DIP Episode 537 - 2024 USMLE Step 2CK Free 120 Discussion Part 13 (Q101-110, worksheet included)

Welcome, my name is Divine. This is episode 537 of the Divine Intervention Podcast. Into this podcast we're going to be contained the series on the free 120 for step 2ck. I am going to be going through questions 101 to 110. Again, if you've missed any other part of the series, I'll link where you can go back and go through it. I think you're going to find it to be very helpful. Let's get right to it. Question 101. A 25-year-old, premier-gravid woman, a 28-weeks gestation, comes to the office for a routine prenatal visit. At 18-weeks gestation, she had vaginal bleeding that results spontaneously. At that time, her blood group was determined to be all-arriage negative and she received a road-D immune globular. She reports good fetal movement. Blood pressure is 120 over 70. Fiddle heart rate is 160. Fondle height is 30. The fetus is in a vertex position. Hemoglobin concentration is 11 grams per decilator and hematocreative is 34%. Serum antibody assay is positive. The anti-detider is 2-week to measure. Results of serologic testing for syphilis and HIV antibody testing are negative. Which of the following is the most appropriate next step in management? Option A says to repeat serum anti-D antibody tighter. Option B says ultrasound sonography of the pelvis. Option C says administration of road-D immune globular. Option D says amuse and T says and option A says induction of labor. If you look at this question, this lady appears to be in her third trimester.

During her pregnancy, she had spontaneous vaginal bleeding and being an arriage negative, which makes sense. The giver, road-D immune globular. Remember, people that are arriage negative, we love to give them roguem at two times during pregnancy. We like to give it at 28 weeks. We like to give it within the first three days after the baby has been delivered within the first 72 hours. You can also give it at other times where you're worried or concerned that mom was exposed to arriage positive blood. Pretty much any time mom bleeds out of the ordinary during pregnancy. Say for example, she's in a trauma and she gets a blood transfusion and maybe mistakenly got arriage positive blood. Or she just has vaginal bleeding or something like that during pregnancy. Or she's getting an amniocent thesis. I know an amniocent thesis doesn't involve bleeding, but there's the potential for mixing between mom and baby's blood. So just keep in mind that there are some unusual times where a woman may get roguem. That is outside of that 28 week and 72 hours postpartum period. So for this one I think I'm going to go ahead and go with option C. This one should certainly get a roady immune globulin. Now I know some people may have been confused that, oh wait, the anti-detider is too weak to measure. So maybe they found something. I almost feel like that term or that small sentence is put there just to kind of mess with people's minds.

Most of this question this woman doesn't seem to be having much of anything going on. Don't over think this thing. Go ahead and pick option C. She's at 28 weeks. She should get roguem because she is arriage negative. Remember if you are a positive you have no business getting roguem. But if for example the anti-detider was very very strong thing, yes in that situation, you should also not give roguem either. So question 102 says, a five year old boy is brought to the office by his parents in July because of a two day history of an itchy rash. The rash began as small red bumps on the right forearm and spread to the left cheek and right ankle within the same day. He has not had fever, vomiting or diarrhea. No other family members have similar symptoms. Medical history is unremarkable and he receives no medications. The family switched to a new brand of bath so last week. They have three pet cats and one dog, three days ago the family attended a picnic at a nearby park. The temperature is 98.6 degrees Fahrenheit, pulse is 90 per minute and respiration is at 20 per minute. The patient is alert and scratching his right forearm. Examination shows mild edema of the left cheek. A photograph of the right forearm is shown. Similar lesions are noted over the left cheek and right ankle. The remainder of the examination shows normalities. Avoidance of which of the following is most likely to have prevented the patient's condition.

Social and e-says dog, daysays flora, caysays peanut butter, daysays perfumed bath soap and e-says sun. So if we look at all these things and of course the MDM is the give you multiple problems here. And we see that in the family, they switched to a new brand of bath soap. But that was last week. The thing that you just see that man, okay, they went to the park, it looks like. Yes, so they went to a park recently like three days ago. That just seems to be the one that is closest to when his symptoms began. So that park is probably the key to his problems. They've had these animals in the family for a long time so I'm not going to go with option A. Peanut butter is not even mentioned in the question so I'm going to skip that. That usually will cause an affelixis if anything. That's a type 1 hypersensitivity reaction. You're not going to have an affelixis for two days. Profumed bath soap, everybody in the family got that bath soap. They've been on infordays. I'm not too concerned. And again, the put option A to make you think of a sunburn. But again, if you have a sunburn, I would hope it comes fairly quickly. After you were exposed to the sun, they went to the park three days ago. That doesn't make any sense. If you look at this image, it sounds an awful lot like poison ivy. So I'm going to go with option B, floor. Basically, it's the stuff that exists in the environment. This child has poison ivy. Remember, it's a delayed hypersensitivity reaction.

