Let's bet on it. Price is right rules.

After some time off, my preceptor is back! So, even though I'm at the same place for another 6 weeks, it'll feel like a slightly different rotation, since every preceptor does things a little differently. All the residents are slowly leaving one by one this week though, so that's sad since they were all awesome. Speaking of the residents, the resident that I was following on rounds and I would sometimes place bets on follow up lab values. This time, a patient's INR was 4.2 on warfarin and azithromycin. The medicine team wanted to bring the INR back down, so the warfarin dose was held for the day and azithromycin was discontinued. The bet was on what the INR would be the next day. The guesses were: 3.0, 3.3, 3.5, and 3.6. The result came back today and it was 3.4...almost therapeutic! This transitions well into a topic that has, again, been coming up this week...

Anticoagulation
For lovenox, if a patient is on a prophylactic dose, the regimen is 40mg qday or 30mg q12h (30mg qday with renal dysfunction). However, if the patient is being treated for a DVT or PE, then the dose is 1mg/kg BID. Speaking of PE/DVT, the Well's score for likeliness of PE/DVT being the diagnosis can be calculated. Here's how to do it:

• Suspected DVT: 3 points
• PE diagnosis more likely than alternative diagnoses: 3 points
• Tachycardia: 1.5 points
• Surgery or immobility in previous 4 weeks: 1.5 points
• History of DVT/PE: 1.5 points
• Hemoptysis (coughing up blood): 1.0 point
• Current cancer: 1.0 point

If a patient scores >6, then the likelihood is high. At this point, I would recommend starting a blood thinner and putting in an order for a chest CT as well (just to confirm). If patient scores 2-6, then there's a moderate likelihood of having a PE/DVT, and <2 is a low likelihood. Some things that can cause a PE include hormone replacement therapy, surgery, and being a smoker among others.

CBC
Pancytopenia means that all 3 cell lines are down: the red blood cells, white blood cells, and platelets (this can be caused by chemotherapy). Neutropenia means a low absolute neutrophil count (ANC). A normal ANC level is >1500cells/microliter, and a low ANC is defined as <500cells/microliter. ANC = (%neutrophils + %bands) x WBC. This value becomes important in diagnosing neutropenic fever, which is a medical emergency. The "neutropenia part" is defined above, and the "fever part" is defined as a temperature of 101'F once or a sustained temperature of 100.4'F over an hour. I learned that for neutropenic fever, you would want to cover for pseudomonas. Another tidbit about CBC is that steroids tend to increase WBC. So, if someone on prednisone presents with a high WBC but no signs of infection, he/she probably doesn't need to be unnecessarily started on antibiotics. I hear this all the time at the hospital...treat the patient, not the numbers. Also, packed red blood cells (PRBC)...1 unit has about 200mg of iron. So, if someone is severely anemic and has a low iron saturation (<20%), and he/she is going to be getting PRBC, then there may not be a need to give supplemental iron.

Heart
We had a few patients come in for atrial fibrillation this week, or at least a history of it. Something interesting that came up was the correlation between a-fib and hypothyroidism. In a patient with both these conditions, despite an elevated TSH level (conferring hypothyroidism), this patient's levothyroxine dose was decreased. Switching gears, when you think of someone with hypERthyroidism, what comes to mind? For me, it's increased metabolic activity, increased heart rate, etc. So, the dose of levothyroxine may have been decreased in an attempt to decrease HR (so it wouldn't exacerbate the a-fib).

Infectious
Now Micromedex has this amazing feature where you type in a bug, and the drug of choice and alternatives are given. I think this will be a great learning tool for me this year. I definitely don't want to constantly rely on it though...it should all be in my head. So, we put in a few bugs to see if we already knew the drugs of choice. Community acquired pneumonia: Azithro 500mg IV x 2 days, and then 500mg PO to complete 7-10 days (+) ceftriaxone 1g q24h x how many ever days depending on the severity of the infection. Hospital acquired pneumonia: Vanco 1g q24h x 10-14 days (+) Zosyn 4.5g q6h x 10-14 days. Listeria: ampicillin 2g IV q4-6h. There was a patient who was in for pneumonia this week, and he was having a horrible non-productive cough. Apparently, things like guaifenesin and robitussin have more of a placebo effect than anything. The only drugs that really suppress cough are narcotics. We gave the patient guaifenesin yesterday, and today he stated that his cough is much better :). Last topic...C.dif (again!). There's a way to categorize the severity of C.dif, and relate it to the most appropriate treatment to give to the patient:

