DIP Episode 1 - DIP Episode 1

Hello, welcome. My name is Divine. I am a fourth-year medical student. This is supposed to be a podcast relating to some high-yield step one topics. I basically created this by going through the different high-yield resources that everyone uses. And I just tried to pick up on some high-yield information and just put it into a keyword format in slides. And then I'm just going to talk about these. I hope you find it marginally helpful. And I guess we'll just go ahead and get started. So keyword number one, the most commonly occluded vessel in an MI. Hopefully you know this to be the left anterior descending artery. Remember this is a branch of the left main coronary artery. And hopefully you'll notice that this will be associated with ST elevations in leads V1 through V4 pretty much. And then the infarcted vessel causing an AV block. Well, the thing with that is that the AV node is supplied by an artery known as the nodal artery. This nodal artery is classically a branch of the posterior descending artery. And as we know, in 85% of individuals, the posterior descending artery comes from the RCA. So an RCA infarct may infarct cause an AV block. And hopefully remember that this will be associated with a PR interval prolongation on an EKG. Now, the papillary muscle that's most susceptible to a rupture. Step one loves this for some bizarre reason. But this is the posterior medial papillary muscle. Okay. The reasoning behind this is this muscle has only one blood supply.

Its blood supply is from the posterior descending artery, again, classically from the RCA. So if you have an RCA infarct, you can rupture, you can have a schemia of the posterior medial papillary muscle. And you can actually have a like a flushary regurgitation, which can cause a massive pulmonary edema. Okay. And contrast this with the anterior lateral papillary muscle has two sources of blood. The left anterior descending and the left circumflex. Okay. So it's less susceptible to a schemia. The only thing that will cause a schemia is if you by some bad luck have those two vessels knocked out or you have your left main coronary artery knocked out because remember it's the precursor to those two vessels. And then coronary vessel dominance. This is just a concept that relates to the source of your posterior descending artery. Okay. Your posterior descending artery in 85% of individuals, it comes from the right coronary artery. So most people are right heart dominant. Okay. In some people it comes from the left circumflex. Okay. This is about 8% of people. And then the least common permutation of that is the posterior descending artery coming both from the left circumflex and the RCA. That will be a codominant heart. Okay. That occurs in about 7% of people. Okay. Now the next question talks about the first line treatment of psoriasis and acne. For this, hopefully you know that this is topical retinoid. Okay. And top retinoids remember that they are vitamin A and analogs.

In fact that's why it puts the 15-17 translocution association. Remember your all trans retinoic acid that is used to treat acute promolyocytic leukemia, which is a kind of AML. Okay. Remember the classic histologic finding of our rods that if they licked into the circulation during surgery chemotherapy for example, the person could have a DIC and it could actually die from that. Okay. And you should also remember that vitamin A, right? With noic acid, sort of want to avoid excess in pregnant women because it's a teradogen. Okay. And the last thing I just put here with regards to the sun and skin cancer. Right. So we know that obviously like, oh don't be the sun or oh still we're from tining salons and tining beds, right? Because oh you could get skin cancer from that. So what's the reasoning behind that, right? So we know that ultraviolet rays cause skin cancer like there's UV arrays and UVB rays. And it so happens that the UVB rays are the ones that are probably more dangerous. Okay. Because they have a shorter wavelength than the UVA rays. The UVA rays have a longer wavelength. So that's why they say, oh you sunscreen and sunscreen, the protective agent in sunscreen, at least against UVB rays, which is the more dangerous one is a papa. Okay. So paramino benzoyic acid. Hopefully you're still remember that papa is an analog that is used is actually a substance that's used in certain microorganisms to make fully cast it. Okay.

Remember that papa is acted on by dihydroetherecentates to make like certain intermediates in the fully synthesis pathway in microorganisms. And remember that their papa analogs, right? Like your so phonomites. They actually look like papa and he worked by inhibiting a dihydroetherecentates. So think about for example like DAPSON or SMX that you find in a trimethoprimsophaneothoxysone. And then if you wanted to block both UV and UVB rays, you would want a sunscreen that contains zinc oxide. Okay. Zinc oxide. So obviously that's probably preferred over something that just contains papa. So next slide. Now hypo-neutrhymia, hypotension, and hypochylemia in a patient with a history of a recent severe and Iceramin-injective infection. Well, what are you thinking about here? Are you thinking of adrenal hemorrhage potentially from water house-free-trixened syndrome? Well, if you're thinking about that then that's great. Okay. Super high-yield out condition to know for step one. So this is basically hemorrhage into the adrenal gland. So this can cause a primary adrenaline-sufficiency. And if you have a primary adrenaline-sufficiency, right? Your adrenal cortex no longer works if it's not working. You basically have reduced outdoor strenghtivity. Remember the zonal glomerulose that ordinarily makes our dose-dure, which is a kind of mineral acridicoyd.

So if you're not making our dose-dure, you have reduced the activity of that in-ex channel at the principal cell of the collecting duct. So you no longer reabsorb sodium. If you're not reabsorbing sodium, you become hypo-neutrhymic. It also so and because sodium is not being reabsorbed, you also have less water absorption. So your blood volume goes down. Okay. That's why you become hypotensive. In addition, remember that your zonal fast-seculada, right? Your source of glucose corticoyd makes cortisol. And cortisol actually has a permissive effect on the sympathetic nervous system. And one of the mechanisms behind that is that cortisol actually helps with epinephrine synthesis in the adrenal medulla by activating the enzyme PNMT, right? That uses sen. S-identusil-methyonine as a cofactor, right? So remember, methyonine is a methyl carrying the body and the big difference between norapinephrine and epinephrine is a methyl group. Okay. So PNMT is activated by cortisol. So that's potentially one mechanism behind the permissive effect of your sympathetic nervous system on, I mean, of cortisol on your sympathetic nervous system. And then jumping back to that fancy principal cell in the collecting duct, right? So remember that in a channel, a sodium comes in, okay? Potassium is extruded in a coupled transport mechanism. So if you have low levels of audustra, right? That in a channel doesn't work, okay? So by virtue of that, that or on the key channel doesn't work as well.

