SlideShare une entreprise Scribd logo
1  sur  27
Critical Alteration
Morphology of Cell Death
Necrosis of Tissue and Organ
Critical Damage and Cell Death
Critical damage it is molecular-sub-
cellular violation of metabolism and
fading of function of
specialized cells.
Cell death it is destruction of
specialized cells in the living
organism under action of critical
damage factors.
Critical Damage and Cell Death
Objects of critical damage are structures of
the cells:
1. mitochondria
2. genetical apparatus (nuclear DNA)
3. plasmatic membrane
4. biosynthetic system
5. cytoskeleton
6. lysosomes and peroxisomes
Changes in cells can’t be determined by
light microscope, it is recognized by
molecular-cytochemical and autography
methods.
Reasons of development:
I. Endogenous metabolic catastrophe:
1.bioenergetics insufficiency of cells (hypoxia of
different genesis)
2.damage of the cells by the surplus of free
oxygen (O-) and oxide nitrogen (NO)
3. damage of the cells by the free radicals
4. increased of the ionized calcium in the cells
5. acid alteration of cells (pH  7)
6. damage of cells by the surplus of own
mediators (exayto-toxical damage)
7. denaturation and/or proteolysis out of control
8. activating of hydroxy-oxidization of lipids
II. Exogenous factors of injury:
1. infectious aggression (viruses, bacteria, fungi's)
2. physical and/or chemical damages (gamma-
and ultraviolet damage, hypo-/hyperthermia,
poisons, mechanical, electric damages)
3. Immunological damages :
а) at overloading of organism by foreign
albumen
в) iatrogenic damage (anesthetics, preparations
of blood, solutions, medicines)
4. damage by enzymes and aggressive molecules
of macrophages and leucocytes (factor of tumor
necrosis, oxide of nitrogen, hydrolytical
enzymes of lysosom - proteases, lipases,
phosphates, hydrolyses)
Consequences of critical damage:
partial necrosis of cell
destruction of cells by necrosis
pathogenic induction apoptosis
immune elimination of cells
reparative regeneration (renewal)
stimulation of neighbors
development of inflammation
damage of genome and appearance of new
tumor generations
NECROSIS
Necrosis - it is death of cells or
tissues in living organism.
Other forms of organ destructions:
Autolysis – post mortem destruction of
organs under action of enzymes,
produced by the dead cells or
bacteria.
Necrobiosis – protracted process of
destruction of tissue (trophic ulcers).
NECROSIS
CELL
1. Necrosis:
-coagulative
-colliquative
2. Apoptosis
3. Immune-
mediated cell
death:
- phagocytosis
TISSUE
1. Coagulative:
- fibrinoid
- caseous
2. Colliquative
3. Fat necrosis
ORGAN
1. Infarction:
- white
- red
- white with
hemorrhagic hal
2. Gangrene:
- wet
- dry
3. Noma
4. Bedsores
- immune-cell killing
- destruction by
activated
fragments of
complement (C5-C9)
It is the premature death and destruction of
cell’s organelles in the living organism under
action of critical damage factors
Phases of development
1. Critical damage
2. Destruction of cells and intercellular
connections:
- cytokaryolysis,
- coagulative necrosis
3. Post-necrotic transformation of cells
Duration: 1 min – 24 hours
NECROSIS of CELL
Classification of Cells Death, based
on the mechanism of development:
Necrosis of specialized cells
 Pathogenic inducted apoptosis
Selective immunological
elimination of cells
Morphology of cell destruction:
1. Karyolysis - the basophilic of the chromatin
may fade, a change that reflects the
activation of the DNA-ses.
2. Pyknosis - characterized by nuclear shrinkage
and increased basophiles. Here the DNA
apparently condenses into a solid, shrunken
basophilic mass.
3. Karyorrhexis - the pyknotic or partially
pyknotic nucleus undergoes fragmentation.
Post-necrotic transformation of
cells in living organism
1.Autolysis – destruction of cells by
ferments of the organism
2. Phagocytosis by macrophages
3.Destruction by free-radical
molecules of leucocytes (at
inflammation)
4.Destruction by ferments of bacteria
(at infected injury)
Pathogenic inducted apoptosis
It is a "programmed by genes cell death"
or cell suicide, that is initiated by internal
or external factors of critical damage.
Features of apoptosis:
1.The process begins at activation of
genes of apoptosis or inhibition of genes
that can stop apoptosis
2. Duration of the process – 10-60min
3.Fragmentation of cell into apoptotic
bodies at the end the process
1. Cell shrinkage. Cell is smaller in
size; the cytoplasm is dense.
2. Chromatin condensation. The chromatin
aggregates peripherally, under the nuclear
membrane, into well-delimited dense
masses of various shapes and sizes. The
nucleus break up, producing two or more
fragments
Morphologic stages of apoptosis
.
Morphologic stages of apoptosis
3. Formation of cytoplasmatical blebs and
apoptotic bodies. The apoptotic cell first shows
extensive surface blebbing, then undergoes
fragmentation into a number of membrane-
