DIP Episode 84 - USMLE Step 1 Rapid Review Series 1

Okay, welcome. My name is Divine. I am a PGI 1 transitional year resident that's going into radiology and this will be the 84th episode of the Divine Intervention Podcasts. In this episode I am going to start a new series that I will just do randomly from time to time. I will title this integrated USML Step 1 review. Basically I've got in some recommendations from people that it may actually be pretty nice for me to essentially have like 30-minute quick podcasts where I pick out like a few high-yield USML topics randomly from the different disciplines that are tested on the exam and then I just talk about like maybe introduce the concept with a case and then talk about like many high-yield facts relating to that case. Explain mechanisms, talk about classic presentations and whatnot. So having gotten that feedback from many people I have decided to just start with that. See the kind of feedback I get. If people like this particular like series I'll just keep making it making a series like this indefinitely. Besides the regular podcasts that I that I make. So I'll just go ahead and try one today. So what if you get a question? So let's I guess begin. So what if you get a question about a woman that's you know slushing her wrists and is in many tenors relationships? Well I hope with that you're thinking about borderline personality disorder. Remember those people have splitting as a as a defensive mechanism. Okay next one.

What if you get a question about a person that you know they hate people let's not say they hate people but they like being alone. They do not train any kind of emotion. They'll rather hang out alone. Work from home. What kind of personality disorder are you thinking about? Well I hope you're saying sketch disorder. Remember sketch soids avoid. Okay. Skits or personality disorder. Those people they don't like people and like their owners and they don't like hanging out with people. Right. And please don't confuse sketch soids with a sketch so type or remember a sketch so type or people are people that you know they kind of have like flamboyant dressing. They have like weird beliefs. It's a personality disorder and then don't confuse I guess these diagnoses were right with some other high yields like electric disorders. Right. So like births psychotic disorder where persons like hearing voices for less than a month or schizophrenia from disorder where the person has you know like psychosis but it between like one to six months versus schizophrenia where they have like the psychosis the hearing voices the flat effect and whatnot for greater than six months. Right. And then also don't forget schizoaffective disorder that's a known that screws up a lot of people on exams. Where basically the patient has like a predominant psychosis and then in addition to that they have some kind of you know like more disorder like depression or menia.

Those are the classic mood disorders on when MBA means. And I mean as an aside right if you get a question about a person you know has a recent stressor and they have like depression like symptoms but you're like man I'm trying to do this CIGI CAHPS 5 out of 9 business and this person is not meeting full criteria right. So it's like maybe they have like CIGI CAHPS symptoms for a week or they have symptoms for more than two weeks but you only count like three out of nine symptoms. If you ever see stuff like that I want I want to encourage you to consider adjustment disorder. That's a very classic where adjustment disorder shows up on on MBA exams. Now what if you get a question about a person that's being treated for bipolar disorder right and then they tell you oh this person was recently diagnosed with hypertension and then they start taking a hydrochlorothia side right and then now they are presenting to the emergency room with tremors. Well if you see that I really really really hope you're thinking about lithium toxicity right so remember diuretics increase the toxicity of lithium. In fact you know let me make life even easier for you. There's a useful principle I've talked about this and multiple podcasts in the past.

Anything that activates the Rinin and Jotensin Outdosterone system will increase your lithium toxicity right because if you think about it if you activate your Rinin and Jotensin Outdosterone system right you make more out of the student and if you make more out of the student remember our dose turn increases the activity of that in the channel that you find at the level of the collecting doctor the principle cells of the collecting doctor and lithium goes into those principle cells through that in the channel. So if you're increasing the activity of that in the channel right because our dose turn is around because you have volume down and you've activated your Rinin and Jotensin Outdosterone system you can imagine it's not very hard to imagine that oh if you increase the activity of that in the channel you'll increase the absorption of lithium through that channel and that can then trigger more lithium symptoms. So that's kind of like a high-yield thing you want to keep at the back of your mind right and again remember lithium in addition to causing like tremors in fact that's like the one of the classic MBME side effects.

