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FM1- Pathology > Cell Adaption and Injury > Flashcards

Cell Adaption and Injury Flashcards

1
Q

(1) Homeostasis

A

the tendency to maintain internal stability by coordinated responses that compensate for environmental changes

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2
Q

(1) Cell adaption

A

reaction of cell to stress where cell is able to adapt, occurs as a result of chronic stimulation by low-level stress

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3
Q

(1) Hyperplasia

A

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

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4
Q

(1) Hypertrophy

A

increase in the size of cells due to increase in structural components of cell, caused by growth factors (physiologic or pathologic)

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5
Q

(1) Atrophy

A

decrease in cell size, due to decreased demand or stimulation (phys or path)

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6
Q

(1) Metaplasia

A

one adult cell type is REPLACED by another adult cell type

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7
Q

(1) Cell injury

A

when severe stress exceeds the adaptive capability of the cell

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8
Q

(1) Hyaline change

A

describes a change in pathological process, often the result of intracellular or extracellular accumulations of proteins

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9
Q

(1) Anthracosis

A

phagocytosis of carbon by macrophages in alveoli leading to black discoloration of the lung tissue and its draining lymph nodes

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10
Q

(1) Necrosis

A

form of cell death associated with damage from an external source that overwhelms the cell’s ability to survive (always pathological)

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11
Q

(1) Capase

A

family of proteins, cysteine proteases are activated when cleaved from pro-enzyme form and lead to activation cascade

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12
Q

(1) Reactive oxygen species

A

oxygen derived free radicals that if excessive cannot be degraded quickly enough and cause oxidative stress

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13
Q

(1) Free radical

A

ion with an unpaired electron in its outer orbit, i.e., ROS is a free radical of an oxygen species

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14
Q

(1) Nuclear pyknosis

A

small, dark chromatin

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15
Q

(1) Karyolysis

A

fading chromatin

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16
Q

(1) Karyorrhexis

A

chromatin fragmentation

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17
Q

(1) Coagulative necrosis

A

dead tissue structure preserved because denatured proteolytic enzymes

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18
Q

(1) Liquefactive necrosis

A

dead cells completely digested, leaving only viscous liquid, often with infection

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19
Q

(1) Caseous necrosis

A

dead tissue transformed into cheesy granular material (TB)

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20
Q

(1) Fat necrosis

A

fatty acid products conbine with calcium to produce chalky-white areas (pancreatitis)

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21
Q

(1)Dystrophic calcification

A

deposition of calcium salts in dying tissues, despite normal serum calcium

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22
Q

(1) Metastatic calcification

A

occurs when increased serum calcium, often in otherwise normal tissue, may also accentuate dystrophic calcification

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23
Q

(2) A normal cell (in resting homeostasis) will respond to stress v. injurious stimulus how?

A

stress –> adaption

injurious stimulus –> cell injury

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24
Q

(2) Name 5 types of cell adaption.

A 
hyperplasia
hypertrophy
atrophy
metaplasia
intracellular accumulations
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25
Q

(2) Contrast the stimulus for hyperplasia v. hypertrophy.

A

hyperplasia: hormone or local growth factor increases mitosis
hypertrophy: increased function of the cell causes more cellular machinery

26
Q

(2) Organ hypertrophy can result from either: (2)

A

cellular hyperplasia or cellular hypertrophy, usually a combination of both to varying degrees

27
Q

(3) List 4 intracellular accumulations.

A

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)

28
Q

(3) Describe intracellular accumulation of triglycerides.

A

steatosis: notable by large round open spaces within the cell

29
Q

(3) Describe intracellular accumulation of cholesterol

A

Intracellular: notable foaming appearance of the cytoplasms of cells, does not usually accumulate into a droplet
Extracellular: athrosclerosis, appears shard-like clear spaces

30
Q

(3) Describe intracellular accumulation of protein.

A

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

31
Q

(3) What are russell bodies?

A

hyaline change in plasma cells due to accumulation of immunoglobulin

32
Q

(3) What does intracellular accumulation of glycogen look like?

A

appears foamy with large amounts, can accumulate in the nucleus

33
Q

(3) Name the different pigments that can accumulate intracellularly.

A

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)

34
Q

(4) Describe the difference between necrosis and apoptosis.

