Pathology Lab Topic: Inflammation - labsstudies

Pathology Lab Topic: Inflammation

Pathology Lab Topic: Inflammation

Definition of Inflammation

  • Is the ability of living vascular tissue to respond to any harmful substances or wounds.
  • It is the internal response of living mammalian tissue to damage caused by the agent.
  • It is an immune response designed to eliminate the original cause of cellular damage as well as necrotic cells and tissues caused by the original damage.
  • This is a complex response involving many other systemic changes, although these have been considered in the field.

Causes of inflammation

  • Physical therapy such as heat, cold, radiation and mechanical injuries.
  • Chemical chemicals such as organic and inorganic toxins.
  • Infectious drugs such as bacterial viruses and their toxins.
  • Antibody and antigen reactions, eg cells mediated by antigen-antibody.

Type of inflammation

  • Depending on host capacity and response time, inflammation can be classified as acute or chronic.

 1. Acute inflammation represents an early response by the body, usually followed by recovery, and is temporary.

2.  Chronic inflammation occurs after a long-term acute inflammatory process or stimulus (example, one that caused chronic inflammation from the start). It’s durable.


  1. Acute inflammation
  • It is a rapid response to injury or bacteria and other foreign substances designed to deliver white blood cells and plasma proteins to the wound site.
  • White blood cells clear the invaders and begin the process of digesting and removing necrotic tissue.

Components of acute inflammation

  • Acute inflammation has composed with two main which are:

o Vascular changes

  • Vascular changes lead to increased blood flow (vasodilation) and structural changes that move plasma proteins out of circulation (increased vascular permeability). 

o Mobile activity

  •  Leukocyte transport (recruiting and promoting cells) from low blood circulation and concentration of damage targets.
  •  The main white blood cells in acute inflammation are neutrophils (polymorphonuclear leukocytes)

Causes of acute inflammation

  • Infections (bacteria, viruses, fungi, parasites) are one of the most common and important health causes of inflammation.
  • Trauma (dull and profound)
  • Physical and chemical substances (thermal wounds such as burning or extreme cold; rays; some environmental chemicals) can damage host particles and cause inflammation.
  • Tissue necrosis (any cause), including ischemia (eg, myocardial infarction) and physical and chemical damage.
  • Foreign objects (debris, dirt, sutures)
  • Immune effects (hypersensitivity) to environmental substances or individual tissues.


Clinical signs and Symptoms of Acute Inflammation

Acute inflammation has the following five main features:

  • Pain and tenderness (days)

o This is an early symptom of acute inflammation.

o Pain in acute inflammation is due to direct nerve damage, tissue irritation chemicals and agents released by cells that cause acute inflammation and stress as accumulated secretions inhibit nerves.

  • Inflammation (tumor)

o This is due to internal accumulation of inflammatory stimuli.

o Vascular changes occur in the affected area, causing fluid and white blood cells to accumulate from the inside of the arteries to the inner tissue of the inflamed area.

  • redness

o This is due to increased internal blood flow, increased permeability, and reddened blood flow to the inflamed area.

o The coloration is less common in people with darker skin.

  • Feeling of hotness (color)

o The swollen area feels warmer than the surrounding area due to increased blood flow to the affected area.

  • Performance loss or reduced efficiency (function laesa)

o The swollen tissue or organ does not function as effectively as normal tissue.

o Temporary or permanent damage to tissue structures may result in loss of function.


Vascular changes in acute inflammation

Transient vasoconstriction

  • This is a very short event lasting a few seconds.

Dilation of arterioles

  • This is a major factor in acute inflammation.
  • This is due to increased blood flow and swelling of the lower capillary bed.
  • This arterial dilation is the cause of redness (erythema) and fever Characteristic manifestations of acute inflammation.
  • As blood vessels thicken, high-protein fluid moves into additional tissue.
  • This makes red blood cells more concentrated, which increases blood viscosity and reduces blood circulation.
  • These changes are reflected under the microscope, with many dilated arteries filled with red blood cells and slow-flowing blood, a process called stasis.
  • As we age, white blood cells (especially neutrophils) begin to accumulate on the posterior surface of the arteries, a process called morphogenesis.
  • This is the first step for white blood cells to travel through the walls of blood vessels to connective tissue (described later).


