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Necrosis
necrosis , MI ppt final.pptx basic to advanced a d it's reasons
necrosis , MI ppt final.pptx basic to advanced a d it's reasons
Necrosis
Definition:-
It is a programmed cell death, largely
resulting from the degradative action of
enzymes on lethally injured cells.
necrosis , MI ppt final.pptx basic to advanced a d it's reasons
necrosis , MI ppt final.pptx basic to advanced a d it's reasons
Hypoxia
Physical agents
Chemical agents
Infectious agents
Immunologic reactions
Genetic make up
Nutritional imbalance
Aging
Causes
External stimuli
↓
ROS(lipid per oxidation)
↓
Increase cytosolic Ca⁺⁺
Pathophysiology
↓
Mitochondrial injury
↓
Mitochondrial permeability transition
↓
Loss of membrane potential
↓
Inability to generate ATP
↓
Cell death (necrosis)
necrosis , MI ppt final.pptx basic to advanced a d it's reasons
necrosis , MI ppt final.pptx basic to advanced a d it's reasons
necrosis , MI ppt final.pptx basic to advanced a d it's reasons
Nuclear degeneration
Increase eosinophillia
Fragmented cell membrane
Glassy appearance due to lack of glycogen
Calcification
Mitochondrial damage
Nuclear damage:- It includes
Pyknosis: Nuclear shrinkage.
Karyolysis: Breakdown of nuclear material.
Karyohexis:- Nuclear fragmentation.
MORPHOLOGY
Type Cause Cell Morphology Examples
(1) Coagulation
Necrosis
 Ischemia  Framework remains intact.
 Cytoplasmic protein degrades.
 Proteolysis is blocked
 Phagocytosis of necrotic cells.
 Myocardial Infarction
(1) Liquefaction Necrosis  Bacterial and Fungal Infection
 Acute Inflammation
 Cell membrane damage.
 Cell contents liquefy.
 Liquid viscous mass is formed.
 Hypoxic death in CNS.
(1) Caseous
Necrosis
 M.Tuberculosis  Cell architecture destroy but cell
contents does not
Liquefy.
 Granuloma formation.
 Lysed cell appears as an amorphous and
granular.
 Lung tuberculosis.
(4) Fat necrosis  Activated pancreatic lipases.
 Acute pancreatitis.
 Cell membrane liquefy.
 Triglyceride esters destroy.
 Calcification.
 White chalky area.
 Necrosis of fat cells.
Slide
Identification
Normal myocardial cells
Myocardial cells in case of
coagulation necrosis
Liquefactive necrosis
Liquefaction necrosis in
the epidermis and
dermis in an abscess of
the skin.
The abscess cavity is
filled with
polymorphonuclear
leukocytes
Caseous Necrosis
Caseous necrosis in a
tuberculosis lymph
node, showing the
typical amorphous,
granular, eosinophilic,
necrotic center
surrounded by
granulomatous
inflammation.
Fat necrosis
Fat necrosis in acute pancreatitis.
The release and activation of
lipolytic pancreatic enzymes
results in the necrosis of
surrounding adipose tissue. The
hydrolysis of the triglycerides
releases free fatty acids, which
precipitate as calcium soaps in
the necrotic debris.
Myocardial Infarction
Definition:-
(Myo means (muscle), (cardial)
means (heart) and (infarction)
means (damage or death).
“The term myocardial infarction
focuses on the myocardium (the
heart muscles) and the changes that
occur in it due to sudden
deprivation of circulating blood. The
main change is necrosis (death) of
myocardial tissue.”
Myocardial Infarction
Causes:-
The major causes are
•Atherosclerotic plaques
•Hypoxia
•Respiratory failure
•Hypercholesterolemia
•Coronary artery vasospasm
•Arrhythmias
•Coronary heart disease
(angina)
Mechanism:-
Coronary artery obstruction (due to atherosclerotic platelet plaque)
Less oxygen supply to heart muscle
Aerobic glycolysis
Inadequate production of ATP
Loss of contractility (within 1 min)
Necrosis (mainly coagulation necrosis) – (within 20-40mins)
Cause
Clinical signs and symptoms: -
It includes
•Sudden and acute chest pain
•Nausea
•Vomiting
•Ventricular fibrillation
•Shortness of breath
•Anxiety
•Palpitation
•Sweating
Diagnostic Tests:-
•ECG
•Troponin Blood test
•Coronary Angiography
•Monitoring of BP, cholesterol level and pulse
rate
Treatment and counseling:-
(1)Patient is shifted to emergency room and oxygen is
given externally.
(2)I.V line is made from which different drug
combinations are given.
(3)Nitroglycerine is given sublingually.
(4)Streptokinase and Clopidogrel can also be given.
(5)Patient may be referred to angioplasty,
thrombolytic therapy and surgery as well.
=> For the protection from second heart attack,
patient is given antiplatelet drugs (e.g. aspirin), β-
blockers and ACE inhibitors are given. Statins are also
used to improve the cholesterol level.
necrosis , MI ppt final.pptx basic to advanced a d it's reasons
Preventive Measures:-
•Control of BP, blood sugar and cholesterol
•Don’t smoke
•Eat healthy and balance diet
•Exercise regularly
•Treatment of depression
•Control weight
Slide
Identification
Normal slide
Pathological
slide