bound apoptotic bodies composed of cytoplasm
and tightly packed organelles, with or without a
nuclear fragment.
4. Phagocytosis of apoptotic cells or bodies by
adjacent healthy cells, either parenchymal cells
or macrophages.
Immune-mediated cell death
It is damage of cells by immunocytes and auto-
antibodies with destruction of cells in living
organism.
By this method can be destroyed:
1. Tumor cells
2. Transplanted cells
3. Infected cells
4. Normal cells (at autoimmune disease)
It is performed by:
- immunocytes
- activated fragments of complement (AB)
Phases of process:
1. Recognition of damaged cells by IS
2. Destroying (killing) of cells
Types of Immune-mediated cell death:
1.Phagocytosis – it is absorbtion and destruction by
macrophages after opsonization in phagolysosoms of
phagocytes, performed by:
professional macrophages
leucocytes (neutrophils)
trombocytes (rarely)
2. Immune-cell killing
3.Destruction by activated fragments of
complement (C5-C9)
Immune-mediated cell death
Cells, that perform immune killing:
 T-lymphocytes killers
 natural killers (NK-cells)
 Zero-cells (K-cell)
 macrophages
Mechanisms of killing:
 Antibody-related killing – against the cell
cytotoxical K-cell registers by antibodies, which
causes elimination.
 AB-independent killing - elimination by killers
(NK-cells, T-killers) without antibodies. Killers
recognize the cells-targets in accordance with
the main complex of histocompeabiality (HLA-1
or HLA-2).
2. Immune-cells killing
NECROSIS OF ORGANS
It is destruction of all
components of organs
(specialized cells, vessels,
stroma, intercellular matrix,
nerves) in the living organism
under action of critical
alteration.
Reasons of development of necrosis:
protracted ischemia
stopping of arterial blood supplying
damage by the mechanical and
chemical factors
inflammatory-destructive action of
infects – bacteria, fungi, viruses
massive damage of organ by
endogenous metabolites
CLASSIFICATION OF NECROSIS OF ORGANS
I According to morphology:
1. Dry necrosis (coagulative) – coagulations of proteins
- caseouse – at syphilis, leprosis, tuberculosis
- fibrinouse – in vessel’s walls at hypertonic disease
2. Wet necrosis (colliquative) – lysis, hydrolysis of soft tissue
3. Fermented necrosis of fat tissue (fat necrosis) – destruction o
fat tissue by ferments of pancreas
II According to spreading:
1. partial necrosis of specialized cells
2. total necrosis
3. selective hearth necrosis of specialized cells
III According to clinic-morphological picture:
1. gangrene
2. infarction (heart attack)
3. noma
4. bedsores
Clinic-morphological forms of necrosis of
organs:
1. Gangrene – total necrosis of the
organ, connected with the external
environment:
а) dry – at the thrombosis of arteries, an
organ acquires the black coloring
b)moist (wet) – at the thrombosis of arteries
and veins + influencing of putrid bacteria
c)gas (anaerobic) – necrotic tissue is
infected by Cl.perfingens
Clinic-morphological forms of necrosis of
organs:
2.Infarction – localized necrosis of part of
organ as a result of stopping of regional
circulation of blood (thrombosis, embolism,
pressuring of the vessel by tumor).
Morphological forms:
а) white (ischemic)
b)red (hemorrhagic)
c) white with hemorrhagic halo
Clinic-morphological forms of necrosis of
organs:
3.Bedsores – necrosis of soft tissue from the
local violation of blood circulation at
immobilized patients
4.Noma – widespread necrosis of soft tissue
under influence of bacterias (Bacterium
fusiformis, spirocheta dentinum) or fungies at
immune insufiency.
Morphological forms of tissue
necrosis:
Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Stages of development of necrosis:
1.Before-necrotic changes – from the beginning
of damage to stopping of implementation of the
specialized functions (8-15 hours).
2.Stage of necrosis – destruction of components
and structures of organ with formation of
biological demarcation of dead tissue (it takes a
few days).
Microscopically: kariocytolysis, coagulative
necrosis of cell, destruction of vessels.
Clinic: functional insufficiency of organ, fever,
leykocytosis.
3.The Postnecrotic changes – reparative
regeneration (remodulation) with complete or
not full regeneration of organ structures.
The outcomes of necrosis are the following:
 organization – the replacement of necrotic tissues by
connective tissue
 incapsulation – formation of connective tissue
capsula around necrotic area
 petrification – accumulation of calcium salts in the
area of necrosis
 cyst formation
 hyaline change – the accumulation of hyaline masses
in the area of necrosis
 sequestration – the formation of sequestrum
 ossification – the appearance of bone tissue in the
area of necrosis
 regeneration – the restoration of necrotic tissues
 purulent fusion of necrotic tissues
 mutilation – spontaneous tearing away of the
necrotic tissues
 autolysis

