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Exam 1: NU 606/ NU606 (Latest 2025/ 2026 Update) Advanced Pathophysiology Review| Questions & Answers| Grade A| 100% Correct (Verified Solutions)- Regis

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Exam 1: NU 606/ NU606 (Latest 2025/ 2026 Update) Advanced Pathophysiology Review| Questions & Answers| Grade A| 100% Correct (Verified Solutions)- Regis QUESTION Why do cellular adaptions occur? Answer: cellular adaptations occur as cells adapt to changes in the internal environment aka increased work demand by changes QUESTION 3 sources of intracellular accumulations and explanation Answer: -normal body substances: lipids, proteins, carbohydrates, melanin etc. -abnormal endogenous products: those resulting from inborn errors of metabolism, aka genetically inherited error in which body can't turn food into energy. e.g. large polymer aka stored glucose -exogenous products: environmental agents and pigments not broken down by the cell, from outside the body e.g. you take drug QUESTION Why is calcium important to the cell? Answer: calcium functions as an important second messenger and cytosolic [fluid portion of the cytoplasm] signal for many cell responses QUESTION Know pathologic calcifications, 2 types Answer: abnormal tissue deposition of calcium salt, together with smaller amount of iron, magnesium and other minerals -dystrophic calcification: occurs in dead of dying tissue. Intracellular accumulation of crystalized calcium phosphate, dying cells release calcium which combine with phosphate. E.g. can occur in advanced artherosclerosis in the aorta or large blood vessels and heart valvues. Can be the result of ischemia - metabolic calcification: occurs in normal tissues as a result of increased serum calcium levels. Most commonly in lungs. Hyperparathyroisism can be a cause, increased mobilization of calcium from bones QUESTION Different causes of cell injury and examples Answer: injury from physical forces -mechansical forces e.g. tissue tears, fractures, blood vessel injury -extreme temperature changes e.g. hypothermia: cold increases blood viscosity, vascular constriction to preserve vital organs, reflex of sympathetic nervous system, hypoxia. Burns and heat stroke: can cause clotting and tissue clumping -electrical forces: impacts neural pathways radiation injury -ionizing radiation: release of free radicals -ultraviolet radiation: sun -nonionizing radiation: microwaves from laser enegery by causing vibrations and rotation of molecules, converted to thermal energy and burns chemical injury -drugs: ethanol hurts liver and gastric mucosa, fetal development. Tylenol detoxified in the liver -carbon tetrachloride: causes damage in liver where detoxified, turns into free radicals which pair with unpaired electrons -lead toxicity can cause cognitive and intellectual deficits, neurobehavioral problems in children. Is stored in bones so can continue to enter blood stream for long time. Children absorb more than adults. demylenation -murcury: can be found in fish, targets CNS and kidneys, thimerisol= extended vaccines shelf life biologic agents -viruses, parasites, bacteria nutritional imbances -excesses and deficnenies, too little folate= spina bifida, too much iron= constipation and increased cancer risk QUESTION 2 patterns of reversible cell injury Answer: impairs cell function but does not result in cell death -cellular swelling: impairment of the energy dependet Na+/K+ APTase membrane pump, usually as the result of hypoxic cell injury. more sodium in cells so fluid comes in too which causes swelling. If oxygen is restored then pumps will work again -fatty changes: linked to intracellular accumulation of fat, most common in liver as liver processes fat QUESTION 3 major mechanisms whereby most injurious agents exert their effects Answer: 1. Free radical and reactive oxygen species (ROS): free radicals are highly reactive chemical species; having an unpaired electron causes them to be unstable and highly reactive. -Radical injury types: lipids, proteins, DNA (histones) 2.Hypoxic cell injury: deprives cell of oxygen and interrupts oxidative metabolism and generation of ATP, acute cellular swelling (edema). The longer the tissue is hypoxic, greater change of perminant damage -causes of hypoxia: inadequate amount of oxygen in the air, respiratory disease [COPD], inability of the cells to use oxygen, edema, ischemia red calcium homeostasis: calcium functions as important secondary messenger and cytosolic signal for many cell responses. -causes: ischemia-induced by calcium disrtuption, inappropriate activation of enzymes QUESTION Apoptosis vs necrosis, define and what's the difference Answer: Apoptosis: 'fallen apart', equated with suicide, REGULATED PROCESS, can occur during regular development, cell shrinks and nucleus decintegrates. process eliminates cells that are worn out, overproduced, developed improperly, genetic damage Necrosis: refers to the cell death of an organ or tissue that is still part of living person. often interfers with cell replacemnt and tissue regeneration. Pathologic, unregulated death. Cells swell and rupture, loss of cell membrane integrity. cellular products sent into intracellular space, causes inflammation QUESTION Types of necrosis Answer: gangrene, wet and dry QUESTION What is gangrene? Answer: occurs when a considerable mass of tissue undergoes necrosis. -dry: affected tissue becomes dry and shrinks, the skin wrinkles and color changes to dark brown or black. spread is slow. typically in extremities. lack of arterial blood flow but venous flow still working -wet: affected area is mostly cold, swollen, and pulseless. skin is moist, black and under tension. blebs form on the surface, liqueficiation occurs and foul oder from bacterial action. spread of tissue damage is rapid. lack of venous blood flow so fluid accumulates -gas gangrene: aka myonecrosis caused by clostudym bacteria [profinges] aerobic bacteria proliferating. good at fermenting carbohydrats such as muscle. gas is prodcuted which seperates muscle fibers. mostly in legs QUESTION A mother who is with her son when a cast is removed from his arm asks the nurse "What is wrong with my son's arm? It looks so small!" What is the nurse's best response? a. "The cells's have atrophied due to lack of use and will regain their size as he starts to use the arm." b. "the cast has squeezed the arm and decreased its size" c. "there is less fluid in the arm due to the arm being compressed" d. "the child has lost weight" Answer: A QUESTION A client receives a phone call from her gynecologists office nurse and is informed that her pap results indentified a mild dysplasia. The best explanation for the nurse to provide her would be: a. "a minor degrees of dysplasia are associated with chronic irritation or inflammation. However, we will need to do additional diagnostic studies to confirm the diagnosis." b. "you need emergency treatment, come into the office today" c. "do not be concerned, this is not abnormal" d." you definitely have cancer" Answer:

