Multiprofessional Critical Care Review: Adult 2024 (MCCRCA24ON)-Board Questions: Kidney, Babies, Blood, and Endocrine Emergencies

Board Questions: Kidney, Babies, Blood, and Endocrine Emergencies

Video Transcription

Okay, let's start with the first border view questions, an endocrine question.  A 34-year-old man with Cushing syndrome is admitted to the ICU from the emergency department with two days of worsening altered mental status  with psychosis, weakness, and fatigue. He has his tachycardic to the 180s, hypertensive, 195 over 110.  Extremely hyperglycemic in the 500s, hypokalemic, and his plasma ACTH is greater than 15. Serum cortisol greater than 75, greater than 20 is usually abnormal,  and his urine-free cortisol is greater than 300 micrograms in 24 hours. The endocrine team recommends medical treatment to reduce the cortisol levels  before surgery for a known adrenocortical carcinoma. Metiropone is started with no effect after six hours of escalating dosage, and his mental status continues to worsen.  He's intubated for airway protection. Here's your question. Which of the following is the most appropriate next intervention to rapidly reduce cortisol concentrations?  So medical management of somebody with Cushing syndrome before surgery to take care of the adrenal carcinoma.  What would be the best medical approach? And here are your choices.  Tomodate,  Lidocaine, Ketoconazole, or Plasma Exchange.  You can select your answers now.  Okay.  Everybody good?  Okay. Whoa. All right. Interesting. So Plasma Exchange was selected by three quarters of you.  So the correct answer is actually Etomidine.  Can you hear me better?  You can turn it on. I don't think you're.  Oh, it's falling down.  How's this? Perfect. So the correct answer is actually Etomidine. So this is a patient that has a very high cortisol level  related to his Cushing syndrome, and the idea here is to try to reduce the cortisol levels. All of these therapies have been tested. Plasma Exchange, however, has not been shown  to be an effective strategy to try to reduce cortisol levels. The other three are drugs,  and they all act in reducing cortisol levels, and the way they do that is they block the conversion of deoxycortisol to cortisol. So the reason Etomidate is the answer  is because Etomidate acts more quickly in reducing cortisol levels than Ketoconazole and Mitotane. So Ketoconazole, Mitotane, and Etomidate, they all act similarly,  but oral treatments take time to work, and so Etomidate, which is used as an anesthesia induction agent, we use it for sedation, for rapid sequence intubations,  is the ideal choice here because it acts more rapidly,  and this is a patient who's extremely clinically symptomatic and needs to have those cortisol levels brought down as quickly as possible  to reduce some of the clinical signs and symptoms. So the correct answer here is Etomidate.  It's an IV infusion, and we require ICU admission, typically central line administration, ICU monitoring.  And here's your short rationale. Etomidate is an IV treatment used if initial measures fail to reduce cortisol. Again, comparing it to Ketoconazole,  it inhibits 11-beta-hydroxylase more potently. It's highly effective. It reduces cortisol concentrations within a few hours. Oral agents just take too long to work.  Plasma exchange has not been shown to be effective, has not been shown to be effective. And although Mitotane can decrease cortisol levels, again, it doesn't act right away,  and it's very specific for treating patients with adrenal cancer specifically. It's almost like a chemo agent for adrenal cancer. It does drop cortisol levels,  but not as fast as you might get with Etomidate. So for the critical care boards, the correct answer here is Etomidate infusion.  So this is a concern, as you know, from the studies that use steroids for septic shock patients. It was somewhat clouded by some patients that got Etomidate, and we know that  that can suppress cortisol levels, and maybe some of those patients might have had  some noise based on the fact that they got Etomidate for intubation. But it just turns out that if you're just giving one intubation, you're not getting  if you're just giving one dose of Etomidate, it's not so much of an issue in terms of adrenal suppression.  So just to remind everybody, renal, metabolic, and endocrine questions, at least for those taking the ABIM Internal Medicine Boards, they comprise about 15% of the questions.  