a blood clot may form as the result of a relatively minor vessel injury and occlude a section of the vascular tree.

A pathologic state in which normal hemostatic processes are activated inappropriately

Manifestations that can occur because of Thrombus and Embolus? (Select all that apply)

Which of the following are TRUE about Thrombus and Embolus? Select all that apply

Arterial Thrombosis (Select all that apply)

Venous Thrombosis (Select all that apply)

Prevent occurrence or enlargement of a thrombus (Select all that apply)

Dissolve already existing clots

Know this

Primary Hemostasis (Select all that apply)

Vascular injury causes

Activated platelets secrete thromboxane A2 (TxA2) and ADP

Tissue factor expressed on activated endothelial cells initiate the steps of the coagulation cascade,

Activates thrombin- Thrombin activates fibrinogen to form fibrin- Fibrin polymerizes with platelets to form hemostatic plug.

Limit the hemostatic process to the site of vascular injury (Select all that apply)

activates the fibrinolytic system

activates inhibitors of the coagulation cascade

inhibits both platelet activation and vasoconstriction

catalyze the inactivation of coagulation factors

 Scanning electron micrographs of (Select all that apply)

Platelets adhere to ___________ that is exposed after vascular injury 

binds to glycoprotein Ib [GPIb] on the platelet membrane and to the exposed collagen.

Platelet glycoprotein VI (GPVI) 

Helps in release of TXA2 causing vasoconstriction & granule release and Important in mediating platelet aggregation (causes platelets to become “sticky” and adhere to one another)

Ca++, ATP, Serotonin, vWF,  Platelet factor 4

Activation in Primary Hemostasis by? Select all that apply

1. Thromboxane A2 (TxA2) is generated from arachidonic acid in activated platelets; cyclooxygenase catalyzes the committed step in this process. 

2. Secreted TxA2 binds to the cell surface TxA2 receptor (TxA2-R), a G protein-coupled receptor. 

3. The Gα isoform Gαq activates phospholipase C (PLC). 

4. PLC hydrolyzes phosphatidylinositol 4,5-bisphosphate (PIP2) to yield inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). 

5. IP3 increases the cytosolic Ca2+concentration by promoting vesicular release of Ca2+ into the cytosol. 

6. DAG activates protein kinase C (PKC). 

7. PKC activates phospholipase A2 (PLA2). 

8. Through an incompletely understood mechanism, activation of PLA2 leads to the activation of GPIIb–IIIa. 

9. Activated GPIIb–IIIa binds to fibrinogen. 

10. Fibrinogen cross-links platelets by binding to GPIIb–IIIa receptors on other platelets. This cross-linking leads to platelet aggregation and formation of a primary hemostatic plug.

1. Binding of ADP to the P2Y(ADP) receptor activates a G_i protein, which inhibits adenylyl cyclase. 

2. Inhibition of adenylyl cyclase decreases the synthesis of cAMP and hence decreases protein kinase A (PKA) activation (dashed arrow). cAMP is metabolized to AMP by phosphodiesterase (PDE). 

3. Decreased PKA activation that results from ADP binding to the P2Y(ADP) receptor causes platelet activation. 

Right panel:

4. Thrombin acts on PAR-1 to activate a G_q protein. 

5. ADP also activates G_q by binding to the P2Y1 receptor. 

6. G_q activation (by either thrombin or ADP) activates phospholipase C (PLC). 

7. PLC activation leads to platelet activation

clopidogrel, prasugrel, and ticagrelor inhibit P2Y (ADP) receptors (Anti-platelet drugs)

Activated fibrinogen-binding protein GPIIb/IIIa bind to other platelets via fibrinogen causing

is activated by tissue factor

can be activated by surface contact with a foreign body

Intrinsic (damaged surface)

Extrinsic (Trauma)

Coagulation cascade is needed to form a stable fibrin clot at the site of vascular injury

What is the process of the coagulation cascade?

The intrinsic and extrinsic pathways converge at the level of

is a cofactor in many of the steps, and that a number of the steps occur on phospholipid surfaces provided by activated platelet and other cells

means there is no injury or damage

This pathway is activated by a stimulus like atherosclerosis [that’s why these patients have a high chance of stroke etc.], heart valve [this is why we use anticoagulants with these patients]

Factor 12a stimulates factor 11 to 11a which then enters the extrinsic pathway and activates factor 9 to 9a and follows the common pathway down 

Coagulation cascade!!!

Thrombin also activates protease-activated receptors (PARs) stimulates these cells to release? Select all that apply

Endogenous anticoagulant factors restrict propagation of the clot beyond the site of injury

The activated endothelium maintains a balance of procoagulant (localized, membrane bound) and anticoagulant factors (non-localized, soluble in blood) to limit hemostasis to the site of vascular injury

What are endogenous anticoagulant factors? Select all that apply

Anti-thrombin III Inactivates

Know this

Physiologically antagonist to TxA2

Prostacyclin (PGI2) Select all that apply

Roles of Thrombin Select all that apply

The binding of heparin to ATIII induces a conformational change in ATIII (A) that allows the ATIII to bind?

The coagulation cascade is arbitrarily divided into the intrinsic pathway, the extrinsic pathway, and the common pathway.

is activated by stimulus like atherosclerosis, artificial heart valve (Select all that apply)

is activated by injury/trauma (Select all that apply)

vitamin K-dependent proteins

Inactivates factors Va and VIIIa

is the cofactor required for activation of Protein C 

Excess thrombin generation leads to activation of __________ helps to prevent the enlarging fibrin clot

Hampers Coagulation

Limits the action of tissue factor (TF) and limits activation of ?

Converts plasminogen to plasmin and Plasmin converts fibrin into fibrin degradation products

Endothelial injury causes (Select all that apply)

Abnormal blood flow

Hypercoagulability refers to

is the longer pathway of secondary hemostasis

is the shorter pathway of secondary hemostasis.