Injuries to cells Flashcards

1
Q

Name the 5 branches of pathology

A
Histology
Haemotology
Immunology
Chemical pathology 
Microbiology
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2
Q

Name the to ways cells respond to stress

A

Adaption

Injury

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3
Q

Injury can be either

A

Reversible

Irreversible

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4
Q

If injury is irreversible this results in what?

A

Cell death

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5
Q

What are the two types of cell death?

A

Apoptosis

Necrosis

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6
Q

Name the different types of cell adaption…

A

Hyperplasia
Hypertrophy
Atrophy
Metplasia

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7
Q

Define hyperplasia

A

Increase in cell number
(Can lead to hypertrophy)
Can be pathological/physiological

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8
Q

Define hypertrophy

A

Increase in cell size
(Can cause increase size of organ)
Can be pathological/physiological

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9
Q

Define atrophy

A

Decrease in cell size

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10
Q

What can cause atrophy?

A
Decrease workload
Decrease blood supply
Inadequate nutrition
Loss of hormonal stimulus
Ageing
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11
Q

Define metplasia

A

One cell replaced by another cell
E.g. oesophagus
*Can be reversible

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12
Q

What are the 3 most common causes of cellular injury

A

Hypoxia (low o2)
Ischaemia (loss of blood supply)
Chemical damage (alcohol etc)

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13
Q

Name other causes of cellular injury

A
Radiation
Lack of nutrients
Infection
Ageing
Immunological changes
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14
Q

What are the 2 most common finding within reversible cellular injury (morphology)?

A

Cellular swelling

Fatty change

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15
Q

Out of necrosis and apoptosis which process is ALWAYS pathological?

A

Necrosis

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16
Q

Out of necrosis and apoptosis which causes local inflammation and why?

A

Necrosis due to cell swelling of cell that then ruptures

17
Q

Out of necrosis and apoptosis which is known as a programmed cell death?

A

Apoptosis

18
Q

Why does necrosis occur?

A

Due to damage of the cell membrane which then allows enzymes to digest the cell

19
Q

Name a common type of necrosis…

A

Ischaemic necrosis

20
Q

What causes apoptosis…

A

Damage to DNA/protein structures resulting in cell death

21
Q

State the process of apoptosis…

A

Cell starts to break into small fragments
Fragments have signals on them that attract resident macrophages
Resident macrophages come and phagocytose
No cellular leakage meaning no danger of inflammatory response

22
Q

Physiological apoptosis is meant to occur when?

A

Embryogenesis (excess tissue is programmed to die away if this doesn’t happen this is bad)
Involution of hormone dependant tissues upon hormone deprivation (e.g. uterus post menopause becomes atrophic and small)
Elimination of cells after they have served their purpose
Elimination of potentially self-reactive lymphocytes

23
Q

When does pathological apoptosis occur?

A
DNA damage
Accumulation of misfiled proteins
Infection
Cell death induced by cytotoxic T cells
Pathological atrophy in parenchymal organs after duct obstruction
24
Q

Apoptosis results from what type of enzymes?

A

Caspases

25
Q

What are the 2 main pathways that result in activation cell death pathway?

A
Mitrochondrial pathway (intrinsic)
Fas death receptor pathway (extrinsic)
26
Q

Name the 4 main types of necrosis

A

Coagulative (commonly occurs after infections/loss of blood supply- most common- causes heart attack/myocardial infarct)
Fat (death of fat tissue due to activation of lypases)
Caseous (usually means TB unless proven otherwise)
Liquefactive (typical of the brain when infarct- hole in the brain)

27
Q

How do cells become injured?

A
ATP depletion 
Mitchondrial damage 
Influx of calcium
Oxidative stress
Damage of cell membrane 
DNA damage
Intracellular accumulation of abnormal material e.g fat cholesterol and proteins
28
Q

ATP depletion causes what?

A

Decrease in cellular energy

It also effects sodium pump which can cause electrolyte imbalances

29
Q

Mitochondrial damage results in what?

A

Decreased levels of ATP

30
Q

An influx of calcium leads to what?

A

Activation of enzymes which can trigger apoptosis and programme cell death

31
Q

Damage to cell membrane results in what?

A

Necrosis

32
Q

Give an example of DNA damage

A

Radiation

33
Q

Give the 3 examples of accumulation of abnormal materials

A

Fat
Cholesterol
Protein