29. Clinicopathological classification of acute inflammation. Organ examples.

Last updated on December 13, 2018 at 14:48

Acute inflammation occurs in the time span of minutes to hours. The most important leukocyte is the neutrophil granulocyte. Vasodilation and permeability increase, which produces all the local signs of acute inflammation.

Signs of an acute inflammation

The local signs are usually these, and you can remember them by using your imagination and thinking about one time you or someone you know had an inflammation:

  • Calor – Heat
  • Rubor- Redness
  • Tumor – Swelling
  • Dolor – Pain
  • Functio laesa – Loss of function

The systemic signs are usually caused by the acute phase reaction:

  • Fever
    • Induced by TNF-α and IL-1
  • Acute phase proteins
    • Induced by IL-6
    • C-reactive protein (CRP), fibrinogen and Serum Amyloid A (SAA) increases.
    • The increased fibrinogen causes increased erythrocyte sedimentation rate (ESR)
  • Leucocytosis
    • Induced by TNF-α and IL-1
  • Pulse increases
  • Loss of appetite
  • Chills

In some severe cases, even sepsis can happen. Sepsis is the life-threatening organ dysfunction caused by a deregulated host response to infection.

Morphological classification of acute inflammation

An acute inflammation can cause the pores and wounds to emit a fluid with exudate (protein rich) composition. There are several types:

  • Serous
  • Fibrinous
  • Pseudomembranous
  • Purulent
  • Haemorrhagic
  • Gangrenous

Let’s take a closer look at them.

  • Serous inflammation

This exudate is protein-poor, almost like transudate, and comes from plasma or mesothelial cells (serous membranes). It can be caused by mild and superficial inflammations, mild trauma or burns and viral and autoimmune inflammations.

Some examples are:

  • Common cold
  • Hay fever
  • Viral meningitis
  • Skin blisters
  • Fibrinous inflammation

As the name suggests, it’s a fibrin rich exudate. The vascular permeability is increased, so fibrinogen can pass through the endothelial barriers and end up as fibrin in the extracellular spaces. This usually happens in the linings of the body cavities, such as meninges, pleura and pericardium.

It can be resolved by fibrinolysis, but sometimes it resists and can cause complications because it leaves fibrous scar tissue, especially in the pericardium as it can cause:

  • Constrictive pericarditis
    Pericardial layers grows together with scar tissue
  • Concretio pericardii
    The layers adhere to eachother
  • Accretio pericardii
    Parietal pericardium adheres to pleura

Causes for fibrinous inflammations are more severe infections than in serous inflammation. It can be caused by:

  • Bacterial infection
  • Early stage autoimmune inflammation
  • Chemical inflammation
  • Rheumatic fever
  • Myocardial infarct
  • Uraemia

Some examples:

  • Fibrinous pericarditis
  • Fibrinous pleuritis

 

  • Pseudomembranous inflammation

The bacteria Clostridium difficile and Corynebacterium Diphtheriae can give a pseudomembranous inflammation. C. difficile produces two toxins called toxin A (enterotoxin) and toxin B (cytotoxin), which damage the lining of the GI tract by destroying tight junctions between epithelial cells and by destroying their cytoskeleton. The epithelial cells loosen from the extracellular matrix, which cause them to undergo a form of apoptosis called anoikis.

  • Purulent inflammation

This inflammation yields a neutrophil-rich exudate together with necrotic cells and oedema, so-called pus, and is caused by pyogenic (pus-forming) bacteria.

We have three classical forms, depending on where the inflammation is:

  1. Abscess – pus in tissue
    • Abscesses leave behind their own cavities, like as seen here.
    • Abscesses are always surrounded by a pyogenic membrane, a membrane formed by the body to limit the spreading of the abscess.
  2. Phlegmone – pus spreading in soft (connective) tissue
    • Like inside the brain parenchyme, or under the skin
    • Has no boundary, unlike abscesses
  3. Empyema – pus in a (pre-existing, anatomically normal) cavity

Some examples are:

Purulent meningitis is a condition caused by bacteria. In infants it’s usually caused by E. coli, but in adults it’s either caused by meningococci, pneumococci or listeria. Symptoms include headache, fever, stiff neck, photophobia and sepsis.

If the purulent meningitis is caused by meningococci, and the patient develops sepsis will the patient develop something called Waterhouse-Friederichsen syndrome. In WFS syndrome will there be a bilateral haemorrhage of the adrenal glands, which causes death due to lack of fluid regulation by aldosterone.

  • Haemorrhagic inflammation

In this type, a large amount of blood is present in the exudate. This can be caused by bacterial, viral and parasitic infections as well as chemical inflammation.

Some examples are:

    • Haemorrhagic cystitis
      • Inflammation in bladder.
      • Can cause further uraemia and haematuria
    • Viral haemorrhagic fever like Ebola
    • Herpes encephalitis
    • Plague
    • Anthrax
    • Uraemic pericarditis

 

  • Gangrenous inflammation

This occurs when there’s both purulent inflammation and ischaemic necrosis in the tissue. The inflammation is caused by bacteria, and diabetes is a risk factor for the ischaemia. More about the different types of gangrene can be studied here.

An example is acute appendicitis. Obstruction by faecalith (stones made of faeces) or food and hyperplasia of lymphatics can compromise the circulation, which results in ischaemia. Bacteria can then grow in the necrotic tissue, producing pus.

Sometimes can a periappendicular abscess develop, which can prevent spreading of the appendicitis.

Other examples of gangrenous inflammation include:

    • Cholecystitis
    • Lung gangrene
    • Feet
Outcome of acute inflammation

So, what happens next after an acute inflammation? We know by now how the immune system reacts, and how the exudate can look like and where it will appear. Let’s study the outcome.

Scar tissue usually forms. The steps of scar formation are as follows:

  • New blood vessels will form (angiogenesis). This begins 2-6 days after the inflammation.
  • Fibroblasts and deposited connective tissue together with abundant vessels form something called granulation tissue.
  • Maturation and organization of the granulation tissue converts it into a stable fibrous scar. Fibrous scar formation takes weeks.

Full recovery

This is only possible if the tissue necrosis or exudate was minimal. It will result in a minimal scar.

Scarring

If the necrosis or exudate was significant, will the tissue have limited regeneration possibilities. Connective tissue accumulates and the tissue will become either fibrotic or sclerotic.

Persistent or chronic inflammation

Here will granulation tissue and later fibrotic scars form. More about chronic inflammation can be studied in the next topic.

Scars

We also distinguish between several types of scarring when they happen in our body. We may not think about them as scars, but they actually are a result of fibrosis.

  • Callus pleurae – pleural fibrosis

Caused by fibrous pleuritis

  • Cirrhosis

Scars of the liver which makes it very hard. Liver damage activates stellate cells (Ito cells), causing them to differentiate into myofibroblasts and start to produce collagen. The scarring produces structures that resemble lobules, so-called pseudolobular scarring.

  • Acquired valve disease

Also called chronic endocarditis. Previous inflammations of valves result in scarring and sclerosis of the valves.

  • Old infarcts

Results in fibrosis and scarring.

 


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28. Vascular and cellular mechanisms and mediators of acute inflammation

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30. Definition, causes, cellular and humoral mechanisms of chronic inflammation

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