It's almost like a kind of contact dermatitis. Typically, people that have these stains, supportive cares, really all they need. But you can use topical steroids. You can use Kalamine lotion that's perfectly fine with these kids. But this child is going to be fine. So again, remember, it's a delayed type hypersensitivity reaction. It's a type 4 hypersensitivity reaction. Now, we're going to go to question 103. Again, one of these HPI studies. These HPI studies again. Scheme in them is not a bad idea. But this person is 56. They're coming to the clinic. It's female. She says she feels tired and doesn't feel well. And she's had fatigue in the least for three months. Tires quickly would physical activity. She has early satiety. She has hypertension and hyperlipidemia. She's on a phyasi diuretic, lotthali-donant, and isihebronastatin. If you look at her vitals, the only thing that jumps out of me is her blood pressure. It's a little bit elevated. 139 over 78. A BMI is 36. So she's obese. And then if we look at the physical examination, nothing really, really, really crazy sticks out at me. So, you know, I don't know the exam may be a little abnormal, but I don't really care much about that. And then, if we look at her blood studies, no, that's where the meat is. So how white count is really high. And a lot of videos neutral fills. You see all these other blood elements. These myeloid elements elevated. Myelocytes, metaminocytes, basal fills, eocinophils.

These are going to be pretty classic, especially in a middle-age person. I'm going to be going with a CML here. This person certainly has a CML. This person absolutely has CML. So, again, what are the key facts here that tell us that this is CML? Just a couple of things, right? So number one, we see that the person is middle-age. Number two, we see the person's white count is elevated. And you see it's mostly myeloid cells. You see neutrophils, myelocytes, metaminocytes, basal fills. Basal fill is a very classic symptom or blood-finding in people that have CML. And remember, CML is caused by this 922 translocation. So the BCL receptor is translocated with ABL. And then your myeloid cells prefer it like crazy. And that can cause problems. And how do we manage CML? Well, manage CML with drugs like the tyrosine kinase inhibitors like immatineb, desatineb, nelotineb. There are many different tyrosine kinase inhibitors. You can use to manage this stuff. And the one thing I'm going to see here is that CML. Remember, that translocation creates that Philadelphia chromosome. Looking at the other answers, option E talks about M-GAS, the monoclonal gamma-pathy of one determined significance. It's almost like a precursor to multiple myeloma, in fact about 1% of people that have M-GAS proceed to multiple myeloma every year. But the key thing here is that in M-GAS, you're going to notice that they're going to have less than 10% plasma cells in the abumar.

And they will not have the crap symptoms. You see multiple myeloma. They won't have hypercocemia. They won't have renal failure. They won't have anemia. They won't have bone pain. And then, if we look at the other answers, ELL, right? Remember, this is usually going to be a pediatric malignancy on the US MLS to get me wrong. Adults can certainly have ELL as well, but usually it's going to be in kids on your exams. And we tend to find any people that have Down syndrome. Remember Down syndrome? It can't go forward. They can have endocardial cushion defects. They can have hersperms disease. Hersperms disease is actually pretty classic in Down syndrome. So many times that hersperms disease will present with chronic constipation. And you see these people, they're having tons of stool in their colon. And they tell you that, oh, this person doesn't pass me a conium early in life. So failure to pass me a conium that can actually be a presentation of hersperms disease on your exams. And then look at an AML. So AML, remember, there are many kinds of AML. But the only one that you only want that you pretty much care about on the US MLS is going to be acute pro-minocelic leukemia. That's like the M3 subtype of AML. And that one tends to be associated with the 15-17 translocation. So you take the PML gene and you're translocated with the RARA, the recnoric acid receptor, aging. You have that translocation. And then that causes your myeloid blasts to proliferate like crazy.

