9/4/13 Flashcards
When there is a vascular injury, what is the first response and what is secreted
neurogenic arteriolar vasonconstriction, endthelin is secreted
what activates platelets during a vascular injury
exposure to ECM
What are three ways that the endothelium prevents platelet aggregation
- Prevent contact with matrix,
- thrombin and cytokines bind to endothelial cells and release NO and PGI-2 which vasodilate and inhibit aggregation
- ADPase degrades ADP
What are three ways that the endothelium prevents coagulation factors
- antithrombin III binds to heparin like molecules and inactivates thrombin and factors XII,XI,X, and IX
- Thrombin binds to thrombomodulin which leads to Protein C inactivating factor V and VIII in the presence of Protein S
- tPA activates plasmin which cleaves fibrin
What promotes platelet adherence to the collagen of the ECM
von willebrand factor
What are the two specific granule types found in platelets
Alpha-granules (contain factor V and VIII), dense core granules (these contain histamin, serotonin, epinephrine, ADP, ATP, Ca2+)
During the secretion phase of prothrombotic activity, what is released and what happens
Ca2+ and ADP released, as granules released phospholipid surfaces of the platelet membrane become available to factors of the intrinsic pathway
During the aggregation phase of prothrombotic activity, what is released in addition to ADP
TXA2
What attracts macrophages and neutrophils to the site of coagulation?
Fibrin split products
Describe the intrinsic pathway of the coagulation cascade
Kallikrein activates XII–> activates XI–> activates IX–> activates X in the presence of VIII, Ca2+ and phospholipid surface–> common pathway
Describe the extrinsic pathway of the coagulation cascade
Tissue factor activates VII–> activates X–> common pathway
Describe the common pathway of the coagulation cascade
X activate thrombin from prothrombin in the presence of V–> thrombin cleaves fibrinogen to fibrin–> factor XIII helps stabilize the fibrin clot
Tissue factor pathway inhibtor inhibts which to coagulation factors
VII, X
Virchow’s triad of thrombosis formation include
- Endothelial injury
- Abnormal blood flow
- Hypercoagulability
Leiden factor is a mutation for which coagulation factor?
V, Protein C resistance
Lines of Zahn are typically more visible in this type of vessel
Artery, rapid blood flow
Thrombus growth is (opposite/same) direction as the direction of flow in arteries
opposite
Thrombus growth is (opposite/same) direction as the direction of flow in veins
same
Describe the effects found in disseminated intravascular coagulation
Small thrombi formation in many tissues and organs–> coagulation proteins are used up–> fibrinolytic mechanisms are activates–> bleeding disorders evolves
Where do most pulmonary thromboembolism originated
DVT
Emboli that get stuck at the bifurcation of the pulmonary trunk
Saddle embolus
What percentage of obstruction in the pulmonary vasculature could cause sudden death
60%
Why are pulmonary emboli not always fatal?
The lung has dual blood supply and bronchial arteries from the aorta can pick up the slack (except in the case of left-sided heart failure)
Systemic thromboembolism arises from the (arterial/venous) system
arterial
Most systemic thromboembolism originate from
cardiac mural thrombi
How does paradoxical emboli occur
A thrombus in the vein becomes an embolus–> right atrium–> right ventricle–> left ventricle via an interventricular septal defect–> systemic distribution
The pathogenesis of the syndrome include mechanical obstruction as well as the release of inflammatory in response to free fatty acids and endothelial cell injury
Fat embolism syndrome
Amniotic fluid embolism can lead to this because of the presence of fetal substances
Disseminated intravascular coagulation
What are the two types of infarcts
Red (soft tissue, secondary blood supply), White (solid organs, single arterial supply)
Infarcts leads to mostly this type of necrosis
Coagulative necrosis
Systemic hypoperfusion is a common outcome in
shock
Cardiogenic shock can result from
MI, Ventricular rupture, arrhythmia
Obstructive shock can result from
pulmonary embolism, cardiac tamponade
Describe the process of Endotoxic shock
LPS binds to LPS binding proteins–> complex binds to CD14 (TLR4) on monocyts, macrophages, and neutrophils–> acute inflammation followed by acute phase reaction (IL-1,6, TNF)–> stimulates synthesis of coagulation proteins
What are the three stages of shock
- Non-progressive–> tries to maintain CO, renin angiotensin
- Progressive–>widespread hypoxia, anaerobic metabolism leads to lower pH
- Irreversible stage–> further damage proceeds due to necrosis and leads to total organ failure
