The usual suspects, again. “Stimuli”, like “etiologic agents” is a very elusive term if you like to think in terms of ultimate causes.
These are the three “phases”, in order, of acute inflammation. Please NOTE they, in no way, are the independent of each other, and as you might suspect by now, quite the contrary, CRUCIALLY all wrapped up with each other!
The three phases of phagocytosis, in correct order.
I must have said THREE patterns, but this looks like four to me. Who cares? Remember, they are only adjectives! (Onelook.com has 133 adjectives to the word “inflammation”)
Acute inflammation by Dr Mohammad Manzoor Mashwani
Acute Inflammation ByDr Mohammad Manzoor Mashwani
Definition• It is a rapid host response that serves to deliver leukocytes and plasma proteins, such as antibodies, to sites of infection or tissue injury.• Minutes- Hours- Days• Less than 48 hours.
Time course Acute inflammation: Less than 48 hours Chronic inflammation: Greater than 48 hours (weeks, months, years)Cell type Acute inflammation: Neutrophils Chronic inflammation: Mononuclear cells (Macrophages, Lymphocytes, Plasma cells).
ACUTE INFLAMMATIONLOCAL MANIFESTATIONS • Heat • Redness • Swelling • Pain • Loss of function 4
Pathogenesis: Three main processes occur at the site of inflammation, due to the release of chemical mediators :1.Increased blood flow (redness and warmth).2.Increased vascular permeability (swelling, pain & loss of function).3.Leukocytic Infiltration.
Cardinal Signs of Inflammation Redness : Hyperaemia. Warm : Hyperaemia. Pain : Nerve, Chemical mediators. Swelling : Exudation Loss of Function: Pain
Major components of Ac. Inflammation• It has three major components:1. Alterations in vascular caliber that lead to an increase in blood flow2. Structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation.3. Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent. 10
Increased Vascular Permeability (Vascular Leakage)• A hallmark of acute inflammation causing edema.• Contraction of endothelial cells resulting in increased interendothelial spaces is elicited by chemical mediators.• It is immediate transient response usually short-lived (15–30 minutes).• In some mild injuries e.g burns, x or ultraviolet radiation, certain bacterial toxins, occurs after a delay of 2 to 12 hours lasting for several hours or days, mild endothelial damage.• Late-appearing sunburn is an example of this type of leakage.• Increased transport of fluids and proteins, called transcytosis, through the endothelial cell. 11
:Lymphatics in inflammationLymphatics are responsible for draining edema.Edema: An excess of fluid in the interstitial tissue or serous cavities; either a transudate or an exudate
EXUDATION• AN EXUDATE: A filtrate of blood plasma. Extravascular fluid High protein concentration Contains cellular debris & High specific gravity.• Its presence implies an increase in the normal permeability of small blood vessels in an area of injury and, therefore, an inflammatory reaction.18
TRANSUDATE: A fluid with low protein content Little or no cellular material & Low specific gravity. It is an ultrafiltrate of plasma, resulting from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability. 19
PUSNeutrophils + Dead cells + Microbes A purulent (infectious) inflammatory exudate. Rich in leukocytes. Mostly neutrophils Debris of dead cells & In many cases microbes. 21
Leukocyte exudation Divided into 4 steps 1. Margination, rolling, and adhesion to endothelium 2. Diapedesis (trans-migration across the endothelium) 3. Migration toward a chemotactic stimuli from the source of tissue injury. 4. Phagocytosis