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Clinical Laboratory Immunology 1st Edition Maahon Tice Test Bank

Clinical Laboratory Immunology 1st Edition Maahon


Tice Test Bank

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Exam

Name___________________________________

MULTIPLE CHOICE. Choose the one alternative that best completes the statement or answers the question.

1) All of the following are functions of complement except 1)


A) chemotaxis.
B) specific, selective antigen binding.
C) anaphylotoxin.
D) cell lysis.
E) opsonization.
Answer: B

2) When antigen binds to antibody, the ________ is (are) activated. 2)


A) mannose binding pathway B) alternate pathway
C) classic pathway D) All of the above
Answer: C

3) The abbreviation C3a in relation to complement gives what information? 3)


A) The capital C indicates this is a complement component.
B) The lower case letter indicates that this is a fragment of the component.
C) The numeral tells which complement component.
D) All of the above.
Answer: D

4) Complement components are completely destroyed if a specimen is 4)


A) kept at body temperature for 30 minutes.
B) kept at room temperature for 30 minutes.
C) frozen.
D) heated to 56° C for 30 minutes.
E) All of the above.
Answer: D

5) What is the recognition unit in the classic complement pathway? 5)


A) Factor B and properdin
B) mannose and mannose binding lectin
C) C2 and C4
D) C1qrs
E) C3
Answer: D

6) Which of the following is TRUE regarding the C3 convertase in the classic complement pathway? 6)
A) Magnesium is required to stabilize the complex.
B) It is incorporated into the membrane attack unit.
C) It is inactivated once it splits a C3 molecule into C3a and C3b.
D) Its composition is C2bC4a.
E) All of the above.
Answer: A

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7) What is (are) the consequence(s) of complement C3 being cleaved into C3a and C3b in the classic 7)
pathway?
A) C3b complexes with C2a4b to form C5 convertase.
B) C3a enters the plasma as an anaphylotoxin.
C) C3b attaches to the cell membrane as an opsonin.
D) All of the above.
Answer: D

8) What is (are) the consequence(s) of complement C5 being cleaved into C5a and C5b? 8)
A) C5a perforates the cell membrane.
B) C5b binds to C6, C7, C8, and C9.
C) C5b is released into the plasma as a potent anaphylotoxin.
D) All of the above.
Answer: B

9) All of the following can activate the alternate pathway of complement except 9)
A) mannose.
B) lipopolysaccharides from gram negative bacteria.
C) teichoic acid from gram positive bacteria.
D) certain fungal cell walls.
E) certain parasites.
Answer: A

10) Which of the following are TRUE regarding the alternate pathway of complement activation? 10)
A) Factor D has a similar function to C1qrs, and Factor B has a similar function to C2.
B) The activation surface of an organism serves to spontaneously cleave C3 into C3a and C3b.
C) Unlike the classic complement pathway, the alternate pathway is independent of calcium and
magnesium.
D) The composition of the C3 convertase is a Factor B/Properdin complex.
Answer: A

11) Which of the following cell wall components can initiate the mannose binding lection pathway of 11)
complement activation?
A) Glucose
B) Mannose
C) Fucose
D) N-acetylglucosamine
E) All of the above
Answer: E

12) Each complement component below is an opsonin except 12)


A) C4a B) C3b C) iC3b D) C1qrs
Answer: D

13) Each complement component below is an anaphylotoxin except 13)


A) C3a B) C4a C) C5a D) C2a
Answer: D

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14) All of the following are properties of complement fragment C5a except 14)
A) promotes ability of neutrophils to adhere to blood vessel walls.
B) serves as initial binding molecule of the membrane attack complex.
C) promotes increases expression of complement 1 receptor on phagocytes.
D) promotes adherence of red blood cells, lymphocytes, and endothelial cells to material
requiring phagocytosis.
E) most potent chemotactic fragment.
Answer: B

15) In what way(s) is complement antiviral? 15)


A) Can opsonize viral particle. B) Can directly disrupt viral particle.
C) Can block viral receptors. D) All of the above.
Answer: D

