Cell injury can occur through various acquired and genetic causes and results in cellular adaptations or cell death. Reversible cell injury causes cellular swelling and fatty change, while irreversible injury leads to necrosis, apoptosis, or autolysis/heterolysis. Necrosis is characterized by loss of membrane integrity and cellular contents, resulting in nuclear changes like pyknosis, karyorrhexis, and karyolysis. In contrast, apoptosis is a programmed form of cell death where the cell activates enzymes to degrade its own DNA and proteins while keeping the plasma membrane intact.
Basic principles of Cell injury and AdaptationAkshayYadav176
Basic principles of Cell injury and Adaptation:
(As per new syllabus of PCI)
Introduction, definitions, Homeostasis, Components and Types of Feedback systems, Causes of cellular injury,Pathogenesis (Cell membrane damage, Mitochondrial damage, Ribosome damage, Nuclear damage),Morphology of cell injury – Adaptive changes (Atrophy, Hypertrophy, hyperplasia, Metaplasia, Dysplasia),Cell swelling, Intra cellular accumulation, Calcification, Enzyme leakage and Cell Death Acidosis & Alkalosis,Electrolyte imbalance.
Pathophysiology B Pharm 2nd semester
CONTENTS
1. Introduction
2. Course Description
3. Course Outcomes
4. Text and Reference Books
5. Syllabus
6. Question Paper Pattern
7. Evaluation Scheme
Pathophysiology is the study of causes of diseases and reactions of the body to such disease producing causes.
This course is designed to impart a thorough knowledge of the relevant aspects of pathology of various conditions with reference to its pharmacological applications, and understanding of basic pathophysiological mechanisms.
Expected outcomes
1. Describe the etiology and pathogenesis of the selected disease states
2. Name the signs and symptoms of the diseases
3. Mention the complications of the diseases.
SYLLABUS
Basic principles of Cell injury and Adaptation
Introduction, definitions, Homeostasis, Components and Types of Feedback systems, Causes of cellular injury, Pathogenesis (Cell membrane damage, Mitochondrial damage, Ribosome damage, Nuclear damage), Morphology of cell injury – Adaptive changes (Atrophy, Hypertrophy, hyperplasia, Metaplasia, Dysplasia), Cell swelling, Intra cellular accumulation, Calcification, Enzyme leakage and Cell Death Acidosis & Alkalosis, Electrolyte imbalance.
Basic mechanism involved in the process of Inflammation and Repair
Introduction, Clinical signs of inflammation, Different types of Inflammation, Mechanism of Inflammation – Alteration in vascular permeability and blood flow, migration of WBC’s, Mediators of inflammation, Basic principles of wound healing in the skin, Pathophysiology of Atherosclerosis
Cardiovascular System
Hypertension, congestive heart failure, ischemic heart disease (angina, myocardial infarction, atherosclerosis and arteriosclerosis)
Respiratory system
Asthma, Chronic obstructive airways diseases.
Renal system
Acute and chronic renal failure
Haematological Diseases
Iron deficiency, megaloblastic anemia (Vit B12 and folic acid), sickle cell anemia, thalasemia, hereditary acquired anemia, hemophilia
Nervous system
Epilepsy, Parkinson’s disease, stroke, psychiatric disorders: depression, schizophrenia and Alzheimer’s disease.
Endocrine system
Diabetes, thyroid diseases, disorders of sex hormones
Gastrointestinal system
Peptic Ulcer
Inflammatory bowel diseases,
jaundice, hepatitis (A,B,C,D,E,F) alcoholic liver disease
Diseases of bones and joints
Rheumatoid Arthritis, Osteoporosis, Gout
Principles of cancer
classification, etiology and pathogenesis of cancer
Infectious diseases
Meningitis, Typhoid, Leprosy, Tuberculosis, Urinary tract infections
Sexually transmitted diseases (STDs)
AIDS, Syphilis, Gonorrhea
#rohitkumartrivedi
Basic principles of Cell injury and AdaptationAkshayYadav176
Basic principles of Cell injury and Adaptation:
(As per new syllabus of PCI)
Introduction, definitions, Homeostasis, Components and Types of Feedback systems, Causes of cellular injury,Pathogenesis (Cell membrane damage, Mitochondrial damage, Ribosome damage, Nuclear damage),Morphology of cell injury – Adaptive changes (Atrophy, Hypertrophy, hyperplasia, Metaplasia, Dysplasia),Cell swelling, Intra cellular accumulation, Calcification, Enzyme leakage and Cell Death Acidosis & Alkalosis,Electrolyte imbalance.