So you do not extro potassium. That's why it gets hyperkalemia, okay? In primary adrenoline sufficiency. And the most common cause of primary adrenoline sufficiency in the US is adicine's disease, okay? That's an autoimmune destruction of the adrenal cortex, okay? Cortex. In developing countries, think more of TB, okay? So if they give you a step one question, where they describe, but they say, oh, microscopic examination of a biopsy specimen from the adrenol cortex reveals case-heating granulomas. You really want to think about TB infection, okay? Cause in our primary adrenoline sufficiency. And then in primary adrenoline sufficiency, you classically get a hyperpigmentation. And the reason behind that is, if your adrenol cortex is not working, there's no cortisol that's going back to give a negative feedback to the anterior pituitary, okay? So you make a ton of VCTH, okay? Now it so happens that ACTH comes from substance known as pop C, okay? Propium melano-quartin. And pop C is a precursor of VCTH. In addition, it's also a precursor of MSH, melano-site stimulating hormone. So if you're making a ton of VCTH, right? You also in the self-sync, we make a ton of MSH. And we can a ton of MSH, you have stimulation on melano-sites, and you can get skin hyperpigmentation. In addition, a person that has primary adrenoline sufficiency as they're making more ACTH and more MSH, they also make a lot of beta endorphine. Beta endorphine is actually also derived from from POMC.

And remember that beta endorphine is a new opioid receptor agonist, okay? Just one of those bizarre things, step one wants you to know. Now if a person has primary adrenoline sufficiency, again, they're making less out ofosterone from the zonal glomerulosa. And if you go to the collecting, doctor, remember there is alpha-intercalidate cells that pump protons into the urine side of the nephron, okay? And that proton pump is activated by our doster. So if you have a low-outosterone state, aka type 4 RTA, you're not pumping protons into the urine side of the nephron, okay? And you get a metabolic acidosis because you're basically retaining protons, okay? And remember that in primary adrenoline sufficiency, you have an eocenophilia, okay? If you remember like your NAACP or D-entry-policyp or caladapy numonic for the differential diagnosis of eocenophilia, one of the ACE in those numonics stands for adhesives disease. Okay, now if a person has secondary adrenoline sufficiency, okay? The problem or the pathophysiology is that these people's anti-operatory no longer works. If a no longer works, you're not making a CT, if you're not making a ton of a CT, you're also not making a ton of a message, okay? So there is no very high yield, there's no skin hyperpigmentation in secondary adrenoline sufficiency. There is also no hyperchylinia, okay? Because again, the problem is your anterior pituitary does not work.

It does not mean that your adrenal cortex is not working as well because remember, yes, if you're not making a CT from the anterior pituitary, your adrenal cortex is not receiving stimulation, okay? But remember that the only parts of the adrenal cortex that depend on ACT's stimulation, primarily include your zona fasciculada that makes lucho-cordicoids and your zona reticularis that makes sex steroids, okay? Remember that your zona glomerulosa that makes mineralocordicoids, kissing points on your dosterone, receive stimulation from the reneinagiotensin adosterone system that basically starts in the afren arterial of your, the JG cells of the afren arterial of your nephra under the control of beta-1 receptors, okay? So if your adrenal cortex is functional, so for example in the setting of secondary adrenoline sufficiency, you actually have normal adosterone levels, so your principal cell with an inect channel and rom-k channel working just fine, okay? So you actually do not get a hyperchylemia in secondary adrenoline sufficiency and if you want to test for adrenoline sufficiency, with regards to sequential testing, right? The first thing you want to do is you want to document that, okay, this person has low levels of cortisol, okay? So one way you can figure that out is just by checking the body's cortisol levels at a time where it's supposed to be high, okay?

For example, if you have a, think about it, if you wake up in the morning, you're about to go for one of your met school lectures or the morning of your step one exam, you're like super stressed, you're like super on edge, right? So your cortisol levels should be crazy, crazy high during that period. Well, if it's low, then you're like, maybe this person has adrenal insufficiency, but the thing you do have to that is to ask yourself, where is the lesion, okay? And one way you can confirm that is by checking the CTH levels, okay? If your CTH levels are super high, then you know that there is lots of negative feedback. So the problem has to be at the adrenal cortex, but if your CTH is super low, okay? That means that the problem has to be a step higher in the anterior pituitary, okay? I could also potentially mean the problem is in the hypothalamus, right? Because if you have low levels of CRH, you also have low levels of CTH, okay? Now, and then you can do something known as a co-syntropin testing, co-syntropin is an ACT channel, if you give co-syntropin and the presence cortisol levels do not rise, then you're also potentially thinking of a primary adrenal insufficiency, right? Because it means that, oh, the adrenal cortex is not responding to ACT to exogenous ACT administration. Okay, now let's look at selected disorders with a metiropon exposure. The thing is, metiropon is an inhibitor of 11 beta hydroxylase.

It so happens that 11 beta hydroxylase helps with the conversion of 11 deoxycodisol to cortisol, okay? So in a normal person, if you give me a tire upon inhibitor, 11 beta hydroxylase, those people's levels of cortisol will go down, okay? And because the cortisol levels are going down, you have a release of negative feedback at the anterior pituitary. If you release negative feedback at the anterior pituitary, okay? The person's ACTH levels will go up and the substrate that lies just before 11 beta hydroxylase, which is 11 deoxycodisol in this case will actually go up as well, okay? Now, let's assume you have primary adrenal insufficiency, okay? If you have primary adrenal insufficiency, you give a person an entire point, okay? Again, metiropon will inhibit 11 beta hydroxylase. I mean, in primary adrenal insufficiency, your cortisol levels are already low, but let's say, oh, it goes down even more, okay? But if you have primary adrenal insufficiency, think about it, right? Your ACTH levels will already be high, okay? So giving metiropon will make it even higher. But think about this, we'll be sure of your levels of 11 deoxycodisol. Well, I'm hoping your singing will be low, right? Because again, if your general cortex is not working in other senses, this, for example, you cannot respond to that ACTH stimulation, okay? So your 11 deoxycodisol levels actually low, okay? Now, let's assume a person has secondary adrenal insufficiency, okay? You give me entire point.

Again, you inhibit 11 beta hydroxylase cortisol levels tank, okay? If your cortisol levels tank, you expect that your ACTH should rise, okay? Because you're releasing that negative feedback. But if your anterior pituitary is not working in the setting of secondary adrenal insufficiency, your ACTH levels will feel too high, so they'll be low. And your 11 deoxycodisol levels will also be low, okay? So because again, if ACTH is not around, 11 deoxycodisol will not be made, okay? So in the normal case, you give me entire point. Your ACTH and 11 deoxycodisol levels increase. If it's primary adrenal insufficiency, the only thing that goes up is ACTH, okay? In secondary adrenal insufficiency, both things are down, both your ACTH and your 11 deoxycodisol. And basically, if a person has a primary adrenal insufficiency, well, you just simply need to give them what they're missing, okay? So the thing that's missing in primary adrenal insufficiency, a glucocorticoids, a mineralocorticoids, okay? So you can replenish the glucocorticoids by giving them some ethosome, okay? You could also give hydrocortisone, for example. And then to replace the mineralocorticoids, you can just give a fluidocortisone, okay? And then if a person has secondary adrenal insufficiency, again, remember that the zona glomerulosa is on the control of the reninant and dratensin out of the sterant system.

