Chapter 9: Alterations Alterations in Immunity and Inflammation MULTIPLE CHOICE
1. Hypersensitivity is Hypersensitivity is best defined as a(an): a. Disturbance in the immunologic tolerance of self-antigens b. Immunologic reaction of one person to the tissue of another person c. Altered immunologic response to an antigen that results in disease d. Undetectable immune response in the presence of antigens ANS:
Hypersensitivity is Hypersensitivity is an altered immunologic response to an antigen that results in disease or damage to the host. !he other options op tions are not accurate definitions of h"persensiti#it". $!S: 1
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. A h"persensiti#it" reaction that produces an allergic response is called: a. *emol"tic shoc+ c. Necroti,ing #asculitis b. Anaph"lais d. S"stemic er"thematosus ANS:
&les of s"stemic anaph"lais are allergic reactions to beestings/ peanuts/ and fish. !he other options are not accurate eamples e amples of h"persensiti#it". h"persensiti#it". $!S: 1
%&': $age 0
0. !he common ha" fe#er allerg" a llerg" is epressed through a reaction that is mediated b" hich class
of immunoglobulins2 a. Ig& b. Ig4
c. Ig3 d. ! cells
ANS: A
!"pe !"pe I reactions are mediated b" antigen-specific Ig& and the products of tissue mast cells (see 'igure 5-1). !he most common allergies (e.g./ pollen allergies) are t"pe I reactions. In addition/ most t"pe I reactions occur against en#ironmental antigens and are therefore allergic. !he other options do not accuratel" ac curatel" identif" the mediation factor related to ha" fe#e r. $!S: 1
%&': $age 0 6 !able 5-1
7. 8hich t"pe of antibod" is in#ol#ed in t"pe I h"persensiti#it" reaction2 a. IgA c. Ig4 b. Ig& d. Ig3 ANS:
!"pe !"pe I reactions are onl" mediated med iated b" antigen-specific Ig& and the products of tissue mast cells (see 'igure 5-1). $!S: 1
%&': $age 0
9. lood transfusion reactions are an eample of: a. Autoimmunit" c. *omoimmunit"
b. Alloimmunit"
d. *"persensiti#it"
ANS:
nl" alloimmunit" (also termed isoimmunity) isoimmunity) occurs hen the immune s"stem of one indi#idual produces an immunologic reaction against tissues of another indi#idual. $!S: 1
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. During an Ig&-mediated h"persensiti#it" reaction/ hich leu+oc"te is acti#ated2 a. Neutrophils c. &osinophils b. 3onoc"tes d. ! l"mphoc"tes ANS:
f the options pro#ided/ onl" eosinophils are acti#ated during Ig&-mediated h"persensiti#it" reactions. $!S: 1
%&': $age 0 6 $age 9
;. During an Ig&-mediated h"persensiti#it" reaction/ hat causes bronchospasm2 a. ronchial edema caused b" the chemotactic factor of anaph"lais b. ronchial edema caused b" binding of the c"totropic antibod" c. Smooth muscle contraction caused b" histamine bound to *1 receptors d. Smooth muscle contraction caused b" histamine bound to * receptors ANS:
During an Ig&-mediated h"persensiti#it" reaction/ onl" smooth muscle contraction caused b" histamine bound to *1 receptors results in bronchospasms. $!S: 1
%&': $age 0 6 $age 9
<. During an Ig&-mediated h"persensiti#it" reaction/ the degranulation of mast cells is a result of
hich receptor action2 a. *istamine bound to * b. hemotactic factor binding to the receptor c. &pinephrine bound to mast cells d. Acet"lcholine bound to mast cells ANS: A
*istamine bound to * results in the degranulation of mast cells during an Ig&-medicated h"persensiti#it" reaction. !he other options do not cause this reaction. $!S: 1
%&': $age 9
5. 8hat characteristic do atopic indi#iduals ha#e that ma+e them geneticall" predisposed to
de#elop allergies2 a. 4reater =uantities of histamine b. 3ore histamine receptors
c. 4reater =uantities of Ig& d. A deficienc" in epinephrine
ANS:
Atopic indi#iduals tend to produce higher =uantities of Ig& and to ha#e more cr"stalline fragment ('c) receptors for Ig& on their mast cells. !he other options do not cause this reaction.