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necrosis , MI ppt final.pptx basic to advanced a d it's reasons

  • 4. Necrosis Definition:- It is a programmed cell death, largely resulting from the degradative action of enzymes on lethally injured cells.
  • 7. Hypoxia Physical agents Chemical agents Infectious agents Immunologic reactions Genetic make up Nutritional imbalance Aging Causes
  • 8. External stimuli ↓ ROS(lipid per oxidation) ↓ Increase cytosolic Ca⁺⁺ Pathophysiology ↓ Mitochondrial injury ↓ Mitochondrial permeability transition ↓ Loss of membrane potential ↓ Inability to generate ATP ↓ Cell death (necrosis)
  • 12. Nuclear degeneration Increase eosinophillia Fragmented cell membrane Glassy appearance due to lack of glycogen Calcification Mitochondrial damage Nuclear damage:- It includes Pyknosis: Nuclear shrinkage. Karyolysis: Breakdown of nuclear material. Karyohexis:- Nuclear fragmentation. MORPHOLOGY
  • 13. Type Cause Cell Morphology Examples (1) Coagulation Necrosis  Ischemia  Framework remains intact.  Cytoplasmic protein degrades.  Proteolysis is blocked  Phagocytosis of necrotic cells.  Myocardial Infarction (1) Liquefaction Necrosis  Bacterial and Fungal Infection  Acute Inflammation  Cell membrane damage.  Cell contents liquefy.  Liquid viscous mass is formed.  Hypoxic death in CNS. (1) Caseous Necrosis  M.Tuberculosis  Cell architecture destroy but cell contents does not Liquefy.  Granuloma formation.  Lysed cell appears as an amorphous and granular.  Lung tuberculosis. (4) Fat necrosis  Activated pancreatic lipases.  Acute pancreatitis.  Cell membrane liquefy.  Triglyceride esters destroy.  Calcification.  White chalky area.  Necrosis of fat cells.
  • 15. Normal myocardial cells Myocardial cells in case of coagulation necrosis
  • 16. Liquefactive necrosis Liquefaction necrosis in the epidermis and dermis in an abscess of the skin. The abscess cavity is filled with polymorphonuclear leukocytes
  • 17. Caseous Necrosis Caseous necrosis in a tuberculosis lymph node, showing the typical amorphous, granular, eosinophilic, necrotic center surrounded by granulomatous inflammation.
  • 18. Fat necrosis Fat necrosis in acute pancreatitis. The release and activation of lipolytic pancreatic enzymes results in the necrosis of surrounding adipose tissue. The hydrolysis of the triglycerides releases free fatty acids, which precipitate as calcium soaps in the necrotic debris.
  • 20. Definition:- (Myo means (muscle), (cardial) means (heart) and (infarction) means (damage or death). “The term myocardial infarction focuses on the myocardium (the heart muscles) and the changes that occur in it due to sudden deprivation of circulating blood. The main change is necrosis (death) of myocardial tissue.” Myocardial Infarction
  • 21. Causes:- The major causes are •Atherosclerotic plaques •Hypoxia •Respiratory failure •Hypercholesterolemia •Coronary artery vasospasm •Arrhythmias •Coronary heart disease (angina)
  • 22. Mechanism:- Coronary artery obstruction (due to atherosclerotic platelet plaque) Less oxygen supply to heart muscle Aerobic glycolysis Inadequate production of ATP Loss of contractility (within 1 min) Necrosis (mainly coagulation necrosis) – (within 20-40mins) Cause
  • 23. Clinical signs and symptoms: - It includes •Sudden and acute chest pain •Nausea •Vomiting •Ventricular fibrillation •Shortness of breath •Anxiety •Palpitation •Sweating
  • 24. Diagnostic Tests:- •ECG •Troponin Blood test •Coronary Angiography •Monitoring of BP, cholesterol level and pulse rate
  • 25. Treatment and counseling:- (1)Patient is shifted to emergency room and oxygen is given externally. (2)I.V line is made from which different drug combinations are given. (3)Nitroglycerine is given sublingually. (4)Streptokinase and Clopidogrel can also be given. (5)Patient may be referred to angioplasty, thrombolytic therapy and surgery as well. => For the protection from second heart attack, patient is given antiplatelet drugs (e.g. aspirin), β- blockers and ACE inhibitors are given. Statins are also used to improve the cholesterol level.
  • 27. Preventive Measures:- •Control of BP, blood sugar and cholesterol •Don’t smoke •Eat healthy and balance diet •Exercise regularly •Treatment of depression •Control weight

Editor's Notes

  • #2: NARCOSIS: a state of stupor, drowsiness, or unconsciousness produced by drugs
  • #8: Lipid Peroxidation Caused by ROS. Cell membranes are sensitive to radical damage due to the presence of polyunsaturated fatty acids.  The cytosolic Ca²⁺ concentration ([Ca²⁺]c) controls virtually every activity of smooth muscle, including contraction, migration, transcription, division and apoptosis.
  • #17: lesion caused by eosinophil-related tissue damage and is associated with various eosinophilia-related conditions such as parasitic infestations, allergic reactions, hypereosinophilic syndrome, and neoplasms