Cell Adaptation, Injury & Death

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Aspects of Pathology

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1. Etiology

2. Pathogenesis

3. Morphologic change

4. Clinical significance

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____ induce a new state that changes the cell but otherwise preserves its viability in the face of ____ stimuli

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Adaptation

exogenous

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increase in size of the cells therefore increase in size of the organ

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Hypertrophy

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increase in cell number due to proliferation of differentiated cells and replacement by tissue stem cells

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Hyperplasia

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shrinkage in cell size by loss of cell substance

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Atrophy

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one adult cell type is replaced by another adult cell type

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Metaplasia

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denotes pathologic cell changes that can e restored to normalcy if the stimulus is removed or if the cause of injury is mild

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Reversible injury

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when stressors exceed the capacity of the cell to adapt and denotes permanent pathologic changes

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Irreversible injury

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occurs primarily through Necrosis and Apoptosis

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Cell Death

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more common type of cell death

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Necrosis

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Necrosis involves (a,b,c,d)

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Denaturation and coagulation of proteins

Organelle breakdown

Cellular swelling

Cell rupture

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occurs when a cell dies by activation of an internal "suicide" program involving orchestrated disassembly of cellular components

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Apoptosis

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Does not elicit an inflammatory response

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Apoptosis

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adaptive response of cells to nutrient deprivation

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Autophagy

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self-cannibalization to maintain viability

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Autophagy

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(Necrosis or Apoptosis)

Enlarged/swelling cell

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Necrosis

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(Necrosis or Apoptosis)

Reduced or shrinkage of cell

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Apoptosis

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(Necrosis or Apoptosis)

Fragmentation of nucleus into nucleosome-size fragments

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Apoptosis

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(Necrosis or Apoptosis)

Disrupted plasma membrane

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Necrosis

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(Necrosis or Apoptosis)

Intact plasma membrane

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Apoptosis

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(Necrosis or Apoptosis)

altered orientation of lipids

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Apoptosis

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(Necrosis or Apoptosis)

enzymatic digestion

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Necrosis

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(Necrosis or Apoptosis)

cellular components are intact and may be released

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Apoptosis

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(Necrosis or Apoptosis)

Frequent adjacent inflammation

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Necrosis

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(Necrosis or Apoptosis)

No adjacent inflammation

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Apoptosis

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Causes of Cell Injury

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Chemical agents

Hypoxia

Infectious agents

Physical agents

Immunologic reactions

Nutritional imbalances

Genetic derangements

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most common cause of hypoxia

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Ischemia

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loss of blood supply

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Ischemia

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Two main correlates of Reversible cellular injury

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Cell swelling

Fatty change

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the sum of the morphologic changes that follow death in living tissue or organ

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Necrosis

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Distinctive features of Necrotic Cells

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1. More eosinophilic than viable cells

2. "Glassy" bec. glycogen loss

3. Vacuolated

4. Fragmented CM

5. Attract Calcium salts = fatty soaps

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Nuclear changes of necrotic cells

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1. Pyknotic

2. Karyorrhexis

3. Karyolysis

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Tissue patterns of necrosis

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1. Coagulative

2. Liquefactive

3. Gangrenous

4. Caseous

5. Fat

6. Fibrinoid

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necrosis in heart and kidney

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Coagulative

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predominated by protein denaturation with preservation of cell and tissue framework

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Coagulative

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undergoes either heterolysis or autolysis

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Coagulative

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Characteristic of Infarcts or "ischemic necrosis" in all solid organs except the brain

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Coagulativeu

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underlying tissue architecture is preserved for at least several days

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Coagulative

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heterolysis or autolysis predominates over protein denaturation

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Liquefactive

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necrotic area is soft and filled with fluid

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Liquefactive

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most frequently seen in localized bacterial infections (abscess) and in the brain

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Liquefactive

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a coagulative necrosis applied to an ISCHEMIC LIMB

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Gangrenous

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superimposed bacterial infection

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wet gangrene

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Characteristic of TUBERCULOUS LESIONS

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Caseous necrosis

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Grossly: soft, cheese-like, friable material

Microscopically: ____

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Caseous necrosis:

- Amorphous eosinophilic material w/ cell debris

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tissue architecture is completely obliterated and cellular outlines cannot be discerned

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Caseous necrosis

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seen in pancreatic tissues

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Fat necrosis

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releases fatty acids from triglycerides, which then complex with calcium to form soaps (fat saponification)

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Lipase activation

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Gross: whie, chalky areas

Micrscopically: ____

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Fat necrosis:

- vague cell outlines and CALCIUM DEPOSITION

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resulting from antigen-antibody immune complex deposition in blood vessels

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Fibrinoid necrosis

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Fibrinoid necrosis:

Microscopically: ____

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- bright pink amorphous material (PROTEIN DEPOSITION)

- in arterial walls

- often associated with INFLAMMATION and THROMBOSIS

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Mechanisms of Cell Injury (3)

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1. Depletion of ATP

2. Mitochondrial damage

3. Influx of Calcium and loss of Ca homeostasis

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mitochondrial damage results in the formation of ____

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Membrane Permeability Transition Pore

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Influx of Calcium and loss of Ca homeostasis activates the following enzymes: ______

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Phospholipase

ATPase

Protease

Endonuclease

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enzyme responsible for membrane damage

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Phospholipase

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enzyme responsible for breakdown of membrane and cytoskeleton proteins

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Protease

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enzyme responsible for hastening ATP depletion

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ATPase

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enzyme responsible for nuclear damage / DNA & chromatin fragmentation

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Endonuclease

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Major forms of Oxygen-Derived Free radicals

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1. Superoxide Anion

2. Hydrogen peroxide

3. Hydroxyl ions

4. Peroxynitrate ion

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Free radicals damage ____ by peroxidizing double bonds and cause chain breakage

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Lipids

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Free radicals damage ____ by oxidizing and fragmenting peptide bonds

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Proteins

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Free radicals damage ____ by single strand breaks

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Nucleic acids

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Free radicals are inactivated or destroyed by... ___

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Antioxidants

Bind to storage and transport protein

Scavenging enzyme systems

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Membrane can be damaged directly by... ____

indirectly by... ___

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Directly:

- Toxins

- Physical & Chemical agents

- Lytic complements components

- Perforins

Indirectly:

- ROS

- Ca activation of phospholipase