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Etiology
Congenital anomalies: posterior urethral valves and urethral strictures,
meatal stenosis, bladder neck obstruction; ureteropelvic junction narrowing
or obstruction; severe vesicoureteral reflux
Urinary calculi
Benign prostatic hypertrophy
Tumors: carcinoma of the prostate, bladder tumors, contiguous malignant
disease (retroperitoneal lymphoma), carcinoma of the cervix or uterus
Inflammation: prostatitis, ureteritis, urethritis, retroperitoneal fibrosis
Sloughed papillae or blood clots
Pregnancy
Uterine prolapse and cystocele
Functional disorders: neurogenic (spinal cord damage or diabetic
nephropathy) and other functional abnormalities of the ureter or bladder
(often termed dysfunctional obstruction)
Clinical features
Acute obstruction
distention of the collecting system or renal capsule pain
Calculi lodged in the ureters renal colic
prostatic enlargements bladder symptoms
Unilateral complete or partial hydronephrosis may remain silent
for long periods
bilateral partial obstruction
inability to concentrate the urine polyuria & nocturia
distal tubular acidosis, renal salt wasting, secondary renal calculi, and
a typical picture of chronic tubulointerstitial nephritis
hypertension
Complete bilateral obstruction
oliguria or anuria
relief postobstructive diuresis
Diagnosis
Examination
A history of difficulty in voiding, pain, infection, or change
in urinary volume is common
Evidence for distention of the kidney or urinary bladder
can often be obtained by palpation and percussion of the
abdomen
rectal examination may reveal enlargement or nodularity
of the prostate, abnormal rectal sphincter tone, or a rectal
or pelvic mass
Penis meatal stenosis or phimosis
vaginal, uterine, and rectal lesions responsible for UTO are
usually revealed by inspection and palpation
Urinalysis may reveal hematuria, pyuria, and bacteriuria
urine sediment is often normal, even when obstruction leads
to marked azotemia and extensive structural damage
abdominal scout film may detect nephrocalcinosis or a
radiopaque stone
Ultrasonography is approximately 90% specific and
sensitive for detection of hydronephrosis
Treatment
relief of obstruction as soon as possible
Drainage (nephrostomy, ureterostomy, or ureteral, urethral,
or suprapubic catheterization)
When infection is not present, immediate surgery often is
not required
Benign prostatic hypertrophy alpha adrenergic blockers
and 5α-reductase inhibitors
Functional obstruction secondary to neurogenic bladder
frequent voiding and cholinergic drugs
Prognosis
Relief of obstruction return of renal function depends
largely on whether irreversible renal damage has occurred
Obstruction not relief obstruction is complete or
incomplete and bilateral or unilateral; whether or not
urinary tract infection is also present
Complete obstruction with infection total destruction of
kidney
Partial return of glomerular filtration rate may follow
relief of complete obstruction of 1 and 2 weeks' duration,
but after 8 weeks of obstruction, recovery is unlikely
LO 1
Menjelaskan batu saluran kemih
Nephrolithiasis
one of the most common urological problems
~13% of men and 7% of women will develop a kidney
stone during their lifetime, and the prevalence is increasing
throughout the industrialized world (United States)
Etiology & type of stones
Manifestations of stones
Asymptomatic until the stones reach the ureter
Stone passage
traverse the ureter without symptoms, but passage usually
produces pain and bleeding
Pain gradually, usually in the flank; increases over the next
20–60 min to become so severe spread downward and
anteriorly toward the ipsilateral loin, testis, or vulva
stone in the portion of the ureter within the bladder
frequency, urgency, and dysuria
Examinations USG, CT, IVP, abdominal x rays
Other syndromes
Staghorn calculi
Struvite, cystine, and uric acid stones grow too large fill the renal
pelvis and may extend to the calyces themselves eventual loss of kidney
function
Nephrocalcinosis
Calcium stones grow on the papillae break lose & cause colic / remain
stay in place (nephrocalcinosis)
e/ hereditary distal renal tubular acidosis (RTA)
Infection
can occur after instrumentation and surgery of the urinary tract
(treatment of stone disease)
due to bacteria that possess the enzyme urease can cause stones
composed of struvite
Activity of stone disease
New stones are forming / preformed stones are growing
Pathogenesis
Supersaturation
Excessive supersaturation is common in stone formation
ex: calcium oxalate crystals will grow in size when it is put in the water with
calcium & oxalate ions
Factors: dehydration, overxcretion (of calcium, oxalate, phosphate,
cystine, or uric acid), urine pH
Crystallization
Cell debris and other crystals present in the urinary tract can serve as
templates for crystal formation multiple crystals aggregated
kidney stone
ex: overgrowth of apatite plaque (Randall’s plaque) calcium oxalate
crystallization
Inhibitors of crystal formation
Inorganic pyrophosphate inhibits calcium phospate formation;
Citrate inhibits crystal growth and nucleation;
glycoproteins inhibit calcium oxalate crystallization
Evaluation
