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Pathology I > Cell injury and necrosis > Flashcards

Cell injury and necrosis Flashcards

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1
Q

what can cause cell injury?

A

lack of oxygen, lack of nutrients, extreme pH, electrolyte imbalances, toxins, oxygen free radical damage, physical disruption

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2
Q

cell injury is an attempt to?

A

return to homeostasis

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3
Q

what are the reversible secondary changes to injury?

A 
cellular swelling
cell membrane blebs
detached ribosomes
chromatin clumping
lipid deposition
vacuole formation
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4
Q

what are irreversible secondary changes to injury?

A

lysosome rupture
dense bodies in mitochrondria (ultrastructural)
cell membrane rupture
karyolysis, karyorrhexis, pyknosis

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5
Q

what is the first thing that happens after cell injury

A

biochemical (can’t see) and ultrastructural happen before any apparent morphological changes

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6
Q

most important feature of necrosis?

A

loss of nucleus

no nucleus-> cell is dead

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7
Q

cellular responses to injury depends on?

A

type of injury, duration and severity

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8
Q

manifestations of cell death take long or quick to appear?

A

more time to develop than those of reversible damage

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9
Q

what is the susceptibility of neurons to ischemic necrosis?

A

High, 3-4 mins

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10
Q

what is the susceptibility of myocardium, hepatocytes, and renal epithelium to ischemic necrosis?

A

intermediate, 30 mins-2 hours

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11
Q

what is the susceptibility of fibroblast, epidermis, skeletal muscle to ischemic necrosis?

A

Low

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12
Q

Fastest injury (minutes) to occur from myocardial infarction?

A

biochemical injury, decrease in membrane function (arrhythmias)

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13
Q

Hours to occur from myocardial infarction?

A

signs of cell injury (cell swelling) giving rise to necrosis and leaking of enzymes

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14
Q

days to occur from myocardial infarction?

A

replacement of necrotic tissue with scar tissue, decrease contractility and heart failure

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15
Q

difference between hypoxia and ischemia?

A

ischemia is loss of blood flow and secondarily leads to lack of oxygen

hypoxia is loss of oxygen

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16
Q

what are some types of injurious agents?

A

ROS, trauma, cold, heat, toxins, receptor blockers, immunological reactions, genetic dearangments, nutritional imbalances

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17
Q

when is the point of no return met?

A

when the mitochondria and cell membrane are disrupted in function

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18
Q

Why does punching holes in the cell kill it?

A

ion transport and channels are disrupted, [ ] of calcium and sodium will be high in the ECF

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19
Q

what are 3 cell injuries that WILL cause cell death?

A

disruption of continuous formation of ATP (mitochondria)
punching holes in cell membrane
activation of self-digestion (proteases, lipases, endonucleases)

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20
Q

mitochondrial damage leads to?

A

ATP depletion, leakage of pro-apoptotic proteins, and multiple downstream effects

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21
Q

What does entry of Calcium into cell lead to?

A

increases mitochondrial permeability, activation of multiple cellular enzymes

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22
Q

an increase in ROS can lead to?

A

damage to lipids, proteins and DNA

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23
Q

damage to cell membrane can lead to?

A

plasma membrane: loss of cellular components

lysosomal membrane: enzymatic digestion of cellular components

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24
Q

protein mis-folding or DNA damage can lead to?

