Hemostasis | Easy Flowchart | Physiology
Hemostasis or haemostasis is a process to prevent and stop bleeding, meaning to keep blood within a damaged blood vessel (the opposite of hemostasis is hemorrhage). It is the first stage of wound healing. This involves coagulation, blood changing from a liquid to a gel. Intact blood vessels are central to moderating blood's tendency to form clots. The endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule and thrombomodulin and prevent platelet aggregation with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor, which initiate the maintenance of hemostasis after injury. Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) blood coagulation, or formation of a fibrin clot. These processes seal the hole until tissues are repaired.Hemostasis occurs when blood is present outside of the body or blood vessels. It is the innate response for the body to stop bleeding and loss of blood. During hemostasis three steps occur in a rapid sequence. Vascular spasm is the first response as the blood vessels constrict to allow less blood to be lost. In the second step, platelet plug formation, platelets stick together to form a temporary seal to cover the break in the vessel wall. The third and last step is called coagulation or blood clotting. Coagulation reinforces the platelet plug with fibrin threads that act as a "molecular glue".[3] Platelets are a large factor in the hemostatic process. They allow for the creation of the "platelet plug" that forms almost directly after a blood vessel has been ruptured. Within seconds of a blood vessel's epithelial wall being disrupted, platelets begin to adhere to the sub-endothelium surface. It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound. After several minutes the platelet plug is completely formed by fibrin.[4] Hemostasis is maintained in the body via three mechanisms:
Vascular spasm (Vasoconstriction) - Vasoconstriction is produced by vascular smooth muscle cells, and is the blood vessel's first response to injury. The smooth muscle cells are controlled by vascular endothelium, which releases intravascular signals to control the contracting properties. When a blood vessel is damaged, there is an immediate reflex, initiated by local sympathetic pain receptors, which helps promote vasoconstriction. The damaged vessels will constrict (vasoconstrict) which reduces the amount of blood flow through the area and limits the amount of blood loss. Collagen is exposed at the site of injury, the collagen promotes platelets to adhere to the injury site. Platelets release cytoplasmic granules which contain serotonin, ADP and thromboxane A2, all of which increase the effect of vasoconstriction. The spasm response becomes more effective as the amount of damage is increased. Vascular spasm is much more effective in smaller blood vessels.[5][6]
Platelet plug formation- Platelets adhere to damaged endothelium to form a platelet plug (primary hemostasis) and then degranulate. This process is regulated through thromboregulation. Plug formation is activated by a glycoprotein called Von Willebrand factor (vWF), which is found in plasma. Platelets play one of major roles in the hemostatic process. When platelets come across the injured endothelium cells, they change shape, release granules and ultimately become ‘sticky’. Platelets express certain receptors, some of which are used for the adhesion of platelets to collagen. When platelets are activated, they express glycoprotein receptors that interact with other platelets, producing aggregation and adhesion. Platelets release cytoplasmic granules such as adenosine diphosphate (ADP), serotonin and thromboxane A2. Adenosine diphosphate (ADP) attracts more platelets to the affected area, serotonin is a vasoconstrictor and thromboxane A2 assists in platelet aggregation, vasoconstriction and degranulation. As more chemicals are released more platelets stick and release their chemicals; creating a platelet plug and continuing the process
Clot formation - Once the platelet plug has been formed by the platelets, the clotting factors (a dozen proteins that travel along the blood plasma in an inactive state) are activated in a sequence of events known as 'coagulation cascade' which leads to the formation of Fibrin from inactive fibrinogen plasma protein.step for wound healing, it has the ability to cause severe health problems if the thrombus becomes detached from the vessel wall and travels through the circulatory system; If it reaches the brain, heart or lungs it could lead to stroke, heart attack, or pulmonary embolism respectively. However, without this process the healing of a wound would not be possible.
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Thank you. You have explained the concept of hemostasis clearly.
Thank you,I am very happy for your easy and simple method of explanation ❤️❤️
Thank you so much, very helpful!!
Most crisped and concised one ..thank you mam
@Dr.KareemaTabassum
2 жыл бұрын
You're welcome, keep watching,❤️
Ahh! What a wonderful expalanation! Really helpful and you saved me a lot of time.
@musicbyej
Жыл бұрын
Seri sootha moodu
@makendratherealityseeker6430
Жыл бұрын
@@musicbyej Nee moodu
@user-cs8zl6mh6n
2 ай бұрын
Please provide pdf notes of this flow charta
Thank u mam good teaching method God bless u
You are amazing genius lady
Wow!! What an easy explanation 👏👏
@Dr.KareemaTabassum
2 жыл бұрын
Thank you, keep watching ❤️
Haha what a coincidence im in class and my teacher is also teaching hemostasis
Please update more and more videos ...thank you 🤗
Sembulingam 🔥🔥🔥
Nicely explained. Thank you🙏 madam
Mem your explain is next level
My question is: Is vasoconstriction part of platelet activation? I've read in many articles that it's not part of platelet activation, but precedes it.
