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MCD Cell Pathology > 1 Cell Injury > Flashcards

1 Cell Injury Flashcards

1
Q

*Q: What does lethal cell injury lead to? What does sublethal cell injury lead to?

A

A: cell death

injury may not amount to cell death but may be reversible/progress to cell death

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2
Q

*Q: Define hypertrophy.

A

A: stress that makes cells adapt and become bigger

Consequently increasing organ size

Trophy= size

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3
Q

*Q: What are the 8 types of cell injury?

A

A: oxygen deprivation- v common

infectious agents- inc drugs

chemical agents

genetic defects

immunological reactions- autoimmune

nutritional imbalances

physical agents- eg lightning, gunshot

ageing

DICGINPA

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4
Q

*Q: What does the cellular response injurious stimuli depend on? (3)

A

A: type of injury, severity, duration

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5
Q

Q: What are the 4 intracellular mechanisms particularly vulnerable to cell injury? Why are they important? Relationship?

A 
A: cell membrane integrity (allows distinguishing from self and non self cells)
ATP generation (important in maintaining cell integrity)
Protein synthesis (affect cell membrane)
Integrity of genetic apparatus (can lead to malfunction in protein synthesis)

integrally related that multiple secondary effects rapidly occur//if one is damaged then leads to problems in others (all feed into eachother)

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6
Q

*Q: What kills the cell first: Morphological changes or loss of function?

A

A: loss of function

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7
Q

*Q: Define atrophy. Example.

A

A: shrinking of size of cell (or organ) by loss of cell substance

Dementia brain = smaller due to smaller cells

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8
Q

*Q: What can cause hypertrophy? (2)

A

A: increased functional demand

Specific hormonal stimulation

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9
Q

*Q: What is hyperplasia? Can be? (2) Describe each.

A

A: plasia= number

Increase in number of cells in organ

Can be physiological or pathological

Physiological can be hormonal or compensatory

pathological is usually due to excessive hormonal or growth factor stimulation

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10
Q

*Q: What is an example of hormonal physiological hyperplasia?

A

A: oestrogenic wave of proliferation of the endometrium (mucous membrane lining the womb/inside on uterus)

(proliferative endometrium stimulated by oestrogen)

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11
Q

*Q: What is an example of pathological hyperplasia?

A

A: carcinoma

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12
Q

*Q: What is tremendous hyperplasia?

A

A: lots of mitosis

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13
Q

*Q: Define metaplasia. May be? (2) Give an example.

A

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

physiological or pathological

when you spoke, columnar epi goes to squamous (returns back when smoking stops)

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14
Q

*Q: Give an example of metaplasia.

A

A: Barrett’s oesophagus- get columnar epithelium instead of squamous lined epithelium due to acid reflu

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15
Q

*Q: What is dysplasia?

A

A: precancerous cells which show genetic and cytological features of malignancy but not invading the underlying tissue (basal lamina)

key features: increased mitoses and increased nuclear cytoplasmic ratio

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16
Q

Q: What is the connection between metaplasia and dysplasia in terms of cancer?

A

A: metaplasia doesn’t give increased risk of cancer but once you’ve got metaplasia, then you may go on to have dysplasia

17
Q

*Q: What are 2 light microscopic changes associated with reversible injury? Examples of?

A

A: fatty change (fat accumulation is seen as holes in images)

Cellular swelling

examples of degenerative changes (ie damage associated with cell and tissue damage)

18
Q

Q: What is necrosis? What’s it associated with being?

A

A: confluent (cells near eachother) cell death associated with inflammation

Whole areas of cells die not just single cell

Associated with being pathological

19
Q

*Q: What are the 4 types of necrosis? (light microscope changes associated with irreversible change)

A

A: coagulative
Liquefactive
Caseous
Fat

20
Q

Q: Describe fat necrosis by aid of an example.

