Transcription
Hey guys, let's resume our discussion on bleeding and coagulation disorders. In the previous video, we have talked about bradykinin. Today, I have a great mnemonic about bradykinin: the son of its mother, the high-molecular-weight kininogen, and this great midwife, plasma kallikrein, which brought him to the world. This could happen when you have lots of bradykinin floating in the plasma. This is called angioedema, swelling of structures in your face and neck, and it could be an emergency. Why? Because your airways are in the neck.
With that being said, now let's get started. [Music] As you know, bradykinin comes from the high-molecular-weight kininogen. High-molecular-weight kininogen activates factor XII and factor XI of the intrinsic coagulation pathway. Kallikrein also activates factor XII, which returns the favor by activating prekallikrein into kallikrein. Kallikrein also activates or releases bradykinin from the tyranny of the high-molecular-weight kininogen. What does bradykinin do? Contract the smooth muscles, the nonvascular smooth muscles to be specific. Increased vessel permeability can lead to angioedema, increased pain—the chronic pain due to chronic inflammation—increased neurasthenia, and vasodilation. Both lead to hypotension. But where's the mnemonic? Wait, honey, good things happen to those who wait. Kallikrein-kallikrein system. If you're in the plasma, kallikrein; the tissue can end up with bradykinin. Either way, yes. You can get all of my hematology cases by going to Patreon. Don't miss on these vignettes because they are just awesome.
Kallikrein helps bring bradykinin into existence. ACE hates kallikrein and its guts. When you are using ACE inhibitors, you are inhibiting ACE and increasing bradykinin, leading to a dry cough, leading to angioedema, hypotension due to vasodilation, by inhibiting the formation of angiotensin II. Also, you have hypotension, you have renal impairment, low sodium, high potassium, hyperkalemia, and acidosis. All of these are side effects of the ACE inhibitors, such as enalapril. Here are again the side effects of ACE inhibitors; they are highlighted here: dry cough, angioedema, hypotension, renal impairment, and acidosis, hyperkalemia, and also add nausea, vomiting, diarrhea. Because what the eff? Here is the renin-angiotensin-aldosterone system. Renin converts angiotensinogen to angiotensin I. ACE converts angiotensin I to angiotensin II. It is attached to the receptor, having two main functions: vasoconstriction of arterioles, aldosterone release. Here is kind of a visual mnemonic or a visual illustration for you: bronchoconstriction, dry cough, increased vessel permeability leading to angioedema, naturally leading to hypotension, visualization into hypotension, pain, especially that chronic pain, and here you have angioedema, which is an emergency. Don't ever forget that.
Let me ask you a question: If you have a kid who has hereditary angioedema, should you give him ACE inhibitors? Never. You'll be an idiot if you do this. ACE inhibitors are contraindicated for patients with hereditary angioedema. Why? Because ACE inhibitors will increase bradykinin, leading to angioedema. That's why. Bradykinin receptors. Bradykinin has two receptors: We have B1 and guess what, B2. The creativity of these scientists is breathtaking. B1 receptor is responsible for pain, acute or chronic, chronic pain due to chronic inflammation. B2 receptor has two functions: vasodilation and increased vessel permeability, which will lead to two things: pus producing and unfitting edema as well as angioedema. So, in brief, B1 has one function, which is pain. B2 has two functions: vasodilation and increased permeability, both of which are related to inflammation. And here is the great bradykinin mnemonic of all time: Bradykinin comes from prekallikrein being converted into, guess what, plasma kallikrein. Now this issue, the plasma kallikrein, and it produces pain through the B1 receptor, as you know, and this pain is not acute; it's chronic, it's perpetual. Bradykinin is pro-inflammation big time. It increases vessel permeability into pus and angioedema, which is perilous, which means high risk. Thank God for the internet. Angioedema is perilous for your upper airway; it can kill you by hypoxia. Bradykinin will lead to bronchoconstriction, big vessel, which means vasodilation. Bradykinin will lead to hyponatremia and hypotension. This mnemonic is just amazing.
Thank you for watching. Subscribe me on Facebook and Instagram. Get all of my notes and the 50 hematology cases by going to patreon.com/medicosays. Thank you guys for watching. Be safe, stay happy, enjoy the moment. Let me know your opinion in a comment. I'll see you soon.