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Excess ACEM Primary cards > Fundamentals: Pathology - Cellular injury and adaptation > Flashcards

Fundamentals: Pathology - Cellular injury and adaptation Flashcards

1
Q

When does cell injury occur?

A

If the limits of adaptive responses are exceeded or if cells are exposed to damaging insults, deprive of critical nutrients, or compromised by mutations that affect essential cellular function

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2
Q

What is the ultimate consequence of persistent or severe cell injury?

A

Cell death

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3
Q

What are the two principal patterns of cell death?

A

Necrosis
Apoptosis

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4
Q

What is the difference between necrosis and apoptosis?

A

Necrosis: severe cell swelling or rupture
Apoptosis: programmed cell death, cells removed with minimum of disruption

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5
Q

List 7 possible causes of cell injury

A

Oxygen deprivation (hypoxia)
Physical agents
Chemical agents and drugs
Infectious agents
Immunologic reactions
Genetic derangements
Nutritional imbalances

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6
Q

What is the difference between hypoxia and ischaemia?

A

Hypoxia: oxygen depravation
Ischaemia: loss of blood supply (one possible cause of hypoxia)

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7
Q

List three possible causes of hypoxia

A

Ischaemia
Inadequate blood oxygenation due to cardiorespiratory failure
Decreased oxygen-carrying capacity of the blood (e.g. anaemia, CO poisoning, blood loss)

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8
Q

Give 5 examples of physical agents that may cause cell injury

A

Mechanical trauma
Extremes of temperature
Sudden changes in atmospheric pressure
Radiation
Electric shock

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9
Q

Why does ischaemia cause tissue injury faster than hypoxia?

A

In contrast to hypoxia, during which glycolytic energy production can continue, ischaemia compromises the availability of metabolic substrates

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10
Q

Cellular response to injurious stimuli is dependent on what three factors?

A

Type, duration, and severity of injury

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11
Q

Consequences of cell injury are determined by what three factors?

A

Type, state and adaptability of injured cell

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12
Q

What four intracellular systems are particularly vulnerable to cell injury?

A

Maintenance of membrane integrity
Aerobic respiration
Protein synthesis
Preservation of the integrity of the genetic apparatus of the cell

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13
Q

Outline 7 general biochemical mechanisms of cell injury and necrosis

A
  1. ATP depletion: results in failure of energy-dependent functions
  2. Mitochondrial damage: results in ATP depletion, ROS formation (due to incomplete oxidative phosphorylation), and leakage of mitochondrial proteins which can trigger apoptosis
  3. Increased permeability of cellular membranes: including plasma membrane, lyosomal membranes, and mitochondrial membranes; caused by ROS, decreased phospholipid synthesis and increased breakdown, and cytoskeleton abnormalities (does not occur in apoptosis)
  4. Accumulation of damaged DNA and misfolded proteins: activates p53-dependent pathways to trigger apoptosis
  5. Accumulation of ROS: results in covalent modification of cellular proteins, lipids, and nucleic acids
  6. Calcium influx: activation of enzymes that damage cellular components (e.g. phospholipases, proteases, ATPases, endonucleases), and may also trigger apoptosis
  7. Unfolded protein response and ER stress: accumulation of misfolded proteins in the ER activates adaptive mechanisms that help the cell to survive, but if their repair capacity is exceeded they trigger apoptosis
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14
Q

Compare and contrast necrosis and apoptosis in terms of cell size

A

Necrosis: enlarged (swelling)
Apoptosis: reduced (shrinkage)

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15
Q

Compare and contrast necrosis and apoptosis in terms of their effect on the nucleus

A

Necrosis: pyknosis, karyorrhexis, karyolysis
Apoptosis: fragmentation into nucleosome-size fragments

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16
Q

Compare and contrast necrosis and apoptosis in terms of their effect on the plasma membrane

A

Necrosis: disrupted
Apoptosis: intact but with altered structure (especially orientation of lipids)

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17
Q

Compare and contrast necrosis and apoptosis in terms of their effect on cellular contents

A

Necrosis: enzymatic digestion (may leak out of cell)
Apoptosis: intact (may be released in apoptotic bodies)

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18
Q

Compare and contrast necrosis and apoptosis in terms of the presence of absence of adjacent inflammation

A

Necrosis: frequent
Apoptosis: no

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19
Q

Compare and contrast necrosis and apoptosis in terms of their physiologic/pathologic roles

A

Necrosis: usually pathologic (culmination of irreversible cell injury)
Apoptosis: often physiologic, means of eliminating unwanted cells (may be pathologic after some forms of cell injury, especially DNA damage)

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20
Q

Explain the phenomenon of reperfusion injury in ischaemia

A

Restoration of blood flow to ischaemic tissues can promote recovery of cells if they reversibly injured but can also paradoxically exacerbate cell injury and cause cell death

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21
Q

What are the two consistent early patterns of reversible cell injury?

A
  1. Cellular swelling
  2. Fatty change
22
Q

What is the first manifestation of almost all forms of injury to cells? Why and how does this occur? What are the macroscopic and microscopic effects?

A

Cellular swelling is the first manifestation of almost all forms of injury to cells
Occurs whenever cells are incapable of maintaining ionic and fluid homeostasis

When it affects all cells in an organ, it causes some pallor, increased turgor and increase in weight of the organ

On microscopic examination, vacuolar degeneration (also known as hydropic change) is observed (small clear vacuoles seen within the cytoplasm)

23
Q

What can be observed microscopically with fatty change as a result of tissue injury?

