Response to Injury I Flashcards

1
Q

What is cell response based on?

A

The type of response a cell undergoes is based on the type, duration and severity of the noxious stimulus.

The type of response a cell undergoes is based on is cell type, status within the cell cycle, capability to regenerate in turn its genetic profile.

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2
Q

What are the different cell types?

A

Labile
Stable
Permanent

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3
Q

Define labile cells.

A

Labile: continually in the cell cycle eg: cells of the epidermis. More susceptible to adaptation.

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4
Q

Define stable cells.

A

Stable: temporarily exit the cell cycle can be recruited back in eg: liver cells

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5
Q

Define permenant cells.

A

Permanent: permanently differentiated once lost cannot be replaced eg: cells of the central nervous system, axons, cardiac myocytes. More susceptible to cell death.

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6
Q

What happens when a cell is injured?

A

Following injury molecular and genetic changes will proceed with functional change. Then structural changes then signs and symptoms.

Adaptative changes may be due to pathological and physiological changes.

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7
Q

Give examples of cellular adaptive response.

A

Hyperplasia
Hypertrophy
Atrophy
Metaplasia
Dysplasia

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8
Q

Define Hyperplasia.

A

Increase in the number of cells occurs in tissues capable of cell division.

Eg: proliferation of glandular tissue in puberty/pregnancy or in the case of the prostate during hormonal imbalance. Dental relevance – can be seen in chronic hyperplastic candidiasis.

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9
Q

Define hypertrophy.

A

Increase in the size of cell.

Eg: skeletal or cardiac muscles. Pathological examples of this is left cardiac hypertrophy following heart failure.

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10
Q

Define atrophy.

A

Reduction in the size of an organ as a result of the reduction in the number of cells.

Eg: vaginal epithelium undergoes atrophy during menopause.

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11
Q

Define metaplasia.

A

Change from one differentiated cell type to another differentiated cell type.

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12
Q

Define dysplasia.

A

Disordered stratification and maturation.

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13
Q

Which cellular adaptive response is reversible.

A

Hyperplasia, hypertrophy, atrophy and metaplasia are all reversible response once stimulus is removed.

Metaplasia may proceed dysplasia (too a degree is reversible and genetic change leaves it irreversible).

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14
Q

Give examples of Causative agents of cell injury.

A

*Physical – E.g. trauma, thermal, radiation
*Chemical – E.g. CO, cigarette smoke, ethanol
*Infectious – E.g. toxins, metabolic products, lysis, DNA damage
*Oxygen deprivation – E.g. hypoxia, ischaemia
*Immunologic – E.g. complement activation, cell mediated cytotoxicity, autoimmune

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15
Q

Explain the mechanism of cell injury through ATP depletion.

A

Most important target of cell injury is disruption of metabolism, through ATP depletion frequently arise from hypoxia.

Mitochondrion is also prone to damage from injury, due to influx of calcium or generation of reactive oxygen species and hypoxic states.

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16
Q

Explain how radical/ROS formation.

A

Free radical/ROS formation has a single unpaired election which can cause serious damage to molecules.

ROS it is a product of cellular metabolism under certain conditions ROS may accumulate and cause damage to the cell.

Excess free radicals may result from ionising radiation, inflammation, drugs and some types of metal. DNA is a target for ROS and DNA damage can trigger death by apoptosis.

17
Q

What are other mechanisms of cell injury?

A
  1. Nutrient/growth factor deprivation is a key mechanism to cell injury.
  2. Another target of free radicles are membranes. Membrane can be disrupted by increased intracellular calcium.
  3. Inflammatory cells are a potent cause of cell death.
18
Q

What is necrosis?

A

Necrosis is morphologically characterised by cell swelling. Pyknosis is the condensation of the nucleus, this does not only occur in necrosis can be seen in apoptosis.

Pyknosis is succeeded by karyorrhexis which is the fragmentation of the nucleus which ultimately leads to karyolysis which is the disintegration and dissolution of the nucleus.

19
Q

What are the different types of necrosis?

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis

20
Q

What is coagulative necrosis?

A

Coagulative necrosis is the most common type of necrosis. The structural pattern of the necrotic tissue is maintained. Ischemia and infarction are common causes of coagulative necrosis.

21
Q

What is liquefactive necrosis?

A

Liquefactive necrosis changes in the organ and tissues results in a collection of liquid and viscous material. Common in necrosis of tissues in CNS or cells affected by bacteria or fungi.

22
Q

What is caseous necrosis?

A

Caseous necrosis is typical for certain types of inflammation. Very common in TB.

23
Q

What is apoptosis?

A

Regulated and targeted programmed cell death. Highly regulated and energy dependant.

24
Q

When does physiological apoptosis occur?

A

Physiological apoptosis occurs during the embryogenesis.

25
Q

When does pathological apoptosis occur?

A

Pathological apoptosis may occur due to DNA damage, protein misfolding or due to viruses.

26
Q

How is apoptosis induced?

A

Death ligand binds to a death receptor which upon activation causes the downstream of apoptotic intermediated called caspases.

There are two pathways:
* Extrinsic – cytotoxic mediated cell death
* Intrinsic /mitochondrial pathway – DNA damage

27
Q

How is apoptosis characterised?

A

It is characterised by shrinkage of the nucleus and cytoplasm this then progresses to membrane bound bodies that contain organelles. These undergo phagocytosis.

28
Q

What is the difference between necrosis and apoptosis?

A

Necrosis:
* Pathological
* Groups of cells
* Cell swelling
* Not energy dependent
* Inflammation

Apoptosis:
* Physiological or pathological
* Individual cells
* Cell shrinkage
* Energy dependent
* No inflammation

29
Q

How may apoptosis be harnessed for beneficial purposes?

A

Cancer treatement

30
Q

What is autophagy?

A

Cell recycles it own contents. Highly regulated.

Starts by the formation of the isolation membrane which elongated to isolate the subcellular organelles which is called autophagosome.

The autophagosome the merges with lysosomes which degrades and deconstructs the components of the organelles rendering it ready for recycling.