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Path Quiz 1 > cell injury and cell death I and II > Flashcards

cell injury and cell death I and II Flashcards

1
Q

what are the three possible consequences of cell injury?

A

reversible injury - altered cell recovers and returns to being a normal cell
permanent cell injury - permanently altered after injury
lethal cell injury - injury leads to cell death - leads to necrosis (ischemia or apoptosis)

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2
Q

what are some characteristics of normal liver tissue (histology)?

A

hepatocytes arranged in trabecular architecture forming sinusoids
lots of pink cytoplasm
blue nuceli that are centrally placed
with electron microscope - mitochondria roundish and in rER

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3
Q

what is steatosis?

A

accumulation of fat (TG) in hepatocytes - often due to alcoholic liver injury
would have elevated white count and elevations of liver enzymes because enzymes leak out of damaged cells

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4
Q

describe an example of reversible cell injury.

A

damage to liver due to alcoholism - steatosis

abstinence from alcohol can result in reversal of cells back to normal hepatocytes

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5
Q

what happens to alcohol in the liver?

A

metabolized to acetate
drives microsomal system that manages toxic agents - role in underlying injury of liver
also drives liver cell into oxidative stress and drive increase in NADH - has effect on liver’s regulation of lipid metabolism

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6
Q

how does NADH (and alcohol) affect lipid metabolism?

A

alcohol increases NADH
NADH decreases FA oxidation
NADH increases TG synthesis

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7
Q

what are the 5 effects of EtOH on hepatic lipid metabolism?

A

1: Mobilization of fatty acids from body stores
2: Decreased fatty acid oxidation
3: Increased triglyceride synthesis
4: Decreased lipoprotein synthesis
5: Decreased transport, glycosylation and secretion of VLDL

all results in buildup of TG in cells cause of decreased export from cells

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8
Q

what would a liver damaged by alcohol (steatosis) look like histologically?

A 
clear spaces (circles) due to lipid buildup - hepatocytes begin to resemble fat cells - eventually will look completely like fat cells  except for portal triads in tissue
nuceli no longer solid blue - have blue rim and dot in center
presence of neutrophils in sinuses - bright red dots much smaller than hepatocyte cells
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9
Q

what is mallory’s hyaline?

A

abnormality in cytoskeleton => aggregation of cytokeratin filaments in liver cells

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10
Q

what happens to hepatocytes after heavy alcohol use in those with mallory’s hyaline?

A

get permanently altered hepatocytes even after abstinence
(note, i don’t think they have mallory’s hyaline until they damage their liver)
get alcoholic hepatitis

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11
Q

what would the liver biopsy of a patient with mallory’s hyaline look like histologically?

A

dense pink “ropes” inside the cells
these are buildup of cytokeratin filaments
hepatocytes die and are removed
neutrophils present

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12
Q

what would a liver biopsy of a patient with hemochromatosis look like histologically?

A

rusty brown/tan color in hepatocytes = buildup of iron
much less pink
check with prussian blue stain - will stain iron blue - so would see liver cells filled with blue

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13
Q

what is hemochromatosis?

A

genetic liver disease that results in abnormal accumulation of iron in tissues
eventually results in cirrhosis - identify by lots of blue with prussian stain

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14
Q

what does prussian blue stain for?

A

iron in tissue - shows up blue

used to diagnose hemosiderosis

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15
Q

what is hemosiderosis? how do you treat it?

A

buildup of iron in tissues due to any cause - can be due to local injury such as local hemorrhage
treat by removing red cell mass and can also restrict diet but iron’s in almost everything

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16
Q

what would a liver with Cirrhosis look like?

A

actual liver (gross) would have lots of green nodules - lots of fibrous tissue - bumpy surface

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17
Q

what are the dangers of having too much iron?

A

causes inflammation and free radical accumulation

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18
Q

what is burkitt lymphoma?

A

malignancy of B lymphocytes with apoptotic cell death of malignant cells and phagocytosis of apoptotic bodies by macrophages
example of apoptosis due to lethal cell injury

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19
Q

what is the process of apoptosis?

