DIP Episode 206 - Family Medicine Shelf Review Series 1

Okay, welcome. My name is Divine, my resident. This is episode 206 of the Divine Intervention Podcast. And in this podcast I'm going to be getting a family medicine shelf exam rapid review series. I'll just be doing a bunch of cases that highlight topics and concepts that are commonly tested on the family medicine exam will be completely random. But hopefully as you listen to this series and as I build up this series you'll find it to be very helpful for the exam. So let's just jump right into it. So the first thing I think I want to start with is talking through like an algorithm that's frequently tested on the family medicine shelf. And that is the algorithm that relates to a thyroid nodule. Right. So if a person has a thyroid nodule what is always your first step in diagnosis? If you're pressing you know physical exam you'll pop it a thyroid nodule what is always your first step in diagnosis? Well I would really hope that you're thinking that you'd want to go ahead and measure the TSH right? Because the thing is when you measure the TSH that will help you deal in it between the person potentially having a hot nodule or a cold nodule okay a hot nodule or a cold nodule. So you measure the TSH. And basically the way I teach people this concept is essentially if the TSH is low you know you're dealing with a hot nodule right? Because the algorithm can get complicated real fast if you try to over-complicate things right?

So the best thing to just say ask yourself is is the TSH low. If the TSH is low it's a hot nodule. If the TSH is not low so any other results be it normal high whatever it doesn't matter then it goes into the TSH not low path. So let's talk about the TSH low path right? So if the TSH is low kind of power right? Then we know we're dealing with a hot nodule right? And once a person has a hot nodule right? The thing is the chance of like thyroid cancer because when you see a thyroid nodule I think that freaks you out this thyroid cancer right? If the TSH is low you know it's a hot nodule super low risk of cancer so your next step in diagnosis on an in-bim exam will be to order a ryu scan okay you want to be able to reinterpret those ryu scan results right? So if for example the person you get a ryu scan and you find like a single hot spot on the ryu scan that's gonna be a toxic at a normal right? That's pretty easy but what if they told you that oh you see multiple hot spots what are you thinking about on those circumstances? Well I hope you're telling me that it's a toxic multi nodule goiter right? Okay and then what if they tell you that there's diffuse there's a diffusely increased optic on the ryu scan what are you thinking about? Well that'll be a gravestis disease right? That'll be gravestis disease right? That'll be gravestis disease right?

So when I see those kinds of things think about again those are kind of like the big things you want to keep at the back of your mind with the ryu scan and I'll see some quick things at the end but let me talk about like the other part of this algorithm right? So the other part of the algorithm if the TSH is not low right? That means you have a cord nodule right? The problem with cord nodules is most of them have been nine about 70% of them 77% they're like colloid cysts in the thyroid but you know you can never be sure of that right? So typically after that you want to do like an f&A with ultrasound right? So you can get like some thyroid tissue and send it off to a pathologist right? And you know if you see a cancer you want to know like some quick for the family medicine shelf you don't need again need to go all super in depth on these cancers but you need to kind of know some of them right? I like some key things right? So say for example right the tell you that you see some of my buddies right from a pathology specimen of a thiccote thyroid nodule what kind of cancer are you thinking about? Well I hope you're thinking about papillary thyroid cancer. Remember papillary thyroid cancer is popular right? So it's the most common kind of thyroid cancer and don't forget the biggest risk factor for that right? Which is a history of exposure to hidden neck radiation right? So remember papillary thyroid cancer actually loves to spread through lymph nodes.

The reason I'm saying that is there is another kind of thyroid cancer, follicular thyroid cancer that loves to spread hematogenously it doesn't spread via lymph nodes right? So that's something we'll keep at the back of your mind for examples right? So follicular thyroid cancer hematogenous spread papillary thyroid cancer loves lymphatic spread it has the best prognosis of all the thyroid cancers it's a huge that would expose you to hidden neck radiation. Another thing you may see on his stologies the often any eye nuclei right? You may see the often any eye nuclei right? So those are the big things there and then what if they give you a question about a person that has like a neck mass and then they tell you that all like the father, the uncle or whatever like just a tomofamily members dying of like some weird neck mass or maybe like this person has had like hypercalcemia for whatever bizarre reason or something. I mean if you see like multiple family members with thyroid cancer right? I would really hope you're thinking about one of the MEN syndrome right? In this case it will be MEN2 E or MEN2 B right? Because they likely have a thyroid cancer. Remember medallary thyroid cancer has a terrible prognosis and all people that have MEN2 E2 B they need a prophylactic thyroidectomy at some point early in their lives because it's not a matter of if they will get thyroid cancer it's just a matter of when they will get the thyroid cancer right?

