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Cellular Pathology > CELL INJURY > Flashcards

CELL INJURY Flashcards

1
Q

Describe Cell Injury

A

1) Occurs when:
1. cells are stressed no longer able to adapt
2. cells are exposed to inherently damaging
agents
3. cells suffer from intrinsic abnormalities.

2) Types of cell injury
1. Reversible (recovery)
2. Irreversible ( Cell death) Apoptosis or necreosis

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2
Q

List the 7 causes of Cell Injury

A
  1. oxygen deprivation (anoxia)
  2. physical agents
  3. chemical agents
  4. infections agents
  5. immunologic reactions
  6. genetic defects
  7. nutritional imbalances
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3
Q

Explain the consequences of OXYGEN DEPREVATION

A

1- Hypoxia is a deficiency of oxygen,
2- causes cell injury by reducing aerobic oxidative respiration by:
1. inadequate oxygenation of the blood due to cardiorespiratory failure
2. decreased oxygen-­carrying capacity of the blood (anemia or carbon
monoxide poisoning severe blood loss)

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4
Q

Examples of PHYSICAL AGENTS

A

1- Cause by:

  1. Mechanical trauma
  2. Extremes of temperature (burns and deep cold)
  3. Changes in atmospheric pressure
  4. Radiation
  5. Electric shock
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5
Q

Examples of CHEMICAL AGENTS and DRUGS

A
  1. Glucose or salt in hypertonic concentrations (electrolyte unbalance)
  2. Oxygen at high concentrations
  3. Poisons such as arsenic, cyanide, or mercuric salts
  4. Environmental and air pollutants
  5. Insecticides, and herbicides
  6. carbon monoxide and asbestos;;
  7. Alcohol
  8. Therapeutic drugs.
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6
Q

Examples of INFECTIOUS AGENTS

A

1- Viruses
2- Bacteria
3- Fungi
4- Parasites

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7
Q

Examples of IMMUNOLOGIC REACTIONS

A

1- Reactions to endogenous self antigens: autoimmune diseases
2- Reactions to many external agents

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8
Q

Explain the consequences of GENETIC DERANGEMENTS

A

DNA sequence variants that are common in human populations (polymorphisms) can also influence the susceptibility of cells to injury by chemicals and other environmental insults.

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9
Q

Examples of NUTRITIONAL IMBALANCES

A

Major causes of cell injury.
1• Protein-­calorie deficiencies
2• Deficiencies of specific vitamins
3• self-­imposed nutritional problems (anorexia nervosa)
4• Nutritional excesses (cholesterol, obesity)
5• composition of the diet

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10
Q

State the principles Cell injury

A
  1. The cellular response to injurious stimuli depends on the type of injury, its duration and its severity.
  2. The consequences of cell injury depend on the type, state, and adaptability of the injured cell
  3. Cell injury results from different biochemical mechanisms acting on several essential cellular
    components
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11
Q

Describe the morphological changes secondary to injury /

Morphological comparison of reversible cell injury from irreversible cell injury

A 
REVERSIBLE
• Cellular swelling
• Cell membrane blebs
• Detached ribosomes
• Chromatin clumping
IRREVERSIBLE
• Lysosomes rupture
• Dense bodies in mitochondria
• Cell membrane rupture
• Karyolysis, karyorrhexis, pyknosis
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12
Q

Explain the transformation of reversible cell injury to irrversibel with respect to time ( in its correct order)

A

Reversible
1- Decrease in cell funtion
Irreversible
2- Increase in biochemical alterations associated with cell death
3- Increase in ultrastructural changes
4- Increase in lighht microscopic changes
5- Increase in morphological changes

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13
Q

Describe the Morphologic Alterations in reversible cell Injury

A 
1• generalized swelling of the cell and
its organelles
2• blebbing of the plasma membrane
3• detachment of ribosomes from the ER
4• clumping of nuclear chromatin
5• decreased generation of ATP
6• loss of cell membrane integrity
7• defects in protein synthesis
8• cytoskeletal damage
9• DNA damage
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14
Q

Explain Specific Morphology of reversible Cells

A

1• KIDNEY-­HYDROPIC CHANGES
• Cellular swelling and vacuole formation (Hydropic changes):
incapacity of maintaining ionic and fluid (failure of energy-­dependent
ion pumps) in the plasma membrane
• Hydropic change is one of the early signs of cellular degeneration in
response to injury.
• Refers to the accumulation of water in the cell.

