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Fundamentals Block 1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What are the four ways cells adapt to physiological or pathological stress?

A
  1. Hypertrophy
  2. Hyperplasia
  3. Atrophy
  4. Metaplasia
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2
Q

What is hypertrophy?

A

an increase in the size of cells that results in transcription of proteins and new organelles.

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3
Q

What are the two major causes of hypertrophy?

A
  1. increased functional demand

2. Increased growth factors or hormonal stimulation

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4
Q

What are three examples of hypertrophy?

A
  1. Enlargement of uterus in pregnancy (increased hormones)
  2. striated or cardiac muscles undergo hypertrophy with use
  3. cardiac enlargement due to functional demand (hypertension)
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5
Q

What is hyperplasia?

A

increased number of cells because of growth factor and hormonal stimulation

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6
Q

What are four examples of hyperplasia?

A
  1. hormonal hyperplasia shown in breast tissue proliferation at puberty
  2. compensatory hyperplasia- when part of the liver is removed, cells will regenerate
  3. endometrial hyperplasia (due to disregulation of estrogen/progesterone balance causing irregular periods)
  4. fibroblast proliferation in would healing
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7
Q

What is atrophy?

A

shrinkage of cell size and loss of cell substance

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8
Q

What causes atrophy?

A
  1. Disuse/decreased workload
  2. loss of innervation
  3. diminished blood supply/nutrients
  4. aging
  5. decreased endocrine stimulation
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9
Q

What are the three major adaptations that occur in atrophy?

A
  1. protein synthesis stops in the cell
  2. Ub-Protease pathway degrades cellular proteins
  3. Autophagy- where the cell eats its own components to survive
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10
Q

What is metaplasia?

A

reversible change of one cell type to another cell type. Stem cells adapt and begin making the new type of cell

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11
Q

What are four examples of metaplasia and what are the cell conversions in each example?

A
  1. smokers lungs- ciliated columnar to stratified squamous
  2. Vitamin A deficiency- squamous metaplasia to stratified keratinized in the eye
  3. GERD- stratified squamous to columnar (to handle acid reflux)
  4. Bone forming in soft tissue as a result of stress
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12
Q

What are the eight main causes of cell injury?

A
  1. O2 deprivation
  2. Chemical agents
  3. Infectious agents
  4. Immunologic reactions
  5. Genetic factors
  6. Nutritional imbalance
  7. Physical agents
  8. Aging
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13
Q

What is the difference between hypoxia and ischemia?

A

Hypoxia is an oxygen deficiency. Ischemia is decreased blood flow to tissue due to impeded arterial flow or decreased venous drainage

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14
Q

What is the morphology of reversible cell injury?

A
  1. Cell swelling

2. Fatty change

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15
Q

Why does the cell swell in reversible cellular injury?

A

Decreased O2-> Decreased ATP-> messed up Na/K pump-> increased Na intracellularly-> increased H20 in cell= swelling

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16
Q

What is “fatty change”?

A

the appearance of lipid vacuoles in the cytoplasm (expecially in liver and myocardial cells)

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17
Q

What are the four intracellular changes associated with reversible cell injury?

A
  1. blebbing of the plasma membrane
  2. mitochondrial changes like swelling
  3. dilation of the ER with detaching polysomes
  4. Clumping chromatin
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18
Q

What cytoplasmic changes are recognized in a necrotic cell?

A
  1. Increased eosinophilia (denatured proteins)
  2. decreased basophilia (less RNA in cytoplasm)
  3. glassy (loss of glycogen)
  4. Vacuolated because of digested organelles
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19
Q

What three patterns can the nucleus of a necrotic cell assume?

A
  1. karyolysis- basophilia fades (dissolution)
  2. pyknosis- nuclear shrinkage and increased basophilia
  3. karyorrhexis- pyknotic nucleus that fragments
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20
Q

What is a pyknotic nucleus that fragments?

A

karyorrhexis

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21
Q

What type of necrosis can only be detected by histologic exam?

A

fibrinoid necrosis

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22
Q

What are the six different kinds of necrosis?

