Inflammation

What is inflammation

A host response to infection or tissue damage: The response of vascularised tissues to injury

Why does inflammation usually not manifest in avascular tissues? Give examples.

Avascular tissues lack blood vessels, so classic inflammation is limited. Examples: cornea, lens, cartilage.

What does the suffix “-itis” mean?

Inflammation of a named site (e.g., appendicitis, meningitis, pancreatitis).

What are major causes of inflammation?

Infections, tissue necrosis, foreign bodies, immune reactions (hypersensitivity/autoimmunity).

What are the “good” outcomes of inflammation?

Dilutes/destroys offending agent, prevents spread, activates immune defences, clears dead cells so healing can occur.

What are the “bad” effects of inflammation?

Can damage delicate tissues (e.g., brain); chronic inflammation → tissue damage; healing may cause fibrosis/scarring and loss of function; causes pain/swelling/systemic effects.

List the main steps in the inflammatory response (sequence).

Recognition → Recruitment → Removal → Regulation → Repair.

Which leukocytes arrive first in acute inflammation? Which come later?

Neutrophils first, then monocytes/macrophages and lymphocytes later.

Define acute inflammation.

Rapid response (hours–weeks) with exudate/oedema, mainly neutrophils, vascular changes, little fibrosis.

Define chronic inflammation.

Prolonged response (weeks–years) with mononuclear cells (macrophages, lymphocytes, plasma cells), tissue destruction, angiogenesis, and fibrosis.

Give causes of chronic inflammation.

Persistent infections (e.g. TB), unresolved acute inflammation, hypersensitivity/autoimmunity, prolonged toxic exposure (e.g. silica, cholesterol crystals).

What are “sentinel cells” in tissues?

Tissue-resident cells that detect injury/pathogens (e.g., macrophages, dendritic cells, mast cells).

What do mast cells do in inflammation?

Release histamine and other mediators (key in vasodilation/permeability).

What is the role of macrophages in chronic inflammation?

Central cell: attempts to eliminate the agent and coordinates inflammation + repair; interacts with T cells.

What causes redness and heat in acute inflammation?

Vasodilation → increased blood flow, mediated largely by histamine (plus prostaglandins).

What causes swelling in inflammation?

Exudate (protein-rich fluid) due to increased vascular permeability → oedema.

What causes pain in inflammation?

Mediators acting on nerve endings, especially prostaglandins and bradykinin (kinins).

What are the steps of neutrophil recruitment?

Margination → Rolling (selectins) → Adhesion (integrins + ICAMs) → Extravasation into tissue.

What is an exudate?

Inflammatory, protein-rich fluid formed due to increased vascular permeability.

What is a transudate?

Fluid due to increased hydrostatic pressure (e.g. heart failure) or decreased osmotic pressure (e.g. nephrotic syndrome), not inflammation.

What are mediators of inflammation?

Chemicals produced/activated at the site that drive inflammation, often causing increased vascular permeability → oedema.

Give examples of cell-derived inflammatory mediators.

Amines (histamine), prostaglandins, leukotrienes, cytokines (from mast cells, macrophages, dendritic cells).

Give examples of plasma-derived inflammatory mediators.

Complement proteins and kinins (inactive in circulation, activated by proteolytic cascades; liver-made).

List the 5 cardinal signs of acute inflammation.

Rubor (redness), calor (heat), tumor (swelling), dolor (pain), functio laesa (loss of function).

What systemic features can occur in acute inflammation?

Fever, leucocytosis, acute phase proteins; severe cases: hypotension, DIC, generalised oedema, organ failure (high cytokines).

What is serous inflammation? Give an example.

Mild, watery, cell-poor exudate; e.g. skin blister (burns), herpes.

What is fibrinous inflammation? Give an example.

Severe permeability → fibrinogen leaks → fibrin deposition; may resolve or scar; e.g. fibrinous pericarditis (rheumatic fever).

What is purulent inflammation/abscess?

Pus (neutrophils + liquefied necrotic debris + oedema); often due to pyogenic bacteria (e.g., Staph aureus). Abscess = localised pus collection.

What is an ulcer? Give examples.

Local surface epithelial defect from sloughing of inflamed necrotic tissue; can be acute or chronic; e.g. peptic ulcer, diabetic leg ulcer.

What are the three main outcomes of acute inflammation?

Resolution, healing by fibrosis (scarring), or progression to chronic inflammation.

What is ESR and when is it raised?

Erythrocyte sedimentation rate; raised in chronic inflammatory disease (normal <30 mm/hr); often replaced by CRP.

What is CRP and what does it indicate?

C-reactive protein made by liver; marker of inflammation and response to treatment (≤8 mg/L).

What leukocyte changes suggest acute vs chronic inflammation?

Acute: neutrophilia; chronic: lymphocytosis; parasites/allergies: eosinophilia.

What is tissue repair?

Restoration of architecture/function after injury, often with angiogenesis; can be by regeneration or fibrosis/scarring.

Outline the phases of wound healing (skin).

• Immediate/early (0–4 days): clot, ↑ blood flow, neutrophils then macrophages

• Proliferation/granulation (4–21 days): angiogenesis, fibroblasts, epithelial closure, matrix, contraction

• Remodelling (3–90 weeks): collagen synthesis, vascular regression, tissue remodelling