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56 Cards in this Set
- Front
- Back
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general pathology
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basic reactions or processes common to most tissues
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systemic pathology
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specific responses or processes in specific organs or tissues
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Aspects of disease (4)
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etiology- causation/origination
morphological changes pathogenesis- mechanism by which disease occurs functional changes |
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manifestations of pathological processes (4)
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gross morphology
histomorphology (light microscop) see with electron microscope (good for kidney analysis) biochemistry (blood tests) |
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how does a cell respond to injury?
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normal homeostatic mechanisms can allow for the cell to adapt in response to some stress (reversible injuries). however if the stress becomes too great, the cell will either undergo apoptosis, or continue with decreased function (like heart muscle during hypertension) which may lead to other disease
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morphology of necrosis
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white/yellow tissue
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etiology of cell injury- acquired (6)
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immunological
nutritional physical chemical infectious (virus, bacteria) hypoxia/ischemia |
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etiology of cell injury- intrinsic (genetic)
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genetic mutations
aging |
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sites of vulnerability to cell injury
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cell membranes, DNA, aerobic respiration, protein synthesis
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morphological change follows...
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biochemical change ergo it is time dependent
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common biochemical themes in cell injury mechanisms (4)
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cell membrane permeability- allows ions to enter cell (increases osmolality of cell- cell swelling)
ATP O2 Calcium- often occurs along with loss of ATP to drive ion pumps |
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loss of ATP results in... (2)
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loss of membrane transport
no biosynthesis (can't make proteins, lipids, etc) |
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calcium excess comes from_______and results in...
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comes from ER and mitochondria intracellular/or extracellular
causes downstream effects like activate ATPases (further run out of energy) activate phospholipases (cleave lipids to damage membrane even more) activate proteases to attack cell membrane and other cytoplasmic proteins can activate nucleases |
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oxygen's role in cell injury (2)
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1) deficiency in O2 results in decreased aerobic respiration
2) too much O2 (sudden reperfusion) triggers--> ROS-->oxidation |
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where do ROS come from (2)
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external agents
from inside certain cells (neutrophils) |
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ROS mechanism in cell injury (3)
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1) lipid peroxidation- breakdown of lipids (especially polyunsaturated fatty acids)
2) oxidative modification of proteins (e.g. sulfylhydryl crosslinking, nitrotyrosine) 3) DNA damage (nuclear/mitochondrial) |
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examples of ROS (3)
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hydrogen peroxide
oxygen free radicals (VERY reactive a.k.a superoxide) hydroxyl free radicals |
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what causes ROS to form? (5)
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radiation
inflammation (e.g. neutrophils) Oxygen toxicity chemicals reperfusion injury |
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hypoxia and it's subtypes (3)
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low amounts of oxygen
1) asphyxia- blockage of breathing 2) anoxia- no oxygen delivery 3) ischemia- blockage of blood supply (not delivering O2 AND nutrients). dmg usually worse due to loss of nutrients in addition to O2 |
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events in cell injury that are reversible (5)
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decreased respiration/loss of ATP- you can make more ATP if you fix it
glycogenolysis/glycogen depletion (again, you can make more) reduction in intracellular pH (lactic acid)- causes clumping of chromatin (due to protein changes?) byproduct of glycogenolysis (why?) Failure of membrane transport systems (water accumulation) Decrease in protein synthesis/detachment of ribosomes |
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events in cell injury that are irreversible (3)
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massive influx of calcium
membrane damage (due to proteases, phospholipases, ROS- get abnormal cytoskeleton) intracellular release of lysosomal enzymes (DNase, RNase, protease) |
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final pathways leading to cell death
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decrease in ATP-->lipid/protein synthesis
increase in Ca++-->production of protease and phospholipase increase in ROS--> peroxidizes membranes CELL MEMBRANE DAMAGE |
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morphology of cell injury- reversible (what are they, what causes them)
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hydropic changes (swelling of cell)
fatty change (e.g. liver cells)- due to alteration of lipid metabolism |
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morphology of cell injury- irreversible
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necrosis: morphology is result of autolysis, denaturation of proteins
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morphology of necrosis (4)
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1) hypereosinophilia- cells become red; breakdown of nuclei acid (which take up blue stain) and also denaturing proteins which makes them take up acid stains (eosin)
2) cytoplasmic vacuolization 3) nuclear changes (pyknosis- condensation of chromatin, karyorrhexis- fragmentation, disappearance) 4) later, coagulation or liquefactive necrosis |
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contraction bands
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denatured contractile proteins
indicative of myocardium necrosis |
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coagulative necrosis (give an example)
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preservation of cell outline
e.g. myocardial infarction |
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liquefactive necrosis (2 properties, and example)
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heterolysis- apoptosis in response to extracellular hydrolytic enzymes
loss of cell outline/structure e.g. bacterial abscess due to collection of neutrophils |
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infarction
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coagulative necrosis with a specific cause, being ischemia
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caseous necrosis (and example)
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"cas" = cheese
granulomatous inflammation that occurs in response to TB cell outlines lost, but does not entirely liquefy (semisolid) |
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granuloma
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small nodule of macrophages attempting to wall off a foreign substance
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fat necrosis (example)
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saponification (digestive enzymes break down fat, which complexes with Ca++, making soap) of fatty tissue
e.g. acute pancreatitis |
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dry gangrene vs. wet gangrene
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specific type of necrosis that is way advanced
dried up before chance of bacterial infection = dry involvement of bacteria = wet |
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gas gangrene
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bacteria release gas, open up tissue to make space for travel.