So typically for those folks you know you go ahead and you go ahead and get a prophylactic thyroidectomy this is medallary thyroid cancer here and what is the key histologic finding on a biopsy the person that has medallary thyroid cancer? Well I hope you're telling me that you'll find amyloid in the thyroid gland right? So if they say something about a person having like apple green birefringents on congruence from like a thyroid biopsy specimen you want to think about medallary thyroid cancer right? And remember that people that have medallary thyroid cancer they can actually come in with like symptomatic hypocalcemia on an mb-mixam because the tumor marker for medallary thyroid cancer is calcium toning so that calcium toning right? Can calcium toned down your blood calcium levels right? So that can cause hypocalcemia or if they want to get like super sneaky they can give you like an e-kg on your family-made shelf in a present that has like a neck mass and then you see like a prolonged acute interval right? You should again think about hypocalcemia from medallary thyroid cancer under those circumstances right? Now I said that at the end I will see some other things about our well let me say one more thing so what if they tell you that oh from this thyroid nodule you get a biopsy specimen of the thyroid and you see a lot of like lymphoid follicles what are you thinking about under those circumstances?

Well I would hope you're thinking about a person having like Hashimoto's right? Remember the most common cause of hypothyroidism in the U.S. is Hashimoto's thyroiditis right? Is Hashimoto's thyroiditis? And those people will have very low levels of like I mean like they can have like a thyrotoxic phase right? Well usually they present with hypothyroid symptoms and the hypothyroidism when you see on your exam will be something along the lines of like bradycardia right? So usually people that are hypothyroid on in-beam exams they have harder usually less than 64-ever bizarre reason and at least probably like 80% of the in-beam equations have seen on hypothyroidism those people almost always have bradycardia right? And you know they will feel tired, they will gain weight, they will have like the pre-tibial mix of demon and all that all that badness right? And they may also have like cholesterol, labyrinthic normalities right? So if you see a ton of lymphoid follicles in a thyroid gland think about Hashimoto's thyroiditis. If you also do a biopsy though right?

Let's say you see a person that has had like a long history of Hashimoto's thyroiditis and then you have like this rapidly expanding neck mass whenever you see stuff like that you obviously want to think about like a thyroid lymphoma remember a thyroid lymphoma is actually one of the new plastic like potential new plastic complications of a person having a long history of Hashimoto's thyroiditis and remember sometimes your friends at the MBM here right they play this game where they will not give you the name of something you're familiar with right? So occasionally instead of putting Hashimoto's thyroiditis they can put lymphocytic thyroiditis as the answer choice on an exam that's just code word for Hashimoto's thyroiditis right? And then if they give you a question about a person that you know has hyperthyroid symptoms like the TSH is low or you get a rye of scan and you notice you're like hmm I'm not seeing any optic whatsoever on a rye of scan what pathologist should you think about? Well I would really really hope that you think about things that have fall along the lines of like like fictitious hyperthyroidism right where a person is like thick and thyroid hormone to like lose with and all that stuff right? Because again if you're taking thyroid hormone exogenously right?

Yeah you know you have hyperthyroid symptoms but I was so impressed you're in dodgy nost TSH so your thyroid gland will no longer be stimulated so you will not have increased optic and other thing you may see that may cause those kinds of symptoms although this person will have like a tender thyroid gland on an MBM exam is the person having like like a dequeous Vince or like the sobacute thyroiditis right? So if a person has hyperthyroid symptoms they have a tender thyroid gland right? But then you see no optic on a rye of scan that's pathologist 1-4 dequeous thyroiditis so you may see divine okay? Well how do I tell dequeous thyroiditis apart from apart from like a person exogenously taking thyroid hormone? Well remember I think I said this in like multiple podcasts in the past right? That there's this thing known as thyroid globulin. Thyroid globulin is like the CPEP type of the thyroid gland so if a person's thyroid hormone is coming from the actual thyroid gland the person's thyroid globulin levels will be inhibited when they are in a state of thyroid toxicosis but if the thyroid hormone is not coming from the thyroid gland the thyroid globulin levels will be really low. So if a person is injecting thyroid hormone or you know taking like orocentral or whatever those people will not have elevated levels of thyroid globulin but if a person has dequeous thyroid itis right? Because remember dequeous thyroiditis is just generalizing inflammation of the thyroid gland right?

