DIP Episode 580 - 2025 USMLE Step 1 Free 120 Discussion Part 1 (Q1-10, super helpful for Step 2 and 3!)

All right welcome my name is divine this is episode 580 of the divine intervention podcasts. In today's podcast we're gonna be starting a new series on the USMLE Step 1 3 120. Now I know some of you may be wondering why is divine making a podcast on Step 1? First I will say is obviously it's not only people that take Step 2 3 and level 2 and 3 that listen to those podcasts. Many people don't actually think of this but actually have like more than a hundred different Step 1 podcasts. Another thing is if you're taking Step 2 or Step 3 I will strongly encourage you to listen to this podcast and I'll also strongly encourage you to do the Step 1 3 120.

The thing is Step 1 has become a heavily clinical exam so there is actually a great number of similarities between the questions you see on Step 1 and the questions that you see on Step 2 and Step 3 right like anybody that attends my classes you see that I emphasize a fair amount of the basic sciences that they have that you may be like wow this we step one material but it's actually like completely step two and step three material as well so just something to keep in mind so this jump right into so this is going to be part one obviously right we're gonna try to do the first 10 questions today God willing all right a 14-year-old boy is brought to the ED by his parents because of a one month history of intermith and right knee pain that has worsened during the pasting he reads his quarantine as a six on a ten point scale and says that it worsens when he walks and lessons when he sits during the past two weeks he has been walking one mile daily in preparation for participation in the school marching band he has not taken any medications for his pain he sustained a right TB and fibula fracture at the age of eight years after a skid body accident which was treated with internal fixation and casting he has asthma treated with in hill buttesan ideally and in hill the biterolas needed his mother has type two diabetes mellitus and his maternal grandmother has osteoporosis the patient is five foot seven inches tall so seventy-fifth seven percentile and weighs 80 kilograms so that's the 90 more than the 95th percentile his BMI is 31 that's in the 98 percentile his temperature pulse and blood pressure are fine physical examination shows hyper pigmented thickened skin at the nape of the neck there is tenderness to population of the anterior aspect of the right hip and limited range of motion on abduction internal rotation and flexion of the hip the left hip and knees are non tend

er range of motion is full in all directions the remainder of the examination discloses no abnormalities which of the following factors in this patient's history most increased his risk for developing this condition so first things first we see a boy that is more than 10 years old and we see that this boy is pretty obese and it appears that he's having issues right he's having issues in his lower extremity especially on the right especially on the right whenever you see something like this we can even see that oh there's tenderness to population of the anterior aspect of the right hip limited range of motion with abduction internal rotation and flexion right this child likely has an issue with the hip and again likely has an issue with something called sciffy so what sciffy sciffy means slipped capital femoral epiphysis to be honest with you for those of you that are taking step one the pediatric hip disorders they're actually easy there is actually a cheat code you can use that you know is mostly step two and step three takers that know this but let me release that cheat code to you right so just use the age if you see a hip problem in a new born a new born on your exams that's gonna be developmental dysplasia of the hip D.D.H.

right and sometimes they use many different names for that sometimes they call that flood as a tabula right but then if you see a child that's less than 10 that has a hip problem they want to think of leg-covy-perthes disease leg-covy-perthes disease is like an austrinecrosis of the femoral head but if you see a child that's over 10 especially a child that is obese that has hip problems you want to think of sciffy slipped capital femoral epiphysis there is actually a very classic hip x-ray finding you miss your exams that you want to be more identify is like the ice cream slipping off the corn that's something I actually want to look into you know many times this the blood person is going to need some kind of surgery so honestly for this if you look at all the answers the one that makes the most sense is option a BMI right sciffy is found almost exclusively in kids that are obese on the US MLE exams so I'm gonna go with option a here option B family history I'm not gonna go with that you know the family history type 2 diabetes osteoporosis it's not a big deal medication use as far as I know this child do I remember seeing any medication here I don't remember okay use this in help you death so an idea and he'll have you to roll yes don't get me wrong can steroids cause osteoporosis yes but that's usually in people that are taking like systemic steroids this person is just taking an inhale cortical steroid so that I would imagine should not be causing issues for this child and then previous fractures no right I would don't go previous fractures don't get me wrong though if you've had joint pathology in the past that can accelerate the development of like osteoarthritis and all these things but those are actually long term problems not an issue in a child that is just 14 years old and in recent physical activity I would discount that because he's been having symptoms for

