Nephro/Urology Flashcards
A 10-year-old boy is seen in the office for evaluation of sudden onset of cola-colored urine. He reports no pain, burning, or passage of blood clots with urination. He has had a sore throat and mild cough for 2 days. He does not have flank pain, fever, rash, or joint pains. He had a similar episode of painless cola-colored urine 6 months ago that resolved without treatment. There is no family history of renal disease. He has a heart rate of 86 beats/min, a respiratory rate of 14 breaths/min, and a blood pressure of 128/82 mm Hg. His chest is clear to auscultation. The rest of his physical examination findings are unremarkable.
Laboratory data are shown:
Laboratory Test
Result
Blood
White blood cell count 7,400/µL (7.4 × 10⁹/L)
Hemoglobin 12.8 g/dL (128 g/L)
Platelet count 360 × 10³/µL (360 × 10⁹/L)
Blood urea nitrogen 36 mg/dL (12.9 mmol/L)
Creatinine 0.9 mg/dL (80 µmol/L)
Complement C3 110 mg/dL (1.10 g/L) (reference range 85-142 mg/dL [0.85-1.42 g/L])
Complement C4 24 mg/dL (0.24 g/L) (reference range 12-41 mg/dL [0.12-0.41 g/L])
Antistreptolysin O < 200 IU
Urine
Blood 3+
White blood cells 5-10/HPF
Red blood cells 50-100/HPF
Protein 3+
Of the following, the MOST likely diagnosis for this child is
A. acute hemorrhagic cystitis
B. immunoglobulin A nephritis
C. poststreptococcal glomerulonephritis D. systemic lupus erythematosus nephritis
immunoglobulin A nephritis
recurrent painless gross hematuria, proteinuria, hypertension, and azotemia favor a diagnosis of acute glomerulonephritis
normal serum complement
Acute glomerulonephritis or nephritic syndrome is characterized by sudden-onset hematuria (macroscopic or microscopic), proteinuria, hypertension, edema, and acute kidney injury
recurrent episodes of gross hematuria triggered by an upper respiratory tract or gastrointestinal illness.
A 7-year-old boy who had surgery for craniopharyngioma 2 days ago now has increased thirst and frequent urination. He has no vomiting, blurry vision, or seizures. His current medication includes phenytoin. He has a heart rate of 102 beats/min, a respiratory rate of 16 breaths/min, and a blood pressure of 102/60 mm Hg. He has no swelling over his body. His craniotomy incision site is clean and healing. He has no neurological deficits, and the rest of his physical examination findings are unremarkable.
Laboratory data are shown:
Laboratory Test
Result
Blood
Sodium 150 mEq/L (150 mmol/L)
Potassium 4.2 mEq/L (4.2 mmol/L)
Chloride 110 mEq/L (110 mmol/L)
Bicarbonate 23 mEq/L (23 mmol/L)
Blood urea nitrogen 28 mg/dL (10.0 mmol/L)
Creatinine 0.5 mg/dL (44 µmol/L)
Glucose 90 mg/dL (5.0 mmol/L)
Serum osmolality 325 mOsm/kg (325 mmol/kg)
Urine
Specific gravity 1.006
Leukocyte esterase Negative
Nitrite Negative
Blood Negative
Protein Negative
Glucose Negative
Of the following, the MOST likely diagnosis for this child is
A. acute kidney injury
B. central diabetes insipidus C. cerebral salt wasting D. syndrome of inappropriate secretion of antidiuretic hormone
central diabetes insipidus
Diabetes insipidus presents with polyuria, new-onset nocturia, and polydipsia.
Laboratory evaluation in diabetes insipidus shows low urine specific gravity on the first-voided morning urine specimen and a normal to high serum sodium level.
