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Pathological Processes > Cell Injury And Death Notes > Flashcards

Cell Injury And Death Notes Flashcards

1
Q

What factors determine the degree of cell injury

A

Type of injury
Severity of injury
Duration of injury
Type of tissue

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2
Q

List the causes of cell injury

A

Environmental:
Hypoxia
Toxins/poisons
Immune mediated
Physical agents
Infections
Nutritional/dietary

Non-environmental:
Genetic
Ageing

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3
Q

Describe the different causes of hypoxia

A
  1. Hypoxaemic hypoxia - arterial content of oxygen is low
  2. Anaemia hypoxia - decreased ability of haemoglobin carry oxygen
  3. Ischaemic hypoxia - interruption to blood supply
  4. Histiotoxic hypoxia - inability to utilise oxygen due to disabled oxidative phosphorylation enzymes
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4
Q

What are the 2 mechanisms of immune mediated cell injury?

A

Hypersensitivity reactions - secondary to excessive immune reaction to non-self antigens

Autoimmune reactions - immune system over reacts to a self antigen causing tissue damage

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5
Q

What are the physical agents that lead to cell injury and death?

A

Trauma
Extreme temperature
Electric currents
Radiotherapy

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6
Q

What can cause infection leading to cell damage?

A

Bacteria
Virus
Parasite
Fungi

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7
Q

What are the nutritional/dietary causes of cell damage?

A

Obesity
Anorexia
Dietary deficiencies or excess

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8
Q

What are the genetic/age causes of cell damage?

A

Inborn errors in metabolism
Enzyme deficiencies
Dysfunctional proteins

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9
Q

What are the 6 mechanisms of cell injury

A

Depletion of ATP
Direct mitochondrial damage
Direct membrane damage
Disruption to calcium homeostasis
Oxidative stress
Direct damage to DNA and proteins

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10
Q

How can calcium influx cause irreversible damage?

A

Can activate ATPases, phospholipases, proteases and endonucleases

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11
Q

What can free radicals damage within cells?

A

Lipids, proteins and DNA

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12
Q

Describe free radical damage of lipids

A

Unsaturated fatty acids get attacked by free radicals. This causes cell membrane and organelle damage, resulting in calcium influx, damage to Na/K pump etc.

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13
Q

Describe free radical damage of protein

A

Promotes protein-protein cross links (disulphide bonds) and oxidation of proteins.
This causes protein fragmentation and thus cell damage

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14
Q

Describe free radical damage of DNA

A

Free radicals target nuclear and mitochondrial DNA
They cause single and double strand breaks in DNA

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15
Q

how does the body remove free radicals?

A

Anti-oxidants
Transport proteins
Enzymes

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16
Q

How does the body control free radical damage?

A

Heat shock proteins e.g. ubiquitin.
They help repair and re-fold damaged proteins, or they label them for degradation
In times of stress, all cells reduce their usual protein synthesis and increase heat shock protein synthesis

17
Q

Describe reversible and irreversible cell injury

A

Reversible:
Swelling
Clumped chromatin
Ribosome dispersion
Cystoplasmic ‘blebs’ (membrane is intact)

Irreversible:
Nuclear changes
Membrane defects
Lysosome rupture
Lysis of endoplasmic reticulum

18
Q

What are the differences between physiological and pathological apoptosis?

A

Physiological - embryogenesis

Pathological - cell death in viral infection

NOTE: in apoptosis, cells shrink, no inflammation, neat and tidy

19
Q

What are the 2 pathways of apoptosis?

A

Intrinsic (mitochondrial) - mitochondria release cytochrome C which activates caspases which induce apoptosis

Extrinsic (death receptor) - death receptors (secreted from T killer cells) attach to the cell membrane which then activate caspases which lead to cell death

20
Q

Describe necrosis

A

Cells swell, disorganised and messy

Characteristic nuclear changes: pyknosis (shrinkage), karyorrhexis (fragmentation), karyolysis (dissolution)

Types of necrosis: coagulative, liquefactive, caseous, fat necrosis, fibrinoid necrosis

21
Q

Describe coagulative necrosis

A

Solid organs
Retains ghost outline of cells and tissue architecture
Protein desaturation prominent in the cell injury/death

22
Q

Describe liquefactive necrosis

A

Damage of ‘loose’ tissue
Complete loss of architecture
Release of enzymes which break down tissue

23
Q

Describe fat necrosis

A

Due to direct trauma to fatty areas and acute pancreatitis

24
Q

What molecules are released by injured cells?

A

Potassium
Enzymes
Myoglobin

25
Q

Cell injury causes deranged metabolism. What can accumulate within cells due to this?

A

Normal cell components - e.g. cerebral oedema: hypoxic cell injury -> sodium enters cell, water follows -> cell swelling

Abnormal cell components - e.g. fatty liver disease: liver cell injury -> deranged metabolism -> fat accumulation within hepatocytes

Pigment - e.g. tattoo: artificial pigment into skin -> pigment phagocytosed by macrophages -> pigment remains in macrophages of dermis

26
Q

What is gangrene?

A

Necrosis visible to the naked eye

27
Q

what is an infarction?

A

Necrosis caused by reduction in arterial blood flow - a cause of necrosis
Can result in gangrene

28
Q

What is ischaemia?

A

Inadequate blood supply to tissue
Can result in infarction

29
Q

Hat is the difference between dry and wet gangrene?

A

Both involve necrosis

Dry - exposure to air. Coagulative necrosis

Wet - infection. Liquefactive necrosis

30
Q

What is the difference between white and red infarct?

A

White:
No associated haemorrhage.
Occlusion of an end artery -> often wedge shaped

Red:
Haemorrhage (into dead tissue)
Organs with a dual blood supply
Previous vascular congestion

31
Q

What is pathological calcification? What are the two different types?

A

Abnormal deposition of calcium within tissues

1) Localised in dying tissue (dystrophic) - most common; nothing to do with calcium metabolism

2) Generalised (metastatic) - deposition in otherwise normal tissue; metabolic error causing high levels of circulating calcium; can be fatal

Pathological Processes (6 decks)

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