• Patient's first experience with C.dif that is mild-moderate: WBC<15000 and no renal dysfunction.
• Treat with PO Flagyl 500mg TID x 10-14days
• Patient's first experience with C. dif that is severe: WBC >15000 and SCr is >1.5x baseline 
• Treat with PO Vanco 135QID x 10-14 days
• Patient's first experience with C dif that is severe and complicated: WBC >15000 and SCr is >1.5x baseline and patient has a megacolon, ileus, or shock. 
• Treat with Flagyl 500mg TID IV and Vanco 500mg QID PO x 10-14 days. Rectal vanco is also an additional option. 
• Patient has recurrent C. dif infections: Vanco taper as mentioned in a previous post.

 Recommendations
I've been noting the recommendations that I've had this week:
Monday: Patient has a saddle embolism (a thrombus that blocks two arterioles, to put it simply), and had an INR of 1.3 on a 5mg dose of warfarin at night. I wanted to increase the dose to 10mg for the night to get the INR up a little faster (goal was 2-3 for her). The dose was changed to 7.5mg and the INR went up to 1.5.

Wednesday (today): Patient came in for a CHF exacerbation. He's on a home dose of Lasix of 80mg in the morning and 40mg in the evening, including a potassium supplement. He had acute kidney injury in the hospital, so the lasix was held; however, the KCl was still kept. The potassium increased from 4.5 to 5.0 (nothing too traumatic, but still trending up). My recommendation was to D/C the KCl unless there were plans to start Lasix again tomorrow.

More again later this week!

2 Down, 5 To Go

Thursday concluded the end of my second rotation (I did an early community rotation in North Carolina last summer). It went by really fast, and as I said before, I'm looking forward to doing another six weeks here. I have some goals for the next month and a half:

*Be more efficient looking through patient charts.
*Think to myself...is this patient on the best medications he/she can be on? If not, then make appropriate recommendations. I want to make some kind of recommendation (even if it's just to my preceptor) once a day, unless all the patients are on the absolute perfect medications.

I have to be careful with my second goal though, because in the acute setting, the one goal is to get the patient back to baseline (or as close to it as possible) and get the patient discharged so they don't get any hospital-acquired anything. So, things like making sure the patient is on the best medications for their comorbidities (for example, conditions listed in their past medical history that aren't directly associated with the reason they are in the hospital) may not be as important. I think the latter would be important in the ambulatory care setting, which I'm curious about. The am care setting appeals to me because of that relationship that I would get to have with my patients, instead of seeing patients in the acute setting, and probably never seeing again. Hopefully I'll have more of an idea after my am care rotation, but as for right now, I'll immerse myself in acute care and keep on learning :).

On a side note, I heard back from the NC clinic, and they approved the rotation :D!! So, I'll be road tripping to NC in August, and I'll be there until about September 18th. It was worth the wait, and definitely worth googling "health clinics in raleigh, NC" and calling random places back in April. There's no pharmacist who works at this clinic, and I'll be there first pharmacy "employee" working directly in their facility, so the pressure's on!

My work area!

Mentees and Mentors :)...there's one person missing in this picture though.

C. Dif GaLoRe!

I finally have a routine when I get to the hospital every morning, and I love it. I'll admit it took me a good 4 weeks to get the hang of how things work and what the heck I'm supposed to be doing, so I'm happy I'll be here for another 6 weeks. On that note, I can't believe the first rotation is over tomorrow. If they all go this fast, graduation will be here before I know it!
My Routine
I'm not sure if all hospitals will have the same computer system/records available to pharmacists as the VA. So, the following may only be useful to people who will be doing their rotation at a VA in the future:

