Renal – Radio/Medicine

The principle of nonmaleficence means “do no harm.”
It obligates healthcare professionals to avoid causing injury or suffering to patients — whether through action or omission.
This is one of the core ethical pillars in medicine, emphasizing that the patient’s safety and well-being come first.

❌ Why Others Are Wrong:

• Beneficence:
  Means doing good or acting in the patient’s best interest — not the same as avoiding harm.

• Justice:
  Refers to fairness in distributing healthcare resources and treatment.

• Autonomy:
  The patient’s right to make their own decisions about care.

• Informed consent:
  A process ensuring patients understand and agree to a proposed treatment — it’s based on autonomy, not nonmaleficence.

The patient has classic signs of congestive heart failure with volume overload:

• ↑ JVP

• Basal crackles

• Pedal edema

To confirm that the symptoms are due to fluid overload from heart failure, the most specific lab marker is:

👉 BNP (B-type natriuretic peptide)
BNP is released when the ventricular walls stretch due to volume and pressure overload.

✔ Why Elevated BNP Is Correct

• BNP rises directly due to increased ventricular filling pressure

• Helps differentiate heart failure vs non-cardiac causes of dyspnea

• High BNP strongly correlates with volume overload

This is the best diagnostic confirmation among the listed options.

❌ Why the Other Options Are Incorrect

Low hematocrit due to chronic anemia — ❌

• Not related to heart failure volume status

• Could occur from many causes (iron deficiency, CKD)

• Does NOT confirm fluid overload

Hyponatremia due to low dietary sodium — ❌

• HF causes dilutional hyponatremia, not dietary deficiency

• Not specific and not confirmatory

Elevated serum creatinine due to dehydration — ❌

• Dehydration is opposite of volume overload

• Heart failure often causes congestion, not dehydration

Hypernatremia due to poor intake — ❌

• Again suggests dehydration

• Not related to fluid overload from heart failure

✅ Computed tomography
Non-contrast CT scan is the gold standard for detecting urinary tract stones.

Non-contrast CT (CT KUB) is considered the most reliable diagnostic test for urolithiasis because it provides high sensitivity and specificity, detects even radiolucent stones (like uric acid), and also reveals complications such as hydronephrosis or obstruction. Unlike X-rays or IVP, CT does not depend on stone composition to visualize them.

Explanation of the Incorrect Options

❌ Intravenous pyelogram (IVP)
Previously the standard test, but less sensitive than CT and involves contrast use, which can be risky in renal impairment.

❌ Magnetic resonance imaging (MRI)
Not preferred for stone detection because stones are poorly visualized on MRI; better for soft tissue and vascular structures.

❌ Blood test
May reveal complications (e.g., renal function, infection) but cannot diagnose stones directly.

❌ X-ray
Can detect radio-opaque stones (like calcium oxalate) but misses radiolucent stones (e.g., uric acid, cystine). Limited sensitivity compared to CT.

The ABG shows:

• pH = 7.49 → alkalosis

• pCO₂ = 3.9 kPa (low) → indicates respiratory cause

• HCO₃⁻ = 22 mmol/L (normal–slightly low) → no significant metabolic compensation yet

This means the patient has a primary respiratory alkalosis, likely due to hyperventilation after surgery (pain, anxiety, or postoperative stress).

❌ Why Others Are Wrong:

• Partial compensatory metabolic acidosis:
  There’s minimal compensation, but the primary disturbance is respiratory, not metabolic.

• Mixed acid–base disturbance:
  No conflicting findings — only one primary process (respiratory alkalosis).

• Respiratory acidosis:
  Would show ↑ pCO₂ and ↓ pH, opposite of this case.

• Metabolic alkalosis:
  Would show ↑ HCO₃⁻ and ↑ pH, not present here.

• The kidneys produce erythropoietin, which stimulates erythropoiesis in the bone marrow.

• In CKD, damaged renal tissue cannot produce enough EPO → reduced RBC production → normocytic, normochromic anemia.

• This type of anemia causes fatigue, pallor, and dyspnea, commonly seen in long-term renal failure.

• Treatment involves recombinant EPO therapy along with iron supplementation if needed.

❌ Why the Other Options Are Wrong:

Hypokalemia:

• CKD usually leads to hyperkalemia due to decreased excretion of potassium.

Hypophosphatemia:

• CKD causes hyperphosphatemia because phosphate is not adequately excreted.

Hypercalcemia:

• CKD often leads to hypocalcemia, not hypercalcemia, because of low vitamin D activation and high phosphate levels.

Hypomagnesemia:

• CKD leads to hypermagnesemia, as magnesium excretion also decreases.

• Micturating cystourethrography (MCUG/VCUG) is an X-ray study in which contrast is instilled into the bladder and images are taken during filling and micturition.