So you have like release of preformed thyroid hormone whenever you see that right? You should suspect the person you know having a and again you also have a tender thyroid gland you should suspect that the cravings of thyroiditis are under those circumstances right? So those are kind of like some big things you want to keep in mind there and again remember your immune syndromes they're just sort of kind of thyroid related so let's talk about those right? So remember right those things have got a zomodominant inheritance and there's immune one way they'll have like parathyroid like primary hyperparathyroid is in right? So they can have hypercalcemia they can have like pituitary adenomas most commonly like a prolactinoma but remember those people can also have um so the prolactinoma right? Obviously it'll cause like an ecomasia, galactoria, infertility because prolactin is a suppressor of gen RH right? And then um they can also have um pituitary pro another pituitary thing they can have right? They can also have like a growth hormone secreting a tumor right? So they can have like a chromegaly right? So like all like the species between the teeth is increased they have frontal bosseine their friends don't recognize their rings don't fit their hats don't fit and they can get like a hypertrophy cardiomyopathy and die from that right? So that's probably that's actually the most common cause of death in people amacromegaly right?

And then um remember that they can also get pancreatic neuroendocrine tumors they can get insulin omas right? Now we have like the classically described weeple striat right? So like they'll have hypoglexemia signs of hypoglexemia and then their symptoms get better with glucose augmentation right? Or they can get like a blue cagonuma right? So if you see a person that's like developing like neon-set diabetes right? They've never had a histro diabetes and then weirdly they develop diabetes and you're like hmm and this person has like a skin rash like a necrotic skin rash uh think about a blue cagonuma on the other circumstances right? So uh the classically described a necrolitic migratoryorythema right? That's a pathonomonic thing emission and ambient exam and then also do not forget that if a person has um another pancreatic neuroendocrine tumor it is that can show up right? It's like a gastrenoma right? So those people can have like the zollinger elicin syndrome so you know you see these people that seem to have like these very virulent ulcers right? Especially if you see ulcers in the genrenum of the small bowel right? That's super unusual that's not hitchpilory that's zollinger elicin syndrome right? And usually those people tend to have chronic diarrhea as well right? And then I guess maybe the final pancreatic neuroendocrine tumor I should talk about here is the viperma right? Remember viperma is tend to represent with the WDHC syndrome right?

Where you have like watery diarrhea you'll have like hypochylemia you'll have echluhedria right? Again those are all classic things you may see with emian 1 and again it's autosomal dominant inheritance emian 2a right? You can have the primary hyperparapartyroidism but those people can also have few chromosidomas right? So uh the fios right? You'll see like the the episodic headache and hypertension and obviously for that you want to check the levels of metanefrens and catecholomins in the right? You'll be elevated and then you do like a CT scan of the abdomen or an MRI of the abdomen or you do like the nucleomedicine test which we classically call like an MIBG scan to establish other diagnosis right? And then those people can also have medallary thyroid cancer which I've talked about already right? And the enemy end to be right? Those people do not get calcium problems they don't get the primary hyperparapartyroidism well they can get the fiochromosidoma right? They can get the marphanoid right? So they can be like super tall and all that jazz right? And then they can also have the fiochromosidomas right? And then they can also have the mucosone aromas like the grotesque on mucososophysususualits, the lips on an MIME exam right? So hopefully you feel comfortable with these are thyroid pathologies again they are all high yield things that tend to pop up on exams right? So that's something I definitely know if I were you preparing for any of these exams.

