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Abnormal growth in tissue
Lecture outcomes
To describe adaptive changes of the cell to
pathological stimuli
To understand abnormalities of cell
differentiation
To define the terms aplasia, agenesis,
dysplasia, hypoplasia, atrophy, hypertrophy,
hyperplasia, metaplasia
To understand each of the above with
appropriate examples
Introduction
Inflammatory, Degenerative & Neoplastic
Growth Increase in size, structure & function. Synthesis of tissue
components.
Differentiation: functional and structural
maturity of cells.
Proliferation- increase in cell population.
Tumour Swelling / new growth / mass
Cell cycle & controls
Cyclins, CDK
Growth factors
Growth Inhibitors
Cancer suppressor
gene p53
Oncogenes
Histologic picture of Mitosis:
Factors affecting growth:
Genetic parents, Pygmies.
Endocrine DM, Iodine, GH.
Nutrition - deficiencies/excess.
Stress psycho-social, diseases.
Neoplasia DNA mutation loss of control
over cell division.
Disorders of Growth
Decreased growth
Hypoplasia, Aplasia, Atrophy
Increased growth
Non Neoplastic Normal DNA
Due to a need.. Controlled.
Neoplastic Abnormal DNA
not needed, auto, uncontrolled.
Non-Neoplastic Proliferation
*Controlled, Reversible, Normal DNA
Hypertrophy *Increase in Size of cells.
Hyperplasia *Increase in Number of cells.
Metaplasia *Change from one type to other
Dysplasia *Disordered, irregular, no
maturation.
Aplasia/ Agenesis
Failure of development of tissue or organ,
which is a developmental abnormality that
presumably develops early in intra uterine life.
Aplastic organs are either totally absent or
represented by small mass of fibrous or fatty
tissue containing a few rudimentary cells.
Paired organs adrenals, kidneys, lungs
Aplasia of aorta or pituitary incompatible
with life.
Hypoplasia
Failure of organ to attain full size
Less severe abnormality than aplasia.
Rudimentary organs, smaller than normal.
Lack full complement of cells, so function may be reduced.
Usually affects same paired & unpaired organs as aplasia.
Aplasia
Hypoplasia
Atrophy
Reduction in size of tissue due to shrinkage in size of cell substance or number of cells or both.
Physiological uterus, thyroglossal duct. Pathological atrophy Disuse atrophy decreased workload muscle
Denervation atrophy Ischaemia Brain, atherosclerosis. Nutrition Protein energy malnutrition, cachexia.
Endocrine breast, endometrium. Senile brain, heart Pressure
Biochemical changes
Balance between protein synthesis and
degradation.
Increased protein degradation proteolytic
enzymes.
Stimulated by Cytokines TNF
Autophagic vacuoles membrane bound
vacuoles within cells containing
mitochondria,
ER.
Pathology of Atrophy
Microscopically - Cells may be fewer (numerical) or smaller than normal (quantitative atrophy).
Grossly - The organ or part is smaller than normal.
Paired organs - one organ is reduced in size & wt
compared with its counterpart.
Fatty atrophy: Missing cells replaced by adipose
tissue as in physiologic atrophy of the thymus
Fibrous atrophy: replaced by fibrous connective
tissue
Hypertrophy
Increase in size of cells and thus increase in size of organ or tissue
Occur in tissue whose cells can not divide-
Striated muscle
Increase in size of many tissues and organs hypertrophy and hyperplasia
Hypertrophy
No new cells, just larger cells.
Not due to cell swelling, but synthesis of more structural compounds
Nuclei have higher DNA content, cell arrests without undergoing mitosis.
Mechanism of hypertrophy
The nature of the signal to the cell is poorly
understood.
There is an increase in total cellular proteins,
including myofibril in muscle cells and
organelles such as mitochondria, ER and
myofilaments.
The anabolic processes exceed catabolic
processes.
Types of hypertrophy
PHYSIOLOGICAL
Skeletal muscles ---- weight lifters, athletes
Hormonal stimulation Uterus smooth muscles during pregnancy oestrogen
Breast lactation prolactin
PATHOLOGICAL
Myocardial hypertrophy stenotic(narrowing) valvular diseases or lung diseases
Cardiac hypertrophy
Hyperplasia
It is the increase in size of an organ due to
increase in number of its constituent
cells
Occur in those organs/ tissues whose cells can divide
Hyperplasia after the removal of the stimuli, does not progress.
Types of hyperplasia
PHYSIOLOGICAL - Increased level of a normal stimulus
(hormonal)
In regeneration liver regeneration after injury.
As a compensatory response, e.g., missing organ in paired
organ, partial resection
PATHOLOGICAL due to excessive response or excessive
stimulation.
thyroid gland (goitre) iodine def.
bronchial epithelium chronic irritation
Hormonal Stimulation uterine, high oestrogen
Excessive growth factor stimulation warts HPV
Goitre Iodine Deficiency
Non neoplastic
Normal DNA
Reversible
Metaplasia
Mature differentiated (highly specialized) cell type is replaced by
another differentiated cell (less
specialized ) type.
Response to better withstand the adverse
environment
Prolonged irritation, chronic infection.
Epithelial metaplasia
Endocervix, gall bladder, urinary bladder, renal pelvis, respiratory tract
(smoking), stomach.
Original columnar or transitional mucosa
changes to squamous.
Stomach change from acid/ enzyme
secreting epithelium to colonic type
intestinal mataplasia.
Connective tissue metaplasia
Most commonly associated with repair
process
Fibroblasts mesenchymal ability to change into other connective tissue
cells, -undergo metaplasia to bone,
cartilage
Dysplasia
Alteration in size, shape and orientation of
epithelial cells.
Is abnormal development of tissue or
disorderly growth, or malformation of tissue.
A proliferative response (non-neoplastic)
accompanied by loss of regular differentiation.
The change is considered as preneoplastic.
Salient features of dysplasia
Commonly associated with chronic inflammation or irritation.
Epithelium of cervix, skin, oesophagus, endometrium.
Cells increase in number with thickening of
epithelium, mitosis increased.
Reversible if irritation removed, however,
changes may persist and progress to
malignancy.
Pathology of dysplasia
Microscopically
Cell atypia and disorderliness
Loss of uniformity of the individual cells and loss of architectural orientation
Cellular atypia is characterized by pleomorphism and hyperchromasia
Mitotic figures are seen in abundant cells
Grossly
No much can be appreciated grossly
Ageing
Cellular ageing is the result of a
progressive
decline in the proliferative capacity and
life
span of cells, with accumulation of
cellular
and molecular damage.
Factors affecting Ageing
Genetic 60%
Age gene on Chromosome 1
Environmental factors (40%)
Trauma
Diseases Atherosclerosis, diabetes
Diet malnutrition, obesity
Psychological & Social health stress
Cellular mechanisms of
ageing Ageing genes
DNA mutation
Free radicle injury
Mitochondrial DNA damage
Loss of DNA repair mech.
Ageing Morphologic changes Easy bruising fragile capillaries Glycosylation of lens proteins Cataract Brown atrophy heart, atrophy uterus Skin elastosis, hair loss, bruising Joints - osteoarthritis Immunity - Immunosuppression CVS Blood vessel hardening atherosclerosis, MI, stroke Neoplasms CNS cerebral degeneration
Questions?
baranikarikalan@imu.edu.my
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