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Questions and Answers
What is the primary reason for rubor (redness) during acute inflammation?
What is the primary reason for rubor (redness) during acute inflammation?
Which of the following is a component of the classical signs of acute inflammation?
Which of the following is a component of the classical signs of acute inflammation?
Which type of exudate is characterized by fluid collection due to burns?
Which type of exudate is characterized by fluid collection due to burns?
What is not a factor contributing to increased vascular permeability?
What is not a factor contributing to increased vascular permeability?
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What is the primary function of opsonization in inflammation?
What is the primary function of opsonization in inflammation?
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Which process significantly contributes to the slowing of microcirculation during inflammation?
Which process significantly contributes to the slowing of microcirculation during inflammation?
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Which of the following is a type of phagocytic cell involved in the inflammatory response?
Which of the following is a type of phagocytic cell involved in the inflammatory response?
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Which inflammatory response is characterized by the formation of purulent material?
Which inflammatory response is characterized by the formation of purulent material?
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What is one of the early vascular events in acute inflammation?
What is one of the early vascular events in acute inflammation?
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What type of injury can lead to increased vascular permeability during inflammation?
What type of injury can lead to increased vascular permeability during inflammation?
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What role do cytokines play in inflammation?
What role do cytokines play in inflammation?
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Which of the following statements about histamines is correct?
Which of the following statements about histamines is correct?
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Which mediators are typically associated with the effects of leukotrienes?
Which mediators are typically associated with the effects of leukotrienes?
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What is a characteristic of chronic inflammation?
What is a characteristic of chronic inflammation?
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What are chemokines primarily responsible for?
What are chemokines primarily responsible for?
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What is a common cause of chronic inflammation?
What is a common cause of chronic inflammation?
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Which of the following statements about prostaglandins is true?
Which of the following statements about prostaglandins is true?
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How do endogenous chemical mediators differ from exogenous mediators?
How do endogenous chemical mediators differ from exogenous mediators?
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What is a common outcome of chronic inflammation regarding tissue appearance?
What is a common outcome of chronic inflammation regarding tissue appearance?
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What effect do leukotrienes have during inflammation?
What effect do leukotrienes have during inflammation?
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Study Notes
Classical Signs of Acute Inflammation
- Rubor (redness): Caused by blood vessel dilation (vasodilation).
- Calor (heat): Resulting from increased blood flow.
- Tumor (swelling): Due to fluid leakage into tissues.
- Dolor (pain): Triggered by chemical mediators and pressure.
- Loss of function: Impaired tissue/organ performance.
Types of Acute Inflammation
- Serous inflammation: Fluid-filled blisters (e.g., burns).
- Fibrinous inflammation: Fibrin leakage, often seen in cancer.
- Suppurative (purulent) inflammation: Pus formation (dead tissue).
- Ulcerative inflammation: Break in epithelial surface; can become chronic.
Formation of Exudate
- Fluid exudate: Accumulation of fluid due to increased hydrostatic pressure.
- Cellular exudate: Leukocytes (especially neutrophils) recruited to the site.
Causes of Acute Inflammation
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Vascular events:
- Persistent vasodilation
- Elevated hydrostatic pressure
- Increased vascular permeability (endothelial cell contraction, injury, increased transcytosis, new blood vessel leakage)
- Microcirculation slowing/stasis.
Phagocytosis and Bacterial Killing
- Phagocytic cells: Neutrophils (early response), monocytes/macrophages.
- Opsonisation: "Markers" on bacteria enhance phagocytosis.
- Phagocytosis process: Engulfment and destruction of pathogens/debris.
- Enzyme release: Neutrophils/macrophages release proteolytic enzymes (e.g., protease, elastase, collagenase, lipase) to degrade pathogens.
Chemical Mediators of Acute Inflammation
- Exogenous mediators: From pathogens (e.g., endotoxins).
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Endogenous mediators: Body-derived (e.g., cytokines, Histamine, Leukotrienes, Prostaglandins, Chemokines).
- Cytokines: Produced by various cells (macrophages, lymphocytes, epithelial cells), regulating immune/inflammatory reactions (pro-inflammatory & anti-inflammatory effects).
- Histamine: Triggers vasodilation.
- Leukotrienes: Increase vascular permeability; cause vasoconstriction.
- Prostaglandins: Lipid compounds; involved in vascular and systemic reactions (vasodilation, fever, pain), derived from mast cells, macrophages, endothelial cells.
- Chemokines: Small proteins attracting specific types of leukocytes.
Chronic Inflammation
- Process: Longer duration, typically with more tissue damage than acute.
- Cells: Predominantly lymphocytes.
- Appearance: More fibrosis.
- Host defense: Unable to effectively clear the insult.
- Granuloma formation: Often present.
Contributing Factors to Chronic Inflammation
- Local: Ischemia, foreign body, infection.
- Systemic: Age, gender, hormones, alcoholism, stress, obesity, nutrition, immune compromise (disease/medication).
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Description
This quiz covers the classical signs of acute inflammation, including redness, heat, swelling, pain, and loss of function. It also explores different types of acute inflammation such as serous, fibrinous, and suppurative inflammation, as well as the formation and causes of exudate. Test your understanding of these essential concepts in inflammation pathology.