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Examl 1:l NUl 606/l NU606l (Latestl 2025/l
2026l Update)l Advancedl Pathophysiologyl
Review|l Questionsl &l Answers|l Gradel A|l
100%l Correctl (Verifiedl Solutions)-l Regis

Q:l Whyl dol cellularl adaptionsl occur?
Answer:
cellularl adaptationsl occurl asl cellsl adaptl tol changesl inl thel internall environmentl akal
increasedl workl demandl byl changes


Q:l 3l sourcesl ofl intracellularl accumulationsl andl explanation
Answer:
-normall bodyl substances:l lipids,l proteins,l carbohydrates,l melaninl etc.
-abnormall endogenousl products:l thosel resultingl froml inbornl errorsl ofl metabolism,l akal
geneticallyl inheritedl errorl inl whichl bodyl can'tl turnl foodl intol energy.l e.g.l largel polymerl
akal storedl glucosel
-exogenousl products:l environmentall agentsl andl pigmentsl notl brokenl downl byl thel cell,l
froml outsidel thel bodyl e.g.l youl takel drug


Q:l Whyl isl calciuml importantl tol thel cell?
Answer:
calciuml functionsl asl anl importantl secondl messengerl andl cytosolicl [fluidl portionl ofl thel
cytoplasm]l signall forl manyl celll responses


