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74 Cards in this Set
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Symptoms
Dysuria, chills/fever, low back pain, perineal pain, frequency. |
Prostatitis
Pathology Escherichia coli (usually aerobic gram-negative rods). Chlamydia, nonspecific inflammation. |
Diagnosis
History and physical, large (boggy if chronic) tender prostate gland. Avoid prostate massage (bacteremia risk). Treatment Steps 1. Antibiotics (e.g., fluoroquinolones, tetracycline), often treated for up to 6 weeks. 2. Nonsteroidal anti-inflammatory drugs (NSAIDs). 3. Sitz baths. |
|
Symptoms
Tender, enlarged testicle and/or epididymis; fever; scrotal thicken- ing. |
Epididymitis
Pathology Organisms include Neisseria gonorrhoeae, E. coli, and Chlamydia |
Diagnosis
History and physical, scrotum may be red/tender. Pyuria, epididymis tender. Urethra/urine culture and Gram stain (if patient is having discharge). Treatment Steps 1. Tetracycline, fluoroquinolones, or antibiotic as per culture. 2. NSAIDs. 3. Scrotal support. |
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Symptoms
Fever, testicular size increase, scrotal pain, and erythema. |
Orchitis (Testicular Inflammation)
Orchitis may be associated with mumps, tuberculosis, or other infections. |
Diagnosis
History and physical, rule out mumps or torsion, usually no urethral symptoms/discharge. Treatment Steps 1. Antibiotic (if bacterial). 2. NSAIDs. 3. Scrotal support. 4. Warm soaks. |
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Symptoms/Diagnosis
Urethral discharge, dysuria. Urethral culture and Gram stain (to rule out sexually transmitted diseases and other infection). |
Urethritis
Pathology Sexual transmission common. Gonococcal and nongonococcal ure- thritis (Chlamydia, Trichomonas, herpes simplex). |
Treatment Steps
Antibiotics tailored to the specific etiology. |
|
Symptoms
Caused by infection with N. gonorrhoeae. Dysuria, urethritis/dis- charge (thick yellow). Less commonly can cause pharyngitis. |
Gonorrhea
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Diagnosis
History and physical, culture/Gram stain (gram-negative intracellular diplococci). TREATMENT OPTIONS FOR GONORRHEA • Cefixime (Suprax) 400 mg PO × 1 • Ceftriaxone (Rocephin) 400 mg PO × 1 • Ciprofloxacin 500 mg PO × 1 • Ofloxacin 400 mg PO × 1 |
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Symptoms
Penile painless lesion: chancre |
Syphilis
See also Chapter 9, section I.C.4. Description STD caused by the spirochete Treponema pallidum. Four stages: primary, secondary, latent, and tertiary. |
Diagnosis
Serologic test for syphilis (rapid plasma reagin [RPR], Venereal Dis- ease Research Laboratory [VDRL]) and fluorescent treponemal antibody absorption (FTA-ABS) studies. Treatment Steps Benzathine penicillin G, 2.4 million U IM (if allergic to penicillin, give doxycycline). For primary disease, one injection. |
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Symptoms
Dysuria, frequency, or asymptomatic. Possible abnormal vaginal dis- charge. Often coinfection with gonorrhea. Caused by infection with Chlamydia trachomatis. |
Chlamydia
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Diagnosis
Urethral culture/Gram stain, Chlamydia culture. Treatment Steps 1. Doxycycline 100 mg twice daily for 1 week (not safe in pregnancy). 2. Azithromycin 1 g PO. 3. Metronidazole 2 g PO. |
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Symptoms
Testicular pain/swelling, vomiting and/or abdominal pain. May have initially only abdominal pain; check scrotum! |
Testicular Torsion
Description Testicular rotation and loss of blood supply. Most common cause of scrotal swelling in children. Testicular torsion is a urologic emergency! If not diagnosed and treated promptly, infarction and loss of testicle may occur Pathology Abnormal tunica vaginalis attachment allowing room for testicular twisting (“bell-clapper deformity”). |
Diagnosis
History and physical, pain unchanged or worse with testicular elevation. Urine negative, and affected testicle may be elevated in position. Treatment Steps Surgery (within 4–6 hours, if possible). |
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Symptoms
None. Pick up on exam only (50% of premature males have undescended testicle). |
Cryptorchidism (Undescended Testicle)
Pathology Failure of testes to descend normally. Exact cause not defined. RYPTORCHIDISM • Undescended testicle has an increased risk of developing cancer. • Risk is not reduced with orchiopexy. |
Diagnosis
History and physical. Rule out retractile testis (hyperactive cremaster muscle pull). In adults, consider computed tomography (CT) Treatment Steps 1. Surgery by age 1 (orchiopexy). 2. Hormones have been tried (human chorionic gonadotropin [hCG]). |
|
Symptoms
Obstruction (hesitancy, dribbling, reduced stream force), and ur- gency, nocturia, frequency. Some cases of BPH can cause near total obstruction of urinary flow and result in renal failure |
Prostate Neoplasm—Benign
