111

USMLE Step 2 (Subject) / Renal/Genitourinary (Lesson)

This lesson was created by estoffel.

Learn lesson

back  |  next 2 / 3

• IgA Nephropathy (Berger's disease) Epidemiology - IgA nephropathy is the most common primary glomerulonephritis- Peak incidence: second to third decade of life- Sex: ♂ > ♀ (2:1)- Ethnicity: more common in Asian and white populations Clinical features:- Recurring episodes of gross hematuria, flank pain, low-grade fever, and/or nephritic syndrome (including hypertension), usually during or immediately following a respiratory or gastrointestinal infection- Can progress to RPGN and/or nephrotic syndrome (< 10% of patients)- Up to 50% of patients progress to end-stage renal disease within 20-25 years. Diagnostics:- Urinalysis: Microhematuria and possibly minor proteinuria- Renal biopsy→ Usually only indicated if there are signs of severe or progressive disease, including: Urinary protein > 0.5-1 g/24 h, ↑ serum creatinine, hypertension→ Light microscopy: mesangial proliferation→ Immunofluorescent microscopy: mesangial IgA deposits→ Electron microscopy: mesangial immune complex deposits- Complement levels (e.g., C3 level) are generally normal. Treatment:- Patients with isolated hematuria: regularly monitor kidney function and initiate treatment if diseases progresses (e.g., occurence of proteinuria)- Patients with proteinuria or hypertension: ACE inhibitors/angiotensin II receptor blockers- For severe/rapidly progressive disease: glucocorticoids + possibly cyclophosphamide/azathioprine Differential diagnoses:- Poststreptococcal glomerulonephritis: Associated with low complement levels; occurs 10-20 days following an infection- Henoch-Schönlein purpura: Assoicated with abdominal symptoms, palpable purpura, arthritis; patients are usually < 10 years of age
• Cystinuria Hereditary defect of renal PCT and intestinal amino acid transporter that prevents reabsorption of Cystine, Ornithine, Lysine, and Arginine (COLA). Autosomal recessive. Common (1:7000). Excess cystine in the urine can lead to recurrent precipitation of hexagonal cystine stones. Treatment: - Urinary alkalinization (eg, potassium citrate, acetazolamide)- Chelating agents (eg, penicillamine)- Good hydration
• Graft-vs-host disease Damage to the host as a result of a systemic inflammatory reaction induced by T lymphocytes present in the graft. Etiology:- Allogenous hematopoietic stem-cell transplantation- Small bowel transplantation- Transfusion of non-irradiated blood products Acute graft-versus-host disease- < 100 days after transplantation- Donor T lymphocytes react with the recipient's organs- Pruritic or painful maculopapular rash- Nausea, vomiting, diarrhea, and/or cramping abdominal pain- Hepatic dysfunction: jaundice- CBC: anemia, thrombocytopenia, leukopenia- ↑ ALP- Confirmatory test: biopsy of skin, rectum, or liver- Prevention: Antithymocyte globulin; Cyclosporine + Methotrexate or Mycophenolate mofetil- Treatment: Corticosteroids Chronic graft-versus-host disease- > 100 days after transplantation- Scleroderma-like and lichenoid skin changes- Sicca syndrome: xerophthalmia, xerostomia, dry pruritic skin- Chronic enteritis (similar to inflammatory bowel disease): bloody diarrhea, abdominal pain, weight loss- Hepatic dysfunction: jaundice- Bronchiolitis obliterans: chronic cough, wheezing, and dyspnea that is not responsive to bronchodilator therapy- Myasthenic symptoms, polymyositis: weakness, muscle pain- Spirometry: obstructive lung disease- Confirmatory test: biopsy of the skin, oral cavity, liver, or lung- Treatment: First-line: corticosteroids; Second-line: cyclosporine and increased corticosteroid dose
• Urethral injury Anterior urethral injury (e.g., perineal straddle injury):- Rupture of this part of the urethra below the urogenital diaphragm causes urine to extravasate into the superficial perineal space and spread into the following areas:- Anterior → around the penis- Superior → in the lower abdominal wall- Inferior → into the scrotum Posterior urethral injury (e.g., due to pelvic fracture):- Rupture of this part of the urethra causes extravasation of urine into the deep perineal space and can spread retropubically, around the bladder, and prostate. Diagnostics:- Retrograde urethrography
