Page 47 - Concise Pathology for Exam Preparation ( PDFDrive )

32 SECTION I General Pathology

TABLE 2.1. Comparison between acute and chronic inflammation

Feature Acute Chronic
Causative agents Physical (heat, radiation and Persistent acute inflammation due to nondegradable
mechanical trauma) pathogens
Chemical agents (organic and Persistent foreign bodies
inorganic poisons)
Infectious agents (bacteria, vi- Autoimmune reactions
ruses and parasites)
Immunological agents (hyper-
sensitivity reactions)
Major cells Mainly neutrophils; also eosino- Mononuclear cells (monocytes, macrophages, lym-
involved phils and basophils phocytes, plasma cells) and fibroblasts
Primary Vasoactive amines, eicosanoids Interferon gamma (IFN-g) and other cytokines,
mediators growth factors, reactive oxygen species, and hy-
drolytic enzymes
Onset Immediate/rapid Insidious/delayed
Duration Few days Up to many months or years
Outcomes Resolution, fibrosis and chronic Tissue destruction and scarring
inflammation
Cardinal signs and 1. Pain (dolour) Absence of any cardinal signs
systemic mani-
festations
2. Heat (calor) Patient is asymptomatic or presents with low-grade
fever, lethargy, loss of appetite and weight loss
3. Redness (rubor) Patient may also present with high-grade fever
4. Swelling (tumour)
5. Loss of function (functio leasa)
Oedema Present Absent
Angiogenesis Absent Present
Tissue destruction Absent Present
Attempts at repair Absent Present
Fibrosis Absent Present

Q. Write briefly on the vascular events in acute inflammation.
Ans. Vascular events in acute inflammation occur in the sequence shown in Flowchart 2.1.

Immediate transient vasoconstriction of arterioles
Histamine, prostaglandins, PAF, kinins and NO
Persistent progressive vasodilatation of arterioles

Opening of new capillary beds (local heat and redness)

Increased blood volume in microcirculation elevating the hydrostatic pressure

Transudation of fluid into the extracellular space
Further injury
Histamine, leukotrienes, PAF, kinins
Increased vascular permeability and escape of exudate into the interstitium
(hallmark of acute inflammation)

Stasis

Leucocytic margination or peripheral orientation of WBCs along the endothelial surface
(neutrophils stick to the endothelium and migrate through vascular wall into the interstitial
tissue. RBCs are smaller, move faster and are oriented centrally)
FLOWCHART 2.1. Vascular events in acute inflammation.
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