Cell Injury Flashcards

Cell injury: list the causes and mechanisms of cell injury, recall the morphological changes associated with reversible and irreversible injury Cell fate: define and recall examples of hyperplasia, hypertrophy, atrophy, metaplasia and dysplasia; define and compare apoptosis and necrosis

1
Q

What is the difference between lethal and sublethal?

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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2
Q

What are the causes of cell injury? (x8) Point to be made about oxygen deprivation – where in the body would there be much decreased risk of this happening? POIGNAnCI [as in, ‘poignancy’].

A

Oxygen deprivation – It’s much rarer when an organ has dual blood supply (e.g. liver: hepatic artery AND portal vein) to get cell injury through oxygen deprivation. Chemical agents Infectious agents Immunological reactions Genetic defects Nutritional imbalances Physical agents Aging

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3
Q

What does the cellular response to cell injury depend on? (x3)

A

Type of injury. Injury duration. Severity of injury.

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4
Q

What do the consequences of an injurious stimulus depend on? (x2)

A

Type of cell e.g. some cells naturally more resistant to injury e.g. heart has high blood supply, but you can cut blood supply for bones for a long period of time. Status of cell e.g. is it in process of dividing.

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5
Q

What four intracellular systems are particularly vulnerable?

A

Cell membrane integrity – defines the cell itself. Creates environment in cell. ATP generation – maintain cell integrity – synthesising components of cell. Protein synthesis. Integrity of genetic apparatus – if damaged, impact on protein synthesis and practically every cellular process.

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6
Q

Why may something not be picked up in a post-mortem in relation to cell injury?

A

CELLS STOP WORKING BEFORE THEY DIE – THIS IS A FACT, ALWAYS! Effects may not ALWAYS be seen in a post-mortem because loss of function COULD kill you before morphological changes takes place in the cell. Usually, there’s loss of function, cells undergo morphological changes, and then you die.

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7
Q

What does atrophy mean?

A

Shrinkage in the size of a cell (or whole organ) by the loss of cell substance.

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8
Q

Example of atrophy?

A

Dementia – brain physically gets smaller because of loss of cell substance.

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9
Q

What is hypertrophy? Two causes? (x2 points about each

A

Increase in the size of a cell and consequently, an increase in organ size. Can be caused by increased functional demand (physiological hypertrophy) or specific hormonal stimulation (pathological hypertrophy).

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10
Q

Example of hypertrophy.

A

Cardiac muscle cells cannot divide, so with increased demand, they adapt by getting bigger.

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11
Q

What is hyperplasia? Classification? (x2)

A

Increase in cell number. Physiological: hormonal or compensatory. Pathological: due to EXCESSIVE hormonal or growth factor stimulation.

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12
Q

Examples of hyperplasia. One for each classification

A

Physiological: Endometrium thickens during menstrual cycle in preparation for possible implantation of an embryo. Pathological: cancer e.g. carcinoma. More active cell proliferation.

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13
Q

What is metaplasia?

A

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

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14
Q

Example of metaplasia.

A

Oesophagus lined by squamous epithelium. As it transitions to stomach, there is transition to columnar epithelium. Physiological: cervix: at pregnancy, cervix expands, and so becomes exposed to acidic environment of vagina. Adapts by changing from columnar to squamous. Pathological: squamous epithelium abnormally transitions to columnar epithelium in lower portion of oesophagus. Called Barrett’s Oesophagus.

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15
Q

What is dysplasia?

A

Precancerous cells which show the genetic and cytological features or malignancy but not invading the underlying tissue. In other words, a tumour is cancerous, but the cells haven’t invaded the basal lamina yet. It therefore may signify a stage preceding the development of cancer.

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16
Q

What ‘-plasia’ is associated with dysplasia? Example?

A

Metaplasia doesn’t give an increased risk of cancer, but once you have metaplasia, you may go on to get dysplasia. That’s why Barrett’s oesophagus is associated with increased risk of oesophageal cancer.

17
Q

What are the light microscopic changes associated with reversible injury? (x2)

A

Fatty change – accumulation of fat WITHIN cells. Cellular swelling.

18
Q

What is necrosis?

A

Confluent cell death associated with inflammation. This inflammation as we already know, is associated with clearing of this necrotic tissue or/and more damage. (Confluent – whole areas of cell.)

19
Q

What are the light microscopic changes associated with irreversible injury? (x4)

A

Coagulative necrosis. Liquefactive necrosis. Caseous necrosis. Fat necrosis.

20
Q

What is coagulative necrosis?

A

Architecture of the dead tissue is preserved. So, dead cells are arranged the same way as if they were alive: difference is the loss of nuclei and migration of cells involved in the inflammatory reaction.

21
Q

What is liquefactive necrosis?

A

Tissue has been liquified. Would not know what that tissue was without seeing what tissue it is around.

22
Q

What is caseous necrosis?

A

Cell death where tissue maintains a cheese-like appearance, so appears soft and white. The area is granular. The presence of a granuloma makes it caseous.

23
Q

What is fat necrosis?

A

Occurs in pancreas, for example, where lipases are released. Fat breaks down and free fatty acids are one of the products. These combine with calcium (found everywhere in the extracellular fluid), which deposits.

24
Q

How does apoptosis differ from necrosis? (x4) – indicated in upper case in the answer

A

Death of SINGLE cells, and NOT associated with inflammation. Apoptosis is an ACTIVE ENERGY DEPENDENT process. Apoptosis can be PHYSIOLOGICAL as well as pathological (necrosis is pathological).

25
Q

Why is there not inflammation in apoptosis?

A

In necrosis, enzymes break down the cell which attracts inflammatory cells to the area. In apoptosis, the nucleus shrinks, and little bits of the cell break off, each surrounded by a membrane. Therefore, the contents of the cell are not exposed extracellularly, so inflammation is not triggered.

26
Q

What are the causes of apoptosis? (x4)

A

Embryogenesis – apoptosis is part of embryo development in forming eye slits… Hormone dependent physiological involution e.g. shedding of endometrium (womb lining). Cell deletion in proliferating populations. When cells divide and proliferate, there is ALWAYS apoptosis. Response to mild injury that cause irreparable DNA damage that triggers cell suicide pathways e.g. virus infection, paracetamol use.