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Nursing class lecture cell injury 2nd class.pptx
1. Cellular adaptation:
Classifcation:
a)Atrophy and Hypertrophy (↑or ↓in size)
b)Hyperplesia (↑number of cells)
c)Metaplasia(change from one type to another
type) and dysplasia (changed phenotypic
differentiation)
2. 2
a. Atrophy
1. Physiologic atrophy: Brain,Gonads,
2. Pathologic atrophy
a) Starvation atrophy
b)Ischaemic atrophy eg, atropic kidney
c)Disuse atrohy eg, atropy of pancreas
d)Neuropathic atrophy eg. Motor neuron
disease
e)Endocrine atrophy eg, atropy of thyroid and
adrenal
7. c. Hyperplasia:
• Temporary Increase in the number of the parenchymal cells.
• Resulting in enlargement of organ.
• Often hypertrophy and hyperplasia occures simultaneously
• Occures due to increased in mitosis of the resting cells.
• Neoplasia causes change in the genetic composition of the cells.
CAUSES:
A. PHYSIOLOGICAL HYPERPLASIA:
I) Hormonal hyperplasia eg: ↑in size of breast during pregnancy
and lactation. Pregnant uterus
ii) Compensatory hyperplasia: Eg: Regenration of liver cells after
hepatectomy,epidermis after skin abrasion.
B.PATHOLOGIC HYPERPLASIA:
I) Endometrial hyperplasia in excess oestrogen
ii) In wound healing: proliferation of fibroblasts cells
iii) Formation of skin warts: papilloma viral infection
8. d. Metaplasia:
• It is defined as a reversible change of one type of epithelial or
mesenchymal cells to another type of adult epithelium or
mesenchymal cells.
• long time metaplasia may result in cancer.
• Divided in 2 types:
A. EPITHELIAL METAPLASIA:
1. Squamous metaplasia:
Eg: In bronchus of chronic smokers
Utreus of old age
2. Columnar metaplasia:
Eg: Intestinal metaplasia in healed chronic gastric ulcer.
B. MESENCHYMAL METAPLASIA:
1. Osseous metaplasia: Eg: arterial wall in old age
2. Cartilaginous metaplasia: Eg; healing of fractures
9. e. Dysplasia:
• Means 'disordered cellular development'.
• Often accompanied with metaplasia and hyperplasia.
• Often occurs in epithelial cells.
• Observed charactertics are
– Increased number of layers of epithelial cells
– Increased mitotic activity
– Disorderly arrangement of cells from basel layer to
surface layer.
– Cellular and nuclear pleomorphism (variability in the size,
shape and staining of cells and/or their nuclei.)
11. 11
Morphology of Irreversible cell
injury
a) Autolysis or self digestion
b) Necrosis
c) Apoptosis
d) Gangrene
e) Calcification
12. 12
CONCEPTS - CELL DEATH
• There is no singal biochemical event that
equates with cell death.
• Necrosis = “cell murder”
• Apoptosis = “programmed cell death or cell suicide”
16. Apoptosis:
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
17. 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.
18. APOPTOSIS IN BIOLOGIC PROCESSES:- Apoptosis is responsible for mediating
cell death in awidevarietyof physiologic and pathologic processes as under:
⚫ Physiologic Processes:
1. Organized cell destruction in sculpting of tissues during development of embryo.
2. Physiologic involution of cells in hormone-dependent tissues
3. Normal cell destruction followed by replacement proliferation such as in intestinal
epithelium.
4. Involution of the thymus in early age.
⚫ Pathologic Processes:
5.Cell death in tumoursexposed to chemotherapeutic agents.
6. Cell death by cytotoxic T cells in immune mechanisms
7. Progressive depletion of CD4+T cells in the pathogenesis of AIDS.
8. Cell death in viral infections e.g. viral hepatitis.
9. Pathologic atrophy of organs and tissues on withdrawal of stimuli e.g. prostatic
atrophy, atrophy of kidney
6. Cell death in response to injurious agents involved in causation of necrosis e.g.
radiation, hypoxiaand mild thermal injury.
7. In degenerative diseases of CNS e.g. in Alzheimer’s disease, Parkinson’sdisease, and
chronic infective dementias.
8. Heart diseases e.g. heart failure, acute myocardial infarction
19.
20. 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.
