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Episode Notes

Source / episode info

  • Episode: 212
  • Title: Divine Intervention Episode 212 – Family Medicine Shelf Review Series 3 (GI).
  • Published: 2020-02-13
  • Source: Episode page

One-liner

Episode 212 provides a comprehensive review of liver pathology, covering the differentiation between hepatocellular and cholestatic patterns; detailing viral hepatitis serologies (A and B); outlining management of cirrhosis complications (bleeding, encephalopathy, HRS); and comparing autoimmune cholangitis syndromes like PBC and PSC.

High-yield summary

  • Liver Injury Patterns: Hepatocellular pattern involves disproportionately elevated AST/ALT; Cholestatic pattern involves disproportionately elevated ALP/GGT. The ratio of direct to total bilirubin is key for diagnosis.
  • Hepatitis Serology (Hep B): Positive H BsAg indicates infection. Anti-H Bc IgM suggests acute infection, while anti-H Bc IgG suggests past or chronic exposure. A positive anti-H Bs alone usually means vaccination or recovery.
  • Cirrhosis Management: Screening for Hepatocellular Carcinoma (HCC) is mandatory every six months via ultrasound in all cirrhotic patients.
  • Autoimmune Cholangitis: PBC affects middle-aged women (40–60 years old), presents with positive Anti-Mitochondrial Antibodies (AMA), and involves intrahepatic ducts. PSC affects younger men, is associated with IBD (especially UC), and can involve both intra- and extrahepatic ducts.
  • Liver Failure Syndromes: Hepato-renal Syndrome (HRS) results from splanchnic vasodilation leading to a pre-renal pattern of AKI; Acute Fatty Liver of Pregnancy (AFLP) is a critical, acute third-trimester complication requiring immediate delivery.

Learning objectives

  • Differentiate between hepatocellular and cholestatic patterns of liver injury using enzyme ratios (AST/ALT vs. ALP/GGT).
  • Recognize the clinical presentation, serology, and management protocols for Hepatitis A and B infections.
  • Master the screening guidelines and differential diagnosis for chronic cholangitis syndromes (PBC vs. PSC).
  • Understand the pathophysiology and acute management of liver failure complications, including HE, HRS, and AFLP.
  • Identify classic signs and symptoms associated with iron overload disorders like Hemochromatosis.

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
Primary Biliary Cholangitis (PBC)Positive Anti-Mitochondrial Antibodies (AMA)Middle-aged women, intrahepatic duct involvementRemember the demographic: 40–60 years old female.
Primary Sclerosing Cholangitis (PSC)String of beads pattern on MRCP/ERCPUlcerative Colitis (UC), men, extra/intrahepatic ductsScreening for colon cancer must start at diagnosis of PSC.
HemochromatosisSkin hyperpigmentation ("bronze skin"), elevated transferrin saturationHFE gene mutation (C282 Y)The classic triad is diabetes, hypogonadism, and arthropathy/arthralgia.
Acute Hepatic FailureCoagulopathy (PT/INR prolongation), Encephalopathy, JaundiceCirrhosis progression; requires immediate interventionMonitor the MELD score for prognosis; consider transplant referral.

Rapid review table

TopicKey PointContextExam Relevance
Liver PatternHepatocellular: AST/ALT >> ALP/GGTViral hepatitis, Drug-induced liver injury (DILI)High transaminases suggest parenchymal damage.
Bilirubin MetabolismGilbert Syndrome: Indirect hyperbilirubinemiaDecreased UDPGT activity; stress/illness triggerNot treated; diagnosis is incidental and benign.
Cirrhosis ScreeningHCC screening every 6 months via ultrasoundAll patients with cirrhosisFailure to screen increases mortality risk.
GI Bleeding AlgorithmUpper endoscopy first, then colonoscopy if negativeAny suspected GI bleed (upper or lower)The initial workup is sequential and non-invasive.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
A 50-year-old woman with fatigue, pruritus, and elevated ALP/GGT, positive AMA, and signs of chronic liver disease.Primary Biliary Cholangitis (PBC)PBC is the most common cause of cholestatic pattern in middle-aged women; AMA is the hallmark antibody.
A young man with a history of ulcerative colitis who presents with jaundice and dilated bile ducts on MRCP.Primary Sclerosing Cholangitis (PSC)PSC strongly correlates with IBD, particularly UC, and affects men, often presenting in younger age groups.
A patient with cirrhosis who develops confusion, asterixis, and elevated ammonia levels.Hepatic Encephalopathy (HE)Cirrhosis impairs the liver's ability to clear toxins like ammonia; management involves Lactulose and Rifaximin.
A man presenting with jaundice, fatigue, skin hyperpigmentation, hypogonadism, and diabetes mellitus.HemochromatosisClassic triad of signs (bronze skin, diabetes, hypogonadism) due to iron overload from excessive absorption.
A pregnant woman in the third trimester who develops coagulopathy, encephalopathy, and elevated transaminases.Acute Fatty Liver of Pregnancy (AFLP)This is a critical, acute liver failure syndrome specific to late pregnancy; requires immediate delivery.
A patient with chronic diarrhea and abdominal pain, showing dilated bile ducts on imaging, but no gallstones are present.Mirizzi SyndromeSuggests extrinsic compression/obstruction of the cystic duct by an adjacent process (e.g., inflamed gallbladder).

Differential diagnosis / distinguishing features

Acute Fatty Liver of Pregnancy (AFLP) vs. HELLP Syndrome

Key FeaturesDistinguishing FindingsNext Step
AFLP: Third trimester, acute liver failure, coagulopathy, encephalopathy.HELLP: Severe preeclampsia + signs: Hemolysis, Elevated Liver enzymes, Low Platelets.Both require immediate delivery and supportive care; AFLP may have high bilirubin/lactate.

Acute Mesenteric Ischemia

Key FeaturesDistinguishing FindingsNext Step
Sudden onset severe abdominal pain ("pain out of proportion to exam").History of Atrial Fibrillation (A Fib) or embolic source; often involves SMA.Immediate surgical consultation and angiography/embolectomy.

Management pearls

  • Cirrhosis Bleeding: Initial management requires large peripheral IV access, fluid resuscitation, and blood products if hemoglobin < 7 g/dL. If refractory, consider TIPS procedure (though carries risk of encephalopathy).
  • GI Bleed Workup: The workup is sequential: EGD first; if negative, proceed to colonoscopy. Only after both are negative should angiography or angioembolization be considered.
  • Cirrhosis Screening: All patients with cirrhosis must undergo HCC screening (ultrasound) every six months. Furthermore, check for underlying causes of coagulopathy and encephalopathy.
  • Portal Hypertension Management: For variceal bleeding refractory to initial measures, IV Octreotide or Vasopressin may be used; TIPS is reserved for severe cases but requires careful monitoring for hepatic encephalopathy.

Don't miss

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PBC vs PSC Demographics: PBC = 40–60yo female + AMA. PSC = Younger male + IBD (UC).
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PSC Screening Protocol: Colonoscopy screening for colon cancer must begin at the time of PSC diagnosis and repeated every 1–2 years, regardless of UC status.
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Iron Overload Triad: Hemochromatosis classically presents with skin hyperpigmentation, diabetes mellitus, and hypogonadism/arthropathy.
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AFLP Timing: AFLP is a critical complication restricted to the third trimester of pregnancy.