Pathophysiology B Pharm 2nd semester
CONTENTS
1. Introduction
2. Course Description
3. Course Outcomes
4. Text and Reference Books
5. Syllabus
6. Question Paper Pattern
7. Evaluation Scheme
Pathophysiology is the study of causes of diseases and reactions of the body to such disease producing causes.
This course is designed to impart a thorough knowledge of the relevant aspects of pathology of various conditions with reference to its pharmacological applications, and understanding of basic pathophysiological mechanisms.
Expected outcomes
1. Describe the etiology and pathogenesis of the selected disease states
2. Name the signs and symptoms of the diseases
3. Mention the complications of the diseases.
SYLLABUS
Basic principles of Cell injury and Adaptation
Introduction, definitions, Homeostasis, Components and Types of Feedback systems, Causes of cellular injury, Pathogenesis (Cell membrane damage, Mitochondrial damage, Ribosome damage, Nuclear damage), Morphology of cell injury – Adaptive changes (Atrophy, Hypertrophy, hyperplasia, Metaplasia, Dysplasia), Cell swelling, Intra cellular accumulation, Calcification, Enzyme leakage and Cell Death Acidosis & Alkalosis, Electrolyte imbalance.
Basic mechanism involved in the process of Inflammation and Repair
Introduction, Clinical signs of inflammation, Different types of Inflammation, Mechanism of Inflammation – Alteration in vascular permeability and blood flow, migration of WBC’s, Mediators of inflammation, Basic principles of wound healing in the skin, Pathophysiology of Atherosclerosis
Cardiovascular System
Hypertension, congestive heart failure, ischemic heart disease (angina, myocardial infarction, atherosclerosis and arteriosclerosis)
Respiratory system
Asthma, Chronic obstructive airways diseases.
Renal system
Acute and chronic renal failure
Haematological Diseases
Iron deficiency, megaloblastic anemia (Vit B12 and folic acid), sickle cell anemia, thalasemia, hereditary acquired anemia, hemophilia
Nervous system
Epilepsy, Parkinson’s disease, stroke, psychiatric disorders: depression, schizophrenia and Alzheimer’s disease.
Endocrine system
Diabetes, thyroid diseases, disorders of sex hormones
Gastrointestinal system
Peptic Ulcer
Inflammatory bowel diseases,
jaundice, hepatitis (A,B,C,D,E,F) alcoholic liver disease
Diseases of bones and joints
Rheumatoid Arthritis, Osteoporosis, Gout
Principles of cancer
classification, etiology and pathogenesis of cancer
Infectious diseases
Meningitis, Typhoid, Leprosy, Tuberculosis, Urinary tract infections
Sexually transmitted diseases (STDs)
AIDS, Syphilis, Gonorrhea
#rohitkumartrivedi
Cell Injury in hindi
Cell injury is defined as the functional and morphologic effects of a variety of stresses on the cell from various etiologic agents which result in change in its internal and external environment.
The term cell injury is used to indicate a state in which the capacity for physiological adaptation is exceeded.
This may occur when the stimulus is excessive or when the cell is no longer capable to adapt without suffering some form of damage.
Cellular response to stress may vary depending upon following two factors:
Host Factors: Type of cell, Nutritional status of cell etc.
Factors pertaining to injurious agent: Its type, dose etc.
Etiology/Causes
Hypoxia and Ischaemia
Physical Agents
Chemicals and Drugs
Microbial Agents
Immunologic Causes
Nutritional Derangements
Ageing
Psychogenic Cause
Iatrogenic Cause
Idiopathic Disease
#rohitkumartrivedi
#cellinjury
#cellinjurypathology
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
Blood disorders can affect any of the three main components of blood:
Red blood cells, which carry oxygen to the body's tissues.
White blood cells, which fight infections.
Platelets, which help blood to clot.
Blood disorders can also affect the liquid portion of blood, called plasma.
Cell Injury in hindi
Cell injury is defined as the functional and morphologic effects of a variety of stresses on the cell from various etiologic agents which result in change in its internal and external environment.
The term cell injury is used to indicate a state in which the capacity for physiological adaptation is exceeded.
This may occur when the stimulus is excessive or when the cell is no longer capable to adapt without suffering some form of damage.
Cellular response to stress may vary depending upon following two factors:
Host Factors: Type of cell, Nutritional status of cell etc.
Factors pertaining to injurious agent: Its type, dose etc.
Etiology/Causes
Hypoxia and Ischaemia
Physical Agents
Chemicals and Drugs
Microbial Agents
Immunologic Causes
Nutritional Derangements
Ageing
Psychogenic Cause
Iatrogenic Cause
Idiopathic Disease
#rohitkumartrivedi
#cellinjury
#cellinjurypathology
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
Blood disorders can affect any of the three main components of blood:
Red blood cells, which carry oxygen to the body's tissues.
