PATHOLOGY

1.01a Cellular Response to Stress and Toxic Insults, Part I

Socorro Cruz-Yanez, MD, FPSP | August 2, 2017

OUTLINE Concept of a multi-factorial basis for disease

Bronchogenic CA was thought to be caused solely by
I. Introduction cigarette smoking; rather, it was later found out that there are
A. Etiology inherent genetic factors, predispositions, and abnormal genes
B. Pathogenesis/Etiopathogenesis that can be associated with higher risk of cancer development of
C. Morphology the lung with exposure to carcinogens.
D. Functionals Derangements and
ClinicalManifestations
B. Pathogenesis/Etiopathogenesis
II. Cellular Adaptation
A. Hypertrophy Mechanism of disease formation
B. Hyperplasia Sequences of cellular, biochemical, genetic, physiological,
C. Atrophy immunological and molecular events following exposure of cells
D. Metaplasia or tissues to an injurious agent and subsequent alterations
III. Cell Injury and Cell Death leading to expression of the disease
A. Causes of Cell Injury Etiopathogenesis linking the cause to the mechanism
B. Important Targets of Cell Injury Etiology refers to WHY a disease ARISES
C. Mechanisms of Cell Injury Pathogenesis describes HOW a disease DEVELOPS
D. Morphology of Injured Cells
C. Morphology
OBJECTIVES: Structural alterations in damaged/injured cells, tissues and
Given a clinical situation, gross specimen, microscopic slide of a case organs as a result of injurious stimuli
with a problem representing lesions with reversible injury/ adaptive o May be subcellular in the form of molecular, biochemical,
change/ necrosis/ apoptosis; the student must be able to: genetic and structural alterations
Describe, discuss, differentiate & understand the terms o Often results in tissue change and/or organ alteration
Demonstrate knowledge and understanding of etio-
pathogenesis and pathophysiology of the disorder D. Functional Derangements and Clinical Manifestations
Describe its subcellular / gross / microscopic morphologic Overt signs and symptoms typically seen in a patient
characteristics including its bio-molecular alterations Functional consequences of the morphological changes
Correlate clinical presentation with the tissue changes o Clinical features of the disease:
Formulating possible clinical importance, outcomes and Signs and symptoms
consequences, complications Laboratory abnormalities
Legend: Clinical course, progression, outcome, complication
Supplementary Book Prognosis
Audio Recording Emphasized Notes
Information
The Study of Pathology
---------
Finding the cause (Etiology) Mechanism of disease formation
(Pathogenesis) Structural effects on the cell (Morphology)
I. INTRODUCTION Resulting clinical manifestations
Study of Pathology: study of suffering brought about by a disease A science that bridges the basic sciences to the clinical sciences
From the Greek word logo study of | pathos suffering Provides the scientific foundation for the practice of medicine
Rudolph Virchow Father of Modern Pathology (Pope of
Medicine)

What is Pathology?
A discipline involving the detailed study of underlying
changes in a cell; structural, biochemical, subcellular &
functional changes in cells/tissues/organs found under the
disease processes.

The Disease Processes

1. Etiology cause
2. Pathogenesis mechanism
3. Morphologic Changes structural alterations induced
4. Functional Derangements and Clinical Manifestations

A. Etiology Figure 1. The Spectrum of Disease Process of Atherosclerosis (PPT)

Cause of the disease
Branches of Pathology
Classes of etiologic factors:
o Intrinsic or genetic General Pathology
o Extrinsic environmental factors o Concerned with the basic reactions of cells and tissues to
Infectious Bacterial, viral or parasitic abnormal stimuli that underlie all diseases
Nutritional Deficiency or in excess of Systemic Pathology
Chemical Toxins or Poison o Concerned with how disease processes affect particular
Physical Thermal injury tissues and organs or organ systems

