Adult Health II Exam 2 2026||with Expertly detailed solutions||Guaranteed
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Terms in this set (222)
What is Polycystic Kidney Disease (PKD) A genetic (autosomal dominant) disorder characterized by:
*Multiple fluid-filled cysts in kidneys
*Progressive nephron destruction
*Enarged kidneys
*Eventual renal failure
IT is progressive and incurable
Why does PKD cause hypertension As cysts grow, they increase renal volume, press on adjacent arteries,
and cause chronic ischemia
The kidney responds by releasing renin, a hormoen that initiates a
cascade (angiotensin II) to tighten vessels, leading to high blood
pressure
What happens in the kidney with PKD? 1. Cysts grow
2. Nephrons are compressed and destroyed
3. Kidney function declines
4. GFR decreases
5. Waste products accumulate
6. RAAS activtes
7. HTN develops
8. Kidney failure eventually occurs
,Clinical Manifestations of PKD Early signs:
*Flank pain
*Increased abdominal girth
*Abdominal distention (enlarged kidneys)
*Hematuria (cyst rupture)
*HTN
GI manifestation:
*Constipation
Why
constipation?
Kidney failure -> fluid imbalance -> decreased fluid movement into intestines -
> stool hardening as well as increased pressure in abdomen which in turn
pushes on other organs slowing movement of stool.
HTN in PKD Kidney damage -> decreased perfusion -> RAAS activation
RAAS causes:
*Vasoconstriction
*Sodium retention
*Fluid retention
*Increased BP
HTN accelerates kidney destruciton
Lab findings for PKD *BUN (↑)
*Creatinine (↑)
*Ka+ (↑)
*Magnesium (↑)
*Phosphorus (↑)
*Calcium ( goes down)
*Proteinuria (glomerular destruction)
*GFR (goes down)
Why do electrolytes matter in PKD? Hyperkalemia -> peaked T waves -> Lethal dysrhythmias so we need to
place these clients on telemetry
Imaging for PKD Best cost-effective diagnostic:
*Renal ultrasound
Also:
*Personal history (HTN)
*Family Hx
*Genetic testing
Blood pressure control for PKD First line:
*ACE inhibitor -> ex: lisinopril
If tolerant: ARB (angiotension receptor blockers) "losartan"
why?
*blocks RAAS
*Protects nephrons
*Slows progression
, Pain management for PKD Flank pain from cyst enlargement ->
*Opioids (careful use)
*Avoid NSAIDs (nephrotoxic)
importance of preventing constipation in PKD *Movement
*High fiber diet
*Stool softeners
Slow progression of PKD and damage to the kidneys Avoid:
*HTN, Hypotension,
dehydration
what is the best indicator of Fluid status? DAILY WEIGHT
Same: Time, clothing, scale
Neurological risk for PKD clients Weaker cerebral blood vessels
*b/c of hypertension from RAAS
Risk:
*Stroke
*Cerrebral aneurysm rupture
*Hypertensive encephalopathy
Nurse must perform:
*Neurological assessments
*Monitor BP closely
Dietary Management of PKD Required restrictions:
*Fluid restriction
*Sodium restriction
*Potassium restriciton
*Phosphorous restriciton
Encourage:
*Fiber
*Wt. maintenance
*Smoking cessation
*Exercise
*Limit alcohol
Why weight matters:
*Overweight -> increased BP
*Underweight -> protein breakdown -> worsens kidney damage
What is Glomerulonephritis? Inflammation of the glomeruli
Most commonly caused by :
*Post- Group A beta-hemolytic strep infection
*Autoimmune disease (systemic lupus)
*Diabetic glomerulosclerosis
*Other immune-mediated processes
success |A+ solution
Terms in this set (222)
What is Polycystic Kidney Disease (PKD) A genetic (autosomal dominant) disorder characterized by:
*Multiple fluid-filled cysts in kidneys
*Progressive nephron destruction
*Enarged kidneys
*Eventual renal failure
IT is progressive and incurable
Why does PKD cause hypertension As cysts grow, they increase renal volume, press on adjacent arteries,
and cause chronic ischemia
The kidney responds by releasing renin, a hormoen that initiates a
cascade (angiotensin II) to tighten vessels, leading to high blood
pressure
What happens in the kidney with PKD? 1. Cysts grow
2. Nephrons are compressed and destroyed
3. Kidney function declines
4. GFR decreases
5. Waste products accumulate
6. RAAS activtes
7. HTN develops
8. Kidney failure eventually occurs
,Clinical Manifestations of PKD Early signs:
*Flank pain
*Increased abdominal girth
*Abdominal distention (enlarged kidneys)
*Hematuria (cyst rupture)
*HTN
GI manifestation:
*Constipation
Why
constipation?
Kidney failure -> fluid imbalance -> decreased fluid movement into intestines -
> stool hardening as well as increased pressure in abdomen which in turn
pushes on other organs slowing movement of stool.
HTN in PKD Kidney damage -> decreased perfusion -> RAAS activation
RAAS causes:
*Vasoconstriction
*Sodium retention
*Fluid retention
*Increased BP
HTN accelerates kidney destruciton
Lab findings for PKD *BUN (↑)
*Creatinine (↑)
*Ka+ (↑)
*Magnesium (↑)
*Phosphorus (↑)
*Calcium ( goes down)
*Proteinuria (glomerular destruction)
*GFR (goes down)
Why do electrolytes matter in PKD? Hyperkalemia -> peaked T waves -> Lethal dysrhythmias so we need to
place these clients on telemetry
Imaging for PKD Best cost-effective diagnostic:
*Renal ultrasound
Also:
*Personal history (HTN)
*Family Hx
*Genetic testing
Blood pressure control for PKD First line:
*ACE inhibitor -> ex: lisinopril
If tolerant: ARB (angiotension receptor blockers) "losartan"
why?
*blocks RAAS
*Protects nephrons
*Slows progression
, Pain management for PKD Flank pain from cyst enlargement ->
*Opioids (careful use)
*Avoid NSAIDs (nephrotoxic)
importance of preventing constipation in PKD *Movement
*High fiber diet
*Stool softeners
Slow progression of PKD and damage to the kidneys Avoid:
*HTN, Hypotension,
dehydration
what is the best indicator of Fluid status? DAILY WEIGHT
Same: Time, clothing, scale
Neurological risk for PKD clients Weaker cerebral blood vessels
*b/c of hypertension from RAAS
Risk:
*Stroke
*Cerrebral aneurysm rupture
*Hypertensive encephalopathy
Nurse must perform:
*Neurological assessments
*Monitor BP closely
Dietary Management of PKD Required restrictions:
*Fluid restriction
*Sodium restriction
*Potassium restriciton
*Phosphorous restriciton
Encourage:
*Fiber
*Wt. maintenance
*Smoking cessation
*Exercise
*Limit alcohol
Why weight matters:
*Overweight -> increased BP
*Underweight -> protein breakdown -> worsens kidney damage
What is Glomerulonephritis? Inflammation of the glomeruli
Most commonly caused by :
*Post- Group A beta-hemolytic strep infection
*Autoimmune disease (systemic lupus)
*Diabetic glomerulosclerosis
*Other immune-mediated processes