So I think for the endocrine section, questions on adrenal insufficiency,  glucose control, and probably Cushing's might be the types of questions you might anticipate for the boards.  It's a standard dose, an IB infusion. A little bit lower than what you might do for somebody that requires sedation. You don't need as much.  Okay, we'll move on to the next question.  Dr. Patel, can you hear me okay? So this is a propofol infusion syndrome question, and it's asking which of the following characteristics  besides metabolic acidosis is comprised of the syndrome itself. So the options are A, hypoglycemia, coagulopathy, endopathic encephalopathy, B, rhabdomyolysis,  myocardial dysfunction, and renal insufficiency, C, hypotension, cardiac dysrhythmias, and status epilepticus, and D, rhabdomyolysis, elevated temperature, and muscle rigidity  are your options. Go ahead and select your answer.  Okay, looks like the vast majority rhabdomyolysis, myocardial dysfunction, and renal insufficiency. And that would be the correct answer.  So you can have changes in at least mental status, but a lot of that it's of course clouded by having a continuous infusion as a sedative, which is what is needed for the patient.  But kind of the hallmark tends to be more related to a mitochondrial and free fatty acid metabolism that's dysfunctional.  And so most of the time what you'll end up finding is a lactic acidosis, elevated triglycerides due to the free fatty acid synthesis that's inhibited.  And then also it'll precipitate, unfortunately as it progresses, to cardiac dysrhythmias. So that could be observed as well.  The arrhythmias may or may not be always observed, but one of the things that has been demonstrated  and shown, and the doses that tend to have this phenomenon tend to be much higher. So if you're kind of in the practice, if you're in fusion pumps, it's usually something the  nurse or maybe a resident intern will alert you of that they've reached a quote upper limit. And most of the time the infusion pumps are set up in mics per kilo per minute.  And that number from the research tends to be right around 67 to 70 mics per kilo per minute in patient populations. It is a little bit more evident in pediatrics.  So the pediatric population is kind of a caveat for those that do or may even interact with the pediatric population more pronounced.  But in adults, it tends to be a lot more duration and dose specific. So at that dose and then generally beyond the 96 hours or four days is when you can  kind of come across this phenomenon.  Any questions on propofol-related infusion syndrome?  The other answers highlight, especially the last one with elevated temperature and muscle rigidity. Those would be kind of things to be ruled out.  So for example, malignant hyperthermia, especially if it's in an immediate timeframe right after  intubation would be something to look for, especially if succinylcholine or if you're getting a patient from the operating room that may have been exposed very, very recently  to anesthetic gas. The others as far as that can be seen, there was one with liver dysfunction as well.  And again, as I had mentioned, you could have acidosis that's present, of course, with liver dysfunction.  But the kind of other hallmark signs, for example, the myocardial dysfunction and the free fatty acid metabolism that's inhibited won't be as present with the other options.  And here are your references.  Our next question is a 22-year-old man who undergoes a resection of small bowel, 100 centimeters, because of mesenteric ischemia. Parenteral nutrition is discontinued.  Enteral nutrition is started. He becomes confused with slurred speech, but is normal glycemic. The initial workup reveals anion gap metabolic acidosis.  Which of the following is the most likely cause of this patient's acidosis? Is it A, ketoacidosis, B, D-lactate, C, pyroglutamic acid, or D, selenium deficiency?  So, more than 50% chose D-lactate, which is the right answer for this question. Essentially, looking at the four options, you've got ketoacidosis.  So this patient, just by looking at it, the way the question is written, starvation ketosis  would definitely be a possibility, but starvation ketosis should not cause neurological changes. D-lactate is essentially a sign of short bowel syndrome.  D-lactate is produced by the gram-positive colonic flora, particularly if a high glycemic load is delivered to the colon, which would be a case in this situation because of the  resection anastomosis. D-lactate is absorbed into the systemic circulation and is slowly metabolized in humans.  