A

The appearance of small or large lipid vacuoles in the cytoplasm

24
Q

Outline 5 ultrastructural changes of reversible cell injury visible by electron microscopy

A
  1. Plasma membrane alterations (e.g. blebbing, blunting, loss of microvilli)
  2. Mitochondrial changes, including swelling and the appearance of small amorphous densities
  3. Accumulation of “myelin figures” in the cytosol composed of phospholipids derived from damaged cellular membranes
  4. Dilation of the ER, with detachment of polysomes
  5. Nuclear alterations, with dissaggregation of granular and fibrillar elements (decreased cytoplasmic RNA results in increased eosinophilia)
25
Q

Define necrosis

A

Pathologic process that is the consequence of severe cell injury

26
Q

What are the four characteristic pathological changes seen in necrosis?

A

Denaturation of cellular proteins
Leakage of cellular contents through damaged membranes
Local inflammation
Enzymatic digestion of the lethally injured cell

27
Q

Outline 5 histological changes observed in necrosis, and the processes that produce each

A

Increased eosinophilia: due to loss of cytoplasmic RNA and accumulation of denatured cytoplasmic proteins
Glassy haemogenous appearance: due to loss of glycogen particles
Vacuolated “moth-eaten” cytoplasm: due to enzymatic digestion of organelles
Dead cells may be replaced by whorled phospholipid precipitates called myelin figures
Nuclear changes (karyolysis, pyknosis, karyorrhexis)

28
Q

Define karyolysis

A

Basophilia of chromatin may fade, reflecting loss of DNA as a result of DNase activity

29
Q

Define pyknosis

A

Characterised by nuclear shrinkage and increased basophilia
DNA condenses into a solid, shrunken basophilic mass

30
Q

Define karyorrhexis

A

Pyknotic nucleus undergoes fragmentation

31
Q

List 5 patterns of necrosis

A

Coagulative
Liquefactive
Caseous
Fat
Fibrinoid

32
Q

What type of nuclear change seen in necrosis can also be seen in apoptosis?

A

Pyknosis

33
Q

How much time does it take for the nucleus of a necrotic cell to disappear?

A

1-2 days

34
Q

What is coagulative necrosis?

A

Pattern of tissue necrosis characterised by preservation of the basic outline of the coagulated cell for a span of time (at least some days) and preservation of the general tissue architecture

35
Q

What is liquefactive necrosis?

A

Pattern of tissue necrosis characterised by digestion of dead cells, resulting in transformation of the tissue into a viscous liquid

36
Q

What is caseous necrosis?

A

Pattern of tissue necrosis seen most often in foci of tuberculous infection

37
Q

Why is tissue architecture preserved in coagulative necrosis?

A

The injury presumably denatures not only structural proteins but also enzymatic proteins and so blocks proteolysis of the cell
As a result, intensely eosinophilic cells with indistinct or reddish nuclei may persist for days or weeks

38
Q

How are necrotic cells eventually broken down in coagulative necrosis?

A

Ultimately the necrotic cells are broken down by the action of lysosomal enzymes from infiltrating leucocytes, which also phagocytose debris of dead cells

39
Q

What kind of injuries typically result in coagulative necrosis? Any exceptions?

A

Characteristic of ischaemic injury in all tissues except the brain

40
Q

What is a localised area of coagulative necrosis called?

A

An infarct

41
Q

What kind of injuries typically result in liquefactive necrosis? Any exceptions?

A

Seen in focal bacterial or, occasionally, fungal infections
Also often occurs in hypoxic injury within the CNS for unknown reasons

42
Q

Describe how liquefactive necrosis occurs

A

Microbes stimulate accumulation of leucocytes and liberation of enzymes from these cells
The necrotic material (called pus) is frequently creamy yellow because of the presence of leucocytes

43
Q

Why is caseous necrosis so-called?

A

Caseous (“cheese-like”) is derived from the friable white appearance of the necrotic area

44
Q

Describe the microscopic appearance of caseous necrosis

A

Microscopic appearance is characteristic of a focus of inflammation known as a known as a granuloma
The necrotic focus appears as structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border

45
Q

What is fat necrosis?

A

Refers to focal areas of fat destruction

46
Q

How does fat necrosis occur?

A

Typically results from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity, as occurs in acute pancreatitis
Activated enzymes liquefy fat cell membranes in the peritoneum, releasing triglyceride esters that are split by pancreatic lipases
Released fatty acids combine with calcium to produce grossly visible chalky white areas (fat saponification)

47
Q

Describe the histological appearance of fat necrosis

A

On histologic examination, the necrotic areas contain shadowy outlines of necrotic fat cells, basophilic calcium deposits, and an inflammatory reaction

48
Q

What is fibrinoid necrosis?

A

Special form of vascular damage usually seen in immune reactions involving blood vessels (i.e. vasculitides)

49
Q

How does fibrinoid necrosis occur?

A

Typically occurs when complexes of antigens and antibodies are deposited in the walls of arteries

50
Q

Describe the histological appearance of fibrinoid necrosis

A

Deposits of these immune complexes, together with plasma proteins that have leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains called “fibrinoid” (fibrin-like)

51
Q

What happens if necrotic cells and cellular debris are not promptly destroyed and reabsorbed?

A

Dystrophic calcification can occur

Excess ACEM Primary cards (1 decks)

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