A
  1. Coagulative
  2. Fibrinoid
  3. Liquifactive
  4. caseous
  5. fat
  6. gangrenous
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23
Q

Where would one see coagulative necrosis?

A

infarcts in all solid organ except the brain

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24
Q

What is the morphology of coagulative necrosis?

A
  • firm tissue
  • can still see cellular structure
  • eosinophilic, aneucleated cells
  • leukocytes to digest dead cells
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25
Q

What is the morphology of liquefactive necrosis?

A

dead cells are completely digested leaving a liquid mass

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26
Q

Where would one identify liquefactive necrosis?

A

1/ hypoxic death of cells in the CNS (brain)

2. Purulent tissue- bacterial/fungal infections

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27
Q

What is the morphology of gangrenous necrosis?

A

lost blood supply and coagulative necrosis in multiple tissue layers

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28
Q

What is the difference between gangrene and wet gangrene?

A

Gangrene is coagulative necrosis of multiple tissue layers

Wet Gangrene is liquefactive necrosis of multiple tissue layers

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29
Q

Where would one see gangrenous necrosis?

A

Limbs

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30
Q

What is the morphology of caseous necrosis?

A
  • cheeselike yellow/white appearance

- fragmented or lysed cells where you cannot discern cell borders

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31
Q

Where would one see caseous necrosis?

A

In the lung because it is associated with TB

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32
Q

What is the morphology of fat necrosis?

A
  • focal areas of fat destruction by pancreatic lipases

- released FAs combine with calcium to make chalky white areas

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33
Q

What are the chalky white areas in fat necrosis called?

A

fat saponification

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34
Q

Where would one find evidence of fat necrosis?

A

pancreas

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35
Q

Where would one identify fibrinoid necrosis?

A

In the walls of arteries due to complexes of antigen and antibodies being deposited

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36
Q

What three things determine the cellular response to injury?

A
  1. cell type
  2. type and severity of injury
  3. duration
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37
Q

What are the four principal targets and biochemical mechanisms of cell injury?

A
  1. mitochondria and its ability to generate ATP and ROS
  2. Ca homeostasis
  3. cellular (plasma and lysosomal) membranes
  4. DNA and misfolding proteins
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38
Q

What are the four major consequences of depletion of cellular ATP during cell injury?

A
  1. Na/K pumps are reduced making high intracellular Na and h20 (cell swelling)
  2. Anaerobic glycolysis-> lactic acidosis-> breakdown of proteins, decreased enzyme activity
  3. Influx of Ca-> activates enzymes-> cell damage
  4. Disrupted protein synthesis b/c ribosomes detach from rough ER
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39
Q

What are the four major responses of mitochondria to cellular injury?

A
  1. failure of oxidative phosphorylation -> decreased ATP
  2. Formation of ROS
  3. form a high conductance channel-> loss of membrane potential
  4. Release proteins to signal apoptosis
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40
Q

What are the major consequences of increased intracellular Ca during cell injury?

A

Ca activates:

  1. phosholipase- cell membrane damage
  2. protease- breaks down cytoskeletal proteins
  3. endonucleases- break down DNA and chromatin
  4. ATPase

Calcium also induces apoptosis by activating caspases and increasing permeability

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41
Q

Why are free radicals dangerous?

A

When in the cell, they attack nucleic acids, proteins and lipids
They react to form more free radicals propogating the cycle

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42
Q

What are the two pathways by which ROS can be generated?

A
  1. As a biproduct of mitochondrial respiration (redox)

2. by phagocytic leukocytes(neutrophils/ macrophages)

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43
Q

What are the ROS intermediates in mitochondrial respiration when reducing O2 to water?

A

oxygen-> superoxide-> peroxide-> hydroxyl free radical

or

oxygen-> superoxide (+NO)–> peroxynitrate (ONOO)

44
Q

What enzyme converts superoxide to hydrogen peroxide?

A

superoxide dismutase

45
Q

What needs to be present to convert hydrogen peroxide to hydroxyl?

A

The presence of iron or other metals. The reaction is the Fenton reaction

46
Q

Why are ROS generated in phagocytic leukocytes?

A

to destroy ingested microbes

47
Q

How does the respiratory redox that generates ROS differ between mitochondria and leukocytes?

