USCSOM: Pathology Cellular Adapt, Injury, Death
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| What are two patterns of cell death? | necrosis and apoptosis
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| What are the four types of cellular adaptation? | hyperplasia, hypertrophy, atrophy, metaplasia
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| What is hyperplasia? | increase in number of cells
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| Example of hormonal hyperplasia. | lactating breast, pregnant uterus
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| Example of compensatory hyperplasia. | liver
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| What is pathologic hyperplasia? | excessive hormonal or growth factor leading to overstiumulation of target cells
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| What is hypertrophy? | increase in size of cells
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| Example of physiologic hypertrophy. | weight training
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| Example of pathologic hypertrophy. | hypertension, post myocardial infarction
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| What is atrophy? | shrinkage in the size of the cell by loss of cell substance
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| Causes of atrophy. | decreased workload, loss of innervation, decreased blood supply, inadequate nutrition, loss of endocrine stimulation, aging, pressure
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| Two key proteolytic systems in atrophy. | lysosomes and ubiquitin-proteasome pathway
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| What is metaplasia? | reversible change in adult cell types
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| What is the most common epithelial metaplasia? | columnar to squamous
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| What is myositis ossificans? | bone mormation in muscle, seen following injury
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| What is a caspase? | enzyme that degrades proteins and DNA
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| What is apoptosis? What is key? | internally programmed series of events to eliminate unwanted cells; cell does NOT spill into extracellular space
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| What are reversible changes in cell injury morphology? | swelling, vacuole formation, blebbing, polysomes detatch from rER, nucleoulus may segregate
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| What are irreversible changes in cell injury? | all ribosomes fall off rER; cytoplasm becomes eosinophilic, holes in membrane, breakdown of DNA in nucleus
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| What is pyknosis? | shrinkage of DNA in cell injury
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| What is karyolysis? | fading of DNA in cell injury
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| What is karyorrhexis? | DNA fragmentation in cell injury
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| What is hydropic change? | cellular swelling (edema) in reversible cell injury
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| What is necrosis? | irreversible cellular injury, always pathologic, associated with karyolysis, contents SPILL out into extracellular space
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| What are the types of necrosis? | Coagulative, Liquefactive, Caseous, Enzymatic Fat, Fibrinoid, Gangrenous
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| What is dysplasia? | disordered growth, usually squamous epithelial cells w/ chronic injury; further down the road than metaplasia
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| Coagulative necrosis. What and Where | ischemia, hypoxia, reperfusion injury; most organs except brain
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| Liquefactive necrosis. What and Where | Abcess filled with puss in non-connective tissue; Brain
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| Caseous necrosis. What and Where | soft, friable, cheesy; granular due to lack of cell wall degredation; TB and Fungi
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| Enzymatic fat necrosis. What and Where | lipase action; calcium and FAs form soap-like, white chalky; pancreatitis and Fat inflammation
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| Fibrinoid necrosis. What and Where | plasma protein build-up in blood vessels; eosinophilic stain
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| Gangrenous necrosis. What and Where | dead limb due to loss of circulation
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| What is wet gangrene? | gangrene plus bacterial infection
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| What are the mechanisms that cause reperfusion injury? | ROS damage (disrupts lipids, DNA, proteins), activation of neutrophils and complement pathway
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| What stimulates the intrinsic pathway of apoptosis? | bax, bak, cyt C, caspases
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| What stimulates the extrinsic pathway of apoptosis? | Fas, TNF, caspases
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| What are the stages of apoptosis? | Initation, signals that commit, execution by caspases and endosomes, removal of dead cell
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| What happens to the ER in cell injury? | dilates; rER loses ribosomes
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| What are characteristics of again? | progressive, gradual, intrinsic, universal, deleterious
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| Describe progeria | acceleration of aging; life span<10; mutation in LMNA gene leading to build up of progerin and disorganization of heterochromatin
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| Describe Werner syndrome | autosomal recessive; loss of fxn of WRN gene that codes for ATPase, helicase, exonuclease, strand annealing
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| What is heterophagy? | materials from external environment taken up through endocytosis
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| What is pinocytosis? | uptake of smaller solubule material
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| What are residual bodies? | undigested material that may persist in the lysosomes
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| Describe lipofuscin pigment granules. | indigestible material resulting from intracellular free radical lipid peroxidation
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| What is induction of smooth ER? | hypertrophy of ER to increase effectiveness of metabolizing compounds
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| What is P-450 modification? | mixed function oxidase system in hepatocyte SER; increases solubility of compounds and facilitates excretion (for detox)
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| What happens to mitochondria in cellular hypertrophy? | increase in the number of mitochondria
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| What are the three categories of substances that can be "stockpiled" in a cell? | normal cellular components in excess; abnormal substances; pigments
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| What are the three pathways for excess intracellular accumulations? | decreased metabolic rate; defects in metabolism/packaging/transport/secretion; exogenous indigestable substance
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| What is steatosis? | any abnormal accumulation of triglycerides within parenchymal cells
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| What are the most common causes of fatty change in the liver in industrialized nations? | alcohol abuse and diabetes associated with obesity
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| How does anoxia affect steatosis? | decrease in fatty acid oxidation
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| What does steatosis look like? | nuclei appear pushed to periphery of fatty vacuoles; seen in liver and heart
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| What are foam cells? | macrophages filled with numerous membrane-bound vacuoles of lipid
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| What are cholesterol clefts? | rupture of foam cells causing crystallization of cholesterol esters
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| What are the fxns of microtubules? | motility, phagocytosis, mitotic spindle
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| What are the fxns of intermediate filaments? | maintain cellular architecture
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| What are the fxns of thin filaments? | movement, phagocytosis
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| What are xanthomas? | acquired and hereditary hyperlipidemic states
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| What organ is affected by cholesterolosis? | galbladder
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| What is microscopic difference between foam cells and hyperlipidemic cells? | nucleus is in the center in foam cells; pushed off to the side in lipids
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| What is a russell body? | round, eosinophilic bodies in plasma cells actively synthesizing immunoglobulins
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| What does a hyaline change look like? | homogenous, glassy pink appearance
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| What is Mallory alcoholic hyalin? | masses of altered intermediate filaments in alcoholic liver disease
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| What is the most common exogenous pigment accumulation? | Carbon (coal dust)
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| What is heavy carbon accumulation called? | anthracosis
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| What is the endogenous "wear and tear" pigment? | Lipofuscin
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| What causes lipofuscin build-up? | Past free radical injury during lipid peroxidation
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| What is the only normal endogenous brown-black pigment? | melanin
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| What pigment is a form of iron storage? | hemosiderin
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| What stain is used to detect hemosiderin? | prussian blue stain
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| What pigment accumulation causes jaundice? | bilirubin
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| What is dystrophic calcification? | sign of previous cell injury, intracellular, extracellular, at NORMAL calcium levels
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| What is metastatic calcification? | calcification in normal tissue during hypercalcemia
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| What are the four main causes of hypercalcemia? | Increased PTH, destruction of bone tissue, Vit-D disorders, renal failure
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