how the body responds to injury

Question 1

What is inflammation?

Answer 1

Inflammation is the body’s response to an irritant, an infectious pathogen, or tissue damage. It is part of the innate immune response and is immediate and non-specific.

Question 2

What are the categories of inflammation?

Answer 2

The categories of inflammation include:

Acute inflammation: It is an immediate response lasting a few days.
Chronic inflammation: It lasts for months or years.
Systemic inflammation (SI): It is a cytokine-induced inflammatory response that follows chronic inflammation. It can lead to the development of conditions such as cardiovascular disease.

Question 3

What are the localized signs of tissue inflammation?

Answer 3

The localized signs of tissue inflammation include:

Redness (Rubor)
Heat (Calor)
Swelling (Tumor)
Pain (Dolor)
Reduction or loss of tissue/organ function (functio laesa)

Question 4

What are the whole body signs of inflammation?

Answer 4

The whole body signs of inflammation include:

Tiredness
General feeling of being unwell
Fever

Question 5

How are diseases associated with inflammation often named?

Answer 5

Diseases associated with inflammation often end with an “itis”. For example: dermatitis, bronchitis, otitis media, cystitis, meningitis, etc.

Question 6

What are the causes of acute inflammation?

Answer 6

The causes of acute inflammation include:

Infection (bacterial, viral)
Exposure to chemicals or radiation
Cell/tissue injury
Excessive immune reaction
Tissue necrosis due to restricted blood flow

Question 7

What are the causes of chronic inflammation?

Answer 7

The causes of chronic inflammation include:

A resistant infectious agent
Prolonged exposure to endogenous (necrotic tissue) or exogenous (chemicals) materials
Some diseases, e.g., chronic inflammatory bowel disease
Autoimmune disease

Question 8

What are the steps in acute inflammation?

Answer 8

The steps in acute inflammation are:

Recognition
Recruitment
Removal
Repair
Regulation

Question 9

What are the characteristics of acute inflammation?

Answer 9

The characteristics of acute inflammation include:

Vessel dilation and increased blood flow
Vascular permeability
Leukocyte (neutrophil/monocyte) movement (migration)
Monocytes are the precursors of macrophages.

Question 10

What happens to blood flow in the capillary network during “normal health”?

Answer 10

In “normal health,” blood flow in the capillary network is intermittent due to capillary sphincters.

Question 11

What happens to arterioles during acute inflammation?

Answer 11

In acute inflammation, arterioles initially dilate, leading to increased blood flow in the tissue capillary network.

Question 12

What happens to vascular permeability during acute inflammation?

Answer 12

In acute inflammation, increased vascular permeability occurs, which leads to the escape of fluid, including blood cells and protein molecules, to the extracellular space. This process is known as exudation.

Question 13

What is the mechanism of vasodilation during inflammation?

Answer 13

The mechanism of vasodilation during inflammation involves histamine produced by mast cells. Histamine relaxes the smooth muscle, through the production of nitric oxide, and causes the contraction of endothelial cells.

Question 14

What happens to capillary pressure during acute inflammation?

Answer 14

In acute inflammation, capillary hydrostatic pressure increases due to vascular dilation and permeability. This increase in pressure allows the release of plasma proteins in tissues.

Question 15

What is the role of vessel permeability in exudation during inflammation?

Answer 15

Vessel permeability, which increases during acute inflammation, allows the release of plasma proteins in tissues. This, in turn, increases the colloid osmotic pressure in the affected area.

Question 16

What are the normal and inflamed capillary pressures?

Answer 16

In normal health, the mean capillary pressure is approximately 12mmHg. However, in acute inflammation, the capillary hydrostatic pressure increases, reaching around 32mmHg.

Question 17

How is histamine released and what is its role in vasodilation?

Answer 17

Histamine is released from granules in mast cells in response to tissue injury, heat, cold, or antibody binding. It binds to G-protein coupled receptors on endothelial cells, leading to vasodilation. Histamine is also released by basophils and platelets. It elicits a fast and short-lived response.

Question 18

What substances increase vascular permeability and contribute to vasodilation?

Answer 18

Bradykinin, which circulates in the blood plasma, and leukotrienes, produced by leukocytes and mast cells, increase vascular permeability. Leukotrienes also act on vascular smooth muscle tissue.

Question 19

What is the role of kinins, such as bradykinin, in vasodilation?

Answer 19

Kinins, including bradykinin, act on vascular smooth muscle tissue. They can cause both contraction and vasodilation of the smooth muscle.

Question 20

where do neutrophils accumulate in inflammation?

Answer 20

Neutrophils accumulate near the endothelium (vascular wall) during inflammation.

Question 21

What role do adhesion molecules play in the adhesion of neutrophils?

Answer 21

Adhesion molecules, specifically selectins, produced by endothelial cells are detected by neutrophil receptors. These adhesion molecules facilitate the initial loose adhesion of neutrophils to the vascular endothelium, allowing them to roll along the endothelium.

