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38 Cards in this Set
- Front
- Back
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Q: Define edema.
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-excess fluid in the interstitial spaces
-depending on the site, fluid collections can be called hydrothorax, hydroperitoneum (ascites), or hydropericardium |
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Q: What is anasarca?
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-when edema is generalized and severe, have profound subQ tissue swelling
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Q: What edementous complication occurs with left heart failure?
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-pulmonary edema is a common problem seen with left heart failure. edema fluid fills alveoli and interstitial tissue. rupture of alveolar capillaries can occur with macrophages ingesting hemosiderin to form heart failure cells
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Q: What is the difference between exudate and transudate?
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-exudate-because of INC vascular permability, inflammatory edema is a protein-rich exudate, with a specific gravity greater than 1.020
-transudate-the edema fluid occurring in hydrodynamic derangements is typically protein-poor transudate, with a specific gravity below 1.012 |
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Q: What are the various causes of edema?
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-INC hydrostatic pressure-as in CHF, cirrhosis of the liver, or dependent edema
-DEC colloid osmotic pressure-loss of protein as in nephritic syndrome, or malnutrition, protein losing gastroenteropathy or cirrhosis of the liver -lymphatic obstruction-post surgical lymphadenopathy, malignancy or filarial -sodium retention-INC sodium intake -inflammation-the tumor resulting form diapedesis of exudate |
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Q: Define active hyperemia.
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-is the INC in blood in an area in response to vascular dilation, as seen in infections of the skin or elsewhere-“tumor, calor, rubor”
-can result from augemented tissue inflow because of arteriolar dilation, as in skeletal muscle during exercise or at sites of inflammation, affected area is redder because of INC blood flow |
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Q: Define passive hyperemia.
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-Passive hyperemia or congestion, as in chronic passive congestion, results from an increase in venous pressure. For example, when the left side of the heart fails and the pressure increases in the pulmonary vascular bed, fluid then leaks into the alveoli (pulmonary edema), oxygen transfer is reduced and the patient becomes cyanotic. When the right side fails, the backup extends to the liver resulting in a “nutmeg liver” chronic passive congestion of the liver) as well as increased pressure in the venous systemic circulation.
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Q: What are the pathological findings associated with hyperemia?
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-hepatomegaly, pulmonary edema, splenomegaly, heart failure cells, ascites
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Q: Define hematoma.
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-accumulation of blood in tissue
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Q: Define petechia/petechiae.
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-minute hemorrhages, pinpoint to pinhead
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Q: Define purpura.
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-larger hemorrhages
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Q: Defin ecchymosis.
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-same as purpura
-get color changes (fresh hemoglobin is red/blue, bilirubin is blue/gree, hemosiderin is golden brown) |
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Q: What is the role of vasoconstriction is hemostasis.
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-after initial injury, there is a brief period of arteriolar vasoconstriction, largely attributable to reflex neurogenic mechanisms and augmented by the local secretion of factors such as endothelin (a potent endothelium-derived vasoconstrictor). the effect is transient however, and bleeding would resume if not for activation of the platelet and coagulation systems
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Q: What is the role of the endothelium in hemostasis?
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-endothelial injury exposes highly thrombogenic subendothelial extracellular matrix (ECM), which allows platelets to adhere and become activated, that is, undergo a shape change and release secretory granules. within minutes, the secreted products have recruited additional platelets (aggregation) to form a hemostatic plug, this is the process of primary hemostasis
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Q: What is the role of tissue factor in hemostasis?
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-tissue factor is exposed at the site of injury. it acts in conjunction with the secreted platelet factors to activate the coagulation cascade, culminating in the activation of thrombin. thrombin converts circulating soluble fibrinogen to insoluble fibrin, resulting in local fibrin deposition, thrombin also induces further platelet recruitement and granule release. this sequence (secondary hemostasis) takes longer than the initial platelet plug
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Q: What is the role of fibrin and platelet aggregates in hemostasis?
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-polymerized fibrin and platelet aggregates form a solid, permanent plug to prevent any further hemorrhage. at this stage, counterregulatory mechanisms are set into motion to limit the hemostatic plug to the site of injury
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Q: What is Virchow’s triad?
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-the three primary influences that predispose one to thrombus formation
-are endothelial injury, stasis or turbulence of blood flow and blood hypercoagulability |
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Q: Describe endothelial injury in Virchow’s triad.
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-can be traumatic or inflammatory, may be caused by hypertension dynamics, bacterial endotoxins or other factors
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Q: Describe alteration of blood flow.
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-turubulence as from atherosclerotic plaques or aneurysms, stasis and turbulence disrupt laminar flow and bring platelets into contact with the endothelium, prevent dilution of activated clotting factors by fresh flowing blood, retard the inflow of clotting factor inhibitors and permit the build of thrombi, and promote endothelial cell activation, predisposing to local thrombosis, leukocyte adhesion and a variety of other endothelial cell effects
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Q: What are the primary (genetic) causes for hypercoagulability?
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-common-mutation in factor V gene, mutation in prothrombin gene, mutation in methyltetrahydrofolate gene
-rare-antithrombin III deficiency, protein C deficiency, protein S deficiency -very rare-fibrinolysis defects |
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Q: What are the secondary (acquired) causes for hypercoagulability?
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-high risk for thrombosis-prolonged bed rest or immobilization, MI, A. fib, tissue damage, cancer, prosthetic cardiac valves, DCI, heparin-induced thrombocytopenia, antiphospholipid Ab syndrome (lupus)
-low risk-cardiomyopathy, nephritic syndrome, hyperestrogenic states (pregnancy), oral contraceptive use, sickle cell anemia, smoking |
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Q: Describe thrombosis.