Prostatic Hyperplasia (BPH) Description Enlargement of the prostate gland due to glandular and/or stromal hyperplasia. Exceedingly common in men as they age. Pathology Hyperplasia or increased tone of bladder neck/prostatic urethra, increasing incidence with age. |
Diagnosis
History and physical. Ultrasound, urodynamics, cystoscopy Treatment Steps 1. Watchful waiting. 2. α-Blocker (prazosin, terazosin, doxazosin [Cardura], tamsulosin [Flomax]). 3. Bulk reducers (finasteride [Proscar]), 5α-reductase inhibitor. In- hibits conversion of testosteron to dihydrotestosterone. 4. Surgical reduction (transurethral prostatectomy [TURP]) |
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SCROTAL MASS
differential diagnosis |
SCROTAL MASS
• Testicular tumor • Hydrocele • Varicocele • Epididymal cyst • Testicular torsion • Epididymal orchitis • Hernia • Inguinal cord tumor • Hematoma |
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Symptoms
None. May be associated with chordee (ventral penile curve). |
Penile Disorders—Hypospadias
Description Most frequent urologic anomaly, with meatus below penis tip. Pathology Urethral ridges do not fuse, possibly hereditary. • Commonly associated with other conditions such as inguinal hernias and cryptorchidism (undescended testes). • The penis is more likely to have chordee, which is ventral shortening and curvature |
Treatment Steps
Surgical if meatus too proximal. Look for associated anomalies. |
|
Symptoms
Nontender scrotal mass. |
Hydrocele and Varicocele
Description Hydrocele—Fluid around testis (in tunica vaginalis layers). Varicocele—Pampiniform plexus vein dilation. Pathology Hydrocele—Patent processus vaginalis. Varicocele—Inefficient pampiniform valves. |
Diagnosis
Transillumination, history and physical, ultrasound. Varicocele may be absent when supine, increase if straining/standing (Valsalva). Treatment Steps 1. Observation. 2. Surgical if not resolving on own, or if resulting in infertility (vari- cocele), or symptoms (pressure). |
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Symptoms
May be asymptomatic, prostatitis, obstruction (abnormal stream an- gle/spraying, or narrow stream), cystitis. |
Urethral Stricture
Pathology May have history of gonorrhea, trauma, or other infections causing fibrotic narrowing of the urethra. |
Diagnosis
Cystourethrogram, history and physical, flow studies, culture, cystoscopy. Treatment Steps 1. Optical internal urethrotomy. 2. Primary resection. 3. Dilation. |
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SIGN OR SYMPTOM:
HEMATURIA |
hink of: Kidney stones,
cystitis, menstrual cycle, anticoagulation/coagulopa- thy, bladder cancer, trauma, Foley catheter manipulation, infections (common as well as uncommon, such as Schistosoma haematobium), renal failure (in some ways |
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Urinary Tract Infection
|
Epidemiology—More frequent in females (except in neonates), and
increases with age. Impact—Recurrent infections and renal damage. Risk Factors—Obstructive uropathy (calculus, stricture/valves), vesicoureteral reflux, diabetes mellitus, sexual activity, and pregnancy. |
Prevention—Patient education, for both prevention/hygiene, early
intervention/treatment, and prophylactic antibiotics where indi- cated. |
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Toxic Nephropathy
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Epidemiology—Common causes include analgesics, penicillin/
sulfa, phenytoin sodium (Dilantin), cimetidine (Tagamet), heavy metals, and aminoglycosides. Noted in chronic pain patients with continued analgesic use. Impact—Papillary necrosis/renal failure. Risk Factors—Compounds listed, occupational/environmental ex- posure to toxins, and both calcium disorders (sarcoid, multiple myeloma, etc.) and antineoplastic agents. |
Prevention—Patient education and early intervention/diagnosis
(discontinue the offending agent). Special consideration is given to the elderly in whom reduced renal function may contribute to elevated serum toxin levels and earlier toxicity. |
|
Renal Failure/Disease
For absorptive hypercalciuria For renal hypercalciuria For hyperuricosuria For struvite/chronic infection stones For hypercystinuria For obstructions |
Renal Failure/Disease Prevention
Prevention of acute renal failure and of urinary tract disease secondary to formation of calculi and/or obstruction. Where absorptive hypercalciuria is noted, reduced-calcium diet, ion-exchange resin (sodium cellulose), hydration, and orthophosphates. For renal hypercalciuria use thiazides. For hyperuricosuria use allopurinol. For struvite/chronic infection stones, use repeat cultures/antibiotics. For hypercystinuria, alkalinize the urine. For obstructions, treat/remove obstruction when indicated |
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Limiting Renal Disease Progression
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Control underlying disorder (hypertension, diabetes mellitus, etc.).
