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Questions and Answers
What outcome of acute inflammation is most likely when there is limited or short-lived injury?
Which condition is characterized by pus formation and is typically caused by pyogenic bacteria?
What triggers the progression of acute inflammation to chronic inflammation?
Which type of inflammation is characterized by an outpouring of thin fluid, associated with plasma or mesothelial secretion?
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What is the primary feature of scarring and fibrosis as an outcome of acute inflammation?
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Which cardinal sign of inflammation is primarily caused by vasodilation and increased blood flow to the area of injury?
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What is the primary characteristic of exudate as compared to transudate?
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Which mechanism is NOT involved in increased vascular permeability during acute inflammation?
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In chronic inflammation, which of the following is primarily involved in the response instead of neutrophils?
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What initiates the active anti-inflammatory mechanisms during the termination phase of inflammation?
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Study Notes
Polymorph Nuclear Leukocyte Emigration
- Neutrophils and macrophages are involved in the process of inflammation.
- This process involves infiltration of lymphocytes.
Cardinal Signs of Inflammation
- The classic signs of inflammation include redness, swelling, heat, pain, and loss of function.
- These signs are typically more pronounced in acute inflammation compared to chronic inflammation.
General Characteristics of Inflammation
- Two main components characterize inflammation: vascular wall response and inflammatory cell response.
- Inflammatory mediators, including circulating plasma proteins and factors produced locally by vessels and inflammatory cells, mediate the effects of inflammation.
- Termination of inflammation occurs when the causative agent is eliminated and secreted mediators are removed.
Acute Inflammation
- Two major components of acute inflammation are vascular changes and inflammatory cell response.
- Increased blood flow due to vasodilation and increased vascular permeability are key vascular changes.
Vascular Changes
- Initial vasoconstriction followed by vasodilation increases blood flow to the area of injury, causing heat and redness.
- Increased vascular permeability leads to the escape of protein-rich fluid (exudate) into the extravascular tissue.
Mechanisms of Vascular Leakage
- Endothelial cell contraction, triggered by histamine, bradykinin, leukotrienes, and other mediators, forms gaps in venules.
- Direct endothelial injury caused by burns or infections also contributes to vascular leakage.
Edema
- Excessive fluid accumulation in interstitial tissue or body cavities can be exudates or transudates.
Exudate
- High protein concentration, cellular debris, and significant alteration in the permeability of blood vessels characterize exudate.
Outcomes of Acute Inflammation
- Factors influencing the outcomes of acute inflammation are the nature and intensity of the injury, the site and tissue affected, and the host's responsiveness.
Resolution
- Resolution involves regaining normal histological and functional tissue.
- It occurs with limited or short-lived injury, minimal or no tissue damage, and tissue capable of replacing injured cells.
Progression to Chronic Inflammation
- If the offending agent is not removed, there is continuing tissue injury, or the affected tissue has a decreased capacity to regenerate, acute inflammation can progress to chronic inflammation.
- Chronic inflammation can lead to scarring or restoration of normal structure and function.
Suppuration
- Suppuration refers to pus formation.
- Pus consists of living and dead neutrophils, bacteria, cellular debris, and edema fluid.
Abscesses
- Abscesses are localized collections of pus, typically with a central necrotic region surrounded by neutrophils and a zone of dilated vessels and fibroblasts.
Scarring and Fibrosis
- Replacement of injured tissue with fibrous connective tissue signifies scarring or fibrosis.
- This occurs with extensive tissue destruction or when inflammation affects tissues with limited regeneration capacity.
Morphology of Acute Inflammation
- Depends on injury type and location, and host's responsiveness.
Types
- Serous inflammation
- Suppurative (purulent) inflammation
- Ulcers
- Fibrinous inflammation
Serous Inflammation
- Characterized by an outpouring of thin fluid (plasma or mesothelial secretion)
- Example: Pleural, pericardial, and peritoneal cavities.
Fibrinous Inflammation
- Inflammation of body cavity linings
- Example: Meninges, pericardium, and pleura.
- Increased vascular permeability allowing large molecules like fibrinogen to pass through.
- Leads to fibrin deposition in the extracellular space.
Suppurative (Purulent) Inflammation
- Characterized by the formation of large amounts of pus or purulent exudate.
- Infiltration of neutrophils with necrotic cells and edema.
- Caused by bacteria, such as Staphylococcus, Streptococcus, and Pneumococcus.
- Example: Acute appendicitis.
Pseudomembranous Inflammation of Mucous Membranes
- Sever injury causes extensive epithelial necrosis and sloughing.
- Forms large, shallow ulcers covered by a mixture of fibrin, dead epithelium, neutrophils, red cells, and bacteria.
- Creates a white-creamy pseudo-membrane.
- Example: Diphtheria.
Abscesses
- Localized collection of purulent inflammatory exudates in tissues or organs.
- Central mass of necrotic leukocytes and debris surrounded by preserved neutrophils without evidence of vascular dilatation.
- May be walled off and replaced by connective tissue.
Ulcer
- Localized defect or excavation on the surface of an organ caused by the shedding of inflammatory necrotic tissue.
- Commonly found in inflammation of mucus-lined cavities (mouth, larynx, stomach) and subcutaneous inflammation in lower extremities, often in older adults with vascular defects.
Effects of Acute Inflammation
Beneficial effects
- Dilution of toxins by edema fluid
- Production of antibodies
- Fibrin network formation providing a scaffold for inflammatory cells and limiting infection spread.
Harmful effects
- Swelling and edema, as seen in acute epiglottitis.
- Increased tissue pressure leading to tissue necrosis.
- Digestion of viable tissue.
- Severe tissue damage in allergic reactions.
- Generalized increased vascular permeability leading to shock, like anaphylactic shock.
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