Inflammation

when is inflammation activated?

when cells or tissues are damaged

purpose of inflammation:

Prevents AG from invading body unchecked, neutralize AG, promotes healing and repair from AG invasion, limits festering of AG in body

what is inflammation dependent on

the activity of cellular and chemical component and the health of the host

the intensity of response for acute inflammation is detemined by:

the type of antigen, severity of injury by antigen, and health of host

which type of inflammation is usually uniform, immediate, non-specific, and has a short duration of edema and emigration of leukocytes

acute

which cells are the first ones to the site of injury

PMNs (neutrophils)

what happens to PMNs once the resolution phase occurs?

PMNs undergo apoptosis and are ingested by macrophages that emigrate rapidly from the inflamed site to the draining lymph nodes. 

what are the hallmark inflammatory signs for acute inflammation?

pain, redness, swelling, loss of function

what occurs in phase one of acute inflammation after the infection is detected?

with inclusion of neutrophils (first), macrophages, and lymphocytes, the pathogen is neutralized and then eradicated

what occurs in phase two of acute inflammation?

based upon the health of host and amount of pathogen, a degree of reversible collateral tissue damage may occur

what occurs in phase three of acute inflammation?

the pathogen is cleared and the resolution/repair phase results

what occurs in phase four of acute inflammation?

the restoration of normal tissue homeostasis

what hemodynamic changes occur with acute inflammation?

vascular permeability changes (edema), leukocyte adhesion and exudation

what is exudate

inflammatory fluid in extravascular space with high protein concentration and great cellular debris

what is pus

inflammatory exudate rich in protein, leukocyte, and lysozymes

what is transudate

low protein fluid in extravascular space with few cells (e.g. ascites or edema due to CHF)

what is chemotaxis?

mediators of inflammation diffuse to the adjoining venules, causing passing phagocytes to adhere to the endothelium. The phagocytes insert pseudopodis between the endothelial cells and dissolve the basement membrane. They pass out of the blood vessels and move up the concentration gradient of the chemotactic mediators in the direction of the site of inflammation

what is phagocytosis?

Phagocytes arrive at a site of inflammation by chemotaxis. They then attach to microorganisms by way of their non-specific cell surface receptors. If the phagocyte membrane now becomes activated, microbicidal oxygen metabolites are formed and the infectious agent is taken into a phagosome by pseudopodia extending around it. Once inside, lysosomes fuse with the phagosome to form a phagolysosome, and the infectious agent is killed. Undigested microbial products may be released to the outside.

chemical mediators of inflammation:

vasoactive amines, prostaglandins, leukotrienes, chemokines, complement system and clotting system

which inflammation may be insidious with low-grade, smoldering response, and has a longer duration

chronic

when may chronic inflammation occur?

May follow acute inflammation due to persistence inflammatory stimuli or may occur due to repeated bouts of acute inflammatory response deformities occurring

which cells are present in chronic inflammation

lymphocytes and macrophages.

which inflammation has a low-grade inflammatory response and recruits neutrophils and macrophages?

chronic

what is phase one for chronic inflammation?

a non-immune pathologic process initiates an indolent sterile inflammatory response through the production of damage-associated molecular patterns (DAMPs)

what is phase two for chronic inflammation?

this inflammatory response intensifies by cytokines and chemokines. Since this inflammatory response does not eradicate the initial pathologic stimulus, continuous inflammation occurs resulting in irreversible tissue damage

T/F: the chronic inflammatory response may provide a positive feedback to continued production of DAMPs

true

which cell death is found in both normal and pathologic tissues to maintain cell homeostasis

apoptosis

which cells are phagocytized with minimal inflammation?

apoptotic

examples of apoptosis

DNA damage thru radiation, toxins, or free radicals, malignant tumors or normal cells exposed to chemotherapy

what type of cell death is accidental as a result of severe injury and represents the summation of cellular changes

necrosis

what is ICAM-1

Is a leukocyte and endothelial-associated transmembrane protein that facilitates cell-cell interactions with leukocyte endothelial migration

what is made in the arachidonic acid cascade

5-lipoxygenase or cyclooxygenase; these lead to formation of prostaglandins or leukotrienes

what is the kinin system

Plasma protein system that increases inflammatory reaction

what is the primary kinin

bradykinin

what does bradykinin cause

vasodilation, acts with prostaglandins to stimulate pain, increases vascular permeability, and may increase leukocyte chemotaxis

what is the complement system

Plasma proteins that activate the complement cascade and potent defense against bacterial infection

what can the complement system do?

Destroy pathogens and cell lysis, Activate or interact with most inflammatory components, C3b adheres to pathogens and is an opsonin, C3a and C5a are chemotactic factors or anaphylatoxins causing mast cell degranulation

which system has a classical and alternative pathway

complement

what is the clotting system

Plasma proteins that form a fibrin mesh at injured or inflamed areas

purpose of clotting system

prevent spread of infections, traps microorganisms, forms a clot to stop bleeding, provides guide for repair and healing

Preformed mediators in secretory granules:

histamine, serotonin, lysosomal enzymes

histamine source

mast cells, basophils, platelets

serotonin source

platelets

lysosomal enyme source

neutrophils, macrophages

Newly synthesized mediators when we have inflammation:

prostaglandins, leukotrienes, platelet-activating factors, activated oxygen species, nitric oxide, cytokines

prostaglandin source

all leukocytes, platelets, EC

leukotriene source

all leukocytes

platelet-activating factors source

ll leukocytes, EC

activated oxygen species source

all leukocytes

nitric oxide source

macrophage

cytokines source

lymphocytes, macrophages, EC

what is fibrosis

 large amounts of tissue destruction and/or damage, unable to completely regenerate damaged tissue

where does fibrous scarring occur

areas of inflammatory damage composed mainly of collagen

what is an abscess

a cavity containing pus, an opaque liquid with dead white blood cells and bacteria with general inflammatory debris from destroyed body cells (i.e. exudate)

what is the itneraction between lymphocytes and phagocytes?

B lymphocytes release antibodies, which bind to pathogens and their products and so aid recognition by phagocytes. Cytokines released by T cells activate the phagocytes to destroy the material they have taken up. In turn, mononuclear phagocytes can present antigen to T cells, thereby activating them

systemic effects of inflammation

fever, leukocytosis, lymphangitis, lymphadenopathy, edema, scar-like tissue

what is healing by primary intention

Wound edges are brought together to be adjacent to each other via suture, glue, etc; Regrowth of basal layer of epidermis; Lysis of fibrin and re-epithelialization; Restoration to intact skin

what is healing by secondary intention

Large defect filled by fibrin clot; New blood vessels and fibroblasts (granulation tissue) grow from the dermis into fibrin; Collagen laid down by granulation tissue fibroblasts to restore integrity; Maturation of collagen achieves structural integrity and allows regrowth of epidermis; Wounds are allowed to granulate. May be packed with gauze or drained; Granulation results in broader scar and healing is often slower