a month and he's a recent physical activity I've been going on for two weeks so his problem started before this physical activity began so I'm gonna go with option A for question one all right now a 14-year-old girl is brought to the office by her mother because of a three-month history of red bumps on her skin the patient says the bumps are not itchy or painful but that she finds them embarrassing she has no history of major medical illness and textual medications for vital signs or within normal limits physical examination shows the findings in the photograph right so this is clearly a derm question we kind of see all these like red goosebumps almost in a sense okay let's look at the answers and see if we can get rid of some and this has been going on for three months right so option A says eczema we should get rid of eczema right eczema is not gonna have this good goosebumps appearance many times he etches a lot and it doesn't just itch you know it's gonna be a thymidose it's gonna be kind of like scaly that's not what we see here so I'm gonna get rid of that option B says folliculitis again usually we're gonna see that around like hair growing regions and chances are you may not have folliculitis for three months right that timeline doesn't really make sense option C says hydrodynamitis right so you're probably thinking of hydrodynamitis superativa that's an inflammation of the apocrynsic red glands that's usually gonna be under the axilla you know your armpits basically on the exam and you know they're gonna have like this chronic drainage false-melting crap I don't see that here so gonna get rid of that and then option D says carotosis pelaris I'm gonna go with that answer I think that's the right answer but let's just roll out option E says on ecare well on ecare literally itches right this day is non-each so we're gonna get rid of the answer is D right so wha

t in the world is carotosis pelaris well look at the name carotosis so that means it's derived from carotene right basically the thing that happens here is that you have excessive carotene deposition right excessive production and you know deposition of of carotene excessive amounts and this thing believe it or not is actually here in an orosomo dominant fashion right and usually this will be tend to have pretty bad symptoms in the cold months right you know these winter months things tend to kind of get worse for these folks right so how does usually look and again I'll encourage you to look up other examples sometimes it's just good to see other examples of something so that if you see it again on your test you can recognize it but you'll have these goosebumps on the arms on the thighs on the face on the back right and the thing is it's more of a cosmetic issue don't get me wrong having it sucks right but it's more of a cosmetic issue but typically you're gonna treat it like moisturizers you can use some lasers and and all that fun stuff but that's I think about as much as you need to know about carotosis of pelaris all right so I'm gonna go to question number three so it says a 50 year old man comes to the office because of a two month history of increasing daytime summer lens he has obstructive sleep apnea for which he has only intermittently used uh common continuous positive airway pressure device and by the way another name you may see for this on your exams is non-invasive positive pressure of ventilation right just to kind of mess with your head a little bit as you're gonna see in this series the USML Es and I'm gonna try to you know make commentary on this we like to take what you know and just use all the terms so just be careful see pop basically means non-invasive positive pressure of ventilation and the trickle into the patient right is obviously gonna be

invasive positive pressure ventilation so this guy's 5 foot 7 inches tall with 400 pounds BMI 63 he's temperature is fine he's pulse is a hundred per minute his repressions are fine blood pressure is 135 over 80 on physical examines a gray blue change to the lips earlobe and nail beds so that's like hypoxia right cardiac examination shows not over abnormalities ebg is on rumours shows a pH of 7.31 pc 1270 and p0 250 so his pH is low his pc to is high and his p0 to is low now which of the following additional findings will be most likely in this patient right so this person clearly has in fact I'm gonna upstage this person from having just USA to OHS so what I mean by OHS OHS means obesity high-poval ventilation syndrome I believe this guy has obesity high-poval ventilation syndrome all right because he has daytime hypercapnia so I'm gonna go with OHS here so let's kind of work this out so option A says decreased serum by carb I'm not gonna go with that yeah I'm not gonna go with that because this guy because of his ciotary tension he has a respiratory acidosis the way your body compensates for respiratory acidosis is the metabolic alkalosis so that doesn't make any sense option B says increase hemoglobin concentration yeah I can I can get on board with that because this guy we can even see on physical exam with his lip findings heirlobe findings nail findings you see those are like the edges of his body right we see hypoxia those those are actually one of the first regions to undergo hypoxia when a person has hypoxia so this guy is hypoxic and whenever you're hypoxic your kidneys respond by making high amounts of Epo and that Epo is gonna drive red blood cell production so this person should have an increase hemoglobin and by the way they can make this a question about a person that has chronic hypoxia for any reason so like a cystic fibrosis patient or a person that