• Methanol poisoning Sources of exposure:- Fuels (highly flammable)- Ingested as ethanol substitute by alcoholics- Self-harm attempts- Accidental ingestion- Improper distillation of spirits Effects:- Metabolism of methanol in the liver → accumulation of formic acid and formaldehyde in the blood → anion gap metabolic acidosis (seen on blood gas analysis) → severe nerve damage- Maximum effect: 48 hours after intoxication Clinical features:- Nausea, abdominal cramps- Headache, altered mental status- Severe acidosis- Optic neuropathy associated with vision problems and blindness
• Cryoglobulinemic vasculitis Cryoglobulin-mediated vasculitis; characterized by temperature dependent deposition of immune complexes in blood vessel walls and subsequent inflammation of involved vessels and surrounding tissue. Etiology: type II and III cryoglobulinemia (mixed cryoglobulinemia)- > 90% association with hepatitis C infection- Formation of hepatitis C IgG and IgM rheumatoid factor → immune complex formation with hepatitis C antigen → complement activation and inflammation of blood vessels. Clinical features:- Nonspecific systemic symptoms: fatigue, malaise, myalgia, arthralgia- Skin lesions (nearly 100% of cases): palpable purpura, ulceration, necrosis- Vasomotor symptoms: Raynaud's phenomenon, acrocyanosis- Polyneuropathy- Hepatosplenomegaly- Glomerulonephritis (severe cases or late complication) Diagnostics:- Cryoglobulinemia: cold-precipitable immune complexes (slow precipitation after 72 hours)- ↑ Rheumatoid factor (in almost all cases)- Hypocomplementemia (90% of cases)- Hepatitis C diagnostics: Hepatitis C RNA and anti-hepatitis C antibodies; ↑ Liver transaminases- Skin or renal biopsy: evaluate inflammatory vascular changes and renal damage; cryoglobulin deposits may be detected in glomeruli. Treatment:- Treatment of underlying diseases: hepatitis C infection (IFN-α, ribavirin)- Immunosuppression
• Fibromuscular dysplasia Women age < 50 with 1 of the following:- Severe or resistant hypertension- Onset of hypertension before age 35- Sudden increase in blood pressure from baseline- Increase in creatinine (≥ 0.5-1 mg/dL) after starting ACE inhibitor or AR-blocker & without significant effect on blood pressure- Systolic-diastolic epigastric bruit Clinical presentation:- Resistant hypertension from renal artery involvement- Cerebrovascular FMD with symptoms of brain ischemia (eg, amaurosis fugax, Horner's syndrome, TIA, stroke)- Nonspecific symptoms (e.g., headache, pulsatile tinnitus, dizziness) from carotid or vertebral artery involvement- Can also involve iliac, subclavian & visceral arteries Diagnosis and follow-up:- Noninvasive testing preferred (e.g., CT angiography, duplex ultrasound)- Catheter-based digital substraction arteriography for patient with inconclusive noninvasive testing- Medically treated patients need follow-up blood pressure & creatinine every 3-4 months & renal ultrasound every 6-12 months Treatment:- Antiplatelet drugs (e.g., aspirin) for stroke prophylaxis is recommended for all patients.- Antihypertensive therapy: ACE inhibitors, angiotensin receptor blockers, calcium channel blocker, beta blockers - Patients who are symptomatic: percutaneous transluminal angioplasty
• Medications that cause hyperkalemia - Nonselective beta-blockers - ACE inhibitor, ARB, K+ sparing diuretics - Digitalis - Cyclosporine (Blocks aldosterone activity) - Heparin (Blocks aldosterone production) - NSAIDs (Decreases renal perfusion resulting in decreased K+ delivery to the collecting ducts) - Succinylcholine (Causes extracellular leakage of potassium through Ach receptors) - Trimethoprim (Block the ENaC channel)
• Hepatorenal syndrome HRS occurs as cirrhosis progresses and patients develop splanchnic arterial dilation and an overall decrease in vascular resistance. This, in turn, activated the RAAS system and results in local renal vasoconstriction with decreased perfusion and glomerular filtration. Precipitating factors:- Reduced renal perfusion- GI bleed, vomiting, sepsis, excessive diuretic use, SBP- Reduced glomerular pressure & GFR Diagnosis:- Renal hypoperfusion- FeNa < 1% (or urine Na < 10 mEq/L)- Absence of tubular injury- No RBCs, protein, or granular casts in urine- No improvement in renal function with fluids Treatment:- Address precipitating factors (eg, hypovolemia, anemia, infection)- Splanchnic vasoconstrictors (midodrine, octreotide, norepinephrine)- Liver transplantation
