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General Pathology (Fall 2014) > Lecture 1-3: Intro/Cell Injury (Castleman) > Flashcards

Lecture 1-3: Intro/Cell Injury (Castleman) Flashcards

1
Q

pathology*

A

study of dz; branch of med. focused on the essential nature of dz, esp. the structural, biochemical and functional changes in tissues and organs of the body that result in or are the result of dz

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2
Q

general pathology*

A

basic reactions of cells and tissues to injury that underlie all diseases. Involves degen, cell necrosis, edema, etc.

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3
Q

systemic or special pathology*

A

specific responses of organs and tissues to more or less well defined stimuli or in well-defined dzs

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4
Q

6 Basic Reactions of Cells and Tissue to Injury**

A

1) cell injury/death
2) tissue depositions and pigments
3) circulatory disturbances
4) inflammation and repair
5) disturbances of growth/neoplasia
6) neoplasia

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5
Q

anatomical path*

A

focuses on tissue changes at the gross, microscopic, ultrastructural, and molecular lvls to identify lesions and to make dx to understand dz and to aid tx and prevention. Includes surgical and necropsy path

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6
Q

necropsy path*

A

exam of animal post-mortem to identify pathologic processes and lesions present at the time of death and to provide info for better future disease treatment and control

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7
Q

surgical path*

A

study changes in samples collected by biopsy procedures

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8
Q

infarct*

A

small localized area of coag. necrosis resulting from failure of blood supply

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9
Q

infarct in dogs most likely caused by:*

A

bacterial endocarditis

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10
Q

deprivation of blood supply to tissue in artery w/o a collateral blood supply –>*

A

coagulation necrosis

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11
Q

how does bacterial dissemination to the kidney result in thrombosis?*

A

via coag. and platelet aggregation

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12
Q

disease*

A

abnormal body process with a char. set of signs/symptoms and lesions that may affect the whole body or any of its parts. Begins with injury at the molecular and cellular level

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13
Q

cell injury*

A

damage or pathologic alterations in cell molecules or cell structures

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14
Q

lesion*

A

cell alteration assoc. with disease

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15
Q

Causes of cell injury (8)*

A

1) hypoxia/hypoxemia
2) physical agents
3) chemicals/drugs
4) infectious agents
5) immunologic rxns
6) genetic defects
7) nutritional imbalances
8) aging

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16
Q

3 Main responses to cell injury**

A

1) Adaptation
2) Reversible cell injury
3) Irreversible cell injury (from necrosis to apoptosis)

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17
Q

necrosis*

A

pattern of cell death that often follows hypoxic, toxic and microbial injury and is char. by cell swelling with nuclear changes such as pyknosis and karyorrhexis. Requires biochem. changes and time to occur

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18
Q

pyknosis*

A

irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis (web)

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19
Q

karyorrhexis*

A

destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distr. irregularly throughout the cytoplasm (web)

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20
Q

apoptosis*

A

pattern of cell death that is induced by a tightly reg. intracellular program in which cells induced to die activate enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins leading to nuclear frag. w/o loss of PM integrity

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21
Q

reversible cell injury*

A
  • cell injury w/ loss of cell fx and structural changes
  • cell CAN revert to normal if insult removed
  • char. by cell swelling, chromatin clumping, lipidosis
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22
Q

cell swelling caused by:*

A

abnormality in the membrane’s ion/water transport mech. so that cell accumulates water (loss of ATP-dependent Na transport system in the plasma membrane causes Na, Ca, H2O influx). Ca influx increases intracellular protease activity and “poisons” mitochondria.

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23
Q

chromatin clumping*

A

chromatin becomes markedly coarse as a result of degen. changes. Decreased oxidative phosphorylation –> increased anaerobic glycolysis –> dec. cell glycogen –> inc. lactic acid –> dec. cell pH –> chromatin clumping

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24
Q

lipidosis*

A

accum. of lipid. Due to decreased protein synthesis leading to decreased lipid transport out of hepatocytes

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25
Q

ultrastructural changes of reversible cell injury*

A

1) dilation of ER
2) ribosomal detachment from RER
3) loss of microvilli/cilia
4) mitochondrial swelling
5) chromatin clumping
6) membrane blebs
7) lipid accum.