• Print inpatient medications and patient's lab values for past three days. 
• Write patient's significant PMH on back of labs sheet. 
• For atrial fibrillation, calculate CHADS score.
• For CHF, find out most recent ejection fraction and BNP (brain natriuretic peptide). 
• For DM, find last A1C recorded.
• On inpatient medication page, circle any of patient's outpatient medications (and write in any dose differences).
• Write in other outpatient meds not continued as inpatient.
• Check abnormal lab values and attribute each one to something.
• Check microbiology results as well, and make sure antibiotics are covering the bugs (if applicable)
• If there a significant drop in H/H, look to see if there's an increase in BUN (possibly upper GI bleed) or increase in SCr (less epo production by kidneys).
• Write down current vital signs.
• Inpatient medications (keep in mind the emergency department administration of drugs sometimes doesn't show up in the inpatient list available to the medicine teams).
• Look up which day of treatment the patients are on for their antibiotics (if applicable). 
• If on IV antibiotics and likely to get discharged, look up oral equivalents. 
• Check to see if ACEI, vancomycin, aminoglycosides are ordered in patients with increasing SCr (suggest dose changes or discontinuation as necessary).
• Check last dose of furosemide if admitted for CHF.
• If patient has high pain level, check last administration of pain drugs. 
• Read the notes to get an overall picture of the patient's situation. 
• Ask yourself what you may be asked as the pharmacist on the rounding team, and be ready with answers (still working on this one!). 

I'm sure this general procedure will change for me in the future, but this is what I'm working with as of now!

Infectious
Ever heard of vancomycin tapering? I hadn't until this week...apparently it's for patients with a second relapse of C. dif within one year. We had a vanco taper that we counseled on, and the ID department recommended the following: 125mg vancomycin QID for 3 weeks, then BID for 1 week, then Qday for 1 week, then QOD for 4 weeks. I really hope this regimen works for this patient. Treating C. dif is tricky, especially if the patient has comorbidities that require antibiotics. If it's a patient's first C. dif infection, then 20-25% of people usually respond to just discontinuing the offending agent. Patients should also avoid PPIs, since the acid is protecting the stomach from the infection. Keep in mind that hand sanitizers don't kill the C. dif spores, and that handwashing with soap is necessary. Once treatment is started, symptoms should get better in 4-6 days, and should resolve in about 2 weeks. Herpes zoster was also relevant to one of our patients this week. The treatments for this include: acyclovir 800mg 5x/day for 7-10 days, valacyclovir 1g TID for 7 days, or famciclovir 500mg or 750mg TID for 7-10 days. Of these three agents, valacyclovir is preferred, but if cost is an issue, then acyclovir is definitely cheaper. Postherpetic neuralgia is also a problem with herpes zoster. In fact, one of the goals of treatment for herpes zoster is to decrease postherpetic pain. Drugs for this include amitriptyline or nortriptyline 25mg x 90 days. Or gabapentin up to 1800mg/day x 90 days. 

TPN (total parenteral nutrition)
20% of lipids for TPN is equivalent to 2kcal/ml. You would think that 10% lipids would equal 1kcal/ml, but it's actually 1.1kcal/ml...weird. 20% dextrose is 3.4kcal/gram, 5% amino acids is 4kcal/gram. 

Heart
CHF doses of beta blockers are as follows: metoprolol 50-100mg BID, bisoprolol 5-10mg once daily, carvedilol 25mg BID (50mg BID in obese patients is what I saw in practice). These three are the beta blockers that were used in the study to see the use of beta blockers in CHF. If someone comes in with chest pain and are diagnosed with unstable angina or NSTEMI, the TIMI risk score is something clinicians might use to predict a patient's risk of death or ischemic events - stands for Thrombolysis in Myocardial Infarction.


 More again tomorrow, and then 1 rotation down, 5 more to go!

Meet Mr. IP Bugs

This past week has been crazy! I did a management conference [AKA doing a 15 minute presentation in front of a bunch of pharmacists who knew more than I did ;)] and a journal club today. Both were 'first-timers' for me. Although the management conference was a bit intimidating, I'm really happy they have us do it on this rotation. My topic was on UTIs, and I wanted to share what I learned, among other things since last Monday.

