Elevated BUN: creatinine ratio favors UPPER over lower GI bleed.
Why?
1) Hb in stomach --> amino acids (aa). 2) aa absorbed by small intestine. 3) aa transported and taken up by liver. 4) In the liver, aa undergo deamination, leading to release of NH3.
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5) NH3 (aka ammonia) is converted to urea by the urea cycle, leading to elevated blood urea levels. 6) Meantime, creatinine is not influenced by the protein/aa bolus. 7) Thus, BUN/creatinine ratio is increased.
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So why does blood cause this bump in urea and increase in BUN/creatinine ratio, whereas a steak dinner does not?
Because blood has poor BIOLOGICAL VALIUE (the protein is poorly utilized by the body).
The LOWER the biological value of a protein, the HIGHER the urea.
I tweeted a poll asking for the next step in a patient with thrombocytopenia and a platelet clumping on a peripheral smear. 62% of you answered correctly, namely to repeat the CBC in a green top (heparin-containing) tube.
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Key points:
1) Pseudothrombocytopenia is mediated by EDTA-dependent antibodies that react with platelets in blood that is anticoagulated with EDTA (chelates calcium, necessary for clotting reactions), causing platelet clumping and falsely low platelet counts.
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2) Pseudothrombocytopenia is purely an in vitro artifact.
3) EDTA-containing collection tubes are preferred for CBCs/peripheral smears because, compared with other anticoagulants, EDTA allows the best preservation of cellular components and blood cell morphology
a. Used to calculate the Hct (Hct = MCV x RBC count)
b. Used by some to predict iron deficiency vs. thalassemia (e.g., Meltzer index)
b. Largely ignored because it says nothing about the size/Hbization of RBCs
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... you could have LOTS of SMALL RBCs or FEWER LARGE RBCs amounting to the same Hct (viscosity) and Hb (oxygen carrying capacity)!
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MCV
a. Ah, now we're talking 😀! MCV is super helpful because it is the first branch point in the ddx of anemia - microcytic vs. normocytic vs. macrocytic. Each has its own specific causes.
1. The clotting cascade in plasma is activated by the addition of a negative charge, which activates the intrinsic pathway (aPTT) or tissue factor, which activates the extrinsic pathway (PT) in presence of Ca2+ and PL.
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2. Once the ingredients are added together, the "stop watch" is started and time to clot formation at 37C is measured (the assays do not discriminate between crosslinked and uncrosslinked fibrin).
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In vivo (the body):
1. The clotting cascade is ALWAYS activated by TF-mediated activation of FVII. TF hides in the subendothelial layer of the blood vessel wall and is expressed on the surface of activated monocytes.
NORMOCYTIC, NORMOCHROMIC IRON DEFICIENCY ANEMIA (IDA)
We tend to think of IDA as being microcytic (more consistently than hypochromic). However, there are certain situations in which the MCV is normal in IDA.
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Examples include:
1. A patient with high-normal baseline MCV whose MCV falls within the normal range in IDA (see first graphic for an example).
2. A patient with baseline macrocytosis, for example from concomitant liver disease, B12 deficiency, MDS or hydroxyurea use.
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3. Rare cases where the MCV simply doesn't budge from baseline despite clear cut evidence of IDA (i.e. anemia +/- low MCHC with low ferritin that responds to iron treatment).