NLE Renal & Urinary Nursing — Acute & Chronic Kidney DiseaseExam Answer Templates

Marks

1

Topic

Acute Kidney Injury (AKI) — Oliguric Phase

Difficulty

easy

Template Id

T1

Examiner Tip

Examiners specifically want 'hyperkalemia' as the answer — NOT 'electrolyte imbalance' or 'metabolic acidosis.' Always specify the exact electrolyte and the cardiac consequence to show clinical understanding.

Model Answer

The most immediate life-threatening complication of the oliguric phase of AKI is HYPERKALEMIA (elevated serum potassium), which can cause fatal cardiac arrhythmias.

Question Type

very_short_answer

Answer Structure

• Line 1: Name the complication correctly — Hyperkalemia [0.5 mark]
• Line 2: State the reason it is life-threatening — fatal cardiac arrhythmias [0.5 mark]

Scoring Breakdown

Common Mark Deductions

• Writing 'fluid overload' alone — while dangerous, hyperkalemia causes more immediate death (arrhythmia) and is the #1 NLE answer.
• Writing only 'electrolyte imbalance' without specifying hyperkalemia — too vague for full marks.
• Confusing the oliguric phase (hyperkalemia) with the diuretic phase (hypokalemia).

Key Phrases To Include

• hyperkalemia
• oliguric phase
• fatal cardiac arrhythmias
• serum potassium
• peaked T waves

Marks

1

Topic

AKI — Prerenal Causes and Diagnostics

Difficulty

easy

Template Id

T2

Examiner Tip

Remember: PreREnal = HIGH BUN:Cr ratio (>20:1) because the kidney is holding on to water and urea. IntraREnal = normal ratio (~10:1) because the tubules are damaged and cannot reabsorb urea.

Model Answer

In prerenal AKI, the BUN:creatinine ratio is greater than 20:1. This is significant because it indicates that decreased renal perfusion (not kidney tissue damage) is the cause — urea is reabsorbed more than creatinine when flow is reduced.

Question Type

very_short_answer

Answer Structure

• Line 1: State the ratio — greater than 20:1 [0.5 mark]
• Line 2: State its significance — indicates decreased perfusion, not intrinsic damage [0.5 mark]

Scoring Breakdown

Common Mark Deductions

• Stating the ratio as 'less than 20:1' — this is the intrarenal pattern.
• Not explaining what the ratio tells us clinically.
• Confusing BUN and creatinine values with GFR.

Key Phrases To Include

• BUN:creatinine ratio
• greater than 20:1
• prerenal
• decreased renal perfusion
• intact kidney tissue

Marks

2

Topic

Chronic Kidney Disease (CKD) — Definition and Staging

Difficulty

easy

Template Id

T3

Examiner Tip

The two words that separate CKD from AKI in any definition are 'progressive' and 'irreversible.' If you omit either word, you risk losing the definition mark. Always pair the GFR value with the Stage number.

Model Answer

Chronic Kidney Disease (CKD) is a progressive, IRREVERSIBLE loss of nephron function over months to years, staged by the Glomerular Filtration Rate (GFR). The top two causes are diabetes mellitus and hypertension. End-Stage Renal Disease (ESRD) corresponds to CKD Stage 5, defined by a GFR of less than 15 mL/min, at which point renal replacement therapy (dialysis or transplant) is required.

Question Type

very_short_answer

Answer Structure

• Line 1: Define CKD — progressive, irreversible loss of nephron function [1 mark]
• Line 2: State ESRD GFR — less than 15 mL/min (Stage 5) [1 mark]

Scoring Breakdown

Common Mark Deductions

• Writing 'CKD is kidney failure' without the key terms 'progressive' and 'irreversible' — loses definition mark.
• Stating ESRD GFR as 'less than 30' (which is Stage 3b) or 'less than 60' (Stage 3a).
• Not mentioning that renal replacement therapy is needed at ESRD.

Key Phrases To Include

• progressive
• irreversible
• Glomerular Filtration Rate (GFR)
• less than 15 mL/min
• Stage 5
• ESRD
• diabetes mellitus
• hypertension
• renal replacement therapy

Marks

2

Topic

Hemodialysis — AV Fistula Care

Difficulty

easy

Template Id

T4

Examiner Tip

Remember the pair: THRILL = felt (palpation); BRUIT = heard (auscultation). Both assess patency of the AV fistula. Absence of EITHER is an emergency — the fistula may be clotted.

