Week 4: Obstruction of the Urinary Tract Flashcards
Normal urinary function
- bladder filling and voiding both occurs under low pressure
- parasympathetic increases bladder contraction and sympathetic decreases (open sphincter)
- this is disturbed when there is obstruction
Division of upper and lower urinary tract.
Bladder and below is Lower
Ureter to kidney is upper
Most common causes of obstruction organized by sites.
- Calyces
- infection TB, trauma, stones, tumors - ureteropelvic junction
- congenital, stones, trauma, extrinsic compression - Ureter
- stones, strictures, trauma, tumor, extrinsic compression - Bladder neck/proximal urethra
- prostatic enlargement!!!
- trauma, bladder neck contractures, prior surgery - Urethra
- most common: strictures
- trauma, prior instrumentation, posterior urethral valves (children-due to embryonic remnant that never dissolves)
Clinical presentation of upper urinary tract obstruction
ACUTE
-renal colic: waves of intense pain, from abdomen, flank, can be in groin
CHRONIC
-recurrent UTIs: stasis of urine–>growth of bacteria
-dull pain, ache, pressure
Clinical presentation of lower urinary tract obstruction
CHRONIC bladder outlet obstruction -bladder hypertrophy -detrusor dysfunction-SM in wall of bladder IRRITATIVE symptoms -urgency -frequency -dysuria -urge incontinence -nocturia OBSTRUCTIVE symptoms -decreased force of stream -dribbling -hesitancy -intermittency -incomplete emptying MAY see renal insufficient in acute or chronic obstruction
Renal changes from obstruction
PHYSIOLOGIC
-altered renal blood flow, changes in GFR, loss of concentrating ability within collecting duct
PHYSICAL/MICRO
-dilation of renal tubules, initial CD then extending proximally
-fibrosis
-apoptosis
-macrophage infiltrate
-hemorrhage, necrosis
-glomeruli is last thing to be affected, only affected with long standing obstruction
Changes that can be detected radiographically from obstruction.
- bladder trabeculation-obstruction below bladder causes hypertrophy that causes scalloped look
- diverticuli (outpouching)
- calculi -due to stasis
- J hooking of ureter: from enlarged prostate pushing upwards
- hydronephrosis
- thinned parenchyma
Describe changes that take place with hydronephrosis
- dilation of renal pelvis and calyces due to outflow tract obstruction
- gross: enlargement of kidneys with blunting of apices of pyramids. Thinning of medulla and cortex
- micro: early dilation of tubules, then tubular compression and atrophy, interstitial fibrosis, glomeruli relatively spared initially
Summarize effects of obstruction of urethra, grossly.
- bladder dilation and hypertrophy
- hydroureter -dilated ureter
- hydronephrosis -dilated renal pelvis and calyces
- bilateral since below bladder
Diagnostic tools for upper urinary tract obstruction.
- based on symptoms and imaging
- renal ultrasound
- CT scan/MRI
- IVP: contrast given and series of x rays at various stages of excretion of the contrast
- diuretic renogram: radioactive isotope given, monitors radioactivity to see how long it takes to leave the urinary tract
- renal resistive index: doppler and blood flow, used mainly in transplants
- whitaker test: old school, using nephrostomy and bladder catheter, infuse saline and measure pressure difference
Benign prostatic hyperplasia (BPH): definition and pathophysiology
- hyperplasia of stroma and epithelium. most common cause of urinary tract obstruction in men.
- beings in 5-6th decade
- little known of pathophysiology
Pathology of BPH
- diffusely nodular surface
- tends to affect medial lobe
- leads to compression of urethra
- associated with tubuloalveolar glands that are either dilated or with infolding of epithelium (serrated edges)
- normally, the glands have 2 layers of cells
Signs and symptoms of BPH
- symptoms: obstructive and irritative symptoms
- signs: bladder hypertrophy, trabeculation of smooth muscle
Describe prostatitis.