$!S: 1
%&': $age ;1
1>. 8hat is the mechanism that results in t"pe II h"persensiti#it" reactions2 a. Antibodies coat mast cells b" binding to receptors that signal its degranulation/
folloed b" a discharge of preformed mediators. b. Antibodies bind to soluble antigens that ere released into bod" fluids/ and the immune complees are then deposited in the tissues. c. "totoic ! l"mphoc"tes or l"mpho+ine-producing helper ! 1 cells directl" attac+ and destro" cellular targets. d. Antibodies bind to the antigens on the cell surface. ANS: D
!he mechanism that results in a t"pe II h"persensiti#it" reaction begins ith antibod" binding to tissue-specific antigens or antigens that ha#e attached to particular tissues. !he cell can be destro"ed b" antibod" Ig4 or Ig3 and acti#ation of the complement cascade through the classical patha". $!S: 1
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11. 8hen mismatched blood is administered causing an A incompatibilit"/ the er"throc"tes are
destro"ed b": a. omplement-mediated cell l"sis b. $hagoc"tosis b" macrophages
c. $hagoc"tosis in the spleen d. Natural +iller cells
ANS: A
&r"throc"tes are destro"ed b" complement-mediated l"sis in indi#iduals ith autoimmune hemol"tic anemia or as a result of an alloimmune reaction to A-mismatched A-mismatched transfused blood cells. !he other options are not in#ol#ed in an A A incompatibilit" reaction. $!S: 1
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1. 8hen antibodies are formed against red blood cell antigens of the %h s"stem/ the blood cells
are destro"ed b": a. omplement-mediated cell l"sis b. $hagoc"tosis b" macrophages c. $hagoc"tosis in the spleen d. Neutrophil granules and toic o"gen products ANS:
Antibodies against platelet-specific antigens or against red blood cell antigens of the %h s"stem coat those cells at lo densit"/ resulting in their preferential remo#al b" phagoc"tosis in the spleen/ rather than b" b " complement-mediated l"sis. !he other options do not cause this reaction. $!S: 1
%&': $ages -;
10. 8hen soluble antigens from infectious agents enter circulation/ tissue damage is a result of: a. omplement-mediated cell l"sis b. $hagoc"tosis b" macrophages c. $hagoc"tosis in the spleen d. Neutrophil granules and toic o"gen products
ANS: D
f the options a#ailable/ onl" the components of neutrophil granules damage the tissue. $!S: 1
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17. *o are target cells destro"ed in a t"pe II h"persensiti#it" reaction2 a. omplement-mediated cell l"sis b. $hagoc"tosis b" macrophages c. Neutrophil granules and toic o"gen products d. Natural +iller cells ANS: D
!he mechanism that results in a t"pe II h"persensiti#it" h "persensiti#it" reaction in#ol#es a subpopulation of c"totoic cells that are not antigen specific (natural +iller ?N@ cells). Antibod" on the target cell is recogni,ed b" 'c receptors on the N@ cells/ hich releases toic substances that destro" the target cell. !he other options do not cause the destruction of target cells related to a t"pe II h"persensiti#it" reaction. $!S: 1
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19. 4ra#es disease (h"perth"roidism) is an eample of hich t"pe II h "persensiti#it" reaction2 a. 3odulation b. Antibod"-dependent cell-mediated c"totoicit" c. Neutrophil-mediated damage d. omplement-mediated l"sis ANS: A
!he antibod" reacts ith the receptors on the target cell surface and modulates the function of the receptor b" pre#enting interactions ith their normal ligands/ replacing the ligand and inappropriatel" stimulating the receptor or destro"ing the receptor. 'or eample/ in the h"perth"roidism (ecessi#e th"roid acti#it") of 4ra#es disease/ autoantibod" binds to and acti#ates receptors for th"roid-stimulating hormone (!S*) (a pituitar" hormone that controls the production of the hormone thyroxine b" thyroxine b" the th"roid). !he other options are not eamples of t"pe II h"persensiti#it" h "persensiti#it" reactions. $!S: 1
%&': $age ; 6 $age 5
