I GET SMASHED. YEAH!

So why in the world would I write about getting smashed on a professional pharmacy rotations blog?! Cause it has to do with pharmacy!!

Pancreatitis
I GET SMASHED are the causes for pancreatitis, and as pharmacists, it's important to know these, since some of the causes are drugs. Idiopathic Gallstone Ethanol Trauma Steroids Mumps Autoimmune Scorpion sting Hypercalcemia ERCP Drugs (Sulfonamides Azathioprine NSAIDS Diuretics). The treatment for pancreatitis is palliative care and the patient should be NPO for a while, since eating will aggravate the pancreas.Palliative care...so that would be treating the pain (cause apparently it's very painful), and using narcotics, correct? Well, narcotics are known to cause spasm of the sphincter of Oddi. Take a look at this picture:

Basically, the gall bladder and the pancreas share a duct that leads into the duodenum. The opening to the duodenum is the sphincter of Oddi. If narcotics, specifically morphine, is used, you would think that the spasm of the sphincter of Oddi would cause increased pressure inside this duct, and cause bile to be kinda back washed back into the pancreas. The other option would be to use meperidine, but the metabolite (nor-meperidine) has an increased half life, and can build up to cause seizures. In this case, it seems that the risk of causing a clinically significant spasm of the sphincter of Oddi outweighs the risk of having a seizure. SO... use morphine for pain in pancreatitis!

Psych
Black Box Warning for quetiapine is increased risk of death (well that sucks). Also, phenytoin can cause nystagmus. The attending on our team said that even if she senses slight side effects of Aricept (donepezil) in a patient, she'll D/C it. Oxybutynin is an anticholinergic that can cause mental problems. Remember...anticholinergics...red as a beet, dry as a something, *mad as a hatter*....

Infectious
Cephalexin is usually dosed every 6 hours. Diverticulitis is inflammation of a pouch in the intestinal wall. This patient was treated with cipro and metronidazole in order to cover anaerobes, enterococcus, and gram negatives. Check, check, and check! Vancomycin toxicity is usually related to peak concentrations. So, if a patient was on 1g vanco q12h, and being treated for hospital-acquired pneumonia, and had a trough concentration of 8mg/mL, what would you do? First of all, the goal concentration here is 15-20mg/mL. You could either increase to 1500mg BID, or 1000mg TID. The latter could decrease toxicity associated with higher peak concentrations, and if the hospital had pre-made bags of 1g vancos sitting around, then why not! For aspiration pneumonia, use clindamycin or Unasyn.

Anticoagulation
If someone is suspected of having a DVT, then try doing a Ddimer test (to rule it out). The problem with this test is that it's useless when it comes out positive, since there are a ton of false positives. For example, if a patient were pregnant or had an infection, the Ddimer would likely come out positive. So, it's only useful if it's a negative result. Also, introducing the FAB Four! Fluconazole, Amiodarone, Bactrim, and Flagyl...if any of these drugs are given with warfarin, then the dose of warfarin must be HALVED so the INR doesn't become supratherapeutic. Also, what's the reversal for bleeding with heparin? PROTAMINE!

That's it for today. I was assigned a DI for IV iron dosing, so I'll have a nice summary about that tomorrow. THEN, off to Vermont for my BFFs wedding!!

HyperBananaNemia

Thought this blog could use some pictures!

AKA hyperkalemia.

Electrolytes 
There was a patient last week on Wednesday who came in with pretty bad hyperkalemia...with a K level of about 8.5. I learned that the first thing the patient is given is calcium gluconate. After that, there are two options: either eliminate the potassium in the body (dialysis, diuretics, Kayexalate) or move the potassium intracellularly (albumin, sodium bicarbonate, dextrose/insulin).

Psych
Flumazenil reverses benzos, but if this happens too quickly, it could lead to seizures :(.

Renal 
No Lovenox or Bactrim for renal failure.

Infectious
The PO equivalent for Zosyn is Augment. The PO equivalent for Vancomycin is Bactrim. Max dose for clindamycin is 1.8g and IV max is 3.6g.

