Inflammation: The Basics Quiz

Inflammation: The Basics

• Inflammation is a non-specific response of the body to local injury, part of the body's second line of defense.
• It can also produce severe effects, like rheumatoid arthritis.
• Various factors can trigger inflammation, including physical agents (trauma, ischemia, extreme temperatures), chemical agents (strong acids, bases, venom), and biological agents (bacteria, fungi).
• The suffix "-itis" indicates inflammation in a specific tissue (e.g., appendicitis).
• Inflammatory responses can be either acute (self-limiting) or chronic (self-perpetuating).

Acute Inflammation: Vascular Response

• Acute inflammation starts almost immediately after injury, involving vasodilation of arterioles and venules.
• Vasodilation leads to increased blood flow, causing redness and heat.
• Increased permeability of capillaries allows fluid to escape into tissues, causing swelling.
• Pain and impaired function result from tissue swelling and the release of chemical mediators.

Inflammation: Vascular Response (Continued)

• Fluid movement into tissues can be beneficial by diluting the injuring agent, carrying plasma proteins and leukocytes to the site, and removing bacterial toxins, dead cells, and debris to the lymphatic system.
• Clotting agents help prevent the spread of microorganisms.

Inflammation: Vascular Response Patterns

• The severity of injury dictates various vascular response patterns.
• Immediate transient response occurs with minor injuries.
• Immediate sustained response occurs with more serious injuries.
• Delayed response happens in injuries like sunburns.

Acute Inflammation: Cellular Response - Mast Cells

• Mast cells are found in connective tissues throughout the body.
• They're especially abundant in the skin and gastrointestinal and respiratory tracts.
• Mast cells contain granules with chemical mediators like histamine and chemotactic factors.
• Degranulation, the release of these mediators, occurs due to physical injury, chemicals, or immunologic means.

Acute Inflammation: Cellular Response - Chemical Mediators

• Histamine causes blood vessel dilation and increased vascular permeability.
• Chemotactic factors attract neutrophils and eosinophils to the injured site.
• Mast cells also synthesize leukotrienes, prostaglandins, and platelet-activating factor to enhance the inflammatory response.

Inflammation: Cellular Response - Neutrophils

• Neutrophils are a type of white blood cell, specifically granulocytes.
• They're usually the first cells at the injury site a few hours after the initial injury.
• Their primary role is cleaning up debris and dead cells.

Inflammation: Cellular Response - Monocytes

• Monocytes are white blood cells that follow neutrophils into the injury site within 24 hours.
• They mature into macrophages.
• Macrophages outlast neutrophils and are crucial for destroying harmful agents (phagocytosis). They are also involved in activating specific immunity.

Inflammation: Cellular Response - Natural Killer (NK) Cells

• NK cells patrol the blood and lymph, identifying and killing cancer cells and virus-infected cells.
• They act non-specifically, targeting cells lacking "self" receptors or having abnormal carbohydrates on their surface.
• NK cells utilize chemicals like perforins to kill target cells.

Inflammation: Cellular Response - Platelets

• Platelets are cytoplasmic fragments circulating in the bloodstream.
• They play a role in clotting processes initiated by injury.
• They release chemical mediators that contribute to inflammation.

Inflammation: Response of White Blood Cells

• White blood cells (primarily neutrophils and monocytes) are integral to the response, including margination to capillary walls, emigration, chemotaxis, and phagocytosis.

Inflammation: Margination (Pavementing)

• Leukocytes slow migration and adhere to endothelial cells via adhesion molecules.
• Chemical mediators (kinins, histamine, leukotrienes, and cytokines) increase leukocyte adhesion molecule (CAM) expression.
• Endothelial cells also express adhesion molecules.

Inflammation: Emigration (Diapedesis)

• Leukocytes send extensions through permeable capillaries and move into tissues.
• This process occurs after adherence to endothelial cells.

Inflammation: Chemotaxis

• Leukocytes move towards the injured site due to chemical signals.
• Chemotactic agents include cytokines, bacterial and cellular debris, and complement fragments (C3a, C5a).

Inflammation: Phagocytosis

• Macrophages and neutrophils engulf bacterial and cellular debris.
• Phagocytosis involves several steps, including adherence, engulfment, phagosome formation, fusion with lysosomes, and intracellular killing.

Inflammation: Phagocytosis (Continued)

• Adherence involves binding of the phagocyte to the target (opsonized), enhancing recognition.
• Engulfment takes place via pseudopods that engulf the microorganism.
• Phagosome formation encapsulates the microorganism.
• Fusion with lysosomes forms a phagolysosome.
• Intracellular killing occurs through oxygen-dependent mechanisms and lysosomal enzymes.

Test your knowledge on the fundamentals of inflammation, including its types, triggers, and effects on the body. This quiz covers the physiological responses associated with acute and chronic inflammation, providing a comprehensive understanding of the topic. Perfect for students in health sciences or those interested in understanding body responses to injury.