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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Document preview page 1

Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 1

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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank

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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 1 preview imageRubin's Pathology: Clinicopathologic Foundations of MedicineTestbank/StudyguideChapter1: Cell Adaptation, Injury and Death1.Ischemiaandothertoxicinjuriesincreasetheaccumulationofintracellularcalciumasaresultof:A)releaseofstoredcalciumfromthemitochondria.B)improvedintracellularvolumeregulation.C)decreasedinfluxacrossthecellmembrane.D)attractionofcalciumtofattyinfiltrates.2.Thepatientisfoundtohaveliverdisease,resultingintheremovalofalobeofhisliver.Adaptationtothereducedsizeoftheliverleadsto___________oftheremaininglivercells.A)metaplasiaB)organatrophyC)compensatoryhyperplasiaD)physiologichypertrophy3.Apersoneatingpeanutsstartschokingandcollapses.Hisairwayobstructionispartiallycleared,butheremainshypoxicuntilhereachesthehospital.Theprolongedcellhypoxiacausedacerebralinfarctionandresulting__________inthebrain.A)caspaseactivationB)coagulationnecrosisC)rapidphagocytosisD)proteinp53deficiency4.Bacteriaandvirusescausecelldamageby_______,whichisuniquefromtheintracellulardamagecausedbyotherinjuriousagents.A)disruptingthesodium/potassiumATPasepumpB)interruptingoxidativemetabolismprocessesC)replicatingandproducingcontinuedinjuryD)decreasingproteinsynthesisandfunction5.Thepatienthasaprolongedinterruptioninarterialbloodflowtohisleftkidney,causinghypoxiccellinjuryandthereleaseoffreeradicals.Freeradicalsdamagecellsby:A)destroyingphospholipidsinthecellmembrane.B)alteringtheimmuneresponseofthecell.C)disruptingcalciumstorageinthecell.D)inactivationofenzymesandmitochondria.
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 2 preview image
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 3 preview image6.Injuredcellshaveimpairedflowofsubstancesthroughthecellmembraneasaresultof:A)increasedfatload.B)alteredpermeability.C)alteredglucoseutilization.D)increasedsurfacereceptors.7.Reversibleadaptiveintracellularresponsesareinitiatedby:A)stimulusoverload.B)geneticmutations.C)chemicalmessengers.D)mitochondrialDNA.8.Injuredcellsbecomeveryswollenasaresultof:A)increasedcellproteinsynthesis.B)alteredcellvolumeregulation.C)passiveentryofpotassiumintothecell.D)blebformationintheplasmamembrane.9.Adiabeticpatienthasimpairedsensation,circulation,andoxygenationofhisfeet.Hestepsonapieceofglass,thewounddoesnotheal,andtheareatissuebecomesnecrotic.Thenecroticcelldeathischaracterizedby:A)rapidapoptosis.B)cellularrupture.C)shrinkageandcollapse.D)chronicinflammation.10.A99-year-oldwomanhasexperiencedthedeclineofcellfunctionassociatedwithage.Agroupoftheoriesofcellularagingfocusonprogrammed:A)changeswithgeneticinfluences.B)eliminationofcellreceptorsites.C)insufficienttelomeraseenzyme.D)DNAmutationorfaultyrepair.11.An89-year-oldfemalepatienthasexperiencedsignificantdecreasesinhermobilityandstaminaduringa3-weekhospitalstayforthetreatmentofafemoralheadfracture.Whichofthefollowingphenomenamostlikelyaccountsforthepatientsdecreaseinmusclefunctionthatunderliesherreducedmobility?A)ImpairedmusclecellmetabolismresultingfrommetaplasiaB)DysplasiaasaconsequenceofinflammationduringboneremodelingC)Disuseatrophyofmusclecellsduringaprolongedperiodofimmobility
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 4 preview imageD)Ischemicatrophyresultingfromvascularchangeswhileonbedrest12.A20-year-oldcollegestudenthaspresentedtohercampusmedicalclinicforascheduledPapanicolaou(Pap)smear.Theclinicianwhowillinterpretthesmearwillexaminecellsamplesforevidenceof:A)changesincellshape,size,andorganization.B)thepresenceofunexpectedcelltypes.C)ischemicchangesincellsamples.D)abnormallyhighnumbersofcellsinaspecifiedfield.13.Whichofthefollowingpathophysiologicprocessesismostlikelytoresultinmetastaticcalcification?A)BenignprostatichyperplasiaB)LivercirrhosisC)ImpairedglycogenmetabolismD)Hyperparathyroidism14.Despitethelowlevelsofradiationusedincontemporaryradiologicimaging,aradiologytechnicianisawareoftheneedtominimizeherexposuretoionizingradiation.Whatistheprimaryrationaleforthetechniciansprecautions?A)Radiationstimulatespathologiccellhypertrophyandhyperplasia.B)Radiationresultsintheaccumulationofendogenouswasteproductsinthecytoplasm.C)RadiationinterfereswithDNAsynthesisandmitosis.D)Radiationdecreasestheactionpotentialofrapidlydividingcells.15.Theparentsofa4-year-oldgirlhavesoughtcarebecausetheirdaughterhasadmittedtochewingandswallowingimportedtoyfigurinesthathavebeendeterminedtobemadeoflead.Whichofthefollowingbloodtestsshouldthecareteamprioritize?A)WhitebloodcelllevelswithdifferentialB)RedbloodcelllevelsandmorphologyC)UreaandcreatininelevelsD)Liverfunctionpanel16.A70-year-oldmalepatienthasbeenadmittedtoahospitalforthetreatmentofarecenthemorrhagicstrokethathaslefthimwithnumerousmotorandsensorydeficits.Thesedeficitsaremostlikelytheresultofwhichofthefollowingmechanismsofcellinjury?A)FreeradicalinjuryB)HypoxiaandATPdepletionC)InterferencewithDNAsynthesisD)Impairedcalciumhomeostasis