16) A person with a genetic deficiency in complement C3 would be predisposed to have 16)
A) immune complex diseases.
B) accelerated, chronic inflammatory reactions.
C) recurrent bacterial infections.
D) autoimmune diseases.
E) no discernible effect since deficiencies in the classic pathway can be compensated for by the
alternate and mannose binding lectin pathways.
Answer: C

17) Which complement regulatory protein(s) below act(s) to prevent initial complement activation? 17)
(Check as many as apply.)
A) C1 inhibitor
B) decay accelerating factor
C) Factor I
D) C4 binding protein
E) Factor H
Answer: A, C

18) Which complement regulatory protein is expressed on red blood cells to prevent them from being 18)
damaged by complement?
A) C4 binding protein
B) C1 inhibitor
C) S protein
D) Factor H
E) decay accelerating factor
Answer: E

19) Which of the following is TRUE regarding paroxysmal nocturnal hemoglobinuria (PNH)? 19)
A) It can be diagnosed by the deficiency of CD55 and CD59 on red blood cells.
B) Red blood cells are deficient in the complement regulatory proteins DAF (decay accelerating
factor) and protectin.
C) Symptoms include lysis of red blood cells with hemoglobin appearing in the urine and a
tendency to develop blood clots.
D) All of the above.
Answer: D

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20) All of the following conditions have been associated with deficiencies in complement regulatory 20)
proteins except
A) hereditary angioedema.
B) paroxysmal nocturnal hemoglobinuria.
C) chronic susceptibility to Neisseria infections.
D) systemic lupus erythematosus.
E) hemolytic-uremic syndrome.
Answer: C

21) How should specimens be collected and stored if they are to be tested for complement activity? 21)
A) Serum can be refrigerated but not frozen.
B) Serum should be separated from red blood cells.
C) Serum can be stored one to two hours at room temperature prior to testing.
D) All of the above.
Answer: B

22) A specimen has a reduced total hemolytic complement as measured by CH50. When individual 22)
components were measured, total C3 was very reduced, but total C4 was within normal limits.
How can these results be best explained?
A) The subject has severe liver disease.
B) There has been a recent significant activation of the mannose binding lectin complement path.
C) There has been a recent significant activation of the alternate complement path.
D) There has been a recent significant activation of the classic complement path.
Answer: C

23) If complement CH50 is decreased and complement AH50 is normal in a specimen, the specimen 23)
may be deficient in factor(s)
A) properdin.
B) C3.
C) C1, C2, or C4.
D) Factor B.
E) C5, C6, C7, C8, or C9.
Answer: C

24) In the complement fixation test, the presence of an antibody/antigen reaction is detected because 24)
A) it precipitates complement proteins.
B) complement C5–9 are consumed in the specimen.
C) complement is bound and is unavailable to lyse sensitized red blood cells.
D) complement is activated and it lyses red blood cells.
E) complement C3 is consumed in the specimen.
Answer: C

25) A complement fixation test is done to see if a specimen contains antibodies to rubella virus. A 25)
control negative for antibodies and a control positive for antibodies are run, and the sensitized
sheep cells are tested alone with no specimen or complement added. Which of reactions below is
correct if the specimen does contain antibodies?
A) Positive control, no lysis; negative control, lysis; specimen, no lysis; red cells no lysis
B) Positive control, lysis; negative control, no lysis; specimen, lysis; red cells lysis
C) Positive control, lysis; negative control, no lysis; specimen, lysis; red cells no lysis
D) Positive control, no lysis; negative control, lysis; specimen, no lysis; red cells lysis
Answer: A

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SHORT ANSWER. Write the word or phrase that best completes each statement or answers the question.

26) The most abundant complement component in plasma is ________. 26)


Answer: C3

27) The cells with receptors for the anaphylotoxins are ________. 27)
Answer: mast cells or basophils

28) Name one complement regulatory protein that inhibits the membrane attack complex. 28)
Answer: CD59, S protein, homologous restriction factor (HRF), or membrane cofactor protein
(MCP)

29) The only complement receptor on red blood cells is ________. 29)
Answer: CR1 or complement receptor 1

30) Hereditary angioedema is associated with a deficiency in ________. 30)


Answer: C1 INH or C1 esterase inhibitor

TRUE/FALSE. Write 'T' if the statement is true and 'F' if the statement is false.

