DENT 301: GENERAL PATHOLOGY | LESSON 1

CELLULAR INJURY – damage that occurs when the

limits of adaptive responses are exceeded; can still be
Lesson 1. Cellular Response and reversible if mild or not persistent
Adaptation
CELL DEATH – end result of progressive injury where
General Pathology the cell ultimately gets killed or kills itself

⎼ Branch of medicine devoted to the study of CELLULAR ACCUMULATIONS – accumulation of

structural and functional changes in cells, substances inside the cell that occur in response to stress
and injury
tissues and organs that underlie different
diseases.
Always Remember
⎼ Specifically concerned with the basic reactions - How a cell responds depends on the NATURE
& SEVERITY of stress, and other variables affecting
of the cells and tissues to abnormal stimuli that
the cell itself – whether it will be an adaptive response,
underlie all kinds of diseases.
reversible injury, or cell death.
⎼ logos study of
CELLULAR ADAPTATIONS
⎼ pathos diseases
⎼ Reversible changes in structure (size, number)
Cellular Responses to Stimuli and function (metabolic activity, phenotype) in
response to stimuli from the environment.
⎼ During this time, new but altered steady states
PHYSIOLOGICAL
are achieved, allowing the cell to survive and
⎼ Good stimulus, part of body’s normal function
continue to function.
PATHOLOGICAL
CELLULAR ADAPTIVE CHANGES
⎼ Bad stimulus, can affect or cause harm to body
structure and/or function
Adaptation Definition
HOMEOSTASIS
ATROPHY Decrease in size &
⎼ A cell is normally in Homeostasis (Steady function
state).
⎼ At this state, the cell is limited to a narrow HYPERTROPHY Increase in size
range of function and structure & capable of
handling physiologic demands. HYPERPLASIA Increase in cell number
EXCESSIVE STIMULATION/STRESS METAPLASIA Change in cell growth
and phenotype
⎼ With excessive physiological stimulation/stress
or with pathologic (harmful) stimuli, the cell
undergoes a series of events or phenomenon
DYSPLASIA * Abnormal growth &
called Cellular Adaptation.
development
⎼ In order to achieve a new altered steady state to
survive and continue to function.

HOMEOSTASIS, ADAPTATION & INJURY

SUMMARY OF CELLULAR RESPONSES

CELLULAR ADAPTATION – reversible changes in

structure & function

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DENT 301: GENERAL PATHOLOGY | LESSON 1

MECHANISMS OF ADAPTIVE CHANGE – Ex. Enlargement of the breast

● Regulation of specific cellular receptors during puberty & pregnancy
– Upregulation (adds more receptors) ● COMPENSATORY
– Downregulation (removes) HYPERPLASIA
– Occurs after damage or partial
● Induction of new proteins removal of a tissue
– Switching of one type of protein to another – Ex. Regeneration of the liver after
damage/surgical removal
ADAPTATION = REVERSIBLE
● It is important to note that these changes are PATHOLOGIC HYPERPLASIA
reversible! ⎼ Response to excess hormones or growth
● Once stress or injurious stimulus is eliminated, factors.
the cell can recover back to its original state ● Benign Protatic Hyperplasia
without suffering any harmful consequences. – Enlargement of prostate from
excess testosterone
1.HYPERTROPHY
⎼ INCREASE IN SIZE ● Endometrial Hyperplasia
of the cell increased size of organ or tissue – Thickening of the uterine wall
⎼ Increased production of proteins in the cell (endometrium) from excessive
⎼ Can be physiologic or pathologic estrogen
⎼ Caused by increased functional demand or – Occurs when the cycle of estrogen
by stimulation by hormones/growth factors and progesterone is disrupted and
⎼ Most common stimulus is increased workload estrogen levels increase excessively
⎼ No new cells, just larger ones – Common cause of abnormal
uterine bleeding
Examples of Hypertrophy: – If estrogen stimulation is removed,
● Uterine smooth muscle – increase in size of the uterine lining returns to its
the uterus in response to hormones of normal thickness
pregnancy (e.g. estrogen, uterine hypertrophy)
● Cardiac muscle – enlargement of the heart due
to increased cardiac muscle size from
prolonged increased workload due to long
standing hypertension or faulty heart
valves(e.g. Cardiac Hypertrophy)
● Skeletal muscle – increase in muscle mass in
response to increased demand from weight
lifting

DIVIDING vs. NON-DIVIDING CELLS

● Keloid formation
● Non-dividing cells – Excessive skin/connective tissue on
– Cells of brain, kidneys, muscle, nerves and scars
heart – In wound healing, granulation
– Respond to stress by increasing tissue mass tissue formation occurs to fill the
through hypertrophy. “gaps” of a wound.

● Cells capable of dividing

– Lining cells of the mouth, stomach and – Excess in mitogenic growth factor in certain people cau
intestines
– Respond to stress by undergoing both
hypertrophy and hyperplasia.