• Chronic bacterial prostatitis Epidemiology:- Young & middle-aged men- ↑ Risk with diabetes, smoking, urinary tract procedure Pathogens:- Coliforms enter from urethra via intraprostatic reflux- E. coli causes > 75% of cases Clinical features:- Recurrent UTIs (with the same organism)- +/- Prostatic tenderness & swelling (often absent)- Pain with ejaculation- History of antibiotic treatment → transient improvement Diagnosis:- Pyuria and bacteriuria on urinalysis- Bacteria in prostatic fluid > bacteria in urine- Fractional urine examination: Four-glass test (according to Meares‑Stamey) Treatment: Fluoroquinolones (eg, ciprofloxacin) for 6 weeks
• Advertisement
• Acute epididymitis Etiology:- Age < 35: sexually transmitted (chlamydia, gonorrhea)- Age > 35: bladder outlet obstruction (coliform bacteria) Clinical features:- Unilateral, posterior testicular pain which develops over several days- Epididymal edema- Tender cord (DD: torsion)- Pain improved with testicular elevation (Prehn sign positive)- Dysuria, frequency Diagnosis:- NAAT for chlamydia & gonorrhea- Urinalysis/culture- Scrotal ultrasound: To rule out testicular torsion or if abscess is suspected Treatment:- Suspected UTI with enteric organisms (> 35 years): Fluoroquinolones- Suspected UTI with chlamydia/gonorrhea (< 35 years): Ceftriaxone and doxycycline- Scrotal elevation, ice packs, NSAIDs
• Male hypogonadism Primary (testicular disease)- ↓ Energy/libido, ↓ body hair- Gynecomastia more likely- ↑ LH/FSH- ↓↓ Testosterone/sperm count Etiology:- Congenital: Klinefelter syndrome, varicocele- Acquired: Radiation, infection (eg, mumps), trauma, medications Evaluation:- Karyotype Secondary (pituitary/hypothalamic disease)- ↓ Energy/libido, ↓ body hair- Gynecomastia less likely- ↓/Normal LH/FSH- ↓ Testosterone/sperm count Etiology:- Congenital: Kallman syndrome- Gonadotropin suppression: Hyperprolactinema, glucocorticoids/opiates- Gonadotroph cell damage: Benign/malignant tumors, pituitary apoplexy, infiltration (eg, hemochromatosis) Evaluation: - Prolactin- Transferrin- +/- MRI
• 5-alpha-reductase deficiency Pathogenesis:- 46, XY genotype- Impaired testosterone to DHT conversion- Impaired virilization during embryogenesis- Normal male testosterone & estrogen levels Clinical features:- Male internal genitalia (eg, testes, vas deferens)- Female external genitalia (eg, blind-ending vagina)- Phenotypically female at birth- Virilization at puberty (↑ testosterone)→ Clitoromegaly→ Increased muscle mass→ Male-pattern hair development→ Nodulocystic acne
• Anal & perianal masses External hemorrhoid:- Dusky/purple lump or polyp- Associated itching, bleeding- Thrombosis: acute enlargement with pain Internal hemorrhoid:- Intermittent itching, painless bleeding, leakage of stool- Detected with digital rectal exam or anoscopy (unless prolapsed) Perianal abscess:- Fluctuant mass/swelling with erythema- Fever- Gradual onset Anogenital wart:- Pink or flesh-colored papules, plaques, or cauliflower-shaped masses- Chronic onset- Mild itching, bleeding Anorectal cancer:- Squamous cell carcinoma most often- Bleeding, pain- Ulcerating, enlarging mass Skin tags:- Small, flesh-colored papules- May represent external terminus of anal fissure (sentinel tag)
• Serum sickness-like reaction Type III hypersensitivity reaction Etiology:- Medications: β-lactams (eg, penicillin, amoxicillin, cefaclor) or TMP-SMX- Antivenom or antitoxin containing animal proteins or serum- Infections: Hepatitis B Clinical features:- Fever- Rash (urticarial or pruritic)- Arthralgias, myalgia- Headache, blurred vision- Abdominal pain, diarrhea, nausea/vomiting- Lymphadenopathy Course:- Symptoms usually appear 1-2 weeks after exposure