Contenu connexe

Tendances

Neoplasia Etiology and pathogenesis of cancer
Neoplasia Etiology and pathogenesis of cancerNeoplasia Etiology and pathogenesis of cancer
Neoplasia Etiology and pathogenesis of cancer
Subramani Parasuraman
 
General pathology lecture 4 cellular adaptation
General pathology lecture 4 cellular adaptationGeneral pathology lecture 4 cellular adaptation
General pathology lecture 4 cellular adaptation
Lheanne Tesoro
 
INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflamma...
INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflamma...INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflamma...
INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflamma...
Bahaudin zakriya university multan pakistan
 

Tendances (20)

Acute leukemia
Acute leukemiaAcute leukemia
Acute leukemia
 
Pathology of Acute Inflammation
Pathology of Acute InflammationPathology of Acute Inflammation
Pathology of Acute Inflammation
 
Cell injury, cell death & adaptations by Dr Nadeem (RMC)
Cell injury, cell death & adaptations by Dr Nadeem (RMC)Cell injury, cell death & adaptations by Dr Nadeem (RMC)
Cell injury, cell death & adaptations by Dr Nadeem (RMC)
 
Ch 2 adaptations, cell injury, cell death
Ch 2 adaptations, cell injury, cell deathCh 2 adaptations, cell injury, cell death
Ch 2 adaptations, cell injury, cell death
 
Cellular adaptation
Cellular adaptationCellular adaptation
Cellular adaptation
 
Neoplasia Etiology and pathogenesis of cancer
Neoplasia Etiology and pathogenesis of cancerNeoplasia Etiology and pathogenesis of cancer
Neoplasia Etiology and pathogenesis of cancer
 
Pathology Lecture - Neoplasia
Pathology Lecture - NeoplasiaPathology Lecture - Neoplasia
Pathology Lecture - Neoplasia
 
Bio 134 Pathology Introduction Part 2
Bio 134 Pathology Introduction Part 2Bio 134 Pathology Introduction Part 2
Bio 134 Pathology Introduction Part 2
 
Pathology of blood
Pathology of bloodPathology of blood
Pathology of blood
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 
Mechanism of cell injury
Mechanism of cell injuryMechanism of cell injury
Mechanism of cell injury
 
Pathology healing and repair stmu
Pathology healing and repair stmuPathology healing and repair stmu
Pathology healing and repair stmu
 
Cellular adaptations, injury and death.. Lecture 1
Cellular adaptations, injury and death.. Lecture 1Cellular adaptations, injury and death.. Lecture 1
Cellular adaptations, injury and death.. Lecture 1
 
General pathology lecture 4 cellular adaptation
General pathology lecture 4 cellular adaptationGeneral pathology lecture 4 cellular adaptation
General pathology lecture 4 cellular adaptation
 
Haemodynamic disorders.
Haemodynamic disorders.Haemodynamic disorders.
Haemodynamic disorders.
 
Neoplasia 4
Neoplasia 4Neoplasia 4
Neoplasia 4
 
clinical aspects of neoplasia
clinical aspects of neoplasiaclinical aspects of neoplasia
clinical aspects of neoplasia
 
Hyperemia and congestion edema
Hyperemia and congestion edema Hyperemia and congestion edema
Hyperemia and congestion edema
 
Morphology of-acute-inflammation
Morphology of-acute-inflammationMorphology of-acute-inflammation
Morphology of-acute-inflammation
 
INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflamma...
INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflamma...INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflamma...
INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflamma...
 

