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
Nutritional imbalances
Deficiencies Overnutrition
26
One cause of congenital anomalies
Cytogenetic disorders/chromosomal aberrations
27
Enzymes defects, eg. Lysosomal storage disease
Mendelian Disorders(mutant genes)
28
Combined effects of environmental factors and 2 or more mutated genes
Multifactorial Inheritance
29
A workload Imbalances which cell injury occurs if stimulus prolonged and/or exceeds ability to adapt.
Overworked cells
30
Prolonged lack of stimulation can lead to atrophy and eventually the loss of cells.
Underworked cells
31
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
Cell Aging
32
Mechanisms of cell injury
General Consideration Biochemical Mechanisms Chemical (toxic) Injury
33
4 intracellular systems are particularly vulnerable to injury.
Cell membranes Mitochondria Protein synthesis Genetic apparatus
34
Are chemicals species with a single unpaired electrons in outer orbit
Free radicals
35
It occurs when free radical generation overwhelms antioxidant defense mechanisms.
Cell injury
36
Generation of free radicals
Cellular metabolism Enzymatic metabolism of exogenous chemicals Ionizing radiation Divalent metals
37
Small amounts produced from cell redox reactions
Cellular metabolism
38
Some intermediary metabolites of chemical/drugs are highly reactive free radicals.
Enzymatic metabolism of exogenous chemicals
39
Hydrolyzes water into hydroxyl (•OH) and hydrogen (H°) free radicals
Ionizing radiation
40
Accept or donate free electrons during certain intracellular reactions
Divalent metals
41
Main sites of damage
Damage of membranes (lipid peroxidation) Damage of Proteins Damage of DNA
42
Protective mechanisms of the cell
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
Enzymes which are involved in neutralizing free radicals:
Glutathione peroxidase Superoxide dismutase (SOD) Catalase
44
A selenium-containing enzyme which catalyzes GSH to GSSG
Glutathione peroxidase
45
All cells are depending on oxidative metabolism for long term survival, regardless of glycolytic ability.
Mitochondrial damage
46
Some chemicals act directly by damaging particular organelles or critical cell molecules
Direct interaction
47
Damages mitochondrial cytochrome oxidase-blocks oxidative phosphorylation
Cyanide
48
Prevents citrate from being used in the citric acid cyclem
Fluoroacetate
49
Major adaptive responses:
Atrophy Hypertrophy Hyperplasia Aplasia Hypoplasia Metaplasia Dysplasia
50
Decrease in the amount of a tissue or organ after normal growth has been attained.
Atrophy
51
Not dead or necessarily badly injured but they have a reduced functional capacity
Atrophic cells
52
Organelles removed by autophagocytosis and decreased proteins by?
Ubiquitin-proteosome pathway
53
Organs are increased in size
Hypertrophy
54
Increase in organ size or tissue mass caused by an increase in the number of constituent cells
Hyperplasia
55
Two features consistently characterize irreversibility
Inability to reverse mitochondrial dysfunction Profound disturbances of membrane function
56
Reasons for irreversible injury
Inability to reverse mitochondrial dysfunction Profound disturbances of membrane function
57
Two main types of reversible cell injury are recognized
Cellular swelling Fatty change
58
The most common and most important response to cellular injuries of all types
Cellular swelling
59
The process continues many vacuoles of variable size appear in the cytoplasm called?
Hydropic or vacuolar degeneration
60
The severe process of continues vacuoles of variable size appear in the cytoplasm
Ballooning degeneration
61
A sick cell, a reversible form of injury, and an adaptive change that may progress to cell death
Degeneration
62
Refers to the rapid death of a limited portion of an organism and is considered to be final stage in irreversible degeneration.
Necrosis
63
Term used for the entire process of degeneration and death of cells
Necrobiosis
64
The morphologic appearance is due to 2 concurrent processes.
Denaturation of proteins Enzymatic digestion of the cell
65
Term often used to describe the changes that occur in all of the cells after an animal has died.
Autolysis
66
Types of necrosis
Coagulation necrosis Liquefactive necrosis Caseous necrosis Gangrenous necrosis Fat necrosis Infarction(Ischemic Necrosis) Zenker's Necrosis
67
Most common manifestation of cell death
Coagulation Necrosis
68
3 patterns of nuclear changes
Karyolysis Pyknosis Karyorrhexis
69
Dissolution/fading of the nucleus
Karyolysis
70
Shrunken and densely basophilic nuclei
Pyknosis
71
Nuclear Fragmentation
Karyorrhexis
72
Occurs when enzymatic digestion of necrotic cells predomjnates over protein denaturation
Liquefactive necrosis
73
Typical lession seen with specific bacterial diseases
Caseous Necrosis
74
Occurs when saprophytic bacteria grow in necrotic tissue.
Gangrenous Necrosis
75
Two types of gangrene
Wet gangrene Dry gangrene
76
Occurs in necrotized portion of the skin with moisture loss due to evaporation and drainage presence of saprophytic bacteria
Dry gangrene
77
When the coagulative necrosis of dry gangrene is modified by the liquefactive action of invading saprophytic/putrefactive bacteria.
Wet gangrene
78
Form of coagulative necrosis resulting from a sudden deprivation of blood supply
Infarct
79
Characterized by loss of striations following necrosis
Zenker's necrosis
80
A shallow area of necrosis confined to epidermis that heals without scarring
Erosion
81
An excavation of a surface produced by necrosis
Ulcer
82
A piece of necrotic tissue in the process of separation from viable tissue
Slough
83
An area of liquefactive necrosis of the nervous tissue. Literally means "softening"
Malacia
84
Isolated necrotic mass
Sequestrum
85
Favorable outcome or Sequela of necrosis
Organization Petrifaction Ossification Aseptic autolysis
86
Falling off
Apoptosis
87
Death of a single cells as a result of activation of a genetically programmed "suicide" pathway.
Apoptosis
88
Pigments and other tissue deposits
Lipid accumulation Glycogen accumulation Protein Accumulation Amyloid and amyloidosis Endogenous pigments Pathologic calcification(mineralization) Crystals Exogenous pigments Parasite pigments
89
Endogenous pigments compised of:
Lipofuscin Ceroid Melanin Copper Hemosiderin Biliburin Hematoidin Acid-Hemalin
90
Other enzymes used to evaluate tissue damage are:
Lactic dehydrogenase(LHD) Creatine phosphokinase(CPK) Alkaline Phosphatase (AP)
91
Post mortem Artifacts
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
Types of calcification
Dystrophic calcification Metastatic Calcification
93
Exogenous pigments
Antracosis Silicosis Asbestosis