Adult Health II Exam 2 2026||with Expertly detailed solutions||Guaranteed
v4 v4 v4 v4 v4 v4 v4 v4
success |A+ solution v4 v4 v4
Terms in this set (222)
v4 v4 v4 v4
What v4is v4Polycystic v4Kidney v4Disease v4(PKD) A v4genetic v 4 (autosomal v4dominant) v4disorder v4characterized v 4 by:
*Multiple v4fluid-filled v4cysts v4in v4kidneys
*Progressive v4nephron v4destruction
*Enarged v 4 kidneys
*Eventual v4renal v4failure
IT v4is v4progressive v4and v4incurable
Why v4does v4PKD v4cause v4hypertension As v4cysts v4grow, v4they v4increase v4renal v4volume, v4press v4on v4adjacent v4arteries,
v4 and v4cause v4chronic v4ischemia
The v4kidney v4responds v4by v4releasing v4renin, v4a v4hormoen v4that v4initiates v4a
cascade v4(angiotensin v4II) v4to v4tighten v4vessels, v4leading v4to v4high v4blood
v4
v4 pressure
What v4happens v4in v4the v4kidney v4with v4PKD? 1. v4Cysts v4grow
2. Nephrons v4are v 4 compressed v4 and v 4 destroyed
3. Kidney v 4 function v 4 declines
4. GFR v4decreases
5. Waste v 4 products v 4 accumulate
6. RAAS v 4 activtes
7. HTN v 4 develops
8. Kidney v4failure v4eventually v4occurs
,Clinical v 4 Manifestations v 4 of v 4 PKD Early v 4 signs:
*Flank v4pain
*Increased v4abdominal v4girth
*Abdominal v4distention v 4 (enlarged v 4 kidneys)
*Hematuria v4(cyst v4rupture)
*HTN
GI v4manifestation:
*Constipation
v 4 Why
v4 constipation?
Kidney v4failure v4-> v4fluid v4imbalance v4-> v4decreased v4fluid v4movement v4into v4intestines v4-
> v4stool v4hardening v4as v4well v4as v4increased v4pressure v4in v4abdomen v4which v4in v4turn
v4 pushes v4on v4other v4organs v4slowing v4movement v4of v4stool.
HTN v 4 in v 4 PKD Kidney v4damage v 4 -> v4decreased v 4 perfusion v 4 -> v 4RAAS v4activation
RAAS v 4 causes:
*Vasoconstriction
*Sodium v4retention
*Fluid v4retention
*Increased v 4 BP
HTN v4accelerates v4kidney v4destruciton
Lab v4findings v4for v4PKD *BUN v 4 (↑)
*Creatinine v4(↑)
*Ka+ v4(↑)
*Magnesium v4(↑)
*Phosphorus v 4 (↑)
*Calcium v4( v4goes v4down)
*Proteinuria v 4(glomerular v4destruction)
*GFR v4(goes v4down)
Why v4do v4electrolytes v4matter v4in v4PKD? Hyperkalemia v4-> v4peaked v4T v4waves v4-> v4Lethal v4dysrhythmias v4so v4we v4need v4to
v4 place v4these v4clients v4on v4telemetry
Imaging v4for v4PKD Best v 4 cost-effective v 4 diagnostic:
*Renal v4ultrasound
Also:
*Personal v4history v 4 (HTN)
*Family v4Hx
*Genetic v 4 testing
Blood v4pressure v4control v4for v4PKD First v 4 line:
*ACE v4inhibitor v4-> v4ex: v4lisinopril
If v4tolerant: v4ARB v4(angiotension v4receptor v4blockers) v4"losartan"
v4 why?
*blocks v4RAAS
*Protects v4nephrons
*Slows v4progression
, Pain v4management v4for v4PKD Flank v4pain v4from v4 cyst v4enlargement v4->
*Opioids v4(careful v4use)
*Avoid v 4NSAIDs v4(nephrotoxic)
importance v4of v4preventing v4constipation v 4in v 4 PKD *Movement
*High v 4 fiber v4diet
*Stool v4softeners
Slow v4progression v4of v4PKD v4and v4damage v4to v4the v4kidneys Avoid:
*HTN, v 4 Hypotension,
v 4 dehydration
what v4is v4the v4best v4indicator v4of v4Fluid v4status? DAILY v4WEIGHT
Same: v4Time, v 4 clothing, v 4 scale
Neurological v 4 risk v 4 for v 4 PKD v 4 clients Weaker v4cerebral v4blood v4vessels
*b/c v4of v4hypertension v4from v4RAAS
Risk:
*Stroke
*Cerrebral v4aneurysm v 4 rupture
*Hypertensive v4encephalopathy
Nurse v4must v4perform:
*Neurological v 4 assessments
*Monitor v4BP v4closely
Dietary v4Management v4of v4PKD Required v 4 restrictions:
*Fluid v4restriction
*Sodium v4restriction
*Potassium v4restriciton
*Phosphorous v4restriciton
Encourage:
*Fiber
*Wt. v4maintenance
*Smoking v4cessation
*Exercise
*Limit v4alcohol
Why v4weight v 4 matters:
*Overweight v4-> v4increased v4BP
*Underweight v 4 -> v 4 protein v 4 breakdown v 4 -> v 4 worsens v 4 kidney v4damage
What v4is v4Glomerulonephritis? Inflammation v4of v4the v4glomeruli
Most v4commonly v4caused v 4 by v4:
*Post- v4Group v4A v4beta-hemolytic v 4 strep v4infection
*Autoimmune v4disease v4(systemic v4lupus)
*Diabetic v4glomerulosclerosis