Q:l Knowl pathologicl calcifications,l 2l types
Answer:
abnormall tissuel depositionl ofl calciuml salt,l togetherl withl smallerl amountl ofl iron,l
magnesiuml andl otherl minerals
-dystrophicl calcification:l occursl inl deadl ofl dyingl tissue.l Intracellularl accumulationl ofl
crystalizedl calciuml phosphate,l dyingl cellsl releasel calciuml whichl combinel withl

,phosphate.l E.g.l canl occurl inl advancedl artherosclerosisl inl thel aortal orl largel bloodl
vesselsl andl heartl valvues.l Canl bel thel resultl ofl ischemial
-l metabolicl calcification:l occursl inl normall tissuesl asl al resultl ofl increasedl seruml
calciuml levels.l Mostl commonlyl inl lungs.l Hyperparathyroisisml canl bel al cause,l increasedl
mobilizationl ofl calciuml froml bones


Q:l Differentl causesl ofl celll injuryl andl examples
Answer:
injuryl froml physicall forces
-mechansicall forcesl e.g.l tissuel tears,l fractures,l bloodl vessell injury
-extremel temperaturel changesl e.g.l hypothermia:l coldl increasesl bloodl viscosity,l vascularl
constrictionl tol preservel vitall organs,l reflexl ofl sympatheticl nervousl system,l hypoxia.l
Burnsl andl heatl stroke:l canl causel clottingl andl tissuel clumping
-electricall forces:l impactsl neurall pathways
radiationl injury
-ionizingl radiation:l releasel ofl freel radicals
-ultravioletl radiation:l sun
-nonionizingl radiation:l microwavesl froml laserl enegeryl byl causingl vibrationsl andl rotationl
ofl molecules,l convertedl tol thermall energyl andl burns
chemicall injury
-drugs:l ethanoll hurtsl liverl andl gastricl mucosa,l fetall development.l Tylenoll detoxifiedl inl
thel liverl
-carbonl tetrachloride:l causesl damagel inl liverl wherel detoxified,l turnsl intol freel radicalsl
whichl pairl withl unpairedl electrons
-leadl toxicityl canl causel cognitivel andl intellectuall deficits,l neurobehaviorall problemsl inl
children.l Isl storedl inl bonesl sol canl continuel tol enterl bloodl streaml forl longl time.l
Childrenl absorbl morel thanl adults.l demylenationl
-murcury:l canl bel foundl inl fish,l targetsl CNSl andl kidneys,l thimerisol=l extendedl vaccinesl
shelfl lifel
biologicl agents
-viruses,l parasites,l bacteria
nutritionall imbances
-excessesl andl deficnenies,l tool littlel folate=l spinal bifida,l tool muchl iron=l constipationl
andl increasedl cancerl risk


Q:l 2l patternsl ofl reversiblel celll injury
Answer:
impairsl celll functionl butl doesl notl resultl inl celll deathl

,-cellularl swelling:l impairmentl ofl thel energyl dependetl Na+/K+l APTasel membranel pump,l
usuallyl asl thel resultl ofl hypoxicl celll injury.l morel sodiuml inl cellsl sol fluidl comesl inl tool
whichl causesl swelling.l Ifl oxygenl isl restoredl thenl pumpsl willl workl again
-fattyl changes:l linkedl tol intracellularl accumulationl ofl fat,l mostl commonl inl liverl asl
liverl processesl fat


Q:l 3l majorl mechanismsl wherebyl mostl injuriousl agentsl exertl theirl effects
Answer:
1.l Freel radicall andl reactivel oxygenl speciesl (ROS):l freel radicalsl arel highlyl reactivel
chemicall species;l havingl anl unpairedl electronl causesl theml tol bel unstablel andl highlyl
reactive.l
-Radicall injuryl types:l lipids,l proteins,l DNAl (histones)
2.Hypoxicl celll injury:l deprivesl celll ofl oxygenl andl interruptsl oxidativel metabolisml andl
generationl ofl ATP,l acutel cellularl swellingl (edema).l Thel longerl thel tissuel isl hypoxic,l
greaterl changel ofl perminantl damage
-causesl ofl hypoxia:l inadequatel amountl ofl oxygenl inl thel air,l respiratoryl diseasel
[COPD],l inabilityl ofl thel cellsl tol usel oxygen,l edema,l ischemial
3.impairedl calciuml homeostasis:l calciuml functionsl asl importantl secondaryl messengerl andl
cytosolicl signall forl manyl celll responses.l
-causes:l ischemia-inducedl byl calciuml disrtuption,l inappropriatel activationl ofl enzymes