Infectious
So, Mr. IP Bugs is an 85 y/o male patient who presents with a UTI. He denies hematuria, dysuria, N/V, fever, and urinary frequency. He has a beta-lactam allergy documented as 'swelling all over the body' with penicillin. His urine culture grew 3 bugs: acinetobacter and 2 species of enterococcus. The team wanted to start him on just one medication to cover all three bugs. The best option, considering susceptibility results, was ciprofloxacin. However, one of the enterococcus strains had an intermediate susceptibility to cipro, and the team was recommended against starting cipro on this patient. Quick review on sensitivity results: Usually done by minimum inhibitory concentrations (MIC), and recall that the smaller this number is, the more susceptible a bug is to a certain drug, since it takes less drug to kill the bacteria. So, therapy for infectious diseases sometimes deals with getting the blood concentration of the drug to concentrations above the MIC. Now, in UTIs, the debate is whether it's sufficient just to get the drug concentrations in the urine above MIC (since renally excreted drugs will concentrate in the urine). It makes sense if you think about it, and I actually found some studies done that show that treating certain kinds of UTIs don't have to correlate with inhibitory drug concentrations in the blood. What kinds of UTIs? What I found was lower UTIs. Now as we go higher up the urinary tract to the ureter and kidneys, it's necessary to have inhibitory drug concentrations in the blood. There's a  review article I read that said with a dose of 500mg PO of cipro, the blood concentration of the drug was 1.6-2.9mg/L and urine concentration was 350mg/L *ding ding ding!* The patient's MIC values for his 3 isolates to cipro were about 1-3mg/L. In this case, the urine concentration that a 500mg dose of cipro results in (350mg/L) is much greater than the patient's MIC values (1-3mg/L). I would argue that cipro could be used in this patient! What actually happened - the patient had to be started on amiodarone for his A-fib (cipro + amio = prolonged QT interval), so he was D/C with other antibiotics for his UTI. This urine vs. serum concentration debate can be extended other drugs and lower UTIs as well.

Hyperlipidemia
The update regarding high dose simvastatin (80mg) recently was to NOT recommend it to new patients due to increased incidence of rhabdomyolysis (which can lead to kidney failure). However, if a patient has already been on this dose for at least 12 months without any myopathy, then this dose is okay. I saw a severe ADR from simvastatin this past week. The patient's creatine kinase (CK) level was about 800, and upper limit of normal (ULN) is about 120. The team was encouraged to decrease the dose of the statin (the patient couldn't be D/C'd completely since he recently had an MI).

Hypertension
There's an interesting class of drugs that can be used to treat hypertension: the alpha1 blockers. These include prazosin, terazosin, and doxazosin. They are also used to treat HTN, BPH, and PTSD (only prazosin for the latter since it crosses the blood brain barrier). If either of these 3 drugs cause orthostatic hypotension, then tamsulosin is used as a back up. Also in relation to HTN, we learned the distinction between HTN emergency and HTN urgency. If a patient's systolic blood pressure goes above 180 OR the diastolic blood pressure goes above 110, then it's consider EITHER HTN emergency OR urgency. The thing that separates these two diagnoses is that HTN emergency has end organ damage as well. With HTN emergency, the common treatments are nifedipine, esmolol, labetolol, diltiazem, and nitroprusside (beware of cyanide toxicity...see picture). These are all drugs of choice because of their fast acting nature.

Look at all those cyanides!

Anticoagulation
My preceptor taught me about certain things to look for when deciding the dose of an anticoagulant to give to a patient. This is important stuff, because this is the fine line between a bleed and a clot. So, first decide whether we're putting the patient on a treatment dose or a prophylaxis dose. For a treatment dose, it's for patients with a recent DVT and a CHADS score of about 4-6. For these patients, you would want to consider direct thrombin inhibitors such as bivalrudin, lepirudin, and argatroban. For a prophylaxis dose, it's for patients with a DVT in the distant past and a lower CHADS score. For these patients, fondaparinux (don't use if CrCl <30ml/min) would be an appropriate choice. Moving onto HITT (heparin-induced thrombocytopenia and thrombus)...what a tricky situation. The patient has a thrombus, so you need to give some kind of blood thinner, and heparin is obviously out of the question...warfarin takes a few days to work, what are the options? In this case, fonda, bivalrudin (0.75mg/kg bolus, 0.25mg/kg/hr infusion), lepirudin, and argatroban (2mcg/kg/min) can be used. Argatroban would be the first choice in this case. Use of lepirudin apparently increases antibodies in your body against the drug, so if there's a history of lepirudin use, may not be a good idea to use it again. An important thing to note with argatroban is that it increases the INR (although the pTT is the monitoring value for argatroban). In such cases of HITT, warfarin is started once platelets reach >150K, and oftentimes while argatroban is still being given. This combination should be continued for 4-5 days, but with INR monitoring (sometimes INR>5 will be seen without risk of major bleed).