Integration & clinical reasoning

  • GI Bleeding & Coagulopathy: Severe liver disease (cirrhosis) impairs synthetic function, leading to coagulopathy (elevated INR/PTT), which complicates any GI bleed and requires careful monitoring.
  • Portal Hypertension Cascade: Cirrhosis leads to portal hypertension -> splanchnic vasodilation -> decreased effective arterial blood volume -> pre-renal AKI pattern (HRS).
  • Autoimmunity Overlap: Autoimmune hepatitis, PBC, and PSC can coexist or mimic each other; always consider the full spectrum of autoimmune markers (AMA, ANA, anti-LKM) when evaluating chronic liver disease.

OMM / COMLEX integration

🦴
For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
  • Standard emergency management (e.g., resuscitation for GI bleed, antibiotics for cholangitis) takes priority over OMT.
  • In cases of suspected septic shock or severe abdominal pain from acute mesenteric ischemia, the focus must be on immediate vascular and surgical stabilization; OMM/OMT is adjunctive only after hemodynamic stability is achieved.

Concept connections / cross-references

  • For detailed management of acute pancreatitis: [ Episode 15 ]
  • For comprehensive review of endocrine disorders/adrenal insufficiency: [ Episode 37 ]
  • For general GI anatomy and motility issues: [ Episode 209 ]

High-yield association table

ConditionAssociationMechanismClinical Significance
Primary Biliary Cholangitis (PBC)Anti-Mitochondrial Antibodies (AMA)Autoimmune destruction of small bile ducts.Requires treatment with Ursodeoxycholic Acid (UDCA).
Primary Sclerosing Cholangitis (PSC)Ulcerative Colitis (UC)Chronic inflammation leads to fibrosis and stricturing of bile ducts.High risk for colorectal cancer; requires aggressive surveillance colonoscopy.
HemochromatosisHFE gene mutation (C282 Y)Excessive intestinal absorption of iron, leading to systemic deposition.Requires regular monitoring of transferrin saturation and phlebotomy for treatment.
Hepato-renal Syndrome (HRS)Splanchnic vasodilation / Portal HypertensionDecreased effective circulating volume perceived by the kidney.Presents as a pre-renal pattern of AKI; treat with vasoconstrictors/lactulose.

Key terms glossary

TermDefinitionContextExample
Hepatocellular PatternLiver injury characterized by high transaminases (AST/ALT).Viral hepatitis, DILI.Acute viral gastroenteritis causing elevated AST/ALT.
Cholestatic PatternLiver injury characterized by high bile duct markers (ALP/GGT).Obstruction of bile flow, PBC, PSC.Gallstone obstruction or Primary Biliary Cholangitis.
Anti-Mitochondrial Antibodies (AMA)Autoantibodies targeting mitochondrial components in liver cells.Diagnosis of Primary Biliary Cholangitis (PBC).Found in the serum of a middle-aged woman with pruritus and elevated ALP.
Hepato-renal Syndrome (HRS)Acute kidney injury secondary to severe portal hypertension/cirrhosis.Splanchnic vasodilation leads to decreased renal perfusion.Seen when creatinine rises despite normal renal anatomy.

Study optimization

TopicStudy ApproachPriorityResources
Liver Patterns & EtiologyUse ratio analysis (AST/ALT vs ALP/GGT) and clinical history (sex, age).HighReview board-style vignettes comparing PBC/PSC.
Cirrhosis ComplicationsCreate flowcharts for bleeding, encephalopathy, and AKI workups.HighestFocus on the next step in management (e.g., EGD vs Colonoscopy).
Autoimmune DisordersMemorize key antibodies (AMA, anti-LKM) and associated demographics/organs.Medium-HighUse mnemonics for PBC (40–60yo female) and PSC (younger male + IBD).

Question pattern recognition

  • Pattern: Red quadrant pain + fever + jaundice: Points to acute cholangitis or cholecystitis; requires imaging (ultrasound/CT) and potential drainage.
  • Pattern: Male, younger age, history of UC, dilated bile ducts on MRCP: Strongly suggests Primary Sclerosing Cholangitis ( PSC ).
  • Pattern: Female, middle-aged age, pruritus, elevated ALP, positive AMA: Highly suggestive of Primary Biliary Cholangitis ( PBC ).

Test yourself

Common mistakes to avoid

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Mistake 1: Confusing PBC and PSC demographics. Remember PBC is typically a middle-aged woman with AMA, while PSC is often associated with IBD in younger men.
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Mistake 2: Assuming all liver failure requires transplant immediately. Use the MELD score to guide prognosis; initial management focuses on supportive care (lactulose/rifaximin).
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Mistake 3: Misunderstanding the GI bleed workup sequence. Never jump straight to angiography or colonoscopy without completing EGD first.

Common traps

⚠️
Trap 1: The "Cholestatic" Trap: Seeing elevated ALP and GGT does not automatically mean obstruction; it can be due to infiltrative disease, PBC, or other causes. Always look for the underlying cause (e.g., AMA).
⚠️
Trap 2: The "Cirrhosis Screening" Trap: Students often forget that HCC screening is mandatory every six months in all cirrhotic patients, regardless of symptoms.
⚠️
Trap 3: The "AFLP vs HELLP" Trap: Both are severe third-trimester complications; remember AFLP involves acute liver failure and coagulopathy, while HELLP is a manifestation of severe preeclampsia.

Original transcript with highlights

Original transcript with highlights

Okay folks, welcome. My name is Divine, I'm a resident. This is episode 212 of the Divine Intervention Podcast. And in this podcast I'll be continuing the Family Medicine shelf review series. This will be series 3 and I'll be focusing on GI. I'll be focusing on GI and I know there's a lot of people that have kind of sent me requests about like when I plan to finish these Family Medicine podcasts. I will try my very best and try to make as many as possible that will be helpful for the shelf and also for step 2 CK. So I will just try to hit on the highest hill topics first and then I'll begin to go after the lorry old ones as time goes up. So let's just jump right into it. So I will say basically today in terms of GI, I think the best way to treat GI is to talk about the other stuff and then talk about the liver. So today I'm gonna focus on the liver. Like the liver and all its pathologies and all the biliary whatever's because that makes up probably like almost half of the GI material that presents on the Family Medicine shelf. So let's jump right into it. So the first thing on MBME exams you want to differentiate is you want to ask yourself is a disease hepatocellular in nature or is it called a static in nature? What do I mean by that?

The thing is a colist static pattern of liver disease is usually a liver disease where you have the outforce disproportionately elevated compared to the AST and ALT and then a hepatocelular pattern of liver disease is when you have the AST and ALT being elevated disproportionately compared to the outforce right. Although remember as a surrogate for outforce you can also use the GGT gamma glutamol transferries that's also a pretty useful test in to tell you that you're dealing with some kind of a colistatic liver disease. So I mean again if you see like this hepatocellular pattern people have like super high AST, ALT's that's usually caused by like you know like a viral hepatitis or you can see people have like drug induced liver injury like from a sediment of a again remember I said a minofin is not an insect that's a common mistake people make on exams.