Remember it can also cause like hypothyroidism it can also cause like Epstein's anomaly remember that whole thing where you have like an actualization of the right ventricle right and remember that lithium is one of those drugs in psychiatry that has been shown to decrease the risk of suicide that's another property that's actually shared with the typical anti-psychotic clasping remember that can cause a granuloseitis and also don't forget lithium can cause nephrogenic diabetes in cipitis so classically you'll talk about a person being treated for bipolar disorder and then they have like hyperneutrimea but they have like hypotonic urine right that basically does not correct with the administration of like an EDH analog like this more present when you do like a water deprivation test right so remember right lithium you know sort of messes up with the signaling cascade of EDH so basically remember EDH does most of his job studying at the principal cell of the collecting duct by acting on those of visual press in a V2 receptors on the blood side of the principal cells of the collecting duct so the thing is if you have nephrogenic diabetes in cipitis the regulation of electrolyte concentrations will be fine all the way till you get to the principal cell of the collecting duct right so I guess you know what maybe to give some more explanation here let me talk about the things that happen on that normal circumstances right so on the normal circumstances right when you get to the proximal convoluted tubule the urine that you find at the PCT will be the same concentration same osmolality as the as basically have the same osmolality as your plasma right because remember you have not on the gunning kind of reabsorption yet now when you get past the proximal convoluted tubule the urine osmolality actually stays similar to plasma osmolality as well right because remember proporti

onal amounts of sodium and water are absorbed at the proximal convoluted tubule right and then after that if you then keep going doop doop doop doop doop through the like the loop of Henley right so like the thin descendant limb of the loop of Henley and then you begin to ascend right your urine actually gets more concentrated so it becomes like hypertonic relative to the plasma right because remember the loop of Henley right especially like the medallary portion remember that's where you have that high salt concentration so that reabsorbs the ton of water right so that actually that's permeable just to water but not permeable to ions so that actually increases the concentration of of your urine and then as you then begin to go up up up traverse the thickest end of the limb of the loop of Henley and then the distal convoluted tubule remember all those transporters like for the thickest end of the limb of the loop of Henley remember you have that sodium potassium a two chloride a transporter and then remember the that reabsorbs sodium potassium and two chloride and they remember you also have a sodium chloride same powder on the urine side of the distal convoluted tubule those transporters are only permeable to salt they are not permeable to water so as urine traverses the thickest end of the limb of the loop of Henley and the distal convoluted tubule the urine actually becomes hypo or smaller relative to the plasma right so it becomes hypotonic relative to the plasma but the thing is on the normal circumstances when you get to the principle cell of the collecting duct ADHD acts on viso pressing v2 receptors okay and helps you insert aqua porines so reabsorba tonal water right from the urine and then your urine becomes hypotonic but if a person has nephrogenic diabetes and syperdose right all these things have said that happen on the normal circumstances happen with th

e exception of the distal nephron right so sort of starting at like the collecting duct area ADHD cannot do his job so your normal hyprothonic urine is not hyprotonically it becomes hypotonic because you essentially just peen out water with your a ton of like free water with your urine right remember you're essentially having like an extension of the hypotenicity coming distal to the thickest end of the loop of Henley and the distal convoluted tubule because ADHD is not doing its job at the level of the principle cell and then I guess to sort around up this case don't forget that the mechlocyling remember it's a tetracycline you actually use it to treat SIDH remember that it actually has a nephrogenic diabetes in syperdose as a side effect in fact we basically use the nephrogenic diabetes in syperdose side effect of the mechlocyling to actually go ahead and treat SIDH and I guess just to sort of round things out remember right if for example you notice a person has hyperneutrymia and hyper hypotonic urine right so hyperneutrymia hypotonic urine and you do what are the probation tests and then you give them the mechlocyling I mean you give them decimal pressing and their urinous molality goes up and then the acermos molality comes down I really hope you are thinking about the central diabetes in syperdose on that those circumstances okay what if you get a question about you know pneumonia right so like you have like an infiltrate right like a low-bind infiltrate in a cystic fibrosis patient right and let's assume the cystic fibrosis patients to in three years old right so what do you think about well I really hope you are thinking about pseudomonol pneumonia remember the most common cause very high of the most common cause of pneumonia in CF patients before the age of like 18 to 20 a staff four years but after the age of like 20 for the most part is pseudomonas right s