Central diabetes insipidus is commonly a result of a primary brain tumor, cranial surgery, or brain injury
polydipsia and polyuria immediately after undergoing cranial surgery with dilute urine and hypernatremia
Central diabetes insipidus is a condition resulting from inadequate secretion of antidiuretic hormone (ADH) from the posterior lobe of the pituitary gland. Other causes of CDI include familial history, Langerhans cell histiocytosis, head trauma, associated brain malformations, and other central nervous system injuries (infectious, vascular, and granulomatous).
A 24-hour urine collection and intake recording is done to confirm polyuria and polydipsia
When the diagnosis is unclear, a water deprivation test is performed to differentiate CDI from nephrogenic diabetes insipidus. Nephrogenic diabetes insipidus results from an inability of the renal tubules to respond to ADH and concentrate the urine despite normal ADH secretion (ADH insensitivity). Urine specific gravity will increase after exogenous ADH administration during a water deprivation test in CDI but will remain unchanged in children with nephrogenic diabetes insipidus.
Management includes desmopressin administration, free access to water, and a close monitoring of serum sodium and urine specific gravity.
A 16-year-old previously healthy adolescent is seen in the emergency department for evaluation after 3 hours of sharp left-sided testicular pain that radiates to the lower abdomen. The pain started suddenly while he was playing video games at home. There was no antecedent trauma, and he is not sexually active. He has no fever, urinary symptoms, or penile discharge. He has vomited twice since the onset of pain. On physical examination, the left hemiscrotum is edematous and exquisitely tender. The left testis appears to be elevated and has a horizontal orientation. The left cremasteric reflex is absent. The right hemiscrotum examination findings are normal.
Of the following, the MOST appropriate next step in management is
A. incision and drainage
B. scrotal ultrasonography
C. urine testing for gonorrhea and chlamydia
D. urological consultation
Urology consult for detorsion
Testicular torsion typically presents with acute onset of unilateral scrotal pain with a swollen and tender hemicrostum on physical examination.
Inguinal or abdominal pain, pain with ambulation, nausea, and/or vomiting
If the diagnosis of testicular torsion can be confirmed with the history and physical examination, urology should be consulted emergently; there is no need for imaging.
If the diagnosis is uncertain, ultrasonography of the testicle with Doppler blood flow can assist in the diagnosis. Torsion is confirmed if blood flow to the affected testicle is significantly decreased or absent
Detorsion should take place in the operating room in conjunction with orchiopexy; however, manual detorsion should be attempted if there will be a significant delay.
A 2-month-old female infant with poor feeding and failure to gain weight is seen for evaluation. She is fed 24 kcal/oz of appropriately prepared infant formula. She was born at 39 weeks’ gestation, and her birth weight was 3 kg. She failed her newborn hearing screening. She had one hospital admission with vomiting and diarrhea at 6 weeks after birth. Her weight is currently at the third percentile, and her height is at the fifth percentile. Her cardiac examination reveals no murmur, and her chest is clear to auscultation. The rest of her physical examination findings are unremarkable.
Laboratory data are shown:
Laboratory Test
Result
Blood
Sodium 134 mEq/L (134 mmol/L)
Potassium 3.2 mEq/L (3.2 mmol/L)
Chloride 110 mEq/L (110 mmol/L)
Bicarbonate 14 mEq/L (14 mmol/L)
Blood urea nitrogen 10 mg/dL (3.6 mmol/L)
Creatinine 0.2 mg/dL (18 µmol/L)
Glucose 90 mg/dL (5.0 mmol/L)
Urine
pH 7.0
Specific gravity 1.015
\Urinalysis with microscopy Normal
Sodium 60 mEq/L (60 mmol/L)
Potassium 10 mEq/L (10 mmol/L)
Chloride 55 mEq/L (55 mmol/L)
Of the following, the MOST likely diagnosis for this child is
A. congenital adrenal hyperplasia
B. distal renal tubular acidosis
C. methylmalonic acidemia
D. postinfectious diarrhea
distal renal tubular acidosis
Diarrhea and renal tubular acidosis are the most common causes of normal anion gap acidosis in children.
The urine anion gap helps differentiate diarrhea from renal tubular acidosis.