Increased blood vessels Permeability

  • During the early stages of inflammation, vasodilation and increased blood flow lead to increased hydrostatic pressure within the arteries, causing fluid to flow from capillaries to tissues.
  • This fluid, called exudate, is basically the main filter of the plasma and contains little protein.
  • However, blood transfusions are quickly overlooked due to increased vascular permeability that allows high protein water and even cells to flow into the interstitium, a fluid protein called exudate.
  • Loss of high protein content in the peripheral space reduces intra-arterial osmotic pressure and increases central fluid osmotic pressure.
  • The real result is the flow of water and ions to the tissue outside the artery.
  • The accumulation of fluid in the area outside the artery is called edema, and the fluid can be exudate or exudate.
  • Although exudate is usually inflammatory, it can accumulate in a variety of non-inflammatory conditions.


  • Due to increased vascular permeability during inflammation, protein-rich fluid increases from the vessel to the center.
  • Exudate composition are:
  •  water
  •  Proteins (immunoglobulins), albumin, and fibrinogen in severe cases
  •  Hormones
  • Antibacterial source opsonin
  •  Cell white blood cells (WBC)

Exudation benefits

  •  Reduces toxins in areas of inflammation
  •  Globulin is a protective antibody
  •  Fibrin helps reduce the spread of inflammatory causes and also aids in wound healing


Mechanism for increased endothelial permeability

  • Squeezing endothelial cells and creating spaces between cells in capillaries is a common cause of increased vascular permeability.

-This is a reversible process derived from histamine, bradykinin, leukotrienes and many other chemical mediators.

– Endothelial cell contractions are usually short-term (15-30 minutes), also known as short-term acute responses.

  • Endothelial damage causes vascular leakage by causing endothelial cell necrosis and disintegration.

– Direct damage to endothelial cells usually follows severe injuries such as burns and multiple infections.

– In most cases, the leak begins immediately after the injury and continues for hours (or days) until the damaged blood vessel is repaired or repaired.

– Therefore, this response is called an immediate continuous response.

  • Direct damage to endothelial cells can also lead to prolonged delayed leakage, which begins after a delay of 2 to 12 hours, persists for hours or even days, and involves veins and capillaries.

– Examples include moderate to severe heat damage, certain bacterial toxins, and X-rays or violet radiation (ie, sunburn that occurs at night in the sun during the day).

  • Ultimate leukocyte-mediated endothelial damage may be the result of leukocyte accumulation along the vessel wall.

– Activated leukocytes provide many toxic mediators that can lead to end-stage damage or disintegration.

  • Leakage of new blood vessels

– Tissue repair involves the formation of new blood vessels (angiogenesis), which remain and leak until endothelial cells mature enough to form cell junctions.


Changes/occurrences during acute inflammation

  • An important function of the inflammatory response is to transport leukocytes to the site of injury and activation.
  • White blood cells ingest harmful substances, kill bacteria and other microorganisms, and remove dead tissue and foreign bodies.
  • Once established, leukocytes can cause tissue damage and prolong inflammation because the products of leukocytes that destroy microorganisms can also damage normal tissue.
  • Key to the normal function of leukocytes in military defense is to ensure that they are recruited and established only when needed (ie, to deal with foreign invaders and dead tissue).

Use of white blood cells

  • The sequence of events that recruit leukocytes from the vascular lumen to the extravascular space includes:
  •  Peripheral: This is the attachment of leukocytes to the endothelium and folds along the vessel wall.
  •  Migration: This is the movement of white blood cells between endothelial cells
  •  Mobility: This is the entry of leukocytes into connective tissue for chemotactic stimulation.
  • Chemical mediators or chemical stimulants and certain cytokines affect these processes by stimulating the orientation of leukocytes.


Activation of leukocytes

  • Once leukocytes are used at sites of infection or tissue necrosis, they must be activated to perform their functions.
  • Facilitating triggers include microorganisms, necrotic cell products, and several mediators.
  • Engagement of these receptors with antimicrobial products or various inflammatory mediators triggers a number of responses in leukocytes that are part of their normal protective function and are classified under the generic term leukocyte activation.