Typical presentation is ethanol intoxication and anion-gap metabolic acidosis. D-lactate is not identified in conventional L-lactate assays.  The other two options, the pyroglutamic acid, it's one of the congenital mitochondrial disorders and then I think selenium deficiency is probably a distractor in this case.  Some of the references, an 18-year-old girl with a history of depression is admitted to the intensive care unit after an apparent suicide attempt where she ingested 100 tablets  of naproxen, 220 milligrams. She's intubated, has a very limited neurological exam. In the past 24 hours, she has had approximately 12 mils per kg per hour of urine output and  her serum lab results are as follows. Sodium of 150, potassium of 3.1, chloride of 104, bicarb of 16, BUN 45, creatinine 1.8,  phosphorus 126, phosphorus 4.5, arterial pH of 7.2, ionized calcium of 1.38, urinalysis is a pH of 7.5, urine sodium of 30, urine creatinine of 72.  The question essentially is which of the following best explains the patient's metabolic acidosis?  RTA type 1, RTA type 2, polyuric, acute kidney injury, and pre-renal azotemia.  Yes.  Go back to the options.  Let's go to our answers. A nice split between all four options. Let's go through, I'll go through the discussion then we'll circle back to the question. The answer is RTA type 1.  RTA type 1 is your distal renal tubular acidosis. We go back to the question. First of all, again, not likely pre-renal because the patient is otherwise stable and  this is an acute event and there is no reason for us to clinically imagine that this patient has not been drinking adequately. It's an 18-year-old girl, apparent suicide attempt.  The naproxen is known to cause or your Cox inhibitors are known to cause renal tubular acidosis. If we fast forward all the way down to the urine pH, urine pH of 7.5, so our kidneys  do acidosis at two places. One is the loop of Henle and the other is the convoluted tubules.  If the problem is in the loop of Henle, your distal tubules are still intact to cause some amount of acidosis. That will reduce your urine pH.  If your distal tubules are problematic, your loop of Henle can cause the acidosis, but because the distal tubules are not working, the urine will again become alkaline.  So when your urine is alkaline, the problem is distal and when the problem is distal, it's RTA 1.  So just a quick way of remembering it, you go into the description for this. Toxic ingestions with direct nephrotoxins such as the NSAIDs can lead to acute interstitial  injury, which manifests with polyuria and acidosis. RTAs can result from such injuries. A patient does have a normal and iron gap and hence it's an RTA, evidence from high  urine pH and low serum bicarb and potassium levels. While there may be some prerenal azotemia, this would not lead to laboratory findings the way they are demonstrated.  In distal RTA, the acidification of urine in the distal tubule by hydrogen ion excretion is not functional, resulting in accumulation of serum hydrogen ions and alkaline.  Go ahead.  Right, so NAND gap is 30 here.  Good catch. I think we will need to sort out the sodium-sodium level in this question. Yeah, I think this sodium might have been a little bit lower.  I think this might have been a typo, because I can see the chloride and the bicarb is 120, and from 150, that would mean the gap is 30. It should have been more of 130.  I think probably it was around 130. Okay. We'll take note of that. Thank you.  So proximal RTA, as I earlier said, with impaired bicarb absorption. But in these patients, the urine pH is generally less than 7, because the distal acidosis is working.  Hypokalemia is common in both. Polyuria can occur after ingestion. And this patient has AKI. This is insufficient to explain the acidosis.  Okay. We'll try to speed up to get through all the questions. A 32-year-old man admitted to the ICU following a traumatic brain injury,  necessitating invasive cerebral monitoring, intubation, ventilation. He has a witnessed GTC seizure. An anti-seizure medication is commenced.  During evaluation, his blood glucose is elevated to 260, and an insulin drip is started. Question for you.  Based on the current recommendations of intensive insulin therapy for glucose control,  which of the following characterizes the most appropriate course regarding insulin therapy in this patient? If you could select your answers.  