Exam 1 (Lecture 4) - Necrosis Flashcards

1
Q

What are the types of necrosis?

A

1) Coagulative
2) Liquefactive (lytic)
3) Caseous
4) Gangrenous (wet vs. dry)
5) Enzymatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is apoptosis and how is it controlled?

A

Programmed cell death; controlled by nucleus.

Many pathologic and physiologic triggers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the extrinsic pathway of apoptosis.

A

1) The “death” ligand binds to “death” ligand receptor on a normal cell.

2) Second messenger system activates procapase 8

3) Procapase 8 activates effector capases (3,6,7, and 12)

4) Initiation of apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the intrinsic pathway of apoptosis.

A

1) Damage to cytocavitary system or irreversible damage to DNA

2) Apoptosome formation and activation and activation of procapase 9

3) Procapase 9 activates effector capases (3,6,and 7)

4) Initiation of apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are useful functions of apoptosis?

A

1) Digit formation (during embryologic development)

2) Cell infection (viral)

3) Neoplastic (DNA damage)

4) Immune system (cells that recognize self)

5) Normal involution (shrinkage) (thymus/uterus)

6) Old/senescent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Necrosis vs. Apoptosis

A

Necrosis: Fragments released into extracellular space (inflammation IS present)

Apoptosis: Fragments are membrane-bound (inflammation IS NOT present)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens to cells during necrosis?

A

1) Cell size: Enlarged (swelling)

2) Nucleus: pyknosis (shinkage), karyorrhexis (exploded nucleus), or karyolysis (faded nucleus)

3) Plasma membrane: disrupted

4) Cellular contents: enzymatic digestion (may leak out of cell)

5) Adjacent inflammation (frequent)

6) Physiologic or Pathologic role: Usually pathologic (culmination of reversible cell injury)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens to cells during apoptosis?

A

1) Cell size: Reduced (shrinkage)

2) Nucleus: Fragmentation into neuclosome-size fragments

3) Plasma membrane: Intact (altered structure, especially orientation of lipids)

4) Cellular contents: Intact (may be released in apoptotic bodies)

5) NO adjacent inflammation

6) Physiologic or Pathologic role: Usually physiologic (means of eliminating unwanted cells); MAY be pathologic after some forms of cell injury (especially DNA damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the causes of free radical injury to cells?

A

1) Inflammation
2) Radiation
3) Oxygen toxicity
4) Chemicals
5) Reperfusion injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some examples of antioxidants?

A

1) SOD
2) Vitamin C
3) Glutathione peroxidase
4) Ferritin
5) Ceruloplasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the histologic hallmarks of necrosis?

A

1) Pyknosis (nuclear condensation with shrinkage and intense basophilia)

2) Karyorrhexis (nuclear fragmentation)

3) Karyolysis (nuclear dissolution or loss)

4) Hypereosinophilic cytoplasm (intensely pink cytoplasm); due to denaturation of proteins, loss of ribosomes

5) Later, the dead cell may have cytoplasmic pallor

6) Become swollen, rounded, and detached from the basement membrane/neighboring cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the characteristics of coagulative necrosis?

A

1) Blood supply has been cut off

2) Loss of differential staining, but retention of cellular structures (can still make out individual cells)

3) Nuclear change: pyknotic

4) Cytoplasm: hypereosinophilic (homogenous)

5) Causes: hypoxia, cell membrane injury, toxins

6) Tissues affected: liver, kidney, muscle, neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the characteristics of caseous necrosis?

A

1) Cells and tissues are unidentifiable

2) Coagulum of debris (more chronic cases); “onion layers” look to lesion

3) Causes: TB granuloma, Mycobacteria sp. and Rhodococcus equi

4) Tissues affected: any site possible (abscesses), lymph nodes, deep skin wounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the characteristics of liquefactive necrosis?

A

1) Cells and tissues are unidentifiable

2) Cavitation or focal loss of structure (liquid debris and fluid)

3) Causes: hypoxia, bacteria

4) Tissues affected: CNS (enzymatic destruction, high lipid content); Abscess (early) (neutrophils, hydrolytic enzymes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the characteristics of gangrenous necrosis?

A

1) Coagulative necrosis + saprophytic bacteria (ischemia or local irritant)

2) Wet Gangrene: Good blood supply; +/- bacteria

3) Dry Gangrene: Is the result of decreased vascular perfusion!! Affects distal extremity (udders/distal ends of appendages); mummification, usually lacks bacteria; dry/leathery appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the characteristic of enzymatic necrosis of fat (fat necrosis)?

A

1) Necrosis of adipose tissue

2) Occurs mainly in peripancreatic adipose tissue (attributed to release of lipases from necrotic pancreatic acinar cells)

3) Grossly appears as chalky-white nodular deposits (the result of saponification = soap formation)

17
Q

Erosion vs. Ulceration

A

Erosion: Necrosis in epithelial surfaces (epidermis or corneal epithelium), or epithelial linings (mucosal epithelium); causes exfoliation or sloughing of dead cells, resulting in erosion of epithelium

Ulceration: Full-thickness necrosis (through mucosa, submucosa, etc)