Dietary measures include protein/potassium/phosphorus restric- tion for chronic renal failure. Limit extra dietary magnesium, treat acidosis, and supply additional calcium when required. |
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Dysuria
|
may be symptom of cystitis, or
urethral syndrome in females. |
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leukocytes in urine
need to r/o |
Pyuria is leukocytes in
urine, but not necessarily infection (pyuria and negative culture: rule out tuberculosis). |
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Hematuria
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may be sign of infection, cancer, found in runners, renal
disease. |
Always
abnormal in males; IVP and cystocope to rule out tumor |
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Casts in urine
leukocyte = RBC cast = |
uggest renal
disease (leukocyte, pyelonephritis; red blood cell [RBC] casts, glomerulitis). |
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Symptoms/Diagnosis
Cystitis presents as dysuria, frequency, nocturia, urgency. Urine dip, urinalysis, and culture used in certain cases. |
Cystitis
Description Cystitis is bladder infection. Pathology Cystitis usually from E. coli. |
Treatment Steps
1. Antibiotics. 2. Intravenous pyelogram (IVP), cystoscopy for recurrent/persistent cases |
|
Symptoms
Severe pain, nausea/vomiting, flank pain, hematuria. Caliceal, may be asymptomatic; proximal ureter, severe intermittent flank pain, colic; distal ureter/ureterovesicle junction, radiating pain, bladder irritation, groin pain. • Pain is often excruciating. |
Nephrolithiasis
Description Calculi (stones) in the urinary tract |
Diagnosis
History and physical, IVP, urine analysis. Uric acid stones not visible on plain x-ray (see Fig. 17–1). Treatment Steps 1. Prevention of further episodes: hydration and medical evalua- tion. 2. Symptomatic stones: small stones (5 mm) supportive measures and spontaneous passage (6 weeks). Larger or completely obstructive stones: upper tract—extracorporeal lithotripsy, lower tract—ureteroscopy. • Requires aggressive hydration and pain medications. • Urinalysis will often show microscopic hematuria. • Calcium-containing stones are seen on x-ray. • CT scanning is now used to visualize calculi. |
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Symptoms
Infection/pyelonephritis, kidney damage/uremia. |
Ureteral Reflux
Description Reflux of urine into ureter with voiding Pathology Short intramural ureter |
Diagnosis
History and physical, urine analysis and culture, IVP, voiding cystourethrography. Treatment Steps 1. Medical (watch and wait, antibiotics). 2. Surgical (ureteral reimplantation) |
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Symptoms
Voiding dysfunction. Failure to empty urine; failure to store urine |
Neurogenic Bladder
Pathology Sensory, motor, uninhibited, reflex, and autonomous. Sensory—No sensation of full bladder, diabetics, herniated disk. Motor—Sensation okay, but cannot initiate contraction, disk, po- lio, tumor. Uninhibited—No control, brain/central nervous system (CNS) le- sion or disease. Reflex Spinal Cord Injury, Autonomous—No connection from bladder to brain, spinal trauma. |
Diagnosis
History and physical, urodynamic testing (cystometrogram [CMG], flowmeter, etc.) Treatment Steps Failure to empty: 1. Clean intermittent catheterization. 2. Sphincterotomy. Failure to store: 1. Anticholinergics. 2. Collagen injections. 3. Bladder sling or artificial sphincter. |
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Symptoms
Loss of urine with activity, coughing, or without reason. |
Stress-Related Urinary Incontinence
Pathology Hypermobility of urethra and/or sphincteric incompetence. |
Diagnosis
History and physical, urinalysis and culture to rule out infection, urodynamic studies, cystoscopy, IVP (see Fig. 17–2). Treatment Steps 1. Pelvic floor exercise (Kegel exercises). 2. Bladder neck suspension. 3. Bladder sling surgery. |
|
Symptoms
Unable to retain urine, day or night, typically nighttime bedwetting |
Enuresis
Pathology Psychological, organic disease, or delayed CNS/neuromuscular de- velopment (most common etiology). |
Diagnosis
History and physical, excretory urogram, urine analysis, and culture Treatment Steps 1. Reassurance. 2. Evening fluid restriction. 3. 1-desamino-8-D-arginine vasopressin (DDAVP) |
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Symptoms
May be asymptomatic, also flank/back pain, decreased urine output, abdominal pain, infections. In infant may have multiple nonspecific symptoms. Pathology Obstruction, in child often uteropelvic junction obstruction; in adult may be BPH, calculus, tumor, aortic aneurysm (see Fig. 17–3) |
Hydronephrosis
Description Kidney/ureter damage from ureter obstruction |
Diagnosis
History and physical, ultrasound, IVP, check electrolytes, blood urea nitrogen (BUN), creatinine Treatment Steps 1. Surgical correction. 2. Stent obstructed area. |
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INCONTINENCE
Urge incontinence |
Detrusor hyperreflexia, neurologic origin, detrusor origin
r/o? |
rule out infection, carcinoma in situ.
