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111 Cards in this Set

  • Front
  • Back
Define inflammation
complex rxn to injurious agents and damaged cells that consist of vascular responses, migration and activation of leukocytes and systemic rxns
what are the three objectives of inflammation
1.neutralize and elimite offending agents

2. demolish necrotic tissue

3. establish conditions for repair and restoration
what are two examples of undesirable effects of inflammation
acute inflammation=asthma

chronic inflammation=rheumatoid arthisis, atherosclerosis
what is atherosclerosis
arterial wall thickened causing lumens of coronary arteries to be narrowed
what leads to a heart attack
decreased blood to heart due to atherosclerosis, chest pain upon exertion, blood clot in cornonary artery, heart attack
What are the three types of leukocytes
1. granulocytes
2. monocytes
3. lymphocytes
what are the three kinds of ganulocytes
1. neutrophils
2. eosinophils
3. basophils
what is another name for a neutrophil

where did this name come from?
polymorphonuclear leukocytes or "poly"

b/c nuclei have variably appearing lobes
what is a result of the nuclei pattern in neutrophils
segmented neutrophils or "segs"
which type of granulocyte is the first to respond at the "scene"
what are neutrophils capable of
amoeboid motion,

phagocytosis and killing offenders intracellularly
in addition to phagocytosis what else do neutrophils ingest
necrotic tissue

ex. after heart attack has occured
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
what do basophils contain?

how many basohphils are present at a time?

what type of cell releases the same chemical as basophils

they exist in small numbers in acute inflammatory response

mast cells
what is the fxn of monocytes
they circulate in the blood and transform into macrophages in tissue
what two actions can a macrophage do when phagocytizing invaders
1. can kill invaders intracellularly

2. stimulate lymphocyte to participate in inflammatory response
what is the difference between neutrophil macrophages and monocyte macrohphages
monocytes arrive much later (clean up site)
what are monocyte macrophages critical for?
resolution of inflammation
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
what are lymphocytes?

are these more important in chronic or acute inflammation?
small, round cells with little cytoplasm

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
what are 3 vascular events assoc. with acute inflammation
2. increased vascular permeability
3. outflow of fluid into extravascular space
what does vasodilation do?

what does increased vasc. permeability do?
increases blood flow

PRO's can now pass through vessel
what things that contribute to the outflow of fluid into the extravascular space in actute inflammation
a. increased vasc. permeability

b. decreased colloid osmotic pressure so water can leave vessel
what is increased hydrostatic pressure in vessels due to

what is extravascular space filled with fluid called?
increased blood flow

what are 4 general cellular events that take place with acute inflammation
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
what i s transmigration?

what is chemotaxis?
leukocytes move into extravascular space

migration of leukocytes to injury site that is mediated by chemicals
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
what two cells macrophage invaders in an amoeboid fashion?
neutrophils and then later macrophages
what are the four clinical signs of inflamation

what is the fifth sign that was added later

functio laesa(loss of fxn)
what is rubor caused by?

what is calor caused by?

what is tumor caused by?

what is dolor caused by?

increased blood flow

outflow of fluid into extravascular space

local pressure from swelling and chemical mediators
what is a preformed cell derived mediator?

why is this important?

what does it do?

causes vasodilation and increased vascular permeability

important in early inflammatory response

releases histamine from mast cells
what is a newly synthesized mediator?

what type of drugs mediate anti-inflammatory actions
arachidonic acid metabolites

glucocorticoid drugs
what are two major oxygenase pathways

what does the cyclooxygenase pathway produce?

what are the effects of the products

vasodilation, pain, fever
what type of drugs inhibit and treat the symptoms assoc. with prostaglandins
(non sterioidal anti-inflammatory drugs)

what do glucocorticoid drugs do?
block arachidonic acid release and prevent production of arachodonic acid metabolites
what is the difference in nomenclature between generic and brand name drugs
the brand name is capitilized while the generic is not
what is the production of the lipooxygenase pathway?

what do they do?

increased vascular permeability; leukocyte chemotaxix, contriction of bronchial passages
what is a major importance of leukotrienes
bring about signs ans symtpoms of asthma
what is used to treat asthma
leukotriene inhibitor

montelukast sodium=generic
what are the 4 major systems in which inactive plasma proteins are activated?
1.complement system
2. kinin system
3. clotting
4. fibrinolytic systems
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
what are the foles proteins play in inflammatory response in the complement system
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
what is the important product in the Kinin system?

what are it's actions?
1. bradykinin

increase vascular permeability, vasocilation, pain
Describe the clotting system?

what is an important product?

what does this product induce?
sequential activation of clotting facotrs result in fibrin clot


what is the major product of the Fibrinolytic System?

What does it do?

activates a complement pro that recruiets WBC's to injury site
What Chemical mediators cause Pain in inflammation?

WHich cause Fever?
Bradykinin and Prostaglandin

Prostaglandin and Cytokines
what causes vasodialtion and increased permability
Mainly Histamine

but also bradykinin, arachidonic acid metabolites, prostaglandins and leukotrienes
what is responsible for intracellular killing and tissue damage
lysosomal enzymes and

oxygen-derived free radicals
what has multiple inflammatory effects
1. arachondonic acid metabolites(prostaglandin and leukotriene)
What are symptoms associated with prostaglandins
vasodilation, fever, pain
what are symtpoms associated with leukotrienes
vasoconstriciotn, bronchospasm, increased vasc. permeability
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
what are the products of the complememnt pathway
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
what drugs relieve allergic symptoms and hayfever respectively?
antihistamines-ex, Benadryl and Zyrtec
what drugs block production of prostaglandins
COX inhibitors drugs
what are the two types of COX inhibitors
Cox1-aspririn, NSAID's

what drugs selectively block leukotriene productio
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?

