Acute Inflammation: Mediators & Patterns

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Questions and Answers

What is the first major component of acute inflammation?

Vascular Changes (correct)

Microvascular Changes

Mediators

Cellular Events

Which of these describes the alteration in permeability of microvasculature in acute inflammation?

Cellular Recruitment

Vasodilation

Increased Vascular Permeability (correct)

Mediators Production

What type of mediators are produced as needed and may originate from cells?

Microbial mediators

Pre-formed mediators

Cell-derived mediators (correct)

Plasma-derived mediators

Which effect is not caused by mediators of inflammation?

Immune System Suppression Signup and view all the answers

What is the role of chemotaxis in inflammation?

Recruitment of leukocytes to injury sites Signup and view all the answers

Which of the following is NOT a feature of acute inflammation?

Vasoconstriction Signup and view all the answers

What initiates the release of active mediators in inflammation?

Necrotic cells Signup and view all the answers

Which of the following is a characteristic of plasma-derived mediators?

Cannot be synthesized as needed Signup and view all the answers

Which of the following is NOT a source of Histamine?

Neutrophils Signup and view all the answers

What is one of the main effects of Prostaglandins?

Vasodilation Signup and view all the answers

What role do Cytokines play in inflammation?

Modulate the functions of other cell types Signup and view all the answers

Which of the following is a key cytokine involved in acute inflammation?

Tumor necrosis factor alpha (TNFa) Signup and view all the answers

Leukotrienes are primarily involved in which of the following processes?

Chemotaxis Signup and view all the answers

Nitric Oxide is known for its primary action as a:

Vasodilator Signup and view all the answers

Which cell type is primarily responsible for producing Platelet Activating Factor?

Mast cells Signup and view all the answers

What is the effect of Tumor Necrosis Factor in the body?

Kills tumor cells and stimulates catabolism Signup and view all the answers

What is the primary role of nitric oxide in inflammation?

It acts as a regulator, decreasing the effects of proinflammatory mediators. Signup and view all the answers

Which of the following is NOT a system involved in plasma protein-derived mediators during inflammation?

Neutrophil Signup and view all the answers

What characterizes fibrinous inflammation?

Deposition of fibrin in extracellular spaces. Signup and view all the answers

In which condition is serous inflammation commonly observed?

Accumulation of skin blisters. Signup and view all the answers

What describes purulent inflammation?

Production of large amounts of pus with neutrophils. Signup and view all the answers

What is an effusion in the context of serous inflammation?

A thin fluid derived from plasma in cavities. Signup and view all the answers

Which of the following is associated with abscess formation?

Localized collection of purulent exudate. Signup and view all the answers

What is a common characteristic of fibrinous exudate?

It occurs with higher vascular permeability allowing larger molecules. Signup and view all the answers

Study Notes

Acute Inflammation: Chemical Mediators & Morphological Patterns

Acute inflammation has four major components: vascular changes, microvascular changes, cellular events, and mediators.
Vascular changes include alterations in vascular caliber (vasodilation), increasing blood flow.
Microvascular changes involve alterations in microvasculature permeability, leading to plasma protein and white blood cell (WBC) leakage.
Cellular events encompass WBC emigration, accumulation, and activation at the injury site.
Mediators are derived from plasma proteins and cells.

Inflammatory Mediators

Inflammatory mediators are chemical substances triggering processes in inflammatory reactions.
Mediators are categorized as cell-derived and plasma-derived.

Cell-Derived Mediators

Preformed mediators stored in secretory granules (e.g., histamine, serotonin, lysosomal enzymes).
Newly synthesized mediators (e.g., prostaglandins, leukotrienes, platelet-activating factors, activated oxygen species, nitric oxide, cytokines).
Examples of sources for these mediators include mast cells, basophils, platelets, neutrophils, macrophages, leukocytes, and various cell types.

Plasma-Derived Mediators

Circulate in an inactive form, requiring activation.
Examples include components of the complement system (e.g., C3a, C5a), kinin system (bradykinin), and coagulation/fibrinolysis system.
The complement system, bradykinin, and factor XII are interrelated protein systems involved in inflammatory reactions.

Principles of Mediators

Initially bind to specific receptors and act.
Stimulate the release of other mediators.
Can act on one or a few target cell types.
Are short-lived after activation.
Can be potentially harmful.

Active Mediators

Active mediators are produced in response to injurious stimuli, such as microbial products and substances released from necrotic cells.
Proteins of the complement, kinin, and coagulation systems activated by microbes and damaged tissues.
Inflammation is triggered only when and where needed.

Roles of Mediators

Mediators affect blood vessels, inflammatory cells, and other body cells.

Effects of Mediators

Vasodilation, vasoconstriction, altered vascular permeability, activation of inflammatory cells, chemotaxis, cytotoxicity, tissue degradation, pain, and fever.

(A) Cell-Derived Mediators

Vasoactive amines (e.g., histamine).
Arachidonic acid derivatives (e.g., prostaglandins, leukotrienes).
Platelet-activating factor (PAF).
Cytokines.
Nitric oxide (NO).

1. Serous Inflammation

Outpouring of thin fluid derived from plasma and mesothelial cells lining cavities (e.g., peritoneal, pleural, pericardial).
Accumulation of fluid is called effusion.
Skin blisters are an example.

2. Fibrinous Inflammation

Characterized by fibrin deposition in extracellular spaces.
Occurs during severe injuries with increased vascular permeability.
Examples include exudates in the meninges, pericardium, and pleura.

3. Purulent Inflammation & Abscess

Production of large amounts of pus (purulent exudate).
Consists of neutrophils, liquefactive necrosis, and edema fluid.
Caused by pyogenic bacteria (e.g., staphylococci).
Abscesses are localized collections of purulent inflammatory exudate (pus).

4. Ulcer

A local defect or excavation on an organ or tissue surface.
Resulting from sloughing (shedding) of inflammatory necrotic tissue.
Occurs when tissue necrosis and inflammation exist on or near a surface.
Common sites include the mucosa of the mouth, stomach, intestines, genitourinary tract, and skin/subcutaneous tissues.

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Description

This quiz explores the key components and chemical mediators of acute inflammation. It covers vascular changes, microvascular alterations, cellular events, and the role of various inflammatory mediators. Test your knowledge on how these elements interact during the inflammation process.