TRANSCRIBERS Piocnacia, Quero, Sie, Vitocruz EDITOR Tilbe (0925 545 2480) 1 of 8
 II. CELLULAR ADAPTATION Cellular Adaptation
Reversible changes in the number, size, phenotype, metabolic
activity, or functions of cells in response to changes in physiologic
or pathologic stress
o Atrophy
Decrease in cell size by the loss of cell substances
Decrease in metabolic activity to conserve energy
o Hypertrophy
Increase in cell size and size of organ
May be due to hormones or increase demand
Observed in non-dividing cells (stable cells/
permanent organs; i.e. heart, skeletal muscle)
o Hyperplasia
Increase in the cell number
Physiologic due to hormones or compensatory
mechanisms
Pathologic may possibly be indicative of
cancer
Figure 2. Stages of the cellular response to stress and injurious stimuli (PPT). o Metaplasia
Change in which one adult cell type (epithelial or
The normal cell maintains a steady state called homeostasis. mesenchymal) is replaced by another adult cell type
Adaptations are reversible responses to changes in physiologic states
and some pathologic stimuli, during which new but altered steady A. Hypertrophy
states are achieved, allowing the cell to survive and continue to Case Scenario
function. When the stress is eliminated, the cell can recover to its A 65-year-old male, known hypertensive with a BP ranging from 160-
original state without having suffered any harmful consequences. If 180 / 100-110 mmHg (normal BP 140/90) for the past 10 years. He
the limits of adaptive responses are exceeded or if cells are exposed feels easily tired upon exertion. A chest x-ray shows enlargement of
to injurious agents or stress, deprived of essential nutrients, or the left ventricle with the LV edge located at the anterior axillary line.
become compromised by mutations that affect essential cellular
constituents, a sequence of events follows that is termed cell injury. Key Elements
Cell injury is reversible up to a certain point, but if the stimulus persists
Elderly person
or is severe enough from the beginning, the cell suffers irreversible
10yrs Hx of Systolic & Diastolic HPN
injury and ultimately undergoes cell death.
Symptoms: Easy fatigability
Cellular Response to Stress and Noxious Stimuli Diagnostic tests: X-ray LV enlargement
Cellular adaptations
Diagnosis & Other Findings
Cell injury (damaged cells unable to adapt)
The patient developed left ventricular hypertrophy due to a long
o Reversible injury no permanent damage, cell is healed
period of sustained high blood pressure.
Mild, transient, small dosages
o Irreversible injury too severe, progressive cell death When seen grossly:
Necrosis always pathologic o LV is enlarged, the dimensions are thick
All the cells/organs of a dead patient are necrotic

o Interventricular septum is prominent
Apoptosis physiologic (programmed cell death) o Coronal section: concentric hypertrophy
Cellular accumulation Observed in tissues incapable of cell division
Why not hyperplasia? Striated muscle cells in the heart and
Cellular aging
skeletal muscles only have a limited capacity for division,
and respond mainly by undergoing hypertrophy to
compensate for the added workload increased production
of cellular proteins.

Figure 3. Cellular Responses to Injury (PPT).

Figure 4. Left ventricular hypertrophy in Hypertensive Heart: Gross (PPT)

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 Figure 6. Breast Histology: Physiologic Hyperplasia in Pregnancy.
The pointed structure shows increased number of mammary glands. (PPT)

Pathologic Hyperplasia may be due to:

Figure 5. Enlarged myocytes and nuclei in left ventricular hypertrophy (PPT) Excessive Hormonal Stimulation
o Benign Prostatic Hyperplasia: Excess androgen stimulation
Hypertrophy o Endometrial Hyperplasia: Excessive estrogen
Increased size & functional capacity in non-dividing cells due Hyperestrinism Endometrial Hyperplasia CA
to: These may be precursors to cancer; thus, premalignant
o Hormonal stimulation Although these forms of pathologic hyperplasias are abnormal,
o Increased functional demand the process remains controlled and the hyperplasia regresses if the
o Increased workload hormonal stimulation is eliminated.
Can be physiologic or pathologic
o Physiologic hypertrophy
Hormonal stimulation (e.g. breast and sex organs in
puberty or pregnant uterus)
Increased functional demand due to exercise
o Pathologic hypertrophy
Abnormal hormone levels (e.g., goiter)
Increased functional demand of abnormal situations
(e.g., LVH in HPN)