So the only thing you really need to give those people glucocorticoids, again, like dexamethosone or hydrocortisone, okay? And then just remember the association that if a person has been on chronic steroid use, has been using steroids for a long time and they get some kind of stressor like surgery or an infection or whatever, okay? You want to go ahead and give those people a stressor dose of corticosteroids, okay? Next slide. So a seven-day-old with a prenatal history of a screening ultrasound, revealing increased the nucleotranslucence as filled to pass meconium. So what's the diagnosis? Well, increased nucleotranslucency, what are you thinking about here? Well, I hope you're thinking about Down syndrome, okay? Try Sumi 21, okay? So if you have Try Sumi 21, it's basically like you see all these disparate findings, but the primary problem is neurocress cell migration, okay? So this kid actually has herchproms disease, okay? You're supposed to pass meconium within 48 hours, okay? Your first poop as a kid. So if you have herchproms disease, you may not pass meconium to keep me, I actually have abdominal distension and all that bad stuff, okay? So the pathophysiology is a failure of neurocress cell migration, okay? To the distal GI tract, okay? So if you were to do some kind of biopsy of the rectum or distal GI tract, for example, you'll not see your micenas and your albax plexi, okay? Remember, your micenas plexus is in the sub-ucosa, okay?

Of the GI tract, your albax plexus is in the muscularis external part of your GI tract. Remember, that's between your inner circular and your outer longitudinal layers, okay? So what are the layers of the GI tract, right? So the layers of the GI tract, basically you have three big layers, okay? You have your mucus, actually, sorry, you have four big layers, you have your mucus, okay? After that, you have your sub-mucus, after that, you have your muscularis external, and then after that, you have your cirrhosa, okay? I remember your cirrhosa is lined by simple squamous epithelium, okay? Which is classically known as mesothelium, okay? So mucosa, sub-mucosa, muscularis external, and cirrhosa. Now, it so happens that the mucosa and your muscularis external have sub-layers, okay? So the sub-layers of your mucosa include the epithelium that's on the surface facing the lumen, okay? Below that, we have supportive connective tissue known as the lamina-proprieh, okay? And then below that, we have a kind of muscle known as a muscularis mucosa, okay? Muscularis mucosa. And then for the muscularis external, it has two sub parts, okay? It has an inner circular layer, okay? And an outer longitudinal layer. And a very easy way to remember that is inner. The eye in inner is the same as the eye, which is the second layer of circular. And then the o in outer is the same as the second layer in longitudinal, okay? Easy way to remember that.

And again, remember that your albax plexus is between that inner circuilli layer and the outer longitudinal layer, okay? Contrast that with your mesothelium plexus that is in the sub-mucosa, okay? Now, what are the distinguishing features of the duodenum? Well, the big thing you want to remember are your bruner's glands, okay? Remember, that nasty acidic stuff coming from your stomach sort of kind of needs some kind of neutralization, okay? So you want to make bicarb to counter that. So the way you counter that is with the bruner's glands. Bruner's glands, they make bicarb, okay? They are found in the sub-mucosa of the duodenum, okay? And then the terminal ilium, the special thing with the terminal ilium at the pyrospatches, okay? They are lymphoid cells, they are basically like lymphoid follicles that you'll find in the laminar appropriate of the terminal ilium, okay? Remember, your terminal ilium is also where you reabsorb vitamin B12 and it's the most common region that's involved in in a, in a cron's disease, okay? And if you torture terminal ilium, in cron's disease, you can have a B12 deficiency. Now the esophagus, the esophagus, it kind of, it's kind of special for certain reasons, okay? We know that in the GI tract, we find primarily smooth muscle, but things are kind of different in the esophagus, okay? The upper third of the esophagus actually has skeletal muscle, the lower third actually has smooth muscle, and then the middle third has a mixture of both, okay?

The middle third has both smooth and skeletal muscle, okay? And the esophagus actually does not have a serosa, like other parts of the GI tract, okay? It actually has an adventition. In fact, this is the lack of an advent, for serosa, is one of the mechanisms behind metastasis of esophageal cancer. And then, for the small intestines, remember we have the fancy veli and micro veli, and we have like the pleikers circularis, those measures all increase absorptive surface area, okay? And please, please, please, please remember, this is one very nice way, we can integrate this concept on step one. If a person has, remember your micro veli, serosa constitute your brush border, okay? There are certain high-yout enzymes that work along that brush border. So remember your lactase, okay? So step one could describe like an asian that has flatulence and diarrhea and blood-enough to consuming milk, think about a lactase deficiency, okay? But they know that everyone has memorized lactase deficiency, so they can just pose that answer choice that says deficiency of a brush border inside, okay? And also remember your diabetes drugs, like acarbose and miglato, okay? They work at the brush border, the inhibitisaccharidasis, okay? In this case, alpha glucose side days, okay? So you do not reabsorb sugar, because you're not converting dysaccharides to monosaccharides, okay?

Remember we have no ability to absorb a dysaccharides, and that's how they treat diabetes, because they basically make you poop out, poop out sugars, okay? Next slide. Now a seven-year-old child in a developing country with a recent history of treatment of severe meningitis presents with palarin fatigue. Palarin fatigue, what do you thinking about with that? Anemia, maybe, okay? Now they say that there's a predominance of adipocytes observed on bone marrow aspiration, right? So this is basically code word for a dry tap on a bone marrow spirit, okay? So hopefully you're thinking of a plastic anemia with this, and then you see developing country, severe meningitis, recent treatment, what drug are you thinking about? I'll give you a hint. This drug causes a great baby syndrome. Well, I hope you're thinking of chlurmphenicol, okay? Chlurmphenicol, it's a 50s inhibitor, okay? And actually inhibits a peptidal transferase, okay? And a common side effect, at least not common, I guess, a classically tested side effect is a plastic anemia, okay? So that's what this kid has. And basically the rectic count will be low because you've injured a person's precursor, precursor blood cells, okay? And the ipo levels will be high because your body is like where am I right? So it tries to compensate by increasing the release of ipo from the particular cells in the nephra, okay?