The thing is these myeloid blasts in AML, they make a lot of pro-inflammatory cytokines so like interlooking one, interlooking 60 NF alpha or whatnot. And that can cause endothelial damage. When you damage the endothelium, you're going to trigger the coagulation cascade. And if you trigger the coagulation cascade, you're going to get in a lot of trouble. You're going to get in a lot of trouble with DIC, right? Remember in DIC, all your platelet labs are out of what? Your bleeding time is up, PT's up, PT's up, D-dimer is elevated, fiber indigradition products elevated, fiber no gene is usually going to be decreased. Those are classic findings in DIC. And remember, don't forget on a blood smear, make sure you can identify those hour routes. You can see what I could promote. Ocelic leukemia, those hour routes. That's a classic blood smear that we see on the USM Lism. Again, we're going to treat this with all trans-retinoic acid. And one thing I want to say about ALL, in fact, many times when kids have ALL or people have ALL, they tend to get interethical chemotherapy because ALL has a predeliction for the central nervous system. Chemotherapies are still in those people's spinal columns. And one thing I'll just say is, before you start a person on therapy for CML, it's usually helpful to go ahead and check their QT interval. Because these tyrosine kinase inhibitors, that sapne about a lot of non-stick and certainly cause a person to have QT interval prolongation.

And one of those weird things you want to keep at the back of your mind for exams. And also, that sapnepe is associated with proteinuria. So that's something I want to keep in mind with that sapnepe. I remember that sapnepe kind of sounds like the signing water. That's a nice way to remember that. And then the final one I think I've not talked about here. CLL is usually going to be in older people. The white count is going to be very, very high. But in contrast with CML, you're going to see an elevation in their lymphocytes. And then you're going to see a big, big, big lymphoid elevation, big, big, big lymphoid elevation. That's the way you know that. Oh, wait, I'm likely dealing with with CLL. And those white cells don't work really great. So those people who tend to be pretty supposed to a lot of infections. Okay, so question 104 says, a 65 year old woman comes to the office because of a six month history of progressive shotness or breath. And a one year history of non-productive cough initially the shotness or breath occurred only with exertion, but now occurs at rest. It does not worsen when she lies down, but is still present. Her symptoms have limited her ability to travel internationally with a peace core. She has not had chest pain fever, chills or blood tinged spirit. She has hypertension, type 2 diabetes and MDD. She is on a load of pain, like synaur pray, and large and sexually. She has smoked one pack of cigarettes daily for 50 years. I have.

She drinks one glass of wine on special occasions. For look at her vital, everything is pretty okay. All socks and room issues and oxygen saturation of 94%. There's no GVD on pulmonary examination and expiratory. Weasers are heard. There's a prolonged expiratory phase. Herd sounds a distant. We should have full age the most appropriate next step in diagnosis. Right. So this person is pretty straightforward. As person seems like they have COPD. They were 50 back years smoking history. We see that they are having like progressive shortness of breath, chronically, worsening disorder. This is COPD. So for this, we're going to do PF Ts. I'm going to go to option E here. I just want to make sure I supply the answers for the other one. So I said that for 103, pretty sure the answer is D, CML. For 102, the answer is flora. 101, the answer is C given our organ. And then, so for 104, I'm going to do PF Ts. This person certainly has COPD. So let's make some integration with COPD. So let me ask you this real quick. So for present COPD, like in Fizima, for example, which is probably what this lady has. What's going to be true of the PBG-02? So the oxygen tension in the LVLI. It was going to be low because the LVLI are just filled with so much CO2 that they are retaining. So the PBG-02 is going to be low. If your PBG-02 is low, or we'll be sure of your P-Liter L2. Well, P-Liter L2 is the oxygen tension in your plasma.

Since they don't have enough oxygen in the LVLI, then they're not going to be able to have enough to send to the plasma. So the P-Liter L2 will be low as well. Okay, how about the P-Liter AC-02? Well, again, these people are CO2 retainers, right? So because they retain so much CO2, they're going to have a ton of CO2 measuring their bloodstream. So the P-Liter AC-02 is going to be increased. How about the S-Liter L2? Remember, the S-Liter L2 refers to the saturation of hemoglobin with oxygen. If you don't have enough blood in oxygen in your plasma, then you're not going to have enough diffusion on hemoglobin to saturated up property. So your S-Liter L2 is going to be decreased. Now, what's going to be true of your EE gradient? Well, again, these people have a cause of hypoxia. The problem is within the lungs. The problem is Litter within the lungs. As per say has COPD, probably has infezima. That's going to mess up because of all those produces. They're going to chew up your pulmonary empire in coma. They're going to chew up the surface area that you use for diffusion. So you're going to have inefficient diffusion of oxygen from your VLI to your pulmonary vessels. So that's going to decrease, that's going to raise the EE gradient that you're going to raise the EE gradient because you're not going to have equilibrium between the two. So you're going to have a equilibrium between the oxygen saturation, oxygen tension. You have VLI versus your pulmonary vessels.

