Cell Adaption and Injury Flashcards
(1) Homeostasis
the tendency to maintain internal stability by coordinated responses that compensate for environmental changes
(1) Cell adaption
reaction of cell to stress where cell is able to adapt, occurs as a result of chronic stimulation by low-level stress
(1) Hyperplasia
increase in the number cells in an organ or tissue usually spurred by hormonal effects (may be physiologic or pathologic), will stop if stimulus is removed
(1) Hypertrophy
increase in the size of cells due to increase in structural components of cell, caused by growth factors (physiologic or pathologic)
(1) Atrophy
decrease in cell size, due to decreased demand or stimulation (phys or path)
(1) Metaplasia
one adult cell type is REPLACED by another adult cell type
(1) Cell injury
when severe stress exceeds the adaptive capability of the cell
(1) Hyaline change
describes a change in pathological process, often the result of intracellular or extracellular accumulations of proteins
(1) Anthracosis
phagocytosis of carbon by macrophages in alveoli leading to black discoloration of the lung tissue and its draining lymph nodes
(1) Necrosis
form of cell death associated with damage from an external source that overwhelms the cell’s ability to survive (always pathological)
(1) Capase
family of proteins, cysteine proteases are activated when cleaved from pro-enzyme form and lead to activation cascade
(1) Reactive oxygen species
oxygen derived free radicals that if excessive cannot be degraded quickly enough and cause oxidative stress
(1) Free radical
ion with an unpaired electron in its outer orbit, i.e., ROS is a free radical of an oxygen species
(1) Nuclear pyknosis
small, dark chromatin
(1) Karyolysis
fading chromatin
(1) Karyorrhexis
chromatin fragmentation
(1) Coagulative necrosis
dead tissue structure preserved because denatured proteolytic enzymes
(1) Liquefactive necrosis
dead cells completely digested, leaving only viscous liquid, often with infection
(1) Caseous necrosis
dead tissue transformed into cheesy granular material (TB)
(1) Fat necrosis
fatty acid products conbine with calcium to produce chalky-white areas (pancreatitis)
(1)Dystrophic calcification
deposition of calcium salts in dying tissues, despite normal serum calcium
(1) Metastatic calcification
occurs when increased serum calcium, often in otherwise normal tissue, may also accentuate dystrophic calcification
(2) A normal cell (in resting homeostasis) will respond to stress v. injurious stimulus how?
stress –> adaption
injurious stimulus –> cell injury
(2) Name 5 types of cell adaption.
hyperplasia hypertrophy atrophy metaplasia intracellular accumulations
(2) Contrast the stimulus for hyperplasia v. hypertrophy.
hyperplasia: hormone or local growth factor increases mitosis
hypertrophy: increased function of the cell causes more cellular machinery
(2) Organ hypertrophy can result from either: (2)
cellular hyperplasia or cellular hypertrophy, usually a combination of both to varying degrees
(3) List 4 intracellular accumulations.
abnormal metabolism, break down at insufficient speed
protein misfiling or transport error
lack of enzyme or breakdown material
accumulation of exogenous materials (deposit and inability to digest)
(3) Describe intracellular accumulation of triglycerides.
steatosis: notable by large round open spaces within the cell
(3) Describe intracellular accumulation of cholesterol
Intracellular: notable foaming appearance of the cytoplasms of cells, does not usually accumulate into a droplet
Extracellular: athrosclerosis, appears shard-like clear spaces
(3) Describe intracellular accumulation of protein.
proteins within the cytoplasm will stain pink with H&S stain, proteins can be found in various different shapes
amalyoid is a word that describes deposits, in this case, non-branching molecules of about the same size (physically similar more than biochemically similar); amyloid picks up congo red stain, under polarized light gives off apple green biofiringence
(3) What are russell bodies?
hyaline change in plasma cells due to accumulation of immunoglobulin
(3) What does intracellular accumulation of glycogen look like?
appears foamy with large amounts, can accumulate in the nucleus
(3) Name the different pigments that can accumulate intracellularly.
carbon (black, phagocytosed)
lipofuscin (wear and tear proteins, yellowish brown)
melanin
hemosiderin (blood breakdown, with iron, Prussian blue specific)
bilirubin (blackish brownish, location can ID)
(4) Describe the difference between necrosis and apoptosis.
necrosis is always pathologic and causes inflammation because is it not membrane bound like apoptosis
(5) Describe the mechanism of intrinsic initiation of apoptosis
cytochrome C is released form mitochondria, which is regulated by Bcl-2 proteins, release of cytochrome C causes initiator caspases to cascade to apoptosis
(5) Describe the mechanism of the extrinsic execution pathway.