Treat with anticholinergics, bladder augmentation when appropriate. |
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INCONTINENCE
Stress incontinence |
Urethral hypermobility, symptoms reproducible, anatomic not neurologic
origin. Subclass of intrisic sphincteric deficiency. |
Treat with pelvic floor strengthening, collagen
injections, surgical urethral suspension |
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BLADDER OUTLET OBSTRUCTION
Bulk obstruction |
Enlarged prostate, high pressure voiding, possible bladder instability. Treat
with bulk reduction |
5α-reductase inhibitor (finasteride) or tissue ablation (TURP, laser ablation,
open enucleation). |
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BLADDER OUTLET OBSTRUCTION
Increased tone |
Increased α-adrenergic tone of bladder neck or prostate/prostate capsule
smooth muscle. |
Treat with α-blockers (organ and CNS affect). Major side effect—orthostasis.
Surgery—bladder neck or prostate incisio |
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BLADDER OUTLET OBSTRUCTION
Urethral stricture |
Occlusion of urethra (usually bulbar).
Status postinfection (gonorrhea), trauma, prior catheterization |
Treatment—dilatation, optical urethrotomy, or surgical repair.
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Symptoms
Chills/fever, vomiting, flank pain, anorexia |
Pyelonephritis (Acute and Chronic)
Description Ascending infxn/inflammation into the kidney Pathology Usually E. coli. Also Pseudomonas. |
Diagnosis
History and physical, urine analysis (white blood cell [WBC] casts, pyuria) and culture, blood culture, complete blood count (CBC). Chronic pyelonephritis: renal damage with persisting infection. Treatment Steps Antibiotics (IV cephalosporin and aminoglycoside). If recurrent/chronic infection, rule out organic disease and coexisting medical conditions. PYELONEPHRITIS • If patient is not seriously ill, may be managed with oral antibiotics. • However, if patient has severe nausea/vomiting or appears ill (dehydration, hypotension), IV hydration and antibiotics may be needed first. • Total duration of treatment usually 10–14 days. |
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Symptoms
Hematuria, proteinuria, reduced glomerular filtration rate (GFR) resulting in hypertension, edema. |
Glomerulonephritis
Description Kidney inflammation with glomeruli as area of disorder. Pathology Inflammation/immune deposits resulting in glomerular injury. |
Diagnosis
History and physical, urine analysis and culture, serologic studies to attempt to define cause. Treatment Steps Varies according to etiology. 1. Acute––diuresis, bed rest, antihypertensives. 2. Rapid progression––steroids, cytotoxics, plasmapheresis |
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Multiple diseases cause
glomerulonephritis Infection Multisystem Drugs |
• Infections: Human
immunodeficiency virus (HIV), hepatitis B, endocarditis, poststreptococcal • Multisystem: Systemic lupus erythematosus, Goodpasture’s, Wegener’s, rheumatoid arthritis, polyarteritis nodosa • Drugs: Penicillamine, hydralazine, allopurinol, rifampin |
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Description/Treatment
MCD refers to a pathologic lesion of the glomerulus. It is the most common cause of nephrotic syndrome in children |
Minimal Change Disease (MCD)
Pathology Under light microscopy, the glomerulus is basically normal. Im- munohistochemistry is also unremarkable. However, changes are seen on electron microscopy: retraction of the epithelial foot processes, sometimes referred to as fusion of the foot processes. |
usually very responsive to steroids (prednisone), with a good prognosis. It is less responsive to steroids and has a slightly worse prognosis in
adults. |
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Symptoms
Gross hematuria after viral infection, fever, proteinuria, dysuria Pathology Immune deposits of IgA on glomeruli |
Immunoglobulin A (IgA) Nephropathy
Description Berger’s disease (a variety of Henoch–Schönlein purpura). |
Diagnosis
History and physical, possible elevated serum IgA, biopsy. Treatment Steps None. |
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Pathology
Microvascular glomerular damage (thickening of the glomerular basement membrane) and Kimmelstiel–Wilson lesions (nodular deposits in glomeruli). |
Diabetic Nephropathy
Description This is a clinical syndrome associated with diabetes, proteinuria, and, if uncontrolled, progressive renal failure. Patients are symptomatic as renal failure develops. It is the leading cause of chronic renal failure. |
TREATMENT OF DIABETIC NEPHROPATHY
• Prevention is of the utmost importance. • Excellent diabetic control (goal: hemoglobin A1C < 7.0). • Excellent blood pressure control (< 120/80). • Routine screening of urine for microalbuminuria (a small but abnormal degree of albumin in the urine, 30–300 mg/day). • Treatment of microalbuminuria with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers. • Early follow-up with a nephrologist is prudent. • If renal insufficiency progresses to failure, counseling and preparation should begin for hemodialysis and/or renal transplant. |
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Symptoms
Polyuria, nocturia, acute renal failure, fever, rash, joint pain. |
Interstitial Nephropathy
Pathology Wide variety of infections, toxins (heavy metals), calcium disorders, drugs, and systemic disorders as etiologic agents. |
Diagnosis
History and physical, eosinophilia, renal biopsy. |
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increase in BUN and
creatinine |
Azotemia
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decreased urine output (100–400mL/day).
