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hemostasis
responsible (platelet)
2 main stage in the process of stopping bleeding (hemostasis) after a blood vessel is injured
primary hemostasis
secondary hemostasis
These stages work together to prevent excessive blood loss while promoting vessel repair.
primary hemostasis
platelet aggregation
no stable and matindi ang clog kasi loose pa
secondary hemostasis
clotting factor
formation of fibrin
make stronger clog
ensures the blood clot remains in place until the blood vessel is healed
characteristics
fibrin-reinforced clot is strong and resistant to blood flow, providing a long-lasting barrier to blood loss.
intrinsic pathway
due to bv damage (platelet, collagen)
extrinsic pathway
due to endothelial damage
common pathway
factor x
Thrombin Production
Thrombin converts fibrinogen into fibrin monomers, which polymerize to form a fibrin mesh.
fibrin cross-linking
Cross-Linking: Factor XIII stabilizes the fibrin by cross-linking the fibrin strands, creating a stable clot that reinforces the platelet plug.
factor 1
fibrinogen
factor 2
prothrombin
factor 3
thromboplastin
factor 4
calcium
factor 5
labile factor
factor 7
stable factor
factor 8
antihemophillic factor a
factor 9
christmas factor
factor 10
stuart prower factor
factor 11
plasma-thromboplastin antecedent
factor 12
hageman factor
factor 13
fibrin stabilizing factor
Plasma fibrinogen
an essential protein in blood plasma that serves as an acute-phase protein and plays a vital role in blood coagulation.
fibrinogen
Produced primarily by the liver
a soluble protein that transforms into fibrin through enzymatic reactions during the clotting process.
Fibrin
in turn, forms a mesh that stabilizes blood clots. thus preventing excessive bleeding
Fibrinogen
acts as a biomarker for inflammation, meaning that its concentration can rise significantly in response to systemic inflammatory processes.
fibrinogen levels change
during inflammation, infection, trauma, or chronic disease, they provide insight into an animal's immune response and coagulation status.
fibrinogen acts as an
This is especially useful in detecting conditions like systemic inflammation, where
acute-phase reactant meaning it increases quickly and significantly in response to infection or tissue injury.
Regular fibrinogen measurement
allows veterinarians to monitor the progression of diseases, evaluate the effectiveness of treatments, and make informed decisions about patient care.
elevated plasma fibrinogen levesl are generally associated with:
Inflammatory diseases
Acute-phase proteins like fibrinogen increase in response to inflammatory stimuli. For example, infections (such as bacterial or viral), immune-mediated diseases, and conditions like arthritis or pancreatitis often cause fibrinogen levels to rise.
elevated plasma fibrinogen levesl are generally associated with:
trauma or surgery
Physical injury or surgical procedures can lead to fibrinogen elevation as the body reacts to potential blood loss and tissue damage.
elevated plasma fibrinogen levesl are generally associated with:
chronic disease
Long-term conditions such as cancers (especially involving the liver or bone marrow) can lead to persistent increases in fibrinogen.
Low plasma fibrinogen levels, though less common, can indicate:
liver disease
Since fibrinogen is produced in the liver, liver dysfunction (e.g., due to cirrhosis or hepatitis) can decrease its production.
Low plasma fibrinogen levels, though less common, can indicate:
coagulopathies
Conditions like disseminated intravascular coagulation (DIC) or other coagulation disorders can result in fibrinogen consumption exceeding production, lowering overall levels.
Low plasma fibrinogen levels, though less common, can indicate:
genetic deficiencies
Some animals may have inherited fibrinogen deficiencies, though rare, which can affect their ability to clot blood properly.
Identifying Coagulopathies
Conditions like DIC or liver disease, where coagulation may be compromised, can be flagged early through abnormal fibrinogen levels, allowing timely interventions.
Preoperative and Postoperative Assessment
Fibrinogen levels provide valuable insight into a patient's coagulation status, helping assess the risk of excessive bleeding or clotting before and after surgeries.
Inflammation Detection
Fibrinogen serves as an indicator of systemic inflammation, helping veterinarians identify and quantify inflammatory responses in animals. For example, a sudden increase in fibrinogen could indicate an infection even before other signs appear.
Monitoring Disease Progression
In chronic conditions or during recovery from surgery, fibrinogen measurements can reveal changes in inflammatory activity, indicating if a condition is worsening or if treatment is effective.
hemostasis
process that stops bleeding at the site of an injury to maintain blood vessel integrity. It involves a series of tightly regulated steps that prevent excessive blood loss and promote tissue repair.
