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91 Cards in this Set
- Front
- Back
Virchow
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"father" of modern pathology; pronounced "Fir-co"
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Virchow's Triad
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elements contributing to thrombosis;
1) Endothelial injury (most important of the three!!) 2) Abnormal blood flow 3) hypercoagulability |
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Pathology
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study of derangement of molecules, cells, tissues, and functions occuring in LIVING organisms in response to injurous agents and deprivations
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Disease
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abnormal body process with characteristic set of signs or symptoms that may affect the whole body or any of its parts
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Etiology
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study of cause of diseases
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Pathogenisis
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step by step development of a disease or how it happened
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Signs or symptoms
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abnormality indicative of disease; signs ONLY in vet med
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Lesion
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abnormality or "hurting"-what happened, functional or morhpological change or both
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Differential diagnosis
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two or more diseases with similar signs; DDX
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Diagnosis
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identification of a disease
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What 4 enzymes does Ca++ stimulate that lead to cell injury?
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1) ATPases-lead to breakdown of ATP, leaving less fuel for the Na/K pump
2) Proteases- disrupt cytoskeleton of the cell 3) Phospholipases-decrease in phospholipids 4) Endonucleases-damage to chromatin in nucleus |
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Prognosis
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prediction of the outcome of a disease
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Pathognomonic
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characteristic or indicative for a specific disease; classic example is Negri bodies seen only in rabies
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Pathogenicity
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ability to cause disease
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Biopsy
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removal of tissue from LIVING patients for diagnostic histopathological exam; removal of tissue from a dead animal is NOT a biopsy
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Zoonosis
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disease transmissible from animal to man
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Injury
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damage or pathologic alterations in molecules and sturcture that can occur in cells and extracellular componants or tissues
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Adaptation
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changes in function and structure that maintain a homeostatic state and maintain cell viability; it must be able to revert back to its original state (ie dysplasia is NOT and example of adaptation)
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Reversible injury
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pathologic alterations in cell molecules and structure that are associated with abnormal function and with loss of homeostatic state; cells MAY recover if injury or stress are removed.
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Homeostasis
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("homeo"-similar, like, resembling) tendency to stability in the normal body states of the organism
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Irreversible cell injury and cell death
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damage to cell reaches magnitude or duration where the cell passes a "point of no return;" the cell cannot recover and dies. Characterized by pyknosis, karyorrhexis, and karyolysis.
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Necrosis
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death of cells or tissues through injury or disease, especially in a localized area of the body; WILL be accompanied by inflammation
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Aoptosis
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programmed celll death or necrobiosis; specialized form of cell death that is often mediated by specific receptor mediated stimuli or by loss of signals on well differentiated cells; occurs both physiologically and pathologically; NO inflammation
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Pyknosis
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nuclear shrinkage with increased basophilia
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Karyorrhexis
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fragmentation of chromatin
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Karyolysis
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dissolution of chromatin
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Autolysis
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hydrolytic changes that occur to cell and tissues after somatic death; the destruction of tissues or cells of an organism by the action of substances, such as enzymes, that are produced within the organism; NO inflammation
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What 3 enzymes inactivate free radicals?
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1) Superoxide dismutase
2) Glutathione peroxidase 3) Catalase |
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Free radical
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chemical species that has a single unpaired electron in an outer orbital; examples are superoxide radicals, hydrogen peroxide, and hydroxyl ion
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Atrophy
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decrease in cell size (decrease in cell substance) due to decrease in functional demand or lack of nutrients, oxygen, endocrine stimulation, or nerve stimulation
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Hypertrophy
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increase in cell size/substance
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Hyperplasia
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increase in cell numbers
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Metaplasia
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replacement of one adult cell type with another (reversible process)
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Zenker's necrosis
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coagulation necrosis in striated muscle
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Dysplasia
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abnormal cell growth-a pre-neoplastic increase in number of epithelial cells; cells are different shapes, sizes, and orientations; localized dysplasia= carcinoma-in-situ (NOT sarcoma!!!)
