lOMoARcPSD|8199574

Cellular Adaptation. Injury, and Death

Pathophysiology (Nova Southeastern University)

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 lOMoARcPSD|8199574

CHAPTER 3 Cellular Adaptation, Injury and Death

Cellular Adaptation
 Cells adapt to changes in the internal environment when confronted with
stresses that endanger normal structure and function
 Cells adapt to increased work demands by changing in
 Size (atrophy and hypertrophy)
 Number (hyperplasia)
 Form or type (metaplasia)
 Adaptive changes also include
 Intracellular accumulations
 Storage of products in abnormal amounts
o Atrophy
 Decrease in cell size→
 Decrease in work demands
 Adverse environmental conditions
EX: Menopause, when a person losses hormonal
stimulation, a cell reverts to a smaller size and a lower and
more efficient level for survival
EX: Endometrium
 Causes (5 Categories)
 Disuse: Occurs when there is a reduction in
skeletal muscle use
o Ex: Plaster casts, b/c Atrophy is adaptive
& Reversible
 Denervation: A form of disused atrophy that
occurs in paralyzed limbs
 Loss of endocrine stimulation
 Inadequate nutrition
 Ischemia or decreased blood flow
Ischemia: Decrease amount of blood flow. IT IS
REVERSABLE, if not fixed in time it could lead to Necrosis
(when cells die, and it is no longer reversible)
o Hypertrophy
 Increase in cell size & functioning tissue mass
 Increased workload (cardiac/skeletal muscle)
 Disease conditions (compensatory or pathologic)
 Cellular Changes
“Hypertrophy may occur as the result of normal
physiologic or abnormal pathologic conditions. The
increase in muscle mass associated with exercise is an
example of physiologic hypertrophy. Pathologic
hypertrophy occurs as the result of disease conditions and
may be adaptive or compensatory.”
Adaptive hypertrophy is the thickening of the urinary
bladder from long-continued obstruction of urinary outflow”

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CHAPTER 3 Cellular Adaptation, Injury and Death

Compensatory: EX: When you take out a liver, or kidney

the other one gets bigger b/c it has to work harder
KNOW DIFF B/W BOTH
o Hyperplasia
 Increase in the number of cells in an organ or tissue
 Occurs in tissues with cells capable of mitotic
division
 Activation of genes which cause replication (?)
 Physiologic or nonphysiologic
“There are two common types of
physiologic hyperplasia: hormonal and compensatory.”
Compensatory: Liver Regeneration

o Metaplasia
 Reversible change in which one adult cell type is replaced by another
adult cell type
 Epithelial
 Mesenchymal
 Chronic irritation, inflammation
One cell type replaces another, they reprogram. Happens
w/ some type of chronic Dx. Ex. oSmoking (Doesn’t
change cell type, still epithelium cell)
o Dysplasia
 Deranged cell growth
 Cells vary in size, shape and organization
 Chronic irritation/inflammation
Drainage, cells start to look very
drained, different. It is potentially
reversible, it’s abnormal but it’s
considered adaptive, strongly indication
as a cancer precursor. BUT IT IS NOT
CANCER!!
Ex: Cervical Dysplasia: Not cancer but
must be monitored
Adaptive and Reversable
o Intracellular Accumulations
 Buildup of substances which cell can’t eliminate or use immediatelyThree
 Normal Body Substances
Lipids, proteins, carbohydrates, melanin, etc.
 Abnormal Endogenous Products
Those resulting from inborn errors of metabolism
 Exogenous Products
Environmental agents and pigments not broken down by
the cell
Question

