Week 4: Obstruction of the Urinary Tract Flashcards

1
Q

Normal urinary function

A
  • 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
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2
Q

Division of upper and lower urinary tract.

A

Bladder and below is Lower

Ureter to kidney is upper

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3
Q

Most common causes of obstruction organized by sites.

A
  1. Calyces
    - infection TB, trauma, stones, tumors
  2. ureteropelvic junction
    - congenital, stones, trauma, extrinsic compression
  3. Ureter
    - stones, strictures, trauma, tumor, extrinsic compression
  4. Bladder neck/proximal urethra
    - prostatic enlargement!!!
    - trauma, bladder neck contractures, prior surgery
  5. Urethra
    - most common: strictures
    - trauma, prior instrumentation, posterior urethral valves (children-due to embryonic remnant that never dissolves)
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4
Q

Clinical presentation of upper urinary tract obstruction

A

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

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5
Q

Clinical presentation of lower urinary tract obstruction

A
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
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6
Q

Renal changes from obstruction

A

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

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7
Q

Changes that can be detected radiographically from obstruction.

A
  • 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
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8
Q

Describe changes that take place with hydronephrosis

A
  • 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
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9
Q

Summarize effects of obstruction of urethra, grossly.

A
  • bladder dilation and hypertrophy
  • hydroureter -dilated ureter
  • hydronephrosis -dilated renal pelvis and calyces
  • bilateral since below bladder
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10
Q

Diagnostic tools for upper urinary tract obstruction.

A
  • 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
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11
Q

Benign prostatic hyperplasia (BPH): definition and pathophysiology

A
  • hyperplasia of stroma and epithelium. most common cause of urinary tract obstruction in men.
  • beings in 5-6th decade
  • little known of pathophysiology
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12
Q

Pathology of BPH

A
  • 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
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13
Q

Signs and symptoms of BPH

A
  • symptoms: obstructive and irritative symptoms

- signs: bladder hypertrophy, trabeculation of smooth muscle

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14
Q

Describe prostatitis.

A
ACUTE
-primary cause: infection 
-periglandular-intraglandular infiltrate
-predominantly PMNs
CHRONIC
-largely interstitial infiltrate
-mononuclear leukocytes
-most cases independent of chronic infection
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15
Q

Complications of benign prostatic hyperplasia

A
  • retention
  • infection
  • bladder decompensation (areflexic-can’t contract anymore)
  • calculi
  • hematuria
  • hydronephrosis
  • renal failure
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16
Q

What is post obstructive diuresis?

A
  • 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
17
Q

What is the epidemiology of kidney stones?

A
  • 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)
18
Q

Types of stones

A
  • calcium oxalate: 80%
  • calcium phosphate
  • struvite
  • uric acid
  • cysteine
19
Q

mechanism of stone formation

A
  • 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)
20
Q

Factors in Stone formation

A
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
21
Q

Formation in calcium oxalate stones

A
  • 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
22
Q

Formation of struvite stones

A
  • Mg ammonium phosphate
  • caused by bacteria with urease enzyme
  • may conform to shape of collecting system–>stag horn
23
Q

Uric acid stones

A
  • product of purine metabolism
  • hyperuricosuria: gout, hereditary conditions. myeloproliferative syndromes, durgs
  • acidic urine
  • dissolved by urine alkalization
24
Q

formation of cystine stones

A
  • 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
25
Q

Presentation of nephrolithiasis

A
Symptoms:
-pain
-hematuria
-UTI
-sepsis
Signs
-CVAT/abdominal tenderness
-UA: RBC, WBC, crystals
26
Q

Treatment principles for nephrolithiasis

A

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)

27
Q

Preventing recurrence of calcium stones

A
  • 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