Dani - ch 5 Flashcards
____: vascular and cellular responses whose purpose is to localize or eliminate the injurious agents
inflammation
2 types of inflammation
acute
chronic
___ inflammation: transient process that occurs within a few minutes of injury and lasts for a short time; usually described by -itis preceded by the organ/tissue
acute
5 causes of acute inflammation
- ____ agents: bacteria, virus, parasites, protozoa
- ____ reaction
- ____ agents: trauma, hot, cold, radiation
- ____ agents: acids, alkalis or bacterial toxins
- tissue ____
infectious hypersensitivity physical chemical necrosis
____: due to blood vessels dilation; redness
rubor
___: due to increased pressure by exudate and by the following mediator; bradykinin and prostaglandins; pain
dolor
___: due to increased blood flow; increased heat
calor
___: due to accumulation of exudate; swelling
tumor
___ ___: due to pain and tissue damage; loss of function
functio laesa
___: fluid, protein, and blood cells escape from the vascular system –> interstitial tissue
exudation
___: ultrafiltrate of blood and plasme, result from imbalance across the vascular endothelium
transudate
___: excess of fluid in the interstitial tissue or body cavities; can be exudate or transudate
edema
___: purulent inflammatory exudate abundant in leukocytes and cell debris
pus
transudate
- ____ permeability
- ___ hydrostatic pressure
normal
increased
transudate
- ___ or ___ protein
no
low
transudate
- only ____ (ultra filtrate)
albumin
transudate
- cells = _____
0
transudate
specific gravity is ____
low
exudate
- ___ permeability
increased
exudate
- ___ protein content
high
exudate
- all proteins except ___
fibrinogen
exudate
- ___ cells
inflammatory
exudate
- specific gravity is ___
high
4 steps in acute inflammation
white line
flush
flare
wheal
3 phases of the triple response
flush
flare
wheal
1st step in triple response:
red line = ____
flush
flush is due to ____ ___
capillary dilation
momentary white line before triple response is due to ___ ___
arteriolar vasoconstriction
2nd step in triple response:
- red irregular area = ____
flare
flare is due to ___ ___
arteriolar dilation
3rd step in tripe response
- a swelling = ____
wheal
wheal is due to ____ caused by ___ permeability
edema
increased
hemodynamics
- changes in blood flow
- transient ____ of arterioles –> ___ of precapillary sphincters –> ___ of arterioles leads to blood flow and opening of new capillary bed
vasoconstriction
relaxation
vasodilation
____: opening of new capillary bed
hyperemia
slowing of circulation:
- vascular permeability and outpouring of fluid into intersitial tissue –> ____ blood viscosity –> ___ rate of blood flow
increased
decreased
hemodynamics - increased vascular permeability
- arteriolar dilation and increased blood flow –> ____ intravascular hydrostatic pressure –> ____
increased
transudate
immediate transient leakage due to ____ injury and ___ reactions
mild
hypersensitivity
immediate transient leakage mediated by ____, ___, and ___
histamine
serotonin
bradykinin
immediate transient leakage
- contraction of endothelial cells –> widening of ___ junctions (gapping)
intercellular
immediate transient leakage
- ____ leakage, ___ lived(___-___min)
immediate short (15-20)
immediate sustained leakage
- caused by ___ injury
sever
immediate sustained leakage
- ___ leakage, ___ for long time till damaged vessel is repaired or thrombosed
immediate
sustained
delayed sustained leakage
- caused by ____ or ___ injury
mild
moderate
severe injury example
burn
mild/moderate injury examples
sunburn
x-ray
bacterial toxins
delayed sustained leakage
- endothelium is injured ___ or ____ causing intracellular gaps
direct
indirect
delayed sustained leakage
- leakge begins after __-__ hours and lasts for several ___ or ___
2-12
hours
days
___ of neutrophils: as blood flow slows, neutrophils fall out of central column and roll along endothelium
margination
___ of neutrophils: neutrophils adhere to endothelium by surface adhesioin molecules
pavementing
adhesion
____ of neutrophils: neutrophils insert pseudopods in intercellular junctions, squeeze their way, traverse basement membrane and escape to extravascular space
diapedesis
emigration
____: passage of blood cells through intact capillary walls and into the surrounding tissue
diapedesis
____: neutrophils move toward site of injury along concentration gradient of chemotactic agents
chemotaxis
neutrophils emigrate 1st in the first 12-24 hours
- later replaced by ___
monocytes
RBCs coalesce into ___ at central axis
rouleaux
____ - like a stack of coins
rouleaux
types of cells in acute inflammation are ____
neutrophils
neutrophils are present __-__hrs
6-24
types of cells in chronic inflammation are ____ and ____
monocytes
macrophages
monocytes and macrophages are present ___-___hrs
24-48
life span of a neutrophil is __-__ hrs
24-48
recognition of phagocytosis is through attachment to agen either directly or indirectly ____ or complement — this is called ____
IgG
opsinization
engulfment in phagocytosis happens when the cytoplasm surrounds an agent, encloses it into a membrane-bound vacuole called a ____
phagosome
intracellular killing - oxygen DEPENDENT mechanism