B. Hyperplasia
Increased number of cells which leads to increased volume,
size, and weight of organ or tissue
Associated with increased DNA synthesis and increased mitotic
division
Can occur together with hypertrophy and also results in an
Figure 7. Endometrial (L) and Benign Prostatic Hyperplasia (R) Histology.
enlarged organ
There is an increased number of glands. (PPT)
Result of growth factor-driven proliferation of mature cells and, in
some cases, by increased output of new cells from tissue cells.
Like hypertrophy, it can also be physiologic or pathologic Effect of growth factors on target organs
o Mitogenic factors Hyperplasia in Wound Healing
o Papilloma virus Skin Wart
Physiologic Hyperplasia
Hormonal Hyperplasia
Hypertrophy vs. Hyperplasia
o Effect of hormonal stimulation
o Ex: Increased breast size in puberty and pregnancy; Uterine Both result in enlargement of the tissue/organ
enlargement in pregnancy Both can occur together and may be triggered by the
Increases the functional capacity of a tissue when needed same stimulus
Compensatory Hyperplasia Both may be physiologic or pathologic
o Increased tissue mass after damage or partial resection
o Ex: Liver and kidney enlargement after partial hepatectomy Hypertrophy increases the cell size of non-dividing cells
and unilateral nephrectomy via transforming growth factor Hyperplasia increases the cell number of actively dividing cells
alpha (counteracted by TGF-beta)
o After restoration of the organ mass, cell proliferation is
turned off by inhibitors. The hyperplastic process remains
controlled. If the signal that initiate it abate, the hyperplasia
disappears.

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C. Atrophy
Decreased size, number of cells, weight of organ and
reduced organ function
Metabolic processes shut down to conserve energy

Physiologic Atrophy
Physiologic atrophy is common during normal development.
o Ex: Thymic atrophy, decrease in the size of the uterus that
occurs shortly after giving birth
Some embryonic structures, such as the notochord and
thyroglossal duct, undergo atrophy during fetal development.
Figure 9: Mammary Lobules in Aging (L), Muscle Atrophy (R). (PPT)
Pathologic Atrophy
Decrease workload (Disuse Atrophy) Atrophy vs. Hypoplasia
o Illustrated when lying down for 6 months due to spine
surgery which leads to shrinkage of muscle Hypoplasia Incomplete development of an organ so that it fails
With more prolonged disuse, skeletal muscle fibers decrease to reach adult size; this is NOT an adaptive response
in number (due to apoptosis) as well as in size. Muscle atrophy Atrophy the organ developed into its full adult size but
can be accompanied by increased bone resorption, leading to decreased in size/function due to noxious stimuli
osteoporosis of disuse.
Loss of Innervation (Denervation Atrophy)
o Damage to the nerves leads to atrophy of the muscle fibers
supplied by those nerves
Decreased Blood Supply
o A gradual decrease in blood supply (ischemia) to a tissue
as a result of slowly developing arterial occlusive disease
results in atrophy of the tissue.
o In late adult life, the brain may undergo progressive
atrophy, mainly because of reduced blood supply as a
result of atherosclerosis. This is called senile atrophy,
which also affects the heart.
Inadequate Nutrition
o Muscle mass is lesser when malnourished, as seen in
protein-calorie malnutrition (marasmus) and cachexia.
Loss of Endocrine Stimulation
o The loss of estrogen stimulation after menopause results in
physiologic atrophy of the endometrium, vaginal epithelium, Figure 10. Hypoplastic Kidney. It is difficult to distinguish between hypoplasia
and breast. and atrophy unless you examine the specimens under the microscope. (PPT)
Pressure Atrophy
Tissue compression for any length of time can cause D. Metaplasia
atrophy. An enlarging benign tumor can cause atrophy in the
surrounding uninvolved tissues. Atrophy in this setting is probably Reversible transformation or replacement of one adult cell
the result of ischemic changes caused by the compromise of type to another adult cell type
blood supply by the pressure exerted by the expanding mass. Examples
o Cervix: from columnar (mucin type) squamous due to
chronic irritation = squamous metaplasia
o Barretts Esophagitis: squamous columnar in order to
adapt to the change in pH in the esophagus due to the
reflux of the gastric juices = intestinal metaplasia
o Chronic Smokers: From columnar ciliated to squamous
cells in the bronchus due to chronic irritation
Mechanism: Metaplastic cells arise from undifferentiated cells
beneath the epithelial lining which can differentiate into
squamous or columnar cells for adaptation.
Metaplasia does not result from a change in the phenotype of an
already differentiated cell type; instead it is the result of a
reprogramming of stem cells that are known to exist in normal
tissues, or of undifferentiated mesenchymal cells present in
connective tissue. In a metaplastic change, these precursor cells
differentiate along a new pathway.
The most common epithelial metaplasia is columnar to
Figure 8. Normal Biceps and Atrophied Biceps (PPT). squamous which occurs in the respiratory tract in response to
chronic irritation.

