Chapter 5: inflammation Flashcards
0
Q
Inflammatory response
A
-after surface barriers are breached
-its a second line defense
-activated to protect the body from further injury, prevent infection of injured tissue, and promote healing
-biochemical and cellular mechanisms that are non-specific
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1
Q
Innante immunity
A
-natural or native immunity, includes natural barriers (physical, mechanical, and biochemical) and inflammation
-form 1st line defense at body’s surfaces and are in place at birth to prevent damage by substances in the environment and infection by pathogenic microorganisms
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2
Q
Adaptive immunity
A
- 3rd line of defense
- known as acquired immunity or specific immunity
- induced in a relatively slower and more specific process and targets particular invading microorganisms for the purpose of eradicating them
- also has “memory”, in which results in a rapid response during future exposure to the same microorganisms
3
Q
what 2 types of defensins contribute to the biochemical barriers?
A
- definsin molecules have 2 subtypes
- the a-definsins often require activation by proteolytic enzymes
- rich in granules of neutrophils and may contribute to the killing of bacterial by those cells
- the b-definsins are synthesized in active forms
- found in a variety of epithelial cells lining the respiratory, urinary, and intestinal tracts, and skin
- help to protect epithelial surfaces from infection w/adenovirus and human immunodeficiency virus
- both classes of antimicrobial peptides can also activate cells of the next levels of defense
4
Q
Normal bacterial flora & it’s role in defense
A
- normal flora is a spectrum of nonpathogenic microorganisms that reside on body surfaces, each surface is colonized by a combination of bacteria and occasionally fungi that is unique to the particular location; including skin, mucous membranes of eyes, upper and lower GI tracts, urinary, and vagina
- normal flora competes with pathogens for nutrients and block attachment to the epithelium and produce chemicals (ammonia, pheols, indols, and other toxic materials) and toxic proteins (bacterioicins) that inhibit colonization by pathogenic microorganisms
5
Q
Inflammation (first response to injury, second line defense)
-the activation of the plasma vascular system
A
- vasodilation: increased size of the blood vessels, causing slower blood velocity, and increase blood flow to the area
- increased vascular permeability: the blood vessels become porous from contraction of endothelial cells, and leakage of fluid out of the vessel (exudation) causes swelling (edema) at the site of injury. As plasma moves outward, blood in the microcirculation becomes more viscous and flows out more slowly, and the increasing concentration of red cells at the site of inflammation cause locally increased redness (erthymea) and warmth
- WBC adherence to the inner walls of vessels and their migration to surrounding tissue
- tissue injury, pain, and swelling contribute to loss of function activated by pain fibers
- the vascular changes delivers leukocytes, plasma proteins, and other biochemical mediators to site of injury where they act in concert
6
Q
Complement System: plasma protein system
A
- activation produces factors that can destroy pathogens directly or can activate or increase the activity of many other components of the inflammatory and adaptive immune response
- large number of proteins that constitute 10% of the total circulating serum protein
- most important function of complement cascade is activation of C3 & C5
- Osponins coat the surface of bacteria and increase their susceptibility to being phagocytized (eaten) and killed by inflammatory cells (ex:neutrophils & macrophages)
- Chemotactic factors diffuse from a site of inflammation & attract phagocytic cells to that site [leukocyte chemotaxis]
- Anaphylatoxins induce rapid vasodilation and increased capillary permeability, a major cellular component of inflammation [mast cell degranulation]
- the most potent complement products are C3b (opsonin), C3a(anaphylatoxin) and C5a(anaphylataoxin, chemotactic factor)
- activation of C5b through C9 results in a complex that creates pores in the outer membranes of cells or bacteria, the pores disrupt the cell’s membrane and permit water to enter->causing the cell to burst and die, or to prevent reproduction (cell lysis)
7
Q
Major pathways that control the activation of the Complement System
A
- 3 major pathways
- classical pathway: antibodies
- alternative pathway: activated by substances found on surface of infectious organisms (endotoxins, gram -). Allows for activation of complementing system w/o antigens. Fungal infections
- Lectin pathway: similar to classical but independent of antigens, activated by plasma proteins Carbohydrates. alternative of alternative pathway
8
Q
Clotting System: plasma protein system that initiates inflammatory response
A
- a group of plasma proteins that form blood clots when activated sequentially [blood clots: mesh work of protein fibrin strands that stabilizes the platelet plug and traps other cells such as erythrocytes]
- Blood clots function to:
- plug damaged vessels and stop bleeding
- trap micro-organisms and prevent future spread to adjacent tissues
- provide framework for healing
-activated by substances that are released during tissue injury and infection (collagen, proteinases, plasmin, endotoxins)
9
Q
Major pathways of the Clotting System
A
- 2 major ways
- tissue factor pathway (extrinsic): activated when there is tissue injury and membrane bound or soluble tissue factor (tissue thromboplastin)
- contact activation (intrinsic): activated when there is abnormal vessel wall and Hageman factor (XII) in plasma contacts negatively charged sub-endothelial substances
- platelets help to contain the area if there is infection, if there is a bleed however small, a clot will form. Things have to stop bleeding so healing can take place. The end result is a fibrin colt. Fibrin is like a spider-web, it holds the clot together, eventually the body will lysis once the body is stabilized and neutrophils will get rid of it
10
Q
Kinin System: major protein plasma system that mediates inflammatory response
A
- initiated through activation of Hagemen factor (XII)/prekillikerin—> final product is bradykinin which causes dilation of blood vessels, acts w/prostaglandins to induce pain, causes smooth muscle contraction, and increases vascular permeability
- functions to activate and assist inflammatory cells, primary kinin is bradykinin which causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability and leukocyte chemotaxis
- interacts closely w/coagulation system
11
Q
Mast cells
A
- are filled with granules and located in the loose connective tissues close to blood vessels near the body’s outer surface (skin and lining of respiratory and GI tract)
- degranulation: in response to a stimulus, biologically active molecules are released from the mast cell granules within seconds and exert their effects immediately, include histamine and chemotactic factors
12
Q
Histamine
A
- a small molecular weight molecule with potent effects on many other cells, those that control circulation
- it is a vasoactive amine–> cause temporary, rapid constriction of smooth muscle and dilation of the post capillary venules (mo9re vasodilation than constriction) , which results in increased microcirculation
- it also causes increased blood flow permeability resulting in retraction of endothelial cells lining the capillaries (causing redness and warmth)
- puffy face, watery eyes
- released within seconds of cellular injury
- increased adherence of leukocytes to the endothelium (causing local swelling from surrounding tissues)
-it affects cells binding to H1 and H2 receptors
13
Q
Synthesis of mediators
A
- leukotrienes (slow reacting substances of anaphylaxis) are sulfur-containing lipids that produce histamine like effects: smooth muscle contraction and increased vascular permeability
- stimulate slower and more prolonged response than histamine, but maintains histamine qualities for a long period of time
-Prostaglandins: caused increased vascular premability, neutrophil chemotaxis, and pain by direct effects on nerves
- Platelet activating factor: produced by removal of fatty acid from plasma membrane phospholipid by phospholipase A2
- can also be produced during inflammation
- causes endothelial cell retraction to increase vascular permeability, leukocyte adhesion to endothelial cells, and platelet aggregation
-at site of tissue damage, inflammation can be caused by mast-cell products
14
Q
Chemotactic factors
A
- Neutrophil chemotactic factor
- attracts neutrophils: needed to kill bacteria in early stages
- Eosinophil chemotactic factor of anaphylaxis (ECF-A)
- attracts eosinophils (mostly parasitic infection)
- helps regulate inflammatory response
