Cellular Injury II Flashcards Preview

NYCPM Pathology > Cellular Injury II > Flashcards

Flashcards in Cellular Injury II Deck (59):
1

examples of bilirubin accumulation

hemolytic jaundice

hepatocellular jaundice

obstructive jaundice

2

hemolytic jaundice is associated with

destruction of red cells.

3

hepatocellular jaundice indicates

parenchymal liver damage

4

obstructive jaundice is either

intra or extrahepatic obstruction of the biliary tract

5

hemosiderin is an

iron-containing pigment that consists of aggregates of ferritin.

6

hemosiderin appears in tissues as

brown amorphous aggregates that stain blue with Prussian blue dye. It is usually in small amounts.

7

hemosiderosis indicates

no damage

8

hemosiderin exists in small amounts within tissue macrophages of the

bone marrow, liver and spleen.

9

hemochronatosis is a

more extensive accumulation of hemosiderin, often within parenchymal cells, with accompanying tissue damage, scarring and organ dysfunction.

it occurs in hereditary (primary) and secondary (blood transfusion) forms.

10

lipofuscin is a

yellowish, fat soluble pigment that is an end product of membrane lipid peroxidation.

11

lipofuscin commonly accumulates in

elderly patients (hepatocytes and myocardial cells), referred to as brown atrophy.

12

necrosis is

the sum of the degradative and inflammatory reactions occurring after tissue death caused by injury.

13

necrosis - general chracteristics

1. occurs within living organisms and pathologic speciments but not fixed cells with well preserved morphology.

2. autolysis is the degradative reactions caused by intracellular enzymes indigenous to the cell.

3. heterolysis is the cellular degradation by enzymes derived from sources extrinsic to the cell.

14

postmortem autolysis occurs after

the death of an organism and is not necrosis.

15

autolysis

degradative reactons in cells caused by intracellular enzymes indigenous to the cell.

16

heterolysis

the cellular degradation by enzymes derived from sources extrinstic to the dying cell.

17

main types of necrosis

coagulative

liquefactive

caseous

18

coagulative necrosis results from

a sudden cutoff of blood sulpply to an organ, paricularly the heart and kidney.

19

in coagulative necrosis,

it is characterized by general preservation of tissue architecture (ghost cells).

increased cytoplasmic eosinophilia occurs because of protein denaturation and loss of cytoplasmic RNA

20

nuclear changes in coagulative necrosis are the

morphologic hallmark of irreversible injury and necrosis. Along with stainable nuclei, they include

pyknosis
karyorrhexis
karyolysis

21

pyknosis

chromatin clumping and shrinking with increased basophilia

22

karyorrhexis

fragmentation of chromatin

23

karyolysis

fading of chromatin material

24

liquefactive necrosis results from

ischemic injury to the CNS. After the death of CNS cells, it is caused by autolysis.

It is also chracterized by digestion of tissue.

25

liquefactive necrosis occurs in

supprative infections characterized by the formation of pus (liquefied tissue debris and neutrophils) by heterolytic mechanisms.

26

caseous necrosis occurs as part of

granulomatous inflammation and is a manifestation of partial immunity caused by the interaction of T lymphocytes, macrophages and cytokines, such as IFN-gamma derived.

27

caseous necrosis is associated most often with

tuberculosis.

28

caseous necrosis has features of both

coagulative necrosis and liquefactive necrosis.

29

caseous necrosis appearance

an amorphous eosinophilic apperanace on histologic examination, usually within the center of granulomas.

30

necrotic cells of caseous necros do not

maintain their cellular outlines but do not undergo lysis (as is seen in liquefactive necrosis).

31

fat necrosis occurs in two forms

traumatic fat necrosis
enzymatic fat necrosis

32

traumatic fat necrosis

occurs after a severe injury to tissue with a high fat content, such as the breast.

33

enzymatic fat necrosis

a complication of acute hemorrhagic pancreatitis, a severe inflammatory disorder of the pancreas.

