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64 Cards in this Set
- Front
- Back
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Hemostasis have 3 major components that when there is injury to the vessels triggers activation of these 3 components and initates coagulation? |
1. platelets 2. endothelial cells 3. blood clotting proteins in plasma |
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hemostasis |
prevents blood loss while maintaining blood in fluid state. |
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Normal hemostasis is made up fo what 4 steps |
1. primary hemostasis (platlets) 2. Secondary hemostasis (coagulation cascade) 3. fibrinolysis 4. regulation of hemostasis |
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what are the 5 steps of hemostasis |
Primary hemostasis: 1. vasoconstriction (i.e smooth muscles try to reduce the blood flow, and endothelin release) 2. platlet plug formation Secondary hemostasis: 3.coagulatino to form fibrin mesh 4. firbrinolysis (restricts the clot to where it needs to be) 5.repair at damaged site |
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what happens during primary hemostasis? |
-Initially there is immeidate vasoconstrtiction reflex and endothelin induced - vessel injury exposes subendothelium -platlets activated when exposed to ECM collagen proteoglycans, fibronectin, glycoproteins (activate platlets. -platelts adhere (von willebrands factor) directly (collagen) -platlet changes shape consolidates platlet plug -platelet degranulation (alpha and dense granules, thromboxane, ADP, Ca2+) -platelet aggredation forming loose plug-->primary hemostatic plug |
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what happens in secondary hemostasis |
1. tissue factor produced by endothelial cells 2. Phospholipid complex (on platelet surface) 3. plasma clotting factors beceom activated 4. results in FIBRIN formation 5. fibrin cements the platlet aggregate--> secondary hemostatic plug |
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what initiates secondary coagulation? |
tissue factor and extrinsic cascade |
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thrombin converts |
fibrinogen to fibrin and it activates platlets and factor V, VII, XI and XII |
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j |
tissue factor 7 is the most crucial |
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why do we have the coagulation cascade |
it allow amplification (allows multiplication) |
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components of the coagulation cascade |
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what are the components of the intrinsic pathway |
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what are the components of the extrinsic pathway |
Tissue factor (TF) -sub-endothelium -activated endothelium Endotoxin, TNF, AL-1, and thrombin also stimulate TF production -sepsis TF-VIIa activates X |
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the common pathway is activated |
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what is fibrin? |
-formed from fibrinogen by THROMBIN -fibrin self-polymerizes and cross linked by factor XIIa -cross-linking of fibrin and platlet contraction produces stong fibrin-platelet thrombus -retraction of the thrombus (by platelet retraction) (allow blood flow around) (pulls damaged vessel edges closer toghether) |
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what stimulates the integrated model of coagulation cascade |
Tissue factor |
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what does thrombin do? |
it |
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k |
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Fibrinolysis |
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f |
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what is the key enzyme in Fibrinolysis |
Plasmin |
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what does anti-thrombin do |
anti-thrombin III (ATIII) binds to the heparan sulfate on endothelium -post potent anticoagulant -degrades all activated coagulation factors except VIIa -can leak through glomerulus in kidney failure |
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too liitle coagulation = |
Hemorrhage |
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too much coagulation = |
thrombosis |
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causes of Hemorrhage |
abnormal function or integrity of major factors that influence hemostasis 1. blood vessels 2. endotheium 3. plateltes 4. coagulation factors |
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how does hemorrhage get cuases through the blood vessel? |
trauma (rhexis) vascualr erosion -inflammatory -invasive tumors -fungi (Aspergillus) Diapedesis -small defects in otherwise intact vessels allows a few RBC to escape Blood vessel wall malformation -Ehlers-Danlos syndrom -vitamin C def. |
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example of blood vessel leading to hemorrhage? |
Aortic rupture strongylus vulgarus larvae... in a horse |
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Diapedesis |
small defects in otherwise intact vessels allows a few RBC to escape |
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a |
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endothelial injury leading to hemorrhage can be due to |
Endotoxemia Vasculitis -virus (canine adenovirus-1) -Tick born diseases Uremic toxins (associated with kidney disease) immune complexes (type III hypersensitivity reaction) |
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how can issues with platelets cause hemorrhage? |
decreased number= thrombocytopenia eg. bone marrow disease abnormal platelet function eg. uremia secondary platelet dysfunction eg. Von Willibrands disease (eg. dobermans) |
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causes of hemorrhage due to coagulation factors |
1. congenital defects (hemophilia) -decreased concentration -funcional deficency 2. Acquired defects -decreased production (liver disease(most factors), Vit K deficentcy (II,VII,IX and X)(Warfarin) -increased consumption (DIC) |
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example of hemorrhage due to coagulation factors |
1. bleeding into leg (Hemophilia) eg. in the dog 2. Cardiac tamponade warfarin toxicity (pericardial effusion) |
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Hemorrhage based on something wrong in the capillaries... |
