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61 Cards in this Set
- Front
- Back
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Pathognomonic lesion |
a lesion that is so characteristic it can only be caused by on disease |
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What should be included in the description of a lesion? |
size (metric) color consistency shape surface distribution margins location |
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What are the Etiologic categories |
Matabolic Inflammatory neoplastic infectious vascular anomalies of development nutritional idiopathic traumatic toxic iatrogenic |
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pathogenesis |
steps involved in development of a lesion or disease |
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Cell injury is ____________, Cell death is ______ |
cell injury is reversible, cell death is not |
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What are causes of cell injury? |
hypoxia/ ischemia free radicals |
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how does hypoxia injure cells? |
1. decreases oxidative phosphorylation and ATP production 2. membrane pumps fail leading to a build up of sodium, water, and calcium 3a. accumulation of water leads to hydroid degeneration 3b. excess calcium activates lots of -ases |
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Build up of calcium in hypoxic cells leads to what? |
activation of: - endonucleases- destroy cell DNA - proteases- destroy proteins - ATPases- destroy what little ATP there is - phospholipases- destroy cell membrane |
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what are sources of free radicals |
radiation injury toxicity inflammation normal cell function (biggest source) |
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What effects to free radicals have on cells? |
membrane lipid peroxidation protein cross linking and peroxidation DNA fragmentation |
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Response to cell injury depends on what? |
type of cell nutrition (antioxidant levels) previous injury reperfusion injury |
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how does previous injury affect a cells response to current injury? |
previous injury up regulates heat shock proteins - these act intracellularly to recognize, bind, refold, chaperone, and degrade proteins - when a cell is injured again it is already primed with these proteins to respond to damage |
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What is reperfusion injury? |
Restoring blood flow to ischemic tissue resulting in increased damage - due to deliver of abundant free radicals with the oxygen -due to neutrophil infiltration which damages what viable tissue there is by attacking all the damage |
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What are examples of intercellular accumulations causing cell injury? |
- fatty change - glycogen accumulation - hydropic degeneration |
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Mechanisms of fatty change |
1. excessive entry of fatty acids 2. defective oxidation of fatty acids- anoxia, toxins 3. decreased apoprotein synthesis- protein malnutrition 4. defective secretion of lipoproteins- toxins (alcohol) |
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Gross morphology of fatty change |
organ is enlarged, friable, and tan-yellow may float if change is severe |
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histologic morphology of fatty change |
clear, round, discrete cytoplasmic vacuoles |
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what is the difference between fatty infiltration and fatty change |
fatty infiltration is the movement of adipose cells into non-adipose tissue- does not affect function fatty change is the accumulation of lipid inside cells- affects function |
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Examples of glycogen accumulation |
1. canine steroid hepatopathy 2. diabetes mellitus 3. Storage diseases 4. Neonatal animals normally have abundant glycogen in hepatocytes |
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what is canine steroid hepatopathy |
excess glucocorticoids cause excess glycogen to be produced and it accumulates in hepatocyte cytoplasm |
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Canine steroid hepatopathy gross morphology |
liver is enlarged, orange-brown, and firable |
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Canine steroid hepatopathy histologic morphology |
midzonal hepatocytes are swollen with cleared cytoplasm (but not completely round like lipid) |
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Hydropic degeneration |
transient and reversible cell swelling that follows ischemia cells are enlarged with clear water cytoplasm (looks identical to glucose accumulation but hardly ever see it because it is so transient) |
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necrosis |
death of cells prior to death of an organism |
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infarct |
focal area of ischemic necrosis |
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gross changes associated with cell death |
softening color change ulceration |
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ulceration |
full thickness necrosis and loss of an epithelial or mucosal surface |
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erosion |
partial thickness loss of an epithelial or mucosal surface |
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malacia |
softening of necrotic tissue in CNS |
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microscopic changes associated with cell death |