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 5 preview image17.Whichofthefollowingprocessesassociatedwithcellularinjuryismostlikelytobereversible?A)CelldamageresultingfromaccumulationoffatinthecytoplasmB)CellularchangesasaresultofionizingradiationC)CelldamagefromaccumulationoffreeradicalsD)Apoptosis18.Theextrinsicpathwayofapoptosiscanbeinitiatedby:A)damagetocellularDNA.B)decreasedATPlevels.C)activationofthep53protein.D)activationofdeathreceptorsonthecellsurface.19.Apatientwithsevereperipheralvasculardiseasehasdevelopedsignsofdrygangreneonthegreattoeofonefoot.Whichofthefollowingpathophysiologicprocessesmostlikelycontributedtothisdiagnosis?A)InappropriateactivationofapoptosisB)BacterialinvasionC)ImpairedarterialbloodsupplyD)Metaplasticcellularchanges20.Whichofthefollowingfactsunderliestheconceptofreplicativesenescence?A)Genescontrollinglongevityarepresentorabsentinvaryingquantitiesamongdifferentindividuals.B)Telomeresbecomeprogressivelyshorterinsuccessivegenerationsofacell.C)Thedamaginginfluenceoffreeradicalsincreasesexponentiallyinlatergenerationsofacell.D)AgingproducesmutationsinDNAanddeficitsinDNArepair.AnswerKey1.A2.C3.B4.C5.A6.B7.C8.B9.B
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 6 preview image10.A11.C12.A13.D14.C15.B16.B17.A18.D19.C20.B
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 7 preview imageChapter2: InflammationMULTIPLECHOICE1.Tears are considered to be part of the:1. first line of defense.2. second line of defense.3. third line of defense.4. specific defenses.5. nonspecific defenses.a.1, 4b.1, 5c.3, 4d.2, 5ANS: B2.A specific defense for the body is:a.phagocytosis.b.sensitized T lymphocytes.c.the inflammatory response.d.intact skin and mucous membranes.ANS: B3.The inflammatory response is anonspecific response to:a.phagocytosis of foreign material.b.local vasodilation.c.any tissue injury.d.formation of purulent exudates.ANS: C4.Chemical mediators released during the inflammatory response include:a.albumin andfibrinogen.b.growth factors and cell enzymes.c.macrophages and neutrophils.d.histamine and prostaglandins.ANS: D5.Which of the following result directly from the release of chemical mediatorsfollowing a moderate burn injury?1. Pain2.Local vasoconstriction3. Increased capillary permeability4. Pallora.1, 2b.1, 3
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 8 preview imagec.2, 3d.2, 4ANS: B 6.Granulation tissue is best described as:a.highly vascular, very fragile, and very susceptible to infection.b.an erosion through thewall of viscera, leading to complications.c.a type of adhesion with no vascularization.d.a form of stenosis, in a duct, that is extremely tough and resists attack by microbes.ANS: A7.Edema associated with inflammation results directly from:a.increased fluid and protein in the interstitial compartment.b.increased phagocytes in the affected area.c.decreased capillary permeability.d.general vasoconstriction.ANS: A8.The warmth and redness related to the inflammatory responseresults from:a.increased interstitial fluid.b.production of complement.c.a large number of white blood cells (WBCs) entering the area.d.increased blood flow into the area.ANS: D9.What is the correct order of the following events in theinflammatory responseimmediately after tissue injury?1. Increased permeability of blood vessels2. Dilation of blood vessels3. Transient vasoconstriction4. Migration of leukocytes to the area5. Hyperemiaa.5, 3, 2, 1, 4b.1, 2, 4, 5, 3c.2, 3, 5,4, 1d.3, 2, 5, 1, 4ANS: D10.The process of phagocytosis involves the:a.ingestion of foreign material and cell debris by leukocytes.b.shift of fluid and protein out of capillaries.c.formation of a fibrin mesh around the infected area.d.movement of erythrocytes through the capillary wall.ANS: A
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 9 preview image11.Systemic effects of severe inflammation include:a.erythema and warmth.b.loss of movement at the affected joint.c.fatigue, anorexia, and mild fever.d.abscess formation.ANS: C12.The termleukocytosismeans:a.increased white blood cells (WBCs) in the blood.b.decreased WBCs in the blood.c.increased number of immature circulating leukocytes.d.significant change in the proportions of WBCs.ANS: A13.Which of the following statements applies to fever?a.Viral infection is usually present.b.Heat-loss mechanisms have been stimulated.c.It is caused by a signal to the thalamus.d.It results from release of pyrogens into thecirculation.ANS: D14.Mechanisms to bring an elevated body temperature down to the normal level include:a.general cutaneous vasodilation.b.generalized shivering.c.increased heart rate.d.increased metabolic rate.ANS: A15.Replacement of damaged tissue by similar functional cells is termed:a.fibrosis.b.regeneration.c.resolution.d.repair by scar tissue.ANS: B16.Scar tissue consists primarily of:a.granulation tissue.b.epithelial cells.c.collagen fibers.d.new capillaries and smooth muscle fibers.ANS: C
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 10 preview image17.Which of the following promotes rapid healing?a.Closely approximated edges of a woundb.Presence of foreign materialc.Exposure to radiationd.Vasoconstriction in the involved areaANS: A18.Glucocorticoids are used to treat inflammation because they directly:a.promote the release of prostaglandins at the site.b.decrease capillary permeability.c.mobilize lymphocytes andneutrophils.d.prevent infection.ANS: B19.Patients taking glucocorticoids for long periods of time are likely to develop all of thefollowing EXCEPT:a.decreased bone density.b.wasting of skeletal muscle.c.opportunistic infections.d.increased leukocyte production.ANS: D20.Which of the following drugs relieves fever and some types of pain but is NOT ananti-inflammatory agent?a.Acetaminophenb.Prednisonec.Aspirind.IbuprofenANS: A21.A burn area in which theepidermis and part of the dermis is destroyed is classified as:a.full-thickness.b.deep partial-thickness.c.superficial partial-thickness.d.first-degree.ANS: B22.A woman has burns on the anterior surfaces of her right arm, chest, andright leg. Thepercentage of body surface area burned is approximately:a.13.5%.b.18%.c.22.5%.