o for this patient right they have pseudomonol pneumonia because they are 23 year old as cystic fibrosis patient so the next question I guess I have is how do you treat pseudomonas on that these circumstances right so you want to definitely want another drug that covers pseudomonas on your NVME exams right so don't forget your amino glycosides right so like gentamysin your mysin amicasein tuberomycin streptomycin streptomycin is used more for TB tuberomycin is used quite a bit in CF patients you can use these amino glycosides they cover pseudomonas remember your amino glycosides like 30s inhibitors they are like bacterial cytol and the stop initiation right and then don't forget your pepteso right so piparasal and tizobactam remember tizobactam is is a bit of lactamys inhibitor pepteso does cover pseudomonas it also covers an aerospority well right and then don't forget your carbopenem right so like meropenem, urna-penem, imipenem, guri-penem those drugs also cover pseudomonas and then don't forget astrayon and remember astrayon is a monobactam right and also those covers pseudomonas astrayon amactually has a rule only covers gram negatives very high you to know that for exams and then don't forget septazidim right that's a third genersion cephalosporin that also covers pseudomonas and then cephepim remember cephepim is also a fourth is a fourth genersion cephalosporin that very specifically covers pseudomonas as well and basically all these drugs are reeled off after you amino glycosides right so like peperacillin tezobactam, urna-penem, astrayon amactythazidim, cephepim these are basically all cell wall inhibitors right so they basically destroy transpeptidids right remember transpeptidids is an example of a penicillin binding protein okay so they inhibit transpeptidids so you don't have cross-linked of alanine residues right so you don't make the bacterial cell wal

l so these drugs are cell wall inhibitors but please don't class I mean astrayon am is also a cell wall inhibitor but remember that the penicillin binding protein binds to his penicillin binding protein 3 okay so that's why for the most part astrayon am has very little cross reactivity with the other cell wall inhibitors and I mean also don't forget your fluoroquine alons can also cover pseudomonas right so like cyprophloxacin, livofoloxacin, gadi-floxacin, moxifloxacin, nalidixic acid, those drugs all cover all cover pseudomonas and I mean remember right your fluoroquine alons they work by inhibiting a DNA chyris right that's a that's a two-piece summaries and I guess well we are talking about like one poster child box pseudomonas let's talk about the drugs that cover another poster child box right Mercer, Mercer remember you can treat Mercer with vancomycin remember vancomycin works by essentially binding to the alanine residues that you find on like diala right remember diala makes up the cross-links of the bacterial cell wall right so vancomycin binds to diala so if you binds to diala transpeptidys does not find any alanine that it can cross-links right that's essentially how how vancomycin works so remember that sort of ties into the mechanism of resistance to vanque where if you chain that alanine residues to lactate then vancomycin has no ability to bind anymore so you essentially evolve resistance to a vancomycin under those circumstances so vanque does in fact cover Mercer don't forget that dapto-mycin right also covers Mercer remember dapto-mycin works by you know basically like inserting like holes in the cell membranes of gram positive bugs remember dapto-mycin only works for gram positives so it inserts holes in the membranes of gram positive bugs remember it can cause myopathy as a side effect that's a high yield thing to know and then don't forget so if

you see a person that's being treated for Mercer and then the accrediting kaini starts growing up you really want to think about to adapt to mycin at toxicity under those circumstances right and then don't forget the nasolid remember linesolid right and also cover Mercer remember linesolid is a bacteriostatic drug it's a 50s inhibitor right he basically shuts down initiation of of what's that process called translation okay and remember right in addition to covering Mercer linesolid actually does have the ability to cover VRE right so vancomycin resistant interococcus and remember that linesolid can in fact triggers serotonin syndrome right because remember it's actually a weak monoamin oxidase inhibitor right so it has like serotonergic activity and then other drugs that can cover Mercer right don't forget yourself power lines remember it's a cell wall inhibitor it's a fifth generation sephalosporine in fact that's probably the only fifth generation sephalosporine you need to know for your USML exams and then other like I guess weaker drugs that can cover Mercer we have like trimethyprim sulfomythoxysone so back trim right actually does cover Mercer remember that back trim right is made up of trimethyphythoxysol and trimethyprim those drugs individually they actually do not they're individually bacteria static when you combine them together they become bacteria side of right and the way so from the thoxysol works remember eating hebits a dihydroethorita synthetase okay and then trimethyprim then goes ahead to inhibit dihydrofolita reductase so those drugs together can be used to treat a Mercer doxycycline right remember that's a tetracycline remember your tetracycline is a 30th inhibitor but they are bacteria static and remember the cause of photosensitivity and they can cause like tooth or discoloration so if a kid is less than seven years old they should probably