nuclear changes - pyknosis - karyorrheis - karyolysis cytoplasmic changes- increased eosinophilia |
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types of stains |
hematoxylin- stains DNA, and RNA mineral blue eosin- stains protein pink to red |
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pyknosis |
shrunken densely basophilic nucleus |
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karyorrhexis |
fragmented nucleus |
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karyolysis |
faded or absent nucleus |
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host reactions to necrosis |
local inflammation- release of cell content stimulates host response systemic reaction- occurs only if significant amount of cell contents enter circulation |
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hyperemia |
sign of local inflammation where a red line surrounds necrotic tissue |
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leukocyte infiltrate |
local inflammatory response to necrosis where white line surrounds necrotic tissue |
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coagulative necrosis |
- can affect any tissue - tissue is dead but maintains architecture |
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causes of coagulative necrosis |
ischemia (infarct)- focal lesion toxins- diffuse lesions |
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liquefactive necrosis |
- can affect any tissue - tissue becomes liquified and architecture is lost |
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causes of liquefactive necrosis |
- bacterial infection - neutrophilic infiltration -- abcesses -- malacia - not necessarily due to bacterial infection, can also be caused by toxins or ischemia |
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caseous necrosis |
- can affect any tissue - architecture is lost, but tissue is solid and friable - frequently present at center of granuloma |
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causes of caseous necrosis |
specific bacterial infections (such as mycobacterium spp. ) - ie. tuberculosis - ie. caseous lymphadenitis |
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Enzymatic fat necrosis |
aka pancreatitis (primary in dogs and cats, secondary in ruminants) 1. pancreas releases enzymes 2. enzymes digest abdominal fat 3. precipitation of calcium (mineralization) to saponify fat |
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appearance of fat necrosis |
gross: chalky, opaque, white spots in abdominal fat (soft or firm, not hard or gritty) microscopic: adipocytes become red (dead) then blue (mineralized) |
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Nutritional/ Toxic fat necrosis in carnivores |
only in fish eating carnivores - cats because they aren't made to eat a lot of fish - herons when they eat a lot of rancid fish fish (particularly when rancid) deplete antioxidants because they are high in oxidized fats--> free-radical damage to adipose tissue |
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Nutritional/ toxic fat necrosis of carnivores appearance |
gross: generalized yellow-orange fat microscopic: adipose cells become red then blue but with additional yellow pigment |
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gross appearance of nutritional/toxic fat necrosis in ruminants |
very firm opaque abdominal fat that may obstruct intestines or mimic pregnancy |
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predisposing factors for nutritional fat necrosis in ruminants |
- grazing fescue - genetics (jersey and guernsey) - increasing age |
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dry gangrene |
coagulative necrosis (typically ischemic) |
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wet gangrene |
liquefactive necrosis (involves bacteria) |
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gas gangrene |
necrosis with gas production (specific bacteria |
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apoptosis |
a distinct form of cell death also called programmed cell death - can be physiologic or pathogenic |
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forms of physiologic apoptosis |
- embryogenesis
- immune tolerance - autoreactive lymphocytes undergo apoptosis - regression of temporary tissues- uterine involution - tissue homeostasis- with mitosis comes apoptosis |
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forms of pathologic apoptosis |
- virus induced - viral inhibition of apoptosis (pox virus) - autoimmunity- mutations decreasing apoptosis - neoplasia- inactivation of genes regulating apoptosis |
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steps of apoptosis |
1. signaling 2. control 3. execution 4. removal (phaogcytosis) |
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signals for apoptosis |
-irreparable DNA damage -binding by a receptor marking for death -lack of necessary factors (growth factors and/or hormones) necessary for continued life |
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control of apoptosis |
determines whether a cell will commit to or abort apoptotic pathway - typically dependent on the action of another molecule outside or within the cell |
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execution of apoptosis |
mediated by capsizes which activate other enzymes to destroy the cell |
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removal of cells following apoptosis |
following destruction, surface membrane phospholipid is flipped to outside phagocytes recognize this and engulf dead cells |
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morphology of apoptosis |
cell shrinkage apoptotic bodies (small dark fragments of nucleus) only affects single cells (contrast necrosis) |