A

activation of cytochrome C - activates enzymatic cascade - cell fragments - macrophages take away debris

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20
Q

what are some examples of things that can induce apoptosis?

A

radiation, some hormones, damage

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21
Q

what does burkitt lymphoma look like histologically?

A

starry sky pattern - lightly stained macrophages with apoptotic bodies surrounded by dense infiltrate of malignant lymphocytes
lymphocytes large and abnormal
macrophages present and contain little blue dots - phagocytized fragments of dead cells

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22
Q

what is ischemia?

A

effect of O2 deprivation on cell function and morphology

can be due to arterial occlusion

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23
Q

what is the result of ischemia on cells?

A

initially injury that leads to altered cells followed by irreversible progression to cell death => necrosis

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24
Q

what are some of the reversible effects of ischemia?

A

decreased oxidative phosphorylation in mitochondria => decreased ATP => decreased Na pump activity; increased glycolysis; detachment of ribosomes so decreased protein synthesis
Na and Ca2+ will come into cell cause of problem with Na/K ATPase (cause of low ATP)
cell swells

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25
Q

what are the irreversible effects of ischemia?

A

at certain point cell can no longer recover - likely due to damage to mitochondria - now no longer reversible
mitochondria releases cytochromes so that apoptosis is triggered

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26
Q

what would heart tissue look like histologically after ischemia?

A

enlarged cells
cells paler because of increased cell volume (cell swelling)
can see space in cells = edema fluid in cell

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27
Q

describe the role of Ca in cell death.

A

affects mitochondria, rER, cell membrane, nucleus adversely

if don’t correct mitochondrial abnormality cells won’t be able to do oxidative phosphorylation

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28
Q

what would mitochondria look like on EM after ischemia? (said he wasn’t going to ask us about this?)

A

mitochondria swell up

inner membranes begin to break down first

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29
Q

what happens to mitochondria after ischemia?

A

become porous, enter low energy state, lose enzymatic systems and cannot recover after a while

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30
Q

what is necrosis?

A 
morphologic changes from cell death in living tissue
cumulative effect of:
- enzymatic degradation of dead cells
- primarily mediated by lysosmal enzymes
- denaturation of proteins
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31
Q

what determines the appearance of necrosis?

A

cause of injury
type of tissue
host response to the injury (inflammation)

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32
Q

what are the two types of necrosis (list)?

A

coagulative necrosis

liquefactive necrosis

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33
Q

what is coagulative necrosis?

A

most common form
denaturation of cell proteins dominates
eg when you fry an egg
infarction (ischemic cell death) is a common example

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34
Q

what is liquefactive necrosis?

A

usually necrosis with extensive acute inflammation (eg bacterial or fungal infections) resulting in fairly complete digestion of tissue (liquification)
abscess and cerebral infarction are common examples
pus

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35
Q

what are examples of coagulative necrosis?

A

1: myocardial infarction
2: renal infarction
3: pulmonary infarction

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36
Q

what would myocardial infarction look like (gross images)?

A

in gross images, thin regions due to long term necrosis and scarring so there’s no muscle there - don’t grow myocardial cells back

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37
Q

what would myocardial infarction look like histologically?

A

dead myocardial fibers - know they’re dead because they’re shrunken and thin and have lost their nuceli - coagulative necrosis - contractile proteins have coagulated
plus tiny dark blue/purple dots = neutrophils

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38
Q

what would renal infarct look like histologically?

A

large spaces with no nuclei - will be paler than surrounding regions - narrow at medulla and wider toward cortex

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39
Q

what would a lung with hemorrhagic pulmonary infarct look like?

A

appears dark red to black - red because there’s a hemmorhage from the bronchial artery even though the pulmonary artery is blocked

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40
Q

what is a reperfusion infarction?

A

red infarct caused when perfusion is immediately restored to the dead tissue

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41
Q

what are examples of liquefactive necrosis?