34

steps of enzymatic fat necrosis

pancreatic enzymes diffuse into inflamed tissue and digest the parenchyma.

fatty acids liberated by the digestion of fat form calcium sats.

vessels are eroded, with resultant hemorrhage.

35

fibrinoid necrosis

marked by deposition of fibrin-like proteinaceous material in the arterial walls, which appears smudgy and acidophilic.

It is often associated with immune-mediated vascular damage.

36

wet gangrene

gangrenous necrosis when complicated by infective heterolysis and liquefactive necrosis

37

dry gangrene

gangrenous necrosis when characterized by coagulative necrosis without liquefaction.

38

apoptosis is used to

remove cells with irreparable DNA damage, protecting against neoplastic formation.

it is also important for embryogenesis and programmed cell cycling (menstruation)

39

apoptosis - morphologic characteristics

1. a tendency to involve single isolated cells or small clusters of cells within a tissue.

2. Progression through a series of changes marked by a lack of inflammatory response.

3. shrinking of affected cells and cell fragments, resulting in small round eosinophilic masses often containing chromatin remnants.

40

the progression of changes in apoptosis

1. blebbing of plasma membrane, cytoplasmic shrinkage, chromatin condensation.

2. budding of cell and separation of apoptotic bodies (membrane bound segments)

3. phagocytosis of apoptotic bodies.

41

diverse injurious stimuli

free radicals
radiation
toxic substances
foreign (viral) DNA
withdrawal of growth factors or hormones.

42

biochemical events of apoptosis

1. initiation of diverse injurious stimuli.

2. Activation of intrinsic/extrinsic pathway or cytotoxic T cell mediated apoptosis

3. activation of caspases

4. Neatly packaged portions of cell membrane with degraded cellular contents are pinched off and form apoptotic bodies which are engulfedby phagocytic macrophages.

43

caspases acrivate

endonucleases, which degrade dNA into nucleosomal chromatin ragments.

they also activate transglutaminases, which cross-link apoptotic cytoplasmic proteins.

44

healthy, stimulated cells contain adequate levels of

anti-apoptotic Bcl-2 (e.g. hormone stimulation)

45

the intrinsic pathway is activated when cells are

deprived of hormonal stimulation.

46

In the intrinsic pathway, lack of growth stimulation results in an excess of

Bax and Bak (pro-apoptotic) over Bcl-2 (anti-apoptotic) and cause release of cytochome-c from mitochondira, causing activation of caspases.

47

caspases are cytosolic cytotoxic proteases that are referred to as

major executioners - they activate intracellular endonucleases and proteases that neatly break down the cellular organelles and contents.

48

the apoptotic cascade is triggered by the

opening of the mitochondrial permeability transition pore and release of cytochrome c, triggering the apoptotic cascade.

49

In the extrinsic pathway,

molecules such as FAS ligand and TNF bind to receptors. The activated receptors signal via transmembrane death domains and activate caspases.

50

in cytotoxic T cell mediated apoptosis, cells that are recognized as

foreign (i.e. contain viral DNA, transplanted organs) are targeted by CD8+ cytotoxic

51

In T cell mediated apoptosis, CD8+ cytotoxic T cells puncture the plasma membranes of target cells via

perforins.

52

through the perforins, _ enters

granzyme B enters the target cell and activates the caspases.

53

bcl-2

gene product that inhibits apoptosis

54

bax

gene product that facilitates apoptosis

55

p53

gene product that facilitates apoptosis by decreasing transcription of bcl-2 and increasing transcription of bax.

56

metastatic calcification is often caused by

hypercalcemia, most often resulting from many things.

57

hypercalcemia often results from

hyperparathyroidism

osteolytic tumors, with resultant mobilization of calcium and phosphorus

hypervitaminosis D

excess calcium intake, such as in the milk-alkali syndrome (nephrocalcinosis and renal stones caused by milk and antacid self therapy for peptic ulcer).

58

dystrophic calcification occurs in

previously damaged tissue, such as areas of old trauma, tuberculosis lesions, scarred heart valves and atherosclerotic lesions.

59

dystrophic calcification is not caused by

hypercalcemia; typically, the serum calcium concentration is normal.