Inflammation Overview

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Questions and Answers

What effect does vitamin C deficiency have on healing?

It inhibits collagen synthesis. (correct)

It accelerates the healing process.

It promotes collagen synthesis.

It has no effect on healing.

How do glucocorticoids affect scar formation?

They inhibit TGF-β production and weaken scars. (correct)

They promote strong scar formation.

They enhance TGF-β production.

They have no effect on fibrosis.

What can mechanical factors like increased local pressure cause?

Decreased inflammation.

Accelerated healing.

Wounds to pull apart (dehisce). (correct)

Improved tissue regeneration.

Which of the following conditions can impair healing due to poor perfusion?

Arteriosclerosis and diabetes. Signup and view all the answers

In which type of tissue healing is scarring inevitable?

In tissues composed of nondividing cells. Signup and view all the answers

What role do proteolytic enzymes of leukocytes play in inflammation?

They help in digesting small exudates. Signup and view all the answers

What is the outcome of extensive injury in tissues capable of proliferation?

Partial loss of function. Signup and view all the answers

What is an effect of foreign bodies on healing?

They impede healing. Signup and view all the answers

What is the primary role of hepcidin in the body?

Reduces the availability of iron during chronic inflammation Signup and view all the answers

Which white blood cell count range is indicative of leukocytosis?

15,000-20,000 cells/uL Signup and view all the answers

What is a common effect of excessive inflammation in the body?

Autoimmune diseases Signup and view all the answers

Which of the following symptoms is NOT typically associated with the acute phase response?

Elevated iron levels Signup and view all the answers

What is a leukemoid reaction characterized by?

A very high increase in white blood cell count Signup and view all the answers

What consequence results from defective inflammation?

Delayed wound healing Signup and view all the answers

In sepsis, what results from large amounts of organisms and endotoxin in the blood?

Increased production of specific cytokines Signup and view all the answers

Which type of infections is primarily associated with an increase in neutrophils?

Bacterial infections Signup and view all the answers

What is the first step in the process of phagocytosis?

Recognition and binding Signup and view all the answers

Which products released by leukocytes can induce tissue injury?

Lysosomal enzymes Signup and view all the answers

What signals the termination of the acute inflammatory response?

Switching metabolites to anti-inflammatory forms Signup and view all the answers

Which of the following is NOT a plasma-derived mediator involved in inflammation?

Histamine Signup and view all the answers

C3a and C5a are known to primarily function in which aspect of inflammation?

Stimulating histamine release Signup and view all the answers

What role does factor XIIa play in the inflammatory response?

Activates plasminogen to produce plasmin Signup and view all the answers

Which mediator is responsible for inducing vasodilation and increased vascular permeability in the kinin system?

Bradykinin Signup and view all the answers

What is a key function of the complement system in the inflammatory process?

Acts as an opsonin for promoting phagocytosis Signup and view all the answers

What are the two main components of inflammation?

Vascular wall response and inflammatory cell response Signup and view all the answers

Which of the following clinical signs is NOT associated with inflammation?

Numbness Signup and view all the answers

What is the primary difference between acute and chronic inflammation regarding duration?

Acute inflammation has a short duration compared to chronic inflammation Signup and view all the answers

Which process involves leukocytes moving toward an injury?

Chemotaxis Signup and view all the answers

Which one of the following changes is a hallmark of acute inflammation?

Leukocyte emigration from blood vessels Signup and view all the answers

What is the effect of increased vascular permeability during the inflammatory response?

Formation of venule intracellular endothelial gaps Signup and view all the answers

Which component is primarily responsible for the early onset of acute inflammation?

Polymorphonuclear cells Signup and view all the answers

What role does hydrostatic pressure play in normal fluid exchange?

It acts as a driving force for fluid movement Signup and view all the answers

What are the main metabolites produced by cyclooxygenase?

Prostaglandins and thromboxanes Signup and view all the answers

Which of the following functions is NOT associated with platelet-activating factor?

Inhibition of leukocyte adhesion Signup and view all the answers

What mediates inflammation as major cytokines produced by activated macrophages?

Tumor necrosis factor and interleukin 1 Signup and view all the answers

Which of the following is a characteristic of serous inflammation?

Tissue fluid accumulation Signup and view all the answers

What is a primary role of nitric oxide in the inflammatory response?

Relaxation of smooth muscles Signup and view all the answers

Which substance acts to protect tissues from reactive oxygen species (ROS)?

Superoxide dismutase Signup and view all the answers

What is a hallmark of acute inflammation morphology?

