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USMLE Step 2 CK Flash Cards > Renal/Genitourinary > Flashcards

Renal/Genitourinary Flashcards

1
Q

Best diagnostic study for evaluating and confirming the diagnosis of bladder cancer

A

Cystoscopy

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2
Q

Treatment of urinary uric acid stone

A
  • Hydration
  • NSAIDs (pain killers)
  • Potassium citrate or potassium bicarbonate→alkalinization of urine►uric acid stone dissolve in an alkaline medium
  • Add allopurinol if stones don’t resolve with initial treatment
  • Radiolucent stones
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3
Q

Why you should avoid sodium bicarbonate for a uric acid stone treatment?

A

Extra salt load→volume expansion►hypercalciuria→formation of calcium stones

*Uric acid is a nidus for calcium oxalate stone formation

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4
Q

Which electrolyte disturbance is caused by Bartter syndrome? Look like which pharmacologic effect?

A
  • Reabsorptive defect in thick ascending loop of Henle→Affect K/Na/Cl cotransporter►hypokalemia, metabolic alkalosis, hypercalciuria
  • Chronic loop diuretic use
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5
Q

Treatment for Bartter syndrome

A
  • Spironolactone→antagonizes effect of ↑aldosterone (↑ by the loss of electrolytes and intravascular volume in Bartter)
  • NSAID→↓excessive prostaglandins (in Bartter ↑PGE)
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6
Q

Potential cause of low urine specific gravity and normal serum sodium

A

Hyposthenuria➡Sicke cell disease or sickle cell trait▶hypoxic, hyperosmolar condition of the renal medulla➡RBC sickle in the vasa recta➡❌water reabsorption and countercurrent exchange

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7
Q

When do you use acute therapy for hyperkalemia?

A
  • ECG changes
  • K>7 mEq/L (with or without ECG changes)
  • Rapidly rising K due to tissue breakdown
  • Dialysis→renal failure or severe life-threatening hyperkalemia unresponsive to initial therapy
  • Calcium gluconate and insulin with glucose
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8
Q

Which metabolic disturbance can be found on diabetic hyporeninism? why?

A
  • Hyperkalemic metabolic acidosis
  • Damage of the juxtaglomerular apparatus→hyporeninemic hypoaldosteronism►”aldosterone deficiency”→Renal tubular acidosis type IV (hyperkalemic RTA)
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9
Q

Pathophysiology of renal tubular acidosis type IV (hyperkalemic RTA) and its metabolic consequence

A
  • Aldosterone insufficiency→Diabetic hyporeninism, ACEI, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency
  • Aldosterone resistance→K sparing diuretics, obstructive nephropathy, TMP/SMX
  • *Impaired function of the cortical collecting tubule►retention of H and K→hyperkalemic Non-anion gap metabolic acidosis
  • Preserved kidney function→at least 20-50 mL/min
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10
Q

Which electrolyte disturbance can occur due to immobilization and its mechanism?

A
  • Hypercalcemia
  • ↑Osteoclastic bone resorption

*Onset around 4 weeks, patients with chronic renal insufficiency develop it in about 3 days

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11
Q

Mechanisms by which Beta-adrenergic agonists cause hypokalemia

A
  • Stimulate Na-K ATPase pump and the Na-K-2Cl cotransporter→potassium shift into the intracellular space
  • Release of Insulin→promotes intracellular K+ shift
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12
Q

Most appropriate initial step in the management of Hyperkalemia with ECG changes

A

Calcium gluconate

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13
Q

Most common cause of Glomerulonephritis in adults

A

IgA Nephropathy

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14
Q

Extrarenal complications of autosomal dominant polycystic kidney disease. What is the most common?

A
  1. Hepatic cyst
  2. Intracranial berry aneurysm (5-15%)
  3. Valvular heart disease (most often mitral valve prolapse and mitral regurgitation)
  4. Colonic diverticula
  5. Abdominal wall and inguinal hernia
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15
Q

Which types of acid-base disorder may cause acute kidney injury and why?

A
  • Non-anion gap metabolic acidosis⇦impaired acid excretion, ammonia generation or bicarbonate reabsorption
  • Anion gap metabolic acidosis⇦retention of unmeasured uremic toxins
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16
Q

Pathophysiologic mechanism of membranoproliferative glomerulonephritis

A
  • Dense intramembranous deposits that stain for C3
  • Deposit disease▶IgG antibodies (C3 nephritic factor) against C3 convertase➡persistent activation of the alternative complement pathway▶kidney damage
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17
Q

What do you have to monitor closely after initiation of Erythropoietin in a CKD patient, and why?

A
  • Blood pressure monitoring
  • Up to 30% patients develop new or worsening hypertension 2-8 wks after initiation

*Large doses or rapidly Hb increase, highest risk

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18
Q

In addition to the classical triad of Renal cell carcinoma, what other features you may find?

