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L34 - Cell Injury and Responses Understand the possible causes of…
L34 - Cell Injury and Responses
- Understand the possible causes of cell/tissue injury.
- Describe the possible outcomes for a cell
subjected to stress or injury
- Describe the changes in cellular appearance and function resulting from cell injury
- Describe how tissues react to cell injury*
You should be able to:
- Describe the important cellular/tissue/organism level events when cells are damaged
- Define the various responses to cell injury
This is important so:
- You can go on to understand the spectrum of disease processes that affect cells/tissues/systems and how the body reacts to them.
- In the context of this unit and major, understand neoplastic disorders (benign and malignant tumours), especially cancer.*
Core Concept: 1
Nearly all acquired diseases are caused by cell injury
This occurs at a molecular, subcellular or cellular level and leads to tissue, organ and organism injury
Core Concept 2:
Severity of injury = Duration X Intensity
Severity of the effect is a function of the duration and intensity of injury
Example
Sunburn
- Sore, red skin
- Blistered skin
Core Concept 3
Cells and Tissues have limited mechanisms for responding to injurious stimuli
The response depends on the nature of the injury/stress, the duration of exposure, the cells affected and the host system/organism response
Example
The response to acute bacterial infection on the lungs may be different in a patient on immuno-suppressive drugs for a lung transplant
Cell Injury
- Non-lethal Reversible Injury (Acute/mild)
- Cell swelling / membrane damage / organelle dysfunction => Return to normal state
- Non-lethal Stress
(long term/chronic)
- Hyperplasia, Hypertrophy, Atrophy, Metaplasia, etc.
- Lethal Irreversible Injury
- Necrosis
- Apoptosis
- Autophagy
IRREVERSIBLE INJURY
Severe, progressive
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Reversible Injury
Mild, transient
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Causes of Cell Injury
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Oxygen Deprivation (Irreversible = infarct)
- Hypoxia
- May be due to reduced oxgenation, reduced hb, reduced blood voume
- Ischaemia (reduced blood flow)
=> Reduced ATP leads to failure of Na+ pump (polarity etc)
- Toxic metabolites, membrane rupture
Physical Agents
- Trauma
- Heat, cold, pressure, radition, electic shock etc
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Immunologic Reactions
- Autoimmunity, excessive inflammation
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Pathways to Cell Death
After reading this, consolidate with slide 38
Necrosis - Irreversible Cell Injury
- Uncontrolled cell death
- Final outcome of severe cell damage
e.g. Ischaemia - Myocardial Infarction
Cytoplasmic Changes
Increased Eosinophila (membrane permeability) - "glassy" cytoplasm, loss of organelles + accumulation of metabolites (lead to vacuolation)
Nuclear Changes
Once nucleus dies, the cell is unsalvageable
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Pyknosis -
shrinkage and basophilia, DNA condenses (darkens)
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Apoptosis - Irreversible Cell Injury
Characterised by regulated enzymatic destruction of proteins and DNA
- Serves to eliminated unwanted or irreparably injured cells, with minimal harm to host
- Unusual variants; necroptosis (regulated) and pyroptosis (pro-inflammatory)
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Hypertrophy and Hyperplasia can occur simultaneously
E.g. Obesity
Both are caused by GFs i response to mechanical stress/hormonal stimulation
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- Ischaemic event →
- Death of myocytes in ischaemic area →
- Vulnerable myocytes at periphery →
- Acute inflammation →
- Death or recovery of vulnerable myocytes →
- Healing / dysfunction / death (early or late)*
Coagulative Necrosis
Dry Gangrene
Caseous Nerosis
Fibrinoid Necrosis
Wet gangrene
Gas Gangrene