Q:l Apoptosisl vsl necrosis,l definel andl what'sl thel difference
Answer:
Apoptosis:l 'fallenl apart',l equatedl withl suicide,l REGULATEDl PROCESS,l canl occurl
duringl regularl development,l celll shrinksl andl nucleusl decintegrates.l processl eliminatesl
cellsl thatl arel wornl out,l overproduced,l developedl improperly,l geneticl damage
Necrosis:l refersl tol thel celll deathl ofl anl organl orl tissuel thatl isl stilll partl ofl livingl
person.l oftenl interfersl withl celll replacemntl andl tissuel regeneration.l Pathologic,l
unregulatedl death.l Cellsl swelll andl rupture,l lossl ofl celll membranel integrity.l cellularl
productsl sentl intol intracellularl space,l causesl inflammation


Q:l Typesl ofl necrosis
Answer:
gangrene,l wetl andl dry


Q:l Whatl isl gangrene?

, Answer:
occursl whenl al considerablel massl ofl tissuel undergoesl necrosis.l
-dry:l affectedl tissuel becomesl dryl andl shrinks,l thel skinl wrinklesl andl colorl changesl tol
darkl brownl orl black.l spreadl isl slow.l typicallyl inl extremities.l lackl ofl arteriall bloodl
flowl butl venousl flowl stilll working
-wet:l affectedl areal isl mostlyl cold,l swollen,l andl pulseless.l skinl isl moist,l blackl andl
underl tension.l blebsl forml onl thel surface,l liqueficiationl occursl andl foull oderl froml
bacteriall action.l spreadl ofl tissuel damagel isl rapid.l lackl ofl venousl bloodl flowl sol fluidl
accumulates
-gasl gangrene:l akal myonecrosisl causedl byl clostudyml bacterial [profinges]l aerobicl
bacterial proliferating.l goodl atl fermentingl carbohydratsl suchl asl muscle.l gasl isl prodcutedl
whichl seperatesl musclel fibers.l mostlyl inl legs


Q:l Al motherl whol isl withl herl sonl whenl al castl isl removedl froml hisl arml asksl thel
nursel "Whatl isl wrongl withl myl son'sl arm?l Itl looksl sol small!"l Whatl isl thel nurse'sl bestl
response?
a.l "Thel cells'sl havel atrophiedl duel tol lackl ofl usel andl willl regainl theirl sizel asl hel startsl
tol usel thel arm."
b.l "thel castl hasl squeezedl thel arml andl decreasedl itsl size"
c.l "therel isl lessl fluidl inl thel arml duel tol thel arml beingl compressed"
d.l "thel childl hasl lostl weight"

Answer:
A


Q:l Al clientl receivesl al phonel calll froml herl gynecologistsl officel nursel andl isl
informedl thatl herl papl resultsl indentifiedl al mildl dysplasia.l Thel bestl explanationl forl thel
nursel tol providel herl wouldl be:
a.l "al minorl degreesl ofl dysplasial arel associatedl withl chronicl irritationl orl inflammation.l
However,l wel willl needl tol dol additionall diagnosticl studiesl tol confirml thel diagnosis."
b.l "youl needl emergencyl treatment,l comel intol thel officel today"
c.l "dol notl bel concerned,l thisl isl notl abnormal"
d."l youl definitelyl havel cancer"

Answer:
A


Q:l Whichl ofl thel followingl canl resultl inl membranel damage
A.inactivationl ofl Na+/K+/ATPase

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