has COPD right or a person that has like pulmonary hypertension or some kind of sanodic congenital heart defect so just be aware of those other kinds of veneants that may be propounded with stuff like this and then option C so the answer I'm pretty sure it's gonna be B option C says increase to the lung capacity no actually when a person is obese it actually causes a restrictive pattern of lung disease I'm gonna say that again when a person is obese it causes a restrictive pattern of lung disease not an obstructive pattern because think about it basically I like to think of the region between the neck and your waist as being one big box that one big box has two tenants what are those tenants number one is your thoracic cavity up high number two is your peritoneal cavity down low so if a person is this obese I mean this guy's BMI is 63 he's weight is 400 pounds then the abdominal cavity is going to take up a bigger chunk it's gonna be the bigger roommate so thoracic cavity is gonna have less space because your thoracic cavity has less space your lungs have less room to expand so you're actually gonna have a restrictive pattern of lung disease so your total lung capacity should actually be low and let me just ask you this because they could actually make an arrow question from this again I if you listen to my podcast you know I love to make integrations I have this sneaky feeling that I will not be able to get a question 10 but don't worry it's gonna be a series we're gonna work through these things but whenever you have restrictive lung disease what's gonna happen to your lung volumes your lung volumes are gonna be low right so we should not expect increased total lung capacity which actually expect decreased total lung capacity now what do you expect to be true of this person's a DLC well again is there any actual problem with the pulmonary architecture no there's no

t so because there is no actual problem with the pulmonary architecture the DLC should be normal and how about the E.E.

ingredient the E.E.

ingredient should also be normal as well because again there's nothing wrong with this person's pulmonary architecture right the lungs are just restricted from expanding why because again there's just less space in the thoracic cavity because of all this obesity that's going around and what would you expect to be true of this person's FVV1 to VC will should be normal or increased because it's a restrictive pattern of lung disease okay what can you tell me about the compliance of this person's lungs or this person's the compliance of their lungs should be because remember an obstructive disease an obstructive disease you have less compliance and high elastance these people's lungs again are kind of restricted from expanding right so because they are lungs are restricted from expanding they should actually not have good compliance the compliance should be low and the elastance should be high right the elastance should be high in this person that has restrictive disease so it's just something I want to keep at the back of your mind for for exams all right so let's go to option D option D says live ventricular hypertrophy well let's think about this for a second let's think about this for a second so if a person has obstructive sleep apnea or obesity hypogenitilation syndrome like I see this guy has let me ask you this what side of the heart is going to be feeling the effects of this think about this for a second think about this for a second what side of the heart is going to be feeling the effects of this is going to be the right side or is it going to be the left side it's going to be the right side or is it going to be the left side it's going to be the right side right because think about it that chronic hypoxia leads to pulmonary hypertension that pulmonary hypertension is actually going to lead to the person having you know right heart failure right we actually cal

l this corpomonali remember corpomonali is when you have right heart failure because of a pulmonary cause right corpomonali is when we have right heart failure because of a pulmonary cause so this person's left heart pressures will actually not be extremely high and I will actually say that this person should not have a leventral eye hypertrophy leventral eye hypertrophy is actually something we're going to see it's something we're going to see when you have something that increases after load for the leventral right something that increases after load for the leventral like what well something like erotic stenosis or severe hypertension you know like systemic hypertension or something like that right and sorry I'm you spoke earlier remember that's kind of moving over this in my head remember in obstructive disease sorry your compliance actually rises and you will you will last dance falls although again you want to be careful you want to be careful actually it depends on the specific kind of disease it depends on the specific kind of disease right because there are certain cases of obstructive long disease where your long compliance will increase but there are certain cases of obstructive long disease where your compliance actually does decrease so let me summarize all of this so that we can kind of get this down pat right so we can get this down pat because I think this is something that is really important to know for you exams so that you don't get in you don't get in trouble on your on your test right you don't get in trouble on your test so here's the thing when a person has obstructive disease in general on the USMLE exams your compliance should move down right think about it something like emphysema right your lungs you know are become like shopping bags right like grocery store shopping bags they don't expand very easily remember compliance is volume of repre

