Renal Alterations, Dialysis Modalities, and Biliary Disorders

Comprehensive flashcards covering pediatric nephrotic syndrome, acute kidney injury (AKI), chronic kidney disease (CKD), hemodialysis and peritoneal dialysis modalities, and biliary tract diseases (cholelithiasis and cholecystitis).

What autoimmune process is believed to trigger nephrotic syndrome, and in what timeframe does it occur?

Nephrotic syndrome is believed to be an autoimmune process occurring $4\text{--}8\text{ days}$ after a viral infection that increases glomerular permeability to protein, especially albumin.

What are the three primary classifications of nephrotic syndrome seen in pediatric care?

1. Primary disease (also termed "idiopathic nephrosis", "childhood nephrosis", or "minimal change nephrotic syndrome" [MCNS])
2. Secondary nephrotic syndrome (associated with systemic glomerular damage)
3. Congenital nephrotic syndrome (an autosomal recessive disorder)

According to this pathophysiologic cascade of nephrotic syndrome, what sequence leads from glomerular basement membrane injury to the development of generalized edema?

Renal glomerular damage causes massive proteinuria and hypoproteinemia, which decreases plasma oncotic pressure. This causes fluid shifts into the interstitial space (edema) and results in hypovolemia, triggering renin release, increased ADH and aldosterone secretion, and renal sodium/water reabsorption.

What are the four hallmark clinical manifestations of nephrotic syndrome?

1. Massive proteinuria
2. Edema
3. Hypoalbuminemia
4. Hypercholesterolemia (hyperlipidemia)

In a child with nephrotic syndrome, what does dark yellow, frothy urine indicate?

It indicates high urine concentration/dehydration combined with significant proteinuria.

What dietary modifications are ordered for a child hospitalized with minimal change nephrotic syndrome (MCNS) experiencing moderate to severe edema?

A $1\text{ g}$ sodium diet (no salt added) and strict fluid restriction.

What pharmacologic agents are key components of medical therapy for minimal change nephrotic syndrome (MCNS)?

Corticosteroids (Prednisone), immunosuppressants (for steroid-unresponsive cases), loop diuretics (Furosemide), and IV Albumin $25\%$.

Why is IV Albumin $25\%$ administered to a child with severe nephrotic syndrome, and what type of solution is it?

IV Albumin $25\%$ is a colloid and volume expander that increases intravascular oncotic pressure, drawing excess interstitial fluid back into the vascular space so that diuretics can promote its excretion.

Based on this anatomical diagram, what are the three etiologic categories of Acute Kidney Injury (AKI) and their primary mechanisms?

1. Prerenal: Factors that reduce systemic circulation and renal perfusion (e.g., severe hypovolemia, blood loss, sepsis, hypotension).
2. Intrarenal: Conditions that cause direct nephron damage and acute tubular necrosis (e.g., nephrotoxic drugs, ischemia, severe infection).
3. Postrenal: Mechanical obstruction of urinary outflow distal to the kidneys (e.g., prostatic hypertrophy, calculi).

What are the adult reference ranges for serum creatinine, BUN, and glomerular filtration rate (GFR)?

Serum Creatinine: $0.6\text{--}1.2\text{ mg/dL}$ Blood Urea Nitrogen (BUN): $10\text{--}20\text{ mg/dL}$ Normal GFR: Approximately $125\text{ mL/min}$

Which laboratory measurement serves as the best indicator of irreversible renal failure damage versus the best indicator of overall renal function?

Serum creatinine is the best indicator of renal failure (reflects irreversible damage), whereas $24\text{-hour}$ urine creatinine clearance is the best indicator of renal function (closely approximates GFR).

What are the four progressive phases of Acute Renal Failure / Acute Kidney Injury?

1. Initiating phase
2. Oliguric phase
3. Diuretic phase
4. Recovery phase

What defines the oliguric phase of Acute Kidney Injury regarding daily urine output and onset?

Urine output decreases to less than $400\text{ mL/day}$, typically developing within $1\text{--}7\text{ days}$ of the initial kidney injury.

