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!
Very good stuff. So, what about reversal of dabigatran? Warfarin? What common foods can alter INR and why? For warfarin's reversal agent, which is the preferred route of administration? How long does it take to work?
ReplyDeleteWhat dose of allopurinol would you use for gout and TLS?
What other uses are there for spironolactone?
Tell us about cardiac remodeling.
There is currently no reversal agent for dabigatran, so if bleeding risk is high for a patient, use of this agent may not be the best choice. For warfarin, short term reversal agents include prothrombin complex concentrates (PCC) or recombinant activated factor VII (rFVIIa). Factor VII has the shortest half life of the clotting factors that warfarin inhibits, so this would work the the quickest. Longer acting reversal agents are Vitamin K and Fresh Frozen Plasma (FFP). FFP is the preferred agent, and I believe this is because it acts faster than Vitamin K (which takes about 24 hours to work regardless of IV or PO route).
ReplyDeleteAllopurinol for gout: Start at 100mg a day, and increase by 100mg a day until uric acid <6mg/dL
Allopurinol for TLS: 600-800mg a day in divided doses.
Need to start renally adjusting allopurinol at CrCl<20ml/min.
Spironolactone: used for edema, hypertension, hyperaldosteronism, hypokalemia and CHF (class III/IV)