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Oliguria
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basically no urine output (< 100mL/day).
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Anuria
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Acute Renal Failure
Description A decline in renal function over a short period of time (hours to days). |
Symptoms
Vary based on cause of the renal failure. Important to assess a de- cline in urine output, change in the quality of the urine flow or color, dysuria, hematuria, increase in abdominal size. Look for signs of volume status: skin turgor, peripheral edema. Diagnosis Assess for symptoms as above. Ask about any new medications that have been started. Routine labs include chemistries (specifically for potassium, CO2, BUN, creatinine, magnesium, phosphate, calcium). Also, urinalysis, urine electrolytes (particularly urine sodium and creatinine). Routine CBC, liver function tests (LFTs), electrocardio- gram (ECG), and chest x-ray (CXR). Other studies (e.g., KUB [kid- neys, ureters, bladder] or CT scan to rule out nephrolithiasis) are done as indicated. |
Treatment Steps
Varies according to the etiology. Some guidelines: 1. Prerenal: Improving renal blood flow may be accomplished with iv hydration, stopping ACE inhibitors, and in certain cases using vasopressors (dopamine). 2. Intrinsic renal: Varies according to etiology. 3. Postrenal: Foley catheter can be curative if obstruction caused by BPH. Removal of kidney stone, or ureteral or urethral stent if there are stenoses causing a blockage. 4. In all cases, meticulous attention paid to urine output and man- agement of electrolyte imbalances (hyperklemia). Also, remove all potentially nephrotoxic medications (NSAIDs, ACE inhibitors) and adjust the doses of necessary medications according the crea- tinine clearance. 5. Dialysis is used in certain cases INDICATIONS FOR DIALYSIS (AIEOU) • Acidosis • Intoxications • Electrolytes • Overload (fluid) • Uremia |
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ACUTE RENAL FAILURE
PRERENAL differential |
PRERENAL
Conditions in which there is decreased flow to the kidney. Commonly includes volume depletion (from gastrointestinal bleed, overdiuresis, severe dehydration). Also includes relative intravascular volume depletion and reduced renal blood flow (i.e., congestive heart failure, cirrhosis). |
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ACUTE RENAL FAILURE
INTRINSIC RENAL differential |
INTRINSIC RENAL
Conditions affecting the kidney directly. Includes the glomerulonephridites, acute tubular necrosis, rhabdomyolysis, multiple myeloma, interstitial nephritis, and amyloidosis. |
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ACUTE RENAL FAILURE
POSTRENAL differential |
POSTRENAL
Obstruction of flow existing somewhere in the urinary tract. In men, common cause is BPH. Also extrinsic compression by pelvic mass, kidney stones. |
One rule of thumb is when a patient is seen
initially, a Foley catheter should be placed. This will help to see if there is distal obstruction. Additionally, a renal ultrasound should be done to rule out hydronephrosis. |
|
Symptoms
May have reduced urine output, lethargy, hypertension, myopathy, pruritus, pericarditis, anemia. |
Chronic Renal Failure
Description Long-term renal function reduction. Diagnosis Assess for symptoms as above. Ask about any new medications that have been started. Routine labs include chemistries (specifically for potassium, CO2, BUN, creatinine, magnesium, phosphate, calcium). Also, urinalysis, urine electrolytes (particularly urine sodium and creatinine). Routine CBC, liver function tests (LFTs), electrocardio- gram (ECG), and chest x-ray (CXR). Other studies (e.g., KUB [kid- neys, ureters, bladder] or CT scan to rule out nephrolithiasis) are done as indicated. Pathology Etiology in numerous disorders. |
Treatment Steps
1. Diet control. 2. Balance electrolytes. 3. Treat anemia, osteodystrophy. 4. Dialysis |
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Symptoms
Children—growth retardation, rickets. Adults—may be asymptomatic, or bone pain, proximal muscle weak- ness. |
Renal Osteodystrophy
Description Skeletal abnormality secondary to chronic renal failure. Diagnose with typical x-ray findings Pathology Subperiosteal bone resorption. Results in osteitis fibrosa and osteomalacia. Most common skeletal lesion in chronic renal failure (CRF): osteitis fibrosa. Lack of erythropoietin results in CRF anemia. Serum phosphate is elevated with reduced GFR (e.g., chronic renal failure). Total serum calcium is reduced in CRF |
Treatment Steps
Control serum calcium/phosphorus (phosphate binders), parathy- roidectomy. Drug of choice for hypocalcemia/secondary hyper- parathyroidism is vitamin D |
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Symptoms
Hematuria, fever, flank pain, renal failure. |
apillary Necrosis