Similaire à Necrosis. critical injury

CELL INJURY,ADAPTATION AND DEATH-2.1.pptx
CELL INJURY,ADAPTATION AND DEATH-2.1.pptxCELL INJURY,ADAPTATION AND DEATH-2.1.pptx
CELL INJURY,ADAPTATION AND DEATH-2.1.pptx
PharmTecM
 
Dr.Jasveer. cell injury presentation.pptx
Dr.Jasveer. cell injury presentation.pptxDr.Jasveer. cell injury presentation.pptx
Dr.Jasveer. cell injury presentation.pptx
jasveer15
 
Cell inj apoptosis
Cell inj apoptosisCell inj apoptosis
Cell inj apoptosis
Aiman Iqbal
 
Mechanism cell deaths
Mechanism cell deathsMechanism cell deaths
Mechanism cell deaths
norazhaniazmi
 

Similaire à Necrosis. critical injury (20)

Cell injury
Cell injuryCell injury
Cell injury
 
Cell injury-necrosis
Cell injury-necrosisCell injury-necrosis
Cell injury-necrosis
 
Cell injury and cell death2
Cell injury and cell death2Cell injury and cell death2
Cell injury and cell death2
 
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injury
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injuryirreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injury
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injury
 
cell injury apotosis necrosis.pptx
cell injury apotosis necrosis.pptxcell injury apotosis necrosis.pptx
cell injury apotosis necrosis.pptx
 
Cell death.pptx
Cell death.pptxCell death.pptx
Cell death.pptx
 
Necrosis and apoptosis
Necrosis and apoptosisNecrosis and apoptosis
Necrosis and apoptosis
 
CELL INJURY,ADAPTATION AND DEATH-2.1.pptx
CELL INJURY,ADAPTATION AND DEATH-2.1.pptxCELL INJURY,ADAPTATION AND DEATH-2.1.pptx
CELL INJURY,ADAPTATION AND DEATH-2.1.pptx
 
introductionofpathology-1903613134414.pdf
introductionofpathology-1903613134414.pdfintroductionofpathology-1903613134414.pdf
introductionofpathology-1903613134414.pdf
 
Introduction of pathology
Introduction of pathologyIntroduction of pathology
Introduction of pathology
 
Cell death and necrosis
Cell death and necrosisCell death and necrosis
Cell death and necrosis
 
Cell injury
Cell injuryCell injury
Cell injury
 
Cell death
Cell deathCell death
Cell death
 
APOPTOSIS by dr Alfarah.pptx
APOPTOSIS by dr Alfarah.pptxAPOPTOSIS by dr Alfarah.pptx
APOPTOSIS by dr Alfarah.pptx
 
Basic principles of cell injury
Basic principles of cell injuryBasic principles of cell injury
Basic principles of cell injury
 
Dr.Jasveer. cell injury presentation.pptx
Dr.Jasveer. cell injury presentation.pptxDr.Jasveer. cell injury presentation.pptx
Dr.Jasveer. cell injury presentation.pptx
 
Cell injury & cell death
Cell injury & cell deathCell injury & cell death
Cell injury & cell death
 
Cell inj apoptosis
Cell inj apoptosisCell inj apoptosis
Cell inj apoptosis
 
NECROSIS by Shabistan.pptx
NECROSIS by Shabistan.pptxNECROSIS by Shabistan.pptx
NECROSIS by Shabistan.pptx
 
Mechanism cell deaths
Mechanism cell deathsMechanism cell deaths
Mechanism cell deaths
 

Plus de Ganapathy Tamilselvan

Plus de Ganapathy Tamilselvan (20)

Rickets Hypervitaminosis spasmophilia
Rickets Hypervitaminosis spasmophiliaRickets Hypervitaminosis spasmophilia
Rickets Hypervitaminosis spasmophilia
 
Protein energy malnutrition in children
Protein energy malnutrition in childrenProtein energy malnutrition in children
Protein energy malnutrition in children
 
Bronchitis lecture in children
Bronchitis lecture in childrenBronchitis lecture in children
Bronchitis lecture in children
 
Bronchial asthma in children
Bronchial asthma in childrenBronchial asthma in children
Bronchial asthma in children
 
Bronchial asthma in children
Bronchial asthma in childrenBronchial asthma in children
Bronchial asthma in children
 
Acute Rheumatic Fever in children
Acute Rheumatic Fever in childrenAcute Rheumatic Fever in children
Acute Rheumatic Fever in children
 
Acute respiratory diseases in children
Acute respiratory diseases in childrenAcute respiratory diseases in children
Acute respiratory diseases in children
 
Pharmacology of the Kidney and Uterus
Pharmacology of the Kidney and UterusPharmacology of the Kidney and Uterus
Pharmacology of the Kidney and Uterus
 