1.01a Cellular Response to Stress and Toxic Insults, Part I 4 of 8

 Figure 13. Dysplasia (PPT)

Table 1. Summary of Cellular Adaptations

Adaptation Mechanism Usually Examples
due to:
Hypertrophy Increase cell Increased Physio: Muscle
size workload exercise
Patho: goiter, LVH
Figure 11. Mechanism of Metaplasia (PPT). Hyperplasia Increase Hormones Physio: Hormones in
Causes number of & other puberty,
o Chronic irritation cells growth compensation due to
o Vit. A Deficiency factors partial resection
Reversible Patho: Prostate and
May precede the development in cancer in some instances endometrial
May arise from reprogramming of stem or undifferentiated cells hyperplasia
that are present in adult tissue. Atrophy Decrease Disuse, Physio: thymic
size/ organ denervation, atrophy
function decreased Patho: Alzheimers,
nutrients senile atrophy
Metaplasia Reversible Chronic Chronic cervicitis,
transformation irritation Barretts esophagus
of one adult
cell type to
another

III. CELL INJURY AND CELL DEATH

Results when cells are stressed so severely that they are no
longer able to adapt or when cells are exposed to damaging
agents
Cell injury can be reversible or irreversible

Figure 12. Barretts esophagus. (PPT) Table 2. Cellular Changes in Injury

Reversible Irreversible
Cellular swelling Lysosome rupture
Cell membrane blebs Cell membrane rupture
Detached ribosomes Dense bodies in mitochondria
Chromatin clumping Karyolysis, karyorrhexis, pyknosis

Karyolysis nucleus dissolves

Karyorrhexis nucleus ruptures
Pyknosis nucleus shrinks into an amorphous, dark blue mass

A. Causes of Cell Injury

1. Oxygen Deprivation (Hypoxia)
Causes:
o Cardio-respiratory insufficiency/ failure
o Reduced blood flow/ ischemia (most common)
Figure 13. Barretts Esophagus Histology. Notice the change from normal Ischemia: The loss of blood supply in a tissue
esophageal squamous mucosa (orange) to columnar intestinal glands (black). due to impeded arterial flow or reduced venous
(PPT) drainage.
o Loss of the oxygen-carrying capacity of the blood;
Dysplasia ex: Anemia or Carbon Monoxide poisoning
Should be differentiated/not be confused with metaplasia 2. Physical Agents
Atypical proliferative changes due to chronic irritation or Mechanical trauma,
inflammation Extremes of temperature: Burns, Deep cold
Premalignant change high risk for cancer Sudden changes in atmospheric pressure

1.01a Cellular Response to Stress and Toxic Insults, Part I 5 of 8

 Radiation, and electric shock of polysomes reduced protein synthesis.
Mechanism: Proteins may become misfolded unfolded protein
o direct irreversible tissue injury cell membrane response cell injury/death
disruption cell organelles breakdown
3. Chemical Agents and Drugs
Oxygen, in high concentrations (high partial pressure)
Poisons: arsenic, cyanide, Hg
o Interfere with cellular metabolism and reduced ATP
Environmental and air pollutants
Insecticides, herbicides, industrial and occupational
hazards
Alcohol
Therapeutic drugs and drugs of abuse
4. Infectious Agents
Bacteria
Fungi
Viruses
Parasites
5. Immunologic Reactions
Anaphylaxis
Hypersensitivity
Autoimmune
Mechanism:
o Inflammatory mediators such as interferons and
interleukins alters gene expression and cellular
metabolism.
o Complement activation direct attack on a cell
membrane
o Cytotoxic T-cells and NK cells direct attack on Figure 14. The functional and morphologic consequences of
target cells & initiate the self-destruct cascade intracellular ATP depletion. (Robbins)
within a target cell.
6. Genetic Derangements
Mitochondrial Damage
Chromosomal abnormalities, congenital malformations. o Causes
Ex: Downs syndrome Hypoxia, Toxins
Deficiency of proteins, deficiency of enzymes, inborn Increase cytosolic Ca2+
errors of metabolism Oxidative stress
7. Nutritional Imbalances Lipid breakdown product
Dietary insufficiency (major cause) o This is the key determinant of cell death
Ex: Protein-calorie malnutrition; vitamin/mineral If the mitochondria is damaged, this is the first
deficiency indication of irreversibility of injury. This is the point of
Dietary excess (predisposed to atherosclerosis) no return.
Ex: Obesity o Damage results to formation of a high conductance channel
called the mitochondrial permeability transition pore
B. Important Targets of Cell Injury loss of membrane potential failure of oxidative
These are the most vulnerable parts of the cell. phosphorylation ATP depletion, formation of reactive
Aerobic respiration: oxygen species (ROS), leakage of cytochrome c and
o ATP depletion or decreased synthesis. other pre-apoptotic proteins like caspases
Cell membranes (plasma membranes, mitochondrial, lysosomal
and other organelle membranes)
Protein synthesis
Cytoskeleton
Genetic apparatus