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Dystrophic calcification
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abnormal calcuim deposit in dead or degenerating tissues; occurs after cell injury
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Metastatic calcification
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abnormal calcium deposition in "normal" tissues SECONDARY TO HYPERCALCEMIA
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Amyloidosis
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accumulation of abnormal proteinaceous substances from several protein sources with eosinophilic staining properties that accumulates between cells; has beta pleated sheet formation
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Pneumoconiosis
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accumulation of particulate matter within the lung (anthracosis, silicosis, asbestosis; asbestosis may cause malignant tumor mesothelioma.
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Endogeouus cell pigments
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substances produced by the organism/cell; accumulate when they are produced in quantities that exceed the cell's ability to metabolize or secrete them; or if the cell is lacking enzymatic capacity to metabolize them
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Exudate
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fluids, cells, or other cellular substances that are slowly discharged from blood vessels usually from inflamed tissues; ACIDIC!! (exudAte and Acidic both have only one A!) thick and more puss-like
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Lipofuscin
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aka ceroid, "pigment of brown atrophy," composed of lipid-protein complexes derived from the peroxidation of lipid in cell membranes (free radical damage); accumulates in cells over time as a "wear and tear" pigment; increased by a vitamin E deficiency; seen most commonly in heart, liver, and brain
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Transudate
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fluids that pass through a membrane or squeeze through tissue or into the extracellular space of tissues; ALKALINE!! (trAnsudAte and AlkAline both have two A's!) thin and watery
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Hemosiderin
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derived from hemoglobin breakdown; erythrocyte phagocytosis leads to release of iron from hemoglobin; do not confuse with artifact acid hematin, hemosiderin stains with Prussian blue.
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Bilirubin
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breakdown product from heme proteins derived from hemoglobin and from other heme groups, such as cytochromes
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Jaundice (icterus)
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yellow discoloration of the skin, sclera, and mucous membranes due to elevated blood levels of bilirubin
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Melanin
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("melas"= black) formed by oxidation of tyrosine to DOPA in melanocytes by tyrosinase; distinguish from post-mortem pseudomelanosis
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Kwashiorkor
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protein malnutrition with adequate calorie intake
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Death
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characterized by cessation of vital signs
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Edema
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accumulation of abnormal amounts of fluid in the intracellular and extracellular tissue spaces of body cavities; may be generalized, such as asasarca, or localized, such as hypopericardium
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Three causes of hyperbilirubinemia (icterus)
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"HOT"
-H = hemolytic (increased breakdown of blood; PRE-HEPATIC) -O = obstructive (bile duct obstruction; POST-HEPATIC) -T = toxic (liver disease; HEPATIC) |
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Anasarca
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severe generalized edema of the subcutis
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Hydrothorx, hydropericardium, hydroperitoneum
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abnormal fluid accumulation on these body cavities
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Ascites
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hydroperitoneum-fluid in the abdominal cavity; often seen in RIGHT HEART FAILURE
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Congestion (aka Passive hyperemia)
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passive process characterized by decreased venous outflow; normal post-mortem occuance; does not indicate a pathologic process antemortem
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Hyperemia
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either active arteriolar dialation (increased inflow) OR passive decreased venous outflow
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2 names for decreased venous outflow:
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congestion or passive hyperemia
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Five causes of edema
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1) increased hydrostatic pressure
2) increased vascular permeability 3) decreased oncotic pressure=HYPOproteinemia/hypoalbuminemia (**HYPERproteinemia is NEVER the cause of edema!!!) 4) lymphatic obstruction 5) sodium retention in renal disease |
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Hemorrhage
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escape of blood from the cardiovascular system; different from congestion or hyperemia, where blood stays in the vascular system
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Petechiae
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pinpoint to 1-2mm diameter areas of hemorrhage
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Purpura
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intermediate size (in between petechiae and ecchymoses) areas of hemorrhage
