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Questions and Answers
What is the primary aim of acute inflammation?
What is the primary aim of acute inflammation?
Which of the following is NOT a clinical sign of acute inflammation?
Which of the following is NOT a clinical sign of acute inflammation?
What is the result of increased permeability of microvasculature during acute inflammation?
What is the result of increased permeability of microvasculature during acute inflammation?
Which system is activated by tissue damage and produces fibrin as an end product?
Which system is activated by tissue damage and produces fibrin as an end product?
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What is the role of thrombin in the coagulation system?
What is the role of thrombin in the coagulation system?
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Which chemical mediator is released in response to physical injury and causes vasodilation?
Which chemical mediator is released in response to physical injury and causes vasodilation?
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What is the characteristic of chronic inflammation that differentiates it from acute inflammation?
What is the characteristic of chronic inflammation that differentiates it from acute inflammation?
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What is the term for the aggregation of macrophages that form in response to chronic inflammation?
What is the term for the aggregation of macrophages that form in response to chronic inflammation?
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Which laboratory test is commonly used to diagnose chronic inflammation?
Which laboratory test is commonly used to diagnose chronic inflammation?
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What is the term for the localised collection of pus surrounded by fibrous tissue?
What is the term for the localised collection of pus surrounded by fibrous tissue?
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Study Notes
Acute Inflammation
- Definition: A complex reaction of vascularised connective tissue to local injury for a short duration of time
- Causes: Local injury
- Aims:
- Contain and isolate the injurious stimulus
- Destroy, dilute, or wall off the agents and neutralise the toxin
- Heal and repair the damage caused
Clinical Signs of Acute Inflammation
- Heat: Hyperaemia
- Redness: Hyperaemia
- Swelling: Exudate
- Pain: Neural damage, chemical mediators
- Loss of function: Pain
Vascular Events
- Calibre change: Rapid transient vasoconstriction followed by vasodilation
- Blood flow change: Initial reduction of blood flow followed by increased blood flow to capillaries
- Permeability change: Increase permeability of microvasculature -> exudate
Cellular Events
- Transmigration towards site of infection
- Degranulation – destroy invading microorganisms
- Phagocytosis
Systemic Effects of Acute Inflammation
- Fever
- Malaise, lethargy, and sleepiness
- Pain
- Leucocytosis
- Tissue damage
- Swelling
- Hyperpyrexia, shock, and death due to too many cytokines
Exudate, Pus, Abscess, and Empyema
- Exudate: Protein-rich fluid that leaks out of blood vessels due to inflammation/infection
- Pus: Inflammatory exudate rich in white blood cells and/or microorganisms
- Abscess: Localised collection of pus surrounded by fibrous tissue
- Empyema: Not mentioned in the text
Coagulation, Kinin, and Complement Cascade Systems
- Coagulation System:
- Activated by tissue damage
- Fibrin is the end product
- Thrombin increases leukocyte adhesion and fibroblast proliferation
- Factor Xa increases vascular permeability and leukocyte exudation
- Fibrin degradation acts as a chemotactic factor for leucocytes and increases endothelial permeability
- Kinin System:
- Activated through Factor XII
- Product: Bradykinin – causes vasodilation, triggers pain
- Complement Cascade System:
- Triggers expression of adhesion molecules on leucocytes
Chemical Mediators of Inflammation
- Vasoactive Mediators:
- Histamine: Released from mast cells, basophils, and platelets
- Histamine causes dilation of arterioles, increasing vascular permeability of venules
- Serotonin: Released from platelets and enterochromaffin cells
- Serotonin actions similar to histamine
Acute Appendicitis
- Illustrates the processes of acute inflammation
Chronic Inflammation
- Pathogenesis:
- Progression from acute inflammation not totally resolved
- Involves macrophages, lymphocytes, and plasma cells
- Mechanism:
- Excessive macrophage accumulation due to:
- Continuous recruitment from circulation
- Local proliferation
- Immobilisation of peripheral macrophages
- Excessive macrophage accumulation due to:
- Morphology:
- Granuloma: Aggregation of macrophages that form in response to chronic inflammation
- Macrophages secrete IL-1, interferon alpha, and TNF
- Macrophage elongation leads to formation of epithelioid histiocytes
- Epithelioid histiocytes and macrophage accumulation leads to giant cell formation
- Necrotising granuloma: Central area of necrosis, occurs in TB
- Non-necrotising granuloma: No necrosis, occurs in Sarcoidosis
- Granulation Tissue: New connective tissue and microscopic blood vessels that form during healing
Differences between Acute and Chronic Inflammation
- To be identified...
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Description
Define acute inflammation, its causes, and how it aims to reduce damage and promote healing and repair. Identify the five clinical signs of acute inflammation.