ssion right they don't expand very easily so since your lungs cannot expand it very easily the compliance is down but your lungs can you know if you cannot expand easily then you can snap back easier right so your elastances is down right I mean your elastances up but when a person has restrictive disease again your lungs are literally restricted from expanding so your compliance also goes down and your elastances those go up because compliance and elastances generally have an inverse relationship right so again because some people they have this erroneous belief that oh whatever happens in obstructive disease the opposite happens in restrictive disease that is not always true okay so just be careful about that so again in summary an obstructive disease generally for you exams compliance goes down elastances goes up for restrictive disease compliance goes down elastances goes up as well right so kind of similar findings so there'll be a similarity between obstructive and restrictive disease I've kind of talked about a few other other differences right I said that hey an obstructive disease you have high long volumes right your FVV1 to FVC should be decreased right but in restrictive disease you should have lower long volumes and your FVV1 to FVC should be normal or increased and then the other things like DLCO and AA gradients you have to analyze the specific situation that you're given right because their situations where a person can have obstructive disease and you have reduced the LCO there are situations where person can have restrictive disease and they will have reduced the LCO or do me have normal DLCO again it kind of depends on your analysis of that specific situation I guess this is one thing I'm gonna say for those of you listening to this podcast you know step one is one of these exams that really emphasized a ton of pathophysiology you know probably more

so than step two and step three so you're gonna see me go off in some of these directions with these questions I think that adds to the richness of our discussion so that you can kind of really see how things work for many different angles all right let's go to question number four question four says that 32 year old man comes to the office because of a one-day history of cough productive of small amounts of blood and a two-day history of shortness or breath and swelling of his ankles he also has a two-week history of progressive fatigue and episodes of dark urine he has no history of major medical illness and taste of medications his temperature is fine his pulse is fine his respiratory versions are fine but his blood pressure is really high 175 over 110 pulse oxon room ensures an auto-sad of 91% that's low diffuse respiratory crackles are heard over all long bases there's two plus pitting the dim of both ankles results of lab studies are shown so his hemoglobin is pretty low his hematocytic is low his BUN is high, his creatinine is high, his urine retails are high your analysis also shows some dysmorphic retails and rare red blood cell cast examination of a kidney biopsy specimen shows chryscientic glomerulina fritis and linear deposition of IgG along the glomerular capillaries this patient most likely has antibodies directly against which of the fluina antigens right this is pretty straightforward right young guy has pulmonary problems has kidney problems and we see dysmorphic retails right those are retail cast again the USML is here they put the word rare red blood cell cast just to see if they can steal you away from nephrodix syndrome no this person has got nephrodix syndrome more specifically this person has got good pastures right remember they can call red blood cell cast on you exams dysmorphic retails just FYI so this person clearly has good pastures righ

t I remember root pastures is an autoimmune disease you pretty much form auto antibodies against the glomerular basement membrane against actually the alpha three chain of type four collagen the alpha three chain of type four collagen so when that happens right well where do we find the type four collagen we find in the lungs we find it in the kidneys so that can cause an ephrodix syndrome more specifically that can cause a rapidly progressive glomerulina fritis rapidly progressive glomerulina fritis right RPG and sometimes on exams they call this chryscientic glomerulina fritis so they can say hey a person that has good pastures what would you find on renal biopsy well you should expect to find chrysents right and they remember you're gonna see this linear the position of IGG along the you know along the glomerular capillaries on immunofluorescence right so this is this is good pastures again auto antibodies against the glomerular basement membrane against the alpha three chain of type four collagen please don't mess up this alpha three chain of type four collagen with the alpha five chain of type four type four collagen that's what is mutated in a person or is defective in a person that has outpork syndrome right remember those who the they'll have hearing problems vision problems and kidney issues right nephrodix syndrome all right so the answer here clearly has to be a right let's look at the other answers option B says double-stranded DNA that's gonna be lupus right anti double-stranded DNA that's gonna be lupus so we're not gonna pick that option C says nucleoloprotein I don't really know what that's associated with maybe a and a with like lupus you know any but that's kind of a bogus answer I wouldn't worry about that and then phospholipid so phospholipids if you make antibodies against phospholipids the one thing I can think of that's pretty close you know is