Anticoagulation
There was a patient in last Wednesday, and the doctor was wondering whether or not the patient should be bridged on heparin while restarting his warfarin therapy. There are some factors that need to be taken into considering to answer this question. The first is whether the patient is at a low, moderate or high risk for clotting. High risk patients would include a mitral valve replacement (MVR), old aortic valve replacement (AVR), A-fib, history of thromboembolism in the last 12 months. Moderate risk patients include AVR with DM, HTN, CHF, >75 y/o, OR stroke. If moderate risk, then bridging therapy is recommended with therapeutic dose LMWH, low dose LMWH, or UFH. HOWEVER, this is a 2C recommendation, meaning it's not that great of a recommendation and the amount of research out there isn't impressive. If high risk, then bridging therapy is recommended with therapeutic dose LMWH or UFH, and this is a 1C recommendation, meaning it's a good recommendation and the amount of research out there isn't impressive. My preceptor said 1C recommendations are good to follow, but not really 2C. The specific patient I'm talking about was at moderate risk, so the doctor decided not to do bridging therapy, and the pharmacist agreed.

Gases
BiPAP vs. CPAP. Bi-level positive airway pressure and continuous positive airway pressure. Both are for patients to get more oxygen into their systems. The difference is that for BiPAP, the air pressure decreases when the patient breathes out, so they're breathing against less pressure. With CPAP, the pressure level is continuous. I can finally tell if someone is in respiratory/metabolic acidosis/alkalosis quickly (I know, about time, right?). So basically, First look to see if the pH is acidic or basic. If acidic, then look at the pCO2 level. If it's high (>45), then you're looking at respiratory acidosis. If the pCO2 level is NOT >45, then you're thinking metabolic acidosis, but take a look at the HCO3 just to be sure (if it's <22, then it's confirmed). If the pH is basic, then look at the pCO2 level. If it's low (<35), then it's respiratory alkalosis). If the pCO2 level is NOT <35, then you're thinking metabolic alkalosis, but take a look at the HCO3 just to be sure (if it's >26, then it's confirmed). If it's a respiratory disorder, then the pCO2 goes in the opposite direction of the pH. If it's a metabolic disorder, then the HCO3 goes in the same direction of the pH. For compensation, the pCO2 will compensate for metabolic disorders by going up if alkalosis and going down if acidosis. For compensation, the HCO3 will compensate for respiratory disorders by going up acidosis and going down if alkalosis. Lastly, if PaO2/FiO2 is <300 then this is Acute Lung Injury...if <200 then it's Acute Respiratory Distress Syndrome. FiO2 is fraction inhaled O2.

Patient Case
There was a patient last week who was sedated beyond belief when we went on rounds. He could barely wake up, even when the doctor shook him. He was given diazepam the day before for alcohol withdrawal. However, the doc had discontinued the patient's benzos and narcotics the day before, because he was concerned about him going into severe respiratory distress. When we went in to check on him, he could barely answer any questions. Turns out he was given 8 percocets within 16 hours. ABGs were done on him, and his pH was 7.2 something and pCO2 level over 100. 0.4mg naloxone was given to him to reverse the narcotic overdose, and I was amazed with how fast it worked. The patient was literally able to answer questions within about 45-60 SECONDS. A few hours later, pCO2 level was <60, and he was improving.

Bugs and Drugs

I have a long ways to go until I can say I feel comfortable with ID. But as a start...

Infectious
Penacillins need to be adjusted for renal deficiency (NO renal adjustment for NO ~nafcillin and oxacillin). These are time-dependent drugs, meaning the effect of the antibiotic will depend on how long the concentration in your body is above the MIC.

• Antistaph penicillins are: nafcillin, oxacillin, dicloxacillin
• DOC for enterococcus: aminopenicillins 
• Pip/tazo covers pseudomonas and acinetobacter but amp/sulbactam does not. 

Cephalosporins need to be adjusted for renal deficiency (except for ceftriaxone), and are time-dependent drugs as well. They are also bacteriocidal. As you move up in generation, you move up in gram negative coverage and down in gram positive coverage.