Description Kidney papilla necrosis. Pathology Ischemic, usually associated infection. Chronic disease, toxins, ob- structions. Often seen in patients with sickle cell disease. May be a complication of pyelonephritis |
Diagnosis
History and physical, IVP, urine analysis, and culture. Treatment Steps 1. Treat primary etiology (infection, etc.). 2. Remove mechanical obstruction |
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Symptoms
Hypertension, may be rapid onset at any age, difficult to control, childhood or older adult onset. |
Renovascular Hypertension
Description Stenosis of the renal arteries can cause systenic hypertension. • In a young female,? • In older patients,? |
RENAL ARTERY STENOSIS
• In a young female, suspect fibromuscular dysplasia, often amenable to stenting. • In older patients, suspect atherosclerosis as the cause. Diagnosis History and physical (epigastric bruit), IVP, renal/digital subtraction angiography (DSA), renal vein renin ratio > 1.5. Treatment Steps 1. Medication (captopril). 2. Surgical (including angioplasty). |
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Symptoms
Often asymptomatic. Over time, signs and symptoms of renal disease develop. Clinical diagnosis. Renal failure, proteinuria, hematuria, small kidneys, or no symptoms. |
Nephrosclerosis
Description A clinical syndrome involving long-standing hypertension, hypertensive retropathy, hypertrophy of the left ventricle, minimal protein- uria, and progressive renal insufficiency/failure. |
Treatment Steps
Control blood pressure and renal disease. |
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Symptoms
Hematuria, proteinuria, hypertension, edema, red cell/hyaline casts |
Lupus Nephritis
Description Lupus may present as interstitial nephritis or glomerulonephritis. Pathology Interstitial fibrosis and inflammation. Includes several histologic types (minimal, mesangial, focal, diffuse, and membranous). |
Diagnosis
History and physical, urine analysis, lupus symptoms (rash, fever, weight loss, joint symptoms, etc.), serologic testing (antinuclear antibodies [ANA], anti-DS-DNA, etc.), renal biopsy. Treatment Steps Prednisone, cyclophosphamide, azathioprine. Close follow-up by nephrologist and rheumatologist. |
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Symptoms
Hematuria, flank pain, hypertension, pyelonephritis, uremia. |
Inherited Disorders—Polycystic
Kidney Disease Description Hereditary cystic kidney disorder. Cysts also in liver and pancreas. Positive association of polycystic kidney disease and intracranial aneurysms. Pathology Adult Polycystic Kidney Disease—autosomal dominant, cysts. Infantile Polycystic Disease—autosomal recessive, collecting duct dila- tion |
Diagnosis
History and physical (enlarged kidney), IVP, ultrasound. Child: bilateral flank mass. Treatment Steps 1. Blood pressure control. 2. Dialysis. 3. Renal transplant |
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Electrolyte Disorder differential
Symptoms Confusion, vomiting, coma, nausea, lethargy |
Hyponatremia
Description Sodium < 130 mEq/L. Pathology Excess salt loss (diuretic use), water retention (renal/cardiac failure, syndrome of inappropriate antidiuretic hormone [SIADH]). (See also Chapter 3. HYPONATREMIA • Diuretics: Generally mild, worsened by free water intake, loss of K+, volume depletion, usually thiazide diuretics. • SIADH: Nonphysiologic release of antidiuretic hormone. Impaired water but normal Na+ excretion. Multiple etiologies: drugs, neuropsychiatric, pulmonary, postsurgical state. Raise serum Na+ at appropriate rate and treat underlying cause. • Edematous states: Renal failure, cardiac failure, cirrhosis. Requires specific therapeutic approaches. |
Treatment Steps
Salt loss—give saline. Water excess—restrict water. • Too rapid correction of hyponatremia can cause central pontine myelinosis (CPM). In CPM, central nervous system sequelae can vary, but the most devastating is known as "locked in syndrome," in which the patient has paralysis of the limbs and lower cranial nerves, but vertical eye movements, blinking, and alertness remain intact. |
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Electrolyte Disorder differential
Symptoms Thirst, hypotension, oliguria, hyperpnea, coma. |
Hypernatremia
Description Elevated sodium, > 145 mEq/L. Pathology Excess water loss, impaired thirst, and solute loss (diabetic ketoacidosis). |
Treatment Steps
Replace free water slowly. If sodium is corrected too rapidly, cerebral edema can result. This can be fatal • Too rapid correction of hypernatremia can cause brain edema. |
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Electrolyte Disorder differential
Symptoms Arrhythmia, muscle weakness/cramps, rhabdomyolysis. Diagnosis History and physical, serum electrolytes, ECG (smaller/wider T wave, U wave, atrioventricular [AV] block). |
Hypokalemia
Description Potassium < 3.5 mEq/L. Pathology Etiology in gastrointestinal (GI) and urinary loss, decreased intake (uncommon), shift into cells (delirium tremens, hypothermia, increased insulin as in hyperglycemia therapy). HYPOKALEMIA • Thiazide and loop diuretics • Low dietary intake • Vomiting or other GI loss • Potassium-free IV fluids • Mineralocorticoid excess • Penicillin derivatives • Periodic paralysis— hypokalemic form |