No one really knows how a sediment of a works is just a fever reducer so that's something I want to keep in mind and then if you see an AST to ALT ratio rated and true right you're probably thinking about some kind of alcoholic hepatitis right and whenever you see a person that has acute liver disease like acute liver injury you notice that they're clotting lapse are beginning to get out of whack so like the PTI nar is getting all screwed up the albuming is getting decreased and all that badness then you want to begin to worry about maybe referring to those people for liver transplant basically once the liver is like kind of like synthetic function like PTI in our PTT begin to get out of whack that's an ominous sign right so that's something you need to watch out for tests and then again colistatic pattern of liver disease the thing that will happen for the most part is those people have again a very outfoss they'll have a very direct bilirubin right proportionally via AST ALT will be much lower and again usually you need to have problems like in the biliratory to have these kinds of problems right and then obviously the person has like hemolytic anemia of any sort right or if they have like a UDPGT problem you have like increases in indirect bilirubin so again those are all things to keep at the back of your mind now what if they give you a question about a patient that you know has like a mild operas for during infection or is just had a surgery and then you have like you know like mild John this mild indirect type of bilirubinemia what's your diagnosis I hope you think about Gilbert syndrome right Gilbert syndrome when breaks like decreased activity of UDPGT so whenever you have decreased activity of UDPGT right you will not be able to convert indirect bilirubin to direct bilirubin so you have an indirect hyperbidirubinemia and remember that Gilbert syndrome is not

treated right he's not treated it's for the most body symptomatic they will just whenever they are stressed or they get like a mild sickness they get like an indirect hyperbidirubinemia so that's fine that's not a huge not a huge issue don't treat it now what if you get a question about a patient that you know maybe trouble to Mexico and then came back and this person you know has like you know pretty severe like red upper cordrum pain the ASTLT like is in the thousands if you see that what are you thinking about I hope you're thinking about like hep A right like acute hep A infection remember hep A doesn't cause chronic infection right then I mean hep A is actually vaccine preventable that's why like if you're traveling to an endemic area or you an IV drug user right or person has like cirrhosis like chronic liver disease or has like one of those hemophiliaes if there's like if you're a man that has sex with other men those people actually do need the hep A vaccine right that's a common example she won't be aware of and again if a person is if a person is given the hep A vaccine then you essentially decrease the risk of them contracting hep A in the first place I remember that hep A for the most part right like the way we present you would be like super acute onset it shall be fatigue you'll have like jaundice you'll have nausea you'll have vomiting there are ASTLT usually above a thousand on MBM exams right and again the way that they will present it in the test they'll give you this kind of presentation and the ask for your next step in diagnosis just go ahead and check for the anti- hep A virus IgM okay because remember IgM is what is elevated in a person that has a acute infection right and then if we're getting to the other hepatitis right like HB right HB for the most part right what are some classic things they'd like to test on exams obviously this vaccine p

reventable I mean if a child is born in the hospital before the child leaves the hospital the child should get the HB vaccine and another classic question you see is if a person gets like a needle stick from HB right you want to give them the HB vaccine and also the HB immune globular right but the thing is if a person already has a history of HB vaccination then you don't need to do any kind of post exposure perphylaxis okay that's a high-yield thing to keep in mind let's say like they tell you that oh this person was recently vaccinated has a positive HB antibody tighter and you don't need to do anything in terms of post exposure perphylaxis for those people now one thing I'm gonna go ahead and say is that when a child contracts HB like when a baby contracts HB the vast majority of them progress to chronic HB but when an adult contracts HB the vast majority of them are really successfully clear the infection that's actually a very high of what subtle factor to keep in mind for the endemic exams right and how do people get HB right like you know sex needle stick injuries like health care worker cannot deal right so those are the things you want to keep at the back of your mind now I know one big bugger book for many many students is that tele-divine how do I memorize all these HB surrogis let me tell you the thing if you keep two rows in mind you probably will be able to and I'll tell you these two rows you'll probably be able to resolve like 90 to 95% of the HB surrogi questions you get and here's here are the two rows if your HB surface antigen is positive you're infected in some way shape or four okay I'll say that again if your HB surface antigen is positive you're infected in some way shape or four now if your the second rule is that if your HB surface antibody is positive then you are not infected okay I'll say that again if your HB surface antibody is positive

you are not infected like literally if you just know those two rows you can usually if you just apply some reasoning figure out exactly what you're testing in a question obviously there are some more derivatives from that but if you remember those two rows I can almost promise you you can probably get like 90% of your questions correct right so what do I mean by that right so say for example a person's HB surface antibody is positive you know they have no infection right so what are two ways you can have no infection well you could have gotten the vaccine where in that case it's only your HB surface antibody that'll be positive or you could have been exposed to HB but you you recovered from the infection in that case your core antibody will be positive right and it will likely be like a core antibody IGG right because remember the core antibody the core antigen that will make your body make the core antibody is not part of the vaccine it's only part of the actual bug right so that's simple HB surface antibody business there and then the surface antigen right again like I said if it's positive then you know you know that you you have an infection and then you may see divine okay how do I know if it's an acute or chronic infection just look at the core look at the core antibody that's it right the core antibody's job is to tell you if you've been exposed to HB or if it's a tell you if you have like an acute or chronic infection if the core antibody is IgM it's an acute infection if the core antibody is IgG it's a chronic infection simple as that and then there's a special case of like the window period right in the window period everything is negative with the exception of the HB core antibody that's it and usually the IgM HB core antibody that's pretty much all you need to know about the HB serologies and in terms of treating and remember that HB has like some associa

tions with some other disorders right so so those disorders you may make that those diagnosis when you tell you that oh this person has a history of HB on an MBM exam right like the classic ones are like polyadrylis nodosa right polyadrylis nodosa those two tend to have like chronic abdominal pain because the vasculitis involves the mesenteric vessels in the GI tract right if a person has membranostinaphyrapathy right remember that's the one that has the it's a kind of nephrodix syndrome is the most common cause of nephrodix syndrome in Caucasians think about HB you know think about HB being an association there right again those are all things they love to test on exams right and then another thing i'd like you to keep at the back of your mind with H Bs in terms of treatment right HB you can treat it like intake of ear right or you can treat it with tenofovir right so intake of ear or tenofovir in some cases right you mean if you don't see the those uncertainures you mean give that person like a pigly fit into fair on right yeah that's that because intake of ear tenofovir those things are kind of like DNA inhibitors right so it will not be ideal to give that to like a person that's like pregnant that's probably not a good idea so you know for persons pregnant and they have HB infection you can treat them with like a pigly fit into fair on and then for person has HIV right you can put them on like I think I'm pretty sure I talked about this in my internal medicine video you put them on a combination of like M3 C the bin and tenofovir right and 3 C the bin and tenofovir as part of because those things also essentially part of anti-retroviral therapy already so it's almost like you're killing two birds with one stone right now the thing is I'll go ahead and see this that one way that your friends at the end of me can integrate HB or HB treatment with psych is to have you r

emember that if a person has a histral depression you absolutely don't want to put them on interferon alpha right interferon alpha is about again a person that has a histral depression because basically it almost puts you into like depression for a year so if a person has a histral like major depressive disorder or they won't have like utropinia right or the azerosis is like super bad with like all these complications interferon alpha is not a great idea in those people right because again remember interferon alpha essentially spursus opulimmune system right so if a person has like really bad cytopanias like they have leukemia thrombocytopenia and nia interferon alpha is not great right because again you don't want to essentially like make those people have like more autoimmune destruction or basically if a person has like an autoimmune thing going on interferon alpha is bad because in general interferon alpha if a mom is speaking I'll have to read some read up some more in this it's not good in people that have autoimmune disorders let's just go ahead and leave it at that and again probably the more common likely thing you see on your exam is where person has like major depressive disorder that's that's a terrible idea right that's a terrible idea and hepsi right like there are some screening guideline questions that pop up on the exam periodically right so if for example a person was born between like 1945 to 1965 on your family medicine shelf you want to make sure you screen those people for hepsi right and usually again blood blood transfusions at the things that give people hepsi on endemic exam so though also being an IV drug user I cannot put you in that situation now one thing that the endemic also does is they may give you again a person just like I said with a B right let me give you a person with a certain disease and your next step in management on an exam

