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PATHOLOGY > CELLULAR INJURY CELL ADAPTATION AND CELL DEATH > Flashcards

CELLULAR INJURY CELL ADAPTATION AND CELL DEATH Flashcards

1
Q

As cells encounter some stresses they may make functional or structural adaptations to maintain viability/homeostasis

A

Cellular Adaptation

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2
Q

Adaptive processes

A

Atrophy
Hypertrophy
Hyperplasia
Metaplasia

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3
Q

Limits of adaptive response are exceeded, or in certain instances when adaptation Is not possible

A

Cell Injury

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4
Q

Removal of stress/injurious stimulus results in complete restoration of structural and functional integrity

A

Reversible cell injury

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5
Q

If stimulus persists the cell will suffer

A

Irreversible cell injury/ cell death

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6
Q

One of the most crucial events in Pathology and can affect any type of cell

A

Cell death

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7
Q

Two principle morphologic patterns that are indicative of cell death

A

Necrosis
Apoptosis

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8
Q

Type of cell death characterized by severe membrane injury and enzymatic degradation; always a pathologic process.

A

Necrosis

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9
Q

Regulated form of cell death; can be a physiologic or pathologic process

A

Apoptosis

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10
Q

Causes of cell injury

A

Hypoxia( oxygen deficiency)
Physical Agents
Chemical, drugs & toxins
Infectious agents
Immunologic radiations
Genetic abnormalities
Nutritional Imbalances
Cell Aging

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11
Q

Hypoxia Occurs with

A

Deficient blood supply
Reduced-oxygen carrying capacity of the blood
Interference with respiratory chain/oxidative phosphorylation

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12
Q

Most important and common causes of cell injury and cell death

A

Hypoxia

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13
Q

Causes impairment of oxidative respiration

A

Hypoxia

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14
Q

Deficiency of blood supply from impedded arterial flow or reduced venous drainage

A

Ischemia

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15
Q

Localized area of ischemic necrosis

A

Infarction

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16
Q

Severity of a physical injury may be increased by tissue hypoxia die to associated local vascular injury

A

Physical Agents

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17
Q

Physical Agents

A

Direct mechanical trauma
Temperature extremes
Radiation
Electrocaution
Sudden changes in atmospheric pressure

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18
Q

Chemical drugs& toxins

A

In organic poisons
Organic poisons
Manufactured chemicals
Physiologic compounds
Plant toxins
Animal toxins
Bacterial toxins/ mycotoxins

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19
Q

Infectious agents

A

Viruses
bacteria/rickettsiae/Chlamydia
Fungi
Protozoa
Metazoan prasite

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20
Q

Immunologic response

A

Immune response
Hypersensitivity (allergic) reactions
Autoimmune diseases

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21
Q

eg. Cells damaged as “innocent bystanders” in immune/inflammatory response.

A

Immune response

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22
Q

eg anaphylactic reaction to a foreign protein or drug

A

Hypersensitivity(allergic) reactions

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23
Q

Reactions to self-antigens

A

Autoimmune diseases

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24
Q

Genetic abnormalities

A

Cytogenetic disorders/chromosomal aberrations
Mendelian disorders(mutant genes)
Multifactorial inheritance

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25
Q

Nutritional imbalances

A

Deficiencies
Overnutrition

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26
Q

One cause of congenital anomalies

A

Cytogenetic disorders/chromosomal aberrations

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27
Q

Enzymes defects, eg. Lysosomal storage disease

A

Mendelian Disorders(mutant genes)

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28
Q

Combined effects of environmental factors and 2 or more mutated genes

A

Multifactorial Inheritance

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29
Q

A workload Imbalances which cell injury occurs if stimulus prolonged and/or exceeds ability to adapt.

A

Overworked cells

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30
Q

Prolonged lack of stimulation can lead to atrophy and eventually the loss of cells.