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 11 preview imaged.31.5%.ANS: C23.The characteristic appearance of a full-thickness burn is:a.painful with multiple blisters.b.heavy bleeding.c.red withsome swelling.d.dry, firm, charred, or hard white surface.ANS: D24.A typical source of infection in burn areas is:a.the skin grafts.b.microbes surviving in the hair follicles in the burn area.c.circulating blood bringing microbes to theburn wound.d.opportunistic virus in digestive tract.ANS: B25.A large burn area predisposes to decreased blood pressure because:a.bleeding occurs under the burn surface.b.the heart is damaged by toxic materials from the burn.c.fluid andprotein shift out of the blood.d.vasoconstriction occurs in the burn area.ANS: C26.During an inflammatory response, hyperemia is caused by:a.increased blood flow in the area.b.increased capillary permeability.c.irritation of sensorynerve endings by histamine.d.increased leukocytes in the area.ANS: A27.The advantages of applying a biosynthetic skin substitute to a large area of full-thickness burns include:1. reduced risk of infection.2. decreased loss of plasma protein andfluid.3. developing stronger fibrous scar tissue.4. more rapid healing.5. regeneration of all glands, nerves, and hair follicles.a.1, 3b.4, 5c.1, 2, 4d.2, 3, 5ANS: C
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 12 preview image28.Purulent exudates usually contain:a.small amounts of plasmaprotein & histamine in water.b.red blood cells & all types of white blood cells.c.numerous leukocytes, bacteria, and cell debris.d.large amounts of water containing a few cells.ANS: C29.Isoenzymes in the circulating blood:a.are a type of plasma protein normally present in the circulating blood.b.often indicate the precise location of an inflammatory response.c.are normally released from leukocytes during the inflammatory response.d.are pyrogens, causinglow-grade fever.ANS: B30.A serous exudate is best described as a:a.thin, watery, colorless exudate.b.thick, sticky, cloudy secretion.c.thick, greenish material containing microbes.d.brownish, clotted material.ANS: A31.Systemic manifestations of an inflammatory response include:a.edema and erythema.b.area of necrosis and loss of function.c.pain and tenderness.d.fever and malaise.ANS: D32.Some local effects of a general inflammatory response wouldinclude:a.high, spiking fever and chills.b.redness, warmth, and swelling.c.leukopenia and reduced erythrocyte sedimentation rate (ESR).d.anorexia and headaches.ANS: B33.Prolonged administration of glucocorticoids such asprednisone may cause:1. atrophy of lymphoid tissue.2. increased resistance to infection.3. thrombocytopenia.4. decreased protein synthesis.a.1, 2b.1, 3
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 13 preview imagec.1, 4d.2, 4ANS: C34.Application of ice to an injured knee reduces edema by:a.promoting return of lymph fluid.b.causing local vasoconstriction.c.increasing the rate of tissue repair.d.causing systemic vasodilation.ANS: B35.Healing of large areas of skin loss (including dermis and epidermis) would be mostsuccessful through:a.rapid mitosis and regeneration of skin layers.b.resolution of damaged cells in the area.c.covering the area with biosynthetic skin substitute.d.graft of fibrous tissue to the area.ANS: C36.Prostaglandins are produced from ___________ and cause ___________.a.activated plasma protein; increased capillary permeabilityb.mast cells; vasodilation and painc.platelets; attraction of neutrophils, chemotaxisd.mast cell granules; activation of histamines and kininsANS: B37.The number of neutrophils in the blood is increased significantly:a.during allergic reactions.b.during chronic inflammation.c.to produce antibodies.d.in order to promote phagocytosis.ANS: D38.An abscess contains:a.serous exudate.b.purulent exudate.c.fibrinous exudate.d.hemorrhagic exudate.ANS: B39.Nonspecific agents that protect uninfected cells against viruses are called:a.neutrophils.b.macrophages.
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 14 preview imagec.interferons.d.pyrogens.ANS: C40.Causes of inflammation include:a.direct physical damage such as cuts and sprains.b.allergic reactions.c.infection.d.All the aboveANS: D41.In normal capillary exchange, what is nethydrostatic pressure based on?a.The difference between the hydrostatic pressure within the capillary, as compared with the hydrostapressure of the interstitial fluidb.The relative osmotic pressures in the blood and the interstitial fluidc.The difference between the hydrostatic pressure and osmotic pressure within the capillaryd.The difference between the concentrations of blood cells, plasma proteins, and dissolved substancesthe blood and the interstitial fluidANS: A42.Thecardinal signs of inflammation include all of the following EXCEPT:a.redness.b.loss of function.c.nausea.d.swelling.ANS: C43.Drugs that have anti-inflammatory, analgesic, and antipyretic activities include:1. COX-2 inhibitors(NSAIDs).2. glucocorticoids (e.g., prednisone).3. ibuprofen (NSAID).4. acetaminophen.5. aspirin (ASA).a.1, 2b.2, 4c.1, 3, 5d.1, 4, 5ANS: C 44.Aspirin (ASA) is discouraged for treatment of viral infection in childrenbecause of:a.decreased bone growth after puberty.b.frequent production of blood clots.c.formation of a granuloma filled with virus.
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 15 preview imaged.the risk of developing Reyes syndrome.ANS: D45.Systemic manifestations of inflammation include all EXCEPT:a.pyrexia.b.malaise.c.local swelling.d.anorexia.ANS: C46.Which of the following cellular elements found in the inflammatory response areresponsible for phagocytosis?a.Macrophagesb.Basophilsc.B lymphocytesd.T lymphocytese.EosinophilsANS: A47.Which chemical mediator is involved in prolonging the inflammatory response?a.Bradykininb.Histaminec.Leukotrienesd.Chemotactic factorsANS: C48.Potential complications after healing by scar formation include allthe followingEXCEPT:a.lack of sensory function in the area.b.contractures and adhesions.c.increased hair growth.d.keloid formation.ANS: C49.All of the following are correct statements regarding wound healing EXCEPT:a.Resolutionoccurs where there is minimal tissue damage and the cells can recover.b.Granulation tissue forms a permanent replacement for damaged tissue.c.Regeneration occurs where the cells are capable of mitosis.d.Scar tissue forms where the surrounding cells are incapable of mitosis.ANS: B50.Which of the following statements regarding inflammation is incorrect?a.Inflammation caused by an allergen or a burn will typically produce a serous exudate.
