William Aird Profile picture
Feb 1, 2023 4 tweets 2 min read Read on X
1/4

#GI #GIbleed #urea

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. Image
2/4

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.
3/4

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.
4/4

For more information see:

thebloodproject.com/cases-archive/…

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More from @WilliamAird4

Jun 11
1/7

RELATIONSHIPS BETWEEN RBC INDICES

RBC count

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 Image
2/7

... you could have LOTS of SMALL RBCs or FEWER LARGE RBCs amounting to the same Hct (viscosity) and Hb (oxygen carrying capacity)!
3/7

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.
Read 7 tweets
May 31
1/4

APPROACH TO NORMOCYTIC ANEMIA

This is the most common type of anemia, and its differential diagnosis can sometimes feel overwhelming, and 'all over the place'.

The following is organizational scheme with simple diagnostic buckets that covers virtually all causes: Image
2/4

BUCKET LIST 1:

Appropriate vs. inappropriate retic response (appropriate defined by absolute retic count > 120 x 10^9/L or 0.12 x 10^12/L)?

BUCKET LIST 2:

If appropriate retic response, is there bleeding or hemolysis? Image
3/4

BUCKET LIST 3:

If inappropriate retic response, is there inflammation or organ dysfunction?

BUCKET LIST 4:

If organ dysfunction, is there chronic liver disease, chronic kidney disease, endocrinopathy or bone marrow dysfunction?
Read 4 tweets
May 30
1/5

COAGULATION IN VITRO/IN VIVO

In vitro (test tube):

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. Image
2/5

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).
3/5

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.
Read 5 tweets
May 21
1/6

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. Image
2/6

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.
3/6

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).
Read 6 tweets
May 1
1/7

ANISOCHROMIA

We are used to considering variation in RBC size (increased variation = anisocytosis) by examining a blood smear or evaluating the RDW.

What about variation in RBC Hb concentration ([Hb]) (anisochromia)? Image
2/7

We can often identify cell-to-cell differences in central pallor on a blood smear.

While we may make mental note of such differences, we rarely incorporate the finding in a summary of the smear. And there is no lab equivalent to the RDW for Hb concentration or "chromia". Image
3/7

Or is there? If we plot single cell [Hb], we would likely find a normal distribution with a bell shaped curve (I have not seen any such data published). The mean would provide us with the MCHC and the standard deviation with the RDW for [Hb]. Image
Read 7 tweets
Apr 5
1/6

TRANSFUSION AS IRON THERAPY

Yesterday I posted a poll showing CBC data from a patient with severe iron deficiency anemia and asked: assuming she receives 4 units pRBCs (which of course would be excessive here), does she need iron therapy on top of that?

70% answered YES. Image
2/6

Each unit of RBC contains about 250 mg Fe. So she will have received about 1000 mg of Fe, not far off from her total needs. However, such is iron is bound up in Hb inside the donor RBCs and is not readily accessible for erythropoiesis. Image
3/6

I ran through some rough numbers (see graphic):

1. Oral iron will deliver about 20 mg Fe to the bone marrow each day.
Read 6 tweets

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