• Its primary indication is to diagnose vesicoureteric reflux (VUR) – the abnormal backward flow of urine from the bladder into the ureters and kidneys.

• It can also evaluate bladder anatomy, posterior urethral valves, strictures, or fistulae, but the main and most common reason is suspected VUR, especially in children with recurrent UTIs.

Why Other Options Are Wrong

• Acute urinary tract infection ❌ – Contraindicated during acute infection; risk of worsening the infection.

• Fistula ❌ – Can be demonstrated, but it is not the primary indication.

• Urethral trauma ❌ – Retrograde urethrography (RUG) is preferred for trauma evaluation, not MCUG.

• Urethral malignancy ❌ – CT urography, MRI, or cystoscopy are better for assessing malignancy.

• Renal calculi are crystalline concretions formed in the kidneys from calcium oxalate, phosphate, uric acid, or cystine.

• Most contain calcium, making them radio-opaque on plain X-rays.

• They typically appear as white opacities in the region of the kidney, ureter, or bladder.

• Associated symptoms include loin pain, hematuria, and urinary obstruction.

• Hence, in this patient’s KUB X-ray, the opaque shadow in the renal calyces represents a renal stone.

❌ Why the Other Options Are Wrong:

Slough off renal papillae:

• Seen in papillary necrosis (e.g., diabetes, analgesic nephropathy); may appear as filling defects on IVP, but not radio-opaque on plain X-ray.

Gravels filtered from glomeruli:

• Glomeruli don’t “filter gravels”; stones form distally in tubules/collecting system, not at glomeruli.

Necrosis with dystrophic calcification:

• May cause calcification but is diffuse and irregular, not a discrete stone shadow in calyces.

Proteins:

• Organic materials (like proteins) are radiolucent, hence invisible on X-ray.

This patient is severely dehydrated due to vomiting and diarrhea, which can quickly lead to hypovolemic shock and organ hypoperfusion if not treated promptly.
The first and most critical step is fluid resuscitation, typically with isotonic fluids (0.9% Normal Saline or Ringer’s lactate) to restore intravascular volume, correct electrolyte imbalance, and stabilize vital signs.

Once the patient is hemodynamically stable, you can proceed with diagnostic tests and targeted therapy.

❌ Why Others Are Wrong:

• Administer intravenous antibiotics:
  Not every case of vomiting and diarrhea is infectious or bacterial; antibiotics are given after confirmation of cause.

• Conduct a thorough physical examination:
  Important but secondary — treat dehydration first; don’t delay life-saving fluids.

• Order CBC and CMP:
  Helpful for evaluation, but initial priority is stabilization, not labs.

• Prescribe antiemetic and antidiarrheal medications:
  These are supportive but not sufficient for severe dehydration.

• The kidneys are highly sensitive to blood volume and pressure.

• In severe dehydration, renal perfusion falls sharply, leading to pre-renal acute kidney injury (AKI).

• The glomeruli cannot filter blood adequately, resulting in decreased urine output (oliguria or anuria).

• If uncorrected, this may progress to acute tubular necrosis and permanent kidney damage.

❌ Why the Other Options Are Wrong:

Liver:

• Has dual blood supply (hepatic artery + portal vein) — remains functional longer even in hypovolemia.

Lungs:

• Usually remain functional unless dehydration leads to severe shock or multi-organ failure.

Pancreas:

• Not directly affected early; ischemia may occur only in prolonged shock.

Eyes:

• May appear sunken in dehydration, but visual function remains intact.

• Ultrasound of the kidneys, ureters, and bladder (KUB) is often considered the first-line investigation in suspected renal colic.

• It is non-invasive, radiation-free, inexpensive, and readily available — making it especially useful in emergency settings, children, and pregnant women.

• It can detect hydronephrosis, renal stones, and bladder pathology. Although not as sensitive as CT for small ureteric stones, it is generally the initial investigation of choice before proceeding to more advanced imaging if required.

Plain radiography KUB ❌

• Can detect only radiopaque stones (calcium oxalate, phosphate, struvite), but misses radiolucent ones (uric acid, cystine).

• Less sensitive overall compared to ultrasound.

MRI scan ❌

• Rarely used in acute stone disease because it does not detect calcifications well.

• More useful for soft tissue or vascular pathology, not acute renal colic.

CT scan ❌

• Non-contrast CT KUB is the most accurate imaging modality, but due to radiation exposure and cost, it is not always the first investigation.

• It is usually reserved for cases where ultrasound is inconclusive.

X-ray KUB ❌

• Similar to plain radiography; limited use in initial diagnosis.

• Cannot detect radiolucent stones and provides less information compared to ultrasound.

