ADAPTATIONS,CELLULAR
INJURY AND DEATH
Richard K.D. Ephraim
ADAPTATIONS
• When a cell is exposed to stress
physiologic (pregnancy, exercise)
or pathologic (hypertension), it
undergoes a reversible functional
and structural response during
which new but altered steady
states are achieved allowing the
cell to survive and continue to
function.
HYPERTROPHY
• Hypertrophy refers to an increase in
the size of cells, that results in an
increase in the size of the affected
organ.
• The increased size of the cells is
due to the synthesis and assembly
of additional intracellular structural
components.
• Example, Cells that cannot multiply
– Muscles in body builder
– Cardiac muscles in hypertension
HYPERPLASIA
• Hyperplasia is defined as an
increase in the number of cells an
organ or tissue in response to a
stimuli.
• Physiologic
Female breast during pregnancy
Bone marrow in response to
supplements
Endometrium after menstruation
• Pathologic
Endometrium in response to
hormones
Hyperplasia of the prostrate
Epidermal hyperplasia (warts) in
response to a viral infection
ATROPHY
• Atrophy is defined as the reduction in the size of an organ
or tissue due to a decrease in cell size and number
• Physiologic
– Embryonic structures – notochord
– Thyroglossal duct
– Post partum uterus
• Pathologic
– Disuse atrophy
– Denervation atrophy
– Ischemic atrophy
– Loss of nutrition
– Loss of endocrine stimulation ( breast after menopause)
METAPLASIA
• Metaplasia is a reversible change in which one
differentiated cell type (epithelial or
mesenchymal) is replaced by another
differentiated cell type.
CELL INJURY
CELL INJURY
• Cell injury refers to any Causes of cell injury
damage or harm caused to 1. Hypoxia – lack of blood supply
or lack of oxygen
cells, which can disrupt 2. Physical agents – Heat ,
their normal functioning mechanical trauma
and potentially lead to cell 3. Chemical agents – glucose or
slat in higher concentrations,
death. poisons
• TYPES OF CELL INJURY 4. Microorganisms causing
infections
– Reversible cell injury 5. Autoimmunity
• Cells can recover from the 6. Genetic derangements-
damage id the cause is accumulation of damaged DNA
removed. can trigger apoptosis
7. Nutritional defects- Anorexia
– Irreversible cell injury nervosa, Atherosclerosis
• Cells cannot recover from the
damage if the cause is
removed leading to cell death.
MECHANISM OF CELL
INJURY
• The cellular response to injurious stimuli
depends on the type of injury, its
duration, and its severity
• The consequences of cell injury depend
on the type, state, and adaptability of
the injured cell
• Cell injury results from functional and
biochemical abnormalities in one or more
several essential cellular components
IRREVERSIBLE CELL INJURY
• NECROSIS – Irreversible cell death caused due
to denaturation of proteins and enzymatic
digestion of cell
• APOPTOSIS – Genetically programmed cell
death
MORPHOLOGY OF NECROSIS
• The morphology of necrosis can be
explained in the following tissue patterns
– Coagulative necrosis
– Liquefactive necrosis
– Gangrenous necrosis
– Fat necrosis
– Fibrinoid necrosis
COAGULATIVE NECROSIS
• Coagulative necrosis is a
form of necrosis in which the
architecture of dead tissues is
preserved
• The injury denatures not only
structural proteins but also
enzymes and so blocks the
proteolysis of the dead cells
• Cause is mainly ischemia
caused by obstruction in a
vessel
Liquefactive necrosis
• Liquefactive necrosis, in contrast to
coagulative necrosis is
characterized by the digestion of the
dead cells, sulting in the
transformation of the tissues into a
liquid viscous mass
• The necrotic material is frequently
creamy yellow because of the
presence of dead leukocytes and is
called PUS.
• Best example is necrosis in the
brain
GANGRENOUS NECROSIS
• It is a type of
coagulative necrosis
with superimposed
bacteria infection
• Best example is a limb,
generally the lower leg,
that has lost its blood
supply
CASEOUS NECROSIS
• Caseous necrosis is encountered most often in
foci of tuberculous infection
• The term “Caseous” (cheese like) is derived
from the friable white appearance of the area of
necrosis
FAT NECROSIS
• It refers to focal areas of fat destruction,
typically resulting from release of activated
pancreatic lipase into the substance of the
pancreas and the peritoneal cavity.
• This occurs in acute pancreatitis
FRIBINOID NECROSIS
• Fibrinoid necrosis is a special form of
necrosis usually seen in immune
reactions involving blood vessels
• This patterns of necrosis typically
occurs when complexes of antigens
and antibodies are deposited in the
walls of arteries
• Deposits of these “immune
complexes”, together with fibrin that
has leaked out of vessels, result in a
bright pink and amorphous
appearance in H&E stains, called
“fibrinoid” (fibrin-like) by pathologist.
APOPTOSIS
• Apoptosis occurs normally both during
development, throughout adulthood, and
serves to remove unwanted, aged or
potentially harmful cells.
– Physiologic apoptosis
– Pathologic apoptosis
PHYSIOLOGIC APOPTOSIS
• Examples of Physiological apoptosis
– Endometrial cell breakdown during the
menstrual cycle
– Ovarian follicular atresia in menopause
– The regression of the lactating breast after
weaning
– Prostatic atrophy after castration
PATHOLOGICAL APOPTOSIS
• DNA damage – Radiation, cytotoxic anticancer drugs, and
hypoxia can damage the DNA
• Accumulation of misfolded proteins – Improper folded
proteins may rise because of mutations. Excessive
accumulation of these proteins in the ER leads to condition
called ER stress
• Cell death in certain infection – Particularly viral infections.
An important host response to viruses consists of cytotoxic T
lymphocytes, which induce apoptosis of infected cells.
• Pathological atrophy in parenchymal organs after duct
obstruction – such as occurs in the pancreas, parotid gland
and kidney.
MORPHOLOGY
• Cell shrinkage
• Chromatin condensation
• Formation of cytoplasmic
blebs and apoptotic bodies
• Phagocytosis of apoptotic
cells or cell bodies, usually
by macrophages
FEATUES OF NECROSIS AND
APOPTOSIS
ASSIGNMENT
• Explain Necroptosis, and its morphology?
• Differentiate between Necrosis and Apoptosis?