Also Read: Pathology Lab topic: Cell Injury and Cell Death


  • It consists of three distinct but related steps.
  •  Recognition and adhesion of particles to swallowed leukocytes;
  •  Phagocytosis with subsequent formation of phagocytic vesicles; and
  •  Kill and destroy swallowed material.
  • Leukocytes bind to and take up most dead organisms and dead cells through special surface receptors that recognize components of microorganisms and dead cells, or host proteins called opsonins that bind to organisms and target them for phagocytosis (a process called conditioning).
  • The most important opsonins are a class of immunoglobulin G (IgG) antibodies that bind to bacterial surface antibodies.


Morphological systems of acute inflammation

Serous inflammation

  • It appears as a fluid-filled, low-protein fluid that, depending on the site of injury, drains serum or from the mucosa of the mesothelial cells surrounding the peritoneal, pleural, and pericardial cavities.
  • Skin burns caused by burns or viral infections are a good example of a serous bath that is collected immediately in or under the skin.
  • The fluid in the slurry chamber is called fluid.

Fibrotic inflammation

  • This is due to more severe damage, resulting in greater vascular permeability, allowing larger molecules (eg, fibrinogen) to pass through the final barrier.
  • Historically, accumulated fibrin was seen as eosinophilic reticular fibers and sometimes as amorphous coagulates.
  • Fibrinous exudates are characteristic of inflammation of the inner layers of the body such as the meninges, pericardium, and pleura.
  •  Such exudates can be destroyed by fibrinolysis, and the accumulated waste can be cleared by macrophages, thereby restoring normal tissue structure (resolution).
  •  Failure to completely remove fibrin can lead to the growth of fibroblasts and blood vessels (tissue), which can lead to scarring that can have serious health consequences.
  •  For example, the arrangement of pericardial fibrin exudates to form dense fibers Scar tissue closes or relaxes the pericardial space and inhibits heart muscle function.

Suppurative ( Purulent) Inflammation

  • This appears as a large amount of pus or pus with neutrophils, necrotic cells and fluid.
  • Some organisms (eg, Staphylococcus) are more likely to cause this internal expansion and are called purulent.
  • A buildup of pus inside called an abscess
  • ulceration
  •  An ulcer is an internal defect or rupture on the surface of a blood vessel or tissue caused by cell necrosis and narrowing of necrotic tissue.
  •  Ulceration occurs only when the effects of tissue necrosis and inflammation are on or near the surface. It is usually accompanied by inflammatory necrosis of the oral, gastric, intestinal, or genitourinary mucosa.
Consequences of acute inflammation
  • Resolution
  •  Complete healing when tissue damage is minimal or the process is short and the tissue has the potential to regenerate.
  • Develop
  •  Acute inflammation can persist to prolonged inflammation when tissue damage is severe or exudate is not completely removed or cleaned.
  • Fibrosis
  •  This occurs when there is severe tissue damage, the exudate is not cleared in time, and the associated tissue cannot regenerate.
  • Spread

o Lymphangiitis progresses to acute lymphadenitis.

o Blood vessels.

  • Pyaemia- the spread of pyogenic microorganisms into small blood clots that travel through the blood a stream that may cause a second abscess (metastatic).
  • Septicaemia – proliferation of organisms in the blood without adequate host protection.

The death due to:

  •  Sepsis, such as endotoxic shock and its complications.
  •  Involvement of key components such as encephalitis, myocarditis.



  • Anne, W. & Grant, A. (2006). Ross and Wilson Anatomy and Physiology in Health and Illness (10th ed.). UK: Churchill Livingstone
  • Kumar, V., Abbas, A.K., Fausto, N. & Mitchell, R. (2007). Robins Basic Pathology (8th ed.). Philadelphia: Saunders Elsevier.
  • Walter, J.B. & Tabot, I.C. (1996). General Pathology (7th ed.). Edinburg: Churchill Livingstone.

You may also like...

Leave a Reply

Your email address will not be published.