What will be discussed here?
There are two types of inflammation: acute, or short lived inflammation, and chronic, or long-term inflammation. I’ll talk about the acute variety here in detail, and briefly discuss acute inflammatory disorders. For more information on chronic inflammation, see the page labelled Intro to Chronic Inflammation and for more info regarding the inflammatory process itself, see the page named Inflammation Mechanisms. This is relevant to other sections in the site as well, as I will be addressing both meningitis and encephalitis (inflammation of the meninges and the brain, respectively). A hint when looking at medical publications about inflammatory conditions is to look for the suffix ‘-itis’: this suffix indicates an inflammatory process going on. As the graphic below demonstrates, inflammation is a common occurrence within the body. Every time that you receive a wound, inflammation starts in order to clean up the area and prepare it for healing.
What are the symptoms of inflammation?
There are five symptoms associated with inflammation: they include the following:
- Pain in the area
- Swelling (or oedema)
- Loss of motion
What triggers acute inflammation?
There are five separate types of stimuli that trigger the acute inflammatory response. They are listed and described in the table above.
What tests can be done to confirm the presence of acute inflammation?
As I mentioned in Inflammation Mechanisms, there are certain acute phase proteins which can be tested for under a biochemistry analyzer. The proteins which are affected include albumin, CRP and alpha-1 and alpha-2 globulins.
In acute inflammation, the following can be seen:
- Normal or decreased albumin
- Increased alpha-1 and alpha-2 globulins
What are the types of acute inflammation?
There are three types of acute inflammation: serous inflammation, fibrinous inflammation, and purulent inflammation.
Serous inflammation is characterized by protein-poor, watery fluid which pours out at the site of injury. The fluid is derived from one of two sources: either the serum within the blood or from the cells lining the body cavities. This tends to happen with second-degree burns, friction-related injuries such as walking in tight shoes and other mild injuries. A good example of serous inflammation is a blister: as seen here, the serum accumulates under the skin.
Fibrinous inflammation tends to occur during more severe injuries. Fibrinogen (the inactive form of the clotting protein fibrin) is able to seep through the endothelial layer of the blood vessels, and this, combined with the regular exudate associated with inflammation, leads to the formation of fibrinous exudate. This particular type of inflammation tends to occur within body cavities (the pleura and pericardium) and the meninges. This can result in one of two outcomes: resolution or scarring.
Purulent inflammation involves the formation of pus, or purulent exudate as seen in this leg picture alongside. Pus consists of oedema fluid, neutrophils and necrotic cells. Some bacteria are capable of localized pus formation and are therefore referred to as pyogenic bacteria: an example of this is Staphylcocci.
Abscesses are basically collections of pus and are typically characterized by a central region of dead cells with an middle layer of neutrophils, and an outer layer of dilated blood vessels and fibroblasts.
An ulcer is a local defect on the surface of an organ or tissue that is produced by cells dying and being sloughed off. There are two scenarios where this can happen:
- Inflammation and necrosis of mucosa of the mouth, stomach, intestines or gastrointestinal tract.
- Tissue necrosis in the lower limbs of older people that have circulatory issues.
What are the plasma protein-derived mediators of inflammation?
There are three different types of plasma proteins associated with the inflammatory process: complement proteins, coagulation proteins and kinins. They are described in more detail in the table below. Chemotaxis is referred to in the page Inflammation Mechanisms. Opsonisation is defined by molecules attaching themselves to an invading microorganism: this makes them stand out.
What are the outcomes that can result from acute inflammation?
There are three possible outcomes, as demonstrated by the Smart Art Graphic:
- The wound gets rid of both the stimuli which caused the injury and of any foreign substances
- The injured cells are successfully replaced
- The acute inflammatory cells are successfully cleared away after their jobs are complete
- Normal functioning of the area is restored.
- The area either first forms an abscess (with pus) and then heals with time, or can heal without the formation of pus.
- However, the area cannot function as it once did because of the hardening of the tissue.
3. Chronic Inflammation
- If the wound does not heal within a short period of time, it can progress to chronic inflammation. This is often triggered by injury from infections from viruses, persistent injury or autoimmune diseases (in where the body is attacking itself).
What are the disorders associated with the acute inflammatory response?
There are several types of disorders associated with the inflammatory response. They are separated into two categories: either through defects in white cell function or through injury from the white blood cells themselves. The latter can happen if the cells are not closely monitored or they go for the incorrect targets. The disorders associated with white cell-related injury is mentioned in the table alongside.
The defects in white cell function include:
- Defects in white cell adhesion
- There are two types of this disorder: leukocyte adhesion deficiency types 1 and 2, or LAD-1 and LAD-2, respectively. Type 1 is more severe than type 2.
2. Defects in activity relating to killing microbes
- An example of this disorder is chronic granulomatus disease, which is genetic in nature.
- Instead of the macrophages being able to directly kill off foreign organisms, they surround them and form granulomas. More of this is discussed in Intro to Chronic Inflammation.
3. Defects in phagolysosome function
- An example of this is Chediak-Higashi syndrome, which is demonstrated in the blood smear alongside.
- This disease is genetic: it is autosomal-recessive, which means that two defective copies have to be present in order for the disease to be present. The genes are located on non-gender related chromosomes in our DNA.
- Chediak-Higashi prevents the fusion of phagosomes (vacuoles within cells) from fusing with the lysosomes (which are discussed in Intro to Normal Cell Structure).