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General Pathology > cell injury and death > Flashcards

cell injury and death Flashcards

1
Q

what are the cellular adaptive responses to stress and injury?

A

–Atrophy
–Hypertrophy
–Hyperplasia
–Metaplasia

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2
Q

what is the difference between hypertrophy and hyperplasia

A

hypertrophy is increase in cell size vs hyperplasia is an increase in cell number

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3
Q

2 ways of irreversible cell injury (cell death)?

A

necrosis and apoptosis

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4
Q

define the atrophy

A

Decrease in size or number of cells due to loss of cell substance (resulting in a decrease in the size of the organ)

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5
Q

atrophy can be both physiologic and pathologic. True/False

A

True.

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6
Q

give examples of atrophy

A

–Decreased workload (atrophy of disuse)
–Loss of innervation
–Diminished blood supply
–Inadequate nutrition (cachexia)
–Loss of endocrine stimulation
–Aging
–Fetal development (atrophy of thyroglossal duct)
–Senile atrophy: due to the physiological aging of cells
Affects all organs; includes the formation of lipofuscin deposits (especially in the heart and liver), which are formed by oxidation and polymerization of lysosomal contents.

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7
Q

define hypertrophy

A

Increase in the size of cells (resulting in an increase in the size of the organ)

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8
Q

what is the mechanism of hypertrophy?

A

– Involves gene activation protein synthesis and production of organelles

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9
Q

what type of cells undergo hypertrophy?

1) labile
2) stable
3) permanent

A

permanent

  • -Occurs in cells incapable of division
  • -No new cells, just larger cells
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10
Q

give examples of physiological vs pathological hypertrophy

A

1)Physiologic
– A skeletal muscle with exercise
2)Pathologic
– Left ventricular hypertrophy in hypertension

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11
Q

define hyperplasia

A

Increase in the number of cells (and usually the size of the organ)

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12
Q

permanent cells can undergo hyperplasia. True/False

A

False.
•Occurs in organs capable of cellular division
•Often associated with hypertrophy

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13
Q

give examples of physiologic and pathologic hyperplasia

A

•Physiologic
– Hormonal (breast/ uterus during pregnancy)
– Compensatory (partial hepatectomy)
•Pathologic
– Excessive hormonal / growth factor (thyroid, endometrial hyperplasia)

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14
Q

hyperplasia is controlled or uncontrolled?

A

Controlled Process but fertile soil for cancer

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15
Q

define metaplasia

A

Reversible change in which one adult cell type is replaced by another adult cell type and involve genetic reprogramming of stem cells

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16
Q

metaplasia is reversible or irreversible?

A

reversible

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17
Q

give examples of metaplasia

A

1) e.g. cigarette smoking- respiratory epithelium à squamous

2) Barrett’s esophagus- squamous epithelium à intestinal epithelium

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18
Q

metaplasia is a precursor for cancer. True/False

A

True.

Barrett metaplasia to adenocarcinoma

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19
Q

what are the causes of cellular injury?

A

• Oxygen deprivation
– Hypoxia- Low oxygen delivery to tissue
– Ischaemia- decrease in blood flow (↓ oxygen and nutrients)
– Shock- decrease in perfusion
• Physical agents (e.g. trauma, thermal injury, radiation)
• Chemical agents (e.g. poisons, environmental pollutants, and drugs)
• Infectious agents
• Immunologic reactions
• Genetic defects
• Nutritional deficiency or excess

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20
Q

give examples of immunologic reactions resulting in cell injury

A

autoimmune diseases

hypersensitivity reactions

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21
Q

give examples of genetic defects resulting in cell injury

A

misdirect cell metabolism (e.g., cystic fibrosis (CFTR gene), hemophilia A (Xq28 gene), α1-antitrypsin deficiency)

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22
Q

give examples of nutritional cellular injury

A

1) Malnutrition
- -Marasmus → decreased intake of calories
- -Kwashiorkor → decreased intake of protein
2) Excess calories: obesity → atherosclerosis → ischemic cell injury
3) Vitamin deficiencies: see the learning card vitamins for more information.
4) Impaired metabolism of glucose or ATP synthesis

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23
Q

cellular response to injury depends on what?