So your EE gradient is going to go up. Your DLCO, your diffusion capacity for carbon monoxide is going to be decreased. Again, these people have reduced surface area because of those produces that I've chewed up the pulmonary empire in coma. And again, since there's so much oxygen in their VLI in their plasma and hemoglobin, that lot of oxygen content is certainly going to be low. I will be sure of these people's hematocrit. I hope you're seeing all the divine this is going to be elevated. Because again, these people have chronic hypoxia from their COPD that's going to cause their Epo to go up. Epo is going to cause them to have polycythemia. This is going to be a very good example of a polycythemia with an elevated Epo. I will be sure of your bicarb. Well again, these people are CO2 retainers. If you retain CO2, you're going to have a respiratory acidosis. And what is going to try to compensate for that by causing a metabolic alkalosis? So your kidney is going to make more bicarb ions. So you're going to have an increase in your bicarb. All right. Now, question 105 says, a 45 year old man comes to the office because of a six month history of difficulty sleeping, nervousness and fatigue. He goes to bed at 11 p.m. every night, falls asleep within 15 minutes, then sleeps, fit fully. After he awakens, he has mild neck pain and feels tired, edgy and tense during the rest of the day.

The company where he worked for 27 years, close six months ago, and he has been unable to find another job. He says he worries about his finances and job prospects. Medical history is remarkable for alcohol use disorder. He has not drunk alcohol for one year. He says he is committed to being sober, but recently has wanted a drink. He currently takes new medications by those signs of within normal limits. Physical examination discloses no abnormalities. Mental status examination shows a constricted, anxious affect, which of the fluency is the most appropriate for macotherapy? So what does this person have? You see this has been going on for six months. Remember, with psych questions, you always want to know your time, your timeframes. That's always a kind of a smart thing to do. So this has been going on for six months, and this person seems to be worried about a ton of stuff. So this seems a lot to me like generalizing anxiety disorder. So remember, GD, you've got to have your symptoms for at least six months. You're worried about so many things in life. So this is GD, and we're going to manage that first line with an SSRI. SSRI, SSRI. Let's see, are there any SSRI answers here? No, so we're going to do that because this nice SSRI answer here. So what can we jump to? We're going to go to the second line treatment, which is bullspirion. Bullspirion is a partial like a list of serotonin receptors that we use to manage, generalize, anxiety disorder.

It's a second line treatment for generalizing anxiety disorder. So, but remember, the first line treatment is in fact an SSRI, but that's not an answer. So looking at these other answers, Kronaza Pam is a benzo. I remember Diffin Hydramine. He's an antihistamine, but he has very powerful anticholinergic properties. It's useful to so many things on the USML Is. Although they like to test it on low in terms of the side effects, right? So remember, it has anticholinergic properties. So you can cause problems like hearing error retention. So your post-order residual volume will actually be elevated. And you can cause delirium, you can cause alterment, those status. And remember, chronic use of these anticholinergic drugs like Diffin Hydramine can be associated with Alzheimer's disease. Which makes sense because in Alzheimer's people usually have a deficiency of acetylcholine. Option D is a TCA, Amy Prome. Amy Prome. That's a tricyclic antidepressant. Remember, tricyclic antidepressants, they cause a bunch of problems, right? So they have antichristamine, energy effects, sodium oxidation. They have anti-alpha-1 effects, so they can cause orthostatic hypotension. They have anti-moschronic effects. So they can cause many of these, uh, hearing error retention, delirium, and whatnot. But remember that your TC Es also block sodium channels. They're sodium channel blockers. They can work in a sense like a class 1 anti-rhythmic.

