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General Pathology VDMP832 > Cell Injury Mechanisms > Flashcards

Cell Injury Mechanisms Flashcards

1
Q

Cell Injury

A
  • Basic cell functions or viability are threatened
  • Injury usually occurs due to situations where the ability of the cell to respond or adapt are exceeded
  • Injury can be reversible or irreversible
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2
Q

Injured Cells

A
  • Changes in available nutrients
    • including oxygen
  • Direct cell damage
    • microorganisms
    • Toxins
    • Physical forces
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3
Q

Cell Injury:

Causes:

Physical Agents

A

Trauma, temperature extremes

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4
Q

Cell injury:

Causes:

Chemical

A

Xenobiotics (toxins), endogenous and exogenouse substances

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5
Q

Cell Injury:

Causes:

Nutrients

A

Too many or Too few

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6
Q

Cell injury:

Causes:

Infectious agents

A

Virus, bacteria

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7
Q

Cell Injury:

Susceptibility

A
  • Cells have widely variable resistance to detrimental stimuli
    • neurons and cardiac myocytes are highly susceptible to hypoxia
    • Fibroblasts or squamous epithelium can survive in the absence of adequate oxygen
  • Metabolic status will influence cell susceptibility
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8
Q

Cell Injury:

Mechanisms:

Loss of membrane integrity

A

Cell membrane breakdown and loose the ability to segregate reactions within the cell

  • Free radical-induced damage
  • Phospholipase-induced damage
  • Direct membrane Damage
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9
Q

Cell injury:

Mechanisms:

Loss of ability to produce energy

A

ATP is insufficient to support cell functions

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10
Q

Cell injury:

Mechanisms:

Genetic Damage

A

Functional changes induced by a mutation

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11
Q

Free Radical Injury

A
  • Free radicals are chemicals with unpaired electrons that readily react with surrounding molecules
  • Chain reaction occurs as the electron passes from molecules to molecule
  • Can damage membranes, as well as other cell components
  • Formed during metabolism and by normal cell reactions
    • Oxidation reduction reactions during areobic respiration
    • Biotransformation of chemical substances
    • Nitric oxide metabolism
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12
Q

Reactive Oxygen Metabolites:

Effects

A
  • Protein and membrane degradation
  • DNA damage
  • Inflammation
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13
Q

Reactive Oxygen metabolites:

Implicated in

A

Aging

Neurodegeneration

Neoplasia

Cell injury and death

Chronic inflammation

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14
Q

Free Radical Injury:

Protective Mechanisms

A
  • Vitamins A, C, and E phytochemicals (Antioxidants)
  • Iron and copper binding proteins
    • ferritin and ceruloplasmin
  • Specific enzymes
    • superoxide dismutase, Catalase, gluthathione peroxidase
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15
Q

Phospholipase-induced injury

A
  • Activated membrane phospholipases cleave phospholipids out of the membrane
    • Can be activated by increased cytoplasmic Ca++
  • Phospholipase activation can also be cause by decreased energy
    • Decreased energy interferes with membrane pump function and increased cytoplasmic Ca++
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16
Q

Direct Membrane Injury

A
  • Certain substances can cause direct injury to membranes
    • Bacterial Toxins
    • xenobiotics
    • Complements
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17
Q

Mechanisms:

Loss of ability to produce Energy

A
  • Cell Injury = ATP
  • ATP produced by
    • oxidative phophorylation
    • Anaerobic glycolysis
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18
Q

Role of Calcium in Cell injury

A

Mitochondrial injury

Phospholipase activation

Protease activation

Endonuclease activation

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19
Q

Mechanisms:

Genetic Injury

A

Damage to cellular nucleic acids is common

Permanent damage to DNA is a mutation

20
Q

Mechanisms:

Genetic Injury

Outcomes

A
  • No effect on the cell or tissues
  • Cell dysfunction leading to disease
  • Cell Transformation leading to neoplasia
  • Cell death
21
Q

Altered and Injured Cells:

Characteristics

A
  • Cell injury can be either sublethal or lethal
    • Sublethal injury can be reversible or progress to cell death
22
Q

Altered and Injured Cells:

Characteristics:

Sublethal

A

Cell swelling

Intracellular accumulations

Neoplastic transformation

23
Q

Altered and Injured Cells:

Characteristics:

Lethal

A

Apoptosis

Necrosis

24
Q

Sublethal Injury:

Cell swelling

A
  • Membrane ion pumps fail to maintain osmotic gradients across the membrane
    • Water enters the cell or an intracellular organelle
  • Morphology:
    • Affected cells or organelles are swollen, and finely vacuolated
    • “Hydropic changes”
25
Q

Sublethal Injury:

Intracellular Accumulations

A
  • Abnormal metabolism, functional demands that exceed the capability of hte cell, or exposure to injurious agents can lead to accumulation of various intracellular substances
    • edogenous
    • Exogenous
26
Q