anti-phospholipid syndrome where you see a woman that has like recurring miscarriages pregnancy losses and she'll have a lot of hypercoglipopipisodes and then option E says proteins in the neutrophilous cytoplasm right this is anca you know many people just memorize the terms anca anca anca anca you know C-enca you know which we find in webinars which we call GPA or P-enca which we find in a truck Strauss which we call E-GPA but again what do you think anca means anca literally means anti-neutrophilous cytoplasmic antibodies you literally making antibodies against antigens within the cytosol of neutrophilous that's why it's called anca anca right but obviously that's not what's going on here right so this person has a collagen issue a type for collagen issue remember Wagner is which we call GPA is associated with issues with your upper earway so the person is going to have like nasal problems or ear problems or whatever and they'll also have issues with their lower airways so they'll have issues with the lungs right and they'll also have nephritic syndrome they'll actually have like rapidly progressive glomerular arthritis right but again a very key differentiating feature is having issues with your nose right we don't usually see that in a person that has good posture syndrome good posture syndrome affects the lower airway it doesn't affect the upper and the lower airway like we see in Wagner's all right so the answer to question four is going to be option a all right now question five says a five-year-old girl is brought to the ED because of a two-day history of fever urinary urgency and burning pain with urination she has had four similar episodes during the past year diagnosis of urinary tract infection is made subsequent renal ultrasoundography shows one large U-shaped kidney which of the following is the most likely embryologic origin of this patient's condition

right so whenever you see a child that has recurring UT Is you're always worried about this child having some kind of anatomical problem and I think we can kind of see the anatomical problem here right you shape kidney I suspect that this child probably has like horseshoe kidney remember this is kind of associated with Turner syndrome where you know the inferior pulls of the kidneys the kind of fuse and then there's kind of stuck on the inferior mesenteric arteries so they don't really rise so I think that's what's going on here so let's look at the answer so option a says failure of the kidneys to rotate 90 degrees medially that's a true statement but that's not the path of his behind horseshoe kidney the kidneys doing fact rotate 90 degrees medially during development so that's wrong option b says failure of no more kidney assent yeah that may be true actually because in horseshoe kidney the kidneys are stuck under the inferior mesenteric artery because the inferior pulls are fused let's keep that answer option C says failure of one uretheric but to develop normally no no no no no right no no it's not it's not this option D says fusion of the inferior pulls of the metanefros during assent so option B and D both look good but option D is just more direct than option B right because really the thing that kind of kick starts all your problems in horseshoe kidneys is that the inferior pulls of your kidneys fuse and then they're stuck on the inferior mesenteric artery so honestly because option D is just a more direct answer than option B I'm gonna go to option D as the right answer here I think that's what we should do for our test so let's go to option D if option D was not an answer they maybe I will think of option B but yeah because option B kind of seems true but option D is like very deep in the path of his right so I like option D a lot let's go with option D all

right question 6 says a 78 year old man comes to the office for a full-up exam it was discharged from the hospital a week ago after being treated for a non-tubacolus mycobacterial infection he started traveling with ciprofloxocin and rifampin at that time he also has hypertension and underwent placement of a mechanical aortic valve six years ago for aortic stenosis other coronamids are HCTZ like Cino Prele and Warframe his Warframe dose was doubled four days ago he says that he's trying to follow a healthier diet drinks to 12 hours beer daily results of lab studies for done four days a month to their show right so we see his I and R from four days ago is his sorry PT 11 seconds PT is from today's 11.2 so it's barely risen that's weird and then his PT is 29 seconds from four days ago and 27 seconds from today and then says which of the four is the most likely cause of this patient's lab findings right so this person we can clearly see we can clearly see that this person in this question they got Warframe and whatever reason this person's you know PT did not rise if they double your dose of Warframe now I would hope that your PT should rise and by the way let me kind of call you attention to this so when you take Warframe your PT and your PT should both rise because many people make this crazy mistake on the exams see many people say oh divine we follow Warframe with PT I in R yes that's true that's how we're following the hospital but it doesn't mean it does not risk PT think about it Warframe we know is an inhibitor of vitamin K epoxide reducties what does vitamin K epoxide reducties do it causes a gamma caboxylation and activation of factors 279 and 10 and protein CNS but if you think about this here well if you inhibit it then you will not activate you will not gamma caboxylate factors 279 and 10 right so pay attention to two clotting factors in that list 2110 2110

