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46 Cards in this Set

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  • Back
the cell which is a key link between the innate and adaptive immune systems
dendritic cells
zymogen
inflammatory mediator that is present in plasma that needs to be activated
how are zymogens usually activated
proteolytic cleavage
why do cytokines take longer to be released
they are synthesized de novo
Factor XII (Hageman factor) and complement are what two types of mediators (where are they found?)
found in plasma - must be activated
how do leukocytes get out of the blood vessel and into the interstitium
diapedesis
the initial step in diapedesis which involves transient adhesions is called? and emplys what kind of cell adhesion molecules
"rolling" - involves selectins
sticking and diapedesis involves what kind of cell adhesion molecules
sticking: selectins and integrins
diapedesis: integrins
histamine and serotonin are what kind of mediators

primary or secondar?
pre-formed
histimine is the principal mediator of
immediate vascular permeability

(through H1 receptors)
serotonin is released from platelet aggregation and causes
increase vascular permeability
how do ABs and C compare when it comes to heat lability
Ab are heat stable and and Complement is heat liable

Complement is needed for Ab activation
what complement is activated by Ag-Ab complexes
classical pathway
what pathway of C is activated by surfaces of pathogens
alternative pathway -


note: complement is highly regulated
two pieces of C that are important in inflammation
C5a and C3a
C that is important for phagocytosis
C3b
Complement that is important for lysis of microbe
MAC
the central component of complement is C3 which is converted to C3a and C3b by
C3 convertatse
C3b proteotypically cleaves
C5
MAC =
C5b+ C6,7,8,9
complement pieces that are known anaphyloxins
C3a and C5a
potent chemoattractant for and activator of PMNs (C)
C5a
Decay accelerating factor (DAF) has what effect on C system

(acts on what part of complement)
deregulation of alternative pathway c3 convertase

it inhibits binding of factor B to cell associated C3B - causes intravascular hemolysis
blocks MAC formation by blocking by blocking C7, C8 binding
membrane inhibitor of reactive lysis MIRL

leads to deregulation of MAC and complement mediated intravascular hemolysis
C1 inhibitor deregulates
classical pathway -
causes HANE - hereditary angioneurotic edema
what inhibits phospholipases which will ultimately inhibit all the formation of all products in the arachidonic acid cascade
steroids
COX inhibitors and aspirin inhibit the production of
the production of prostaglandins
prostaglanding that causes vasoconstricution, promotes platelet aggregation
TXA2
prostaglanding that causes vasodilation and inhibits platelet aggregation
Prostacylin (PGI2)
prostaglanding that causes vasodilation and potentiates edme
PGE2
Lipoxins cause what three things
vasodilation
inhibit neutrophil chemotaxis
stimulate monocyte adhesion
Leukotriene which is important for chemotaxis
B4
in general what is the effect of leukotrienes
vasoconstriction
bronchospasm
increased permeability
produced by the arachidonic cascade

local, short range hormones, formed rapidly, local effects, short lived
eicosanoids

formed in specialized cellular domains called lipid bodies that have high concentraitons of synthetic enzymes
eicosanoids that cause increase in vascular permeability
LTC4, D4, E4
eicosanoids that cause vasodilation
PGI2,E2,E1, D2
4 eicosanoids that cause vasoconstriction
TXA2, LTC4, D4, E4
eicosanoid that caused chemotaxis and leukocyte adhesion
LTB4, HETE, lipoxins (inhibit)
a chemokine w/ one a.a. separating first two conserved cys residues
CXC (alpha)
a chemokine with the first two cysteines are adjacent
C-C (beta)

others
C = gamma
CxxxC
what kind of receptor do chemokine bind
7TM receptor - activating G proteins
NO is released from
endothelial cells

acts as a local paracrine factor, short lived,
effect of NO
vasodilation -

forms adducts with thiol groups on protein
Hemoglobin can function as NO sink - may be important function of hemoglobin
two forms of NO that are constitutive at low levels and are ACTIVATED by Ca
e-NOS, n-NOS
iNOS is inducible and requires de novo synthesis w/in macrophages, does it require Ca
no
NF-kB induces the transcription of what cytokines
TNF, IL-1

NF-kB is also stimulated BY these