Hats off👍👍🙏
amazing explanation
Nice 🙂 easily explained
Amazing.
Its very hard to understand the concept.now i got concept from ur lecture .thankyou so much
@Dr.KareemaTabassum
3 жыл бұрын
You're welcome 😊
Thank you so much...
Mashallah nice method of teaching
@Dr.KareemaTabassum
3 жыл бұрын
Jazakallah 😊
is this the flowchart of primary and secondary hemostatis?
Thank you ma'am this video is very helpful 🙂🥰🙂
@Dr.KareemaTabassum
2 жыл бұрын
You're welcome, keep watching ❤️
Hi! Does serotonin cause increased vascualar permeability due to vasoconstriction? If yes, how exactly? Thanks in advance.
@Dr.KareemaTabassum
3 жыл бұрын
Serotonin is an important inflammation mediator and exerts its effects by initiating vasodilation as well as increasing vascular permeability. Molecular regulators of vascular permeability include growth factors and inflammatory cytokines,that is where the serotonin is included. As serotonin is an inflammatory mediator,Acute inflammation can be characterized by vasodilatation, the exudation of protein-rich fluid (plasma), increase of vascular permeability, and cell migration (primarily neutrophil) into the site of inflammation. So, Serotonin is an important inflammation mediator and exerts its effects by initiating vasodilation as well as increasing vascular permeability . Serotonin possesses both vasoconstrictor and vasodilator properties. The constrictor action of the monoamine can be due to: (a) direct activation of vascular smooth muscle; in most blood vessels, this is mediated by S2-serotonergic receptors. (b) augmentation (amplification) of the action of other endogenous vasoconstrictors such as catecholamines, angiotensin II and the prostanoids. (c) release of norepinephrine from adrenergic nerves. Thank you.
@alinzavada8566
3 жыл бұрын
@@Dr.KareemaTabassum This was so helpful. Keep up the good work! You literally rock!!
@Dr.KareemaTabassum
3 жыл бұрын
Thank you, ☺️
clear explanation mam ....thank you🤗
@Dr.KareemaTabassum
3 жыл бұрын
Glad you liked it,thank you ❤😊
Thank you🙏 ma'am...
Thank you so much Mam❤️
you are the best!!!!
@Dr.KareemaTabassum
8 ай бұрын
Thank you❤, keep watching.
Very nice
Crystal clear explanation mam 👌👌👌👌..plz make video on regulation of respiration mam
@Dr.KareemaTabassum
3 жыл бұрын
Thank you, sure 😊
Thank u so much mam.helped a lot.plz do make more videos,😇😇
@Dr.KareemaTabassum
2 жыл бұрын
You're welcome ❤️
It is very helpful for me akka...
@Dr.KareemaTabassum
2 жыл бұрын
Glad it was helpful, keep watching ❤️
❤
Mam i need any diagrammatic representation for it.
Nice video
Thank u sis😊
Way of explaination is quite good. ...👍 And video editing is nice... Saving our time👌
@fayeramorketa3508
Жыл бұрын
Thank you 💕💕
Well explained mam❤️
@Dr.KareemaTabassum
2 жыл бұрын
Thank you❤️
Mam can you plzz tell what pens do u use with brand name ?😅
😍👌
Hemostasis and stages of hemostasis flow chart explained
Medam mechamisam of hemostasis tell me
Kindly mam make vedios on circulation topics
@Dr.KareemaTabassum
3 жыл бұрын
Okey sure 😊
Mam can you please disclose the physiology textbook from which you got these points?
@Dr.KareemaTabassum
Жыл бұрын
Hello, its from shembulingam textbook
@varshajprakash
Жыл бұрын
@@Dr.KareemaTabassum thank you mam
Thank you ma'am, please make much more videos
@Dr.KareemaTabassum
3 жыл бұрын
You're welcome 😊, sure
Mam please share full screenshot.
Thank you mam... Good explanation 😘😘😘
@Dr.KareemaTabassum
3 жыл бұрын
You're welcome 😊
@ayshafathi7687
3 жыл бұрын
@@Dr.KareemaTabassum mam please make more videos
@ayshafathi7687
3 жыл бұрын
@@Dr.KareemaTabassum normal Spirogram, erythropoiesis, regulation of stroke volume
Mam iska mechanism bhi bta do
Mam pdf kaise milega
Helpful video. But due to many, many cuts it looks glitched.
@Dr.KareemaTabassum
3 жыл бұрын
Thank you, will be looking at it!.😊
Sambu ka same bol rahe ho
You are amazing genius lady
@Dr.KareemaTabassum
2 жыл бұрын
thank you , keep watching😊
Nice video
@Dr.KareemaTabassum
3 жыл бұрын
Thanks 😊