I remember on the third week of Clinical Orientation, one of my patients came in and was HIV-positive. There was an order in the chart. “Pharmacy to assess HIV therapy and restart if appropriate.” I panicked. I didn’t know what to do. Luckily, I had my preceptor to give me a crash course in how to assess appropriateness of HIV therapy (and who had access to the CfE’s labwork and database – this was at St Paul’s). So, I really appreciated this session’s practical approach to evaluating HIV medications. Lots of resources were introduced. The take-home points I got:
– Although I have heard this before, it still is amazing to think that HIV is now treated as a chronic medical condition, and not the life-ending illness it was.
– Always, always, always check drug interactions when encountering a patient who is HIV positive and on HAART
– Do NOT assume anyone knows about their diagnosis.
– Always err on the side of continuity of care. If you have the opportunity to initiate HIV therapy but the patient is leaving in a day or two (and there is no opportunity to liaise with CfE before they are discharged), refer them to CfE for a complete assessment.
– Half-lives of medications play a role into clinical decision making, and whether to abandon a treatment regimen, or alter a regimen slightly in order to ensure continuity of care
One of the scenarios that I found myself scratching my head over the past few months on rotation is this: what are the pharmaceutical implications for a patient receiving TPN or enteral nutrition (EN)? Does it matter? Is there a difference? Do we need to care, as pharmacists?
Spoiler alert – Yes, we do.
Some take-home points:
– Don’t overcomplicate. TPN = EN except by delivery system
– There are tons of different kinds of tubes depending on entrance and exit points. For pharmacists, we just have to make sure it goes down the thicker lumen
– 25 kcal/kg total calories –> divide 50% carbs, 30% fat, 20% protein
– Carbs and protein roughly are 4 kcal/g; fat is 10 kcal/g
– The commercially available MVI and Micro +6 concentrate will do the job for vitamins and minerals
– MAINTAIN ELECTROLYTES WITH TPN/EN, SUPPLEMENT REACTIVELY THROUGH DIFFERENT ACCESS
– As a pharmacist, for a clogged EN tube, you can save the day by recommending Cotazym (make sure it’s NOT enteric-coated – 1 capsule should do it given through the tube), but you should give it ASAP before the clogged stuff becomes hard rock!
– A lot of things such as nausea, vomiting, constipation are blamed on the tube. Do not succumb to this temptation, and reassess for other causes (medical conditions, MEDICATIONS, procedures)
This was an imposing topic with lots to cover – it’s great that there weren’t any pictures of Mucor spp. infections – not for the weak of stomach!
In a way, I find mycoses therapeutics to be more straightforward than bacterial infection therapeutics – however, monitoring is more complex with the antifungals, what with therapeutic drug monitoring added to the mix. It was helpful for me to review the risk factors associated with invasive candidiasis, as empiric fluconazole is started on some patients destined for ICU, but it’s always a judgement call whether empiric antifungal coverage is warranted.
Overall, it was a good overview of antifungal susceptibilities and empiric treatment – I had certainly forgotten some of them since undergrad (and I had barely seen any fungal infections during my time on the AMS service).
Delirium is linked with higher mortality, and delirium can complicate a patient’s stay. I had encountered delirium a few times before on rotation, and I remember one previous resident’s project was comparing prescribing practices between first-gen antipsychotics and second-gen antipsychotics for delirium on a general medicine ward. I knew delirium had negative clinical outcomes associated with it (a patient on my CICU rotation was delirious for nearly the entirety of his CICU stay), but what I gained from the ADS was a way of assessing delirium, from hypoactive, hyperactive, and mixed.
More importantly, as is a common refrain during residency – try to find the cause! I look forward to applying these skills when I get out there as a staff pharmacist, and also on my Psychiatry rotation.
I have written many a resume before residency. I remember for Science Co-op, sending them out in hopes of catching an employer’s eye. I had heard of the term “curriculum vitae” before but never truly grasped the difference between the two. I am in no ways a seasoned veteran of the professional world, but I couldn’t help saying to myself – why was I not aware of this? It also made me reflect – what would I put on my CV?
What I think was striking was that I thought that a CV was purely academic – however, in a field of similar candidates, maybe it’s the non-academic, non-professional stuff that sets you apart.
I now have a framework by which to form a CV – I’m sure the skills acquired through this seminar will serve me well for future opportunities that may arise in my career.