maybe to actually screen them for hepsi right classic ones will be a person that has like mixed cryoglubulinemia right remember where those people have like renotes phenomenon kind of deal right with those called agglutinins right and then another classic one is profereic utenia tarda remember profereic utenia tarda is a deficiency of urod right like urobophereinogen decarboxylis so those people right again they tend to they tend to they tend to there is a very strong association hepsi right so that's something you want to keep at the back of your mind and exams and I mean if you suspect the presid has hepsi the first thing you want to do on an MB is just check the anti hepsi the antibody right that's always your first step in diagnosis check the anti hepsi the antibody right if the anti hepsi this antibody is positive then you just check the hepsi RNA right because the thing is when you know the hepsi RNA that tells you if the person has active infection or not right if the hepsi RNA is negative then person does have active infection if the hepsi RNA is positive then for sure they do have active infection going up right and the thing is we also do all that because you need to do you know like genotyping right before you can start them on like hepsi treatment and the thing is when a person gets hepsi treatment right you know you can put them on one of those direct acting agents like sofosbovia and ledi pasvia I think that's the one that's known as harvoni that you may hear about on tv and then you can also give like sofosbovia and semeprovia right so sofosbovia ledi pasvia sofosbovia semeprovia there are many other regimens but I feel like those two I just mentioned probably the high sia who wants to know for exams just basically look for drugs that end in like the start with look for sofosbovia right it will likely be as it will likely be one of the answers you see

on your test right so that's why you typically want to do genotyping right because genotyping is the most common one in the US is like 70-ish percent of cases of hepsi right so you put those people on those drugs and you know you kind of essentially cures them and the thing is when a person is cured right when a person is cured of hepsi the hepsi hepsi RNA will be negative it's only the antibodies that will remain positive right and one weird kind of vasculitis that you may actually find if people would hepsi is something called like a lyucocytoclastic vasculitis right so those people essentially have like poppable preparer usually on the lower extremities especially like the legs right like the legs the feet right that's one thing you want to watch out for on exams and if a person has cirrhosis so this is again another screening guideline thing we see on exam on an exam if a person has cirrhosis and they have hepsi you do actually need to um um because they have a high risk of hepatocellococytoclomerate those people actually deserve ultrasound every six months right just again to screen them for hepatocellococytoclomerate and then also don't forget right that before you start a person on a treatment for hepsi you do actually need to check the hepatocellocytoclomerate that you want to check the hepatocellocytoclomerate because the thing is when again a person is studied on anti-varietary before hepsi that may actually cause a reactivation of the hepatocellocytoclomerate so again just something to watch out for on an exam and then again if a person is an alcoholic right usually they are AST to ALT which will be greater than 2 to 1 on an in-bim exam um and then another thing you may also see is they will have like increased levels of gamma glutamol transfer is right and again if a person drinks so hard that he going to acute liver failure watch out for if the aptin R is

bad or things like that those people may need like referral to like a transplant center right and usually um there's this thing called like the melt score i would not memorize the components if i were you or the madri score again i would the thing is people in family medicine love their scores right but i'm not saying to memorize the components but i'm just into memorize like some numbers right so if for example a person is like melt score is 18 or higher right or the amadri score is like 32 or higher one thing that's usually prudent to do on an in-bim exams right again from alcohol it's a guy here that give those people steroids okay that's just one of those ribb is our things you mission an exam uh steroids have been shown to like you know like help with like their liver lapse and almost like preserve liver function right so that's just something you want to keep at the back of your mind with uh with these tests and then um what did they give you a question about a patient that you know has a history of like Hashimoto's thyroiditis or type 1 diabetes or video ligo or other sins disease and then um they tell you that oh this person you know has like red opacorgent pain um and they show you that the ASTLT is you know pretty high and they tell you that all the A&E is positive on your exam what are you thinking about well i hope you're thinking about like autoimmune hepatitis right and for autoimmune hepatitis unfortunately your friends at the mbim expect you to know the positive auto antibodies right so the positive auto antibodies tend to be like the anti-smote muscle antibodies right another one mission an mbim exam that anti-liberal kidney micro-summon antibodies right so anti-smote muscle antibodies and the anti-lk m or the liver kidney micro-summon antibodies again it's an autoimmune disease remember whenever you when it almost always i'll say like a pretty great

majority of the when a person has one autoimmune disease when they are presenting an autoimmune disease question to you on an mbim exam they'll usually give you like some autoimmune disease pre-existing autoimmune disease the patient already has and for the most part the way you treat these people is you know you just give them steroids you can also give them isophyalprin um and unfortunately whenever you stop treatment usually the disease comes right back right so it's kind of an unfortunate situation there and then again autoimmune pancreatitis just if the tell you that a person has like um a sausage-shaped pancreas think about autoimmune pancreatitis on mbim exams it's one of those IGG4 related diseases where the levels of IGG4 are kind of high right so that's something in keeping in mind and then what if they give you a question about like a 65 year old man on your shelf you know he has erectile dysfunction he has like this new onset diabetes he has like skin hyperpigmanum condition um or you may even have like signs and symptoms of like uh pituitary dysfunction um if you see that what are you thinking about well i hope you think about hemochromatosis right heterochromatosis remember it's a little more recessive inheritance that's a high-em factor no right and because basically these people have like you know they just reabsorb a creptone of iron and all that stuff right and the iron name the positive and different organs triggers the fainting reaction and then causes like a reactive oxygen species and like uh fibertic destruction of those organs right so one of the classic things in mycena your exam skin hyperpigmentation right neon state diabetes in a super like kind of like an older person it's almost always in a guy on tests um they may also have like um because again the iron deposits in the pancreas uh again they may have like erectile dysfunction they may

have like cppd right so calcium pyrophosphate deposition disease right especially if you won't see like a person having like arthritis like in unusual areas right like arthritis like in the shoulders in the ankles and the elbows um and again they have like again these other things that kind of talked about think about here hemochromatosis under those circumstances right and for the most part you check these patients transfer and saturation to you know kind of screen them um and then you want to know the genetic underpinnings right for this right so usually people that have hair deterioration macromatosis they have like the C2 H2 Y mutation right so if they are homozygous for the C2 A2 Y mutation or sometimes you may even find people that are like compound heterozygous where they don't have like two C2 A2 Y mutations but they have one C2 H2 Y mutation and then you also have like a H63 D mutation that's what's known as a compound heterozygous that can also trigger symptoms of heterozygous macromatosis right and again sometimes you may just see them say that oh the person has a HFE gene mutation right so again that's these things are all just higher than important to know for tests right and again if a person uh has basically when a person has like something that can cause cirrhosis when they actually get cirrhosis as a general principle the screening guideline is to check those people for hepatocelular carcinoma every six months with ultrasound right and again um hyaluracrymatozygous again like I said you can check the transfer incertoration alternatively you can naturally um go ahead and check the affair team level so be elevated the transfer incertation will be elevated as well right and the way treat you want comatosis is phlobotum right phlobotum is basically a treatment for hemocromatosis polycythemia there and uh prefer cutina tart on an endemic exam right and then if you