Okay, 71% of the group got the correct answer. As you know, in the early 2000, there was this landmark study that suggested that intensive insulin therapy with tight control,  70 to 110 milligrams per deciliter, led to an improved outcome in a surgical ICU population. But in the mid 2000s, 2006, another study showing in a medical ICU population  that there was no benefit to intensive insulin therapy for medically critically ill patients, but only a higher incidence of hypoglycemic events.  In the neurocritical care setting, there is literature to support  certainly avoiding hyperglycemia, but the current recommendations are to treat glucose levels, to try to maintain them more in the 140 to 180 milligrams per deciliter range.  And that is also the recommendations from the surviving sepsis guidelines. So we've gone away from very tight control, but on the other side,  not dismissing elevated glucose levels above 200. So insulin therapy, choice A is incorrect.  Choice C, again, is also incorrect.  Loose control is actually harmful in neurocritical care patients because of that U-shaped curve that they have. So the correct answer here is intensive insulin therapy  may lead to more hypoglycemic events, but in the neurocritical care patient population, hyperglycemia should be avoided. And the suggestions, even for septic patients,  is to try to maintain a goal somewhere between 140 to 180 milligrams per deciliter. And these are your references over here.  Next question, a 62-year-old woman with CAD and hyperlipidemia is admitted with MRSA bacteremia from a skin infection. She's lethargic, tachypneic, hypotensive, tachycardic.  She's volume resuscitated. A central line is placed. Vasopressors are started. They're titrated quickly. Six hours later, she's on near maximal doses of two vasopressor agents.  Question for you, under which of the following circumstances should IV hydrocortisone be appropriate in this patient? You could select your answers.  Pretty much, great, everybody got it.  The correct answer is hydrocortisone, 200 milligrams a day, either by continuous infusion or 50 milligrams IVQ-6, is recommended for septic shock patients  who are refractory to fluid and require vasopressor therapy to maintain their mean arterial pressure. We no longer need to do the ACTH-TIM test  to decide who gets hydrocortisone therapy. We don't have a good way of diagnosing this secondary or what we call relative adrenal insufficiency,  which has a new acronym, as you know, critical illness-related corticosteroid insufficiency, or CIRSI, but traditionally, clinicians use a cortisol level below 10,  random, or a failure to respond to the ACTH-TIM test, but we no longer need to do any testing if we are seeing a patient who's in septic shock who requires double pressors,  despite fluid resuscitation, to maintain a blood pressure, and free cortisol levels can be checked. However, they are cumbersome to do  and not generally advocated anymore for clinical practice.  The rationale for this question is very extensive, but you can just read it at your leisure,  but I pretty much went over the high points for the question, and all of you got it correctly, so we'll move on to the next question.  72-year-old woman without significant medical history is admitted with UTI and septic shock. She requires resuscitation and norepinephrine. To prevent acute kidney injury,  which of the following interventions is most indicated? Is it A, normalized mixed venous oxygen saturation,  B, continue resuscitating the patient with lactated ringers, C, titrate vasopressors to a mean arterial pressure of 90, D, add inotropes to get a cardiac index  of four and a half liters per minute per meter square, or E, place a pulmonary artery cateter to guide hemodynamic goals?  Can you go back to the question one more time, sorry.  UTI, septic shock, requires resuscitation and norepinephrine.  The question is, which of the following interventions is most indicated to prevent acute kidney injury?  90% of you got this correct. I'm OK. This should be OK. So as we discussed earlier, there is old literature that has looked at increasing your MAP goals to improve kidney function.  Those goals are still in the 65 to 75 to 80 range. They're not all the way up to 90. The analysis that has been done to look at the renal function  or prevention of AKI has not shown significant benefit of improving the MAP to improve the AKI incidence. And actually, it's a really long description.  But if you go all the way down to the lower middle part, titration of vasopressors to a MAP of 85 mmHg versus 65 mmHg has been tested in two small clinical trials  using norepinephrine. In both studies, higher MAP was associated with increased cardiac output, but no difference in the urine output or creatinine clearance.  