And then one thing I found to be high yield for these family medicine exams is knowing the cholesterol screening guidelines right? So those are things that people unfortunately tend to not know very well. They're kind of detailed so you know the kind of one of those annoying things that you need to like sort of finish in the back of your mind for exams right? So again there are many guidelines here but let me give you like the Cliffs Notes version that you want to keep at the back of your mind right? So they are basically four groups of people that should get statins on MIME exam right? So the first group is easy. Do you have an LDL cholesterol? Not total cholesterol? Because the MIME they love to give people with this on exams you know they'll put like people that have like elevated like total cholesterol and try to get you to pick giving those people statins that's not always the case right? So if a person has an LDL cholesterol not total cholesterol LDL cholesterol more than you know 190 right? So 190 or higher so if it's 1.89 doesn't fall but 190 or higher right? Go ahead and give those people a statin right? And again usually you give like high intensity statins like at overstatin or overstatin right? And then if a person has like a really bad like atherosclerotic cardiovascular disease right?

Like the have coronary artery disease, the fat stroke, they have peripheral anterior disease whatever for those people they also deserve high intensity statins and again remember at overstatin and overstatin are your high intensity statins right? And then if you have diabetes and your LDL cholesterol is more than 70 right? And you are over the you're basically between the ages of 40 to 75. The way I just think about it is are you a diabetic? Is your cholesterol more than 70? Are you more than 40 years old? That's it. You get a high intensity statin as well. But if you also over the age of 40 and your cholesterol is just above 70 right? But you notice that this person's acvd risk is more than 7.5% so 7.5% those people also deserve a high intensity statins right? So again I'll reel them out. So LDL greater than 190. So greater than or equal to 190 right? If you have like really bad atherosclerotic cardiovascular disease so that the classic ones are an exam. MI stroke, PD right? Or if you're a diabetic, your cholesterol is greater than 70 and you're over the age of 40 right? You LDL cholesterol greater than 70 and you're over the age of 40. You also get a high intensity statin and then if you are over the age of 40 right? I mean if you want to be more strict like the 2040 and 75 and you don't again you don't have the diabetes but your LDL cholesterol is over 70 but your acvd risk is more than 7.5% those people also desire the deserve high intensity statins on an mb-mixer right?

And that acvd score you don't need to memorize how to calculate it is something that you would typically get on an mb-mixer right? And again remember your high intensity statins are things like a tovers statin and a rozovers statin right? And then one other thing that your friends at the mb-mixer love to test on exams are like these vitamin deficiencies right? So let's maybe run through the vitamins that's probably where I'll stop today because it's a fairly it's a fairly large topic right? So let's maybe go through the b vitamins right? So vitamin b1 right? So vitamin b1 is thiamine right? So what are the higher things you want to keep at the back of your mind for your family medicine for your family medicine shelf with thiamine? The big ones you want to keep at the back of your mind one you want to think about like an alcoholic right? So alcoholics right? They can get winykey cursor cough syndrome. Remember winykey cursor cough syndrome arises because you have issues with transketolise. Transketolise is one of those key enzymes in the non-oxidative fees of the pentose phosphate pathway right? So transketolise uses thiamine vitamin b1 as a cofactor. So if you're an alcoholic you know you deplete your b1 if you deplete your b1 then you can get into trouble right? Like having a winykey cursor cough syndrome. And remember winykey is right? Is the trade of a person having a confusion right? Optimal plegia.

Optimal plegia is just code word for any eye problem and then a taxia right? If you see that that's winykey is that reversible right? You give ivy thiamine for that and you give the thiamine before you give glucose right? But if you take that trade and add on to it things like a person making stuff up right? So like confabulations or the person having like this organized movements like it, taxia then that's cofacocops. Cofacocops is also treated with ivy thiamine but it's irreversible right? It's irreversible. And then one other thing that you may see with thiamine problems on an exam is a person that has high premises, gravity, direct, or if they describe a feist trimester pregnant woman, woman and a ton. Those people actually have a pretty high risk of winykey's. So those people actually deserve vitamin B1 like ivy vitamin B1 when they come to the hospital in addition to the anti-emetics that you're giving them right? And usually on mbimics and those people have a metabolic acidosis they'll have like a hypochalemic hypochalemic metabolic acido sorry hypochalemic hypochalemic metabolic alkalosis whoops I think that but metabolic alkalosis right? Because your vomitting stomach acid right? So you become alkalotic from that and also because your vomitting at ton right to become volume depleted so the activity of urine and trotense in our dust urine system goes up right?

