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pathology > apoptosis and necrosis > Flashcards

apoptosis and necrosis Flashcards

1
Q

define apoptosis

A

programmed cell death
nothing has killed them they are kind of just killing themselves

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2
Q

whats a trigger to apoptosis

A

dna damage
a signalling messanger causes this

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3
Q

give an example of apoptosis during foetal depelopment

A

our fingers grow all stuck together, apoptosis allows us to have individual fingers

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4
Q

give an example of apoptosis in disease

A
  • B53 gene faulty - lack of apoptosis - cancer development
  • too much B53 gene is what HIV used to kill T-cells
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5
Q

define necrosis and give some examples

A
  • death of a large number of cells all at once
  • traumatic cell death
  • frostbite
  • toxic spider venom
  • cerebral infarction
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6
Q

what is the gene P53?

A

detects DNA damage and can then trigger apoptosis

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7
Q

how does a cell apoptose?

A
  • the cell triggers a series of proteins which lead to the release of enzymes
  • these digest the cell
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8
Q

why is apoptosis beneficial in health?

A

development - removal of cells during development

cell turnover - removal of cells during normal turnover

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9
Q

outline the differences between apoptosis and necrosis.

A

apoptosis:
- programmed, controlled
- caused by signals, dna damage and cell stress
- orderly and systematic process
- maintained membrane until final stages
- no inflammation or affect on surrounding tissues

necrosis:
- uncontrolled, accidental
- caused by external injury, infections, toxins, ischemia
- unregulated and chaotic
- membrane is lost early, cellular contents spill
- inflammation occurs due to the release of cellular contents
- examples are trauma, infection and ischemia

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10
Q

when cells die by necrosis, they exhibit 2 major types of microscopic or macroscopic appearances, what are these?

A
  • liquefactive / colliquative
  • coagulative
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11
Q

what catagorises liquefactive / colliquative necrosis?

A
  • partial or complete destruction of dead tissue and transformation into a liquid, viscous mass
  • The loss of tissue and cellular profile occurs within hours - short amount of time
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12
Q

what catagorises coagulative necrosis?

A

maintenance of normal architecture of necrotic tissue for several days after cell death

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13
Q

Q: What is the main microscopic or macroscopic appearance of liquefactive necrosis?

A

A: Tissues undergoing liquefactive necrosis appear slimy and liquid-like due to tissue dissolution.

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14
Q

Q: What causes the dissolution of tissue in liquefactive necrosis?

A

A: Hydrolytic enzymes break down cellular organelles, leading to liquefaction.

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15
Q

Q: Where do the hydrolytic enzymes in liquefactive necrosis come from?

A

A: They are derived from bacterial enzymes or the cell’s own lysosomal enzymes.

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16
Q

Q: How does coagulative necrosis differ from liquefactive necrosis in terms of tissue structure?

A

A: In coagulative necrosis, the tissue structure is maintained temporarily, unlike in liquefactive necrosis, where tissue is quickly dissolved.

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17
Q

Q: Which type of necrosis is commonly seen in ischemic events like myocardial infarction?

A

A: Coagulative necrosis is typically associated with ischemic injury, such as myocardial infarction.

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18
Q

Q: In what conditions is liquefactive necrosis most commonly observed?

A

A: Liquefactive necrosis is commonly seen in brain infarcts and abscesses due to bacterial or fungal infections.

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19
Q

Q: What role do lysosomes play in liquefactive necrosis?

A

A: Lysosomes release hydrolytic enzymes that break down cell components, leading to liquefaction.

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20
Q

Q: What is the key difference in enzyme activity between liquefactive and coagulative necrosis?

A

A: Liquefactive necrosis involves active hydrolytic enzyme activity that digests tissue, while coagulative necrosis maintains tissue architecture due to less enzymatic breakdown.

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21
Q

in addition to the main types of necrosis: coagulative and liquefaction, what are the other types of necrosis?

A

Caseous Necrosis
Fat Necrosis
Gangrenous Necrosis
Fibrinoid necrosis

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22
Q

Q: What is the default pattern of necrosis associated with ischemia or hypoxia in most organs?

A

A: Coagulative necrosis is the default pattern of necrosis associated with ischemia or hypoxia in every organ in the body except the brain.

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23
Q

Q: What is the gross appearance of tissue undergoing coagulative necrosis?

A

A: The tissue appears firm, and its architecture is maintained for days after cell death.

24
Q

Q: What is the microscopic appearance of cells in coagulative necrosis?

A

A: Cell outlines are preserved, but the cells lack nuclei.

25
Q

Q: In what conditions is liquefactive necrosis typically seen?

A

A: Liquefactive necrosis is commonly seen with infections and following ischemic injury in the brain.

26
Q

Q: Why does liquefactive necrosis occur in infections?

A

A: In infections, liquefactive necrosis is caused by the release of digestive enzymes and contents from neutrophils, leading to tissue liquefaction.

27
Q

Q: What is the gross appearance of tissue undergoing liquefactive necrosis?

A

A: The tissue is in a liquid form and may appear creamy yellow due to pus formation.

28
Q

Q: What is the microscopic appearance of liquefactive necrosis?

A

A: inflammatory cells with numerous neutrophils.

29
Q

when does caseous necrosis occur?

A

a unique case
only tuberculosis

30
Q

what is the microscopic appearance of cells undergoing caseous necrosis?

