It is always a challenging task to identify the “highest yield” topics for the ABSITE. Everything you study seems important in some way, whether it doubles as useful information for your everyday rounding or is strictly a scenario you run into in an exam setting (see: any question about a pulmonary artery catheter). Below I’ve selected three questions from TrueLearn’s ABSITE 2021 SmartBank for discussion, each of which represents a different interpretation of the term “high yield.”
Question 1: Hypovolemic Shock
Which of the following sets of parameters is consistent with the diagnosis of hypovolemic shock?
A. pulmonary capillary wedge pressure = 6 mm Hg, cardiac output = 1.5 L/min/m2, systemic vascular resistance = 1800 dynes/sec/cm-5, venous O2 saturation = 50%
B. pulmonary capillary wedge pressure = 20 mm Hg, cardiac output = 1.5 L/min/m2, systemic vascular resistance = 1800 dynes/sec/cm-5, venous O2 saturation = 50%
C. pulmonary capillary wedge pressure = 10 mm Hg, cardiac output = 8 L/min/m2, systemic vascular resistance = 400 dynes/sec/cm-5, venous O2 saturation = 80%
D. pulmonary capillary wedge pressure = 6 mm Hg, cardiac output = 1.5 L/min/m2, systemic vascular resistance = 400 dynes/sec/cm-5, venous O2 saturation = 50%
E. pulmonary capillary wedge pressure = 10 mm Hg, cardiac output = 5 L/min/m2, systemic vascular resistance = 1000 dynes/sec/cm-5, venous O2 saturation = 70%
The correct answer is: A
Hypovolemic shock is the most common cause of shock. It occurs as a result of hemorrhage or loss of plasma volume only through extravascular fluid sequestration or gastrointestinal, urinary, and insensible losses. The diagnosis of hypovolemic is easily made when there is an obvious source of volume loss and when overt signs of hemodynamic instability are present.
If the clinical diagnosis is in doubt, then invasive monitoring using a pulmonary artery catheter (PAC) might be helpful. Low pulmonary capillary wedge pressure, depressed cardiac output, elevated systemic vascular resistance, and low venous O2 saturation indicates a hypovolemic state.
Listed below are the normal ranges for the cardiac index, pulmonary capillary wedge pressure, and systemic vascular resistance.
Answer B: Pulmonary capillary wedge pressure = 20 mm Hg, cardiac output = 1.5 L/min/m2, systemic vascular resistance = 1800 dynes/sec/cm-5, and venous O2 saturation = 50% is consistent with cardiogenic shock.
Answer C: Pulmonary capillary wedge pressure = 10 mm Hg, cardiac output = 8 L/min/m2, systemic vascular resistance = 400 dynes/sec/cm-5, and venous O2 saturation = 80% is consistent with septic shock.
Answer D: Pulmonary capillary wedge pressure = 6 mm Hg, cardiac output = 1.5 L/min/m2, systemic vascular resistance = 400 dynes/sec/cm-5, and venous O2 saturation = 50% is consistent with neurogenic shock.
Answer E: Pulmonary capillary wedge pressure = 10 mm Hg, cardiac output = 5 L/min/m2, systemic vascular resistance = 1000, dynes/sec/cm-5, and venous O2 saturation = 70% is consistent with a normal state.
Bottom Line: Low pulmonary capillary wedge pressure, depressed cardiac output, elevated systemic vascular resistance, and low venous O2 saturation indicates a hypovolemic state.
For more information, see:
Pugh A. Chapter 12: Shock. In: The Mont Reid Surgical Handbook. 7th ed. Elsevier; 2018:159-170.
This question is not a particularly difficult one, but it shows up every year in some way or another on the exam. It is featured on the TrueLearn SmartBank this year and I am bringing it up because it is a giant time-sink for many test-takers. I call these questions speedbumps, because they are meant to slow you down. The sheer cumbersome layout and word-bulk of the answer choices makes it easy to get lost in the numbers and takes minutes away from more challenging questions that require your time.
However, you can make these questions work in your favor by memorizing the following chart:
Memorizing this chart allows you to stave off the in-test rationalization and doodling on the whiteboard. Just because you understand the concepts of physiology doesn’t mean you should have to re-enact the mental gymnastics in real-time.
Question 2: Tumor Immunology
A 63-year-old woman is diagnosed with stage IV colorectal cancer. Her medical oncologist wants to add a targeted epidermal growth factor receptor (EGFR) inhibitor. Which of the following genotypes must be confirmed prior to beginning the corresponding therapy?
A. programmed cell death protein 1 (PD-1), wild type; pembrolizumab
B. Kirsten rat sarcoma viral oncogene homolog (KRAS), mutation; panitumumab
C. cytotoxic T-lymphocyte antigen-4 (CTLA-4), mutation; ipilimumab
D. Kirsten rat sarcoma viral oncogene homolog (KRAS), wild type; cetuximab
E. human epidermal growth factor receptor 2 (HER-2), wild type; trastuzumab
The correct answer is: D
It is important to know the targets of major monoclonal antibody therapies. Both cetuximab and panitumumab target and inhibit the epidermal growth factor receptor (EGFR) and are effective in colorectal cancer. However, it has been shown that in patients with a Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation in exon 2, these targeted therapies have poor response rates. Oncologists will confirm that a patient is KRAS wild type prior to initiating cetuximab or panitumumab.