• Anal fissures A longitudinal tear of the perianal skin distal to the dentate line, often due to increased anal sphincter tone. Etiology:- Local trauma (eg, constipation, prolonged diarrhea, anal sex)→ located at the posterior commisure (6 o'clock in the lithotomy position)- Inflammatory bowel disesase (eg, Crohn disease)- Malignancy Clinical features:- Pain with bowel movements- Bright red blood on toilet paper or stool surface- Perianal pruritus- Chronic fissure may have skin tag at distal end Treatment:- High-fiber diet & adequate fluid intake- Stool softeners- Sitz baths- Topic anesthetics & vasodilators (eg, nifedipine, nitroglycerin)
• Urethral stricture Etiology:- M > F- Urethral trauma (eg, catheterization)- Urethritis- Radiotherapy Clinical features:- Weak or spraying stream- Incomplete emptying- Irritative voiding (eg, dysuria, frequency) Complications:- Acute urinary retention- Recurrent urinary tract infection- Bladder stones Diagnostics:- Postvoid residual, uroflowmetry- Urethrography- Cystourethroscopy Management:- Dilation- Urethroplasty
• Interstitial cystitis (bladder pain syndrome) Epidemiology:- W > M- Associated with psychiatric & pain disorders (eg, fibromyalgia) Clinical features:- Bladder pain with filling, relief with voiding- ↑ Urinary frequency, urgency- Dyspareunia Diagnosis:- Bladder pain with no other cause for ≥ 6 weeks- Normal urinalysis Treatment:- Not curative, focus is on improving quality of life- Behavioral modification, avoidance of triggers, physical therapy- Amitriptyline, pentosan polysulfate sodium- Analgesics for acute exacerbations
• Hypercalcemia of malignancy Etiology:- PTHrP secretion (80%) of cases: Squamous cell, renal/bladder, gynecological malignancy, breast- 1,25(OH) vitamin D: Lymphoma- Bone metastasis: Breast, multiple myeloma, lymphoma Clinical features:- Mild to moderate: Nausea, fatigue, constipation, ileus- Severe (> 12 mg/dL): Confusion, weakness, delirium, coma- Tumor related: Anorexia/cachexia, local pain, mass effects Diagnosis:- Serum calcium often severely elevated- Elevated PTHrP, suppressed PTH- Localization, identification of primary tumor
• Urge incontinence Sudden, overwhelming, or frequent need to void Pathophysiology: Detrusor overactivity Treatment:- Lifestyle modifications- Bladder training- Antimuscarinic drugs (eg, oxybutynin)
• Stress incontinence Leakage with Valsalva (coughing, sneezing, laughing) Treatment:- Lifestyle modifications- Pelvic floor exercises- Pessary- Pelvic floor surgery
• Overflow incontinence Constant, involuntary dribbling & incomplete emptying Pathophysiology: Impaired detrusor contractility or bladder outlet obstruction → chronically distended bladder with ↑ bladder pressure → dribbling of urine when intravesical pressure > outlet resistance Treatment:- Identify & correct underlying cause- Cholinergic agonists (eg, bethanechol)- Intermittent self-catheterization
• Crystal-induced acute kidney injury Common etiologies:- Acyclovir- Sulfonamides- Methotrexate- Ethylene glycol- Protease inhibitors- Uric acid (tumor lysis syndrome) Clinical features:- Usually asymptomatic- AKI ≤ 7 days of starting drug- Urinalysis: Hematuria, pyuria, & crystals- Increased risk with volume depletion, CKD Treatment:- Discontinuation of drug- Volume repletion- Loop diuretic
• Peyronie disease Fibroproliferative disorder affecting the tunica albuginea of the penis. Pathophysiology: Repetitive blunt trauma to the penis during sexual intercourse with subsequent aberrant wound healing. Clinical features:- Penile pain- Curvature- Dosal nodules or plaques Treatment:- Resolves over 1-2 years- NSAIDs for pain- Pentoxifylline to reduce fibrosis- Intralesional injections of collagenase- Surgery in refractory cases
• Genitourinary syndrome of menopause Symptoms:- Vulvovaginal dryness, irritation, pruritus- Dyspareunia- Vaginal bleeding- Urinary incontinence, recurrent UTIs- Pelvic pressure Physical examination:- Narrowed introitus- Pale mucosa, ↓ elasticity, ↓ rugae- Petechiae, fissures- Loss of labial volume Treatment:- Vaginal moisturizer & lubricant- Topical vaginal estrogen
• Acute bacterial prostatitis Etiology:- Intraprostatic reflux of pathogens in urine- Primarily gram-negative bacilli (E coli ~75%) Clinical features:- Flu-like illness (eg, fever, chills, malaise, myalgia)- Lower urinary symptoms (eg, dysuria, urine retention, pelvic pain) Diagnosis:- Digital rectal exam – tender, swollen prostate- Urine culture Treatment:- 6 weeks of TMP-SMX or fluoroquinolone
