HISTOPATH LEC (MODULE 2) stimuli, during which new but altered steady

states are achieved, allowing the cell to survive

Cellular Adaptations, Cellular Injury and Cell and continue to function.
Death
 Cellular response to cell injury
Cell injury occurs for many reasons. Some
represent spontaneous alterations in the ability CELL INJURY:
of a cell to proliferate and function normally,
 Irreversible – if reversible injury progress
and in other cases, disease results when external
this may lead to cell death, severe
stimuli produce changes in the cell's
progressive
environment that make it impossible for the cell
o Cell death – either by necrosis or
to maintain homeostasis. In such situations, cells
apoptosis
must adapt to the new environment. These
adaptations include hyperplasia, hypertrophy,
atrophy, and metaplasia which can be classified
as physiologic or pathologic depending upon
whether the stimulus is normal or abnormal. A
cell can adapt to a certain point, but if the
stimulus continues beyond that point, failure of
the cell, and hence the organ, can result. If cells
cannot adapt to the pathologic stimulus, they
can die.
 Reversible – once the stimulus is remove
the cell may be back to normal or may
return to homeostasis, mild, transient

Cell Death - This refers to an end result of

progressive cell injury.
Homeostasis - Characteristic of cell being in
a steady state. This may also refer to absence of CAUSES OF CELL INJURY
cell injury brought about by stress or injurious
1. Oxygen deprivation of cells/Hypoxia -
agent.
decreased partial pressure of oxygen in
 Steady state – equilibrium, characteristic blood, reduction in aerobic oxidative
of the cell being in balance, absence of respiration of the cell
cell injury, the cell is normal a. Ischemia – reduce blood flow to a
particular tissue/organ
Cell injury- This refers to exposure of cells to b. Cardio respiratory failure
stress or injurious agent causing injury to cell c. Carbon monoxide poisoning in
and disruption of cell's homeostasis. cases of anemia
Once cell is expose to stress or injury stimuli 2. Chemicals, drugs, toxins
there is only 2 outcomes: a. glucose, salt in hypertonic
solution could result to cellular
 Adapt injury
 Development of cellular injury b. air pollutants (asbestos,
insecticides, herbicides, oxides)
Cell Adaptation - reversible functional and
c. mercury, recreational drugs such
structural responses to changes in physiologic
as alcohol
states (e.g., pregnancy) and some pathologic
d. carbon monoxide
 3. Microbiologic/Infectious agents  Programed destruction of
a. bacteria, viruses, fungi, parasites cells during embryogenesis
4. Physical agents  Hormone-dependent
a. Mechanical trauma (nauntog, involution in aging
nadulas)  Cell deletion in
b. Extreme temperature changes proliferating cell
(extreme heat and cold) populations
c. Sudden changes in atmospheric  Death of host cells that
pressure (radiation, electric have served its purpose
shock)  Elimination of potentially
5. Immunologic reactions harmful self-reactive
a. autoimmune diseases lymphocytes
b. immune reactions to external  Cell death induced by
agents such as viruses, cytotoxic T cells
environmental substances  Necrosis - “accidental” and unregulated
6. Genetic defects/derangement form of cell death resulting from damage
a. enzyme defects in cases of inborn to cell membranes and loss of ion
errors of metabolism homeostasis. Sum of all the morphologic
b. deficiency in proteins changes that follow after cell death. The
c. defect in DNA sequence morphologic appearance of necrosis is
d. accumulation of damage DNA the result of denaturation of intercellular
e. errors in chromosome proteins and enzyme digestion of injured
7. Nutritional imbalance cell. Happens on pathologic conditions.
a. Severe vitamin deficiency o Liquefaction necrosis – result
b. Nutritional problems (anorexia from action of powerful hydrolytic
nervosa) enzymes which is characterized
c. Aging – normal process, paghina generally by digestion of dead
ng cells cells.
 best exemplified by brain
TARGETS OF INJURIOUS STIMULI
infarction (kinulang ng
1. Aerobic respiration – once aerobic oxygen supply ang brain)
respiration of the cell is disrupted or brought about by ischemic
targeted by particular stimuli expect destruction of brain tissue.
hypoxia to occur and eventually cellular  Common “pus”/nana or
damage/injury present of dead leukocyte
2. Integrity of cell membranes (creamy yellow material),
3. Protein synthesis abscess. Another example
4. Cytoskeletal system is suppurative appendicitis
5. Integrity of the genetic apparatus of the there is also presence of
cell – targets DNA and RNA pus.
o Coagulative necrosis – the
PATHWAYS/TYPES OF CELL DEATH
architecture of dead tissues is
 Apoptosis - refers to "programmed cell preserved for a span of at least
death", usually regulated but may also be few days. Results from total
pathogenic. occlusion of supplying vessels
o Tightly regulated intracellular especially in solid organs resulting
program whereby cells destined to to:
die activate enzymes that degrade  conversion of the cell to
the cell’s own nuclear DNA and acidophilic tombstone
nucleo-cytoplasmic protein.  loss of nucleus but cell
o Regulated cell death by the cells. architecture preserved
o Sometimes it can be pathologic  protein denaturation
(precipitation)
but most of the time it is normal
regulated type of cell death.  exemplified by myocardial
infarction leading to AMI
 o Enzymatic fat necrosis – size of cells, that results in an
destruction of fat resulting from increase in the size of the
abnormal release of enzymes affected organ
especially lipases o
 Exemplified by acute o Physiologic - caused by
pancreatitis increased functional
 Saponification: action of demand or by
lipase on fat results in stimulation by hormones
dissolution together with and growth factors (e.i.
hydroxyl ions (-OH) will enlargement of skeletal
produce soap with addition muscle during vigorous
of calcium will result in exercise, enlargement
formation of “chalky” of uterus during
material pregnancy)
o Caseous necrosis – combination of a. Hormonal –
liquefaction and coagulative estrogen
necrosis. Caseous means cheese stimulation of
like. uterus in
 only seen in tuberculosis pregnancy
process/infection b. Compensatory –
 characteristic “cheesy increased
appearance”, white friable functional
appearance on necrotic demand
area 1. If skeletal
 structureless, only
muscle is
composed of live cell and
overworked
amorphous granular debris
like pag
o Gangrenous necrosis – according
nag ggym
to robins’ it is not a specific
nalaki
pattern of cell death. However,
muscle
this is use in clinical practice.
2. Liver
Applied to describe a limb, lower
regeneratio
leg that has lost its blood supply.
n
Combination of liquefaction and
o Pathologic – due to
coagulative necrosis.
disease process, occurs
 2 types: dry & wet
due to an abnormal
 Depends on
stressor (e.i. increase in
predominance
the size of the heart due
necrosis
to aortic stenosis).
 Gangrene of the foot due
to diabetes mellitus is
a. excessive
classified as DRY.
hormonal
 Gangrene of loose organs, stimulation
e.g., appendix is classified b. viral-induced –
as WET. growth factors
produced by virus
PRINCIPLES AND CONCEPTS OR FOUR like papilloma
TYPES OF CELLULAR ADAPTATIONS viruses
Adaptations are reversible changes in the
size, number, phenotype, metabolic
activity, or functions of cells in response to
changes in their environment.

