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Cell Pathology > Cell Pathology 4- Cell Injury > Flashcards

Cell Pathology 4- Cell Injury Flashcards

1
Q

Describe the two situations that can lead to cell injury

A

Injurious stimulus

Stress and increased demand above a point where the cells can no longer adapt to the increase in demand.

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2
Q

What happens when cells adapt

A

They exist in a new equilibrium and homeostasis.

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3
Q

What preceded cell death

A

Cell injury

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4
Q

What are the two types of cell death

A

Lethal:
produces cell death

Sublethal:
produces injury not amounting to cell death
may be reversible or progress to cell death

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5
Q

What can we do to sublethal injuries

A

Reverse the cells to their normal or adapted state.

Limit their progression to cell death.

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6
Q

What are the two types of stress

A

Physiological- Exercise
Pathological- High Blood Pressure
Both cause hypertrophy- more myofilaments needed to cope with increased demand for work.

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7
Q

What causes a myocardial infarction

A

muscle death due to ischaemia; atheroma block coronary arteries

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8
Q

What do chemical agents include

A

Iatrogenic injuries- side-effects of prescribed drugs

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9
Q

What does the mechanism of cell injury depend on

A

The cellular response to injurious stimuli depends on:
the type of injury,
its duration and
its severity
e.g ischaemia to the bone will have a long duration as bone is not metabolically active. However ischaemia to the brain will have a short duration, we try to mitigate duration in medicine.

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10
Q

What do the consequences of cell injury depend on

A

on the type of cell
its status
dividing cells are more susceptible to injury- dividing cells in the cervix are more susceptible to damage from HPV.

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11
Q

Which 4 intracellular systems are particularly vulnerable to cell injury

A

cell membrane integrity,
ATP generation,
protein synthesis and
the integrity of the genetic apparatus

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12
Q

What is fundamental to the existence of the cell

A

The cell membrane

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13
Q

Describe the interrelationship between these 4 systems

A

Genetic issues- cannot synthesise proteins or divide. No protein synthesis, no synthesis of proteins involved in generation of ATP- thus no cell membrane stability.
The structural and biochemical components of a cell are so integrally related that multiple secondary effects rapidly occur

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14
Q

Describe the temporal relationship between loss of cell function and cell death

A

Cellular function is lost before cell death occurs which in turn occurs before the morphological changes are seen

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15
Q

What is meant by atrophy

A

Shrinkage in the size of the cell (or organ) by the loss of cell substance- loss of cell number too.

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16
Q

When is atrophy pathological

A

Dementia

Damaged nerves can have atrophic effects on muscle- Muscle atrophy secondary to denervation

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17
Q

What is meant by hypertrophy

A

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

18
Q

What can hypertrophy be caused by

A

Can be physiological or pathological
It is caused either by increased functional demand or specific hormonal stimulation

Hormones- overproduction of TSH- increases size of follicular cells in thyroid gland.

Physiological; e.g. Uterus in pregnancy increases in size

Pathological- associated with disease state; e.g. Increased demand leads to hypertrophy

19
Q

What is a key characteristic of muscle

A

They rarely divide- thus when the demand is increased they get bigger.

20
Q

Define Hyperplasia

A

An increase in the number of cells in an organ.

21
Q

Describe the causes of hyperplasia

A

Can be physiological or pathological
Physiological hyperplasia can be either hormonal or compensatory
Pathological hyperplasia is usually due to excessive hormonal or growth factor stimulation

Physiological; with every menstrual cycle, endometrial cells increase in number and in breasts during oestrogenic phase - hormones very important- hypertrophy also occurs here- increased TSH also causes hyperplasia of follicular cells.

Pathological- carcinomas.

22
Q

Define metaplasia

A

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

23
Q

What are the causes of metaplasia

A

May be physiological / pathological

Pathological- smoking changes epithelium from columnar to squamous- if you stop smoking it will reverse.

Physiological- puberty- cervix expands- opens canal- columnar exposed to acid- squamous- pregnancy reverses this

Pathological; Barrett’s oesophagus - in acid reflux, normal stratified squamous epithelia metaplase to columnar due to acid, but reversible if stop acid production as will become stratified squamous again.

24
Q

Define dysplasia

A

Precancerous cells which show the genetic and cytological features or malignancy but not invading the underlying tissue

25
Q

Describe some of the characteristics of dysplasia

A

Key state between normal cells and cancer

Large nuclei, large number of mitoses, increased nuclei: cytoplasm raito

26
Q

What are the light microscopic changes associated with reversible cell injury

A

Fatty change
Cellular swelling

These are examples of degenerative changes
i.e. changes associated with cell and tissue damage.

27
Q

What is a metabolic consequence of excess alcohol

A

Fatty Liver

28
Q

Describe ballooning degeneration

A

cell membrane damaged- fluid leaks in cell appears swollen.

29
Q

What are the key aims of cervical and breast screening

A

Diagnose dysplastic changes- to prevent progression to cancer

30
Q

Define necrosis

A

Confluent cell death associated with inflammation.

Confluent = lots of cells next to each other.

31
Q

What are the light microscopic changes associated with irreversible injury

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat Necrosis

32
Q

Describe coagulative necrosis

A

Cells are dead- but you can see where they were- keeps its structure and shape- myocardial infarction.

33
Q

Describe liquefactive necrosis

A

nothing there but liquid- old cerebral infarct.

34
Q

Describe caseous necrosis

A

Cheesy appearance- oozes out when cut- TB of lungs

35
Q

Describe Fat necrosis

A

Inflammation of the pancreas- makes lipase when damaged. Lipase hydrolyses triglycerides into FFAs and glycerol. The FFAs react wit calcium ions in the ECF to form calcium fat salts which are deposited on the pancreas. Appear white where the calcium has precipitated out; dense blue on microscope.

36
Q

Define apoptosis

A

Programmed cell death- usually a single cell

37
Q

Explain why apoptosis is not associated with inflammation

A

Cell contents are not released in apoptosis- they bud off and are enclosed in membranes- like vesicles- where they are phagocytosed.
No cell contents to stimulate inflammation- unlike necrosis.

38
Q

What are the 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.

Endometrium after menstrual cycle
Apoptosis also seen pathologically in cancers.

39
Q

Describe how the p53 acts as the guardian of the genome

A

Holds cells in mitotic arrest to allow DNA to be repaired if damaged. If the DNA cannot be repaired- they will be deleted by apoptosis - ‘safe’ way to die.

40
Q

What are the key differences between apoptosis and necrosis

A

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

41
Q

What is meant by necroptosis

A

Programmed cell death associated with inflammation

Many causes e.g. viral infections

42
Q

What is a consequence of the inflammation associated with necrosis

A

Damages healthy tissue- innocent bystander effect seen in pulmonary TB.

Cell Pathology (6 decks)

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