• Uric acid kidney stones Risk factors:- Increased uric acid excretion: Gout, myeloproliferative disorders- Increased urine concentration: Hot, arid climates; dehydration- Low urine pH: Chronic diarrhea (GI bicarbonate loss), metabolic syndrome/diabetes mellitus Pathophysiology:- Acidic urine favors formation of uric acid (insoluble) over urate (soluble)- Supersaturation of urine with uric acid precipitates crystal formation Clinical features:- Radiolucent stones (not visible on x-ray)- Uric acid crystals on urine microscopy- Urine pH usually < 5.5 Treatment: Alkalinization of urine (potassium citrate)
• Testicular torsion Testicular torsion is caused by twisting of the spermatic cord due to inadequate fixation of the lower pole of the testes to the tunica vaginalis. The twisting leads to compression of the pampiniform plexus and reduced venous outflow. Epidemiology:- Most common in adolescents Clinical features:- Testicular, inguinal, abdominal pain- Nausea, vomiting- Horizontal testicular lie with elevated testicle- Absent cremasteric reflex- Swollen, erythematous scrotum Imaging: Only in ambiguous cases!- No blood flow on scrotal ultrasound with Doppler Management:- Testicular torsion is a medical emergency and should be treated upon suspicion within 6 hours of the onset - Surgical detorsion & fixation with exploration of the contralateral side- Manual detorsion (if immediate surgery is not available)
• Treatment of acute cystitis Uncomplicated cystitis:- Nitrofurantoin for 5 days (avoid in suspected pyelonephritis or creatinine clearance < 60 mL/min)- Trimethoprim-sulfamethoxazole for 3 days (avoid if local resistance rate > 20%)- Fosfomycin single dose- No urine culture needed Complicated cystitis:*- Fluoroquinolones (5-14 days), extended-spectrum antibiotic (e.g., ampicillin/gentamicin) for more severe cases- Obtain sample for urine culture prior to initiating therapy & adjust antibiotic as needed *Associated with diabetes, pregnancy, renal failure, urinary tract obstruction, indwelling catheter, urinary procedure, immunosuppression & hospital-acquired Children: Third-generation cephalosporin (e.g., cefixime)
• Cryptorchidism Risk factures:- Prematurity- Small for gestational age- Low birth weight (< 2.5 kg)- Genetic disorders Clinical features:- Empty, hypoplasitc, poorly rugated scrotum or hemiscrotum- ± Inguinal fullness Treatment: Orchiopexy before age 1 Complications:- Inguinal hernia- Testicular torsion- Subfertility- Testicular cancer (the risk of cancer is not necessarily eliminated by surgery)
• Advertisement
• Glomerular vs. nonglomerular hematuria Glomerular hematuria- Microscopic > gross- Etiologies:→ Glomerulonephritis: Poststreptococcal, IgA nephropathy→ Basement membrane disorder: Alport syndrome- Presentation: nonspecific, nephritic syndrome- Urinalysis: Blood & protein; RBC casts, dysmorphic RBCs Nonglomerular hematuria- Gross > microscopic- Etiologies:→ Nephrolithiasis→ Cancer (eg, renal, prostate)→ Polycystic kidney disease→ Infection (eg, cystitis)→ Papillary necrosis- Presentation: Dysuria, urinary obstruction- Urinalysis: Blood but no protein; normal-appearing RBCs
• Management of hypercalcemia Severe (calcium > 14 mg/dL) or symptomatic:- Short-term (immediate) treatment→ Normal saline hydration plus calcitonin→ Avoid loop diuretics unless volume overload (heart failure) exists- Long-term treatment→ Bisphosphonate (zoledronic acid) Moderate (calcium 12-14 mg/dL):- Usually no immediate treatment required unless symptomatic- Treatment is similar to that for severe hypercalcemia Asymptomatic or mild (calcium < 12 mg/dL)- No immediate treatment required- Avoid thiazide diuretics, lithium, volume depletion & prolonged bed rest
• Varicocele Clinical presentation:- Soft scrotal mass ("bag of worms")→ ↓ In supine position→ ↑ With standing/Valsalva maneuvers- Subfertility- Testicular atrophy Ultrasound findings:- Retrograde venous flow- Tortuous, anechoic tubules adjacent to testis- Dilation of pampiniform plexus veins Treatment:- Gonadal vein ligation (boys & young men with testicular atrophy)- Scrotal support & NSAIDs (older men who do not desire additional children)