Question 22

What happens when integrin ligands bind on neutrophil integrins during inflammation?

Answer 22

When integrin ligands bind strongly on neutrophil integrins, the rolling motion of neutrophils stops, and transmigration through the endothelium begins.

Question 23

What are the ligands involved in activating leukocytes (neutrophils or monocytes/macrophages) during inflammation?

Answer 23

The ligands involved in activating leukocytes through receptor-ligand binding include lipopolysaccharides (LPS) on the surface of pathogens.

Question 24

What specific receptors are macrophage-specific in inflammation?

Answer 24

Toll-like receptors (TLRs) are macrophage-specific receptors involved in the recognition and activation of immune responses.

Question 25

What are some examples of phagocytic receptors?

Answer 25

Phagocytic receptors involved in phagocytosis include mannose receptors, scavenger receptors, and opsonin receptors.

Question 26

What is the role of reactive oxygen species (ROS) and lysosomal enzymes in phagocytosis?

Answer 26

Phagocytosis relies on reactive oxygen species (ROS) and lysosomal enzymes. ROS are formed in the membrane of phagosomes in activated phagocytes following pathogen recognition. Inside the phagosome, ROS and nitric oxide (NO) contribute to killing pathogens, while lysosomes carry enzymes that destroy proteins.

Question 27

Besides pathogens, what else can phagocytosis eliminate?

Answer 27

Phagocytosis is also used to eliminate necrotic cells.

Question 28

What are the cell types involved in the histology of acute inflammation?

Answer 28

The cell types involved in the histology of acute inflammation are neutrophils and monocytes.

Question 29

What are the mediators of the inflammatory response and their sources?

Answer 29

The mediators of the inflammatory response and their sources include:

Histamine: Produced by mast cells, basophils, and platelets. It causes vasodilation and increased vascular permeability.
Prostaglandins: Produced by mast cells and leukocytes. They cause vasodilation, pain, and fever.
Cytokines (TNF, IL-1, IL-6): Produced by macrophages, endothelial cells, and mast cells. They contribute to endothelial activation, adhesion molecule expression, fever, and hypotension (shock).
Chemokines: Produced by leukocytes and activated macrophages. They promote chemotaxis and leukocyte activation.
Complement factors: Produced in the plasma (primarily in the liver). They contribute to leukocyte chemotaxis and inflammation, pathogen killing (membrane attack complex formation), and mast cell stimulation.

Question 30

What is the role of complement factors in inflammation?

Answer 30

Complement factors circulate in the plasma in their inactive form. Upon cleavage, they become active and function in various aspects of inflammation, including histamine release, chemotaxis (recruitment of leukocytes), and pathogen opsonization (recognition of a pathogen by a phagocyte). The most abundant complement factor is C3, which is cleaved to C3a and C3b. C3b participates in the cleavage of C5 to C5a and C5b, thereby amplifying the signaling involving other complement factors.

Question 31

How is the inflammatory response terminated?

Answer 31

The mediator molecules involved in the inflammatory response are only expressed in response to a stimulus, such as infectious microbes or necrotic cells. These mediator molecules have short half-lives and decay quickly. Neutrophils, which are important inflammatory cells, have relatively short half-lives and can survive for a couple of days after transmigration to tissues. Additionally, anti-inflammatory molecules, such as lipoxins, are produced in parallel with pro-inflammatory molecules. Lipoxins inhibit neutrophil recruitment, including chemotaxis and adhesion to the vascular endothelium.

Question 32

What are the potential consequences of prolonged inflammation?

Answer 32

Prolonged inflammation or unchecked release of enzyme-rich leukocyte granules can lead to tissue damage. Leukocytes, when the inflammatory response is prolonged, can also attack host tissues, contributing to autoimmune diseases

Question 33

What are the local benefits of inflammation?

Answer 33

The local benefits of inflammation include:

Increased vascular permeability assists in the transportation of blood-circulating antibodies and drugs, such as antibiotics, to the site of infection.
Exudation and fluid release can dilute the concentration of toxins produced by pathogens.
Vascular exudate includes fibrinogen, a precursor of fibrin. Fibrin is a fibrous protein that participates in blood coagulation and wound healing. It forms a fiber-rich network at the site of infection that can trap microbes.

Question 34

What are the outcomes of the end of an acute inflammatory response?

Answer 34

The end of an acute inflammatory response can have the following outcomes:

Complete resolution, where the inflammation subsides and the tissue returns to its normal state.
Healing by tissue replacement, where the body recovers from the injury by replacing damaged tissue with new tissue.
Progression to chronic inflammation, where the inflammation persists and can lead to long-term tissue damage.

Question 35

Can acute inflammation resolve completely?

Answer 35

Yes, in most cases, acute inflammation resolves completely.

Question 36

Can chronic inflammation develop without a prior acute phase?

Answer 36

Yes, chronic inflammation can develop without a prior acute phase. This is known as primary chronic inflammation and can occur in conditions such as tuberculosis, autoimmune diseases (e.g., rheumatoid arthritis), chronic inflammatory bowel disease, or necrotic adipose tissue.

