The following interest group meetings have been arranged to give you the opportunity to meet and talk with the program directors and fellows within UCSD’s program. All are welcome to attend! We encourage you to attend as many meetings as you’d like! Feel free to reach out to the program directors or chief residents, if you have any questions! We will continue to update this post as meetings are arranged.
This afternoon was full of great kidney talk! Our senior residents started out the afternoon working through cases of both nephrotic and nephritic syndromes with Dr. Cunard. Once our interns joined the group, we moved on to a discussion of CKD management with Dr. Woodell. He did note the current controversy surrounding the role of Race in calculating eGFR – more to come next week! Finally, Dr. Carreira from Family Medicine/Psych, taught us about healthcare for patients experiencing homelessness and about the resources available in San Diego. She reminded us that “just being homeless is trauma,” and we took time to share our own stories of the barriers we see our patients face when accessing healthcare. The best thing we can do is be human and connect with this population.
UCSD is hosting a virtual event on Wednesday, September 29th at 5:30pm featuring health science experts working at the front line of the COVID-19 pandemic. They will be giving an in-depth look into the COVID-19 vaccine and variant situation. If you are interested, you can register for the event here!
This morning our residents reviewed a case of an older female who presented after 3 weeks of shortness of breath and 2 weeks of atypical chest pain. Reviewing her medical history we learned she has a long history of hypertension and also multiple myeloma and was currently on steroid therapy and carfilzomib. We then focused on her exam and found the patient to be volume overloaded on exam with elevated JVP, crackles, and lower extremity edema.
We then discussed our initial differential which included ACS, PE, pericarditis, myocarditis, heart failure, aortic dissection, and PHTN. Residents then came up with next steps: EKG, CXR, cardiac markers, BNPP, and echocardiogram. With the help of our expert discussant, the UCSD IM alum Dr. Gary Ma, we read the EKG and CXR. The patient then got an echocardiogram and with the help of Dr. Ma we reviewed the imaging ourselves and found that the patient had an EF of 20%!! We reviewed that the most common etiology of new systolic dysfunction is ischemia! We then debated the pros and cons of CTA Coronary vs MIBI vs Cardiac catheterization. Our patient ultimately underwent cardiac catheterization and had normal vessels without significant blockages. Tune in next week for part 2 where we evaluate for non-ischemic causes of systolic heart failure.
This morning at Hillcrest, we talked about a patient who was recently admitted with DKA. He was sent to the ED by his wife for hyperglycemia, generalized weakness, nausea, epigastric pain, and diarrhea. He also endorsed recent polyuria and polydipsia. He had a history of type 2 diabetes “for many years,” which was currently being treated with insulin. Our audience appropriately asked questions about potential underlying precipitants, including MI, CVA, sepsis, pancreatitis, medication non-adherence, new medications (SGLT-2 inhibitors, glucocorticoids, thiazides, sympathomimetics), and undiagnosed or inappropriately treated DM1. This did not reveal a clear precipitant, though.
On exam, he was afebrile, hypotensive, and with a BMI of 26. He had dry mucus membranes, bilateral lower extremity edema, and no localizing signs of infection. We then broke up into teams to analyze his lab abnormalities. We specifically highlighted:
Leukocytosis – this may be reactive or a clue to an underlying precipitant of DKA. Team 1 appropriately recommended an infectious workup.
Hyperosmolar hyponatremia – Team 2 explained that this was due to the higher serum tonicity caused by marked hyperglycemia, which pulls water into the intravascular space and thereby dilutes the serum sodium concentration. We discussed calculations for serum osm and corrected Na.
Hyperkalemia – though the patient’s initial serum K was elevated, Team 3 appropriately identified that he was likely total body deficient in K. With treatment, we expect that the serum K will fall, due to both insulin stimulation of K transport into cells and improvement in the metabolic acidosis (which allows H to move out of cells and K to move into cells).
