lab Flashcards

1
Q

A form of cell death in which cellular membranes fall apart and cellular enzymes leak out and, ultimately, digest the cell.

A

Necrosis

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2
Q

Elicits a local host reaction (inflammation) that is induced by substances released from dying or dead cells.

A

Necrosis

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3
Q

Often the culmination of irreversible cell injury that cannot be corrected.

A

Necrosis

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4
Q

Shows increased eosinophilia due to increased binding of eosin to denatured cytoplasmic proteins and loss of basophilic RNA in the cytoplasm
Loss of glycogen particles.
Prominent myelin figures.

A

Cytoplasm Changes during Necrosis

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5
Q

nuclear shrinkage

A

Pyknosis (nucleus changes during necrosis)

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6
Q

fragmentation of the pyknotic nuclei

A

Karyorrhexis (nucleus changes during necrosis)

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7
Q

nucleus and DNA fades due to DNAse activity.

A

Karyolysis (nucleus changes during necrosis)

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8
Q

(nucleus changes during necrosis)

A

Pyknosis
Karyorrhexis
Karyolysis

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9
Q

The underlying tissue architecture is preserved for several days.
Affected tissues take on a firm texture
Injury denatures enzymes blocking proteolysis of dead cells – eosinophilic, anucleate cells persist
Leucocytes are recruited to the site of necrosis.
Cellular debris are removed by phagocytosis
Characteristic of infarcts in all solid organs except the brain.
example: kidney

A

Coagulative Necrosis

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10
Q

Seen in focal bacterial and fungal infections
Because microbes stimulate the accumulation of inflammatory cells.
Enzymes of leukocytes digest the tissue.
The dead cells are completely digested, transforming the tissue into a liquid viscous mass.
The digested tissue is removed by phagocytosis
If the process was initiated by acute inflammation – the material is creamy yellow
Pus
Seen in abscesses
Ischemic destruction of brain tissue
example: heart

A

Liquefactive Necrosis

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11
Q

This is a combination of coagulative and liquefactive necrosis encountered principally in the center of tuberculous infections.
Characteristic appearance is that of a soft, friable, whitish-gray debris resembling clumped cheesy material.
On microscopic examination, the necrotic focus appears as a collection of fragmented or lysed cells.
With amorphous granular pink appearance
Tissue architecture is completely obliterated.
often enclosed within an inflammatory border granulomas

example: lungs

A

Caseous Necrosis

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12
Q

due to the action of lipases on triglycerides resulting to saponification.
The released fatty acids combine with calcium to produce the visible chalky white areas.
occurs in the female breast, mesenteries and in the omentum.
There is no enzymatic lipolysis but there is apparent rupture of the cell membrane with release of neutral fat. Subsequent phagocytosis of the fat follows.
example: acute pancreatitis

A

Enzymatic and Traumatic Fat Necrosis

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13
Q

If produced by ischemia with a superimposed saprophytic bacterial infections

A

wet gangrene

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14
Q

When bacterial infection does not supervene

A

Dry gangrene or mummification

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15
Q

may be cause by: arteriosclerosis, Buerger’s disease, Raynaud’s disease, Ergot poisoning (ABRE)

A

Dry gangrene

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16
Q

Marked by deposition of fibrin-like proteinaceous material in arterial walls
smudgy and eosinophilic on light microscopy
e.g. immune vaculitis, malignant hypertension

A

fibrinoid necrosis

17
Q

cell injury causes (OTGAIIN)

A
O2 deprivation 
Trauma (physical, chemical, radiation)
Genetics
Aging
Infectious agents
Immunologic reaction 
Nutritional Imbalance
18
Q

stress is present

A

irreversible

19
Q

stress is removed

A

reversible

20
Q

steps in paraffin preparation (OFDCECSO)

A
Obtain fresh specimen 
Fixation 
Dehydration 
Cleansing 
Embedding 
Cutting 
Staining 
Observe under microscope
21
Q

fat necrosis appears as yellowish-white and firm deposits. Formation of calcium soaps imparts the necrosed foci firmer and chalky white appearance

A

Grossly

22
Q

necrosed fat cells have cloudy appearance ; surrounded by inflammatory reaction

A

microscopically

23
Q

“falling off”, fragments of apoptotic cells break off

A pathway of cell death in which cells activate enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins.

A

Apoptosis

24
Q

Replacement of worn out cells.
Highly proliferative and hormone responsive tissues undergo cycles of proliferation and cell loss.
In immunity, elimination of excess leukocytes left at the end of an immune response.

A

Physiologic Apoptosis (causes)

25
Q

When DNA is severely damaged.
Accumulation of misfolded proteins
Some viruses induce apoptotic death of infected cells

A

Pathologic Apoptosis (causes)