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IVP: Veterinary Pathogenesis > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

When does cell injury occur

A

Once the adaptive capacity of the cell is surpassed is it is no longer able to respond to functional demands

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2
Q

Broad definition of cell injury

A

Any change in a cell which, if not reversed, could lead to the death of that cell. In other words, a loss of ability to respond to functional demands

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3
Q

Causes of cell injury

A
  1. Hypoxia
  2. Physical agents
  3. Genetic factors
  4. Inflammation
  5. Immunological responses
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4
Q

What are the two most important requirements for the maintenance of homeostasis and normal cell function?

A
  1. Intact membranes

2. Energy supply

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5
Q

Outline the importance of intact cell membranes to maintaining homeostasis

A

Selective barrier which maintains correct internal osmolarity

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6
Q

What is the result of damaged cell membrane?

A
  • -> influx of NA, Ca2+, H2O
  • -> Swelling
  • -> Altered spatial arrangement
  • -> Substrates diffuse around cell
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7
Q

What is the most common cause of a damaged membrane

A

Free radicals = highly reactive small molecules with unpaired electrons, often O2 mols

“Leak” out of many normal biochemical reactions - usually mopped up by cell’s own antioxidants, but when they are released faster than the cell can mop up –> cell injury

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8
Q

Enzyme induction

A

Cell injury resulting from excess free radicals

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9
Q

How do free radicals cause damage to membranes?

A

Perioxidation of membrane lipids = free radicals react with membrane lipids –> membrane damage –> inc permeability

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10
Q

Examples of agents that cause direct damage to cell membranes

A

Irradiation, toxins, complement, deficiency of Vitamin E or selenium

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11
Q

Protection against oxidative injury

A

Superoxide dismutases - catalyse conversion of superoxide anion to hydrogen perioxide

Antioxidants - remove free radicals by becoming oxidised themselves

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12
Q

Are free radicals always harmful?

A

No!

They are actually utilised by the phagocytic leukocytes as mechanisms for the killing of micro-organisms

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13
Q

What do cells need energy for?

A
  • Driving ion pumps to maintain osmotic gradients
  • Synthesis of structural molecules and enzymes
  • Heat production
  • Carrying out specialised functions (e.g. contraction)
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14
Q

What is the earliest and most significant manifestation of energy depletion?

A

Swelling of the cell and its organelles due to failure of the energy dependent Na-K-ATPase ion pump

Mitochondria are most affected by the swelling –> energy shortage is accentuated and protein synthesis is disrupted

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15
Q

Anaerobic glycolysis

A

Stimulated following mitochondrial damage as a result of swelling

Less efficient, causes build up of lactic acid –> further inhibits the respiratory and other enzymes

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16
Q

What is the most common cause of energy (ATP) depletion?

A

Hypoxia (oxygen shortage) –> failure of aerobic respiration

No O2 –> electron transport cannot occur
–> ATP production via oxidative phosphorylation inhibited

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17
Q

Potential causes of hypoxia

A
  • Oxygen not reaching the blood
  • Oxygenated blood not reaching the tissues
  • “Respiratory poisons” - O2 available but cannot be utilised
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18
Q

Which cells are most susceptible to hypoxia?

A

Cells with high metabolic rates

e.g. brain, heart, kidney

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19
Q

What is the most common manifestation of cell injury?

A

Cellular swelling, sometimes referred to as oncosis

  1. Cell becomes enlarged
  2. Staining characteristics alter
  3. Formation of intracellular vacuoles
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20
Q

Vacuolar degeneration/hydropic degeneration

A

Cellular swelling and the formation of intracellular vacuoles

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21
Q

Why do intracellular vacuoles from?

A
  • Failure of membrane function and resulting influx of water
  • Loss of cytoplasmic organelles in particular areas
  • Accumulation of small lipid droplets in cytoplasm
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22
Q

What does reversible cell injury usually involve?

A

Cloudy swelling, hydropic change or fatty degeneration or fatty change

  • Cells often able to maintain homeostasis and stay alive but unable to carry out normal functions
23
Q

What is an example of reversible cell injury?

Outline the mechanisms involved, and the gross and histological pathology

A

Hepatic Lipidosis

24
Q

Mechanisms of lipidosis

A
  1. Excess delivery of free fatty acids to liver when body fat is rapidly metabolised
  2. Reduced capacity to syntesis apolipoprotein

(both impact ability to export triglycerides)

25
Q

Gross pathology of hepatic lipidosis

A

Liver appears pale yellow

26
Q

Histopathology of hepatic lipidosis

A

Lipid evident as vacuoles, either large or multiple small ones

27
Q

At what point does cell damage become irreversible?

