4. Cell injury Flashcards

1
Q

Lethal cell injury

A

Causes cell death

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2
Q

Sublethal cell injury

A

produces injury not amounting to cell death

may be reversible or progress to cell death

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3
Q

Cell stress

A

can lead to adaptation which may be reversible
inability to adapt will lead to cell injury and death
excess stress leads straight to damage

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4
Q

Give an example of physiological cell stress

A

Exercise
Muscle cells increase in size as need more myofilaments to deal with increased work they have to do
Increases size of heart

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5
Q

Give an example of pathological cell stress

A

High blood pressure
Causes muscles to adapt (hypertrophy)
Increases size of heart

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6
Q

List 8 causes of cell injury

A
Oxygen deprivation
Chemical agents (Inc. drugs)
Infectious agents (Viruses, parasites etc)
Immunological reactions (Inc. Autoimmune)
Genetic defects
Nutritional imbalances
Physical agents
Aging
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7
Q

Myocardial infarction

A

Muscle death due to ischaemia

Atheroma blocks artery

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8
Q

Cellular response to injurious stimuli depends on

A

Type of injury
Duration
Severity

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9
Q

Consequences of injurious stimuli depend on

A

Type of cell

The cell’s status e.g. dividing cells are more vulnerable than non-dividing

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10
Q

Which 4 intracellular systems are particularly vulnerable to injury?

A

Cell membrane integrity- separates self from non-self
ATP generation- cells NEED energy
Protein synthesis- essential for growth, enzyme systems
Integrity of the genetic apparatus- DNA & RNA=problems with cell division and protein synthesis

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11
Q

structural and biochemical components of a cell are integrally related, this means that

A

multiple secondary effects rapidly occur

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12
Q

Atrophy

A

Shrinkage in size of cells (or organs) by loss of cell substance (Cell size and Number)

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13
Q

5 Cellular adaptations to injury

A
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
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14
Q

Example of atrophy

A

Dementia: Loss of neurones

Muscle atrophy secondary to denervation

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15
Q

Hypertrophy

A

Increase in size of cells and consequently an increase in size of the organ

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16
Q

Types of hypertrophy and examples of each

A

Physiological e.g. Pregnancy, Exercise

Pathological e.g. High BP

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17
Q

What is hypertrophy caused by?

A

increased functional demand or specific hormonal stimulation

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18
Q

Hyperplasia

A

An increase in number of cells in an organ

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19
Q

Types of hyperplasia

A

Physiological

Pathological

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20
Q

Physiological hyperplasia

A

either hormonal or compensatory

e.g. Proliferative Endometrium

21
Q

Pathological hyperplasia

A

usually due to excessive hormonal or growth factor stimulation
e.g. Carcinoma

22
Q

Metaplasia

A

A reversible change in which one adult cell type is replaced by another

23
Q

types of metaplasia

A

Physiological

Pathological

24
Q

Physiological metaplasia example

A

At puberty and during pregnancy cervix expands, opens canal, columnar exposed to acid pH causing columnar to become Squamous
If no pregnancy, cervix closes Squamous become Columnar

25
Q

How is the Cervix lined?

A

internally by columnar

Externally by stratified squamous epithelium.

26
Q

Pathological metaplasia example

A

Barrett’s Oesophagus

Acid reflux causes Squamous to become Columnar.

27
Q

How is the oesophagus normally lined?

A

with stratified squamous epithelium

28
Q

What happens if Barrets oesophagus is treated with a PPI, which inhibits acid production?

A

Columnar revert to being Squamous

29
Q

Dysplasia

A

Precancerous cells which show the genetic and cytological features of malignancy but not invading the underlying tissue. E.g.
High nuclear cytoplasmic ratio
Increased mitosis

30
Q

What are the light microscope changes associated with reversible injury?

A

Fatty change

Cellular swelling

31
Q

Alcoholic fatty change

A

Excessive alcohol leads to fatty change in liver.

If stop drinking, fat goes away

32
Q

Ballooning degeneration

A

Cells increase in size as cell membrane is damaged and fluid floods in, cells become swollen

33
Q

Necrosis

A

Confluent (lots of cells next to each other) cell death associated with inflammation

34
Q

What are the 4 light microscope changes associated with irreversible injury?

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat Necrosis

35
Q

Coagulative necrosis

A

Cells dead, but still visible and recognisable

36
Q

Example of coagulative necrosis

A

Myocardial infarct

37
Q

Liquefactive necrosis

A

Cells die and disappear, with just liquid remaining

38
Q

Example of Liquefactive necrosis

A

seen in brain in cerebral infarct

39
Q

Caseous necrosis

A

Tissue maintains a cheese-like appearance

On cutting, is ‘creamy’, oozes out

40
Q

Where is Caseous necrosis often seen?

A

Pulmonary TB

41
Q

Fat necrosis

A

seen in inflammation of pancreas
Lipase hydrolyses triglycerides to free fatty acids and glycerol
Free fatty acids bind to calcium in ECF to form calcium fat salts which deposit in pancreas (chalky)

42
Q

When is fat necrosis seen?

A

In acute pancreatitis

43
Q

Apoptosis

A

Programmed cell death
Single cell
No inflammation
Requires ATP

44
Q

Characteristics of Necrosis

A

Mass cell death
Inflammation
Occurs when run out of ATP

45
Q

Causes of apoptosis

A

Embryogenesis
Deletion of auto-reactive T cells in the thymus
Hormone-dependent physiological involution
Cell deletion in proliferating populations
A variety of mild injurious stimuli that cause irreparable DNA damage that triggers cell suicide pathways

46
Q

What are the major differences between apoptosis & necrosis?

A

Apoptosis may be physiological
Apoptosis is an active energy dependent process
Apoptosis is not associated with inflammation

47
Q

Necroptosis

A

Programmed cell death associated with inflammation

48
Q

What could cause necroptosis?

A

Viral infection