Model Answer

Priority nursing assessments for a patient with an AV fistula include: 1. Palpate the access site for a THRILL (a buzzing vibration) to assess patency — absence of thrill indicates possible clotting and must be reported immediately. 2. Auscultate the access site with a stethoscope for a BRUIT (a swooshing sound) to confirm blood flow — absence of bruit also indicates clotting.

Question Type

short_answer

Answer Structure

• Point 1: Palpate for THRILL — name the assessment + state normal finding + state what absence means [1 mark]
• Point 2: Auscultate for BRUIT — name the assessment + state normal finding + state what absence means [1 mark]

Scoring Breakdown

Common Mark Deductions

• Writing 'check for swelling' or 'assess for infection' — these are important but NOT the priority patency assessments.
• Listing 'thrill and bruit' without explaining what they indicate — incomplete answers lose partial marks.
• Confusing thrill (palpated) with bruit (auscultated).

Key Phrases To Include

• thrill
• bruit
• palpate
• auscultate
• patency
• AV fistula
• clotting
• report immediately

Marks

2

Topic

CKD Pharmacology — Phosphate Binders

Difficulty

medium

Template Id

T5

Examiner Tip

A common NLE trap is confusing the timing of phosphate binders (WITH meals) with other CKD medications. If you remember 'the binder needs to MEET the food in the gut,' the timing will always be correct.

Model Answer

Phosphate binders are given WITH meals because they need to be present in the gastrointestinal tract at the same time as food. When food containing phosphate enters the GI tract, the binder physically binds to the dietary phosphate and prevents its absorption into the bloodstream. This reduces serum phosphate levels and helps prevent hyperphosphatemia and related complications such as hypocalcemia and renal osteodystrophy. Example: Calcium carbonate (Titralac) is a commonly used phosphate binder in CKD patients.

Question Type

short_answer

Answer Structure

• Sentence 1: State WHY timing with meals is essential — must be present in the GI tract with dietary phosphate [1 mark]
• Sentence 2: Name one phosphate binder correctly [1 mark]

Scoring Breakdown

Common Mark Deductions

• Saying 'take on an empty stomach' or 'take before meals' — this is the opposite of the correct instruction and is a dangerous error.
• Listing an antacid or vitamin D analog as a phosphate binder — e.g., calcitriol is NOT a phosphate binder.
• Explaining the action without mentioning the GI/meal timing rationale.

Key Phrases To Include

• with meals
• bind dietary phosphate
• GI tract
• prevent absorption
• hyperphosphatemia
• calcium carbonate
• sevelamer
• renal osteodystrophy

Marks

2

Topic

Peritoneal Dialysis — Complications

Difficulty

medium

Template Id

T6

Examiner Tip

For ANY peritoneal dialysis question about an abnormal finding, the answer almost always involves peritonitis as the complication and 'report immediately + strict asepsis' as the nursing response. Memorize this pair.

Model Answer

Cloudy outflow (turbid drained dialysate) in peritoneal dialysis is a SIGNIFICANT finding because it indicates PERITONITIS — infection of the peritoneal cavity. This is the most serious and most common complication of peritoneal dialysis. Normal drained dialysate should be clear and pale yellow. Priority nursing action: Report the finding IMMEDIATELY to the physician, document the time and appearance of the drainage, assess the patient for associated signs of peritonitis (fever, abdominal pain, rebound tenderness), and obtain a specimen of the dialysate for culture and sensitivity as ordered. Maintain strict aseptic technique throughout.

Question Type

short_answer

Answer Structure

• Sentence 1: State significance — cloudy outflow = peritonitis, the most serious complication [1 mark]
• Sentence 2: State priority nursing action — report immediately, assess for fever/abdominal pain, send culture [1 mark]

Scoring Breakdown

Common Mark Deductions

• Writing 'adjust the dialysate temperature' — this does not address cloudy outflow.
• Identifying peritonitis but failing to state the priority nursing action.
• Writing 'monitor' without specifying what to report or do.

Key Phrases To Include

• cloudy outflow
• peritonitis
• most serious complication
• report immediately
• fever and abdominal pain
• culture and sensitivity
• strict aseptic technique
• pale yellow and clear

Marks

3

Topic

AKI — Four Phases

Difficulty

medium

Template Id

T7

Examiner Tip

The NLE loves to test whether students know that OLIGURIC = dangerous (hyperkalemia) while DIURETIC = deceptively dangerous in the OPPOSITE direction (hypokalemia, dehydration). These two phases are frequently the trap in AKI MCQs.