!"pe III h"persensiti#it" h "persensiti#it" reactions are a result of hich of the folloing2 1. !"pe a. Antibodies coating mast cells b" binding to receptors that signal its degranulation/ folloed b" the discharge of preformed mediators b. Antibodies binding to soluble antigens that ere released into bod" fluids and the immune complees being deposited in the tissues c. !c cells or l"mpho+ine-producing !h1 cells directl" attac+ing and destro"ing cellular targets d. Antibodies binding to the antigen on the cell surface ANS:
Antigen-antibod" (immune) complees that are formed in the circulation and then deposited later in #essel alls or etra#ascular tissues (see 'igure 5-0) cause most t"pe III h"persensiti#it" diseases. !he other options do not cause this t"pe of reaction. $!S: 1
%&': $age 5
1;. A t"pe IB h"persensiti#it" reaction causes hich result2 a. Antibodies coating mast cells b" binding to receptors that signal its degranulation/
folloed b" the discharge of preformed mediators b. Antibodies binding to soluble antigens that ere released into bod" fluids and the immune complees being deposited in the tissues c. C"mpho+ine-producing C"mpho+ine-producing !h1 cells ce lls directl" attac+ing and destro"ing cellular targets d. Antibodies binding to the antigen on the cell surface ANS:
!"pes !"pes I/ II/ and III h"persensiti#it" reactions are mediated b" antibod"/ t"pe IB reactions are mediated b" ! l"mphoc"tes and do not in#ol#e antibod". !"pe !"pe IB mechanisms occur through either !c cells or l"mpho+ine-producing !h1 cells. !c cells directl" attac+ and destro" cellular targets. $!S: 1
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1<. In a t"pe III h"persensiti#it" reaction/ the harmful effects after the immune complees that are
deposited in tissues are a result of: a. "totoic ! cells b. Natural +iller cells
c. omplement acti#ation d. Degranulation of mast cells
ANS:
omplement acti#ation/ particularl" through the generation of ch emotactic factors for neutrophils/ causes the harmful effects of immune comple deposition. !he neutrophils bind to antibod" and 0b contained in the complees and attempt to ingest the immune complees. !"pe !"pe III h"persensiti#it" reactions as described are not the result of an" of the other options. $!S: 1
%&': $age 5
15. %a"naud phenomenon is classified as a t"pe III h"persensiti#it" reaction and is due to: a. Immune complees that are deposited in capillar" beds/ bloc+ing circulation b. 3ast cells that are bound to specific endothe lial receptors/ causing them to
degranulate and creating a locali,ed inflammator" reaction that occludes capillar" circulation c. "totoic ! cells that attac+ and destro" the capillaries so that the" are unable to perfuse local tissues d. Antibodies that detect the capillaries as foreign protein and de stro" them using l"sosomal en,"mes and toic o"gen species ANS: A
%a"naud phenomenon is a condition caused b" the temperature-dependent deposition of immune complees in the capillar" beds of o f the peripheral circulation. None of the other options are in#ol#ed in causing this condition. $!S: 1
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>. Deficiencies in hich element can produce depression of both - and !-cell function2 function2 a. Iron c. Iodine b. inc d. 3agnesium ANS:
f the options a#ailable/ onl" deficient ,inc inta+e can profoundl" depress !- and -cell function. $!S: 1
%&': $age 51
1. 8hen the maternal immune s"stem becomes sensiti,ed against antigens epressed b " the
fetus/ hat reaction occurs2 a. !-cell immunit" b. Alloimmunit"
c. 'etal immunit" d. Autoimmunit"
ANS:
Alloimmunit" occurs hen an indi#idualEs immune s"stem reacts against antigens on the tissues of other members of the same species. Sensiti,ation against fetal antigens is not the cause of an" other a#ailable option. $!S: 1
%&': $age ;
. !issue damage caused b" the deposition of circulating immune complees containing an
antibod" against the host DNA is the cause of hich disease2 a. *emol"tic anemia c. S"stemic lupus er"thematosus b. $ernicious anemia d. 3"asthenia gra#is ANS:
nl" the deposition of circulating immune complees containing an antibod" against the host DNA produce tissue damage in indi#iduals ith s"stemic lupus er"thematosus (SC&). $!S: 1
%&': $age ;;
0. 8h" does tissue damage occurs in acute acu te reFection after organ transplantation2 a. !h1 cells release c"to+ines that acti#ate infiltrating macrophages/ and c"totoic !
