Acute inflammation. Morphologic patterns of acute inflammation, types of inflammatory cells, tissue alterations
Acute inflammation is an inflammatory response which occurs over seconds to days (while chronic is measured in weeks).
It is initiated by resident macrophages, dendritic cells, kupffer cells and mast cells, which release inflammatory mediators (described above). This triggers the vasodilation (leading to redness and heat) and increased permeability (which triggers edema). The release of bradykinins increase the sensitivity to pain.
We have spoken above about the vessel dilation, cellular changes and leukocyte infiltration of the interstitial space, here we are going to focus on certain morphological patterns of acute inflammation.
- Serous inflammation
- Accumulation of thin, protein-poor fluid from plasma (exudate) or mesothelial cells (effusion)
- Blisters are one such example
- Typical of burning and viral infections (e.g. Herpes)
- Fibrinous inflammation
- Increase in vascular permeability is greater than in serous inflammation
- We have protein rich exudate which contains fibrin (and others)
- Accompanied by pro-coagulative stimulus and is characteristic of the lining of body cavities (especially serous membranes)
- Hemorrhagic inflammation
- Characterised by extravasation of blood, often combined with fibrin (fibrinohemorrhagic)
- Examples include Epidemic hemorrhagic fever, Leptospirosis and Plague
- Suppurative inflammation
- Characterised by formation of pus. A cell rich exudate, typical of bacterial infections.
- Dead neutrophils and liquefied tissue leave cellular fragments in extracellular space
- If bacteria penetrates deep into organ, an abscess can be formed (an example of liquefactive necrosis)
- Ulcer
- Damages to organ surface due to shedding of superficial necrotic tissue
- Commonly found in mucosas of hollow organs (e.g. GI tract) and lower limbs of those with circulatory diseases or diabetes
H&E, fibrinous pericarditis: shaggy pink fibrin (top) deposited on the serous surface, with inflammatory cells in the tissue beneath.
Image: “Pericarditis fibrinosa” by dr n. med. Krystyna Bielnik, lek. med. Dariusz Młoczkowski, dr n. med. Tadeusz Modrzewski, lek. med. Dorota Snopkowska, , CC BY-SA 3.0, via Wikimedia Commons.
Examples: a typical lesion of each pattern:
- Serous: the blister of a second-degree burn
- Fibrinous: "bread-and-butter" pericarditis in uremia, rheumatic fever or after myocardial infarction
- Suppurative: staphylococcal skin abscess, acute appendicitis
- Ulcer: peptic ulcer of the stomach or duodenum
The cells predominantly involved in inflammation vary depending on the time frame:
- Neutrophils
- Dominate in the first 24 hours, but disappear quickly after this
- They respond more rapidly to chemokines than others, and attach more firmly to adhesion molecules
- Monocytes
- Take over from Neutrophils after about 24 hours as the the predominating leukocyte