Inflammation and Abscesses Quiz

Introduction to Inflammation

• Inflammation is a local vascular and cellular response of living tissue to an injurious agent.

Objectives

• Define inflammation
• Differentiate between acute and chronic inflammation
• Recognize the steps of extravasation of inflammatory cells
• Recognize the process of chemotaxis and phagocytosis
• Identify different examples of inflammation

Aims of Inflammation

• Fighting bacteria
• Localizing infection
• Removing damaged tissue

Causes of Inflammation

• Allergic reactions
• Chemical irritants
• Infections
• Trauma
• Burns
• Lacerations, cuts, wounds
• Frostbite
• Cardiovascular disease
• Neurological disease
• Autoimmune diseases (e.g., rheumatoid arthritis)
• Cancer
• Lupus
• Fibromyalgia
• Chronic fatigue syndrome

Types of Inflammation

• Acute inflammation
• Chronic inflammation

Cells in Acute and Chronic Inflammation

• Acute: Neutrophils (phagocytosis, pus cells)
• Chronic: Lymphocytes, plasma cells, histiocytes (chronic phagocytosis, monocytes), eosinophils (allergy, parasitic), mast cells (allergy, histamine, serotonin), giant cells (phagocytosis, histiocytes)

Acute vs. Chronic Inflammation (Features)

Local Signs of Inflammation

• Heat
• Redness
• Swelling
• Pain
• Loss of function

Systemic Effects of Inflammation

• Fever
• Leukocytosis
• Malaise
• Nausea
• Anorexia
• Lymphoid hyperplasia
• CRP, ESR raised

Main Events of Inflammation

• Vascular response
• Inflammatory fluid exudate
• Inflammatory cellular exudate

Vascular Response

• Changes in vascular flow and caliber (vasodilation, stasis, increased viscosity, swollen end, open capillaries)
• Increased permeability and formation of fluid exudate (histamine, kinins, endothelial gaps, direct endothelial injury)

Inflammatory Fluid Exudate

• Formation: Increased vascular permeability, interstitial osmotic pressure, reduced hydrostatic pressure.
• Function: Dilutes toxins, brings antibodies, supplies nutrients, supplies fibrinogen for localization and movement of inflammatory cells and fibroblasts.

Composition of Exudate

• Appearance: Turbid
• Consistency: Viscous (like pus)
• Protein content: High (4-8 g/dL)
• Specific gravity: High (>1018)
• Cell content: Numerous neutrophils
• On standing: Clots

Cellular Exudate (Extravasation of neutrophils):

• Margination (PMNs toward wall)
• Rolling (tumbling and EAPING) via selectine-glycoprotein and adhesion via integrine-lg
• Transmigration (diapedesis) via PCAM
• Role of activating substances (bacteria, damaged tissues) and mediators (lipopolysaccharides, cytokines).

Chemotaxis

• Movement of neutrophils and macrophages toward inflammatory irritant.
• Mediated by exogenous bacteria products and endogenous mediators (complement, arachidonic acid metabolites, chemokines) leading to actin polymerization.

Leukocyte "Activation"

1. Produce eicosanoids
2. Undergo degranulation
3. Secrete cytokines

Phagocytosis

• Ingestion and destruction of bacteria, necrotic debris, and foreign particles by phagocytic inflammatory cells (e.g., neutrophils, macrophages).

Cellular Responses (Recognition, Engulfment, Killing)

• Recognition: Opsonization (Ig, complement) ,C3b receptor, Fc receptor
• Engulfment: phagocyte ingests the target
• Killing/degradation/digestion: via oxidative burst (reactive oxygen metabolites, lysosomal enzymes).

Chemical Mediators

• Cellular: Histamine, serotonin, eicosanoids, nitric oxide, platelet activating factor (PAF)
• Plasma: Complement, kinins, clotting factors, fibrinolytic factors

Outcome of Acute Inflammation

• Resolution
• Regression & Healing
• Progression & spread
• Progression & chronicity

Summary of Sequence of Events

• Vasodilation → Increased vascular permeability → Leakage of exudate, stasis → Extravasation, margination, rolling, adhesion, transmigration (diapedesis) → Chemotaxis → PMN activation → Phagocytosis (recognition, attachment, engulfment, killing) → Termination → 100% resolution, scar, or chronic inflammation

Types of Acute Inflammation

• Suppurative (pus-forming)
  • Localized (e.g., abscess, furuncle, carbuncle)
  • Diffuse (e.g., cellulitis, appendicitis, peritonitis)
• Non-suppurative (non-pus-forming)

Characteristics and Composition of Pus

• Non-coagulable, creamy, alkaline, yellowish or yellow-green fluid
• Fluid exudate, without fibrin
• Pus cells (neutrophils, macrophages), RBCs
• Liquified necrotic tissue
• Bacteria and pigments

Abscess

• Localized suppurative inflammation
• Cause: Often Staphylococci, excess fibrin
• Site: Skin, organs
• Microscopically: Central necrotic zone, peripheral inflamed tissue, granulation tissue, fibrosis
• Clinical: Red, hot, swollen
• Fate: Healing or complications

Boil (Furuncle), Carbuncle

• Boil (Furuncle): small abscess around hair follicle or sebaceous gland
• Carbuncle: multiple communicating abscesses, common in diabetics, commonly back of neck

Diffuse Suppurative Inflammation

• Cause: Often Streptococci producing enzymes (fibrinolysin, hyaluronidase, spreading factor).
• Examples: Cellulitis, appendicitis, peritonitis

Comparison of Abscess and Cellulitis

Types of Acute Non-Suppurative Inflammation

• Catarrhal (e.g., rhinitis, excess mucous)
• Serous (e.g., pleuritis, excess watery fluid exudate)
• Membranous (e.g., diphtheria, fibrin patches)

Chronic Inflammation

• Causes: Persistence of infection, prolonged exposure to insult
• Types: Non-specific, specific (granuloma)

Granulomas

• Chronic, specific type of inflammation
• Collection of epithelioid cells, lymphocytes, and giant cells (e.g., Langhan's)
• Etiology: Infective (TB, leprosy, syphilis, Bilharzia, Leishmania, fungi like Madura foot), non-infective (foreign bodies, sarcoidosis)

Components of Granuloma

• Epithelioid cells (main component)
• Giant cells (Langhans' type or foreign body type)
• Lymphocytes
• Fibroblasts
• Types of granuloma: granuloma with caseation (tuberculosis), granuloma without caseation (sarcoidosis, Crohn's, silicosis), suppurative granuloma (cat scratch disease), foreign body granuloma.