So our dust urine will dump all those protons at the level of the infar intercanid cell of the collecting of the distonephrine right? So you get a metabolic alkalosis there and your hypochalemic right? Because you have vomiting hydrochloric acid literally right? So those are the big things to know with thiamine and remember thiamine has that neuronatomicula association with hemorrhagic infarctions of the mammillary bodies right? So that's something you want to keep in mind. And then having a thiamine deficiency right? And also cause uh wet berry berry right? That's like a diluted cardiomyopathy again that you can find in the chronic alcoholic right? Because again if thiamine is not working you may see the fine why is that? Well if thiamine doesn't work I don't know some key pathways in your body I don't know like maybe like uh like the pyruid dehydrogen is complex not going to work so your TC is basically the gateway to your TC cycle is shot right? So you're not going to be able to make it EP right? And if you're not making it EP right? Your cells will begin to feel they'll be essentially have like it's almost like a metabolic ischemia in a sense right? So you get into trouble and you can get a diluted cardiomyopathy which is essentially wet berry berry. It's called wet berry berry because if your heart doesn't work you have a dimi everywhere right?

Now vitamin B2 uh riboflavin that's not really tested on the family match also I'm going to move on from that uh vitamin B3 is nice and right? Nice and certainly is tested right? Pelagra right? Pelagra right? And there are many things that can cause pelagra in your test right? So you know if you don't eat foods that are rich and often B3 well you're kind of screwed there that's one but another thing that can kind of screw you over as well is if you have like carcinolid syndrome right? Remember carcinolid syndrome is what you have like a GI mask that makes a ton of our serotonin? Well think about it. Serotonin is known as 5-HT for a reason right? 5-hydroxy triptophan right? So that means it's derived from triptophan. Well guess what? What do you think we used to make um niacin? We also used triptophan to make niacin right? So if you shunt all your triptophan towards making serotonin well you're going to get pelagra with that right? Or if you have like heart and obd disease where you have trouble reabsorbing like neutral amino acids like triptophan at the level of the proximal convoluted tubule right? You'll also get a niacin deficiency and you can get into you can get into trouble all right? And then um what are the things you find with niacin deficiency? E.K. pelagra right? You know you have the 4 Ds right? So like diarrhea, dermatitis, dimension death right? So those are all things to keep at the back of your mind for exams um vitamin B5.

So then it can say that's step one so I'm going to skip that. There's no vitamin B4 at least I don't think yeah I'm pretty sure actually I'm certain there's no vitamin B4. So only if they discovered vitamin B4 and I'm not aware of it. But vitamin B6 is definitely high yield to know for exams right? That's paradoxal phosphate. There are many different contexts that you could see this in on an ambient exam right? So especially on a family medicine shelf right? The probably the classic one will be like TB treatment right? Your doctor says ooh you're taking it so nice is it? I would really love you to take this vitamin alongside right? You're like uh doc I don't think you really know what you're talking about or maybe you read like Dr. Google and you know read some crap online well fine I wish all the best with uh with your pseudo-roblastic anemia right? So uh what are the things that B6 can cause right? So B6 can cause pseudo-roblastic anemia right? Because remember if you remember from step one there's this enzyme known as alas like elisin thase that's like the reclimiting enzyme of hym synthesis well it needs B6 as a cofactor right? So you know if your B6 is not working if you don't have B6 because I so nice it depletes your B6 uh depletes your B6 if your B6 is not working right? Then alas will not work you won't make him so you get a pseudo-roblastic anemia. Another thing that can also happen is you can also get seizures right from a B6 deficiency right?

So um because again remember glutamate is an excitatory neurotransmitter at least of the central nervous system like the brain and then gabai is the inhibitory neurotransmitter of the brain right? So gabai is inhibitory it kind of comes you down glutamate is super excitatory it kind of spurses you up right? So if you have like uh B6 deficiency there's this enzyme known as gad glutamate decarboxylis that will not work and gad converts glutamate to gabab right? So if gad doesn't work because the cofactor is not around and your glutamate will raise your gabab will plummet and because you have high glutamate you have too much excitation can get seizures right? And then you can also get like LFT abnormalities right? Because again you see all those transaminases that you learn about ELT, EST, blah blah blah blah blah blah right? Well what's the cofactor used by your transaminases? It's vitamin B6 right? So if your vitamin B6 does not work that explains why isonize it is potentially hepatotoxic as well right? So those are all things you want to keep in mind on exams um vitamin B7 biotin yeah I'm going to skip that that's most step one further um B8 there's nobody in B8 at least as far as I know but B9 folate you know kind of high up to no right? So if you're the kind of person that does a T and two stiate well you can get a fully problem right? And folate can cause a mega-loblastic anemia right?

