This document discusses tissue response to injury at the cellular level. It defines cell injury and outlines the cellular responses, which can include adaptations, reversible injury, or irreversible injury. The causes of cell injury are also categorized, including genetic, hypoxic/ischemic, physical, chemical, microbial, immunological, nutritional, and psychological factors. The key stages of reversible injury are decreased ATP generation, reduced pH, sodium pump damage, decreased protein synthesis, and functional/ultrastructural changes. Irreversible injury is marked by mitochondrial dysfunction and membrane damage, leading to cell death through autolysis, necrosis, apoptosis, or gangrene. Aging is also discussed in terms of genetic, environmental, and oxidative stress factors.
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PHAGOCYTOSIS- History • Introduction • Phases of phagocytosis :- a) Margination b) Diapedesis c) Chemotaxis d) Opsonization or Attachment e) Engulfment orIngestion f) Secretion or Degranulation g) Killing or Degradation • Applied Aspects • Recent Advances
This is a powerpoint presentation on the Topic of Diseases of the immune system, part 1 - Chapter 6, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics. Instagram handle @pathologybasics
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PHAGOCYTOSIS- History • Introduction • Phases of phagocytosis :- a) Margination b) Diapedesis c) Chemotaxis d) Opsonization or Attachment e) Engulfment orIngestion f) Secretion or Degranulation g) Killing or Degradation • Applied Aspects • Recent Advances
This is a powerpoint presentation on the Topic of Diseases of the immune system, part 1 - Chapter 6, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics. Instagram handle @pathologybasics
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
Adaptive immunity is an immunity that occurs after exposure to an antigen either from a pathogen or a vaccination. This part of the immune system is activated when the innate immune response is insufficient to control an infection. In fact, without information from the innate immune system, the adaptive response could not be mobilized. There are two types of adaptive responses: the cell-mediated immune response, which is carried out by T cells, and the humoral immune response, which is controlled by activated B cells and antibodies.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
Adaptive immunity is an immunity that occurs after exposure to an antigen either from a pathogen or a vaccination. This part of the immune system is activated when the innate immune response is insufficient to control an infection. In fact, without information from the innate immune system, the adaptive response could not be mobilized. There are two types of adaptive responses: the cell-mediated immune response, which is carried out by T cells, and the humoral immune response, which is controlled by activated B cells and antibodies.
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
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.
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The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
We all have good and bad thoughts from time to time and situation to situation. We are bombarded daily with spiraling thoughts(both negative and positive) creating all-consuming feel , making us difficult to manage with associated suffering. Good thoughts are like our Mob Signal (Positive thought) amidst noise(negative thought) in the atmosphere. Negative thoughts like noise outweigh positive thoughts. These thoughts often create unwanted confusion, trouble, stress and frustration in our mind as well as chaos in our physical world. Negative thoughts are also known as “distorted thinking”.
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The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
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The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
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2. OBJECTIVES
• Highlight the basic concepts & principles of
tissue response to injury.
• Differentiate between normal tissue &
pathologic tissue.
2
3. CONTENTS
3.1: Definitions & Concepts of Tissue Response To
Injury
3.2: Etiology of Cell Injury
3.3: Pathogenesis of Cell Injury
3.4: Morphology of Reversible & Irreversible Cell
Injury
3.5: Aging
3
4. 3.1 Definitions & Concepts of Tissue Response
To Injury
• Cell injury; defined as a variety of stresses as a result
of changes in internal & external
environment.
• All cells of the body have inbuilt mechanism to deal
with changes in environment.
• The cellular response to stress varies & depends on:
i. Type of cell & tissue involved
ii. Type of cell injury
4
5. • Cellular responses to injury may be as follows:
i. Cellular adaptations
ii. Reversible cell injury & Irreversible cell injury
iii. Subcellular changes & Intracellular
accumulations
5
6. • Molecular interactions between cells;
i. Cell adhesions molecules (CAMs)
ii. Cytokines
iii. Membrane receptors
i. Cell adhesions molecules (CAMs); these are
chemicals which mediate the interaction
between cells (cell-cell interaction) & between
cells and extracellular matrix (cell-ECM
interaction).