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26
Q

consequence of decreased protein synthesis*

A

accumulation of neutral triglycerides

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27
Q

Irreversible cell injury*

A
  • cell passes point of no return/can’t recover
  • nuclear changes (hallmark) ie. nuclear condensation, fragmentation, dissolution:
    • pyknosis
    • karyorrhexis
    • chromatolysis
  • high amplitude mitochondrial swelling
  • membrane defects
  • lysosomal membrane rupture
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28
Q

chromatolysis*

A

DNA broken down enzymatically and loses ability to be stained by various dyes such as hematotoxylin. Char. by loss of basophilic stain and increased eosinophilia

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29
Q

kidney convoluted tubules undergo ____ when blood supply is interrupted*

A

coagulation necrosis

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30
Q

EXAM Q: Which of the following are changes seen in reversible cell injury?***

A

A: mitochondrial swelling and swelling of ER. NOT pyknosis/karyorrhexis

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31
Q

EXAM Q: Which of the following are defining chars. of necrotic cells?***

A

A: pyknosis/karyorrhexis and nuclear chromatolysis

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32
Q

Chars. of coagulative necrosis*

A
  • nuclear changes
  • pyknosis
  • karyorrhexis
  • chromatolysis
  • increased eosinophilia of cytoplasm
  • cell borders still visible**
  • cooked appearance grossly
  • calcification may occur
  • vacuolization (moth-eaten appearance)
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33
Q

Patterns of necrosis*

A 
coagulative
liquefactive
caseous
gangrenous
fat
fibrinoid
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34
Q

Chars. of liquefactive necrosis*

A
  • loss of cell borders
  • granular basophilic and eosinophilic debris with nuclear fragments
  • tissue structure obliterated
  • often occurs in tissues with high fat content
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35
Q

Liquefactive necrosis pathogenesis*

A
  • high neutrophil influx (protease destruction)

- high fat content of tissue (i.e. brain)

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36
Q

chars. of caseous necrosis*

A
  • “cheese-like” quality grossly
  • loss of cell borders
  • tissue structure obliterated
  • center of lesions homogeously eosinophilic with scattered nuclear basophilia
  • hallmark: recruits macrophages, rather than neutrophils**
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37
Q

pathogenesis of caseous necrosis*

A
  • recruitment of macrophages with persistence of stimulus and inflammatory cell component breakdown
  • common in mycobacterial infections
38
Q

pathogenesis of gangrenous necrosis *

A
  • loss of blood supply to distal extremities

- hypoxia-induced necrosis

39
Q

apoptosis*

A

specialized form of cell death that is often triggered by specific receptor-mediated stimuli or by loss of signals on well differentiated cells. Occurs both physiologically and pathologically. Cell breaks up into smaller fragments and then phagocytized

40
Q

Physiologic examples of apoptosis*

A
  • embryogenesis
  • hormone-dependent physiologic involution and cycling
  • cell depletion in proliferating populations during tissue repair
  • deletion of autoreactive T cells in thymus
  • death of virus-infected cells induced by cytotoxic T cells
41
Q

Pathologic examples of apoptosis*

A
  • DNA damage
  • accum. of misfolded proteins
  • drug/cytokine induced cell death
  • viral induced cell death
  • pathologic atrophy of organs after duct obstruction
42
Q

Examples of pathologic inhibition of apoptosis*

A
  • neoplasm (i.e. p53 mutation)