By being able to work that way, they can cause a widening of your curious complex. Because you have depolarization that just digs longer. Because remember, the sodium channels are involved in depolarization. So, and the curious complex presents depolarization on an e-key G. So, of the ventricles at least. So, because they're blocking sodium channels, depolarization is taking longer. Your carriers is going to get wider. Remember, we're going to treat that with a sodium bicarb. To overcome that sodium channel blockade. Option E. So, this e-key G, uh, that you see in the worksheet is, is showing a Y-Q-R. So, that's, that's going to be a pretty much an option D very, very well here. And then, um, don't forget that with the IP is, is an e-typical anti-psychotic. The Maze Pan is a benzo. That's all I'm going to see here. Alright, so let's go to question 106. So, 56-year-old man. Comes to the clinic with his wife because of a six month history of restlessness while sleeping. The wife says he motions as if he were throwing or kicking a ball. And sometimes punches the pillow during the night. He has hit her twice. Recently, he began talking in his sleep and yelling expletives. Occasionally, he seems to be acting out a dream twice. He has a weekend and hotel his wife, what the dream was about. Otherwise, he's on a way of these episodes and feels well rested in the mornings. He has a history of constipation treated with polyethylene glycol.

He takes northern medications, vital signs that within normal limits. Excevenations shows no abnormalities. The patient is at greatest risk for developing which of the following. This is one of those things where you either know the association or you don't know it. There's nowhere around it. But you see a person and they've had like years before, they start having the neurologic disease. I'm trying to be here to kind of give you a presentation. You notice that they have like anosmia. They have like chronic, they have a lot of constipation. You can see that they act out a lot of their dreams. That's pretty classical Parkinson's disease. You can see people that have Parkinson's disease having those three symptoms. Those three symptoms before years before they even have Parkinson's. Constipation, anosmia, actin out dreams. So the answer here is going to be e. Remember when a person has Parkinson's disease, we're going to manage it with. Carbidopa-livo-dopa. Remember, Carbidopa-livo-dopa have an association with people developing like compulsive behaviors, gambling, hypersexuality and things of that nature. So you see a person, you know, they are being treated for an neurologic disease. And then they go like on a spending spree or they start seeing inappropriate things. They'll try to trick you on your exam. Tell you that, ooh, they've developed for them to temper out dementia. No, that's just Carbidopa-livo-dopa. Toxicity kind of showing forth.

So the answer here is going to be e. So I'm not going to go in our collapse. In our collapse, he's more of a sleep disorder. They tend to just fall asleep on a whim. They go straight into REM sleep. This is not a stroke, right? This person doesn't seem to have many risk factors for strokes. And with the biggest risk factor for stroke is hypertension. This person does not have a history of hypertension. ELS, you're going to have a lot of motor neuron problems. It's an operand lower motor neuron disease. There's just not many things here. Alzheimer's disease, I can use more of dementia. To be honest with you, I'm just going to say this. This question, there's no way you can get it right without knowing the association. That's all I'm going to see there. All right, let's go to question 107. So a 77-year-old woman is brought to the ED by her son. Because of a 3-day history of pain in her right wrist. The patient has advanced dementia, Alzheimer type, and is unable to provide her medical history. She's completely dependent on her son, with whom she lives, and who is her only caregiver. The son says he's unaware of any trauma to the patient's wrist. The son says the patient has no other history of serocelness. Only medication is memantin. That's an N-indie receptor antagonist that can be used to manage Alzheimer's. That's more like a second line. Remember, in Alzheimer's, we're going to start off with the acetylcholinesteries inhibitors like dunepezil gallantamine or rivestidine.

She's nonverbal and has a flat effect. She appears on chemt. And she appears on chemt and to half poor hygiene. If we look at her vitals, they're completely... Okay, blood pressure is up actually 150 over 90. The patient moves when the physician touches the right wrist. Examination shows multiple bruises over both forearms and wrists. The remainder of the examination shows not normalities. Excerpt the right wrist shows a distalrio fracture. The fracture is treated with cast immobilization, which will influence the most appropriate next step in management. Sounds like this woman is being abused. So we're going to contact the no-protective services. This is a pretty easy question. You see an elderly person usually is going to be able to dementia, they will have a bed bound. People that depend on other people for help. And they notice all these bruises on them. And the person doesn't see much. And that's going to be an elderly abuse. So we're going to go ahead and contact the no-protective services. All right. That's not a question. 108. So 27-year old man comes to the emergency department because of a four-week history of progressive shortness of breath and swelling of the lower extremities. During this time, he has also had shortness of breath during the night while lying down. He also has a six-month history of intermittent, moderate, substernal chest pain, and pressure while exercising. He has not had syncopy. He has no history of serocelness and textual medications.