*Other v4immune-mediated v4processes
v4 v4 v4 v4 v4 v4 v4 v4
success |A+ solution v4 v4 v4
Terms in this set (222)
v4 v4 v4 v4
What v4is v4Polycystic v4Kidney v4Disease v4(PKD) A v4genetic v 4 (autosomal v4dominant) v4disorder v4characterized v 4 by:
*Multiple v4fluid-filled v4cysts v4in v4kidneys
*Progressive v4nephron v4destruction
*Enarged v 4 kidneys
*Eventual v4renal v4failure
IT v4is v4progressive v4and v4incurable
Why v4does v4PKD v4cause v4hypertension As v4cysts v4grow, v4they v4increase v4renal v4volume, v4press v4on v4adjacent v4arteries,
v4 and v4cause v4chronic v4ischemia
The v4kidney v4responds v4by v4releasing v4renin, v4a v4hormoen v4that v4initiates v4a
cascade v4(angiotensin v4II) v4to v4tighten v4vessels, v4leading v4to v4high v4blood
v4
v4 pressure
What v4happens v4in v4the v4kidney v4with v4PKD? 1. v4Cysts v4grow
2. Nephrons v4are v 4 compressed v4 and v 4 destroyed
3. Kidney v 4 function v 4 declines
4. GFR v4decreases
5. Waste v 4 products v 4 accumulate
6. RAAS v 4 activtes
7. HTN v 4 develops
8. Kidney v4failure v4eventually v4occurs
,Clinical v 4 Manifestations v 4 of v 4 PKD Early v 4 signs:
*Flank v4pain
*Increased v4abdominal v4girth
*Abdominal v4distention v 4 (enlarged v 4 kidneys)
*Hematuria v4(cyst v4rupture)
*HTN
GI v4manifestation:
*Constipation
v 4 Why
v4 constipation?
Kidney v4failure v4-> v4fluid v4imbalance v4-> v4decreased v4fluid v4movement v4into v4intestines v4-
> v4stool v4hardening v4as v4well v4as v4increased v4pressure v4in v4abdomen v4which v4in v4turn
v4 pushes v4on v4other v4organs v4slowing v4movement v4of v4stool.
HTN v 4 in v 4 PKD Kidney v4damage v 4 -> v4decreased v 4 perfusion v 4 -> v 4RAAS v4activation
RAAS v 4 causes:
*Vasoconstriction
*Sodium v4retention
*Fluid v4retention
*Increased v 4 BP
HTN v4accelerates v4kidney v4destruciton
Lab v4findings v4for v4PKD *BUN v 4 (↑)
*Creatinine v4(↑)
*Ka+ v4(↑)
*Magnesium v4(↑)
*Phosphorus v 4 (↑)
*Calcium v4( v4goes v4down)
*Proteinuria v 4(glomerular v4destruction)
*GFR v4(goes v4down)
Why v4do v4electrolytes v4matter v4in v4PKD? Hyperkalemia v4-> v4peaked v4T v4waves v4-> v4Lethal v4dysrhythmias v4so v4we v4need v4to
v4 place v4these v4clients v4on v4telemetry
Imaging v4for v4PKD Best v 4 cost-effective v 4 diagnostic:
*Renal v4ultrasound
Also:
*Personal v4history v 4 (HTN)
*Family v4Hx
*Genetic v 4 testing
Blood v4pressure v4control v4for v4PKD First v 4 line:
*ACE v4inhibitor v4-> v4ex: v4lisinopril
If v4tolerant: v4ARB v4(angiotension v4receptor v4blockers) v4"losartan"
v4 why?
*blocks v4RAAS
*Protects v4nephrons
*Slows v4progression
, Pain v4management v4for v4PKD Flank v4pain v4from v4 cyst v4enlargement v4->
*Opioids v4(careful v4use)
*Avoid v 4NSAIDs v4(nephrotoxic)
importance v4of v4preventing v4constipation v 4in v 4 PKD *Movement
*High v 4 fiber v4diet
*Stool v4softeners
Slow v4progression v4of v4PKD v4and v4damage v4to v4the v4kidneys Avoid:
*HTN, v 4 Hypotension,
v 4 dehydration
what v4is v4the v4best v4indicator v4of v4Fluid v4status? DAILY v4WEIGHT
Same: v4Time, v 4 clothing, v 4 scale
Neurological v 4 risk v 4 for v 4 PKD v 4 clients Weaker v4cerebral v4blood v4vessels
*b/c v4of v4hypertension v4from v4RAAS
Risk:
*Stroke
*Cerrebral v4aneurysm v 4 rupture
*Hypertensive v4encephalopathy
Nurse v4must v4perform:
*Neurological v 4 assessments
*Monitor v4BP v4closely
Dietary v4Management v4of v4PKD Required v 4 restrictions:
*Fluid v4restriction
*Sodium v4restriction
*Potassium v4restriciton
*Phosphorous v4restriciton
Encourage:
*Fiber
*Wt. v4maintenance
*Smoking v4cessation
*Exercise
*Limit v4alcohol
Why v4weight v 4 matters:
*Overweight v4-> v4increased v4BP
*Underweight v 4 -> v 4 protein v 4 breakdown v 4 -> v 4 worsens v 4 kidney v4damage
What v4is v4Glomerulonephritis? Inflammation v4of v4the v4glomeruli
Most v4commonly v4caused v 4 by v4:
*Post- v4Group v4A v4beta-hemolytic v 4 strep v4infection
*Autoimmune v4disease v4(systemic v4lupus)
*Diabetic v4glomerulosclerosis
*Other v4immune-mediated v4processes