give your question about a patient that you know has like insulin resistance versus in super obese has type 2 diabetes and then has like you know like mild elevations in their ASTLT um think about any FLD right so I like I like to call this disease Nafold right Nafold non alcoholic fat-eliver disease right uh basically for the most part the symptoms will resolve if you treat your diabetes have them lose weight treat your hyperliplagemia and that's pretty much that's pretty much it um and then don't forget your classic disorders PVC right PVC so it's gonna be in a woman on your test right um show have a colistatic pattern of liver disease so outfoss will be elevated G2 will be elevated and don't forget your auto antipadus right the anti mitochondrial antipadus right and the thing is because these people have these obstructive problems they may actually have like a fat soluble vitamin deficiency so that's actually like an unusual kind of question in me seeing your test so they may have an incidence of like vitamin A deficiency like my blindness or vitamin D deficiency where they have like um osteovalesia right or vitamin E deficiency where they have like etaxia and acanthosytosis on a blood smear or they may bleed from a vitamin K deficiency right and again they can also have like osteoporosis osteomalysia and uh again it's a problem PVC primary bilirical angiostrum remember before the old name was a primary biliric cirrhosis uh so PVC is something that you treat it also dial right that's essentially what you do and again it's a problem with the intran hepatic bowel docs only right contrast this with PSC that again we're shopping men usually men with ulcerative colitis on an endemic exam right and it will show be much younger men because PVC is usually like a women that are like 40 to 60 years old PSC is usually men that are 20 or 40 years old right and again they almos

t always have you seen and unlike PDC that affects the intran hepatic bowel docs only PSC tends to affect the intran and extra hepatic bowel docs and again they'll have jundes they'll have paritis they'll have also be elevated um um and for the most part right you can make the insure diagnosis by doing an ultrasound um and then if you notice that hmm this person has like diluted bowel bowel docs right you can then go ahead and do an MRCP or ERCP to establish the diagnosis and the screening things you want to keep at the back of your mind with um with use and with a PSC actually kind of high yield to know right so the thing is these people they have like very high risk of like colon cancer very high risk of like gobladder cancer very high risk of colanducarcinoma so the thing is um if one patient is diagnosed with PSC right we need to start screening them for colon cancer or colonoscopy at the time of diagnosis right and then you screen them like everyone to two years this is floridae high yield I promise you this is actually floridae high yield to know because I know some people may be saying but divine night thought it was eight years so let me clear this up for you for pressing is diagnosis also rid of colitis you start screening them with colonoscopies for colon cancer eight years after the initial diagnosis of UC is made but if a patient is found to have PSC you need to start screening them from colon cancer at the moment that the diagnosis is made and then you screen them every one to two years without colonoscopy for colon cancer for those people is usually not appropriate to do like those hemocall tests or the fet test or whatever you just go straight for the juggerna you go straight for for colonoscopy right and then these people you also need to do like annual MRC Ps right you need to do annual MRC Ps for these people you help you kind of screen them for coland

ucarcinoma and again if you have cirrhosis with PSC you need to consider again every six months ultrasound to screen for hepatocellular carcinoma right and again just again let me just real quick help you differentiate PBC PSC again PBC woman 40 to 60 years old affecting hepatic bowel docs only they usually have some other kind of autoimmune disease on board right you have positive anti-mythocontriol antibody is treated also diol sometimes they may call also diol on the exam cell also the oxycolic acid PSC will be in a guy that's much younger 20 to 30-ish years old right you'll have again intra hepatic bowel docs are affected they'll have a history of IBD right and if you do an MRCP erc you see the string of beats pattern right but the most part again these people don't give them also diol it doesn't work right essentially the way you treat these people is you can do a liver transplant to cure or you can use like an ERCP or you can do like some kind of endoscopic therapy to to dilate like big-time strictures that are causing the patient a lot of symptoms right and again PSC you do an ultrasound first if it's positive then you proceed to doing an ERCPR MRCP right and then if a person you know has a bad liver you know like cirrhosis there are many classic things you'll see on the test right so they can have like hepatic cancer fallopathy from the beautiful vanomonia right because the the urecyle stops working they can have a sideys they can tell you that oh they have been kind of acting weird and they have like mild abdominal pain they have a low-grade fever and obviously you're thinking about SBP under those circumstances and I hope you choose to do a parasyntesis in those people and look for the more than 250 neutrophils right to establish the diagnosis of SBP right and then don't forget right these people can have like a pardorino syndrome they can get a pardopominar

y syndrome and all that stuff and for the most part right like again they can have like big splints from polo hypertension which and I mean if your splin is big remember your spin I think comes the question up to 30% of your total plebplepone right so those people can have a thrombus eye opinear with that right and then obviously they'll have like low levels of albumin they'll have like blim problems right because again they're not able to make adequate amounts of of clotting factors so some things right with cirrhosis right so again hepatic cancer fallopathy right again the patient will have like you know like all these weird cognitive issues they may be comatose you know they will there are many things that can trigger it right so they may have like an infection they may have a GI bleed right those things can all trigger hepatic cancer fallopathy and we should hepatic cancer fallopathy right you give lactolose if they are not responding very well to lactolose you can consider giving those people a faxamine on a test right and then if they give you a question about a person that has cirrhosis and you know these persons like shot of breath they have pied the ox the tereloxygen tension is low so they have like an increase the a gradient and then they tell you that oh when the person sits up they feel super shot of breath when the lie back the assortment of breath gets better if you see that think about a hepato pulmonary syndrome right that's basically that thing I just described is what's known as like orthodioxia platypnea syndrome right it's classic for hepato pulmonary syndrome and we make the diagnosis of hepato pulmonary syndrome is actually to go ahead and get an echo get an echo cardiogram and then the detail is that the person has like you know like very elevated again shotness of breath but you don't necessarily have any pulmonary dima but you notice that the

aryventral pressure is a real high right and they have cirrhosis you want to think about pulmonary hypertension so pulmonary hypertension on those circumstances again those people need an echo cardiogram yeah it's a bad situation for the most part and then hepato renal syndrome right again you see a person that has cirrhosis and they're they're creatinine you know kind of keeps rising and the thing is when they give you urine labs in those people the urine labs look exactly like pre-rinolizotemia kind of labs I kind of explained the pathophysiology behind this is one of my GI step one podcast but I don't think pathophysiology is like super-descestry basically like when a person is serotic they may have like splatonic visual dimension so that was still profusional away from the kidneys right so the hyper-perfusion the kidneys so essentially those people like the kidneys have like completely normal anatomy completely normal architecture right but the kidneys are just feeling right that's classic for hepato renal syndrome and then don't forget right like again if you have like liver disease you're not going to be able to make calcium dial which on embian is the occasionally called a 25 hydroxy vitamin D so if you're not able to do any of those stents right you're not going to be able to make because there's nothing that you can send to the kidneys right to act on throw one alpha hydroxyl is to make calcium trial so your calcium will be low your phosphoryl will be low because you don't have active vitamin D that will raise your parathetic level and that'll begin again to resolve your bone and all that stuff so you can have like like osteoporosis osteopenia like you can get like an osteodystrophy right so again those are all just high yield to keep in mind essentially those people have like a secondary hyper-paraphrilism and really the way for these people is you give the

m calcium trial right or can give them calcium trial and that one is fine and typically what you do is if they have osteoporosis right you know consider giving them like you know like a bisphosphanate to the most part like you normally would do for osteoporosis right and since we're kind of talking about serosis let me just maybe talk about the GI bleed algorithm it's something that people tend to get wrong and it kind of hurts my heart I don't want that to be the case GI bleed that easy picking so name me an example they are always easy points because they are treated the same way upper lower GI bleed doesn't matter right the reason I'm talking about the GI bleed now I'm talking about serosis is well literally people that are serotic at high risk of bleeding right from it so of geoviruses for person comes over to the GI bleed right oh they have vomiting blood, pulping blood or whatever the first thing you do is you insert too large peripheral I Vs that's it that's first step give them fluids if they're hemodynamicly unstable and you know fluids are not calling it you can give them some blood and then the third thing is you just do upper endoscopy right you do an GI and it's so far go gastroid water andoscopy right if the EGD shows you what you're looking for you intervene and you're done but if the EGD does not show what you're looking for your next step is a colonoscopy on an example and then if your colonoscopy is wrong then one thing can do you can do like a tag the rib blood self scan or anything of that sort right so again these all things to keep in mind for the purposes of these are exams and then again SVPU dual parts and TC is already kind of talked about that already and don't forget your sag gradient right don't forget your sag gradient if your sag gradient is more than 1.1 then basically anything that increases hydrostatic pressures or decreases on cortic