not be on a on doxycycline the only exception to that will be a kid with a Rocky Mountain spotted fever if a kid is less than seven and they have Rocky Mountains spotted fever you can actually infact give them a doxycycline because Rocky Mountains spotted fever is rapidly fetal if it's not treated so a doxycycline does in fact cover Mercer and trimethyprim that's another 50th bacteria static agent that's also effective against Mercer right and other like you know like anaerobic infections and I mean I'm not saying that you necessarily choose bacteria as your treatment of choice for a Mercer infection you probably go with vancomycin but I'm just basically trying to walk you through all the different drugs that can cover Mercer and the mechanisms of action so hopefully that was a very good quick high odontai about it review for you there okay now let's talk about I guess another case right so what if you get a question right so you have a lady that's in fertile she's been trying to have kids for a while it's not working out so well and she has like a BMI of 34 and you can see like signs of her sutism on a physical exam and then they tell you that she has like dark velvet lesions on her skin if you see that I really really really hope you're thinking about PCOS right so polycystic ovarian syndrome right then what is PCOS basically PCOS is a no big guy in the solder and you make the diagnosis if you meet two out of three criteria right so don't forget your three criteria right so one is um uh come on divine think one is like having signs of hyperandrogenism right unlike a physical exam or if a person has like polycystic ovaries on ultrasound right that's kind of easy to remember or if they have signs of an ovulation right so like irregular means is that essentially counts as a sign of an ovulation if you see that if you meet two out of those three criteria you can make th

e diagnosis of PCOS right now one classic thing they will try to mess up with your head with on exams is they'll say oh uh which of the following is criteria for the diagnosis of PCOS and you'll put like LH to FSH being a greater than two to one that is wrong okay that's a classic finding in PCOS but that is not part of the defining characteristics of PCOS that's not one of the diagnostic criteria so you don't want to mess that up on an exam right so how do we treat PCOS right so obviously PCOS you can treat it with like OC Ps OCP is actually helping two is right they can sort of shut down the hyperandrogenism that you find in PCOS but they can also help with like you know kind of regularizing the menstrual the menstrual cycles now you should definitely keep in mind right that these people that have PCOS right if they're less than 50 years old and they have like a prolonged history of PCOS and they have like abnormal like vaginal bleeding you actually want to go ahead and do like an endometrial biopsy sometimes they call it endometrial sampling on NVME exams you want to go ahead and do endometrial sampling to roll out endometrial cancer in those people right because they've been exposed to like prolonged levels of estrogen on opposed estrogen for long periods of time so that's one thing you'd want to screen those people for and I mean if they infertile like this patient right you know you probably want to consider giving them a Serm right so like a selective estrogen receptor modulator right like clomifin I remember clomifin works by it's essentially like a partial estrogen receptor agonist at the level of the hypothalamus right so think about it if you're a partial agonist right in the presence of a full agonist you essentially actin as an antagonist so basically it's like you could normally get fully effect from activating this receptor but now you're getting partial

effect too essentially actin as an antagonist so think about it right if you give clomifin it performs like again its real mechanism of action is it's a partial estrogen receptor agonist but the thing is it essentially acts as an antagonist for reasons I just explained so that effectively releases the negative feedback of estrogen at the level of the hypothalamus right then as you know if you kill that negative feedback you operate your HPG axis right your hypothalamic agonadala axis and that leads to fertility right so that's how you treat the infertility that accompanies a PCOS and one thing I actually want to see here is this concept of a partial agonist right remember again partial agonists are full intents and purposes antagonists right so it's a concept you want to be able to link across multiple fields of learning multiple fields of learning on the USMLE step one right so I just talked about how clomifin is a serum that works by being a partial agonist at estrogen receptors so it's effectively an estrogen receptor antagonist don't forget if you're thinking about bitter blockers right like as a bitter law and pin the law remember those are partial bitter receptor agonists but again they're effectively acting as antagonists and if you're also going to the land of schizophrenia and uetipical anti-psychotics don't forget drugs like RIP personal RIP personal is a partial dopamine receptor agonist what it effectively acts as a dopamine receptor antagonist that is why it is used in the treatment of of schizophrenia and I mean I guess since I mentioned terms don't forget your other terms right so like tamoxifen tamoxifen remember right it's like an estrogen receptor antagonist in the breast but it's an agonist everywhere right so like the uterus and bone right so if because it's an estrogen receptor agonist in the uterus it can op your risk of endometrial cancer and b