are common to both the extrinsic and the intrinsic correlation cascade so because it's founding both if you take Warframe you're gonna mess up both so your PT and your PT should both rise so just be careful about that common area people make on the exams same thing with Heparin right Heparin activates and activates anti-thomping 3 to inhibit factors 2 and 10 so Heparin even if we follow it with the PT it also does raise your PT because it affects clotting factors that are common to both the extrinsic and the intrinsic correlation cascade so the big question here is why did this person's PT not rise why did PT not even really rise by much well so let's see option A says decrease protein binding I don't know if I'm gonna buy that option B says their educational got flora yeah that could be a problem actually right especially when you're eradicate got flora in a person that is on Warframe it's kind of a problem because at least your God for her makes some vitamin K for you to temper the effects of Warframe what if anything you should have like a lot of bleeding because you you're now like vitamin K deficient because you've eradicated the God floor not barely raising your PT so that's a bug or something I'm not gonna pick that option C says increased alcohol intake well alcoholism especially if you're chronic alcoholic can rev up cytochrome P450 and remember Warframe is metabolized by Cycrom P450 so if you take a ton of alcohol that can cause you to rev up say P450 that can accelerate the metabolism of Warframe and that can cause you to not respond as well to Warframe so let's keep that answer although I don't think this guy has been taking more alcohol it seems like he's been taking his regular amount of alcohol let's keep that option D says increased vegetable consumption that's ridiculous we're not gonna pick that answer right I'm not gonna pick that pick that answer

and again we're told that is full in a healthier diet we're not told that is consuming veggies healthy diet can mean many things to many people just FYI prison can be drinking students in the a healthy diet all right option E says induction of cytochrome enzymes I like that answer a lot because this person is already fumping as well and we know that right fumping is a pretty bona fide inducer of CP450 enzymes remember whenever you induce cytochrome P450 enzymes you're gonna accelerate the metabolism of drugs that are metabolized by the cytochrome P450 system so what are the so option E's certainly I'll see the right answer because again it kind of hits the pathophase those pathophase answers are usually right from the exams so what are the CP450 inducers well don't forget grizzio fulvin right caramazepine finitoin babiteritz rifampin st.

John's words and also if you're a chronic alcoholic if you're chronic alcoholic but again this guy he started taking rifampin like pretty recently you know so I like rifampin better than alcohol alcohol alcohol has been doing it for a long time not a big deal but this rifampin has been doing it for a short time so that's a big deal some good good option E for question number six let's trade out let's see if we can get to 10 if possible okay question seven says a 32 year old man comes to the office because of a two week history of fever and throat pain his 5 foot 18 inches tall and weighs 140 pounds it's BMI's 21 this boss is 110 that's high respiration is refined not pressure is 90 to 68 physical exam shows scattered 2 to 4 centimeter lymph nodes in the neck axillary and inguinal regions there is a bilateral tonsular x-udate right bilateral tonsular x-udate but no oscarations results of lab studies are shown okay it's hemoglobin is low hematocrate is low white count is low pleatly count is low a heterophyll antibody test result is negative so that's like a monospot test right is negative so which of the following is the most likely diagnosis okay so the monospot is negative person has a mononuclosis like syndrome but the monospot is negative so I don't think I want to pick option a here so I'm gonna cross that off and also if you think about it like this person has like almost like a pancidopini that's gonna be a little bit unusual for eb V infection right now we see this you know scattered lymphodonopathy and this person symptoms are kind of bad I'm not gonna go with eb V though this person has a mononuclosis like syndrome with a negative monospot so I'm not gonna pick option a option b says gonna coca-coclophyrinjaides no gonna coca-coclophyrinjaides is not gonna cause you to have pancidopini if anything it's actually gonna cause you to have a local cytosis right it's