Question 37

What can cause the transition from acute to chronic inflammation?

Answer 37

The transition from acute to chronic inflammation can occur as a result of repeated episodes of acute inflammation or persistent triggers.

Question 38

Can you provide an example of the transition from acute to chronic inflammation?

Answer 38

Yes, an example of the transition from acute to chronic inflammation is abscess formation. An abscess starts as an acute inflammatory response to an infection, but if the infection persists or is not adequately resolved, it can progress to a chronic inflammatory state.

Question 39

What are the cellular changes observed in chronic inflammation?

Answer 39

Chronic inflammation is characterized by increased numbers of lymphocytes, plasma cells (antibody-secreting lymphocytes), and macrophages. Necrotic tissue may also be present.

Question 40

What is the impact of inflammatory cells in chronic inflammation?

Answer 40

Inflammatory cells in chronic inflammation can cause tissue damage due to their persistent presence and activity.

Question 41

What processes are initiated in chronic inflammation for tissue repair and angiogenesis?

Answer 41

In chronic inflammation, tissue repair mechanisms and angiogenesis (formation of new blood vessels) are initiated to facilitate healing and restoration of damaged tissue.

Question 42

Can you provide the histological features of chronic inflammation?

Answer 42

Histologically, chronic inflammation is characterized by the presence of plasma cells (P), lymphocytes (L), and macrophages (Ma).

Question 43

What are the principal sources and actions of cytokines in acute inflammation?

Answer 43

• TNF (Tumor Necrosis Factor): Macrophages, mast cells, T lymphocytes. It stimulates the expression of endothelial adhesion molecules and secretion of other cytokines. It also has systemic effects.

IL-1 (Interleukin-1): Macrophages, endothelial cells, some epithelial cells. Similar to TNF, it plays a role in fever and stimulates the expression of adhesion molecules and other cytokines.
IL-6 (Interleukin-6): Macrophages and other cells. It has systemic effects and contributes to the acute inflammatory response.
Chemokines: Macrophages, endothelial cells, T lymphocytes, mast cells, and other cell types. They play a key role in the recruitment of leukocytes to sites of inflammation and the migration of cells in normal tissues.
IL-17 (Interleukin-17): T lymphocytes. It is involved in the recruitment of neutrophils and monocytes to the site of inflammation.

Question 44

What are the principal sources and actions of cytokines in chronic inflammation?

Answer 44

IL-12 (Interleukin-12): Dendritic cells, macrophages. It increases the production of IFN-γ (Interferon-gamma).

IFN-γ (Interferon-gamma): T lymphocytes, NK cells. It activates macrophages, enhancing their ability to kill microbes and tumor cells.
IL-17 (Interleukin-17): T lymphocytes. It plays a role in the recruitment of neutrophils and monocytes to the site of inflammation.

Question 45

What is granulomatous inflammation characterized by?

Answer 45

Granulomatous inflammation is characterized by the presence of macrophages, lymphocytes, and central necrosis.

Question 46

How do activated macrophages change in granulomatous inflammation?

Answer 46

Activated macrophages in granulomatous inflammation can undergo changes and begin to resemble epithelial cells, known as epithelioid cells. They can also fuse together to form cells with multiple nuclei, known as giant cells.

Question 47

What are some diseases that can cause granulomatous inflammation?

Answer 47

Diseases that can cause granulomatous inflammation include tuberculosis, leprosy, syphilis, and Crohn’s disease.

Question 48

What is responsible for the prolonged recruitment of macrophages and the formation of granulomas in persistent pathogen infections?

Answer 48

In the event of persistent pathogen infection, lymphocytes (T-cells) are responsible for the prolonged recruitment of macrophages and the formation of a granuloma.

Question 49

What are other causes of granulomas besides infections?

Answer 49

Granulomas can also be caused by foreign bodies, such as sutures.

Question 50

What causes the systemic effects of inflammation in the acute phase?

Answer 50

The systemic effects of inflammation in the acute phase are caused by the production of cytokines in response to pathogen infection. Cytokines such as TNF, IL-1, IL-6, and type I interferons contribute to these systemic effects.

Question 51

What is the role of cytokines in systemic inflammation?

Answer 51

Cytokines, including TNF, IL-1, and IL-6, are involved in the systemic effects of inflammation. They can lead to increased production of leukocytes in the bone marrow and, in severe cases such as sepsis or severe bacterial infection, cause a series of severe pathological events known as septic shock. Similar systemic effects can occur in non-infectious diseases, resulting in Systemic Inflammatory Response Syndrome (SIRS).

Question 52

How is fever induced during inflammation?

Answer 52

Fever is induced by pyrogens, which include endogenous pyrogens such as TNF, IL-1, and IL-6. These cytokines stimulate the production of prostaglandins that act on the hypothalamus, releasing neurotransmitters that raise the body temperature. The synthesis of prostaglandins can be inhibited by aspirin.