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CHAPTER 3 Cellular Adaptation, Injury and Death

o Which of the following best describes the cellular adaptation seen in chronic
cigarette smokers?
 A. Atrophy
 B. Hypertrophy
 C. Hyperplasia
 D. Metaplasia
 E. Dysplasia
 Rationale: As cells are damaged, a hardier version replaces the
normal strata of cells.
Pathologic Calcifications
o Definition
 Abnormal tissue deposition of calcium salts, together with smaller
amounts of iron, magnesium, and other minerals
o Types
 Dystrophic calcification
 occurs in dead or dying tissue
 Metastatic calcification
 occurs in normal tissue as a result of elevated Ca levels
KNOW Diff b/w both is that Dystrophic only occurs in
injured tissue, whereas Metastatic occurs in normal tissues
as the result of increased Ca levels (hypercalcemia)
Question
o Is the following statement true or false?
 Dystrophic calcification can result from prolonged ischemia
True, Rationale stresses the tissue, it dies, and calcium
precipitates out of solution.
Causes of Cell Injury
o Injury from Physical Agents
 Mechanical forces: Body Impact w/ another object
 Extremes of temperature
 Electrical forces
o Radiation Injury
 Ionizing radiation
 Ultraviolet radiation
 Nonionizing radiation
o Chemical Injury
 Drugs
 Carbon tetrachloride
 Lead toxicity
 Mercury
o Injury from Biologic Agents
 Virus, parasites, bacteria
o Injury from Nutritional Imbalances
 Excesses and deficiencies
 EX: Obesity & extreme diet
Thermal Injury

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CHAPTER 3 Cellular Adaptation, Injury and Death

Mechanisms of Cell Injury

o Free radical and reactive oxygen species (ROS) formation
 Free radicals are highly reactive chemical species; having an unpaired
electron causes them to be unstable and highly reactive.
o Free radical injury
 Lipid peroxidation
 Oxidative modification of proteins
 DNA effects
Hypoxic Cell Injury
o Deprives cell of oxygen and interrupts oxidative metabolism and the generation
of ATP
 Acute cellular swelling (edema)
o The longer tissue is hypoxic, the greater chance of irreversible cellular injury
o Causes of hypoxia
 Inadequate amount of oxygen in the air
 Respiratory disease
 Inability of the cells to use oxygen
 Edema
 Ischemia
Impaired Calcium Homeostasis
o Calcium functions as an important second messenger and cytosolic signal for
many cell responses.
o Cytosolic calcium levels are kept low by energetic mechanisms.
 Ischemia-induced calcium disruption
 Inappropriate activation of enzymes
Calcified Aortic Stenosis

Question
o Which of the following can result in membrane damage?
 A. Inactivation of Na+/K+ ATPase
 B. Oxidation of phospholipid
 C. Ischemic activation of Ca2+-regulated protease
 D. All the above
 E. None of the above
 Rationale: Each of these can result in membrane damage
Programmed Cell Death
o Number of cells in tissues regulated by cell proliferation balanced with cell death
 This process eliminates cells that
 Are worn out
 Have been produced in excess
 Have developed improperly
 Have genetic damage
o Cell death occurs via→
 Necrosis

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CHAPTER 3 Cellular Adaptation, Injury and Death

“Necrosis differs from apoptosis because it causes loss of

cell membrane integrity and enzymatic breakdown of cell
parts and triggers the inflammatory process.1 In contrast to
apoptosis, which functions in removing cells so new cells
can replace them”
 Apoptosis (programmed cell death)
“Is a highly selective process that eliminates injured and
aged cells, thereby controlling tissue regeneration”
EX: Menstrual cycle, after breast feeding
Reversible Cell Injury
o Impairs cell function but does not result in cell death
o Two patterns of reversible cell injury occur:
 Cellular swelling: impairment of the energy-dependent Na+/K+ ATPase
membrane pump, usually as the result of hypoxic cell injury.
 Fatty change: linked to intracellular accumulation of fat
Programmed Cell Death
o Necrosis
 Refers to cell death in an organ or tissues that is still part of a living
person
 Often interferes with cell replacement and tissue regeneration
o Gangrene
 The term gangrene is applied when a considerable mass of tissue
undergoes necrosis.
Gangrene
o Wet ( Moist) Gangrene
 Affected area
 cold, swollen, pulseless
 skin is moist, black, and under tension
 blebs form on the surface, liquefaction
occurs, and a foul odor is caused by
bacterial action.
 The spread of tissue damage is rapid
o Dry Gangrene
 Affected tissue
 dry and shrinks
 skin wrinkles and its color changes to dark
brown or black
Can affect internal organs
 The spread of dry gangrene is slow
“Dry gangrene usually results from interference with the
arterial blood supply” Mostly extremities

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