pressures in your blood stream will cause those are like I almost think of like a sag gradient being greater than 1.1 as almost like trans-UD it's kind of a side is right so it's like high high low on cortic pressure high hydrostatic pressure things that give rise to these problems right so things like like your person has like like cirrhosis so they have like butchery syndrome or like right side in heart from like RC in fact to something like that right and then if you list at 1.1 if your sag gradient is not even greater than 1.1 then you are so SAG right you're right about like like cancer for the most part right cancer for the most part and again if a person has cirrhosis please don't free like I think this probably like the fourth time I'm seeing this right please don't get this wrong on a test for person has cirrhosis you need to screen them for if I don't say lockers you know my every every six months with an ultrasound right and then so let's talk about how you treat like some of these bad things with cirrhosis right so if for example again you want to profile out the person like against like a virus so bleed right the best thing you can do on an MBM exam is to consider giving like a bit of blocker and non-selective bit of blocker right so like for parallel needle all you can also use like carvidi law right I remember carvidi law is an alpha bit of blocker right and then if for example that's not an option let's say for example they have like a Hishov like severe asthma or severe activity with disease then you can profilistically do like op-renoscopy and do like a band ligation of those are of those are very six right and then if a person is like you know bleeding like an active virus you bleed again kind of like what I said already peripheral I Vs fluids plus or minus blood easy to intervene right and typically right there are some drugs you need to give and th

ese drugs are kind of high you to know an example right you want to go ahead and give those people IV up to your time right and then you also need to place them on like prophylactic antibiotics it's usually of the fluoroquinolone variety right so you can give them like or like nor flocks the same you can give them super flocks the same you can even give them safe tracks and actually and then let's say you try out those things you've done the band ligation nothing is working then you have to call interventional radiology those people need the tips procedure right then either tips procedure although remember the tips right one common complication is hepatic and cephalopathy because you essentially connect it putting a conduit between the hepatic artery and like the sorry between the portal vein and the hepatic vein right that's great that's I mean that's great I know right but you do need to be mindful of the fact that be essentially bypassing the liver you're bypassing the ureth cycle so those people can get a hyperamonymia for person is bleeding right and again the hemoglobin is less than seven you need to give them blood right to help with like the acides right you can give them like spironolactone you can give them like lexics right so like ferozomide and if you notice that this person's acides right like you've tried diuretics you've tried everything doesn't seem to be working these still keep building up a ton of like acytic fluid once more thing can actually do an anemone examine is to do like serial press and T Cs like serial like large volume and press and T Cs and one magic number you probably want to remember here is five liters if you strip a person more than five liters of acytic fluid you need to give them argument right you need to give them argument and again if you want to profile acts against SBP give fluoroquino loans that's kind of like the big thing y

ou should take away from that or if a person has SBP for the most part SBP is treated with argument plus a third generation cephalosporine so like safe triaxone cephotaxine kind of deal right and again I've talked about it buddy can cephalopathy you give Latula's first if that doesn't cause it to have refaxing remember refaxing is an RNA polymerizing inhibitor but as far as I know it's extremely expensive and yeah I feel like I've pretty much talked talked about most problems with most problems with people that have zero sensory so I think I'm gonna go ahead and kind of pause there and then again acutely ventricular like these people just usually it's some toxin or some drug usually acid aminofin the STALT just go through the roof like really quickly right acutely ventricular can lead you to acutely verifilure right where you begin to have like insephalopathy your PTI in our your PTC goes out of whack that's bad right and again for the most part what are the things that cause acutely ventricular in immune exams acetaminofin big big big one right sometimes drug reactions right acut viral hepatitis right another one maybe also be it if a person like consumes mushrooms remember like mushrooms contain like aminida aminida aminida like mushrooms and all that stuff right so you know just kind of watch out for those things right so and also if a person has like systemic hypertension right that can cause like massive massive elevation in EST ELT that's something that people call like shock liver right so that those are all things to watch out for in your test right so basically right if you see a person that has a amino phenofin overdose your next step in my event on an in-bim exam is you know measure the serum acetaminofin level right and then go ahead and you know get use of nomogram to see the qualify for an acetyl if a person has like hepatitis A right then it's causing l

ike acutely verine jury you know just supportive care give them fluids give them anti medics that's pretty much all you can do there's no like relantibiotic treatment right and then if they give you a question about a person that has like elevated EST ELT and the person has like psych style maybe like this he's trouble like psych style problems partying sonia problems like peripheral movements and they tell you that all they have like chisaflash earrings in the eye may not be about aero consider will since disease right usually for those people you measure the levels of serum copper measure the acetyloplasmic levels and you can also even check the auring copper excretion and the way you treat that right you treat that with like triantine right or you can treat them with penicillin triantines TRIIN that's high or two now remember triantine though can not just kill it copper can kill it zinc right so if they give you a question about a person with a histral will since disease that's well controlled with medication and then they have like alopecia and they have like poe and healing you know like or rational the skin and think about a zinc deficiency from the medications they are taking again those are all high or things to know and then mushroom poisoning for the most part right like you want to think about giving those people like a penicillin G right that's a thing that it's unusual I can pretty much combine them most people get wrong on a test but you won't get it wrong because you listen to ampede attention to this podcast and then some of these like pregnancy related squabbles right again remember your family medicine exam right has OB questions that's one of those things you you should expect right so you know be able to identify some of these liver associated OB gene pathologies right so like like hypermessage gravidarim right you'll be a first trimester woman tha

t has like severe vomiting right the ALT is really pretty pretty elevated and these people actually have risk of a renegade and cephalopathy so you typically want to go ahead and give them like IV thymine and you usually check their ketone levels when they come into the hospital right and when you treat these people you hydrate them right you give them anti antimerics give them IV thymine and then you tell them you know when you go home it's more males you can give them like vitamin B6 plus doxilamine that also usually helps as well right and then if they give you a question about a woman like in the second or third trimester she has like really bad paritis um and then they show you some labs you notice that the ALT is like super high the alcohol is super high um but other than that she has more symptoms other than like the paritis and stuff you want to think about like intraepatic holostasis and your treatment of choice on in-beaming exams actually is also dial right so remember also dial is useful for like two things on exams PBC and intraepatic holostasis of pregnancy PBC meaning primary bilirical angitis right and then if they give you a question about the woman that you know a blood pressure is really high she has like low extremity edema has protein positive in her urine that's pretty clumsy right those people you again you want to you know kind of be careful want to be looking towards delivering the baby right and again this would be a third trimester problem not a second trimester third trimester problem when you examine and then obviously ready for person has you know like antecedents of preeclampsia where you notice that they have like an indirect type of urubinemia they have like low playclips and all that stuff that's helps syndrome H.E.