C. Mechanisms of Cell Injury

Depletion of ATP
o Underlying cause: hypoxia, ischemia, exposure to chemical
substance
Reduced activity of Na+/ K+-ATPase Na+ enters and
accumulates in the cell and K+ dissolves out isosmotic gain of
water cell swelling because of water and sodium inflow
ATP AMP Increased anaerobic glycolysis rapid
depletion of glycogen stores and accumulation of lactic acid
reduces intracellular pH reduces activity of cellular enzymes;
clumping of nuclear chromatin
With prolonged or worsening depletion of ATP, structural
disruption of the protein synthetic apparatus occurs
Figure 15. Role of mitochondria in cell injury and death (Robbins)
detachment of ribosomes from the rough ER and dissociation

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 Influx of Intracellular Ca2+ and Loss of Ca2+ Homeostasis Protein damage oxidation of AA, protein
o Calcium ions are important mediators of cell injury fragmentation, formation of protein-protein cross
o Normally, most intracellular calcium is sequestered in linkages (i.e., disulfide bonds)
mitochondria and the ER Lesions in the DNA
To help protect cells from injury, cytosolic free calcium is
normally maintained at very low concentrations (~0.1 mol)
compared with extracellular levels which are 15x higher
Ischemia and certain toxins cause an increase in cytosolic
calcium concentration
Initially because of release of Ca2+ from mitochondria
and ER
Later due to increased influx across the plasma
membrane
Increased intracellular Ca2+ causes cell injury by several
mechanisms: Figure 17. The generation, removal, and role of ROS in cell injury.
Ca2+ accumulates in mitochondria opening of the
mitochondrial permeability transition pore ATP Defects in Membrane Permeability
intracellular Ca2+ activates phospholipases, o Early loss of selective membrane permeability, leading
proteases, endonucleases, and ATPases ultimately to overt membrane damage, is a consistent
Induction of apoptosis by: (1) direct activation of feature of most forms of cell injury (except apoptosis)
caspases and (2) increasing mitochondrial Mechanisms of membrane damage
permeability ATP depletion
Calcium-mediated activation of phospholipases
Direct damage by various bacterial toxins, viral
proteins, lytic complement components
Physical and chemical agents
Biochemical mechanisms:
Reactive oxygen species
Decreased phospholipid synthesis
(leading to ATP production)
Increased phospholipid breakdown
Cytoskeletal abnormalities (due to
activation of proteases by Ca2+)

Figure 16. The role of increased cytosolic calcium in cell injury (Robbins).

Accumulation of Oxygen-Derived Free Radicals (Oxidative

stress) Figure 18. Mechanisms of membrane damage in cell injury.
o Highly reactive species that have a single unpaired electron
in an outer orbit Consequences of Membrane Damage
o Produced normally during mitochondrial respiration and Mitochondrial membrane damage ATP, release
energy generation, but are degraded and removed by of proteins that trigger apoptosis
cellular defense systems Plasma membrane damage loss of osmotic
o Anti - Free Radicals: balance, influx of fluids and ions, loss of cellular
Antioxidants (block initiation and inactivate ROS) contents, ATP
Vitamins C, E, A; glutathione Lysosomal membrane damage enzymatic digestion
Binding of iron and copper through transport and of proteins, RNA, DNA, and glycogen necrosis
storage proteins (transferrin, ferritin, lactoferrin,
ceruloplasmin)
IV. MORPHOLOGY OF INJURED CELLS
Enzymes catalase, superoxide dismutase,
glutathione peroxidase Reversible Injuries (non-lethal)
o production and/or scavenging of ROS (superoxide, OH o Cellular swelling
radicals, H2O2, etc.) oxidative stress o Fatty Change
o Pathologic effects of ROS: Irreversible Injuries (lethal) lead to cell death/necrosis
Lipid peroxidation in membranes

