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Questions and Answers
What is the primary difference between reversible and irreversible cellular injury?
What is the primary difference between reversible and irreversible cellular injury?
Which of the following accurately describes pathogenesis?
Which of the following accurately describes pathogenesis?
What initiates a cascade of damaging events at the cellular level?
What initiates a cascade of damaging events at the cellular level?
Which change is NOT typically associated with reversible cellular injury?
Which change is NOT typically associated with reversible cellular injury?
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Which of the following best describes the outcome of persistent or intensified cellular injury?
Which of the following best describes the outcome of persistent or intensified cellular injury?
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What is the primary consequence of anaerobic glycolysis when oxidative phosphorylation is compromised?
What is the primary consequence of anaerobic glycolysis when oxidative phosphorylation is compromised?
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Which of the following is a direct effect of mitochondrial damage?
Which of the following is a direct effect of mitochondrial damage?
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What is the role of DAMPs in cellular injury?
What is the role of DAMPs in cellular injury?
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Which of the following cells can survive the longest without a blood supply?
Which of the following cells can survive the longest without a blood supply?
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What occurs as a result of ATP depletion in cells?
What occurs as a result of ATP depletion in cells?
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Which molecules are released during cellular damage that signal to the immune system?
Which molecules are released during cellular damage that signal to the immune system?
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What cellular abnormality is associated with necrosis?
What cellular abnormality is associated with necrosis?
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Which condition primarily leads to fat necrosis due to the digestion of fat tissue?
Which condition primarily leads to fat necrosis due to the digestion of fat tissue?
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What role do lipases play in the process of fat necrosis?
What role do lipases play in the process of fat necrosis?
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In pancreatitis, ischemia results from which of the following?
In pancreatitis, ischemia results from which of the following?
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What is formed during the process of saponification in fat necrosis?
What is formed during the process of saponification in fat necrosis?
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Which of the following is a secondary reaction that highlights the involvement of calcium in fat necrosis?
Which of the following is a secondary reaction that highlights the involvement of calcium in fat necrosis?
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What triggers the premature release of digestive enzymes in acinar cell injury?
What triggers the premature release of digestive enzymes in acinar cell injury?
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Duct obstruction can lead to fat necrosis primarily due to which underlying mechanism?
Duct obstruction can lead to fat necrosis primarily due to which underlying mechanism?
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What pathological change drives inflammation in the context of fat necrosis?
What pathological change drives inflammation in the context of fat necrosis?
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What effect does chronic alcoholism have on pancreatic acinar cells?
What effect does chronic alcoholism have on pancreatic acinar cells?
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What is primarily responsible for the chalky white deposits seen in fat necrosis?
What is primarily responsible for the chalky white deposits seen in fat necrosis?
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What characteristic appearance is associated with caseous necrosis?
What characteristic appearance is associated with caseous necrosis?
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What types of cells typically surround the necrotic core in caseous necrosis?
What types of cells typically surround the necrotic core in caseous necrosis?
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Which statement is true regarding fibrinoid necrosis?
Which statement is true regarding fibrinoid necrosis?
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What is a common mechanism that triggers fibrinoid necrosis?
What is a common mechanism that triggers fibrinoid necrosis?
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Which type of necrosis is primarily associated with Mycobacterium tuberculosis?
Which type of necrosis is primarily associated with Mycobacterium tuberculosis?
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In which disease is fibrinoid necrosis prominently observed?
In which disease is fibrinoid necrosis prominently observed?
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What does the pink staining in caseous necrosis represent?
What does the pink staining in caseous necrosis represent?
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Which of the following is NOT a common cause of fibrinoid necrosis?
Which of the following is NOT a common cause of fibrinoid necrosis?
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What histological feature distinguishes caseous necrosis from coagulative necrosis?
What histological feature distinguishes caseous necrosis from coagulative necrosis?
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Which type of necrosis primarily results from immune-mediated vascular damage?
