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Foundations of Pathology > L3 - Cell Injury and Death > Flashcards

L3 - Cell Injury and Death Flashcards

1
Q

How do cells survive?

A
  • Constant energy supply
  • Intact plasma membrane
  • Efficient cellular activities
  • Genomic integrity
  • Controlled cell division
  • Internal homeostatic mechanism

Disturbance of these factors can lead to cell injury or death

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2
Q

How are mechanisms of cell injury classified?

A

Classified according to:

• Causative agents
• Cellular target
• Pattern of cell death
apoptosis/necrosis

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3
Q

Physical causative agents

A
  • Passive cell destruction (membrane disruption lead to catastrophic functional impairment)
  • Trauma and thermal injury (Microwave leads to thermal injury, Laser breaks intramolecular bonds, Disrupt cells & denature proteins)
  • Freezing (Mechanical damage leads to ice crystals and membrane disruption)
  • Shearing forces (Structures move relative to each other)
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4
Q

Chemical and biological causative agents

A
  • Chemical agents (Naturally occurring or synthetic, Toxic to specific metabolic pathways)

Biological agents:
- Enzymes & toxins secreted by microorganisms
- Bacterial endotoxin (lipopolysaccharide, LPS) that damage nearby cells
- Viruses (Physical rupture of infected cells , local tissue damage from immune response)
-

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5
Q

Cellular target: DNA damage

A
  • Non-lethal damage inherited by daughter cells: neoplastic transformation
  • Lethal damage can occur if multiple mutations accumulate
  • If cells unable to repair, cell will die (Apoptosis)
  • Strand breaks, base alterations, cross linking
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6
Q

Characteristics of irreversibility in cell damage

A
  • Irreversible mitochondrial dysfunction (earliest sign)

- Profound membrane dysfunction

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7
Q

Reversible cell injury

A

Hydropic change:

  • Accumulation of fluid
  • cytoplasm pale & swollen

Fatty change:
- Vacuolation of cells, accumulation of lipid droplets

Autophagy

  • Cellular response to stress, e.g. lack of nutrients or growth factors
  • Cell components isolated into vacuoles, lysosomes
  • can proceed to apoptosis if stimulus not removed
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8
Q

Reversible cell swelling/ hydropic change can be caused by

A
  • Interference with membrane structure
  • Interruption of energy supplies
  • Both lead to dysregulated ion and water movement in/out of cell
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9
Q

Features of reversible cell swelling/hydropic change

A
  • Cell cytoplasm - pale and swollen

- Fluid accumulation

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10
Q

Cells can survive for weeks after reversible swelling and hydropic change if:

A
  • no membrane and internal structures rupture;

* Enough membrane function is present so that metabolic processes are functioning

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11
Q

Reversible Fatty changes (locations where it can be seen)

A

Seen in cells which have a high lipid content/ high lipid synthesis (Liver, heart, kidney)

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12
Q

Reversible Fatty changes (common causes)

A
  • Toxins - alcohol and hydrocarbons such as chloroform - Chronic hypoxia
  • Diabetes mellitus.
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13
Q

Irreversible cell death is due to:

A
  • Free radicals
  • Calcium ions
  • Energy shortage (ATP depletion)
  • Cell membrane dysfunction (increased permeability)
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14
Q

Ischaemia

A

lack of blood supply to an organ

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15
Q

Hypoxia

A

lack of oxygen

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16
Q

Necrosis (irreversible cell death) is caused by

A
  • Ischemia (leading to hypoxia, lack of oxygen)
  • Metabolic blockade
  • Trauma
17
Q

Time to death of organs with hypoxia

A
  • Brain < 3 minutes
  • Heart 1-2 hours
  • Kidney 2-3 hours
  • Skin fibroblasts < 24 hours
18
Q

Coagulative necrosis

A
  • protein denaturation is the main process
  • enzymes in the cells are broken down, preventing normal function
  • seen in hypoxic/ ischaemic cell death everywhere except the brain
  • loss of nuclear stain and cytoplasmic detail after tissue has been consumed by macrophages
19
Q

Caseous necrosis

A
  • Characteristic of TB in lungs
  • Dead cells/tissue has no structure
  • Histology: amorphous eosinophilic area with haematoxylin-stained nuclear debris
  • Granulomas have a centre that contains cells that mediate chronic inflammatory reaction
  • Cheesy looking; Grey/white, soft & friable
  • Combination of coagulative and colliquative necrosis
20
Q

Gangrene

A
  • Necrosis with putrefaction of tissues
  • Black areas are deposition of iron sulphide from degraded haemoglobin
  • Sometimes due to bacterial infection e.g. clostridia
  • Can also be due to poor blood supply, e.g. to feet in diabetic patients
  • Dry form > usually seen in toes, due to lack of blood supply
  • Wet form > bowel gangrene
21
Q

Fibrinoid necrosis

A
  • Immune-complex-mediated hypersensitivity
  • These antigen-antibody complexes stick to vessel walls, attract inflammatory cells, activate complement.
  • Inflammation damages the vessel wall and wall becomes necrotic.
  • The “fibrinoid” part of the name implies fibrin has a central role in this type of necrosis – it doesn’t
  • The name is because the bright pink staining in an H&E (due to immune complexes and debris) looks like fibrin.
22
Q

Fat necrosis (direct)

A
  • Seen in adipose tissue of thigh, breast, other locations subject to impact
  • Physical injury to adipocytes releases triglycerides > hydrolysed by serum lipases > fatty acids > saponification > formation of chalky material
23
Q

Fat necrosis (pancreatitis)

A
  • Lysis of fat due to lipase release > leaks from pancreas into surrounding tissue
  • Fat split into fatty acids, combines with calcium/sodium/potassium > precipitates as white soaps
24
Q

Fat necrosis (inflammatory response)

A
  • Neutrophils and macrophages phagocytose the fat

- End result > fibrosis – can have palpable mass

25
Q

Apoptosis

A
  • No inflammatory reaction (intact cell membrane)
  • Death of scattered single cells
  • Form rounded membrane bound bodies
  • Eventually phagocytized by unaffected neighbouring cells
  • Occurs in most living cells
  • Energy-dependent
26
Q

Apoptosis - intrinsic pathway

A
  • Bcl-2 inhibits apoptosis
  • Bax stimulates apoptosis
  • Ratio of Bcl-2: Bax influence how susceptible a cell is to apoptotic stimuli
  • The Bcl-2 family govern mitochondrial outer membrane permeability
27
Q

Apoptosis - extrinsic pathway

A
  • Ligand binding at death receptors on cell surface
  • Receptors include (TNF Receptor 1, Fas (CD95))
  • Ligand binding leads to clustering of receptors on cell surface
  • Initiation of a signaling cascade resulting in caspase activation
28
Q

Factors affecting repair of tissues

A
  • Damage to fetus can affect subsequent development (e.g. rubella, thalidomide)
  • Children generally heal quickly, but there can be growth disturbance following tissue damage (e.g. pulmonary airways permanently damaged by whooping cough)
  • Nutritional deficiencies (Vitamin C disturbs collagen synthesis and causes scurvy, malnutrition impairs repair)
  • In old age, reserve capacity is reduced, healing is slower (ischaemia contributes to this)

Foundations of Pathology (15 decks)

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