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-usually occurs in the legs or pelvis
-superficially are usually benign and characterized by erythema, heat, pain and edema (treat with elevation, heat and ASA) -deep ones (popliteal), about 50% have silent PE (treat with anticoagulants) |
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Q: What are the diagnostic tests for thrombosis?
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-venography, impedance plethysmography, and venous duplex (pulse wave Doppler with ultrasound (gold standard))
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Q: What is the difference between ante morten thrombi and post mortem clots?
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-ante mortem thrombi are firm, friable and adherent
-post mortem clots are soft and rubbery, elastic, not adherent and associated with a yellow coagulum “chicken-fat” clot -A thrombus is an ante mortem structured solid mass of blood constituents that form in the cardiovascular system. It is composed of platelets, fibrin and entrapped rbcs. Layers of platelets then fibrin and varying numbers of red cells form distinct definable lines which are called the lines of Zahn. |
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Q: What is a mural thrombi?
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-Mural thrombi form on the wall of a structure, such as a heart chamber or aneurysm.
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Q: What is the difference between phlebotrhombosis and thrombophlebitis?
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-Phlebothrombosis and thrombophlebitis are terms used synonymously, but by definition phlebothrombosis is formation of a thrombus in a vein without primary inflammation and thrombophlebitis implies inflammation of a vein with secondary thrombus formation.
-An entity named “migratory thrombophlebitis” or “thrombophlebitis migrans” in which thrombi form spontaneously in various veins and disappear, also known as Trousseau’s sign, is associated with visceral cancers. |
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Q: What is the fate of a thrombus?
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1. propagation-the thrombus may accumulate more platelets and fibrin, eventually leading to vessel obstruction
2. embolization-thrombi may dislodge and travel to other sites in the vasculature 3. dissolution-thrombi may be removed by fibrinolytic activity 4. organization and recanalization-thrombi may induce inflammation and fibrosis (organization) and may eventually become recanalized, that is, may reestablish vascular flow, or may be incorporated into a thickened vascular wall |
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Q: Define embolism.
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-Practically all emboli result from a dislodged part of a thrombus. Rarely, other substances can act as emboli, such as fat, air, nitrogen, cholesterol as atherosclerotic debris, tumor fragments, bone marrow, amniotic fluid, foreign bodies
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Q: Describe a pulmonary thromboemoblism.
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-origin from deep leg veins(calf, popliteal, femoral, iliac can be small and usually does not cause infarction)
-large saddle emboli can obstruct 60% or more of the pulmonary artery and cause sudden death. -pulmonary embolism is extremely common and preventable, dyspnea is the most common symptom -diagnose with scan, radiography or angiography |
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Q: Define infarction.
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-Most common cause is obstruction of arterial blood supply resulting in ischemic (coagulative) necrosis
-Venous obstruction as would occur after twisting about a pedicle, such as testicular torsion, or volvulus. The venous drainage becomes occluded. The arterial supply continues though decreased. The tissue becomes engorged. Oxygen is depleted and ischemic necrosis occurs. -A single source of blood as an end artery occlusion results in a pale or bloodless or white infarct. -If there is a dual blood supply, as in the lung or numerous collateral vessels as in the intestine, then blood can flow into the necrotic area and the infarct is red (hemorrhagic). |
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Q: What is the fate of an infarct?
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-Infarcts will heal and fibrous scar is the eventual result
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Q: Define shock.
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-Shock constitutes systemic hypoperfusion due to reduction either in cardiac output or in the effective circulating blood volume. This results in hypotension followed by impaired tissue perfusion and cellular hypoxia.
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Q: What are the three general categories of shock?
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-cardiogenic, hypovolemic, septic
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Q: Describe cardiogenic shock.
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-results from myocardial pump failure, this may be caused by intrinsic myocardial damage (infarction), ventricular arrhythmias, extrinsic compression, or outflow obstruction
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Q: Describe hypovolemic shock.
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-results from loss of blood or plasma volume, this may be caused by hemorrhage, fluid loss form severe burns or trauma
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Q: Describe septic shock.
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-is caused by systemic microbial infection, most commonly, this occurs in the setting of gram-negative infections (endotoxic shock), but it can also occur with gram-positive and fungal infections
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Q: Describe the pathogenesis of septic shock.
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1. Recent reviews indicate that gram negative bacteria producing endotoxin and gram positive bacteria are about equal as causative factors. Other causative agents include viruses, fungi and protozoa and other certain bacterial proteins.
2. Lipopolysaccharides (LPS) are released when bacterial cell walls are degraded. 3. LPS activates monocytes and macrophages (devours offending organism) 4. LPS directly activates complement (bacteria removal ) 5. Monocytes respond to LPS producing tumor necrosis factor (TNF) 6. TNF induces (interleukin) IL-1 synthesis (enhanced inflammatory response) 7. The degree of involvement varies from local inflammatory reactions to systemic effects to septic shock. |
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Q: Describe the morphology of shock.
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-The changes in vital organs are related to the degree of susceptibility of cells to hypoperfusion and anoxia.
-Examples include Brain (ischemic encephalopathy), Heart (focal and widespread coagulation necrosis), Kidneys (acute tubular necrosis), lungs (ARDS (Adult Respiratory Distress Syndrome)), Adrenals (cortical lipid cell depletion), GI tract (mucosal hemorrhage and necrosis), Liver (fatty change and centrolobular necrosis) |
