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Cell Adap,Inj,Death

USCSOM: Pathology Cellular Adapt, Injury, Death

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

 



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