1. wk 5 inflammation Flashcards
stopped at S; 37
___: vascular and cellular response whose purpose is to localize / elimainate the injurious agents
inflammation
what are the two types of inflammation
acute
chronic
___: transient process that occurs within few min of injury and lasts for short time
acute inflammation
infectious agents are (4)
bact
viruses
parasites
protozoa
name 5 causes of inflam
- infectious agents
- hypersensitivity rxn
- physical agents
- chem agents
- tiss necrosis
___: redness due to blood vessel dilation
rubor
___: pain due to incr. pressure by exudate
dolor
___: increa. heat due to increase in blood flow
calor
___: swelling due to acc of exudate
tumor
___: loss of fxn due to pain and tiss damage
funtio laesa
What are two mediators of dolor
bradykinin
prostaglandin
what are the 5 cardinal signs of acute inflam
rubor dolor calor tumor functio laesa
____: fluid, protein, and blood escaping from the vascular system into tiss
exudation
aka edema
____: ultrafiltrate of blood and plasma, results from imbalance across vascular endothelium
transudate
____: excess of fluid in the interstitial tis of body cavitites (can be exudate or transudate)
edema
______: purulent inflam exudate abundant
pus
abundant in leukocytes and cell debris
edema can be ___ or ___
exudate or transudate
_____ will only form in a bact. infection
pus
There is normal permeability and increa. hydrostatic pressure in ______
trandsudate
increase permeability in exudate
There is an increase in permeability in _____
exudate
_____ only has albumin
trandsudate
After a strike to the skin there is a white line bc of _______
arteriolar vasoconstriction
What is involved in “triple Response”
- flush (due to cap. dialation)
- flare (due to arteriolar dilation
- wheal (due to edema caused by incr. permeability )
the flush during triple response is due to _____
capillary dilation
the flare during triple response is due to ____
arteriolar dilation
the wheal during triple response is due to _____
edema caused by incr. permeability
vascular changes is called _____
hemohynamics
there is ____ leakage , ___ for a long time till damage vessel is repaired during “immediate sustained (prolonged) leakage
immediate leakage , sustained for a long time
leakage begins after ___ & lasts for _____ during “delayed systained leakage”
begins 2-12 hrs
lasts: several hrs or days
lates awhile to begin and a while to end
as blood flow slows, ___ fall out of the central column and roll along the endothelium
neutrophils
______: is the neutrophils adhering to endothelium by surface adhesion mole
pavementing
during _______ neutophils insert pseudopods in intercellular jxn , squeeze their way, & exscpe into extravascular space
emigration
____: the passage of blood cells (WBC) through intact cap. walls and into surrounding tis
diapedesis
there is recognition of the phagocyte by attachment to agent either directly or indirectly by ____
IgG or complement (opsonization )
cytoplasm of a phagocyte surrounds agent, encloses it into a membrane bound vacuole called _____
phagosome
_____emigrate first, and then are later replaced by monocytes
neutraphils
______: neutrophils mnove toward site of injury along conc. gradient of chemotact agents
chemotaxis
if inflam process and lynmph nodes fail to defend against bact. it goes into the ______
venous circulation
(bad!)
–> bacteremia septicemia
what is the first line of defense after damage
inflam process
if the inflam process fails to stop the damage , the bact. is carried to the _____
lymph node to be filtered
fxn of neutrophils
phagocytosis
_____ make up the majority of WBC
neutrophils (60-70%)
what is the 1st inflam cell to respond
neutrophils
_____ respond to allergy and parasitic infections
eosinophils
____ make up 1-4% of total WBC
eosinophils
_____cyte respond to chronic inflam & acute viral or fungal infections
lymphocytes
25-30% of WBC
_____cyte make up 25-30% of WBC
lymphocytes
fxn of monocytes is ____
phagocytosis
___cyte are long lived. they replace neutrophils 1-2 days later
monocyte
What is the plasmatic zone during inflm
layer of plasma protecting endoth.
RBC sludging during inflam is called ___
Rouleaux formation
_____ mechanism of intracellular killing: phagocytosis stim cellular oxidative mechanism (respiratory burst)
oxygen dependent mechanism
_____mechanism of intracellular killing: phagosome fuses with lysosome
oxygen independent
What are 2 vasoactive amines
histamine and serotonin
source: mast cells, basophils, platets
Action of histamine and serotonin (vasoactive amines)
dilation of arterioles
incr permeability
short lived , immediate
Fxn of plasma proteaase bradykinins
dilation of arterioles
incr permeability
** pain
short lived
activation of ____ leads to production of thrombin from prothrombin
factor XII (hageman factor)
What arachidonic acid cycle is blocked by aspirin and ibuprofen
cyclooxygenase cycle
fxn of the lipoxygenase cycle (under the arachidonic acid)
leukotrienes : increase permeability , chemotasix
fxn of the cyclooxygenase cycle
prostagladin (vesodil)
thromboxane (vasocon)
prostacyclin (vasodilation)
what are 4 products released by leukoproducts
02 derived free radicals
lysosomal enzymes
platlet activating factor
cytokinase
tumor necrosis agent
TNF
fxn of the hageman factor activation
clotting system
kinin system
What cells are histamine and serotonin derived from
mast cells
blood basophils
blood platelets
3 systemic clinical signs of inflammation
fever
change in WBC count
incr. erythrocyte sedimentation rate
healing as a result of inflammation will result in (3)
complete resolution
healing by scar
progression to chronic inflam
