All of the following responses are seen in acute inflammation except: March 2005
Ans. C: Granuloma formationSequence of vascular changes:Transient vasoconstriction of aerioles may be due to:- Direct mechanical stimulation of capillaries- Local axon reflex (vasoconstrictor fibres).Persistent vasodilation- first aerioles, followed by opening of capillary beds, caused by chemical mediators.Increased blood flow mainly due to aeriolar dilatation and opening of capillary beds.Slowing of the circulation (Stasis) due to- Increased viscosity of blood due to fluid loss- Swollen capillary endothelium due to toxin.Flow of protein-rich fluid into extra-vascular space called inflammatory exudates.Inflammatory Exudate: due to:- Increased intra-vascular hydrostatic pressure.- Increased permeability due to endothelial contraction with increased intercellular gaps, of the venules.- Direct endothelial injury and detachment, involving venules, capillaries and aerioles.- Increased tissue osmotic pressure.Margination and immigration of leucocytes:Normally red and white cells flow intermingled in the center of the vessel forming axial stream, separated from vessel wall by a clear cell-free plasmatic zone.Due to slowing of the circulation, leucocytes fall out of the axial stream and come to plasmatic zone known as margination of leucocytes.Leucocytes gradually adhere to the vessel wall known as pavementing of the leucocytes.Leucocytes squeeze between the endothelial cells by the process of diapedesis and migrate through the vessel wall into the interstitial tissue, a process known as emigration of leucocytes (first neutrophils followed by monocytes and lymphocytes).Emigrated leucocytes move towards the site of injury under the influence of chemotactic agents and the process is called chemotaxis.Granuloma formation is a distinctive pattern of chronic inflammation.
Vasodilatation
Neutrophil migration
Granuloma formation
Increased vascular permeability