Pharmacology of the Respiratory System
Pharmacology of the Respiratory SystemPharmacology of the Respiratory System
Pharmacology of the Respiratory System
 
Adverse Drugs Reactions
Adverse Drugs ReactionsAdverse Drugs Reactions
Adverse Drugs Reactions
 
Pharmacology of Antihelmintic and Antisyphilitic Drugs
Pharmacology of Antihelmintic and Antisyphilitic DrugsPharmacology of Antihelmintic and Antisyphilitic Drugs
Pharmacology of Antihelmintic and Antisyphilitic Drugs
 
Sulfonamides, Fluoroquinolones, Oxiquinolines, Nitrofurans,Quinoxalines, Oxaz...
Sulfonamides, Fluoroquinolones, Oxiquinolines, Nitrofurans,Quinoxalines, Oxaz...Sulfonamides, Fluoroquinolones, Oxiquinolines, Nitrofurans,Quinoxalines, Oxaz...
Sulfonamides, Fluoroquinolones, Oxiquinolines, Nitrofurans,Quinoxalines, Oxaz...
 
Pharmacology of Antibiotics
Pharmacology of AntibioticsPharmacology of Antibiotics
Pharmacology of Antibiotics
 
Pharmacology of Antihistamine agents. Immunopharmacology
Pharmacology of Antihistamine agents. ImmunopharmacologyPharmacology of Antihistamine agents. Immunopharmacology
Pharmacology of Antihistamine agents. Immunopharmacology
 
Pharmacology of drugs used in Endocrine Disorders
Pharmacology of drugs used in Endocrine DisordersPharmacology of drugs used in Endocrine Disorders
Pharmacology of drugs used in Endocrine Disorders
 
Pharmacology of Drugs Affecting Blood
Pharmacology of Drugs Affecting BloodPharmacology of Drugs Affecting Blood
Pharmacology of Drugs Affecting Blood
 
Antihypertensive and Lipid Lowering Drugs
Antihypertensive and Lipid Lowering DrugsAntihypertensive and Lipid Lowering Drugs
Antihypertensive and Lipid Lowering Drugs
 
Antianginal Drugs
Antianginal DrugsAntianginal Drugs
Antianginal Drugs
 
Cardiotonic Drugs. Antiarrhythmic Agents
Cardiotonic Drugs. Antiarrhythmic AgentsCardiotonic Drugs. Antiarrhythmic Agents
Cardiotonic Drugs. Antiarrhythmic Agents
 
Pharmacology of Gastrointestinal Diseases
Pharmacology of Gastrointestinal DiseasesPharmacology of Gastrointestinal Diseases
Pharmacology of Gastrointestinal Diseases
 

Dernier

Salient Features of India constitution especially power and functions
Salient Features of India constitution especially power and functionsSalient Features of India constitution especially power and functions
Salient Features of India constitution especially power and functions
KarakKing
 

Dernier (20)

Accessible Digital Futures project (20/03/2024)
Accessible Digital Futures project (20/03/2024)Accessible Digital Futures project (20/03/2024)
Accessible Digital Futures project (20/03/2024)
 
Jamworks pilot and AI at Jisc (20/03/2024)
Jamworks pilot and AI at Jisc (20/03/2024)Jamworks pilot and AI at Jisc (20/03/2024)
Jamworks pilot and AI at Jisc (20/03/2024)
 
How to setup Pycharm environment for Odoo 17.pptx
How to setup Pycharm environment for Odoo 17.pptxHow to setup Pycharm environment for Odoo 17.pptx
How to setup Pycharm environment for Odoo 17.pptx
 
Micro-Scholarship, What it is, How can it help me.pdf
Micro-Scholarship, What it is, How can it help me.pdfMicro-Scholarship, What it is, How can it help me.pdf
Micro-Scholarship, What it is, How can it help me.pdf
 
Unit 3 Emotional Intelligence and Spiritual Intelligence.pdf
Unit 3 Emotional Intelligence and Spiritual Intelligence.pdfUnit 3 Emotional Intelligence and Spiritual Intelligence.pdf
Unit 3 Emotional Intelligence and Spiritual Intelligence.pdf
 
Mehran University Newsletter Vol-X, Issue-I, 2024
Mehran University Newsletter Vol-X, Issue-I, 2024Mehran University Newsletter Vol-X, Issue-I, 2024
Mehran University Newsletter Vol-X, Issue-I, 2024
 
Google Gemini An AI Revolution in Education.pptx
Google Gemini An AI Revolution in Education.pptxGoogle Gemini An AI Revolution in Education.pptx
Google Gemini An AI Revolution in Education.pptx
 
NO1 Top Black Magic Specialist In Lahore Black magic In Pakistan Kala Ilam Ex...
NO1 Top Black Magic Specialist In Lahore Black magic In Pakistan Kala Ilam Ex...NO1 Top Black Magic Specialist In Lahore Black magic In Pakistan Kala Ilam Ex...
NO1 Top Black Magic Specialist In Lahore Black magic In Pakistan Kala Ilam Ex...
 
