Complement Proteins

Question 1

edema

Answer 1

accumulation of fluid within extravascular compartment

Question 2

Exudate

Answer 2

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

Question 3

Transudate

Answer 3

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

Question 4

fibrinous exudate

Answer 4

large amounts of fibrin from activation of blood coagulation components

Question 5

purulent exudate

Answer 5

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

Question 6

background levels and origin of complement proteins?

Answer 6

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

Question 7

main roles of the complement system

Answer 7

enhance inflammation, enhance immune response, and eliminate pathogens

Question 8

Immune complex diseases like lupus erythmatosus and complement system

Answer 8

these disorders are often due to a deficiency in a complement protein…

Question 9

alternative complement pathway

Answer 9

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

Question 10

role of c3b

Answer 10

helps make convertase, and is an opsonin

Question 11

lectin complement pathway

Answer 11

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

Question 12

Classic pathway

Answer 12

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

Question 13

c3a, c4a, c5a roles

Answer 13

these are all anaphylatoxins that increase vascular permeability

c3a and c5a are also chemoattractants that attract neutrophils and monocytes

Question 14

c5b-c9 roles

Answer 14

these are the proteins in charge of making the membrane attack complex that pokes holes in the pathogen and eventually makes it lyse

Question 15

c4b2b3b convertase

Answer 15

converts c5 to c5a and c5b

Question 16

c3bBd3b convertase

Answer 16

converts c5 to c5a and c5b

Question 17

membrane attack complex

Answer 17

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

Question 18

decay accelerating factor

Answer 18

DAF is a protein that regulates the function of C3bBd convertase, so it inhibits it from working

Question 19

decay accelerating factor deficiency

Answer 19

leads to unregulated activity of the C3bBd convertase that will lead to lysis of RBCs due to overactivity of C3 convertase

Question 20

paroxysmal nocturnal hemoglobinuria

Answer 20

lysis of RBCs due to deficiency in decay accelerating factor

Question 21

C1-inhibitor

Answer 21

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!!

Question 22

c1-inhibitor deficiency

Answer 22

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

Question 23

c3 deficiency

Answer 23

profound risk of encapsulated bacteria infection

Question 24

C1, c2 and c4 deficiency

Answer 24

risk of immune complex diseases like lupes

Question 25

c1-inhibitor deficiency

Answer 25

excessive amounts of bradykinin, a vasoactive peptide, are made…hereditary angiodema

Question 26

c5b, c6,c7,c8,c9 deficiency

Answer 26

deficient in any one and MAC does not work…so susceptible to niesseria diseases like gono and meningitis

Question 27

treatment for niesseria meningitidis

Answer 27

penicillin and ceftriaxone…super susceptible

prophylaxis use rifampin, ceftriaxone, cipro, or azithromycin

Question 28

most commone nisseria meningitidis infections

Answer 28

meningococcemis (in blood) meningitis, arthritis, conjuctivits, and pericarditis

Question 29

nisseria meningitidis structure and info

Answer 29

gram negative cocci, with capsule

serotypes of ABCY and W-135

vaccines ow

Question 30

purpura fulminans

Answer 30

petechia or bleeding to skin can lead to clotting off and leads to loss of extremities

Question 31

petechiae

Answer 31

common rash with non blanching spots on the skin in neisseria meningitidis

Question 32

risk factors for Neisseria meningitidis

Answer 32

asplenia, low numbers of terminal complement proteins and no MAC

Question 33

hereditary angiodema sites of attack

Answer 33

skin, upper airway, and Gi tract due to angiodema that is causes by no c1 inhibitor so not inhibition of bradykinin and super vasoactivity

Question 34

changes in complement proteins during hereditary angiodema

Answer 34

decrease in c4 and decrease in c1 esterase inhibitor

c4 down because C1 is super active and will clip more C4

Question 35

treatment for hereditary angiodema

Answer 35

can be a medication you take daily that supplements the c1 esterase inhibitor or you can have purified c1 inhibitor shots available and give when have flare up

does not respond to epinephrine but can be good if airway blocked

does not respond to anthistamines or corticosteroids