A

1: cerebral infarction (stroke)
2: necrotizing fungal pneumonia

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42
Q

why does the brain undergo liquefactive necrosis? what would it look like (gross)?

A

structure and circulation

get hemmorhage and that makes the area appear black, but the area itself is gone

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43
Q

what would a lung with fungal pneumonia look like?

A

on xray, opaque white
in autopsy, grey regions, developing abscess, eventually get hole in lung
in histology - lots of actue inflammation and abundance of neutrophils

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44
Q

what type of necrosis is gangrenous necrosis?

A

both coagulative (typically ischemic but can also be due to frostbite) mixed with superimposed bacterial infection that causes liqueficative necrosis

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45
Q

what does gangrenous necrosis look like?

A

tissue turns black

46
Q

what is enzymatic fat necrosis?

A

necrosis of fat by pancreatic lipases
FA released from fat cells combine with Ca2+ resulting in saponification
results in chalky yellow deposits

47
Q

what does enzymatic fat necrosis look like?

A

chalky yellow deposits on pancreas (can be in other areas of body sometimes too)
when becomes really bad gets black due to hemorrhage

48
Q

what is caseous necrosis? (type of necrosis and what disease it’s associated with)

A

type of necrosis classically associated with TB - combination of coagulative and liquifactive necrosus

49
Q

what does caseous necrosis look like?

A

looks like cheese (or mold)
amorphous eosinophilic acellular material in center of granulomas
in histology - liquefied tissue that leaves a cavity
can see cavity in gross disection

50
Q

what are the two major classes of etiologic factors?

A

genetic - eg inherited mutations, disease-associated variants, polymorphisms
acquired - infectious, nutritional, chemical, physical

51
Q

what is pathogenesis?

A

sequence of events in the response of cells or tissues to the etiologic agent, from the initial stimulus to the ultimate expression of the disease

52
Q

what are examples of adaptive responses in cells to altered physiological stimuli and some nonlethal injurious stimuli (reversible)?

A

1: hypertrophy - increase in size of cells
2: hyperplasia - increase in number of cells
3: atrophy - decrease in size and number of cells
4: metaplasia - change in phenotype of cells

53
Q

what are some examples of altered physiological stimuli and nonlethal injurious stimuli?

A

increased demand, increased stimulation (eg by growth factors, hormones)
decreased nutrients, decreased stimulation
chronic irritation (physical or chemical)

54
Q

what are adaptations?

A

reversible functional and structural responses to more severe physiologic stresses and some pathological stimuli, during which a new but altered steady state is achieved, allowing the cells to continue to survive and function

55
Q

what results in cell injury?

A

when the limits of adaptive responses are exceeded or if cells are exposed to injurious agents or stress, deprived of essential nutrients, or become compromised by mutations that affect essential cellular constituents

56
Q

what are the two pathways of cell death?

A

necrosis and apoptosis

autophagy can also occur in response to nutrient deprivation

57
Q

what is pathologic calcification?

A

when cell death results in the deposition of Ca

58
Q

what are the hallmarks of reversible cell injury?

A

reduced oxidative phosphorlyation with resultant depletion of energy stores (ATP)
cellular swelling due to changes in ion concentrations and water influx
intercellular organelles may should alterations

59
Q

when does necrosis versus apoptosis occur?

A

necrosis = when damage to membranes is severe, lysosomal enzymes enter the cytoplasm and digest the cell, cellular contents leak out

apoptosis = when when DNA or proteins are damaged beyond repair and cell kills itself

necrosis is always pathologic, whereas apop has many normal physiological functions

60
Q

what is hypoxia? what is its effect on cells?

A

deficiency of O2

reduces oxidative respiration - cells will adapt, undergo injury, or die

61
Q

what are some causes of hypoxia?

A

reduced blood flow (ischemia)
inadequate oxygenation of blood due to cardiorespiratory failure
decreased O2 carrying capacity of blood (anemia and CO poisoning)
severe blood loss

62
Q

what are the two features of reversible cell injury that can be recognized under a light microscope?