Treatment Steps
1. Oral potassium replacement. 2. IV replacement under 20 mEq/hour. |
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Electrolyte Disorder differential
Symptoms Diarrhea, weakness. Diagnosis History and physical, serum electrolytes, ECG (wide QRS, peaked T). |
Hyperkalemia
Description Potassium > 5 mEq/L. Pathology Reduced renal excretion, excess intake, adrenocortical insufficiency Periodic paralysis: low, normal, or high potassium, muscle weakness. |
Treatment Steps
1. Stop potassium. 2. Exchange resin (sodium polystyrene sulfonate [Kayexalate]). 3. Insulin/50% glucose. 4. Dialysis in certain cases. HYPERKALEMIA WITH ECG CHANGES Acute treatment includes: 1. Calcium IV to stabilize the cardiac myocyte membrane. 2. Insulin and glucose to facilitate potassium exchange into the cells. 3. Sodium bicarb used in certain situations. 4. Kayexalate must also be given to facilitate removal of potassium from the body |
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Electrolyte Disorder differential
Symptoms Thirst, dehydration (sunken eyes, reduced skin turgor, etc.), coma. Diagnosis History and physical, increased serum sodium, BUN, and osmolality. |
Volume Depletion
Excessive water loss, reduced intake, or “third spacing.” |
Treatment Steps
1. Slow replacement of free water. 2. Replace sodium as needed. |
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Electrolyte Disorder differential
Symptoms Weakness, nausea, seizure, coma. Diagnosis History and physical, electrolytes (low sodium, BUN). |
Volume Excess
Description Free water excess. Pathology SIADH, renal failure, congestive heart failure (CHF). |
Treatment Steps
Restrict free water. Subcategory: water intoxication—psychiatric component, restrict fluids. |
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Electrolyte Disorder differential
Symptoms May have symptoms of hypokalemia, lethargy, tetany, volume depletion. Diagnosis History and physical, elevated anion gap, blood gas (elevated pH and serum bicarbonate). |
Metabolic Alkalosis
Description Elevated pH and elevated carbon dioxide. Reduced acid or gain of bicarbonate. Often caused or worsened by volume depletion, diuretics. |
Treatment Steps
Correct electrolyte abnormality and primary cause. |
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Electrolyte Disorder differential
Symptoms Syncope, tetany, anxiety, perioral paresthesias. |
Respiratory Alkalosis
Description Elevated pH with low carbon dioxide, caused by hyperventilation. RESPIRATORY ALKALOSIS Patient is breathing rapidly. Etiology could be as simple as anxiety or as serious as pulmonary embolism. Look for underlying cause and treat appropriately. |
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Electrolyte Disorder differential
Symptoms Thirst, lethargy, coma, dehydration, and primary disease symptoms |
Metabolic Acidosis
Description Reduced blood pH and bicarbonate. Separate into elevated or nonelevated anion gap. Anion gap = sodium – (bicarb + chloride). Pathology Elevated Anion Gap—Diabetic ketoacidosis, lactic acidosis, starvation, methanol/salicylate/ethylene glycol ingestion. Commonly used mnemonic is MUDPILES: Methanol Uremia DKA Paraldehyde (very rare cause) Iron or Isoniazid ingestion Lactic acidosis (which itself has many causes) Ethanol, ethylene glycol Salicylates Normal Anion Gap—Diarrhea, renal tubular acidosis. |
Diagnosis
History and physical, arterial blood gas. Evaluation of individual disorders Treatment Steps Correct primary etiology. Lactic acidosis: acidosis associated with shock and metabolic disorders, significant mortality. |
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Electrolyte Disorder differential
Symptoms Lethargy, disorientation, coma, headache, anxiety. |
Respiratory Acidosis
Description Reduced pH and elevated PCO2. Often occurs in respiratory failure, commonly in patients with underlying chronic obstructive pulmonary disease (COPD). Pathology Inadequate ventilation. |
Diagnosis
History and physical, arterial blood gas (hypercapnia). Treatment Steps This is a medical emergency, and ventilation needs to be improved in order to lower the PCO2 level. Treatment of the underlying condition is warranted; however, mechanical ventilation is often needed. In certain scenarios, “noninvasive” ventilation can be used (continuous positive airway pressure [CPAP] or bilevel positive airway pressure [BiPAP]) via face mask, but often intubation with mechanical ventilation is needed. |
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RENAL TUBULAR ACIDOSIS
• Distal differential |
Primary, inherited,
drugs, nephrocalcinosis, idiopathic hypercalciuria, hypervitaminosis D, hyperthyroidism, multiple myeloma, hyperparathyroidism. |
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RENAL TUBULAR ACIDOSIS