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 16 preview imageb.Infection is one cause ofinflammation.c.Inflammation is the bodys nonspecific response to tissue injury.d.Disorders are named using the ending-sarcomato indicate inflammation.ANS: D51.Which of the following helps to localize and wall off the foreign materialduring aninflammatory response?a.Lymphocytesb.Increased fluidc.Fibrinogend.AntibodiesANS: C52.Why is an application of cold recommended as part of the RICE first aid measuresimmediately following an inflammatory response due toinjury?a.It improves circulation in the area removing chemical mediators.b.It causes local vasoconstriction to reduce local edema.c.It draws more phagocytic cells to the area to remove debris.d.It promotes immediate healing.ANS: B53.One goal for current research in tissue engineering is to:a.create a functional replacement tissue when regeneration is not possible.b.adapt cells from the injured organ to produce replacement tissue.c.design a nonliving synthetic replacement tissue.d.use stem cells as a temporary covering for damaged tissue.ANS: A54.Identify the proper sequence in the healing process.a.A blood clot forms; granulation tissue grows into the gap; new blood vessels develop; phagocytosisforeignmaterial and cell debris occurs; and collagen fibers form a tight, strong scar.b.A blood clot forms; phagocytes remove foreign material and cell debris; granulation tissue grows ingap; new blood vessels form; and collagen fibers promote formationof a tight, strong scar.c.Collagen fibers form in the damaged area; a blood clot forms; granulation tissue grows into the gapangiogenesis takes place; and foreign material and cell debris are removed by phagocytes.d.Foreign material and cell debris are removed by phagocytes; a blood clot forms; granulation tissueinto the gap; new blood vessels form; and collagen fibers grow and cross-link.ANS: B55.All of the following are factors that promote healing EXCEPT:a.good nutrition:protein, vitamins A and C.b.a clean, undisturbed wound.c.effective circulation.
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 17 preview imaged.advanced age.ANS: D56.Identify the correct statement about burns:a.The severity of the burn depends on the temperature, duration, and extent of the burn.b.Young children are less likely to suffer severe burns from immersion in excessively hot water.c.Burns to the palms of the hands are more damaging than burns on the face.d.With a major burn, excessive bleeding usually causes shock.ANS: A57.Which statement applies to the recommended emergency care for burns?a.Drop and lie completely still on your back.b.Call a neighbor for help if the burn appears to be extensive.c.Apply lotion and cover burn tightly with a sheet or towel.d.Cover the burn area with clean, cool, or tepid water and remove nonsticking clothing.ANS: D58.Inhalation of carbon monoxide is a threat for many burn patients because this gas:a.causes swelling in the trachea.b.quickly reduces the availableoxygen in the blood.c.prevents full expansion of the lungs.d.is toxic to the nervous system.ANS: B59.How does scar tissue usually cause obstructions to develop in tube-like structures?a.Scar tissue continues to grow and spread, causing ablockage.b.Scar tissue does not stretch, but rather shrinks in time, causing narrowing.c.Scar tissue twists and forms knots as it develops.d.Scar tissue attaches to nearby normal tissue, causing obstruction.ANS: B60.Which of thefollowing is a serious potential complication found only with the anti-inflammatory COX-2 inhibitor drugs?a.Increased risk of infection at the site of inflammationb.Reyes syndrome developing in children and young adultsc.Increased incidence of heart attacksd.Greatly delayed blood clottingANS: CChapter3: Repair, Regeneration and FibrosisMULTIPLECHOICE
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 18 preview image1.Apublichealthnurseisteachingthecommunityabouthealthpromotion.Whichinformationshouldthenurseincludeforinnateimmunity?Innateimmunityisgained:a.Followinganillnessb.Atbirthc.Viainjectionofspecificantibodiesd.InadulthoodANS:BInnateimmunityispresentatbirth.Innateimmunityispresentatbirthanddoesnotrequireanillness.Innateimmunityispresentatbirthanddoesnotrequireinjection.Innateimmunityispresentatbirth.REF:2.Whichstatementindicatesteachingwassuccessfulregardingcollectins?Collectinsareproducedbythe:a.Kidneysb.Bowelc.Lungsd.IntegumentANS:CCollectinsareproducedbythelungs.Collectinsareproducedbythelungs,notthekidneys.Collectinsareproducedbythelungs,notthebowel.Collectinsareproducedbythelungs,nottheintegument.REF:3.A20-year-oldmalereceivedaknifewoundtothearmduringanaltercation.Whichofthefollowingtypesofimmunitywascompromised?a.Innateimmunityb.Inflammatoryresponsec.Adaptiveimmunityd.SpecificimmunityANS:ATheepithelialcellsoftheskinareapartofinnateimmunity.Theinflammatoryresponseisnotatypeofimmunity.Adaptiveimmunityisrepresentedbythenormalfloraofthebowel.Specificimmunityisatypeofadaptiveimmunityandisnotassociatedwithabreakinskinintegrity.REF:4.Biochemicalsecretionsthattrapandkillmicroorganismsinclude:a.Hormonesb.Neurotransmitters