In an earlier investigation, the rate of AKI was not decreased by normalization of mixed venous oxygen saturations or by increasing the oxygen delivery to supernormal levels.  So fluids are still the answer. And here are your references.  OK, another renal question. An 85-year-old patient presents to the ICU three days after hip replacement with severe pneumonia and respiratory failure.  He's adequately volume resuscitated. Baseline creatinine is 1.3. It's now 3.6. And his BUN has increased to 86. He's not vasopressor dependent.  His potassium and CO2 levels are normal. He gets boluses of IV furosemide. And his respiratory status is slowly improving. Tube feeds are started two days after ICU admission.  His creatinine is 5.7. BUN is now 115. Potassium, 5.1. CO2, 21. He's making 1,500 urine per day. His family wants to pursue renal replacement therapy.  Which of the following statements is correct? A, if the patient has been started on renal replacement therapy on admission to the ICU, his chances of survival would be higher.  B, continuing diuresis on hospital day 5, ICU day 2, instead of starting RRT, will improve his chances of successful intubation. C, delaying renal replacement therapy  will decrease his risk for dialysis catheter-related central line bloodstream infection. Or D, delaying renal replacement therapy until his BUN hits greater than 140  may be associated with higher mortality.  So if you remember the big slide that I had with multiple renal studies that have looked at the timing of renal replacement therapy, the answer here is D.  You can go to the next part. So this is essentially, so if you remember, we looked at the START-AKI study. They actually went ahead and did the next study, which  is called the AKIKI-2 study, which looked at the delayed group. And in the delayed group, they did a further subgroup analysis where they looked at a BUN level as being an indicator  for initiating dialysis. And in that subgroup analysis, or in that analysis, they essentially identified that once your BUN hits a particular level and you go above that,  at that point in time, those patients were associated with higher mortality. The biggest critique for that study has been that they used BUN as an isolated criteria.  And if you go back to the chunk of this question, if you look at the other five things, this patient obviously has a good long-term outcome. This is all very acute.  85 years old, understandable. But otherwise, without any descriptions, has no other comorbidities that are listed. When you look at the trend of the BUN and creatinine  in this patient, 1.3 is baseline, 3.6. And in two days, it's gone up to 5.7. When you look at the trajectory of the disease,  you look at the trajectory of BUN, this is not looking good. The patient is in a polyureic AKI phase. You obviously would rely on your nephrologist to make the final assessment.  But when your numbers are reaching that high, the evidence suggests that you can initiate CVVH. And it is associated with improved mortality if your BUN hits a particular threshold.  That threshold is a variable. The study did not define 140 as the threshold at that point. But again, I think within this question, that is the threshold.  Okay, next question. 26-year-old man with history of opioid abuse is found unresponsive by family members at home. It's unknown how long he was unconscious  during ambulance transport. Naloxone is administered with rapid return of normal mental status. He reports injecting heroin the night before,  but has no recollection of overnight events. You can see a normal hemogram, normal white count. He has acute kidney injury with creatinine of 2.6, potassium of 5.8.  His CK is elevated at 15,000. His dipstick in the urine is positive for blood. And microscopy reveals only granular cast. He is admitted to the ICU.  And the question is, which of the following is the most appropriate management of his acute kidney injury? Said A, give furosemide. B, mannitol. C, pentoxifilin.  D, aggressive hydration with isotonic crystalloid. Or E, alkalize the urine with sodium bicarbonate.  Yep, that is the correct answer. 90% people got the correct answer. The other two things that are utilized for rhabdomyolysis  associated AKI, you can use furosemide, but it is only recommended after your volume overloaded the patient. And the  alkalization of urine with sodium bicarbonate is recommended, but it's only recommended after your first two things of fluid and Lasix has failed. So the answer in this situation is  aggressive hydration with isotonic.  