Changes in Flow Flashcards
three phases of unilateral ureteral obstruction
initial phase - urine back-flow increase intra-luminal hydrostatic pressure - offset by simultaneous increase in glomerular capillary pressure at the afferent to maintain GFR - activates RAAS –>
Second phase - decrease glomerular blood flow d/t afferent arteriole vasoconstriction
third phase - decreased luminal hydrostatic pressure AND renal blood flow –> 50% drop in GFR (one kidney out)
two phases of bilateral ureteral obstruction
initial phase - urine back flow increases intraluminal hydrostatic pressure, increase in glomerular capillary pressure induced by afferent arteriolar vasodilation to maintain GFR - activates RAAS
second phase - decrease glomerular blood flow d/t afferent arteriole vasoconstriction, persistent efferent and partial afferent arteriole vasoconstriction maintains GFR
sodium reabsorption changesi n unilateral ureteral obstruction
inability to reabsorb Na throughout the nephron leads to salt wasting
volume changes in bilateral ureteral obstruction
volume expansion
ANP blocks effects of renin –> decreased angiotensin OO therefore net result in diuresis and natriuresis
how does the urinary concentration change in obstruction?
inability to absorb Na in the ascending limb and dilute the filtrate in the DCT leads to excretion of solute
defective urea recycling : transporter defect reduces concentrating effect and allows urea to be excreted
tubular dsyfuction changes potassium concentration in which direction
leads to hyperkalemia
low-flow luminal states lead to high urinary k+ concentrations in the collecting duct result in a loss of the graident between cell and lumen
RTA type that occurs in tubular dysfunction d/t low-flow luminal states
RTA type I
generalized tubular defect
change in RBF, GFR, medullary blood flow and vasodilator concentrations of prostaglandin and nitric oxide in acute bilateral ureteral obstruction
increased RBF
decreased GFR
decreased medullary blood flow
increased concentration of vasodilators prostaglandin and nitric oxide
acute bilateral ureteral obstruction effects on tubules
increased ureteral and tubule pressures
increased reabosroption of Na, urea and water
change in RBF, GFR, vasoconstrictor porstaglandins and RAAS system in chronic bilateral ureteral obstruction
decreased RBF
double decreased GFR
increased vasoconstrictor prostaglandins
icnreased RAAS stimulation
chronic bilateral ureteral obstruction effects on tubules
decreased medullary osmolarity
decreased concentrating ability
parenchymal atrophy
decreased transport functions for Na. K. H
clinical features of chronic bilateral ureteral obstruction
azotemia hypertension avp-insensitive polyuria natriuresis hyperkalemic hyperchloremic acidosis
after release of bilateral ureteral obstruction, what change can be expected in the GFR
slow rise in GFR
after release of bilateral ureteral obstruction, what change can be expected in the tubules
postobstructive diuresis
decreased tubule pressure
increase solute load per nephron
natriuretic factors present
patient presentation for urinary tract obstruction
azotemia
HYPERkalemia
metabolic acidosis
congenital causes for mechanical urinary tract obstruction
UJP narrowing or obstruction
uretovesical junction narrowing or obstruction and reflux
ureterocele
retrocaval ureter
congenital causes for mechanical bladder outlet obstruction
bladder neck bostruction
ureterocele
congenital causes for mechanical blockage of the urethra
posterior urethral valves anterior urethral valves stricture meatal stenosis phimosis
aqcuired intrinsic defects in ureters leading to mechanical obstruction
calculi inflammation infection trauma sloughed papillae tumor blood clots
acquired intrinsic defects in bladder outlet leading to mechanical obstruction
BPH cancer of prostate cancer of bladder calculi diabetic neuropathy spinal cord disease anticholinergic drugs and alpha adrenergic antagonists
acquired intrinsic defects in the urethra leading to mechanical obstruction
stricture tumor calculi trauma phimosis
acquired extrinsic defects in ureter leading to mechanical obstruction
pregnant uterus retroperitoneal fibrosis AA uterine leiomyomata carcionoma of the uterus, prostate, bladder, colon, rectum lymphoma PID, endometriosis accidental surgical ligation
acquired extrinsic defcts in bladder outletleading to mechanical obstruction
carcinoma of cervix, colon
trauma
while acute urinary obstruction is often assocaited with obvious clinical symptoms, chronic obstruction
may be insidious or clinically silent
most common inherited anomaly of the GU tract
vesicoureteral reflux
vesicoureteral reflux is clinically important becuase it presents with
frequent UTI or pyelonephritis
more common in males
clinical presentation of BPH
slow stream increase urgency dribbling after finishing incomplete emptying nocturia eventualy pressure in the bladder will icnrease such that urine is forced into the ureters, causing hydronephrosis
cycle of BPH obstruction
incomplete emptying –>
stretch of bladder wall and muscle –>
ineffective bladder contraction –>
incomplete emptying
ultrasound evalutation of post-void residual urine can be easily performed after instructing the patient to void when bladder feels full and using USG to estimate volume left in the bladder
what residual volume indicates incomplete emptying
100mL
neurogenic bladder causes include:
spinal cord trauma
spinal myelomeningocele
less commonly: spinal stenosis and herniated discs
why is it important to tmonitor patients iwth a neurogenic bladder
> 40cm H2O increase risk of hydronephrisis and subsequent decrease in GFR
want to monitor for hydronpehrosis to subvert before irreversible injury occurs
preferred radiography for diagnosis of renal lithiasis
CT
not all stones are radiographic however
tx is to remove the stone
pregnant patient presents with mild hydronephrosis in the first trimester on routine fetal USG but otherwise patient is asymptomatic: what do you do
monitor until it becomes symptomatic
if it does relieve the obstruction with a stent
pathophys of postobstructive diruesis following BUO
combination of fluid overload, urea accumulation, electrolyte imbalance
results from donwregulatino of Na transporters during obstruction
ANP released in reponse to cardiac preolaod during obstruction
tx for postobstructive diuresis
fluid replacement and careful monitoring of urine and serum osmolality as well as serum electrolytes
