Netter for the iPhone
Would have loved this during anatomy. Looking at the video, I can almost smell the gristle and formaldehyde again. This is one of the few medical apps I haven't used, though — any medical students find it helpful?
Would have loved this during anatomy. Looking at the video, I can almost smell the gristle and formaldehyde again. This is one of the few medical apps I haven't used, though — any medical students find it helpful?
Image via Wikipedia
Yesterday I gave a great lecture on interpreting ABG results. I added a problems set for gap-gap analysis and added a section on the osmolar gap. I also improved the anion gap section with my new favorite mnemonic. Forget PLUMSEEDS, forget MUDSLEEPS, forget MUDPILES. The new hotness is GOLD MARK:
* G Glycols
* O 5-Oxoproline (pyroglutamic acid)
* L L-Lactic acid
* D D-Lactic acid
* M Methanol
* A Aspirin
* R Renal failure
* K Ketoacidosis

I'm transitioning Kidney Notes' blog commenting system to Disqus. The old comments will — hopefully — still be there, but things may look strange for a bit.
Image via Wikipedia
A few minutes later, Dr. Hecht studied the results. As he had expected, the angiogram revealed that Mr. Franks’s arteries were healthy. In some places, plaque had blocked 25 percent of their blood flow, but in general, cardiologists do not consider blockages clinically relevant until they reduce blood flow at least 70 percent.The article attempts to reconcile two sharply opposing points of view. In my opinion — and I hasten to add that I'm not a cardiologist or radiologist — cardiac CTAs are at the same level of clinical usefulness and acceptance now that CTAs of the pulmonary arteries were several years ago. It took years for a CTA of the pulmonary arteries to a widely accepted test for diagnosing or excluding pulmonary emboli. Within the next several years, I would expect that CTAs of the coronary arteries will become a well-accepted test for diagnosing or excluding coronary disease.
After Mr. Franks finished dressing, he joined Dr. Hecht, who went over the results, explaining that his heart appeared healthy and that he would not need a stent. Still, Dr. Hecht recommended that Mr. Franks have another CT angiogram next year to check that the plaque was not thickening. Mr. Franks agreed, pronounced himself satisfied and left.
For Mr. Franks, the test was quick and painless. But it subjected him to a significant dose of radiation.
Based on a reporter’s notes about the duration of the scan and the power output reported by the scanner, Dr. Brenner of the Center for Radiological Research estimated that Mr. Franks had received 21 millisieverts of radiation — even more than a typical test, equal to about 1,050 conventional chest X-rays.
Given the radiation risks, Dr. Ralph Brindis, another cardiologist, said Dr. Hecht had erred. Because Mr. Franks had already taken a nuclear stress test with normal results, he did not need a CT angiogram, said Dr. Brindis, vice president of the American College of Cardiology. And particularly because the scan’s results were benign, he said, Dr. Hecht should not have recommended a follow-up test.
“The biggest problem we have with radiation is that the doses are cumulative and additive,” Dr. Brindis said. “So the concept of doing serial CT testing on asymptomatic patients, I think, is abhorrent. I cannot justify that.”
Dr. Hecht said he sharply disagreed with Dr. Brindis. The scan was appropriate for Mr. Franks, despite his normal results from the nuclear stress test, because of Mr. Franks’s other risk factors for heart disease, including his higher-than-average calcium score, Dr. Hecht said. And he said he recommended a follow-up scan next year so he could see how quickly the plaque in Mr. Franks’s arteries was thickening.