Model Answer

The four phases of Acute Kidney Injury (AKI) are: 1. ONSET (Initiating) Phase: Begins from the time of the insult (e.g., nephrotoxin exposure, hemorrhage) until signs of renal dysfunction appear. Nursing concern: identify and eliminate the causative factor early to prevent progression. 2. OLIGURIC Phase: Urine output falls to LESS THAN 400 mL/day, lasting approximately 1–3 weeks. This is the MOST DANGEROUS phase. Nursing concerns: monitor for HYPERKALEMIA (peaked T waves on ECG), fluid overload (edema, hypertension, crackles), and metabolic acidosis (low bicarbonate, Kussmaul breathing). Strict intake and output monitoring and daily weights are essential. 3. DIURETIC Phase: Tubules begin to recover, and urine output increases dramatically (up to 3–5 liters/day). However, tubules cannot yet concentrate urine. Nursing concerns: risk of DEHYDRATION, HYPOKALEMIA, and HYPONATREMIA — monitor for fluid and electrolyte LOSS. 4. RECOVERY (Convalescent) Phase: Gradual return of renal function over weeks to months. Some permanent deficit may remain. Nursing concern: monitor GFR and educate the patient about prevention of further renal injury.

Question Type

short_answer

Answer Structure

• Phase 1: Name the phase (Onset) + key nursing concern [0.5 mark]
• Phase 2: Name the phase (Oliguric) + state <400 mL/day + identify hyperkalemia and fluid overload [1 mark]
• Phase 3: Name the phase (Diuretic) + state high urine output + identify hypokalemia/dehydration risk [1 mark]
• Phase 4: Name the phase (Recovery) + key nursing concern [0.5 mark]

Scoring Breakdown

Common Mark Deductions

• Confusing the oliguric and diuretic phases — this is the most common error; stating 'hypokalemia' in the oliguric phase or 'hyperkalemia' in the diuretic phase.
• Omitting the onset or recovery phase entirely.
• Not providing a nursing concern for each phase — the question asks for BOTH the phase AND the concern.

Key Phrases To Include

• onset
• oliguric
• less than 400 mL/day
• most dangerous
• hyperkalemia
• diuretic
• hypokalemia
• dehydration
• recovery
• metabolic acidosis
• fluid overload

Marks

3

Topic

CKD — Anemia and Erythropoietin

Difficulty

medium

Template Id

T8

Examiner Tip

The keyword examiners look for in CKD anemia pathophysiology is 'erythropoietin.' You must establish the cause-and-effect chain: nephron damage → reduced EPO → reduced RBC production → anemia. Without this chain, you cannot earn full pathophysiology marks.

Model Answer

Pathophysiology of Anemia in CKD: The kidneys are responsible for producing ERYTHROPOIETIN, a hormone that stimulates the bone marrow to produce red blood cells (RBCs). In CKD, progressive nephron destruction reduces erythropoietin production. Without adequate erythropoietin, the bone marrow cannot produce sufficient RBCs, leading to NORMOCYTIC, NORMOCHROMIC ANEMIA. Additionally, uremia impairs platelet function, causing a bleeding tendency that worsens anemia. Nursing Management: 1. Administer ERYTHROPOIETIN-STIMULATING AGENTS (ESAs) such as epoetin alfa (Eprex) as ordered, typically subcutaneously, to stimulate RBC production. 2. Administer supplemental IRON therapy (oral or IV iron) as ordered, since adequate iron stores are needed for ESAs to be effective. 3. Monitor hemoglobin and hematocrit levels regularly to evaluate treatment response. 4. Assess for signs of severe anemia: fatigue, pallor, dyspnea, tachycardia, and dizziness. 5. Provide rest periods and prioritize energy conservation activities. 6. Educate the patient to report worsening fatigue or shortness of breath.

Question Type

short_answer

Answer Structure

• Paragraph 1: Pathophysiology — state kidneys produce erythropoietin; nephron loss reduces EPO; bone marrow cannot produce enough RBCs [1.5 marks]
• Paragraph 2: Nursing management — ESAs (epoetin alfa), iron supplementation, monitoring Hgb/Hct, activity management [1.5 marks]

Scoring Breakdown

Common Mark Deductions

• Stating 'CKD causes anemia' without explaining the erythropoietin mechanism — earns zero for the pathophysiology portion.
• Writing only drug names without explaining the nursing monitoring responsibilities.
• Confusing CKD anemia (EPO deficiency) with iron-deficiency anemia without mentioning the renal EPO connection.