Salient Features of India constitution especially power and functions
Salient Features of India constitution especially power and functionsSalient Features of India constitution especially power and functions
Salient Features of India constitution especially power and functions
 
Fostering Friendships - Enhancing Social Bonds in the Classroom
Fostering Friendships - Enhancing Social Bonds  in the ClassroomFostering Friendships - Enhancing Social Bonds  in the Classroom
Fostering Friendships - Enhancing Social Bonds in the Classroom
 
How to Create and Manage Wizard in Odoo 17
How to Create and Manage Wizard in Odoo 17How to Create and Manage Wizard in Odoo 17
How to Create and Manage Wizard in Odoo 17
 
Basic Civil Engineering first year Notes- Chapter 4 Building.pptx
Basic Civil Engineering first year Notes- Chapter 4 Building.pptxBasic Civil Engineering first year Notes- Chapter 4 Building.pptx
Basic Civil Engineering first year Notes- Chapter 4 Building.pptx
 
Beyond_Borders_Understanding_Anime_and_Manga_Fandom_A_Comprehensive_Audience_...
Beyond_Borders_Understanding_Anime_and_Manga_Fandom_A_Comprehensive_Audience_...Beyond_Borders_Understanding_Anime_and_Manga_Fandom_A_Comprehensive_Audience_...
Beyond_Borders_Understanding_Anime_and_Manga_Fandom_A_Comprehensive_Audience_...
 
This PowerPoint helps students to consider the concept of infinity.
This PowerPoint helps students to consider the concept of infinity.This PowerPoint helps students to consider the concept of infinity.
This PowerPoint helps students to consider the concept of infinity.
 
Python Notes for mca i year students osmania university.docx
Python Notes for mca i year students osmania university.docxPython Notes for mca i year students osmania university.docx
Python Notes for mca i year students osmania university.docx
 
Application orientated numerical on hev.ppt
Application orientated numerical on hev.pptApplication orientated numerical on hev.ppt
Application orientated numerical on hev.ppt
 
Understanding Accommodations and Modifications
Understanding  Accommodations and ModificationsUnderstanding  Accommodations and Modifications
Understanding Accommodations and Modifications
 
Exploring_the_Narrative_Style_of_Amitav_Ghoshs_Gun_Island.pptx
Exploring_the_Narrative_Style_of_Amitav_Ghoshs_Gun_Island.pptxExploring_the_Narrative_Style_of_Amitav_Ghoshs_Gun_Island.pptx
Exploring_the_Narrative_Style_of_Amitav_Ghoshs_Gun_Island.pptx
 
Sensory_Experience_and_Emotional_Resonance_in_Gabriel_Okaras_The_Piano_and_Th...
Sensory_Experience_and_Emotional_Resonance_in_Gabriel_Okaras_The_Piano_and_Th...Sensory_Experience_and_Emotional_Resonance_in_Gabriel_Okaras_The_Piano_and_Th...
Sensory_Experience_and_Emotional_Resonance_in_Gabriel_Okaras_The_Piano_and_Th...
 
Food safety_Challenges food safety laboratories_.pdf
Food safety_Challenges food safety laboratories_.pdfFood safety_Challenges food safety laboratories_.pdf
Food safety_Challenges food safety laboratories_.pdf
 