A

In mitochondria, hydrogen peroxide gets converted to hydroxyl via the fenton reaction.
In leukocytes, hydrogen peroxide is converted to hypochlorite via myeloperoxidase.
Leukocytes also have NO which forms peroxynitrite

48
Q

What determines the amount of damage causes by ROS?

A

the rates of production and removal

49
Q

Why three notable occurances increase the production of ROS?

A
  1. absorbing radiant energy (UV, Xray)
  2. enzymatic metabolism (tetrachloride)
  3. Inflammation
50
Q

What are the four major ways the cell limits ROS concentration and effect?

A
  1. superoxide dismutase converts to peroxide
  2. Glutathione Peroxidase (GSH) breaks peroxide down to water
  3. Catalase in peroxisomes breaks down h2o2
  4. Endogenous or exogenous antioxidants (vitamin AEC or b-carotene)
51
Q

What are the three main reactions that allow ROS to cause cell damage?

A
  1. Lipid peroxidation by attacking double bonds in membrane polyunsaturated lipids
  2. Sulfhydryl-mediated protein crosslinking to enhance degradation and loss of enzyme activity
  3. Free radical reaction with thymine to cause DNA damage
52
Q

What are major causes for membrane damage?

A
  1. decreased production of phospholipids because of reduced ATP
  2. Phospholipid breakdown due to increase Ca
  3. ROS lipid peroxidation
  4. Detergents
  5. cytoskeletal abnormalities by protease breakdown
53
Q

How do changes in membrane permeability affect the cell?

A
  1. Mitochondrial membrane damage-> decreased ATP, increased ROS
  2. Plasma membrane damage-> loss of osmotic balance, influx of fluid and ions, loss of cellular content
  3. Lysosomal membrane damage-> enzymes leaked into cytoplasm, acidic pH, digestion of cell components
54
Q

What is the result of damaged DNA and misfolded proteins?

A

the cell initiates apoptosis and dies

55
Q

What is the major context of physiological apoptosis?

A

It is a normal phenomenon that eliminates cells no longer needed to maintain a constant number of cells in a certain tissue type

56
Q

What are examples of physiological apoptosis?

A
  1. embryogenesis
  2. involution of hormone dependent tissue after hormone withdraw (endometrial cells in menstruation/lactating breast cells after weaning)
  3. Cell loss in proliferating populations (intestinal crypt cells)
  4. Neutrophils in acute inflammation when they have served their purpose
  5. Elimination of self-reactive lymphocytes
  6. cytotoxic T-cells to kill virally infected cells
57
Q

What is the major context of pathological apoptosis?

A

Apoptosis eliminates cells that have been injured or genetically altered beyond repair.

  • No severe host reaction
  • keep tissue damage to a minimum
58
Q

What are examples of pathological apoptosis?

A
  1. DNA damage- elimination may be better than risking mutation
  2. Accumulation of misfolded proteins-> ER stress
  3. Viral infection which causes cell injury
  4. Atrophy in parenchymal organs after duct obstruction
59
Q

What is the major context of physiological apoptosis?

A

It is a normal phenomenon that eliminates cells no longer needed to maintain a constant number of cells in a certain tissue type

60
Q

What are examples of physiological apoptosis?

A
  1. embryogenesis
  2. involution of hormone dependent tissue after hormone withdraw (endometrial cells in menstruation/lactating breast cells after weaning)
  3. Cell loss in proliferating populations (intestinal crypt cells)
  4. Neutrophils in acute inflammation when they have served their purpose
  5. Elimination of self-reactive lymphocytes
  6. cytotoxic T-cells to kill virally infected cells
61
Q

What is the major context of pathological apoptosis?

A

Apoptosis eliminates cells that have been injured or genetically altered beyond repair.

  • No severe host reaction
  • keep tissue damage to a minimum
62
Q

What are examples of pathological apoptosis?

A
  1. DNA damage- elimination may be better than risking mutation
  2. Accumulation of misfolded proteins-> ER stress
  3. Viral infection which causes cell injury
  4. Atrophy in parenchymal organs after duct obstruction
63
Q

What is the major context of physiological apoptosis?

