General Pathology 601 for Dental Students

Cell Injury and Death, and Cellular Adaptation 
 

Nitya Ghatak, MD
Autopsy Pathology & Neuropathology
Sanger Hall, 5th Floor
(804) 828-9739
nrghatak@hsc.vcu.edu

II. Cellular Adaptation

Objectives
Upon completion of this lecture you will be able to:

1. Define atrophy,  hypertrophy, hyperplasia, metaplasia.
2. List at least four examples of abnormal intracellular accumulation of various substances.
3. Describe two general types of pathologic calcification.
4. Discuss two factors thought to influence aging.
   

Important Terms
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
lipofuscin
hemosiderin
bilirubin
Dystrophic calcification
Metastatic calcification
telomeres

Various Types of Adaptations

Cells may undergo various adaptations in physiological and pathological conditions. These are controlled by complex molecular mechanisms. The following are common types of cellular adaptation:

1. Atrophy--shrinkage of cells; classified as:
   • Physiologic--due to decreased work load (e.g., decreased size of uterus following child birth, or disease)
   • Pathologic--primarily due to denervation of muscle, diminished blood supply, nutritional deficiency
    
2. Hypertrophy--increase in the size of cells which results in enlargement of the organs. It is mostly seen in cells that cannot divide, such as skeletal muscle (pumping iron), and cardiac muscle (hypertension). These changes usually revert to normal if the cause is removed. Hypertrophy is mediated by different mechanisms.
   
3. Hyperplasia--increased number of cells in an organ or tissue. Hyperplasia may sometimes co-exist with hypertrophy. Hyperplasia can be classified as:
   • physiologic--hormonal (e.g., breast and uterus during pregnancy)
   • compensatory--regeneration of liver following partial hepatectomy. Various growth factors and interluekins are important in such hyperplasia.
   • pathologic--excessive hormonal stimulation viral infection (papilloma viruses); neoplasms
     
4. Metaplasia--transformation or replacement of one adult cell type to another adult cell type (e.g., the change from columnar to squamous cells in respiratory tract, from squamous to columnar in Barrett esophagitis). Metaplasia also occurs in mesenchymal tissue (e.g., formation of bone in skeletal muscle).

Metaplastic changes usually result from chronic irritation. Metaplastic changes seem to precede the development of cancer, in some instances. Metaplasia is thought to arise from reprogramming of stem or undifferentiated cells that are present in adult tissue.

Intracellular Accumulation

• Accumulation of pigments: 
  • Exogenous--carbon dust (anthracosis) 
  • Endogenous-- 
    • lipofuscin (aging pigment) in liver, heart, neurons, etc.
    • hemosiderin--in lungs following congestive heart failure; called hemosiderosis when found in a number of tissues and organs
    • bilirubin--in jaundice

Pathologic Calcification

1. Dystrophic--deposition of calcium and other minerals in dead tissue (e.g., atherosoma in blood vessels, heart valves in elderly individuals, old tuberculosis lesions)
2. Metastatic--calcium deposits in normal tissues in hypercalcemic states

Cellular Aging

Many cell functions decline, and morphologic changes occur with aging. Aging is thought to be influenced by an intrinsic molecular program, called the "programmed aging hypothesis." It states that sequential shortening of telomeres (the natural ends of chromosomes) may lead to loss of genes, causing cellular aging. 

Aging is also thought to be influenced by cumulative effects of various extrinsic factors. Progressive effects of free radical damage throughout life may be an important factor in cellular aging. Free radicals can induce damage to mitochondria and DNA.

Digital Legends for Labs
Lab 1 | Lab 2 | Lab 3 | Lab 4 | Lab 5 | Lab 6 | Lab 6b | Lab 7 | Lab 8 | Lab 9 | Lab 9b | Lab10 |
Lab 10b | Lab11 | Lab 12 | Lab 13 | Lab 14 | Lab 15 | Lab 15b | Lab 16 | Lab 16b | Lab 17 |

Lab 18

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Updated September 5, 2007