NURSl 5315/l NURS5315l Finall Examl –l
Advancedl Pathophysiologyl Guidel |l UTAl
(Latestl 2026l Update)l 100%l Verifiedl
Questionsl &l Answersl |l Gradel A
Q:l Whatl dol cellsl inl thel urinel measure?
Answer:
1.l RBCs.l
l a.l Glomerularl nephritis.l
l b.l Trauma.l
l c.l Kidneyl stones.l
2.l WBC
l a.l Ingection
3.l Casts
l a.l Coagulatedl portiens.l
l i.l Cellularl debris
l 1.l Acutel kidneyl injury
l b.l RBCl
l i.l Tubularl orl glomerularl injury.l
l c.l WBC
l i.l Inflammation
l d.l Epithelial
l i.l Tubularl injury.l
l e.l Broadl waxy
l i.l Stasisl andl tubularl injury
l a.l Notl al goodl sign.l
Q:l Whatl dol biomarkersl inl thel urinel measure?
Answer:
a.l )l NGALl
l 1.l Neutrophill gelatinase-associatedl lipcalinl (plasma,l urine)
,b.l )l KIMl 1l
l 1.l Kidneyl injuryl moleculel 1l (urine)
c.l )l IL-18
l 1.l Interleukinl -18l (urine)
d.l )l IDFl BIP7
l 1.l Insulinl likel growthl factorl bindingl proteinl (urine)
e.l )l TIMP-2
l 1.l Tissuel inhibitorl ofl metallopretinases-2l (urine)
f.l )l Urokinase-typel plasminogenl activatorl receptor.l
Q:l Whatl changesl occurl inl thel kidneyl withl aging?
Answer:
a.l )l Mayl hypertrophyl asl compensatoryl mechanism
l i.l Kidneyl donation,l trauma,l disease
b.l )l Numberl ofl nephronsl decreasedl withl agel (beginningl atl agel 40)l
l i.l Decreasedl renall bloodl flowl andl GFR.l
c.l )l Tubularl atrophy
l i.l Decreasedl glucose,l bicarb,l andl sodiuml reabsorption.l
d.l Decreasedl productionl ofl Vitaminl D-changesl inl Calciuml absorption.l
e.l )l Bladderl symptomsl morel common.l
l i.l Neurogenicl changesl andl otherl externall causes.l
l 1.l Hormonall changes
l 2.l Prostaticl hypertrophy
l 3.l CVl disease
l 4.l Positionl changes
l a.l Diurnall nocturia.l
Q:l Evaluatel thel etiology,l pathophysiology,l andl manifestationsl ofl nephrolithiasisl andl
urolithiasis
Answer:
Etiology:l Massesl ofl crystals,l protein,l substratesl causel obstructionl ofl urinaryl tractl
(usuallyl unilateral)
Pathophysiology:l Saltsl inl urinel precipitatel andl forml crystalsl thatl frowl (calciuml oxalatel
orl Ph;l uricl acid;l struvite:l Mag,l ammonium,l Ph)
,Manifestations:l pHl ofl urinel (>-7-Calcium,l Ph,l struvite;l <5l uricl acid-relatedl tol
movementl (pain)l orl obstruction.l
Q:l Evaluatel thel etiology,l pathophysiology,l andl manifestationsl ofl nephrotic
Answer:
Etiology:l Glomerulonephritis,l drugs,l infections,l thrombo-embolism.l
Pathophysiology:l Increasedl permeabilityl throughl damagedl basementl membrane.l
Manifestations:l Proteinuria;l hypoalbuminemia,l edema,l hyperlipidemia,l lipiduria
Q:l Evaluatel thel etiology,l pathophysiology,l andl manifestationsl ofl nephriticl syndrome
Answer:
Etiology:l Infectionl relatedl andl rapidlyl progressivel glomerulonephritis
Pathophysiology:l Inflammationl ofl thel glomerulus
Manifestations:l Hematurial andl RBCl castsl (proteinurial lessl significant);l HPTN,l oliguria.l
Q:l Explainl thel etiology,l pathophysiology,l andl manifestationsl ofl acutel glomerularl
