This document provides an overview of cell injury and adaptation. It discusses various causes of cell injury including hypoxia, infections, physical and chemical agents. The pathogenesis and morphology of reversible and irreversible cell injury is explained. Cellular adaptations such as atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia are defined. Necrosis and apoptosis are compared as two types of cell death. Specific examples of cell injuries and adaptations in different organ systems are also presented.
This presentation is for those who want to understand the basics of reversible cell injury.
You can also get more idea from my youtube channel:
Harshit Jadav I Medical Wala
This presentation is for those who want to understand the basics of reversible cell injury.
You can also get more idea from my youtube channel:
Harshit Jadav I Medical Wala
Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
The study of the blood flow is called hemodynamics.
Thus hemodynamics deals with the dynamics of blood flow. The circulatory system is controlled by homeostatic mechanisms, much as hydraulic circuits and are controlled by control systems.
Hemodynamic response continuously monitors and adjusts to conditions in the body and its environment. Thus hemodynamics explains the physical laws that govern the flow of blood in the blood vessels.
Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
The study of the blood flow is called hemodynamics.
Thus hemodynamics deals with the dynamics of blood flow. The circulatory system is controlled by homeostatic mechanisms, much as hydraulic circuits and are controlled by control systems.
Hemodynamic response continuously monitors and adjusts to conditions in the body and its environment. Thus hemodynamics explains the physical laws that govern the flow of blood in the blood vessels.
Cellular adaptations, injury and death.. Lecture 1Ashish Jawarkar
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Notes for Cellular Injury.
Prepared for B.pharm I year II sem students for study purpose.
Contact email : drxmathinanotech@gmail.com
Regards,
Mrs.S.Mathivanan., M.Pharm
Assistant Professor,
SMVEC Pharmacy college,
Puducherry.
This is the brief overview on the topic CELL INJURY. After reading this you will get to know about adaptations, types, etiology, pathogenesis of cell injury.
This report, prepared by the student at the College of Dentistry, Hassan Atheed , in the third phase discusses scientific topics, but it maybe did not be 100% complete.
Cell injury (cell death): it is the variable changes in morphological and functional properties of cell occurs due to internal or external causes (ex. Chemical, physical, infectious and genetic agents), that obligate cell to respond for preserving normal hemostasis (adaptation) or death (necrosis) when the injury factors sever cell unable to adept, cell may also killed by another pathway even when it have the ability to adept for saving other cells and tissue by programed cell death (apoptosis).
حسن عضيد
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Chapter 3 - Islamic Banking Products and Services.pptx
Principles of cell injury and cellular adaptation .ppt
1. ChapterChapter :1:1
PrinciplesPrinciples ofof cellcell injuryinjury andand
adaptationadaptation
Presented by: Prof.Mirza Anwar BaigPresented by: Prof.Mirza Anwar Baig
Anjuman-I-Islam's Kalsekar Technical CampusAnjuman-I-Islam's Kalsekar Technical Campus
School of Pharmacy,New Pavel,NaviSchool of Pharmacy,New Pavel,Navi
Mumbai,MaharashtraMumbai,Maharashtra
11
2. Contents:
• Causes of cell injury
• Pathogenesis and morphology of
cell injury.
• Cellular adaptation
• Cellular atrophy and hypertrophy.
3. CELL INJURY
• Cell injury results from a disruption of one
or more of the cellular components that
maintain cell viability.
• Defined as variety of stresses a cell encounters
as a result of internal or external environmental
changes.
• Cell injury is common to all pathologic
processes.
3
4. CELL INJURY
• Cellular adaptation
• Reversible or irrversible cell injury
• Subcellular changes and intracellular accumlation
Injury at one point induces a cascade
of effects.
4
10. Pathogenesis of cell injury
• General principles of pathogenesis
1. Type, duration and severity of injurious agents
2. Type, status and adaptability of target cell
3. Underlying intracellular phenomena
eg. Mitochondrial damage, cell wall damage, free
radicals
4. Morphological consequences
eg. Ultrastrucal changes, swelling
10
11. OUTCOMES OF CELL INJURY
REVERSIBLE CELL DEATH CELL
ADAPTATIONS
NORMAL CELL
CELL INJURY / CELL STRESS
ACUTE CHRONIC
11
12. 1.Pathogenesis of ischemic and
hypoxic injury
Reversible cell injury:
1. Decreased generation of cellular ATP
2. Intracellualar lactic acidosis: Nuclear clumping
3. Damage to plasma membrane pump
- ATP dependent Na /K pump, Ca pump
4. Reduced protein synthesis- Dispersed ribosomes
Irreversible cell injury:
1. Mitochondrial damage- ↑ca influx
2. Activated phospholipase- membrane damage
3. Intracellular proteases- cytoskeleton damage
4. Activated endonucleases- nuclear damage
12
13. 1.1: Ischemia reperfusion injury and free
radical mediated cell injury
3 different consequences:
1. from ischaemia to reversible injury
2. from ischaemia to reperfusion injury
3. from ischaemia to irreversible injury
Mechanism:
1. Calcium overload: ↑lipid peroxidation of cell
membrane
2. Generation of ROS:
3. Subsequent inflammatory reactions neutrophils
utilize oxygen and gives free radicals 13
14. 2. Pathogenesis of chemical injury:
• Direct cytotoxic effect
– Direct cytotoxic effect: Hgcl2 poisoning,
Anticancer agents
Conversion to reactive toxic metabolites
metabolites kills the cells eg, CCl4 affects liver
Acetaminophen poisoning
3. Pathogenesis of physical injury:
Ionizing radiations.- cell membrane & DNA
damage
14
15. 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)
16. 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
16
21. 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
22. 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
23. 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.)
25. Morphology of Irreversible cell
injury
a) Autolysis or self digestion
b) Necrosis
c) Apoptosis
d) Gangrene
e) Calcification
25
26. CONCEPTS - CELL DEATH
• There is no singal biochemical event that
equates with cell death.
• Necrosis = “cell murder”
• Apoptosis = “programmed cell death or cell suicide”
26
27. NECROSIS
• Morphologic types of necrosis
– Coagulative
– Liquifactive
– Caseous
– Enzymatic (fat)
• The type of necrosis is dependent upon patterns of
enzymatic degradation of cells and extracellular
matrix, the type of necrotic debris, and by
bacterial products when present.
27
28. Coagulative necrosis:
• Common type of necrosis
• caused by irreversible focal injury,ischemia.
• Foci are pale,firm and slightly swollen.
• Hall mark is presence of tombstones.
Liquefaction necrosis:
Caused due to ischaemic injury or bacterial
infection.
Eg: infarct brain.
Affected area is soft containing necrotic debris.
Caseous necrosis:
Found in foci of tuberclosis infection.
have the features of coagulative and liquefaction
necrosis.
Appears like dry cheese,soft, granular and yellowish.
29. Fat necrosis:
• Present at pancrease and breast.
• Yellowish white firm deposits.
• Fat cells have cloudy appearance and
surrounded by inflammatory reactions.
• Calcium soaps are present in the cells.
Fibrinoid necrosis:
• Deposition of fibrin like material.
• Present in immunological tissue injuries.
• Arterioles of hypertension,peptic ulcers.
• Appears like brightly eosinophillic in vessel
wall.
33. 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 CD4 cells in AIDS.
4. Cell death in viral infection
5. Pathological atropy
6. Cell death after exposure of radiations, hypoxia etc
7. Degenerative diseases of CNS eg: Alzheimers disease etc
8. Heart diseases