If you look at his vital, he is tachycotic, he is hypertensive, he is decapnic. Examination shows severe defuse gingivitis. Crackles are heard halfway of the posterior lung bases by laterally. On cardiac examination, a permanent S3 is heard. So that means this person has systolic heart failure. There's three plus pitting and dima of the lower extremities, ECG shows sinus tachycardia, which of the following is the most likely substance used. So we'll see this person in the hypertensive. They've developed heart failure. They have gingivol problems or problems with the tooth, with the mouth. This is pretty classic, right? It's going to be meth. So I'm going to go with option D here. I'm going to go with option D here. So this person has meth, toxicity. Remember meth, it kind of works like cocaine in a sense. So you can increase the cadacolamine, sodium synapsis, and that can cause you to have hypertension. All those cadacolamines, they can stimulate alpha-1 receptors and that can cause viso-construction. So you can have coronary viso-construction when every half-credits ischemia, myocardial cells are going to start dying. They're going to start dying, dying, dying. And if myocardial cells die, then your heart is not going to be able to pump blood effectively. You're going to develop a systolic heart failure.

And the death of those myocardial cells, as your myocardial cells feel to contract well, volume fluid is just going to keep accumulating, accumulating, accumulating within your heart. That chronic volume over and over can cause your sacramir to be added, eccentrically, added in series. Again, that can cause you to have a diluted cardiomyopathy. So this person has meth. You know some of you may be like, well, they're not a white, they're not cocaine. The thing is, could it be cocaine? Yes. Cookeen can also cause a cardiomyopathy. But the thing is, we see this person having the severe diffuse gingivitis. Those mouth problems tend to be more meth-associated. Look at how these other answers, remember, to allowing can cause sodium cardiac death. You're going to see these people that just, the people inhale, to allowing, they sniff it, because it can cause a europhoria. But the thing is, to allowing, a message of a person's brain, message of a person's kidneys, message of a person's heart. So many times you can see them have a nasty cardiac arrhythmias that can cause sudden death, they can have like, renal problems. So just going to keep that in the back of your mind. That's usually pretty classic with, with to allowing. And in heroin, right, that's an opioid. So it's going to cause respiratory depression. So the person is going to be superhypoxic. But remember, it's not like your lungs are bad. This is that the heroin tells you to not breathe, basically.

So the person's lungs are completely fine. So they'll be hypoxia because they're not breathing enough. They have like profound respiratory depression. But they're going to have a normal e-gridion because oxygen can diffuse just finding their lungs. Their pulmonary architecture is completely okay. Now, can lead to polymorphine ventricular tachycardia? I remember methadone. Methadone methadone methadone. We use it for opioid rehab. It's kind of like a weak or opioid. But obviously it can prolong your QT interval. And that's why you want to be sure that a person doesn't have a prolonged QT when you're studying them on methadone. This person probably, if you put a problem on methadone, it can prolong the QT interval. And that can lead to torsada plant. Remember, I know the name on the exams for torsada plant is polymorphic V-tack. I remember for torsada plant, we're going to manage that with magnesium. Now, one other thing I want to say about methadone, right? So we use it in opioid rehab. Does it make sense to put a person that is on methadone on now-trexone? It doesn't make any sense, right? Because now-trexone is also used to treat some addictive disorders. So if you put that person, they already on methadone, they're putting on now-trexone. Now, trickson is a mere receptor antagonist. It's going to reverse the methadone. You're going to throw them into opioid withdrawal. That doesn't seem like a very smart smart idea. Does it?