In a patient with renal artery stenosis (suggested by renal bruit and hypertension), the use of ACE inhibitors can lead to a sharp rise in serum creatinine and hyperkalemia.
ACE inhibitors block angiotensin II, which normally constricts the efferent arteriole to maintain glomerular filtration pressure. Blocking this mechanism reduces GFR, especially in bilateral renal artery stenosis or a single functional kidney, leading to acute kidney injury.

Why others are wrong:
❌ Alpha blockers — reduce peripheral resistance, no major effect on renal filtration.
❌ Beta blockers — lower cardiac output and renin release but do not cause acute renal failure.
❌ Calcium channel blockers — cause vasodilation and reduce BP safely in renal artery stenosis.
❌ Thiazide diuretics — may cause mild electrolyte disturbances but not a sharp rise in creatinine.

• The creatinine clearance test estimates the glomerular filtration rate (GFR) — the most comprehensive indicator of overall kidney function.

• It measures how efficiently creatinine (a constant by-product of muscle metabolism) is cleared from blood into urine.

• The test requires 24-hour urine collection and plasma creatinine measurement to calculate Creatinine Clearance

• This gives a direct estimate of GFR, helping evaluate both kidneys’ performance and any damage caused by obstruction or infection.

❌ Why the Other Options Are Wrong:

Urine D/R (detailed report):

• Checks for protein, blood, pus cells, crystals, etc.

• Useful for infection or hematuria, but not for functional assessment.

X-ray KUB:

• Provides anatomical information (stones, calcifications), not kidney function.

Urea, creatinine, electrolytes:

• Reflect biochemical changes in blood but cannot measure GFR precisely — a rise in serum creatinine only appears after significant nephron loss.

Urine acidification test:

• Assesses tubular function, not overall glomerular function.

Chronic Kidney Disease (CKD) is staged according to eGFR (mL/min/1.73 m²) as follows:

This patient’s eGFR = 45, which falls in the Stage 3 CKD range — indicating moderate kidney dysfunction.

❌ Why Others Are Wrong:

• Stage 1: Normal eGFR (>90) — not applicable.

• Stage 2: 60–89 — mild, higher than his value.

• Stage 4: 15–29 — more severe than his current status.

• Stage 5: <15 — end-stage renal disease, not yet reached.

Chronic or repeated NSAID use can lead to drug-induced interstitial nephritis, an inflammatory reaction in the renal interstitium.
Key supporting features here are:

• History of prolonged NSAID use

• Eosinophilia (E = 12%)

• Mild proteinuria

• Raised urea and creatinine

These are classic for chronic interstitial nephritis rather than glomerular disease.

Why others are wrong:
❌ Nephrotic syndrome — shows massive proteinuria (>3.5 g/day) and severe edema, not mild protein +.
❌ Acute tubular necrosis — usually due to ischemia or toxins (e.g., radiocontrast), not hypersensitivity to NSAIDs.
❌ Nephritic syndrome — characterized by hematuria, hypertension, and RBC casts, absent here.
❌ End-stage renal disease — represents the final stage of chronic damage, but this presentation reflects an active, reversible inflammatory process.

• The pH indicates whether the blood is acidic (<7.35) or alkaline (>7.45).

• Once pH is known, the next steps are:

  1. Determine if it’s acidosis or alkalosis (based on pH).

  2. Look at PCO₂ → if it changes in the same direction as pH, it’s respiratory.

  3. Look at HCO₃⁻ → if it changes in the opposite direction to pH, it’s metabolic.

  4. Calculate anion gap or delta–delta only after the primary disorder is identified.

So in this COPD patient, the ABG shows respiratory acidosis, but the first thing to check is the pH to confirm acidemia before determining the cause.

❌ Why the Other Options Are Wrong:

Anion gap:

• Used only for metabolic acidosis to identify the cause — not the first step.

Delta–delta gap:

• Used in mixed metabolic disorders, much later in interpretation.

HCO₃⁻ level:

• Evaluated after pH and PCO₂ to decide if it’s metabolic or compensatory.

PCO₂:

• Important for determining respiratory involvement, but only after pH is assessed.

I’ll confirm this from a Medicine Professor, but according to the slides :-

Dehydration in children is classified based on percentage of body-weight fluid loss:

• Mild: 3–5%

• Moderate: 6–9%

• Severe: ≥10%

This child has 8% fluid loss, which is borderline, but:

👉 The clinical signs take priority over the number.

✔ Why This Is Considered Severe Dehydration

The child shows:

• Irritability

• Sunken eyes

• Dry tongue / dry mucosa

• Slow skin pinch (poor skin turgor)

• Reduced urine output (oliguria)

These are classic signs of SEVERE dehydration, regardless of exact % estimate.

