0:00 - 29:40 When a cell is irreversibly damaged, either it undergoes necrosis or apoptosis. Necrosis always follows pathological cell injury by toxins, radiations, trauma, hypoxia. Apoptosis may be physiological (during embryogenesis) or pathological. NECROSIS: Necrosis is a series of morphological changes in a lethally and irreversibly injured cell. These changes may be recognized by light microscope only after a few hours. When cell is lethally injured, it cannot produce ATPs. Reserve of ATPs run out. In case of hypoxia, pyruvic acid produced from glucose cannot enter Krebs cycle. So they get converted into lactic acid. So intracellular environment becomes acidic. And structural and functional proteins get denatured. This will translate into morphological changes in cell. There is also enzymatic digestion of severely injured cell. a. These enzymes are from burst lysosomes.(autolysis) b. And also may be from inflammatory cells like neutrophils and macrophages. These enzymes also may be from proliferating microbes (Heterolysis) So causes of morphological changes: a. Enzymatic digestion b. Denaturation of proteins c. Loss of integrity of plasma membrane. Intracellular components leaks out and injure surrounding cells. This causes inflammation at the site. This will summon the leucocytes. This process does not happen in apoptosis. The summoned leucocytes eat the cell debris and produce factors that cause proliferation of cells at the site for repair or conversion of fibrocyte into fibroblast. DEATH OF PATIENT IMMEDIATELY AFTER LETHAL CELL INJURY: For example, a person dies within an hour of severe myocardial ischemia. The section of heart under light does not show necrotic changes. Because necrotic changes take some hours to manifest and can happen only in a live person. Other sign like plaque in coronary artery sections and past MI scars may be seen in dead person. However, in this case, because of loss of membrane integrity, intracellular myocardial proteins may leak in to blood and act as evidence of myocardial death. These proteins may be cardia Troponin T, cardiac Troponin I, CK-MB. These markers are also used to diagnose MI in live persons. ECG can also be used. If the person were to live, local inflammation would be produced and leucocytes would be summoned forming a necrotic picture and later fibrosis would have occurred at the site of necrosis. 29:40 - 49:30 MORPHOLOGICAL CHANGES IN NECROSIS: Normally cytoplasmic proteins bind eosinophillic stain. Ribosomes binds hemotoxyllin. DNA is basophilic and binds hematoxyllin. After irreversible injury, light microscopic changes seen are 1. Cell becomes intensely eosinophillic because a. Denatured intracellular proteins unfold and bind more eosinophil and cell becomes intensely eosinophillic. b. Disintegration of basophilic ribosomes. 2. Moth eaten appearance due to digestion of organalles and unstained pockets. 3. Granularity present in normal because of glycogen granules. 4. During necrosis, glycogen granules are lost and cell appearance becomes glassy and homogenous 5. Myelin figures are formed which are whorled phospholipid membrane formed from disintegrated membrane of organelles and cell. These will be ultimately be cleared by macrophages or undergo dystrophic calcification since they are difficult to digest. Ultra structural changes under Electron Microscope: 1. Plasma and organelle membrane discontinuity 2. Mitrochondrial swelling. 3. Amorphous bodies inside mitochondria 4. Intracellular myelin figures 5. Cytoplasmic amorphous deposits which are denatured proteins. DNA is also digested by DNAases Nuclear changes during necrosis may be any one of the following types 1. Karyolysis: Gradual disappearance of nucleus by gradual digestion of nuclear material 2. Pyknosis: Nucleus becomes intensely condensed and 3. Karyorrhexis: Nucleus becomes condensed and fragmented 49:30 - 1:20:12 DIFFERENT TYPES OF NECROSIS Coagulative necrosis: Hallmark: Maintenance of cellular architecture for few days but nucleus is lost within 1 or 2 days. Both structural and functional proteins undergo denaturation simultaneously. So enzymes are also denatured. So enzymatic digestion does not occur. So autolysis cannot occur. Example: Myocardial Infarction, Severe hypoxic injury of Spleen, Kidney, Liver Localised areas of coagulative necrosis is called infarct. After a few days, heterolysis by neutrophils and macrophages occurs. Brain cannot undergo coagulative necrosis. Liquefactive Necrosis: Severe hypoxia of brain causes liquefactive necrosis. Cellullar architecture not maintained. Enzymatic digestion occurs here( autolysis). Also heterolysis occurs by leucocytes and microbes. Other examples: necrosis by infection. Why do neutrophils come early than mcrophages? a. The chemotactic factors produced at first attract neutrophils. That which attract monocytes are produces later. b. Neutrophils are abundant c. Neutrophils are mobile In the later part of inflammation, macrophages are abundant than neutrophils. PUS: It is a product of liquefactive necrosis constitutes of alive, dead and dying local cells, microbes and neutrophils all covered with protein rich inflammatory exudates. ABCESS: Localised pus formation. Center of the collection consists of dead local cells, microbes, neutrophils. This is surrounded by active and alive local cells, microbes and neutrophils. This is further surrounded by blood vessels that is dilated and permeable. And finally, the periphery is made of fibrotic tissue and proliferating local tissue
I watched the video because I thought it was about studying apoptosis in detail, but the wonderful explanation of necrosis prevented me from leaving until the end!❤
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0:00 - 29:40
When a cell is irreversibly damaged, either it undergoes necrosis or apoptosis. Necrosis always follows pathological cell injury by toxins, radiations, trauma, hypoxia. Apoptosis may be physiological (during embryogenesis) or pathological.
NECROSIS:
Necrosis is a series of morphological changes in a lethally and irreversibly injured cell.
These changes may be recognized by light microscope only after a few hours.