A

– Type
– Severity
– Duration of injury

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24
Q

consequences to the cell after injury depends on what?

A

cell
–Type
–State
–Adaptability

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25
Q

what cell structures are most vulnerable to injury?

A

–Mitochondria (aerobic respiration and ATP-synthesis)
–Cell membrane
–Synthetic apparatus (protein and enzymes)
–Cytoskeleton
–Genetic apparatus (DNA)

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26
Q

mitochondria are stable to injury.True/False

A

False.

  • -increased mitochondrial membrane permeability → cytochrome c release from mitochondria → activates apoptosis
  • -Decreased oxidative phosphorylation within mitochondria –↓ ATP
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27
Q

what are the mechanisms by which cells are injured?

A
  • Inhibition of aerobic respiration à ATP depletion
  • Generation of oxygen species (free radicals)
  • Defects in membrane permeability (membrane damage)
  • Disruption of calcium homeostasis (calcium influx)
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28
Q

how free radicals cause cell injury?

A

Reactive oxygen species cause damage to:
–DNA (via fragmentation)
–Cell membranes: via direct damage and lipid peroxidation → increased permeability
→ ↑ intracellular Ca2+ → activates numerous enzymes causing damage to the cytoskeleton, nuclear chromatin, activates apoptosis
→ leakage of cellular proteins → apoptosis and necrosis
–Mitochondrial membranes: via lipid peroxidation and transition pores → increased permeability
→ cytochrome c escapes from mitochondria and activate caspases → apoptosis
→ increased permeability to small molecules → draw in water → swelling → rupture → apoptosis and necrosis
–Cellular proteins
–Microvessels: microvascular injury → increased permeability of capillaries and arterioles → increased diffusion and fluid filtration → tissue swelling
–Recruit and activate platelets → increase coagulation
–Recruit and activate WBCs → worsen the immune response started by ischemia
–React with DNA and cause mutation

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29
Q

what are the features of reversible cell injury?

A

reversible cell injury→ results in cellular swelling (e.g., hydropic degeneration), nuclear chromatin clumping, decreased protein sysnthesis
1)Tissue hypoxia → decreased ATP production:
Decreased Na+/K+ ATPase → diffusion of Na+ and water into the cell → ↓ passive Ca2+ efflux and cellular/mitochondrial swelling
Disrupted Ca2+ ATPase pump activity → ↓ active Ca2+ removal from the cytoplasm into the extracellular space → Ca2+ accumulates inside the cell and activates degradative enzymes.
2)Low oxygen and ATP result in anaerobic respiration → ↑ lactate and ↓ intracellular pH → denatures proteins and causes clumping of nuclear chromatin
3)Detachment of ribosomes and polysomes → decreased protein synthesis

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30
Q

how activation of cellular enzymes result in cell injury?

A

–ATPase à decreased ATP
–Phospholipase à decreased phospholipids
–Endonuclease à nuclear chromatin damage
–Protease à disruption of the membrane and cytoskeletal proteins

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31
Q

what are the features of irreversible cell injury?

A

1)Mitochondrial changes
2)Extensive plasma membrane damage
3)Injury to lysosomal membranes
–Activation of enzymesà degrades the damaged cells
–Release of enzymes à damage to the surrounding cells

mechanism: degradation of phospholipids in the plasma membrane → rupture of the cell membrane → release of cytosolic enzymes into the serum and influx of Ca2+ into the cytoplasm → activation of lysosomal enzymes and protease (e.g., calpain) → ↑ breakdown of cellular proteins and damage cytoskeleton → autolysis
Rupture of lysosomes and release of lysosomal enzymes → autolysis
Increased mitochondrial membrane permeability → cytochrome c release from mitochondria → activates apoptosis

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32
Q

what are the nuclear changes seen with irreversible cell injury?

A

1) Pyknosis: shrinkage of the nucleus due to chromatin condensation
2) Karyorrhexis: fragmentation of the nucleus (mediated by endonucleases)
3) Karyolysis: disintegration or dissolution of the nucleus))

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33
Q

what are free radicals?

A

Extremely unstable, highly reactive chemical species with a single unpaired electron in the outer orbit

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34
Q

give examples of free radicals

A

– Superoxide O2.-
– Hydrogen peroxide H2O2
– Hydroxyl ion OH.