Clinical classifications (WHO) say:
If two or more severe signs → classify as severe dehydration.

This child has more than two.

❌ Why the Other Options Are Incorrect

No dehydration — ❌

• Would look normal

• No signs like sunken eyes or poor turgor

Mild dehydration — ❌

• Thirsty but alert

• Normal skin turgor

• No sunken eyes

• NOT matching exam findings

Moderate dehydration — ❌

• Some dryness and mild sunken eyes

• But skin pinch usually returns slowly ONLY in severe, not moderate

• Reduced urine output & irritability more typical of severe

Hyperhydration — ❌

• Opposite condition

• Would show edema or puffy appearance

• Not possible with vomiting + diarrhea

• Severe dehydration leads to hypovolemia, hypotension, and impaired consciousness.

• Since the patient is semi-conscious, oral fluids are unsafe (risk of aspiration) and ineffective.

• IV fluid therapy (e.g., Ringer’s lactate or normal saline) is the first line of management to restore:

  • Circulating volume

  • Electrolyte balance

  • Blood pressure

  • Renal perfusion

Once stable, oral rehydration and further management (antibiotics if indicated) can follow.

❌ Why the Other Options Are Wrong:

IV antibiotics:
❌ Not the first priority. Infection may be present, but immediate correction of shock and dehydration takes precedence.

Oral fluid replacement:
❌ Contraindicated in semi-conscious patients due to risk of aspiration. Suitable only for mild to moderate dehydration in alert patients.

Oral antibiotics:
❌ Not useful in acute management; hydration comes first. Antibiotics are only given if bacterial infection is confirmed or strongly suspected (e.g., cholera, dysentery).

KYB diet (Keep Your Balance / light diet):
❌ Dietary changes are not part of emergency stabilization and only apply later during recovery.

For routine UDR (urinalysis)—especially when evaluating dysuria / possible UTI—the gold-standard specimen is:

👉 Midstream clean-catch urine, after cleaning the perineal area,
👉 Processed within 2 hours, or refrigerated to prevent bacterial overgrowth.

This reduces contamination and ensures accurate dipstick + microscopy.

✔ Why This Option Is Correct

• Perineal cleansing ↓ contamination

• Midstream sample avoids first flush flora

• Analyzing within 2 hours maintains sample integrity

• Refrigeration prevents false positives (e.g., nitrites) and false negatives (e.g., cell lysis)

This is exactly what labs recommend.

❌ Why the Other Options Are Incorrect

First-void early-morning urine without cleansing — ❌

• High contamination risk

• First-void is for STI testing, not UTI urinalysis

• Also can’t wait 6 hours—cells and casts deteriorate

Catheterized urine in all women — ❌

• Not indicated routinely

• Used only when patients cannot void, are critically ill, or need sterile sample

• Unnecessary + risk of iatrogenic UTI

Random urine kept in warm pocket for 12 hours — ❌

• Warm environment → bacterial overgrowth

• Nitrite changes, pH rises, WBCs break down

• Completely unacceptable handling

24-hour urine mandatory for all tests — ❌

• 24-hour urine is for quantitative tests (e.g., protein, creatinine clearance)

• NEVER for dipstick or routine UDR

• Completely incorrect for UTI evaluation

• Pre-renal acute kidney failure occurs when there is a drop in blood flow to the kidneys, leading to reduced glomerular filtration rate (GFR).

• Profuse diarrhea causes severe fluid and electrolyte loss, resulting in hypovolemia and decreased renal perfusion.

• If uncorrected, this can progress to ischemic injury and acute tubular necrosis (ATN).

• It is reversible if treated early by restoring fluid balance.

❌ Why the Other Options Are Wrong:

Nephrotic syndrome:

• ⚠️ Primarily a glomerular disease causing protein loss, not a perfusion issue — classified as renal (intrinsic).

Prostatic hypertrophy:

• 🚫 Causes urinary outflow obstruction, leading to post-renal failure.

Cancer of prostate:

• 🚫 Also causes post-renal failure through obstruction of the urethra.

Acute glomerulonephritis:

• 🚫 A renal (intrinsic) cause — inflammation within the glomeruli impairs filtration directly.

Urine-specific gravity (USG) measures the concentration of solutes in urine, reflecting the kidney’s ability to conserve water.
In dehydration, the kidneys retain water → urine becomes concentrated, leading to high specific gravity (usually >1.020).
Therefore, USG is a quick, sensitive indicator for assessing the severity of dehydration.

❌ Why Others Are Wrong:

• Blood test:
  Too vague — doesn’t specify what’s being measured.

• Serum creatinine:
  Rises in renal failure, not specifically in simple dehydration.

• Serum sodium:
  Can vary — may be normal, high, or low depending on fluid type loss.