- viral-induced proliferative diseases

43
Q

Cell functions that may be critical to tissue function and organismal survival

A
  • contractility
  • communication
  • absorption
  • secretion of glycosaminoglycans
  • secretion of proteolytic enzymes
  • nutrient storage
  • defense against microbial and parasitic invaders
44
Q

adaptation

A

changes in function and structure that maintain a homeostatic state and maintain cell viability. Cells may revert to previous structure and fx when the stress or injury is removed

45
Q

karyolysis

A

dissolution of chromatin

46
Q

Extrinsic pathway of apoptosis (6 steps)*

A

In general: FAS-Fas-ligand, TNF-TNF receptor interactions activate caspases

1) stim. of receptor by ligand
2) alteration in second signals
3) activation of capsases
4) activation of endonucleases and cytoskeleton breakdown
5) nuclear and cytoplasmic fragmentation
6) phagocytosis of apoptotic bodies
* no swelling/inflammation*

47
Q

What are caspases?*

A

enzyme cascade system

48
Q

withdrawal of growth factors initiates stim. of membrane pro-apoptotic molecules –>*

A

activates caspases –> apoptosis

49
Q

cytotoxic T-cells initiate necrosis by:*

A

bringing FAS ligand to FAS receptor. They help kill cells that become targeted by the cellular or adapted immune response

50
Q

what does granzyme B do?*

A

activates apoptotic pathway

51
Q

What does Bcl-2 do?*

A

inihibit mitochondrial permeability and therefore inhibits apoptosis

52
Q

Intrinsic (mitochondrial) pathway of apoptosis*

A

loss of stimuli or positive stimuli induce increased mitochondrial permeability and release of cytochrome c or other activators of the caspase system. mitochondrial permeability a critical event

53
Q

What circumstances can induce intrinsic pathway of apoptosis?*

A
  • mitochondrial injury/dysfunction
  • increased cytosolic Ca2+
  • oxidative stress
  • lipid peroxidation
54
Q

Does apoptosis have gross changes? Microscopic?*

A

RARELY gross. (i.e. lymphoid atrophy). Detectable microscopically

55
Q

Clicker Q: Mitochondrial release of cytochrome c contributes to the initiation of:*

A

apoptosis

56
Q

Clicker: Cell death is rarely assoc. with inflammation in: *

A

apoptosis

57
Q

Mitochondrial and ER swelling often accompanies:*

A

necrosis

58
Q

T/F: some injuries can induce both apoptosis and necrosis*

A

True. Dominance depends on severity/duration of injury

59
Q

Pyroptosis*

A

microbial products induce activation of inflammasome and apoptotic-like changes (i.e. activation of caspase 1 or IL-1)

60
Q

T/F: apoptosis and necroptosis can be regulated or programmed*

A

T

61
Q

activation of caspase 1 results in*

A

cell death with cell swelling due to membrane pores that are induced

62
Q

activation of IL-1 results in:*

A

fever and leukocyte recruitment

63
Q

post-mortem autolysis*

A

“self-digestion” after somatic death. Char. by diffuse gross changes (i.e. pale tissue) and NO tissue response microscopically

64
Q

Mechanisms of cell injury*** (7)

A 
ATP depletion
mitochondrial damage/dysfunction
influx of calcium
oxygen-derived free radicals
membrane permeability defects
DNA damage
protein misfolding
65
Q

Common pathways in cell death (4)*

A
  • ischemic/hypoxic injury
  • free radical injury
  • chemical injury
  • injury by infectious agents
66
Q

what is the result of Ca intracellular release? What do these results lead to? (4 things)*

A

Activation of enzyme systems including:

  • ATPase –> decreased ATP
  • Phospholipase –> decreased phospholipids
  • Protease –> disruption of membrane and cytoskeletal proteins
  • Endonuclease –> chromatin clumping
  • protease and phospholipase ultimately lead to membrane damage*
67
Q

Describe the flow of events resulting from hypoxic damage in REVERSIBLE injury?*

A

ischemia –> decreased mitochondrial ox. phos. –> decreased ATP –> decreased Na/K pump, increased glycolysis, detachment of ribosomes