• First generation: cefazolin and cephalexin
• Second generation: cefoxitin (IV), cefuroxime (PO and good e. coli coverage)
• Third generation: cefpodoxime (PO), ceftriaxone (IV and no pseudomonas coverage), ceftazadime (IV and yes pseudomonas coverage)
• Fourth generation: cefepime (covers pseudomonas and acinetobacter)
• Fifth generation: ceftobiprole (covers MRSA*** and pseudomonas)

Vancomycin covers gram positive, and is DOC for MRSA. It's a 'cidal drug, and is renally eliminated. The loading dose is 15-25mg/kg actual body weight, and maintenance is determined with CrCl.

Carbapenems are 'cidal antibiotics as well.

• Ertapenem does not cover pseudomonas
• Imipenem (AKA Seizurpenem), meropenem, doripenem DO! 
• If a patient has a history of seizures and has poor kidney function, then don't give imipenem.

Aztreonam only covers Gram negative!!
Linezolid only covers Gram positive!! This includes VRE and MRSA, and oddly, its PO bioavailability is greater than its IV bioavailability. Oh, and don't give this drug with an SSRI.

Daptomycin is a 'cidal and concentration-dependent drug.

• Covers MRSA and VRE
• Doesn't work in lung infections like pneumonia, since pulmonary surfactants inactivate it. 

Polymyxins

• Usually reserved for multi drug resistant gram negatives 
• Examples polymyxin B and E

Macrolides cover atypicals

• Clarithromycin is good for H. pylori
• Azithromycin is good for pneumonia, including S. pneumonia 

Clindamycin is the biggest cause of drug-induced C.dif

Tetracyclines cover atypicals as well

• Atypicals = chlamydia, mycoplasma, and legionella 
• Demecocycline is best for SIADH (Syndrome of Inappropriate Secretion of Antidiuretic Hormone)
• Tigecycline does not cover pseudomonas 

Bactrim

• Covers gram positive and negative, MRSA. 
• There's 5x more sulfamethoxazole than trimethoprim in dosage forms 

Aminoglycosides

• Have a post antibiotic effect - it doesn't mean the drug will keep killing the bugs after the medication is stopped...what it means is that there won't be any more growth of the bug.
• Nephrotoxic side effects are reversible, but ototoxic side effects are irreversible. 

Metronidazole cover anaerobes!!

Fluoroquinolones are 'cidal

• Moxifloxacin and levofloxacin are respiratory quinolones, and do cover strep pneumonia. They don't cover pseudomonas.
• Ciprofloxacin is not a respiratory quinolone, doesn't cover strep pneumonia. It does cover pseudomonas.
• If the QTc > 500 when on these drugs, then action needs to be taken.

As a general rule, if an antibiotic works on the cell wall, then it's bacteriocidal. If it works on protein synthesis, then it's bacteriostatic. The exception is aminoglycosides - they work on protein synthesis, and are bacteriocidal! This was a very basic overview of antibiotics. I needed a basic review, since I feel like I forgot almost everything from second year ID, so my preceptor gave a presentation that he had prepared for a talk a while ago :).

Adam Fights Elephants This SATurday

(5/24 stuff)

I'm rounding with a new team this week and it's been fun! Just as a side note, when I say team, I mean the medicine team that discusses each patient assigned to them every morning before going and seeing each one individually. There's the Attending, Resident, 2 Interns (all doctors), Pharmacist, Nurse, sometimes social worker, and then some students. As always, I've learned a lot this week.

Diuretics
Adam Fights Elephants This SATurday. Acetazolamide works on the proximal tubule, Furosemide and Ethacrynic acid work on the loop of Henle, Thiazides work on the distal tubule, and Spironolactone, Amiloride, and Triamterene work on the collecting duct. Often times, if a patient isn't getting rid of all the fluid they need to on just Lasix, metolazone (thiazide-like) will be adding to his/her regimen (metolazone 30 minutes before Lasix). It makes sense if you think about it. The Lasix is working on the loop of Henle, but when the fluid gets to the distal tubule, some of it is reabsorbed back into the body. With metolazone, this is prevented. To get an idea of how much more fluid a patient can get rid of...it could be 500ml with just Lasix, and 1500 with both. Spironolactone can be used if the SCr <2.5, and the K <5.5.