A

Underworked cells

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31
Q

The cumulative effects of a life time of cell damage leads to a diminished capacity of aged cells/tissues to maintain homeostasis and adapt to harmful stimuli

A

Cell Aging

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32
Q

Mechanisms of cell injury

A

General Consideration
Biochemical Mechanisms
Chemical (toxic) Injury

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33
Q

4 intracellular systems are particularly vulnerable to injury.

A

Cell membranes
Mitochondria
Protein synthesis
Genetic apparatus

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34
Q

Are chemicals species with a single unpaired electrons in outer orbit

A

Free radicals

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35
Q

It occurs when free radical generation overwhelms antioxidant defense mechanisms.

A

Cell injury

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36
Q

Generation of free radicals

A

Cellular metabolism
Enzymatic metabolism of exogenous chemicals
Ionizing radiation
Divalent metals

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37
Q

Small amounts produced from cell redox reactions

A

Cellular metabolism

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38
Q

Some intermediary metabolites of chemical/drugs are highly reactive free radicals.

A

Enzymatic metabolism of exogenous chemicals

39
Q

Hydrolyzes water into hydroxyl (•OH) and hydrogen (H°) free radicals

A

Ionizing radiation

40
Q

Accept or donate free electrons during certain intracellular reactions

A

Divalent metals

41
Q

Main sites of damage

A

Damage of membranes (lipid peroxidation)
Damage of Proteins
Damage of DNA

42
Q

Protective mechanisms of the cell

A

Storage and transport proteins
Antioxidants
Enzymes which are involved in neutralizing free radicals
Intracellular calcium and loss of calcium homeostasis
Mitochondrial damage
Defects in membrane permeability

43
Q

Enzymes which are involved in neutralizing free radicals:

A

Glutathione peroxidase
Superoxide dismutase (SOD)
Catalase

44
Q

A selenium-containing enzyme which catalyzes GSH to GSSG

A

Glutathione peroxidase

45
Q

All cells are depending on oxidative metabolism for long term survival, regardless of glycolytic ability.

A

Mitochondrial damage

46
Q

Some chemicals act directly by damaging particular organelles or critical cell molecules

A

Direct interaction

47
Q

Damages mitochondrial cytochrome oxidase-blocks oxidative phosphorylation

A

Cyanide

48
Q

Prevents citrate from being used in the citric acid cyclem

A

Fluoroacetate

49
Q

Major adaptive responses:

A

Atrophy
Hypertrophy
Hyperplasia
Aplasia
Hypoplasia
Metaplasia
Dysplasia

50
Q

Decrease in the amount of a tissue or organ after normal growth has been attained.

A

Atrophy

51
Q

Not dead or necessarily badly injured but they have a reduced functional capacity

A

Atrophic cells

52
Q

Organelles removed by autophagocytosis and decreased proteins by?

A

Ubiquitin-proteosome pathway

53
Q

Organs are increased in size

A

Hypertrophy

54
Q

Increase in organ size or tissue mass caused by an increase in the number of constituent cells

A

Hyperplasia

55
Q

Two features consistently characterize irreversibility

A

Inability to reverse mitochondrial dysfunction
Profound disturbances of membrane function

56
Q

Reasons for irreversible injury

A

Inability to reverse mitochondrial dysfunction
Profound disturbances of membrane function

57
Q

Two main types of reversible cell injury are recognized

A

Cellular swelling
Fatty change

58
Q

The most common and most important response to cellular injuries of all types

A

Cellular swelling

59
Q

The process continues many vacuoles of variable size appear in the cytoplasm called?

A

Hydropic or vacuolar degeneration

60
Q

The severe process of continues vacuoles of variable size appear in the cytoplasm

A

Ballooning degeneration

61
Q

A sick cell, a reversible form of injury, and an adaptive change that may progress to cell death

A

Degeneration

62
Q

Refers to the rapid death of a limited portion of an organism and is considered to be final stage in irreversible degeneration.