3 stage of hemostasis
vascular spasm
platelet plug formation
coagulation (clot formation)
vascular spasm (vasoconstriction)
Purpose: Reduces blood flow to the injured area to minimize blood loss.
Mechanism: When a blood vessel is damaged, smooth muscles in the vessel wall contract, causing vasoconstriction. This spasm is triggered by nerve reflexes and the release of signaling molecules from damaged endothelial cells.
Duration: This is a quick, temporary response that lasts only a few minutes but is crucial for reducing blood flow immediately after injury.
platelet plug formation
Purpose: Forms a temporary seal over the injury.
Mechanism:
Platelet Adhesion: Platelets adhere to exposed collagen fibers at the injury site.
Platelet Activation: Once attached, platelets become activated and release signaling molecules like ADP, thromboxane A2, and serotonin. These chemicals recruit and activate more platelets to the site.
Platelet Aggregation: Activated platelets stick together, forming a plug that temporarily seals small breaks in the vessel wall.
Outcome: The platelet plug provides an initial barrier to prevent blood loss, especially effective for small injuries.
coagulation
Purpose: Forms a stable, insoluble clot that reinforces the platelet plug.
Mechanism:
Intrinsic and Extrinsic Pathways: Coagulation is triggered by either internal vessel injury (intrinsic pathway) or external trauma (extrinsic pathway), which activate a series of clotting factors in a cascade.
Common Pathway: Both pathways converge to activate factor X, leading to the conversion of prothrombin to thrombin.
Fibrin Formation: Thrombin converts fibrinogen into fibrin, which forms a mesh around the platelet plug.
Clot Stabilization: Factor XIII cross-links fibrin strands, solidifying the clot and anchoring it to the wound site.
Outcome: The resulting fibrin clot provides a stable barrier that prevents blood loss until tissue repair occurs.
clot retraction and repair
Clot Retraction: Platelets contract, pulling the edges of the wound closer together,
reducing the size of the injury.
Tissue Repair: Endothelial cells begin the healing process, regenerating the blood
vessel wall beneath the clot.
clot removal (fibrinolysis)
Purpose: Dissolves the clot after the vessel has been repaired to restore normal blood
flow.
Mechanism:
Plasminogen, an inactive enzyme within the clot, is converted to plasmin, which breaks down fibrin into smaller fragments.
Outcome: Fibrinolysis ensures that the clot is removed once it has fulfilled its function, preventing obstruction in the vessel.
Calcium Deficiency:
Can impair blood clotting, increasing the risk of hemorrhage
Vitamin K Deficiency
Leads to a reduction in functional clotting factors, necessitating vitamin K supplementation in cases of deficiency or poisoning (e.g. anticoagulant rodenticide ingestion)
Thrombin and Anticoagulants:
Thrombin's central role means it’s a target for
anticoagulant medications to prevent abnormal clotting
hemophilia A (factor 8 deficiency)
Description
results from an inherited deficiency in Factor VIII, a crucial clotting factor in the intrinsic pathway of the coagulation cascade. Factor VIII forms a complex with Factor IX to activate Factor X, which is necessary for thrombin production.
Prevalence
Commonly seen in dogs, especially in breeds like German Shepherds, Golden Retrievers, and others with a genetic predisposition. Cats can also be affected but less frequently.
Effect
Without sufficient Factor VIII, the intrinsic pathway is impaired, leading to a decreased production of fibrin, the protein mesh that stabilizes blood clots. Animals with Hemophilia A often experience spontaneous bleeding or excessive bleeding following minor injuries. • Hemophilia B (Factor IX Deficiency):
hemophilia B (factor 9 deficiency)
Description
Also known as Christmas disease, ______ is due to a deficiency in Factor IX, another critical clotting factor in the intrinsic pathway.
Effect
Similar to Hemophilia A, this deficiency hampers the formation of the Factor VIII-IX complex, which delays clot formation. Affected animals are prone to bleeding episodes, though severity varies by the level of deficiency.
Von Willebrand Disease (vWD)
Cause
arises from a deficiency or abnormal function of von Willebrand factor (vWF), which plays a dual role in clotting:
Facilitating Platelet Adhesion: vWF helps platelets adhere to the exposed collagen at the injury site, forming the initial platelet plug.