nephritis
Answer:
Etiology:
1.l Post-infectious
2.l Auto-ummune0antibodiesl formedl in-situ;l
3.l Rapidlyl progressivel glomerulonephritis
Pathophysiology:
1.l Depositsl ofl IgGl andl complementl complexes.l Kids:l Groupl Al beta-hemolyticl strep;l
adultsl postl staphylococcus;l IgAl nephropathyl depositsl ofl IgAl (lupus/earlyl diabeticl
nephropathy)l
2.l Membranousl glomerulonephritis
, 3.l Accumulationl ofl macrophagesl andl proliferationl ofl epitheliall cellsl inl Bowmansl spacel
forml crescentsl andl occludesl capillaryl flow.l
Manifestations:l Fatigue,l HTN,l edema/ascites,l proteinuria/hematuria,l decreasedl urinel output
Q:l Explainl thel etiology,l pathophysiology,l andl manifestationsl ofl chronicl glomerularl
nephritis
Answer:
Etiology:l Chronicl inflammationl (slowl tol develop):l diabeticl nephropathy;l lupusl nephritis.l
Pathophysiology:l Podocytel injury,l thickeningl ofl basementl membranel andl
glomerulosclerosis.l
Manifestations:l Nausea,l vomiting,l hematuria,l proteinuria,l HTN,l edema,l decreasedl urinel
output.l
Q:l Listl thel definition,l onset,l andl commonl etiologiesl ofl acutel kidneyl injury.l
Answer:
Definition:l Declinel inl GFRl (notl enoughl bloodl atl sufficientl pressurel forl perfusion)l urinel
outputl andl clearancel ofl wastel productsl andl electrolytesl
Stagel 1:l Baselinel creatininel 1.l 5-1.l 9l orl </=l 0.l 3mg/dll increased.l
Stagel 2:l Creatininel 2-2.l 9l xl baselinel
Stagel 3:l Creatininel 3xl baselinel orl usel ofl renall replacementl therapy
Onset:l Sudden
Manifestations:l Elevatedl creatinine,l oliguria
Electrolytes:l K,l Ph,l BUN,l metabolicl acidosis,l edema,l dysnpea,l fatigue,l AMS,l muddyl
urine.l
Commonl etiologies:l Pre,l intrinsic,l post-renal
Q:l Listl thel definition,l onset,l andl commonl etiologiesl ofl chronicl kidneyl disease
Answer:
Advancedl Pathophysiologyl Guidel |l UTAl
(Latestl 2026l Update)l 100%l Verifiedl
Questionsl &l Answersl |l Gradel A
Q:l Whatl dol cellsl inl thel urinel measure?
Answer:
1.l RBCs.l
l a.l Glomerularl nephritis.l
l b.l Trauma.l
l c.l Kidneyl stones.l
2.l WBC
l a.l Ingection
3.l Casts
l a.l Coagulatedl portiens.l
l i.l Cellularl debris
l 1.l Acutel kidneyl injury
l b.l RBCl
l i.l Tubularl orl glomerularl injury.l
l c.l WBC
l i.l Inflammation
l d.l Epithelial
l i.l Tubularl injury.l
l e.l Broadl waxy
l i.l Stasisl andl tubularl injury
l a.l Notl al goodl sign.l
Q:l Whatl dol biomarkersl inl thel urinel measure?
Answer:
a.l )l NGALl
l 1.l Neutrophill gelatinase-associatedl lipcalinl (plasma,l urine)
,b.l )l KIMl 1l
l 1.l Kidneyl injuryl moleculel 1l (urine)
c.l )l IL-18
l 1.l Interleukinl -18l (urine)
d.l )l IDFl BIP7
l 1.l Insulinl likel growthl factorl bindingl proteinl (urine)
e.l )l TIMP-2
l 1.l Tissuel inhibitorl ofl metallopretinases-2l (urine)
f.l )l Urokinase-typel plasminogenl activatorl receptor.l
Q:l Whatl changesl occurl inl thel kidneyl withl aging?