31) The complement system is a group of proteins solely comprised of activators and substrates for the 31)
system.
Answer: True False

32) Complement fragments only attach to foreign cells, not host cells. 32)
Answer: True False

33) For each of the three complement pathways, once C5 is split into C5a and C5b, formation of the 33)
membrane attack complex is identical for all three paths.
Answer: True False

34) The alternate complement activation path and the mannose binding lectin path both function 34)
completely independent of antibody.
Answer: True False

35) The C3 convertases for the classic and mannose binding lectin paths of complement activation are 35)
identical.
Answer: True False

36) The activated components of complement are generally very stable to promote a long period of 36)
activity and shortened time of infection.
Answer: True False

37) The only complement receptor on red blood cells is CR4. 37)
Answer: True False

38) Systemic lupus erythematosus is highly associated with C1q genetic deficiency. 38)
Answer: True False

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39) When there is a complement deficiency, the CH50 increases. 39)
Answer: True False

40) Complement activity of the alternate pathway can be assessed using rabbit red blood cells. 40)
Answer: True False

SHORT ANSWER. Write the word or phrase that best completes each statement or answers the question.

41) List the three stages of complement cascade. 41)


Answer: 1. Recognition—identifying a situation in which complement needs to be activated.
2. Activation—sequence that creates the active enzyme needed to form the membrane
attack complex.
3. Membrane attack—assembling the components of the membrane attack complex
and lysing a cell.

42) Explain why one molecule of IgM can activate complement but it takes about 1000 42)
molecules of IgG on a cell surface to activate complement.
Answer: Complement is activated by the classic pathway when antigen binds to antibody,
altering the structure of the antibody to reveal the C1q binding site. In order for C1q
to be activated, it must be bound to two adjacent C1q binding sites. Thus, if two IgG
molecules are close together, C1q is activated. IgM, because of its pentameric
structure, naturally has two C1q binding sites adjacent, and one molecule of IgM can
easily activate complement. Since IgG is a monomer and single IgG cannot activate
complement, a cell must be coated with enough IgG to eventually put two IgG
molecules in close proximity. Statistically, it takes about 1000 IgG molecules to bind
to the cell before two molecules are sufficiently close enough.

43) Discuss how the anaphylotoxin complement fragments promote a better immune 43)
response.
Answer: The complement fragments that function as anaphylotoxins are C3a, C4a, and C5a.
When they attach to basophils/mast cells, the cells degranulate, releasing
inflammatory mediators such as histamine. The inflammatory mediators promote
vascular permeability, smooth muscle contraction, release of lysosomal enzymes,
and induction of increased white blood cell metabolism (respiratory burst). This
promotes the transfer of humoral immune components and white blood cells to the
affected area.

44) Describe the mechanism of acquired (nongenetic) complement deficiency. 44)


Answer: Complement components can become deficient if they are consumed in excess or
produced insufficiently. An excessive amount of immune complexes can activate the
complement cascade and cause a consumption of available complement
components. There are some chronic conditions, autoimmunity, for example, that
are associated with the constant generation of immune complexes and thus a
chronic deficiency of complement components. Since most of the complement
components are produced by the liver, liver disease is also associated with chronic
deficiency of complement components.

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Clinical Laboratory Immunology 1st Edition Maahon Tice Test Bank

45) Explain how genetic deficiencies of early complement components are associated with 45)
immune complex and autoimmune disorders such as systemic lupus erythematosus.
Answer: Complement plays a role in the recognition and clearance of immune complexes, as
well as dead host tissue. Lack of early complement components that are key in
recognizing that an antigen/antibody reaction has occurred will result in an
increased life span of circulating immune complexes. Further, if dead host cells are
not cleared efficiently, there is increased exposure time of their antigens to the
immune system and an increased risk of autoimmunity.

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