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35
Q

how activated oxygen species are produced?

A 
–Physiologic generation during oxidative phosphorylation 
–Radiation
–Inflammation
–Oxygen toxicity
–Chemicals and drugs (Paracetamol) 
–Metals (copper and iron)
–Reperfusion injury
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36
Q

overdose with what medication result in extensive production of ROS and liver injury?

A

paracetamol (acetaminophen)

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37
Q

what hereditary diseases result in extensive production of ROS and damage to the liver?

A

Hemochromatosis (iron accumulation) and Wilson disease (copper accumulation)

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38
Q

why reperfusion after myocardial infarction results in cell injury?

A

Oxygen is reintroduced to the previously ischemic tissue (oxygen toxicity) → activated endothelial cells and leukocytes generate reactive oxygen species (ROS)

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39
Q

what are the protective mechanisms against ROS

A

– Unstable with spontaneous decay
– Inactivation by enzymes
– Antioxidants (vitamin E, C)

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40
Q

what are the morphologic changes seen with reversible cell injury?

A

1)Cellular swelling (hydropic change, vacuolar degeneration)
2)Ultrastructural changes
– Plasma membrane alteration-blebbing
– Loss of microvilli
– Mitochondrial swelling
– Dilation of endoplasmic reticulum with the detachment of ribosomes
– Nuclear alterations

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41
Q

why cell swell in response to reversible injury?

A

Tissue hypoxia → decreased ATP production:
Decreased Na+/K+ ATPase → diffusion of Na+ and water into the cell → ↓ passive Ca2+ efflux and cellular/mitochondrial swelling
Na+/K+ ATPase pump functions to keep Na+ and water outside the cell and K+ inside the cell. When impaired, Na+ and water diffuse inside the cell leading to cellular swelling. Na+/Ca2+ exchanger, located on the plasma membrane, uses the chemical energy of the Na+ gradient to pump out Ca2+ ions out of the cytosol. When there are fewer Na+ ions outside the cell, more Ca2+ ions remain inside the cell.

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42
Q

what are the morphologic signs seen with irreversible cell injury?

A

Membrane damage
– cellular enzymes released (eg Troponin, amylase)
– Mitochondrial membrane– the release of cytochrome c
– Lysosome (lytic enzymes)-degradation of cell membrane phospholipids

43
Q

what is necrosis?

A

collective term for unprogrammed cell death and tissue destruction

44
Q

necrosis can be physiologic. True/False.

A

False.
Never physiologically induced
Always associated with an inflammatory reaction

45
Q

heterolysis vs autolysis?

A

cell death induced by hydrolytic enzymes from surrounding (usually inflammatory) cells. On the other hand, Autolysis is a death cell by its own enzymes.

46
Q

necrosis is always associated with inflammation. True/False

A

True.

In contrast, there is never inflammation with apoptosis

47
Q

if there is breakdown plasma membrane of the mitochondrial membrane, the injury is reversible. true/False

A

False

if the membrane is damaged, it is always irreversible!!!!!!!!!!!!!!!!!!!!!!!!

48
Q

why necrosis is associated with cytoplasmic eosinophilia?

A

Increased red staining (eosinophilia) is predominant in H&E staining because of the binding of eosin to denatured intracellular proteins.

49
Q

list types of necrosis

A

1) Coagulative necrosis
2) Liquefactive necrosis
3) Caseous necrosis
4) Fat necrosis
5) Fibrinoid necrosis
6) Gangrenous necrosis

50
Q

describe coagulation necrosis

A

1) A specific morphologic pattern of necrosis with preservation of the structural outlines
2) Characteristic of hypoxic cell death except in the brain
3) Cell shape and organ structure are preserved
4) Nuclei disappear

51
Q

what is the pathophysiology of coagulation necrosis?