• Proximal: differential |
Primary,
Wilson’s disease, heavy metals, carbonic anhydrase inhibitors, scleroderma, tetracycline, amyloid, nephrotic syndrome, acute |
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Electrolyte Disorder differential
Symptoms Tetany, lethargy, delirium, CNS irritability, muscle cramps. ECG findings are nonspecific but can include ST depression, loss of voltage, PR prolongation, and widened QRS. |
Hypomagnesemia
Pathology Etiology includes alcoholism, malnutrition, diabetic ketoacidosis, diuretics. |
Treatment Steps
Replace magnesium (IV or IM). |
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Electrolyte Disorder differential
Symptoms Renal failure, nausea/vomiting, confusion, ECG (short QT, long PR). |
Hypercalcemia
Description Serum calcium > 10.2 mg/dL. Pathology Etiology includes sarcoidosis, cancer, milk-alkali, hyperthyroid/hyperparathyroidism. CALCIUM • Do not forget to correct the calcium level when the albumin is abnormal. • Corrected calcium = 0.8 times (normal albumin – measured albumin) + |
HYPERCALCEMIA
• The most common etiology in the outpatient setting is primary hyperparathyroidism (see Chapter 3) • The most common etiology in the inpatient setting is malignancy. • If asymptomatic, investigate etiology and follow calcium levels. • If symptomatic, inpatient treatment: • Initially, aggressive hydration with normal saline, followed by diuresis with loop diuretics (furosemide), not thiazides. • Bisphosphonates are very effective. Pamidronate (Aredia) is given as a one-time intravenous dose. |
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Electrolyte Disorder differential
Symptoms Tetany, Chvostek’s sign, Trousseau’s sign, perioral paresthesia, muscle cramps. |
Hypocalcemia
Description Low serum calcium (< 8.4 mg/dL). Pathology Etiology includes renal failure, vitamin D deficiency, hypoparathyroidism, malabsorption. CALCIUM • Do not forget to correct the calcium level when the albumin is abnormal. • Corrected calcium = 0.8 times (normal albumin – measured albumin) + |
Treatment Steps
1. Control etiology. 2. Administer calcium and vitamin D. HYPOCALCEMIA AND NEONATES Rule out DiGeorge anomaly, a rare but serious condition (see Chapter 7). |
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Symptoms
Pain, shock, flank ecchymosis. Injury to ?—Hematuria. Injury to ?—Blood at meatus, distended bladder, voiding difficulty. ? Ligation—Presents as pain, nausea/vomiting, fever postop. |
Kidney and Urinary System Trauma
Description Renal injury, minor (contusion, cut, hematoma), and major (deeper cut/rupture, pedicle injury). Ureteral injury: most often surgical mishap, external cause most often gunshot. Injury to Upper Urinary Tract—Hematuria. Injury to Posterior Urethra—Blood at meatus, distended bladder, voiding difficulty. Ureter Ligation—Presents as pain, nausea/vomiting, fever postop. retrograde cystography to evaluate bladder. Pathology Renal—Blunt, by auto accident most common. Pedicle Injury—Left renal vein most often injured, usually penetrating injury. Ureter—Often surgical injury, hysterectomy commonly. |
Diagnosis
History and physical, IVP, CT, angiography, KUB. Evaluate urethra with retrograde study. If blood at meatus: do not catheterize. Do retrograde cystography to evaluate bladder. Treatment Steps Kidney—Penetrating, surgical exploration; blunt, medical, or surgical. Bladder—Contusion, catheter; rupture, surgery. Ureter—Surgical (may need stent, anastomosis, bladder reimplantation, depending on injury). Urethra—Partial rupture, suprapubic cystotomy; complete rupture, drainage, and suprapubic cystotomy. |
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Symptoms
Lethargy, edema, oliguria, fever. Elevated blood pressure, diminishing renal function and proteinuria may indicate chronic graft rejection. |
Kidney Transplant Rejection
Description Allograft rejection. Acute type most common. Pathology Immunologic host reaction, where activated helper T cells and macrophages damage donor tissue. |
Diagnosis
History and physical, renal scan, renal biopsy. Treatment Steps Rejection types: Hyperacute (immediate, no treatment, nephrectomy), acute accelerated (after several days, no treatment, nephrectomy), acute (after 1–3 weeks, immunosuppression), chronic (no treatment). Rule out muscular or obstructive pathology. |
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Symptoms
Cirrhosis (jaundice, ascites, etc.), renal failure (azotemia, oliguria). |
Hepatorenal Syndrome
Description Cirrhosis and renal failure. HEPATORENAL SYNDROME • The kidneys retain the ability to function normally. • If a patient with hepatorenal syndrome restores hepatic function (or gets a liver transplant), the kidneys can again function normally. |
Diagnosis
History and physical, clinical picture (oliguria and severe liver disease), no urine sediment. Low wedge pressure may suggest prerenal azotemia, not hepatorenal syndrome Treatment Steps Treat etiology if possible, dialysis(?), fluids to rule out hypovolemia. |