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M1 General Pathology > Cell Damage > Flashcards

Cell Damage Flashcards

1
Q

What are the 3 cellular outcomes of prolonged decreased functional demand?

A

1) Atrophy (↓ cell size)
2) Involution/Hypoplasia (↓ cell no.)
3) Metaplasia

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2
Q

What are the 3 cellular outcomes of prolonged increased functional demand?

A

1) Hypertrophy (↑ cell size)
2) Hyperplasia (↑ cell no.)
3) Metaplasia

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3
Q

What is the difference between metaplasia and dysplasia?

A

Metaplasia transforms a cell from one form to another; caused by external stimulus; can be reversible; less likely to lead to cancer.

Dysplasia transforms a cell into an abnormal version of itself; caused by internal stimulus; is irreversible and more likely leads to cancer.

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4
Q

What can stimulate cellular metaplasia?

A

Injurious stimuli (eg. Gastroenteritis, H. pylori infection, CMV)

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5
Q

What are the 4 mechanisms of cell injury?

A

1) Cell membrane damage (eg. complement-mediated lysis via MAC, bacteria toxins, free radicals)

2) Mitochondrial damage (eg. Hypoxia, Cyanide poisoning)

3) Ribosomal damage (eg. alcohol in hepatocytes, antibiotics in bacteria)

4) Nuclear damage (eg. virus, radiation, free radicals)

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6
Q

How can increased cytosolic Ca2+ cause cell damage?

A

Ca2+ ions can activate hydrolytic enzymes
i) ATPase→↓ATP
ii) Phospholipase→↓phospholipids
iii) proteases → membrane dmg
iv) endonuclease → chromatin dmg

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7
Q

How can tissue ischaemia cause cell damage?

A

Decreased OXPHOS and ATP prod.
i) Ribosome detachment
ii) ↑ Anaerobic glycolysis → ↓pH
iii) ↓Na pump f(x) → cell swelling

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8
Q

Are all early cellular changes after injury reversible?

A

Yes

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9
Q

Are all late cellular changes after injury irreversible?

A

Yes

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10
Q

What factors determine whether cellular changes in response to injury are reversible or irreversible?

A

1) Type of injury
2) Exposure time
3) Severity

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11
Q

What are 4 early/reversible cellular changes after injury?

A

1) Cytoplasmic swelling & Vacuolation
2) Mitochondrial & ER swelling
3) Chromatin clumping
4) Fatty changes

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12
Q

What are 4 late/irreversible cellular changes after injury?

A

1) Densities in mitochondria
2) Cell membrane disruption
3) Lysosomal rupture
4) Atypical nucleus
4a) Pyknosis (nuclear shrinkage)
4b) Karyolysis (nuclear dissolution)
4c) Karyorrhexis (nuclear breakup)

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13
Q

How can fat change occur in hepatocytes?

A

Anythingthat changes FFA Ss or metabolism
1) DM/Starvation → change FFA Ss
2) Ethanol → ↑FFA Ss and ↓Esterification
3) Hypoxia → ↓FFA oxidation and ↓ esterification
4) Toxins → ↓FFA oxidation and ↓apoprotein availability
5) Protein malnutrition → ↓apoprotein availability

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14
Q

What are 2 cellular non-death responses to injury?

A

1) Cell stress response (↑exp. of protective proteins)
1a) molecular chaperones (refold misfolded proteins)
1b) Ubiquitination of damaged proteins

2) Autophagy (digest own organelles)

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15
Q

What are the histological characteristics of cell stress response?

A

Inclusion bodies (Aggregates of ubiquitin & damaged proteins)

eg. Mallory’s hyaline bodies in Hepatocytes with Alcoholic Liver Damage, Lewy Bodies in Substantia Nigra with Parkinson’s

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16
Q

What are the histological characteristics of Autophagy

A

Residual bodies (accumulation of lipofuscin: wear and tear pigment)

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17
Q

What are “wear and tear pigments”.

A

Lipofuscin

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18
Q

What are the 3 forms of cell death?

A

1) autolysis
2) apoptosis
3) necrosis

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19
Q

What are the differences between Autolysis, Apoptosis, Necrosis?

A

Autolysis is the death of tissues after the death of the organism.

Apoptosis is the death of cells in living tissues and programmed. It can be physiological or pathological.

Necrosis is the death of cells in living tissues and is always pathological.

20
Q

Compare and contrast between Apoptosis and Necrosis.

A

Apoptosis:
- can be physiological or pathological
- membrane preserved
- no inflammation
- single cells
- active process

Necrosis:
- always pathological
- membrane breached
- inflammatory
- contiguous (connecting) cells
- passive process

21
Q

Which form of necrosis is associated with ghost outlines?

A

Coagulative necrosis

22
Q

What are 8 forms of necrosis?

A

1) Coagulative
2) Caseous
3) Liquefactive
4) Suppurative
5) Hemorrhagic
6) Fat
7) Gangrenous
8) Fibrinoid

23
Q

Which form of necrosis is common secondary to hypoxia, ischaemia, infarction, and skin burns?

A

Coagulative necrosis

24
Q

Which form of necrosis is associated with associated with friable and “cheesy” tissue?

A

Caseous necrosis

25
Q

Which form of necrosis is associated with mycobacterium infections (eg. TB)?

A

Caseous necrosis

26
Q

What cell is associated with caseous necrosis in TB infections?

A

Langhan’s giant cell

27
Q

What are the components of granuloma?

A

Epithelioid macrophages, neutrophils, T lymphocytes, multinucleated giant cells, (central caseous necrosis)

28
Q

How do multinucleated giant cells form?

A

via frustrated phagocytosis
(macrophages from tissue stroma NOT epithelium)

29
Q

What is the most common form of necrosis in the brain?

A

Liquefactive necrosis

30
Q

What form of necrosis does liquefactive necrosis often overlap with?

A

Suppurative necrosis

31
Q

Which form of necrosis is associated with a cystic “liquefied” appearance?

A

Liquefactive necrosis

32
Q

Where does the “liquefactive” part of liquefactive necrosis come from?

A

The lipids from breakdown of myelin

33
Q

Which form of necrosis describes abscess formation?

A

Suppurative necrosis

34
Q

Which form of necrosis describes ulcers?

A

Suppurative necrosis

35
Q

Which form(s) of necrosis is associated with large collections of dead neutrophils?

A

Suppurative (and also Liquefactive) necrosis

36
Q

Which form of necrosis is common secondary to bacterial infections?

A

Suppurative necrosis

37
Q

Which form of necrosis occurs in organs with dual blood supply (eg. lungs and liver)?

A

Haemorrhagic necrosis

38
Q

Which form of necrosis is associated with reperfusion injury?

A

Haemorrhagic necrosis

39
Q

Which form of necrosis is common secondary to venous congestion?

A

Haemorrhagic necrosis

40
Q

What are 6 possible mechanisms of cellular aging?

A

1) ↓ replication
2) telomere shortening
3) Accumulated dmg
4) Genetic and environmental insult
5) DNA repair defects
6) Abnormal growth factor

41
Q

What is the macroscopic appearance indicative of haemorrhagic necrosis?

A

Redness

42
Q

What is the macroscopic appearance indicative of coagulative necrosis?

A

White tissue

43
Q

How does coagulative necrosis occur?

A

Hypoxia → Ischaemia → Infarction → Coagulative necrosis

44
Q

Where does fat necrosis occur?

A

Breast, Buttock (high fat content)

45
Q

Where does fibrinoid necrosis occur?

A

Blood vessels?

M1 General Pathology (4 decks)

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