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
How is the Cervix lined?
internally by columnar | Externally by stratified squamous epithelium.
26
Pathological metaplasia example
Barrett’s Oesophagus | Acid reflux causes Squamous to become Columnar.
27
How is the oesophagus normally lined?
with stratified squamous epithelium
28
What happens if Barrets oesophagus is treated with a PPI, which inhibits acid production?
Columnar revert to being Squamous
29
Dysplasia
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
What are the light microscope changes associated with reversible injury?
Fatty change | Cellular swelling
31
Alcoholic fatty change
Excessive alcohol leads to fatty change in liver. | If stop drinking, fat goes away
32
Ballooning degeneration
Cells increase in size as cell membrane is damaged and fluid floods in, cells become swollen
33
Necrosis
Confluent (lots of cells next to each other) cell death associated with inflammation
34
What are the 4 light microscope changes associated with irreversible injury?
Coagulative necrosis Liquefactive necrosis Caseous necrosis Fat Necrosis
35
Coagulative necrosis
Cells dead, but still visible and recognisable
36
Example of coagulative necrosis
Myocardial infarct
37
Liquefactive necrosis
Cells die and disappear, with just liquid remaining
38
Example of Liquefactive necrosis
seen in brain in cerebral infarct
39
Caseous necrosis
Tissue maintains a cheese-like appearance | On cutting, is ‘creamy’, oozes out
40
Where is Caseous necrosis often seen?
Pulmonary TB
41
Fat necrosis
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
When is fat necrosis seen?
In acute pancreatitis
43
Apoptosis
Programmed cell death Single cell No inflammation Requires ATP
44
Characteristics of Necrosis
Mass cell death Inflammation Occurs when run out of ATP
45
Causes of apoptosis
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
What are the major differences between apoptosis & necrosis?
Apoptosis may be physiological Apoptosis is an active energy dependent process Apoptosis is not associated with inflammation
47
Necroptosis
Programmed cell death associated with inflammation
48
What could cause necroptosis?
Viral infection