Cell injury, adaptation and death
Diperkenalkan| English | Makna |
|---|---|
| cell swelling | cell swelling |
| fatty change | fatty change |
| necrosis | The opposite: many cells, swelling, leaking and inflammation. |
| coagulative necrosis | coagulative necrosis |
| liquefactive necrosis | liquefactive necrosis |
| caseous necrosis | caseous necrosis |
| apoptosis/əpəpˈtəʊsɪs/ | A programme: single cells shrink and break into neat fragments, driven by caspases, and are eaten without inflammation. |
| atrophy | atrophy |
| hypertrophy | hypertrophy |
| hyperplasia | hyperplasia |
| metaplasia | metaplasia |
Twenty minutes to save a heart cell
- When a coronary artery blocks, heart muscle cells can still recover if blood returns within about 20–30 minutes. After that, they begin to die.
- All disease starts as stressed cells. Whether they recover or die, and how they die, is where pathology begins.
Reversible injury
- Without oxygen, ATP falls, the Na⁺/K⁺ pump fails, sodium and water flood in, and the cell swells (cell swelling 细胞水肿).
- Lipid droplets can collect in liver and heart cells: fatty change 脂肪变. Restore the supply and both reverse.
Which change is still reversible?
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Swelling and fatty change reverse when oxygen returns; membrane damage does not.
The point of no return
- Membranes are damaged, calcium floods in and mitochondria fail. The cell cannot recover.
- Leaky membranes release cell contents into the blood: troponin from heart muscle, ALT from liver cells. Those blood tests date the injury.
Put the events of ischaemic cell injury in order.
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The reversible steps come first; membrane damage marks the point of no return.
Patterns of necrosis
- Necrosis 坏死 has patterns that name the cause. Coagulative necrosis 凝固性坏死 keeps the cell outlines (ischaemia in heart or kidney); liquefactive necrosis 液化性坏死 turns tissue to liquid (brain, abscess).
- Caseous necrosis 干酪样坏死 is cheese-like, inside granulomas (classically tuberculosis); fat necrosis follows enzyme release in the pancreas; fibrinoid necrosis damages vessel walls.
Match each pattern of necrosis to its typical setting.
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The pattern names the cause.
Apoptosis
- Apoptosis 细胞凋亡 is a programme: single cells shrink and break into neat fragments, driven by caspases, and are eaten without inflammation.
- It removes cells during development, ends immune responses and deletes damaged cells. Necrosis is the opposite: many cells, swelling, leaking and inflammation.
Apoptosis causes a strong inflammatory reaction.
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Apoptotic fragments are eaten quietly; it is necrosis that leaks and inflames.
Four adaptations
- Atrophy 萎缩: cells shrink (disuse). Hypertrophy 肥大: cells enlarge (the heart against high blood pressure, with no new muscle cells).
- Hyperplasia 增生: more cells (the endometrium under oestrogen). Metaplasia 化生: one cell type replaces another (squamous cells in a smoker's bronchus).
A smoker's bronchial lining changes from ciliated columnar to squamous cells. What is this?
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One differentiated cell type has replaced another.
A heart grows from 300 g to 450 g with no new muscle cells. By what percentage has the average cell's mass grown?
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Same number of cells, so each grows by 150 ÷ 300 = 50%, which is hypertrophy.
Worked example: the adaptation quartet
- (Fictional set) A plastered leg's muscles shrink: atrophy. A hypertensive heart thickens: hypertrophy. A healing liver after part is removed: hyperplasia.
- A smoker's airway lining turns from ciliated columnar to squamous: metaplasia. It resists smoke better but can no longer clear mucus.
Worked example: the 20-minute window
- (Fictional) Kidney tubule cells deprived of blood for 20 minutes are swollen with low ATP; when blood returns, they recover.
- After hours without blood, their membranes leak enzymes such as LDH into the blood and calcium has flooded in: the cells are dead, and the blood test shows it.
Kidney tubule cells are swollen with low ATP after 20 minutes without blood. What happens if blood returns now?
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Swelling with intact membranes is reversible injury.
Three common slips
- Calling apoptosis a kind of necrosis. It is a tidy programme with no inflammation.
- "Caseous means tuberculosis." It means a necrotic granuloma; tuberculosis is the classic but not the only cause.
- Treating fatty change as death. It is an early, reversible sign.
Recap
- Low ATP → swelling and fatty change (reversible); membrane damage and Ca²⁺ entry → death.
- Coagulative (ischaemia), liquefactive (brain, abscess), caseous (granuloma), fat (pancreas), fibrinoid (vessels).
- Apoptosis is tidy and silent; adaptations are atrophy, hypertrophy, hyperplasia and metaplasia.