chemical analyses of serum and urine
24-h urine collections, with a corresponding blood sample
measurements of serum and urine
calcium,
uric acid,
electrolytes
creatinine,
urine pH,
volume,
oxalate,
citrate
Treatment
avoid dehydration and to drink copious amounts of water
Oral α1-adrenergic blockers relax ureteral muscle
general, severe obstruction, infection, intractable pain, and
serious bleeding removal
Extracorporeal lithotripsy shock wave
Percutaneous nephrolithotomy cystoscope-like instrument
into the renal pelvis through a small incision in the flank
ultrasound manuver or holmium laser
Ureteroscopy holmium laser
Calcium oxalate stone
Hypercalcemia & hypercalciuria (hyperparathyroidism, diffuse
bone disease, sarcoidosis, and other hypercalcemic states)
5%
Hypercalciuria without hypercalcemia 55%
Pathogenesis
hyperabsorption of calcium from the intestine (absorptive hypercalciuria)
an intrinsic impairment in renal tubular reabsorption of calcium (renal
hypercalciuria)
idiopathic fasting hypercalciuria with normal parathyroid function
Uric acid secretion > (hyperuricosuric calcium nephrolithiasis),
with or without hypercalciuria 20%
Hyperoxaluria 5%
Hypocitraturia, associated with acidosis and chronic diarrhea of
unknown cause
Treatment (hypercalciuria)
Low-sodium and low-protein diets
Thiazide diuretics lower urine calcium
Thiazide-induced hypokalemia should be treated, hypokalemia will reduce urine
citrate formation of stone
Treatment (hyperoxaluria)
diet low in oxalate and with a normal intake of calcium and magnesium to
reduce oxalate absorption
Enteric hyperoxaluria low-fat, low-oxalate diet and calcium
supplements, given with meals, to bind oxalate in the gut lumen
oxalate-binding resin cholestyramine at a dose of 8–16 g/d additional
high fluid intake, neutral phosphate, and pyridoxine (25–200 mg/d)
primary
Citrate suplementation
Magnesium ammonium phospate stones ~ struvite stones
formed largely after infections by bacteria (e.g., Proteus and
some staphylococci) convert urea -> ammonia
Alkaline urine precipitation magnesium ammonium phospate
salts largest stone (staghorn calculi)
Treatment
Percutaneous nephrolithotomy
extracorporeal lithotripsy
Irrigation of the renal pelvis and calyces with hemiacidrin
Antimicrobial treatment
acetohydroxamic acid (many side effects limit), an inhibitor of
urease
Uric acid stones
common in individuals with hyperuricemia (gout, diseases
involving rapid cell turnover, such as the leukemias)
hyperuricemia nor increased urinary excretion of uric acid half
of patients
Urine pH , 5,5 predisposing factors
Radiolucent stones
Treatment
Supplemental alkali, 1–3 mmol/kg (3-4 divided dose, one given at
bedtime)
A low-purine diet
Cystine stones
genetic defects in the renal reabsorption of amino acids
(cysteine, lysine, arginine, and ornithine) cystinuria
Form at low urine pH
Treatment
High fluid intake, even at night; Daily urine volume should exceed 3 L
Raising urine pH with alkali
A low-salt diet (100 mmol/d)
penicillamine and tiopronin (use only when fluid loading, salt reduction,
and alkali therapy are ineffective)
LO 2
Menjelaskan infeksi saluran kemih
Definiton
growth of >=105 organisms/ml from a properly collected
midstream "clean-catch" urine sample
fewer bacteria (102–104/mL) may signify infection
Suprapubic aspiration colony counts of 102–104/mL
infection
Classifications
lower tract infection (urethritis and cystitis) superficial / mucosal
infection
upper tract infection (acute pyelonephritis, prostatitis, and intrarenal
and perinephric abscesses) tissue invasion
Epidemiology
Acute community-acquired UTIs 7 million office visits
annually in the United States
female population, these infections occur in 1–3% of
schoolgirls
UTIs are unusual in male patients under the age of 50
common among women between 20 and 50
Asymptomatic bacteriuria is more common among elderly
men and women 40-50%
acute uncomplicated pyelonephritis among community-
dwelling women (18–49 yo) 28 cases per 10,000
women
Etiology
Most common gram-negative bacilli
E. coli (~80%),
Men (and women) who are infected with HIV and who have CD4+ T
cell counts of <200/microL UTI risk >>
lack of circumcision has been identified as a risk factor for UTI in both
male neonates and young men
Pregnancy
detected in 2–8% of pregnant women
20–30% of pregnant women with asymptomatic bacteriuria
subsequently develop pyelonephritis
Predisposing fx
decreased ureteral tone,
decreased ureteral peristalsis,
temporary incompetence of the vesicoureteral valves
low birth weight, premature delivery, and neonatal death
result from UTIs
Obstruction
tumor, stricture, stone, or prostatic hypertrophy
hydronephrosis UTI >>
lead to rapid destruction of renal tissue
Physical exam
tenderness of the urethra or the suprapubic area
Genital lesion / vaginal discharge + <105 bacteria/ml urine
urethritis, vaginitis, or cervicitis (e.g., C. trachomatis, N. gonorrhoeae,
Trichomonas, Candida, and HSV)
temperature of >38.3°C (>101°F), nausea, and vomiting
costovertebral angle tenderness
Physical exam
fever, tachycardia, and generalized muscle tenderness
tenderness on deep pressure in one or both costovertebral angles or on
deep abdominal palpation