ecause it's an estrogen receptor agonist in bone it can actually decrease your risk of osteoporosis and then we have a relax if it relax if it's an estrogen receptor antagonist in the breast and uterus right so it actually does not increase your risk it does not increase your risk of endometrial cancer but it's actually an estrogen receptor agonist in the breasts I mean in bone so it actually decreases your risk of of osteoporosis remember we said that anything that has estrogenic activity will increase the synthesis of osteoportagring and osteoportagring basically is a dummy receptor for rank ligand so if you bind up your rank ligand rank ligand that comes from osteoblasts will never interact with the rank receptor that is found on osteoclasts so you not have bone resorption in fact that's why women that are less than 50 years old are kind of protected from osteoporosis but after the heat the age of 50 and they are ovaries basically shrink down and then they lose their estrogen then they have a higher risk of osteoporosis remember that's also kind of the wheel this drug they not swim up works they not swim up is a monoclonal antibody against a rank ligand right so if you bind up rank ligand again rank ligand does not interact with the rank receptor and you do not reserve your bone okay so let's jump up to another case right so what if you get a question about you know like hyponytremia and hyperkelimia in a college student with so hyponytremia so low sodium and hyperkelimia so hypotassium in a college student with neck stiffness right if you see that I really really hope you're thinking about like an isyrimin angiolis and waterhouse of fredricksinac syndrome right so remember an isyrimin angiolis can actually like infect the adrenal glands and then the person can have like adrenal hemorrhage and that can essentially cause a waterhouse of fredricksinac waterhouse of f

redricksinac syndrome right and the thing is you should really think of this as a diagnosis if you have like a meningitis patient that you know just suddenly decompensates and then they begin to present with like signs and symptoms of like adrenaline and sufficiency right so like they have like hyponytremia and like hyperkelimia remember our dosterum right helps with reabsorbing sodium and wasting potassium in the urine so if you have a low dose term because your adrenal gland is like all screwed up you'll be hyponytremic and you'll be hyperkelimic right and these patients will usually on exams also have like prominent hypertension because they're effectively going into like a kind of shock now what if you get a question right about a patient you know they're septic and they have been recently studied treatment for our paroxysmal and nocturnal hemoglobinuria well if you see this right again sort of going with a nice ear theme theme here I remember that P&E tried paroxysmal nocturnal hemoglobinuria it arises when a person has like a peak age in mutation if you have that peak age in mutation well guess what you don't have on your rib lot cells GPI anchors so if you don't have GPI anchors on your rib lot cells like CD55 and CD59 you will effectively be unable to protect yourself against a complemented medial damage right remember that membrane attack complex that goes with like C5 to C9 so to basically treat that condition you make a monoclonal antibody gain C5 like it will assume that okay but the thing is remember that your terminal complement components starting from C5 actually help with protection against my cereal infections so the thing is patients that have terminal complement component deficiencies at increased risk of recurring my cereal infections right so if a person is actually taking aculosium for P&H you actually it's clinically indicated that you actually

vaccinate against a nice cereal meningitis so if a person has a if a person has a stichinic elusium ab and then they get next stiffness they become septic bloody bloody blood think about a nice cereal infection that will be a very nice way to link up him on and infectious disease on on an NV Me exam that's a kind of like a nifty question there and I mean right don't forget the virulence factors for nice germ meningitis right so remember it has like an Ig protease that's why can infect I mean it's it's you get the infection through like the respiratory tract right if you if you want to be able to survive in the respiratory tract you need to be protected against the guardian of the mucosa Ig right so if you have it should make sense that nice germ meningitis should have a Ig protease as a as a virulence factor remember it also has a capsule right so nice germ meningitis that three does have a capsule so that sort of prevents a phagocyteosis in a sense right so again classically on exams nice germ meningitis will shop as like next stiffness in the setting of like particular and a preparic like red dot-like lesions on the skin and remember right because it's a gram negative bug you're most likely cause sepsis through like the endotoxin in the hatch right so like a lipopolisaccharide LPS instead of exotoxins remember endotoxins are more the purview of gram negative organisms exotoxins are more than the purview of gram positive organisms right and remember though that yeah I've given that general robot gram negative organisms can in fact make exotoxin I mean I can give you one example right now right don't forget like your exotoxin A with like a pseudomonas right so again gram negatives for the most part they work with endotoxin as their causal as their means of medialin sepsis but they can in fact produce a exotoxin as well but gram positives almost exclusively make a exot

