Inflammation Quiz for Medical Students

Inflammation - Definitions, Classification, and Causes

• Inflammation is a defensive reaction of the organism to harmful agents.
• The aim is to remove or destroy the cause of damage or affected cells and tissues.
• Causes include physical agents (extreme temperatures, electric shock, radiation, mechanical injuries), chemical agents (metabolism products, acids, alkalis, drugs, tissue necrosis), and biological agents (microorganisms, parasites, immune cells and complexes).

Comparison Between Acute and Chronic Inflammation

• Acute inflammation:

  • Short-term (minutes to days)
  • Rich in protein exudate
  • Neutrophils are the primary cell type

• Chronic inflammation:

  • Long-term (days to years)
  • Lymphocytes and macrophages are the primary cell type
  • Granulation tissue, vascular hyperplasia, and scar formation are common

Signs of Inflammation (Symptomatology)

• Local signs:
  • Heat
  • Redness
  • Swelling
  • Pain
  • Loss of function
• Systemic signs:
  • Fever (TNF, IL-1, IL-6)
  • Increased erythrocyte sedimentation rate
  • Leukocytosis (increased WBC count)
    • Bacteria → neutrophils
    • Parasites → eosinophils
    • Viruses → lymphocytes
  • Leukopenia (decreased WBC count)
    • Viral infections, salmonella infections, ricketttsiosis
  • Increased levels of some substances (C-reactive protein) in response to immune reactions

Sequence of Vascular and Cellular Changes in Acute Inflammation and Their Purpose

• The sequence of events includes initial vasoconstriction, followed by vasodilation of arterioles, capillaries, and venules, leading to increased blood flow and vascular permeability.
• This permits plasma proteins and leukocytes to leave the circulation.
• Leukocytes then migrate to the site of injury, engulf and destroy pathogens, and initiate tissue repair.

Consequences and Outcome of Inflammation

• Resolution:
  • Clearance of injurious stimuli
  • Removal of mediators and inflammatory cells.
  • Replacement of damaged cells with normal tissue.
• Healing:
  • Tissue repair may involve regeneration (replacement with identical tissue)
    • or scar formation (replacement with fibrous tissue).
• Pus formation (abscess):
  • Necrotic tissue, dead and decayed cells surrounded by living cells.

Morphologic Patterns of Inflammation

• Alteration: Damage (e.g., necrosis).
• Exudation: Reaction of microcirculation; exudate formation; leukocyte migration; phagocytosis.
• Proliferation: Cell proliferation (macrophages, lymphocytes, and fibroblasts)

Classification of Inflammation

• Length: acute, chronic (subacute, hyperacute)
• Predominant component:
  • Alterative (necrosis, e.g., diphtheria)
  • Exudative (e.g., pleuritis)
  • Proliferative (tissue thickening, e.g., cholecystitis)
• Histological feature: nonspecific / specific (e.g., tuberculosis)
• Causative agent: aseptic (sterile) / septic (caused by living organisms).

Types of Exudate

• Serous (fibrin-free serum)
  • Initial response. Dilution of harmful agents
• Catarrhal (watery exudate of serum and mucus exclusively on mucous membranes)
• Fibrinous (exudation of fibrin outside blood vessels)
  • Initial temporary barrier against inflammation
• Purulent (primarily neutrophils, cellular debris)
  • Pathogen destruction, damaged tissue dissolution.
• Gangrenous (massive destruction of tissue, extensive necrosis)
• Hemorrhagic (extensive microvascular bleeding, with blood as the principal exudate)

Steps of an Acute Inflammatory Response

1. Recognition of the injurious agent
2. Recruitment of leukocytes
3. Removal of the agent
4. Regulation (control) of the response
5. Resolution

Mechanisms of Acute Inflammation

• Vascular: Change in diameter and permeability (vasoconstriction/vasodilation)
• Cellular: Rolling, adhesion, diapedesis; and chemotaxis (movement of cells along a chemical gradient).

Roles of Cells and Molecules in Inflammation

• Leukocytes (blood cells): neutrophils, macrophages, eosinophils, basophils, lymphocytes, plasma cells, mast cells

• Vascular cells (blood vessels): endothelial cells, smooth muscle cells

• Plasma proteins (kininogens, complement)

• Cells in connective tissue: Mast cells, fibroblasts, other cells

• Chemotaxis of Leukocytes

  • Chemotaxis is the locomotion of cells along a chemical gradient
  • Agents acting as chemoattractants can be exogeneous (e.g., bacterial products) or endogeneous (e.g., complement system components, cytokines).

Phagocytosis

• Adhesion - invagination into cytoplasm
• Lysosomes - destruction of pathogens
• Highly virulent microorganisms cause leukocyte death
• Highly resistant microbes persist in macrophages, causing sustained activation and inflammation.

Mediators of Inflammation

• Necrosis-derived (kinins): result from necrosis.
• Cell-derived (histamine, serotonin, cytokines, arachidonic acid derivatives, platelet-activating factor).
• Plasma-derived (kinin system, complement system, C-reactive protein).

Morphologies of Inflammation

• Alterative Inflammation: (characterized by cellular injury) - ulcerative, pseudomembranous, necrotic
• Exudative Inflammation: (characterized by exudation of blood components and emigration of blood cells) - serous, catarrhal, fibrinous, purulent, gangrenous, hemorrhagic
• Proliferative (Productive) Inflammation: (characterized by cell proliferation) - primarily/ secondarily (e.g., in the case of cholecystitis)
  • Granulomatous Inflammation (distinctive chronic inflammation with cell-mediated immune reaction; macrophages aggregates, multinucleated giant cells)
    • Tuberculosis, sarcoidosis, cat scratch disease, lymphogranuloma inguinale, leprosy, syphilis, mycotic infections, autoimmune diseases

Outcomes of Acute Inflammation

• Abscess formation
• Resolution; healing (regeneration or scarring); fibrosis

Complications of Suppurative Inflammation

• Bacteremia
• Sepsis
• Septic shock
• Thrombophlebitis
• Lymphangiitis, lymphadenitis