Key Phrases To Include

• erythropoietin
• EPO production reduced
• bone marrow
• erythropoietin-stimulating agent
• epoetin alfa
• iron supplementation
• normocytic normochromic anemia
• hemoglobin and hematocrit
• fatigue and pallor

Marks

3

Topic

AKI — Classification by Cause

Difficulty

easy

Template Id

T9

Examiner Tip

Use the PRE-INTRA-POST mnemonic with the key mechanisms: PRE = poor perfusion; INTRA = inside damage (ATN/nephrotoxins); POST = outflow obstruction. Each mechanism requires a DIFFERENT treatment approach.

Model Answer

The three categories of AKI causes based on anatomical location are: 1. PRERENAL AKI — Caused by DECREASED RENAL PERFUSION (the kidney tissue is intact; the problem is inadequate blood flow reaching the kidneys). Example: Severe dehydration, hemorrhage, cardiogenic shock, or sepsis causing hypotension. 2. INTRARENAL (Intrinsic) AKI — Caused by DIRECT DAMAGE TO KIDNEY TISSUE, most commonly Acute Tubular Necrosis (ATN). Example: Nephrotoxic drugs (aminoglycoside antibiotics, contrast dye, NSAIDs) or prolonged ischemia destroying the renal tubules. 3. POSTRENAL AKI — Caused by OBSTRUCTION of urine outflow BELOW the kidneys. Example: Benign Prostatic Hyperplasia (BPH) in elderly men, kidney stones (urolithiasis), or urethral stricture blocking urine drainage.

Question Type

short_answer

Answer Structure

• Point 1: Prerenal — decreased perfusion + clinical example [1 mark]
• Point 2: Intrarenal — direct tissue damage/ATN + clinical example [1 mark]
• Point 3: Postrenal — obstruction + clinical example [1 mark]

Scoring Breakdown

Common Mark Deductions

• Listing only the category names without explaining the mechanism — loses half the mark for each point.
• Misclassifying NSAIDs/contrast dye as postrenal (they are intrarenal nephrotoxins).
• Misclassifying BPH as intrarenal (BPH causes obstruction = postrenal).

Key Phrases To Include

• prerenal
• intrarenal
• postrenal
• decreased renal perfusion
• acute tubular necrosis (ATN)
• obstruction
• nephrotoxins
• BPH
• kidney stones

Marks

5

Topic

BPH — Post-TURP Nursing Care

Difficulty

hard

Template Id

T10

Examiner Tip

Post-TURP questions in the NLE almost always test three things: (1) recognizing normal vs. abnormal drainage color, (2) knowing to INCREASE CBI for hemorrhage, and (3) the true urine output formula. If you know these three, you have a strong foundation for a full-score answer.

Model Answer

ASSESSMENT FINDINGS: The clinical picture — bright red drainage with visible clots and sluggish catheter outflow after TURP — indicates SURGICAL HEMORRHAGE and POSSIBLE CLOT OBSTRUCTION of the urinary catheter. Normal post-TURP drainage is expected to be pink to light red initially, clearing gradually over hours. Bright red, thick (ketchup-consistency) drainage with clots is ABNORMAL and signals hemorrhage. A sluggishly draining catheter suggests a developing clot obstruction, which can lead to bladder distension, pain, and worsening hemorrhage. Clinical parameters to assess immediately: - Vital signs for signs of hemorrhage: tachycardia, hypotension, falling BP - Bladder distension (suprapubic fullness or pain) - Rate of CBI irrigation vs. drainage output discrepancy - Signs of TUR syndrome (fluid absorption into systemic circulation): confusion, hyponatremia, bradycardia PRIORITY NURSING DIAGNOSIS (NANDA): Risk for Deficient Fluid Volume related to post-operative hemorrhage as evidenced by bright red drainage with clots and sluggish catheter output. SECONDARY DIAGNOSIS: Acute Pain related to bladder distension secondary to clot obstruction. NURSING INTERVENTIONS: 1. INCREASE CBI flow rate IMMEDIATELY — speeding up the irrigation helps flush clots and prevents further obstruction. This is the PRIORITY nursing action. 2. Report the finding to the physician/surgeon IMMEDIATELY — bright red drainage with clots is a hemorrhage emergency requiring medical intervention. 3. Monitor vital signs every 15 minutes for signs of hypovolemic shock (falling BP, rising heart rate, cool clammy skin). 4. Calculate TRUE urine output by subtracting the total irrigation fluid instilled from the total drained output to accurately assess renal function and blood loss. Formula: True Urine Output = Total Drained − Total Irrigation Instilled 5. Assess for signs of TUR syndrome (dilutional hyponatremia from absorbed irrigation fluid): confusion, headache, bradycardia — report immediately. 6. Maintain catheter patency: ensure no kinks in the tubing; position the drainage bag below the level of the bladder. 7. Provide patient reassurance and keep the patient on bed rest to reduce physical activity that may increase bleeding. 8. Document all findings, time, actions taken, and patient response accurately per RA 9173 standards of nursing documentation.