A

It is a normal phenomenon that eliminates cells no longer needed to maintain a constant number of cells in a certain tissue type

64
Q

What are examples of physiological apoptosis?

A
  1. embryogenesis
  2. involution of hormone dependent tissue after hormone withdraw (endometrial cells in menstruation/lactating breast cells after weaning)
  3. Cell loss in proliferating populations (intestinal crypt cells)
  4. Neutrophils in acute inflammation when they have served their purpose
  5. Elimination of self-reactive lymphocytes
  6. cytotoxic T-cells to kill virally infected cells
65
Q

What is the major context of pathological apoptosis?

A

Apoptosis eliminates cells that have been injured or genetically altered beyond repair.

  • No severe host reaction
  • keep tissue damage to a minimum
66
Q

What are examples of pathological apoptosis?

A
  1. DNA damage- elimination may be better than risking mutation
  2. Accumulation of misfolded proteins-> ER stress
  3. Viral infection which causes cell injury
  4. Atrophy in parenchymal organs after duct obstruction
67
Q

What is the major context of physiological apoptosis?

A

It is a normal phenomenon that eliminates cells no longer needed to maintain a constant number of cells in a certain tissue type

68
Q

What are examples of physiological apoptosis?

A
  1. embryogenesis
  2. involution of hormone dependent tissue after hormone withdraw (endometrial cells in menstruation/lactating breast cells after weaning)
  3. Cell loss in proliferating populations (intestinal crypt cells)
  4. Neutrophils in acute inflammation when they have served their purpose
  5. Elimination of self-reactive lymphocytes
  6. cytotoxic T-cells to kill virally infected cells
69
Q

What is the major context of pathological apoptosis?

A

Apoptosis eliminates cells that have been injured or genetically altered beyond repair.

  • No severe host reaction
  • keep tissue damage to a minimum
70
Q

What are examples of pathological apoptosis?

A
  1. DNA damage- elimination may be better than risking mutation
  2. Accumulation of misfolded proteins-> ER stress
  3. Viral infection which causes cell injury
  4. Atrophy in parenchymal organs after duct obstruction
71
Q

What is the alternative name for the intrinsic pathway of apoptosis?

A

Mitochondrial pathway

72
Q

What is the alternative name for the extrinisic pathway of apoptosis?

A

The death receptor pathway

73
Q

The choice between cell death and cell survival depends on the __________ of the motochondria which is controlled by the ______ family of proteins./

A

permeability; BCL2

74
Q

What proteins in mitochondria sense damaged DNA, misfolded proteins, or deprivation of growth factors?
What factors do these proteins activate?

A

BH3 proteins

They activate Bak and Bax

75
Q

What activates Bak and Bax?

What do they do?

A

They are activated by BH3 proteins and are proapoptotic. They form a channel through which cytochrome C can escape to the cytosol.

76
Q

What inhibits Bak and Bax?

A

Bcl2 and Bclx

77
Q

What does cytochrome C activate?

A

Caspase 9

78
Q

What organ does one typically see an excess of glycogen?

A

renal tubular epithelium, cardiac myocytes, pancreatic b-cells (islets of langerhaans)

79
Q

Describe the steps in the extrinsic apoptotic pathway.

A
  1. TNF receptors or Fas on the surface of the cell sense a ligand that triggers apoptosis
  2. Caspase 8 is recruited which is a central mediator that activates pro-apoptotic members of Bcl2
80
Q

Where do the intrinsic and extrinsic apoptotic pathways converge?

A

initiator caspase 9 (intrinsic) and 8 (extrinsic) activate an executer caspase = caspase 3

81
Q

What is autophagy?

When does it occur?

A

“self-eating” where the lysosome digests the cells own components.This occurs when there is nutrient deprivation

82
Q

Why would defective autophagy be a cause of neuronal death?

A

autophagy is involved in the clearance of misfolded proteins (mainly in neurons and hepatocytes).
If autophagy is defective, the misfolded proteins can build up which would trigger apoptosis–> neuronal death

83
Q

What are the four major pathways for abnormal intracellular accumulations?

