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Basic Hemostasis

Hemostasis is the process by which bleeding is stopped. It involves vascular constriction, platelet plug formation, and fibrin clot formation through the coagulation cascade. Hypocoagulation is a condition where blood does not clot normally, increasing risk of hemorrhage. It can be caused by low platelets, genetic disorders, diseases, or medications. Hypercoagulation is an excessive clotting tendency that increases risk of thrombosis. It can be inherited or acquired through factors like cancer, medications, pregnancy, or smoking. The vascular system includes arteries and veins. Arteries have thicker walls to handle high blood pressure from the heart. Veins have thinner walls and return blood to the heart at lower

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47 views

Basic Hemostasis

Hemostasis is the process by which bleeding is stopped. It involves vascular constriction, platelet plug formation, and fibrin clot formation through the coagulation cascade. Hypocoagulation is a condition where blood does not clot normally, increasing risk of hemorrhage. It can be caused by low platelets, genetic disorders, diseases, or medications. Hypercoagulation is an excessive clotting tendency that increases risk of thrombosis. It can be inherited or acquired through factors like cancer, medications, pregnancy, or smoking. The vascular system includes arteries and veins. Arteries have thicker walls to handle high blood pressure from the heart. Veins have thinner walls and return blood to the heart at lower

Uploaded by

Marvin Simbulan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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CENTRAL LUZON DOCTORS’ HOSPITAL EDUCATIONAL INSTITUTION

Romulo Hi-way, San Pablo, Tarlac City, Tarlac, Philippines

MEDICAL TECHNOLOGY DEPARTMENT

MODULE IN
HEMATOLOGY
2

--BASIC HEMOSTASIS--

Prepared by: Alton Joshua S. Masanque, RMT, DTA


HEMOSTASIS

Hemostasis is a complex physiologic process that keeps circulating blood in a fluid state
and then, when an injury occurs, produces a clot to stop the bleeding, confines the clot to the site
of injury, and finally dissolves the clot as the wound heals. When hemostasis systems are out of
balance, hemorrhage (bleeding) or thrombosis (pathological clotting) can be life-threatening.
The absence of a single plasma procoagulant may destine the individual to lifelong anatomic
hemorrhage, chronic inflammation, and transfusion dependence. Conversely, absence of a
control protein allows coagulation to proceed unchecked and results in thrombosis, stroke,
pulmonary embolism, deep vein thrombosis, and cardiovascular events.

Hemostasis is coagulation that occurs in a physiological (as opposed to pathological)


setting and results in sealing a break in the vasculature. This process has a number of
components, including adhesion and activation of platelets coupled with ordered reactions of the
protein coagulation factors.

Hemostasis, the arresting of bleeding, depends on several components. The four major
components are the vascular system, platelets (thrombocytes), blood coagulation factors, and
fibrinolysis and ultimate tissue repair. Three other less important components are the
complement and kinin systems as well as serine protease inhibitors. Functionally, several
processes are involved in hemostasis following injury to a small blood vessel:

➢ Blood vessel spasm/constriction


➢ Formation of a platelet plug
➢ Contact among damaged blood vessel, blood platelet, and coagulation proteins
➢ Development of a blood clot around the injury
➢ Fibrinolytic removal of excess hemostatic material to reestablish vascular
integrity

Primary hemostasis refers to the role of blood vessels and platelets in response to a
vascular injury, or to the commonplace desquamation of dying or damaged endothelial cells.
Blood vessels contract to seal the wound or reduce the blood flow (vasoconstriction). Platelets
become activated, adhere to the site of injury, secrete the contents of their granules, and
aggregate with other platelets to form a platelet plug. Vasoconstriction and platelet plug
formation comprise the initial, rapid, short-lived response to vessel damage, but to control major
bleeding in the long term, the plug must be reinforced by fibrin. Defects in primary hemostasis
such as collagen abnormalities, thrombocytopenia, qualitative platelet disorders, or von
Willebrand disease can cause debilitating, sometimes fatal, chronic hemorrhage.

Secondary hemostasis is defined as the formation of insoluble, cross-linked fibrin by


activated coagulation factors, specifically thrombin. Fibrin stabilizes the primary platelet plug,
particularly in larger blood vessels where the platelet plug is insufficient alone to stop
hemorrhage.
Coagulation is the process that leads to fibrin formation; this process involves controlled
interactions between protein coagulation factors.

HYPOCOAGULATION

Hypocoagulation is the condition that occurs when the blood doesn't clot normally. If left
untreated, the disorder may lead to hemorrhage, bleeding on the brain or gastrointestinal
bleeding. Conditions that may prevent blood from clotting normally are:

➢ Thrombocytopenia, or low platelet count


➢ Genetic diseases like hemophilia or von Willebrand disease
➢ Blood, bone marrow or liver disease
➢ Certain medications, like blood thinners
➢ Vitamin K deficiency

HYPERCOAGULATION

Hypercoagulation is a condition that causes your blood to clot more easily than normal.
Hypercoagulation can be an acquired or inherited condition. Acquired hypercoagulation is
caused by a disease or other condition. Examples include obesity, pregnancy, use of birth control
pills, or cancer. Inherited coagulation is caused by genes that have been passed to you from a
parent. These genes cause problems with how your blood clots.

➢ Hereditary predisposition
➢ Certain medications, such as birth control pills
➢ Certain cancers, like pancreatic, prostate, or breast
➢ Pregnancy
➢ Smoking

VASCULAR SYSTEM

ARTERIES AND VEINS

Arteries are the distributing vessels that leave the heart, and veins are the collecting
vessels that return to the heart. Arteries have the thickest walls of the vascular system. Although
variations in the size and type of vessel exist, the tissue in a vessel wall is divided into three coats
or tunics. These coats are the tunica intima, tunica media, and tunica adventitia. The tunica
intima forms the smooth glistening surface of endothelium that lines the lumen (inner tubular
cavity) of all blood and lymphatic vessels and the heart. The simple squamous epithelium that
lines these vessels is referred to as endothelium. The tunica intima consists of a single layer of
endothelial cells thickened by a subendothelial connective tissue layer containing elastic fibers.
The tunica media, the thickest coat, is composed of smooth muscle and elastic fibers. The tunica
adventitia consists of fibrous connective tissue that contains autonomic nerve endings and the
vasa vasorum, small networks of blood vessels that supply nutrients to the tissues of the wall.

Veins are larger and have a


more irregular lumen than arteries.
In comparison with arteries, veins
are relatively thin-walled with a
weaker middle coat. Elastin fibers
are usually found only in larger
veins, and there are fewer nerves
distributed to the veins than to the
arteries.

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