So the MCV will be more than 100 um and those people can also get like hyper homosystememia although remember that people that have a folate deficiency will not get a methylmalonic acidemia right? Because remember it's B12 deficiency that's cobalamin it's B12 deficiency that will cause the the methylmalonic acidemia in addition to the mega-loblastic anemia and hyper homosystememia because if you remember from step one with your OCHA fatty acids right? Like if you want to go from like methyl from from methylmalono coa to succino coa you need methylmalono coa imutes for that to happen right? So you know if you have a B12 deficiency the enzyme methylmalono coa imutes will not work because B12 is its cofactor so you get a methylmalonic acidemia from that and then remember B12 can also cause all these other problems right? Like subacute combined degeneration of the spinal cord so like your nostal columns your corticospinal tract won't work so those people have problems with like fine touch vibration per perception they'll have like opal moron neurons in thumbs kind of deal right? you know so those are things to keep in mind and then remember right fully deficiency or classic in people that are taken on type elliptic drugs and B12 deficiency right if you're vegan right? Like an onwise vegan you know you don't take like B12 supplements because remember B12 comes from animal products right? Remember fully it comes from fully each right?

So if you're taking if you're vegan you're not going to get a fully deficiency but you'll definitely get a B12 deficiency especially if you're like a prolonged like you're like a long term you're a long vegan right? So let's see is they know the vitamin stuff want to talk about or mineral stuff? if a person has like this gusia so you know like imparity sensation or person has alopecia right? that's classic zinc deficiency and I mean there are many things that can cause zinc deficiency right? Like if you're on TPN for a long time right? Or if you have Wilson's disease believe it or not right? If you have Wilson's disease and it's being treated and you're not supplementing zinc that can also cause problems because one of the treatments for Wilson's disease is a copper chelator known as triantine so TRIE and TINE well in addition to being able to kill it copper it's actually pretty good at killing zinc right? So you can get a zinc deficiency that way right? And then vitamin C deficiency right? So the person will have like mucosol bleeds you'll have because collagen doesn't work very well because remember from step one if you want to like hydroxylate like pruline and lysine residues you kind of need vitamin C for that so you have like you know like a kind of like screwed up collagen synthesis when you have a vitamin C deficiency so you essentially have like scurvy they'll have like bleeding gums and all that crap and then don't forget right?

If they give you a question about a person that has like a malabsorptive disorder right? That's basically like a gateway to like fat soluble vitamin deficiency questions on exams right? So like night blindness with like vitamin A deficiency or like osteoporosis or secondary hyperparthyroidism with a vitamin D deficiency right? Because remember right like if you have a fat malabsorption then by default you are not able to resolve your ADE and key vitamins or vitamin E deficiency right? They'll be like the person may have like e-conthocyteosis on a blood smear and they will also have e-taxia because again if you remember from step one it's kind of phenomenal how step one actually is really helpful for step two like doing like knowing your step one material well really helps on step two at least in my experience. But I mean e-deficiency can cause e-taxia right? Because from step one if you remember your spinal cerebellar tracts the proper malination of those tracts depends on a vitamin E right? And then vitamin K they can get like all these vitamin K deficiency they can get all these bleeds so I guess your major question here may be like oh divine. One of the things that can cause fat malabsorption well a bunch of stuff right? So let's assume your terminal ilium has been reset fed because you have current disease well you're not going to be reabsorbing many fats that way and that can also cause B2 of deficiency right?

