1/11 I like this flowchart, but my brain starts to melt. If yours does to, follow along and we'll take it from the top! This is my first #tweetorial on hypercortisolism!
2/11 Let's start with a question. Which of the following are TRUE?
a. Cushing disease = hypercortisolism
b. Cushing disease is a type of Cushing syndrome
c. Cushing syndrome is a type of Cushing disease
3/11 a. and b. are correct! Here are some physical exam features of hypercortisolism.
4/11 Once we suspect hypercortisolism, the next step is to:
5/11 Take that history! Our goal is to figure out if the patient is taking any steroids (inhaled, oral, topical, injectable). If they are, this is EXOGENOUS hypercortisolism.
6/11 If you are concerned about ENDOGENOUS hypercortisolism, we have to start looking at tests, but before that, let's start getting our paradigm straightened out.
7/11 Before we continue, we have to look at the HPA axis. Here is one of the clearest versions that I can find:
8/11 Let's go back to ENDOGENOUS hypercortisolism. We have two think of two types. 1. ACTH-dependent 2. ACTH-independent
9/11 In ACTH-dependent hypercortisolism:
Something is ⬆️ circulating ACTH, leading to ⬆️ serum cortisol (go look at the HPA axis in tweet 7!)
10/11 In ACTH-independent hypercortisolism
Something is ⬆️ circulating cortisol, leading to ⬇️ ACTH levels (go look at the HPA axis in tweet 7!)
Note: EXOGENOUS hypercortisolism is also ACTH-independent
11/11 If we combine all of this, we get this paradigm for hypercortisolism. There is nuance with this, and we will get there in a stepwise fashion. As always, feedback is welcome!
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The primary focus of this thread is going to be on the history (a heads up - the flowchart at the end will go a little bit out of order)!
3/18 When taking a chest pain history, we ask lots of questions about associated symptoms and alleviating/aggravating factors, mostly because we were taught to obtain and report this history. But is there a more focused way to approach this?
Note: the original post was deleted due to a mathematical error
2/5 While the CHADSVASc is helpful for annual estimation of ischemic stroke risk (and other events), what is the risk of DAILY risk? Turns out we can do some math to derive it from the annual risk estimation!
3/5 The math here doesn't EXACTLY reflect the daily risk of for patients because there are countless variables that we cannot control. @JessieCurrier17 describes the rationale using probability quite nicely.
1/7 Considering how to manage community-acquired pneumonia (CAP)? Is it CURB-65 or should it be CARB-65? No idea what I am talking about? Let's talk about azotemia and uremia!
2/7 The CURB-65 score has been used for diagnosis and treatment of adults with community-acquired pneumonia (CAP). The most recent IDSA CAP guidelines in 2019 (pubmed.ncbi.nlm.nih.gov/31573350/) referenced the 2007 IDSA CAP criteria for defining severity
3/7 The original article that describes validation of the CURB scoring system (ncbi.nlm.nih.gov/pmc/articles/P…) does NOT use the word "uremia," but instead references an serum urea level cutoff.
2/9 The cornerstone of treatment is to treat the underlying cause. Everything else is just a 🩹. It can sometimes be very hard to treat the underlying cause immediately (assuming you can identify it).
3/9 Free water restriction is going to help (to a certain degree), but make sure that it’s feasible for the patient (they often need to do this beyond hospitalization). Consider restricting 500 cc below their 24-hour urine output:
2/8
💥Fludrocortisone will increase ⬆️ RAAS and can cause volume overload, so you should avoid it here
💥 Caffeine and ibuprofen are last-line agents to manage orthostatic hypotension
💥 Midodrine is probably your best bet here
3/8 You prescribe midodrine 2.5 mg PO q8h and end up titrating it up to 5 mg PO q8h over the course of a few weeks. The patient shows you their BP log and you notice that their nighttime supine BPs are elevated. What do you do next?
1/5 A 78 yo F with no prior medical history p/w progressive pill-rolling tremor, shuffling gait, and dizziness upon standing. She takes no meds. Orthostatics are ➕. What is the likely cause of her orthostatic hypotension? #MedTwitter#MedEd#FOAMEd#GeriTwitter#NeuroTwitter
2/5 The answer is Parkinsonism! Parkinsonism is a synucleinopathy (the protein alpha-synuclein accumulates in neurons and glia) leading to autonomic dysfunction. Review this approach on orthostatic hypotension here:
3/5 She is diagnosed with Parkinsonism, and started on carbidopa-levodopa BID with improvement in symptoms. Her family has hired 24/7 caregivers who ensure her PO intake is adequate.