And other drug causes, again, remember your C's like carbamazepine, carbamazepine is a classic cause, remember your antithyroid medications like PT and methemazole, those also cause an aplastic anemia, okay? And if a person has sickle cell, okay? Remember those people are really, really, really depend on the production of their cells. So they could potentially have an aplastic crisis with a parvo B19, okay? Remember parvo B19, remember your classic slap-cheek rash, and remember that it's one of those high-yield singles stranded in fights, probably the only singles stranded in the virus that you do need to know for step one, okay? Now finally in the bottom part of this slide, I talk about Caffeole spots, a small head, hypoplastic thumbs, and a type 2 RTA. So what are we thinking about here? Caffeole spots, Caffeole spots are not only found in neurofibromatosis, or only in all bright hair, deterosidious to dystrophy. If you see Caffeole spots and you see the qualifier that, oh, this person has hypoplastic thumbs and a type 2 RTA or proximal RTA. Well, hopefully you're thinking about Fankone syndrome, okay? Fankone syndrome. Fankone syndrome usually presents with like thumb problems, okay? It can also present within anemia every now and then. You can basically have problems with the transporters in your proximal tubule, so you can actually present with a type 2 RTA, okay? And the pathophysiology here is just a problem with a double stranded DNA break repair, okay?

So your non-homologous end joining essentially does not work, okay? So this is Fankone syndrome, okay? Fankone syndrome. Okay? So, next slide says recurring UT Is in a patient on chronic treatment for type 2 diabetes, okay? So for person who's been treated for type 2 diabetes and they get a ton of UT Is, what's the drug you're thinking of? Well, I hope you're thinking of an SGLT2 inhibitor, okay? Like a canagly flosen, the pagly flosen or impagly flosen, so it inhibits SGLT2, so you do not reabsorb sodium and glucose in the nephra, okay? So glucose shows up in your urine, okay? That's how the lower your blood glucose levels. But again, if you really think about this, if you put more glucose in the urine, right? You're essentially creating a Valentine's Day for bugs, okay? So you could potentially get recurring UT Is with the SGLT2 inhibitors, okay? Now, the proximal convoluted tubule, remember it has microvli, just like the small intestine, and that should mix in because again, it's the workhorse, okay? So it reabsorbs a ton of uh, a ton of nutrients, okay? Now, PTH, I remember PTH stands for phosphate trashing hormone, okay? So the mechanism behind PTH trashing force feet is that it actually inhibits a core transporter of sodium and phosphate at the proximal tubule, okay?

Remember, sodium is primarily an extracellular ion, so as it flows down its gradient, you can pump things against their own radiant, like taking force feet from the proximal convoluted tubule to, like I mean from the urine side of the proximal convoluted tubule into the actual PCT cell, okay? So PTH works by inhibiting that sodium phosphate core transporter. Now, and you're tensing two, and you're tensing two actually increases the activity of a sodium hydrogen antipoder that you find at the proximal tubule, right? So why is this an antipoder and not a same potter? Again, this should hopefully make sense. If sodium is flowing down its gradient into a cell, okay? If you're bringing in positive charges into a cell, you want to sort of counterbalance that by bringing out positive charges, okay? So the positive charge you bring out in this case are protons, okay? So those protons, they basically bind with bicarb that has been filtered from woman's space, yeah, from woman's capsule, okay? They combine with the bicarb under the activity of carbonic and hydrates, okay? Which you find on the microv-light of the proximal tubule. You form carbonic acid, that splits off to form CO2 and water, okay? You reabsorb that, and you basically have the CO2 being converted back to bicarb, which is reabsorbed on the blood side and the protons, which again take that route through the sodium hydrogen antipoder, okay?

So, and you're tensing two actually increases the activity of this sodium hydrogen antipoder. So if it increases its activity, you should sort of realize that you'll be dumping more protons in the urine side of the proximal tubule, and by doing, as you're dumping more of those protons, you actually reabsorb it more of the bicarb, okay? That's the mechanism behind the contraction alkalosis that you get with, that you get in a person that is volume down from taking a diuretic, for example, okay? Because they are volume down, okay? So the volume is contracted, that volume down state increases the activity of the reining and juteins in our dosterone system, so you make reining from the jg cells of the nephor of the afrin arterial that converts a juteincinogen from the liver to a juteincinone, okay? And then the long endothelial cells convert a juteincinone to a juteincin tube, okay? And a juteincin two, one of the things it does again is to increase the activity of that sodium hydrogen antipoder, okay? And just remember that if you go to an experimental question, for example, and they were like, oh, a person has, if you're looking at levels of angiotensin one and two in the pulmonary artery versus the pulmonary vein, where would you have higher concentrations of angiotensin two? Well, I really hope you're thinking about the pulmonary vein, okay? Because it's the endothelium of long capillaries that contain angiotensin, converting enzyme, okay?

So you're angiotensin two levels are pretty much higher in the pulmonary vein because they are distal to the pulmonary capillaries, okay? Compared with the pulmonary arteries, okay? Good. Now, the RTS, as you know, dorsolomyc used dorsolomyc is just like I said, a zolomyc, I remember your sulfur allergies, these drugs work by inhibiting carbonych and hydrates, okay? And when you're even carbonych and hydrates, you can basically replicate some of the findings you'll get in type two or proximal RTA, okay? So remember, it's one of those R Ts where you have hypochylemia, okay? And you'll get an anion gap metabolic acidosis with that, okay? And just real quick, as an aside, what is the bone disorder associated with a mutational carbonic and hydrates too? Well, the answer to that is osteopatrosis, okay? Next slide. Now, these are just some quick, newer associations, right? So what's the infarctate CNS structure in a chronic alcoholic? Well, I hope you're thinking of the mammillary bodies, okay? They look like breasts, you find them around the pineal gland, and that's in renegade course of cough syndrome, okay? Now, the atrophied CNS structure in a patient with a C-EG-train nucleotide repeat the disorder, okay? Well, I hope you're thinking about the Codate nucleus, okay? It's atrophied in Huntington's disease, okay? So you could potentially have something known as hydrocephalus X-Vacua, okay?