A
  • Unintentional weight loss
  • Intermittent fever
  • Paraneoplastic syndromes (ectopic EPO, hypercalcemia)
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19
Q

How do you expect to find the urinary sodium, fractional excretion of sodium, urine sediment, urine WBC and BUN/creatinine ratio in a patient with sepsis?

A
  • Renal hypoperfusion➡activation of RAAS➡⬆Na reabsorption➡⬇Urinary sodium (<20mEq/mL), ⬇Fractional excretion of Na (<1%)
  • No intrinsic kidney damage➡urine sediment bland (acellular, no WBC or RBC)
  • Urea follows reabsorption of Na and water➡⬆BUN/creatinine ratio >20:1
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20
Q

How are the urinary sodium, urine osmolality and urine sediment in acute tubular necrosis?

A
  • ❌reabsorption of Na by the injured tubules➡⬆Urinary Na (>20mEq/mL)
  • ⬇Urine Osmolality (300-350)
  • Muddy brown granular urinary casts
  • BUN/creatinine ratio 10-15:1
  • FENa>2%

*Contrast-induced ATN may have ⬇Urinary Na (<20mEq/mL)

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21
Q

Urine sodium and urine sediment on glomerulonephritis

A
  • RBC casts, mild ⬆WBC, hematuria
  • ⬇Urine Na (<20mEq/mL)

*Hypertension

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22
Q

Which conditions may present with very high urinary sodium levels?

A
  • Syndrome of inappropriate antidiuretic hormone (SIADH)

- Diuretics

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23
Q

What can damage the renal distal tubule? What is the consequence?

A
  • Drugs: Amphotericin, Topiramate
  • Autoimmune diseases: SLE, Sjögren syndrome
  • Distal Renal Tubular Acidosis (Type I)➡❌H+ secretion
24
Q

What can damage the renal proximal tubule? What is the consequence?

A
  • Amyloidosis, myeloma, Fanconi syndrome, acetazolamide, heavy metals, Tenofovir
  • Proximal Renal Tubular Acidosis (Type II)➡❌HCO3- reabsorption
25
Q

Best initial test and most accurate test for proximal renal tubular acidosis

A
  • Best initial: Urianalysis➡Variable pH; Basic at first (>5.5), until most HCO3 is lost, pH <5.5
  • Most accurate: Give HCO3 and test urine pH➡⬆⬆urine pH
26
Q

Treatment for proximal renal tubular acidosis

A

Thiazide➡volumen depletion➡⬆HCO3 absorption

27
Q

Complication of proximal renal tubular acidosis and why does it happen?

A

Acid can’t be excreted into de the tubule➡⬆Urine pH (alkaline urine)➡⬆formation of calcium oxalate stones in kidneys

28
Q

Treatment of renal tubular acidosis type IV

A

Fludrocortisone➡”Aldosterone like” effect

29
Q

Which drug may help to avoid the recurrence of calcium kidney stones?

A

Hydrochlorothiazide➡⬆distal tubular reabsorption of Ca➡removes Ca from urine

30
Q

Treatment for distal renal tubular acidosis

A

Replace HCO3-➡will be absorbed in the proximal tubule

31
Q

Mechanism of renal dysfunction in an end-stage liver disease

A

Hepatorenal syndrome➡splanchnic arterial dilation ➡⬇vascular resistance➡➕RAAS➡local renal vasoconstriction (renal arterioles)➡⬇perfusion and glomerular filtration

32
Q

Best next step when unilateral varicoceles fail to empty when a patient is recumbent

A

Suspicion of underlying mass (eg, Renal cell carcinoma)➡obstructs venous flow▶CT scan of the abdomen

33
Q

Mechanism of calcineurin inhibitor toxicity (tacrolimus, cyclosporine). Most common toxicities.

A

Vasoconstrictive properties

  • Acute: Hypertension and AKI [prerenal] (constriction of afferent and efferent arteriole, reversible)
  • Chronic: slow decline in renal function (prolonged vasoconstrictive renal ischemia, tubular toxicity, irreversible)

*Elicit by impairment in hepatic clearance (Ex, add drugs metabolized by cytochrome P450)

34
Q

Which test might detect eosinophils in the urine? What may suggest?

A

Wright and Hensel stains➡Allergic interstitial nephritis

*Most accurate test for AIN

35
Q

What is Isosthenuria and why does it happen?

A
  • Urine Osmolality similar to blood Osmolality (about 300 mOsm/L)
  • Acute tubular necrosis➡tubule cells cannot reabsorb water

*Renal tubular concentrating defect

36
Q

Most probable cause of acute kidney injury in a patient with hematologic malignancy who is beginning chemotherapy

A

Tumor lysis syndrome➡hyperuricemia

37
Q

How do you prevent renal failure from tumor lysis syndrome?