oxin now um how do you treat um a nice germ meningitis try you want to go ahead and give the third genertion sephalosporin sephteryaxone and if you wear actually a close contact of a person with meningitis you do actually need treatment as well I remember in general you can treat with rifampin or sephteryaxone or superflexicin although the preferred agent is actually rifampin but if you're pregnant right for example you don't want to give a pregnant woman right fampin that's not very safe you go ahead and escalate to a sephteryaxone you also do no one to give superflexicin right to a pregnant woman because that can cause a problems with like cartilage I mean those kids right like rupture of like tendons and all that crap right so you don't want to do that with a pregnant woman so if a pregnant woman was around the person meningitis you definitely want to go ahead and um um give a sephteryaxone right but for every other person go ahead and consider right fampin um so a classic mbmi question me be a person that intubated a person with my sebum meningitis that person does in fact need um need uh um profilaxis right because in the presence of intubation you were probably exposed to like the bad stuff the like my sebum meningitis through your respiratory tree and that can cause a cause a lot of trouble for you okay now um I guess since I'm talking about my sebum meningitis let me talk about it's close cousin right so like my sebum meningitis right so remember my sebum meningitis it's also a gram negative organism to gram negative diplococcus just like the insure meningitis remember it does not have a capsule okay and it can only ferment glucose glucose right contrast down my sebum meningitis that does in fact have a capsule is a gram negative diplococcus and can ferment maltose and glucose okay but my sebum meningitis does not have a capsule there's no vaccine against it a

nd it actually cannot ferment maltose it can only ferment very high yield to know that for example right then my sebum meningitis right can cause lots of infection right like ST Gs or I guess ST Is these days that's what they call it um for that you want to give like septraxone is it through my sin because many people that have like my sebum meningitis also have like coin infection with um with the chlamydia right so though is it through my sin we help with covering that um remember my sebum meningitis can also cause like PID right so like bimonol tenderness in a young female with like risky behaviors like you know sex without condoms and whatnot uh think about a uh PID what does PID even stand for pelvic inflammatory disease right so pelvic inflammatory disease uh think about it under those circumstances um and then don't forget this one this one is something that most people get wrong on the USML this was some reason but it's called like FID's here Curtis syndrome that's basically where you have like an infection of the hepatic of the liver capsule um with a nice urinary okay and you may wonder divine why does nice urinary gonna have love to mess with uh the urinary tract well the reason behind that is that it has like a PID it's essentially like fem like fembre and that helps with sort of attaching to the epithelial cells that line the urinary tract I mean it's kind of like the same deal with like E.

coli remember E.

coli loves to attach to the epithelial cells of urinary tract that's why it's actually the most common cause of urinary tract infections right and I mean if you uh guess if you want that to add another question here what's the second most common cause of urinary tract infections in the US or just say second most common cause of urinary tract infections right that'll be stuff uh saprophilicus right stuff saprophilicus classically an example is in a sexually active younger younger female so I think I've covered what I want to at least the things that I've come to mind with this case so let me go ahead and uh you know talk about some thinnest right so what if you get a question about a patient you know that has like severe abdominal pain and difficulty breathing and like lip swelling after like recently studying like synopro um well I really hope with this you're thinking about a hereditrengeodema right so remember that usually arises like in the setting of like a c1stries inhibitor deficiency the key concept you want to remember here is that c1stries inhibitor and and you're tensing, converting enzyme both of those actually helping the breakdown of really kind right so if you have a deficiency of one of those enzymes you really do depend on the other enzyme right so if you then kill the second pathway by giving a niece inhibitor in a person that's already deficient in c1stries inhibitor well guess what happens you're essentially setting up the person for a build up of bradykining which can cause you know with pretty severe problems right like air week compromise or the lip swell or they have like a dima of the agi mucosa so they have abdominal pain um so that's a classic we hereditrengeodema can actually present on on exempts right and then please don't forget right your ace inhibitors they actually contraindicated in patients with bilateral renal adristinosis as well s

