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Pathology > Cell Adaption, Injury and Death > Flashcards

Cell Adaption, Injury and Death Flashcards

1
Q

Etiology

A

The underlying cause. (Genetic, acquired, or both)

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2
Q

Pathogenesis

A

Sequence of events that occurs in response to the injurious event. How the disease occurs.

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3
Q

Morphologic Changes

A

Appearances of tissues or cells that are characteristic in a given disease process. (Diagnostic pathology) Biochemical and molecular changes.

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4
Q

Functional derangement.

A

Symptoms (What a patient feels) and signs (What a physician sees), clinical course, outcome

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5
Q

Metabolic cause of cell/tissue injury.

A

Oxygen deprivation. HYPOXIA. Glucose and nutritional imbalance, etc.

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6
Q

Hypoxia

A

Oxygen deprivation. Neutrophils.

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7
Q

Physical causes of cell/tissue injury.

A

Cold, heat trauma, etc.

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8
Q

Chemical causes of cell/tissue injury.

A

Tylenol, alcohol, recreational drugs, pollutants, ingestion of toxic substances.

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9
Q

Immunologic Reactions that cause cell/tissue injury.

A

Allergies, autoimmune

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10
Q

Genetic causes of cell/tissue injury.

A

Chromosomal (Down’s), gene-specific (CF), etc.

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11
Q

Infectious causes of cell/tissue injury.

A

Bacteria, viruses, parasites, fungi, prions.

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12
Q

What is homeostasis?

A

Cell is in balance with environment and in a steady state, functioning as intended.

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13
Q

What is adaption?

A

Generally reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.

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14
Q

What does it mean when the damage is irreversible?

A

Terminal disease.

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15
Q

Hypertrophy

A

Increase in size in cells, often resulting in increase in size of organ. (Ex. Heart)

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16
Q

Atrophy

A

Decreased in cell size and number, resulting in reduced size of organ or tissue. (Ex. Brain, muscles)

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17
Q

Hyperplasia

A

Increase in number of cells. (Ex. Liver regeneration)

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18
Q

Metaplasia

A

Conversion of one cell type to another. (Ex. Bronchus, esophagus and heart burn)

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19
Q

Dysplasia

A

Alteration in size, shape and organization of cells within tissue. (Cancer)

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20
Q

What are the vulnerable systems of the cells?

A

Cell membranes, mitochondria and aerobic respiration, ER and synthesis of proteins and enzymes, DNA integrity and preservation of the genetic apparatus

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21
Q

Why is the cell membrane so easily injured?

A

Membrane faces the external environment and sustains trauma, extracellular oxidants, proteases, etc.

Requires a constant supply of ATP for normal function (ion pumps)

Lipid molecules in the membrane are easily oxidized and support an oxidative chain reaction called lipid peroxidation.

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22
Q

What are the 6 mechanisms of cell injury?

A
  1. Decrease in ATP
  2. Mitochondrial damage
  3. Entry of Ca2+
  4. Increase in ROS
  5. Membrane damage
  6. Protein misfolding, DNA damage
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23
Q

What effect does mitochondrial damage have on a cell?

A

Leakage of pro-appoptotic proteins and a decrease of ATP which leads to multiple downstream effects.

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24
Q

What effect does the entry of Ca2+ have on a cell?

A

Increase of mitochondrial permeability and activation of multiple cellular enzymes.

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25
Q

What effect does an increase of ROS (Reactive Oxygen Species) have on a cell?

A

Damage to lipids, proteins and DNA/

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26
Q

How does membrane damage affect the cell?

A

Plasma membrane: Loss of cellular components.

Lysosomal membrane: Enzymatic digestion of cellular components.

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27
Q

What effect does protein misfolding and DNA damage have on a cell?

A

Activation of pro-apoptotic proteins.

28
Q

What is the morphological evidence of a sublethal injury.

A

Swelling of ER and mitochondria. Loss of ribosomes. Cell stress response operates.

29
Q

What happens during recovery following a sublethal injury?

A

Removal of damaged components through autophagy, returning to a normal cell.

30
Q

What is the morphological evidence of a cell undergoing necrosis?

A

Early dead cell shows loss of nucleolus, no ribosomes, swelling of all mitochondria and ER.

It then undergoes nuclear condensadtion, membrane blebs and holes, and the lysosomes rupture.

Finally, there is fragmentation of all inner membranse and nuclear breakup.

31
Q

What is this an example of?

A

Hypertrophy

32
Q

What is pyknosis?

A

Cytoplasmic RNA is removes, resulting in a more intensely eosinophilic cytoplasm. The nucleolus is lost and the nucleus condenses, shrinks, and becomes intensely basophilic.

Dark, condensed, purple nucleus.

33
Q

What is karyorrhexis?

A

The pyknotic nucleus fragments.

34
Q

What is autolysis?

A

The process of dissolution of dead cells by intrinisc and extrinsic hydrolases.

35
Q

What stages of of cellular injury are reversible?

A

Cellular swelling in the early stages associated with the mitochondria and ER are still reverisble. The breakdown of plasma membrane, organelles and nucleus is irreversible.

It is thought that a critcally damaged membrane in association with cytoplasmic calcium accumulation and enzyme activation may be the point at which cellular damage is irreversible and cell death occurs.

36
Q

What is the general definition of necrosis?

A

Spectrum of morphologic changes that follow cell death in living tissure. Necrotic cells are usually found in contiguous sheets and often associated with accute inflammation.

37
Q

What is coagulative necrosis?