Endogenous Intracellular Accumulations

A
  • Excess normal or abnormal metabolic products that accumulate in a cell
  • Causes:
    • Abnormal metabolism
    • demand exceeds capability of the cell
    • Cell injury that inhibits cell functions
  • Examples:
    • Metabolic storage disease
    • Lipidosis
    • Glycogenosis
    • Intracellular Pigments
27
Q

Endogenous Accumulations:

Lipidosis

A
  • Metabolic pathways in cells are inhibited by injury or overwhelmed by excess demand
    • Triglyceride accumulation is one common manifestation of metabolic change
  • It can be physiological as well as pathological
    *
28
Q

Endogenous Accumulations:

Lipidosis:

Physiologic causes

A

High fat ration

Increased periparturient engergy need

Anorexia

29
Q

Endogenous Accumulations:

Lipidosis:

Pathologic Causes

A

Hyptotoxins

Hypoxia

Starvation

30
Q

Endogenous Accumulations:

Glycogenosis

A
  • Glycogen accumulates due to abnormal metabolism
    • Hypatocytes of animals with diabetes mellitus
  • Cells look “swollen”
31
Q

Endogenous Accumulations:

Hemosiderin

A
  • Intracellular Aggregates of Ferritin
  • Commonly Associated with:
    • Increased RBC sensecences
    • Hemolysis
32
Q

Endogenous Accumulations:

Lipofuscin-ceroid

A

Undegradable remnants of oxidized membrane lipid

It can accumulate as a part of aging or due to excessive membrane oxidation

33
Q

Exogenous Intracellular Accumulations

A

The substances that accumulate are not native to the cell environment

These Include:

Viral Proteins and Nucleic Acids

Carbon

Non-Nutritive minerals

34
Q

Sublethal Injury:

Transformation

A
  • As a result of genetic injury soem cells undergo neoplastic transformation
  • Transformed cells may have abnormal growth, often abnormal function, and abnormal morphology
  • They are not injured, in the traditional sense, they are detrimentally changed
35
Q

Sublethal Injury:

Transformation:

Morphology

A
  • Cells may appear normal
    • some degree of hyperplasia may be present
  • Some cells appear poorly differentiated
    • Anaplasia
  • Some cells have vairable sizes/shapes/appearance
    • Pleomorphism
36
Q

Lethal Cell Injury

A
  • The insult to the cell exceeds the cells ability to adapt or respond
    • Lethal injury is immediate
  • Sublethal injury can progress to lethal injury
    • The severity of the insult may determine the outcome for the cell
      • Many of the causes of lethal injury are the same as those for sublethal injury
37
Q

Lethal Cell Injury:

Apoptosis

A
  • Physiological Cell Death
    • the mechanism to remove damaged or unneeded cells in the least disruptive way possible
  • Apoptosis maintains homeostasis, but can also be involved in pathological states
  • Apoptosis is an active process that requires energy from the cell
38
Q

Apoptosis:

Causes:

Physiological

A
  • Patterned death during embrygenesis
  • Hormone/cytokine induced death
    • tissue involution
  • Maintain balance in proliferating populations
  • Removal of cells following completion of their purpose
  • Removal of self-reactive lymphocytes
39
Q

Apoptosis:

Causes:

Pathologic

A

Unrepaired DNA damage

Heat

Hypoxia

Viral infections

Physical pressure

40
Q

Lethal Cell injury:

Necrosis

A
  • Death due to injury that disrupts the ability of the cell to continue to function
  • Degradative process that occurs after the cell is dead
  • Passive process, that does NOT require energy from the cell
41
Q

Autolysis

A

self-digestion of a cell or tissue

42
Q

Necrosis

A

Autolysis of a cell/tissue in a living animal

43
Q

Postmortem Autolysis

A

Self-digestion of cells/tissues/organs after an animal dies

44
Q

Necrosis:

Causes

A
  • Direct Injury to the cell
    • Hypoxia
    • Direct Membrane Injury
  • Many of the same facotrs that initiate apoptosis when the stimulus is mild, initiate necrosis when more severe
45
Q

Necrosis:

Mechanisms

A
  • Degradative Activity fo lytic enzymes
    • Lysosomal enzymes degreade cell components
    • Enzymes may come from the same cell
    • Enzymes may come from other cells
46
Q

Necrosis:

Morphology

A
  • Eosinophilia
    • protein denaturation
  • Smooth, Homogenous cytoplasm “ground glass”
  • Cytoplasmic vacuolation
  • Nuclear degeneration
  • Inflammation in response to necrosis
47
Q

Post Mortem Autolysis

A
  • Cells and tissues degradation that occurs following the death of an animal
    • Changes that occur in cells are similar to those associated with antemortem necrosis
  • Occurs ina predictable fashion
  • All cells are affected and are at the same stage of autolysis
  • There is no inflammation of host response

General Pathology VDMP832 (26 decks)

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