• Chronic pelvic pain syndrome Clinical features:- Pain in pelvis, perineum, genitalia- Irritative voiding symptoms (eg, urgency, hesitancy)- Hematospermia, pain with ejaculation Diagnosis:- No or mild prostate tenderness- Sterile urine culture Management:- Alpha blockers (eg, tamusolin)- Antibiotics (eg, ciprofloxacin), especially if history of UTI- 5-alpha-reductase inhibitors (eg, finasteride)
• Analgesic nephropathy Etiology: - NSAIDs- AcetaminophenPatients commonly present with a history of chronic headaches or chronic back pain. Pathophysiology: Inhibition of prostacyclin synthesis → vasoconstriction of the medullary blood vessels → papillary ischemia and papillary necrosis Clinical features:- Painless hematuria- Pyuria- Fatigue- Nausea- Can have chronic tubulointerstitial nephritis or hematuria due to papillary necrosis Diagnosis:- Elevated creatinine with urinalysis showing hematuria or sterile pyuria- Can have mild proteinuria (< 1.5 g/day)- CT can show small kidneys with bilateral renal papillary calcifications
• Urethritis in men Etiology:- Neisseria gonorrheoae (most common)- Chlamydia trachomatis- Mycoplasma genitalium- Trichomonas (rare) Clinical features:- Dysuria- Discharge- Urgency- ↑ Voiding frequency Diagnosis:- Urinalysis- Gram stain & culture- NAATDysuria with urethral discharge and no organism on Gram staining suggests C. trachomatis or M. genitalium! Treatment:- Azithromycin OR doxycyclinePLUS ceftriaxone if gonococcus is suspected or not ruled out
• Magnesium toxicity Clinical features:- Mild: Nausea, flushing, headache, hyporeflexia- Moderate: Areflexia, hypocalcemia, somnolence- Severe: Respiratory paralysis, cardiac arrest Treatment:- Stop magnesium therapy- Give IV calcium gluconate bolus
• Penile fracture Traumatic rupture of the tunica albuginea and the corpora cavernosa of the erect penis. Etiology:- During sexual intercourse; most commonly occurs with the penetrative partner on top- Aggressive masturbation methods Clinical features:- Cracking, snapping, or popping sound- Immediate detumescence (loss of erection)- Pain- Pronounced soft tissue swelling, curving, and hematoma ("eggplant appearance")- Blood at the urethral meatus in concomittant urethral injury Diagnostics:- Retrograde urethrography: performed if urethral injury is suspected→ Blood at the meatus→ Hematuria→ Dysuria→ Urinary retention Treatment:- Surgical → Exploration and evacuation of hematoma→ Suture of rupture in the tunica albuginea
• Acute tubular necrosis Causes ∼ 85% of intrinsic AKIs Location: - Ischemic damage: straight segment of the proximal tubule and the straight segment of the distal tubule (i.e., the thick ascending limb) - Toxic damage: convoluted segment of the proximal tubule  Etiology:- Ischemic: Prolonged hypovolemia/shock, thromboembolism, thrombotic microangiopathy, cholesterol embolism (atheroemboli)- Toxic: → Contrast-induced nephropathy→ Medication: aminoglycosides, cisplatin→ Pigment nephropathy: Myoglobinuria due to rhabdomyolysis (crush syndrome), hemoglobinuria associated with hemolysis→ Acute uric acid nephropathy Urinary sediment: brownish ("muddy") granular epithelial cell casts, renal tubular epithelial cells (due to denudation of tubular basement membrane)
• Contrast-induced nephropathy Acute kidney injury after IV administration of iodinated contrast medium Risk factors:- Chronic kidney disease (esp. in patients with diabetes mellitus, multiple myeloma)- Congestive heart failure, arterial hypotension- Nephrotoxic drugs (esp. NSAIDs)- Anemia- Dehydration Course:- Creatinine is highest after 3-5 days and usually falls back to the patient's baseline level within 1 week.- The course is usually mild (end-stage renal disease usually only occurs in patients with pre-existing CKD). Prevention:- Always evaluate kidney function before administering contrast agent.- Use low dose and concentration of contrast medium.- Discontinue nephrotoxic substances before administration.- Ensure hydration: isotonic NaCl before and after administration of contrast medium (isotonic bicarbonate can also be used - Acetylcysteine 