Why does hypocalcemia occur during the oliguric phase of AKI, and what secondary endocrine response does it trigger?

The failing kidneys cannot activate vitamin D, impairing gastrointestinal calcium absorption. In response, the parathyroid glands secrete parathyroid hormone (PTH), causing bone demineralization that releases both calcium and phosphate into the bloodstream, worsening hyperphosphatemia.

What characterizes the diuretic phase of AKI, and what major clinical risks are present?

Daily urine output gradually increases to $1\text{--}3\text{ L/day}$ (and may exceed $3\text{--}5\text{ L/day}$) over $1\text{--}3\text{ weeks}$. Because nephrons are not yet fully functional, patients face high risks of hypovolemia, dehydration, hypotension, and persistent uremia.

What marks the beginning of the recovery phase in AKI, and how long can renal function take to stabilize?

It begins when the GFR increases, allowing BUN and serum creatinine levels to plateau and then decrease. Kidney function can take $3\text{--}12\text{ months}$ to fully stabilize.

What are the primary clinical indications for initiating Renal Replacement Therapy (dialysis) in Acute Kidney Injury?

Severe volume overload, refractory hyperkalemia, severe metabolic acidosis, BUN level $> 120\text{ mg/dL}$ ($43\text{ mmol/L}$), significant changes in mental status, or uremic pericarditis/pericardial effusion/cardiac tamponade.

Why are older adults at heightened risk for acute renal failure?

They possess a decreased number of functioning nephrons, an aging kidney less capable of compensating for fluid and electrolyte fluctuations, and a higher prevalence of comorbid conditions.

What is the priority nursing intervention when a patient's serum potassium level returns at $6.8\text{ mEq/L}$?

Immediately place the patient on a continuous cardiac monitor to detect and respond to potentially fatal dysrhythmias.

How is Chronic Kidney Disease (CKD) clinically defined?

A progressive, irreversible loss of kidney function manifested by kidney damage (markers in blood, urine, or imaging) or a Glomerular Filtration Rate (GFR) $< 60\text{ mL/min/1.73m}^2$ persisting for $3\text{ months}$ or longer.

What are the two leading causes of Chronic Kidney Disease in adults?

Diabetes mellitus ($50\%$) and hypertension ($25\%$).

How is uremia distinguished from oliguria and anuria in chronic renal disease?

Uremia is a systemic syndrome of multiorgan dysfunction due to waste retention (typically when GFR is $\le 15\text{ mL/min}$); oliguria is a daily urine output of $300\text{--}500\text{ mL/day}$; anuria is a daily output of less than $40\text{ mL/day}$.

At what GFR threshold is End-Stage Renal Disease (ESRD) diagnosed, necessitating renal replacement therapy?

ESRD occurs when the GFR drops to $< 15\text{ mL/min}$, indicating that conservative management is no longer sufficient and dialysis or transplantation is required.

Why might a diabetic patient who develops uremic CKD require less exogenous insulin than before the onset of renal disease?

Because insulin excretion depends on functioning kidneys; diminished renal clearance causes insulin to remain active in circulation longer.

What causes severe pruritus and "uremic frost" in patients with advanced Chronic Kidney Disease?

Pruritus results from dry skin, sensory neuropathy, and calcium-phosphate crystals depositing in the skin; uremic frost occurs when extremely high concentrations of urea crystallize on the skin surface upon sweat evaporation.

What are the recommended dietary limits for sodium, potassium, and phosphate in conservative CKD management?

Sodium: Restricted to $2\text{--}4\text{ g/day}$ Potassium: Restricted to $2\text{--}3\text{ g/day}$ Phosphate: Restricted to $1000\text{ mg/day}$ (limiting dairy intake)

Based on this diagram of dialysis transport principles, what defines diffusion, osmosis, and ultrafiltration?

1. Diffusion: Movement of solutes down a concentration gradient from an area of higher concentration to lower concentration.
2. Osmosis: Movement of fluid across a semipermeable membrane toward an area of higher solute concentration.
3. Ultrafiltration: Water and waste removal driven across a semipermeable membrane by an osmotic or hydrostatic pressure gradient.