That's all from a few days last week...correct me if I didn't quite get something right :)

Current Status: Status Epilepticus

Today on rounds, a rapid response team was called because someone was suffering from status epilepticus. My preceptor asked me what I would give first, and then next if that didn't work...and I had no idea. Then I thought to myself, if I was the actual pharmacist on that team, and they were counting on me to know the doses of these medications...the patient may not have made it. So0o, definitely went home and looked up the drugs and doses...

Psych
If someone is have tonic clonic seizures for more than 30 minutes, then consider status epilepticus as the diagnosis. It can be caused by antiseizure medication withdrawal as well. First, give lorazepam 0.1mg/kg or diazepam 0.2mg/kg over 2 minutes. This will work right away but won't last very long, so phenytoin or fosphenytoin should be started as well. Fosphenytoin is better than phenytoin in the following ways: minimizes CV depression, improved IV infusion tolerance, and it's also available as an IM route. It's dosed as phenytoin equivalents (PE: 1.5 fosphenytoin is equivalent to 1.0 phenytoin). The dose is 15-20mg PE/kg and max of 150 PE/minute. If the concentration is needed, then it should be taken 2 hours after the end of the IV infusion to give time for the fosphenytoin to be converted to phenytoin. If this doesn't work, then phenobarbital could be added at 20mg/kg at a rate no greater than 1.5mg/kg/minute. As a side note, the therapeutic range for valproic acid is 50-125mcg/ml.

Renal
CIN stands for contrast induced nephropathy. Say there's a patient who has kidney dysfunction and needs to go into the cath lab after having a heart attack. Well, CIN is a possibility...but two drugs can be used to minimize this. Acetylcysteine PO 600-1200mg or bicarbonate infusion (30amps in dextrose) at 3ml/kg/hr.

Heart
What's the physiological difference between NSTEMI and STEMI? STEMI is a complete occlusion, while NSTEMI is a partial occlusion in the heart. Also for a STEMI, the "door to balloon (balloon angioplasty)" time is 90 minutes or less. Switching gears, there's a patient at the hospital who has been admitted and readmitted multiple times due to his heart. The EF is 25%, he's tried everything, and is allergic to ACEs and ARBs. So, cardiology was considering starting ranolazine (an anti-anginal drug). The dose is 500-1000mg BID, starting dose is 500 BID. Basically, it changes sodium current in the body to ultimately decrease calcium overload. The nice thing about ranolazine is that it doesn't change HR and BP. The not so nice thing about it is that it's contraindicated in patients with hypokalemia, hepatic failure, renal failure, and prolonged QTc. The QTc was already 570, so ranolazine was not started.

Liver
In a healthy person, the AST/ALT ratio is 1:1. In a patient with a sudden ratio of 2:1, it's likely due to an alcohol binge. What are three lab values to look out for to determine liver function? INR, Tbili, and albumin.

Diabetes
A patient diagnosed with DKA was in the hospital a few days ago. A few things to remember about DKA - insulin is the only treatment for DKA. If you start the insulin drip, the patient's glucose level goes back down to normal, you can't stop the insulin, because glucose levels will go back up. The end goal is to correct the acidosis in the patient. Also, KCl is usually added to the patient's fluids. This is because the acidosis will eventually be resolved, so you would expect the potassium to decrease. With the KCl, you're ready for this, and can replenish the patient's potassium simultaneously. Also don't forget about MUDPILES as the causes for metabolic acidosis. Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates.

P.S. lame title today, I know! :)

"You're a Gemini? Sorry, no ASA for you." - Awesome stats review

Let's face it. Stats is incredibly dry, but pretty important to know when we want to back our drug recommendations with some data. Today, my preceptor gave a talk about the important things to know about stats in about 30 mins. Here goes stats in bullet points...