In terms of efficacy, panitumumab has been shown to be non-inferior to cetuximab in a randomized, multicenter, open-label trial (ASPECCT). Panitumumab has been shown to have more favorable outcomes in patients previously treated with anti-vascular endothelial growth factor (VEGF) therapy in a retrospective study.
Answer A: Pembrolizumab is approved for programmed cell death protein 1 (PD-1) blockade in treatment refractory melanoma. There is no genotyping required for use of this therapy.
Answer B: Patients with metastatic colorectal cancer who are KRAS wild type, not KRAS mutated, may be expected to have a response to panitumumab.
Answer C: Ipilimumab targets cytotoxic T-lymphocyte antigen-4 (CTLA-4) in melanoma. There is no mutational status to check for this therapy.
Answer E: Patients with human epidermal growth factor receptor 2 (HER-2) positive breast cancer may benefit from trastuzumab.
Bottom Line: Patients with colorectal cancer who are being considered for epidermal growth factor receptor (EGFR) targeted therapy should be tested for Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations as there is compelling evidence that only patients with wild-type genotypes benefit from cetuximab and panitumumab.
For more information, see:
Hayashi K, et al. Panitumumab provides better survival outcomes compared to cetuximab for metastatic colorectal cancer patients treated with prior bevacizumab within 6 months. Oncology. 2019;96(3):132-139.
This is a personal favorite of mine, which I refer to as my “buy-low, high-yield” question. As targeted EGFR inhibitors move to the first-line of colorectal cancer chemotherapy and multidisciplinary care becomes a staple of both patient care and resident education, this question is coming up more and more. It is only fitting that it now makes its way onto the ABSITE.
KRAS is downstream of the EGFR protein, thereby making EGFR inhibitors ineffective for patients who have a constitutively active KRAS protein (the most common result of mutation). Knowing this will come in handy, both on the ABSITE and for your multidisciplinary colorectal conferences.
Question 3: Repair of Ureteral Injury
A 23-year-old man presents after sustaining a gunshot wound to the abdomen. The patient is taken to the operating room for exploration. He is found to be hemorrhaging from a splenic laceration, which is managed with a splenectomy. Hemostasis is achieved and upon further exploration, the patient is found also to have a transecting injury to the lower third of the left ureter. Which of the following is the most appropriate strategy for repair of the ureteral injury?
A. Foley catheter placement and observation
B. primary ureteroureterostomy over stent
C. reimplantation of the proximal ureter into bladder
D. renal autotransplantation
Injuries to the ureter can be approached by dividing the ureter into thirds. Lower ureter injuries are commonly managed with reimplantation of the proximal ureter into the bladder. If the ureter has been ligated without transection, repair can be attempted with primary ureteroureterostomy over a stent.
Answer A: Foley catheter placement and observation is not indicated due to morbidity from urinoma development.
Answer B: Proximal ureteral injuries are typically managed with primary ureteroureterostomy. If there is significant ureteral loss, a segment of ileum may be used for ureteral replacement.
Answer D: Autotransplantation is rarely performed for ureteral injury and is not advisable in trauma situations due to increased operative times.
Answer E: Injuries to the midureter can be managed by primary ureteroureterostomy or transureteroureterostomy. Distal mobilization of the ureter provides additional length, but it is important to avoid devascularizing the ureter.
Bottom Line: Traumatic distal ureteral transaction is best managed with reimplantation of the proximal ureter into the bladder.
For more information, see:
McAninch JW, Master V. Chapter 180: Genitourinary tract trauma. In: Fischer J, ed. Fischer’s Mastery of Surgery. 7th ed. Wolters Kluwer; 2018.
To conclude the series, I call this one my “do as I say, not as I do” question. We’ve all been in the OR for ureteral transections, so we all know they can come in a variety of flavors: high, low, left, right, traumatic, electrothermal, stapled… you name it, someone has done it. The one thing I always hear from residents when discussing this question is: “but when this happened, we did ______.” This is understandable, because in the OR, we do what we think has the highest chance of succeeding for that particular patient and that particular injury.
But alas, the ABSITE demands order. In this question, note that the injury is traumatic, which leads us to believe that the defect may be larger and the transected ends less “clean” than if you, say, came across it with the old William T. (“Bovie”). The safe answer in a traumatic transection in the lower-third is reimplantation, even if your Urology attending does a mean Boari flap.
Thanks for reading! I hope you found these questions helpful. If nothing else, I hope you take away the following three key points:
1. Having a shortcut to the right answer isn’t cheating, it’s strategizing. Boiling down concepts in physiology to simple relationships, as we saw in question #1, can save you a lot of time.
2. Cancer care is multi-disciplinary, which makes medical oncology, radiation oncology, and immuno-oncology fair game for the ABSITE. Keep an eye out for questions on checkpoint inhibitors and small molecule inhibitors (e.g., anti-PD1, anti-PDL1 anti-BRAF/MEK) that have attained highly publicized FDA approvals in the last 10 years.
3. When it comes to the ABSITE, go with the textbook. It hurts a little sometimes, but you’ll be thankful for it when you get your score back. Situations where you may find yourself splitting hairs between textbook and clinical management include ureteral injuries, bowel resections, drain placement/management, and minimally invasive versus open approaches.
For hundreds of other high-yield ABSITE practice questions, along with authoritative answer explanations, illustrative figures and tables, supporting references, focused Bottom Line statements, and test-taking tips, check out TrueLearn’s ABSITE 2021 SmartBank.
The author would like to acknowledge Ben Shragge for contributions made to this post.