double LP this one is bad right you want to go ahead and deliver the child quickly and then obviously for president has a clumsy are you give IV magnesium and deliver the baby right my magnesium helps with the seizures is being shown to be better than benzo's right and treating the seizures that are associated with preeclampsia right and then if they give you a question again and again helps syndrome mean the third trimester so again hyperemesis gravity darum first trimester intraepatic holostasis second of third trimester all these other pathologies I'm mentioning are all third trimester problems right so they give you a question about a patient that you know has like severe you know like signs of like preeclampsia has like severe abdominal pain filling STLT crazy high low playclips indirect hyperbular binemia they have like an encephalopathy they have like you know their liver function is just all out of what ptt is high i and r is high and it's like acute onset think about acute fatty liver of pregnancy they may even have high pulg Lycemia on an inbim exam you need to go ahead and deliver that baby pronto right so I also have you maybe saying okay define how do I differentiate help syndrome from acute fatty liver of pregnancy for the most part helps in drug tends to have like those people tend to have more like a micro and apatic chymolytic anemia but acute fatty liver of pregnancy they tend to be like comatose they tend to have like many liver functional laba normalize like ptt out of whack and they also tend to have like an encephalopathy right and then one thing I want to go through with your real quick again I'm going to end this podcast very soon I promise if they give you a question about a patient so let's just run through these vignetial quick like a patient that has like redubacorjan pain or sometimes on inbim is to be deceitful they'll put that this perso

n has a big astric pain right and then you notice that this person's you know has like fever but they have no jundis and they're astlty just mildly elevated if you see that and maybe they say oh they get an ultrasound are you see like a thickened gobladder or paracolacistic fluid this is a cure colisistitis right remember for those people you get a redubacorjan ultrasound first if that's a pivot or you get a high-discamp right and you feel the colisistectomy right and then if for example the person has like like no intermittent redubacorjan pain you do an ultrasound you don't see any ghost stones that person has something called a like biliric sludge right or say for example they give you a question about a patient sorry I'm just running through this quick because I may actually need to like run to somewhere so they give you a question about a person that has like you know like fever of 103 redubacorjan pain jundis that shakos triad right you know this ascending colonitis or they may add like altered mental status hypertension then that's renal spent time your first day being management and diagnosis for those people is boom go straight for go straight for an ERCP okay that's your you're not going to be doing an ultrasound and then you're going to give them like broad spectrum antibiotics right and then what if they give you a question about a patient that is like you know like super ill stuck in the ICU super septic right and you know they have like redubacorjan pain they have like a mild fever and you know you check they're ultrasound you don't see any ghost stones or whatever what you may see like pericolacistic fluid and all that stuff if you see that I was hoping thinking about ecalculus colisestitis the way you treat that is you do like a colisestostomy right you don't do a colisestectomy right that's bad you know a colisestostomy you call interventional radiolo

gy that put a tube in the to kind of drain and decompress the gold blood right and then again if a patient has like a big astrophim going to the back that's pancreatitis if you have like the classic pattern of abdominal pain and elevated lipis like three four-operative normal then you know that's kind of that's kind of bad right so you don't need to get any kind of image and you know you just make them MPO so they're not eating anymore you give them pain control you give them a ton of fluid right that's pretty much it and then don't forget your rancin criteria or encourage you to look those up right like if those people are like hypocalcemic like your calcium is like low right or they have like like a big decrease in the hemo globin or their AS Ts markedly elevated or their LDG is markedly elevated or they have like a lucosytosis their white clonysmode and 16,000 those are all poor prognostic factors right you know a person that has acute pancreatitis and then if they give you a question about a patient right that you know has like bilateral like nestle tenderness like they tell you that this person has like like a like purulent vaginal discharge and they have like red opera cordrant pain I hope you're thinking about like feats you pretty syndrome right that's essentially like a very hepatitis from like chlamydia or gonorrhea obviously you want to give those people safe traxone and and is it through my cyloncyphytroaxone from the doctor's cycling and then if they give you a question about a patient they tell you that oh this patient has like on usually they will give you the image and finding in these kinds of questions the theory that oh this patient's are common hepatic dot is dilated and you notice that there is a gallstone in the cystic dot and they have like jaundice right because jaundice is not a classic finding people call this isitis right so if you see a pers

on that has like a stone obstructing the cystic dot which you're like oh the van bodaju be call this isitis but you notice that they have jaundice right and they tell you in the question that oh their hepatic dots are dilated that's something known as merizis syndrome m i r i double z i that's something that you may also see on a surgery shell factory right and then if a person you know has like a history of like intermitter and right upper cordron pain and then this like you know like for the last two days they've been having like vomiting basically like small bowel obstruction symptoms I hope you're thinking about like a coli like a like a coli cis to enteric fistula right they've essentially formed like a fistula between like the gallbladder and the GI tract usually like the distal small bowel and then a stone has traveled and obstructed a small bowel and do the circumstances great so again those are just kind of like big things to keep at the back of your mind I don't know is there any other thing I want to talk about I think they've pretty much talked about everything I want to say um there's nothing I want to talk about well let me just say some real quick things right so they give you a question about like an old person that has you know like a painless lorgie I believe does that particularly low-six right you can do like barium studies to make the diagnosis you can also do a CT scan if you see like a person over the age of 50 that has an iron deficiency anemia with hemocorpositives tools right that's colon cancer that's pretty easy or they may even have like a colonic like angiotusplasia and then if they give you a question about a patient there has a history of aphid and they have like sodium nonsense severe abdominal pain where you want to think about like a acute mesenteric ischemia under those circumstances right and then if again if you notice the person

has like GI bleeds or hemocorpositives tools and they tell you in the custom that the person has a history of like erotic stenosis you want to think about like something called high-d syndrome like he wide it's like an angiotusplasia right you want to do like some kind of colonoscopy or something to find like the vascular problem there right and then if you tell you that oh a person has GI bleeds and they've had like a triple leaf fixed in the past that's something known as an erotic phystula right and then if you see like a very young person on your test like a young kid with like you know painless like like bloody poop think about mecos that are particular you know do like a technician scan like the mechal scan you really find the lesion in the right lower quadrant right and then if you notice that a person has all these bleeding and then they have like like especially like on their lips they have like these telangetisia you want to think about a hemorrhagic like heritage of hemorrhagic telangetisia I think that's what's also known as like Oslo Viborandus syndrome right so just something to keep in mind so I think I'm going to go ahead and pause here as I do at the end of every podcast I four one or one tutoring for a ton of exams step one two CK two C S step three preclinical med school exams 30-ish of exams basically all the medicine residency exams like the in training the ibi imports and then I do these booster courses it's 15 hours for two CK and step three 20 hours for step one basically it's a couple of sessions one on one rapid fire review the most knows for those are exams don't know the ton of people defund it to be really helpful and then if you're a college student or you need to end cut tutoring like gen chem or chem physics biochem histology physiology I tutor for all those things and then I also do like coaching right for like if you're a med student

applying to residency so like an ira sap or a college student applying to med school so like an amcassap again I do offer like one on one tutoring and coaching for those things again I have like one year's worth of admissions committee experience at the top two med school right so if you need like helping any of those areas or you know some that needs helping any of those areas just go ahead and have them reach out to me and then also I'm going to be studying this private study group soon I'll probably audit like weekly but it's going to come up soon I'll put out some more information on that soon it'll be like a nominal fee usually before like an hour or two right and if you if you sign up right it will usually be like a theme where I cover like cardiology or this or that and again I suspect it's something that people will find helpful I've done this many times in the past that's something I want to study will probably be through zoom or some kind of good online media so if you're interested in any of these things reach out to me through the website divine intervention reach out to me that through the website you can send me an email divine intervention podcasts with an essay at the end at gmail.com and please subscribe to the You Tube channel the podcast website and also have all these podcasts on like Apple podcasts Spotify and Google Play so please feel free to subscribe and I appreciate any extra subscription so have a wonderful rest of your day God bless you I'll see you in the next podcast thank you

Practice questions — USMLE style

Question 1 — Hepatology/Liver Pattern Recognition

A 25-year-old male presents to the clinic with fatigue and mild jaundice. Laboratory studies reveal an elevated total bilirubin, which is predominantly indirect. Liver function tests show mildly elevated AST and ALT levels, but no signs of acute hepatitis or other liver injury. The physician suspects a common cause for this pattern of hyperbilirubinemia. Which condition best explains the patient's findings?