a bacterial infection option c says HIV I'm gonna keep HIV because HIV is one of those causes of a mononuclosis like syndrome with a negative monospot so let's keep option c option d says lymphogram luma venerium infection well that's a climideal infection that actually affects the growing on the exam especially men not the throat and stuff so that's wrong strap fire angiitis again it's gonna be wrong because you should expect lucositis I like option c a lot for this I wish the mbme's to make this question even better if you could have put an answer that says cytomegalovirus I'm sure a lot of people jump on that and that'll be wrong because remember that's another cause of a mononuclosis like syndrome with a negative monospot test this person has got HIV so I'm gonna go to option c for this one all right this person has like an acute ritual viral syndrome all right question eight says a 50-year-old man comes to the office for a full-of examination he has a two-month history of headaches and shortness of breath with exertion he also has hypertension treated HCTZ for the past two years his blood pressure is 180 over 105 that's pretty high up that most copy examination is most likely to show which of the following in this patient right so this person has crazy hypertension and they're asking what are we're gonna see in this person's eye okay option a says a two-year-old man sneaking let's keep that that's probably the right answer that's something we tend to find people that are hypertensive and this guy is hypertensive option b says melanocytes in the uvia no that really doesn't have any as your hypertension option c says optic neuritis no that's a zero multiple sclerosis right that's gonna cause a painful in a lateral vision loss we tend to find that in MS option d says posterior sub capsula cataracts no cataracts are found in old people don't get me wrong because age

is actually the biggest risk factor for cataracts but it's not really a serious hypertension option e says structural retinal detachment we tend to find that in people that have diabetes right I'm not especially people that have a proliferative ethnopathy with their diabetes I'm not gonna pick that I'm gonna pick option a let's go for the simple answer here right remember when you have bar hypertension you can develop a ton of atherosclerosis in your vessels especially in your arteries when that happens right your arteries can begin to almost like in pain because remember arteries and veins sometimes they can run together so that artery that is kind of kinked can impingion of vein so or like a venial and you know you see like a bulge or a dilation before that artery sneaking and you see a dilation afterwards right I like to think of this as like an hourglass venial you the venial kind of looks like an hourglass so I'm gonna go to option if for that right so by the way please be careful even nicking something you can find the person that has anything that causes really bad hypertension like renal arteries stenosis fibromuscular dysplasia also of these vasculidities just something I want to keep out the back of your mind for for example so I'm gonna go to option a for question 8 and then question 9 yeah questions like question 9 is one of these either know it or you don't if you don't know it then you're gonna get it wrong sadly all right so question 9 says a 65 year old woman and I'm gonna refer you to two things here so number one I was strongly encourage you if you can listen to my risk factors podcast if you notice I've talked about risk factors a lot in this podcast and I'll probably talk about it some more in this series risk factors are things that are heavily tested on before it was only tested on like step two step three but not the also heavily tested on step

one right so one of the earliest podcasts I have on my website episode 37 it's a very good risk factor podcast another good risk factor podcast is episodes 97 and also 184 so other good podcasts on that in that regard at 97 and 184 so 37 97 and 184 and then you know for question 9 you can clearly see a depiction of the circle of willis you you really should listen to so for the sake of time I'm not gonna go too deep on this question but listen to my circle of willis podcast I do have a podcast I'm pretty sure of meeting in the past called like literally circle of willis podcast so just go and go go type in circle of willis podcast divine intervention I think you're gonna find it right so this is one of those questions where if you don't recognize the image there's almost no way you're gonna get this right so question 9 says 65-year-old woman with a history of rheumatic mitrovov disease is brought to the ED 30 minutes after the sodium onset of right-sided weakness and ill-ability to speak neurologic examination shows weakness of the right lower side of the face and difficulty swallowing okay most of strength is three out of five on the right side she can understand what is said to her but she cannot repeat words to answer questions sounds a lot like broke us a feature to me an ECG shows a fib the most likely cause of the neurologic findings in this patient is occlusion of which occlusion occlusion of which of the following liberal arteries in the photograph of a normal brain right so again we can clearly see the circle of willis we can see like the like the basilar artery we can see the superior cerebellar can see the poster cerebral was actually kind of labeled here right but this person right you see this person has broke us a feature and the person's a lower face control at our lower face and stuff is all messed up this is pretty easy right this is a left MC stroke