A

—Decreased oxygen delivery → decreased ATP
Anaerobic metabolism → increased lactic acid production → decreased pH → denaturation of proteins (including proteolytic enzymes) → cell death
—Impaired Na+/K+-ATPase → ↑ intracellular Na+ → ↑ intracellular H2 → cell swelling

52
Q

in coagulation necrosis cell architecture is preserved. True/False

A

True

vs caseous necrosis

53
Q

give examples of coagulation necrosis

A

1) Myocardial, splenic, hepatic, and renal infarction
2) Gangrene (wet gangrene is liquefactive)
3) Organ damage caused by acidic solutions

54
Q

describe liquefactive necrosis

A

1) Transformation of solid tissue into a liquid mass
2) Complete digestion of the dead cells
3) Tissue structure destroyed
4) Enzymatic lysis of cells
5) Characteristic of bacterial and some fungal infection (abscess) and hypoxic cell death in the central nervous system

55
Q

hypoxic damage in all organs result in coagulation necrosis.True/False

A

False

except in brain

56
Q

what is the pathophysiology of liquefactive necrosis

A

Release of hydrolytic enzymes from neutrophilic lysosomes that digest the affected tissue

57
Q

what is the microscopic appearance of liquefactive necrosis

A

1) Macrophages and cellular debris (early) followed by cystic spaces or cavitations (late)
2) In bacterial infections → cellular debris and neutrophils

58
Q

does tissue structure is preserved in liquefactive necrosis?

A

no, destroyed

59
Q

give examples of liquefactive necrosis

A

1) Bacterial abscesses (purulent infection)
2) Stroke
3) Pancreatitis (due to enzymatic damage to the parenchyma)
4) Organ damage caused by alkaline solutions

60
Q

acidic vs alkaline solutions cause what type of necrosis?

A

coagulation vs liquefactive

61
Q

describe caseous necrosis

A

1) Distinctive form of necrosis, characteristic of tuberculous infection
2) Cheesy, crumbly, white gross appearance
3) Granular debris surrounded by a ring of granulomatous inflammation
4) Macrophages, epitheloid cells, and multinucleated giant cells (Langhans giant cell) surround a focus of infection

62
Q

Cellular debris in a granular pattern, epitheloid cells and multinucleated giant cells that form granulomas are characteristic of what type of necrosis?

A

caseous

63
Q

give examples of infections causing caseous necrosis

A

Tuberculosis
Histoplasmosis
Nocardiosis

64
Q

describe fat necrosis

A

1) Necrosis of fat, induced by lipases (pancreas or macrophages)
2) Fatty acids complex with Calcium to create calcium soaps
3) Fat trauma, fat necrosis in pancreatitis

65
Q

what is the pathophysiology of fat necrosis?

A

Release of lipase and triglycerides from the cytoplasm of damaged cells → lipase breaks down triglycerides → fatty acids bind calcium → saponification (esp. in acute pancreatitis, traumatic breast injury)

66
Q

what is the microscopic appearance of fat necrosis

A

1) Adipocytes with no nuclei

2) Saponification: dark blue appearance on H&E staining

67
Q

describe fibrinoid necrosis

A

1) Necrotic damage to the blood vessel wall

2) Associated with malignant hypertension and vasculitis

68
Q

what is the pathophysiology of fibrinoid necrosis

A

Vessel wall damage by immune complexes (type III hypersensitivity reaction) → fragmentation of collagenous and elastic fibers

69
Q

what is the microscopic appearance of fibrinoid necrosis

A

Vessel wall damage with fragments of embedded cellular debris, serum, and fibrin
Necrotic areas stain intense red

70
Q

causes of fibrinoid necrosis?

A
  • Polyarteritis nodosa
  • Rheumatoid arthritis
  • Preeclampsia
  • Hypertensive emergency
71
Q

describe gangrenous necrosis

A

1) Not a distinctive pattern of cell death (clinical term)
2) Coagulative necrosis (mummified tissue- dry gangrene)
3) Characteristic of ischaemia of the lower limb
4) Ischaemia with secondary bacterial infection (liquefactive necrosis- Wet gangrene)
5) Gas gangrene- Clostridium infection

72
Q

what is the cause of wet gangrene?

A

caused by superinfection of dry gangrene

73
Q

what bacteria can cause gangrene?

