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91 Cards in this Set

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Virchow
"father" of modern pathology; pronounced "Fir-co"
Virchow's Triad
elements contributing to thrombosis;
1) Endothelial injury (most important of the three!!)
2) Abnormal blood flow
3) hypercoagulability
Pathology
study of derangement of molecules, cells, tissues, and functions occuring in LIVING organisms in response to injurous agents and deprivations
Disease
abnormal body process with characteristic set of signs or symptoms that may affect the whole body or any of its parts
Etiology
study of cause of diseases
Pathogenisis
step by step development of a disease or how it happened
Signs or symptoms
abnormality indicative of disease; signs ONLY in vet med
Lesion
abnormality or "hurting"-what happened, functional or morhpological change or both
Differential diagnosis
two or more diseases with similar signs; DDX
Diagnosis
identification of a disease
What 4 enzymes does Ca++ stimulate that lead to cell injury?
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
Prognosis
prediction of the outcome of a disease
Pathognomonic
characteristic or indicative for a specific disease; classic example is Negri bodies seen only in rabies
Pathogenicity
ability to cause disease
Biopsy
removal of tissue from LIVING patients for diagnostic histopathological exam; removal of tissue from a dead animal is NOT a biopsy
Zoonosis
disease transmissible from animal to man
Injury
damage or pathologic alterations in molecules and sturcture that can occur in cells and extracellular componants or tissues
Adaptation
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)
Reversible injury
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.
Homeostasis
("homeo"-similar, like, resembling) tendency to stability in the normal body states of the organism
Irreversible cell injury and cell death
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.
Necrosis
death of cells or tissues through injury or disease, especially in a localized area of the body; WILL be accompanied by inflammation
Aoptosis
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
Pyknosis
nuclear shrinkage with increased basophilia
Karyorrhexis
fragmentation of chromatin
Karyolysis
dissolution of chromatin
Autolysis
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
What 3 enzymes inactivate free radicals?
1) Superoxide dismutase
2) Glutathione peroxidase
3) Catalase
Free radical
chemical species that has a single unpaired electron in an outer orbital; examples are superoxide radicals, hydrogen peroxide, and hydroxyl ion
Atrophy
decrease in cell size (decrease in cell substance) due to decrease in functional demand or lack of nutrients, oxygen, endocrine stimulation, or nerve stimulation
Hypertrophy
increase in cell size/substance
Hyperplasia
increase in cell numbers
Metaplasia
replacement of one adult cell type with another (reversible process)
Zenker's necrosis
coagulation necrosis in striated muscle
Dysplasia
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!!!)
Dystrophic calcification
abnormal calcuim deposit in dead or degenerating tissues; occurs after cell injury
Metastatic calcification
abnormal calcium deposition in "normal" tissues SECONDARY TO HYPERCALCEMIA
Amyloidosis
accumulation of abnormal proteinaceous substances from several protein sources with eosinophilic staining properties that accumulates between cells; has beta pleated sheet formation
Pneumoconiosis
accumulation of particulate matter within the lung (anthracosis, silicosis, asbestosis; asbestosis may cause malignant tumor mesothelioma.
Endogeouus cell pigments
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
Exudate
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
Lipofuscin
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
Transudate
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
Hemosiderin
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.
Bilirubin
breakdown product from heme proteins derived from hemoglobin and from other heme groups, such as cytochromes
Jaundice (icterus)
yellow discoloration of the skin, sclera, and mucous membranes due to elevated blood levels of bilirubin
Melanin
("melas"= black) formed by oxidation of tyrosine to DOPA in melanocytes by tyrosinase; distinguish from post-mortem pseudomelanosis
Kwashiorkor
protein malnutrition with adequate calorie intake
Death
characterized by cessation of vital signs
Edema
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
Three causes of hyperbilirubinemia (icterus)
"HOT"
-H = hemolytic (increased breakdown of blood; PRE-HEPATIC)
-O = obstructive (bile duct obstruction; POST-HEPATIC)
-T = toxic (liver disease; HEPATIC)
Anasarca
severe generalized edema of the subcutis
Hydrothorx, hydropericardium, hydroperitoneum
abnormal fluid accumulation on these body cavities
Ascites
hydroperitoneum-fluid in the abdominal cavity; often seen in RIGHT HEART FAILURE
Congestion (aka Passive hyperemia)
passive process characterized by decreased venous outflow; normal post-mortem occuance; does not indicate a pathologic process antemortem
Hyperemia
either active arteriolar dialation (increased inflow) OR passive decreased venous outflow
2 names for decreased venous outflow:
congestion or passive hyperemia
Five causes of edema
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
Hemorrhage
escape of blood from the cardiovascular system; different from congestion or hyperemia, where blood stays in the vascular system
Petechiae
pinpoint to 1-2mm diameter areas of hemorrhage
Purpura
intermediate size (in between petechiae and ecchymoses) areas of hemorrhage
Ecchymoses
blotchy, irregular, greater than 2-3cm diameter areas of hemorrhage
Hematoma
three diamentional area of hemorrhage trapped in tissue resulting in a grossly visable mass
Hemorrhage per rhexis
vessel rupture leading to hemorrhage
Thrombosis
process of INTRAVASCULAR (or intracardiac) formation of a clot of fibrin and platelets DURING LIFE
Thrombus
intravascular clot attached to the cardiovascular wall; its attachment to the wall is what lets you know it was formed ante mortem
Embolus
physical mass carries from its site of origin in the vessel wall to a more distant site; may be solid, liquid, or gas
Thromboembolus
embolus formed from a thrombus
Blood clot
clot of blood formed INTRAVASCULARLY AFTER DEATH or EXTRAVASCULARLY DURING LIFE OR AFTER DEATH
Lines of Zahn
concentric lines in an arterial thrombus formd by layers of platelets, fibrin, WBC's, and RBC's; not found in venous thrombi
Hemostasis
process resulting in termination of hemorrhage (like blood clotting)
Coagulation
formation of a fibrin clot
Chicken fat clot
clot formed in vitro or postmortem from leukocytes and plasma of sedimentatd blood; yellow color
Currant jelly clot
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
Disseminated intravascular coagulation (DIC)
widespread thrombosis of micorvascular bed with concurrent fibrinolysis and consumption of coagulation factors; sometimes called consumptive coagulopathy
Infarct
localized area of ischemic necrosis (**coagulative!!**) resulting from occlusion of the arterial or venous supply
Shock
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.
Heart failure cells
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.
Epistaxis
*spelling!
hemorrhage from the nose
Hematemesis
*spelling!
vomiting blood
Hemoptysis
*spelling!
coughing blood
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
Hematuria
*spelling!
blood in urine
Hematorrhea
*spelling!
copious hemorrhage
Hemangioma
*spelling!
tumor of newly formed blood vessels
Hamartoma
*spelling!
excessive but focal overgrowth of cells and tissues native to the area or site in which they occur (different from hematoma!!!)
Hematochezia
*spelling!
passage of blood in feces
Hyperhidrosis
excessive sweating
Venous thrombi
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
Arterial thrombi
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)
Cardiac Tamponade
fluid accumulation in the pericardial sack, resulting in ineffective pumping of blood, shock and possible death