binding of ligand like Fas protein to Fas receptor causes initiator caspases to be activated
(6) List the major causes of cell injury/death. (7)
hypoxia/ ischemia physical agents chemical agents infection immunologic reactions and derangements genetic derangements nutritional deficiencies and imbalances
(7) List the 4 major targets of cell damage.
machinery for energy production
cell membranes
machinery for protein synthesis
genetic apparatus
(8) List the major mechanism of cell damage (7)
depletion of ATP (failure of energy dependent cell systems)
mitochondrial damage
loss of Ca2+ homeostasis
oxidative stress
defects in membrane permeability (necrosis not apoptosis)
DNA damage
unfolded or misfiled proteins
(8) Describe how depletion of ATP leads to cell injury
failure of energy dependent systems (membrane potential and electrolyte balance) and increased lactic acid/decreased pH
(8) What is a mitochondrial permeability transition pore?
leads to the destruction of mitochondria due to lack of gradient for oxidative phosphorylation and caused by increase in intracellular Ca2+ levels
(8) Describe the pathological effects of oxidative stress. (3)
lipid peroxidation of membranes
oxidative modification of proteins (can destroy active site)
lesions in DNA
(8) Site 5 sources of oxidative stress free radicals
mitochondrial oxidative phosphorylation radiant energy leukocytes during inflammatory response oxidizing metals (iron, copper, etc.) nitric oxide
(8) Site 3 ways biological systems remove free radicals.
antioxidant scavengers
transport proteins that bind reactive metals and
enzymes that convert free radicals
(8) What events around defect in membrane permeability contribute to cell injury?
phospholipase activated by increased cytoplasmic Ca2+
detergent action of phopholipid breakdown products
damage to cytoskeleton
(9) Using high power LM on a cell undergoing apoptosis, what would you call the reddish blobs found in defecting cells?
apoptotic bodies, notice there would be no inflammation associated with this change (apoptosis morphology is subtle
(9) What signs are morphologically characteristic of necrosis?
robust neutrophilic (lobulated) infiltration; extra neutrophil nuclei
(9) Describe the cellular features of necrosis.
swelling of mitochondria and ER and break down of plasma membranes and organelles
(9) Describe the cell size in necrosis and apoptosis.
necrosis (cell swelling, sometimes shrinkage), apoptosis (cell shrinkage)
(9) What features would you see in reversible cell injury under EM.
early changes include loss of microvilli and blabbing, mitochondrial swelling and dilated ER (honeycomb looking)
(9) What features would you expect to see in reversible cell injury under LM.
ballooning degeneration, extra fluid causes cells to enlarge, cytoplasm is foamy; steatosis is reversible, notice lobules of triglyceride in this case
(9) What features are apparent for irreversible cell injury under electron microscope. (2)
- super dilated mitochondria and membrane discontinuity
2. myelin figures - black whorls, cell membranes that curl on self
(9) What features are apparent for irreversible cell injury under light microscope. (3)
- nuclear pyknosis (dark shrunk and irregular)
- karylosis (fading of nucleus- nucleus disintegrates)
- karyorrhexis (chromatin fragmentation; loss of nuclei)
(9) Describe the mechanism for dystrophic calcification.
excess calcium binds to phopholipid membranes and is cleaved off by phophatases, the high concentration of Ca2+ eventually leads to crystallization of calcium
(9) Describe the features of coagulative necrosis.
usually due to ischemia, tissue will still be recognizable in form, and be accompanied by anucleated cells and neutrophilic infiltration
(9) Describe the features of liqufactive necrosis.
tissue is reduced to liquid, leaving a light or cyst-like space, which is hard to process; this pattern is common in CNS infarct as well as fungal or bacterial infection
(9) Describe the patter of caseous necrosis.
granular gunk in place where tissue is no longer recognizable (characteristically between coagulative and liquifactive) it is classic of TB granuloma and appears “cheese-like” in texture
(9) Describe the pattern of fat necrosis.
occurs within fatty tissue resulting in white nodules formed by calcium deposit; space is typically left where adipocytes were, without the presence of nuclei (fat necrosis is common near pancreas where leaking lipase can induce fat necrosis)
(9) What is metastatic calcification?
not associated with necrosis, is the result of pathologically high levels of Ca2+ serum
(9) Describe a basic scenario of events in myocyte tissue occurring after coronary artery blockage.
hypoxia stops cellular respiration, ischemia leads to glycolysis, lower pH; declining ATP levels lead to K/Na pump stops working, cells draw in swelling and blabbing and increase in Ca++ can activate caspases and self-digesting enzymes within the cell as well as a mitochondrial permeability transition pore leading to more disintegration
