Hemostasis and Clotting

Learning Objectives – Hemostasis (Ch 10)

1. Recall the function of: thrombopoietin, platelets, TXA2, vWf,

coagulation factors (in general), Factor X, thrombin, fibrin, plasmin.

Thrombopoietin: released by liver. Bone marrow and platelet protection. 

Platelets: made in bone marrow. Clotting initiation.

TXA2: released from injured cells in the endothelium. Activates platelets. Stimulates aggregation.  

vWf: from endothelial cells. Adhesion for platelets (glue)

Coagulation factors: 

Factor X: creates thrombin from prothrombin 

Thrombin: creates fibrin from fibrinogen 

Fibrin: thread to hold platelets in place 

Plasmin: breaks down fibrin 


2. Provide examples of normal vs abnormal hemostasis.

Normal: stops loss of blood 

Abnormal: Clots form when the shouldn’t or don’t form when they should.


3. Describe role of endothelium in hemostasis

Endothelium inhibits coagulation → released Prostaglandins, Nitric oxide and vWF = no platelets stick uninjured vessel walls. 

4. Provide the purpose and key activities of each of the four stages of

hemostasis. Relate to #1.

  1. Vasoconstriction: smooth muscle around bv constricts. Stop blood loss

  2. Formation of a platelet plug: Platelets attracted by exposed collagen in bv wall= aggregation. vWF released.

  3. Blood Coagulation: factor X → fibrin cascade 

*Calcium and Vit K necessary cofactors 

  1. Fibrinolysis: thrombin synthesizes plasmin from plasminogen, breaks down thread. 


5. Compare and contrast the intrinsic and extrinsic pathways of

Coagulation

Intrinsic → slower, damaged blood vessel

Extrinsic → immediate, faster, damaged tissue, more factor 10 released


6. Recognize the action of anticoagulants (Warfarin, Heparin),

acetylsalicylic acid (Aspirin), and thrombolytics (Tissue Plasminogen

Activators) on ability to clot.

Warfarin: decrease thrombin (anticoagulant) 

Heparin: decrease thrombin (anticoagulant) 

Acetylsalicylic acid: blocks platelet aggregation 

Thrombolytics and Tissue Plasminogen Activators : increases plasminogen (clot buster)  

Learning Objectives – Blood-Clotting Disorders

• Recognize common indications of blood clotting disorders and

why they occur.

Blood clotting disorders occurs with decreased platelet levels or impaired platelet function: suppression of bone marrow, cancer, autoimmune, viral infection, previous clot, von willebrand disease, liver or kidney disease.  

• Define each, and when relevant, explain the etiology pathogenesis, manifestations, and potential complications of

Thrombocytopenia
Etiology: Bone marrow suppression
Pathogenesis: Suppression of bone marrow decreases platelet production
Manifestations: Not enough platelets to aggregate properly
Complications: Easy bleeding, impaired clotting

Von Willebrand Disease
Etiology: Hereditary
Pathogenesis: Deficiency of von Willebrand factor, a clotting factor that helps platelets clump and stick to blood vessel walls where damage has occurred
Manifestations:
• Skin rashes
• Frequent nosebleeds
• Easy bruising
• Bleeding of the gums
• Abnormal menstrual bleeding
Complications: Prolonged bleeding episodes

Prolonged ASA Use
Etiology: Prolonged use of ASA (aspirin)
Pathogenesis: Decreased cyclooxygenase activity leads to reduced production of thromboxanes from the endothelium
Manifestations: Easy bleeding, difficulty clotting
Complications: Excessive bleeding

Deep Vein Thrombosis (DVT)
Etiology: Clot formation in deep veins, mostly in lower extremities
Pathogenesis:
• Hypercoagulable state
• Vessel injury
• Venous stasis
Manifestations:
• Asymptomatic at first
• Aching and tenderness
Complications: Thromboembolism (leading to pulmonary embolism)