AGMA with insufficient respiratory compensation (concurrent respiratory acidosis) and a NAGMA – Teams 4 & 5 tackled this patient’s acid/base status. They appropriately classified his primary disorder as an elevated anion-gap metabolic acidosis. They then evaluated his respiratory compensation. Because the PCO2 was not quite as low as one would expect for appropriate compensation, he was deemed to have a concurrent respiratory acidosis. Finally, they used delta/delta to evaluate for a coexistent NAGMA. Because his delta/delta was <1, he was confirmed to also have a NAGMA, likely due to diarrhea and/or renal dysfunction.
We then reviewed the basic principles of DKA management – IV fluids, insulin, potassium, and treatment of any underlying precipitants! We highlighted the awesome resources available to us here at Hillcrest, including the Medication Resources tab on Pulse and the DKA/HHS order set in Epic.
Finally, we discussed the consideration for DM1/LADA in this patient. Because of his near-normal BMI, relatively low insulin requirements, and presentation with DKA, his care team questioned whether he actually had type 1 diabetes, rather than type 2. The patient was found to have a positive GAD65 Ab, which further supported the diagnosis of DM1/LADA. He was discharged home on insulin and will follow up with his PCP and Endocrinology in clinic.
When evaluating a patient with DKA/HHS, investigate for both symptoms of the DKA/HHS itself AND signs/symptoms of potential underlying precipitants (MI, CVA, sepsis, pancreatitis, medication non-adherence, new medications like steroids and SGLT-2 inhibitors, and undiagnosed or inappropriately treated DM1).
Recognize that the hyponatremia seen in DKA/HHS is at least in part due to water shifts in response to the hyperosmolar state. Correct for this with the following equation:
Recognize that the perceived hyperkalemia in DKA/HHS is due to shifts in K from the intracellular to the extracellular space in the setting of acidosis and insulin deficiency. With insulin treatment, the potassium will shift back into the cells and serum K will fall. Aggressively monitor and replete K in these patients!
Corrected Na = Measured Na + 2 x [(Measured glucose – 100) / 100]
Use a systematic approach to acid/base disorders. Remember to characterize the primary disorder, evaluate for appropriate vs inappropriate compensation, and check the delta/delta.
Remember the basic principles of DKA management – IV fluids, insulin, potassium, and treatment of any underlying precipitants. A VERY helpful management flowchart can be found under “Tools & Resources –> Medication Resources –> Glucose Management –> DKA & HHS Management” on Pulse (or in the intern handbook)!
Do NOT stop the insulin drip until the anion gap has normalized on two repeat BMPs. If a patient with DKA has a BG < 250 but they still have an elevated anion gap, CONTINUE the insulin drip to treat the ongoing ketoacidosis and ADD dextrose to their continuous fluids to prevent hypoglycemia.
Medical Spanish Words of the Day: diabetes = la diabetes; pancreas = el páncreas
Today Dr. Sandip Patel taught us about using immunotherapy in lung cancer!
Here are some key pearls:
Diagnosis: the initial workup for lung cancer (and many other cancers) includes imaging (CT CAP or PET, sometimes CNS imaging), pathologic diagnosis and stage (biopsy of the highest stage non bone lesion), and molecular diagnosis (cfDNA or tissue based multiplex for tumor markers)
In NSCLC patients benefit from chemotherapy + immunotherapy or targeted therapy
Immunotherapy adverse events: include pneumonitis, colitis, adrenal insufficiency, rash, hepatitis. Treatment of these adverse events often includes steroids with a taper over at least 3-4 weeks.
For Jacob’s Report today we discussed the case of a 70-year-old gentleman with a history of Waldenström Macroglobulinemia who presented to clinic for chronic shortness of breath. We followed his course over the next 90 days as he was worked up for SOB. Over the course of multiple clinic visits, ED visits, and hospitalizations, he was found to have Afib with RVR, a subdural hematoma and hyperviscosity as a result of progression of his Waldenström Macroglobulinemia. He was ultimately transferred to Jacobs where he underwent plasmapharesis and re-initiation of chemotherapy for his WM.