Because the Codate is getting smaller, your third ventricle could actually look bigger than normal, okay? Actually, your lateral ventricle could look bigger than normal, sorry about that. Now, arterially schemia, associated with contralateral loss of all sensory and auto function. This is very highly tested on step one. Remember, it's your fancy lenticular stride arteries, okay? Remember, these are derived from the middle cerebral artery, okay? So if you have ischemia of your lenticular strides, basically your posterior limb of the internal capsule doesn't work anymore, okay? And if it doesn't work anymore, all your somato-sensory information is gone because they also are crowding to that space and also all your motor information is gone, okay? The reason you get contralateral motor problems is that by infarcting, remember, your motor, your descending motor fibers, primarily your corticospinal tract that you see at the medallary pyramids, okay? Now, the reason you got also get contralateral sensory losses, again, a lot of your sensory information sort of crosses on the way up through the thalamus, okay? As they go on to the post-central gyros of your of your cerebral cortex, okay? And then lose it in trouble, subsequent coma, athlete hitting the head with a bat. Well, I hope you're thinking of your lenticular epidural hematomas with that. So that's a fracture of like the temporal bone. So your midomelin jolary is gone, okay?

Remember, it's one of the branches of your external carotid, okay? And then crescent chip lesion in a shaking baby, that's a subduro-timatoma, and yeah, remember, besides the shaking baby syndrome, subduro-timatomas may also be found in like, I don't know, like chronic alcoholics because their heads get tiny or person that is old because again, as you get older, your cerebral cortex are shrinks, okay? And remember, it's involvement of the bridging veins that creates a subduro-timatoma. Okay, now, next slide, proximal muscle weakness, skin findings in a smoker with new onset hyponytremia and a CT-detective thoracic mass. So this person is a smoker, right? You've seen a mass, they have lung cancer, okay? We have hyponytremia. So is there a particular kind of lung cancer you're thinking about here? Well, I hope you're thinking about small cell lung cancer, okay? Remember, it's perneoplastica phenomena like SIDH, which can cause a hyponytremia. Remember, it's more hyposmolar, uvolimic hyponytremia. It can also make a ton of ACTH, okay? So you can get a topic ACTH secretion. Remember, that's the one that is not suppressible with high dose dexamethosol, okay? And you can also make autoantibodies against the presynaptic calcium channel, okay? So you have something known as LAMBRED 18 amyestenic syndrome. And when you have that, remember, that's the muscle weakness that gets better with use, okay?

Because the more you use the muscle, the more you recruit calcium to that presynaptic calcium channel, be outcompete the nasty autoantibodies, okay? And then the presynz amosol weakness that improves, okay? So proximal muscle weakness in this case, with skin findings. I added this qualifier of skin findings to get you thinking more of like dermatomyocytes. Okay? The thing is dermatomyocytes actually is relatively common perneoplastic phenomenon. Also, as she said with small cell lung cancer, okay? So what's the difference between polyversus and metomyocytes? Right? So polymyocytes has no skin findings, okay? That means it may always be true, but on MBM is generally true. No skin findings in polymyocytes is. In dermatomyocytes, you do actually have skin findings, right? And it's easy to remember that because there's derm in dermatomyocytes, okay? And the skin findings you get in dermatomyocytes include things like the racoon ice, okay? So that's like the heliotroprasia around the eye. There's the there like if you think of an anti-rhodness of your neck and your like the anterior thoracic cavity, you're thinking more of like the V sign, okay? But if you go to the back, you're thinking more of the shell sign, okay? And then remember those gotron's papules. Now you also get on the on the fingers, okay? You could actually also have a Miller rash, okay? Just like lupus. It's just the Miller rash in lupus does not involve the, it actually spares the nizolibial folds.

The Miller rash actually getting dermatomyocytes does not spare the nizolibial folds, okay? And in dermatomyocytes is the cells that I involved, okay? Are your CD4 positive T cells, okay? And I guess B cells as well, but for polymyocytes is actually more your CD positive T cells that I involved, okay? And those cells, the cause inflammation of your perimysium, okay? And basically the structure around the facecaubs of your skeletal muscle, okay? That's more dermatomyocytes. So you find perimysium and perifacicular inflammation in dermatomyocytes. In polymyocytes, you actually find more of, what am I thinking about here? You have inflammation more around the capsule that surrounds individual skeletal muscle fibers, okay? You have endomysyl inflammation in polymyocytes. And dermatomyocytes is more common in kids compared with polymyocytes that's more common in adults, okay? So think of dermatomyocytes, the D has been an earlier letter in the alphabet that's kids, polymyocytes is being a P letter letter in the alphabet that's more adults, okay? And classically like your muscle markers, right? Like your LDH, so Lathid dehydrogenase, your creatine kinase, okay? Those are classically elevated in in dermatomyocytes, okay? And then you also, chelidodonantibodies, there's your anti-jewel and antibody, okay? That's an antibody against like a TRN into these, I think it's like histidio-ferinase, if these are something like that. We have the anti-MI2 antibodies, okay?

Those antibodies against the helicase, okay? And then we also have antibodies again, the signal recognition particle, SRP, okay? Remember, your signal recognition particle is what sort of threads, partially synthesized proteins through the into the lumen of the endoplasmic reticulum in the process of our protein synthesis, okay? And really the way you do your diagnostic testing here is, classically you've checked for, you observe like, oh, this person's creatine kinase is elevated. And then you're like, okay, let's do some extra stuff here. Every now and then you can do an MRI, okay? But if the MRI doesn't pan out, you could potentially do like an EMG or some kind of muscle biopsy, okay? And the way you treat their models, slash polymyocytes is with steroids, okay? You give us systemic of local, uh, local quadicoids to induce a remission. Now, plural inflammation within and without pain, this is a classic anatomy question for step one. Remember, we have the visceral plurum, and then we also have the parietal plurum, okay? The visceral plurum does not have pain innervation, okay? But the parietal plurum does. So if you have pluritis that involves just your parietal plurum, it hurts, okay? So remember like your intercostal nerves doing factor innervate your parietal plurum, okay? But your visceral plurum generally do not get pain if you have just, if you have inflammation, limit that specifically to the visceral plurum, okay?

And then transudidi versus exudidi-refusions, right? So your transudidi-refusions, they are certain causes, right? So like, I mean, there's tons of causes, but I'll just say in general, like anything that raises the hydrostatic pressure, pressures in the pulmonary vasculature or decreases on cortic pressures would potentially cause a transudidi-refusion, so anything like CHF, CHF raises hydrostatic pressures, if a person has nephrodix syndrome, in nephrodix syndrome, right? Remember your peanut, our human, so your oncotic pressures in the blood go down, okay? Those things can all cause a transudidi-refueral effusion, okay? Remember, a transudidi-refueral effusion is transparent, okay? So the specific gravity should be less than your magic number of 1.012, okay? And then your exudidi-refusions, I would just say to think of an exudidi-refusion as something that arises from increased vascular permeability, okay? And the classic causes of exudidi-refusions include things like cancer, okay? Like neoplasms, infections could also cause exudidi-refusions. Actually, a pretty high yield factor noise that pulmonary amline caused both transudidi-ref and exudidi-refusions, not exactly sure about this, but I'm just proposing a mechanism. My proposed mechanism is that initially when you have those pulmonary amline, you have an increase in hydrostatic pressures that causes a transudidi-refusion, okay?

