• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/25

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

25 Cards in this Set

  • Front
  • Back

Protein system that provide a biochemical barrier against invading pathos

complement system


clotting system


kinin system

Cellular Mediators

Mast cells,


granulocytes (neutrophils, eosinophils, basophils)


Monocytes and macrophages


NK cells and lymphocytes


Cellular fragments (platelets)

Mast Cells

most important activators of inflammation


Chemokines or sytokines

regulate innate or adaptive resistance:


pro or anti inflammatory


actions are pleiotropic


either synergic or antagonistic


include interleukins, interferons, and tumor necrosis factors (TNF)

interleukins (ILs)

Cytokines: that are produced by microphages and lymphocytes. they help regulate inflammation.


IL-1, 6, 10,

Interferons (INFs)

cytokines- protect against viral infections; produced and released by virally infected host cells in response to viral double-stranded RNA ; doesn't directly kill viruses but prevents them from infecting additional healthy cells .



INF-a- INF-b - induce antiviral protein production


INF-y - increase microbiocidal activity of macrophages

Chemokines

More than 40 diff kinds exist.


-induce wbc chemotaxis


-produced by macrophages, fibroblasts, and endothelial cells.


Mast cells

in connective tissue close to blood vessels. Skin, Digestive lining, and resp tract



Activated by physical injury, chem agents, adaptive immunity, and TLRs (detects invasion of microbial pathogens)

how are mast cells chemicals released?

1. degranulation


2. Synthesis of Lipid-derived chemical mediators

exudate

fluids and cells, such as protein and debris

serous exudate

watery exudate; indicate early inflammation

fibrinous exudate

thick, clotted exudate; indicate more advanced inflammation

purulent (suppurative) exudate

PUS: indicates a bacterial infection

Hemorrhagic exudate

exudate containing blood: indicates bleeding

Systemic Maifestations of inflammation includes

Fever- caused by exogenous and endogenous pyrogens. On hypothalamus.


LEUKOCYTOSIS- increase # of circulating leukocytes


Increase plasma protein synthesis

Chronic Inflammation

lasts 2wks-months-yrs


related to unsuccessful acute inflammatory response


Causes- high lipid and wax content of micros; ability to survive inside the macrophage; toxins; chemicals, physical irritants



Regeneration

most favorable outcome

Resolution

returning injured tissue to the original structure and function

Repair

replacement of destroyed tissue with scar tissue

Debridement

cleaning up dissolved clots, microorgs, erythrocytes, and dead tissue cells

healing

filling in the wound, sealing the wound (epitheliazation), shrinking the wound (contraction)

Acute inflammation (stage 1)

present in exudate.


macrophages release angiogenesis factors to attract epithelial cells and vascular endothelia cells.



fibroblast-activation factor to attract fibroblasts

Reconstructive phase (stage 2)

wound begins to heal 3-4 days after injury and cont for 2 wks.


fibroblast proliferation occurs. Collagens synthesis by fibroblasts.


Epithelialization


wound contract through actions of myofibroblasts


cellular differentiation occurs

Maturation Phase

healed wound os remodeled. Wks-2yrs after injury.


Cellular diff continues, scar tissue forms, scar remodeling occurs

dehiscence

wounds pull apart at the suture line.


Causes are excessive strain, wound sepsis, and obesity


5-12 days after suture



characteristics are - serious drainage is increased; feels like something gave away; surgery is required