cells directl" attac+ the endothelial cells of the transplanted tissue. b. irculating immune complees are deposited in the endothelial cells of transplanted tissue/ here the complement cascade l"ses tissue. c. %eceptors on natural +iller cells recogni,e antigens on the cell surface of transplanted tissue/ hich releases l"sosomal en,"mes that destro" tissue. d. Antibodies coat the surface of transplanted tissue to hich mast cells bind and liberate preformed chemical mediators that destro" tissue. ANS: A
!he recipientEs l"mphoc"tes interacting ith the donorEs dendritic cells ithin the transplanted tissue usuall" initiate sensiti,ation/ resulting in the induction of recipient !h1 and !c cells against the donorEs antigens. !he !h1 cells release c"to+ines that acti#ate infiltrating macrophages/ and the !c cells directl" attac+ the endothelial cells in the transplanted tissue. !he other options do not accuratel" ac curatel" describe ho acute reFection after organ transplantation results in tissue damage. $!S: 1
%&': $age <>
7. 8hich blood cell carries the carboh"drate antigens for blood t"pe2 a. $latelets c. C"mphoc"tes b. Neutrophils d. &r"throc"tes
ANS: D
!he reaction that causes a blood transfusion recipientEs recipientEs red blood cells to clump together is related to the A antigens located on the surface of onl" er "throc"tes. $!S: 1
%&': $age ;<
9. A person ith t"pe blood is li+el" to ha#e high titers of hich anti-antibodies2 a. A c. A and b. d. ANS:
!"pe !"pe indi#iduals ha#e neither A or antigen but ha#e both anti-A and anti- antibodies and therefore cannot accept blood from an" of the other three t"pes. $!S: 1
%&': $age ;<
. 8hich class of immunoglobulins forms isohemagglutinins2 a. IgA c. Ig4 b. Ig& d. Ig3 ANS: D
Naturall" occurring antibodies/ called isohemagglutinins/ isohemagglutinins/ are immunoglobulins of onl" the Ig3 class. $!S: 1
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;. 8hich component of the immune s"stem s "stem is deficient in indi#iduals ith infections caused b"
#iruses/ fungi/ or "east2 a. Natural +iller cells b. 3acrophages
c. cells d. ! cells
ANS: D
f the a#ailable options/ deficiencies in !-cell !-cell immune responses are suggested hen certain #iruses (e.g./ #aricella/ #accinia/ herpes/ c"tomegalo#irus)/ fungi/ and "easts (e.g./ Candida, (e.g./ Pneumocystis jiroveci Histoplasma) Histoplasma) or certain at"pical microorganisms (e.g./ Pneumocystis jiroveci)) cause recurrent infections. $!S: 1
%&': $age <1
<. In hich primar" immune deficienc" is there a partial-to-complete absence of !-cell !-cell
immunit"2 a. ruton disease b. Di4eorge s"ndrome
c. %eticular d"sgenesis d. Adenosine deaminase deficienc"
ANS:
!he principal immunologic defect in Di4eorge s"ndrome is the partial or co mplete absence of !-cell !-cell immunit". !he !he other options are not the result of either a partial or complete absence absenc e of !-cell immunit". $!S: 1
%&': $age <1
5. *o man" months does it ta+e for the neborn to be sufficientl" protected b" antibodies
produced b" its on cells2 a. 1 to b. 7 to 9
c. to < d. 1> to 1
ANS:
" to < months/ the neborn should be efficientl" protected b" antibodies produced b" its on cells. $!S: 1
%&': $age 5>
0>. onsidering the effects of nutritional deficiencies on the immune s"stem/ se#ere deficits in
calories and protein lead to deficiencies in the formation of hich immune cells2 a. cells c. Natural +iller cells b. ! cells d. Neutrophils ANS:
Se#ere deficits in calorie or protein inta+e lead to deficiencies in !-cell !-cell function and numbers. !he other options are not necessaril" affected. $!S: 1
%&': $ages 5>-51
01. Urticaria are a manifestation of a hich t"pe of h"persensiti#it" reaction2 a. IB c. II b. III d. I ANS: D
Urticaria/ or hi#es/ is a dermal (s+in) manifestation of onl" t"pe I allergic reactions. $!S: 1
%&': $age ;
0. 4ra#es disease is a result of: a. Increased le#els of circulating immunoglobulins b. !he infiltration of the th"roid ith ! l"mphoc"tes c. Autoantibodies binding to th"roid-stimulating th "roid-stimulating hormone (!S*)-receptor sites d. &posure to acet"lates in substances such as rubber ANS:
In the h"perth"roidism (ecessi#e th"roid acti#it") of 4ra#es disease/ autoantibod" binds to and acti#ates receptors for !S* (a pituitar" hormone that controls the produ ction of the hormone thyroxine b" thyroxine b" the th"roid). !he other options do not accuratel" describe the cause of 4ra#es disease. $!S: 1
%&': $age ; 6 $age 5
00. %a"naud phenomenon is an eample of hich t"pe of h"persensiti#it"2 a. IB c. II b. III d. I ANS:
!he characteristics of serum sic+ness are obser#ed in onl" s"stemic t"pe III autoimmune diseases such as %a"naud phenomenon.
$!S: 1
%&': $age ;>
07. 8hich statement is true concerning true concerning an atopic indi#idual2 a. !he" tend to produce less Ig&. b. !he" tend to produce more 'c receptors. c. !he" tend to attract #er" fe mast cells. d. !he" tend to produce #er" high le#els of Ig3. ANS:
Atopic indi#iduals tend to produce higher =uantities of Ig& and ha#e more 'c ' c receptors for Ig& on their mast cells. !he other a#ailable options are not true. $!S: 1
%&': $age ;1
09. 8hich statement is true regarding true regarding immunodeficienc"2 a. Immunodeficienc" is generall" not present in other famil" members. b. Immunodeficienc" is ne#er ac=uiredG rather/ it is congenital. c. Immunodeficienc" is almost immediatel" s"mptomatic. d. Immunodeficienc" is a result of a postnatal mutation. ANS: A
4enerall"/ the mutations mutations are sporadic and not n ot inheritedG a famil" histor" eists in onl" approimatel" 9H of indi#iduals. !he sporadic mutations occur before birth/ but the onset of s"mptoms ma" be earl" or later/ depending on the particular s"ndrome. !he immunodeficienc" can be either congenital or ac=uired. $!S: 1
%&': $age <1
0. A person ith t"pe blood is considered to be the un i#ersal blood donor because t"pe
blood contains hich of the folloing2 a. No antigens b. No antibodies
c. oth A and antigens d. oth A and antibodies
ANS: A
ecause indi#iduals ith t"pe blood lac+ both t"pes of antigens/ the" are considered con sidered uni#ersal donors/ meaning that an"one can accept their red blood cells. !"pe indi#iduals/ ho ha#e neither A or antigen but ha#e both anti-A and anti- antibodies/ cannot accept blood from an" of the other three t"pes. $!S: 1
%&': $age ;<
0;. Immunoglobulin & (Ig&) is associated ith hich t"pe of h "persensiti#it" reaction2 a. I c. III b. II d. IB ANS: A
*"persensiti#it" reactions ha#e been di#ided into four distinct t"pes: t"pe I (Ig&-mediated) h"persensiti#it" reactions/ t"pe II (tissue-specific) h"persensiti#it" reactions/ t"pe III (immune complemediated) h"persensiti#it" reactions/ and t"pe IB (cell-mediated) h"persensiti#it" reactions. $!S: 1
%&': $age 0