Statistics

• The null hypothesis = no difference between the groups.
• Type 1 error: We say A>B, but A=B
• Probability of making a Type 1 error = alpha = p-value = 0.05 (usually)
• Only consider Type 1 error if you REJECT your null hypothesis (there is a difference)
• Type 2 error: We say A=B, but A>B
• Probability of making a Type 2 error = beta = 0.20 (usually), and this is related to the POWER of a study (1-beta = power)
• Only consider Type 2 error if you ACCEPT your null hypothesis (there is NO difference found)
• Confidence Intervals: We're used to seeing 95% CI, related to p=0.05
• Prospective studies: if the interval includes 0, NOT significant
• Retrospective and Odds Ratio: if the interval includes 1, NOT significant
• Example: If Drug A makes you lose 10 pounds, and Drug B makes you lose 2 pounds. Then the difference is 8, correct? Say the results of this study say Drug A is better since it makes you lose 8 pounds more with a 95% CI of 6-10. What does this mean? It means that if you do this study over and over again, you're 95% certain that study subjects will lose between 6-10 pounds. If another drug has a result of 95% CI of 1-15, then which drug would you want to be on? The drug where you're 95% sure you'll lose at least 6 pounds, or the drug where you're 95% sure you'll lose at least 1 pound?
• Absolute Risk Reduction (ARR): If the risk of dying with placebo is 5%, and the risk of dying with Drug A is 2%, what is the ARR? Simple: 5-2 = 3%. **This is the clinically important number**
• Relative Risk Reduction (RRR): (Placebo risk - Drug risk)/Placebo risk. (5-2)/5 = 0.6 = 60%. This is the number that drug manufacturers will use to sell their product. Doesn't a relative risk reduction of death of 60% sound so much better than an absolute risk reduction of 3%? Don't be fooled! 
• Number Needed to Treat (NNT): This is the number of patients you would have to treat to get a specific effect. If the drug is to reduce death, then it's the number of patients you would have to treat to save a life. The formula for this is: 100/ARR. The lower this number the better. The way to interpret it is according to whoever is treating a specific patient, and things like cost of medication, length of treatment, etc. must be taken into account in order to make a good call. 
• Number Needed to Harm (NNH): This is the number of patients you would have to treat to get a specific adverse event to happen from the drug. If the adverse effect is causing death, then it's the number of patients that would be treated before a death happens. The formula for this is 100/percent increase in ADR. The denominator is found in whatever study you're looking at. So, if the study says Drug X caused 5% headaches, and 2% headaches on placebo, then the denominator would be the difference (3%). 
• Lastly, subgroup analysis is BS for the most part. If researchers don't find a difference between the groups they're analyzing, they might try and subgroup their analyses to find some kind of difference. For example, there was a study about to be published for the use of aspirin after a heart attack. However, the reviewers of that journal (Lancet) wanted the researchers to perform a subgroup analysis on patients with diabetes and without diabetes. The researchers also decided to do a subgroup analysis on which astrological sign the patients were (Gemini/Libra or other). There was no difference between diabetic and non-diabetic patients and their use of aspirin after a heart attack. However, apparently, if the patients were Gemini or Libra, they had a higher death rate after using aspirin. Pretty crazy! Oh and the astrological sign data is actually published in this article! 

COPD
GOLD guidelines: Stage 1 - FEV% predicted >80%. Stage 2 - FEV% predicted 50-79%. Stage 3 - FEV% predicted 30-49%. Stage 4. FEV% predicted <30% or respiratory failure symptoms. In COPD, anticholinergics tend to be better than beta-2 agonists. Steroids and theophylline are used as well.

Anticoagulation 
If a patient is having A-fib symptoms for more than 2 days, then the guidelines say to anticoagulate them 3-4 weeks before cardioversion, and then 1 month afterwards. If a patient is having A-fib symptoms for less than 2 days (and no mitral valve issues, prosthetic values, or history of embolism), then the patient will be fine with heparin throughout pericardioversion and 24 hours after cardioversion. OR the patient can be put on warfarin or dabigatran until therapeutic anticoagulation is reached (INR 2-3). If immediate cardioversion is needed, then patient would be put on heparin, and then warfarin for 4 weeks after cardioversion.

hot cross BUNs!

Apparently when I say I’ll post again “tomorrow,” I mean in a week! No more weddings this summer [:( ], so won’t happen again!