A

Clostridium perfringens: gas gangrene

74
Q

describe apoptosis

A

1) programmed cell death
2) Greek word for “falling off”
3) Involves single cells or small clusters
4) Physiologic and pathologic processes

75
Q

apoptosis can be both physiologic and pathologic. True/False

A

True

76
Q

apoptosis is always associated with inflammation.True/False

A

False.

vs necrosis

77
Q

give examples of physiologic apoptosis

A

– during embryogenesis
– Hormone (involution of breast, endometrial shedding)
– Death of inflammatory cells after inflammation
– Cell deletion in proliferating populations-intestinal epithelium
– Deletion of autoreactive T cells in thymus (failure might result in autoimmunity)

78
Q

give examples of pathologic apoptosis

A

– Virus-infected cells
– Cells with DNA damage
– Tumor cells

79
Q

apoptosis is energy dependent. True/False

A

true

80
Q

Usually affects individual cells and not groups of cells

True/False

A

True

vs necrosis

81
Q

list anti- vs pro-apoptotic genes

A

Bad and Bax have a proapoptotic effect, whereas Bcl-2 and Bcl-xL have an antiapoptotic effect!

82
Q

does plasma membrane is destroyed in apoptosis?

A

no, intact

83
Q

what are the histopathological features of apoptosis?

A

1) Shrunken and irregularly shaped cells with membrane blebbing
2) The cell detaches from other cells or the extracellular matrix.
3) Nuclear changes (pyknosis, karyorrhexis, karyolysis)
4) Degradation of the cell into apoptotic bodies
5) Phagocytosis by macrophages
6) DNA laddering (fragments in multiples of 180 base pairs) is seen on gel electrophoresis
7) Eosinophilia of the cytoplasm

84
Q

what are apoptotic bodies?

A

The cytoplasm and cell organelles form small bubbles and the endonucleases degrade the chromatin in the nucleus, resulting in nuclear fragmentation and apoptotic bodies.

85
Q

what are the stimuli to induce apoptosis?

A

– Internal signals- mitochondrial damage, DNA damage, decreased hormonal stimulation
– Hypoxia and other types of exogenous damage to the cell (radicals, irradiation, toxins)
– Growth factor withdrawal
– Specific signals such as TNF-alpha and ligands (TRAIL, FasL) activate the apoptotic program of the cells via binding to death receptors (DR 4/5, Fas, TNF-R).
Cytotoxic T cells, which recognize a pathogen on the target cell
– Denervation

86
Q

describe intrinsic pathway (mitochondrial) of apoptosis

A

1) p53 is activated through DNA damage (e.g., chemical toxins, radiation).
2) p53 leads to an intracellular increase of proapoptotic proteins of the Bcl-2 family (e.g., Bax or Bad).
3) These proteins increase the permeability of the mitochondrial outer membrane, e.g., through the formation of a membrane channel by the heterodimer Bax/Bad.
4) Cytochrome c enters the cytosol from mitochondria through the membrane.
5) Cytochrome c binds to APAF-1 (apoptotic protease activating factor-1) in the cytosol, forming a wheel-like structure, known as an apoptosome.
6) The complex of cytochrome c and APAF-1 converts procaspase 9 into active caspase 9.
7) Caspase 9 activates executioner caspases such as caspase 3.

87
Q

describe the extrinsic pathway of apoptosis

A

1) extracellular ligands (e.g., TNF-α, TRAIL, or FasL) bind to a death receptor on the cell surface.
2) The receptor-ligand complex activates initiator caspases such as caspase 8.
3) Initiator caspase activates executioner caspases such as caspase 3.

88
Q

what are caspases?

A

1)Enzymes from the group “Cysteine-ASpartic ProteASES” that cleave proteins and peptides and attack the cell membrane, nucleus, and cytoplasm
Association: Caspase 8 is not only a part of the extrinsic pathway but also stimulates the intrinsic pathway by altering the permeability of the inner mitochondrial membrane.
2)Caspases involved in apoptosis can be differentiated into initiator caspases (caspases 2, 8, 9, and 10), which can initiate apoptosis via activation of executioner caspases, and executioner caspases (caspases 3, 6, and 7), which induce cell death through cleavage of other cell proteins (structural proteins, DNases, etc.).

89
Q

what is endonuclease?

A

An enzyme that is responsible for the cleavage of nucleotides and the release of DNA bases.