A

Give prior chemotherapy: Allopurinol, hydration and rasburicase

38
Q

What type of kidney damage may cause rhabdomyolysis and why?

A

⬆Myoglobin➡severe oxidant stress on the tubular cells▶Acute tubular necrosis

39
Q

Best initial and most specific test for rhabdomyolysis during ATN

A
  • Best initial: ⬆⬆blood on urine dipstick, no RBC on microscopic examination
  • Most: Urine myoglobin
40
Q

Which electrolyte disturbances might be identified in rhabdomyolysis?

A

Hyperkalemia
Hyperuricemia
Hyperphosphatemia
Hypocalcemia (⬆Ca binding to damaged muscle)

41
Q

Treatment for rhabdomyolysis

A
  • Saline hydration

- Mannitol➡osmotic diuretic

42
Q

Most common medications causing acute (allergic) interstitial nephritis

A
  • Penicillins and cephalosporins
  • Sulfa drugs (include furosemide and thiazide)

*Drugs overall are the cause in 70% of cases

43
Q

Most likely clinical presentation of acute (allergic) interstitial nephritis

A
  • Acute renal failure
  • Fever (80%)
  • Rash (50%)
  • Arthralgias
  • Eosinophilia and Eosinophiluria (80%)
  • ⬆BUN:Creatinine (but <20)
  • 10% of patients have simultaneously all the findings
  • Urine eosinophils not found in AIN from NSAIDs
44
Q

Treatment for acute interstitial nephritis

A
  • Stop drug or control infection➡usually resolves spontaneously
  • Severe disease➡Dialysis
  • ⬆⬆creatinine even stopping drug➡Glucocorticoids
45
Q

Most accurate test for papillary necrosis

A

CT Scan➡abnormal internal structures of the kidney from the loss of the papillae

46
Q

What is postictal lactic acidosis and how do you manage it?

A
  • Anion gap metabolic acidosis typically following tonic-clonic seizure➡skeletal muscle hypoxia, ⬇hepatic lactic acid uptake▶⬆⬆lactic acid
  • Transient and self-limited in 90 minutes➡observe and repeat chemistry in 2 hours
47
Q

How do you suspect an acute renal allograft rejection? How do you confirm it?

A
  • Typically within the first 6 months after a transplant
  • Asymptomatic usually
  • Acutely ⬆creatinine, proteinuria
  • Confirmation by Bx➡Lymphocytic infiltration of the intima, inflammatory tubular disruption, intimal arteritis.
  • Mostly Reversible (⬆dose glucocorticoids)
48
Q

How do the calcineurin inhibitors cause acute toxicity to kidneys? What do you expect to find?

A

Vasoconstriction of afferent and efferent renal arterioles➡prerenal acute kidney injury and hypertension

49
Q

When do you suspect a BK virus reactivation in a patient with a renal transplant? What is the finding in the most accurate test?

A
  • Excessive immunosuppression in renal allograft recipients➡tubulointerstitial nephritis
  • Asymptomatic ⬆creatinine
  • Bx➡intranuclear inclusions, mixed lymphocytic and neutrophilic infiltrate
50
Q

Common findings on urinalysis in a patient with glomerulonephritis

A
  • Hematuria
  • Dysmorphic red cells
  • Red cell casts
  • Proteinuria
51
Q

Treatment of nephrogenic diabetes insipidus

A
  • Correct potassium and calcium
  • Stop lithium or demeclocycline
  • Hydrochlorothiazide or NSAIDs (still having NDI despite previous interventions)
52
Q

Best initial and most accurate test for distal renal tubular acidosis (Type I)

A
  • Best initial: Urinalysis➡⬆pH>5.5

- Most accurate: infuse acid (ammonium chloride)➡urine pH remains basic >5.5. Normal response is ⬇pH

53
Q

In addition to drugs, which other cause of acute interstitial nephritis there might be?

A
  • Autoimmune diseases (20%): SLE, Sjögren, Sarcoidosis

- Infections or Idiopathic (10%)

54
Q

Best next step in management when a male patient has a penile fracture and suspects urethral injury

A

Retrograde urethrography (urethroscopy)➡rule out urethral injury (20% of PF) before surgery

*Possible urethral injury: urinary retention/blood at the meatus/hematuria/dysuria

55
Q

What additional studies do you do on adult patients with membranous nephropathy?

A
  • Hepatitis B serology, HCV, syphilis, studies for autoimmune disease, malignancy because evaluation for secondary causes should be done in adults
  • MN is often idiopathic or primary

USMLE Step 2 CK Flash Cards (17 decks)

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