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2 types of cell death
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necrosis- irreversible cell injury
apoptosis |
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apoptosis is involved in what biological processes? (4)
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1) development
2) proliferating tissues 3) hormone-related (breast, uterus) 4) response to injury |
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apoptotic bodies
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breakage of cytoplasm from cell for engulfment by phagocytes (flipping of cell membranes become receptors for phagocytes)
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histology of apoptosis
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small, shrunken and hyperchromatic (dark) nuclei, some of which are broken into small fragments.
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necrosis vs. apoptosis:
physiological/non-physiological regulation energy requirements effects on DNA effects on cell membrane inflammatory response? death of groups of cells or individual |
1) necrosis is non-physiological, apoptosis can be both
2) necrosis is not regulated, apoptosis is 3) apoptosis requires ATP, while necrosis does not 4) necrosis DNA is cleaved randomly, while apoptosis DNA is cleaved by endonuclease (phosphodiester bonds) 5) necrosis cell membrane dissolves/leaky, apoptosis is fine 6) necrosis involves death of groups/areas, apoptosis is single cell 7) necrosis gives rise to inflammatory, apoptosis does not because they are taken up rapidly by macrophages |
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2 inducers of apoptosis and pathway
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withdrawal of trophic factors (hormones, growth factors)-->cytochrome C released from mitochondria-->activates caspases-->cascade-->protein/DNA breakdown
OR activation of death receptors (fas) directly activates caspase cascade |
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bcl-2
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regulatory protein
inhibits release of cytochrome C |
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3 kinds of initiation for apoptosis
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1) withdrawal of trophic factors
2) injury- ROS, radiation, toxins 3) death receptor ligand interactions (fas, TNF) |
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3 pathways of integration for apoptosis after initiation
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1) trophic-->cytochrome C-->caspase
2) injury-->DNA affected-->p53 3) death receptor activation-->caspase |
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2 execution pathways for apoptosis (what does caspase do)
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activates endonucleases
catabolizes cytoskeleton into apoptotic bodies |
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adaptions to cell injury (2)
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1) induction of smooth ER- more ER = more toxin removal (esp. in liver)
2) lysosomal degradation of damaged organelles (autophagy) |
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responses that are adaptive but also pathological (2)
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hypertrophy and hyperplasia
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benign prostatic hyperplasia
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hyperdivision of cells in prostate; bigger prostate. sometimes mistakenly referred to as prostatic hypertrophy
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what can cause hypertrophy of muscle, and specifically in the heart, what will that lead to?
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stressing the muscle constantly
loss of contractile function-->CHF |
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alzheimer brain in the late stages shows...
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atrophy of brain tissue
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metaplasia
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replacement of one type of differentiated cell by another type
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barretts metaplasia of the esophagus
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stratified squamous epithelial cells of esophagus changes into columnar cells-->high risk for adenocarcinoma
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many diseases have this at the root of the problem
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accumulation of abnormal material or excessive accumulation of normal material
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mechanisms of intracellular accumulation (4)
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abnormal metabolism
abnormal protein folding or transport (e.g. protein cannot be transported from liver = liver dmg) genetic enzymatic effect incomplete lysosomal degradation |
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some examples of accumulation and pathological effects (2)
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1) iron accumulation in liver cells
2) cholesterol accumulation in macrophages (especially on inner lining of vessel walls = atherosclerosis) |
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stenosis
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abnormal narrowing of blood vessels
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coronary artery atherosclerosis
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deposition of cholesterol and other lipids causes proliferation of cells in vessel wall
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