6
7. • The ECM is the ground substances or matrix of
connective tissue which provides environment to
the cells & consists of 3 components;
i. Fibrillar structural proteins (collagen, elastin)
ii. Adhesion proteins (fibronectin, laminin)
iii. Molecules of proteoglycans &
glycosaminoglycans
(heparan sulphate, hyaluronic acid)
7
8. • There are 5 groups of CAMs;
i. Integrins – have a role in cell-ECM interactions & in
leucocyte - endothelial cell interaction.
ii. Cadherins – these are calcium-dependent adhesion
molecules which bind adjacent cells.
iii. Selectins – which bind to glycoproteins & glycolipids on
the cell surface.
iv. Immunoglobulin superfamily – have a major role in
recognition binding of immunocompetent cells.
v. CD44 – involved in leucocyte-leucocyte-endothelial
interactions & cell-ECM interaction.
8
9. ii. Cytokines; main role is in activation of
immune system.
• 6 categories of cytokines;
i. Interferons (IFN)
ii. Interleukins (IL)
iii. Tumor necrosis factor (TNF)
iv. Transforming growth factor (TGF)
v. Colony stimulating factor (CSF)
vi. Growth factors
9
10. iii. Cell membrane receptor; molecules consists of
proteins, glycoproteins or lipoproteins & may be
located on the outer cell membrane, inside the cell or
trans-membranous.
• There are 3 main types of receptors;
i. Enzymed - linked receptors (involved in control of
cell growth)
ii. Ion channels (for ion exchange)
iii. G-protein receptors (activate phosphorylating
enzymes for metabolic & synthetic functions of cells)
10
11. 3.2 Etiology of Cell Injury
• The causes of cell injury (reversible or irreversible)
can be classified into 2 large groups;
i. Genetic causes (Down’s syndrome)
ii. Acquired causes
11
12. • Acquired causes of cell injury can be further
categorised as follows;
i. Hypoxia & Ischaemia
ii. Physical agents
iii. Chemical agents & drugs
iv. Microbial agents
v. Immunologic agents
vi. Nutritional derangements
vii. Psychological factors
12
13. 1.Hypoxia (deficiency of oxygen) & Ischaemia
• Hypoxia is the most common cause of cell injury
• Causes of hypoxia are as below;
i. by reduced blood supply to cells e.g. ischaemia
ii. oxygen deprivation of tissues e.g. anaemia
2. Physical agents
• Causes of physical agents are as below;
i. mechanical trauma e.g. road accidents
ii. thermal trauma e.g. heat or cold
iii. electricity
iv. radiation e.g. ultraviolet
v. rapid changes in atmospheric pressure
13
14. 3. Chemicals & Drugs;
• Causes of chemicals & drugs are as below;
i. chemical poisons
ii. strong acids & alkalis
iii. environmental pollutants
iv. insecticides & pesticides
v. oxygen at high concentrations
vi. hypertonic glucose & salt
4. Microbial agents
5. Immunologic agents;
• Causes of chemiclas & drugs are as below;
i. hypersensitivity reactions
ii. anaphylactic reactions
iii. autoimmune diseases
14
15. 6. Nutritional derangements;
• Causes of nutritional derangements are as below;
i. nutritional deficiency e.g. starvation
ii. nutritional excess e.g. heart disease
7. Psychologic factors;
• Causes of psychologic factors are as below;
i. mental stress
ii. overwork
iii. frustration
15
16. 3.3 Pathogenesis of Cell Injury
• In general, the following principles apply in
pathogenesis of most forms of cell injury by
various agents;
i. Type, duration & severity of injurious agent
ii. Type, status & adaptability of target cell
iii. Underlying intracellular phenomena
iv. Morphologic consequences
16
17. Reversible Cell Injury
• If the ischaemia or hypoxia is short duration, the effects
are reversible e.g. coronary artery occlusion, myocardial
contractility.
• The sequential changes in reversible cell injury are as
under;
i. Decreased generation of cellular ATP
ii. Reduced intracellular pH
iii. Damage to plasma membrane sodium pump
iv. Reduced protein synthesis
v. Functional consequences
vi. Ultrastructural changes
17
18. i. Decreased generation of cellular ATP
• - Ischaemia & hypoxia both limit the supply of
oxygen to the cells, thus causing decreased
ATP generation from ADP.
• - In ischaemia, aerobic respiration as well as
glucose availability are both compromised
resulting in more severe effects of cell injury.
• - In hypoxia, anaerobic glycolytic energy
production continues and thus cell injury is
less severe.