Okay, so I think we've kind of hit most of the leisure points here. So I think I'm going to go ahead and continue. So question 109. Question 109. So a 39-year-old man comes to the office because of a three-month history of episodes of headaches, poppetitions, and sweating. Episodic headache, poppetitions, and sweating. I would hope that you kind of know what's going on with that. The episodes occur two to three times monthly. He has hypertension, and he knows the calcium channel blocker, and an ACE inhibitor. He has blood pressure 166 over 112. Examination shows noctub normalities, CT scan, of the abdomen shows a 4 centimeter effigrinal mass. Which of the following is the most appropriate next step in management? So we'll see your presence in episodic headache, hypertension, and poppetition, sweating. This is pretty classic for a few chromosyctoma. So we're going to check the plasma, metaneference, normative, and effigrine. So we're going to go to option D for that. Let's look at the other answers here. The option A. So in four-year-old collection, for measurement of one-leumandeli-cacid, hmm. Sure, but I don't like the second half of that answer. Five-hydroxyindolaceli-cacid. That's five-heat-IAA. That's what we measure levels off to screen a person for carstenoid syndrome. What this person does not have carstenoid syndrome. So we're going to cross out option A. Remember, a carstenoid syndrome. You have your mass, making a ton of serotonin.

Usually it's going to be in the appendix, but... I'm usually not going to cause any symptoms because it's in the appendix. It makes the serotonin. Liver breaks it down. We're all happy. But once you spread to the liver, once you have met to the liver, then you're going to start having problems. Because that serotonin is... If you've bypassed the liver, it can cause right-sided heart problems. So it can cause like tract constipation and sufficiency. It can cause pulmonic stenosis. You can see a lot of wheezing, bronchospasin in carstenoid syndrome. And remember, blood-haffcarstenoid also tends to be flushed. They tend to have a lot of diarrhea. Just something to keep in mind. So this person does not have carstenoid syndrome. I'm going to get rid of that. Adrenaline sampling is something that we sometimes do in con syndrome management. This person doesn't have con syndrome. They don't have primary high-proudosteronism. So we're going to skip that. Option C is something you may do to treat again. Like an adrenal... Option C kind of seems like something you may do as a treatment measure. But like, gee, we've not figured out. Let's figure out what's going on with this guy first. Before we start treating, right? So we said the right answer is option D. And option E transphenoidal hypophysic to me. That's a surgical procedure we use for pituitary adenomas.

Although I remember usually, if a person has a prolectinoma, which is probably the most chronic kind of functional pituitary adenoma, we're going to money that would dobumin agonists, like bromo-cryptinocarbagoline. We almost never do surgery for people to have a prolectinomas. But there are other kinds of pituitary adenomas that we definitely do surgery for. A pituitary adenoma that's making growth hormone, you can certainly do a transphenoidal hypophysic to me. Before surgery for those people, you can say, oh, fine, let's put it on octetiotide. Let's put it on pig visomant. Pig visomant is a growth hormone receptor antagonist. But just in general, you can do surgery for those people. Transphenoidal surgery. I believe I've actually seen one of those back in the day. So like a growth hormone secreting to my... So how are a growth hormone secreting to my present? Well, my growth hormone is a diabetes or genic hormone. So you're going to see this person having a very high fast-impot glucose. And it causes visceromagol. So many of your organs are going to get big. So you're going to have heart failure. You'll see increased spacing between the teeth. The hearts don't feel any more. Blah, blah, blah, blah. And typically, you're going to work that stuff out by checking the presence IGF1 levels. Because remember, growth hormone desecration is kind of weird. So you cannot depend on those levels to say, Oh, I'm going to screen you for a growth hormone secreting tumor like that.

No, you're going to measure the IGF1 levels. You're going to notice I elevated. And after that, you're going to do an oral glucose suppression test. Remember, whenever you have a tumor in endocrinology, or whenever you have a disorder in endocrinology associated with hypersecretion of something, the confirmatory test is really going to be some kind of suppression test. I've talked about this schema many times in different podcasts. Like if a person has like primary hyper-adostroenism con syndrome, they're making a ton of... ...adosture. Well, you can do like a ceiling infusion test. Because you give the person ceiling, it raises the upload volume when you want to see the outdo serum suppresses. So those suppression tests are good for hypersecretive tumors. So for growth hormone tumor, because it's a diabetes genocormone, give the person a glucose load and see if you are a growth hormone suppresses. That's how you confirm actually the diagnosis of growth hormone suppresses. Obviously, if you're less than 18, that's gigantic. More than 18 is going to be... We're going to call that acromegaly. All right, so let's go to the final question here. Question 110. So, for the one-year old woman has been prepared for a discharge from the hospital, I have to treatment for acute pancreatitis. She has already done a good job for the past 12 hours. She has had three prayer admissions for pancreatitis. Medical history also is remarkable.