this is a left MC stroke the MCA is one of the big arteries here is it's gonna be already it's gonna be already right again make sure you can label circle of willis diagrams is actually something also go for in a quite a number of my of my classes all right so the answer is D this one if you don't know it then you're that's it right sorry so so make sure you know the labels of the circle of willis right be able to know how your vertebrals come together from your basilar artery and coming off of your vertebrals you have paika right and then you know you you have your basilar artery that gives rise to AI cap right and then the terminal regions of the basilar artery you have your superior cerebral artery and then you have your posterior cerebral right and then your posterior cerebral is connected by p-com to your anterior cerebral and then your two anterior cerebrals are connected by a-com the anterior comically in artery right remember a com is where you many times have aneurysms in the circle of willis right and they remember the you know MCA kind of comes through again I've proved these labeled arteries and pretty much a discussed them again I don't want to go into a lot of detail on this just listen to the circle of willis podcasts look at images of circle of willis they're gonna be fine but this question for sure the answer is D all right we're gonna go to question number 10 so 51 year old man with a 10 year history of gird and suspected by its esophagus comes to the office because his home apprazo doesn't work around the Christmas holidays I wonder why he states that he prides himself on having a large appetite no kidding and holding his lecker during the holidays no kidding he currently takes the maximum dose of home apprazole which of the following is the most appropriate initial action by the physician so this guy seems like he's a home apprazole doesn't work d

uring Christmas I wonder why you'll me perso will no work around the holiday let's find out why right this guy is non-adherent let's say fine okay I don't want to be judgmental but I'm pretty sure this guy is not adhering to therapy so option a ask the patient how much he's eating and drinking during the holidays I like that answer a lot let's keep option a option b says explain the hazards of untreated reflux in the presence of baritone esophagus well the problem is this guy doesn't seem to be eating reasonably right so I'm not gonna pick option b option c says order an operating doscape no the home apprazole seems to work at all the times of the year just not during holidays no option d says refer the patient to a gastroenterologist no option e says switch to home apprazole to pan to a person no right no this guy home apprazole works here on the except during holidays he's eating a lot right your diet can really increase your risk of baritone of girl to kind of worsening things so I'm gonna go to option a here right option a the USM is they love to test this concept of a medication non-adherence especially when it's a medication you need to take chronically for issues remember home apprazole is for good because it inhibits that hydrogen potassium at the hydrogen potassium pp spam that we find in the in the stomach right with those pridele cells right that's how it works as an acid a reducer okay so let's go ahead and stop here again I hope you found this podcast to be helpful again I'm gonna try to make integrations with all these questions as we go and yeah so I'm gonna stop here if you're interested in any of my classes I have a series of classes first they want to step three study next Tuesday the 18th of March I have a testing in class on Tuesday bio stats class on Wednesday and social sciences QI healthcare systems class on Thursday that's all these classes are

first step one step three and then on Friday at Friday you know I have a last minute review for step two step three and then the following week after that have a 20 hour step two step three review and the first week in May I have a 25 hour step one review and also the first two weeks in June I have a 50 hour step two step through review that's the only one of its kinds gonna be held this year if you're interested in any of these classes just shoot me an email I can give you some more information and then also offer one or one tutoring for all the USML and complex exams and I help with your applications personal statements rec letters and things like that and then I have these podcasts on Apple Google on Spotify so just check those out and I also have a You Tube channel where I post the videos that I make and then many of you know a Christian there's this on the website I have a divine intervention life lessons dot com divine intervention life lessons dot com every week I post like two or three podcasts where from a biblical perspective I address a life lesson many people have actually listened to those podcasts and found them to be helpful there's actually an Apple podcast associated with that it's called the Divine Intervention Life Lessons Podcast so thank you for listening to me today I will see you in episode 581 have a wonderful day good bless you and bye for now thank you

The patient is over 10 years old AND obese (BMI).

Daytime somnolence, severe OSA, obesity, cyanosis/hypoxia signs, and chronic respiratory acidosis.

The alpha three chain of Type IV collagen ($\alpha_3$ chain).

Linear deposition of IgG along the glomerular capillaries.

Increased hemoglobin concentration (due to erythropoietin release).

Right-sided weakness and expressive aphasia.

Carotosis pilaris.

Compliance decreases, and Elastance increases.

Fusion of the inferior poles of the kidneys during descent.

Rifampin (or Phenytoin, Carbamazepine).

$\alpha_3$ chain of Type IV collagen.

HIV or Cytomegalovirus (CMV).

Carotosis pilaris.

Compliance decreases, and Elastance increases.

Fusion of the inferior poles of the kidneys during descent.

Rifampin (or Phenytoin, Carbamazepine).

$\alpha_3$ chain of Type IV collagen.

HIV or Cytomegalovirus (CMV).