Week 2: Acute Inflammation Flashcards
What is inflammation? What common medical terminology is associated with it?
Inflammation is a response of vascularized tissues that deliver leukocytes and molecules of defense from circulation to sites of infection. Inflammatory events are often denoted by the suffix “itis” including
Vasculitis
Gastritis
Meningitis
What general events are occurring during inflammation? What are the two major forms?
Acts to destroy, dilute or wall off the offending agent
Triggers events of repair simultaneously
Two major forms are acute and chronic
What are the five general steps of inflammation?
“Five R’s”
1) Recognition of the offending agent
2) Recruitment of inflammatory cells
3) Removal of agent
4) Regulation of the reaction (termination)
5) Repair of tissue
What cells are common recognition agents in inflammatory pathways?
Macrophages
Dendritic cells
Mast cells/basophils
Granulocytes
Platelets
What are the components of innate and adaptive inflammatory responses?
Innate: physical barriers, secretions, phagocytosis and complement
Adaptive: B/T cells, humoral/antibodies (B cells), and cell-mediated (cytotoxic and other T cells)
What are the characteristics of acute inflammation?
Rapid onset
Short duration
Edema
Neutrophils observed
Symptoms: redness, swelling, heat and pain
What are the characteristics of chronic inflammation?
Variable onset
Longer duration
Fibrosis
Macrophages
Define exudate and transudate
Exudate - extravascular fluid that has a high protein concentration and cell debris
Transudate - fluiud with low protein concent, little to no cell material–essentially an ultrafiltrate of blood plasma due to high hydrostatic pressure and/or pressure imbalance across a vessel wall without an increase in permeability
Define edema and pus
Edema - excess fluid in the interstitial tissue or serous cavities, can be either an exudate or transudate
Pus - purulent exudate–inflammatory exudate rich in leukocytes (mostly neutrophils), the debris in dead cells and, in many cases, microbes
What are some stimuli of acute inflammation?
Bacterial infection, like meningitis in the brain
Tissue injury, like a cut
Physical or chemical injury, like necrosis from frostbite
Tissue damage, like ischemia
Foreign bodies, like a splinter
Overall: infection (bacterial/fungal), trauma (physical/chemical), tissue necrosis
What are the three components of acute inflammation?
Vascular response
Cellular response
Chemical mediators
What vascular events occur during inflammation?
Increased blood flow due to vasodilation–delivers necessary proteins and cells
Increased vessel permeability–vascular leakage allows cells/proteins to move into target tissue
What event in inflammation occurs first, and what induces it?
Vasodilation occurs due to nitric oxide and histamine signaling. This is immediately followed by increased permeability.
What event in inflammation occurs second, and what are its major mechanisms? Where does it occur most often?
Vascular leakage in the post-capillary venules occurs via:
1) retraction (separation) of endothelial cells and
2) endothelial injury
What are the general time frames of vascular events, and what is their ultimate purpose?
Vascular leakage involves
Immediate transient response (15-30m)
Delayed response (2-12h)
Prolonged response (burns)
Purpose: Allows plasma proteins and leukocytes to arrive at the site of infection or tissue damage
What are the main cellular events that occur in recruiting WBCs from plasma to sites of infection?
Many Apes Might Cause Removal
Margination
Adhesion
Migration
Chemotaxis
Recognition and removal
What kind of tissue is this? What cells involved in inflammation are observed here, and how do we know they are involved?
This is a blood vessel (main pink area is lumen) with neutrophils surrounding the endothelial surface. We know these are neutrophils from their dark staining and multilobulated nuclei.
What cell elements mediate adhesion?
Selectins mediate rolling interaction
Integrins mediate firm adhesion
Cytokines enhance this process
What is chemotaxis and what stimuli are involved in this process?
Chemotaxis is the movement of leukocytes in tissue towards a chemical gradient. At the micro level, this occurs due to polymerization of actin and locomotion.
Exogenous stimuli: bacterial products
Endogenous stimuli: complement, leukotrienes, cytokines
What cell receptors mediate recognition?
Tall Guys Of Course
Toll-like receptors (TLRs) - bacterial lipopolysaccharides, proteoglycans and lipids
GPCRs - short bacterial peptides, chemokines, lipid mediators
Opsonin receptors (opsonins coat the microbe) - antibodies, complement, lectins
Cytokine receptors - interferon
Other than destroying microbes, what are some other functions of leukocytes?
Production of growth factors that stimulate repair
Production of mediators tha further stimulate the inflammatory response
Production of mediators that inhibit the inflammatory response
What are the three general steps of cell events leading to the destruction of microbial cells?
1) Leukocytes brought to the site of injury through blood stasis, the expression of adhesion molecules, and chemoattractants
2) Leukocytes functionally respond with the release of enzymes and chemicals
3) Phagocytosis acts as an important means of eliminating the microbe
What are the general concepts (5) of chemical mediators of inflammation?
Derived from plasma or from cells
Production is triggered by microbial products
Mediators bind to specific receptors
Often a progressive process with amplification potential
Mediators are relatively short-lived and capable of harmful effects
What are the kinds of chemical mediators in the body (8)?
He Probably Likes Chess Cause Players Can Knight
Histamine
Prostaglandins
Leukotrienes
Cytokines
Chemokines
Platelet activating factor
Complement
Kinins
What is complement? What is it’s major role?
Complement is a collection of proteins that are activated and bind to receptors with the following functions to enhance the immune response:
Increased vascular permeability
Chemotaxis
Opsonization
It is involved in innate and adaptive immunity, and can be activated by microbes and antibodies
What is occurring here and how do we know?
This is glandular gastritis, likely in the stomach. We can observe the high volume of neutrophils in the area, which are acting to resolve tissue damage or infection. This is occuring within 24h of infection.
What is occurring here and how do we know?
This is the necrotizing of lung tissue, with tissue destruction as well as the invasion of acute inflammatory cells–especially neutrophils.
What patterns of infection are observed here?
This is fibrinous inflammation, where fibrin is produced in abundance in response to tissue damage. Fibrin is the end product of the coagulation cascade.
What patterns of inflammation are observed here?
This is suppurative (purulent) inflammation, characterized by large amounts of pus.
What are the four possible outcomes of acute inflammation?
Progression:
chronic inflammation (angiogenesis, fibrosis/scarring)
Healing:
fibrosis (loss of function)
pus formation (abcess)
resolution (clearance of stimuli, mediators, and inflammatory cells, replacement of injured with normal cells)
What are the three general outcomes of acute inflammation?
Resolution
Fibrosis
Chronic inflammation
What are the possible complications of inflammation?
Ulcers, a local defect in the skin or mucosal surface–loss of superficial surface with a base consisting of inflammatory exudate
Abcesses, a walled-off collection of pus, which can be treated by drainage