P450 cytochrome system
how do lymphatic channels drain?

what do the lymph channels return
distally to proximally (drain far to near)

extravascular fluit to venous system
what are lymph nodes?

what do they contain?
discrete structures with a capsule

marcrophages and lymphocytes
what is the lymphatic system's role in inflammation?
resolution of inflammation via
-draining edema
-removing leukocytes and cell debris
what do lymph nodes filter out?
invaders as a secondary line of defense
what are complications of the lymph systems
lymphangitis-2ndary inflammation of lymphatic CHANNELS draining infectious organisms

lymphadenitis-2ndary inflammation of lymph NODES draining infectious organisms
what are the red streaks that form from a bite mark
the course of the lymphatic channels
what are 4 possible outcomes of acute inflammation?
1.complete resolution
2.abscess formation
3.healing by scarring
4.progression to chronic inflammation
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

what are some examples of when inflammation begins as a chronic inflammation as opposed to acute
autoimmune diseases such as tuberculosis and rheumatoid arthritis
what is chronic inflammation?
inflammation of prolonged duration (week or months) in which active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously
what are three settings in which chronic inflammation arises
1. persisten infection by certain microorganisms

2. prolonged exposure to potentially toxic agents

3. chronic autoimmune disease
what are examples of chronic inflammatory causing:


toxic agents?

autoimmune diseases?
TB and Syphilis causing, viruses and fungi


rheumatoid arthritis, systemic lupus erythematosus
what cells are present in chronic inflammation

2. lymphocytes

3. T lymphocytes
what are the key players in chronic inflammation?

what activates the macrophages

bactgerial toxins and cytokines produced by lymphocytes
what are the effects of the chemical mediators produced by macrophages?
1. recruitment of leukocytes to inflammatory site

2. tissue destruction

3. repair by scarring
what destroys the tissue in chronic inflammation?

how is scar formed
toxic oxygen metabolitesw, proteases and NO

fibroblast proliferation and collagen production
what type of immunity do B lymphocytes participate in?

what activates lymphocytes

cytokines produced by macrophages
what do b cells produce?

what do antibodies inactivate?

how do they aid phagocytosis?

what can they activate?

toxins and viruses

sticking to invaders and signaling cells to engulf them

the complement system
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
define gramulomatous inflammation

what is it characterized by?
type of chronic inflammatory rxn

predominance of activated macrophages, multinucleated giant cells and lymphocytes
what are multinucleated giant cells?

what are activated macrophages called?

what do lymphocytes surround
fused epithelial cells

epitheloid cells

define granuloma
nodule of granulomatous inflammation
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
what are immune granulomas caused by?
poorly degradable microogranisms that incite a cell mediated immune response

ex, TB, syphilis, cat scratch disease
what is a system type of immune granulomatous disease?

what is the cause

it is unknown
what result in the morphologic variations in the patters of acute and chronic inflammation
severity of rxn, specific cause and particular tissue and site involved
what is the location of the inflammatory rxn given by?
the organ or tissue name followed by -itis
what is the least severe type of inflammation?

what is the definition of this type?

an outpouring of a thin fluid with low PRO and cell content which is derived from serum
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
what is fibrinous inflammation?
inflammation of the pleura which is inflammatory disease within the lungs

ex. TB pneumonia, lung abscess, necrosis of lung tissue
what is another type of fibrinous inflammation?
pericarditis caused by necrosis of cardiac muscle
what is purulent inflammation?

what is another name?

how does pus come about?
thick edema fluid rich in neutrophilsnecrotic tissue cells and bacteria


neutrophils digest tissue and cause necrosis
what is pyogenic bacteria
bacteria causing purulent inflammation

ex staphylocoal aureua
describe pus

what are examples of purulent inflammation
creamy yellow due to necrotic white blood cells

acute appendicitis, acute bacterial meningitis
what is an abcess?

what are central necrotic cells surrounded by?
localized collection of pus buried in a tissue or organ

living neutrophils
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
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
what are systemic effects of inflammation
1. fever

2. behavioral changes
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
what is the role of fever
an increase of body temp to improve efficiency of leukocyte killing
how is fever surpressed
with anti-prostaglandin drugs

ex NSAIDs, ibuprofen
what are behavioral changes associated with inflammation
1. chills
2. rigors
3. sleepiness, decreased appetite, malaise
what is a feeling of chills due to?

what is malaise?

a feeling of general discomfort or uneasiness; feeling out of sorts
what is C-reactive protein a marker of
inflammation and in cardiology is a marker for heart attacks
what does an increased CRP serum or plasma level increase the risk of
heart attack, for people at risk for atherosclerosis and coronary artery disease

recurrent heart attack for patients with established cornonary artery disease
what is leukocytosis
elevation of leukocyte count
what do most bacterial infections give rise to
what is lymphocytosis
elevation of lymphocyte count associated with some viral infections and pertussis
what is eosinophilia
elevation of eosinophil count associated with asthma, hay fever and parasitic infections
what is leukopenia
low white blood cell count which may be cause dby overwhelming bacterial infections in compromised patients