• Urinary sodium level:
  Low (<20 mEq/L) in dehydration, but it’s less immediate and more complex to assess than USG.

The estimated glomerular filtration rate (eGFR) is the most accurate and specific test to determine the stage and chronicity of chronic kidney disease (CKD). It reflects the kidneys’ filtration ability and helps classify CKD into stages (1–5). In long-standing diabetes with elevated creatinine and recurrent hypoglycemia (due to decreased insulin clearance), a low eGFR confirms chronic renal impairment.

Why others are wrong:
❌ Urine DR for proteinuria — supports diagnosis but does not quantify renal function or stage CKD.
❌ Serum albumin — may fall in nephrotic states but is not diagnostic for CKD.
❌ Urea and creatinine — indicate renal dysfunction but are less reliable for staging or early detection.
❌ Electrolytes and ABGs — show complications (e.g., acidosis, hyperkalemia) but not disease chronicity.

• In ultrasound, hyperechoic structures (very dense, like bone or stones) reflect most of the ultrasound waves, so they appear bright white.

• Behind them, there’s an acoustic shadow (dark area) because no sound waves pass through.

• Calculi (stones) are classic examples — they produce a bright echogenic focus with posterior acoustic shadowing.

• Fluid → appears black (anechoic), not bright.

• Cortex/Medulla/Fat → have intermediate echogenicity, not associated with shadowing.

Answer breakdown:

• Fluid → black (anechoic).

• Medulla → hypoechoic relative to cortex, not bright.

• Fat → hyperechoic but doesn’t make strong posterior shadows.

• Cortex → intermediate echogenicity.

• Calculus → bright focus with acoustic shadow → correct.

0.9% Normal saline (isotonic saline) has an osmolality (~308 mOsm/L) close to that of plasma, making it isotonic.
It neither causes cell swelling (as hypotonic fluids do) nor cell shrinkage (as hypertonic fluids do).
In this pregnant woman with vomiting and dehydration, isotonic saline safely restores extracellular fluid volume without disturbing cellular balance.

❌ Why Others Are Wrong:

• 5% Dextrose:
  Initially isotonic, but once glucose is metabolized, it becomes hypotonic, leading to cell swelling.

• 10% Dextrose water:
  Hypertonic; may cause osmotic diuresis or vein irritation.

• 3% Saline:
  Hypertonic saline, used in severe hyponatremia, not for general rehydration — can cause cell shrinkage.

• 25% Dextrose water:
  Extremely hypertonic, used to treat hypoglycemia, not dehydration.

A dipstick pattern of:

• Leukocyte esterase: Positive → WBCs present → inflammation/UTI

• Nitrite: Negative → organism does NOT convert nitrate → nitrite

Only certain Gram-positive organisms and some Gram-negatives lack nitrate reductase.

👉 Enterococcus faecalis is the classic nitrite-negative UTI organism.

✔ Why This Option Is Correct

Enterococcus faecalis — ✅

• Causes UTI

• Does NOT reduce nitrate to nitrite

• Hence: LE positive / Nitrite negative pattern
  Perfect match.

❌ Why the Other Options Are Incorrect

Escherichia coli — ❌

• Strong nitrate reducers

• Should give nitrite-positive dipstick

• Most common cause of nitrite-positive UTI

Klebsiella pneumoniae — ❌

• Also nitrate-reducing

• Usually nitrite-positive

Proteus mirabilis — ❌

• Nitrate-reducing + urease-producing

• Causes nitrite-positive AND alkaline urine

Corynebacterium — ❌

• Rare UTI cause, but LE may be positive

• However Enterococcus is the classic exam answer

• Corynebacterium is not the common choice here

Urolithiasis (kidney stones) requires imaging for diagnosis. Among available modalities:

• Non-contrast CT scan of the kidneys, ureters, and bladder (NCCT KUB) is the most sensitive and specific test for detecting urinary stones.

  • Detects stones as small as 1–2 mm.

  • Identifies stone location, size, and density.

  • Can detect stones of all compositions except very rare radiolucent stones (like some uric acid stones).

• X-ray (KUB) – Can detect radio-opaque stones (like calcium stones) but misses radiolucent stones.

• Intravenous pyelogram (IVP) – Older method; uses contrast to outline urinary tract; less commonly used now due to CT availability and speed.

• MRI – Poor for stones; not used routinely for urolithiasis.

• Blood test – Cannot reliably detect stones; may show secondary effects like elevated creatinine or uric acid, but not diagnostic.

• When a renal mass is incidentally found on ultrasound, the gold standard next step is a contrast-enhanced CT scan of the abdomen (CT KUB/CT abdomen with contrast).

• CT allows:

  • Differentiation between solid vs cystic masses.

  • Assessment of vascularity, calcification, fat content, necrosis.