Infectious
PO antibiotics for bacteremia is crappy, BUT the exceptions are: quinolones and linezolid (the latter for Gram (+) only), because the blood concentration when given PO is good. When thinking about ID, think about where you want the antibiotic to concentrate...is it the blood, the urine? Cipro definitely concentrates in the urine, and is about 70% bioavailable in the blood. In general, ampicillin PO can be used when necessary, but the dose is 500mg BID whereas the IV dose is 2g TID. If someone has bacteremia, would you use the IV or PO dose (if the drug adequately covers the bugs)? Probably IV. The attending in our team asked a question that no one in the room knew the answer to...he wanted to know which bug is covered by Augmentin but NOT Zosyn (pip/tazo). The answer is Stenotrophomonas. Maybe it won't be useful in clinical practice, but now you know for trivia! The following drugs are used for treating MRSA PO: Clindamycin, Bactrim, doxycycline. Bacterial meningitis...what are two tests you could do to test for severe neck stiffness? Brudzinski's and Kernig's. The following link shows a positive Brudzinski's sign: http://www.youtube.com/watch?v=jO9PAPi-yus, and the first suggested link shows a positive Kernig's sign. I realize a pharmacist won't be doing these tests, but it may be mentioned in rounds, so it's good to know.

Heart
Tuesday was a big Congestive Heart Failure (CHF) day. A few of our patients had CHF, so our preceptor gave a really good talk about it. Labs: look at ejection fraction (normal is 60-70%), brain natriuretic peptide (BNP...>500 is bad, and a patient this week had around 10K). The classification for the severity of CHF is by the New York Heart Association (NYHA Classification). Class I is no limitations during normal activity. Class II is mild symptoms on exertion/during normal activity. Class III is pretty bad symptoms on exertion, or during less than normal activity. Class IV is symptoms at rest. Treatment: Loop diuretics will relieve symptoms but doesn't prolong life. Spironolactone, ACEI/ARBs, BB, and Hydralazine/ISDN all improve survival. The only BBs that have actually been studied are: carvedilol, metoprolol XL, and bisoprolol. Digoxin has no affect on mortality. If a patient comes in with CHF exacerbation, look to see if he/she is taking DM meds like the glitazones, pain meds like NSAIDS, and dihydropyridines (d/t dilation).

Miscellaneous
If phosphate is elevated above 5, don't use vitamin D because vitamin D will increase phosphate.

Interesting incident...a nurse found a joint filled with "goodies" under one of the patient's pillows! But of course he found it on the floor in the hospital, and was going to turn it in. Riiight ;)

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

So I got asked a lot of questions today. Unfortunately, my preceptor didn’t get a lot of answers. And when I say “get answers,” I don’t mean that I eventually stumbled upon the answer after a couple minutes of staring off into space…I mean that I knew the answer 110% and said it with conviction! No medicine team is going to accept a recommendation that was stumbled upon. So here comes the phrase, the 9 magic words, that will make this year that much more of an enriching experience:

“I don’t know, but I’ll get back to you.” (technically 11 words I guess)

Here are some questions I was asked today, and used this respectful phrase.

