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PH-FD03

Acute and chronic inflammation

How injured tissue calls in fluid and white cells: why vessels dilate and leak, how neutrophils leave the blood, which mediators cause the cardinal signs, and what happens when inflammation persists.

By the end, you can

  • Explain how vascular changes produce redness, heat, swelling and pain.
  • Describe the steps by which neutrophils leave the blood and reach the injury.
  • Relate the main chemical mediators to the effects they cause, local and systemic.
  • Distinguish acute from chronic inflammation and describe a granuloma.
  • Describe the possible outcomes: resolution, abscess, scarring or chronic inflammation.
  • Recognise the classic patterns of acute and chronic inflammation under the microscope, and explain how NSAIDs, glucocorticoids and cytokine blockers act on the mediators.

What it is

Inflammation is the response of vascularised tissue to infection or injury: blood vessels dilate and leak, and white cells are brought in to remove the cause and the dead tissue. Acute inflammation develops within minutes to hours, is dominated by fluid and neutrophils, and usually resolves. Chronic inflammation lasts weeks to years, is dominated by macrophages, lymphocytes and plasma cells, and combines ongoing damage with attempted repair.

3 types to tell apart
Acute inflammation
Fast and short: vasodilation, a protein-rich exudate and neutrophils. Typical of bacterial infection and fresh tissue injury.
Chronic inflammation
Slow and persistent: macrophages, lymphocytes and plasma cells, with tissue destruction, new vessels and fibrosis at the same time.
Granulomatous inflammation
A form of chronic inflammation in which activated macrophages cluster into granulomas, as in tuberculosis, sarcoidosis and reactions to foreign material.

Normal function

Quiet vessels and sentinel cells

In loose connective tissue, a fine network carries blood between arterioles and post-capillary venules. Its endothelium keeps most plasma proteins and white cells inside the vessel, while water and small solutes cross into the .

Sentinel cells wait in the tissue. are packed with granules of histamine; carry receptors (such as toll-like receptors) that recognise molecules made by microbes and molecules released from damaged cells. When they detect either, they release the signals that start inflammation.

Point to it on the model