In distal renal tubular acidosis, the urine anion gap is positive and ammonium (NH4+) excretion is low.
Anion gap (mEq/L) = sodium (Na+) − [chloride (Cl−) + bicarbonate (HCO3−)]
A normal anion gap ranges from 8 mEq/L to 12 mEq/L
The higher-than-expected urinary pH and positive urine anion gap favors a diagnosis of distal renal tubular acidosis.
To differentiate between diarrhea and RTA, urine electrolytes should be obtained and the urine anion gap (UAG) calculated.
Urine anion gap = {urine sodium (Na+) + urine potassium (K+)} - urine chloride (Cl−)
The UAG can be positive (urine [Na+] + urine [K+] is > urine [Cl−]) or negative (urine [Na+] + urine [K+] is < urine [Cl−]). Diarrhea causes Negative
type 1 (distal; failure to excrete H+ ion), type 2 (proximal; failure to reabsorb HCO3−), and type 4 (hyperkalemic, disruption of renin-angiotensin-aldosterone axis)
A 10-month-old male infant is seen for follow-up. He was diagnosed with bilateral acute otitis media 3 days ago after developing fever and otalgia with abnormal tympanic membrane findings. He was prescribed a 10-day course of high-dose amoxicillin and ibuprofen as needed. He has received 6 doses of amoxicillin, but the fever persists despite administration of ibuprofen every 6 hours. He has had a poor appetite and a few episodes of nonbloody, nonbilious emesis. His parents have also noted that his eyes seem swollen and he is urinating less frequently. His history includes a previous history of otitis media treated successfully with amoxicillin at 4 months of age. He appears to be nontoxic and well hydrated. His weight and length are in the 75th percentile, and his blood pressure is in the 87th percentile. There is mild periorbital edema without conjunctival or scleral injection and no discharge. Other significant findings include erythematous, opaque, and bulging tympanic membranes bilaterally. The remainder of the physical examination findings are within normal limits. Laboratory findings reveal sterile pyuria, proteinuria, hematuria, and elevated levels of blood urea nitrogen and creatinine. Findings of a urine culture are negative.
Of the following, the BEST initial step in management is to
A. admit for intravenous fluid administration B. admit for intravenous steroid administration C. discontinue amoxicillin D. discontinue ibuprofen
discontinue ibuprofen
Drug-induced acute interstitial nephritis is commonly caused by nonsteroidal anti-inflammatory drugs, such as ibuprofen.
The mainstay of initial treatment for drug-induced acute interstitial nephritis is discontinuation of the offending agent. The majority of patients improve after the offending medication is withdrawn.
Supportive interventions for acute interstitial nephritis may include fluid and electrolyte management, adequate hydration, and avoidance of nephrotoxic drugs.
Nonsteroidal anti-inflammatory drug–induced AIN does not typically respond to glucocorticoid therapy. Other supportive interventions may include fluid and electrolyte management, adequate hydration, and avoidance of nephrotoxic drugs.
An 8-year-old boy is brought to the office for evaluation of nighttime bedwetting. He has never been dry at night and has urinary accidents 5 nights per week. The boy’s parents report that he has been completely continent during the day since 3 years of age. He has no history of urinary frequency, urgency, or hesitancy. He has a normal daily bowel movement and has not had fecal soiling. He is described as a deep sleeper. He is embarrassed to sleep at his cousin’s house. His father also had nighttime bedwetting until he was 9 years old. The boy’s parents decreased his fluid intake before bedtime and tried bedwetting alarms, but with no improvement in the boy’s frequency of nighttime bedwetting.
He is at the 50th percentile for weight and height. He has no skin lesions on his back. His abdomen is soft with no organomegaly. His neurological examination findings are normal.
A urinalysis performed in the office has normal results. A 48-hour voiding diary shows that the boy voids 4 to 6 times per day with a normal maximum urine volume of 300 mL.