Stabilizing Factor VIII: vWF binds to Factor VIII, protecting it from premature degradation in the blood.
Prevalence
disease is the most common inherited bleeding disorder in dogs, affecting breeds like Doberman Pinschers, Shetland Sheepdogs, and others. It’s less common in cats.
Effect
A lack of functional vWF disrupts both platelet adhesion and Factor VIII stability, leading to a heightened risk of bleeding, especially from mucosal surfaces such as the gums or nose. Animals may also experience prolonged bleeding after surgeries or injuries.
vitamin K deficiency
Cause
Vitamin K is an essential nutrient for activating several key clotting factors, including Factors II (prothrombin), VII, IX, and X, by enabling gamma-carboxylation of these proteins. This chemical modification allows the factors to bind calcium ions, which is essential for their role in the cascade.
Prevalence
Vitamin K deficiency in animals can result from dietary insufficiency, malabsorption issues, or more commonly, ingestion of anticoagulant rodenticides that inhibit vitamin K recycling.
Effect
Without vitamin K, the affected clotting factors cannot bind calcium, rendering them inactive and disrupting both the intrinsic and extrinsic pathways. This leads to an increased bleeding tendency, and animals may exhibit symptoms like bruising, bleeding gums, or severe internal bleeding in critical cases.
Disseminated Intravascular Coagulation (DIC)
Cause
DIC is often secondary to severe underlying conditions like infections (sepsis), trauma, cancer, or systemic inflammation. It triggers widespread activation of the coagulation cascade throughout the bloodstream rather than at a localized injury site.
Effect
DIC leads to the formation of numerous small clots in the bloodstream, which consume platelets and clotting factors faster than the body can replenish them. As the cascade progresses, the excessive clotting depletes these components, causing a paradoxical bleeding tendency (since clotting factors and platelets are exhausted).
Clinical Implications
DIC is a medical emergency that requires immediate intervention. It’s challenging to treat because of the dual risk of clotting and bleeding. Common symptoms include widespread bruising, bleeding from various sites, and organ damage due to microclots in blood vessels.
Factor XII Deficiency
Cause
Factor XII deficiency is usually an inherited condition where Factor XII, which initiates the intrinsic pathway, is either absent or defective.
Prevalence
Common in cats and may be seen in some dog breeds, but this deficiency is generally asymptomatic.
Effect
Unlike other clotting factors, a deficiency in Factor XII does not typically cause
bleeding issues. Instead, it prolongs the activated partial thromboplastin time (APTT), a laboratory test that measures intrinsic pathway activity. This prolonged APTT can be misleading, suggesting a bleeding risk that is not actually present.
Factor XI Deficiency
Cause
Factor XI deficiency is another inherited condition that impairs the intrinsic pathway.
Prevalence
Seen in certain dog breeds, such as Great Pyrenees and Kerry Blue Terriers.
Effect
Deficiency in Factor XI usually results in mild to moderate bleeding tendencies. Animals with this deficiency may experience bleeding after surgery or trauma, but spontaneous bleeding is rare. This condition highlights the variability in bleeding severity depending on which clotting factor is deficient.
Factor VII Deficiency
Cause
Factor VII, essential in the extrinsic pathway, can be deficient due to genetic mutation
Prevalence
Commonly affects certain breeds, including Beagles and Alaskan Malamutes.
Effect
Since Factor VII is involved early in the extrinsic pathway, its deficiency impairs the ability to activate Factor X via this pathway. This results in a bleeding tendency that varies from mild to moderate, depending on the severity of the deficiency. Factor VII deficiency mainly affects clotting in response to external trauma.
Liver Disease-Associated Coagulopathies
Cause
Most clotting factors are synthesized in the liver. Liver disease, such as cirrhosis or hepatitis, reduces the production of these factors, leading to a decrease in clotting capability.
Effect
Animals with liver disease often exhibit prolonged clotting times, particularly the prothrombin time (PT), which reflects the extrinsic pathway. Because the liver also produces regulatory proteins for coagulation, liver dysfunction can cause imbalances that lead to either excessive bleeding or clotting, complicating treatment.
Coagulation cascade
a complex series of steps that lead to blood clot formation to stop bleeding. It involves a chain reaction among clotting factors that ultimately results in the conversion of fibrinogen to fibrin, forming a stable blood clot
