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nursing class cellularadaptation and apoptosis.pptx
1.
2. ⦁ Adaptations are reversible changes in the size,
number, phenotype, metabolic activity, or
functions of cells in response to changes in
their environment
⦁ Cells must constantly adapt, even under
normal conditions, to changes in their
environment.
⦁ These physiological adaptations usually
represent responses of cells to normal
stimulation by hormones or endogenous
chemical substances.
◦ For example, as in the enlargement of the breast and
induction of lactation by pregnancy.
3. ⦁ Pathologic adaptations may share the same
underlying mechanisms, but they provide the
cells with the ability to survive in their
environment and perhaps escape injury.
⦁ Cellular adaptation is a state that lies
intermediate between the normal, unstressed
cell and the injured, overstressed cell.
4. ⦁ Cell can adapt themselves by undergoing 5
different conditions
1. Hyperplasia
2. Hypertrophy
3. Atrophy
4. Metaplasia
5. Dysplasia
7. a. Hormonal : influence of hormonal stimulation
🞄 h
.
pregnant uterus
🞄 normal endometrium after a normal menstrual cycle.
🞄 Prostatic hyperplasia in old age
b. Compensatory: hyperplasia occurring following
removal of part of an organ or a contralateral
organ in paired organ
🞄 Regeneration of the liver following partial
hepatectomy
🞄 Regeneration of epidermis after skin abrasion
🞄 Following nephrectomy on one side, there is
hyperplasia of nephrons of the other kidney.
8. ⦁ Excessive stimulation of hormones or growth
factors
◦ Endometrial hyperplasia
◦ wound healing - of granulation tissue due to
proliferation of fibroblasts and endothelial cells.
◦ skin warts from hyperplasia of epidermis due to
human papilloma virus.
◦ Pseudocarcinomatous hyperplasia of the skin
9. Definition: An increase in the size of cells, and
with such change, an increase in the size of
the organ.
Types:
• Physiologic: physiologic growth of the uterus
during pregnancy involves both hypertrophy
and hyperplasia.
• Pathologic causes: increased workload,
hormonal stimulation and growth factors
stimulation.
• hypertrophy of heart the most common stimulus is
chronic hemodynamic overload
12. Although hypertrophy and hyperplasia are
two distinct processes, frequently both
occur together, and they well be triggered
by the same mechanism.
13. Definition: Acquired loss of size due to
number of
reduction of cell size or
parenchyma cells in an organ
Types: Physiologic or Pathological
Left Normal
Atrophy
Right
14. ⦁ A normal process of
aging in some tissues,
which could be due to
loss of endocrine
stimulation or
arteriosclerosis.
◦ Atrophy of lymphoid
tissue in lymph nodes,
appendix and thymus.
◦ Atrophy of gonads after
menopause.
◦ Atrophy of brain with
aging.
16. Definition: Metaplasia is a reversible change in
which one adult cell type is replaced by
another adult cell type.
Causes
⦁ Changes in environment
⦁ Irritation or inflammation
⦁ Nutritional
17. ⦁ There are basically 2 types of metaplasia
⦁ EPITHELIAL METAPLASIA
◦ Squamous metaplasia: changes in bronchus, uterine
endocervix, gallbladder, prostate, renal pelvis and
urinary bladder
🞄 vitamin A deficiency: squamous metaplasia in the nose,
bronchi, urinary tract, lacrimal and salivary glands
◦ Columnar metaplasia: Intestinal metaplasia in healed
chronic gastric ulcer and Barrett’s oesophagus
⦁ MESENCHYMAL METAPLASIA
◦ Osseous metaplasia.
◦ Cartilaginous metaplasia.
20. ⦁ disordered cellular development.
⦁ also referred to as atypical hyperplasia
⦁ Epithelial dysplasia is characterised by cellular
proliferation and cytologic changes
◦ Increased number of layers of epithelial cells
◦ Disorderly arrangement of cells from basal layer to the
surface layer
◦ Loss of basal polarity i.e. nuclei lying away from basement
membrane
◦ Cellular and nuclear pleomorphism
◦ Increased nucleocytoplasmic ratio
◦ Nuclear hyperchromatism
◦ Increased mitotic activity.
• The two most common examples of dysplastic
changes are the uterine cervix and respiratory
tract
21.
22. APOPTOSIS
⚫It is a form of ‘coordinated and internally programmed
cell death’ having significance in avarietyof
physiologicand pathologicconditions (apoptosis is a
Greek word meaning ‘falling off’ or ‘dropping off’).
⚫The term was first introduced in 1972 as distinct from
necrosis by being a formof cell death which is
controlled and regulated by the rateof cell division;
when thecell is not needed, pathwayof cell death is
activated (‘cell suicide’) and is unaccompanied byany
inflammation and collateral tissuedamage.
23. In 2 process:
A. Physiological process:
1. During development of embryo
2. Cells of hormone dependent tissues eg: endometrial sheeding,
regression of lactating breast.
3. Involution of thymus gland in early age.
B. Pathological process:
1. Cell death in tumour exposed to chemotherapeutic agents
2. Cell death by cytotoxic T cells in graft rejection.
3. Progressive depletion of CD4cells in AIDS.
4. Cell death in viral infection
5. Pathological atropy
6. Cell death after exposure of radiations, hypoxia etc
7. Degenerative diseases of CNSeg:Alzheimers diseaseetc
8. Heart diseases
24.
25. MOLECULAR MECHANISMS OF APOPTOSIS Several physiologic and
pathologic processesactivate apoptosis in avariety of ways. However, in general
the following events sum up thesequence involved in apoptosis:
Initiatorsof apoptosis:- Triggers forsignalling programmed cell death actat the
cell membrane, either intracellularlyorextracellularly
i) Withdrawal of signals required for normal cell survival
(e.g. absenceof certain hormones, growth factors, cytokines).
ii) Extracellularsignals triggering of programmed cell death (e.g. activation of FAS
receptor belonging toTNF-R family).
iii) Intracellularstimuli e.g. heat, radiation, hypoxiaetc.
Processof programmed cell death:- After thecell has been initiated into self-
destruct mode, the programme inbuilt in thecell getsactivated as under:
i) Activation of caspases
ii) Activation of death receptors
iii) Activation of growth controlling genes (BCL-2 and p53)
iv) Cell death.
Phagocytosis:- Thedead apoptotic cellsdevelop membrane changeswhich
promote their phagocytosis. Phosphatidylserine and thrombospondin
molecules whichare normally presenton the inside of thecell membrane,
appearon theoutersurfaceof thecells in apoptosis, which facilitate their
identification byadjacent phagocytesand promotes phagocytosis.