A
  1. Inability to reverse mitochondrial dysfunction –> ATP depletion
  2. Profound disturbances in membrane function
28
Q

What is the best indicator of the onset of irreversible cell damage?

A

Severe ultrastructural mitochondrial change (prolonged reduction in ATP leads to irreversible cell injury)

29
Q

Role of calcium in cell injury

A

Increase in intracellular calcium is a consistent feature of necrosis. Necrotic cells may even contain deposits of calcium salts.

A combination of membrane damage and calcium influx are critical to lethal cell injury

30
Q

What are the two mechanisms of irreversible cell injury?

A
  1. Apoptosis - programmed cell death

2. Necrosis - damage to membranes and organelles becomes lethal (cells die in an uncontrolled fashion)

31
Q

Necrosis

A

Refers to the morphological changes to the cell after cell death

32
Q

What is involved in apoptosis?

A
  1. Cell shrinkage, rapid condensation of nuclear chromatin and cytoplasm, convolution of cell
  2. Separation of cell into apoptotic bodies
  3. Phagocytosis of apoptotic bodies by adjacent healthy cells
33
Q

Does apoptosis provoke an inflammatory reaction?

A

No - apoptotic cells do not release cellular constituents –> do not provoke immune response

34
Q

Examples of when apoptosis occurs

A
  • Cell death in tumours
  • Death of neutrophils during acute inflammatory response
  • Death of immune cells - both B and T cells
35
Q

How does distribution differ in apoptosis and necrosis

A

Apoptosis - usually single cells

Necrosis - often contiguous cells

36
Q

How does cell size and shape differ in apoptosis and necrosis

A

A - shrinkage and convolution

N - Swelling

37
Q

How does nuclear morphology differ in apoptosis and necrosis

A

A - chromatin condensation, nuclear fragmentation

N - lysis

38
Q

How does plasma membrane differ in apoptosis and necrosis

A

A - intact until phagocytosed

N - Damaged, leaky

39
Q

How does cytoplasm differ in apoptosis and necrosis

A

A - retained in apoptotic bodies

N - contents released

40
Q

How does inflammation differ in apoptosis and necrosis

A

A - absent

N - typically present

41
Q

Macroscopic changes that occur in necrosis

A
  • Lighter colour than surrounding tissues
  • Haemorrhage possible
  • Swollen tissue OR reduced volume due to degeneration
  • Surrounding zone of inflammation
42
Q

Microscopic changes that occur in necrosis

A

Cytoplasm - cytoplasmic swelling

Nucleus - clumping of chromatin, pyknosis (shrinkage) or karyolysis (disintegration)

43
Q

Pyknosis

A

Nuclear shrinkage and intense basophilia

  • result of necrosis
44
Q

Karyolysis

A

Disintegration of nucleus

  • result of necrosis
45
Q

Coagulation Necrosis

A
  • Cellular detail lost
  • Shape and tissue organisation remain
  • Eventual phagocytosis of these dead cells
46
Q

Liquefaction Necrosis

A
  • Malacia (softening of the tissue)
  • Often seen in inflammatory lesions
  • Lots of neutrophils present
47
Q

Caseous Necrosis

A
  • Tissue becomes soft and pasty - likened to cheese

- Often seen in bacterial infections

48
Q

Gangrenous Necrosis

A

Ischaemic necrosis of extremities

49
Q

Gry gangrene

A

Ischaemic necrosis of extremities with coagulative pattern

50
Q

Wet gangrene

A

Ischaemic necrosis of extremities with liquefactive pattern due to bacterial products

51
Q

Response of surrounding tissue to necrosis

A

Inflammatory response

  • Vascular engorgement and congestion +/- haemorrhage
  • Infiltration by neutrophils and macrophages - provide hydrolytic enzymes to break down dead tissue and phagocytose necrotic tissue
52
Q

What do the consequences of cell injury depend on?

A
  • Degree of damage (severity)
  • Extent of damage (no of cells)
  • Tissue affected
53
Q

What is the practical significance of post mortem changes?

A

They may:

  • Obscure or obliterate gross and microscopic lesions
  • Mimic true lesions
  • Adversely affect the quality of lab specimens
54
Q

Under what conditions are post mortem changes hastened?

A
  • High ambient temperature
  • Raised body temp prior to death
  • Excessive fat or wool - slows cooling of carcase

IVP: Veterinary Pathogenesis (8 decks)

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