Heart

It’s not well known that amiodarone can cause delirium. So, if one of your a-fib patients start acting a little weird after starting amiodarone, it might be the culprit. If a patient has aortic stenosis, then the opening in the aorta where the blood is pumped becomes smaller…goes from “O” to “o.” In this case, you would NOT want to give diuretics and nitroglycerin. NYHA Classes for CHF are useful when choosing drug therapies. Class I: BB or ACEI/ARB. Class II: Add the one you didn’t use the first time around. Class III: Spironolactone (increases potassium, so increased monitoring is required) or furosemide. Class IV: heart transplant, hospice, and some people may consider digoxin (although this is falling out of favor). Be cautious if you ever see furosemide and spironolactone given together. Often times, furosemide will be given with potassium supplements, since it’s a loop diuretic. If spironolactone is given on top of this, then the patient is at high chance of hyperkalemia and having serious heart problems. Also, why is low magnesium an issue? Torsades de pointes!

Renal

Yesterday, we revisited what the BUN:Cr ratio means in the context of kidney dysfunction.

>20:1: Prerenal. This is due to dehydration or hypovolemia. ACEI, NSAIDS, and diuretics can cause this. As seen in this diagram, ACEI inhibitors cause dilation of the efferent vessel by blocking angiotensin. On the afferent side, prostaglandins usually cause dilation of vessels, and when NSAIDS block COX, prostaglandin synthesis goes down, so the afferent vessel gets constricted. Both of these processes result in decreased GFR.

10-20:1: Postrenal. This is due to obstruction like BPH or kidney stones.

<10:1: Intrinsic. Due to drugs. This can manifest in one of two ways: AIN (acute interstitial nephritis – from beta-lactams, sulfa drugs, and you’ll usually see eosinophils in the urine) or ATN (acute tubular necrosis – from aminoglycosides, vancomycin, contrast dye, amphoterrible).

Anticoagulation

I had mentioned last week that protamine reversed heparin, but left out the dose – I’ve learned it as 10mg of protamine per 1000U of heparin in the last 3 hours. A patient may get an IVC (inferior vena cava) filter to prevent pulmonary embolisms. This is usually done if a patient fails anticoagulation, if anticoagulation is contraindicated, if large clots are present, or if there's a high risk for a PE. Also, dabigatron is an alternative to warfarin (except it can't be used in patients with renal dysfunction of CrCl < 30ml/min).

Infectious

If a patient has a catheter, and if the culture finds coagulase-negative staph in it, then what bug is it? Staph epidermidis like catheters. If you're treating a UTI with vanco, it's not necessary to get a blood level of 10-20, since vanco will concentrate in the urine anyway. Yesterday, I saw a serratia UTI treated with ceftriaxone, then switched to cipro for outpatient.

Conversions

IV >> PO Lasix: half the dose. IV methylprednisone >> PO prednisone: keep the dose the same.

Liver

For ascites patients, the goal spironolactone goal is 300mg a day and the goal heart rate if on a beta blocker is 50-60.

Lipids

Atorvastatin is the only statin that has to be renally dosed. If a patient is on both simvastatin and gemfibrozil, then the max dose of simvastatin is 20mg, due to increased risk of rhabdomyolysis. Also, an OTC product is great for lower triglycerides when the LDL is under control...Fish Oil! Speaking of TG's, the "Oh crap" point isn't until it's >500.

Cancer

Allopurinol is indicated for tumor lysis syndrome. TLS is an increase of uric acid in the blood when "zapping" cancer cells during chemotherapy. There's increased risk for a gout attack if the size of the tumor is big. For example, leukemias are bulky cancers, so allopurinol may be given to the patient for gout prophylaxis.

GI Bleed

If a patient has a GI bleed, the usual therapy is IV PPI for 72 hours, and then discharge with PO PPI for 6-8 weeks. If a patient has an upper GI bleed, then BUN levels tend to increase, because your body would try to reabsorb BUN back into the body. Also, when would you transfuse a patient? Is it for all patients who lose some blood? Nope! In a study, more people died when they were transfused blood, mainly due to immune reaction to foreign material in the body. So, it's better to avoid it if possible. Basically, if Hgb is less than 8.0, then transfusion is acceptable, and if there's a CV risk and Hgb < 10, then it's also acceptable to transfuse.

That's it for today!