A

A: Associated with acute pancreatitis where you get the release of lipases which digests fats and hydrolyses triglycerides -> free FA and glycerol

Free FA combine with calcium in the extra cellular fluid and deposits

Each deposit (appears as white part on real life image) are areas of fat necrosis

21
Q

Q: What is apoptosis?

A

A: programmed cell death of single cells not associated with inflammation

Active cell death that needs energy

Can be pathological or physiological

22
Q

Q: How does apoptosis occur?

A

A: nucleus shrinks
Little bits of the cell break off (lined by cytoplasm)
Nothing from inside cell is exposed to outside so there is no inflammation

It is phagocytosed by macrophages

23
Q

*Q: What are the differences between apoptosis and necrosis? (4)

A

A: A may be physiological

A is an active energy dependent process
N is what happens when ATP runs out

A is not associated with inflammation
N includes a damaged plasma membrane

N is a response to severe injury
A is a response to mild injury

24
Q

Q: Describe the stress triangle involving a normal cell.

A

A: can stress the normal cell and it will adapt -> adapted state (eg heart cells work harder when low bp)

normal cell-> too much stress -> cell injury which leads to cell death (eg. myocardial infarction where blood supply is cut off)

adapted state-> continually put pressure on -> reach point where no longer adapt -> cell injury …

25
Q

Q: What are the 2 types of cell injury?

A

A: lethal and sublethal

26
Q

Q: Describe the 2 types of stress exerted on cells.

A

A: physiological- that healthy people have eg. when exercising

pathological- associated with a diseased state eg. HBP

27
Q

*Q: What do the consequences of an injurious stimulus depend on? (4)

A

A: type of cell (some are more susceptible to injury)

status (cell that is dividing is more vulnerable)

adaptability

genetic makeup

28
Q

*Q: Define hypertrophy. Can be? (2)

A

A: increase in cell size and consequently an increase in the size of the organ

pathological or physiological

29
Q

*Q: What’s an example of physiological hypertrophy? pathological?

A

A: uterus is larger during pregnancy (more fibres)

HBP

30
Q

Q: Describe an alcoholic fatty change? Ballooning degeneration?

A

A: -single metabolic consequence

  • (liver disease)
  • reversible change
  • fluid leaks in
  • cells are much bigger as are swollen
31
Q

Q: How does necrosis occur?

A

A: contents are released-> attract neutrophils and cause necrosis (membrane is damaged)

32
Q

*Q: What are 5 causes of apoptosis that are normal physiological processes?

A

A: embryogenisis (separate fingers)

deletion of auto reactive T cells in the thymus

hormone dependent physiological involution

cell deletion in proliferating populations

variety of mild injurious stimuli that cause irreparable DNA damage that triggers cell suicide pathways

33
Q

Q: What’s a third type of cell death? Describe. Circumstance?

A

A: necroptosis

programmed cell death associated with inflammation

only in pathological circumstances eg viral infections

34
Q

*Q: Define ulcer.

A

A: open sore on an external or internal surface of the body, caused by a break in the skin or mucous membrane which fails to heal

35
Q

*Q: Define degeneration.

A

A: process by which tissue deteriorates and loses its functional ability due to traumatic injury, aging and wear and tear

36
Q

Q: Describe caseous necrosis. What is it associated with?

A

A: ‘cheesy’ necrosis

Necrotic area is granular (that’s what makes it caseous)

Associated with pulmonary TB

37
Q

Q: Describe liquefactive necrosis using an example. Identified?

A

A: brain has totally liquified

Is an empty space and can only identify cells by looking at cells around the cyst

38
Q

Q: Describe coagulative necrosis. (3) Appearance? Example.

A

A: cell shape does not change- tissue keeps structure

Nuclei are gone

Loss of cell substance

On images- see inflammatory cells between

In images appear like ‘ghost cells’ due to loss of proteins etc so stain isn’t picked up as much

myocardal infarct (dead cells are still recognisable)

MCD Cell Pathology (6 decks)

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