  • Accurate staging if malignancy (e.g., renal cell carcinoma) is suspected.

• This is essential for guiding management decisions.

Plain radiography KUB ❌

• Useful for detecting renal calculi, but not for characterizing renal masses.

• Cannot differentiate solid vs cystic lesions.

MRI pelvis ❌

• MRI is helpful in renal mass characterization, particularly in patients with contraindications to contrast CT (e.g., allergy, poor renal function).

• However, it is not the first-line follow-up after an incidental ultrasound finding.

Ultrasound KUB ❌

• The mass was already found on ultrasound.

• Repeat ultrasound adds little value for further characterization.

X-ray KUB ❌

• Similar to plain radiography, used for stones, not renal mass evaluation.

• No role in staging or characterizing renal tumors.

This CKD patient has severe fluid overload:

• Pitting edema up to thighs

• Bilateral crackles (pulmonary congestion)

• Rapid 4 kg weight gain (≈ 4 L fluid)

• Oliguria despite fluid restriction

The next step in management is:

👉 Give a loop diuretic (e.g., furosemide) — the strongest diuretic effective even at low GFR.

✔ Why This Option Is Correct

Loop diuretics are:

• Most potent diuretics

• Effective in CKD, even when thiazides fail

• Reduce pulmonary congestion quickly

• Improve edema and shortness of breath

This is the standard first-line treatment for fluid overload in CKD or heart failure.

❌ Why The Other Options Are Incorrect

Thiazide diuretics — ❌

• Very ineffective when GFR is low

• CKD patients do NOT respond well

• Not useful in marked overhydration

Increase oral fluid intake — ❌

• Patient is already volume overloaded

• Would worsen edema and lung congestion

• Dangerous

Hypertonic saline infusion — ❌

• Used for severe symptomatic hyponatremia, not volume overload

• Would massively worsen fluid retention

Withholding all medications and observing — ❌

• Patient already has pulmonary congestion + edema + oliguria

• Needs active management, not observation

• MCUG (also called Voiding Cystourethrogram) is the gold standard test to confirm vesico-ureteric reflux.

• The procedure involves:

  1. Filling the bladder with a radiopaque contrast through a catheter.

  2. Taking X-rays during filling and voiding.

  3. Observing for retrograde flow of contrast from the bladder into the ureters or kidneys.

• It also helps detect posterior urethral valves and other structural abnormalities of the bladder outlet — important in male toddlers.

❌ Why the Other Options Are Wrong:

CT Urography:

• ❌ High radiation exposure and not routinely used in children; poor sensitivity for reflux.

Intravenous urography (IVU):

• ❌ Outdated for VUR; mainly shows anatomy, not functional reflux.

MR Urography:

• ⚠️ Can show urinary tract anatomy without radiation but is less practical and not the investigation of choice for reflux detection in toddlers.

Ultrasound bladder with pre and post-void volumes:

• ⚠️ Useful for assessing residual urine or hydronephrosis, but cannot detect reflux.

A patient with:

• Sudden severe flank → groin pain

• Hematuria

• Normal X-ray (so the stone is likely radiolucent, e.g., uric acid, cystine)

👉 The best investigation is Non-contrast CT KUB, which detects all stones—radiopaque and radiolucent—with the highest sensitivity.

✔ Why Plain CT KUB Is Correct

• Gold standard for suspected ureteric colic

• Detects even non-opaque stones not visible on X-ray

• Fast, accurate, widely used in emergency

• Shows exact location, size, and obstruction

Perfect match.

❌ Why the Other Options Are Incorrect

Cystography — ❌

• Used for bladder injuries, fistulas, VUR

• NOT for ureteric stones

Intravenous Urography (IVU) — ❌

• Old test, replaced by CT KUB

• Uses contrast → harmful in renal impairment

• Misses very small or radiolucent stones

Ultrasound Abdomen — ❌

• Good for hydronephrosis, pregnancy

• Poor at detecting ureteric stones, especially small distal ones

• Misses many radiolucent stones

MRI Abdomen — ❌

• Excellent for soft tissues, but

• Stones appear poorly

• Not recommended for stone evaluation

Voiding cystourethrogram (VCUG)

• Posterior urethral valves (PUV) are congenital obstructive membranes in the male posterior urethra.

• Antenatal ultrasound signs: bilateral hydronephrosis, hydroureters, distended bladder, “keyhole sign.”

• After birth, the investigation of choice to confirm the diagnosis is Voiding cystourethrogram (VCUG).

Why VCUG?

• It visualizes the bladder during filling and voiding.

• Demonstrates bladder trabeculations, dilated posterior urethra, and reflux if present.

• Gold standard for diagnosing PUV.