A

cellular swelling and fatty change

63
Q

when does cellular swelling occur?

A

when cell are incapable of maintaining ionic and fluid homeostasis
result of failure of energy-dependent ion pumps in the plasma membrane

64
Q

when does fatty change occur? how does it appear under microscope? what cells does it occur in?

A

in hypoxic injury and various forms of toxic or metabolic injury
see lipid vacuoles in cytoplasm
seen mainly in cells dependent on fat metabolism (ie hepatocytes, myocardial cells)

65
Q

what are the histological ultrastructural changes of reversible cell injury?

A

1: plasma membrane alterations (blebbing, blunting, loss of microvilli)
2: mitochondrial changes (swelling, appearance of small amorphous densities
3: dilation of the ER (with detachment of polysomes, intracytoplamic myelin figures may occur)
4: nuclear alterations (disaggregation of granular and fibrillar elements)

66
Q

what is the morphology of necrotic cells?

A

increased eosinophilia in H&E stains (due to loss of cytoplasmic RNA and denatured cytoplasmic proteins)
may have more glassy, homogenous appearance (due to loss of glycogen particles)
cytoplasm vacuolated (appears moth-eaten)
dead cells replaced by myelin figures
nuclear changes

67
Q

what are myelin figures?

A

large, whorled phospholipid masses derived from damaged cell membranes that replace necrotic cells
these are then phagocytised or calcified

68
Q

what are the nuclear changes that can occur in necrotic cells?

A

three possible patterns:

1: karyolysis - bacsopilia of the chromatin fades (loss of DNA because of enzymatic degradation by endonucleases)
2: pyknosis - nuclear shrinkage and increased basophilia (chromatin condenses into solid mass)
3: karyorrhexis - pyknotic nucleus undergoes fragmentation

nucleus will disappear eventually

69
Q

what is an infarct?

A

localized area of coagulative necrosis

70
Q

what is fibrinoid necrosis?

A

seen in immune reactions involving blood vessels
when complexes of antigens and antibodies are deposited in the walls of arteries
these deposits and fibrin that’s leaked out of vessels make bright pink and amorphous appearance in H&E

71
Q

what is dystrophic calcification?

A

if necrotic cells and debris are not removed promptly - attract Ca salts and other minerals => calcification

72
Q

how is ATP produced?

A

oxidative phosphorylation of adenosine diphosphate => reduction of O2 by the ETC
glycolytic pathway - makes ATP in absence of O2

73
Q

what are the major causes of ATP depletion?

A

reduced O2 supply
reduced nutrient supply
mitochondrial damage
actions of some toxins (eg cyanide)

74
Q

what are the consequences of depletion of ATP?

A

reduced Na/K ATPase
cellular energy metabolism altered - oxidative phos ceases ==> increased rate of anaerobic glycolysis => glycogen stores rapidly depleted
failure of Ca pump => influx of Ca
if prolonged, structural disruption of protein synthetic apparatus => reduction in protein synthesis
proteins may be misfolded => misfolded protein response
eventually irreversible damage to mitochondrial and lysosomal membranes => necrosis

75
Q

what can cause mitochondrial damage?

A 
increases of cytosolic Ca
reactive O2 species
O2 deprivation
(hypoxia and toxins)
mutations due to inherited diseases
76
Q

what are the consequences of mitochondrial damage?

A

formation fo high-conductance channel in membrane = mitochondrial permeability pore => loss of mitochondrial membrane potential => failure of oxidative phos => depletion of ATP => necrosis

proteins sequestered between inner and outer membranes released - these can trigger apoptotic pathways

77
Q

what is the role of cyclophilin D?

A

structural component of mitochondrial permeability transition pore
target of immunosuppressive drug cyclosporine

78
Q

what causes an increase in cytosolic Ca concentration?

A

ischemia
certain toxins

initially due to release from intracellular stores
later due to increased influx across plasma membrane

79
Q

how does influx of Ca cause cell injury?