We were lucky to be joined by one of our oncologists, Dr. Tiffany Tanaka, who helped us along the way! She highlighted some key points about Waldenström Macroglobulinemia:
WM is an indolent B-cell lymphoma of clonal lymphoplasmacytic cells that secrete clonal IgM into the blood
IgM is the largest of the immunoglobulins, and it can span RBCs resulting in aggregations (rouleaux) as seen in this patient’s blood smear shown above
It is rare with only about 5,000 new cases/year in the U.S.
It primarily involves the bone marrow but can involve the spleen and LNs
Hyperviscosity syndrome from high levels of IgM can occur resulting in diverse CNS symptoms
Symptomatic hyperviscosity syndrome is a medical emergency requiring plasmapheresis to remove excess IgM
Ibrutinib (a tyrosine kinase inhibitor) is approved for treatment of WM
It has many possible side effects include cytopenias, atrial fibrillation (thought to be the cause of this patients Afib), and dyspnea
Thank you so much to Dr. Tanaka for joining us today for this interesting case!
Today’s Grand Rounds were presented by Tony Reid, MD, PhD. Dr. Reid reviewed many of his interesting oncology research studies on reversing tumor immunosuppression through the use of oncolytic viruses. His research focuses on AdAPT-001, an oncolytic virus that is injected directly into tumors. Dr. Reid developed this “viral vector” off of an adenovirus after decades of research. The oncolytic virus works by infecting and replicating inside cancer cells resulting in cancer cell lysis while leaving healthy cells undamaged.
The AdAPT-001 virus builds off of the Onyx-015 virus to improve tumor-selectivity, oncolytic potency, and add TGF-beta trap transgene expression. This virus results in oncolysis independent of tumor oncogenes such as Kras mutations. It also results in activation of the immune response by turning immunologically “cold tumors” to “hot tumors” and induction of memory response to tumors.
AdAPT-001 has now entered Phase 1 of clinical testing.
Thank you to Dr. Reid for joining us today and discussing your amazing research with us!
One of our very own third-year residents, Aram Namavar, has created the first ever Society of Hospital Medicine San Diego Chapter Virtual Research, Innovations, and Clinical Vignettes (RIV) Poster Competition, and it is now open for abstract submission. We encourage you to submit an abstract! Details below: — The SHM San Diego Chapter is hosting their first ever Virtual RIV Poster Competition for trainees. Abstract submissions are now open and will close on October 31, 2021 at 11:59 PM PST. One overall abstract winner will be announced on November 14, 2021 and will be granted automatic acceptance to SHM Converge 2022 in Nashville, TN. Please see the attached flyer for more details. Abstract submission link with example of abstract submission from the 2020 SHM National Meeting can be found here: https://docs.google.com/forms/d/e/1FAIpQLSezWHwkSzjKYBZt16rqm32O9Q6uQtFLQhnPVfSWs8VIHLrB4A/viewform?usp=sf_link.
Today Dr. Beben took time to teach us about AKI! He started by providing a framework for evaluating AKI. Here are some key learning points:
Urine electrolytes can be helpful, but remember that FENa and FEUrea have limitations!
Similarly, urine microscopy can be helpful, though not always
Other workup includes serologic workup, ultrasound (formal or POCUS), and biopsy
Obstructive uropathy: caused by high tubular and glomerular pressure. This can lead to fibrosis and ultimately tubular atrophy and interstitial fibrosis (usually after months of obstruction)
Infection related GN: it’s most common with staph (strep is most common association in children, and it most common WITH infection instead of after the infection. This is an immune complex mediated injury, so complement levels will be lower and UA will show hematuria.
Prerenal AKI: remember that kidney recovers quickly with fluid resuscitation. If the creatinine doesn’t improve quickly look for other causes of AKI
Contrast induced nephropathy: a controversial topic (we discussed this at journal club last week). Remember that the FENa is paradoxically low in this situation (even though tubules are damaged)