As someone who has been treating COVID patients since early April, my working theory has been that many if not most of the secondary disease processes (non-respiratory effects of the virus), and even to some extent the worsening of respiratory function, have been largely driven by micro-thrombotic disease. Delicate capillary beds, like the ones seen in the lungs and kidneys, are highly susceptible to becoming blocked in this sort of setting. When these small vessels get plugged up, end-organ dysfunction necessarily follows. The kidney won't work properly if the blood needing filtration can't reach the nephron (functional unit of the kidney).
I'm in large part guessing here based on clinical observation, but my feeling is that you can extend this logic to other syndromes that accompany COVID-19. For example, we often see worsening liver function in the setting of this illness (albeit delayed by a few days). This could be explained in a number of ways, one of which is by impaired perfusion within capillary beds in the liver. Further, there is a myocarditis-like picture we sometimes see as well that could be explained by direct viral infection or again by impaired perfusion of the cardiac muscle by small vessel clotting.
When the thrombotic disease progresses, you start to see a more macro version: think strokes and pulmonary emboli in patients who are otherwise low risk at baseline. Thus, there's some interpolation going on here.
Hey, it's great to see something from a professional !!!
A dear friend is dying of pancreatic cancer. And one of the key reasons that she's still alive was getting thrombosis under control. Initially with IV heparin, and now with Lovenox.
Are those commonly used for COVID patients? Or do they use oral anticoagulants?
I'm sorry to hear about your friend. Unfortunately, cancer is one of the big predisposing factors for thromboembolic disease, so I'm glad to hear that controlling this issue has helped her along.
Based on our institutional protocol, hospitalized COVID-19 patients receive therapeutic dose Lovenox, Eliquis, or IV heparin.[1] Lovenox is the first line treatment, but is contraindicated in patients with, among others things, severely impaired renal function. If these patients are able to tolerate oral medications, they can be given Eliquis. If not, they’re typically put on IV heparin drips (and are subject to the uncomfortable and burdensome blood draws that come with them).
Typically, all of these patients are discharged on two weeks of Eliquis if there are no major contraindications. The thinking is that the risk of damage to the body by microthrombi doesn’t necessarily end just because the patient is stable enough to go home.
Of course, with all of these medications, preventing clotting has to be balanced with preventing bleeding. We’ve had to stay vigilant for things like GI bleeds and hemorrhagic strokes, as these things become more common when everyone in the hospital is being heavily anticoagulated.
[1] Therapeutic dosing in this case is higher than typical prophylactic dosing. In the case of Lovenox, it would be something like 40 mg twice a day for the therapeutic dose versus 40 mg once a day for the prophylactic dose, which is what would be used in non-COVID-19 patients to prevent thromboembolism.
You fail to appreciate that there is quite a bit of skills development and problem solving training. The first two years are more memorization heavy, as you have to learn the language and basics. Years 3 and 4 are more focused on navigating the health care system, interacting with patients, performing technical skills, physical examination, use of imaging, diagnosis, etc. Memorization is only a fraction of what you do to become a competent physician.
First two years of medical school are in classroom, second two years are clinical rotations.
Residency is after medical school, and that's the first time you start earning a meager paycheck. In medical school, even when you're "working" with patients, you still pay tuition.
Or the opposite. The ramp-up period (4-8 weeks before the brain rebalances its chemistry in response to the drug) is hell, and cessation of the drug (or running out without access to a pharmacy) causes near-total loss of cognitive ability for a few days (with brain zaps to boot).
That's why I'm not using my bupropion. I got a prescription last month to treat seasonal affective disorder, and my psychiatrist wants me to use it every winter then cycle off in the spring, but the side effects both coming on and off seem awful.
My wife is a psychiatrist and sees a psychiatrist off the record because she’s afraid of the stigma affecting her career. It’s just one data point but I find it telling that a psychiatrist is afraid that other psychiatrists will know she takes med to treat a psychiatric condition. Hers is anxiety related.
In my view it's pretty widespread that people are hesitant to seek certain kinds of care because of the potential effect of a "pre existing condition" on their employability.
Exactly. I don't think it's because the medical board itself would stop them, but more because the stigma attached to it would lead to people questioning them and their ability to do their job, not to mention the issues with insurance. I'd say that likely has a lot more to do with doctors wanting to see others off-the-record... I know of some teachers who do the same thing with psychiatrists, because they don't want it getting out to the students' parents.
The issue for me is the "average commute to work". I need to be on the 6 (or 4/5). Anywhere outside of Manhattan makes my commute ~1 hour instead of ~35 min. I don't currently live in the EV, but I'd entertain doing so if I could get a bit more for the money.
Crown Heights close to Nostrand to Grand Central should take you 30-45min, and you can have a semi-luxury building or renovated apartment for the same price as the author of the article posted. There are other similar neighborhoods in BK. UES or East Harlem could work too.
If you don't mind a bit of grungy asthetics, the areas near the JMZ trains just on the other side of Manhattan in Williamsburg and the Bed Stuy/Bushwick border have a relatively fast commute - much faster than far more expensive neighborhoods in Brooklyn.
For example, it's like 10m from Marcy Ave to Essex St. in the LES. The J goes downtown in the Wall St. area while the M takes much of the same path as the F along 6th Ave, and both of those trains follow the same lines up until Myrtle-Broadway. In fact, it's literally two stops from Essex St. during rush hour as the J runs express (sometimes it sees itself as a Z).
I live in Brooklyn, east of Prospect Park, and am on the 5. I can also take the Q/B which are express to Manhattan and switch to the 6 or 5 at 14th. My commute is to Midtown, and it takes about 35 minutes.
For many years, I lived in Westchester, took metro-north to grand central (30 minutes on an express train), then the 4/5/6 to work (10 minutes. 15 when things were slow).
I looked at this before leaving NYC and the problem is that once you add the time to get to the metro-north station, time to switch from metro north to subway, time from subway to office, and time waiting for trains, elevators, etc, you can easily have a 75-90 minute commute. And that's when things go right on two different transit systems, which seems far too rare these days.
Lately, Grand Central Station has become an overcrowded tourist nightmare where you have to do breathing exercises to stay calm getting from the station to the subway.
I cannot believe they put an Apple store in there. It should be a crime to choose profits over efficiency.
It's worth noting that temperature control is only half the equation. In places like Houston, A/C plays a big part in controlling indoor humidity as well(for both comfort purposes and to prevent mildew from growing all over everything).
There's other (read: more efficient) ways to control humidity than using an A/C. Including making buildings more "airtight" so the dampness doesn't leak into the house (as long as you don't open doors/windows too much, of couse).
I'm in large part guessing here based on clinical observation, but my feeling is that you can extend this logic to other syndromes that accompany COVID-19. For example, we often see worsening liver function in the setting of this illness (albeit delayed by a few days). This could be explained in a number of ways, one of which is by impaired perfusion within capillary beds in the liver. Further, there is a myocarditis-like picture we sometimes see as well that could be explained by direct viral infection or again by impaired perfusion of the cardiac muscle by small vessel clotting.
When the thrombotic disease progresses, you start to see a more macro version: think strokes and pulmonary emboli in patients who are otherwise low risk at baseline. Thus, there's some interpolation going on here.
Hope that makes some sense.