2• LIVER and MYOCARDIAL CELLS-­FATTY CHANGES
• lipid vacuoles in the cytoplasm
• Changes at this stage are better appreciated by EM that may show blebbing of the plasma membrane, swelling of mitochondria and dilatation of ER

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15
Q

What are the Susceptibility of Cells to

Ischemic Necrosis ?

A

High – Neurons (3-­4 min)

Intermediate -- Myocardium, hepatocytes,
renal epithelium (30 min-­2hr)

Low – Fibroblasts, epidermis, skeletal
muscle (many hours)

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16
Q

3rd Principle of Cell Injury: Cell injury results from different biochemical
mechanisms acting on several essential cellular
components

List the biochemical mechanism

A 
1- Depletion of ATP
2- MItochondrial damage
3- Influx of Ca2+
4- Accumulation of ROS
5- Membrane damage
6- Protein misfolding, DNA damage
17
Q

Explain the depletion of ATP

A

1• Mitochondria -­ reduced oxidative phosphorylation.

2• Cell membrane -­ reduced sodium pump.

3• Endoplasmic reticulum dilates, the cell swells, blebs appear.

4• Anaerobic glycolysis occurs with loss of glycogen,
accumulation of lactic acid, acid pH which interferes with
enzymes.

5• Failure of the calcium pump leads to influx of Ca++ into the cell, activate various enzymes to the detriment of the cell.

6• RER loses ribosomes and
protein synthesis falls

18
Q

Explain Mitochndrial Damage

A

3 Major consequences

  1. Formation of a high-­conductance
    mitochondrial permeability transition pore
    (MTP). Loss of mitochondrial membrane
    potential, resulting in failure of oxidative
    phosphorylation
    • cyclosporine (immunosuppressive drug
    used to prevent graft rejection) targets the
    protein cyclophilin D (one of the structural
    components of the mitochondrial
    permeability transition pore). It blocks the
    opening of the pore and blocks necrosis.
    • Clinical trials for cyclosporine use to
    reduce ischemic myocardial injury in
    humans.

2 Production of reactive oxygen species

3 Leakage of pro-­apoptotic proteins

19
Q

Explain the Influx of Calcium

A

1) Extracellular Ca2+ is 15X > Cytosolic Ca2+
2) Influx of cytosolic calcium is from the extracellular fluid and ER
3) Increase Ca2+ activates:
1- Phospholipases: damage cell membranes
2- Proteases: Damage cell membranes and cytoskeleton
3- Endonucleases: damages DNA

4) Mechanism of cell death:
1- Severe damage to membranes of lysosomes
2- leakage of lysosomal enzymes
3- Triggering of apoptosis

5) Occurs particularly in hypoxia and ischaemia with certain toxins

20
Q

Explain the accumulation of O2-derived free radicals (Oxidative stress)

A

1• Free radicals have a single unpaired electron in the outer orbit. They are highly
reactive with adjacent molecules.
2• Are usually derived from oxygen to produce reactive oxygen species, superoxide,
hydroxyl radicals,H2O2,etc.
3• Are normally produced during cellular respiration.
4• Protective molecules include superoxide dismutase, glutathione peroxidase, vitamin
E, vitamin C, catalase.
5• They damage proteins, lipids, carbohydrates, nucleic acids.
6• These damaged molecules may themselves be reactive species with a chain
reaction being set up with widespread damage.

21
Q

Examples of diseases related to oxidative stress

A

1– oxygen toxicity, ischaemia/reperfusion injury, radiation injury (hydrolyses H2O to OH & H), metabolism of drugs,toxins,pollutants (eg Paracetamol to reactive metabolite,cigarette smoke);;
2– leukocyte killing of bacteria or in non-­bacterial inflammations, release of iron in hemorrhages
enhances oxidative stress (important in CNS),
3– lipid peroxidation of low-­density lipoproteins in atherosclerosis, cancer production (damage to DNA), ageing.

treatment with antioxidants and/or free-­radical scavengers.

Cellular Pathology (5 decks)

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