Why the Other Options Are Wrong ❌

Kidney, ureter, and bladder (KUB) X-ray

• Poor sensitivity for soft tissue or valve obstruction.

• Might show secondary calcifications, but not diagnostic.

Magnetic resonance imaging (MRI)

• Good soft tissue detail, but not the first-line or most practical investigation in neonates.

Computed tomography scan (CT scan)

• Not indicated in infants for PUV due to radiation exposure and limited functional information.

Repeat ultrasound KUB + Prostate

• Helpful for screening and follow-up, but not confirmatory.

• Cannot directly visualize urethral valves.

🔎 Step 1: Key Clinical Features

• Patient: 32-year-old pregnant woman

• Ultrasound findings in fetus:

  • Bilateral hydronephrosis

  • Hydroureters

  • Distended bladder with “keyhole sign”

• Suspected diagnosis: Posterior urethral valves (PUV)

The keyhole sign indicates obstruction at the level of the posterior urethra, leading to bladder distension and proximal urinary tract dilation.

🔎 Step 2: Postnatal Investigation Choice

• Goal: Confirm obstructive uropathy and assess anatomy of bladder and urethra

• Investigation options:

1. Kidney, ureter, and bladder (KUB) X-ray

   • Cannot visualize urethra or bladder obstruction in detail

2. Voiding cystourethrogram (VCUG)

   • Gold standard for diagnosing posterior urethral valves

   • Evaluates:

     • Bladder morphology

     • Posterior urethra

     • Vesicoureteral reflux

   • Performed postnatally with catheterization and contrast

3. CT scan / MRI

   • Rarely used in neonates for PUV

   • Radiation (CT) or impractical (MRI)

4. Repeat ultrasound

   • Useful for follow-up

   • Cannot definitively identify urethral obstruction

✅ Correct Answer: Voiding cystourethrogram (VCUG)

• Definitive postnatal investigation for suspected posterior urethral valves

❌ Why the Other Options Are Incorrect

• KUB X-ray → Cannot show urethral obstruction

• CT scan / MRI → Not first-line in neonates for PUV

• Repeat ultrasound → Helpful for monitoring, not diagnostic

The low pH (7.10) with low HCO₃⁻ (6 mEq/L) indicates a primary metabolic acidosis. The compensatory low PCO₂ (20 mmHg) shows respiratory compensation through Kussmaul breathing — rapid, deep respirations helping to blow off CO₂.

This presentation (abdominal pain, dehydration, altered consciousness, Kussmaul breathing) is classic for diabetic ketoacidosis (DKA) or another high anion gap metabolic acidosis (e.g., lactic acidosis).

Why others are wrong:
❌ Metabolic alkalosis — would have high pH and high HCO₃⁻, opposite findings.
❌ Respiratory acidosis — would have high PCO₂, not low.
❌ Respiratory alkalosis — would have high pH and low PCO₂, not low HCO₃⁻.

The patient has acute kidney injury (AKI) secondary to severe dehydration from profuse watery diarrhea. The raised urea and creatinine, along with low bicarbonate, point to prerenal azotemia and metabolic acidosis due to fluid loss.
The immediate and life-saving step is rapid rehydration with IV fluids (e.g., isotonic saline or Ringer’s lactate) to restore perfusion and renal function.

Why others are wrong:
❌ Bicarbonate replacement — metabolic acidosis will usually correct once hydration is restored.
❌ Antibiotics — not indicated unless there’s evidence of infection (fever, blood in stool).
❌ Hemodialysis — considered only if renal function fails to recover after adequate rehydration.
❌ ORS — useful for mild to moderate dehydration; this patient is severely dehydrated and needs IV fluids.

✅ Creation of arteriovenous fistula
An AV fistula provides durable vascular access with high blood flow for hemodialysis.

For hemodialysis, a patient requires a vascular access that can:

• Provide high blood flow (200–400 mL/min).

• Be long-lasting with low infection risk.

• Withstand repeated needle punctures.

The arteriovenous (AV) fistula, usually created surgically between the radial artery and cephalic vein at the wrist, is the gold standard. Over weeks, the vein becomes arterialized (thick-walled, high flow), making it suitable for dialysis needles.

Alternative access methods include AV grafts or central venous catheters, but these have higher complication rates compared to fistulas.

Explanation of the Incorrect Options

❌ Ventriculogallbladder shunt
Not a recognized procedure in nephrology; irrelevant here.

❌ Ventriculoperitoneal shunt
Used to treat hydrocephalus by draining CSF into the peritoneal cavity.

❌ Ventriculoatrial shunt
Also used in hydrocephalus; drains CSF into the right atrium.

❌ Lumboperitoneal shunt
CSF diversion procedure from lumbar subarachnoid space to peritoneum, not for dialysis.