A

activation of pro-apoptotic proteins

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25
what are the 6 mechanisms of cell injury?
1. ) ATP depletion 2. ) irreversible mitochondrial damage 3. ) disturbances in calcium homeostasis 4. ) free radical formation 5. ) defects in cell membrane permeability 6. ) accumulated DNA and protein damage
26
what causes ATP depletion?
lack of oxygen, lack of substrates, decrease mitochondrial function
27
what does ATP depletion result in?
1. ) Loss of ATP dependent processes: increase in Na into the cell-> swelling and dilation of ER 2. ) switch to anaerobic glycolysis-> uses glycogen instead of glucose/glycogen stores depleted 3. ) accumulation of lactic acid with intracellular acidosis-> decrease functional capacity of cell 4. ) damage to protein synthesis apparatus-> detachment of ribosome from the rough ER (increase in smooth ER) 5. ) lack of oxygen and glucose results in mis-folding of protein-> unfolding protein response (apoptosis) 6. ) loss of calcium homeostasis-> sequestration of calcium requires ATP
28
irreversible damage to mitochondria will?
ULTIMATELY KILL THE CELL
29
what can damage mitochondria?
decreased oxygen, increased cytosolic Ca, activation of lipases, free radical damage
30
what is a mitochondrial permeability transition pore?
formation of a high conductance channel - non-selective pores - inability to maintain membrane potential - POINT OF NO RETURN
31
what can cause a disturbance in calcium homeostasis?
- loss of ATP-> shuts down calcium pumps - loss of membrane integrity allows influx of calcium - activation of enzymes - increase mito permeability and apoptosis
32
normal metabolism produces which ROS?
superoxide anion, hydrogen peroxide, hydroxyl ion, superoxide
33
ROS damages what?
lipids, protein and DNA - lipid peroxidation of membrane - chain breakage in proteins - formation of thymidine dimers and single-stranded breaks in DNA
34
how do we protect against ROS?
- by removing free radicals - catalase, superoxide dismutase - antioxidants and scavengers (Vit. E and A) - glutathione peroxidase - transport molecule binding of metals that can cause free radical formation
35
Defects in cell membrane permeability result in?
- mitochondrial dysfunction which leads to decreased phospholipid synthesis and activation of lipases due to increase in calcium in cytosol (calcium activated lipases) - increased cytosolic calcium - reactive oxygen species (lipid peroxidation) `
36
what can accumulation of DNA and protein damage cause?
interfere with specific gene transcription faulty transcription failure to repair DNA dysfunction protein synthesis mis-folded proteins (toxins accumulate, apoptosis)
37
again, what is point of no return?
damage to mito and inability to make ATP
38
What does the release of lysosomal enzymes and membrane damage result in?
necrosis | loss of structural integrity, loss of nucleus, and leakage of cell contents
39
what can cause hypoxia?
ischemia, low oxygen tension, carbon monoxide poisoning, severe anemia -all lead to inability to make ATP
40
duration of hypoxia to induce necrosis in brain? Liver?
Brain: 3-5 mins Liver: 1-2 hours
41
which injures tissue faster, ischemia or hypoxia?
Ischemia -b/c of decreased oxygen, loss of nutrients, decreased delivery of metabolic requirements for the glycolytic pathway, and inability to carry away damaging agents, build up of lactic acid
42
what are some consequences of hypoxia?
low oxidative phosphorlyation increased anaerobic metabolism-> +lactic acid, dec pH impairment of Na pump-> swelling, blebbing, mito swelling disaggregation of ribosomes-> dec protein syn-> lipid deposition
43
what are free radicals highly toxic to in particular?
membranes and nucleic acids
44
what kind of damage do free radicals cause?
peroxidation of membrane lipids single strand DNA breaks->thymidine dimers oxidative modification of proteins-> sulfhydral X linking of sulfur containing amino acids
45
what diseases are associated with cancer associated with chronic inflammation?
chronic hep C, gastric reflux, smoking, chronic gastritis
46
Fenton reaction deals with?
iron and oxygen can't get rid of iron, too much iron over DECADES hereditary hemochromatosis: see in 40's and usually die of liver cancer iron is deposited in tissues like liver, heart, and pancreas-> can lead to cirrhosis, diabetes, heart failure -damage done by free radicals formed by fenton reaction
47
reperfusion injury is caused by what?
re-establishment of blood flow to an ischemic area may actually enhance tissue damage-> as blood flow returns oxygen is converted to ROS by damaged cells - mediated by oxygen free radicals - ROS further compromise mito function and permeability - contraction bands-> indicative of reperfusion injury
48
what does CCl3 mainly react with?
-auto-oxidation of fatty acids in membrane phospholipids with formation of organic peroxides -damages to lipoprotein synthesis and lipid export-> fatty liver mild exposure-> fatty liver severe exposure-> necrosis
49
order in which changes associated with cell injury?
