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24 Cards in this Set
- Front
- Back
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What are hemorrhages and how are they most often caused?
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escape of blood from the vasculature into surrounding tissues, a hollow organ or body cavity, or to the outside
trauma |
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Hematoma?
Hemothorax? Hemopericardium? hemoperitoneum? hemarthrosis? |
localized hemorrhage occurs within a tissue or organ
hemorrhage in pleural cavity hemorrhage in pericardial sac hemorrhage in peritoneal cavity hemorrhage in synovial space |
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Petechial hemorrhages, petechiae, or purpura?
Ecchymosis? |
small hemorrhages in the skin, mucous membranes, or serosal surfaces
diffuse hemorrhage in skin and subcutaneous tissue |
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hyperemia?
active hyperemia is caused by ___. passive hyperemia is caused by ___ and also called passive ___. |
localized increase in the volume of blood in caps and small vessels
localized arteriolar dilation (blushing, inflammation) obstructed venous return or increased back pressure from congestive heart failure (CHF) passive congestion |
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When does acute passive congestion occur?
When does chronic passive congestion of the lung occur? When does chronic passive congestion of the liver and lower extremities occur? |
shock, acute inflammation, or sudden right-sided heart failure
left-sided heart failure or mitral stenosis right-sided heart failure |
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In chronic passive congestion of the lung, congestion of the ____ leads to capillary ____ and passage of ____ into the alveoli. What happens to the red cells? what does this cause?
In long standing congestion, what happens to the lung? |
alveolar capillaries; rupture; RBC
phagocytised; intra-alveolar hemosiderin-laden macrophages (heart failure cells) fibrosis and hemosiderin deposition result in brown induration of the lung |
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What is nutmeg liver and when does it occur?
What produces the nutmeg liver? |
nutmeg liver- a speckled, nutmeg-like appearance on a cut section; appears with chronic passive congestion of the liver and lower extremities
combination of dilated, congested central veins and the surrounding brownish-yellow, fatty, liver cells |
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What is infarction?
What are anemic infarcts and where can you find them? |
necrosis resulting from ischemia
white or pale; arterial occlusions in heart, spleen, and kidney |
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What are hemorrhagic infarcts?
Where can you find them? What happens to the nonobstructed portion of the vasculature? When are these infarcts caused by venous occlusion? |
red infarcts in which red cells ooze into the necrotic area
GI tract and lung hemorrhages into the infarct volvulus, incarcerated hernias, and postoperative adhesions |
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What is thrombosis and what does it cause?
What are some pathological predispositions of thrombosis? |
intravascular coagulation of blood; interruption of blood flow
venous stasis, usually from immobilization, polycythemia, sickle cell disease, oral contraceptives in associated with cigarette smoking |
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Thrombogenesis results from the interaction of ____, ____, and ____.
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platelets, damaged endothelial cells, and the coagulation cascade
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What are the four main functions of platelets?
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1) maintain physical integrity of vascular endothelium
2) endothelial repair through platelet-derived growth factor (PDGF) 3) formation of platelet plugs 4) promote the coagulation cascade through the platelet phospholipid complex |
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What is platelet adhesion and what mediates this?
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interaction of platelet surface glycoprotein receptors and subendothelial collagen during vessel injury; von Willebrand factor
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What occurs during the platelet release reaction?
How do platelets affect the coagulation cascade? |
soon after adhesion platelets release ADP, histamine, serotonin, and PDGF.
conformational changes in the platelet membrane makes the platelet phospholipid complex available, contributing to the coagulation cascade, leading to the formation of thrombin |
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Activation of the platelet phospholipid complex provides _____, which proceeds through the ____pathway to the production of ____.
What are the functions of thromboxane A2? What does asprin do? |
Arachidonic acid; cyclooxygenase; thromboxane A2
potent vasoconstrictor and platelet aggregant inhibits cyclooxeganse, which in turn inhibits coagulation |
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What happens during platelet aggregation?
Why are additional platelets recruited? What mediates this process? How are the platelets linked? |
platelets stick to each other
to form the initial hemostatic platelet plug glycoprotein IIb-IIIa complex on the surface of platelets fibrinogen bridges |
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What are some agonists that promote aggregation?
What is an antagonist that limits platelet aggregation? |
ADP, thrombin, thromboxane A2, collagen, epinephrine, and platelet-activating factor
prostacyclin PGI2 which is produced by endothelial cells |
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Endothelial cells are ____ to platelets and coagulation proteins.
Endothelial cells produce ____, which neutralizes thrombin and other coagulation factors. |
resistant
antithrombin III |
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Endothelial cells secrete ____, degrade ____, and take up, inactivate, and clear ____.
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tissue plasminogen activator (TPA- activates plasminogens); ADP; thrombin
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Endothelial cells synthesize 4 things?
What is thrombomodulin? |
thrombomodulin, protein S, PGI2, and NO
cell-surface protein that binds thrombin and converts it to an activator of protein C (inhibiting coagulation) |
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What initiates the extrinsic pathway of coagulation?
It activates ____ and forms a ____. It activates ____ to ____, which activates____ to ____, and finally ____ to ____. What is the cofactor in the conversion of prothrombin to thrombin? Thrombin converts ____ to ____. |
tissue factor
factor VII; tissue factor-factor VII complex factor X to factor Xa; factor IX to factor IXa; prothromb (factor II) into thrombin (factor IIa) Va fibrinogen to fibrin |
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What stabilizes the fibrin monomer, thus forming the fibrin clot?
How is the extrinsic pathway evaluated? what factors does it measure? |
factor XIII
prothrombin time (PT) factors II, V, VII, X, and fibrinogen |
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The intrinsic pathway of coagulation involves the activation of which clotting factors?
This pathway may involve ___ activation by which factors? What are the two options for activation of the intrinsic pathway? |
all but VII and XIII
contact; contact factors: XII (Hageman), prekallikrein, and high-molecular weight kininogen, as well as factor XI. tissue factor-factor VIIa complex or platelet phospholipid complex |
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How is the intrinsic pathway of coagulation evaluated?
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partial thromboplastin time (PTT) which measures factors II, V, VIII, IX, X, XI, XII, and fibrinogen
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