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 19 preview imagec.Earwaxd.GastricacidANS:CEpithelialcellssecreteseveralsubstancesthatprotectagainstinfection,includingearwax.Hormonesdonotcontainbiochemicalsecretionsthattrapandkillmicroorganisms.Neurotransmitterscarryimportantmessages,buttheydonotcontainbiochemicalsecretions.Gastricacidhelpsbreakdownfoodintoitscomponentparts,butdoesnotcontainbiochemicalsecretions.5.A25-year-oldfemalepresentstoherprimarycareproviderreportingvaginaldischargeofawhite,viscous,andfoul-smellingsubstance.Shereportsthatshehasbeentakingantibioticsforthepast6months.Whichfindingwillthenursemostlikelyseeonthemicroorganismreport?a.Clostridiumdifficileovergrowthb.DecreasedLactobacillusc.Streptococcusovergrowthd.DecreasedCandidaalbicansANS:BDiminishedcolonizationwithLactobacillusthatoccursasaresultofprolongedantibiotictreatmentincreasestheriskforvaginalinfections,suchasvaginosis.Clostridiumdifficileoccursinthecolon,notthevagina.Streptococcusovergrowthwilloccurinthemouth.Candidaalbicansoccursinthecolon,notthevagina.6.Whenanaideasksthenursewhatisapurposeoftheinflammatoryprocess,howshouldthenurserespond?a.Toprovidespecificresponsestowardantigensb.Tolysecellmembranesofmicroorganismsc.Topreventinfectionoftheinjuredtissued.TocreateimmunityagainstsubsequenttissueinjuryANS:COnepurposeoftheinflammatoryprocessistopreventinfectionandfurtherdamagebycontaminatingmicroorganisms.Specificresponsetowardantigensisapartofthecomplementsystemthatassistsintheinflammatoryresponse,butnotitspurpose.Lysisofcellmembranesispartoftheprocessofphagocytosis,whichremovesforeignmaterial,butthisisnotthepurposeoftheinflammatoryresponse.Immunitycannotbeachievedagainstfuturetissueinjury.7.Achildfellofftheswingandscrapedtherightknee.Theinjuredareabecomespainful.Whatelsewillthenurseobserveuponassessment?a.Vasoconstrictionatinjuredsiteb.DecreasedRBCconcentrationatinjuredsite
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 20 preview imagec.Paleskinatinjuredsited.EdemaatinjuredsiteANS:DIncreasedvascularpermeabilityandleakageoffluidoutofthevesselcauseedemaatthesiteofinjury.Vasodilationoccurs,notvasoconstriction.IncreasedRBCscometothesite,notfewer.Rednessoccurs,notpaleness,duringinflammation.8.Anurserecallsthemastcell,amajoractivatorofinflammation,initiatestheinflammatoryresponsethroughtheprocessof:a.Chemotaxisb.Endocytosisc.Degranulationd.OpsonizationANS:CDegranulationofmastcellsisamajorcellularcomponentofinflammation.Chemotaxisistheprocessofwhitecellmigration.Endocytosisisapartofphagocytosisandisnotafactorinmastcellresponse.Opsonizationispartofphagocytosisandisnotafactorinmastcellresponse.9.Whichofthefollowingindividualswouldbeatgreatestriskforanopportunisticinfection?a.18-year-oldwithdiabetesb.70-year-oldwithcongestiveheartfailurec.24-year-oldwhoisimmunocompromisedd.30-year-oldwithpneumoniaANS:COpportunisticmicroorganismscancausediseaseiftheindividualsdefensesarecompromised.An18-year-oldwithdiabeteswouldnotbeimmunocompromisedandwouldnotbeatrisk.A70-year-oldwithcongestiveheartfailurewouldnotbeimmunocompromisedandwouldnotbeatrisk.A30-year-oldwithpneumoniawouldnotbeimmunocompromisedandwouldnotbeatrisk.10.Thedirectionalmigrationofleukocytesalongachemicalgradientistermed:a.Chemotaxisb.Endocytosisc.Marginationd.DiapedesisANS:A
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 21 preview imageChemotaxisistheprocessbywhichleukocytesundergodirectedmigration.Endocytosisisaformofengulfmentandapartofphagocytosis.Marginationoccurswhenleukocytesadheretoendothelialcellsinthewallsofvessels.Diapedesisistheemigrationofthecellsthroughcelljunctionsthathaveloosenedinresponsetoinflammatorymediators.11.A20-year-oldmaleshootshishandwithanailgunwhilereplacingroofingshingles.Whichofthefollowingcelltypeswouldbethefirsttoaidinkillingbacteriatopreventinfectioninhishand?a.Eosinophilsb.Neutrophilsc.Leukotrienesd.MonocytesANS:BNeutrophilsarethepredominantphagocytesintheearlyinflammatorysite,arrivingwithin6to12hoursaftertheinitialinjury.Eosinophilshelplimitandcontrolinflammation.Leukotrienesareactivatorsoftheinflammatoryresponse.Monocytesentermuchlaterandreplaceleukocytes.12.Thepredominantphagocyteofearlyinflammationisthe:a.Eosinophilb.Neutrophilc.Lymphocyted.MacrophageANS:BNeutrophilsarethepredominantphagocytesintheearlyinflammatorysite,arrivingwithin6to12hoursaftertheinitialinjury.Eosinophilshelplimitandcontrolinflammation,buttheyarenottheprominentphagocyte.Lymphocytesarepartoftheinnateimmuneresponse.Macrophageskillmicroorganisms.13.A25-year-oldfemaleexperiencesaheadacheandtakesaspirinforrelief.Anurserecallsaspirinrelievestheheadacheby:a.Decreasingleukotrieneproductionb.Increasinghistaminereleasec.Decreasingprostaglandinproductiond.Increasingplatelet-activatingfactorANS:CAspirinisaprostaglandininhibitor.Aspirininhibitsprostaglandins;itdoesnotaffectleukotrieneproduction.Aspirininhibitsprostaglandins;itdoesnotaffecthistaminerelease.Aspirindoesnotplayaroleintheplateletactivatingfactor;thisisaleukotrieneresponse.14.Whichfactorwillhelpthenursedifferentiateleukotrienesfromhistamine?
