1/ #UncleBob started medical school 50 years ago. Medicine is always progressing. Here are some things we did not have:

Diseases: HIV, Lyme, Takasabu, MRSA

infectious disease Medications: Only 1st generation cephalosporins, no fluoroquinolones, a variety of MRSA drugs, etc.
2/Treatment for HFrEF - first study of decreasing mortality in the 80s, no ACE-I, ARB, beta-blockers, neprolysin inhibitors, Calcium channel blockers

No interventional cardiology - CABG or nothing

M-mode Echo was in its infancy - no 2D echo

No nuclear medicine stress testing
3/ No home oxygen, no home IV infusions

No CT scanning, very little ultrasound (clearly in its infancy), no MRI, no PET

Limited endoscopy and colonoscopy

No "scopic" surgeries - think laparoscopic, arthroscopic, etc

I cannot even describe cancer chemotherapy
4/ Now the good stuff

No P4P, no RVUs, no guidelines (expert opinions only)
No computerized medical records - we actually wrote our notes
5/ No work hour restrictions
Only 10% of our class were women
6/ Medicine is always progressing. Once you reach 20 years, start looking back with amazement at both progress and things you consider worse. The scientific advances continue to amaze me. The administrative requirements and intrusions continue to aggravate me.

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More from @medrants

27 Sep
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.
Read 6 tweets
31 May
#UncleBob - eGFR Tweetorial

eGFR - estimated GFR
mGFR - measured GFR

@UnremarkableLab
1/ So what is GFR? Glomerular Filtration Rate - how much blood do the kidneys filter per minute

Perfect mGFR -> stable measurable molecule that is perfectly filtered and neither reabsorbed nor secreted
2/ mGFR continued

Measure the plasma value of the molecule and measure the quantity in urine over a specific number of minutes.

Clearance formula - (Um*V/time)/Pm

Since Um is cc and V/time (# of minutes)
The result is cc/ min.
Read 21 tweets
28 Feb
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.
Read 6 tweets
27 Feb
#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# . ,.,. .
#UncleBob is a huge @uva basketball fan. Our coach, Tony Bennett learned this 5 pillars from his dad (also a great coach). I believe they will resonate with great educators
@UABGIM @CPSolvers @gradydoctor @DxRxEdu @rabihmgeha @andrewolsonmd @LisaWillett13 #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.
Read 8 tweets
15 Dec 20
1/ The classic presentation at morning report for hypercalcemia starts with polyuria, constipation and confusion. #UncleBob wanted to understand why - stimulated by @CuriousClinPod ? @HannahRAbrams @tony_breu @AvrahamCooperMD
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.
Read 11 tweets
25 Nov 20
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…

@UnremarkableLab @kidney_boy @hswapnil @CPSolvers
@uabimres @UAB_NRTC
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%)
Read 9 tweets

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