Lecture 19: Cell Injury and Necrosis

Question 1

What is the difference between Necrosis and Apoptosis

Answer 1

Necrosis: always pathological
Apoptosis: programmed cell death (safe cell death)

Question 2

What are the critical functions of cells?

How long can a neuron, a cardiac cell or liver last without o2

Answer 2

1. Cell membranes
2. Aerobic Respiration
3. Protein Synthesis
4. Genetic Function

neuron- 3-5mins
heart 30-60 mins
liver/kidney 1-2h

Question 3

What are the types/cause of cell injury?

Answer 3

• Ischaemic (> metabolites, <blood flow)
• age
• hypoxia (anemia etc)
• nutritional, biological (virus, bacteria, fungi etc)
• immunological (diabetes, hypothyroidism)
• chemical
• physical (trauma, temp)
• genetic

Question 4

Describe the Chart on slide 7 of Reversible cellular response to injury

Answer 4

What happens first? Hypoxia etc cause a drop in oxidative phosphorylation, so cells are poor in ATP. So the energy dpendant reactions occuring cant eg is the sodium potassium pump. To keep Na outside etc. When this happens, the cell membranes start to leak and Sodium, chloride and K cells swell along with their micro-organnelle. (Hydropic –balooning of cell).

• So then glycolysis occurs but they produce organic acids eg pyruvate decreasing pH, causing further functional consquences.
• Energy deficiency can lead to

Question 5

Reversible changes 1 slide 9

Liver acute hepatitis

Answer 5

The foamy appearance is due to swelling of organelles, as noted in the previous slide.
Ballooning degeneration can see the cells swelling. The cell membrane is in tact. Some leakage though, and the nucleus is still present. All assosiated with inflow of fluid.

Question 6

Reversible change 2
Alcoholic fatty liver
alisw 11

Answer 6

It is diffusely pale and yellow, rather than the normal dark brown of healthy liver. This would be greasy to the touch, due to accumulated fat.

next slide
These vacuoles have very sharp, ‘punched’out’ appearance, typical of fat vacuoles, and different from the foamy hydropic change shown earlier.

Question 7

Irreversible changes are characterised by

Answer 7

• swelling (oncotic necrosis) (patho)

- wheras apoptosis is characterised by shrinking? (physiological)

Question 8

Necrosis

Answer 8

Local cell death and degradation in a living organism (excludes apoptosis)
Oncotic necrosis increased activity and release of dangerous enzymes, which digest the carbs in the cell, the proteolytic enzymes are released and cause autoolysis which kills the cell itself.
More dangeroud form is the heterolysis which release exogenous enzymes (snake venom) cellular damage then death of cell.

Question 9

Irreversible changes slide 18

describe the chart

Answer 9

Mitochondrial damage (energy source of the cell0  cell looses the energy source. When energy isnt available there are more serious morphological consequences eg pyknosis.
Cell membranes are responsible to keep the goods inside and the bad outside so when there damaged there is consequences.
May be assosiated with leakage of the contents of the cells important in diagnostic work.
May be assoisiated with ionised calcium etc which is dangerous can kill the cells.

Question 10

slide 19 Histology section of cell necrosis describe the changes

Answer 10

Marked cellular injury, cell death. This microscopic appearance of myocardium is a mess because so many cells have died that the tissue is not recognizable. Many nuclei have become pyknotic (shrunken and dark) and have then undergone karyorrhexis (fragmentation) and karyolysis (dissolution).
The cytoplasm and cell borders are not recognizable. In this case, loss of the blood supply from a major coronary artery led to ischemia and cell death.

Question 11

Oncotic Necrosis (Oncotic pressure is Colloid Osmotic Pressure)
Can be divided into which 5 groups

Answer 11

1. Coagulative
2. Liquefactive
3. Caseous
4. Fat necrosis
5. Gangrene
   - wet gangrene
   - dry gangrene

Question 12

Describe Coagulative Necrosis

slide 21

Answer 12

‘infarct’- coagulative necrosis (rapid proteon denature) because of sudden uschaemua e.g. thromboembolus

Question 13

Describe the histo on slide 22

Answer 13

This is a example of coagulative necrosis

• cells appear pale and ghost like
• cells are dying or haven’t quite died
• normal renal parenchyma on the right

Question 14

describe slide 23

Answer 14

This liver has areas where the cells have reddened (eosinophilic) cytoplasm, and a shrunken (pycnotic) and even fragmented (karyorrhectic) nucleus, that eventually dissolves (karyolysis). So, the outlines of the cells remain as ‘ghostly’ outlines, but clearly, with the nucleus broken down or lost, this is an irreverisble change – the cells are dead. This is coagulative necrosis again.

Question 15

Describe slide 24

Answer 15

It is easy to overlook the changes on the left. But in fact the lack of nuclei, and the overall eosinophilic appearance are key features that show cell death. Normal muscle on the right has clearly visible nuclei, in contrast. Because the outlines are preserved on the left, this form of necrosis is called coagulative necrosis, again.

Question 16

describe the Liquefactive necrosis on slide 25

What is liquefactive

Answer 16

Liquefactive necrosis (or colliquative necrosis) is a type of necrosis which results in a transformation of the tissue into a liquid viscous mass.[1] Often it is associated with focal bacterial or fungal infections. In liquefactive necrosis, the affected cell is completely digested by hydrolytic enzymes, resulting in a soft, circumscribed lesion consisting of pus and the fluid remains of necrotic tissue.

At high magnification, liquefactive (moist) necrosis of the brain demonstrates many macrophages at the right which are cleaning up the necrotic cellular debris. The job description of a macrophage includes janitorial services such as this, particularly when there is lipid .
When tissue is liquefied by venom, the effects of neutrophils (enzymes etc), or bacterial toxins, then liquefactive necrosis occurs. This sort of necrosis is common in the brain. The tissue architecture, and the cells outlines, are all lost in this process.

Question 17

describe slide 26

Answer 17

The top left diagonal half of pancreas is now unrecognisable due to liquefactive necrosis. The pink material is necrotic cell debris, as well as fibrin and some nuclear debris. This example also has some neutrophils present in both the remaining pancreas and the necrotic area (within the oval at top left). The enzymes made in the pancreas mean that pancreatic inflammation often results in liquefactive necrosis as these enzymes are released from the cells… the pancreas then digests itself, assisted by the neutrophils enzymes also.

Question 18

What is Caseous necrosis
27
28

Answer 18

Caseous necrosis is a form of cell death in which the tissue maintains a cheese-like appearance.[1] The dead tissue appears as a soft and white proteinaceous dead cell mass.
This is classic for tuberculosis, for example. The tissue here is not recognisable from this picture.
Microscopically, caseous necrosis is characterized by acellular pink areas of necrosis, as seen here at the upper right, surrounded by a granulomatous inflammatory process.

Question 19

Fat necrosis slide 29

and 30

Answer 19

When fat is dissolved by lipases, as happens in pancreatitis, or in other inflammatory conditions of fat, then a special term ‘fat necrosis’ is applied. There are often chalky white deposits present grossly, which represent soap formation as the fatty acids react with calcium.

Question 20

Wet Gangrene

31, 32

Answer 20

This is gangrene of the lower extremity. Gangrene is a localised death of tissue associated with loss of blood supply, so, firstly it is coagulative necrosis. When bacterial invasion is present, lytic enzymes cause predominantly liquefactive necrosis. This is WET GANGRENE. Dark colour is due to precipitating ferrous sulphide, FeS. Putrefaction of tissues causes an unpleasant odour.
This patient had diabetes mellitus.