Image via Wikipedia
Resistant hypertension is a common clinical problem faced by both primary care clinicians and specialists. While the exact prevalence of resistant hypertension is unknown, clinical trials suggest that it is not rare, involving perhaps 20% to 30% of study participants. As older age and obesity are 2 of the strongest risk factors for uncontrolled hypertension, the incidence of resistant hypertension will likely increase as the population becomes more elderly and heavier. The prognosis of resistant hypertension is unknown, but cardiovascular risk is undoubtedly increased as patients often have a history of long-standing, severe hypertension complicated by multiple other cardiovascular risk factors such as obesity, sleep apnea, diabetes, and chronic kidney disease. The diagnosis of resistant hypertension requires use of good blood pressure technique to confirm persistently elevated blood pressure levels. Pseudoresistance, including lack of blood pressure control secondary to poor medication adherence or white coat hypertension, must be excluded. Resistant hypertension is almost always multifactorial in etiology. Successful treatment requires identification and reversal of lifestyle factors contributing to treatment resistance; diagnosis and appropriate treatment of secondary causes of hypertension; and use of effective multidrug regimens. As a subgroup, patients with resistant hypertension have not been widely studied. Observational assessments have allowed for identification of demographic and lifestyle characteristics associated with resistant hypertension, and the role of secondary causes of hypertension in promoting treatment resistance is well documented; however, identification of broader mechanisms of treatment resistance is lacking. In particular, attempts to elucidate potential genetic causes of resistant hypertension have been limited. Recommendations for the pharmacological treatment of resistant hypertension remain largely empiric due to the lack of systematic assessments of 3 or 4 drug combinations. Studies of resistant hypertension are limited by the high cardiovascular risk of patients within this subgroup, which generally precludes safe withdrawal of medications; the presence of multiple disease processes (eg, sleep apnea, diabetes, chronic kidney disease, atherosclerotic disease) and their associated medical therapies, which confound interpretation of study results; and the difficulty in enrolling large numbers of study participants. Expanding our understanding of the causes of resistant hypertension and thereby potentially allowing for more effective prevention and/or treatment will be essential to improve the long-term clinical management of this disorder.
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Patients with morbid obesity who also have chronic renal disease (CRD) may improve or stabilize renal function after gastric bypass, according to a study presented here at the American Society for Metabolic & Bariatric Surgery 25th Annual Meeting.[Interesting. Obesity related glomerulopathy is mediated by hyperfiltration, which might theoretically be reversible with gastric bypass.]
Just received this email:
Your slideshow Life Hacks For Doctors has been selected as the 'Slideshow of the Day' on the SlideShare homepage.Nice start to the week. On the home page, Slideshare also highlights other slideshows on Doctors, Medicine, and Web 2.0.
Our editorial team would like to thank you for this awesome creation.
- The SlideShare team
Visit the Efficient MD Wiki at http://wiki.efficientmd.com.
Wikis — collaborative websites — are powerful tools for education. The Efficient MD Wiki is designed to help healthcare professionals and medical students discover clinical pearls, useful resources, life hacks, and strategies to improve the practice of medicine.
Although this Wiki is currently in its infancy, it is growing rapidly and needs your help. Please post your ideas, mnemonics, best practices, tricks, timesavers, presentations, helpful links, or other advice you'd care to share. (Don't worry if your writing is disorganized. Someone will always edit it later.)
While posting anonymously is allowed, if you'd like to have a link to your personal website added to the home page — as our way of saying thanks — please join the wiki and send us a message.
Please see the posting guidelines and disclaimer. The Efficient MD Wiki is an ongoing experiment, and comments are welcome.
Sincerely,
Joshua Schwimmer, MD, FACP, FASN; The Efficient MD Blog (in association with the American College of Physicians); Clinical Instructor in Medicine, Columbia University College of Physicians & Surgeons and Clinical Assistant Professor of Medicine, New York University School of Medicine
Ves Dimov, MD; Clinical Cases and Images; Clinical Assistant Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University
(Also posted on The Efficient MD Blog.)
Lipitor Image via WikipediaThree Vytotin/Zetia reps just came to me and said, "When do you feel comfortable using Zetia? After all, Lipitor titration is a failed step. It only reduces LDL by 6%."
I gently referred them to the PROVE IT trial, asked them to come back when they had positive mortality data, and walked away.
Has anyone else encountered this strategy by the Zetia reps?
Image via WikipediaI'm still puzzling over this article in the New York Times, "Some Diabetics Don't Have What They Thought They Had." The article seems to imply -- and some other news outlets have picked up -- that some children diagnosed with type 1 diabetes mellitus (DM) actually have diabetes insipidus (DI). What the article means to imply, I think, is that some children with type 1 DM actually have maturity onset diabetes of the young (MODY). (I've looked, but I could not find a situation in which you'd ever confuse type 1 DM and DI. In DI, for example, you wouldn't have glucose in the urine.)
Why is this important? Because if the myth propagates through the media that you can easily confuse DI and DM, countless younger adult patients with DM will approach their doctors demanding that they be tested for DI, which will require a lengthy explanation of how the two could not be confused...