ACUTE -primary cause: infection -periglandular-intraglandular infiltrate -predominantly PMNs CHRONIC -largely interstitial infiltrate -mononuclear leukocytes -most cases independent of chronic infection
Complications of benign prostatic hyperplasia
- retention
- infection
- bladder decompensation (areflexic-can’t contract anymore)
- calculi
- hematuria
- hydronephrosis
- renal failure
What is post obstructive diuresis?
- can happen after unilateral or bilateral obstruction has been relieved
- physiologic: is common and self limiting, will go away on its own
- pathologic: rare, impared concentrating ability or Na reabsorption
What is the epidemiology of kidney stones?
- increasing in women, almost as same as men now
- relapse rate is 50-75% from 5-20 years
- relapse is associated with: young age of onset, family hx, infection stones, underlying predisposing conditions (hPTH)
Types of stones
- calcium oxalate: 80%
- calcium phosphate
- struvite
- uric acid
- cysteine
mechanism of stone formation
- supersaturation: spontanous nucleation and crystal growth (homogenous nucleation)
- heterogenous nucleation: small crystal of one type serves as nidus on which another compound precipitates (major mechanism)
Factors in Stone formation
INHIBITORS -citrate is most important URINARY pH -determines solubility -uric acid and cysteine poorly soluble in acidic media -calcium salts poorly soluble at alkaline pH CONTRIBUTING factors -predisposing factors -dehydration -hypercalcemic conditions -bladder obstruction -congenital disorders: e.g. PKD
Formation in calcium oxalate stones
- dihydrate–>monohydrate (soft to hard)
- Randall’s plaques: stones form on these plaques. true pathogenesis unknown
- accumulation of crystal deposits around loop of Henle
- initially deposits in papillary tissue
- hypercalcuria: most common abnormality found in calcium stone formers. Can be idiopathic or secondary: hPTH, sarcoidosis, immobilization, hyperthyroidism, malignancy, excessive intake
- hyperoxaluria: excess ascorbic acid intake
- hyperuricosuria: uric acid crystals serve as nidus for heterogenous nucleation of calcium crystals
Formation of struvite stones
- Mg ammonium phosphate
- caused by bacteria with urease enzyme
- may conform to shape of collecting system–>stag horn
Uric acid stones
- product of purine metabolism
- hyperuricosuria: gout, hereditary conditions. myeloproliferative syndromes, durgs
- acidic urine
- dissolved by urine alkalization
formation of cystine stones
- genetic defect: inability to reabsorb cysteine, ornithine, lysine, arginine in PT
- family hx
- stones are very hard, and difficult to treat
- crysinuria: crystine is poorly soluble in water. excreted 5-10x the normal rate in affected individuals
Presentation of nephrolithiasis
Symptoms: -pain -hematuria -UTI -sepsis Signs -CVAT/abdominal tenderness -UA: RBC, WBC, crystals
Treatment principles for nephrolithiasis
Acute colic
-pain management with analgesia
-hydration
-hospitalization if systemic infection
Most stones pass on their own 80-90%
TREATMENT OPTIONS
-observation for small stones
-alpha blockers/Ca blockers to relax SM and expulse stone faster
-immediate attention: infection, solitary kidney, intractable pain, renal failure
-ESWL: extracorporeal shock wave lithotripsy, for small stones
-ureteroscopy: scope, if WSWL fails
-can combine with percutaneous nepehrolithotomy to break up stones (laser?)
MEDICAL Rx
-tx hyperoxaluria hypercalcinuria by taking in Ca2+(free oxalate is absorbed when Ca bound by bile salts or FA)
Preventing recurrence of calcium stones
- dietary modification: more fluid intake,
- drink citrate: increases solubility of calcium salts
- less Na intake: leads to hypercalcuria
- don’t restrict Ca
- avoid carbs/sugar
- moderation of protein intake: can lead to hypocitraturia, hypercalciuria, hyperuricosuria