A

accumulation of Ca in mitochondria => opening of mitochondrial permeability transition pore ==> failure of ATP generation

increased cytosolic Ca activates some enzymes

increased cellular Ca => apoptosis via direct activation of caspases and increasing mitochondrial permeability

80
Q

how are free radicals generated?

A

reduction-oxidation reactions that occur during normal metabolic processes

absorption of radiant energy

produced in activated lymphocytes during inflammation

enzymatic metabolism of exogenous chemicals or drugs

transition metals donate or accept

NO can act as free radical

81
Q

what does glutathione peroxidase do?

A

protects against injury by catalyzing free radical breakdown

82
Q

what are the pathologic effects of free radicals?

A

lipid peroxidation in membranes => peroxides, membrane damage

oxidative modification of proteins

lesions in DNA (single and double strand breaks, crosslinking, adducts)

83
Q

what are the mechanisms that create membrane damage?

A

reactive O2 species
decreased phospholipid synthesis
increased phospholipid breakdown
cytoskeletal abnormalities

84
Q

what are the consequences of membrane damage?

A
  • mitochondrial membrane damage => opening of mitochondrial permeability pore and decreased ATP production and release of apoptotic proteins

plasma membrane damage => loss of osmotic balance and influx of fluids and ions and loss of cellular contents

injury to lysosomal membranes => leakage of enzymes into cytoplasm and activation of acid hydrolases

85
Q

what could create DNA damage that can’t be corrected?

A

exposure to DNA damaging drugs
radiation
oxidative stress

86
Q

what are the two phenomena that characterize irreversible damage?

A

inability to reverse mitochondrial dysfunction

profound disturbances in membrane function

87
Q

which is worse: hypoxia or ischemia? why?

A

ischemia is worse because the cells are deprived of glycolytic substrates as well as O2, so can’t make up for the O2 lack with anaerobic glycolysis, whereas hypoxic tissue still has access to arterial glycogen supplies

88
Q

what is the mechanism behind cell swelling due to hypoxia or ischemia?

A

depletion of ATP => failure of Na pump => loss of K => influx of Na and H2O => cell swelling

89
Q

what are the morphological steps of ischemia?

A

associated with severe swelling of the mitochondria, extensive damage to plasma membranes, swelling of lysosomes

large, flocculent, amorphous densities develop in mitochondrial matrix

influx of Ca occurs

death by necrosis but apoptosis also contributes

90
Q

what does hypoxia-inducible factor-1 do?

A

promotes new blood vessel formation
stimulates cell survival pathways
enhances anaerobic glycolysis

protective response to hypoxic stress

91
Q

what is ischemia-reperfusion injury?

A

reperfused tissues may sustain loss of cells in addition to cells that are irreversibly damaged at the end of ischemia

92
Q

how does reperfusion injury occur?

A

new damaging processess are set in motion during reperfusion => death of cells that might have recovered otherwise

93
Q

what pathologic states can induce apoptosis?

A
  • DNA damage (radiation, chemo, hypoxia)
  • accumulation of misfolded proteins - in ER => ER stress
  • cell death in certain infections
  • pathologic atrophy in parencymal organs after duct obstruction
94
Q

what are the morphologic changes seen in apoptosis?

A
  • cell shrinkage
  • chromatin condensation
  • formation of cytoplasmic blebs and apoptotic bodies
  • phagocytosis of apoptotic cells or cell bodies, usually by macrophages

plasma membranes remain intact until last stages - become permeable

95
Q

what are the phases of apoptosis and what occurs during them?

A

initiation phase: some caspases become catalytically active

execution phase: other caspases trigger degradation of critical cellular components

96
Q

where do the signals for initiation of apoptosis come from?

A

intrinsic (mitochondrial)

extrinsic (death receptor-initiated)

97
Q

how do mitochondria regulate apoptosis?