- phagocytosis stimulates other cellular oxidative mechanism (____ ___) –> microbicidal derivatives and antimicrobil (___,___ and ___)
respiratory burst
O2
H2O2
HOCl
intracellular killing - oxygen INDEPENDENT mechanism
- phagosome fuses with ____(phagolysosome) –> release of ____ enzymes –> ___ agent
lysosome
lysosomal
degrade
inflammation process –> ___ to stop damage –> still alive bacteria is carried to ___ ___ to be filtered –> if fails –> lymph system –> ventricular circulation –> ____ or ____
fails
lymph node
bacteremia
septicemia
neutrophils account for ___-___% of all WBCs
60-70
neutrophils
- ___ nucleus
- __-__ lobes
segmented
1-4
___ are the 1st acute inflammatory cell
neutrophils
function of neutrophils is ____
phagocytosis (oxygen dependent and independent)
monocyte = _____ = ____ ____
macrophage
tissue histiocyte
monocyte accounts for ___-___ of all WBCs
4-8
monocyte has a ___ shaped nucleus
kidney
monocytes are ___-lived; replace neutrophils after __-__ days
long
1-2
monocytes are in the blood for ___ days and the tissues for ____ months
4
several
function of monocytes: ____
phagocytosis (large particles)
lymphocytes account for __-__% of all WBCs
25-30
lymphocytes are present in ___ inflammation and ___ viral or fungal infections
chronic
acute
eosinophils account for __-__% of all WBCs
1-4
eosinophils are present in ___ and ___ infections
allergy
parasitic
2 vasoactive amines
histamine
serotonin
3 sources of vasoactive amines
mast cells
basophils
platelets
action of vasoactive amines
- ___ of arterioles
- ___ permeability (intercellular gaps)
dilation
increased
duration of vasoactive amines
- ___ release
- ____ lived
immediate
short
bradykinin causes ___ of arterioles, ___ permeability, ___ and is __ lived and deactivated by ____
dilation increased pain short kininase
bradykinin is made through ____
kallikrein
fibrinopeptides
- ___ permeability
- ____ for neutrophils
increased
chemotactic
C3b: favors ____ (____)
phagocytosis
opsonin
C3a, C4a, C5a:
- ____ and ___ permeability
- ____
- stimulate mast cells to release ____
vasodilation
increase
anaphylatoxins
histamine
C5a: ___ to neutrophils and macrophages
chemotactic
cell membrane phospholipids release ___ __ which are activated by ____
arachidonic
phospholipase
____ inhibit phospholipase
corticosteroids
lipoxygenase cycle of AA produce ____
leukotrienes
leukotienes
- ___ permeability
- _____
increase
chemotaxis
cyclooxygenase cycle of AA produce 3 things
prostaglandin
thromboxane
prostacyclin
prostaglandin favors ____
thromboxane favors ____
prostacyclin favors ____
vasodilation
vasoconstriction
vasodilation
leukocyte product:
- oxygen derived free radicals
___ damage –> ___ permeability
endothelial
increased
leukocyte product:
- lysosomal enzymes
neutral proteases
____ damage –> ___ leakage
capillary
sustained
leukocyte product:
- acid proteases
___ bacteria and ___ debis
degrade
cellular
leukocyte product
- platelet activating factor:
____ of platelets –> release of ___ and ___ –> _____ vascular permeability
aggregation
histamine
serotonin
increase
2 cytokines
Interleukin - 1 (IL-1)
tumor necrosis factor (TNF)
IL-1 and TNF are produced by ____ and ___
lymphocytes
macrophages
action of cytokines:
- ___ effect: ___ synthesis of endothelial ___ molecules and ____
endothelial
adhesion
prostaglandins
action of cytokines
- release of ___ from basement membrane
neutrophils
action of cytokines
- ____ phase reaction
acute
3 acute phase reactions due to cytokines
fever
sleepiness
anorexia
endothelial cells make ____
prostaglandins
3 systemic clinical signs
fever
changes in WBC count
increased erythrocyte sedimentation rate
3 sequelaes of acute inflammation
- complete ____
- healing by ___
- progression to ___ ____
resolution
scar
chronic inflammation
serous acute inflammation
- ___ type
- excess thin ___ __ __ fluid
mildes
watery clear serous
examples of serous acute inflammation
- ____ in burn
- ___ ___ in herpes
- ___ of serous sacs
blisters
skin vesicles
inflammation
fibrinous inflammation:
____ form, virulent bacteria
rich in ___
severe
fibrinogen
examples of fibrinous inflammation
- lobar ___
- ____ of serous sacs
pneumonia
inflammation
catarrhal inflammation
___ inflammation of ___ ____
exudate rich with ____
mild
mucous membrane
mucus
exmaple of catarrhal inflammation
common cold
allergic inflammation
- ____
- many ____
hypersensitivity
eosinophils
2 examples of allergic inflammation
bronchial asthma
urticaria
pseudomembranous inflammation
- ___, affect mucous membrane, by ____ bacteria
- necrotic epithelium and inflammatory exudate –> ___ membrane replacing mucosa
severe
toxigenic
false
example of pseudomembranous inflammation
diphtheria
hemorrhagic inflammation
- ____, by highly virulent bacteria, viral or fungal agents
- excessive tissue ___ and ____
severe
necrosis
hemorrhage
3 examples of hemorrhagic inflammation
anthrax
plague
herpes simplex
suppurative inflammation
- ___ bacteria
- aggregation of neutrophils, tissue ____ and ____ into pus
necrosis
liquefaction
acute inflammation without neutrophils
- ___ and ___ infections
viral
rickettsial
inflammatory cells in acute inflammation without neutrophils
lymphocytes
plasma cells
lyphocytosis
neutropenia