On the other hand, I've seen patients with MODY misdiagnosed as having type 1 DM -- and they eventually are able to stop insulin and switch to oral therapy. This is the real message of the NYT article, I think, and it's great when it happens.
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The moral of the story? Do not get injections of silicone in the buttocks by an unlicensed practitioner. Via the MMWR:
Soft-tissue fillers are substances injected to augment or enhance the appearance of lips, breasts, buttocks, or other soft tissues. Previous reports have linked the administration of soft-tissue fillers, usually liquid silicone, by unlicensed practitioners to severe adverse events, including death On December 27, 2007, the North Carolina Division of Public Health (NCDPH) was notified of three cases of renal failure occurring among women who had received cosmetic soft-tissue filler injections at a facility in North Carolina (facility A). This report summarizes the clinical findings for these cases and describes the subsequent public health investigation. All injections were administered by a practitioner with no medical training or supervision (practitioner A). Investigators were not able to identify the substances injected. Although records indicated that the injections contained liquid silicone, this substance has not been associated previously with renal failure. These findings underscore the risks posed by cosmetic injections administered by unlicensed practitioners. Public health officials should be alert for adverse events associated with these injections and take all necessary actions to prevent additional injuries.Image: Wikipedia
Case Reports
Case 1. On December 8, 2007, a District of Columbia woman aged 42 years, who was previously healthy except for a history of anemia, received cosmetic soft-tissue filler injections in her buttocks at facility A. Records specifying the substance injected were unavailable. On December 22, the woman received additional injections at facility A. According to facility records, 300 mL of "dermal silicone/saline solution" were injected into each buttock (600 mL total) during the December 22 visit. The woman experienced headache and vomiting within 30 minutes of these injections and noted that her urine looked like purple blood. She went to an emergency department (ED) in Maryland on December 24 with fatigue, vomiting, and headache and was found to be in acute renal failure, with a serum creatinine level of 4.2 mg/dL (normal: 0.8--1.4 mg/dL). Laboratory investigations, including urine testing for heavy metals, did not reveal a specific etiology. Her serum creatine phosphokinase (CPK) level was 411 U/L on the day of admission (normal: 25--200 U/L). She remained hospitalized for 10 days. Hemodialysis was not required, and her serum creatinine level subsequently returned to normal.
Case 2. On December 8, 2007, a previously healthy Illinois woman aged 26 years received cosmetic soft-tissue filler injections in her buttocks at facility A. Records indicated that she received 500 mL of "25% silicone dermal filler and 75% saline solution" in each buttock (1,000 mL total). She received additional injections at facility A on December 22. Records from December 22 indicate that 400 mL of a "50% concentration of silicone oil dermal filler and saline solution" were injected into each buttock (800 mL total). Within 1 hour of these injections, she experienced headache and nausea and noted that her urine had a burgundy color. She went to an Illinois ED on December 23 with nausea, headache, and fatigue and was found to be in acute renal failure, with a serum creatinine level of 4.0 mg/dL. Serum CPK was 517 U/L on the day of admission. The patient's renal function worsened, and hemodialysis was initiated. A renal biopsy on December 27 revealed severe acute tubular necrosis with cast formation. The casts were not myoglobin or hemoglobin; pathologists were unable to determine their composition, despite the use of specialized stains. No heavy metals were identified in urine specimens, and no other specific etiology was identified. The woman remained in the hospital for 13 days. Hemodialysis was discontinued after 5 weeks, and the woman subsequently regained normal kidney function.
Case 3. A previously healthy Maryland woman aged 26 years received soft-tissue filler injections in her buttocks at facility A on December 8, 2007, and again on December 22. No records were available from either date. The woman developed abdominal pain, lightheadedness, and nausea within 1 hour after the second procedure. She went to an ED on December 26 with fatigue and vomiting and was found to have a serum creatinine level of 11 mg/dL. Hemodialysis was initiated. A renal biopsy on January 11, 2008, demonstrated acute interstitial nephritis with substantial numbers of eosinophils, consistent with a toxic or allergic etiology. Eosinophilia was not found on peripheral blood smears. No heavy metals were identified in urine specimens. She remained in the hospital for 14 days; hemodialysis was discontinued within 1 week after discharge, and her serum creatinine level subsequently returned to normal.