What catheter is surgically placed through the anterior abdominal wall to provide long-term access for peritoneal dialysis?

A Tenckhoff catheter, which accesses the peritoneal cavity through the anterior abdominal wall.

What are the three sequential steps of a peritoneal dialysis exchange, and what are their typical time parameters?

1. Inflow (fill): Infusing the prescribed dialysate volume over approximately $10\text{ minutes}$, then clamping the line.
2. Dwell: Allowing solutes and fluid to equilibrate across the peritoneal membrane; duration varies by protocol.
3. Drain: Draining the effluent over $15\text{--}30\text{ minutes}$, which should yield more fluid than was infused and appear clear-yellow.

What glucose concentrations are standardly available in peritoneal dialysis solutions, and how do they alter fluid removal?

Solutions are available in $1.5\%$, $2.5\%$, and $4.25\%$ glucose concentrations; higher glucose percentages create higher osmotic gradients that draw greater volumes of fluid out of the vasculature.

How does Automated Peritoneal Dialysis (APD) differ mechanically from Continuous Ambulatory Peritoneal Dialysis (CAPD)?

APD utilizes an automated automated cycler machine to program and execute fill, dwell, and drain phases (often while the patient sleeps), whereas CAPD relies on manual exchanges performed several times throughout the day.

What distinguishes an arteriovenous (AV) fistula from an AV graft as shown in diagrams A and B?

Diagram A shows an AV fistula, created by directly anastomosing a native artery to a vein (e.g., radial artery to basilic vein), allowing arterial pressure to dilate and toughen the vein over several weeks. Diagram B shows an AV graft, which uses a synthetic looped tube implanted under the skin to connect an artery and a vein.

What essential physical assessment findings confirm the patency of an active arteriovenous (AV) fistula?

Palpating a continuous vibration (thrill) over the vascular access and auscultating a rushing sound (bruit) with a stethoscope.

What nursing precautions are required for an extremity with a hemodialysis AV fistula or graft?

Never perform blood pressure measurements, venipunctures, or IV line placements on that arm; post warning signs in the room and place an alert wristband on the affected extremity.

Why do central venous temporary hemodialysis catheters require special handling by trained dialysis nurses?

These double-lumen central venous catheters (internal jugular or femoral) are locked with highly concentrated heparin to prevent thrombosis, which must be completely aspirated and discarded before accessing the lumen for dialysis.

What are the common causes of hypotension and muscle cramps during hemodialysis sessions?

Hypotension results from rapid intravascular volume depletion, reduced cardiac output, and lowered peripheral vascular resistance; muscle cramps stem from rapid ultrafiltration rates, hypovolemia, hypotension, and low-sodium dialysate.

How do cholelithiasis and cholecystitis differ in pathophysiology?

Cholelithiasis refers to the presence or formation of gallstones in the gallbladder; cholecystitis refers to inflammation of the gallbladder wall, most commonly triggered by obstruction from gallstones or biliary sludge.

What hallmark clinical manifestations and physical findings characterize acute cholecystitis?

Fever, leukocytosis, right upper quadrant (RUQ) tenderness or abdominal rigidity, and severe biliary colic that radiates to the right shoulder or back, often intensifying $3\text{--}6\text{ hours}$ after consuming a high-fat meal or when lying down.

What clinical signs indicate total obstruction of the common bile duct by gallstones?

Jaundice, dark amber urine, clay-colored stools, steatorrhea (fatty stools), pruritus, bleeding tendencies, and marked intolerance to dietary fats.

What is the purpose of placing a T-tube into the common bile duct following an open (incisional) cholecystectomy?

The T-tube maintains patency of the common bile duct and allows excess bile to drain externally until postoperative ductal edema subsides.

How does postoperative dietary progression differ between a laparoscopic cholecystectomy and an open incisional cholecystectomy?

After laparoscopic surgery, patients consume liquids on day $1$ and advance to light meals over several days; after open surgery, patients advance from liquids to regular food only after bowel sounds return and must restrict dietary fats for $4\text{--}6\text{ weeks}$.