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 22 preview imagea.Siteofproductionb.Vasculareffectc.Chemotacticabilityd.TimeofreleaseANS:DLeukotrienesarereleasedslowerandlongerthanhistamine.Leukotrienesandhistamineareproducedfrommastcells.Leukotrienesandhistaminehavesimilarvasculareffects.Leukotrienesandhistaminehavesimilarchemotacticability.15.A25-year-oldmaleisinacaraccidentandsustainsafracturetohisleftfemurwithextensivesofttissueinjury.Thepainassociatedwiththeinjuryisrelatedto:a.Histamineandserotoninb.Kininsandprostaglandinsc.Vasoconstrictiond.ImmunecomplexformationANS:BProstaglandinscauseincreasedvascularpermeability,neutrophilchemotaxis,andpainbydirecteffectsonnerves.Kininsalsopromotepain.Prostaglandinsproducepain;histaminepromotesvasodilation.Prostaglandinsproducepain,notvasoconstriction.Prostaglandinsproducepain,nottheimmunecomplex.16.Thecomplement,clotting,andkininsystemssharewhichofthefollowingcharacteristics?a.Activationofaseriesofproenzymesb.Phagocytosisinitiationc.Granulocyteproductiond.ActivatedbyinterferonANS:AThecomplementsystem,theclottingsystem,andthekininsystemarenormallyininactiveforms,butcanactivateinaseriesasproenzymesandareinvolvedintheinflammatoryprocess.Thecomplementsystem,theclottingsystem,andthekininsystemdonotplayaroleinphagocytosis,butdoplayaroleintheinflammatoryresponseasproenzymes.Thecomplementsystem,theclottingsystem,andtjekininsystemdonotplayaroleingranulocyteproduction,buttheyfunctionasproenzymesintheinflammatoryresponse.Thecomplementsystem,theclottingsystem,andthekininsystemarenotactivatedbyinterferon,butareactivatedbyenzymaticaction.17.Whichstatementindicatesteachingwassuccessfulregardingtheclassicpathwayofthecomplementsystem?Theclassicpathwayofthecomplementsystemisactivatedby:a.Histamineb.Antigen-antibodycomplexes
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 23 preview imagec.Leukotrienesd.ProstaglandinsANS:BTheclassicpathwayofthecomplementsystemisactivatedbyantibodiesoftheimmunesystem.Theclassicpathwayofthecomplementsystemisactivatedbyantibodies,notbyhistamine.Theclassicpathwayofthecomplementsystemisactivatedbyantibodies,notbyleukotrienes.Theclassicpathwayofthecomplementsystemisactivatedbyantibodies,notbyprostaglandins.18.ApatienthasresearchedbradykininontheInternet.Whichinformationindicatesthepatientunderstandsthefunctionsofbradykinin?Bradykininisinvolvedin:a.Increasingvascularpermeabilityb.Vasoconstrictingbloodvesselsc.Stimulatingtheclottingsystemd.IncreasingdegradationofprostaglandinsANS:ABradykininincreasesvascularpermeability.Bradykininincreasesvascularpermeability;itdoesnotpromotevasoconstriction.Bradykininincreasesvascularpermeability;itdoesnotstimulateclotting.Bradykininpromotespain;thus,itdoesnotdegradeprostaglandinsbutsupportsthem.19.Afterteachingthestaffabouttheclottingsystem,whichstatementindicatesteachingwassuccessful?Theendproductoftheclottingsystemis:a.Plasminb.Fibrinc.Collagend.FactorXANS:BTheendproductoftheclottingsystemisfibrin.Plasminactivatesthecomplementcascade.Collagenplaysafactorinwoundhealing.FactorXisafirststepintheclottingsystem.20.A5-year-oldmaleisdiagnosedwithabacterialinfection.Culturesofthebacteriarevealedlipopolysaccharidesonthebacterialcellsurface.Whichofthecomplementpathwayswouldbeactivatedinthiscase?a.Classicalpathwayb.Lectinpathwayc.Alternativepathwayd.KininpathwayANS:C
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 24 preview imageThealternativepathwayisactivatedbyseveralsubstancesfoundonthesurfaceofinfectiousorganisms,suchasthosecontaininglipopolysaccharides.Theclassicalpathwayisprimarilyactivatedbyantibodiesthatareproteinsoftheacquiredimmunesystem.Thelectinpathwayissimilartotheclassicpathwaybutisindependentofantibody.Itisactivatedbyseveralplasmaproteins.Thekininpathwayisinvolvedincoagulation.21.An8-year-oldfemalepresentswithedemaofthecutaneousandmucosaltissuelayers.Hermotherreportsthattheconditionisrecurrentandseemstooccurmoreoftenduringstressfulsituations.Thechildisdiagnosedwithhereditaryangioedema.Whichofthefollowingisdeficientinthischild?a.C1esteraseinhibitorb.Carboxypeptidasec.Neutrophilsd.PlasminANS:AAgeneticdefectinC1esteraseinhibitor(C1INHdeficiency)resultsinhereditaryangioedema.HereditaryangioedemaisduetoC1esteraseinhibitor.Carboxypeptidasedegradeskinins.HereditaryangioedemaisduetoC1esteraseinhibitor,notadisorderofneutrophils.Plasminisnotassociatedwithhereditaryangioedema,butisassociatedwithclots.22.Anurseispreparingtoteachonthesubjectofopsonins.Whichinformationshouldthenurseinclude?Opsoninsaremoleculesthat:a.Arecomposedoffattyacidsb.Regulateinflammationc.Degranulatemastcellsd.EnhancephagocytosisANS:DOpsoninscoatthesurfaceofbacteriaandincreasetheirsusceptibilitytobeingphagocytized.Opsoninsarenotcomposedoffattyacids;theyareantibodies.Opsoninscoatthesurfaceofbacteriaandincreasetheirsusceptibilitytobeingphagocytized.Theydonotregulateinflammation;mastcellsdo.Opsoninscoatthesurfaceofbacteriaandincreasetheirsusceptibilitytobeingphagocytized;theydonotreactwithmastcells.23.A10-year-oldmaleisdiagnosedwithaparasite.Whichlabresultshouldthenursecheckforaresponsetotheparasite?a.Monocytesb.Eosinophilsc.Neutrophilsd.MacrophagesANS:B
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 25 preview imageEosinophilsserveasthebodysprimarydefenseagainstparasites.Monocytesarenotthebodysprimarydefenseagainstparasite;eosinophilsare.Monocytesarephagocytic.Neutrophilsarephagocytic;theyarenotthebodysdefenseagainstparasites.Macrophagesarenotactiveagainstparasites;theyactaslong-termdefenseagainstinfections.24.A65-year-oldfemaleisdiagnosedwithmetastaticbreastcancer.Shehasdevelopedmusclewasting.Whichofthefollowingsubstanceswouldbeproducedinlargequantitiestoeliminatethetumorcellsandcausemusclewasting?a.Interleukin-6b.Eosinophilsc.Tumornecrosisfactord.PlateletsANS:CTumornecrosisfactorcausesmusclewasting.Interleukin-6stimulatesgrowthanddifferentiationofbloodcells.Eosinophilsarestimulatedforparasites.Plateletsstimulateclotting.25.Whenphagocytesbegintostickavidlytocapillarywalls,whichprocessisoccurring?a.Marginationb.Exudationc.Integrationd.EmigrationANS:ABothleukocytesandendothelialcellssecretesubstancesthatincreaseadhesion,orstickiness,causingtheleukocytestoadheremoreavidlytotheendothelialcellsinthewallsofthecapillariesandvenulesinaprocesscalledmargination.Exudationistheprocessofpusformationanddoesnotresultinstickiness.Integrationoccursincellsbutisnotamajorfunctionanddoesnotleadtostickiness.Emigrationissimilartodiapedesisandisnotassociatedwithincreasedstickiness.26.Aninfantdevelopsafeversecondarytoabacterialinfection.Whichofthefollowingmostlikelytriggeredthefever?a.Interleukin-1b.Interleukin-6c.Interleukin-10d.Interferons(INFs)ANS:AInterleukin-1isresponsibleforfeverproduction.Interleukin-6stimulatesgrowthanddifferentiationofbloodcells.Interleukin-10helpsdecreasetheimmuneresponse.INFsaremembersofafamilyofcytokinesthatprotectagainstviralinfections.