But as those hydrostatic pressures get too high, you begin to blow out those pulmonary vessels, you then have increased vascular permeability, and you then get an exudidi-refusion. I'm also imagining that maybe as your immune system cells try to come and take care of the clot, the inflammation, increases vascular permeability as well and could potentially create the exudidi-refusion. But again, this is my own teleological explanation, doesn't necessarily mean it's true. Okay, now, light's criteria. This is more of a 30-year concept, but basically just is a set of criteria that says the ratio of your pleural fluid to your serum protein should be less than 0.5, the ratio of your pleural fluid LDH to your serum LDH should be less than 0.6, and your LDH should be no more than two-thirds the upper limit of normal of some magic lab value, okay? Basically, if you meet all three criteria, you have a transudidi-refusion. If you fail to meet, even if it's just one of those criteria, okay? You have an exudidi-refusion. So, see, for example, the pleural fluid protein to serum fluid protein is greater than 0.5, okay? That will be associated more with an exudidi-refusion, okay? So you need to meet all three criteria to be judged as a transudidi-refusion. Okay? I remember your exudidi-refusion is not transparent, okay? So the specific gravity should be greater than 1.012, okay? Now, so those are all light's criteria.

Now, if they describe a sodium-oncete chest pain in a patient with a histro-infosima, I hope you're thinking of the rupture of some kind of blebabola, okay? So that'll be a pneumothorax, okay? And next one says, don't ask super caution with chest drainage revealing fluid of high lipid content, right? So the lipid you're seeing is chial, okay? So chialo, that's a chialo thorax, okay? So you go get that from, I don't know, let's say you have like some kind of lymphatic obstruction by a malignancy or you've transsected thoracic duct, okay? Because remember chialo-microns traveling your lymphatic system, okay? And then if you have a recent victim of a stab wound, and they say, oh, a scotation reveals doneness to precaution and decreased ductile fremmetis. Well, hopefully you're thinking of some kind of liquid involvement in the pleural space, okay? Of a hemothorax because president stabbed, so they probably bled into the pleural species, okay? Now, next slide. The three zones of the prostate, again, this is how they can test histogen or anatomy in step one, okay? If you're going from outside in, okay, there's the peripheral zone of the prostate, okay? If you come to the middle, you have the central zone of the prostate, okay? And then if you come to the area of the prostate that is juxtaposed to the prosthetic urethra, okay? We're dealing with the transitional zone of the prostate, okay?

So the way to remember that the mnemonic is like PCT, like proximal convoluted tubule, you have like peripheral, central, and transitional zone, okay? The transitional zone is also called the peri-rythrozone, again, because it juxtaposed to the prosthetic urethra, okay? Now, if you then understand what I just said, it should then make sense that it's that transitional or peri-rythrozone that overgrows in BPH, that's a benign prosthetic hyperplegia, okay? Because if that region overgrows, that can begin to compress the urethra and you can get BPH symptoms, okay? And the hormone that drives the growth of the prostate, okay, is dihydrotestosterone, remember? Dihydrotestosterone is derived from testosterone by the enzyme known as five-alphoreoductase, okay? So if you inhibit that five-alphoreoductase with a drug like finasteride or detastoride, you decrease the synthesis of DHT. If you decrease DHT synthesis, you can over a time, like, over like six months shrink the size of the prostate and chronically relieve the symptoms of BPH. But if you're like, I don't like patient away for six months, or you're like, okay, I'll give you this six-month medication, but let me also give you something that can sort of immediately relieve your symptoms. Think of giving an awful one blocker, okay? Like Tamsulocin, for example, Tamsulocin is an awful one blocker.

Most specifically, the alpha-1 AD receptors in the prostate, and by opening up the urinary sphincter, the person's urine can drain up pretty well, okay? You can also give other drugs like Prasusin, Doxazusin, Terasusin, but those drugs are less specific for the alpha-1 receptors in the prostate because they are also blocked the alpha-1 receptors you find on the vasculature, so they can decrease the systemic vascular resistance and cause an orthostatic hypertension as a side effect, okay? And other things you could do for a BPH, you could chop off some part of the prostate, so you can do like a trans-uritrory section or whatever it's called. Let's see, another alternative. Let's see the person, they could give you like a mean step one question where they say, well, this person has like superpubic fullness, right? And they have like post-terrinolyzotemia picture where their B-wing to creatin is like, at least in the early phase, yeah, the B-wing to creatinine could be like, I don't know, like less than 20 and phenol, the phenol could be like greater than 1% and stuff like that. You're seeing like, oh, post-emerrinolyzotemia and you can see what's like the quickest way to relieve these person symptoms. You can do that by inserting like a catheter into the bladder, like a fully, okay? So you can drain that bladder, okay? You can very quickly relieve the obstruction because remember an obstructive neuropathy is the most common cause of a post-terrino-accururinophilia, okay?

Now the common location of prosthetic malignancies, think more of the peripheral zone, okay? That's where most prostate cancers are right, right? That's why when you go for a digital rifle exam, they try to, and guys, again, remember to go for those kinds of exams when you get older, but basically you'll pop it the peripheral region of the prostate and you could potentially try to detect a malignancy of the malignancies can also arise in other regions, okay? So I guess that's why a prostate biopsy may ultimately be helpful. Okay, now blood supply to the prostate, blood supply to the prostate comes primarily from the inferior vesicle artery, okay? That's branch of the internal iliac, okay? And in general, if you remember the arteries, you will remember the venous drain, right? So you should make sense that some, they probably exist like some inferior vesicle vein that drains the prostate, that then supplies a drain's blood into the internal iliac vein, which then becomes the IVC at some point, okay? And 55-year-old female with, oops, not female, originally or female, let me change that to male, because females do not have prostate, okay, but to the reward. So 55-year-old female with, sorry, male, oh, divine, come on. 55-year-old male with a history of treated prostate cancer presents with low back pain, low back pain, low back pain, okay?