18
19. ii. Reduced intracellular pH
• Due to low oxygen supply to the cell, aerobic
respiration by mitochondria fails first.
• This is followed by switch to anaerobic
glycolytic pathway for the energy
requirement.
• This results in rapid depletion of glycogen and
accumulation of lactic acid lowering the
intracellular pH.
19
20. iii. Damage to plasma membrane
sodium pump
• Normally, the energy-dependent sodium
pump operating at the plasma membrane
allows active transport of sodium out of the
cell and diffusion of potassium into the cell.
• Lowered ATP in the cell and consequent
increased ATPase activity interfere with this
membrane-regulated process.
• This result in intracellular accumulation of
sodium and diffusion of potassium out of cell.
20
21. iv. Reduced protein synthesis
• Ribosomes are detached from granular
endoplasmic, reticulum & polysomes are
degraded to monosomes, thus causing
reduced protein synthesis.
21
24. Irreversible Cell Injury
• If the ischaemia or hypoxia is persistence, the
effects are irreversible.
• 2 essential phenomena always distinguish
irreversible from reversible cell injury;
i. mitochondrial dysfunction
ii. disturbance in cell membrane function
24
25. 3.4 Morphology of Reversible & Irreversible Cell
Injury
Reversible Cell Injury
• Following morphologic forms of reversible cell injury;
i. Cellular swelling =the commonest & earliest form of cell injury
from almost all causes, common cause of cellular swelling include
bacterial toxins, chemicals, poisons, burns, high fever,
intravenous administration of hypertonic glucose or saline,
cloudy swelling results from impaired regulation of cellular
volume especially for sodium.
• ii. Fatty change =the intracellular accumulation of neutral fat
within parenchymal cells, especially common in the liver but may
occur in other non-fatty tissues like the heart, skeletal muscle,
kidneys and other organs.
25
26. • iii. Hyaline change =is a descriptive histologic
term for glassy,homogenous, eosinophilic
appearance of material in H & E stained
sections and does not refer to any specific
substance, hyaline change is associated with
heterogenous pathologic conditions and may
be intracellular or extracellular.
iv. Mucoid change =is a combination of
proteins complexed with
mucopolysaccharides, it’s chief constituent,
normally produced by epithelial cells of
mucous membranes and mucous glands .
26
27. Irreversible Cell Injury
• Cell death is a state of irreversible injury
• It may occur in the living body as a local or
focal change e.g. autolysis, necrosis &
apoptosis & the changes that follow it e.g.
gangrene.
27
28. • The pathologic processes involved in cell death
are described below;
i. autolysis
ii. necrosis
iii. apoptosis
iv. gangrene
v. atrophy
vi. hypertrophy
vii. hyperplasia
viii. metaplasia
ix. dysplasia
28
39. 3.5 Aging
• In general, the life expectancy of an individual
depends upon the following factors;
i. intrinsic genetic process
ii. environmental factors
iii. lifestyle of the individual
iv. age-related diseases
39
40. Cellular mechanisms of aging
i. Cross linking proteins & DNA
ii. Accumulation of toxic by products
iii. Aging genes
iv. Loss of repair mechanism
v. Free radical injury
vi. Telomerase shortening
40
41. • Experimental cellular senescene with every cell
division, there is progressive shortening of
telomerase present at the tips of chromosomes
which is normal cell is repaired by the presence
of RNA enzyme, telomerase. However, due to
aging, due to inadequate presence of
telomerase enzyme, lost telomerase is not
repaired resulting in interference in viability of
cell
• Genetic control in invertebrates-clock genes
responsible for controlling the rate and time of
aging that slowing metabolic function.
41
42. • Disease of accelerated aging : aging is under
genetic control in human beings supported by
the observation of high concordance in
lifespan.
• Oxidative stress hypothesis : aging is partly
caused by progressive and reversible
molecular oxidative damage due to persistent
oxidative stress on the human cell.
42
44. • Organ changes in aging;
i. Cardiovascular system
ii. Nervous system
iii. Musculoskeletal system
iv. Eyes
v. Hearing
vi. Immune system
vii. Skin
44
46. • Factors affecting aging;
o Diminished stress
o Stress
response
o Infections
o Diminished immune
o Diseases
response
o Malnutrition
o Good health
o Accidents
46
47. "No matter how dark things seem to
be or actually are, raise your sights
and see the possibilities – always
see them, for they're always there.“
Norman Vincent Peale
47