Which type of necrosis primarily results from immune-mediated vascular damage?
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What is the primary characteristic of a white kidney infarct?
What is the primary characteristic of a white kidney infarct?
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Which process mainly results in the formation of a depressed scar on the renal surface following an infarct?
Which process mainly results in the formation of a depressed scar on the renal surface following an infarct?
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What indicates the absence of cell viability in an acute kidney infarct?
What indicates the absence of cell viability in an acute kidney infarct?
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What triggers the inflammatory response after a kidney infarct?
What triggers the inflammatory response after a kidney infarct?
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What condition is predominantly associated with the occurrence of kidney infarcts?
What condition is predominantly associated with the occurrence of kidney infarcts?
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Which histological feature is indicative of a white infarct?
Which histological feature is indicative of a white infarct?
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What is the mechanism by which coagulative necrosis occurs following ischemia?
What is the mechanism by which coagulative necrosis occurs following ischemia?
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How does a red infarct differ from a white infarct?
How does a red infarct differ from a white infarct?
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Which factor contributes to the histological absence of neutrophils in early stages of kidney infarction?
Which factor contributes to the histological absence of neutrophils in early stages of kidney infarction?
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Study Notes
I. Introduction to Pathology and Cell Injury
- Pathology is the study of structural, biochemical, and functional changes in cells, tissues, and organs.
- General pathology focuses on common reactions of cells and tissues to injuries.
- Systemic pathology focuses on specific organ systems.
II. Cellular Responses to Stress and Noxious Stimuli
- Homeostasis in cells maintains a steady state, adapting to physiological changes.
- Adaptations include hypertrophy (increased cell size), hyperplasia (increased cell number), atrophy (decreased cell size and metabolic activity), and metaplasia (change in cell type).
- Beyond a threshold, stress can lead to reversible or irreversible injury.
III. Cellular Adaptations
- Hypertrophy – increase in cell size due to increased workload or growth factors.
- Hyperplasia – increase in cell number due to hormonal or compensatory stimuli.
- Atrophy – decrease in cell size and metabolic activity due to reduced use.
- Metaplasia – a change from one adult cell type to another, typically for better resistance to conditions.
IV. Mechanisms of Cell Injury and Death
- Reversible cell injury involves changes that are correctable if the stimulus is removed (cellular swelling and organelle changes).
- Irreversible cell injury leads to cell death, either through necrosis (uncontrolled, inflammatory death) or apoptosis (programmed, non-inflammatory cell death).
V. Intracellular and Extracellular Accumulations
- Intracellular accumulations involve the buildup of substances inside cells, caused by metabolic disorders, or by genetic problems.
- Pathological calcification is the deposition of calcium in normally not calcium-rich areas of the body, and it is most likely caused by tissue damage.
- Dystrophic calcification develops in necrotic or degenerating tissue.
- Metastatic calcification develops in healthy tissues due to increased blood calcium levels.
II. Necrosis
- Necrosis is tissue death accompanied by inflammation, occurring as a result of severe or prolonged injury.
- Types of necrosis include coagulative (e.g., in myocardial infarction/kidney injury), liquefactive (e.g., brain and abscesses), caseous (e.g., tuberculous lesions), fat (e.g., pancreatitis), and fibrinoid (e.g., vasculitis).
III. Apoptosis – programmed cell death
- Apoptosis is a regulated, orderly process of programmed cell death that helps maintain homeostasis.
- This process involves specific steps and is characterized by chromatin condensation, membrane blebbing, and fragmentation into apoptotic bodies.
- Two major pathways regulate apoptosis: intrinsic and extrinsic.
IV. Comparative Summary of Necrosis Types
- Provides a table summarizing different necrosis types, their appearance, and the factors associated with them.
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Description
This quiz explores the fundamentals of pathology and the cellular responses to stress and injury. It covers key concepts such as homeostasis, adaptations, and the types of cellular injuries that can occur. Test your understanding of how cells respond to various stimuli.