So when I see that an MRI or bone-slash bone scan reveals a singular lumbar lesion, well, I hope you're thinking about a metastatic prostate cancer, okay? Remember prostate cancer tends to cause plastic lesions, okay? So one of the higher causes of plastic lesions, okay? And the way you can treat this is potentially give, because remember, Androgen's drive the growth of the prostate, so you can give an Androgen receptor blocker like a flutamide or bicarlutamide, okay? Like flutamide or bicarlutamide, okay? And then, yep, next slide. So 45-year-old male presents with 10 out of 10, sodium onset abdominal pain. Now, here's the kicker. EKG reveals an irregularly irregular interval. What is this? Well, I hope you're telling me that this person has acutemizontaric ischemia, okay? If you have an irregularly irregular interval, you have e-fit, okay? If you have e-fit, you could potentially have like stasis of blood in the left-itrella pendage. You can create an embolus, okay? Remember, stasis is part of your sheenomonic and vericostriode, okay? So you can form an embolus, you can flick off and go to the, go to one of the blood vessels in the, you can actually go to one of the blood vessels in the brain, you could get a stroke, or you go to one of the blood vessels in the GI tract, classically, the supermizontaric artery, okay? The supermizontaric artery. So this person has acutemizontaric ischemia from embolization of clot, okay, to a GI tract blood vessel, okay?

Again, most commonly on exams, it's the supermizontaric artery. So what are the branches of the supermizontaric artery? You may be like, hmm, there's no way you need to know these things for step one. Well, think again, okay? You do actually need to know the branches of the SMA, okay? The other branches of your GI tract blood vessels like your cilia artery and stuff like that, okay? So the SMA, it's the blood supply to the mid-gut, okay? Remember, your cilia artery is the blood supply to the foregut, and your IMA is the blood supply to the hindgut, okay? So your supermizontaric artery may basically supply blood from, basically supply to like your ascending colon, supplies the proximal two-thirds of your transverse colon, up on, basically like approximately up until the splenic fracture, okay? So remember, the splenic fracture is a watershed area, okay? Because that is where like SMA blood flow stops, and that's sort of where IMA blood flow stops as well, okay? So again, I could have easily said in this question that a person had left of a quadrant pain, okay? Because the splenic fracture was his schemic, okay? And remember that that splenic fracture is where vagus nerve, your crinon nerve 10, vagus nerve inner vision ends, okay? So the branches of the supermizontaric artery, one branch is the right colic artery, okay?

That supplies your ascending colon, then there's the middle colic artery that supplies your transverse colon, at least the proximal two-thirds, and then I believe there's also an iliosyco branch that sort of supplies your elium, okay? Your elium, your appendix, your sycam and stuff like that, so iliosyco, so ilium plus sycam, okay? Remember, the appendix is sort of in that iliosyco area, so that should sort of, you can sort of make that knowledge leap. And then there is another branch known I believe as the, let's see, the inferior pancreatic adenolodory, okay? The inferior pancreatic adenolodory. Remember, the inferior pancreatic adenolodory is anastomosis with the anterior superior pancreatic adenolodory. And hopefully you remember from anatomy that the anterior superior pancreatic adenolodory is a branch of the gastro adenolodory, okay? The gastro adenolodory. Remember that gastro adenolodory supplies, basically forms a part of the right gastro amental artery that supplies like the greater curvature of the stomach, at least one half of it. And that gastro adenolodory also happens to be a branch of the, common hepatic artery, which is a branch of the cilia artery, which is the blood supply to the foregut, okay? So again, cilia artery forms the common hepatic artery, which has the gastro adenolodory as a branch. The gastro adenolodory is the creator of the right gastro-omental, we can call it gastreypipluic artery, that supplies the greater curvature of the stomach, okay?

But another branch of the gastro adenolodory is the anterior superior pancreatic adenolodory, that an asthmosis with the inferior pancreatic adenolodory, which is a branch of the superior mesenteric artery, which is the blood supply to the midgut, okay? No, that was kind of a lot, but it's one of those things you probably want to know for step one. Okay, now differentiating not cracker and SMA syndromes, okay? So not cracker versus SMA syndromes, so not cracker syndrome. Basically, these two syndromes involve something that's been compressed between the superior mesenteric artery and the yoder, okay? In not cracker syndrome, the thing that is compressed is the left reno vein, okay? If you compress the left reno vein, right? You won't have good drainage of your left testicular vein. And if your left testicular vein is not draining well, you could potentially imagine that you could have like a left-sided varicoseal, you could have like biny or testicles, okay? So an easy way to remember that it's the left reno vein that's compressed is to remember that in not cracker syndrome, your nuts hurt, okay? My belief people refer to the nuts as, you know what I'm talking about, okay? So I'm going to keep going from there, but not cracker syndrome is left reno vein compression between the superior mesenteric artery and the abdominal yoder, okay? Now, SMA syndrome, the thing that's compressed between the SMA and the yoder in this case is your duodenum, okay?

So if you compress your duodenum, you could potentially imagine a person presenting with like signs of a GI tract obstruction, okay? And just real quick, let's assume you've got a question about a person with a history of like a low posterior heraline, lymphedema around the neck, elevated blood pressures in the arms, but low blood pressures in the legs, and they tell you that the person has recurrent UT Is, and they say that, oh, you see a GI anomaly with a CT scan or an MRI of the abdomen. Well, I hope you're thinking about Horseshoe kidney, this patient has tunnel syndrome, okay? Horseshoe kidney, where the inferior pool of the kidney fuses, okay? And it's stuck under the inferior mesenteric artery, okay? So next slide. So comparing means of two groups, so how do you compare means of two groups, okay? Use the T test, okay? T for two. How do you compare means of three groups? You use the another test, okay? Analysis of variance, so three words, so you compare means of three groups, okay? Now, what's the test that helps you calculate differences between categorical variables? Well, I hope you're thinking about the chi-square test, okay? And when a confidence interval results insignificant? Well, they love to test this on step one because it's sort of something people maybe don't realize for some reason, right? So remember, if two numbers are the same, if you take the difference between those numbers, you get a zero, okay?

So if there are no significant differences between like difference of means, for example, if your confidence, it means your confidence interval will cross zero, okay? So if your confidence interval crosses zero, okay? There's no significant difference between like difference of means, okay? Now, remember relative risk is a ratio, okay? If you have the same number in the numerator and the denominator of a ratio, okay? If you take that ratio, you get a value of one, okay? So what do I mean by that? The thing I mean by that is whenever you have a relative risk and you get a confidence interval and it crosses one, there are no significant differences between the two relative risks that you're trying to compare. You can also extrapolate that knowledge to another ratio like the odds ratio, okay? Now, the mean, okay? How do you get the mean? You take a series of numbers, add them up, divide by the number of numbers and boom, your mean shows up, okay? Now, how do you calculate the variance? Well, I'll just sort of talk you through this, but basically what you do is, each of the numbers in your numbers set, you subtract the mean from those numbers, okay? And then that mean difference for each of the numbers, you'll basically square all of them, okay? And when you square all of them, you add those numbers all together, okay? So you get a sum of the difference of means, okay?