Answer:
a.l )l Mayl hypertrophyl asl compensatoryl mechanism
l i.l Kidneyl donation,l trauma,l disease
b.l )l Numberl ofl nephronsl decreasedl withl agel (beginningl atl agel 40)l
l i.l Decreasedl renall bloodl flowl andl GFR.l
c.l )l Tubularl atrophy
l i.l Decreasedl glucose,l bicarb,l andl sodiuml reabsorption.l
d.l Decreasedl productionl ofl Vitaminl D-changesl inl Calciuml absorption.l
e.l )l Bladderl symptomsl morel common.l
l i.l Neurogenicl changesl andl otherl externall causes.l
l 1.l Hormonall changes
l 2.l Prostaticl hypertrophy
l 3.l CVl disease
l 4.l Positionl changes
l a.l Diurnall nocturia.l
Q:l Evaluatel thel etiology,l pathophysiology,l andl manifestationsl ofl nephrolithiasisl andl
urolithiasis
Answer:
Etiology:l Massesl ofl crystals,l protein,l substratesl causel obstructionl ofl urinaryl tractl
(usuallyl unilateral)
Pathophysiology:l Saltsl inl urinel precipitatel andl forml crystalsl thatl frowl (calciuml oxalatel
orl Ph;l uricl acid;l struvite:l Mag,l ammonium,l Ph)
,Manifestations:l pHl ofl urinel (>-7-Calcium,l Ph,l struvite;l <5l uricl acid-relatedl tol
movementl (pain)l orl obstruction.l
Q:l Evaluatel thel etiology,l pathophysiology,l andl manifestationsl ofl nephrotic
Answer:
Etiology:l Glomerulonephritis,l drugs,l infections,l thrombo-embolism.l
Pathophysiology:l Increasedl permeabilityl throughl damagedl basementl membrane.l
Manifestations:l Proteinuria;l hypoalbuminemia,l edema,l hyperlipidemia,l lipiduria
Q:l Evaluatel thel etiology,l pathophysiology,l andl manifestationsl ofl nephriticl syndrome
Answer:
Etiology:l Infectionl relatedl andl rapidlyl progressivel glomerulonephritis
Pathophysiology:l Inflammationl ofl thel glomerulus
Manifestations:l Hematurial andl RBCl castsl (proteinurial lessl significant);l HPTN,l oliguria.l
Q:l Explainl thel etiology,l pathophysiology,l andl manifestationsl ofl acutel glomerularl
nephritis
Answer:
Etiology:
1.l Post-infectious
2.l Auto-ummune0antibodiesl formedl in-situ;l
3.l Rapidlyl progressivel glomerulonephritis
Pathophysiology:
1.l Depositsl ofl IgGl andl complementl complexes.l Kids:l Groupl Al beta-hemolyticl strep;l
adultsl postl staphylococcus;l IgAl nephropathyl depositsl ofl IgAl (lupus/earlyl diabeticl
nephropathy)l
2.l Membranousl glomerulonephritis
, 3.l Accumulationl ofl macrophagesl andl proliferationl ofl epitheliall cellsl inl Bowmansl spacel
forml crescentsl andl occludesl capillaryl flow.l
Manifestations:l Fatigue,l HTN,l edema/ascites,l proteinuria/hematuria,l decreasedl urinel output
Q:l Explainl thel etiology,l pathophysiology,l andl manifestationsl ofl chronicl glomerularl
nephritis
Answer:
Etiology:l Chronicl inflammationl (slowl tol develop):l diabeticl nephropathy;l lupusl nephritis.l
Pathophysiology:l Podocytel injury,l thickeningl ofl basementl membranel andl
glomerulosclerosis.l
Manifestations:l Nausea,l vomiting,l hematuria,l proteinuria,l HTN,l edema,l decreasedl urinel
output.l
Q:l Listl thel definition,l onset,l andl commonl etiologiesl ofl acutel kidneyl injury.l
Answer:
Definition:l Declinel inl GFRl (notl enoughl bloodl atl sufficientl pressurel forl perfusion)l urinel
outputl andl clearancel ofl wastel productsl andl electrolytesl
Stagel 1:l Baselinel creatininel 1.l 5-1.l 9l orl </=l 0.l 3mg/dll increased.l
Stagel 2:l Creatininel 2-2.l 9l xl baselinel
Stagel 3:l Creatininel 3xl baselinel orl usel ofl renall replacementl therapy
Onset:l Sudden
Manifestations:l Elevatedl creatinine,l oliguria
Electrolytes:l K,l Ph,l BUN,l metabolicl acidosis,l edema,l dysnpea,l fatigue,l AMS,l muddyl
urine.l
Commonl etiologies:l Pre,l intrinsic,l post-renal
Q:l Listl thel definition,l onset,l andl commonl etiologiesl ofl chronicl kidneyl disease
Answer:
