Free CDN Exam Flashcards

Stage 3a: GFR 45-59 mL/min/1.73 m²; Stage 3b: GFR 30-44; Stage 4: GFR 15-29 (severe reduction); Stage 5: GFR below 15 or on dialysis (kidney failure). Staging guides planning for renal replacement therapy and complication management.

Prerenal AKI: low urine sodium, FENa under 1%, responds to volume. Acute tubular necrosis: muddy brown casts, FENa over 2%. Postrenal AKI: obstruction history, hydronephrosis on imaging, may have fluctuating output. Nursing priority is identifying reversible causes quickly.

Heavy proteinuria (typically over 3.5 g/24 h), hypoalbuminemia, generalized edema, and hyperlipidemia. Results from increased glomerular permeability. Nurses monitor fluid balance, infection risk, and thrombosis risk from urinary protein loss.

Hematuria with dysmorphic red cells and red-cell casts, hypertension, oliguria, and variable proteinuria (usually not nephrotic-range). Reflects glomerular inflammation. Differs from nephrotic syndrome, which features massive protein loss with relatively little hematuria.

Failing kidneys excrete phosphorus poorly and cannot activate vitamin D to calcitriol. Hyperphosphatemia and hypocalcemia stimulate parathyroid hormone, causing bone resorption and vascular calcification. Diet, binders, and vitamin D analogs are core management tools.

Erythropoietin is made by peritubular interstitial cells in the renal cortex. Nephron loss reduces EPO production, causing normocytic anemia. Treatment includes iron repletion and erythropoiesis-stimulating agents when indicated, with blood pressure and hemoglobin targets monitored.

Peaked T waves appear first, then PR prolongation, QRS widening, and loss of P waves — progressing toward ventricular fibrillation. IV calcium gluconate or calcium chloride stabilizes the myocardial membrane immediately while definitive lowering therapy is prepared.

Asterixis, confusion or encephalopathy, pericarditis, intractable nausea or vomiting, refractory hyperkalemia, pulmonary edema unresponsive to diuretics, and severe metabolic acidosis. These are clinical indications for emergent renal replacement therapy beyond routine outpatient scheduling.

A1 normal to mildly increased: under 30 mg/g. A2 moderately increased: 30-300 mg/g. A3 severely increased: over 300 mg/g. Higher categories predict faster CKD progression and cardiovascular risk; repeat testing confirms persistence.

Retention of organic acids produces a normal anion-gap or elevated anion-gap metabolic acidosis depending on cause. Lungs compensate with Kussmaul respirations (deep, rapid breathing). Severe acidosis contributes to muscle wasting, bone disease, and hyperkalemia.

Use lowest effective contrast volume, avoid nephrotoxic combinations when possible, and ensure periprocedural hydration per protocol. Hold metformin around contrast when eGFR is reduced. Monitor creatinine after exposure; at-risk patients include CKD, diabetes, and dehydration.

Angiotensin II normally constricts the efferent arteriole to maintain glomerular filtration pressure. Blocking that mechanism with bilateral stenosis can precipitate acute kidney injury. Report acute creatinine rise after starting these drugs.

Overload: hypertension, pulmonary crackles, jugular distension, edema, weight gain above dry weight. Hypovolemia: hypotension, tachycardia, poor access flow, cramps, dizziness. Accurate pre-dialysis weight compared to dry weight guides ultrafiltration goals.

Moderate protein restriction may be recommended to reduce uremic toxin production while maintaining adequate nutrition. Phosphorus restriction and binder timing with meals limit CKD-MBD. Dietitian collaboration is essential; malnutrition worsens outcomes.

Solutes move down a concentration gradient from blood across the semipermeable membrane into dialysate. Countercurrent dialysate flow maintains the gradient along the fiber length. Small molecules such as urea and potassium clear faster than larger ones.

Hydrostatic pressure across the membrane exceeds oncotic pressure, forcing plasma water out of blood while solutes remain. The ultrafiltration rate (mL/h) multiplied by treatment time equals fluid removed. Excessive UF rate risks hypotension and cramping.

Kt/V quantifies dialysis dose: clearance (K) times treatment time (t) divided by urea distribution volume (V). A single-pool Kt/V of at least 1.2 per session (or equivalent URR) is a common adequacy benchmark for thrice-weekly in-center hemodialysis.

URR compares pre- and post-dialysis BUN: (pre minus post) divided by pre, times 100. A URR of at least 65% is widely used as an adequacy threshold for conventional hemodialysis schedules. Low URR signals insufficient clearance or shortened treatments.

Native arteriovenous fistula (AVF) is preferred: lowest infection and thrombosis rates, longest patency, and lowest long-term cost. Requires maturation (often 6-12 weeks) before cannulation. Plan access well before anticipated dialysis start.

AV graft uses synthetic conduit; cannulation possible sooner than fistula but higher thrombosis and infection risk than AVF. Tunneled cuffed catheter is for temporary or bridge access — highest infection and central stenosis risk; avoid as permanent access when possible.

Distal hand ischemia from diversion of arterial flow into the access: pain, numbness, cool pale fingers, weak pulse distally. May require surgical revision. Assess neurovascular status before and after access creation and during dialysis.

Rotate needle sites along the access length to allow aneurysm-free healing and preserve access life. Avoid repeated puncture in one spot (area cannulation) except in buttonhole programs with strict sterile technique. Document sites each treatment.

Prevents circuit clotting; dose individualized by weight and bleeding risk. Monitor for access site bleeding post-treatment. Heparin is contraindicated or reduced with active bleeding; protamine sulfate reverses heparin in overdose emergencies.

Causes include excessive ultrafiltration, rapid UF rate, eating during dialysis, cardiac dysfunction, and antihypertensive timing. Interventions: Trendelenburg, reduce UF, saline bolus per protocol, lower blood pump speed, and reassess dry weight.

Often related to rapid fluid removal, sodium shifts, or hypovolemia. Slow UF rate, adjust sodium profiling, and give normal saline per protocol. Review dry weight and dietary sodium intake. Cramps may signal excessive fluid gain between sessions.

Occurs when urea is cleared faster than the brain equilibrates, causing cerebral edema. Highest risk in first treatments or very high pre-dialysis BUN. Symptoms: headache, nausea, restlessness, seizures, decreased consciousness. Prevention includes shorter initial treatments.

Sudden dyspnea, chest pain, hypotension, altered mental status, or cardiac arrest. Clamp blood lines, place patient on left side with head down, administer oxygen, and notify provider immediately. Prevention: prime lines completely and secure connections.

The post-dialysis weight below which the patient develops hypotension or cramps without overt edema. It changes with nutrition status and cardiac function. Accurate dry weight is the foundation for setting ultrafiltration goals each session.

Many protocols limit UF rate to about 10-13 mL/kg/hour to reduce hypotension and cardiac stress. Higher rates increase cramping and intradialytic events. Interdialytic weight gain control through fluid and sodium counseling reduces required UF.

Varies dialysate sodium during treatment to reduce osmotic shifts that cause cramps and hypotension while still achieving fluid removal goals. Individualized profiles balance comfort against interdialytic thirst and weight gain.

RO removes dissolved ions, bacteria, and endotoxins from feed water. Dialysis water must meet AAMI/ISO purity standards because impurities cross into blood. Daily chlorine/chloramine testing and bacterial cultures per facility policy are mandatory.

Chloramine can pass carbon prefilters and cause hemolytic anemia in patients if not removed. Total chlorine testing before each shift confirms removal. Standard chlorine alone is easier to eliminate; chloramine requires specific treatment design.

Typically contains sodium, potassium, calcium, magnesium, bicarbonate (or acetate precursor), and glucose optional. Potassium bath of 0-4 mEq/L is matched to serum K and arrhythmia risk. Bicarbonate corrects metabolic acidosis during treatment.

Optical sensor detects blood in effluent dialysate line, indicating membrane rupture or disconnect. Machine stops blood pump automatically. Do not bypass without investigating; patient blood loss can be rapid.

Needle dislodgement, kinked venous line, clot in drip chamber or fiber, or stenosis in outflow tract. Inspect access and tubing immediately. High venous pressure can indicate impending access failure.

Access recirculation, needle against vessel wall, suction from blood pump too high, or line kink on arterial side. May reduce clearance and damage access. Reposition needles or reduce pump speed per protocol.

Treated blood returns to arterial needle without full circuit transit, lowering effective clearance. Suspected with poor Kt/V despite adequate time, high access flows, or reversed lines. Access imaging or dilution studies confirm.

Type A (anaphylactic): within minutes — chest pain, dyspnea, hypotension; often ethylene oxide or membrane sensitizer. Type B (complement-mediated): back pain, chest pain, often 15-30 minutes in; may resolve with continued treatment. Stop blood flow for severe Type A.

All susceptible patients and staff should complete HBV vaccination series. HBsAg-positive patients dialyze in dedicated room or station with dedicated equipment per CDC guidelines. Serologic surveillance guides station assignments.

Exit-site: erythema, drainage at skin exit — often topical or oral antibiotics. Tunnel infection: tenderness along subcutaneous tract, may have drainage; higher risk of bacteremia and often requires catheter removal plus systemic antibiotics.

CAPD uses manual bag exchanges throughout the day without a machine. APD (automated peritoneal dialysis) runs cycles overnight with a cycler. Both use the peritoneal membrane as the filter; choice depends on lifestyle, ultrafiltration needs, and residual kidney function.

New catheters need healing time before full-volume exchanges (often 2 weeks per surgeon protocol) to reduce leaks and infection. Low-volume dwells may start earlier. Train patients on sterile connection technique before independent exchanges.

Cloudy dialysate with abdominal pain and fever suggests peritonitis. Send effluent for cell count, Gram stain, and culture before broad antibiotics per protocol. Do not routinely remove catheter unless refractory or fungal infection.

Membrane transport changes reduce fluid removal, causing volume overload and possible modality failure. May require increased hypertonic dwells temporarily or transition to hemodialysis. Monitor daily weights and blood pressure closely.

Longer dwells improve small-solute clearance early but may reduce ultrafiltration as osmotic gradient dissipates. Prescription balances exchanges per day, dwell duration, and glucose concentration to meet adequacy (Kt/V or PET results).

Classifies membrane transport as low, low-average, high-average, or high transporter. High transporters clear small solutes quickly but may need shorter dwells; low transporters may need longer dwells. Guides individualized PD prescription.

Increased intra-abdominal pressure from dialysate volume raises inguinal and umbilical hernia risk. Avoid heavy lifting, treat constipation, and report bulges or pain. Surgical repair may be needed before continuing PD safely.

Hypertonic dextrose creates osmotic gradient pulling fluid into peritoneal cavity. Higher concentrations remove more fluid but accelerate membrane changes and metabolic load. Icodextrin solutions provide sustained ultrafiltration for long dwells.

Watch rising creatinine, decreased urine output, fever, graft tenderness, and hypertension. Biopsy confirms rejection type. Immunosuppressant levels and adherence are critical; teach patients never to stop medications without transplant team approval.

Continuous renal replacement therapy runs 24 hours with gentler fluid and solute shifts — preferred in hemodynamically unstable ICU patients. Conventional HD is intermittent with higher UF rates. Nursing monitors anticoagulation, filter clotting, and fluid balance hourly on CRRT.