Now, you have that sum of the difference of means, you then go ahead and divide that number by your sample size, so your number of numbers, okay? When you make that division, you get your variance, okay? So your variance in words, because again, it's much easier to just sort of think about certain things, it makes more sense than trying to memorize the will inily. But basically your variance is the sum of differences in means divided by your sample size, okay? And if you so happen to take the average, I mean, the square root of that variance number, you essentially get your standard deviation, okay? Your standard deviation, if you took that number and divided it by the square root of your sample size, your n, you'll get the standard error of the mean, okay? And that standard error of the mean is kind of useful, because it helps you calculate your confidence intervals, okay? So how do you calculate your confidence intervals? You basically take your mean, okay? And you go plus or minus some number, multiply by the standard error of the mean, okay? So what do I mean by some number? Some number relates to whether you're trying to find a 95% confidence interval or the 99% confidence interval. There's the 95% confidence interval you're looking for. You multiply your standard error of the mean by 1.96, just use two for step one. And then if you're trying to do that for your 99% confidence interval, you go ahead and multiply by 2.58, okay? Just use 2.64 step one.

Okay, and then your confidence intervals, what do they tell you? They essentially tell you that for the sample mean you've gotten, the population mean with 95% confidence falls within whatever boundary you derive from the calculation we just mentioned, okay? So there'll be a 5% chance that the population means does not fall within your confidence intervals. If you're going with a 95% confidence interval, for example, okay? And then remember your correlation coefficients, they basically show your relationship between like your dependent and independent variables, okay? If it's plus one, it means that there's a positive correlation, if it's minus one, it means there's a negative correlation. And the closer your R value is to the absolute value of like one, okay? You have a stronger correlation that way, okay? But remember, correlation does not imply causation. So next slide, 13b, so that's our last slide. So as you've in a class mean score of 80 on step one, sample size of 16 and a standard deviation of five, how many students scored above the 95th okay? So you could use all these numbers, I gave you or you could just think, okay? You actually do not need to use these numbers. So think about it. If I'm asking for how many students scored above, okay?

So notice, this question is very, so asking a question that says how many students scored above the 95th 95th percent confidence interval versus a question that says how many students scored outside of the 95th percent confidence interval? Those are different questions. If I'm asking, or how many people scored outside the 95th, the 95th percent confidence interval? And thinking more of the people that are like the extra, the 5% that I'm not accounting for, that 5% at the 2.5% that scored on the low end of things and the 2.5% that scored on the high end of things, okay? But if I 'm asking for the people that just scored above the 95th percentile, I'm asking only for that 2.5% okay? That's scored above the 95th percentile in this question. And I mean we can easily calculate that, right? We know that the standard deviation is five and the sample size is 16, okay? So we'll calculate the standard error of the mean, okay? So standard error of the mean will be five divided by the squared of 16, which I believe is one and a quarter, so that's 1.25, okay? So this is where the 95th percent confidence interval, we do 1.25 multiplied by 2, okay? So that's a 2.5. So basically, any score above an 82.5, okay, is higher than the 95th percentile, okay? So if we want to detect the actual number of students that scored above the 95th percentile, we just want to take 2.5% of the total sample size, which is 16, okay? So how do we do that?

Well, let's see, I don't have a calculator of me, but 10% of 16 is 1.6, right? And 2.5% is a quarter of 10%. So that means if you take a quarter of 1.6, that means 0.4 students scored above the 95th percentile, okay? And again, remember, this is outside two standard deviations and you can increase the power of a study by just increasing your sample size, okay? Increasing your sample size, okay? Another way you can increase the power of your studies to increase the effect size, right? So think about it, if you're trying to measure differences between like the wealth of Bill Gates and like the average match student, like that's a large effect size. Bill Gates is a billionaire. Match students, unfortunately, do not have as much money as Bill Gates. So that's a big effect size. The power of your study will be good, okay? But if you're trying to compare the incomes between two average match students, right? The income differences will not be big. The effect size is kind of small in that group, okay? So that's the end of today's discussion. I hope you find this helpful. I just tried to integrate as much as possible with these slides and I'll see you at the next podcast. Thank you.

The Left Anterior Descending Artery (LAD).

Right Coronary Artery (RCA) infarct; associated with PR interval prolongation.

The posterior medial papillary muscle; it has only one blood supply from the PDA/RCA.

ACTH (derived from POMC), which also acts as a precursor for MSH.

Primary AI causes hyperpigmentation and hyperkalemia; Secondary AI does not cause hyperpigmentation or hyperkalemia because ACTH/MSH are low.

The muscularis externa.

To secrete bicarbonate ($\text{HCO}_3^-$) to neutralize acidic chyme from the stomach.

The anterior superior pancreaticoduodenal artery anastomoses with the inferior pancreaticoduodenal artery.

AV block (due to nodal artery supply) and rupture of the posterior medial papillary muscle.

Glucocorticoids (e.g., Hydrocortisone), Mineralocorticoids (e.g., Fludrocortisone). (Note: The transcript mentions replacing both.)

Dermatomyositis involves perimysium/perifascicular inflammation; skin findings include Gottron's papules and heliotrophorasia (raccoon eyes).

Duodenum has Brunner's glands ($\text{HCO}_3^-$); Terminal ileum absorbs Vitamin B12. Crohn's disease most commonly affects the terminal ileum.

Co-syntropin testing (ACTH challenge). Primary AI: Cortisol fails to rise. Secondary AI: ACTH levels are low.

Compression of the left renal vein between the SMA and abdominal aorta; presents with left-sided varicocele/varicular signs.

AV block (due to nodal artery supply) and rupture of the posterior medial papillary muscle.

Glucocorticoids (e.g., Hydrocortisone), Mineralocorticoids (e.g., Fludrocortisone). (Note: The transcript mentions replacing both.)

Dermatomyositis involves perimysium/perifascicular inflammation; skin findings include Gottron's papules and heliotrophorasia (raccoon eyes).

Duodenum has Brunner's glands ($\text{HCO}_3^-$); Terminal ileum absorbs Vitamin B12. Crohn's disease most commonly affects the terminal ileum.

Co-syntropin testing (ACTH challenge). Primary AI: Cortisol fails to rise. Secondary AI: ACTH levels are low.

Compression of the left renal vein between the SMA and abdominal aorta; presents with left-sided varicocele/varicular signs.