1. Hypertrophy – increase in size of

cells, refers to an increase in the
 o CAUSES OF ATROPHY:
a. Decreased workload –
also known as atrophy of
disuse
a. i.e., fractured
bones,
b. Loss of innervation –
loss of stimuli, also
known as denervation
atrophy
c. Diminished blood
supply – gradual
2. Hyperplasia - as an increase in the decrease in a blood
number of cells in an organ or supply particularly in the
tissue in response to a stimulus cases of ischemia this
o Physiologic- due to the could lead to a gradual
action of hormones or decrease of organ or
growth factors occurs in could also lead to
several circumstances atrophy – pag nagkaroon
(e.i. enlargement of ng decrease of blood
breast during puberty) supply sa tissue this
o Pathologic- most are could lead to arterial
caused by excessive or occlusive disease which
inappropriate actions of is common in late adult
hormones or growth life particularly in brain
factors acting on target d. Inadequate nutrition –
cells (e.i.  growth of skeletal muscles need
adrenal glands due to proteins as a source of
production of energy
adrenocorticotropic a. Can develop
hormone (ACTH) by a cachexia
pituitary adenoma). e. Loss of endocrine
3.  Atrophy – decrease in size cells, stimulation – concerned
defined as a reduction in the size with hormones, if wala
of an organ or tissue due to a ng hormones na mag
decrease in cell size and number. stimulate this could lead
o Results from decreased protein to gradual atrophy of
synthesis and increased protein organs
degradation in cells. Reduced a. Breast and
metabolic activity could lead to reproductive
decreased protein synthesis. organs
a. Ubiquitin-proteasome b. Loss of estrogen
pathway after menopause
a. Activates could result to
ubiquitin ligases atrophy of
b. Accelerated endometrium,
proteolysis vagina, vaginal
b. Accompanied by epithelium and
increased autophagy – breast
consumption of the f. Aging
body’s own tissue as g. Pressure/tissue
metabolic process compression
occurring in starvation a. Presence of
and certain disease, enlarged benign
more like cell eating
 tumor surrounding o Not an adaptive mechanism but
tissue a change for the worse
o Physiologic- common
during normal
development (e.i. 
atrophy of thyroglossal
duct during fetal
development)
o Pathologic - occurs due
to many causes (e.i. 
Decreased workload
(atrophy of disuse, Loss
of innervation
(denervation atrophy),
diminished blood
supply, inadequate
nutrition, aging, loss of
endocrine stimulation,
pressure)
4. Metaplasia – replace adult cell by
another type, refers to
a reversible change in which one
differentiated cell type (epithelial
or mesenchymal) is replaced by
another cell type (e.i. epithelial
metaplasia, change of normal
columnar epithelial cells to
squamous cells in the respiratory
tract)
o CAUSES OF METAPLASIA:
a. Persistent irritation
b. Infection
c. Malnutrition

5. (not a cell adaptation response,

only an addition) Dysplasia
o DERANGED DEVELOPMENT
a. Proliferation and
atypical cytologic
alterations
b. Change in size, shape
and organization