• Albright hereditary osteodystrophy A constellation of physical findings that occur in patients with pseudohypoparathyroidism type 1a and pseudopseudohypoparathyroidism. Mode of inheritance: usually autosomal dominant Pathophysiology: the body does not respond to parathyroid hormone Clinical features:- Short stature, round face, as well as metacarpal and metatarsal shortening (shortened fourth and fifth digits)- Intellectual disability (oligophrenia)- Additionally signs of hypoparathyroidism: hypocalcemia, tetany, cerebral seizures, intracranial calcifications, and tooth anomalies Laboratory findings:- Pseudohypoparathyroidism type 1a: ↑ PTH, ↓ calcitriol, ↓ calcium, ↑ phosphate- Pseudopseudohypoparathyroidism: normal PTH, calcitriol, calcium, and phosphate
• Familial hypocalciuric hypercalcemia Etiology: autosomal dominant inactivating mutation in the CaSR gene → decreased sensitivity of calcium-sensing receptors in the kidneys and parathyroid gland Clinical features:- Usually asymptomatic (incidental finding)- Neonatal hypocalcemia in children of mothers with FHHDuring pregnancy, the maternal hypercalcemia results in hypercalcemia in the fetus and supresses their endogenous PTH production. After birth, when the mother is not supplying the child with calcium via the placenta anymore, the neonate presents with hypoparathyroidism and hypocalcemia. Diagnosis:- Hypercalcemia and normal or increased PTH- Hypocalciuria:→ ↓ 24-hour urinary calcium excretion (< 200 mg/ day)→ ↓ Ca/Cr clearance ratio (< 0.01) Therapy: no treatment necessary
• Type 1 renal tubular acidosis Pathophysiology: inability of the intercalated cells of the distal tubule to secrete H+ Etiology:- Sporadic, familial- Autoimmune diseases (e.g., Sjögren's syndrome, rheumatoid arthritis, SLE, primary biliary cirrhosis, autoimmune hepatitis, Hashimoto's thyroiditis)- Nephrocalcinosis (e.g., hyperparathyroidism, vitamin D toxicity)- Sickle cell nephropathy- Drugs: ifosfamide, amphotericin B, lithium, NSAIDs Clinical features:- Nephrocalcinosis- Polyuria → polydipsia, dehydration- Impaired growth Diagnostics:- Non-anion gap metabolic acidosis (i.e., normal anion gap)- Hypokalemia- Hypocalcemia- Urine pH > 5.5 Treatment: alkalinization therapy with sodium bicarbonate
• Type 2 renal tubular acidosis Pathophysiology: Inability of the proximal convoluted tubule to reabsorb HCO3-- Fanconi syndrome: Associated with other defects of resorption (e.g., potassium, glucose, phosphate, amino acids) Etiology:- Sporadic, familial- Cystinosis, tyrosinemia, galactosemia- Multiple myeloma- Amyloidosis- Drugs: Acetazolamide, ifosfamide, tetracyclines, aminoglycosides Clinical features:- Stunted growth- Polyuria → polydipsia, dehydration Diagnostics:- Non-anion gap metabolic acidosis- Hypokalemia- Fanconi syndrome: Hypouricemia, hypophosphatemia- Urine pH < 5.5- Bicarbonate infusion test: Urine pH rises above 7.5- Negative urine anion gap Treatment:- Alkaline therapy with potassium citrate
• Hydrocele Painless accumulation of fluid in a sac around one or both testicles which derives from the tunica vaginalis, a tissue covering the testes.Etiology:- Idiopathic (most common)- Secondary to underlying pathology (e.g., trauma, tumor, torsion)- Wuchereria bancrofti infection is the most common cause worldwide, but is basically nonexistent in the US Communicating or noncommunicating:- Communicating hydrocele (usually discovered in infancy): failed closure of processus vaginalis during development- Noncommunicating hydroceles: The fluid in noncommunicating hydroceles derives from the tunica vaginalis and is due to extensive secretion and/or reduced reabsorption of fluid.  Clinical features:- Fluctuant, painless swelling of affected scrotum- May be present since infancy or childhood.- May or may not be reducible.- Palpation above the swelling is possible: a normal spermatic cord and inguinal ring are present. - Positive transillumination Diagnosis:- Usually a clinical diagnosis- Ultrasound: hypoechoic fluid confirms the diagnosis. Treatment:- Usually resolves spontaneously within 6 months of birth- Indications for surgery→ If spontaneous resolution does not occur in children by 1 year of age→ Excessive discomfort and/or if scrotal skin integrity is compromised→ An underlying pathology is suspected→ Testicle not palpable→ If infertility is a concern Procedures:- Surgical excision of the hydrocele sac- Percutaneous aspiration of the hydrocele fluid combined with instillation of a sclerosing promoter into the sac 
