1/ #UncleBob is working to better understand hepcidin. Please critique this so that we can have a better understanding.
Hepcidin is a peptide hormone. Its main function is the regulator of iron entry into the circulation
2/ As hepcidin levels increase, iron transport into the circulation decreases. It does this by binding to ferroportin - the transport channel.
Thus - decreased dietary iron absorption. It also leads to iron sequestration in macrophages.
3/ Why should we care? IL-6 (a proinflammatory cytokine) stimulates hepcidin. Thus the anemia of chronic inflammation results from increased hepcidin which in turn makes iron less available to the bone marrow.
4/ When we ingest iron, we also stimulate hepcidin - thus taking too much oral iron has the paradoxical effect of decrease iron absorption and iron access. This likely explains the newer concept of once daily or every other day oral iron.
5/ We can overcome some of hepcidin's absorption problems with IV iron. I suspect this is why many CKD 4&5 patients get anemia improvement with IV iron (and do not always need EPO.
6/ In working on this tweetorial I did much extra reading to better understand this important hormone. I'm certain that I have more to learn. Please teach me.
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1/ #UncleBob asks you to consider the implications of the famous Nietzsche quote, “There are no facts, only interpretations” These tweets inspired by following @VPrasadMDMPH
We all interpret data differently weighing the risks & benefits.
2/ How else can one explain competing guidelines? Committees look at the same data and make different recommendations. This is the potential flaw in "evidence based medicine".
Confirmation bias influences all these decisions.
3/ The critical care community developed a very aggressive guideline for early treatment of possible sepsis. The ID community left the joint committee and wrote a strong editorial about the risk of over use of antibiotics secondary to this guideline.
#UncleBob is a huge @UVA basketball fan and very proud of our coach Tony Bennett. He took these 5 pillars of our program from his dad (also a great basketball coach. These are very applicable to #MedEd# . ,.,. .
1/ HUMILITY: KNOW WHO WE ARE
Never overestimate our abilities, but do not underestimate them either. Humility is not modesty, rather it involves knowing who you are and never pretending to be more. Avoid narcissism.
2/ Let's start with confusion. Finding information on this is very non-specific but I think this quote helps: High calcium levels can be a catalyst for neuronal demise, possibly due to glutaminergic excitotoxicity and dopaminergic and serotonergic dysfunction.
3/ But colleagues and learners know that I am most interested in the polyuria. I have taught that hypercalcemia can cause nephrogenic diabetes insipidus, but the mechanism was unclear. Let's review how ADH works and then look at an interesting study that suggests an answer.
1/ #UncleBob on treating metabolic acidosis. First, get this article:
Sabatini, S., Kurtzman, N. (2009). Bicarbonate Therapy in Severe Metabolic Acidosis JASN 20(4), 692-695. dx.doi.org/10.1681/asn.20…
2/ Here is the quick chalk talk.
For increased anion gap metabolic acidosis, treat the underlying cause. Do not give bicarbonate unless you have an extraordinarily low pH (debate whether this is < 7.2 or 7.1 or 7. And with DKA, NEVER.
3/ For normal gap metabolic acidosis ALWAYS give bicarbonate with a goal of ~ 22 for the bicarbonate.
How?
Estimate bicarbonate deficit = 22 - current bicarb
Multiply by bicarbonate space = TBW = 50% wt in kg (+/- 10%)
Deliver a succinct HPI - start with chief complaint - insert RELEVANT PMH as desired. Tell the story chronologically if possible. Include related review of systems, social history, health behavior history, medication list as pertinent.
3/ Stop after HPI and we will discuss the HPI. The goal of the discussion is to improve how each learner tells the story. The goal is complete, yet succinct. Don't give too much information. Avoid redundancy. We call this discussion IMMEDIATE FEEDBACK.