hemostasis Flashcards
what is homeostasis
stopping bleeding - homeostasis is the process that stops bleeding when blood vessel walls are damaged
maintaining circulatory integrity - haemostats ensures the integrity of the circulatory system by preventing excessive blood loss
complex series of events - haemostats involves a complex series that lead to the formation of a stable blood clot
blood clot formation - the process of blood clot formation is a crucial part of haemostats, which stops bleeding and maintains the integrity of the circulatory system
steps involved in hemostasis
vessel constriction
platelet plug formation
coagulation cascade
fibrin clot formation
vessel constriction
The first step in haemostasis is vessel constriction, where the blood vessels immediately constrict or narrow in response to injury. This helps to reduce blood flow and slow the bleeding
platelet plug formation
Next, platelets begin to adhere to the site of injury and aggregate to form a temporary platelet plug. The platelets release chemical signals that activate the coagulation cascade.
coagulation cascade
The coagulation cascade is a series of enzymatic reactions that lead to the formation of fibrin, a insoluble protein that forms a mesh-like clot to stabilize the platelet plug.
fibrin clot formation
The final step is the formation of a stable fibrin clot. The fibrin strands crosslink and trap red blood cells, forming a solid clot that seals the wound and prevents further bleeding.
vascular constriction
vascular injury
vasospasm
sustained vasoconstriction
vascular injury
when the blood vessel in injured, the smooth muscle in the vessel walls is stimulated to constrict
vasospasm
the initial reflex contraction occurs, narrowing the blood vessel to reduce blood flow and limit blood loss
sustained vasoconstriction
The combination of vascular spasm and the release of chemical signals continues to maintain vessel constriction until a stable clot is formed.
platelet plug formation
injury to blood vessel
platelet adhesion
platelet aggregation
platelet activation
platelet plug formation
injury to the blood vessel
When a blood vessel is injured, the endothelial cells lining the vessel release chemicals that trigger the activation of platelets.
platelet adhesion
Activated platelets adhere to the site of injury, forming a temporary plug to stop the bleeding. This is facilitated by the interaction between platelet receptors and proteins exposed in the damaged vessel wall.
platelet aggregation
the adhered platelets release additional chemicals that attract more platelets to the site, causing them to aggregate and form a growing plug to seal the injured vessel
platelet activation
activated platelets become further activates, changing shape and releasing the contents of their granules, which help to stabilise the platelet plug and initiate the clotting process
platelet plug formation
the final result is a platelet plug that seals the injured vessel and prevents further blood loss, allowing the body to begin the process of of repairing the damaged tissue
disorders of haemostats
platelet disorders
coagulation disorders
vascular disorders
anticoagulant disorders
platelet disorders
related to the production, function or destruction of platelets, leading to abnormal bleeding or clotting
coagulation disorders
disorders affecting the proteins in the blood clotting process, resulting in impaired haemostasis
vascular disorders
including structural and functional abnormalities that can impact haemostasis
anticoagulant disorders
disorders involving the overproduction or dysfunction of anticoagulant proteins, leading to an increased risk of bleeding
platelet disorders
condition whether the platelet count is lower than normal, leading to increased risk of bleeding
thrombocytosis
platelet count is higher than normal, increasing the risk of blood clots
platelet function disorders
conditions whether platelets are unable to function, despite normal platelet count
immune thrombocytopenia purpura
autoimmune disorder where the body’s own immune system attacks and destroys platelets
coagulation disorders
haemophilia
von willebrand disease
disseminated intravascular coagulation
antiphospholipids syndrome
haemophilia
genetic disorder that impairs the body’s ability to control blood clotting, leading to excessive bleeding
von willebrand disease
Most common inherited bleeding disorder, caused by a deficiency or dysfunction of von Willebrand factor, a protein involved in blood clotting.
disseminated intravascular coagulation
Serious condition where blood clots form throughout the body, leading to excessive bleeding and organ damage.
antiphospholipid syndrome
Autoimmune disorder that increases the risk of abnormal blood clots, potentially leading to stroke, heart attack, or pregnancy complications.
vascular disorders
atherosclerosis
aneurysm
varicose veins
deep vein thrombosis
atherosclerosis
Build-up of plaque in the arteries, leading to restricted blood flow and increased risk of heart attack or stroke.
aneurysm
Weakening and bulging of the arterial wall, which can lead to rupture and internal bleeding.
varicose veins
swollen, twisted veins, often found in the legs caused, caused by the valves in the veins not functioning properly
deep vein thrombosis
Formation of a blood clot in a deep vein, typically in the leg, which can potentially dislodge and travel to the lungs (pulmonary embolism).
anticoagulant disorders
thrombophilia
factor V leiden
protein c and protein s deficiency
antiphospholipid syndrome
thrombophilia
Inherited or acquired conditions that increase the risk of abnormal blood clot formation
factor V leiden
The most common inherited thrombophilia, caused by a mutation in the Factor V gene
protein c and protein s deficiency
Rare genetic disorders that impair the body’s natural anticoagulant system
antiphospholipid syndrome
An autoimmune disorder that increases the risk of blood clots and pregnancy complications
factors affecting haemostasis
platelet function
coagulation cascade
anticoagulant mechanisms
vascular integrity
hormonal influences
platelet function
Platelets play a crucial role in the initial response to vascular injury, adhering to the site of damage and aggregating to form a platelet plug.
coagulation cascade
The coagulation cascade involves a series of enzymatic reactions that ultimately lead to the formation of a fibrin clot, stabilizing the platelet plug
anticoagulant mechanisms
Regulatory mechanisms, such as the protein C system and antithrombin III, help control and limit the coagulation process to prevent excessive clot formation.
vascular integrity
The integrity and health of the vascular endothelium, which lines the blood vessels, can influence hemostasis by regulating the balance between pro- and anti-coagulant factors.
hormonal influences
Hormonal changes, such as fluctuations in estrogen and progesterone levels, can affect the expression of coagulation factors and the overall hemostatic balance.
patients at risk for bleeding
patients on anticoagulants
liver disease
thrombocytopenia
renal impairment
trauma or surgery
patients on anticoagulants
Individuals taking medications like warfarin, heparin, or direct-acting oral anticoagulants (DOACs) are at increased risk of bleeding complications.
liver disease
Patients with liver dysfunction may have impaired clotting factor production, leading to a higher bleeding tendency.
thrombocytopenia
A low platelet count (thrombocytopenia) can result in impaired clot formation and increased bleeding risk.
renal impairment
Individuals with kidney disease or failure may have altered drug metabolism and clearance, increasing the risk of bleeding.
trauma or surgery
Patients who have recently experienced physical trauma or undergone surgical procedures are at higher risk of bleeding complications.
drugs influencing haemostasis
anticoagulants
antiplatelet agents
fribinolytic agents
haemophilia treatment
anticoagulants
Drugs that inhibit the blood clotting process, such as warfarin, heparin, and direct-acting oral anticoagulants (DOACs)
antiplatelet agents
Drugs that prevent platelet aggregation and thrombus formation, like aspirin, clopidogrel, and ticagrelor
fribinolytic agents
Drugs that dissolve existing blood clots, such as tissue plasminogen activator (tPA) and streptokinase
haemophilia
Drugs that replace or enhance deficient clotting factors in individuals with haemophilia, including factor VIII and IX concentrates