Dilation of small blood vessels Signup and view all the answers

Which statement accurately describes fibrinous inflammation?

Involves high amounts of fibrinogen in exudates Signup and view all the answers

Study Notes

Inflammation

Inflammation is the body's protective response to injury or infection.
The main objective is to eliminate the initial cause of injury, the necrotic cells, and tissue.
It can be both beneficial and harmful.
- Beneficial responses include: the delivery of leukocytes and plasma proteins to the site of injury, and subsequent removal of harmful stimuli and debris.
- Harmful responses include: hypersensitivity reactions and organ damage.

General Characteristics

Vascular wall response - Changes in blood vessels, like dilation and increased permeability.
Inflammatory cell response - Recruitment of cells like neutrophils and macrophages to the site of injury.

Patterns of Inflammation

Acute inflammation - Occurs early, short duration, fluid exudation, involves polymorphonuclear cell emigration.
Chronic inflammation - Occurs later, longer duration, involves blood vessel proliferation and scarring, lymphocytes, and macrophages.

5 Signs of Inflammation

Heat (Calor)
Redness (Rubor)
Edema (Tumor)
Pain (Dolor)
Loss of Function (Functio Laesa)

Acute Inflammation

Alteration in vascular caliber - Vasodilation, an initial transient vasoconstriction can occur but quickly shifts to vasodilation.
Structural changes in the microvasculature - Increased vascular permeability and exudation.
Leukocyte emigration - Leukocytes move from the blood vessels to the site of injury.

Vascular Changes

Hydrostatic pressure - The force pushing fluid out of blood vessels (the "kicking force").
Plasma colloid osmotic pressure - The force pulling fluid into blood vessels (the "keeping force").
Increased vascular permeability - Endothelial cells in blood vessels become leaky, allowing fluid and proteins into the tissue leading to edema.

Cellular Events

Leukocyte extravasation - The process of leukocytes moving from the bloodstream to the site of injury.
- Margination: leukocytes rolling along the endothelium.
- Adhesion: leukocytes adhere to the endothelium.
- Transmigration (Diapedesis): leukocytes cross the endothelial lining of the blood vessel.
- Migration in interstitial tissues: leukocytes move towards the site of injury following chemotactic factors.

Chemotaxis

Leukocytes are attracted to and move towards an injury through chemotaxis, mediated by chemical agents.

Phagocytosis

This is the process by which leukocytes engulf and destroy microbes and cell debris.
Steps:
- Recognition & binding: The leukocytes recognize and bind to targets, usually via opsonin receptors.
- Engulfment: Leukocytes engulf the target into a phagocytic vacuole (phagosome).
- Killing & degradation: The leukocytes destroy the target and degrade cell debris.

Products Released by Leukocytes

Lysosomal enzymes - These can damage tissues by degrading extracellular matrix components.
Oxygen-derived active metabolites - Reactive oxygen species (ROS) can cause damage to surrounding tissues.
Products of arachidonic acid metabolism - These can contribute to the inflammatory response by inducing vasodilation and chemotaxis.

Termination of Acute Inflammation

The inflammatory response must be tightly regulated to prevent damage to healthy tissues.
Mechanisms of termination:
- Switching the production of arachidonate metabolites towards anti-inflammatory forms.
- Production of anti-inflammatory cytokines like TGF-β.

Chemical Mediators

Complement system: This is a cascade of plasma proteins that plays a critical role in inflammation, phagocytosis, and cell lysis.
- C3a and C5a: Induce histamine release which causes increased vascular permeability and vasodilation.
- C5a: is also chemotactic for various leukocytes and activates the lipoxygenase pathway in neutrophils and monocytes.
- C3b: Acts as an opsonin promoting phagocytosis.
- MAC (membrane attack complex): Cell lysis by forming pores in cell membranes.
Kinin system: Leads to the production of bradykinin, which causes vasodilation and increased vascular permeability.
Clotting system:
- Fibrinopeptides: Induce vascular permeability and chemoattract leukocytes.
- Thrombin: Increases leukocyte adhesion to endothelium.
- Plasmin: Cleaves C3 and generates fragments that increase vascular permeability.
Arachidonic acid metabolites: These are produced by the cyclooxygenase and lipoxygenase pathways.
- Cyclooxygenase: produces prostaglandins (pro-inflammatory) and thromboxane (platelet aggregation).
- Lipoxygenase: produces leukotrienes (pro-inflammatory) and lipoxins (anti-inflammatory).

