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111 Cards in this Set
- Front
- Back
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Define inflammation
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complex rxn to injurious agents and damaged cells that consist of vascular responses, migration and activation of leukocytes and systemic rxns
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what are the three objectives of inflammation
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1.neutralize and elimite offending agents
2. demolish necrotic tissue 3. establish conditions for repair and restoration |
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what are two examples of undesirable effects of inflammation
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acute inflammation=asthma
chronic inflammation=rheumatoid arthisis, atherosclerosis |
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what is atherosclerosis
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arterial wall thickened causing lumens of coronary arteries to be narrowed
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what leads to a heart attack
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decreased blood to heart due to atherosclerosis, chest pain upon exertion, blood clot in cornonary artery, heart attack
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What are the three types of leukocytes
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1. granulocytes
2. monocytes 3. lymphocytes |
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what are the three kinds of ganulocytes
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1. neutrophils
2. eosinophils 3. basophils |
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what is another name for a neutrophil
where did this name come from? |
polymorphonuclear leukocytes or "poly"
b/c nuclei have variably appearing lobes |
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what is a result of the nuclei pattern in neutrophils
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segmented neutrophils or "segs"
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which type of granulocyte is the first to respond at the "scene"
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neutrophil
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what are neutrophils capable of
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amoeboid motion,
phagocytosis and killing offenders intracellularly |
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in addition to phagocytosis what else do neutrophils ingest
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necrotic tissue
ex. after heart attack has occured |
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what do eosinophils contain?
why are these cells important? |
a major basic protein that is toxic to parasites
important in allergic rxns and parasitic infections |
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what do basophils contain?
how many basohphils are present at a time? what type of cell releases the same chemical as basophils |
histamine
they exist in small numbers in acute inflammatory response mast cells |
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what is the fxn of monocytes
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they circulate in the blood and transform into macrophages in tissue
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what two actions can a macrophage do when phagocytizing invaders
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1. can kill invaders intracellularly
2. stimulate lymphocyte to participate in inflammatory response |
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what is the difference between neutrophil macrophages and monocyte macrohphages
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monocytes arrive much later (clean up site)
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what are monocyte macrophages critical for?
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resolution of inflammation
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why do monocytes dominate chronic inflammation?
what does this p romote |
can continue to accumulate at site and divide
coexistence ofinflammation , tissue destruction and tissue repair |
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what are lymphocytes?
are these more important in chronic or acute inflammation? |
small, round cells with little cytoplasm
chronic |
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what is acute inflammation?
what are the events of acute inflammation? |
immediate and early response to an injurious agent
chemical mediators bring about events of inflammatory response |
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what are 3 vascular events assoc. with acute inflammation
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1.vasodilation
2. increased vascular permeability 3. outflow of fluid into extravascular space |
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what does vasodilation do?
what does increased vasc. permeability do? |
increases blood flow
PRO's can now pass through vessel |
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what things that contribute to the outflow of fluid into the extravascular space in actute inflammation
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a. increased vasc. permeability
b. decreased colloid osmotic pressure so water can leave vessel |
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what is increased hydrostatic pressure in vessels due to
what is extravascular space filled with fluid called? |
increased blood flow
edema |
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what are 4 general cellular events that take place with acute inflammation
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1.margination
2.adhesion 3.transmigration 4.chemotaxis |
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what is margination?
what is margination a result of? what is adhesion? what is another name for this? |
the lining up of the white blood cells along vascular walls
a result of slowing circulation leukocytes stick to endothelial cells "pavementing" due to cobblestone street appearance |
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what i s transmigration?
what is chemotaxis? |
leukocytes move into extravascular space
migration of leukocytes to injury site that is mediated by chemicals |
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what is exudite?
why does it accumulate? |
fluid which is high in PRO and white blood cell content
as a result of vascular and cellular events |
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what two cells macrophage invaders in an amoeboid fashion?
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neutrophils and then later macrophages
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what are the four clinical signs of inflamation
what is the fifth sign that was added later |
rubor-redness
calor-heat tumor-swelling dolor-pain functio laesa(loss of fxn) |
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what is rubor caused by?
what is calor caused by? what is tumor caused by? what is dolor caused by? |
vasodilation
increased blood flow outflow of fluid into extravascular space local pressure from swelling and chemical mediators |
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what is a preformed cell derived mediator?
why is this important? what does it do? |
histamine
causes vasodilation and increased vascular permeability important in early inflammatory response releases histamine from mast cells |
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what is a newly synthesized mediator?
what type of drugs mediate anti-inflammatory actions |
arachidonic acid metabolites
glucocorticoid drugs |
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what are two major oxygenase pathways
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1.cyclooxygenase
2.lipoxygenase |
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what does the cyclooxygenase pathway produce?
what are the effects of the products |
prostaglandins
vasodilation, pain, fever |
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what type of drugs inhibit and treat the symptoms assoc. with prostaglandins
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NSAID's
(non sterioidal anti-inflammatory drugs) asprin |
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what do glucocorticoid drugs do?