Necrosis. critical injury

  • 1. Critical Alteration Morphology of Cell Death Necrosis of Tissue and Organ
  • 2. Critical Damage and Cell Death Critical damage it is molecular-sub- cellular violation of metabolism and fading of function of specialized cells. Cell death it is destruction of specialized cells in the living organism under action of critical damage factors.
  • 3. Critical Damage and Cell Death Objects of critical damage are structures of the cells: 1. mitochondria 2. genetical apparatus (nuclear DNA) 3. plasmatic membrane 4. biosynthetic system 5. cytoskeleton 6. lysosomes and peroxisomes Changes in cells can’t be determined by light microscope, it is recognized by molecular-cytochemical and autography methods.
  • 4. Reasons of development: I. Endogenous metabolic catastrophe: 1.bioenergetics insufficiency of cells (hypoxia of different genesis) 2.damage of the cells by the surplus of free oxygen (O-) and oxide nitrogen (NO) 3. damage of the cells by the free radicals 4. increased of the ionized calcium in the cells 5. acid alteration of cells (pH  7) 6. damage of cells by the surplus of own mediators (exayto-toxical damage) 7. denaturation and/or proteolysis out of control 8. activating of hydroxy-oxidization of lipids
  • 5. II. Exogenous factors of injury: 1. infectious aggression (viruses, bacteria, fungi's) 2. physical and/or chemical damages (gamma- and ultraviolet damage, hypo-/hyperthermia, poisons, mechanical, electric damages) 3. Immunological damages : а) at overloading of organism by foreign albumen в) iatrogenic damage (anesthetics, preparations of blood, solutions, medicines) 4. damage by enzymes and aggressive molecules of macrophages and leucocytes (factor of tumor necrosis, oxide of nitrogen, hydrolytical enzymes of lysosom - proteases, lipases, phosphates, hydrolyses)
  • 6. Consequences of critical damage: partial necrosis of cell destruction of cells by necrosis pathogenic induction apoptosis immune elimination of cells reparative regeneration (renewal) stimulation of neighbors development of inflammation damage of genome and appearance of new tumor generations
  • 7. NECROSIS Necrosis - it is death of cells or tissues in living organism. Other forms of organ destructions: Autolysis – post mortem destruction of organs under action of enzymes, produced by the dead cells or bacteria. Necrobiosis – protracted process of destruction of tissue (trophic ulcers).
  • 8. NECROSIS CELL 1. Necrosis: -coagulative -colliquative 2. Apoptosis 3. Immune- mediated cell death: - phagocytosis TISSUE 1. Coagulative: - fibrinoid - caseous 2. Colliquative 3. Fat necrosis ORGAN 1. Infarction: - white - red - white with hemorrhagic hal 2. Gangrene: - wet - dry 3. Noma 4. Bedsores - immune-cell killing - destruction by activated fragments of complement (C5-C9)
  • 9. It is the premature death and destruction of cell’s organelles in the living organism under action of critical damage factors Phases of development 1. Critical damage 2. Destruction of cells and intercellular connections: - cytokaryolysis, - coagulative necrosis 3. Post-necrotic transformation of cells Duration: 1 min – 24 hours NECROSIS of CELL
  • 10. Classification of Cells Death, based on the mechanism of development: Necrosis of specialized cells  Pathogenic inducted apoptosis Selective immunological elimination of cells
  • 11. Morphology of cell destruction: 1. Karyolysis - the basophilic of the chromatin may fade, a change that reflects the activation of the DNA-ses. 2. Pyknosis - characterized by nuclear shrinkage and increased basophiles. Here the DNA apparently condenses into a solid, shrunken basophilic mass. 3. Karyorrhexis - the pyknotic or partially pyknotic nucleus undergoes fragmentation.
  • 12. Post-necrotic transformation of cells in living organism 1.Autolysis – destruction of cells by ferments of the organism 2. Phagocytosis by macrophages 3.Destruction by free-radical molecules of leucocytes (at inflammation) 4.Destruction by ferments of bacteria (at infected injury)
  • 13. Pathogenic inducted apoptosis It is a "programmed by genes cell death" or cell suicide, that is initiated by internal or external factors of critical damage. Features of apoptosis: 1.The process begins at activation of genes of apoptosis or inhibition of genes that can stop apoptosis 2. Duration of the process – 10-60min 3.Fragmentation of cell into apoptotic bodies at the end the process
  • 14. 1. Cell shrinkage. Cell is smaller in size; the cytoplasm is dense. 2. Chromatin condensation. The chromatin aggregates peripherally, under the nuclear membrane, into well-delimited dense masses of various shapes and sizes. The nucleus break up, producing two or more fragments Morphologic stages of apoptosis .
  • 15. Morphologic stages of apoptosis 3. Formation of cytoplasmatical blebs and apoptotic bodies. The apoptotic cell first shows extensive surface blebbing, then undergoes fragmentation into a number of membrane- bound apoptotic bodies composed of cytoplasm and tightly packed organelles, with or without a nuclear fragment. 4. Phagocytosis of apoptotic cells or bodies by adjacent healthy cells, either parenchymal cells or macrophages.
