Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how



what are the goals of inflammation? respond, remove, restore
what are stimulators/ initiators of inflammation infections, trauma, physical or chemical agents, tissue necrosis, foreign bodies, hypersensitivity immune reactions
what are the five cardinal signs of inflammation? redness, pain, heat, loss of function,
general responses to inflammation: processes vascular, activation of chemical mediators (plasma and cell derived) migration and activation of cells termination/resolution
in an acute inflammatory response, describe the timing, specificity, predominant cell type, vascular response, and tissue response immediate response, mostly innate immunity, neutrophils, prominent edema, and structure and function may be restored
in a chronic inflammatory response, describe the timing, specificity, predominant cell type, vascular response, and tissue response, slower activation, cell mediated immunity, lymphocytes/macrophages/plasma cells, less prominent edema, typically a loss of function
what are the components of the inflammation process vasculature (fluid, chemicals, cells), connective tissue (matrix, cells) parenchyma
describe what vascular changes take place during inflammation altered hemodynamics (vasoconstriction, vasodilation), altered vascular structure (contraction of endothelial cells, increased vascular permeability, increased interstitial fluid and cells that exit vessels)
what are the two types of edema transudate and exudate
describe the transudate fluid in terms of hydrostatic and colloid osmotic pressure its more watery, less cellular components present. hydrostatic pressure is increased and colloid osmotic pressure is decreased significantly..it is noninflammatory
describe exudate fluid the fluid is leaving with a lot of protein and cells because they leak out of the vasculature...it is inflammatory. there is increased vascular permeability
describe the source of chemical mediators of inflammation plasma derived, cell derived, extracellular matrix
list preformed chemical mediators of inflammation in secretory granules of cells(cell derived) histamine, seratonin. the source is from mast cells, basophils, platelets
list several newly synthesized chemical mediators of inflammation (cell derived) prostaglandins, leukotrienes, platelet activating factor, reactive oxygen species, nitric oxide, cytokines, neuropeptides
list chemical mediators that are plasma derived (come from liver) complement activation proteins: C3a, C5a, C3b, C5b-9, bradykinin, coagulation, fibronolysis system
describe some functions of the complement system phagosytosis/destruction (opsonization: coating bacteria for phagocytosis), vascular inflammatory effects (anaphylotoxins: increase vascular permeability/vasodilation), cellular inflammatory effects (wbc adhesion, activaiton, chemotaxis)
what are the vasoactive amine chemical mediators histamine and seratonin (preformed and released from storage vacuoles within mast cells)
these chemical mediators are generated from cell membrane phospholipids and consist of prostaglandins, leukotrienes, and lipoxins arachidonic acid metabolites
these chemical mediators are generated from membrane phospholipids and have broad range effects on inflammation platelet activating factor (PAF)
these chemical mediators are proteins produced by many cell types and consist of TNF and IL cytokines
these chemical mediators are small proteins that function in chemotaxis chemokines
this chemical mediator is a soluble gas, is a potent vasodilator, and a toxic free radical NO-nitrous oxide
these chemical mediators are acid and neutral proteases that degrade cellular and ECM proteins and result in cell death and slow tissue destruction, also allow for migration of inflammatory cells into tissues: one example is alpha 1 antitrypsin, lysosomal molecules.
in this disease, there is an imbalance of lysosomal molecules. the imbalance between protease and antiprotease results in destruction of the alveolar wall emphysema
this chemical mediator is involved in NADPH oxidative system within RBC's ROS
this chemical mediator is involved with pain (substance P) neuropeptides
what are the chemical mediators which are potent vasodilators? NO, prostaglandins, histamine
what are the chemical mediators involved with fever? IL1, TNF, prostaglandins
what are the chemical mediators involved with pain? prostaglandins, bradykinin
what are the chemical mediators involved with tissue damage? lysosomal enzymes of leukocytes, ROS, NO
what are the chemical mediators involved with chemotaxis, and leukocyte recruitment and activation TNF, IL1, chemochines, C3a, C5a, leukotriene, bacterial products
what are the chemical mediators involved with increased vascular permeability? histamine and seratonin, C3a and C5a, bradykinin, leukotrienes, PAF, substance P
what cell is involved with acute inflammation? neutrophils
what cells are involved with chronic inflammation? lymphocytes, macrophages, plasma cells
what are the possible outcomes of inflammation resolution, healing by fibrosis, or ongoing chronic inflammation
what is one example of an acute inflammation? gastric ulcer
what are three possible causes of chronic inflammation? persistent infection or injurious stimulus, prolonged exposure to injurious stimulus, autoimmunity
in chronic inflammation, what disease is an example of persistent infection or injurious stimulus tuberculosis
in chronic inflammation, what is an example of prolonged exposure to an injurious stimulus silicosis, athersclerosis
in a chronic inflammation, what are examples of autoimmunity rheumatoid arthritis, hashimotos, lupus
what are the processes of chronic inflammation tissue infiltration by mononuclear cells (macrophages, lymphocytes, plasma cells), tissue destruction, tissue repair (angiogenesis, fibrosis)
longstanding resident of macrophages in tissues are called this histiocytes
this is a distinctive pattern of chronic inflammation that forms aggregates of activated macrophages that assume and epitheliod appearance. some macrophages coalesce to form a syncytium: multinucleated giant cell that surround mononuclear inflammatorycell granulomatous inflammation
this is a granulomatous inflammation with necrosis caseating granuloma
this is a granulomatous inflammaiton with no necrosis noncaseating granuloma
this disease is an example of caseating granuloma tuberculosis
this disease is an example of noncaseating granuloma sarcoidosis
what are some systemic effects of inflammation fever, elevated plasma, elevated WBC's
when blood cells stack because of increased plasma cell concentration, it's called this rouleaux
what does increased sed rate mean there is increased cells in the plasma
Created by: aferdo01