Cell Injury & Cell Death Flashcards

1
Q

Two main morphological correlates of reversible cell injury

A

Fatty Change & Cellular Swelling

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2
Q

3 Characterizations of Irreversible injury

A

Inability to restore mitochondrial function

Loss of structure and function of plasma membrane and intracellular membranes

Loss of DNA and chromatin structural integrity

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3
Q

Beginning of necrosis is initiated by

A

Injury to lysosomal membranes of injured cells.

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4
Q

Necrosis

A

“Accidental” cell injury

  • occurs in diseased cells only
  • Caused by toxins, infections, trauma and ischemia.
  • elicits inflammation
  • cells lose their membrane and cellular enzymes leak out and digest the cell and cytoplasmic organelles.
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5
Q

Apoptosis

A

“Regulated” cell death

  • occurs in healthy or diseased cells
  • occurs via therapeutic agents, genetic mutations, and infections.
  • cells do not lose their membrane
  • no inflammation
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6
Q

Pyknosis

A

Breakdown of DNA and chrome in characterized by nuclear shrinkage and increased basophila.

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7
Q

Karyorrhexis

A

Fragmentation of the pyknotic nucleus

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8
Q

Karyolysis

A

Digestion of DNA via DNase activity inside a pyknotic nucleus.

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9
Q

Coagulative necrosis

A

Underlying tissue architecture tube is preserved while the inside cells undergo necrosis.

  • marked increase in eosinophilia
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10
Q

Liquefactive necrosis

A

Rapid accumulation of leukocytes “liquify” the tissue

  • seen in bacterial and some fungal infections
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11
Q

Gangrenous Necrosis

A

Coagulative necrosis that is marked via a Loss of blood supply

  • when combined with a bacterial infection, becomes liquefactive necrosis. “Wet gangrene”
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12
Q

Caseous Necrosis

A

Possess a yellow-white cheese like appearance from TB infections.

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13
Q

Fat necrosis

A

Fat destruction, typically caused via pancreatic lipase.

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14
Q

Fibrinoid necrosis

A

Caused via immune reactions and mostly found in blood vessels

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15
Q

Mitochondrial pathway of apoptosis

A

Most used form

Mitochondria releases cytochrome c, which triggers caspase: the initiator of apoptosis.

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16
Q

Proteins that control cytochrome c permeability

A

Bcl-2

  • holds the Bax and Bak pathways back
17
Q

Death Receptor pathway of apoptosis

A

Type 1 TNF and FAS (CD95) receptors are unregulated on infected cells.

CD-8 T cells posses fas-L and bind to these receptors, activating caspase: the initiator of apoptosis

18
Q

Oxidative stress

A

Damage to the cell is generated via Reactive oxygen species (ROS)

Can be upregulated with additional stress factors

Can induce apoptosis or necrosis

19
Q

Ways of cellular adaption to stress

A

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

20
Q

Autophagy

A

Lysosomal digestion of the cells own organelles and components

  • done it times of severe nutrient deprivation
21
Q

Pyroptosis

A

Inflammasome activation causes caspase activation

  • produces cytokines and is essentially inflammation mixed with apoptosis
22
Q

Necroptosis

A

TNF receptor triggering causes RIP kinases to activate.

Causes membrane dissolution and apoptosis bodies. Is essentially necrosis mixed with apoptosis.

23
Q

4 pathways of abnormal intracellular accumulations

A

Defects in packaging/transport mechanisms

Genetic or acquired defects in protein folding

Failure to degrade a metabolite via enzyme deficiencies

Enzyme and transport failure altogether

24
Q

Abnormal metabolism

A

Can’t metabolize products in cells

Ex: steatosis: accumulation of triglycerides writhing parenchyma cells

25
Q

Alpha 1 antitrypsin deficency

A

Mutation in proteins causes very slow folding. ER stress

26
Q

Glycogenoses

A

Cell doesn’t have the enzymes to break down glucose

27
Q

Most exogenous pigment

A

Carbon

28
Q

Dystrophic calcification

A

Calcium metabolism is normal but deposits in injured or dead tissue

29
Q

Metastatic calcification

A

Acclimation of calcium in any tissue via hypercalcemia.

30
Q

Causes of hypercalcemia

A

Increased secretion of PT hormone

Accelerated Destruction of bone

Vitamin-D related disorders

Renal failure