White blood cells, which fight infections.
Platelets, which help blood to clot.
Blood disorders can also affect the liquid portion of blood, called plasma.
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
It is the study of nature & cause of disease which involves changes in structure and function
The aspects of a disease process that form the core of pathology include:
its cause, the pathogenesis that is the sequence of events which give rise to the manifestations of the disease), and
the morphologic changes (structural alterations induced in cells & tissues by the disease
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
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3. Introduction to Pathology (Greek Word)
Pathos = Suffering
Logos = Study
Definition:
It is the scientific study of structure and function of the body in disease.
(or)
Pathology consists of the abnormalities that occur in normal anatomy and physiology
leading to disease.
It mainly involves the investigation of the causes of disease and associated changes at the
levels of cells, tissues, and organs, which in turn give rise to the presenting signs and
symptoms of the patient.
4. Important terms in pathology and medicine:
1) Patient: Is the person affected by disease.
2) Lesions: Are the characteristic changes in tissues and cells produced by disease
in an individual (or) experimental animal.
3) Morphology: It consists of examination of diseased tissues (Blood & Urine Tests)
4) Etiology: Includes the underlying causes and modifying factors. (Why of Disease)
Eg: Diseases with unknown etiology: Hypertension, Diabetes, Cancer etc.
5) Pathogenesis: Refers to the steps in the development of disease. (How of Disease)
5. Cell Injury
Definition: It is defined as a variety of stresses a cell encounters as a result of changes in its
Internal and external environment.
(Stress may be Physiologic (or) Pathologic stimuli)
7. Examples of Acquired causes:
Hypoxia & Ischemia : Due to ↓ Blood Supply, Heart & Lung diseases or
Anaemia.
Physical Agents: Eg Road Accidents, Extreme Heat & Cold, Electricity
Radiation etc.,
Chemical & Drugs: Eg Chemical poisons like Cyanide, Arsenic,
Mercury, strong acids, insecticides, pesticides, alcohol, narcotic drugs
etc.,
Microbial agents: Eg Bacteria, Viruses, Fungi etc.,
Immunological agents: Used in Autoimmune disorders.
Nutritional derangements: Nutritional deficiency (Anaemia,
Marasmus, Kwashiorkor etc.,)
8. Aging: Eg Inability to repair in cellular aging.
Psychogenic diseases: (Depression, Schizophrenia) Eg Drug
addiction, Alcoholism, Smoking results in liver damage, Chronic
bronchitis, Lung Cancer etc.,
Iatrogenic Causes: Errors due to Physician (Unwanted
Prescription)
Idiopathic diseases: Diseases/Disorders due to Unknown causes
Eg: Hypertension, Cancer, Diabetes etc.,
9. Cellular Adaptations to Stress:
Adaptations are reversible changes in the number, size,
phenotype, metabolic activity, or functions of cells in response to
changes in their environment.
Cellular Adaptations
Physiologic
adaptations
Pathologic
adaptations
10. Physiologic adaptations: Usually represent responses of cells to
normal stimulation by hormones (Eg: The hormone-induced
enlargement of breast and uterus during pregancy.)
Pathologic adaptations: are responses to stress that allow cells to
modulate their structure and function and thus escape injury.
Types of Cellular adaptations
Hypertrophy (Increase in Cell size)
Hyperplasia (Increase in Cell number)
Atrophy & (Decrease in Cell size or Cell shrinkage)
Metaplasia (Change of one form of cell to other, Eg: Columnar
epithelium to Simple Squamous epithelium.)
12. Atrophy: Due to decreased workload or decreased metabolic
activity.
A. Normal Brain B. Atrophy of Brain
13. “Mechanisms of Cell Injury”:
ATP
DEPLETION
Leading To
Multiple Effects
MITOCHONDRIAL
DAMAGE
Leading To Leakage of Pro-
Apoptotic
Molecules
1
2
↑↑ Ca2+
ENTRY
3
Leading To ↑ Mitochondrial
Permeability
Activation of
Enzymes
14. “Mechanisms of Cell Injury”:
ROS
(Reactive o2
Species)
Damage To
Lipids, Proteins &
DNA
4
MEMBRANE
DAMAGE
5
Damage To
Cell Membrane
Lysosomal
Membrane
Misfolded
Protein &
DNA Damage
6
Leading To Leakage of Pro-
Apoptotic
Molecules
19. ROS
(Reactive o2 Species)
ROS are o2 derived free radicals ( Free radicals are special type of
molecules that have an unpaired electron in their outer orbit.)