Question Type

case_study

Answer Structure

• Section 1: Assessment — correctly interpret bright red drainage with clots as hemorrhage, NOT normal post-TURP drainage [1 mark]
• Section 2: Priority NANDA nursing diagnosis — correctly formatted with Problem + Related Factor + AEB [1 mark]
• Section 3: Priority intervention — increase CBI flow rate first + report to physician [1 mark]
• Section 4: Monitoring — VS q15min for shock, true urine output calculation, TUR syndrome [1 mark]
• Section 5: Ongoing care — catheter patency, rest, documentation per RA 9173 [1 mark]

Scoring Breakdown

Common Mark Deductions

• Writing 'slow down the CBI' — this is WRONG; bright red output with clots requires INCREASING the flow rate to flush clots.
• Listing nursing interventions without a NANDA priority diagnosis when the question explicitly asks for one.
• Not calculating true urine output — examiners specifically look for this formula after TURP.
• Confusing TUR syndrome (hyponatremia — too much water absorbed) with hyperkalemia or other electrolyte problems.
• Ignoring the sluggish catheter — failing to recognize clot obstruction as a component of the clinical problem.

Key Phrases To Include

• bright red drainage = hemorrhage
• increase CBI flow rate
• report immediately
• true urine output = total drained minus irrigation
• TUR syndrome
• hyponatremia
• hypovolemic shock
• tachycardia and hypotension
• catheter patency
• NANDA nursing diagnosis
• RA 9173 documentation

Marks

5

Topic

AKI — Hyperkalemia Emergency Management

Difficulty

hard

Template Id

T11

Examiner Tip

The most powerful way to structure a hyperkalemia management answer is the 'Protect-Shift-Remove' framework. Examiners look for: (1) the correct sequence, (2) the correct rationale for calcium gluconate, and (3) the insulin+dextrose combination. These three elements alone can earn 3 of the 5 marks.

Model Answer

OVERVIEW: Hyperkalemia (serum potassium greater than 5.0 mEq/L) is the MOST IMMEDIATELY LIFE-THREATENING complication of AKI, particularly in the oliguric phase, because elevated potassium disrupts cardiac membrane excitability, causing fatal arrhythmias. Emergency management follows a three-step framework: PROTECT the heart, SHIFT potassium into cells, and REMOVE potassium from the body. STEP 1 — PROTECT THE HEART (Immediate): Intervention: Administer IV CALCIUM GLUCONATE (or calcium chloride) as ordered. Rationale: Calcium does NOT lower serum potassium. Instead, it STABILIZES the cardiac cell membrane, raising the threshold for arrhythmia and temporarily protecting the heart from fatal effects while other interventions lower the potassium level. Monitor ECG continuously — early signs of hyperkalemia include peaked T waves, progressing to widened QRS, sine wave pattern, and ventricular fibrillation. STEP 2 — SHIFT POTASSIUM INTO CELLS (Rapid onset, temporary): Intervention A: Administer IV REGULAR INSULIN with IV DEXTROSE (to prevent hypoglycemia). Rationale: Insulin activates the sodium-potassium ATPase pump, driving potassium from the extracellular fluid into the cells. Dextrose prevents hypoglycemia caused by insulin. Intervention B: Administer IV SODIUM BICARBONATE. Rationale: Corrects metabolic acidosis; in an acidotic state, hydrogen ions move into cells and potassium moves out. Correcting the acidosis reverses this shift. Intervention C: Inhaled beta-2 agonists (e.g., albuterol/salbutamol) can also shift K⁺ into cells. STEP 3 — REMOVE POTASSIUM FROM THE BODY (Definitive): Intervention A: Administer SODIUM POLYSTYRENE SULFONATE (KAYEXALATE) orally or rectally. Rationale: This ion-exchange resin binds potassium in the GI tract and eliminates it through the feces, actually reducing total body potassium over hours. Intervention B: DIALYSIS (hemodialysis) — if hyperkalemia is refractory to the above measures. Rationale: Dialysis is the most efficient method for removing potassium from the blood and is indicated when the patient has severe hyperkalemia with cardiac compromise, uremia, or volume overload. ADDITIONAL NURSING ACTIONS: - Place patient on continuous CARDIAC MONITORING (ECG); report arrhythmias immediately. - Monitor serum potassium and serum calcium levels frequently. - Restrict DIETARY POTASSIUM (avoid bananas, oranges, potatoes, tomatoes — common Filipino foods high in potassium). - Hold or adjust any medications that raise potassium (ACE inhibitors, ARBs, potassium-sparing diuretics). - Establish IV access and ensure emergency resuscitation equipment is at the bedside. - Document all interventions per RA 9173 nursing practice standards.