ince I just talked about these inhibitors with hereditrengeodema and the contraindication it sort of makes sense to talk about another contraindication to give an niece inhibitor right so if you have bilateral renal adristinosis you're already not profusing your kidneys as well because you don't have enough blood flow through the afferent arterios right so the way your kidneys respond right they will rev up the renal adjutancing system they'll make a ton of angiotensin 2 and that angiotensin 2 right in the setting of renal hypo profusion will profancially constrict the efferent arterial right as a means of increasing GFR so if you give an ace inhibitor right you will inhibit an adjutancing convertin enzyme you will decrease the production of angiotensin 2 so you will essentially blunt that angiotensin 2 constrictive response at the level of the efferent arterial and if you do that you essentially plummet in the hydrostatic pressures that you'll find in your glomerular capillary so guess what will happen your GFR will go down and that can trigger renal failure so that is the mechanism behind ace inhibitors being contraindicated in patients that have a bilateral renal adristinosis the same warning will also apply for your angiotensin 2 receptor blockers and I guess so this is going for 33 minutes so let me try to round this up probably within the next like two three minutes another close-re-related abdominal pain sort of concept after taking something may be acutelyntamethan poffiria on NBME exams remember this is I've talked about this in one of the hiparkas where I talked about like a deficiency in a poffobili nogin diamines I mean sometimes I call it like peanut butter and jelly diamines it's like another sumo just dominant at the solder you have a deficiency of PBG diamines and if you have that deficiency remember that's one of the enzymes in the synthesis pathway f

or him so your poffobili nogin levels will go up okay and then you begin to have symptoms right so AIP right acutelyntamethan poffiria right so remember it's one of the poffirias that classically on exams you'll present with like dark red urine like potwine sting urine basically and you usually have that in the setting of pretty severe abdominal pain but here's a higher thing you want to remember they have the severe abdominal pain they do not have diarrhea very high you to know that they have severe colic abdominal pain but they do not have diarrhea right and the thing is what could trigger the symptom some things that could actually trigger these symptoms that things like like consummate alcohol right remember if you consume ethanol that will increase the activity of the cytochrome P450 system and that will sort of increase flux through that him synthesis pathway another classic trigger right is like weight loss right so or you know like weight loss or you'll pick up one of these like new diets that sort of like restricts your your carbohydrates those things can actually trigger trigger pretty nasty exacerbations of acutelyntamethan poffiria so you may say to find how does losing weight cause triggers I mean how does each trigger acutelyntamethan poffiria so the thing is if you read the literature apparently if you actually if you lose weight that actually increases the activity of amino level liniac acid synthase right so like alas and if you have an increase in the activity of alas right you begin to again make more precursors to profitable in origin and if you have a PBG um the aminist deficiency your profitable in origin levels will go up right um and the thing is you may just see that actually in if you look at the literature because this is something that's bugged me for a very long period of time right if you really look at the literature all you see is oh if

you're losing weight or you on a low calorie diet that can increase the activity of alas there's really no mechanisms that have been um proposed in the literature but I guess since this is my own podcast let me try to provide a teleologic explanation um so teleologic right so there's no real basis for it does not be proven but it makes sense to me if you sort of reasoned through the biochemistry right so think about it right if you restrict carbs right um you begin to burn fat when you burn fat you begin to make a ton of aceroque right and aceroque can flux through the tca cycle to help you make more ATP right in the fasting state so that gluconeogenesis can happen the thing that happens is one of the byproducts of the of the tca cycle is succinoque right I remember succinoque marys glycine to make delta aminolevone nica acid in the first step of him synthesis under the activity of alas right so that's one potential mechanism behind weight loss, triggering attacks acute attacks of acute intamethanthapofiri another potential theory right is like thinking about watching fatty acids right because when you're in the fasting state you're bringing down fatty acids and right to you watching fatty acids are a kind of fatty acid right so if you're bringing down a watching fatty acids remember they can use the vomit pathway to ultimately make um succinoque coi remember I talked about this in my biochem podcast remember your vomit pathway are things that can uh basically bypass the early steps of the tca cycle and sort of shifting to uh gluconeogenesis right so um that's why they are certain glucogenic um amino acids right so that vomit pathway the v stands for veilin the o stands for all chain fatty acids right so remember in general fatty acids cannot be used to make glucose with one exception all chain fatty acids right so veilin um watching fatty acids is the o the m stands

