Chapter 4, Cell Injury, Aging, & Death

Reversible cell injury

mild/short lived injury

Hydropic swelling

cellular swelling due to accumulation of water intracellular accumulations

• excessive amounts of fat

• accumulation of abnormal substances produced by cell & pigments and particles cell cannot digest

(reversible cell injury)

Cellular adaptation

persistent sublethal injury

• atrophy

• hypertrophy

• hyperplasia

• metaplasia

• dysplasia

• anaplasia

• neoplasia

Atrophy

cells shrink and reduce differentiated functions

• Causes: Disuse, enervation, ischemia, nutrient deficiency, interruption of endocrine signals, persistent cell injury

Hypertrophy

increase in cell mass, augmented functional capacity

• Causes: Response to increased physiologic or pathophysiologic demands

Hyperplasia

increased number of cells + functional capacity

• Increased physiologic demands and persistent cell injury

Metaplasia

replacement of one differentiated cell type with another (reversible)

• Causes: adaptation to persistent injury with replacement of a cell type better suited for situation

Dysplasia

disorganized appearance of cells because of abnormal variations in size, shape and arrangement

• Causes: adaptive effort gone wrong

• VERY high chance to go cancerous

Anaplasia

cellular deviance characterized by a loss of differentiation and structural organization. Anaplastic cells lose their specialized functions, vary wildly in size and shape, and are a hallmark feature of aggressive, malignant tumors.

Neoplasia

"new growth"; an abnormal, unregulated, and autonomous proliferation of cells that continues even after the original stimulus is removed. Neoplasms can be benign (non-cancerous and localized) or malignant (cancerous and capable of invading surrounding tissue or metastasizing)

Irreversible cell injury

• Necrosis

• Apoptosis

Necrosis

cell death resulting from inflammation/consequence of ischemia or toxins. characterized by cell membrane rupture, spilling of contents into surrounding fluid, and subsequent inflammation

Has 4 types:

• Coagulative

• Liquefactive

• Fat necrosis

• Caseous

Coagulative

the most common type; begins with ischemia and ends in tissue degradation (ex. dry gangrene)

Liquefactive

occurs when dead cells dissolve quickly due to lysosomal enzymes, often forming an abscess or cyst (ex. wet gangrene)

Fat necrosis

death of adipose tissue resulting from trauma or pancreatitis, appearing as chalky white areas

Caseous

characteristic of lung damage from tuberculosis; leaves tissue looking soft and clumpy like cheese

Apoptosis

programmed cellular suicide triggered by internal signaling pathways. Response to injury that does not directly kill the cell. Does not cause inflammation and not always pathological

Ischemia

interruption of blood flow to an area; it is the most common cause of tissue hypoxia and overall cell injury

Ischemia stages

1. Blockage in artery

2. Decreased oxygenation

3. Decreased cellular metabolism

4. Vital organs becoming hypoxic

5. ATP production inhibited

6. Failure of sodium pump causing cells to enlarge and rupture

Ischemia-Reprefusion Injury

additional cellular damage that occurs after blood supply is restored, driven by calcium overload, formation of reactive oxygen species (free radicals), and localized inflammation

Hypoxia

insufficient oxygen reaching tissues, which deprives cells of the energy required to maintain basic physiological function

_____ _____ is caused by ischemia.

Tissue hypoxia

Bacteria

single-celled microorganisms that primarily cause cell injury externally by producing toxins or competing for nutrients. MOST DAMAGE CELLS FROM THE OUTSIDE

Viruses

obligate intracellular agents that must enter inside host cells to replicate, causing cell injury directly from the inside. ENTER A CELL TO DAMAGE FROM THE INSIDE

Immune responses do more damage than the direct effects of the _______ _____.

Infectious agent

Somatic death

the death of the entire organism, characterized by the absence of respiration and heartbeat. Key postmortem changes include rigor mortis (stiffening of muscles within 6 hours) and postmortem autolysis (widespread tissue deterioration within 24 to 48 hours)