up. I wanted to do graphic design, art, writing. But in high school I had a chemistry teacher who believed in me. On the very last day of my high school career, she gifted me a pen with a pull out periodic table and that was the spark I think I needed to believe that I actually maybe was good at science. She was followed by a college chemistry professor who believed in me, and then an organic chemistry professor who absolutely kicked my butt, but also believed in me even though he'd be hard pressed to admit it. He recruited me in my sophomore year to do research in his lab, building a library of molecule fragments. Although I loved the challenge, I knew research wasn't for me in the long run.

Finding My Place (And My Pharmily)
I eventually realized that despite years of feeling pretty indifferent to almost every school subject and telling myself I was no good at science, I felt impassioned by medicine and chemistry. The subject I felt married the both of those subjects, was pharmacy. It made sense to me: a healthcare profession, medicinal chemistry and pharmacology were two subjects I gravitated toward all through undergrad, and I got to help people. It wasn't long after that I started taking prerequisite courses needed to get me into a pharmacy program. 

Pharmacy is different from other medical graduate programs, like MD or DO because you don't need a degree going into the program as long as you take the basic prerequisite courses (which are essentially just your sciences). In fact, my class is split 50/50 between kids with undergraduate degrees, and kids like me. I labored through the final classes I needed, and applied to pharmacy school in the fall of my junior year of college. I took my PCATs about a month later, interviewed the weekend before Christmas and learned of my acceptance that same day. 

It seems cliche to say all of that is only the beginning but it's so true. I had no idea how much I would be challenged, and how for almost every day in those four following years I would also surprise myself. I surprised myself with my dedication, my resilience and the passion I had for the subject. As someone who kind of floated all through high school, I never expected that I could funnel such love and energy into a career choice. The more I learned why medicine and how medicine worked the more I fell in love, the more questions I had, the more I had to know everything I could about the drugs we use.  Don't get me wrong though, it was hard work and a lot of work. I spent mostly everyday studying or in class dawn to dusk. I became that weird person at the cocktail party who wants to tell everyone how alcohol is metabolized. My life was entirely riddled with studying, assignments, projects, and work ups. Luckily, I was able to lean on my classmates, many of which became like family (or Pharmily as we affectionately term it!). 

It also helped that the rotations I had were the perfect supplement to my didactic work and honestly kept my spirits up during some of my hardest weeks. My program had us do our IPPE rotations during the school year, so every week I had a designated day to show up and learn real life practices. It really did keep me sane some weeks. I rotated between a HIV clinic, a community center for blind folks, an emergency room, and so many more interesting places. They all inspired me in one way or another to keep going. 

Three Years Down, One to Go
That is ultimately the story of how I ended up where I am today, in my fourth year on my APPE rotations, set to graduate with my PharmD in just 9 months. I still have a very long road ahead of me to become the pharmacist I dream of being, but I'm on my way and trying to absorb as much as I can from my didactic experience and apply it to my rotations. I think my 9 year old self would laugh if I went back and told her one day she'd learn that there are way cooler drugs out there than lidocaine to write essays on.
August 15, 2017 No comments
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About Me


|Gianna|
Previously titled "The Philly Pharm Student", The Pink Apothecary is a documentation of my adventures in pharmacy. From graduating pharmacy school with my PharmD to starting residency away from my home of Philadelphia, I hope to share tips, advice and commentary on how I've made it through and fell in love with my career.



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