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Ecchymoses
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blotchy, irregular, greater than 2-3cm diameter areas of hemorrhage
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Hematoma
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three diamentional area of hemorrhage trapped in tissue resulting in a grossly visable mass
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Hemorrhage per rhexis
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vessel rupture leading to hemorrhage
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Thrombosis
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process of INTRAVASCULAR (or intracardiac) formation of a clot of fibrin and platelets DURING LIFE
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Thrombus
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intravascular clot attached to the cardiovascular wall; its attachment to the wall is what lets you know it was formed ante mortem
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Embolus
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physical mass carries from its site of origin in the vessel wall to a more distant site; may be solid, liquid, or gas
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Thromboembolus
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embolus formed from a thrombus
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Blood clot
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clot of blood formed INTRAVASCULARLY AFTER DEATH or EXTRAVASCULARLY DURING LIFE OR AFTER DEATH
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Lines of Zahn
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concentric lines in an arterial thrombus formd by layers of platelets, fibrin, WBC's, and RBC's; not found in venous thrombi
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Hemostasis
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process resulting in termination of hemorrhage (like blood clotting)
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Coagulation
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formation of a fibrin clot
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Chicken fat clot
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clot formed in vitro or postmortem from leukocytes and plasma of sedimentatd blood; yellow color
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Currant jelly clot
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jelly-like mass of red blood cells and fibrin fromed by the in vitro or post-mortem clotting of whole or sedimentated blood; dark red in color
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Disseminated intravascular coagulation (DIC)
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widespread thrombosis of micorvascular bed with concurrent fibrinolysis and consumption of coagulation factors; sometimes called consumptive coagulopathy
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Infarct
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localized area of ischemic necrosis (**coagulative!!**) resulting from occlusion of the arterial or venous supply
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Shock
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a condition characterized by a reduction in tissue profusion and oxygen delivery below the levels required to meet normal demands; cardiogenic, hypovolemic, septic, or neurogenic shock; loss of fluid volume leading to hypovolemic shock might be from hemorrhage, vomiting, diarrhea, excessive sweating (hyperhidrosis), etc.
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Heart failure cells
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found in the LUNGS, not heart!! are macrophages full of hemosiderin as a result of chronic passive hyperemia (congestion) of the lung due to heart failure (left heart isn't beating effectively and not sending blood back out to the body, so blood becomes backed up in the lungs, leading to congestion). The RBC's squeeze out of the capillaries due to the pressure and the macrophages pick them up and break them down, eventually becoming full of hemosiderin.
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Epistaxis
*spelling! |
hemorrhage from the nose
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Hematemesis
*spelling! |
vomiting blood
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Hemoptysis
*spelling! |
coughing blood
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Melena
*spelling! |
black feces (particularly digested blood in feces); observed in animals with gastric ulcers; blood from lower in the GI tract (therefore undigested blood which will be red in color) is generally called hematochezia
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Hematuria
*spelling! |
blood in urine
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Hematorrhea
*spelling! |
copious hemorrhage
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Hemangioma
*spelling! |
tumor of newly formed blood vessels
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Hamartoma
*spelling! |
excessive but focal overgrowth of cells and tissues native to the area or site in which they occur (different from hematoma!!!)
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Hematochezia
*spelling! |
passage of blood in feces
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Hyperhidrosis
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excessive sweating
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Venous thrombi
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uniformly red in color, no Lines of Zhan (because of slower flow, RBC's have mixed with other cells and do not form these laminations); lumen of the vein is usually completely occluded
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Arterial thrombi
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usually only partially occluded (blocked) vessel; pale or white in color; has Lines of Zhan (because the blood is flowing quickly, the blood is not evenly mixed, resulting in laminations)
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Cardiac Tamponade
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fluid accumulation in the pericardial sack, resulting in ineffective pumping of blood, shock and possible death
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