for methyonine the i stands for isoleusine the t stands for three-onine okay um so the vomit pathway those are all um things that can fit stock into succino um coi right so if you're fasting you're breaking down all chain fatty acids you're increasing the production of succino coi as you are beta oxy essentially beta oxydizing those watching fatty acids and that succino coi can paraphriclycein under the activity of alas to make delta mille levelemic acid so those are like my two proposals as to why weight loss or like carburestriction or like calorie counting or like you know just basically if you get on a diet you could trigger acute attacks of acute intamithenta pothiri so um how do you treat acute intamithenta pothiri you treat it by you know basically avoiding the triggers um like alcohol or like losing weight in a prudent fashion right and you can also treat it with something called himin himin is basically an elisin thizin hybride right and i guess to round this up i promise uh and again i apologize as i talk about these things more and more good ideas just on the fly coming to my mind right so aip is one pothiri disorder another classic one that shows up on exams right is pothiri cutinia tartar right that's where you have like a urod deficiency right so like europe pothiri nogin decarboxylis pct you know tends to present more with like cutaneous symptoms right so like skin symptoms that's why it's called pothiri acuteinia tartar right um so they'll have like you know like a lot of hair growth under the dorsum of your hands they have like a lot of skin blisters really the way you treat it is with phlobotomy um because really if you bleed out a patient right by bleeding that out that patient you essentially induce an iron deficiency right and the thing is remember if you want to synthesize him you need two things for him right him is made of iron and pothiri so

if you bleed out a patient and induce like a mild iron deficiency your body is like crap i don't have iron to help me synthesize him so he makes absolutely no sense for me to synthesize him um to synthesize a pothiri remember pothiri is part of that him synthesis pathway so you bleed out the patient they have an iron deficiency the body shuts down the synthesis of protoprofring so that decreases flux through the him synthesis pathway and that basically reduces the attacks of pothiri cutaneous tartar okay so i think uh we'll go ahead and end here so please please please i'm actually begging for feedback on this specific podcast it's a format you like let me know and i can definitely make a ton of other podcasts uh like this these are like free flowing podcasts i just literally come up with like six or seven high yield scenarios in my head and then as i sort of get into it and discuss the scenarios i just discuss like high yield things that just pop up into my mind um over a time span so it's kind of like a freestyle um freestyle uh podcast and before i round up remember um i do offer a tutoring for the usml step one step two ck step two cs and step three exams um have tutor thousands and thousands of people that have done extremely well on those tests i also offer a tutoring for the internal medicine in training exam and the internal medicine board exams and i um also prepare applications and provide like consultant for like era's applications if you're a med student applying to residency or amcass applications for college students applying to med school in fact i've been on an admissions committee at a top three med school in the country so i have a lot of admissions committee experience so i can definitely assist in that regard and then on the off chance that you're studying for an organic chemistry exam or a med school preclinical exam or a third year shelf exam i a

lso offer tutoring for all those things so i wish all the best have a wonderful blessed Sunday and i will see you in the next podcast thank you and god bless

Signs of hyperandrogenism (physical exam), polycystic ovaries on ultrasound, or evidence of anovulation/irregular menses.

Pseudomonas aeruginosa.

Neck stiffness, septic appearance, and petechial/purpuric rash.

Linezolid and Daptomycin.

N. meningitidis has a capsule, can ferment maltose/glucose, and causes septicemia via LPS; M. pneumoniae lacks a capsule and cannot ferment maltose.

It will decrease Angiotensin II production, blunting the efferent arteriolar constriction needed to maintain GFR, leading to acute kidney injury.

Borderline Personality Disorder (BPD).

It binds to the D-Ala-D-Ala termini on the peptidoglycan cross-links, preventing transpeptidation and cell wall synthesis.

Thiazide diuretics or loop diuretics (though the underlying issue is ADH resistance at the collecting duct). Correction/Better Answer: The mechanism involves increasing urinary free water excretion, often requiring careful management rather than a single drug class.

Petechial or purpuric rash, neck stiffness, and signs of septic shock.

Tamoxifen (SERM).

Acute Intermittent Porphyria Attack (AIP).

C5 monoclonal antibody.

Borderline Personality Disorder (BPD).

It binds to the D-Ala-D-Ala termini on the peptidoglycan cross-links, preventing transpeptidation and cell wall synthesis.

Thiazide diuretics or loop diuretics (though the underlying issue is ADH resistance at the collecting duct). Correction/Better Answer: The mechanism involves increasing urinary free water excretion, often requiring careful management rather than a single drug class.

Petechial or purpuric rash, neck stiffness, and signs of septic shock.

Tamoxifen (SERM).

Acute Intermittent Porphyria Attack (AIP).

C5 monoclonal antibody.