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Cell Adap,Inj,Death
USCSOM: Pathology Cellular Adapt, Injury, Death
| Question | Answer |
|---|---|
| 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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