And this is your rationale here and some references.  Okay, let's start going to some toxicology questions. A 24 year old man is evaluated on a New Year's Eve for mental status change.  It's an elevated creatinine, normal BUN, normal pH, anion gap,  normal no blood alcohol concentration. His osmolar gap is increased and he has an increased acetone level.  Ingestion of which of the following types of alcohol is most likely causing this patient's presentation? Is it isopropyl alcohol,  B, methanol, C, ethylene glycol, or D, ethanol?  You can always expect an alcohol question on the IM critical care boards. They love these questions.  Dr. Patel. So the majority selected isopropyl alcohol, which is the correct answer.  And we can go through each one of these scenarios.  What ends up happening is your  osmolar gap will be elevated with the alcohols, but your anion gap  predominantly would not necessarily be with the isopropyl or the ethanol.  What's actually kind of interesting is that the isopropyl alcohol metabolized to acetone, so this is one that  unfortunately is also, fortunately or unfortunately depending on your perspective, because if you see the admissions, but is at home and it's in nail polish remover.  So sometimes you'll see this a little bit more in kids, but in pediatric patients if they get their hands on it,  it's something that's ingested, but it's metabolized, which the isopropyl is, but the acetone is a common  product still at home. The  methanol, which was also an option,  is also predominant in different areas depending on, you know, where you're serving your population. But one area where it's been a little bit more, we found increased admissions,  and it comes up maybe just two or three times a year, actually is in morticians.  So in mortuaries, right, their predominant preservative is formaldehyde, and so what we could see sometimes are similarities  since the methanol is metabolized forward to that, and you could see a lot of similarities with that particular agent.  But one of the hallmark ones for that one, at least for methanol, tends to be more related to ophthalmology, so blindness, and then liver pain or  abdominal pain, rather, and abnormalities in the liver enzymes. The others, as far as like intoxications,  I would agree, it's almost one that everybody's always come back and said, yeah, there was a question on alcohols,  but the key is also looking at the history, and I think one of the other ones at the bottom was ethylene glycol.  One of the hallmark findings with that one is  oxalate crystals in the urine, and so that generally is depicted either in the history or  in one of the findings. So if you see that in the question, that's kind of your hint that ethylene glycol is present.  Great, thank you.  And here are your references.  56-year-old man is brought to the ED, found confused, agitated, having a seizure, witness seizure, following 24 hours of nausea and vomiting.  He's unable to provide a history, but his sister reports that he has a long history of bipolar disorder,  had been doing well since being on lithium for about two years.  She thinks he has recently started taking ibuprofen for his aches and pains in his back. His lithium level is 5.3 millimoles per liter.  Based on these clinical manifestations and the level of lithium,  treatment with IV fluid and which of the following acute therapies should be initiated in this patient?  Is it A, enteral activated charcoal, B, charcoal hemoperfusion, C, hemodialysis, or D, plasmapheresis? If you could select your answer.  And it looks like the vast majority selected hemodialysis as the answer, which is a correct one.  And we can go through, just briefly, one of the things that, and we've seen a little bit more of a resurgence of lithium in the population.  But it is a compound and a medication that's very easily dialyzable. But one of the keys in the finding of the question itself is the acuity and the onset  and the presentation, at least in toxicology sense. And when you come across anything with mental status changes, one of the hallmark things  of at least trying to administer, for those that have had to do it, activated charcoal, is your patient's going to have to be interactive enough and coherent enough with the mental  status to actually, A, take the activated charcoal, and B, keep it down. So aspiration is still a very unfortunate event.  But due to the acuity and the mental status change, changes that's been presented in very acute onset, the hemodialysis would be the preferred and the right answer.  