| 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 |
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