  • A) Acute viral hepatitis
  • B) Primary biliary cholangitis (PBC)
  • C) Gilbert syndrome
  • D) Hemolytic anemia

Answer: C. Gilbert syndrome. This condition is characterized by decreased activity of UDPGT, leading to an inability to efficiently convert indirect bilirubin to direct bilirubin, resulting in unconjugated hyperbilirubinemia. The diagnosis is typically incidental and requires no specific treatment. Acute viral hepatitis would present with significantly higher AST/ALT levels (hepatocellular pattern), while PBC involves cholestasis and usually presents with elevated alkaline phosphatase and pruritus.

Question 2 — Gastroenterology/GI Bleeding Algorithm

A 68-year-old man presents to the emergency department with hematemesis and melena. He has a history of chronic alcohol use and hypertension. Initial labs show signs of coagulopathy (elevated INR). The patient is hemodynamically stable but requires urgent evaluation for the source of bleeding. What is the most appropriate initial diagnostic step in the workup of this acute upper gastrointestinal bleed?

  • A) Colonoscopy
  • B) CT angiography of the abdomen
  • C) Upper endoscopy (EGD)
  • D) Barium swallow study

Answer: C. Upper endoscopy (EGD). In any patient presenting with an acute GI bleed, regardless of whether it is suspected to be upper or lower in origin, the initial diagnostic step is usually EGD. The transcript emphasizes that the workup must start at the top; if the EGD does not identify a source, then the next step would be colonoscopy.

Question 3 — Hepatology/Chronic Liver Disease

A 55-year-old woman with a history of inflammatory bowel disease (IBD) and chronic cholestasis presents for follow-up. She has elevated alkaline phosphatase and bilirubin levels. Imaging reveals dilated bile ducts, and the patient's clinical picture is highly suggestive of a progressive biliary obstruction process. Which diagnosis is most likely, and what is the key differentiating feature from Primary Biliary Cholangitis (PBC)?

  • A) PBC; associated with positive anti-mitochondrial antibodies (AMA).
  • B) Primary sclerosing cholangitis (PSC); strongly associated with IBD and affects both intra- and extrahepatic bile ducts.
  • C) Autoimmune hepatitis; characterized by elevated IgG4 levels.
  • D) Mirizzi syndrome; typically presents with a gallstone obstructing the cystic duct.

Answer: B. Primary sclerosing cholangitis (PSC). PSC is strongly associated with IBD, particularly ulcerative colitis, and affects both intrahepatic and extrahepatic bile ducts. The key differentiator from PBC is its association with male gender and IBD history, as well as the typical finding of a "string of beads" pattern on imaging.

Question 4 — Hepatology/Cirrhosis Complications

A 70-year-old man with known cirrhosis due to chronic hepatitis C presents with mild abdominal pain, low-grade fever, and altered mental status (encephalopathy). Physical examination reveals spider angiomata and gynecomastia. Laboratory tests show an elevated ammonia level. Which of the following interventions is most appropriate for managing this patient's acute decompensation?

  • A) Administering high-dose ursodeoxycholic acid
  • B) Initiating a course of oral antibiotics (e.g., fluoroquinolones)
  • C) Performing a paracentesis to measure total fluid volume
  • D) Starting lactulose and monitoring ammonia levels

Answer: D. Starting lactulose and monitoring ammonia levels. The patient's presentation—encephalopathy, elevated ammonia, and signs of cirrhosis—is highly suggestive of hepatic encephalopathy (HE). Lactulose is the primary treatment for HE as it reduces ammonia absorption in the gut. While antibiotics are used to treat precipitating factors (like infection), the initial management step for confirmed HE involves reducing nitrogenous waste products like ammonia using lactulose.

Quick fire review

What is the key difference between a hepatocellular pattern and a cholestatic pattern of liver injury?

Hepatocellular involves disproportionately elevated AST/ALT; Cholestatic involves disproportionately elevated ALP/GGT.

What specific finding in HBV serology indicates an acute infection?

Positive anti-H BcIgM (and often H BsAg).

Which two rules are sufficient to interpret most Hepatitis B serologies?

1) If H BsAg is positive, the person is infected. 2) If anti-H Bs is positive, the person is NOT infected.

What is the classic presentation of Primary Biliary Cholangitis (PBC)?

Woman, aged 40–60 years old, with elevated ALP and positive Anti-Mitochondrial Antibodies (AMA).

What are the two most common causes of secondary hyperparathyroidism in advanced cirrhosis?

Chronic kidney disease or severe vitamin D deficiency/malabsorption.

What is the primary screening recommendation for a patient diagnosed with Primary Sclerosing Cholangitis (PSC)?

Colonoscopy screening for colon cancer must start at the time of diagnosis, and subsequent surveillance should occur every 1–2 years.

If a patient has elevated ALP/GGT but normal AST/ALT, what pattern of liver injury is suspected?

Cholestatic pattern (suggests bile duct obstruction).

What condition causes indirect hyperbilirubinemia due to decreased UDPGT activity and is not treated?

Gilbert syndrome.

In the context of HBV serology, what does a positive anti-H BcIgG suggest?

Past or chronic exposure/infection (non-acute).

What are the two classic associations for Primary Sclerosing Cholangitis (PSC)?

1) Men, usually younger (20–40 years old). 2) History of Inflammatory Bowel Disease (IBD), especially UC.

Which specific lab test is used to screen for Hemochromatosis?

Serum ferritin and transferrin saturation (or checking the HFE gene mutation status).

What are the key components of the workup for suspected acute mesenteric ischemia in a patient with abdominal pain?

CT angiography/CT scan, looking for bowel wall thickening or pneumatosis intestinalis.

If a cirrhotic patient presents with severe lower extremity edema and rising creatinine, what syndrome should be considered?

Hepatorenal Syndrome (HRS).

Quick recall / Anki-style questions

If a patient has elevated ALP/GGT but normal AST/ALT, what pattern of liver injury is suspected?

Cholestatic pattern (suggests bile duct obstruction).

What condition causes indirect hyperbilirubinemia due to decreased UDPGT activity and is not treated?

Gilbert syndrome.

In the context of HBV serology, what does a positive anti-H BcIgG suggest?

Past or chronic exposure/infection (non-acute).

What are the two classic associations for Primary Sclerosing Cholangitis (PSC)?

1) Men, usually younger (20–40 years old). 2) History of Inflammatory Bowel Disease (IBD), especially UC.

Which specific lab test is used to screen for Hemochromatosis?

Serum ferritin and transferrin saturation (or checking the HFE gene mutation status).

What are the key components of the workup for suspected acute mesenteric ischemia in a patient with abdominal pain?

CT angiography/CT scan, looking for bowel wall thickening or pneumatosis intestinalis.

If a cirrhotic patient presents with severe lower extremity edema and rising creatinine, what syndrome should be considered?

Hepatorenal Syndrome (HRS).