A

necrosis is always pathologic and causes inflammation because is it not membrane bound like apoptosis

35
Q

(5) Describe the mechanism of intrinsic initiation of apoptosis

A

cytochrome C is released form mitochondria, which is regulated by Bcl-2 proteins, release of cytochrome C causes initiator caspases to cascade to apoptosis

36
Q

(5) Describe the mechanism of the extrinsic execution pathway.

A

binding of ligand like Fas protein to Fas receptor causes initiator caspases to be activated

37
Q

(6) List the major causes of cell injury/death. (7)

A 
hypoxia/ ischemia
physical agents
chemical agents
infection
immunologic reactions and derangements
genetic derangements 
nutritional deficiencies and imbalances
38
Q

(7) List the 4 major targets of cell damage.

A

machinery for energy production
cell membranes
machinery for protein synthesis
genetic apparatus

39
Q

(8) List the major mechanism of cell damage (7)

A

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

40
Q

(8) Describe how depletion of ATP leads to cell injury

A

failure of energy dependent systems (membrane potential and electrolyte balance) and increased lactic acid/decreased pH

41
Q

(8) What is a mitochondrial permeability transition pore?

A

leads to the destruction of mitochondria due to lack of gradient for oxidative phosphorylation and caused by increase in intracellular Ca2+ levels

42
Q

(8) Describe the pathological effects of oxidative stress. (3)

A

lipid peroxidation of membranes
oxidative modification of proteins (can destroy active site)
lesions in DNA

43
Q

(8) Site 5 sources of oxidative stress free radicals

A 
mitochondrial oxidative phosphorylation
radiant energy
leukocytes during inflammatory response
oxidizing metals (iron, copper, etc.)
nitric oxide
44
Q

(8) Site 3 ways biological systems remove free radicals.

A

antioxidant scavengers
transport proteins that bind reactive metals and
enzymes that convert free radicals

45
Q

(8) What events around defect in membrane permeability contribute to cell injury?

A

phospholipase activated by increased cytoplasmic Ca2+
detergent action of phopholipid breakdown products
damage to cytoskeleton

46
Q

(9) Using high power LM on a cell undergoing apoptosis, what would you call the reddish blobs found in defecting cells?

A

apoptotic bodies, notice there would be no inflammation associated with this change (apoptosis morphology is subtle

47
Q

(9) What signs are morphologically characteristic of necrosis?

A

robust neutrophilic (lobulated) infiltration; extra neutrophil nuclei

48
Q

(9) Describe the cellular features of necrosis.

A

swelling of mitochondria and ER and break down of plasma membranes and organelles

49
Q

(9) Describe the cell size in necrosis and apoptosis.

A

necrosis (cell swelling, sometimes shrinkage), apoptosis (cell shrinkage)

50
Q

(9) What features would you see in reversible cell injury under EM.

A

early changes include loss of microvilli and blabbing, mitochondrial swelling and dilated ER (honeycomb looking)

51
Q

(9) What features would you expect to see in reversible cell injury under LM.

A

ballooning degeneration, extra fluid causes cells to enlarge, cytoplasm is foamy; steatosis is reversible, notice lobules of triglyceride in this case

52
Q

(9) What features are apparent for irreversible cell injury under electron microscope. (2)

A
  1. super dilated mitochondria and membrane discontinuity

2. myelin figures - black whorls, cell membranes that curl on self

53
Q

(9) What features are apparent for irreversible cell injury under light microscope. (3)

A
  1. nuclear pyknosis (dark shrunk and irregular)
  2. karylosis (fading of nucleus- nucleus disintegrates)
  3. karyorrhexis (chromatin fragmentation; loss of nuclei)
54
Q

(9) Describe the mechanism for dystrophic calcification.

A

excess calcium binds to phopholipid membranes and is cleaved off by phophatases, the high concentration of Ca2+ eventually leads to crystallization of calcium

55
Q

(9) Describe the features of coagulative necrosis.

A

usually due to ischemia, tissue will still be recognizable in form, and be accompanied by anucleated cells and neutrophilic infiltration

56
Q

(9) Describe the features of liqufactive necrosis.

A

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

57
Q

(9) Describe the patter of caseous necrosis.

A

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

58
Q

(9) Describe the pattern of fat necrosis.

A

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)

59
Q

(9) What is metastatic calcification?

A

not associated with necrosis, is the result of pathologically high levels of Ca2+ serum

60
Q

(9) Describe a basic scenario of events in myocyte tissue occurring after coronary artery blockage.

A

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

FM1- Pathology (6 decks)

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