Complement Proteins Flashcards
edema
accumulation of fluid within extravascular compartment
Exudate
fluid rich in protein and cellular elements that oozes out of blood vessels due to inflammation
specific gravity higher than 1 due to proteins etc
Transudate
fluid that has filtered out a lot of the protein and cellular elements and yields a watery solution, with low levels of protein from blood
specific gravity closest to 1…like water
fibrinous exudate
large amounts of fibrin from activation of blood coagulation components
purulent exudate
contains prominent cellular components but mainly neutrophils, can be green color due to peroxidase from neutrophils, if yellow then due to massive amounts of neutrophils
background levels and origin of complement proteins?
these are typically made in the liver and are found circulating the blood stream in normal function…when a pathogen is introduced they will start their cascade and binding and clipping to activate though
main roles of the complement system
enhance inflammation, enhance immune response, and eliminate pathogens
Immune complex diseases like lupus erythmatosus and complement system
these disorders are often due to a deficiency in a complement protein…
alternative complement pathway
circulating levels of c3b, they find proteins b and d to make c3 convertase called c3bBd, which can then clip C3 into c3a and c3b
role of c3b
helps make convertase, and is an opsonin
lectin complement pathway
binds mannose on pathogens…leads to C1 complex converting c4 into c4a and c4b, c4b then combines with c2b and makes a convertase for c3 called c4bc2b that can convert c3 into c3b and c3a
Classic pathway
anitgen and antibody binding, c1q interacts with Fc portion of antibody , leads to a C1 complex including c1qrs, that can convert c2 into c2a and c2b, c2b then combines with the c4b to make c4bc2b convertase and change c3 into c3b and c3a
c3a, c4a, c5a roles
these are all anaphylatoxins that increase vascular permeability
c3a and c5a are also chemoattractants that attract neutrophils and monocytes
c5b-c9 roles
these are the proteins in charge of making the membrane attack complex that pokes holes in the pathogen and eventually makes it lyse
c4b2b3b convertase
converts c5 to c5a and c5b
c3bBd3b convertase
converts c5 to c5a and c5b
membrane attack complex
made of c5b to c9…only works against organisms with very thin cell walls like the Neiserria species
leads to lysis of cells by poking holes in membranes
decay accelerating factor
DAF is a protein that regulates the function of C3bBd convertase, so it inhibits it from working
decay accelerating factor deficiency
leads to unregulated activity of the C3bBd convertase that will lead to lysis of RBCs due to overactivity of C3 convertase
paroxysmal nocturnal hemoglobinuria
lysis of RBCs due to deficiency in decay accelerating factor
C1-inhibitor
protein that inhibits the activity of the C1 complex in the classical complement system, it down regulates the c1r and c1s proteins
made in liver!!
c1-inhibitor deficiency
leads to uncontrolled C1 activity, so makes a lot of the proteins involved in vasoactivity, also c1 inhibitor is an inhibitor of the bradykinin pathway so if this is not inhibited then can see increase in vasoactivity
means patient will have high vasoactivity due to low c1 inhibitor…hereditary angiodema
c3 deficiency
profound risk of encapsulated bacteria infection
C1, c2 and c4 deficiency
risk of immune complex diseases like lupes