Platelet-Activating Factor (PAF)

Produced by mast cells and other leukocytes.
Has multiple effects:
- Platelet aggregation and release
- Bronchoconstriction
- Vasodilation
- Increased vascular permeability
- Increased leukocyte adhesion and chemotaxis

Cytokines and Chemokines

Cytokines: These are protein signaling molecules produced by activated lymphocytes and macrophages.
Chemokines: A subgroup of cytokines that specifically attract and activate leukocytes.

Tumor Necrosis Factor (TNF) and Interleukin 1 (IL-1)

Major cytokines involved in inflammation that are produced by activated macrophages.

Nitric Oxide (NO)

A free radical that causes relaxation of smooth muscles, inhibits platelet aggregation and adhesion, and has antimicrobial and anti-tumor properties.

Oxygen-Derived Free Radicals (ROS)

Can cause damage to endothelial cells, red cells, and other cell types.

Protective Mechanisms Against ROS

Ceruloplasmin: A protein that binds free iron, which is important for reducing the production of ROS.
Transferrin: Another protein that binds free iron.
Superoxide dismutase: Enzym that converts superoxide to hydrogen peroxide, which is less harmful.
Catalase: Enzyme that breaks down hydrogen peroxide into water and oxygen.
Glutathione peroxidase: Enzyme that reduces hydrogen peroxide and other ROS.

Outcomes of Acute Inflammation

Resolution: Complete restoration of normal tissue structure and function.
Chronic inflammation: Persistent inflammation that can lead to tissue damage and scarring.
Abscess formation: Localized collection of pus (dead leukocytes, bacteria, and inflammatory exudate).

Morphologic Patterns of Acute Inflammation

Dilation of small blood vessels
Slowing of blood flow due to increased vessel permeability and leukocyte accumulation.
Accumulation of leukocytes and fluid in the extravascular tissue (edema and exudate formation).
Serous inflammation: Characterized by the accumulation of serous fluid (thin, watery).
Fibrinous inflammation: Characterized by the accumulation of fibrin, resulting in a thicker, more sticky exudate.

Hepcidin

A peptide hormone that regulates iron availability in the body.
chronically elevated hepcidin levels are associated with the anemia of chronic inflammation.

Leukocytes and Leukocytosis

Leukocytosis: Increase in the number of leukocytes in the blood.
Neutrophils: Commonly elevated in bacterial infections.
Lymphocytes: Commonly elevated in viral infections.
Eosinophils: Commonly elevated in parasitic infections and allergic reactions.

Other Manifestations of the Acute Phase Response

Increased pulse and blood pressure.
Decreased sweating.
Rigors (muscle spasms and shivering).
Chills.
Anorexia (loss of appetite).
Somnolence (drowsiness).
Malaise (general discomfort).

Sepsis

A life-threatening organ dysfunction caused by a dysregulated host response to infection; commonly associated with high levels of inflammatory cytokines like TNF and IL-1.

Consequences of Defective Inflammation

Increased susceptibility to infections: Due to ineffective removal of pathogens.
Delayed wound healing: Due to the lack of proper inflammatory response to repair tissue damage.

Consequences of Excessive Inflammation

Allergies: Immune system overreacts to common environmental antigens.
Autoimmune diseases: Immune system attacks self-antigens.
Atherosclerosis and ischemic heart disease: Chronic inflammation contributes to plaque formation in arteries.
Alzheimer disease: Inflammation is implicated in the development of this neurodegenerative disease.

Factors Affecting Wound Healing

Infection: Can delay healing by prolonging inflammation and harming tissues.
Diabetes: High blood sugar levels can impair the healing process.
Nutritional status - Deficiencies in protein and Vitamin C can impede collagen synthesis and healing.
Glucocorticoids: These medications suppress inflammation and can weaken scar formation.
Mechanical factors: Increased pressure or tension on a wound can cause it to split open (dehisce).
Poor perfusion: Reduced blood flow due to conditions like arteriosclerosis or venous obstruction can impair healing.
Foreign bodies: Can interfere with healing and create risks of infection.
Type and extent of tissue injury: Tissues with a higher capacity for cell division are more likely to regenerate, while those composed of non-dividing cells may heal with scarring.
Location of injury: Inflammation in enclosed spaces (pleural, synovial, peritoneal) can sometimes resolve without scarring.

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Description

This quiz explores the key concepts of inflammation, discussing its role as the body's protective response to injury and infection. Participants will learn about the general characteristics, patterns, and the dual nature of inflammation, encompassing both beneficial and harmful effects. Test your knowledge on the vascular and inflammatory cell responses involved in acute and chronic inflammation.