A

some proteins in mitochondria initiate suicide program - eg cytochrome c
controlled by Bcl family of proteins esp. Bcl-2, Bcl-x, Mcl-1
all normally regulate mitochondrial permeability and prevent leakage of mitochondrial proteins
if DNA damaged or ER stress occurs, other members of the Bcl family (Bim, Bid, Bad) activate Bax and Bak => oligodimers => insert into mitochondrial membrane => channels that allow proteins from inner mitochondrial membrane to leak out into the cytoplasm
cytochrome c released into cytosol and binds to Apaf-1 => apoptosome
binds caspase 9

98
Q

how can apoptosis be activated extrinsically?

A

death receptors (TNF family) activated
eg Fas
FasL = fas ligand - expressed on T cells that recognize self antigens
Fas trimerizes - form binding site for FADD - binds inactive form of caspase-8 and multipule caspase-8 accumulate - cleave one another - triggers chain of caspase activation

can be inhibited by FLIP

99
Q

what is autophagy? when does it occur?

A

when cell eats its own contents
survival mechanism in times of nutrient deprivation
intracellular organelles and portions of cytosol are sequestered in autophagic vacuole - fuses with lysosomes => autophagosome

100
Q

what are the two types of substances that can accumulate in cells?

A

1: normal cellular constituents (water, lipids, proteins, carbs)
2: abnormal substances (exogenous like mineral or products of infectious agents, endogenous like products of abnormal synthesis or metabolism)

101
Q

what are the four types of abnormalities that can result in abnormal intracellular accumulations?

A

1: normal endogenous substance produced at normal or increased rate but rate of metabolism is inadequate
2: abnormal endogenous substance due to defects in protein folding and transport and inability to degrade abnormal protein
3: normal endogenous substance accumulates because of defects in enzymes required for metabolism of the substance
4: abnormal exogenous substance is deposited and accumulates because the cell has neither the enzymatic machinery to degrade the substance nor the ability to transport it to other sites

102
Q

what is steatosis?

A

abnormal accumulation of TG in parenchymal cells

103
Q

what are the causes of steatosis?

A 
toxins
protein malnutrition
diabetes mellitus
obesity
anoxia
104
Q

what is MI? what are the consequences?

A

death of cardiac muscle due to prolonged severe ischemia

initially, cessation of aerobic metabolism => inadequate production of ATP and accumulation of potentially noxious metabolites (lactic acid)
loss of contractility
if fixed within 20-30 minutes, reversible

105
Q

what are the events leading up to MI?

A

1: sudden change in atheromatous plaque
2: platelets adhere to exposed subendothelial collagen and necrotic plaque contents
3: platelets become activated and release granule contents
4: aggregate to form microthromi
5: vasospasm stimulated by mediators released from platelets
6: tissue factor activates the coagulation pathway - adds to bulk of thrombus
7: thrombus evolves to occlude lumen

106
Q

what does triphenyltetrazolium chloride stain for?

A

highlights area of necrosis after infarct

imparts brick-red color to intact, non-infarcted myocardium where dehydrogenase activity is preserved

107
Q

what is myocytolysis?

A

vacuolar degeneration
on margins of infarcts
large vacuolar space within cells that probably contain water

108
Q

what is the extension of an infarct? why does it occur?

A

when infarcts expand beyond their original borders over a period of days to weeks via a process of repetitive necrosis of adjacent regions
central zone where healing is more advanced than in the periphery

can be due to retrograde propagation of thrombus, proximal vasospasm, progressively impaired cardiac contractility, deposition of platelet-fibrin microemboli or arrythmia

109
Q

what are the clinical symptoms of MI?

A

myocardial proteins in plasma (myoglobin, cardiac troponins T and I, MB fraction of creatine kinase, lactate dehydrogenase)
ECG changes
rapid, weak pulse, profuse sweating
dyspnea

but can be entirely asymptomatic

110
Q

what is hemochromatosis? how do you get it? what tissues does it affect?

A

excessive accumulation of body iron - most deposited in parenchymal organs (liver, pancreas) - heart, joints, endocrine organs

primary = homozygous-recessive inherited disorder due to excessive iron absorption

Path Quiz 1 (12 decks)

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