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Document Text Contents
Page 1

Intracellular accumulations; calcifications3. Metabolic alterations, genetic or acquired

Cellular aging4. Prolonged life span with cumulative sublethal injury

Subcellular alterations in various organellesMild chronic injury

Irreversible injury  cell death (necrosis, apoptosis)Progressive and severe (incl. DNA damage)

Acute reversible injuryAcute and self-limited

Cell Injury2. Reduced O2; Chemical Injury; Microbial Infection

MetaplasiaChronic irritation (chemical or physical)

AtrophyDecreased nutrients, stimulation

Hyperplasia, hypertrophyIncreased demand, trophic stimulation

Cellular Adaptations1. Altered Physiologic Stimuli

Cellular ResponseNature and Severity of Injurious Stimuli

Figure 1-1

Page 2

1. Physiologic

• Hormonal
• Compensatory

2. Pathologic
• Excessive hormonal stimulation
or GFs
• Fertile soil for cancer

1. Physiologic

• Functional demand
• Specific hormonal stimulation

2. Pathologic
3. Genes that induce hypertrophy

a. Genes that encode transcription factors
c-fos; c-jun

b. Growth factors

c. Vasoactive agent
α-adrenergic agonist; endothelin-1;

angiotensin II

Atrophy (Physiologic or Pathologic)
1. Decreased workload
2. Loss of innervation
3. Diminished blood supply
4. Inadequate nutrition
5. Loss of endocrine stimulation
6. Aging (senile atrophy)
7. Pressure

1. Reversible change
2. Most common = columnar to squamous
3. Vitamin A deficiency
4. May induce malignant transformation

Figure 1-4

Page 9

Figure 1-15

Defects in Membrane Permeability Result In:

1. Mitochondrial dysfunction
2. Loss of membrane phospholipids
3. Cytoskeletal abnormalities
4. Reactive oxygen species
5. Lipid breakdown products  detergent effect on membranes

1. Injury to lysosomal membranes results in
leakage of their enzymes into the cytoplasm
and activation of these enzymes

2. Lysosomes contain:
- RNases
- DNases
- proteases
- phosphatases
- glucosidases
- cathepsins

3. Activation of enzymes leads to enzymatic
digestion of cell components

Page 10

Figure 1-17 Morphologic changes in reversible and irreversible cell injury.
A, Electron micrograph of a normal epithelial cell of the proximal kidney tubule. Note abundant microvilli (mv) lining the lumen (L). N, nucleus; V, apical vacuoles (which
are normal structures in this cell type).

B, Epithelial cell of the proximal tubule showing reversible ischemic changes. The microvilli (mv) are lost and have been incorporated in apical cytoplasm; blebs have
formed and are extruded in the lumen (L). Mitochondria are slightly dilated. (Compare with A.)

C, Proximal tubular cell showing irreversible ischemic injury. Note the markedly swollen mitochondria containing amorphous densities, disrupted cell membranes, and
dense pyknotic nucleus. (Courtesy of Dr. M.A. Venkatachalam, University of Texas, San Antonio, TX.)

Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 1 March 2005 09:25 PM)
© 2005 Elsevier

Figure 1-17

Two phenomena consistently characterize irreversibility:
1. Inability to reverse mitochondrial dysfunction
2. Development of profound disturbances in membrane

Histological Reversible Cell Injury:
1. Cellular swelling
2. Fatty change

Ultrastructural Reversible Cell Injury:
1. Plasma membrane alterations
- blebbing, blunting, distortion of microvilli, creation of
myelin figures, loosening of intercellular attachments
2. Mitochondrial changes
- swelling, rarefaction, small amorphous densities
3. Dilation of the ER
- detachment and disaggregation of polysomes
4. Nuclear alterations
- disaggregation of granular and fibrillar elements

Page 17

Figure 1-35

Intracellular accumulation of abnormal amounts of substances:
1. a normal cellular constituent accumulates
2. an abnormal substance –exogenous or endogenous
3. a pigment

Three types of abnormalities:
1. normal endogenous substance; rate of metabolism is inadequate
2. normal or abnormal endogenous substance accumulates; genetic
or acquired defect in metabolism, packing, transport, secretion
3. abnormal exogenous substance is deposited and accumulates

Types of Accumulations:
1. Lipids
- steatosis and fatty change (LIVER, HEART, MUSCLE, KIDNEY)
- cholesterol and cholesterol esters (atherosclerosis, xanthomas,
inflammation and necrosis, cholesterolosis, Niemann-Pick disease type C
2. Proteins
- reabsorption droplets in PCT kidneys
- synthesis of excessive amounts
- defects in protein folding  may lead to “unfolded protein response”
3. Hyaline change
4. Glycogen
- glycogen storage diseases
- DM
5. Pigments
- exogenous pigments (carbon, tattoo)
- endogenous pigments (lipofuscin, melanin, hemosiderin)

**Systemic overload of iron, hemosiderin is deposited in many organs and tissues;
a condition called hemosiderosis and is seen with:
1. increased absorption of dietary iron
2. impaired use of iron
3. hemolytic anemias
4. transfusions

Page 18

Figure 1-43

Pathologic Calcification
1. Dystrophic calcification –occurs locally in dying tissues; NORMAL serum Ca++ levels

2. Metastatic calcification – occurs in normal tissues; almost always results from HYPERCALCEMIA
- increased secretion of PTH
- destruction of bone tissue
- vitamin D-related disorders
- renal failure

Metastatic calcification occurs in the following:
1. Gastric mucosa
2. Kidneys
3. Lungs
4. Systemic arteries
5. Pulmonary veins

Cellular Aging
1. Telomere shortening utimately
results in cell cycle arrest
2. Telomerase = lengthens the telomeres
by nucleotide addition

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