Question Type

long_answer

Answer Structure

• Introduction: Define hyperkalemia as #1 life threat in AKI + state the three-step framework [0.5 mark]
• Step 1: IV calcium gluconate + correct rationale (protects heart membrane, does NOT lower K) [1 mark]
• Step 2: Insulin + dextrose + sodium bicarbonate + rationale (shift K into cells) [1.5 marks]
• Step 3: Kayexalate + dialysis + rationale (remove K from body) [1.5 marks]
• Additional nursing actions: ECG monitoring, dietary restriction, documentation [0.5 mark]

Scoring Breakdown

Common Mark Deductions

• Stating that calcium gluconate 'lowers potassium' — this is factually incorrect; it only protects the heart membrane.
• Forgetting dextrose when giving insulin — failure to prevent hypoglycemia is an important omission.
• Confusing Kayexalate's mechanism (removes K via stool) with insulin's mechanism (shifts K into cells).
• Not organizing the answer by mechanism (protect, shift, remove) — unstructured answers are harder to score and lose marks.
• Omitting ECG monitoring — for a cardiac emergency, continuous monitoring is essential.

Key Phrases To Include

• IV calcium gluconate
• stabilizes cardiac membrane
• peaked T waves
• widened QRS
• insulin with dextrose
• Na-K ATPase pump
• sodium bicarbonate
• metabolic acidosis
• sodium polystyrene sulfonate
• Kayexalate
• dialysis
• dietary potassium restriction
• ECG monitoring
• three-step framework: protect, shift, remove

Marks

5

Topic

Renal Replacement Therapy — Hemodialysis vs Peritoneal Dialysis

Difficulty

hard

Template Id

T12

Examiner Tip

Comparison questions are worth significant marks precisely because they require organized, parallel thinking. Use a table format in your answer if allowed — it shows the examiner that you understand BOTH modalities and can contrast them clearly. Each row earns marks independently.

Model Answer

COMPARISON OF HEMODIALYSIS (HD) AND PERITONEAL DIALYSIS (PD): 1. MECHANISM: - Hemodialysis: Blood is circulated OUTSIDE the body through an artificial dialyzer (extracorporeal circuit). Wastes and excess fluid are removed by diffusion across a semipermeable membrane and returned to the patient. - Peritoneal Dialysis: Uses the patient's own PERITONEAL MEMBRANE as the dialyzing surface. Dialysate is infused into the peritoneal cavity, dwells while diffusion and osmosis occur, then is drained — the 'fill-dwell-drain' cycle. 2. VASCULAR/PERITONEAL ACCESS: - Hemodialysis: Requires VASCULAR ACCESS — preferred is an ARTERIOVENOUS (AV) FISTULA (surgically created anastomosis between an artery and a vein; needs 6–12 weeks to mature). Other options: AV graft or temporary central venous catheter. - Peritoneal Dialysis: Requires a PERITONEAL CATHETER (Tenckhoff catheter) surgically inserted into the peritoneal cavity. 3. FREQUENCY: - Hemodialysis: Typically performed 3 times per week for approximately 3–4 hours per session. - Peritoneal Dialysis: More continuous — Continuous Ambulatory Peritoneal Dialysis (CAPD) involves 3–4 exchanges per day, every day; more gentle and closer to natural kidney function. 4. MAJOR COMPLICATION: - Hemodialysis: HYPOTENSION (from rapid fluid removal) and DISEQUILIBRIUM SYNDROME (rapid solute shifts causing cerebral edema — headache, nausea, confusion). - Peritoneal Dialysis: PERITONITIS (infection of the peritoneal cavity) — signaled by CLOUDY outflow, fever, and abdominal pain. 5. KEY NURSING ACTION: - Hemodialysis: Assess the AV fistula for THRILL (palpation) and BRUIT (auscultation) before each session. Never take BP, draw blood, or insert IV in the access arm. Weigh patient before and after to calculate fluid removal. - Peritoneal Dialysis: WARM the dialysate to body temperature before infusion (prevents cramping). Use STRICT ASEPTIC TECHNIQUE at every catheter connection. Monitor outflow for clarity — CLOUDY outflow = report immediately.

