Cell Injury Flashcards

1
Q

Characterized by nuclear shrinkage and increased basophilia.

A

Pyknosis

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2
Q

Characterized by the pyknotic nucleus undergoing fragmentation.

A

Karyorrhexis

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3
Q

Characterized by fading of the chromatin.

A

Karyolysis

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4
Q

The formation of a hydroxyl molecule due to the interaction with transition metals.

A

Fenton Reaction

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5
Q

The formation of a hydroxyl molecule due to the interaction of hydrogen peroxide and superoxide.

A

Harber - Weiss Reaction

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6
Q

Basic form of necrosis resulting from ischemia; predominately autolytic.

A

Coagulative Necrosis

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7
Q

Basic form of necrosis generally the result of heterolytic digestion (lysins/enzymes); an autolytic form is seen with ischemic injury to the central nervous system.

A

Liquefactive Necrosis

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8
Q

A combined form of necrosis (coagulative + liquefactive) associated with mycobacterial infections but may be seen with fungal diseases, tularemia and lymphogranuloma venereum.

A

Caseous Necrosis

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9
Q

In destructive pancreatic diseases, pancreatic lipases and other enzymes may be liberated into the surrounding adipose tissue where they hydrolyze the extracellular fat, in addition to other tissues (leads to soap formation).

A

Fat Necrosis

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10
Q

This necrosis has no enzymatic degradation of fat, but only release of fat from cells into the tissue due to rupture or damage of cell membranes.

A

Traumatic Fat Necrosis

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11
Q

Where is traumatic fat necrosis most commonly found?

A

In the breast but also in subcutaneous areas.

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12
Q

This necrosis is not a distinctive form of cell death. Generally applied to necrosis involving the distal portion of a limb.

A

Gangrenous Necrosis

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13
Q

What are the two forms of gangrenous necrosis?

A
  • Dry gangrene

- Wet gangrene

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14
Q

Predominately coagulative necrosis of a portion of an extremity. The tissue dries out, becomes greenish-yellow, and finally dark brown to black (mummification).

A

Dry Gangrene

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15
Q

Occurs when the gangrenous area becomes infected, inducing a significant amount of liquefactive necrosis.

A

Wet Gangrene

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16
Q

A special tissue reaction in which the connective tissue stains highly eosinophilic like fibrin.

A

Fibrinoid Necrosis

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17
Q

What type of necrosis is seen with certain immunologic reactions and arterioles in association with malignant (high grade) hypertension.

A

Fibrinoid Necrosis

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18
Q

An oxidative enzyme that behaves like an intracellular asphyxiant, which inactivates cytochrome oxidase.

A

Cyanide

19
Q

Oxygen hemoglobin of red blood cells; most damaging effects is on neurons.

A

Carbon Monoxide

20
Q

Binds to sulfhydryl group of cell membranes and other protein causing increased permeability and inhibiting ATPase - dependent transport.

A

Mercury

21
Q

Contains phospholipases, which attack the phospholipids of cell membranes.

A

Exotoxin of Clostridium Perfringes

22
Q

What are two types of virus induced cell injuries?

A
  1. Cytolytic/Cytopathic

2. Oncogenic replication of infected cells

23
Q

Rapidly replicating viruses that interfere with cellular metabolism (thereby inducing an immunologic response).

A

Cytolytic/Cytopathic

24
Q

The accumulation of adipose tissue between parenchymal cells of an organ.

A

Stromal Infiltration/Fatty Ingrowth

25
Q

What type of accumulation happens in the epithelial cells of the proximal convoluted tubules of kidney in mercury poisoning.

A

Protein Accumulation

26
Q

Eosinophilic (alcoholic hyaline) masses within degenerating liver cells in active nutritional cirrhosis representing accumulation of intermediate pre-keratin filaments.

A

Mallory Bodies

27
Q

Spherical hyaline masses within plasma cells in many forms of chronic inflammation (representing aggregates of immunoglobulins synthesized by the plasma cells).

A

Russell Bodies

28
Q

Degenerative hyaline changes in voluntary muscle in typhoid fever and other severe febrile infections.

A

Zenker (Waxy)

29
Q

Blackened carbon pigments in the tissues of the lungs and the regional lymph nodes without significant fibroblastic reaction (due to repeated air pollution exposure).

A

Anthracosis

30
Q

Pigmentation of the pulmonary tissue which may induce an extensive fibroblastic response or emphysema leading to coal worker’s pneumoconiosis.

A

Carbon Dust Aggregates (Coal Miners)

31
Q

What are two exogenous pigments?

A
  1. Anthracosis

2. Carbon Dust Aggregates (Coal Miners)

32
Q

What are two endogenous pigments?

A
  1. Lipofuscin

2. Melanin

33
Q

For all practical purposes, the only brown-black endogenous pigment.

A

Melanin

34
Q

Ingestible residue of lipid peroxidation of sub-cellular membranous structures seen in cells undergoing slow regressive changes.

A

Lipofuscin

35
Q

Hemoglobin derived, golden-yellow to brown pigment.

A

Hemosiderin

36
Q

Seen in association with tissue damage characterized by broad/wide zones of basophilia.

A

Dystrophic Calcification

37
Q

Seen in association with hypercalcemia characterized by fine basophilic strippling around small blood vessels (perivascular).

A

Metastatic Calcification

38
Q

What are some causes of hypercalcemia?

A

CHIMPS

C - Cancer
H - Hyperparathyroidism
 I  - Intoxication of vit D
M - Multiple myeloma/Milk alkali syndrome
P  - Paget disease of the bone
S  - Sarcoidosis
39
Q

What are two types of reversible cell injury?

A
  • Hydropic Change

- Fatty Change

40
Q

Explain the gross morphology and microscopic features of hydropic change.

A
  • Gross: Pallor, increased weight, INCREASED turgor

- Microscopic: Enlarged cells, fine cytoplasmic vacuolization WITHOUT nuclear displacement, and normal nuclei

41
Q

Explain the gross morphology and microscopic features of fatty change.

A
  • Gross: Pallor, increased weight, DECREASED turgor

- Microscopic: Enlarged cells, large vacuoles with peripheral displacement of nuclei, normal nuclei

42
Q

What are two types of irreversible cell injury?

A
  • ATP depletions

- Cell membrane damage

43
Q

Explain Carbon Tetrachloride injury and explain what CCL3 does to the body.

A
  • This is where a biologically inactive chemical like CCL4, is converted into something toxic, like free radical CCL3 in the SER (via mixed oxidase system).
  • CCL3 initiates lipid peroxidation; leading to ER swelling, dissociation of ribosomes, disaggregation of polysomes, and lipid accumulation.