When cell is lethally injured, it cannot produce ATPs. Reserve of ATPs run out.
In case of hypoxia, pyruvic acid produced from glucose cannot enter Krebs cycle. So they get converted into lactic acid. So intracellular environment becomes acidic. And structural and functional proteins get denatured. This will translate into morphological changes in cell.
There is also enzymatic digestion of severely injured cell.
a. These enzymes are from burst lysosomes.(autolysis)
b. And also may be from inflammatory cells like neutrophils and macrophages. These enzymes also may be from proliferating microbes (Heterolysis)
So causes of morphological changes:
a. Enzymatic digestion
b. Denaturation of proteins
c. Loss of integrity of plasma membrane. Intracellular components leaks out and injure surrounding cells. This causes inflammation at the site. This will summon the leucocytes. This process does not happen in apoptosis.
The summoned leucocytes eat the cell debris and produce factors that cause proliferation of cells at the site for repair or conversion of fibrocyte into fibroblast.
DEATH OF PATIENT IMMEDIATELY AFTER LETHAL CELL INJURY:
For example, a person dies within an hour of severe myocardial ischemia. The section of heart under light does not show necrotic changes. Because necrotic changes take some hours to manifest and can happen only in a live person. Other sign like plaque in coronary artery sections and past MI scars may be seen in dead person.
However, in this case, because of loss of membrane integrity, intracellular myocardial proteins may leak in to blood and act as evidence of myocardial death. These proteins may be cardia Troponin T, cardiac Troponin I, CK-MB.
These markers are also used to diagnose MI in live persons. ECG can also be used.
If the person were to live, local inflammation would be produced and leucocytes would be summoned forming a necrotic picture and later fibrosis would have occurred at the site of necrosis.
29:40 - 49:30
MORPHOLOGICAL CHANGES IN NECROSIS:
Normally cytoplasmic proteins bind eosinophillic stain. Ribosomes binds hemotoxyllin. DNA is basophilic and binds hematoxyllin.
After irreversible injury, light microscopic changes seen are
1. Cell becomes intensely eosinophillic because
a. Denatured intracellular proteins unfold and bind more eosinophil and cell becomes intensely eosinophillic.
b. Disintegration of basophilic ribosomes.
2. Moth eaten appearance due to digestion of organalles and unstained pockets.
3. Granularity present in normal because of glycogen granules.
4. During necrosis, glycogen granules are lost and cell appearance becomes glassy and homogenous
5. Myelin figures are formed which are whorled phospholipid membrane formed from disintegrated membrane of organelles and cell. These will be ultimately be cleared by macrophages or undergo dystrophic calcification since they are difficult to digest.
Ultra structural changes under Electron Microscope:
1. Plasma and organelle membrane discontinuity
2. Mitrochondrial swelling.
3. Amorphous bodies inside mitochondria
4. Intracellular myelin figures
5. Cytoplasmic amorphous deposits which are denatured proteins.
DNA is also digested by DNAases
Nuclear changes during necrosis may be any one of the following types
1. Karyolysis: Gradual disappearance of nucleus by gradual digestion of nuclear material
2. Pyknosis: Nucleus becomes intensely condensed and
3. Karyorrhexis: Nucleus becomes condensed and fragmented
49:30 - 1:20:12
DIFFERENT TYPES OF NECROSIS
Coagulative necrosis: Hallmark: Maintenance of cellular architecture for few days but nucleus is lost within 1 or 2 days. Both structural and functional proteins undergo denaturation simultaneously. So enzymes are also denatured. So enzymatic digestion does not occur. So autolysis cannot occur. Example: Myocardial Infarction, Severe hypoxic injury of Spleen, Kidney, Liver Localised areas of coagulative necrosis is called infarct. After a few days, heterolysis by neutrophils and macrophages occurs. Brain cannot undergo coagulative necrosis.
Liquefactive Necrosis: Severe hypoxia of brain causes liquefactive necrosis. Cellullar architecture not maintained. Enzymatic digestion occurs here( autolysis). Also heterolysis occurs by leucocytes and microbes. Other examples: necrosis by infection.
Why do neutrophils come early than mcrophages?
a. The chemotactic factors produced at first attract neutrophils. That which attract monocytes are produces later.
b. Neutrophils are abundant
c. Neutrophils are mobile
In the later part of inflammation, macrophages are abundant than neutrophils.
PUS: It is a product of liquefactive necrosis constitutes of alive, dead and dying local cells, microbes and neutrophils all covered with protein rich inflammatory exudates.
ABCESS: Localised pus formation. Center of the collection consists of dead local cells, microbes, neutrophils. This is surrounded by active and alive local cells, microbes and neutrophils. This is further surrounded by blood vessels that is dilated and permeable. And finally, the periphery is made of fibrotic tissue and proliferating local tissue
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I watched the video because I thought it was about studying apoptosis in detail, but the wonderful explanation of necrosis prevented me from leaving until the end!❤
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Sir, i am watching your lectures from class 9th....today I am in class 11th and I am still watching your lectures.Your lectures helps me a lot... especially in my 11th class.....
Sir, I am very thankful to you....💜💜...
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@@DoctorNajeeb sir, i have a doubt...is the following stem T/F
- The light microscopy changes precede ultra structural changes during necrosis
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Thank you so much Dr.Najeeb and happy holidays, where can I find the other part of necrosis (caseous, gangrenous, fibroid)?
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Excuse me is there are videos for all general pathology chapters?
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I find your basic lectures of medical science free where should I search for it: please help me sir
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Is it true that Necrotic cells do not generate ATP in the intracellular space?
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What is necrosis❤
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