A
  • eosinophilic center surrounded lymphocytes and activated macrophages
  • known as a granuloma.
31
Q

when does fat necrosis occur?

A
  • occurs from acute inflammation
  • affects tissues with numerous adipocytes
  • damaged cells release enzymes which break down lipids into fatty acids
32
Q

what is the gross appearance of cells being broken down during fat necrosis?

A

Whitish deposits as a result of the formation of calcium soaps.

33
Q

what is the microscopic appearance of cells being broken down during fat necrosis?

A

Anucleated adipocytes with deposits of calcium

34
Q

when does fibrinoid necrosis occur?

A

vascular damage (autoimmunity, immune-complex deposition, infections (viruses, spirochetes, rickettsiae)).

35
Q

what is the gross appearance of cells broken down by fibrinoid necrosis?

A

Usually not grossly discernible.

36
Q

what is the microscopic appearance of cells broken down by fibrinoid necrosis?

A

Deposition of fibrin within blood vessels.

37
Q

what does gangrenous necrosis describe?

A
  • used in clinic to describe the necrosis of the lower limbs
38
Q

whats the gross appearance of cells affected by gengrenous necrosis?

A

Black skin with varying degree of decay.

39
Q

whats the microscopic appearance of cells affected by gengrenous necrosis?

A

Combination of coagulative necrosis, due to ischemia (dry gangrene); and liquefactive necrosis (wet gangrene) if a bacterial infection is superimposed.

40
Q

in what tissues does liquefactive necrosis occur and under what circumstances?

A
  • solid organs - infections
  • brain - hypoxia/ischemia
41
Q

what 3 main factors drive liquefactive necrosis?

A
  • enzymatic digestion of cellular debris
  • enzymatic digestion of surrounding tissues
  • denaturation of proteins

infections are a major cause of this because it produces these enzymes and causes for an immune response causing immune cells to further release enzymes

42
Q

what are the main digestive enzymes leading to liquefaction?

A
  • proteases
  • DNases
  • lysosomal enzymes
43
Q

outline the difference in enzymatic digestion of coagulative vs liquefactive necrosis and why this is.

A
  • liquefactive - both autolysis and heterolysis
  • coagulative - only heterolysis because ishemia would have damaged the enzymes in the tissue effected - only the inflammatory cells have enzymes - also explains the late onset of digestion and removal of dead tissue
44
Q

explain how fat necrosis occurs

A
  • pancreatitis causes pancreatic cells to release lipases and amylases
  • in breast tissue, the trigger is usually trauma
45
Q

explain the occurance of fibrinoid necrosis

A
  • endothelial damage and exudate lasma proteins
46
Q

what triggers apoptosis?

A

intracellular and extracellular signals

intracellular:
- dna damage
- failure to conduct cell devision properly

extracellular:
- detachment ffrom the extracellular matrix
- withdrawal of growth factors
- specific signals from other cells

47
Q

name a few inhibitors for apoptosis

A
  • growth factor
  • sex steroid
48
Q

name some inducers of apoptosis

A
  • growth factor withdrawal
  • free radicals
  • dna damage
  • loss of matrix attachment
  • viruses
  • glucocorticoids
49
Q

describe what occurs in the intrinsic pathway of undergoing apoptosis

A
  • proteins from the Bcl-2 family decide
  • both pro and anti apoptosis proteins in ratio to each other - whichever is higher is the decider
  • Bcl-2 - prevents apoptosis - blocks cell death signals
  • bax - promotes apoptosis - forms bax-bax dimers that enhance cell death signals
50
Q

What is the extrinsic pathway of apoptosis, and how does it function?

A

A: - “death receptors” on the cell surface (e.g., TNFR1 and Fas/CD95) bind to ligands
- receptors cluster together
- This activates caspases, enzymes that initiate cell death

51
Q

Q: What happens during the execution phase of apoptosis?

A

A: - Initiator caspases (like caspase-8) activate executioner caspases (like caspase-3).
- These degrade the cytoskeleton and nuclear proteins, causing DNA fragmentation
- The nucleus shrinks (pyknosis) and breaks apart (karyorrhexis).
- The cell shrinks but keeps its membrane intact, signaling phagocytosis.
- Dead cells form apoptotic bodies and are cleared without causing inflammation.

52
Q

describe briefly a couple of the abnormal apoptotic responses detailing the cells involved

A
  • neurons - neurodegenerative disease
  • t lymphocytes - autoimmune disease
53
Q

what actually is liquefactive necrosis and when is it likely to happen?

A
  • type of tissue death
  • cells rapidly digested by enzymes
  • forms soft liquid mass
  • commonly occurs in tissues with high enzymatic content eg brain after ischemic injury and infections
  • this is the type of necrosis which results in pus or fluid accumulation due to cellular destruction
54
Q

Why does liquefactive necrosis occur in the brain after ischemia, while coagulative necrosis occurs in other solid organs?

A

Liquefactive necrosis occurs in the brain because its lipid-rich neurons and glial cells contain high concentrations of enzymes that quickly digest tissue into a liquid form after ischemia. In solid organs like the heart or kidneys, structural proteins denature and coagulate after ischemia, preserving tissue architecture temporarily, leading to coagulative necrosis instead.

55
Q

thinking about immunity and haematapoesis, when would apoptosis occur?

A
  • if the MHC molecules weren’t there or working
  • if they didn’t bind to TCR
  • if they bound to readily to self-antigens

pathology (14 decks)

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