Question Type

long_answer

Answer Structure

• Row 1: Mechanism — HD (extracorporeal dialyzer) vs PD (peritoneal membrane/fill-dwell-drain) [1 mark]
• Row 2: Access — HD (AV fistula) vs PD (Tenckhoff catheter) [1 mark]
• Row 3: Frequency — HD (3x/week, 3-4 hrs) vs PD (daily CAPD) [0.5 mark]
• Row 4: Major complication — HD (hypotension/disequilibrium) vs PD (peritonitis) [1 mark]
• Row 5: Key nursing action — HD (thrill/bruit check, no BP in access arm) vs PD (warm dialysate, asepsis, clear outflow) [1.5 marks]

Scoring Breakdown

Common Mark Deductions

• Describing only one modality in depth and neglecting the other — comparison questions REQUIRE both sides.
• Stating that PD uses an 'artificial kidney machine' — PD uses the patient's own peritoneal membrane; no machine is required.
• Omitting disequilibrium syndrome as an HD complication — many students only write 'hypotension.'
• Writing 'maintain hygiene' as the PD nursing action without specifically stating 'strict aseptic technique' — too vague.

Key Phrases To Include

• extracorporeal
• dialyzer
• peritoneal membrane
• fill-dwell-drain
• AV fistula
• Tenckhoff catheter
• 3 times per week
• CAPD
• hypotension
• disequilibrium syndrome
• peritonitis
• thrill and bruit
• no BP in access arm
• warm the dialysate
• strict aseptic technique
• cloudy outflow

Marks

2

Topic

BPH — Pharmacological Management

Difficulty

medium

Template Id

T13

Examiner Tip

The NLE specifically tests: (1) '-osin' ending = alpha blocker = teach dizziness/orthostasis; (2) finasteride/dutasteride = 5-ARI = teratogenic. Memorize these two drug-teaching pairs as a unit — they appear together in almost every BPH pharmacology question.

Model Answer

1. ALPHA-1 BLOCKERS (e.g., TAMSULOSIN/Harnal, TERAZOSIN/Hytrin, DOXAZOSIN/Cardura): These relax smooth muscle in the prostate and bladder neck to improve urine flow. Patient teaching: Teach the patient about ORTHOSTATIC HYPOTENSION — rise slowly from a lying or sitting position to prevent dizziness and falls, especially after the first dose. Avoid standing up suddenly. Take the medication at bedtime initially to reduce the risk of falls from dizziness. 2. 5-ALPHA-REDUCTASE INHIBITORS (e.g., FINASTERIDE/Proscar, DUTASTERIDE/Avodart): These shrink the prostate by blocking conversion of testosterone to DHT. Full effect takes several months. Patient teaching: TERATOGENICITY WARNING — pregnant women and women of childbearing age must NOT handle crushed or broken tablets, as the drug can be absorbed through the skin and cause fetal harm (feminization of a male fetus). The male patient must also use contraception if his partner is or could become pregnant.

Question Type

short_answer

Answer Structure

• Drug 1: Name the drug class + example + state the specific patient teaching (orthostatic hypotension) [1 mark]
• Drug 2: Name the drug class + example + state the specific patient teaching (teratogenicity) [1 mark]

Scoring Breakdown

Common Mark Deductions

• Naming an alpha-1 blocker but teaching about teratogenicity — and naming finasteride but teaching about hypotension — this reversal of teachings loses both marks.
• Stating only 'monitor blood pressure' without the specific teaching about orthostatic hypotension and rising slowly.
• Not specifying 'crushed' tablets for the finasteride warning — intact tablets have a coating that prevents absorption.

Key Phrases To Include

• tamsulosin
• alpha-1 blocker
• orthostatic hypotension
• rise slowly
• dizziness and falls
• finasteride
• 5-alpha-reductase inhibitor
• teratogenic
• pregnant women should not handle
• crushed tablets

Marks

2

Topic

Kidney Transplant — Rejection Signs

Difficulty

medium

Template Id

T14

Examiner Tip

Use the mnemonic DFPC for transplant rejection signs: Decreased urine output, Fever, Pain over graft, Creatinine rising. These four are the core NLE answer. Bonus marks if you also mention weight gain and hypertension from fluid retention.

Model Answer

The nurse should monitor and report the following signs of kidney transplant rejection: 1. DECREASED URINE OUTPUT (oliguria) — the first and most sensitive indicator that the transplanted kidney is losing function. 2. FEVER — indicates systemic immune activation or infection; any temperature elevation in an immunosuppressed transplant patient must be reported. 3. PAIN AND TENDERNESS over the graft site (iliac fossa) — local inflammation from the immune response attacking the donor kidney. 4. RISING SERUM CREATININE — laboratory confirmation that the transplanted kidney's GFR is declining; also watch for rising BUN.