1st: biochemical and functional changes (minutes) 2nd: ultrastructural changes (hours) 3rd: microscopic changes (hours to days) 4th: gross tissue changes (days)
50
what are the ultrastructural changes of reversible cell injury?
1. ) plasma membrane alterations: blebbing, blunting, distortion of microvilli, myelin figures 2. ) mitochondrial changes: mito swelling, appearance of amorphous densities 3. ) dilation of ER/detachment of polysomes 4. ) nuclear alterations
51
what are the light microscopic characteristics of degeneration?
1st morphologic change: cytoplasmic swelling and pallor cytoplasmic vacuolization-> distention of ER by water, pinched off segments form vacuoles ballooning degeneration: swollen eosinophilic cytoplasm without vacuoles clumping chromatin
52
is fatty change a reversible injury?
Yes | with continued cell injury-> cells will eventually die (irreversible)
53
characteristics of Necrosis
disintegration of nucleus disruption of cellular membrane leakage of intracellular contents-> inflammation is set up to heal in response to necrosis loss of function
54
Two key features to Necrosis?
1. ) disruption of membrane leading to dissolution of cell | 2. ) destruction of nucleus
55
what is used to monitor presence of necrosis in myocardial infarctions?
leakage of intracellular into circulation (troponins, creatine kinase) useful because leakage occurs within minutes to hours
56
morphological changes from necrosis? (irreversible)
enzymatic digestion-> release of enzymes from lysosomes, infiltration of leukocytes denaturation of proteins, lipids, nucleic acids disruption of membrane
57
light microscopic characteristics from necrosis?
cytoplasmic changes - increased eosinophilia due to loss/dissolution of RNA/ribosomes - hyalinization-> glassy/homogenous appearance-> due to loss of glycogen, dissolution of organelles - vacuolation - calcification
58
what are the microscopic characteristics of pyknosis?
solid, shrunken basophilic mass | increased basophilia of the chromatin
59
what are the microscopic characteristics of karyorrhexis?
pykonotic nucleus undergoes fragmentation
60
what are the microscopic characteristics of karyolysis
``` dissolving of the nucleus into amorphic mass decreased basophila (NO FRAGMENTATION) dissolution of DNA-> activation of DNAase ```
61
reversible light microscopic characteristics of necrosis?
cell swelling hydropic change fatty change chromatin clumping
62
irreversible light microscopic characteristics of necrosis?
``` increased eosinophilia hyalinization nuclear condensation (P, Karyorrh, Karyol) vacuolization calcification ```
63
what are the Gross changes that are seen with necrosis?
pallor-> occurs within minutes Soft: disruption of tissue architecture (hours to days) raised or depressed
64
what are the classical morphological patterns with necrosis?
``` coagulative necrosis liquefactive necrosis gangrenous caseous fat fibrinoid apoptosis reperfusion ```
65
what are the three subtypes of coagulative?
gangrenous, caseous, fat
66
coagulative necrosis characteristics?
nucleus absent cytoplasm-> eosinophilia cell outlines is preserved tissue remains firm for several days before softening
67
coagulative necrosis mechanism
intracellular acidosis denatures structural proteins and proteolytic enzymes so autolysis is minimized
68
what is coagulative necrosis usually associated with?
ischemia, except in brain
69
liquefactive necrosis
- infiltration of tissue by large numbers of neutrophils - destructive enzyme from PMN - tissue architecture usually destroyed - liquefied remains of tissue, neutrophils (pus)
70
liquefactive necrosis in brain
caused by ischemia, most necrosis in CNS | -not necessarily neutrophils
71
Gangrenous necrosis
associated with loss of blood supply, dry gangrene usually associated with limbs if secondary liquefactive necrosis-> wet gangrene (infection)
72
Caseous necrosis
common with Mycobacteria | gross appearance: yellow-white cheese like material
73
Caseous necrosis light microscopic characteristics
cell outlines indistinct but not liquefied central areas of amorphous eosinophilic granuloma material surrounded by macrophages and multinucleated giant cells granulomatous inflammation
74
Fat necrosis general features
- destruction of adipose tissue - trauma-> breasts - pancreatitis-> associated with abnormal release of activated pancreatic lipase into the substances of the pancreas and peritoneal cavity - formation of calcium soaps-> combination of calcium and degrading lipids and proteins
75
Fat necrosis light microscopic characteristics
- eosinophilic ghost outlines of necrotic adipocytes - basophilic calcium deposits - surrounded by inflammation - Gross appearance: white chalky firm areas, saponification
76
fibrinoid necrosis
- special necrosis within walls of blood vessels - results from immune-mediated forms of vasculitis-> deposition of antibody and immune complexes within the walls of blood vessels together with fibrin - looks like deposition of fibrin in tissues-> fibrinoid

Pathology I (8 decks)

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