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Thread: A case for you

  1. #1
    Statia Graduate is offline Junior Member 510 points
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    A case for you

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    Here is one for you guys, this comes from a real case last month:

    63 year-old white male is admitted for dizziness, confusion, mild SOB, and 2+ bilateral lower ext edema. He has a history of Hep C, treated with tenofovir for 1 week before stopping due to side effects. Liver biopsy in 8/2000 showed Stage 1 bridging fibrosis. Medications at home include spironolactone 80mg once a day, lasix 100mg twice a day, omeprazole 40mg once a day, aspirin 81mg, amlodipine 10mg once a day.

    Labs:
    WBC: 4.2
    Hg/HCT: 10.2/30.4
    plt: 102

    Na: 130
    Cl: 112
    K: 3.8
    Bicarb: 24
    BUN: 18
    Cr: 1.2
    Total protein: 7.4
    Alb: 3.0
    AP: 91
    ALT: 52
    AST: 24
    Tbili: 1.9
    Bilic: 1.4
    Ca: 9.4

    PTT: 24.1
    INR: 1.4

    Upper endoscopy in March/2009 showed:
    Grade 1-2 esophageal varices, normal GE junction

    Transthoracic ECHO in 3/2007 showed:
    Normal LV function
    Stage I dystolic dysfunction
    Mild aortic stenosis, valve area 1.5 cm2

    Question one:
    The patient's abnormal labs are due to:
    A. Congestive heart failure
    B. Overdiuresis
    C. Cirrhosis
    D. GI bleeding
    E. Multiple myeloma

    The patient's symptoms are due to:
    A. Pulmonary embolism
    B. Hepatic encephalopathy
    C. Critical aortic stenosis
    D. GI bleeding
    E. None of the above

    Okay, so think this one out, feel free to ask questions, and I'll answer them for you!
    Last edited by Statia Graduate; 05-08-2009 at 11:35 PM.

  2. #2
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    ok i guess i'll be the first to take a stab.. first what i'd like to know is physical exam findings? any jaundice? any scleral icterus? hepatic enlargement? also what's his T billi? what's his Retic count? what's his RDW and MCV? Did you guys do fecal occult blood test? did you do an anemia work up like TIBC and Fe levels? Did he report any blood in the stool or coffee ground stools? Also does he look pale? is he sweating? does he have tachycardia, orthostatic hypotension? I mean you totally missed the vitals, and they're always important..

    For question 1 he has a lot of abnormal labs and it's possible a combination of a few things. like for example his low CBC could be from a chronic GI bleed. his high INR and ALT and low Albumin and is probably from his liver cirrhosis and his low Na, high Cl is probably from the lasix. So at least for me it's hard to to pick out one thing. if you asked why the cbc is abnormal i'd say GI bleed (D) if you asked why the INR is high i'd say cirrhosis (C) if you asked why the electrolyte imbalance i'd say Over diursesis (B).

    #2) A)we can rule out PE cause his INR is 1.4 and he has no history of immobilization, i know the INR isn't that high and a clot could still form but not likely, and he takes a daily asprin.

    B) for hepatic encepholopathy we need physical exam findings and t. billi maybe also blood ammonia levels? depending on this results this could be the answer, cause his liver isn't doing so well, it's not making protiens very well hence the edema and the high INR, and the low albumin. so we can't rule this out just yet.

    C) critical aortic stenosis, can be ruled out cause the echo says "mild aortic stenosis" lol

    D) GI bleed, I can't rule the out as well. because lets face it I need the info above and depending on what it says this could be the answer.

    E) of course if the test results come back negative for both B and D then this would be the answer. but some how i doubt is.

    So if i had to make a guess as to what the answer to #2 is I would say D) GI bleed, cause lets face it how common is hepatic encephalopathy compared to a GI bleed, and common things happen commonly. Also his LFT's aren't that high, his BUN isn't that high, he's still making some protien and other stuff so he's liver isn't totally shot for it to cause encephelopathy.

    so my final answers are 1) it depends on which lab value you want. if you're talking about all lab values in general i would say D, GI bleed

    and for q #2) my answer is D.


    if you don't want to reveal the answers just yet can you please at least private message me if i am correct or not. I kind of did it with out looking anything up and so would like to know how accurate I am.

    thanks and it's a great post!
    Hollywood Upstairs School of Medicology, Class of 2010
    Due to the high volume of private messages, I can only answer questions that are posted in a forum. Private messages will be ignored.
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    Statia Graduate is offline Junior Member 510 points
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    Hi RJ,

    I structured the question like this because this is how some of mine were structured on Step 2 and 3. I apologize about the Tbili! Totally my fault. The Tbili was 1.9. I will add it in up above. So, I want you guys to be able to look at the entire picture and out of the box.

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    Statia Graduate is offline Junior Member 510 points
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    The clinical cases on the steps may not give you all the info you would like (ie vitals). So, just think out of the box.

    Ok, so this is what I want you guys to learn from this:

    Just by looking at this patient's lab work, you can tell that he has cirrhosis. He has hyponatremia, thrombocytopenia, anemia, elevated INR, hypoalbuminemia, hyperbilirubinemia. These lab values are classic for liver cirrhosis. His last liver bx was 9 years ago with only stage 1 fibrosis (Stage 4 is cirrhosis). Obviously, his disease has progressed.

    I know not all the information is presented to you, but when you hear liver+confusion, always consider hepatic encephalopathy. You do not need all the info to start a differential. Any liver patient is at risk for hepatic encephalopathy.