This might be one of our few final questions. A 24-year, 20-year-old patient, significant past history of depression, anxiety, is evaluated  in the ED, found unconscious, obtunded, his GCS is 8, he's subsequently intubated for area protection, his pH is 7.19, PCO2 17, you can see his electrolytes, bicarb of 10,  he's got elevated AST, ALT, and alkaline phosphatase levels, serum ethanol is 56, a smaller gap is 42, urinalysis reveals microscopic hematuria and calcium oxalate crystals.  Which of the following treatments is most appropriate? Is it A, NAC, N-acetylcysteine, B, formepizole, C, activated charcoal, or D, methylene blue?  Okay, it looks like the vast majority selected Fomepazole, which is the correct answer. Again, activated charcoal won't obviously be an option  because it won't bind necessarily the alcohols at all. The N-acetylcysteine, you may see time to time used for either acetaminophen overdose and or hepatic insufficiency  when you have elevated transaminases in the tens of thousands. The Fomepazole is an interesting drug. It's been around now for some time  when it's available, actually, I should say as a caveat. And one of the interesting pieces of it is that it's almost 500-fold more potent at the alcohol dehydrogenase enzyme,  which is responsible for pushing this whole metabolism chain forward. And so by inhibiting it with Fomepazole is one avenue to actually address alcohol intoxications,  more so others outside of ethanol itself,  but it can be in extreme circumstances. And you can also see, one of the caveats though, I will mention, and you may see this in a question time to time,  is that it has to be redosed and dosed more frequently if the patient ends up transitioning to hemodialysis as well. So there are scenarios where there's a combination  of hemodialysis used in addition to Fomepazole, but the Fomepazole needs to be more frequently dosed in those case scenarios. But Fomepazole is the correct answer.  And here are your references. Okay, this might be our last question. 65-year-old woman with hypertension, AFib, CHF, and GERD, admitted from the ED with hypertensive urgency,  tachycardia, headache. She has a palpable abdominal mass. Her blood sugar is 286. She's anxious. Urine metanephrines are positive.  You see her vital signs, extremely high blood pressure. O2 sat, 92 on four liters. Nasal cannula, and the question is, which of the following is the first step  in this patient's management?  First of all, what condition, what endocrine disorder does she have?  Pheochromocytoma, correct. So what would be the immediate management for this particular patient?  Okay, 60% of you got the correct answer.  Again, it's important to first make sure that the patients are volume replete, so you don't wanna be rushing to give diuretics in patients like this.  You have to control the heart rate, and you wanna try to avoid beta blockers early. So the key here is to give agents that what we call alpha blockers.  So phenoxybenzamine, for example, if that was a choice, that might be the correct answer. But in this case, they're telling you another alpha blocker to consider using.  So this is a pheochromocytoma case with tachycardia, headache, extreme high blood pressure, urine methanephrines, catecholamines are high. Confirmation is done by CT or MRI,  and it's telling you to avoid conditions that can precipitate pheo-crisis, like dopamine receptor antagonists, beta blockers, zypotomimetics, opioid analgesics,  SSRI agents, MAO inhibitors, steroids. Treatment is surgical, but before you take care of the pheochromocytoma, you have to minimize complications  such as MI and CVAs, which can occur, and so you need to control medical management. And typically, we use phenoxybenzamine, but in the selection that we had,  you can see the explanation as to why another agent like doxazosin is favored. And ensuring hypo-euvolemia is critical because many of these patients may be depleted,  so you don't wanna be just rushing to give diuretics. And avoid beta blockers, and only after you've given the alpha blocker and you have persistent tachycardia,  you have to consider the use of agents such as propranolol.  And those are the only questions we have for this section. So, thank you very much.

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Rajat Kapoor, MBA, MD (Kidney); Gourang Patel, BCCCP, BCPS, MSc (Toxicology); Stephen M. Pastores MD, MACP, FCCP, FCCM (Endocrine)

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