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block arachidonic acid release and prevent production of arachodonic acid metabolites
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what is the difference in nomenclature between generic and brand name drugs
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the brand name is capitilized while the generic is not
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what is the production of the lipooxygenase pathway?
what do they do? |
leukotrienes
increased vascular permeability; leukocyte chemotaxix, contriction of bronchial passages |
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what is a major importance of leukotrienes
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bring about signs ans symtpoms of asthma
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what is used to treat asthma
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leukotriene inhibitor
Singulair-brand montelukast sodium=generic |
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what are the 4 major systems in which inactive plasma proteins are activated?
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1.complement system
2. kinin system 3. clotting 4. fibrinolytic systems |
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what are all 4 induced by?
what is it activated by? what are all these rxns important in |
a Hageman factor protein
exposed collagen in injured vessels or other mechanisms inflammatory response and blood clotting |
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what are the foles proteins play in inflammatory response in the complement system
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1. vasodilation
2. promote phagocytosis of invaders by acting as "flags" 3. directly kill the invader cells 4.recurit WBC's to site of inflammation |
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what is the important product in the Kinin system?
what are it's actions? |
1. bradykinin
increase vascular permeability, vasocilation, pain |
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Describe the clotting system?
what is an important product? what does this product induce? |
sequential activation of clotting facotrs result in fibrin clot
thrombin inflammation |
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what is the major product of the Fibrinolytic System?
What does it do? |
plasmin
activates a complement pro that recruiets WBC's to injury site |
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What Chemical mediators cause Pain in inflammation?
WHich cause Fever? |
Bradykinin and Prostaglandin
Prostaglandin and Cytokines |
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what causes vasodialtion and increased permability
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Mainly Histamine
but also bradykinin, arachidonic acid metabolites, prostaglandins and leukotrienes |
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what is responsible for intracellular killing and tissue damage
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lysosomal enzymes and
oxygen-derived free radicals |
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what has multiple inflammatory effects
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1. arachondonic acid metabolites(prostaglandin and leukotriene)
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What are symptoms associated with prostaglandins
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vasodilation, fever, pain
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what are symtpoms associated with leukotrienes
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vasoconstriciotn, bronchospasm, increased vasc. permeability
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what is the fxn of cytokins?
what is a major fxn |
systemic effects of inflammation ex, fever, sleepiness
stimulate repair and recruit WBC's to injury site |
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what are the products of the complememnt pathway
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1.vasodilation and increased vascular permeability
2.promote phagocytosis of invaders 3.directly kill invader cells 4.recruit white blood cells to site of inflammation |
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what drugs relieve allergic symptoms and hayfever respectively?
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antihistamines-ex, Benadryl and Zyrtec
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what drugs block production of prostaglandins
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COX inhibitors drugs
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what are the two types of COX inhibitors
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Cox1-aspririn, NSAID's
Cox2-Celebrex |
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what drugs selectively block leukotriene productio
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Singulair
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what is a poor Cox inhibitor that is oxidized in the brain to lower fever and relieve pain?
where is it oxidized in the brain? |
tylenol(acetiminophen)
P450 cytochrome system |
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how do lymphatic channels drain?
what do the lymph channels return |
distally to proximally (drain far to near)
extravascular fluit to venous system |
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what are lymph nodes?
what do they contain? |
discrete structures with a capsule
marcrophages and lymphocytes |
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what is the lymphatic system's role in inflammation?
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resolution of inflammation via
-draining edema -removing leukocytes and cell debris |
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what do lymph nodes filter out?
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invaders as a secondary line of defense
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what are complications of the lymph systems
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lymphangitis-2ndary inflammation of lymphatic CHANNELS draining infectious organisms
lymphadenitis-2ndary inflammation of lymph NODES draining infectious organisms |
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what are the red streaks that form from a bite mark
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the course of the lymphatic channels
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what are 4 possible outcomes of acute inflammation?
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1.complete resolution
2.abscess formation 3.healing by scarring 4.progression to chronic inflammation |
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what is complete resolution?
what is the "clean up crew"? what must tissues be capable of? |
restoration of tissue to normal histology fxn
clean up crew are lymphatics and macrophages that mop up the extra fluid, necrotic tissue and leukocytes regeneration |
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what are some examples of when inflammation begins as a chronic inflammation as opposed to acute
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autoimmune diseases such as tuberculosis and rheumatoid arthritis
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what is chronic inflammation?
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inflammation of prolonged duration (week or months) in which active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously
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what are three settings in which chronic inflammation arises
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1. persisten infection by certain microorganisms
2. prolonged exposure to potentially toxic agents 3. chronic autoimmune disease |
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what are examples of chronic inflammatory causing:
microorganisms? toxic agents? autoimmune diseases? |
TB and Syphilis causing, viruses and fungi
silica rheumatoid arthritis, systemic lupus erythematosus |
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what cells are present in chronic inflammation
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1.marcrophages
2. lymphocytes 3. T lymphocytes |
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what are the key players in chronic inflammation?
what activates the macrophages |
macrophages
bactgerial toxins and cytokines produced by lymphocytes |
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what are the effects of the chemical mediators produced by macrophages?