1. What lab parameters would you look at if you suspect acute kidney injury on top of chronic kidney injury? Serum creatinine and BUN (and do the serum: creatinine ratio).
2. When would you not bridge a patient for anticoagulation in the hospital? If the INR is more than 1.7.
3. What’s the calcium phosphate product and how would you interpret it? First of all, the equation is [corrected calcium] x [phosphate]. If this is >55, it’s bad for the kidney, but if it’s >70 it’s really bad.
4. What are some PTH lowering agents? Calcitriol, doxycalciferol, cinacalcet.
5. What’s different about cinacalcet between these three agents? It not only lowers PTH, it also lowers calcium and phosphate.
6. How would you treat hyperphosphatemia? Foslo, TUMS, aluminum hydroxide, lanthanum [thanks Connie!]. 
7. How would you define orthostatic hypotension? If your BP drops by 20 for systolic and by 10 for diastolic when you stand  up (from your sitting BP).
8. What’s the difference between carvedilol and metoprolol in terms of effects on BP and HR? Carvedilol effectively decreases both. Metoprolol decreases the HR the same, but doesn’t lower BP as much.
9. What does CIWA stand for? Clinical Institute Withdrawal Assessment. It’s for alcohol withdrawal…there’s a grading scale of 10 things you would look for in a patient, and if this score is more than a certain defined threshold (different for each institution), then you would give lorazepam or diazepam.
10. What do you look at to determine a Child Pugh score? Total bilirubin, albumin, INR, ascites, hepatic encephalopathy. The interpretation would be 1 and 2 year survival percentages.
11. What’s MELD? Model for End-stage Liver Disease. The equation for this is: 3.78 [Total bilirubin] + 11.2 [INR] + 9.57 [SCr] + 6.43. The interpretation for this is 3-month mortality.
12. What’s the link between using lactulose in cirrhosis patients? Increased levels of ammonia that the liver isn’t able to break down could lead to hepatic encephalopathy. The lactulose increases the passage of ammonia from tissues into gut lumen and blocks the intestinal ammonia production.

And that’s about it for today!

Code Brown (wait, what?)

So, I’ve heard of Code Blue, but anyone heard of Code Brown? Thankfully I asked my preceptor what exactly Code Brown entails before saying something embarrassing. “Code Brown” = when a patient has C. dif, and (for lack of better words) takes a huge dump and it gets everywhere!

Today [5/19] was my third 10 hour day, but the time is starting to go by faster J. Learned a lot, as always.

Anticoagulation

Heparin-induced thrombocytopenia. I did some research on this topic today, and I’ll now attempt to type up everything I remember. There are 3 types of HIT: type 1, type 2, and HITT. Type 1 is not immune-mediated, and it happens when heparin directly activates platelets, and aggregation begins. Type 2 is the clinically relevant HIT. Basically, if a patient has a type of anti-PF4-heparin antibody, then it will see the heparin-PF4 complex as a threat to the body and begin the immune response…eventually resulting in a high risk for thrombosis. BTW, PF4 stands for platelet factor 4. It’s just a pretty crazy paradox, because a blood thinner eventually causes high risk for clotting. The treatments are direct thrombin inhibitors like bivalrudin, lepirudin, and argatroban. There’s also a factor Xa antagonist called danaparoid that can be used. Why wouldn’t warfarin be used? It’s because of the initial procoagulation effect of warfarin via quick depletion of proteins C and S. So, it’s generally recommended to stay off the warfarin until INR is therapeutic, and possibly bridging him onto the warfarin. Also, HIT is diagnosed by the 4 T’s: timing, severity of the thrombocytopenia, the occurrence of new thrombosis, and the presence of alternative explanations for the thrombocytopenia.

Infectious

Atypical pneumonia. Bugs: Legionella pneumonia, Mycoplasma pneumonia, Chlamydia. Drugs: I believe these bugs are covered by azithromycin, clarithromycin, erythromycin, fluoroquinolones, and tetracyclines. With C. dificile, there are two main therapies: metronidazole (500mg TID for 7-14 days) and vancomycin (150 or 250mg QID for 10-14 days). Metronidazole is for low risk and vanco is for high risk. Hospital Acquired Pneumonia. Something I learned about HAP – the risk factors for this include previously being in a hospital for 72 hours or more within the past 90 days, being in a hospital in general, antibiotics, and being immunocompromised. Ampicillin/sulbactam covers Gram positive, negative, anaerobes, but NOT pseudomonas. Piperacillin/tazo covers the same plus pseudomonas. For aspiration pneumonia, you want to cover anaerobes. Ampicillin has a 50% bioavailability, and amoxicillin has a 80-90% bioavailability.