If pharmacological therapy is pursued, the BEST initial agent is
A. desmopressin
B. imipramine
C. oxybutynin
D. polyethylene glycol
desmopressin
Primary monosymptomatic nocturnal enuresis is defined as enuresis without symptoms of lower urinary tract abnormalities or bladder dysfunction.
Treatment of nocturnal enuresis includes limiting the fluid intake before bedtime, emptying the bladder before going to sleep, and establishing a consistent bedtime routine.
For primary monosymptomatic nocturnal enuresis, bedwetting alarms are among the most effective treatment options, and desmopressin is the first-line pharmacological therapy.
questions about the following: number of nighttime bedwetting episodes per week, perceived nocturnal volume, child’s bedtime routine and fluid consumption, whether the child has had a dry period of 6 months or longer, daytime incontinence, frequency, urgency, urinary retention, and other features of voiding dysfunction. A thorough history regarding stooling habits, fecal incontinence, and constipation is also required.
A healthy 2-month-old male infant, born at full term, is seen for a health supervision visit. The family recently moved from another state. His mother reports persistent drainage of clear fluid from his umbilicus despite several cauterization procedures with silver nitrate by his previous pediatrician. The infant is otherwise doing well and has remained afebrile. He has had normal intake and output. His vital signs and growth parameters are normal. His physical examination findings are normal except for a 3-mm-diameter umbilical granuloma with serous drainage. There is no erythema or tenderness around the umbilicus.
Of the following, the BEST next step in management is to
A. ligate the umbilical stump with absorbable sutures B. perform ultrasonography of the umbilicus C. prescribe oral cephalexin D. provide parental reassurance
perform ultrasonography of the umbilicus
Ultrasonography is the preferred imaging modality to evaluate infants with persistent umbilical granulomas or drainage; surgical referral should be considered.
Dry cord care is recommended for infants delivered under hygienic conditions.
Most umbilical hernias close spontaneously by age 6 years.
A 4-month-old female infant with a 5-day history of diarrhea is brought to the emergency department. She has been refusing to drink formula for 2 days. She has no history of vomiting, fever, or abdominal distension. She is sleepy but has a high-pitched cry on stimulation. She has a heart rate of 160 beats/min, a respiratory rate of 22 breaths/min, and a blood pressure of 70/38 mm Hg. Her skin feels doughy. Her mucous membranes are dry. The rest of her physical examination findings are unremarkable.
Laboratory results are as follows:
Laboratory Test
Result
Sodium
162 mEq/L (162 mmol/L)
Potassium
3.1 mEq/L (3.1 mmol/L)
Chloride
115 mEq/L (115 mmol/L)
Bicarbonate
18 mEq/L (18 mmol/L)
Blood urea nitrogen
28 mg/dL (10.0 mmol/L)
Creatinine
0.5 mg/dL (44 µmol/L)
Glucose
90 mg/dL (5.0 mmol/L)
Osmolality
340 mOsm/kg (340 mmol/kg) (reference range, 275-295 mOsm/kg [275-295 mmol/kg])
Of the following, the MOST likely complication of rapid correction of this infant’s condition is
A. central pontine myelinolysis B. cerebral edema C. dural sinus thrombosis D. subdural hemorrhage
cerebral edema
Hypernatremic dehydration, commonly seen in infants with acute diarrhea, reflects excess water loss as compared with solute loss.
Infants with hypernatremic dehydration may have a high-pitched cry on stimulation and a doughy feel to the skin on examination.
Hypernatremic dehydration should be corrected slowly to prevent cerebral edema.
A rapid correction of the high serum sodium can result in shifting of water from the extracellular fluid (ECF) compartment to the intracellular fluid (ICF) compartment, leading to cerebral edema.
Initially, the serum sodium may need to be monitored every 4 to 6 hours. Infants with serum sodium greater than 160 mEq/L should undergo sodium correction over a period of 48 to 72 hours. The target drop in the serum sodium is less than 0.5 mEq/L per hour or 10 to 12 mEq/L per day.