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 26 preview image27.A54-year-oldmaleintravenous(IV)druguserisdiagnosedwithchronichepatitisC.Testingrevealedthatheisacandidatefortreatment.Whichofthefollowingcouldbeusedtotreathiscondition?a.Interleukin-1b.Interleukin-6c.Interleukin-10d.INFsANS:DINFsaremembersofafamilyofcytokinesthatprotectagainstviralinfections.Interleukin-1isresponsibleforfeverproduction.Interleukin-6stimulatesgrowthanddifferentiationofbloodcells.Interleukin-10helpsdecreasetheimmuneresponse.28.A35-year-oldmaleisdiagnosedwithlobarpneumonia(lunginfection).Whichofthefollowingexudateswouldbepresentinhighestconcentrationatthesiteofthisadvancedinflammatoryresponse?a.Serousb.Purulentc.Hemorrhagicd.FibrinousANS:DFibrinousexudatesoccurinthelungsofindividualswithpneumonia.Serousfluidiswateryfluid,asinablister.Purulentischaracterizedbyanabscess,suchaspus.Hemorrhagicoccurswhentheexudatesarefilledwitherythrocytes.29.Duringinflammation,theliverisstimulatedtoreleaseplasmaproteins,collectivelyknownas:a.Opsoninsb.Acutephasereactantsc.Antibodiesd.PhagolysosomeANS:BThesynthesisofmanyplasmaproteinsbytheliverisincreasedduringinflammation.Theseproteins,whichcanbeeitherproinflammatoryorantiinflammatoryinnature,arereferredtoasacutephasereactants.Opsoninscoatthesurfaceofbacteriaandincreasetheirsusceptibilitytobeingphagocytized.Antibodiesareproteinsoftheimmunesystem.Phagolysosomedestroysbacterium.30.A3-year-oldismakingplaycakesinasandboxandiseatingtheplaycakes.Thesandwasalsobeingusedbycatsasalitterboxandwascontaminatedwithtoxoplasmosis.Whichofthefollowingwouldmostlikelyalsobepresent?
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 27 preview imagea.Granulomaformationb.Degranulationc.Bloodclotsd.ExudateproductionANS:AInfectionscausedbybacteriasuchastoxoplasmosiscanresultingranulomaformation.Degranulationisapartofmastcelldestruction.Bloodclotsarenotexpectedwithchronicinflammation.Exudateproductionispusformation.31.A12-year-oldmaleisfightingwithanotherchildwhenhereceivesapuncturewoundfromapencil.Theschoolnursecleansandbandagesthewound.Afterabout1week,thewoundwouldbeinwhichphaseofhealing?a.Debridementb.Primaryintentionc.Resolutiond.MaturationANS:CResolutionoccurswhenrepairedtissueisapproachingclosetonormal.Debridementisthescrapingawayofdeadtissueandisnotaphaseofwoundhealing.Primaryintentionisthestageofhealingofwoundsthatarecloselyproximated.Maturationistheresultofseverewoundswhichwouldbeginseveralweeksafterinjuryandmaytake2years.32.Themacrophagesecretionthatstimulatesprocollagensynthesisandsecretionis:a.Angiogenesisfactorb.Matrixmetalloproteinasec.Vascularendothelialgrowthfactord.Transforminggrowthfactor-betaANS:DMacrophagessecretetransforminggrowthfactor-betatostimulatefibroblaststosecretethecollagenprecursorprocollagen.Angiogenesisfactorsupportsthegrowthofnewvessels.Matrixmetalloproteinaseremodelsproteinsatthesiteofinjury.Vascularendothelialgrowthfactorsarealsoinvolvedinvesselgrowth.33.A30-year-oldmalewasinvolvedinamotorvehicleaccident.Theglassfromtheshatteredwindowcuthisfaceandneck.Thescar,however,wasraisedandextendedbeyondtheoriginalboundariesofthewound.Thispatternofscarringiscausedbyimpaired:a.Nutritionalstatusb.Collagensynthesisc.Epithelialization
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 28 preview imaged.ContractionANS:BImpairedproductionofcollagencancausesurfaceoverhealing,leadingtoakeloidorahypertrophicscar.Nutritionaldeficiencieswouldleadtohealingproblems,butnotextendedscarring.Necrosisorsteroiduseleadstoimpairedepithelialization.Impairedcontractionwouldleadtodrawingoftissues,notraised.34.Thenurseisreviewingthelabdataofanewlyadmittedpatient.Thenursenotesthepatienthadanerythrocytesedimentationdone,andtheresultsarequiteelevated.Thenursewouldfocusthecareplanonwhichofthefollowingconditions?a.Anemiab.Infectionc.Inflammationd.ElectrolyteimbalanceANS:CCommonlaboratorytestsforinflammationmeasurelevelsofacutephasereactants.Anincreaseinfibrinogenisassociatedwithanincreasederythrocytesedimentationrate,whichisconsideredagoodindicatorofanacuteinflammatoryresponse.Anemiawouldnotresultinanincreasederythrocytesedimentationrate.Aninfectionwouldresultinanincreaseinwhitebloodcellcount,butnottheerythrocytesedimentationrate.Anelectrolyteimbalancewouldnotcauseariseinthesedimentationrate.35.Healingbysecondaryintentionwouldoccurinwhichofthefollowingpatients?Apatientwitha:a.Suturedsurgicalwoundb.StageIVpressureulcerc.Papercutd.SunburnANS:BApatientwithastageIVpressureulcerwouldhealbysecondaryintention.Apatientwithasurgicalwoundwouldhealbyprimaryintention.Apatientwithapapercutwouldhealbyprimaryintention.Apatientwithasunburnwouldhealwithoutneedingeitherprimaryorsecondaryintention.36.Thepost-surgicalpatientisexperiencingdelayedwoundhealing.Thedieticianbelievesthedelayisrelatedtonutritionalintake.Adeficiencyinwhichofthefollowingsubstancescoulddirectlyaffecthealing?a.VitaminDb.Ascorbicacidc.Melanind.Cholesterol
