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47 Cards in this Set
- Front
- Back
Anthracosis
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Anthracosis: Accumulation of carbon in the lungs from inhaled smoke or coal dust
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Pneumoconiosis
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Pneumoconiosis: A disease of the lungs, such as asbestosis or silicosis, Anthracosis) caused by long-term inhalation of particulate matter, especially mineral or metallic dust.
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Carotenoid pigments
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Fat soluble pigments of plant origin, includes precursors of Vit-A (B-carotene)
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cyanosis
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Non Oxygenated Hb: giving bluish appearance to skin & tissues, term cyanosis
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hemosiderosis
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hemosiderin accumulation is called: hemosiderosis
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Thrombosis
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Formation of a blood clot inside of a blood vessel
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Virchow's triad leading to thrombus formation
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endothelial injury
Abnormal Blood flow Hypercoagulability |
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Endothelial Cell Injury Pathogenesis
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EC injury leads to exposure of TF or subendothelial collagen or fibronectin which is the stimuli for platet aggregation and coagulation
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Some etiologies for endothelium injury
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CAV-1, Equine Morbillivirus ( hendra), EHV-1, Equine arteritis virus ( EAV), Pestviruses ( Hog cholera, BVD, Border dz., flaviviruses: WNV), Elephant endotheliotropic Herpesvirus
Bacteria: Salmonella typhimurium, manheimia haemolytic, erysipelothrix rhusiopathiae, hemophilus somnus |
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Altered Blood flow
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Stasis: reduced blood flow is more important in veins: Venous thrombosis ( Common in horses with occlusion of intestinal veins)
Turbulent flow: happens at narrowing of the vessel lumenor venous or lymphatic valves (disrupts laminar blood flow, physically can damage EC, and mixing of the blood can lead to a greater opportunity for coagulation factors) |
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Causes of Altered blood Flow
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Cardiac diseases, Hypovolemia, Aneurysm
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Hypercoagulabiliy ( thrombophilia)
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it is the lesser than frequent contributor to thrombotic states, it is associated with alteration of coagulation pathways
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Causes of Hypercoagulability
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-Inflammation, tissue necrosis ( increase in factor I)
-Trauma, acute illness, surgery, increased metabolism ( increase in Factors I, VIII) - Nephrotic syndrome ( Deficient ATIII, which is lost through damaged glomeruli) - heartworm disease, nephrotic syndrome, neoplasia ( increase in platelet activation) |
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Thrombus
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can develop anywhere in the cardiovascular system ( Cardiac chambers, valves, arteries, veins ,capillaries. Focally attached to the underlying vascular surface
***Propagation portion of a thrombus is often poorly attached and so it is prone to fragmentation --> emboli |
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Recanalization
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regrowth of endothelium over the surface of the scar produce narrowing of the vessel lumen.
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Embolus
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detached intravascular solid, liquid, gaseous masses that are carried by the blood to a site distant from its point of origin
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Venous Thromboemboli
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Typically end up in the pulmonary circulation ...pulmonary infarcts or right side heart failure
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Arteral Thromboemboli
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end up mostly within a smaller artery downstream from the site of the thrombuis, near a bifucation; infarction
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Cardiac Thromemboli
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end up mostly at the birfurcation of the external iliac arteries therefore producign a saddle thrombus
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infarcts
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seen in areas of ischemic necrosis
caused by occlusion of either arterial supply or the venous drainage The dominant histologic characteristic of infarcts is coagulative necrosis |
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Red Infarcts
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occur with venous occlusion in losse tissue, tissue with dual circulation ( lung, small intestine). Also seen when flow is reestablised to a site of previous arterial occusion and necrosis
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White infarcts
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occur with arterial occlusionin solid organs with end arterial circulation ( heart, spleen, kidney)
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What do factors I, V, and VIII all have in common?