• Priapism A sustained erection that lasts more than 4 hours, is not caused by sexual excitation, and is not relieved by ejaculation. Etiology:- Drugs: Treatment of erectile dysfunction (e.g., sildenafil), trazodone, prazosin- Hypercoagulable states: Sickle cell disease, leukostasis reactions associated with leukemia- Autonomic dysfunction: spinal cord stenosis, autonomic neuropathy, cauda equina syndrome- Renal pelvic tumors: bladder cancer, prostatic cancer Clinical features:- Painful erection (differential diagnosis: Peyronie's disease) - The corpus cavernosum is completely rigid.- No clinical features of perineal trauma are present.- Recurrent priapism (stuttering priapism): a form of ischemic priapism that occurs in men with sickle cell disease Diagnostics:- Penile blood gas analysis→ Low-flow priapism: dark blood with hypoxia, hypercapnia, and acidosis→ High-flow priapism: bright red blood with normal arterial values- Doppler ultrasound→ Low-flow priapism: poor arterial influx→ High-flow priapism: high arterial influx and adequate outflow Treatment:- First-line therapy→ Repeating intracavernosal injections of phenylephrine (alpha receptor agonist) up to an hour → Aspiration of sludged blood (up to 500 mL) from the corpus cavernosum with/without irrigation with normal saline- Second-line therapy (if detumescence does not occur): decompression of the penis by creating a shunt between the corpus cavernosum and either the glans or the corpus spongiosum (e.g., Winter or Ebbehoj techniques)- Supportive measures: Oxygen, adequate analgesia (with opiates if necessary), and hydration with IV fluids- Patients with sickle cell disease who develop priapism require exchange transfusion.
• Chancroid Chancroid (also known as soft chancre) is a highly contagious sexually transmitted infection (STI) caused by Haemophilus ducreyi. Clinical features:- Very painful genital ulcers- Deep, small (∼ 10-20 mm in diameter), well-demarcated lesions with a grayish necrotic base- Painful inguinal lymphadenopathy- An asymptomatic course is more likely in women. Diagnostics: Clinical- Gram-stain: gram-negative rods in ulcer exudate (swab sample) suggestive of Haemophilus ducreyi infection Treatment:- Antibiotic treatment: single dose oral azithromycin or IM ceftriaxone- Examine and treat sexual partner(s).
• Kallmann syndrome More common in men Characterized by delayed onset of puberty and hyposmia/anosmia Often associated with structural/developmental abnormalities: cryptorchidism, cleft palate, scoliosis, renal agenesis
• Urinary tract infection (UTI) Etiology:- Escherichia coli: in ∼ 80% of UTIs- Proteus mirabilis: urease-producing → causes alkaline urine with an ammonia smell- Klebsiella pneumoniae- Enterobacter species- Staphylococcus saprophyticus: Urinary nitrates are negative- Enterococci (e.g. Enterococcus faecalis)- Ureaplasma urealyticum- Viruses: Adenoviruses can cause hemorrhagic cystitis in children and immunocompromised patients. Predisposing factors:- Female sex- Sexual intercourse- Catheter-associated urinary tract infection (CAUTI): caused by indwelling urinary catheters; most common cause of iatrogenic or nosocomial urinary tract infection- Structural or functional abnormalities of the urinary tract (e.g., BPH, vesicoureteral reflux, urinary bladder diverticulum, neurogenic bladder, calculi or stones)- Pregnancy- Diabetes mellitus- Immunocompromise- Uncircumcised males- Chronic constipation in toddlers
• Treatment of pyelonephritis Uncomplicated pyelonephritis- Outpatient treatment- Fluoroquinolones (e.g., ciprofloxacin, levofloxacin) for 7 days Complicated pyelonephritis- Characterized by: Urinary tract abnormalities (e.g., obstruction, indwelling catheter), recent surgery to the urinary tract, renal impairment, immunosuppression and/or severe comorbidities- Inpatient- Intravenous antibiotics (e.g., fluoroquinolone, aminoglycoside ± ampicillin) for 14 days - Obtain sample for urine culture prior to initiating therapy & adjust antibiotic as needed

back  |  next 2 / 3