1. What are the physiological benefits of inflammation? (there are 4)
2. What are pahophysiological effects of inflammation? (name 3)
1. dilute, destroy damaged tissue or invading microorganisms, isolate, initiate repair
2. wide-spread inflammation (sepsis), re-occuring inflammation (allergies), chronic inflammation (autoimmunity)
(Inflammation - normal physiological effects)
1. What are the cardinal clinical signs of acute/early inflammation (localized)? What is all of this due to?
2. What are the systemic effects of inflammation? (there are 5)
1. redness, heat, swelling, pain, and loss of function; vascular events
Figure is on ipad - look at it too
2. fever, weight loss, systemic lymph node enlargment, hematological changes, acute phase proteins
(Inflammation - Vascular effects)
1. What is the process of stopping blood leakage from a damaged blood vessel? Involves what?
2. What increases net blood flow resulting in heat, redness, and swelling/edema? Fluid escaping the blood vessels during vasodilation is referred to as what?
3. How is swelling important?
1. hemostasis; vasoconstriction and clot formation (coagulation and platelet aggregation)
2. vasodilation; transudate (extravascular fluid with low protein)
*look at attached figure - just use dropbox
3. dilutes the toxins - also extra fluid gets sent through lymph to draining lymph nodes
(Inflammation - Vascular effects cont)
1. What is it called when endothelial cells contract permiiting th passage of protein rich fluid (called what?) and the cells becomes sticky allowing for attachment and migration of what?
2. Exudate contents vary and are useful for diagnostic purposes
(He said that knowing the type of exudate isn't all that important - pretty much just read these and don't worry about memorizing)
3. Which kind is watery with no cells (blister fluid)?
4. Thick fluid that contatins WBC, bacteria, cellular debris?
5. contains blood
6. contains high concentrations of fibrinogen and fibrin resulting in a sticky meshwork
7. What is transudate vs. exudate?
1. exudate; leukocyte; increased vascular permeability and adhesiveness
3. serous exudate
4. purlent/suppurative exudate
5. hemoragic exudate
6. fibrinous exudate
7. transudate is low protein fluid, exudate is high
(Inflammattion-Mechanisms - Initiated by early signals that are then amplified)
1. What are the initial events that cause inflammation (3 of them)
2. When cells become damaged they release kinds of signals that do what?
2.1 What are these signals referred to as?
3. What do these DAMPS bind to? Then what happens?
4. What are PAMPS? What do they do?
5. What else do signalling factors released by leukocytes act on?
1. trauma, heat, chemicals
2. pro-inflammatory factors signal to leukocytes that these cells have been damaged and that they need to be cleared, removed, and repaired
2.1 DAMPS (damage-associated molecular patterns)
3. bind to leukocytes (macrophages, mast cells); leukocyte releases a whole bunch more signalling molecules and amplifies the signal
4. pathogen associated molecular patterns; they also send signals to leukocytes - and the same kind of things occur as with DAMPS
5. Act on blood vessels and other leukocytes
(Inflammation - Proinflammatory Factors)
1. What are the localized effects?
2. What are the systemic effects?
1. increased vasodilation and permeability, increased leukocyte recruitment and activation
2. - fever
- increased blood pressure
- loss of appetite
- acute-phase proteins
(Inflammation - proinflammatory factors)
- Leukocytes release numerous soluble factors that regulate inflammation
1. Lipid mediators do what? examples of these?
+learn this graph - but do not worry about platelet-activating factor, thromboxanes, and prostacyclins
1. attract leukocytes and have various vascular effects; leukotrines and prostaglandins
(Inflammation - proinflammatory factors)
1. Amines and peptides do what?
Name that compound
2. Source - leukocytes and platelets. Derived from the amino acid histidine
3. Source - platelets. Derived from the amino acid tryptophan and is stored inside platelet granules
4. Source - endothelial cells, leukocytes, etc. Is a soluble gas derived from the amino acid arginine
5. Source - Nerve Cells. Peptide products from nerve cells that function directly and indirectly in inflammation (substance P)
6. eg. IL-1beta, IL-6, TNFalpha
1. increase vasodilation and permeability
4. nitric oxide (NO)
1. What is the most predominant white blood cell (leukocyte) in blood of mammals? found in tissue sites? important in inflammation? life span?
2. What is the hallmark of acute inflammation?
3. Neutrophils are stored where?
1. neutrophil; not usually; yes; 2 days
3. bone marrow
1. What do blood vessels get upon activation?
2. What process do neutrophils go through upon sticking?
3. Does it occur in arteries? venules? capillaries? Where does it occur?
4. What are the three main families of adhesion molecules and where expressed?
1. very sticky
2. rolling --> adherence --> immigration
3. no; no; no; as capillaries converge back into venules (post capillary venules)
4. Selectins (WBC or endothelial cell), integrins (WBC), immunoglobulin superfamily (endothelial cells)