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1. recruitment of leukocytes to inflammatory site
2. tissue destruction 3. repair by scarring |
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what destroys the tissue in chronic inflammation?
how is scar formed |
toxic oxygen metabolitesw, proteases and NO
fibroblast proliferation and collagen production |
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what type of immunity do B lymphocytes participate in?
what activates lymphocytes |
humoral
cytokines produced by macrophages |
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what do b cells produce?
what do antibodies inactivate? how do they aid phagocytosis? what can they activate? |
antibodies
toxins and viruses sticking to invaders and signaling cells to engulf them the complement system |
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what type of immunity do T cells participate in?
what are T cells directed against what do they kill what do they regulate? |
against fungi and Mycobacterium
kill virus infected cells and tumor cells regulate humoral response from B cells |
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define gramulomatous inflammation
what is it characterized by? |
type of chronic inflammatory rxn
predominance of activated macrophages, multinucleated giant cells and lymphocytes |
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what are multinucleated giant cells?
what are activated macrophages called? what do lymphocytes surround |
fused epithelial cells
epitheloid cells macrophages |
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define granuloma
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nodule of granulomatous inflammation
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what are foreing body gramulomas?
what happens |
irritants which cannot be phagocytized ex. sutures, tale from IV drug abues
epitheloid cells and giant cells surround the foreign body without any specific immune response |
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what are immune granulomas caused by?
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poorly degradable microogranisms that incite a cell mediated immune response
ex, TB, syphilis, cat scratch disease |
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what is a system type of immune granulomatous disease?
what is the cause |
sarcidosis
it is unknown |
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what result in the morphologic variations in the patters of acute and chronic inflammation
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severity of rxn, specific cause and particular tissue and site involved
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what is the location of the inflammatory rxn given by?
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the organ or tissue name followed by -itis
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what is the least severe type of inflammation?
what is the definition of this type? |
serous
an outpouring of a thin fluid with low PRO and cell content which is derived from serum |
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what is an example of serous inflammation?
what is plasma? what is serum? |
skin blister-fluid within or directly u nderneath epidermis
blood without cells fluid remaining after blood haS clotted |
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what is fibrinous inflammation?
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inflammation of the pleura which is inflammatory disease within the lungs
ex. TB pneumonia, lung abscess, necrosis of lung tissue |
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what is another type of fibrinous inflammation?
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pericarditis caused by necrosis of cardiac muscle
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what is purulent inflammation?
what is another name? how does pus come about? |
thick edema fluid rich in neutrophilsnecrotic tissue cells and bacteria
pus neutrophils digest tissue and cause necrosis |
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what is pyogenic bacteria
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bacteria causing purulent inflammation
ex staphylocoal aureua |
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describe pus
what are examples of purulent inflammation |
creamy yellow due to necrotic white blood cells
acute appendicitis, acute bacterial meningitis |
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what is an abcess?
what are central necrotic cells surrounded by? |
localized collection of pus buried in a tissue or organ
living neutrophils |
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what eventually happens to an abcess?
how are abcess's treated? |
gets walled off with fibrous tissue
difficult to treat with antibiotic alone, require surgical drainage |
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what is an ulcer?
what caused it? |
an excavated area on the surface of a tissue or organ
sloughing off of necrotic, superficial inflammatory tissue ex. peptic ulcer of stomach or duodenum |
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what are systemic effects of inflammation
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1. fever
2. behavioral changes |
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what causes fever?
how is signal transmitted what nervous system is stimulated what happens to skin and core body temp |
cytokines released in response to infections stimulate release of prostaglandins
vasomotor center sympathetic nerves skin vasoconstriction and increases core body temp |
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what is the role of fever
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an increase of body temp to improve efficiency of leukocyte killing
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how is fever surpressed
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with anti-prostaglandin drugs
ex NSAIDs, ibuprofen |
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what are behavioral changes associated with inflammation
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1. chills
2. rigors 3. sleepiness, decreased appetite, malaise |
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what is a feeling of chills due to?
what is malaise? |
vasoconstriction
a feeling of general discomfort or uneasiness; feeling out of sorts |
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what is C-reactive protein a marker of
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inflammation and in cardiology is a marker for heart attacks
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what does an increased CRP serum or plasma level increase the risk of
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heart attack, for people at risk for atherosclerosis and coronary artery disease
recurrent heart attack for patients with established cornonary artery disease |
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what is leukocytosis
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elevation of leukocyte count
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what do most bacterial infections give rise to
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neutrophilia
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what is lymphocytosis
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elevation of lymphocyte count associated with some viral infections and pertussis
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what is eosinophilia
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elevation of eosinophil count associated with asthma, hay fever and parasitic infections
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what is leukopenia
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low white blood cell count which may be cause dby overwhelming bacterial infections in compromised patients
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