Week 4: Obstruction of the Urinary Tract Flashcards Preview

Renal > Week 4: Obstruction of the Urinary Tract > Flashcards

Flashcards in Week 4: Obstruction of the Urinary Tract Deck (27):
1

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

2

Division of upper and lower urinary tract.

Bladder and below is Lower
Ureter to kidney is upper

3

Most common causes of obstruction organized by sites.

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)

4

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

5

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

6

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

7

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

8

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

9

Summarize effects of obstruction of urethra, grossly.

-bladder dilation and hypertrophy
-hydroureter -dilated ureter
-hydronephrosis -dilated renal pelvis and calyces
-bilateral since below bladder

10

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

11

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

12

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

13

Signs and symptoms of BPH

-symptoms: obstructive and irritative symptoms
-signs: bladder hypertrophy, trabeculation of smooth muscle

14

Describe prostatitis.

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

15

Complications of benign prostatic hyperplasia

-retention
-infection
-bladder decompensation (areflexic-can't contract anymore)
-calculi
-hematuria
-hydronephrosis
-renal failure

16

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

17

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)

18

Types of stones

-calcium oxalate: 80%
-calcium phosphate
-struvite
-uric acid
-cysteine

19

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)

20

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

21

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

22

Formation of struvite stones

-Mg ammonium phosphate
-caused by bacteria with urease enzyme
-may conform to shape of collecting system-->stag horn

23

Uric acid stones

-product of purine metabolism
-hyperuricosuria: gout, hereditary conditions. myeloproliferative syndromes, durgs
-acidic urine
-dissolved by urine alkalization

24

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

25

Presentation of nephrolithiasis

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

26

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)

27

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