Necrosis And Dystrophy

Front 1

1. How many percent formaldehyde is used in formalin solution?

Back 1

37% formaldehyde is used to prepare 10% formalin solution

Front 2

2. During necrosis, describe and name the morphological changes of nucleus?

Back 2

- all ncl changes are due to breakdown of DNA and chromatin by lysosomal enzymes (proteases and nucleases)

pyknosis - condensation and clumping of nucleus which becomes dark basophilic

karyorrhexis - Nuclear fragmentation in to small bitsdispersed in the cytoplasm

karyolysis - dissolution of the nucleus

Front 3

3. What is pyknosis, and when does it occur?

Back 3

- nucleus becomes smaller and stains deeplybasophilic as chromatin clumping continues (shrinkage of ncl, chromatin forms shrunken solid mass)

- seen in apoptosis as well as necrosis of the cells

Front 4

4. What is karyorrhexis, and when does it occur?

Back 4

- pyknotic nucleus breaks up into many smaller fragments scattered about the cytoplasm

- apoptotic cells

Front 5

5. What is karyolysis, and when does it occur?

Back 5

- pyknotic nucleus may be extruded from the cell or it may manifest progressive loss of chromatin staining

- necrotic cells

Front 6

6. What are the main causes of necrosis?

Back 6

- reduced oxygen supply (arteriosclerosis, hypoxaemia...)

- physical agents (crush)

- chemical agents (acid, lye)

- toxins (corrosive sublimate)

- viruses

- abnormal immunological reaction

- nutritional deficiencies (qualitative, quantitative)

- genetic abnormalities (aging)

Front 7

7. Name the 5 different types of necrosis

Back 7

1. Coagulative necrosis

2. Liquefactive (colliquative) necrosis

3. Caseous necrosis

4. Fat necrosis

5. Fibrinoid necrosis

Front 8

8. What is typical in coagulative necrosis, in which tissues does it occur, and does the tissuecontain much or less protein?

Back 8

- most common type (irreversible focal injury)

- in infarcts in any tissue (except brain)

- Due to loss of blood

- Gross: tissue is firm and pale

- Micro: Cell outlines are preserved (cells look ghostly), and everything looks red

Front 9

9. White infarct in tissues is a result of what?

Back 9

- white infarct (anemic)

- result of arterial occlusions in solidorgans with end-arterial circulations (e.g., heart, spleen, andkidney)

Front 10

10. Which tissues are mostly associated with white infarct?

Back 10

- solidorgans with end-arterial circulations (e.g., heart, spleen, andkidney), and where tissue density limits the seepage of bloodfrom adjoining patent vascular beds

Front 11

11. What tissues are most likely to undergo coagulative necrosis?

Back 11

- all tissues except of brain (solely liquefactive )

- spleen, heart, kidney

Front 12

12. What is liquefactive (colliquative) necrosis, and such a name as “liquefactive”?

Back 12

- in infections and in brain infarcts

- Due to lots of neutrophils around releasing their toxic contents, “liquefying” the tissue

- Gross: center of the tissue is liquid and creamy yellow (pus), later cyst wall is formed

- Micro: lots of neutrophils and cell debris

Front 13

13. What tissues are more likely to undergo liquefactive necrosis and why?

Back 13

- tissues must rich in lipids

- dissolution of the tissue by the action of hydrolytic enzymes

- necrosis caused by bacterial infection

- ischemia of CNS

Front 14

14. Which organ is mostly associated with liquefactive necrosis?

Back 14

brain, CNS

Front 15

15. What is caseous necrosis?

Back 15

- typical for tuberculosis (centre of foci)

- combines signs of coagulative and liquefactive necrosis

- Due to the body trying to wall off and kill the bacilli with macrophages

- Gross: White, soft, cheesy-looking (“caseous”) material

- Micro: fragmented cells and debris surrounded by a collar of lymphocytes and macrophages (granuloma)

Front 16

16. What is the most commonly causative agent for caseous necrosis?

Back 16

Mycobacterium tuberculosis

Front 17

17. What hypersensitivity is associated with caseous necrosis?

Back 17

delayed hypersensitivity reaction (granulommatous inflammatory reaction)

Front 18

18. Caseous necrosis is a combination of two other types of necrosis, which?

Back 18

causeous and liquefactive

Front 19

19. What is the etiology of fat-necrosis?

Back 19

- in acute pancreatitis

- Damaged cells release lipases, which split the triglyceride esters within fat cells

- Gross: chalky, white areas from the combination of the newly-formed free fatty acids with calcium (saponification)

- Micro: shadowy outlines of dead fat cells (see image above); sometimes there is a bluish cast from the calcium deposits, which are basophilic

Front 20

20. Which organs are most prone to fat-necrosis, and why?

Back 20

- pancreas (following acute pancreatic necrosis) - may affect fat depots through abdominal cavity - sometimes extra-abdominal as well

- breast (traumatic fat necrosis)

Front 21

21. What is saponification?

Back 21

lipases split the triglyceride esters containedwithin fat cells - released fatty acids combine withcalcium to produce grossly visible chalky white areas

Front 22

22. What is fibrinoid necrosis?

Back 22

- immune reactions in vessels

- Complexes of antigens and antibodies (immune complexes) combine with fibrin

- Gross: changes too small to see grossly

- Micro: vessel walls are thickened and pinkish-red (called “fibrinoid” because it looks like fibrin but has other stuff in there too

Front 23

23. What is microscopical typical feature of fibrinoid necrosis?

Back 23

- brightly eosinophilic, hyaline-like deposition in the vessels wall (thickening)

- leucocytoclasis (necrotic focus surrounded by nuclear debris of neutrophils)

- local haemorrhage may occur due to rupture of blood vessels

Front 24

24. What is the etiology of fibrinoid necrosis?

Back 24

inflammation of vessels or hypertenion

Front 25

25. Can hypertension lead to fibrinoid necrosis, and why?

Back 25

yes - it is unclear, but the following sequence is suggested:

- initialevent = some form of vascular damage to thekidneys

- this most commonly results from long-standinghypertension, with eventual injury to the arteriolar walls.

- result is increased permeability of the small vessels to fibrinogenand other plasma proteins, endothelial injury, and plateletdeposition

- appearance of fibrinoidnecrosis of arterioles and small arteries and intravascularthrombosis.

Front 26

26. What is gangrene?

Back 26

for of necrotic tissue with super-added putrefaction

Front 27

27. What is putrefaction?

Back 27

anaerobic decomposition of organic matter by bacteria and fungi that results in obnoxiously odorous products; rotting.

Front 28

28. What is responsible for the black color in gangrenous tissue?

Back 28

liberation of hemoglobin from haemolysed RBC which is acted upon by H2S produced by bacteria resulting in formation of black iron sulfide

Front 29

29. There are 3 basic types of gangrene, which?

Back 29

dry, wet, gas

Front 30

30. What kind of gangrene is associated with diabetic foot?

Back 30

wet gangrene (high sugar content favours bacteria)

Front 31

31. What kind of gangrene is associated with bed sores?

Back 31

wet gangrene (increased pressure - blockage of venous, less commonly arterial blood flow = affected part is stuffed with blood)

Front 32

32. Which bacteria is associated with gas gangrene?

Back 32

Clostridia (gram-positive anaerobic bacteria)

Front 33

33. What is the most common cause of dry gangrene?

Back 33

ischemia of the distal part of the limb

Front 34

34. Which places is wet gangrene most likely to occur?

Back 34

moist tissues and organs (mouth, bowel, lung, cervix, vulva)