Injuries To Cells & Tissue Injury And Repair Flashcards

1
Q

What are the 4 types of cell adaptation?

A

Hyperplasia, Hypertrophy, Atrophy & Metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Hypertrophy?

A

The increase in cell size resulting in the increase in size of the organ.

  • Physiological example - body builders muscles
  • Pathological example - heart from hypertension (common cause of heart failure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which 2 types of cell adaptation can occur together?

A

Hypertrophy & Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Hyperplasia?

A

The increase in number of cells resulting in a larger (hypertrophied) organ.

  • Physiological example - menstrual cycle
  • Pathological example - endometrial hyperplasia (if hormonal stimuli persists) > can progress to cancers and other diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Atrophy?

A

Shrinkage in size of the cell > due to loss of cell substance.
Could be due to; decrease in workload, reduced blood supply, inadequate nutrition, loss of hormonal stimulation and ageing.
EXAMPLE - body builders stopping lifting weights.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Metaplasia?

A

When one cell type is replaced by another cell type.
This adaptation is in order to cope with stimulus. It is a reversible process and the new type of cell can withstand stress of environment.
EXAMPLE - Barrett’s Oesophagus - stratified squamous changes to simple columnar with goblet cells to cope with acid reflux.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name 8 causes of cell injury.

A

Hypoxia - low oxygen supply
Ischaemia - loss of blood supply > oxygen and nutrients
Chemical exposure - cigarette smoke, alcohol, paracetamol ( and other drugs)
Infection
Radiation
Lack of nutrients
Ageing
Immunologic reactions (cells attack themselves e.g. HIV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 2 reversible forms of cell injury?

A

Cellular swelling & fatty change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 2 types of cell death?

A

Necrosis & Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Necrosis?

A

Damage to cell membranes, allow enzymes to digest the cell > this causes local inflammation.
Necrosis is always pathological.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is ischaemic necrosis?

A

Lack of blood supply to cells > leading to cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Apoptosis?

A

“Programmed cell death” - cells killing themselves.
Irreparable damage to cells protein/DNA OR cell deprivation of growth factors.
Can be pathological or physiological.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the method of necrosis.

A

Normal cell > cellular swelling > break down of cell membrane + leakage of cell contents into surrounding tissues causing inflammatory response to prevent further damage > cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the method of apoptosis.

A

Normal cell > proteins break down and cell begins to digest itself (no inflammatory response occurs as no leakage of cell contents) > bits of cell fall off and phagocytosis occurs (macrophages engulf dead bits of cell) > cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe physiological apoptosis.

A

Embryogenesis > shrinkage of hormone dependent tissues (e.g. Womb) as a result of hormone deprivation > elimination of cells which have served their purpose > elimination of potentially harmful self-reactive lymphocytes.
(This process does not cause any further damage and helps in the prevention of auto immune diseases).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 2 mechanisms of apoptosis?

A

Mitochondrial pathway (intrinsic pathway)
Fans (death) receptor pathway (extrinsic pathway)
Both these pathways result in cell death and occur from the activation of enzymes called caspases.

17
Q

Name the 4 types of necrosis.

A
  • Coagulative - most common & occurs after loss of blood supply and after infections
  • Liquefactive
  • Caseous
  • Fat
    The names of the types of necrosis are due to their appearance.
18
Q

Coagulative necrosis…

A
  • lack of blood supply
  • lack of oxygen
    Also called ischaemic necrosis.
19
Q

Caseous necrosis…

A

It can be caused by fungal infections- it should be assumed that caseous necrosis is a sign of TB unless proven otherwise.
Lump - looks like cheese.

20
Q

Liquefactive necrosis…

A

Typically occurs in the brain - effect of stroke.
Causes a hole in the brain - the brain doesn’t heal by scarring, holes occur which are areas of necrosis.
Areas of liquefactive necrosis can have abscesses growing within them - this usually comes secondary to infection.

21
Q

Fat necrosis…

A

Occurs due to activation of lipase’s.
Result of fat cell death, commonly occur in breast diseases as lumps.
Can mimic tumours secondary to breast trauma.

22
Q

Name the 6 mechanisms of cell injury.

A
  • Depletion of ATP
  • Mitochondrial damage
  • Increased intracellular calcium
  • Oxidative stress
  • Damage to the cell membrane
  • DNA damage
23
Q

Depletion of ATP…

A

Energy store of cells - decrease in cellular energy if process is effected.
Reduced supply of oxygen and nutrients, mitochondrial damage and poisons.
Effects; ATP dependant sodium pumps - electrolyte inbalance
Increased intercellular lactic acid (noxious stimuli), failure of calcium pumps and damage to protein structures.

24
Q

Mitochondrial damage…

A

Causes proton leakage, depletion of ATP and leakage of cytochrome C which triggers apoptosis.
A decreased level in ATP, radiation can affect mitochondria directly > leads to decreased production of energy.

25
Q

Increased intracellular calcium…

A

Activates enzymes which further deplete ATP.
Effects; increased intracellular calcium > activation of enzymes > damage to cellular components.
Can be a trigger of apoptosis.

26
Q

Oxidative stress…

A

Accumulation of reactive oxygen species (free radicals).
Produced by normal cellular function - excess can lead to cell damage.
Some insults increase their production e.g. Paracetamol overdose - increase in production of free radicals + cell death in the liver.
Removed by antioxidants. React with and damage proteins, fat, DNA and reproduce causing further damage.

27
Q

Damage to the cell membrane…

A

Results in necrosis and damages various sites such as; damage of the mitochondrial membrane, lysosomal membrane and plasma membrane > proteins in wrong place = cell death.
Mechanisms of damage - decrease in phospholipid synthesis = decreased levels of ATP, oxygen free radicals and lipid breakdown.

28
Q

What may occur post radiation/oxidative stress?

A

Damage to DNA and proteins

29
Q

What is NEOPLASIA?

A

Gene mutation due to mild DNA damage.

Mutations gather and eventually lead to abnormal cells > cancers.

30
Q

What is DYSPLASIA?

A

Disordered abnormal growths secondary to Metaplasia.

31
Q

DNA and protein damage…

A

If beyond repair, can directly trigger apoptosis.

32
Q

What is tissue regeneration?

A

Complete reconstitution.

E.g. The epithelium of the GI tract can continuously renew itself after injury.

33
Q

What is tissue repair?

A

A combination of regeneration and scar formation - depends on capacity to regenerate, extent of injury and extent of scarring.

34
Q

What are parenchymal cells?

A

Cells that make up the bulk of an organ and performs the specific functions of that organ.

35
Q

How to cells respond to noxious stimuli?

A

Normal cells - narrow range of functions and structure.
Stressors or noxious stimuli cause cell adaptation > is cell in unable to recover, then cell injury occurs. (Response depends on type of injury, duration and severity).