A

Necrosis

63
Q

Term used for the entire process of degeneration and death of cells

A

Necrobiosis

64
Q

The morphologic appearance is due to 2 concurrent processes.

A

Denaturation of proteins
Enzymatic digestion of the cell

65
Q

Term often used to describe the changes that occur in all of the cells after an animal has died.

A

Autolysis

66
Q

Types of necrosis

A

Coagulation necrosis
Liquefactive necrosis
Caseous necrosis
Gangrenous necrosis
Fat necrosis
Infarction(Ischemic Necrosis)
Zenker’s Necrosis

67
Q

Most common manifestation of cell death

A

Coagulation Necrosis

68
Q

3 patterns of nuclear changes

A

Karyolysis
Pyknosis
Karyorrhexis

69
Q

Dissolution/fading of the nucleus

A

Karyolysis

70
Q

Shrunken and densely basophilic nuclei

A

Pyknosis

71
Q

Nuclear Fragmentation

A

Karyorrhexis

72
Q

Occurs when enzymatic digestion of necrotic cells predomjnates over protein denaturation

A

Liquefactive necrosis

73
Q

Typical lession seen with specific bacterial diseases

A

Caseous Necrosis

74
Q

Occurs when saprophytic bacteria grow in necrotic tissue.

A

Gangrenous Necrosis

75
Q

Two types of gangrene

A

Wet gangrene
Dry gangrene

76
Q

Occurs in necrotized portion of the skin with moisture loss due to evaporation and drainage presence of saprophytic bacteria

A

Dry gangrene

77
Q

When the coagulative necrosis of dry gangrene is modified by the liquefactive action of invading saprophytic/putrefactive bacteria.

A

Wet gangrene

78
Q

Form of coagulative necrosis resulting from a sudden deprivation of blood supply

A

Infarct

79
Q

Characterized by loss of striations following necrosis

A

Zenker’s necrosis

80
Q

A shallow area of necrosis confined to epidermis that heals without scarring

A

Erosion

81
Q

An excavation of a surface produced by necrosis

A

Ulcer

82
Q

A piece of necrotic tissue in the process of separation from viable tissue

A

Slough

83
Q

An area of liquefactive necrosis of the nervous tissue. Literally means “softening”

A

Malacia

84
Q

Isolated necrotic mass

A

Sequestrum

85
Q

Favorable outcome or Sequela of necrosis

A

Organization
Petrifaction
Ossification
Aseptic autolysis

86
Q

Falling off

A

Apoptosis

87
Q

Death of a single cells as a result of activation of a genetically programmed “suicide” pathway.

A

Apoptosis

88
Q

Pigments and other tissue deposits

A

Lipid accumulation
Glycogen accumulation
Protein Accumulation
Amyloid and amyloidosis
Endogenous pigments
Pathologic calcification(mineralization)
Crystals
Exogenous pigments
Parasite pigments

89
Q

Endogenous pigments compised of:

A

Lipofuscin
Ceroid
Melanin
Copper
Hemosiderin
Biliburin
Hematoidin
Acid-Hemalin

90
Q

Other enzymes used to evaluate tissue damage are:

A

Lactic dehydrogenase(LHD)
Creatine phosphokinase(CPK)
Alkaline Phosphatase (AP)

91
Q

Post mortem Artifacts

A

Postmortem scavenging vs. predation
Rigor mortis
Algor mortis
Livor mortis
Postmortem clotting
Hemoglobin imbibition
Bile imbibition
Pseudomelanosis
Postmortem autolysis/decomposition
Putrefaction and postmortem emphysema(bloating)
Postmortem ruptures and organ displacements
Other abnormalities

92
Q

Types of calcification

A

Dystrophic calcification
Metastatic Calcification

93
Q

Exogenous pigments

A

Antracosis
Silicosis
Asbestosis

PATHOLOGY (4 decks)

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