Inflammation Flashcards
What is inflammation?
- It is a dynamic response of vascularized tissue to injury which brings defense and healing to the site of injury
What are the steps involved in an inflammatory response?
- The 5R’s
1) Recognition
2) Recruitment
3) Removal
4) Regulation
5) Resolution
What are the cardinal signs of inflammation?
1) Rubor (Redness, hyperemia)
2) Calor (Warm, hyperemia)
3) Dolor (Pain-nerve)
4) Tumor (swelling-exudation)
5) Loss of function
What are the systemic effects of inflammation?
1) Fever
2) Malaise
3) Loss of appetite
4) Leukocytosis
What are the different types of inflammation?
1) Acute inflammation: is RAPID response. In addition, it’s a response to sudden body damage, such as cutting your finger
2) Chronic inflammation: PROLONGE process, can take weeks/months, or years.
What is meant by the systemic effect?
For example sometimes when we injure our hand we might have inflammation in the lungs, due to the systemic effects caused by various factors like the cytokines secreted by the mast cells into the vascular bed
What are the causes of inflammation?
1) Trauma (blunt & penetrating)
2) Immune reactions (hypersensitivity)
3) Foreign bodies
4) Tissue necrosis (cell releases inflammatory substance)
5) Physical and chemical agents (burns, frostbite, irradiation)
6) Infections
Who are the inflammatory players?
- In general, they are cells and BV:
1) Mast cells (histamines, etc)
2) monocyte - macrophages (elimination of microbes, dead tissue, and source of mediators “cytokine, etc”)
3) PMNL (Eliminates microbes and dead tissue)
4) plasma proteins (Complement) mediate inflammation and elimination of microbe
5) Endothelium: source of mediator, nitric oxide, cytokines, etc
6) Fibroblast, and ECM both mediate repair
Which type of lymphocyte is considered the hallmark of acute inflammation?
Neutrophils (As they are very fast-acting)
- Macrophages (slow-acting imp in chronic)
What are the manifestations of acute inflammation?
1) Vascular dilation & increased blood flow (erythema and warmth)
2) Extravasation and deposition of plasma fluid & proteins (edema)
3) Leukocyte emigration (accumulates at the site of injury)
What is the causes of pain in inflammation?
As the endothelial cells shrink creating gaps (due to histamine and bradykinin), plasma fluid will leak out causing edema, this fluid compression on a pain receptor will make us feel the pain
What are the vascular changes in inflammation?
1) Changes in vascular caliber & Flow
2) Vasodilation (induced by histamine and nitric oxide)
3) Increase microvasculature permeability
4) Stasis (fluid loss concentrates RBC, increasing the viscosity)
- Antihistamines are given to minimize inflammation severity
What is a transudate?
- There is no increase in permeability
Transudate is when there is an increase in hydrostatic pressure (water wants to leave), a decrease in the blood colloid osmotic (there is fewer proteins available for it to catch the water in place) pressure which leads to the formation of a “transudate” with low protein content, and few cells, mainly fluid
- it could be due to liver disease (protein synthesis) or kidney diseases (increased protein loss in urine)
What is an exudate?
- Happens during inflammation as a normal process, due to increased vascular permeability, protein-rich fluid and RBC start moving
- Fluid, plasma proteins (mainly albumin) & cells are found
What are the differences between exudate and transudate?
1) Mechanism:
- Exudate: increased vascular permeability
- Transudate: Increased Hydrostatic or decreased colloid osmotic pressure
2) Protein content:
- Exudate: High more than 1gm%
- Transudate: Low, less than 1gm%
3) Type of protein:
- Exudate: All plasma proteins including fibrinogen
- Transudate: Small molecules, mainly albumin
4) Number of cells:
- Exudate: many
- Transudate: few
5) Cause:
- Exudate: Inflammation
- Transudate: Hypoproteinemia, Heart failure (Increases Hp), Lymphatic congestion, Liver failure, Kidney disease
What are the different classes of cell surface receptors present on leukocytes?