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 2. This poor medical student is also a chronic smoker. Which of the
following best describes the mechanism of the cellular adaptation
that the affected organ will undergo?
a. The lung epithelium will undergo uncontrolled
proliferation due to chronic irritation
b. Stem cells from the columnar epithelial lining will
differentiate into squamous cells for adaptation
c. The differentiated columnar epithelial cells will gradually
shift to become squamous epithelium
d. All of the above
e. B and C
3. The damage to the poor medical students lung tissue becomes
extensive that the injury to the tissue becomes irreversible. Which
of the following would most probably be evident in the medical
students lung tissues?
a. Cell membrane blebs
Figure 20. Continuum of morphologic changes in Renal Tubular Epithelium in b. Detached ribosomes
reversible and irreversible cell injury. (A) Normal: Cell outlines and nuclei are c. Chromatin clumping
well-defined; cytoplasm is well visualized. (B) Cellular Swelling which is a form d. Dense bodies in mitochondria
of reversible injury: cytoplasm appears hazy because of water, nuclei remain e. Cellular swelling
well-defined (C) Acute Tubular Necrosis which is a form of irreversible injury: 4. Smoking, in this case, is considered the __________ of the
nuclei shrunken and not well-defined, chromatin appear clumped (PPT and disease.
Audio Record) a. Etiology
b. Pathogenesis
c. Morphological alteration
d. Clinical manifestation
5. Which of the following pairs is CORRECTLY matched?
a. Physiologic atrophy: Failure of the Thymus to develop
b. Hypoplasia: Regression of the thyroglossal duct
c. Physiologic hyperplasia: Benign Prostatic Hyperplasia
d. Pathologic hyperplasia: Skin Wart due to Papilloma
virus
e. Pathologic hypertrophy: Breast development in puberty
6. Injury to the cell will cause which of the following ion imbalances?
a. Na+, Ca2+ intracellularly; K+ extracellularly
b. Na+ intracellularly; Ca2+, K+ extracellularly
c. Na+, Ca2+ intracellularly; K+ extracellularly
d. Na+ intracellularly; Ca2+, K+ extracellularly
e. Na+, Ca2+ intracellularly; K+ extracellularly
7. Depletion of ATP in an injured cell will lead to the following
EXCEPT
a. Decrease in glycogen
b. Increase in pH
c. Decrease protein synthesis
d. Clumping of nuclear chromatin
e. Increase in AMP
8. Which of the following best indicates that the cell is about to die?
Figure 21. Sequential development of biochemical and morphologic changes in a. Depletion of ATP
cell injury. Cells may become rapidly nonfunctional after the onset of injury, b. Accumulation of ROS
although they may still be viable, with potentially reversible damage; a longer c. Mitochondrial damage
duration of injury may lead to irreversible injury and cell death. Note that d. Chromatin clumping
irreversible biochemical alterations may cause cell death, and typically this e. Cellular atrophy
precedes ultrastructural, light microscopic, and grossly visible morphologic 9. A 63-year-old male experienced severe chest pain. EKG and
changes (Robbins). lab studies indicates MI. The irreversible injury of the cardiac
muscle would occur in the presence of which cellular change?
REFERENCES a. Depletion of glycogen stores
1. Robbins 3. Audio Recording b. Increase of intra-cytoplasmic Na+ levels
2. Lecture Notes 4. Yanez PPT c. Karyorrhexis of nuclei
d. Reduction of intracellular pH levels
QUIZ
10. Which of the following is an effect of ROS accumulation?
1. A poor medical student decides to sell his left kidney to the black a. Cross-linking of DNA strands
market so that he can afford a ticket to the Coldplay concert. b. Protein misfolding
Which of the following cellular adaptations will most likely occur to c. Lipid peroxidation
the right kidney? d. All of the above
a. Physiologic Hyperplasia
b. Pathologic Hyperplasia
c. Pathologic Hypertrophy Answer key: 1a, 2b, 3d, 4a, 5d, 6e, 7b, 8c, 9c, 10d
d. Physiologic Atrophy
e. B and C

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