Diabetes mellitus is the leading cause of end-stage renal disease (ESRD) worldwide.
Chronic hyperglycemia damages glomerular capillaries, leading to glomerulosclerosis, proteinuria, and progressive loss of renal function.
The process typically evolves from microalbuminuria → macroalbuminuria → declining GFR → ESRD.

❌ Why Others Are Wrong:

• Hypertension:
  A major cause of ESRD, but secondary to diabetes globally and often contributes alongside it.

• Polycystic kidney disease:
  A genetic cause of ESRD, but much less common overall.

• Glomerulonephritis:
  Can cause ESRD but accounts for a smaller percentage of chronic kidney failure cases compared to diabetes.

• Kidney stones:
  Rarely cause ESRD unless there’s chronic obstruction or infection over many years.

Cola-colored urine + RBC casts + dysmorphic RBCs = Glomerular bleeding.

These findings are diagnostic of a glomerular origin (e.g., PSGN, IgA nephropathy, GN).

✔ Why This Option Is Correct

Glomerular source of hematuria — ✅

• RBC casts = formed inside renal tubules → must come from glomeruli

• Dysmorphic RBCs = RBCs squeezed through damaged GBM

• Cola-colored urine = oxidized heme pigments seen in glomerular disease
  This triad is CLASSIC.

❌ Why the Other Options Are Incorrect

Lower urinary tract bleeding (cystitis) — ❌

• Has no casts

• RBCs are normal in shape

• Color is usually pink/red, not tea-/cola-colored

Contamination from menstruation — ❌

• No casts

• Normal-shaped RBCs

• No dysmorphic RBCs

• Urine color usually bright red

Interstitial nephritis — ❌

• WBC casts, eosinophils

• NOT RBC casts

• No dysmorphic RBCs

Nephrolithiasis — ❌

• Causes gross hematuria, often red

• No casts

• RBCs are normal in morphology

Severe watery diarrhea causes significant loss of potassium and bicarbonate from intestinal secretions, leading to hypokalemia and metabolic acidosis. The dehydration and vomiting further worsen electrolyte depletion. Clinically, this may present with muscle weakness, fatigue, or cardiac arrhythmias if untreated.

Why others are wrong:
❌ Hyponatremia — sodium loss does occur, but dehydration often concentrates plasma sodium, keeping it near normal or slightly elevated.
❌ Hypocalcemia — not typically associated with diarrheal losses.
❌ Hyperkalemia — opposite effect; potassium is lost, not retained.
❌ Hypernatremia — can occur in pure water loss, but diarrhea causes more isotonic or potassium-rich loss.

The patient has:

• Hypernatremia (Na⁺ 156 mmol/L)

• Signs of hypovolemia → low BP, tachycardia, delayed capillary refill, dry mucosa

• Confusion + lethargy from dehydration

• Chronic kidney disease history → delicate fluid balance needed

👉 FIRST priority is volume resuscitation, not immediate sodium correction.

Therefore: Start with isotonic saline (0.9% NaCl) to restore intravascular volume.

Once stable, you can later switch to hypotonic fluids to correct sodium slowly.

✔ Why This Option Is Correct

Slow IV 0.9% saline — ✅

• Treats hypovolemic shock, which is the biggest immediate danger

• Restores perfusion to brain and kidneys

• Prevents worsening AKI

• DOES NOT rapidly drop sodium → avoids cerebral edema

Correct emergency approach.

❌ Why the Other Options Are Incorrect

Rapid correction with 5% dextrose — ❌

• Drops sodium too fast → risk of cerebral edema, seizures, herniation

• Dangerous in chronic hypernatremia

Oral rehydration — ❌

• Patient is lethargic and confused → unsafe

• Too slow in shock

• Not appropriate in severe dehydration + hypotension

Half-normal saline (0.45%) — ❌

• Hypotonic → will lower sodium too fast

• Only used after volume is restored

• Dangerous in unstable patients

Vasopressin (ADH) — ❌

• Not used in hypovolemic hypernatremia

• Would worsen sodium retention

• Indicated only for central diabetes insipidus

The low pH (7.10) with high PCO₂ (80 mmHg) and normal HCO₃⁻ (27 mEq/L) indicates a primary respiratory acidosis. This results from hypoventilation, which causes CO₂ retention.
The pin-point pupils and respiratory rate of 6/min point toward opioid poisoning — a classic cause of acute respiratory acidosis due to depression of the medullary respiratory center.

Why others are wrong:
❌ Metabolic acidosis — would show low pH and low HCO₃⁻, not elevated CO₂.
❌ Metabolic alkalosis — would have high pH and high HCO₃⁻.
❌ Respiratory alkalosis — would have high pH and low PCO₂ from hyperventilation.