  • 16. Immune-mediated cell death It is damage of cells by immunocytes and auto- antibodies with destruction of cells in living organism. By this method can be destroyed: 1. Tumor cells 2. Transplanted cells 3. Infected cells 4. Normal cells (at autoimmune disease) It is performed by: - immunocytes - activated fragments of complement (AB)
  • 17. Phases of process: 1. Recognition of damaged cells by IS 2. Destroying (killing) of cells Types of Immune-mediated cell death: 1.Phagocytosis – it is absorbtion and destruction by macrophages after opsonization in phagolysosoms of phagocytes, performed by: professional macrophages leucocytes (neutrophils) trombocytes (rarely) 2. Immune-cell killing 3.Destruction by activated fragments of complement (C5-C9) Immune-mediated cell death
  • 18. Cells, that perform immune killing:  T-lymphocytes killers  natural killers (NK-cells)  Zero-cells (K-cell)  macrophages Mechanisms of killing:  Antibody-related killing – against the cell cytotoxical K-cell registers by antibodies, which causes elimination.  AB-independent killing - elimination by killers (NK-cells, T-killers) without antibodies. Killers recognize the cells-targets in accordance with the main complex of histocompeabiality (HLA-1 or HLA-2). 2. Immune-cells killing
  • 19. NECROSIS OF ORGANS It is destruction of all components of organs (specialized cells, vessels, stroma, intercellular matrix, nerves) in the living organism under action of critical alteration.
  • 20. Reasons of development of necrosis: protracted ischemia stopping of arterial blood supplying damage by the mechanical and chemical factors inflammatory-destructive action of infects – bacteria, fungi, viruses massive damage of organ by endogenous metabolites
  • 21. CLASSIFICATION OF NECROSIS OF ORGANS I According to morphology: 1. Dry necrosis (coagulative) – coagulations of proteins - caseouse – at syphilis, leprosis, tuberculosis - fibrinouse – in vessel’s walls at hypertonic disease 2. Wet necrosis (colliquative) – lysis, hydrolysis of soft tissue 3. Fermented necrosis of fat tissue (fat necrosis) – destruction o fat tissue by ferments of pancreas II According to spreading: 1. partial necrosis of specialized cells 2. total necrosis 3. selective hearth necrosis of specialized cells III According to clinic-morphological picture: 1. gangrene 2. infarction (heart attack) 3. noma 4. bedsores
  • 22. Clinic-morphological forms of necrosis of organs: 1. Gangrene – total necrosis of the organ, connected with the external environment: а) dry – at the thrombosis of arteries, an organ acquires the black coloring b)moist (wet) – at the thrombosis of arteries and veins + influencing of putrid bacteria c)gas (anaerobic) – necrotic tissue is infected by Cl.perfingens
  • 23. Clinic-morphological forms of necrosis of organs: 2.Infarction – localized necrosis of part of organ as a result of stopping of regional circulation of blood (thrombosis, embolism, pressuring of the vessel by tumor). Morphological forms: а) white (ischemic) b)red (hemorrhagic) c) white with hemorrhagic halo
  • 24. Clinic-morphological forms of necrosis of organs: 3.Bedsores – necrosis of soft tissue from the local violation of blood circulation at immobilized patients 4.Noma – widespread necrosis of soft tissue under influence of bacterias (Bacterium fusiformis, spirocheta dentinum) or fungies at immune insufiency.
  • 25. Morphological forms of tissue necrosis: Coagulative necrosis Liquefactive necrosis Caseous necrosis Fat necrosis
  • 26. Stages of development of necrosis: 1.Before-necrotic changes – from the beginning of damage to stopping of implementation of the specialized functions (8-15 hours). 2.Stage of necrosis – destruction of components and structures of organ with formation of biological demarcation of dead tissue (it takes a few days). Microscopically: kariocytolysis, coagulative necrosis of cell, destruction of vessels. Clinic: functional insufficiency of organ, fever, leykocytosis. 3.The Postnecrotic changes – reparative regeneration (remodulation) with complete or not full regeneration of organ structures.
  • 27. The outcomes of necrosis are the following:  organization – the replacement of necrotic tissues by connective tissue  incapsulation – formation of connective tissue capsula around necrotic area  petrification – accumulation of calcium salts in the area of necrosis  cyst formation  hyaline change – the accumulation of hyaline masses in the area of necrosis  sequestration – the formation of sequestrum  ossification – the appearance of bone tissue in the area of necrosis  regeneration – the restoration of necrotic tissues  purulent fusion of necrotic tissues  mutilation – spontaneous tearing away of the necrotic tissues  autolysis