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68 Cards in this Set
- Front
- Back
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Why does edema results from a decreased plasma colloid pressure?
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water will not move into the capillaries from tissue fluid; high colloid pressure is needed to create a gradient to force water back into the capillaries
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Why might heart failure lead to edema?
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heart failure = back up of blood in veins = higher hydrostatic pressure = water won't go back into capillaries = more water in tissue fluid
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What is transudate?
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protein-poor fluid that can cause edema
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If tissue fluid is rich with exudate, what is a likely cause of the edema?
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inflammation; exudate = protein-rich extravascular fluid (leukocytes and other responsive elements)
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Why might liver cirrhosis cause edema?
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liver makes albumin. no albumin = low plasma colloid pressure = no tissue fluid re-enters the capillaries = edema
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Why does sodium retention in the capillaries lead to edema?
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sodium retention = water retention in the capillary = high venous hydrostatic pressure = water wont enter capillaries from tissue fluid
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What is lymphedema?
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edema caused by poor lymphatic drainage
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What is hyperemia?
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active increase of blood flow due to vasodilation; causes erythema
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What causes cyanosis?
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high levels of deoxygenated hemoglobin
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What are "heart failure cells"?
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hemosiderin filled macrophages as a result of blood back up in the pulmonary circuit
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What is a hemotoma?
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hemorrhage that leads to accumulation of blood
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Petechiae usually is associated with (high or low) platelet levels?
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low platelet levels
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What is a purpura?
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hemorrhage larger than petechiae, smaller than ecchymoses
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Why is there a brief period of vasoconstriction after vascular injury?
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to reduce amount of blood flowing to the injury = less blood loss
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What forms the "hemostatic plug"?
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platelets aggregating on the endothelium; this is primary hemostasis
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What is "tissue factor"?
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also known as factor 3; initiates coagulation cascade = high thrombin
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What is secondary hemostasis?
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second plug formation by fibrin meshwork
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What is thrombin's function in secondary hemostasis?
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cleave fibrinogen into fibrin; fibrin then forms the secondary plug
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Once a permanent plug is formed, after vascular injury, why do we want to release t-PA?
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t-PA activates plasmin that will degrade the clots and temporary plugs that were made during repair; also limit the coagulation cascade
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What affect do NO and PGI2 have on platelet adhesion to the endothelium?
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inhibit platelet aggregation to endothelium
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Function of thrombumodulin?
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convert thrombin from a coagulant to an anti-coagulant
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Protein C function
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limit factor V activation = limit coagulation cascade
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t-PA function
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cleave plasminogen into plasmin; plasmin can cleave fibrin to degrade the thrombus
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Function of vWF (von Willebrand Factor)
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allow for platelet binding to endothelium
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When platelets adhere to the endothelial wall, why do neutrophils also attach?
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platelets bind P-selectin on the , which also has receptors for neutrophils
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Why might a patient with a defective GpIb platelet protein exhibit hemophilia?
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GpIb binds to vWF in the endothelium to initiate platelet binding to the endothelium; this is Bernard- Soulier syndrome
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What is Bernard-Soulier syndrome?
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defective GpIb protein on platelets = no binding to vWF on endothelial wall
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Thromboxane A2's affect on platelet aggregation
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promotes aggregation
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How does aspirin help patients avoid clotting?
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inhibiting thromboxanes (they also inhibit cyclooxygenases and PGI, but COX can be reformed)
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What does coumadin do?
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anti-coagulant drug; antagonizes vitamin K in the coagulation cascade
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"Tissue factor"/thromboplastin are found to initiate coagulation from which pathway?
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Extrinsic
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What test screens for clotting disorders of the extrinsic pathway?
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PT (Prothrombin Time)
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What test screens for clotting disorders of the intrinsic pathway?
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PTT (Partial Thromboplastin Time)
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What does a D-dimer test tell us?
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D-dimer tests for fibrinolytic split particles in circulation; high particles = more fibrinolysis = more clotting
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What protein is responsible for fibrinolysis?
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plasmin
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How does t-PA work to dissolve clots?
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promotes plasminogen activation
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Function of PAIs (plasminogen activator inhibitors)
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inhibit fibrinolysis/t-PA binding fibrin
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What is Virchow's triad?
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3 major factors leading to thrombosis; endothelial injury, stasis/turbulence, hyper-coagulable state
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What is urokinase?
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acts like t-PA; promotes fibrinolysis
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Why does endothelial damage lead to more platelet aggregation?
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sub-endothelial ECM has a much higher affinity for platelets
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How does turbulence/stasis contribute to thrombosis?
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turbulence = more elements of the blood (like platelets) flow closer towards the endothelium= endothelial activation and adhesion
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What is laminar flow?
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elements of blood flow towards the center of the vessel
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Why can hyper-viscosity lead to a thrombus?
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high viscosity leads to stasis and turbulence = more platelets interacting/damaging the endothelium
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Most common mutation in patients with hyper-coagulable states
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factor V (Leiden); mutation in factor V makes it resistant to protein C regulation so it is always on
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What are mural thrombi?
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thrombi in the heart chambers of aorta
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What are "vegetations"?
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thrombi on heart valves
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Why is it important to administer t-PA within a few hours of clot formation?
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older thrombi have extensive fibrin linking and are more resistant to fibrinolysis
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What is "recanalization"?
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remodeling of the capillary to create a lumen around the clot, to restore blood flow around a clot
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What is phlebothrombosis?
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venous thrombosis
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A thrombus in the larger leg veins (saphenous) will likely become lodged where?
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pulmonary artery
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What is an embolism?
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a detached intravascular mass carried to a site distant from where it was formed
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What is a "saddle embolus"?
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pulmonary embolism that is between the pulmonary artery bifurcation
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What is a paradoxical embolism?
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an embolism that passes through a cardiac septum and enters from venous to systemic circulation (rather than becoming a pulmonary embolism); occurs in patients with septal defects
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Most systemic thrombi come form where?
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intercardiac mural thrombi (in the heart chambers)
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What type of embolism is seen in decompression sickness?
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gas/air embolism; nitrogen bubbles in circulation
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How does do deep sea divers get decompression sickness?
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underwater in high pressure, they breath nitrogen which enters blood in solution. but as they "depressurize/ascend to normal level", this nitrogen is no longer a solid particle in the blood solution, but now its a gas
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What is infarction?
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ischemic necrosis
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Why does the nature of the vascular supply determine whether or not infarction will occur?
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if an organ has multiple blood supplies (liver, lungs etc.), an occlusions may not lead to total ischemia
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What causes septic shock?
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inflammation as a result of bacterial infections leads to severe vasodilation and pooling of blood
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What causes cardiogenic shock?
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low cardiac output due to heart failure
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What causes hypovolemic shock?
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low blood volume after severe bleeding or burns perhaps
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What causes anaphylactic shock?
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allergic reaction; IgE hypersensitivity
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Toll-like receptors on neutrophils bind to what ligand?
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bacterial products
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Increased PAI leads to (more or less) fibrinolysis?
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more PAI =less t-PA = less fibrinolysis
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Hyperglycemia leads to (more or less) neutrophil function?
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less; diabetics are more likely to have bacterial infection
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What occurs during the progressive stage of shock?
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tissue hypo-perfusion/ischemia, acidosis; leads up to irreversible stage
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During the progressive stage of shock, why do we see acidosis?
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decreased oxygen to the tissue = more glycolysis = more lactic acid = acidosis
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What are some mechanisms the body can use as a reflex to combat shock?
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tachycardia, vasoconstriction, retention of fluid from kidneys; all serve to increase blood volume and pressure
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