90
Q

examples of disorders associated with increased apoptosis?

A

– AIDS (T cells)

– Neurodegenerative diseases (neurons)

91
Q

examples of diseases associated with decreased cell apoptosis?

A

– Neoplasia
– Autoimmune disorders
1)Follicular lymphoma → translocation t(14;18) → Blc-2 (regulator of apoptosis) on chromosome 18 is translocated to the immunoglobulin heavy chain locus on chromosome 14 → overexpression of Bcl-2 → abnormal lymphocytes never died and produce cancer.
2)Burkitt lymphoma → translocation t (8;14) → c-myc (nuclear regulator protein) on chromosome 8 is translocated to the immunoglobulin heavy chain locus on chromosome 14 → overexpression of c-myc → associates with Bcl-2 → overexpression of c-myc and Bcl-2 → lymphoma
3) HPV encodes for protein E6 → E6 binds to p53 → inactivation of p53 → inability of p53 to arrest the cell cycle and to activate DNA repair genes → proliferation of abnormal cells → low-grade dysplasia → high-grade dysplasia → carcinoma in situ → invasive cervical carcinoma
4) HPV encodes for protein E7 → E7 binds to Rb → inability of Rb to bind to E2F and arrest the cell cycle → proliferation of abnormal cells → low-grade dysplasia → high-grade dysplasia → carcinoma in situ → invasive cervical carcinoma

92
Q

list few endogenous substances that accumulate inside cell with time

A

Lipofuscin is a pigment-like waste product, rich in lipid, accumulates in old age
Lipofuscin deposits are normal wear-and-tear, yellow-brown, granular pigments found in organs such as the heart, lung kidneys, liver, etc.

93
Q

list exogenous substances that can accumulate inside the cell

A

– Cell cannot degrade substance (carbon, tattoos)

94
Q

what is pathologic calcification?

A

Abnormal deposition of calcium salts with smaller amounts of iron, magnesium and other mineral salts

95
Q

2 types of pathologic calcification?

A

– Dystrophic calcification

– Metastatic calcification

96
Q

describe dystrophic calcification

A

A localized calcification in abnormal, damaged tissue in patients with normal serum calcium levels. Often seen in tissues that have been affected by the general “wear and tear” of aging (e.g., calcific aortic stenosis). Associated with fat necrosis (pancreatitis), infarcts, thrombi, congenital CMV, CREST syndrome, and atherosclerotic plaques

97
Q

what is the histology of dystrophic calcification?

A
  • Basophilic granules

- Psammoma bodies

98
Q

describe metastatic calcification

A

diffuse calcification of normal tissue (especially lung, kidney, and gastric mucosa) caused by chronic hypercalcemia or a high phosphate-calcium solubility product. Calcinosis of collecting ducts may lead to nephrogenic diabetes and renal failure. Associated with conditions that cause hypercalcemia (e.g., hyperparathyroidism, sarcoidosis, multiple myeloma).

99
Q

serum calcium level in metastatic vs dystrophic calcification?

A

increased vs normal

100
Q

hyperphosphatemia can cause metastatic calcification. True/False

A

True
eg. in chronic renal failure
increased phosphate bind calcium and deposit in tissues

101
Q

what organs are primarily affected in metastatic calcification?

A

–Primarily affects vessels, kidneys, lungs, and gastric mucosa

102
Q

what tissues are involved in dystrophic calcification?

A

Abnormal necrotic tissues or degenerated inflammatory sites

103
Q

what are the 2 theories of cellular aging

A

1)Wear-and-tear (accumulation of metabolic and genetic damage)
– Free radical damage throughout life
2)Intrinsic cellular aging (replicative senescence)
– Predetermined genetic programming
– Telomere shortening (incomplete replication of chromosome ends which ultimately result in cell arrest)

104
Q

what is a telomere?

A

The distal end of a chromosome that contains a non-coding, repetitive base sequence (TTAAGGG in humans). A chromosome is shortened with every successive cycle of DNA replication because the enzymes that replicate DNA cannot proceed all the way to the end of a DNA sequence. The presence of expendable, non-coding telomeres at the end of a chromosome ensures that important genetic information is not lost with every cycle of cell division.

General Pathology (9 decks)

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