    So to answer your questions directly:
    A. You can never rule out a PE in a patient who "autocoagulates." These patients still develop clots. Daily ASA use, even 325mg does not lower the risk of DVT. Risk factors for DVT include: hypercoagulable states-such as CA, phosopholipid antibody, Protein C and S deficiency, lupus anticoagulant, Factor V Leiden deficiency, immobility, dehydration, destruption of vascular integrity (lines, trauma), old age.

    B. I just wanted you to consider hepatic encephalopathy without even a PE. Should always be in the back of your mind with liver pts. Ammonia levels are great for an one-time baseline. But they do not correlate with clinical presentation or severity of disease.

    C. I put in aortic stenosis as a red herring.

    D. You are right, by this case, you cannot rule out a GI bleed. But, I didn't mention melena did I? By the way, fecal occult test are positive so much of the time, we rarely do them in the clnical setting. Every patient with a suspected GI bleed should be rectalized to eval for fresh blood or melena. Usually when a varix decides to bleed, there is no question about it.

    E. not the correct answer.

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    Statia Graduate is offline Junior Member 510 points
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    The case will continue...

    So here is a bit more for you:

    What is this guy's MELD score?

    Why is the MELD score significant?

    This guy has varices, what medication should he be on and why?

    These may be a bit tough:

    How often do you screen pts with hep C and ETOH cirrhosis for HCC? and with what test?

    What is the one chronic liver disease where you screen for HCC even if they don't have cirrhosis?

  6. #6
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    Quote Originally Posted by Statia Graduate View Post
    Hi RJ,

    I structured the question like this because this is how some of mine were structured on Step 2 and 3. I apologize about the Tbili! Totally my fault. The Tbili was 1.9. I will add it in up above. So, I want you guys to be able to look at the entire picture and out of the box.
    so can you private message me the answers of what he had? i guess after your hints. 1) is cirrhosis 2) PE? encephalopathy?

    How does the liver failure produce anemia? I haven't gone over any IM notes yet. and I don't think I learned that in school maybe i just forgot. I know renal failure can cause anemia but liver? do you mind going over the pathophysiology?
    Hollywood Upstairs School of Medicology, Class of 2010
    Due to the high volume of private messages, I can only answer questions that are posted in a forum. Private messages will be ignored.
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    Quote Originally Posted by Statia Graduate View Post
    So here is a bit more for you:

    What is this guy's MELD score?

    Why is the MELD score significant?

    This guy has varices, what medication should he be on and why?

    These may be a bit tough:

    How often do you screen pts with hep C and ETOH cirrhosis for HCC? and with what test?

    What is the one chronic liver disease where you screen for HCC even if they don't have cirrhosis?
    these are much harder lol.. I haven't even heard of the MELD score till now.. I had to look all these up so i guess posting on here would be pointless since i didn't know the answers..but maybe for the sake of being complete i'll post.

    1) his MELD is over 40 so that means 100% mortality rate.

    2) MELD tells you mortality and liver transplant need i guess cause it's used by UNOS.
    3) propranolol to reduce the portal hypertension.
    4) This I couldn't find i bet it's anually. an diagnosis can be made by CT or even better by MRI so would you use those as the screening tools as well?
    5) Hep B and C can cause HCC without cirrhosis.
    Hollywood Upstairs School of Medicology, Class of 2010
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    Statia Graduate is offline Junior Member 510 points
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    Very close

    Very close again!

    His MELD is actually 14. When you use the MELD calulators online, make sure you calcuate for someone who is not on dialysis.

    This guy's Cr rose to 1.3 the next day, and so his MELD became 15. At discharge, I referred him for transplant evaluation.

    The MELD score is a scale that ranges from 4-40. It predicts motality from end-stage liver disease. A MELD of 15 is usually the threshold most hepatologists have to start the transplant workup.

    The screening tool usually used for HCC is a 4-phase CT scan of the liver. It is done annually. If someone has renal failure, an MRI can be done. Screening is usually done in cirrhotic patients (cirrhosis of any cause), and chronic viral hepatitis patients.

    Non-selective beta-blockers such as propranolol and nadalol do reduce portal hypertension. They are given to patients with varices. Reduce the portal hypertension=reduce the size of the varices, and therefore reduce the chance the varx may bleed.

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    RussianJoo's Avatar
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    Quote Originally Posted by Statia Graduate View Post
    Very close again!

    His MELD is actually 14. When you use the MELD calulators online, make sure you calcuate for someone who is not on dialysis.

    This guy's Cr rose to 1.3 the next day, and so his MELD became 15. At discharge, I referred him for transplant evaluation.

    The MELD score is a scale that ranges from 4-40. It predicts motality from end-stage liver disease. A MELD of 15 is usually the threshold most hepatologists have to start the transplant workup.

    The screening tool usually used for HCC is a 4-phase CT scan of the liver. It is done annually. If someone has renal failure, an MRI can be done. Screening is usually done in cirrhotic patients (cirrhosis of any cause), and chronic viral hepatitis patients.

    Non-selective beta-blockers such as propranolol and nadalol do reduce portal hypertension. They are given to patients with varices. Reduce the portal hypertension=reduce the size of the varices, and therefore reduce the chance the varx may bleed.

    what formula did you use for the MELD equation?

    Also so what were the answers to questions 1 and 2 on your original post?
    Hollywood Upstairs School of Medicology, Class of 2010
    Due to the high volume of private messages, I can only answer questions that are posted in a forum. Private messages will be ignored.
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    RussianJoo's Avatar
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    Also could you please explain how liver disease or liver failure causes anemia? and what type of anemia should you see with liver failure?

    thank you for doing this by the way. this is very helpful.
    Hollywood Upstairs School of Medicology, Class of 2010
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