Labs

If BUN is increased, then it could be due to things like kidney dysfunction or upper GI bleed (labs will show decreased H/H). Fever is defined as a temperature of 101’F one time or 100.4’F x2. The FeNa is the fraction excreted sodium. The equation is: [Urine Na x Urine Cr]/[Serum Na x Serum  Cr] x 100. If this number is >1.0, it’s not prerenal kidney injury. If it’s <1.0, it is prerenal kidney injury (so think dehydration/hypovolemia). 

P.S. If I didn’t make it clear enough, Code Brown isn’t a real code!

Some MONA(BS) Stat, Please!

Although I was very disappointed that my ID rotation (#3) got canceled, I’m pretty happy with the amount of ID information I’m getting everyday. It’s mostly pneumonia and UTI, but hey, if it’s common infections, might as well know the therapy like the back of my hand.

Anyway, about the medicine team – I think they’re all awesome. The attending is great, and is very receptive to suggestions my preceptor has regarding drug therapy. For example, one of the medical interns had a patient who developed tachycardia for no apparent reason. The pharmacist noticed that one of the patient’s outpatient meds was carvedilol, and was D/C’d in the hospital. He suggested starting up a beta blocker again to try and control the tachycardia, and metoprolol was ordered for the patient :).

As for things I learned in the last two days that I think are actually going to stick…

Anticoagulation

DVT prophylaxis is always assessed for every patient, and is important in the acute setting. Enoxaparin is much more expensive than UFH, so UFH is more commonly used (although more inconvenient, given the TID dosing). The UFH DVT prophylaxis dose is 5000U SQ TID. The enoxaparin dose is commonly 40mg SQ once daily, can go up to 30mg SQ BID, and adjusted for renal dysfunction (CrCl<30ml/min) at 30mg SQ once daily. Scenario: say a patient takes warfarin regularly, gets admitted to the hospital, and  has a supratherapeutic INR (~5.0), causing the warfarin to be D/C’d. Well, what if the INR suddenly drops to 1.8? At this point, we'd need to restart the warfarin, but it takes a few days to work…soo BRIDING therapy with heparin comes into play! I remember learning this last month in kinetics, but now that it's clinically relevant, it should stick ;). Also on the topic of INR…the following antibiotics will almost always raise INR when given with warfarin: Bactrim, and Azithromycin, Metronidazole. Last tidbit about INR – if it gets too high, it can be reversed with Vitamin K or fresh plasma (the latter is quicker, but also doesn’t last very long).

Heart

If someone comes into the hospital with chest pain, what do you give them? MONA(BS)!! So we learned MONAB in school. Now there’s also the “S” component, which apparently has shown to be beneficial. The acronym stands for Morphine, Oxygen, Nitrogen, Aspirin (+/-clopidogrel), Beta Blocker, Statin. The morphine isn’t only for pain – it can actually improve oxygenation to the heart…I believe it’s by decreasing the demand for oxygen. Oxygen is given for obvious reasons. Nitro dilates the vessels to get more blood through, and ASA to thin the blood a little bit. BB is helpful in decreasing the demand of oxygen, and I’ll look into exactly why statins are beneficial. Also, all chest pain doesn’t have to do with the heart. If someone receives nitroglycerin, and the chest pain doesn’t improve, then it could be because of epigastric pain or extreme GERD as well.

Liver

What’s the relationship between a patient having ascites and receiving albumin? I had no idea until about 4:15pm today. So basically, if a patient is receiving a tap to remove the ascites, an oncotic agent such as hetastarch or albumin will be given to the patient so the fluid from the intravascular won’t get into the abdomen to replace the ascites fluid. If an oncotic agent isn’t given, there’s a chance for hypotension, since there will be less fluid in the intravascular, since it'll move to the abdomen. 

Lab Values

SAAG is the serum-ascites albumin gradient, and it helps determine the cause of ascites. SAAG = (albumin concentration of serum) – (albumin concentration of ascitic fluid). If this value is >1.1g/dL, the ascites is likely due to portal hypertension. More specifically, if the value is >2.5, then it’s likely due to heart failure and if <2.5 (but still >1.1), then it’s likely due to cirrhosis. If <1.1, then the ascites is more associated with tuberculosis or various types of cancers.