Or if a person has like 65 broses on a family medicine shelf if you have CF right your pancreas right? You have like an endocrine and exocrine pancreatic defect right? Because your pancreatic secretions are very fake right? So you're not making lipes you know so that can cause problems or let's assume you have celiac disease right? celiac disease can also cause a fat malabsorption because again one of the areas you can torture your GI tract is your terminal ilium in celiac right? Remember you want to avoid a gluten containing foods in those people and then if you know if you drank alcohol for you know pretty long portion of your life and then they tell you that oh the prisoner has had recurring the episodes of abdominal pain that's chronic pancreatitis right? pancreas is shot no more lipes right? So you're kind of screwed from that perspective. So I think those are kind of like the key vitamins and minerals you know you want to commit to memory for your exams. One thing that just dropped in my mind let me just see this for completeness seek because again the family medicine shelf covers like kids to adults right? So if you see a newborn with like big tongue like a big tongue beefy red tongue has an umbilical hernia, hazmaco glossia right? That's pretty classic for congenital hypothyroidism right? And usually the most common cause there's like thyroid is genesis right?

So again these are just all things you want to keep at the back of your mind and I will try really hard it's just again time that's my big limiting factor here but I'll try really hard to hopefully make some more family medicine related shelf podcasts as time goes on but I'll just make them rapid review series. It will be a comprehensive library at the end. It will just take a while to to get to right? So I'm going to go ahead and pause here again as I do at the end of every podcast I do offer one or one to learn for many exams step one two CK two C.S.

Step three preclinical medical exams 30th shelf exams if you're if you're a medicine resident the ABI M board exam the medicine in treating exam um or if you're a college student that needs to learn for the MCAT um or you need to learn for like general chemistry organic chemistry physics biochemistry histology physiology I tutor for all those things and then I do like these booster courses it's like 15 hours for step two CK step three it's like 20 hours for step one where again I review like the most notes like right before you take it like your USMLE exams again I've done it with a ton of people super successful with that stuff and then I do like comprehensive USMLE reviews um I just need a group of five to seven people so if you have a group um you know just reach out to me and I'll be happy to kind of give you some more details um and then again as I've said in prior podcasts I think I that's maybe like a episode two or four or something like that um there's this podcast I made recently on USMLE and the military so the USMLE has started focusing these days on like military servicemen and women and also like geriatric like folks um I'll make a geriatric podcast like actually very soon um but that's of tested on the exam so please before you take step two CK or step one or step three I promise you you'll literally be changing yourself if you do not listen to the podcast on like USMLE and the military it's one of the more recent podcasts I made it's like some episode above 200 or something like that so um you know just listen to it get your three points and move on from that so um if you need details and again on any of these things or let's say you're a medicine applying to residences or like an era's application or college student applying to med school so like an Amcass application so you know you need help with like editing your application editing your personal s

tatements doing more interviews rec letters again reach out to me um again I've done this with a ton of people more than 90% of the people have worked with have much of their first choices um and I also have like admissions committee experience I've been on the admissions committee of a top two med school for a year um so again I have a lot of experience with this stuff so you know if you need any of those things either reach out to me through the website or send me an email at divine intervention podcasts with an sbn.gmail.com so have a wonderful rest of your day um god bless you I'll see you next time thank you

The non-oxidative branch of the pentose phosphate pathway; Wernicke-Kefler-Cornelly Syndrome (WKS).

De Quervain's thyroiditis.

Amyloid deposition (and elevated calcitonin).

Folate (B9) deficiency.

Cardiomyopathy.

VI Poma (Vasopressin-Intimin-Peptide-related tumor).

Confusion/Encephalopathy, Ataxia, and Ophthalmoplegia.

Vitamin C (Ascorbic Acid).

Amyloid deposition in the thyroid gland and elevated calcitonin.

B12 is required as a cofactor for Methylmalonyl-CoA mutase, leading to accumulation of methylmalonic acid.

Celiac disease or terminal ileum resection/Crohn's disease.

Papillary loves lymphatic spread; Follicular loves hematogenous spread.

Vitamin B6 (Pyridoxine).

Confusion/Encephalopathy, Ataxia, and Ophthalmoplegia.

Vitamin C (Ascorbic Acid).

Amyloid deposition in the thyroid gland and elevated calcitonin.

B12 is required as a cofactor for Methylmalonyl-CoA mutase, leading to accumulation of methylmalonic acid.

Celiac disease or terminal ileum resection/Crohn's disease.

Papillary loves lymphatic spread; Follicular loves hematogenous spread.

Vitamin B6 (Pyridoxine).