Being on CCU currently, I don’t think that I’ll get a chance to outperform the cardiologists in terms of interpreting an ECG, but I hope to take these skills to CTU or Critical Care and try to apply findings to drug therapy. The main take-home points I got:
– Have an approach: rate, rhythm, axis, conduction, hypertrophy, injury/infarction/ischemia
– Examine leads systematically: doesn’t matter which ones first, just have an approach
– Have a checklist in mind of what pertains to drug therapy
– Look for things that will kill the patient first, e.g. big ST-elevations in anterior leads
If nurses and paramedics can do it, why not us?
I personally feel that Cardiology has been my toughest rotation so far – the sheer volume of trials and information to incorporate, synthesize and apply has been quite challenging. It was quite fortunate that we had this ADS to round out my experiences so far on CCU. Throughout the seminar, I tried to relate the material back to the patients I encountered, and relate the guidelines to what is actually done in practice.
I won’t go over take home points since there are numerous ones, but rather say that Cardiology is like peeling back an onion – no matter how well you think you know the material, there is always another layer to the trial or concept, or another clinical situation where in the absence of good RCTs, clinical decisions have to be made. We all try to fit patients into compartments and boxes and fit them into typical patient profiles for trials, but it most often doesn’t work that way.
This ADS was a good reminder of the main things that one may encounter in a CKD or ESRD patient dependent on HD or PD. It was a bit of a challenge digging out what I learned during the renal elective in undergrad, and all the antibiotic recommendations for line infections in HD and peritonitis in PD… some take-homes I got:
- The ferritin target is higher in HD vs non-HD patients (including PD)
- For MBD: lower the PO4, lower the iPTH, lower the Ca, but DON’T raise the Ca unless the patient is symptomatic.
- The contraindication of malignancy in patients receiving ESAs depends on the type of malignancy – solid tumours are at higher risk
- Double-cephalosporin coverage is recommended as first line for peritonitis in PD
- Fluconazole 100 mg PO daily is recommended as fungal prophylaxis if the patient has had peritonitis in the past, has had exposure to broad spectrum ABX recently, had recent GI surgery, or is immunocompromised
- Vancomycin +/- gentamicin (if unstable) is recommended for HD catheter-related infections – I assume the vancomycin is preferred over cefazolin because it would cover Enterococcus faecium.
This was an ADS that was more geared for a primer to diabetes care in hospital. Some take-home points I got:
- Overall, poor glycemic control in the hospital setting leads to delayed wound healing, increased stay in hospital, and other negative outcomes (retrospective data)
- NICE-SUGAR showed that in the ICU setting, aiming for <10 mmol/L as a BG target resulted in less mortality vs. more strict control (4.5-6 mmol/L)
- RABBIT-2 showed that despite more control with blood glucose and less hypoglycemia, there were no differences in length of stay between basal-bolus-correctional and sliding scale only insulin regimens. However, for seamless care, a BBC-based regimen would afford more glycemic control in the long run for a diabetic who is primarily dependent on insulin.
- DKA and HHS are mostly managed in the same manner: fluids, insulin, and potassium supplementation.
Overall, this was a good rehash of DKA and HHS (which I went over in detail with Dr Zed in Emerg), and a good reminder of the importance of the varying recommendations in glycemic control depending on the care setting.
Before I could even blink, it’s already seven months through the residency year. I definitely do not feel ready to enter practice without the comforting safety net of a preceptor (and I shouldn’t; there’s so much more to learn and experience)…so this ADS was a bit of an awakening for me. I may be expected to precept students in the next year, along with the rest of my colleagues! Isn’t that scary?
What is comforting is that if I know what makes a good preceptor, I can model myself to be that way too, but it takes practice and commitment. I’ve done teaching and mentoring before, but never in a clinical or pharmaceutical context. Some take-home messages I got:
– Always understand your student has a life outside of their rotation, and even if they’re putting in 110% into the rotation, life happens, and sometimes they’ll slip, and that’s okay.
– Don’t use the sandwich method: it’s insincere and belittles positive feedback.
– Instruct, model, coach, facilitate, repeat.
– My preceptors wrestle with a lot of dilemmas on a daily basis: do I step back and observe? Do I let my resident make this recommendation on their own? Should I give them the answer, or have them find it on their own without compromising patient care?
Excited to get my first student already – and hopeful that I’ll be up to the challenge when the time comes.