Definitions & Key takeaways

Vitamin K plays a crucial role in blood coagulation, which is the process by which the body forms clots to stop bleeding. Vitamin K acts as a cofactor for a group of proteins known as the vitamin K-dependent clotting factors (II, VII, IX, and X ), which are involved in the activation of blood-clotting proteins. To be useful, vitamin K undergoes a series of oxidation and reduction reactions called the vitamin K cycle.

Vitamin K deficiency can result in impaired blood clotting, leading to spontaneous bleeding or excessive bleeding from cuts or injuries. Newborn infants are at particular risk because they have limited stores of vitamin K, and are often not able to produce enough of the vitamin on their own. This is why they are typically given a single injection of vitamin K shortly after birth.

Chapters:

Introduction0:00–0:35

Vitamin K helps to regulate the process of blood coagulation by assisting in the conversion of certain coagulation factors into their mature forms.
Without Vitamin K our bodies would be unable to control clot formation. Imagine being unable to form blood clots effectively.
That would mean we would lose all of our blood volume from something as simple as a pinprick. Oh To prevent this extreme scenario, Vitamin K must be ingested metabolized and utilized to create mature coagulation factors.
Now, to understand the regulation of clot formation, we first need to talk briefly about hemostasis in which hemo refers to the blood and stasis means to halt or stop hemostasis is divided into two phases.

Hemostasis0:35–1:20

Primary and secondary hemostasis. Primary hemostasis involves the formation of a platelet plug around the site of an injured blood vessel and secondary hemostasis reinforces that platelet plug with the creation of a protein mesh called fibrin.
To get to fibrin. A set of coagulation factors.
Each of which are enzymes need to be activated. These enzymes are activated via a process called proteolysis, which is where a portion of the protein is clipped off.
In total. There are 12 coagulation factors.

Coagulation factors1:20–1:42

Numbered factors. One through 13, there is no factor six.
Most of these factors are produced by liver cells and it turns out that producing coagulation factors. 279 and 10 requires an enzyme that uses Vitamin K Vitamin K is found in abundance in green leafy foods.

Vitamin K1:42–3:43

Things like spinach, kale and chard. It's a fat soluble vitamin along with vitamins ad and e meaning that it can be stored in fat cells instead of being excreted by the kidneys.
Vitamin K is also synthesized by bacteria in our gastrointestinal tract as a byproduct of their metabolism, which further contributes to overall intake.
Now, when Vitamin K is mobilized from fat cells or the digestive tract to the liver, it's in its dietary form and it's called Vitamin K quinone.
An enzyme called quinone reductase takes electrons from NADPH and donates them to Vitamin K quinone, converting it into the reduced form, which is called Vitamin K hydroquinone.
Then Vitamin K hydroquinone acts as a cofactor by donating its electrons to an enzyme called gamma glutamyl carboxylase which converts the nonfunctional forms of coagulation factors 279 and 10 into their functional forms.
Gamma glutamyl carboxylase adds a carboxyl group. A chemical group made up of one carbon, two hydrogens and one oxygen onto the end of glutamic acid residues on the protein.
After the carboxylation step, Vitamin K is in an oxidized form where it can accept electrons and it's called Vitamin K epoxide.
Vitamin K epoxide gets converted back into Vitamin K quinone by another enzyme called epoxide reductase, which donates electrons to Vitamin K epoxide.
Using a thiol group. In this fashion, a single molecule of Vitamin K can be reused many times as it turns out the drug warfarin, which was first used as a rat poison blocks the function of this enzyme which blocks Vitamin K from getting recycled.
And as a result factors 279 and 10, don't get activated. Now, let's take a closer look at the coagulation cascade to see where these coagulation factors play their respective roles.

Coagulation cascade3:43–3:58

The coagulation cascade begins via two pathways. The extrinsic and intrinsic pathways.
The intrinsic pathway starts when circulating factor 12 comes into contact with the surface of activated platelets or collagen activated factor 12 then activates factor 11, which activates factor nine, which activates factor 10.

Intrinsic pathway3:58–4:47

Factor 10 starts the common pathway where it activates factor two, which activates factor one that builds the fibrin mesh.
When factor two gets activated, it also activates four other factors 589 and 13. Factor five gets activated and acts as a cofactor for 10.
Factor eight acts as a cofactor for factor nine. And factor 13 helps factor one or fibrin form crosslinks in the extrinsic pathway.

Extrinsic pathway4:47–5:21

Exposed tissue factor activates factor seven which activates factor 10 and starts the common pathway. So without Vitamin K the loss of factor seven means that the extrinsic pathway won't function.
And without factor nine, the intrinsic pathway won't function. And without factor 10 and two, the common pathway won't function since these factors are utilized in all three pathways.
It's easy to see how clot formation does not function properly unless our body properly utilizes Vitamin K All right is a quick recap.

Review5:21–5:51

Vitamin K plays an essential role in clot formation because it's used in synthesis of clotting factors. 279 and 10.
In order to be useful, Vitamin K undergoes a series of oxidation and reduction reactions called the Vitamin K cycle. An important enemy of this system is the drug warfarin which inhibits epoxide reductase to prevent maturation of these factors.