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 29 preview imageANS:BMostofthefactorsthatinterferewiththeproductionofcollageninhealingtissuesarenutritional.Scurvy,forexample,iscausedbylackofascorbicacidoneofthecofactorsrequiredforcollagenformationbyfibroblasts.Theresultsofscurvyarepoorlyformedconnectivetissueandgreatlyimpairedhealing.VitaminDdeficiencywillnotdirectlyaffecthealing;ascorbicaciddoes.Melanindeficiencywillnotdirectlyaffecthealing;ascorbicaciddoes.Cholesteroldeficiencywillnotdirectlyaffecthealing;ascorbicaciddoes.MULTIPLERESPONSE1.Anurserememberstheprimaryactionsofthecomplementcascadeinclude(selectallthatapply):a.Increasedvascularpermeabilityb.Vasoconstrictionc.Chemotaxisd.Opsonizatione.Cellkillingf.IncreasedclottingANS:A,C,D,ETheactionsofthecomplementcascadeincludeincreasedvascularpermeabilityandvasodilation,chemotaxis,opsonization,andcellkilling.Itdoesnotinvolvevasoconstrictionorincreasedclotting.2.Thenurseisassessingapatientwithadiagnosisofinflammation.Thenursewouldexpecttofindwhichofthefollowingsignsandsymptomsconsistentwithacuteinflammation?(Selectallthatapply.)a.Heatb.Erythemac.Paind.Swellinge.Exudatesf.LossoffunctionANS:A,B,C,D,FTheclassicsymptomsofacuteinflammationincluderedness(erythema),heat,swelling,pain,andlossoffunction.Exudateswouldindicateinfection,notinflammation.3.Thenurseidentifiedeachofthefollowingclinicalmanifestationsofinflammation.Whichwouldthenurseclassifyasalocalresponse?(Selectallthatapply.)a.Feverb.Rednessc.Swellingd.Heate.Pain
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 30 preview imageANS:B,C,D,ELocalmanifestationsofinflammationaretheresultofthevascularchangesassociatedwiththeinflammatoryprocess,includingvasodilationandincreasedcapillarypermeability.Thesymptomsincluderedness,heat,swelling,andpain.4.Physicalbarriersthatofferthebodyprotectionfromdamageandinfectionarelocatedinthe(selectallthatapply):a.Gastrointestinaltractb.Genitourinarytractc.Respiratorytractd.Lymphsysteme.HematopoieticsystemANS:A,B,CThephysicalbarriersthatcovertheexternalpartsofthehumanbodyofferconsiderableprotectionfromdamageandinfection.Thesebarriersarecomposedoftightlyassociatedepithelialcellsoftheskinandoftheliningsofthegastrointestinal,genitourinary,andrespiratorytracts.Chapter4: ImmunopathologyMULTIPLECHOICE1.Neutrophils:a.are phagocytic cells.b.produce histamine.c.produceantibodies.d.are elevated during an allergic response.ANS: A
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Rubin's Pathology: Clinicopathologic Foundations of Medicine Seventh Edition Test Bank - Page 31 preview image2.Which cells are required to process and present antigens from foreign material as theinitial step in the immune response?a.Thelper cellsb.Macrophagesc.Eosinophilsd.MonocytesANS: B3.Humoral immunity is mediated by:a.natural killer cells.b.T lymphocytes (T cells).c.B lymphocytes (B cells).d.neutrophils.ANS: C4.A secondary immune response differs from the primary immune response in that:a.it ismore rapid than the primary response and results in higher antibody levels.b.it is slower than the primary response and doesnt change the antibody levels.c.it occurs at the same time as the primary response but results in a decrease inantibodies.d.it only occurs in hyperallergic reactions and results in a decrease of antibodies.ANS: A5.Which type of immunity is provided by a vaccination?a.Active naturalb.Active artificialc.Passive naturald.Passive artificialANS: B6.When an allergen binds with IgE antibodies on mast cells, resulting in release ofchemical mediators, this reaction is called:a.cytotoxic hypersensitivity.b.immune complex hypersensitivity.c.type I hypersensitivity.d.type IVhypersensitivity.ANS: C7.The role of memory cells is to:a.change into an antibody-secreting cell following activation.b.immediately secrete antibodies following the first exposure to antigen.c.recognize the antigen and stimulate theimmune response.d.bind complement to the antibody.
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