For alcohol use disorder, the patient does not have secure housing, which of the following recommendations is most likely to reduce this patient's risk for future hospital admissions. So, option E says abstinence from alcoholic beverages, option B says, in a rooming and a health insurance plan, option C says nutritional canceling, option D says placement in a women's shelter. This person has acute pancreatitis. She has alcohol use disorder. Alcohol causes pancreatitis. Stop drinking and pancreatitis will go away. We'll go to option A here. Don't overthink this thing. Remember, there are many other causes of pancreatitis. You're missing on your exams, moms, hyper-tribalistroidemia, and many drugs that can cause pancreatitis. Like, the ozempic-like drugs, the gel-pywan agonist, the DPP-point inhibitors, those in the cause pancreatitis. There are many drugs that can cause pancreatitis. Remember, if you'll smash your belly or like a handlebar or whatever, that can also cause you to have a pancreatitis like a traumatic pancreatitis. Goldstones can also cause pancreatitis. There are many things that can cause pancreatitis on the exam. So, I think we should stop here. I hope you... So, I'll encourage you. There's a worksheet included with this podcast. So, just... I will tell you to pre-read the worksheet before you listen to the podcast. And then after you... And then you can do one of two things.

You can either fill out the worksheet as you listen to the podcast or use the worksheet as a quiz after you listen to the podcast. Basically, these worksheets are designed for you to be able to answer all the questions if you listen to the podcast closely. If you listen to the podcast closely, all the answers to the questions are in the podcast. So, that's all I'm going to say there. So, as I wrap up, I offer classes for step one to step three, starting next week Tuesday. And if you're interested in many of those, I've made a separate podcast where I talk about those. If you go to my website, you see the dates and times. The all over Zoom, the classes are not lectures. They're all clinical scenarios, MDME style questions that I used to meet in integrations and explain pathophase. So, I'm not a person that's usually dumping you for you. Now, I'm going to explain the material to you. I'm going to explain pathophase. I'm going to help you make integrations. And I'm going to show you how the test things on the exams. I just want to see many people on the side of it in preparing for these tests. And then I also want to want to learn and I have these podcasts on the major platforms Apple Google Spotify. I forget to show you can check out. And I also help with your applications and personal statements and rec letters and things of that nature. And then I have another website that I call Devine Intervention Lifelesses.com.

Every week I post about two podcasts where from a biblical perspective, I address a life lesson. So, Devine Intervention Lifelesses.com. There's actually an Apple podcast associated with that call the Devine Intervention Life Lessons podcast. So, thank you for listening to me today. I will see you in the next episode. I guess that will be 538. So, God bless you. Have a wonderful weekend and bye for now. Thank you.

Delayed type IV hypersensitivity reaction (contact dermatitis) caused by urushiol exposure.

Constipation, anosmia (loss of smell), and REM sleep behavior disorder (acting out dreams).

The Philadelphia chromosome ($\text{t}(9;22)$) translocation, fusing $BCR$ with $ABL$.

Low $\text{PaO}_2$, high $\text{PaCO}_2$, low $\text{SaO}_2$, and a widened alveolar-arterial gradient.

Carbidopa-levodopa therapy, which can lead to compulsive behaviors (e.g., gambling).

Administer Rho D immune globulin (Rho GAM) to prevent alloimmunization.

Delayed Type IV Hypersensitivity Reaction (Contact Dermatitis).

Tyrosine Kinase Inhibitors (TK Is), such as imatinib, dasatinib, or nilotinib.

Because they are chronic $\text{CO}_2$ retainers due to impaired gas exchange and ventilation issues.

Constipation, anosmia, and REM sleep behavior disorder (the classic triad).

Selective Serotonin Reuptake Inhibitors (SSR Is).

Administer Rho D immune globulin (Rho GAM) to prevent alloimmunization.

Delayed Type IV Hypersensitivity Reaction (Contact Dermatitis).

Tyrosine Kinase Inhibitors (TK Is), such as imatinib, dasatinib, or nilotinib.

Because they are chronic $\text{CO}_2$ retainers due to impaired gas exchange and ventilation issues.

Constipation, anosmia, and REM sleep behavior disorder (the classic triad).

Selective Serotonin Reuptake Inhibitors (SSR Is).