B5.078 Ureteral Obstruction Flashcards
normal pathway of urine from formation to excretion?
glomerulus > PCT > loop of henle > DCT > collecting duct > minor calyx > major calyx > renal pelvis > bladder > urethra
variation in presentation of urinary obstruction
can be permanent if not treated
congenital or acquired
acute or chronic
unilateral or bilateral
what is hydronephrosis
dilated renal pelvis, calix, or ureter
can be present without obstruction
need radiologic findings to confirm
typical symptoms of acute obstruction
flank pain secondary to stretch of renal collecting system
nausea/vomiting
anuria- severe and urgent issue
lab studies for diagnosis of obstruction
UA
BMP (can assess renal fxn)
fractional excretion of Na+
GFR calculated for you
what can fractional excretion of Na+ tell you about obstructive symptoms
prerenal <1%
intrarenal
post renal >4%
main 2 imaging modalities for urinary obstruction
US and CT
pros and cons of US
first line modality
widely available, cheap, no radiation, no contrast
can visualize hydronephrosis, but can not necessarily see obstruction (can’t prove w ultrasound alone)
can’t see ureters well
pros and cons of CT
great anatomic detail
fast, accurate, safe
high sens for most calculi
limited in seeing obstructive processes that aren’t stones (tumors and strictures): need to use 3 phase CT, urogram
excretory radiography
used in developing countries without CT available
single plate films sequentially (5 min intervals)
retrograde/anterograde pyelography
injection of contrast into renal system to determine site of obstruction
commonly done in surgery
Whitaker test
very invasive
percutaneous nephrostomy, tests pressures along urinary tract
rarely performed
change in GFR with unilateral urinary obstruction
acute: GFR preserved
mid/late: GFR declines
change in GFR with bilateral urinary obstruction
GFR immediately decreases and persists until fixed
path of damage in obstruction
pressure form obstruction moves distal to proximal
glomerulus is the last impacted structure, most preserved
effects of severe obstruction
urine produced will exit renal pelvis by lymphatic/venous drainage
impacts tubular function (poor concentrating ability)
as obstruction progresses, AQPs are down regulated so urine is not concentrated
2 types of post obstructive diuresis
- physiological: elimination of excess free water and solutes that have accumulated
- pathological: loss of renal concentrating ability due to down regulation of AQP and Na+ channels
impact of pathological post obstructive diuresis
sodium transport decreases salt wasting concentrating defects deficit in ability to acidify urine Mg2+ excretion markedly increased
gross appearance of kidney after 2 days of obstruction
dilation of collecting system
blunting of papilla tips
increased weight due to edema
thinning of kidney parenchyma due to increased dilations
large cystic appearance w weight loss due to loss of renal tissue
microscopic appearance of kidney after 2 days of obstruction
tubulointerstitial effects
dilation of tubules
fibrosis, inflammatory cells, apoptosis
glomerulosclerosis over time due to hyperfiltration injury/chronic inflammation
clinical impacts after 2 days of obstruction
HTN (upregulation of RAA)
relief of block and blocking angiotensin 2 receptors will help combat rise in BP
clinical impacts of chronic obstruction
compensatory growth in other kidney
increase due to cell hypertrophy, not hyperplasia (no more nephrons)
first step in treatment of renal stones
pain management, symptom control
how is pain managed in renal stones
opioids first line: rapid onset
NSAIDs for renal colic pain, but don’t use for people with compromised renal fxn
hydration