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The all rely on thrombin to be activated
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Disseminated Intrvascular coagulation (DIC)
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manifestation of abnormal coagulation ( not a primary disease)
cause: any condition associated with widespread activation of thrombin |
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Septicmia
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Systemic infection of the blood with virulent bacteria that release their toxins
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Endotoxemia
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endotoxins (derived from gram negative bactera) Circulating in the blood
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Bacteremia
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presence of ive bacteria in the blood. Bacteremia precedes septicemia
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Shock
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it is the final common pathway for several potentially lethal clinical events including severe hemorrhage, extensive trauma or burns, diarrhea, microbial sepsis
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Three Types of Shock
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Cardiogenic shock
Hypovolemic shock septic shock |
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Cardiogenic shock
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failure of the heart to adequately pump blood
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Hypovolemic shock
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Decrease in circulating blood volume due to loss
caused by hemorrhage, fluid loss secondary to vomiting, diarrhea, burns. Leads to hypoperfusionS |
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Septic Shock
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Peripheral vasodilation and pooling of blood, endothelial cell activation/ injury, WBC induced damage, DIC, activation of cytokine cascade
causes: systemic immune reaction ( release of excessive vascular and inflammatory mediators) to bacterial or fungal infection, most commonly initiated by endotoxins ( LPS complex), less common: peptidoglycans, lipotheichic acids or G+. |
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What are the Effects of LPS on endothelium
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Inhibit production of anticoagulants ( TFPI, Thrombomodulin)
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What are the Effects of LPS on Monocytes and Macrophages
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Direct and indirect release of TNF, IL-2, IL-6, Chemokines
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LPS directly activates Factor XII
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initiates intrinsic coagulation pathway; and related XIIa activated pathways ( Kinin, fibrinolysis, complement)
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LPS directly activates the complement pathway
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generation on anaphylations ( C3a, C5a)
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Detrimental effects of LPS
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IL-1, TNFa and other cytokines; the secondary effects of these cytokines become more prominent
WHen? if the response is very pronounced like in heavy bacterial infections or when prolonged intestinal ischemia results in breakdown of the muscosal integrety and leakage of bacteria and toxins into the blood |
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Effects of inflammatory mediators: IL-1
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activates lymphacytes, increase EC expression of adhesion molecules (E-selectin, ICAM-1, 2, VCAM-1) that mediate WBC extravasation and secrete chemokines (CXCL8) that lead to the activation of WBCs
- Stimulate the production of nuetrophils and platelets by the BM - Acute-phase reaction: stimulates hepatocytes to synthesize increase levels of acute phase proteins in response to inflammation -In nervous system: acts on the brain to cause fever, lethargy, malaise, lack of appetite |
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Effects of inflammatory mediator: TNF
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activated vascular endothelium to express adhesion molecules and synthesis of chemokines
- Activates nuetrophile, macrophages, enhancing their microbialcidal activities -stimulates synthesis of acute phase proteins -In very large amounts it is the principal mediator in septic shock which leads to inhibition of muscle tone and cardiac contractility decrease blood pressure and shock |
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Stages of Shock
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- Non progessive: during which reflex compensatory mechanism are activated and perfusion of vital organs is maintained
-Progressive stage: characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances - Irreversible Stage: sets in after the body has incurred cellular and tissue injury that is so severe that even if the hemodynamic defects are corrected, no way to survive |
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Neurogenic shock
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Peripheral vasodilation
Mechanism: autonomic discharges lead to loss of vascular tone, peripheral pooling of blood as it occurs due to trauma, stress to the nervous system |
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Effects of inflammatory mediators: IL-1
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activates lymphacytes, increase EC expression of adhesion molecules (E-selectin, ICAM-1, 2, VCAM-1) that mediate WBC extravasation and secrete chemokines (CXCL8) that lead to the activation of WBCs
- Stimulate the production of nuetrophils and platelets by the BM - Acute-phase reaction: stimulates hepatocytes to synthesize increase levels of acute phase proteins in response to inflammation -In nervous system: acts on the brain to cause fever, lethargy, malaise, lack of appetite |
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Anaphylactic shock
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Systemic vasodilation and increase vascular permeability leads to hypptension and tissue hypoperfusion
Mechanism: interaction of Ag ( allergen, drug, vaccine) with Ig-E bound to mast cells which leads to widespread MC degranulation and realease of histamine and vasoactive mediators ( Type 1 hypersensitivity) |
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Effects of inflammatory mediator: TNF
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activated vascular endothelium to express adhesion molecules and synthesis of chemokines
- Activates nuetrophile, macrophages, enhancing their microbialcidal activities -stimulates synthesis of acute phase proteins -In very large amounts it is the principal mediator in septic shock which leads to inhibition of muscle tone and cardiac contractility decrease blood pressure and shock |
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Stages of Shock
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- Non progessive: during which reflex compensatory mechanism are activated and perfusion of vital organs is maintained
-Progressive stage: characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances - Irreversible Stage: sets in after the body has incurred cellular and tissue injury that is so severe that even if the hemodynamic defects are corrected, no way to survive |
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Neurogenic shock
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Peripheral vasodilation
Mechanism: autonomic discharges lead to loss of vascular tone, peripheral pooling of blood as it occurs due to trauma, stress to the nervous system |
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Anaphylactic shock
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Systemic vasodilation and increase vascular permeability leads to hypptension and tissue hypoperfusion
Mechanism: interaction of Ag ( allergen, drug, vaccine) with Ig-E bound to mast cells which leads to widespread MC degranulation and realease of histamine and vasoactive mediators ( Type 1 hypersensitivity) |