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Questions and Answers
In the context of cellular injury, at what stage is necrosis considered inevitable, assuming no therapeutic intervention?
In the context of cellular injury, at what stage is necrosis considered inevitable, assuming no therapeutic intervention?
- Immediately following exposure to an injurious stimulus, regardless of its severity.
- Once the cell reaches a 'point of no return' characterized by irreversible damage. (correct)
- After the cell has initiated adaptive mechanisms to counteract the stressor.
- During the initial exposure to a reversible stressor, before any cellular changes occur.
Why does oncosis, as an initial mechanism of necrosis, lead to cell swelling and eventual lysis?
Why does oncosis, as an initial mechanism of necrosis, lead to cell swelling and eventual lysis?
- The cell actively uptakes water in an attempt to dilute intracellular toxins.
- Cell membrane integrity is immediately compromised, leading to uncontrolled water entry.
- Increased activity of sodium-potassium pumps causes excessive ion influx.
- Mitochondrial damage impairs ATP production, disrupting ion balance and causing water influx. (correct)
What is the primary reason coagulative necrosis results in the preservation of tissue architecture, albeit in a non-functional state?
What is the primary reason coagulative necrosis results in the preservation of tissue architecture, albeit in a non-functional state?
- The affected tissues are rapidly replaced by fibrous connective tissue.
- The inflammatory response is suppressed, limiting the activity of immune cells.
- Denaturation of structural proteins inhibits proteolytic enzymes, preventing complete cell breakdown. (correct)
- Rapid calcification of the dead cells prevents enzymatic degradation.
In liquefactive necrosis, what is the role of hydrolytic enzymes in the transformation of tissue into a liquid-like substance?
In liquefactive necrosis, what is the role of hydrolytic enzymes in the transformation of tissue into a liquid-like substance?
Why does gangrenous necrosis, particularly in its 'dry' form, result in tissue that appears desiccated and mummified?
Why does gangrenous necrosis, particularly in its 'dry' form, result in tissue that appears desiccated and mummified?
How does the unique pathophysiology of caseous necrosis, typically seen in tuberculosis, contribute to its characteristic 'cottage cheese-like' appearance?
How does the unique pathophysiology of caseous necrosis, typically seen in tuberculosis, contribute to its characteristic 'cottage cheese-like' appearance?
In fat necrosis, what is the mechanism by which saponification leads to the formation of dystrophic calcifications?
In fat necrosis, what is the mechanism by which saponification leads to the formation of dystrophic calcifications?
How does malignant hypertension induce fibrinoid necrosis in arteriolar walls?
How does malignant hypertension induce fibrinoid necrosis in arteriolar walls?
What is the significance of Karyolysis in necrotic cells, and how does it contrast with the nuclear changes observed in apoptosis?
What is the significance of Karyolysis in necrotic cells, and how does it contrast with the nuclear changes observed in apoptosis?
Why is the measurement of intracellular proteins released into circulation clinically useful in diagnosing specific types of tissue necrosis?
Why is the measurement of intracellular proteins released into circulation clinically useful in diagnosing specific types of tissue necrosis?
Flashcards
Necrosis
Necrosis
Cell death where membranes fall apart, usually after irreversible injury, causing enzyme leakage and inflammation.
Oncosis
Oncosis
A type of necrosis initiated by toxins or ischemia, leading to mitochondrial damage and cell swelling.
Coagulative Necrosis
Coagulative Necrosis
Necrosis due to hypoxia, causing protein denaturation and gel-like tissue with wedge-shaped infarcts. Often in heart, kidneys, or spleen.
Liquefactive Necrosis
Liquefactive Necrosis
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Gangrenous Necrosis
Gangrenous Necrosis
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Necrosis (Nuclear features)
Necrosis (Nuclear features)
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Pyknosis
Pyknosis
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Karyorrhexis
Karyorrhexis
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Karyolysis
Karyolysis
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Caseous Necrosis
Caseous Necrosis
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Study Notes
- Necrosis originates from the Greek word "Necros," meaning dead body
- It is a form of cell death characterized by the breakdown of cell membranes
- It typically occurs after irreversible cell injury
Pathophysiology and Mechanisms
- Cell injury progresses to a point of no return
- If the injurious stimulus is not removed, the cell undergoes necrosis
- Cellular enzymes leak out, leading to cell digestion
- An inflammatory response is triggered
Necrosis Initiation: Oncosis
- Oncosis is initiated by toxins or ischemia damaging the mitochondria
- Mitochondrial damage stops ATP synthesis
- Failure of ionic pumps increases the influx of sodium and water into the cell
- Increased sodium and water causes the cell to swell and rupture
- Immune cells release proteases and reactive oxygen species (ROS)
- Proteases degrade proteins
- Reactive oxygen species further damage tissues
- Tissue destruction can lead to organ dysfunction.
Types of Necrosis
Coagulative Necrosis
- Caused by hypoxia, most commonly due to ischemia
- Structural proteins denature
- Lysosomal enzymes become ineffective
- Dead tissue remains somewhat intact, appearing gel-like
- Pale wedge-shaped infarcts occur, with the apex pointing toward the obstruction
- Reperfusion injury can cause red infarcts
- It commonly occurs in the heart, kidneys, and spleen
Liquefactive Necrosis
- Caused by hydrolytic enzyme activity
- Enzymes digest cells into a creamy substance filled with dead immune cells
- Microglial cells in the brain liquefy necrotic tissue
- Pancreatic enzymes (like trypsin) digest pancreatic cells in pancreatitis
- Neutrophils liquefy tissue in abscesses, forming pus
- It commonly occurs in the brain, pancreas, and abscesses
Gangrenous Necrosis
- Caused by hypoxia affecting extremities or the gastrointestinal (GI) tract
- Dry gangrene resembles coagulative necrosis with mummified tissue
- If infected, it leads to liquefactive necrosis and becomes wet gangrene
Caseous Necrosis
- Caused by fungal or mycobacterial infections
- Mycobacterium tuberculosis classically is a cause
- Dead cells disintegrate but are not fully digested
- Tissue has a characteristic cottage cheese consistency
Fat Necrosis
- Caused by trauma to fatty organs, such as the pancreas or breast
- Adipose cells rupture, releasing fatty acids
- Fatty acids bind calcium, forming dystrophic calcifications (chalky deposits)
- In pancreatitis, lipase digests surrounding fat
Fibrinoid Necrosis
- Caused by malignant hypertension and vasculitis
- High blood pressure damages arterial walls, allowing fibrin deposition
- Vasculitis causes inflammation and vessel destruction
Necrosis vs. Apoptosis
Necrosis Features
- Pyknosis: nuclear shrinkage
- Karyorrhexis: fragmentation
- Karyolysis: nuclear fading
- Cell membrane breakdown, enzyme leakage, inflammation
Apoptosis Features
- Shrinkage and fragmentation of the nucleus but no karyolysis
- No inflammation occurs
- Rather, apoptotic bodies are phagocytosed cleanly
Clinical Correlation and Lab Tests
- Leakage of intracellular proteins can be detected through testing
- Myocardial infarction elevates troponin and creatine kinase-MB (CK-MB)
- Hepatocyte injury elevates AST and ALT
- Bile duct injury elevates alkaline phosphatase (ALP)
- Skeletal muscle injury elevates creatine kinase-MM (CK-MM) and aldolase
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