2. HYPERPLASIA HYPERTROPHY & HYPERPLASIA

⎼ INCREASE IN NUMBER ● Hypertrophy & Hyperplasia can occur together
of cells increased growth andEx. Pregnant
mass of organuterus – both the uterine endothelium and
or tissue
uterine smooth muscle cells undergo increased DNA
⎼ Occurs when the cell is capable of dividing
synthesis & enlargement of cells
⎼ Proliferation of cells due to growth factor, or
increased formation of cells from stem cells
⎼ Can either be physiologic or pathologic
CANCER VS. HYPERPLASIA
● Hyperplasia is distinct from cancer.
● Pathologic hyperplasia however constitutes a
PHYSIOLOGIC HYPERPLASIA
fertile soil for cancerous proliferation to arise.
⎼ Response to a normal functional stimulus
– Those with endometrial hyperplasia are at an increased
⎼ Can either be hormonal or compensatory
risk of developing endometrial cancer
● HORMONAL HYPERPLASIA
– Response to hormone stimulation
3. ATROPHY

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DENT 301: GENERAL PATHOLOGY | LESSON 1

⎼ Reduced size of an organ or tissue due to a METAPLASIA

decrease in cell size and loss of cell contents. ⎼ Most common form of metaplasia
⎼ Cells shrink but are not dead ⎼ Mucus-secreting columnar epithelium is
⎼ Can be physiologic or pathologic. replaced by the protective stratified squamous
epithelium
PHYSIOLOGIC ATROPHY Examples:
⎼ Occurs during embryonic development where – In the respiratory tract in response to prolonged
embryonic structures not useful in life are irritation (e.g. smoking) or Vitamin A deficiency
removed – In the ducts of glands, pancreas or bile tree in response
⎼ Occurs shortly after delivery of the baby where to unremoved stones
the uterus shrinks back to near nonpregnant ⎼ The normal lining of ducts & respiratory tract
size is composed of simple or pseudostratified
columnar cells that secretes mucus and
PATHOLOGIC ATROPHY contains cilia.
Common causes: ⎼ In squamous metaplasia, the more protective
1. Decreased workload (atrophy of disuse) stratified squamous epithelium takes over
– e.g. skeletal muscle shrinkage for patients
with fractured bone immobilized in plaster SQUAMOUS-TO-COLUMNAR
cast, or stroke & senile patients on prolonged METAPLASIA
bed rest. ⎼ May occur, as in Barrett’s esophagus
2. Loss of nerve supply (denervation atrophy) ⎼ Esophageal squamous epithelium is replaced
– e.g. shrinkage of base of thumb (the fat part by intestinal-like columnar epithelium in
of your hand) in patients suffering from Carpal prolonged exposure to gastric acid reflux
Tunnel Syndrome
3. Diminished blood supply CONNECTIVE TISSUE METAPLASIA
– e.g. arterial occlusive disease in chronic ⎼ Formation of mesenchymal tissues such as
smokers, causing blackening of digits and cartilage, bone or adipose in tissues that
gangrene normally do not contain these elements
4. Inadequate nutrition ⎼ Ex. Myositis ossificans
– e.g. marasmus, a protein calorie malnutrition
disorder, causes cachexia (“skin and bones” SEQUELAE OF METAPLASIA
appearance) ⎼ Change to metaplastic squamous epithelium
5. Loss of endocrine stimulation comes with a price.
– e.g. shrinkage and sagging of breasts due to ⎼ Although becoming tough and protective,
loss of estrogen stimulation after menopause important mechanisms of protection against
6. Pressure infection become lost
– e.g. prolonged compression of an organ by an
enlarging tumor 5. DYSPLASIA
7. Aging (senile atrophy) ⎼ NOT a true adaptation
⎼ Refers to an abnormal development of cells
Examples of Atrophy: causing abnormal changes in shape, size and/or
TESTICULAR ATROPHY organization
⎼ Shrinkage of the testis due to reduced ⎼ Thought to be related to hyperplasia, and is
hormonal stimulation and/or blood supply sometimes called “Atypical hyperplasia”
CEREBRAL ATROPHY ⎼ Can be seen in the lining of squamous
⎼ Shrinkage of brain tissue, causing deepening epithelium thickened by hyperplasia of basal
and widening of the depression (sulcus) and cells with abnormal maturation of cells
narrowing of the folds (gyri) ⎼ Dysplatic changes (e.g. mitotic figures,
ATROPHY OF DISUSE abnormally large nuclei, abnormally large
⎼ Shrinkage of muscles after prolonged cells) can act as a precursor to cancer.
immobilization or loss of use/function ⎼ A.K.A. Stage 0 cancer
⎼ e.g. leg of stroke patients with one-sided ⎼ This is still REVERSIBLE at this point!
paralysis DYSPLASIA of the CERVIX
(Cervical Intraepithelial Neoplasia or CIN)
4. METAPLASIA ⎼ Cells appear different in size, shape and
⎼ Reversible change in phenotype nuclear appearance
⎼ One mature cell type is replaced by another
⎼ It may be an adaptive replacement of a weaker
stress-sensitive type by a more resistant type.
⎼ Can be a result of reprogramming of stem cells SUMMARY TABLE
existing in normal tissue, or by undifferentiated
mesenchymal cells.
⎼ In a metaplastic change, precursor cells mature
along a different pathway
METAmorphosis

COLUMNAR-TO-SQUAMOUS

Gracelle Joy Suelto Sebua DDM3