Question Type

short_answer

Answer Structure

• Sign 1: Decreased urine output + brief explanation [0.5 mark]
• Sign 2: Fever [0.5 mark]
• Sign 3: Graft site pain/tenderness [0.5 mark]
• Sign 4: Rising serum creatinine [0.5 mark]

Scoring Breakdown

Common Mark Deductions

• Listing only two signs when four are requested — a direct mark loss.
• Writing 'decreased renal function' without specifying which measurable sign indicates it (urine output or creatinine).
• Listing 'increased urine output' as a sign of rejection — DECREASED, not increased, output indicates rejection.

Key Phrases To Include

• decreased urine output
• oliguria
• fever
• graft site pain
• iliac fossa tenderness
• rising serum creatinine
• weight gain
• hypertension
• report immediately

Marks

3

Topic

CKD — Renal Osteodystrophy and Calcium-Phosphate Imbalance

Difficulty

hard

Template Id

T15

Examiner Tip

The bone disease pathway in CKD is a chain reaction: No active Vit D → Low Ca → High PTH → Bone breakdown → Fractures. Also: No phosphate excretion → High phosphate → binds Ca → Low Ca (worsens the cycle). Drawing a quick diagram in your exam answer can earn you bonus clarity marks and make the chain reaction obvious to the examiner.

Model Answer

VITAMIN D AND RENAL OSTEODYSTROPHY: The kidneys are responsible for the FINAL ACTIVATION of Vitamin D into its active form, CALCITRIOL (1,25-dihydroxyvitamin D). In CKD, damaged kidneys cannot perform this activation, resulting in a deficiency of active Vitamin D. Active Vitamin D is essential for CALCIUM ABSORPTION from the GI tract. Without it, serum calcium FALLS (HYPOCALCEMIA). In response to low calcium, the PARATHYROID GLANDS secrete excess PARATHYROID HORMONE (PTH) — a condition called SECONDARY HYPERPARATHYROIDISM. PTH, in an attempt to raise serum calcium, mobilizes calcium FROM THE BONES, leading to BONE DEMINERALIZATION (renal osteodystrophy), fractures, and skeletal pain. Additionally, impaired kidneys cannot excrete phosphate, causing HYPERPHOSPHATEMIA. Elevated phosphate binds to calcium, further lowering serum calcium and worsening the cycle. NURSING IMPLICATIONS: 1. Monitor serum CALCIUM (low in CKD — report symptoms of hypocalcemia: muscle cramps, Chvostek's sign, Trousseau's sign, tetany) and PHOSPHATE (high — assess for itching and ectopic calcification). 2. Administer CALCITRIOL (active Vitamin D) as ordered to supplement deficient active Vitamin D and improve calcium absorption. 3. Administer PHOSPHATE BINDERS (calcium carbonate, sevelamer) WITH MEALS to reduce dietary phosphate absorption and lower serum phosphate. 4. Advise the patient to avoid phosphate-rich foods (dairy products, processed foods, dark colas, instant noodles — relevant in Philippine diet context). 5. Educate the patient about fall and fracture prevention due to weakened bones.

Question Type

short_answer

Answer Structure

• Paragraph 1: Explain that kidneys activate vitamin D to calcitriol; CKD → no active Vit D → hypocalcemia [1 mark]
• Paragraph 2: Explain secondary hyperparathyroidism → PTH mobilizes calcium from bones → osteodystrophy [0.5 mark]
• Paragraph 3: Explain hyperphosphatemia binding calcium → worsens hypocalcemia [0.5 mark]
• Paragraph 4: Nursing implications — monitor Ca/Phosphate, calcitriol, phosphate binders with meals, diet, fall prevention [1 mark]

Scoring Breakdown

Common Mark Deductions

• Saying 'CKD patients lack Vitamin D' without explaining the kidney's role in ACTIVATING Vitamin D — loses the pathophysiology mark.
• Confusing HYPOCALCEMIA (low calcium in CKD) with hypercalcemia.
• Not explaining the PTH/parathyroid feedback loop — this is the mechanism of bone disease and is essential for full marks.
• Listing nursing interventions without explaining their rationale (e.g., 'give calcitriol' without saying 'to supplement deficient active Vitamin D').

Key Phrases To Include

• calcitriol
• 1,25-dihydroxyvitamin D
• activation of Vitamin D
• hypocalcemia
• secondary hyperparathyroidism
• PTH
• bone demineralization
• renal osteodystrophy
• hyperphosphatemia
• phosphate binders with meals
• Chvostek's sign
• Trousseau's sign
• fall and fracture prevention