A

Dead cell remains a ghost like remnant of its former self. Classically seen in the heart, but occurs in all organs except for the brain. Cytoplasm is more eosiniphilic than normal. Nucleus undergoes pyknosis, karyorrhexis and karyolysis. Ultimately removed by scavenger white cells.

38
Q

What is liquefactive necrosis?

A

Dead cells dissolve away as lysosomal hydrolases digest cellular components and transforms it into a **liquid viscous mass. **Commonly seen in the brain and spleen and with acute bacterial infection.

39
Q

What is caseous necrosis?

A

Classically seen in tuberculosis. Chalky white appearance. A combination of coagulative and liquefactive necrosis.

40
Q

What is fat necrosis?

A

Occurs in adipose tissue. Typically follows acute pancreaitis aor pancreatic trauma. Saponification (soap production) happens due to the hydrolyzation of fats into free faty acids that then percipitate with calcium.

41
Q

What is hemorrhagic necrosis?

A

Dead tissue is suffused with extravasated RBCs. Happens when venous dranaige of a tissue is blocked and the tissue becomes severly congested.

42
Q

What is fibrinoid necrosis?

A

Used to describe the histologic appearance of arteries in cases of vasculitis and hyper tension when fibrin is deposited in the damaged necrotic arterial wall.

43
Q

What is gummatous necrosis?

A

Necrosis in the spirochaetal infection syphilis. The dead tissue is firm, rubbery with necrotic proteinaceous mass.

44
Q

What is apoptosis?

A

Programmed cell death or cellular suicide. It is tightly regulated.

45
Q

How is Apoptosis distinct from necrosis?

A
  1. No inflammatory reaction
  2. No loss of cell membrane integrity or leakage of cellular contents.
  3. Can coexist with necrosis.
  4. not necessarily a response to injury.
46
Q

When does apoptosis classically occur?

A

During embryogenesis. Hormone-dependent involution such as the menstrual cell. Tumors. Cytotoxic T cells. etc.

47
Q

What is the most characteristic feature of apoptosis?

A

Chromatin condensation.

48
Q

What are the morphological changes in apoptosis?

A
  1. Cell shrinkage
  2. Chromatin condensation
  3. Cytoplasmic blebs.
  4. Apoptotic or acidophilic bodies.
  5. Phagocytosis of apoptotic bodies.
49
Q

What is this an example of?

A

Atrophy

50
Q

What is this an example of?

A

Atrophy of the brain.

51
Q

What is this an example of?

A

Metaplasia of the respiratory tract.

52
Q

Explain why this is reversible damage?

A

Fluid has leaked in and there is damage, but hte membranes are not compromised.

53
Q

Explain why this is reversible damage.

A

It is mitochondrial swelling. A common first step, but can be reversed.

54
Q

What is karyolysis?

A

The complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases. The whole cell will eventually stain uniformly with eosin after karyolysis. It is usually preceded by karyorrhexis and occurs mainly as a result of necrosis, while in apoptosis after karyorrhexis the nucleus usually dissolves into apoptotic bodies.

55
Q

What are 2 common causes of mitochondrial damage?

A

Supply of oxogyen to the cell is interrupted (Hypoxia) or various toxins

56
Q

How is damage to the mitochondria commonly expressed?

A

Formation of a high conductance channel (mitochondrial permeability transition) in the inner mitochondrial membrane and by leakage of cytochrom c into the cytoplasm of cells.

57
Q

What do these various mechanisms of mitochondrial damage result in?

A

Decrease in the O2 dependent synthesis of ATP, which is required to fuel the ion pumps of the mitochondrial membrane. Failure of the ion pumps leads to ingress of fluid and mitochondrial swelling, secondarily effecting oxidative metabolism necessary for cell survival.

58
Q

What is usually the first cellular component to be damaged?

A

The outer cell membrane.

59
Q

What does damage to the membrane tht physically inactivate the ion pumps result in?

A

Cell swelling and messing up of the concentration gradients accross the membrane that the cell requires. (Na+, K+ and Ca++)

60
Q

What does ATP depletion result in?

A

Failure of the membrane and ER Na?K ion pump, membrane transport, protein syntesis, lipogenesis, reactions necessary for phospholipid turnover and deacytilation.

61
Q

What does the breakdown of membrane calcium pumps lead to?

A

Accumularion of free cytoplasmic calcium. (Also released from mitochondria and ER) The Ca leads to activation of a number of enzymes and proteases. It is thought that a critcally damaged membrane in association with cytoplasmic calcium accumulation and enzyme activation may be the point at which cellular damage is irreversible and cell death occurs.

62
Q

What happens when the cisternae of the ER are distended and the polyribosomes detach from the RER?

A

A decrease in the ability of the cell to synthesize new protein. Aditionally, DNA damage and nucleolar damage occurs, which als oresults in decreased protein synthesis.

63
Q

What is calpain?

A

One of the proteases that is activated by calcium. It causes disassembly of cytoskeletal proteins which cases cells to be abnormally fragile.

64
Q

What does extremely high levels of oxygen cause?

A

Production of activated O2 radicals and species. Have toxic effects on cells, especially in the lung.

65
Q

What is reperfusion injury?

A

In hypoxia, xanthine dehydrogenase is proteolytically converted to xanthine oxidase. Once the hypoxia is corrected, the xanthine oxidase produces activated oxygen species.

66
Q

How does acute inflammation cause cell tissue and injury?

A

Neutrophils have enxymes such as myeloperoxidase which produce 02 radicals. Many hypoxic tissues are inflitrated with neutrophils.

67
Q
A

Pathology (6 decks)

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