That’s it for the last couple days. I promise I have been learning ID stuff, but I wanted to organize the bugs and drugs for pneumonia in my head before posting about it! 

And about rotations in general...not only my 3rd, but my 4th rotation was canceled as well...awesome! I got the 4th one replaced at Shea Health Care in Scottsdale, and working on getting a contract with a clinic in North Carolina for #3 :). 

T-0 Days!

Today was the first day of rotations...first part of the day was more orientation, and needless to say, pretty uneventful. The pace picked up at 1:00 pm, when I met with my preceptor. I listened to the resident presenting about 15 patient cases, and before I knew it, it was time to go home.

I've been assigned 3 patients to begin with, and as time goes on and I become more comfortable suggesting ways to optimize drug therapy, I'll probably be assigned a few more.

I learned a few things today though!

Infectious 
When a patient is on IV antibiotics, and will likely need them at discharge, look up the oral equivalents to any IV-only antibiotics. This keeps you ahead of the game. Also, the trough drug concentrations of Vancomycin are measured, and the therapeutic range is between 10-20mg/dL. However, the range is 15-20mg/dL for complicated skin infections, bone infections, bacterial meningitis [thanks Edric] bacteremia, and hospital acquired pneumonia.

Renal
If there's a 30% or a 0.5 increase of serum creatinine in a patient, then that's defined as Acute Kidney Injury (divided into prerenal -usually dehydration issues-, intrinsic -actual damage due to medications-, and post renal, where there is obstruction). The different categories can be defined by the BUN:SCr ratio.

Heart
If a patient undergoes CABG, he/she is at risk for Afib shortly after the surgery. If <48 hours, then warfarin is used for cardioconverstion. If >48hours, then chemical conversion with amiodarone (or similar drugs) is done. (I need to double check on this one though...not sure if I write it down correctly). Also, for a CHAD2 score, being >75y/o is the biggest risk. Lastly, when a patient is post MI, troponin levels tend to rise after 3-12 hours. 3 consecutive negative troponin lab results must be done in order to discharge the patient. Need to be careful, because troponin levels don't increase right after the MI, and may take some time.

That's about it for today. I go on rounds tomorrow, so more to come...!

Meaning Behind the Name

“The end of the beginning” is what the Master of Ceremonies at my White Coat called this upcoming year…the year of clinical clerkships/rotations/etc. It’s not quite the end of school, since graduation is still a year away, but it’s not exactly the beginning of the next chapter either. It’s sort of a bridge between the didactic classroom setting and a taste of “the life of a pharmacist.” The life of a pharmacist, huh? Makes it sound exhilarating and cutting edge and exciting…well that’s because IT IS!! Seriously, when I think of my future career, there’s always action hero, “save the world” music playing in the background…I wake up every morning excited to get to work and round with doctors, nurses, and other health care professionals…I picture other members of the team directing drug therapy questions at me, and expecting me to be the drug expert…I can usually answer them off the top of my head, only sometimes relying on my smart phone. I picture my future career as a life long learning path, so nothing ever gets old. Most importantly, I picture what I do as a living as something that positively impacts the life of patients everyday…whether it’s holding a newly diagnosed diabetic’s hand when they’re picking up their insulin for the first time, or saving someone on a tight budget $100 a month by switching them to a combination product for his/her asthma after completing medication therapy management (MTM), or making an important recommendation to a physician who wants to know, “What do you suggest?”

Now I understand that I have heard a lot about the pharmacist’s role in health care, but have yet to experience it first hand. I understand that it may not live up to my idealistic day dream, and that I might actually not wake up to action hero music every morning! But honestly, my career will be what I make it. The perception of how valuable a pharmacist is to everyone I interact with will depend not only on what I know, but how I communicate it. It takes well-rounded knowledge and confidence to gain trust with both patients and other health care professionals, and the road to both of those things begins now with rotations. This is why this next year is significant to me, and why I decided to start this blog to capture the highlights of “the beginning of the end” [in accordance with HIPAA of course ;) ].