68
Q

decreased Na/K pump function –> ??*

A

influx of Ca H2O, Na into cell. Efflux of K. Results in cell swelling, loss of microvilli, membrane blebs ER swelling, myelin figures

69
Q

increased glycolysis –> ??*

A

decreased pH/glycogen in the cell. Results in chromatin clumping, intracellular release and activation of lysosomal enzymes, decreased basophilia, nuclear changes, and protein digestion

70
Q

detachment of ribosomes –> ??*

A

decreased protein synthesis–> lipid deposition

71
Q

At what point does reversible cell injury from hypoxia become irreversible?*

A

Once membrane injury, intracellular release/activate of lysosomal enzymes, and/or influx of Ca occurs

72
Q

Review green star slide flow chart slide 22 and practice drawing on whiteboard

A

:)

73
Q

Free radical*

A

a chemical species that has a single unpaired electron in an outer orbital. I.e. OH, O2-

74
Q

Sources of free radicals*

A
  • absorption of radiant energy
  • redox rxns (i.e. Fenton rxn)
  • exposure to toxins
  • inflammation
  • aging
  • repurfusion injury
75
Q

Fenton rxn*

A

generates ferric iron and hydroxyl radical from ferrous iron and hydrogen peroxide. anything that leads to an abundance of ferrous iron will eventually kill cell via Fenton rxn due to generation of free radicals

76
Q

superoxide dismutase (SOD)*

A

breaks down superoxides into hydrogen peroxide and oxygen

77
Q

Damage induced by free radicals*

A
  • lipid peroxidation of membranes –> increased permeability and lipid autoperoxidation rxn
  • DNA damage leading to mutations and death
  • cross linking of proteins (esp. sulfhydryl rich proteins)
  • interaction with cytosolic molecules such as Hb

free radicals propagate more free radicals!

78
Q

fxn of catalase*

A

breaks down hydrogen peroxide to H2O and O2

79
Q

Common antioxidants, and their mech. of action*

A
  • sulfhydryl rich molecules (free radical scavengers)
  • Vitamin E (terminate lipid peroxidation)
  • Ceruplasmin and transferrin (bind copper and Fe+2, preventing Fenton rxn)
80
Q

glutathione peroxidase*

A

catalyzes conversion of hydroxyl free radicals to water

81
Q

most free iron in the body is in what state?

A

ferric iron (Fe+3)

82
Q

Reperfusion Injury is a combo of:*

A

hypoxic and free radical damage. Tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen (web)

83
Q

Series of events in reperfusion injury*

A
  • reduced blood flow –> hypoxic damage
  • increased xanthine oxidase activity
  • re-est. of blood-flow brings O2, Ca, inflammatory cells
  • O2 converted to superoxide anion and OH
  • inflamm. cells generate oxygen free rads
  • membrane damage, increased Ca, cell death
84
Q

2 examples of toxin-induced cell injury*

A

CCl4, Cyclophosphamide

85
Q

CCl4 effects*

A

activation of free-radical intermediate, lipid peroxidation, necrosis

86
Q

Cyclophosphamide effects*

A

(a chemo drug) induces apoptosis via caspases

87
Q

2 methods of bacterial-induced cell injury*

A

1) exotoxin (i.e. by Clostridia) –> indirect membrane damage
2) endotoxin –> direct membrane damage, apoptosis, indirect membrane damage via TNF-alpha

88
Q

Clicker: Which of the following contribute to formation of free radicals that initiate cell injury?**

A

UV radiation, Fenton rxn, and CCl4 metabolism in the liver (all of the above)

89
Q

Clicker: Which of the following mechs. contributes most to cell death in hypoxic tissue injury?**

A

ATP depletion

90
Q

Clicker: Ischemia reperfusion injury is characterized by which of the following mechs. of injury?**

A

ATP depletion and free radical injury. (NOT protein misfolding and apoptosis)

General Pathology (Fall 2014) (6 decks)

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