Causes of free radical generation:
Via normal reduction and oxidation reactions (o2
-, H2O2, OH-)
Ionization radiations .Eg: X-rays etc.,
Inflammation
Metabolism of exogenous molecules
Metals
24. Morphology of Reversible Cell Injury
The two main morphological correlates of reversible cell injury
are:
Cellular Swelling : it is the result of failure of energy-
dependent ion pumps in the plasma membrane, leading to an in
ability to maintain ionic and fluid homeostasis. Cellular swelling
the first manifestation of almost all forms of cell injury to cells, is
a reversible alteration that may be difficult to appreciate with the
light microscope, but it may be apparent at the level of the whole
organ.
Eg: It causes increase in weight of organ.
25. Fatty change: It occurs in hypoxic injury and in various forms
of toxic or metabolic injury and is manifested by the appearance
of small or large lipid vacuoles in the cytoplasm.
It is principally encountered in cells participating in fat
metabolism (e.g., hepatocytes, myocardial cells) and is also
reversible.
Other morphological characteristic includes:
Plasma membrane blebbing and loss of microvilli,
Mitochondrial swelling,
Dilation of the ER,
Eosinophilia.
26. Morphology of Irreversible Cell Injury
Autolysis (i.e. self-digestion) is disintegration of cell by its own
hydrolytic enzymes liberated from lysosomes. Autolysis is rapid
in some tissues rich in hydrolytic enzymes such as in the
pancreas, and gastric mucosa; intermediate in tissues like the
heart, liver and kidney; and slow in fibrous tissue.
Heterolysis is disintegration of cell by the hydrolytic enzymes
liberated from inflammatory mediators like Neutrophils etc.,
Necrosis is a series of morphological changes which occurs in
a lethally injured cell.
Apoptosis is also known as Programmed Cell death.
27. Morphology of Necrosis
Necrosis is the type of cell death that is associated with loss of
membrane integrity and leakage of cellular contents resulting in
dissolution of cells, largely resulting from the degradative action
of enzymes on lethally injured cells.
(Or)
It is a spectrum of morphological changes that follow cell death
in living due to progressive degradation action of enzyme
(present with in the cell) on lethally injured cell.
28. Morphological changes are due to:
1) Intracellular protein denaturation.
E.g. Both structural and functional proteins.
2) Enzymatic digestion of severely injured cell.
E.g. Leading to Autolysis & Heterolysis.
3) Loss of integrity of plasma membrane of necrotic cell.
Necrosis is characterized by changes in the cytoplasm and
nuclei of the injured cells.
29.
30. Cytoplasmic changes: Necrotic cells show increased
eosinophilia. Compared with viable cells, the cell may have a
more glassy, homogeneous appearance, mostly because of the
loss of glycogen particles.
Myelin figures are more prominent in necrotic cells than
during reversible injury.
Necrotic cells are characterized by discontinuities in plasma
and organelle membranes, marked dilation of mitochondria,
disruption of lysosomes.
31. Nuclear changes: Nuclear changes due to breakdown of DNA
and chromatin. It includes:
Pyknosis: Characterized by nuclear shrinkage and increased
basophilia.
Karyorrehexis: Fragmentation of Nucleas
Karyolysis: Fading of basophilia & chromatin.
Fates of necrotic cells:
Necrotic cells may persist for some time or may be digested by
enzymes and disappear.
Dead cells may be replaced by myelin figures, which are either
phagocytosed by other cells or further degraded into fatty acids.
32. Morphologically, there are six types of necrosis
1) Coagulative necrosis: Characteristic of Infarcts
Types of Necrosis
38. Apoptosis
• Apoptosis is a pathway of cell death in which cells
activate enzymes that degrade the cells’ own nuclear
DNA and nuclear and cytoplasmic proteins.
• The plasma membrane of the apoptotic cell remains
intact, but the membrane is altered in such a way
that the cell and its fragments become avid targets
for phagocytes.
• Apoptotic cell death does not elicit an inflammatory
reaction in the host
• In contrast to Necrosis, Apoptosis takes place in both
physiologic and pathologic situations. Were the
prior occurs only in pathological conditions.
39. • This process helps to eliminate unwanted cells by an
internally programmed series of events effected by
dedicated gene products. It serves several vital
functions and is seen under various settings.
During development for removal of excess cells during
embryogenesis
To maintain cell population in tissues with high turnover
of cells, such as skin, bowels.
To eliminate immune cells after cytokine depletion, and
autoreactive T-cells in developing thymus.
To remove damaged cells by virus
To eliminate cells with DNA damage by radiation,
cytotoxic agents etc.
Hormone-dependent involution - Endometrium, ovary,
breasts etc.
Cell death in tumours.