0<. 4ra#es disease is an autoimmune disease that results in hich maternal antibod"2 a. inding ith receptors for neural transmitters on muscle cells/ causing neonatal
muscular ea+ness b. Affecting the receptor for !S*/ causing neonatal h"perth"roidism c. Inducing anomalies in the fetus or causing pregnanc" loss d. Destro"ing platelets in the fetus and neonate ANS:
4ra#es disease is an autoimmune disease in hich maternal antibod" against the receptor for !S* causes neonatal h"perth"roidism. 3"asthenia gra#is is an autoimmune disease in hich maternal antibod" binds ith receptors for neural transmitters on muscle cells (acet"lcholine receptors)/ causing neonatal muscular ea+ness. S"stemic lupus er"thematosus is an autoimmune disease in hich di#erse maternal autoantibodies induce anomalies (e.g./ congenital heart defects) in the fetus or cause pregnanc" loss. Immune thromboc"topenic purpura causes both autoimmune and alloimmune #ariants to occur/ during hich maternal antiplatelet antibod" destro"s platelets in the fetus and neonate. $!S: 1
%&': $age ;;
MULTIPLE REPO!E
05. 8hen a tuberculin s+in test is positi#e/ the hard center and er"thema surrounding the
induration are a result of hich of the folloing2 (Select folloing2 (Select all that apply.) a. *istamine d. $roducts of complement b. ! l"mphoc"tes e. 3acrophages c. Immune complees ANS: / &
!he reaction site is infiltrated ith onl" ! l"mphoc"tes and macrophages/ resulting in a c lear hard center (induration) and a reddish surrounding area (er"thema). $!S: 1
%&': $age ;>
7>. &posure to hich of the folloing could result in a t"pe IB h"persensiti#it" reaction2 (Select
all that apply.) a pply.) a. $oison i#" b. Neom"cin c.
d. Nic+el e. Detergents
Dair" products
ANS: ANS: A/ / / D/ D/ &
Allergens that primaril" elicit t"pe IB allergic h"persensiti#ities include plant resins (e.g./ poison i#"/ poison poison oa+)G metals (e.g./ nic+el/ chromium)G acet"lates and chemicals in rubber/ cosmetics/ detergentsG and topical antibiotics (e.g./ neom"cin). $!S: 1
%&': $age ;1
71. 8hich disorders are considered autoimmune2 (Select autoimmune2 (Select all that apply.) a. rohn disease d. S"stemic lupus er"thematosus b. Addison disease e. Noninsulin-dependent diabetes c. %heumatoid arthritis
ANS: ANS: A/ / / / / D
rohn disease/ Addison disease/ rheumatoid arthritis/ and s"stemic lupus er"thematosus are all diseases that result from autoimmune pathologic conditions. Insulin-dependent diabetes is also an autoimmune disorder/ but noninsulin-dependent diabetes is not. $!S: 1
%&': $ages 7-9 6 !able 5-
7. 8hich statements best define acute reFection2 (Select all that apply.) a. Acute reFection is a cell-mediated immune response. b. Acute reFection is usuall" a t"pe III reFection. c. Immunosuppressi#e drugs dela" or lessen the intensit" of an acute reFection. d. Acute reFection is associated ith the bod"Es response to an organ transplant. e. Acute reFection is a response against unmatched human leu+oc"te antigens (*CAs). ANS: ANS: A/ / / D/ D/ &
Acute reFection is primaril" a cell-mediated immune response that occurs ithin da "s to months after transplantation. !his t"pe of reFection occurs hen the recipient de#e lops an immune response against unmatched *CAs after transplantation. A biops" of the reFected organ usuall" shos an infiltration of l"mphoc"tes and macrophages characteristic of a t"pe IB reaction. Immunosuppressi#e drugs ma" dela" or lessen the intensit" of an acute reFection. $!S: 1