1) G-protein coupled receptor
- Cytoskeletal changes, signal transduction that induces chemotaxis and increases integrin avidity (adhesion is increased)
2) CD-14 & TLR (produces mediators “arachidonic acid metabolites and cytokines” that amplify the inflammatory reaction)
3) Cytokine receptor (eg. IFN-y): Produces ROS and lysosomal enzymes which kills the microbe
4) Phagocytic receptor: Phagocytise microbes into phagosomes killing them, and produces ROS
What is meant by extravasation?
- The events which lead the leukocytes from the vessel lumen to the interstitial fluid
What are the steps in Leukocyte extravasation?
In the lumen:
1) Margination ()
2) Rolling (via selectins)
3) Adhesion (via integrins)
4) Transmigration (diapedesis, under the effect of CD31)
5) Migration in interstitial tissue (via chemotactic stimuli)
What happens when leukocytes are activated?
It enhances:
- Phagocytosis of particles
- Intracellular destruction of phagocytosed microbes and dead cells by the substances produced in a phagosome (like reactive oxygen and nitrogen species)
- Liberation of substances that destroy extracellular microbes and dead tissue
- Mediator production like arachidonic acid metabolites, cytokines
What are the types of inflammation?
- Depending on the severity of the reaction, specific causes, and the particular tissue involved
1) Fibrinous inflammation (characterized by fibrin deposition)
2) Purulent inflammation (neutrophil exudation, with different degrees of tissue necrosis and pus formation)
3) Serous inflammation
4) Hemorrhagic inflammation
Describe the serous inflammation
- Cell poor fluid (Transudate)
- Marked by the outpouring (effusion) of a thin fluid that is derived from either the plasma or the secretions of mesothelial cells lining the peritoneal, pleural and pericardial cavities
- Example includes blisters (epidermis separated from the dermis)
Describe the fibrinous inflammation
-In more severe injuries, vascular permeability is increased, larger molecules like fibrinogen can escape the vascular barrier forming fibrin in the extracellular space
- It is a characteristic of inflammation of the body cavities (meningis and pericardium)
- Fibrin (water-insoluble) appears as an eosinophilic meshwork and sometimes as an amorphous coagulum
Describe the purulent inflammation
Due to the production of large amounts of pus or purulent exudate that contains neutrophils, necrotic cells, and edema fluid
- Can be due to certain bacteria (Staphylococci, species that produce such a reaction are called “pyogenic”)
PMNs in the lungs indicate what?
Acute bronchopneumonia, due to the dilation of the capillary
What is an abscess?
- Produced by deep seeding pyogenic bacteria, Localized collection of purulent inflammatory tissue due to tissue, organ, or a confined suppuration
- They have a central region that appears as a mass of necrotic leukocyte and tissue cells
- Liquified center can appear as an air-fluid
What is an ulcer?
- Local defect on the surface of an organ or a tissue
- Produced by the sloughing “shedding” of the inflammatory necrotic tissue
- “ULCERATION” can occur when tissue necrosis and inflammations exist near/on a surface
- They are deeper than erosions
What are the different outcomes of an acute inflammation?
1) Resolution
2) Healing by connective tissue replacement (Fibrosis)
3) Chronic inflammation (Fungus, cancer, T.B.)
4) pus formation (abscess)
What is the difference between acute inflammation and a chronic one?
1) Onset:
- Acute: fast (min-hours)
- Chronis: Slow (days)
2) Cellular infiltrate:
- Acute: mainly neutrophils
- Chronic: Monocytes/macrophages & lymphocytes
3) Tissue injury (fibrosis)
- Acute: mild and self-limited
- Chronic: Severe and progressive
4) Local and systemic signs:
- Acute: Prominent
- chronic: Less prominent and may be subtle
Which type of lymphocyte is prominant in breastfeeding inflammation?
Neutrophils
Which inflammatory cell plays the most important role in the healing process?
Macrophages