A
  1. abnormal metabolism (fatty liver)
  2. defect in protein folding, transport
  3. Lack of an enzyme leads to a build up of substrate
  4. ingestion of indigestible material (pigments)
84
Q

Where does intracellular accumulations of fat normally occur?
What is the morphological appearance?

A

In the parenchyma of the liver where triglycerides accumulate.
The morphological appearance is frothy because there are a lot of small lipid bubbles in the hepatocyte

85
Q

What stain would you use to check for excess Fe?

A

Prussian blue

86
Q

Where does cholesterol accumulate in cells?

A

phagocytic cells that become overloaded with triglycerides, cholesterol and cholesteryl ester

87
Q

Where would one see protein accumulations in cells?

A

When excess is presented to the cells or if the cells synthesize excessive amounts.

  • kidney–> large reabosorption of protein
  • ER–> new Ig in RER of plasma cells = eosinophilic Russel bodies
88
Q

What does protein accumulation look like morphologically?

A

pink, hyaline cytoplasm droplets

89
Q

If you see a Russel body (eosinophilic) in a plasma cell, you know there is an accumulation of what?

A

protein

90
Q

What organ does one typically see an excess of glycogen?

A

renal tubular epithelium, cardiac myocytes, pancreatic b-cells (islets of langerhaans)

91
Q

What is the most common exogenous pigment?

A

carbon dust (anthracotic pigment)

92
Q

Where would one identify anthracotic pigment (carbon dust)?

A

In the alveolar macrophages (because it is ingested via air pollution) and then in lymph nodes

93
Q

Where would one see lipofuscin granules?

What is the appearance?

A

This is “wear and tear pigment” so it is seen in heart liver and brain tissue with age and atrophy.
It appears brownish-yellow and granular.

94
Q

Where would one see melanin?

What is the appearance?

A

It is a brown-black pigment that is synthesized by melanocytes in the epidermous

95
Q

What is hemosiderin?
Where would one find its accumulation?
What is the appearance?

A

It is a Hb derived granular pigment.
It is gold-brown and accumulates in tissue where there is local or systemic accumulation of Fe.
Usually pathogenic, but can be seen in small amounts in bone marrow, spleen and liver where RBCs are degraded.

96
Q

What is an excess of hemosiderin called?

A

hemosiderosis –> hemochromatosis

97
Q

What stain would you use to check for excess Fe?

A

Prussian blue

98
Q

What is the deposition of Ca salts with smaller amounts of Fe, Mg and other mineral in dead or dying tissue?

A

dystrophic calcification

99
Q

What are the major differences between dystrophic and metastatic calcification?

A

Dystrophic is calcium build up in dead/dying tissue
Metastatic is calcium build up in normal tissue.

Metastatic has elevated serum Ca and is a result of a derangement of Ca metabolism.
Dystrophic has normal serum levels and is NOT a result of dearangement of Ca metabolism

100
Q

What is the most common situation where one would see dystrophic calcification>

A

atherosclerosis

101
Q

What is the ultimate end product of dystrophic calcification?

A

calcium phosphate

102
Q

What are common causes of hypercalcemia which leads to metastatic calcification?

A
  1. increases parathyroid hormone
  2. destruction of bone
  3. vitamin-D disorders
  4. renal failure
103
Q

What is the deposition of Ca salts with smaller amounts of Fe, Mg and other mineral in dead or dying tissue?

A

dystrophic calcification

104
Q

What are the major differences between dystrophic and metastatic calcification?

A

Dystrophic is calcium build up in dead/dying tissue
Metastatic is calcium build up in normal tissue.

Metastatic has elevated serum Ca and is a result of a derangement of Ca metabolism.
Dystrophic has normal serum levels and is NOT a result of dearangement of Ca metabolism

105
Q

What is the most common situation where one would see dystrophic calcification>

A

atherosclerosis

106
Q

What is the ultimate end product of dystrophic calcification?

A

calcium phosphate

107
Q

What are common causes of hypercalcemia which leads to metastatic calcification?

A
  1. increases parathyroid hormone
  2. destruction of bone
  3. vitamin-D disorders
  4. renal failure

Fundamentals Block 1 (7 decks)

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