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Proposed COVID-19 Pathophysiology [Part 3 of (now) 4]:

Coagulopathy Strikes Back.

What happens when #COVID19 clashes with the world of hematology?

Buckle up again for a long one.

...let’s dive in like this macrophage (exploring all directions):
First, what do you think is the predominant mechanism by which thrombosis occurs in COVID-19?
Where does thrombosis typically first occur?
Read 38 tweets
Proposed COVID-19 Pathophysiology [Part 2 of 3]:

Enter the magnificent macrophage.

What do #COVID-19 and hemophagocytic lymphohistiocytosis (#HLH) potentially have in common?

...let’s continue our journey onward into the cytokine storm.
First, let’s briefly summarize what we covered before:

What mechanism may be partly responsible for heterogeneity of COVID-19 disease phenotype as well as its severity?
Correct! Antibody-dependent enhancement (ADE) is the result of producing sub-neutralizing antibodies which paradoxically enhance the rate of viral replication and severity of viremia.
Read 24 tweets
Proposed COVID-19 Pathophysiology [Part 1 of 3]

What do #COVID-19 and #Dengue fever potentially have in common?

The answers have significant potential clinical implications in COVID-19.

Buckle up. It's a long one.

Let’s take a hematological walk on the zoonotic side.
Dengue is a flavivirus that is called “breakbone fever”, a nod to bone-breaking pains that occur during the infection.

There are four serotypes of the dengue virus.

Infection with one serotype does not fully protect one from contracting a different serotype.
True or false: The second or later infection with dengue is often much more dangerous.
Read 26 tweets
A hematology @tony_breu-style tweetorial:

Why does lymphopenia occur in #COVID19?

A normal WBC count and lymphopenia are seen in patients affected by COVID-19, but why it occurs has bothered me since the pandemic onset.

The potential answer is surprising and interesting.
First, what do you think the mechanism is?
Does the degree of lymphopenia correlate with survival?
Read 26 tweets

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