We describe based on the size Petechia (1-2mm)- -diapedesis -minor vascular damage eg. Thrombocytopenia |
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Purpura? |
Type of hemorrhage >3mm<2cm somehting wrong with the lymph nodes purpura hemorrhagica (in the horse teeth) |
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Ecchymosis (ses) |
Type of hemorrage 2-3cm more extensive vascular damage elephant herpesviral myocarditis --in the heart of the elephant |
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Suffusive |
Type of hemorrhage larger contiguous areas larger vessel damage (artery or vein)..due to decreased collagen strength eg. Vit C deficency in a guinea pig |
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Hematoma |
a type of hemorrhage localized area of hemorrhage -hemorrhage within a confined space eg. Aural Hematoma in the dog eg. Ethmoid Hematoma |
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Hemorrhage within the body cavity blood in the abdomeb blood in the thoacic cavity blood in the pericardium |
hemoabdomen hemothroax hemopericardium |
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what are the clinical consequences of hemorrhage |
-Rapid loss of up to 20% and slow rate of loss can be tolerated -rapid loss (>20%) results in hypovolemic shock location specific (cranial cavity) (cardiac tamponade) -loss of iron and subsequent iron deficiency anemia -external hemorrhage predominantyly (From GIT) -Internal hemorrhage, iron is preserved and recycled |
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what happens during the resoltuion of hemorrhage |
1. Resorption -small amount 2. organization -larger amounts -phagocytosis and digestion of hemoglobin -Hemoglobin converts to bilirubin and then turns to Hemosiderin 3. Organizing hematoma |
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what are the steps of hemorrhage resolution in terms of the chagnes that happen on the surface of the skin? |
Hemoglobin (red-blue)-->Bilirubin(blue-green)-->Hemosiderin (yellow-brown) |
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WHat is Thrombosis |
the formation of inappropriate (excessive) thrombus in wall of blood or lymphatic vessel, or heart or free in lumen (thromboembolism) |
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what is Virchows Triad of Thrombosis? |
Endothelial injury (tissue factor) + Hypercoagulability (of the blood) + Abnormal blood flow (because you have turbulent blood flow it can thrombosis) can all lead to thrombosis |
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Thrombosis due to endothelial damage |
1. Endothelial injury exposes -tissue factor (extrinsic coagulation) -collagen and fibrinonectin 2. loss of endothelial anti-thrombotic mechanisms |
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Cuases of thrombosis due to endothelial injury |
-vasculitis (viral, bacterial, fungi) -immune mediated -toxic -DIC eg. pulmonary thrombosis Dirofilaria in the dog |
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Thrombosis due to alteration of blood flow causes |
1. reduced blood flow: -systemic heart failure -local congestion 2. Turbulent blood flow: -Aneurysm -narrowing vessels 3. increased contact of platelets and endothelal cells 4. accumulation of activated coagulation factors |
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example of thrombosis due to alteration in blood flow |
Horse colon: colonic torsion and venous thrombosis |
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Reasons for thrombosis due to hypercoagulability |
1. increased concentration of activated clotting factors -increased activation( due to inflammation, surgery, preg, renal disease) -decreased degradation (liver disease) 2. Decreased concentration of anti-coagulation factors -decreased ATIII (anti-coagulation factor) with renal disease in dogs |
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what is the appearance of Thrombus in the cardiac and arterial thrombi |
-usually due to endothelial damage -predominantly platelets and firbin (pale) -large thrombi laminations (lines of zahn) eg. Pulmonary artery thrombi (HCM) |
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What is the appearance of Venous thrombi |
-usuallly due to blood stasis -Erythrocytes commonly incorporated (red) eg. Jugular vein thrombus |
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Post morten coagulation pic |
l |
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Propagation |
Accumulate more and more platelets and fibrin eventually leading to vessel obstruction (thromus fate) |
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what are the steps in the fate of thrombus |
-propogation -dissolution -organization and recanalization -embolism |
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Dissolution |
removal by fibrinolytic activity |
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organization and recanalization in the fate of thrombus? |
fibrosis |
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Embolism |
Dislodge and travel to other sites Thromboemboli: -dislodged fragments of thrombus -lodge in smaller caliber vessels |
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what are three types of Thromboemboli
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1. venous thromboemboli- typically lodge in pulmonaty circulation 2. Arterial thromboemboli- lodge downstream usually at vascular bifurcation 3. Cardiac thromboemboli-often lodge at iliac bifurcation (saddle thromus) |
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Types of Emboli |
Bacterial emboli- abscess or valvular endocarditis fat emboli - fracture releasing bone marrow - usually lodge in pulmonary circulation fibrocartilaginous emboli- intravascular parasites malignant neoplasms ????? |
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Disseminated intracascular coagulation (DIC)( |
-severe malfunction of hemostasis -serious consequences (often results in death) -excessive (systemic) generation of THROMBIN -Excessive generation of tissue factor |
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causes of DIC (Disseninated intravascular coagulation |
-diffuse vascular damage (trauma, vasculitis, burns) exposure of endothelial tissue factor -bacteremia and systemic infections intravascular generation of TF by endothelial cells and monosytes |
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